FECAVA 2018 abstracts by Publicon OÜ

............................................................................ 2 ....................................................................... 3 Anesthesia & Critical care................................................................................... 7 Behavior ........................................................................................................... 13 Cardiology ........................................................................................................ 25 Clinical pathology ............................................................................................. 37 Dentistry .......................................................................................................... 42 Dermatology .................................................................................................... 76 Diagnostic imaging ........................................................................................... 89 Exotic animals .................................................................................................. 98 Gastroenterology ........................................................................................... 108 Infectious diseases ......................................................................................... 119 Internal medicine ........................................................................................... 132 Neurology ...................................................................................................... 137 Opthalmology ................................................................................................ 153 Orthopedics ................................................................................................... 165 Reproduction & Neonatology......................................................................... 184 Soft tisuse surgery .......................................................................................... 191 Nurses’ programme ....................................................................................... 216 Poster presentations ...................................................................................... 224

The abstracts have first been sorted alphabetically according to the session’s title, after which the abstracts were sorted alphabetically according to the authors’ surnames within the session.

Short Table of Contents...................................................................................... 2 Detailed Table of Contents ................................................................................. 3 Anesthesia & Critical care................................................................................... 7 Capnography saves lives...................................................................................................................... 7 I'm broken - fix me. Stabilisation and anaesthesia of the emergency trauma patient. ...................... 9 The cold cat and other dying patients (about perianaesthetic morbidity and mortality) ................ 11

Behavior ........................................................................................................... 13 Gut feelings â&#x20AC;&#x201C; the merging field of interaction between guts and emotions ................................... 13 Infectious or behavioral problem? .................................................................................................... 15 Neurological or behavioral problem? ............................................................................................... 16 Interest and validity of comparison between hypersensitivity - hyperactivity syndrome (HS-HA) in dogs and attention deficit hyperactivity disorder (ADHD) in humans; can intraspecific and interspecific relationships be triggers of emotional or mood disorders in cats?.............................. 17 Idiopathic cystitis: Does a behavioral management improve the results? ....................................... 21 Link between gastric chronic diseases and anxiety in dogs .............................................................. 22 Acral lick dermatitis or behavioral problem? .................................................................................... 23

Cardiology ........................................................................................................ 25 Approach to the cat with an incidental murmur ............................................................................... 25 Approach to the cat with suspected heart failure ............................................................................ 27 Approach to the dog with acute or refractory heart failure ............................................................. 29 Approach to the dog with an incidental murmur ............................................................................. 31

Clinical pathology ............................................................................................. 37 Artefacts and false results in lab results - how to recognize them ................................................... 37 In-house laboratory evaluation of body fluids .................................................................................. 40

Dentistry .......................................................................................................... 42 Imaging in oral and maxillofacial conditions ..................................................................................... 42 Interceptive orthodontics in veterinary dentistry ............................................................................. 46 Juvenile dentistry .............................................................................................................................. 48 Dental/oral problems commonly encountered in toy breeds .......................................................... 52

Extractions ......................................................................................................................................... 53 Periodontal disease and therapy....................................................................................................... 59 Oral pathology ................................................................................................................................... 67

Dermatology .................................................................................................... 76 How I diagnose CAD .......................................................................................................................... 76 Skin diseases I diagnose with a DNA test .......................................................................................... 78 New drugs to control CAD ................................................................................................................. 80 Skin diseases I diagnose with a biopsy .............................................................................................. 82 How I control severely pruritic cat .................................................................................................... 83 How I treat otitis media in a dog ....................................................................................................... 85 How I approach a pruritic cat ............................................................................................................ 87 How I treat allergic otitis externa in a dog? ...................................................................................... 88

Diagnostic imaging ........................................................................................... 89 Radiographic signs of cardiac disease ............................................................................................... 89 Systematic approach to thoracic radiology ....................................................................................... 91 A systematic approach to the interpretation of abdominal radiographs ......................................... 93

Exotic animals .................................................................................................. 98 Anesthesia, Pain Management and basic Surgery in Birds, Reptiles and Small Mammals - an approach from privat practice........................................................................................................... 98 How to get samples in Birds, Reptiles and Small Mammals ........................................................... 100 Cardiology and lung problems in Exotics - a first overview ............................................................ 102 Feather abnormalities in birds ........................................................................................................ 104 Skin abnormalities in small mammals ............................................................................................. 106

Gastroenterology ........................................................................................... 108 Updates on canine and feline acute pancreatitis ............................................................................ 108 Updates on canine and feline cobalamin deficiency ....................................................................... 111 Updates on canine acute hemorrhagic diarrhea syndrome............................................................ 114 Updates on canine and feline exocrine pancreatic insufficiency .................................................... 117

Infectious diseases ......................................................................................... 119 Best vaccination schedule – how to vaccinate a healthy and an immunosuppressed cat? ........... 119 In-house test – how useful are they really? .................................................................................... 121 Potential adverse effects of vaccination – feline injection-side sarcoma and chronic kidney disease ......................................................................................................................................................... 123 What’s new in antiviral treatment? ................................................................................................ 125 What’s new in immunomodulatory treatment? ............................................................................. 127 PCR, antibodies, antigen – what is the difference and when to use what? .................................... 129

What’s new in antibacterial treatment? ......................................................................................... 130 What’s new in treatment of protozoal diseases? ........................................................................... 131

Internal medicine ........................................................................................... 132 Interpreting the numbers – do all animals with azotaemia have kidney disease? ......................... 132 Interpreting the numbers – making sense of liver and pancreatic clinical pathology .................... 133 Approach to fever of unknown origin ............................................................................................. 134 Urinary tract infections ................................................................................................................... 135

Neurology ...................................................................................................... 137 Disc disease: an update ................................................................................................................... 137 Spine: conditions we see on x-rays, but are they to blame? .......................................................... 139 Spine and spinal cord: syringomyelia, neuropathic pain and its management .............................. 141 Treatment of epilepsy and status epilepticus: when, what and how? ........................................... 143 Epilepsy reminding conditions: looks like a seizure, but is it? ........................................................ 145 What’s new in classification, genetics and comorbidities in epilepsy patients? ............................ 147 Looks like a patient with back pain, but is it? Neurologist perspective .......................................... 149 Spine and spinal cord: diseases we do not see on x-rays................................................................ 151

Opthalmology ................................................................................................ 153 Is glaucoma treatment possible? .................................................................................................... 153 Is this eye disease inherited? .......................................................................................................... 155 Conjunctivitis. A cat Is not a small dog!........................................................................................... 157 The “Bulging eye”. How do I know? How do I treat? ...................................................................... 162

Orthopedics ................................................................................................... 165 Elbow dysplasia, early diagnosis, kinematics and treatment .......................................................... 165 Shoulder lameness, diagnosis and treatment ................................................................................. 169 Hip dysplasia, Early diagnosis and treatment ................................................................................. 175 Modern approach to patellar luxation ............................................................................................ 180

Reproduction & Neonatology......................................................................... 184 Neonatology .................................................................................................................................... 184 Do's and dont's in infertility, abortion, dystocia and c- section ...................................................... 187 Gynecological and andrological cases in small animal clinics, diagnostic work-up and treatment options............................................................................................................................................. 189

Soft tisuse surgery .......................................................................................... 191 Are you an oncologic surgeon? ....................................................................................................... 191 Complications: the great taboo ....................................................................................................... 196 From fresh wound to wound closure .............................................................................................. 199

How to be a better surgeon? .......................................................................................................... 203 How to close these wounds. Clinical cases from the daily practice ................................................ 206

Nurses’ programme ....................................................................................... 216 Anesthesia: Why are anaesthetists obsessed with oxygen? ........................................................... 216 Behavior: Intercat tension in multicat households ......................................................................... 218 Reproduction: Kitten neonates ....................................................................................................... 220 Reproduction: Dystocia. Is it time for C-section? ............................................................................ 222

Poster presentations ...................................................................................... 224 Faecal microbiota comparisons between obese and normal weight pet dogs .............................. 224 The occurrence of methicillin-resistant staphylococci and acinetobacteria in the environment of small animal clinics during the non-outbreak period in Estonia ..................................................... 226 A case of multilobular tumor involving the zygomatic bone in a dog ............................................. 228 Herpesviruses in pet tortoises and turtles in Europe ...................................................................... 229 Rabbit haemorrhagic disease viruses in pet rabbits in Europe ....................................................... 231 Estimation of optimal breeding time in the bitch by urinary hormone measurements ................. 233 The impact of the dialyzer type in hemodialysis in dogs ................................................................ 234 Child and Pets: Bidirectional Exchange of Microbiota .................................................................... 235

The abstracts have first been sorted alphabetically according to the session’s title, after which the abstracts were sorted alphabetically according to the authors’ surnames within the session.

The role of the respiratory system is to transfer oxygen (O2) and carbon dioxide (CO2) between the body and the atmosphere. CO2 is the end-product of cellular metabolism. It is transferred from the cells to the lungs by circulation, and from the lungs it is expelled to the atmosphere by ventilation. Lungs are the only route for CO2 elimination. Ventilation is the product of respiratory rate and tidal volume. Anaesthetised animals may be able to maintain a normal respiratory rate but their tidal volume often falls leading to insufficient ventilation (hypoventilation). Even animals with high respiratory rates may hypoventilate under anaesthesia, leading to accumulation of CO2 (hypercapnia). Hypercapnia can have severe negative consequences, such as respiratory acidosis, cardiac arrhythmias and hypoxaemia if supplemental oxygen is not provided. Ventilation is a measure of the animalâ&#x20AC;&#x2122;s ability to regulate the level of CO2 within the body. Therefore, the only way to assess the adequacy of ventilation is to measure either the arterial or alveolar partial pressure of CO2. Measuring the partial pressure of CO2 in the arterial blood is invasive and requires expensive blood gas equipment. Alveolar CO2 cannot easily be measured, but end-tidal CO2 (EtCO2) measured at the end of each expiration, approximates alveolar CO2 levels under normal conditions. EtCO2 can be measured non-invasively with capnography. In addition to the EtCO2, capnography measures the inspired carbon dioxide which should always be zero. Capnographs are very easy to use. They provide continuous information not only on the adequacy of ventilation but also on anaesthesia and equipment-related problems, such as decreased cardiac output, airway obstruction and faulty breathing system.

Capnographs are especially useful in assessing adequacy of cardiopulmonary resuscitation, because CO2 cannot get from the cells to the lungs without sufficient cardiac output and circulation. For the same reason, a sudden fall in EtCO2 may indicate failing cardiac output or even cardiac arrest.

References •

Flaherty D and Musk G (2005) Anaesthetic monitoring equipment for small animals. In Practice, 27; 512-521.

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Lumb AB. Nunn’s Applied Respiratory Physiology. 6th edition. Elsevier 2009.

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Marshall M (2004) Capnography in dogs. Compendium, 26; 761-778.

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McMillan M (2017) Pitfalls and common errors of anaesthetic monitoring devices part 3: Capnography. Veterinary Nursing Journal, 32; 265-269. https://doi.org/10.1080/17415349.2017.1351601

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Power I. And Kam P. Principles of Physiology for the Anaesthetist. 2nd edition. Hodder Arnold 2008.

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Simpson K (2014) Capnography for veterinary nurses. Part One: The Basics. Veterinary Nursing Journal, 29;358-361. https://doi.org/10.1111/vnj.12191

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Simpson K (2014) Capnography for veterinary nurses. Part Two: Capnograms and the respiratory cycle. Veterinary Nursing Journal, 29;395-397. https://doi.org/10.1111/vnj.12201

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Simpson K (2015) Capnography for veterinary nurses. Part Three: Interpretation. Veterinary Nursing Journal, 30; 22-25. https://doi.org/10.1080/17415349.2014.985491

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Spiegel J (2013) End-tidal carbon dioxide: the most vital of vital signs. Review article. Anesthesiology News.

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West JB. Respiratory Physiology - The Essentials. 9th edition. Lippincott Williams & Wilkins 2012.

Triage is derived from French word ”trier”, which means “sorting”. Trauma patients presented for emergency care may have a wide range of injuries ranging from minor to life threatening. These patients must be sorted (triaged) so that the patients with most serious injuries are treated first. When resources are limited, prioritization by triage is essential. Very brief history and brief, but thorough initial physical examination is the gold standard of triage: evaluate airway, breathing, and circulation to identify immediate life-threatening abnormalities of these systems. During the physical exam, observe for exsanguinating external haemorrhage or neurologic (brain or spinal cord) injury, because these might also need immediate management. Remember during your evaluation that most trauma patients benefit from minimizing stress levels and optimizing oxygen delivery. Pain control in the trauma patient should be a high priority; untreated pain can adversely affect the patient. Venous access is imperative in the seriously injured patient because it will allow administration of intravenous fluids and analgesic drugs. Hypovolaemia, blood loss and electrolyte deficits should be corrected first, while providing supplemental oxygen and monitoring the patient. Once the patient has been stabilized and analgesia has been provided, diagnostics procedures such as radiographs, ultrasound and comprehensive blood work can be performed if needed to gain more information about the patient’s condition. It is often necessary to either anaesthetise or sedate the trauma patient for these diagnostic procedures; in order to do this safely, thorough knowledge and understanding of the anaesthetic drugs is required. Remember that stabilization of the trauma patient before any anaesthetic drug administration is necessary due to the fact that anaesthesia in an unstable patient greatly increases the risk of complications. Sedation or anaesthesia of the trauma patient should not be taken lightly. Many trauma patients are in shock, meaning that oxygen delivery to the tissues is compromised. The sympathetic nervous system is stimulated in the emergency situation in an attempt to maintain blood flow and oxygen delivery; however almost all anaesthetic drugs blunt the

response of the sympathetic nervous system. Therefore, the patient that is in compensatory shock may decompensate when given a sedative or anaesthetic agent. In addition to interfering with the cardiovascular system, sedatives and anaesthetics can decrease lung ventilation thus increasing carbon dioxide retention, which in turn leads to respiratory acidosis and even hypoxaemia if supplemental oxygen is not provided. Any respiratory system compromise can be detrimental in a patient that is in respiratory distress.

References •

Drobatz KJ, Beal MW and Syring RS (editors): Manual of Trauma Management in the Dog and Cat. Wiley-Blackwell 2011.

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Lisciandro GR: Abdominal and thoracic focused assessment with sonography for trauma, triage, and monitoring in small animals. Journal of Veterinary Emergency and Critical Care 2011, 21; 104–122.

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Macintire DK, Drobatz KJ, Haskins SC, Saxon WD: Manual of Small Animal Emergency and Critical Care Medicine, 2nd edition, Blackwell Publishing 2012.

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Martin M: Small Animal ECGs – an introductory guide, 2nd edition, Blackwell Publishing 2007.

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Matthews KA: Veterinary Emergency + Critical Care Manual, 2nd edition, Lifelearn 2007.

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Silverstein DC, Hopper K (editors): Small Animal Critical Care Medicine, 2nd edition, Elsevier 2015.

Studies suggest that veterinary anaesthetic mortality is considerably higher than that of humans, and anaesthetic deaths are over two times more common in healthy cats than in healthy dogs. Death occurs most commonly when the animal is not under close supervision, and the risk of death is at its highest during the postoperative phase; nearly half of the dogs and over 60% of cats that die due to anaesthesia-related causes die in recovery. Due to their smaller size, cats are more likely than dogs to develop hypothermia under general anaesthesia. Hypothermia, although common, is detrimental to the patient and leads to numerous negative and even life-threatening consequences, including metabolic, respiratory, cardiovascular, neurologic and immunologic, and it should never be taken lightly. Other potential causes of higher perianaesthetic morbidity and mortality in cats compared to dogs include accidental anaesthetic overdose, excessive fluid administration and fluid overload, difficult intubation leading to airway obstruction or tracheal rupture, and unique anatomy affecting the blood supply of the feline brain. In order to decrease veterinary perianaesthetic mortality, we need to improve our current practice: close monitoring of patients both during anaesthesia and in recovery, supplemental oxygen administration, and active warming of anaesthetised patients throughout the procedure should be routine in all cases. References ď&#x201A;ˇ ď&#x201A;ˇ

Armstrong SR et al (2005) Perioperative hypothermia. Journal of Veterinary Emergency and Critical Care, 15; 32-37. Bainbrigde et al (2012) Perioperative and anaesthetic-related mortality in developed and developing countries: a systematic review and meta-analysis. Lancet, 30;10751081.

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Barton-Lamb A et al (2013) Evaluation of maxillary arterial blood flow in anesthetized cats. The Veterinary Journal, 196; 325-331. Brodbelt D et al (2008) The risk of death: the Conﬁdential Enquiry into Perioperative Small Animal Fatalities. Veterinary Anaesthesia and Analgesia, 35; 365-373. Brodbelt D (2012) Anaesthetic deaths in cats in practice. Veterinary Ireland Journal, 2(3); 151-156. Clarke K, Hall L (1990) A survey of anaesthesia in small animal practice: AVA/BSAVA report. Journal of Veterinary Anaesthesia,17; 4-10. Hoad J (2013) Immediate postoperative recovery: Part 1. Veterinary Nursing Journal, 28; 44-46. https://doi.org/10.1111/vnj.12009 Killner J (2014) The ups and downs of anaesthesia monitoring: Part 2. Veterinary Nursing Journal, 24; 21-23. https://doi.org/10.1080/17415349.2009.11013148 Pottie RG et al (2007) Effect of hypothermia on recovery from general anaesthesia in the dog. Australian Veterinary Journal, 85; 158-162. Stevens-Sparks C, Strain G (2010) Post-anesthesia deafness in dogs and cats following dental and ear cleaning procedures. Veterinary Anaesthesia and Analgesia, 37; 347351. Stiles J et al (2012) Post-anesthetic cortical blindness in cats: Twenty cases. The Veterinary Journal, 193; 367-373. Sullivan L et al (2011) Comparison of tissue oxygen saturation in ovariohysterectomized dogs recovering on room air versus nasal oxygen insufflation. Journal of Veterinary Emergency and Critical Care, 21; 633-638.

This session is supported by FECAVA

There has been an appreciation of the link between gastrointenstinal health and mental health in humans for some time and this is a very active and current field in terms of research, with new information being published on a regular basis. The veterinary field has been slower to embrace the reality that emotional and physical health are inextricably linked but recently there has been increasing interest in this interplay. One area in which research has raised interesting questions about the need for a more integrated approach to veterinary medicine is the gastrointestinal field. Enteric disease can lead to malabsorption of nutrients (e.g. cobalamin, tocopherol) that can affect both neurologic and enteric function. For example, cobalamin deficiency can cause glossitis, affect taste perception, impair enterocyte function, cause psychiatric disorders, retinal degeneration and frank encephalopathy. However we now know that there are other more sophisticated links between enteric and neurological function. There are more neurons in the alimentary canal than in the spinal cord and the enteric and central nervous systems are closely integrated; we are just beginning to understand some of those relationships and their mechanisms. While the connection of the brain to the gut via the vagus nerve has been

well known for years, more than 90% of the information passes from the gut to the brain, and not the other way around! The enteric nervous system contains many neurotransmitters that are also present in the brain, and in some cases, such as serotonin, 95% of the bodyâ&#x20AC;&#x2122;s content is present in the gut. Some antidepressant drugs can affect gut function positively, and procedures such as vagal stimulation can help in some human patients with depression. It is also clear that many species of microbiota present in the gut produce, and react to, neurotransmitters and hormones known to be vital to normal functioning of higher mammals. Recent evidence has shown that probiotics can improve depression in people and manifest ions of anxiety in dogs. Diets and their prebiotic components may also have more systemic effects than we ever suspected. The primary areas of interest when investigating the link between gastrointestinal and emotional health are those of deficiencies and dysbiosis. Both of these issues can be related to compromised gut function or to inappropriate dietary intake. Investigation of the potential for dietary supplementation to improve emotional health has resulted in some exciting findings. Areas of interest include the use of MCTs, essential fatty acids and antioxidants in the management of cognitive dysfunction in dogs and cats. Extensive research which began in relation to management of Alzheimerâ&#x20AC;&#x2122;s disease in humans has led to the availability of a range of diets and supplements which are used in clinical veterinary practice. Other areas in which dietary supplementation has been investigated are cobalamin and B.Longum and it is an exciting time in these areas of research. Irritable bowel syndrome in humans has been shown to be responsive to medication affecting gut motility and availability of serotonin. Whilst IBS has not been confirmed as a diagnosis in companion animals the presence of a range of idiopathic chronic enteropathies raises questions about the interplay between emotional state and gut function. Gathering information about gastrointenstinal health is well established during history taking in the field of behavioural medicine but asking questions about lifestyle, social and physical environment and emotional health is still not routine in gastrointestinal investigations. A number of myths and misconceptions have developed in the field of companion animal nutrition and a multidisciplinary approach by those working in the fields of gastroenterology and behavioural medicine can only be of benefit for our patients and their owners.

There are many conditions in companion animals which demonstrate the interplay between emotional and physical health. The physiological stress response may play a part in the development or worsening of clinical signs of disease and the onset of clinical illness can also affect emotional responses. In this lecture, Drs. Heath and Lappin will use case examples to emphasise some of the most common scenarios. In the field of feline medicine infectious disease is of particular concern to those involved in breeding and those working in shelter medicine but cats in domestic homes are also commonly affected by these conditions. Concerns over Feline infectious peritonitis has led to changes in breeding practices which have concentrated on the reduction of exposure to viral load but failed to address the role of emotional challenge. Indeed early separation of kittens presents concerns from a behavioural development perspective and may be a risk factor for increased vulnerability in terms of negative emotional bias. Negative emotional arousal is commonly associated with suboptimal feline environments and routine investigation of social and physical circumstances is therefore an important part of infectious disease investigation. Recurrent clinical signs of upper respiratory infections are most commonly associated with feline herpesvirus 1. Drs. Heath and Lappin will discuss the role of emotional distress in this syndrome, review the current FHV-1 management practices including the current doses of famciclovir (40 to 90 mg/kg, PO, up to 3 times daily) and review use of pheromones to attempt to promote positive emotional motivation in cats. Dr. Lappin will present the results from a recent study showing the use of a facial pheromone delivered by diffusor to lessen signs of FHV-1 in a stress model. It is also important to consider the interplay between physical and emotional health in canine patients and canine infectious respiratory disease complex offers a good example of the potential for overcrowded or stress inducing environments to be a risk factor for infectious disease. There are a range of pathogens which have been implicated this condition and many owners are misled by the â&#x20AC;&#x153;kennel coughâ&#x20AC;? label into believing that this is a condition which can only occur in dogs that have spent time in boarding kennels. This lecture will explore the physical and emotional influences on this relatively common clinical presentation and discuss the importance of prevention and management strategies as well as treatment protocols.

There are many medical conditions that stress may play a part in the development or worsening of clinical signs of disease. It then appears that the condition in â&#x20AC;&#x153;medicalâ&#x20AC;? when behavioral components may be the primary cause of the illness. In this lecture, Dr. Lappin will use case examples to emphasize several of the most common scenarios that stress can induce clinical signs of disease in dogs confused with infections. Feline interstitial cystitis (FIC) is one of the more common clinical syndromes that develops in cats and most specialist believe the syndrome is related to stress. While the clinical signs associated with FIC are similar to primary infections or stones, one of the major treatments is to manage stress. Diarrhea is also very common in dogs and cats and have multiple causes that have primary treatments. However, it is now recognized that stress can play a role in chronic recurrent diarrhea in dogs or cats, particularly related to overgrowth of the normal flora bacterium Clostridium perfringens. Dr. Lappin will discuss the diagnostic workups associated with these 2 common syndromes, emphasizing clinical historical findings that suggest a behavioral component. Recently, it has been shown that stress affects the intestinal microbiome and Dr. Lappin will show how use of probiotics and high fiber diets may be able to lessen clinical signs of stress diarrhea. Practical tips for environmental modification to lessen stress will be emphasized by both speakers. Recurrent clinical signs of upper respiratory infections are most commonly associated with feline herpesvirus 1 in cats. Dr. Lappin will discuss the role of stress in this syndrome, review the current FHV-1 management practices including the current doses of famciclovir (40 to 90 mg/kg, PO, up to 3 times daily) and review use of pheromones to attempt to lessen stress in cats. Dr. Lappin will present the results from a recent study showing the use of a facial pheromone delivered by diffusor to lessen signs of FHV-1 in a stress model.

Interest and validity of comparison between Hypersensitivity-Hyperactivity syndrome (HSHA) in dogs and Attention-Deficit Hyperactivity Disorder (ADHD) in humans Strictly speaking, cats cannot be described as either a territorial or a social species. However, cats develop a wide range of relationships with other cats or with humans. The sociabilization period determines how the individual develops communication skills and the ability to form harmonious relationships with other cats and members of other species. French zoopsychiatry has defined a syndrome linked to impaired relationships that is called schezipathy, based on Greek etymology: schezi (relationship) and pathy (suffering). Since relationships may be an important dimension of catsâ&#x20AC;&#x2122; lives, they may be a source of suffering when they go wrong, for various reasons and independent of the quality of the living environment. Suffering is manifested by emotional or mood disturbances.

Vulnerability factors Early developmental conditions, the level of autocontrol, and health status have a strong influence. The quality of the environment must always be considered, and when it plays a real role in the disease, this is referred to as bioto-schezipathy.

The origin of a schezipathy may be ontogenic, post-traumatic, or due to changes to which the cat does not adapt. Relationships are at the centre of the disorder.

Normal versus pathological Relationships are not compulsory for cats, and cats may avoid relationships without being pathological. E.G, a cat may exhibit threatening behaviours to keep a new cat at a distance. While the two cats are not friends, they do not show signs of suffering. A bit later, there may be no more aggressive behaviours, though the cats are still not friends. Another possibility is that one cat becomes more and more aggressive, the fights cause wounds, and the second cat becomes more and more inhibited. At this stage, both cats suffer from a pathological condition. Both protagonists must be considered in an intraspecific schezipathy.

Emotional and mood disorders Different states have been described: -

Phobic state: the symptoms occur only in the presence of the other individual. Symptoms of fear such as shaking, mydriasis, piloerection, urinating, and defecation occur, in combination with escape, inhibition or aggressive behaviours.

Anxiety states: the symptoms can include: anticipation, hypervigilance and obnubilation, agitation, aggressive behaviour, redirected aggression, changes in facial marking behaviour, urinary marking, house soiling, and hyperaesthesia. o Intermittent anxiety produces a variety of these symptoms. o In permanent anxiety, inhibition is predominant, and substitutive activity such as bulimia or alopecia occurs.

Depression: chronic depression is more frequent, but acute depression can occur after a trauma. Symptoms are: dysorexia, sleep perturbations, inhibition, withdrawal, house soiling, grooming deficits, and changes in facial marking behaviour. Some acute emotional reactions may occasionally appear.

Consequences The inability to adapt exacerbates the symptoms and misunderstanding of the catâ&#x20AC;&#x2122;s behaviour. Frequent punishments worsen the catâ&#x20AC;&#x2122;s disorder. The diagnosis of a mood or emotional disorder should lead to a pharmacological prescription. There are currently a wide variety of options that can be used to help the cat. The selected treatment must be based on analysis of the symptoms and associated neuromodulators. Environmental and behavioural modifications are prescribed.

Beata C. et al. Pathologie comportementale du chat. 2016. AFVAC Editions Paris. Turner D., Bateson P. ed. The domestic cat: the biology of its behaviour. 2000. Cambridge University Press.

Can Intraspecific and interspecific relationships be triggers of emotional or mood disorders in cats? Psychiatry has always used animal models for experimentation, all of which are approximations. They can present construct validity (if they have the same aetiology), face validity, or predictive validity. Experimental models of ADHD, including spontaneously hyperactive rats, dopamine-depleted rats, dopamine transporter knock out mice, or measuring delayed reward in rats or monkeys, have been used, although there is a risk of something being â&#x20AC;&#x153;lost in translationâ&#x20AC;? (4). New imaging techniques have made in vitro animal models obsolete, and allow exploration of many aspects, as ADHD is considered to be a heterogeneous disorder. Spontaneous in vivo animal models are used less frequently. Pageat (3) has described HSHA syndrome in dogs, which has been further compared to ADHD (2). In addition, ADHD-like behaviours are more and more commonly described in dogs (1). The comparison is relevant in several ways, and may be useful for human and veterinary psychiatry. Face validity is the first line of evidence. ADHD and HSHA are both developmental disorders. The core symptoms include varying intensities of attention deficit, hyperactivity, and impulsivity, which must be present from an early age. In both conditions, these symptoms cannot be better explained by other conditions such as organic disease, endocrine disorder, or neurological or mental disease, or by the living conditions. The symptoms have a real impact on the patientâ&#x20AC;&#x2122;s quality of life and impair his or her functioning; they are not simply a variation in the level of activity in a normal individual. Aetiology: both are considered to be syndromes, so construct validity at this stage is difficult to assess. -

In dogs, early-age environmental conditions are important, and can lead to impaired activation of the neurological regulatory system. Genetics research has highlighted convergences in genes polymorphisms.

Treatment: the dopaminergic and serotoninergic systems are the target of prescribed drugs. The treatments are multimodal (both behavioural and environmental) and present some similarities.

Similar difficulties -

Patients’ behaviour leads them to be rejected. They are scolded, punished, and (in the case of dogs) given up. They can accidentally hurt others or themselves due to their impulsivity and lack of autocontrol. Many of them become anxious. The patient’s family feels exhausted, in check, rejected, and judged by a society that thinks the problem is educational. Very early diagnosis is quite difficult, and may lead to delays in initiating management of the disorder. Originally, ADHD was not recognised in adulthood, while it has always been diagnosed in adult dogs. Symptoms are usually different in adults, and comorbidity often appears. The diagnosis is still subject to discussion in both species.

The comparison between HSHA in dogs and ADHD in humans may highlight new perspectives for research and management in both species.

Lit, L., Schweitzer, J., Iosif, AM., Oberbauer, A. (2010). Owner reports of attention, activity, and impulsivity in dogs: a replication study. Behav Brain Funct., 6:1.

Marlois, N. (2001). Hyperactivity in dogs, a model for human pathology: Discrepancies between different approaches. Proceeding of the third International Congress on veterinary behavioural medecine. Vancouver. 212-214.

Pageat, P. (1998) Pathologie du comportement du chien, 2ème édition. MaisonsAlfort : Point Vet.

Wickens, J.R, Hyland, B., Tripp, G. (2011) Review Animal models to guide clinical drug development in ADHD: lost in translation? BJP, 164 1107–1128.

Lower urinary tract infection (LUTI) in cats is a clinical syndrome that is frequently encountered by practitioners and is characterized by clinical signs including dysuria, frequent urination, strangury, periuria and hematuria. When the diagnostic evaluation of cats presenting with such clinical manifestations does not lead to the identification of a specific cause, it is referred to as idiopathic cystitis. This entity, which is similar to the interstitial cystitis that is encountered in women, represents the primary cause of LUTIs in cats under 10 years of age. While the cause of idiopathic cystitis is not currently known, it appears that this disease is not limited simply to the urinary system, but can also be considered to be a complex functional disorder involving systemic neuro-hormonal dysfunctions, and in which the emotional stability of the cat plays a key role. A multimodal approach is therefore fully justified in managing this disease. Implementing environmental and social changes with the aim of decreasing signs of anxiety in the cat enables a significant reduction in the clinical signs of cystitis, and in particular the risk of relapse. Together with environmental changes, when signs of anxiety are identified in a cat, the use of anxiolytic treatments is indicated. These treatments include pheromones, nutraceuticals, essential oils, anxiolytics and antidepressants. Many treatments are currently available, although none are marketed for use in cats. For many animals with severe anxiety, a prescription lasting several months is required. This prescription is accompanied by therapeutic measures, without which a relapse is probable. Including questions about the animalâ&#x20AC;&#x2122;s behavior from the beginning of the consultation enables better observance of treatment (psychotropic and therapeutic). For example, if during the examination it is apparent that the cat does not respond well to the presence of unfamiliar individuals, but is fine the rest of the time, providing occasional treatment when guests are present and organizing a few easily accessible areas where the cat can be alone will be sufficient. In contrast, if the questions reveal daily instability, the prescription should be accompanied by personalized and more comprehensive therapeutic measures. Therefore, in order to be relevant and tailored, the therapy must be supported by a precise diagnosis. General measures constitute a first step, but cannot be considered a substitute for a complete medical approach including a behavioral component.

Many dogs suffer from episodes of vomiting without any apparent organic or alimentary cause. Owners often describe them as stressed animals. The aim of this study was to verify the existence of a link between vomiting and anxiety. The Evaluation of Emotional Disorders in Dogs (EDED) scale was used to score anxiety in dogs (1,2,3). We compared two populations ¬¬– anxious dogs and normal dogs ¬– which were distinguished based on their EDED scores. The first population consisted of 20 animals suffering from chronic gastric disease without organic lesions. All selected animals are under medical treatment and/or on a hyperdigestible diet. The second population consisted of 20 animals without any chronic gastric disease that were matched by gender, age and breed to each individual in the first group. We used a specific statistical analysis for paired series (Wilcoxon test). The average EDED scores of the two populations were significantly different (p<0.01), which allowed us to conclude that anxiety is a possible etiology of chronic gastric disease. Differential diagnosis of chronic gastric disease should include anxiety, and should not be only a diagnosis of exclusion. Scoring chronic and relapsing dogs on an EDED scale can save time. Treating anxiety improves outcomes in these dogs. References 1. Patent CA 2122780.2004. 2. Reiwald, D., Pillonel, C., Villars, AM., Cadore, J.L.2013. Rev. Med.Vet 164(3), 145-149. 3. Pageat, P., Lafont, C., Falewee, C., Bonnafous, L., Gaultier, E., Silliart, B. 2007. Appl Anim Behav Sci 105(4), 342-350.

Acral lick dermatitis is a descriptive diagnosis of a disease complex characterised by prominent licking of a small area typically on the dorsal aspect of a carpus. Clinically it is characterised by alopecia, erosive to ulcerative changes with a yellowish raised border of the central erosion or ulcer. This syndrome can be due to a large number of reasons. Orthopedic problems, allergies, bacterial infections and behavioural problems are all potential causes of acral lick dermatitis. Thus, a thorough history should specifically enquire about potential past trauma, life style, seasonality, changes in diet, and other clinical signs such as pruritus elsewhere on the body. As acral lick dermatitis can also have a behavioural component, while ruling out other medical causes, particular focus should be also be on the behavioural history. The temperament of the dog, when the licking started (any obvious stimuli), any increase or decrease in frequency, duration and intensity and any other behavioural signs should also be considered. Physical examination looking particularly for cutaneous signs elsewhere on the body as well as depth of lesion and pain of the carpus will determine further proceedings. Many dogs with acral lick dermatitis have a secondary deep bacterial infection thus impression smears of the lesion to evaluate the patient for bacterial pyoderma are always indicated. Allergic skin diseases as causes of acral lick dermatitis are often associated with mild erythema and salivary staining of the paws, ventrum and perianal area and pruritus of those body locations. An elimination diet may be helpful in some patients with acral lick dermatitis. Previous trauma leading to joint pains or neurologic pains may also be identified on radiographs, another frequent diagnostic measure for dogs with acral lick dermatitis. Treatment of acral lick dermatitis is aimed at the underlying cause. Bacterial infections often require longer courses of systemic antibiotics chosen after culture and sensitivity due to the

deep nature of the lesion. With adverse food reactions, avoidance of the offending allergens is the treatment of choice. Environmental allergies can be treated with allergen immunotherapy or symptomatic drugs. Orthopedic problems will often necessitate analgesic and anti-inflammatory therapy, usually NSAIAs. If the cause is determined to have a behavioural component (which may persist after other medical reasons have been eliminated), then the 3 M plus 1 approach should be utilized. Environmental management, behaviour modification and often psychotropic medication should be implemented and then the patient carefully monitored or a regular basis.

Heart murmurs are common in cats. In some cats a murmur is a sign of life-threatening heart disease, whereas in other cats it may be a completely innocent finding. Ideally, we need to be able to identify which cats with murmurs are most at risk of cardiac death. Diagnostic tests Murmur characterisation based on auscultation is much more challenging in cats than in dogs. Murmurs that vary with stress are heard with hypertrophic cardiomyopathy (HCM) and functional murmurs. These murmurs may vary from moment to moment, so a change in intensity has no prognostic significance. Very loud murmurs (≥6/6) are most likely to be associated with congenital heart disease. Anemia, hyperthyroidism and systemic hypertension are easily ruled out as causes of a murmur. It may be more practical to direct efforts at distinguishing cats at high risk of developing congestive heart failure (CHF) or arterial thromboembolism (ATE) from low risk cats, or normal cats with a functional murmur. It is more important to stage the heart disease than to identify the specific cardiomyopathy. Identifying the ‘High Risk’ cat Echocardiographic examination by a cardiologist is the gold standard, but this is not an option chosen by every owner. Presence of a heart murmur is not a reliable indication of heart disease. The louder the murmur, the more likely the cat is to have heart disease, but not all cats with HCM should be consider ‘High Risk’. Auscultation findings that more reliably indicate ‘High Risk’ cats are gallop sounds and audible arrhythmias.

Thoracic radiography: The advantages of thoracic radiography are its wide availability, and ability to demonstrate cardiomegaly in ‘High Risk’ cats. The disadvantages are the challenges of positioning cats with heart disease in order to obtain diagnostic films, the challenges of finding a sedative combination that will enable such films to be taken, and the relatively poor sensitivity at detecting mild-moderate LA dilation. ECG: For cats with a regular heart rhythm, there is little value from an ECG for identifying high risk cats. Plasma biomarkers: Troponin-I and NT-proBNP concentrations may increase in cats with CHF. NT-proBNP is often higher in cats with preclinical cardiomyopathy than in normal cats but biomarkers do not offer the same reliability in staging heart disease as echocardiography carried out by an experienced cardiologist, but they may be more reliable than some longer established diagnostic techniques. Biomarkers may help with pre-screening which cats with a murmur should be referred and which cats can be considered ‘Low-risk’ and therefore do not need further diagnostic tests. In-house Echocardiography: Ultrasound is the ideal technique to identify LA enlargement, usually from a short axis right parasternal view that includes the LA and the aortic valve. The LA diameter should be no more than 1.6 x the aortic diameter. Most ‘High risk’ cats have an unequivocally dilated LA. Identifying mild LV hypertrophy or identifying the source of a murmur in a cat is much more challenging, and requires considerable training and experience. Specialist Echocardiography: Referring to a cardiologist is not always an option, although echo performed by a Specialist is the most reliable way to identify high-risk cats. If the echocardiography results show the cat is at high risk of CHF or ATE, then antiplatelet therapy should be started. The owner should also start monitoring resting respiratory rate at home in order to identify the early signs of CHF. Treatment ‘Low risk’ cats: As HCM is believed to be very common and prognosis is good in many cats, for many cats no treatment is necessary. ‘High risk’ cats: The prognosis is worse in cats with LA enlargement, as they are predisposed to both CHF and ATE. There are no studies reporting any benefit with any treatment in preventing CHF in cats with HCM. Cats at risk of ATE could benefit from antithrombotic treatment, and currently the first choice treatment is clopidogrel (18.75mg per cat, q24h PO). Other cats that may require treatment include cats with congenital heart disease (the ductus should be closed in cats with a patent ductus arteriosus) and cats with dynamic left ventricular outflow tract obstruction.

Dyspneic cats are fragile, and will easily arrest if not handled with great care. REDUCING STRESS IS VITALLY IMPORTANT so sedation (eg. with butorphanol) is often helpful. Fortunately, observation is of great value when determining the underlying cause of dyspnea, and this can be done while the cat is in an oxygen-enriched environment. Restrictive respiratory diseases (pleural effusion, parenchymal disorders such as pulmonary oedema) cause rapid respiratory motions. Obstructive disorders (asthma) result in slow, deep breathing. Increased expiratory effort, prolonged expiratory time and abdominal effort on expiration suggests chronic lower airway disease. Upper airway obstruction results in prolonged and laboured inspiration with noise. Physical exam should be completed once the cat is stable. Cats with heart disease are generally in good body condition unless heart failure is advanced. Cats with hyperthyroidism may have marked weight loss, and some cats with severe congenital heart disease may be stunted. Pale mucous membranes can indicate anemia, but can also be associated with severe peripheral vasoconstriction in low output states or conditions of elevated sympathetic tone. Cyanosis is most often seen with severe hypoxemia resulting from respiratory disease (including pulmonary edema or pleural effusion with congestive heart failure) but can also be seen with a right-to-left congenital shunt. Distended jugular veins indicate elevation of right atrial pressures. Femoral pulses may be absent with systemic thromboembolism, although blood flow may return within a few hours to a few days following acute embolization. The presence or absence of a murmur is not a reliable way to identify congestive heart failure, whereas a gallop sound or arrhythmia is likely to indicate significant cardiac disease. Presence of a gallop sound in a cat with respiratory distress justifies commencement of heart failure treatment. Severe tachycardia (>220/min) is most likely to be associated with cardiac disease, but most cats with CHF are not tachycardic. Cats with severe signs of low cardiac output may actually be bradycardic. Cats with persistent 3rd degree atrioventricular block may be only moderately bradycardic, and an ECG should always be recorded in cats with a heart rate <130/min. Auscultation of lung sounds can be helpful: presence of crackles can indicate pulmonary edema, but are sometimes heard with airway disease. Wheezes are more likely to be heard with chronic bronchial disease. Absent lung sounds can indicate pneumothorax or pleural effusion.

Diagnostic tests Radiography: Although often considered the gold standard for confirmation of cause of dyspnea, radiography can be risky. Cats with severe respiratory distress should not be subjected to radiography, and physical exam and/or ultrasound is likely to be safer. Cardiogenic pulmonary edema is extremely variable in distribution in cats and there is no characteristic radiographic pattern. Echocardiography: Ultrasound is extremely helpful for identification of pleural effusions in unstable cats, although physical exam should be sufficient for raising suspicion. Pulmonary edema results in â&#x20AC;&#x2DC;B-linesâ&#x20AC;&#x2122; which can be detected with thoracic ultrasound. Echocardiography is also invaluable for identifying left atrial enlargement, which almost always accompanies left heart failure in cats.

Management Oxygen should be administered in a stress-free way, and butorphanol (0.25mg/kg IM) should be given as an anxiolytic. Furosemide should be given IV to effect, starting at 2 mg/kg with subsequent doses of 1-2mg/kg every 45-60 mins until respiratory rate decreases. Significant pleural effusions should be drained while causing minimal stress (generally with a butterfly cannula). Use ultrasound if available for locating effusions. If blood pressure is normal, furosemide forms the basis of acute treatment. For hypotensive cats without a murmur, pimobendan (1.25mg PER CAT PO) can be given. IV fluids should be avoided, as this will worsen CHF. Beta-blockers (such as atenolol) should also be avoided.

The approach to treating dogs with heart failure depends on the stage of the disease. A different approach is needed for acute and long term management, and another approach is needed for when those approaches fail. Short term goals - optimize hemodynamic function • •

Treat life-threatening congestive signs Increase cardiac output

Long term goals - eliminate abnormal fluid accumulation, control abnormal neurohormonal responses that are harmful to the heart • • • •

Reduce sodium and water retention Support hemodynamic function Counteract vasoconstriction Try to preserve adequate renal function

Treatment of acute heart failure (ACVIM Stage C) The main short term goals are to improve oxygenation and tissue perfusion without compromising renal function. This usually involves administering oxygen in a non-stressful way. Furosemide is administered intravenously at 2 – 4 mg/kg and smaller doses are repeated as necessary until respiratory rate has decreased. Severe pleural effusions should be drained. Furosemide will reduce preload, which will help reduce atrial and venous pressures. Although a reduction in preload can reduce cardiac output (and therefore blood pressure) in normal patients, furosemide rarely does this in dogs with congestive heart failure (CHF). In hypotensive patients, the aim should be to increase blood pressure by increasing cardiac output, NOT by increasing peripheral vascular resistance. This can sometimes be achieved by optimizing heart rhythm and sometimes rate but positive inotropes such as dobutamine or pimobendan are often needed. ACE inhibitors are not used for short term management of critical congestive failure patients.

Treatment of chronic heart failure (ACVIM Stage C) For chronic heart failure, the aim is to prevent abnormal fluid retention, and minimize effects of harmful neurohormones. A number of randomized clinical trials have been reported of therapy for dogs with chronic heart failure, and this provides a rational basis for selecting treatment.

Maintain control of abnormal fluid accumulation Furosemide is the main treatment for eliminating retained fluid. The usual maintenance dose is 12mg/kg q12h, but higher doses are often needed after long-term use. The dose of furosemide should be carefully titrated to effect. Azotemia and hypochloremia are common. The dose should be reduced once congestive signs are well-controlled or if an animal is excessively polyuric/ polydipsic. Pimobendan has beneficial effects on survival in chronic mitral valve disease and dilated cardiomyopathy in dogs, and is standard treatment for chronic heart failure in dogs. ACE inhibitors & Spironolactone are also widely used in treatment of CHF.

Treatment of refractory heart failure (ACVIM Stage D) Most canine cardiac disease is progressive, and tolerance to furosemide develops with chronic use. It can be difficult to determine which is responsible for recurrent CHF, but dogs that are refractory to furosemide do not show polyuria/polydipsia, azotemia, or hypochloremia. The dose of oral furosemide can be increased, or subcutaneous furosemide injections can be added. An alternative loop diuretic such as torasemide can be substituted for furosemide at 1/10 of the furosemide dose. Other diuretics can be added, including spironolactone and thiazides. Thiazides should be started at a low dose and titrated to effect. Other complications seen with refractory heart failure include cachexia, azotemia, arrhythmias and pulmonary hypertension.

Presentation is supported by the Estonian Veterinary Association

Introduction Finding a murmur is most commonly raising a suspicion of a heart disease. The murmur itself is not a disease, but it is likely to indicate a disturbance of the blood flow caused by a congenital or acquired structural abnormality of the heart or great vessels, or, in the absence of a structural disease, caused by other physiological mechanisms (innocent or functional murmurs). Therefore, discovery of a murmur generally warrants further investigations to detect the underlying mechanism and cause. The signalment of the animal and a thorough history are likely to provide essential clues and help in narrowing down the differential diagnosis list, thus helping to select the appropriate approach to the patient. Physiological principles of the generation of the murmurs The normal blood flow through the heart is laminar (sheet-like) and therefore will not causing audible murmurs. When the flowing blood encounters an obstruction, the parallel streams of flow are disrupted, and the flow becomes turbulent. As the vibrations are transmitted to the thoracic wall they can be picked up with a stethoscope and heard as the murmur. When the vibrations are very intense, they can be felt by the bare hand placed on the skin surface (â&#x20AC;&#x2DC;thrillâ&#x20AC;&#x2122;). The factors influencing the ease of generating the turbulence are best described by the Reynolds number (NR) - a dimensionless quantity in fluid mechanics that helps to predict the flow pattern. At low Reynolds numbers flow tends to be laminar; at high Reynolds numbers the flow becomes turbulent. The Reynolds number is defined by the following equation đ?&#x2018; đ?&#x2018;&#x2026; = đ?&#x153;&#x152;đ??ˇđ?&#x2018;ŁĚ&#x2026; /đ?&#x153;&#x201A; where Ď is density, D is the tube diameter, v Ě&#x2026; is the mean velocity and Îˇ is the viscosity. This equation indicates that large diameter, high velocity and low viscosity favour generation of turbulence.

The viscosity of blood is mainly determined by the haematocrit: anaemia reduces viscosity, thus increasing the occurrence of the murmurs. Furthermore, anaemia generally leads to an increased cardiac output, i.e. higher flow velocities through the cardiac structures. The opposite is true for polycythaemia: the viscosity is increased and the flow velocity reduced, and as a result the flow is less likely to become turbulent. Turbulence also occurs when the cross-sectional area of the bloodstream changes, causing an increase in the flow velocity - a typical example of this would be blood flow through a stenotic valve. The third most common cause for generation of turbulence is the flow through abnormal connections between the cardiac chambers or vascular structures. The flow velocity through such connections is determined by the pressure gradient between the two connected chambers or vessels as well as by the diameter of the connection. A large pressure gradient (e.g. between the left and the right ventricles) leads to a faster flow and therefore to a more intense turbulence, compared to a flow caused by a smaller pressure gradient (e.g. between the two atria). If a connection is very wide (e.g. a large ventricular septal defect) the flow velocity will reduce, as the pressures within the chambers will equalise. In case of smaller connections between the chambers (e.g. in degenerative valvular lesions), the intensity of the murmur is dependent on the volume of abnormal blood flow - the larger the regurgitant volume, the louder the murmur. Characteristics of the murmurs Timing - Cardiac murmurs are described by the timing within the cardiac cycle as systolic, diastolic or continuous. Although the timing can be further classified as early- (proto-), mid(meso-) or late (tele-) systolic or diastolic the differentiation of these may be difficult due to the relatively high heart rates. Systolic murmurs start after the first heart sound (S1) and end before the second heart sound (S2) (holosystolic), or start at the beginning of S1 and last until the end of S2, obscuring the normal heart sounds (pansystolic). The differentiation between holo- and pansystolic is mainly academic as the causes for the two are similar. Pansystolic murmurs are generally louder, therefore â&#x20AC;&#x2DC;maskingâ&#x20AC;&#x2122; the normal heart sounds. Diastolic murmurs occur between S2 and S1 and they are significantly less common in veterinary patients. The most common cause of a diastolic murmur is aortic valve insufficiency that can be present concurrently with aortic stenosis or result from the valve damage secondary to infective endocarditis. Pulmonic insufficiency in the absence of pulmonary hypertension does not usually lead to development of a murmur due to a small diastolic pressure gradient between the pulmonary artery and the right ventricle. However, pulmonic insufficiency murmur can be heard if pulmonary hypertension is present. Continuous murmurs occur throughout the cardiac cycle without interruption indicating that a substantial pressure gradient is continuously present between the two connected chambers or vessels. Usually the diastolic component is quieter due to the lower pressure gradient. Furthermore, it can disappear completely at the end of diastole at lower heart rates. Continuous murmurs can be confused with simultaneous presence of a systolic and

diastolic murmurs ('to-and-fro murmurs'), e.g. in combination of aortic stenosis and insufficiency. Other important characteristics of a murmur that will further help to determine the cause of the murmur are the localization, or the point of maximal intensity (PMI) and the direction where the same murmur can be heard over other regions of the thorax - the radiation. Most of murmurs can be heard over the left hemithorax. The mitral valve region is normally in the area where the apex beat can be felt on palpation. To auscultate the aortic and pulmonic valve regions the stethoscope must be moved cranially and dorsally, whilst the thoracic limb is rotated laterally. The next region to be auscultated is the cranial thoracic inlet in the area that is used to raise the left jugular vein for venepuncture. Typically, the murmurs caused by aortic stenosis radiate towards this area. The cardiac auscultation is completed by carefully auscultating the right hemithorax with a special attention to tricuspid region almost directly opposite to the mitral valve region. Intensity - The murmurs can be graded based on their intensity on a scale from I to VI, with one being the quietest and six the loudest; grade V and VI murmurs are associated with a palpable thrill. To detect quiet murmurs and for consistency of the grading it is essential that auscultation is always performed in a quiet environment and on a calm animal. The animal should preferably be in a standing position facing away from the clinician, as this allows better access to all regions to be auscultated, as well as reduces the risk of animal attacks. Classification of the murmurs â&#x20AC;&#x201C; physiological vs pathological Physiological murmurs can occur secondary to decreased blood viscosity or increased cardiac output and they are most commonly detected in animals with anaemia, fever, increased sympathetic tone, hyperthyroidism or pregnancy. Typically, the PMI of such murmurs is on the left hemithorax near the left ventricular outflow tract and thus they can be heard at the left base or between the mitral and aortic regions. These murmurs are usually soft (grade I to III), early- to mid-systolic and they don't radiate extensively. In very young animals the haematocrit is lower, and the stroke volume is relatively larger compared to the diameter of the great vessels and these factors can result in an 'innocent' murmur. Innocent murmurs generally disappear as the dog matures. Pathological murmurs result from valvular lesions (stenosis or insufficiency), abnormal connections between the cardiac chambers (atrial or ventricular septal defect), or large vessels (persistent ductus arteriosus - PDA). Majority of the pathological murmurs are heard in the region of the affected structure. One major exception to this rule is the murmur caused by the atrial septal defect, where the murmur is caused by an increased volume of flow through the pulmonic valve, thus resulting in a â&#x20AC;&#x2DC;relative pulmonic stenosisâ&#x20AC;&#x2122; and the PMI of the murmur being in the pulmonic valve region. Diagnostic approach to a newly detected murmur As the vast majority of the murmurs in dogs are caused by a structural heart disease, in most cases further investigations should be considered. The gold standard for assessment of cardiac diseases is echocardiography including spectral Doppler imaging. However, it is not

always available, feasible, or necessary. To decide whether to pursue with additional diagnostic evaluations, the following factors should be considered: •

Patient – signalment, features of the murmur, concurrent signs and conditions

•

Veterinarian – confidence in the findings, perception of the cause

•

Client – financial aspect, uncertainty and concern

The main approaches to newly detected murmurs are: •

ruling out the causes of physiological murmurs (e.g. anaemia, fever, elevated sympathetic tone)

•

‘watchful waiting’, i.e. repeating the auscultation after a certain period (e.g. at the next vaccination in a puppy with suspected innocent murmur)

•

cardiac biomarkers (‘blood tests for the heart’)

•

thoracic radiography

•

basic heart ultrasound

•

full specialist Doppler echocardiography

Heart murmurs in paediatric patients The estimated prevalence of congenital malformations in dogs is 5-9 per 1000 dogs. Most of the haemodynamically significant congenital defects are associated with an audible murmur and therefore a detection of a murmur should alert the clinician of the possibility of a structural heart disease. Although ‘innocent’ murmurs can occur in young dogs, it may not always be appropriate to recommend a watchful waiting approach, as this can lead to an unnecessary delay in reaching a diagnosis and providing treatment if possible or necessary. Furthermore, the uncertainty is also likely to cause unnecessary stress for the owners. The innocent murmurs are usually very soft (grade I-II), short and early systolic and the PMI in the mitral or left ventricular outflow tract regions. It is important to note that auscultation alone cannot differentiate pathological and non-pathological murmurs. The following features of the murmur are unlikely to be associated with functional murmurs and therefore additional investigations should be recommended: •

continuous

•

diastolic

•

PMI left base

•

radiating to cranial thoracic inlet

•

PMI over right hemithorax

•

murmur intensity >III/VI

•

associated with jugular pulsations/distension

â&#x20AC;˘

weak, pounding or late rising femoral pulses

â&#x20AC;˘

abnormal mucous membrane colour

â&#x20AC;˘

presence of arrhythmias.

Murmurs in adult dogs Systolic murmurs are more common, and signalment, thorough history and careful auscultation in combination with ruling out systemic diseases help to narrow down the differential list. Diastolic murmurs are always pathological. In case of uncertainty of the cause, it is safer to presume that a murmur is pathological and recommend further investigations. Doppler echocardiography will provide a superior quality of information and generally a more accurate diagnosis. Radiography, although widely available, has limited sensitivity and specificity in detection of heart disease. Furthermore, patient safety needs to be taken into consideration, especially if sedation or anaesthesia is required. Biomarkers may help in determination whether the murmurs are associated with cardiac stretch (natriuretic peptides) or cardiomyocyte damage (cardiac troponin I). In small breed dogs the most common cause of a systolic left apical murmur is degenerative mitral valve disease, in which the murmur loudness often correlates with the severity of the regurgitation. In large breed dogs systolic dysfunction and resulting left ventricular dilation (DCM-phenotype) is more common, and it is important to note, that the associated systolic apical murmur is often mild even in advanced disease states due to a small regurgitant fraction and lower pressure gradient between the two chambers. Degenerative mitral valve can also be present in large breed dogs, although the regurgitant fraction also tends to be smaller than in similarly affected small breed dogs. Murmurs in geriatric dogs In small breed dogs degenerative atrioventricular valve disease is the most common cause of left apical systolic murmurs. Biomarkers, especially natriuretic peptides, help to determine the severity of myocardial stretch resulting from volume overloading. Radiographs are helpful in assessing the degree of cardiac remodelling, may be useful for prognostic purposes, and help to detect the presence of congestive heart failure. Echocardiography is helpful in quantifying the severity of the defects and may be especially useful if the murmur is detected on right hemithorax, or physical examination reveals femoral pulse abnormalities, jugular distension or arrhythmias. In large breed dogs, echocardiography is the test of choice, as it helps in quantifying the severity of systolic function. Degenerative mitral valve disease can also be diagnosed in large breed dogs, and its progression tends to be more rapid compared to the disease in small breed. Therefore, echocardiography can be considered the test of choice in large breed geriatric dogs presented with an incidental murmur. Conclusions Finding of an incidental murmur should alert the clinician of the possibility of a structural heart disease, although diseases of other organ systems and physiologic causes of the

murmurs should also be considered. The test of choice for investigations of the murmurs is echocardiography, allowing direct visualization of the intracardiac and vascular structures, as well as quantification of the severity of the defects. Cardiac biomarkers may help in determination of the origin of the disease (cardiac vs. non-cardiac), but sensitivity and specificity of these tests may limit the use of these as a sole test. Thoracic radiography is useful in assessment of cardiac and pulmonary disease, but in isolation from the clinical information (signalment, history, physical examination findings) is unlikely to provide a conclusive diagnosis. â&#x20AC;&#x2DC;Watchful waitingâ&#x20AC;&#x2122; is generally an unsafe approach to newly detected murmurs and may only be acceptable in a small number of selected cases - young dogs with low-grade early systolic murmurs with a PMI over left outflow tract region, in which other systemic or structural heart diseases are considered unlikely or ruled out. In these cases, the likely differentials as well as diagnostic modalities should be discussed with the owners to allow for an educated decision to be reached.

Laboratory tests, if used wisely, can make a significant contribution to the diagnostic workup and management of the patient. However, not all results received from the laboratory should trigger action. Some results should be noted, others ignored. Ignorable results can be either accurate ones that do not help in decision making or erroneous results caused by a mistake in the long laboratory testing cycle (Figure 1). The testing cycle starts with the clinician deciding to perform the test and involves all the subsequent steps up to the time when the clinician interprets the results. Frequently, false or inaccurate laboratory results are attributed to the analytical phase of the cycle. Recent study showed that preanalytical errors constituted biggest part of the total encountered errors.

Decision to perform the test

Action taken

Order

Results interpreted

placed

Sample acquisition

Report generated

Sample

Transportation

analysed

Figure 1. The full laboratory testing cycle. This is a sequence of events that starts with the decision to perform the test, moving through sample acquisition, submission, analysis, until the results are obtained and interpreted. In this schematic diagram - events that take place in the clinic (pre-analytical phase) are in orange; the intermediate steps where clinic and laboratory intersect are in yellow and laboratory (analytical phase) is in red. The most common causes of unreliable and artefactual test results are: •

failure to obtain adequate sample (half-empty, overfilled, clotted collection tube, wrong test tube)

•

submission errors (specimen identification errors, wrong choice of test, test request errors).

A term “laboratory artefact” here is used to describe a change in the sample that is not present in vivo - in patient. Artefacts can affect any type of the sample - hematology, biochemistry, urine etc. The steps before the analytical testing phase are the most important in terms of avoiding and/or recognizing the possibility of erroneous results or mistakes. Special attention should be paid to: •

sampling and sample preparation o technique, smear thickness, drying, staining o time between the sampling and testing (<30 minutes for urine samples) o sampling of the fasted patients, selection of the accurate test tube and test

•

environment

o sample storage and transportation - in room temperature or refrigerator o drying the smear with the hairdryer/ flame o over and under filled hematology test tubes •

contamination after/during the sampling procedure o blood contamination while performing an FNA o old, unfiltered cytology stains - bacteria, yeast contamination o voided urine sample - material from the ground.

All information included in the submission form and the laboratory report form should be equally important to the clinician and the laboratory. Careful and complete evaluation of the patient is always the most important procedure that you have at your disposal!

References 1.

Clinical Laboratory Tests: Which, Why, and What Do The Results Mean? Lab Med. 2015;40(2):105-113. doi:10.1309/LM4O4L0HHUTWWUDD Lab Med | © American Society of Clinical Pathologists

Wians FH Jr Baskin LB Chapter 2: The Use of Clinical Laboratory Tests in Diagnostic Decision-Making. In: Handbook of Clinical Pathology, ASCP Press: Chicago; 2000:9–24

Carraro P Plebani M, Errors in a stat laboratory: Types and frequencies 10 years later. Clin Chem. 2007;53:1338–1342

Elston DM, Laboratory results that should be ignored. MedGenMed.2006;8:4-9

Minuscule amounts of fluid that escapes capillaries ends up in the interstitium where in conjunction with cellular membrane glycoproteins it forms a gel like substance that lubricates the tissue surfaces. The amount of interstitial fluid is dependent on the balance between plasma and tissue oncotic and hydrodynamic pressures. Laboratory analysis of the effusion can: • • •

provide a specific diagnosis identify the cause of the effusion point to other diagnostic procedures.

Examination of the fluid: • •

•

visual evaluation: colour, clarity, odour, viscosity cell counts – analysers provide total nucleated cell counts, including white blood cells, mesothelial cells, cancer cells and sometimes even non-cellular material, i.e. bacteria or cellular debris. All results should be confirmed by microscopic assessment of the smear. protein content – supernatant is tested after centrifugation. Automated analyzer results will be most precise. A refractometer may be used in the clinic for assessing protein and specific gravity. cytology – cellular components can be evaluated microscopically in stained direct smear, smear of the sediment, or smear of the buffy coat.

The following table briefly shows the typical features of the specific, potentially clinically important effusions. Microscopy -

Predominant cells Low numbers! Macrophages Mesothelial cells Neutrophils Lymphocytes Nondegenerate neutrophils Macrophages

Other findings/notes - Total nucleated cell numbers <1.5 x109/L - Cytocentrifuged sample for microscopy

Effusion Transudate

- Cells can appear aged, phagocytic, do not Inflammatory confuse with degenerative changes. non-septic - Look/test for possible causes of the effusion: bile – macrophages may contain blue-green

to yellow bile pigment (can test total bilirubin in serum and effusion), for uroabdomen test for creatinine (in serum and effusion) - Total nucleated counts>7x109/L - Degenerate neutrophils - Macrophages

- Intracellular bacteria, +/- free bacteria. Inflammatory - Lack of bacteria does not rule out septic septic process (ongoing antibiotic therapy, low number of bacteria). - Cytology cannot identify the bacterial species. - Total nucleated counts>7x109/L

- Erythrocytes - Nondegenerate neutrophils (variable #) - Macrophages (variable #) - Mesothelial cells

- Main objective: to rule out inflammation, Haemorrhagic infection. - PCV usually >5% - Chronic hemorrhagic effusion- erythrocyte breakdown products within the cytoplasm – hemosiderin (blue black, amorphous pigment), in anaerobic environment - yellow, rectangular hematoidin crystals. - If platelets present – assume blood contamination, instead of true hemorrhagic process.

- Lymphocytes - Nondegenerate neutrophils - Macrophages

- Lymphocytes are small, morphologically Chylous normal. - Cells may contain small, clear cytoplasmic vacuoles. - With time, neutrophils and macrophages may outnumber the lymphocytes. - To distinguish between chylous and pseudochylous effusion – test serum and effusion trigliceride and cholesterol concentration.

+/- Neoplastic cells +/- Inflammatory cells +/- Reactive cells

- Difficult to differentiate between reactivity Neoplastic and neoplasia.

Dental and maxillofacial radiology is quickly becoming the standard of care in veterinary dentistry. This is due not only to the fact that it is crucial for proper patient care, but also because of a significant increase in client expectations. Finally, providing dental radiographs as a routine service can create significant income for a veterinary practice. To obtain high-quality skull radiographs, positioning of the head and the rest of the body must be ideal. Therefore, patient positioning devices are necessary for appropriate placement of the body and head. Cassettes used for full-body images limit their intraoral use to certain parts of the mandibles and maxillae. However, with precise extraoral positioning it is possible to obtain an image of the entire area of interest. As the number of clinics offering CT scans increases and the value of such technology is proven, many specialists will begin offering 3D imaging. If CT/MRI is not available within the practice, standard radiographs should be performed rather that referring the patient immediately. It is important to begin the standard diagnostic plan with skull radiographs in the following clinical situations: 1.

2. 3. 4. 5.

Emergency: after head trauma when an overview is necessary to plan the final diagnostic and treatment plan. It is particularly important in unconscious patients with visible head injuries to estimate the severity of trauma Generalized problems affecting larger anatomic regions Suspicion and/or confirmation of presence of foreign bodies Prior to 3D imaging to predefine areas of interest Any skeletal deformities and defects present in oral cavity and maxillofacial part of the head

6. 7. 8.

Cephalometric and orthodontic assessment to evaluate skull symmetry in dogs and cats As part of the diagnostic plan for orofacial pain, masticatory muscle disorders, malfunction of the temporomandibular joint (TMJ), and nasal problems In small mammals it is standard to obtain entire skull radiographs.

Dental radiography in most cases is based on intraoral projections. Interpreting dental radiographs starts with the appropriate orientation. First, place the convex side of the dot towards you. This means you are looking at the teeth as if your eyes are the x-ray beam. This step is done for you on most digital systems. The dot should always be located in such a way that it is not superimposed on structures being imaged. When chemical development is performed, place the clip to hold the film adjacent to the dot. This will provide an area of interest free of interfering artifacts. Next, rotate the film so that the roots are in their natural position (pointing up on maxillary views and down on mandibular). When this is done, it is necessary to determine if it is the left or right side of the patient. For lateral oblique projections (canine, premolar, and maxillary molar teeth) or parallel projections (mandibular molar teeth), the side of the film where the more mesial teeth are located indicates the side that was imaged. In other words, if the mesial teeth are on the right side of the film, it is an image of the right side of the patient. With other projections, such as dorsoventral (DV) or ventrodorsal (VD) images (i.e incisors or canines), the right side of the mouth is on the left side of the film and vice versa for the left side of the mouth. This is similar to a VD image of the abdomen. To distinguish between mandibular and maxillary images, certain landmarks should be evaluated. For mandible the presence of the mandibular canal, mental foramina, mandibular symphysis and ventral mandibular margin (cortex).The most rostral mental foramen is located in the second incisor area, the middle at the level of apex of the second premolar, and the caudal is at the level of the third premolar. In dogs, the mandibular second, third, and fourth premolars and the first and second molars should have two roots. In cats there are normally only three teeth caudal to the canine. There are obviously exceptions to these rules (e.g. third root in a molar, fused roots or the presence of the second premolar in cats, and supernumerary teeth) In maxilla the presence of palatine fissures, incisive canal; the conchal crest rostrally and pterygopalatine fossa caudally. The radiopaque line running across the canine root and just dorsally to the roots of the premolars and molars is the nasal surface of the alveolar process of the maxilla. Nasal structures are visible above the conceal crest with symmetric turbinate details. Typical structures for the nasal cavity are the palatine fissures and incisive foramen. In dogs, the fourth premolar as well as two maxillary molars normally have three roots; however, the second molar often has fused roots. In cats, the zygomatic arch is typically superimposed on the maxillary cheek teeth.

Normal radiographic anatomy. There are numerous structures within the oral cavity that mimic pathologic states depending on the projection. Knowledge of normal radiographic anatomy will help avoid over interpretation. Normal alveolar bone will appear gray and relatively uniform throughout the arcade. It is slightly more radiopaque â&#x20AC;&#x153;darkerâ&#x20AC;? than tooth roots. In addition, it appears slightly but regularly mottled. Alveolar bone should completely fill the area between the roots (furcation) and end at the cementoenamel junction (CEJ).The root canals should all be the same width; allowing for differences in the diameters of the root. There should be no radiolucent areas in teeth or bone. A regular thin dark line (periodontal ligament) should be visualized around the roots. Periodontal disease. Periodontal bone loss results from the combination of bacterial induced inflammation and host response creating osteoclastic resorption of bone. This resorption will result in crestal bone loss to a level below the cementoenamel junction. This decrease in bone height may also create furcational exposure. Horizontal bone loss is the most common pattern in veterinary patients is horizontal. This appears as generalized bone loss of a similar level across all or part of an arcade. The other pattern is angular (vertical) bone loss. The radiographic appearance of angular bone loss is one area of recession below the surrounding bone. The surrounding bone may be normal or be undergoing horizontal bone loss. Therefore it is common to have a combination of the two types in the same arcade. Bone loss does not become radiographically evident until 30-50% of the mineralization is lost. Therefore, radiographic findings will always underestimate bone loss. In addition, bone loss on only on surface (i.e. lingual, palatal, or facial) may be hidden by superimposition of bone or tooth. This may resulting in a non-diagnosed bony pocket. Always interpret radiographs in light of the complete oral examination findings. Endodontic disease. Endodontic disease may be demonstrated radiographically in several ways. An individual tooth may have one, some, or all of the different changes listed below. However, only one need be present to establish a presumptive diagnosis of endodontic disease. Radiographic changes can be broken into two major classifications: 1) changes in the surrounding bone, or 2) changes within the tooth itself. Tooth Resorption. Physiologically, tooth resorption occurs during changing of dentition from deciduous to permanent teeth. The erupting permanent tooth causes resorption of the deciduous tooth root. Persistent deciduous dentition teeth very often undergo resorption even without permanent tooth eruption,and therefore the lifespan and time of functionality of these teeth is often very limited. The radiographic appearance of different types of resorption does not always relate to the type of disease, however replacement resorption has some typical features. In addition, localization of the lesion also could be linked to the specific type. The importance of dental radiography in TR cases cannot be overstated. Type 1 lesions typically retain a viable root canal system, and will result in pain and endodontic infection if the roots are not completely extracted. However, the concurrent presence of a normal periodontal ligament makes these extractions routine. With type 2 lesions, there are areas lacking a normal periodontal ligament (ankylosis) which also demonstrate varying degrees of root resorption, which

makes extraction by conventional elevation difficult to impossible. The continued resorption in type 2 teeth is the basis for crown amputation therapy. Neoplasia. Neoplasia is defined as the abnormal growth of cells that is not responsive to normal growth control. Neoplasms can be further classified by their biologic behavior as benign or malignant. Benign masses: Most benign neoplastic growths will have no boney involvement on dental radiographs. If bone involvement does occur with a benign growth it will be expansive, resulting in the bone “pulling away” from the advancing tumor leaving a decalcified soft tissue filled space in the tumor site. Bony margins are usually distinct. Finally, this expansive growth will typically result in tooth movement. Malignant neoplasia: Malignant oral neoplasms typically invade bone early in the course of disease, resulting in irregular, ragged bone destruction. Initially, the bone will have a mottled “moth eaten” appearance, but radiographs late in the disease course will reveal a complete loss of bone (the teeth will appear to float in space). If the cortex is involved, an irregular periosteal reaction will be seen. Diagnosis of temporomandibular joint is based on a series of well positioned radiographs or, ideally, 3D imaging. CT is superior for TMJ evaluation than standard radiography,3 whereas MRI provides more accurate evaluation of the soft tissues. In standard 2D radiography diagnostic imaging of temporomandibular joints, the mandibular area is visualized by performing three projections: lateral oblique, dorsoventral (DV), and oblique DV.

Further reading 1. 2.

Niemiec B. Gawor J, Jekl V. Practical Veterinary Dental Radiography CRC Press 2018. Dupont GG, Debowes LJ. Atlas of Dental Radiography in Dogs and Cats, Elsevier, 2009

Interceptive orthodontics (IO) occurs when the problem has been already manifested. Any procedure that may include minor local tooth movement or extraction which eliminates or reduce the severity of malocclusion in the developing dentition. Interceptive orthodontics is often the first phase of orthodontic treatment. It may not prevent the need for braces, retainers, or other orthodontic techniques in later years but it can minimize the second phase of treatment. The most common indications of IO include: persistent deciduous dentition, crowding of the teeth, uneven development of maxilla and mandible, impaction of the teeth caused by mechanical reasons and supernumerary teeth. Interceptive orthodontics involves the selective extraction of any deciduous teeth that would impede the development of a proper bite. The general rule is to extract the teeth from the short jaw. For a class 2 malocclusion, extraction of the deciduous mandibular canines and incisors will alleviate the dental interlock. These procedures do not alter the animalâ&#x20AC;&#x2122;s genetic make-up nor do they make anything happen. Rather, they allow the animal to express its full genetic potential by removing any mechanical impediment to growth. Owners and breeders should be cautioned that, even if the animal undergoes successful treatment, it did require intervention and has to potential to pass the malocclusion on to offspring.1 To maximize the benefit of interceptive orthodontics, extractions should be performed as early as possible. The hope is that the jaw length relationship will normalize before the permanent teeth erupt and recreate dental interlock. The more time between deciduous tooth extraction and permanent tooth eruption, the better the chances of success. However, the owners should be made aware that most animals with jaw length discrepancies at eight weeks of age will not â&#x20AC;&#x2DC;go normalâ&#x20AC;&#x2122;, regardless of treatment, and there will very likely be orthodontic problems when the permanent teeth erupt. The removal of the abnormal interlock does not make the short jaw grow fast and catch up, rather it allows the animal to express its full genetic potential. If the programming is faulty, interceptive orthodontics will not change that. A second (and much more predictable) benefit of interceptive orthodontics is that it immediately relieves the oral trauma and pain associated with abnormal tooth-to-

Niemiec BA Pathology in the Pediatric Patient in A Color Handbook Small Animal Dental, Oral and Maxillofacial Disease, Manson 2010, 89-126

tooth or tooth-to-soft tissue contacts. This on its own is sufficient cause to recommend the surgery. In deciding if interceptive orthodontic extraction is required (and if so which tooth or teeth should be extracted), one should be familiar with the normal location of the permanent teeth. Except for the permanent maxillary canines (which erupt mesial to the deciduous), permanent teeth erupt lingual to their deciduous counterparts. Besides relative positioning, other clues to differentiate deciduous teeth from permanent teeth include comparative whiteness, diminutive size, and degree of root development. When performing pure interceptive orthodontics, the simple rule is to extract the teeth on the jaw that needs to grow. However, recent texts recommend extracting any deciduous tooth that is or is likely to become a hindrance to movement, while not extracting teeth that may be creating a favorable dental interlock. Favorable dental interlocks most commonly occur with class III malocclusions where the mandibular canines are close but still distal to the maxillary lateral incisors. Among other procedures which may act as interceptive orthodontics are also extractions of the permanent dentition, operculectomy and odontoplasty. All these actions can allow the patient to correct itself during the growth phase. IO by changing the trajectory of permanent teeth eruption can improve relations and position of erupted teeth. Often such procedures are combined with minor teeth movement. Further reading: 1. 2. 3.

1.Niemiec BA Pathology in the Pediatric Patient in A Color Handbook Small Animal Dental, Oral and Maxillofacial Disease, Manson 2010, 89-126 2.Niemiec BA ed. Veterinary Orthodontics. Practical Veterinary Publishing, San Diego 2013 3.Harvey CE, Emily PP : Orthodontics, In: Small Animal Dentistry. St. Louis, Mosby. 266-96. 1993

Pediatric or juvenile dentistry is considered the time between birth and seven months of age when the adult teeth are fully erupted. There are numerous problems that can occur during this time. Some of these are similar to problems seen in the adult dentition, and others are only seen in juvenile patients. Deciduous dental formula: Canine: Three incisors, one canine, and three premolars in each quadrant for a total of 28 teeth Feline: Three incisors, one canine, per quadrant. Three maxillary premolars per side and two mandibular premolars per side for a total of 26 teeth. There are no deciduous molars; however the deciduous fourth premolars function as mandibular first molars.

1. Problems with the teeth themselves: The most common problem seen in pediatric dentistry is retained deciduous dentition. This is most common in toy and small breed dogs, but can occur in any breed as well as cats. The most common teeth that are retained are the cuspids, followed by the incisors and then premolars. This is a serious condition since they cause both orthodontic and periodontal problems. Orthodontically, the adult tooth will erupt in an unnatural position which can cause tooth, gingival, or palatine trauma. The sooner these are removed, the better the chances of self correction. The classic belief is that the deciduous tooth being retained caused the adult tooth to erupt in an unnatural position. Current knowledge, however, is that the adult tooth erupted in the wrong place thus CAUSING the deciduous to be retained. The periodontal problems occur due to the fact that the gingival and periodontal attachment is attached to the retained deciduous in that area and therefore does not form a normal attachment to the erupting permanent tooth. This results in a weakened periodontal attachment and susceptibility to future periodontal disease. This is even more concerning given the fact that the patients who tend to retain teeth (toy and small breeds) tend to be worse with periodontal disease.

The adult tooth does not need to be completely erupted for these problems to occur, in fact, the problems begin as soon as the permanent tooth begins to erupt. Therefore, the teeth should be extracted as early as possible to lessen the untoward effects. Do not wait until six months of age to perform the extractions along with neutering.

Malocclusions in deciduous teeth are fairly common. In some cases, the patient may be genetically programmed for a normal bite and only temporarily maloccluded. This is due to the fact that the maxilla and mandible grow at varying rates. However, the dentition may interfere with the jaw movement and subsequent correction. This is called an adverse dental interlock. This interlock can be removed by extraction the deciduous teeth that are causing it. This is called interceptive orthodontics and if performed properly in a patient that is genetically programmed to have a normal bite may result in self correction. In general, extract the teeth on the jaw in which movement is desired. However it is also recommended to remove any tooth that may cause a problem. Interceptive orthodontics should be performed as soon as possible (6-8 weeks) for maximum effect. In class II (overshot) and IV (wry) malocclusions the patient may have palatine trauma secondary to the tooth malalignment. This hurts the patient just like a thorn in the foot. The extractions will alleviate this discomfort as well as possibly allow movement of the jaw. Malocclusions in the adult dentition can be treated in various ways. These include extraction, coronal amputation and vital pulp therapy, and orthodontic appliances. Early recognition and proper therapy is essential to proper outcomes. Deciduous teeth are weaker than adult teeth and therefore are of increased susceptibility to fracture. This combined with the fact that the pulp chamber is very large makes pulp (nerve) exposure a fairly common occurrence. This is a very painful experience for the patient. In addition, these teeth may become infected in the same manner of a permanent tooth. These teeth need to be extracted; ignoring them is NOT an option. Do not wait until neutering to remove them as they are painful to the patient on a daily basis.

Unerupted teeth can occur due to a variety of reasons. Generally this is due to failure of passive eruption. There is no therapy for this condition. On occasion, however, there can be bony or soft tissue interference with eruption. If this is suspected, an operculectomy should be performed. This consists of removal of the barrier to eruption surgically. If this fails to bring about resolution of the problem, it is likely due to failure of passive eruption. On occasion unerupted teeth may result in dentigerous cysts. These are caused by the reduced enamel epithelium with remnants of ameloblasts (which would normally have been exfoliated during eruption) creating fluid and thus creating the cyst. These growths can become quite large and disfiguring which will result in major surgical correction. For this reason, all unerupted teeth should be radiographed at an early age. The radiographic appearance of these cystic structures is classic. If a cyst is found, treatment should be

performed right away. Currently surgical extraction of the offending tooth and cystic lining or radiation therapy is acceptable.

Enamel hypoplasia results from a malformation of the enamel prior to tooth eruption. Once the tooth erupts into the mouth the weakened enamel will fracture off thus resulting in exposure of the underlying dentin. The dentinal exposure will result in significant discomfort for the patient as the dentinal tubules will cause significant pain. In addition, the exposed dentinal tubules can act as a conduit for bacterial infection of the pulp (or root canal system), thus initiating endodontic disease. The dentinal surface is much rougher than enamel, and its exposure results in increased plaque and calculus deposition which in turn increases periodontal inflammation. Finally, the dentin will become stained which is much less esthetic. For all of these reasons, prompt therapy of these teeth is critical to the health of the patient. The best therapy is bonded composite restoration. A properly placed restoration will alleviate all of the deleterious effects associated with this condition.

Other anatomic anomalies include gemination, fusion, concrescence of the teeth as well as presence of supernumerary teeth, supernumerary roots, dilaceration of teeth, invagination of teeth, enamel pearls. Intrinsic tooth discoloration may be caused by systemic and local factors. Although changes caused by systemic tetracycline administrationn do not require treatment - other staining may be associated with internal resorption or pulp disease and it is reasonable to evaluate them radiographically.

2. Problems of the oral soft tissues Cleft Palates are a fairly uncommon occurrence. They can be fairly mild to major or it can involve the hard and/or soft palate. The length of these clefts is not the major prognostic factor, rather it is the width. The wider the cleft the more guarded the prognosis. These can generally be corrected surgically, however they can be quite challenging due to the lack of pliability of the palate. Many flap techniques have been devised for the correction of these defects. The practitioner is encouraged to study and practice these techniques prior to attempting them on an actual patient. The major point to consider in these cases is to create closure without tension. In addition, you must make every effort to successfully cure the problem the first time, as subsequent surgeries will be more difficult due to scar tissue formation. Oral pappillomas are a fairly common occurrence as well. These appear as whitish cauliflower growths on the gingiva. They are viral induces and are generally self limiting. However, they can become infected as well as mimic more aggressive tumors. Therefore excisional biopsy is recommended to ensure the diagnosis.

Oral tumors: Odontomas are benign odontogenic tumors typically diagnosed in young dogs at the age between 6-18 months of age. Depending on radiographic appearance we can distinguish either compound odontoma with dental-like structures or complex odontoma organized into conglomerate of dental tissue. Canine Oral Papillary Squamous Cell Carcinoma (COPSCC) used to be regarded as typical for young individuals, however the recent literature does not confirm this fact. The juvenile rhabdomyosarcoma, similarly to human being is more prone to occur in young dogs, however this tumor is extremely rare.

Eruptive gingivitis is a fairly common problem in small animal patients. This is inflammation of the gingiva during and just after tooth eruption. This is self limiting in most cases, however home care (brushing or chlorhexidine rinses are recommended to decrease the inflammation. If the condition does not resolve in a short period of time, additional diagnostics and therapy is recommended as this could b e juvenile periodontitis (see below). Juvenile periodontitis is a very difficult problem to treat and or cure. This condition is similar to rapidly progressive periodontitis in adult patients. In rare cases it can begin in the deciduous dentition. On occasion it can be transient and resolve with proper therapy (cleaning and homecare). If this does not solve the problem, advanced periodontal therapies with strict and consistent homecare may be required. This condition generally caries a poor prognosis.

Further reading 1. Hale FA Juvenile Veterinary Dentistry in Vet Clin North Am Small Anim Pract 2005; 35; 789-817 2. Fulton AJ, Fiani N, Verstraete FJM Canine Pediatric Dentistry Vet Clin Small Anim 44 (2014) 303â&#x20AC;&#x201C;324

Small dogs, big problems? Small and toy dogs have become increasingly numerous and popular within the pet population, and often make up the majority of dental patients in our practices. A review of oral pathologies and complications more commonly encountered in small and toy sized dogs compared to large breed dogs is presented.

Step 1: OBTAIN CONSENT NEVER extract teeth without owner consent (preferably written), no matter how bad the problem, or how obvious the decision is. Make sure that you have a valid daytime number (or numbers) for the client and inform them they must be available during surgery hours. Consider loaning pagers to clients for the day, as this author has found this to be a very effective means to contact clients. If the client cannot be reached and prior consent was not obtained, DO NOT PULL THE TOOTH. Document the problem, recover the patient, and reschedule the work. Remember, the tooth can always be extracted later, but it cannot be put back in!

Step 2: DENTAL RADIOGRAPHS Dental radiographs should be exposed on all teeth prior to extraction. Dental radiographs are invaluable resources for the practiconer. Radiographs allow the practitioner to determine the amount of disease present, any root abnormalities or ankylosis. Help with radiographic interpretation is available while the patient is under anesthesia at www.vetdentalrad.com. In addition, the radiographs will serve as evidence for the extraction in the medical record. Radiographs should also be exposed post-extraction to document complete removal of the tooth.

Step 3: OBTAIN PROPER VISABILITY AND ACCESSABILITY The patient should be positioned in such a way as to allow maximum visibility of the area as well as make the surgeon most comfortable. Note that during the extraction procedure the ideal position may change and the patient should be adjusted appropriately. The lighting should be bright and focusable on the surgical field. Suction, air/water syringes, and gauze should be utilized continually to keep the surgical field clear, and mouth gags can be used to hold the mouth in proper position for surgery. Finally, magnification may help the surgeon locate furcations or retained root tips.

Step 4: PAIN MANAGEMENT Extractions are surgical procedures and are moderately to severely painful for the patient. Depending on patient health, a multimodal approach (combination of opioids, NSAIDs, local anesthetics, and dissociative) should be employed, as this provides superior analgesia.

Preemptive analgesia is proven to be more effective than post-operative, and it is therefore important to administer the drugs BEFORE the painful procedure.

SINGLE ROOT EXTRACTIONS Step 5: INCISE THE GINGIVAL ATTACHMENT This is accomplished with a scalpel blade (number 11 or 15), elevator, or luxator. The selected instrument is placed into the gingival sulcus with the tip of the blade angled toward the tooth (this will help avoid going outside the bone and creating a defect or cutting through the gingiva). The blade is then advanced apically to the level of the alveolar bone, and the instrument is carefully worked around the entire tooth circumference. This step is very helpful as the gingival attachment contributes approximately15% of the retentive strength of the periodontal apparatus. More importantly, however, this procedure will keep the gingiva from tearing during the extraction procedure. This is most important with mobile teeth where little elevation is needed, but one edge is still attached. Gingival tearing can cause defects that require closure or can make a planned closure more difficult.

Step 6: ELEVATE THE TOOTH Elevation is the most dangerous step in the extraction procedure. Remember that you are holding a sharp surgical instrument and working in an area of numerous critical and delicate structures. There have been many reports of eyes that have been gouged and lost by extraction instruments as well as at least one confirmed fatality due to an elevator puncturing a patientâ&#x20AC;&#x2122;s brain. The index finger is placed near the tip of the instrument to avoid causing iatrogenic trauma in the event of instrument slippage or encountering diseased bone. In addition, the jaw should be gently held with the opposite hand to provide stability and avoid mandibular fracture. First, select an instrument which matches the curvature and size of the root. There are numerous instruments available including the classic elevator, the luxating elevator, and the winged elevators. Classic elevators and winged elevators are used in an â&#x20AC;&#x153;insert and twistâ&#x20AC;? motion to tear the periodontal ligament, whereas luxators are used in a rocking motion during insertion to fatigue as well as cut the periodontal ligament. Luxators can be GENTLY twisted for elevation, but they are not designed for this and can be easily damaged when used in this manner. Elevation is initiated by inserting the elevator or luxator firmly yet gently into the periodontal space. The insertion should be performed while keeping the instrument at about a 10 to 20 degree angle toward the tooth, to avoid slippage. Once in the space between the bone and the tooth, the instrument is gently twisted with two-finger pressure. This is not to say that the instrument should be held with two fingers, rather the entire hand should be used to hold the instrument. Twist only with the force that you could generate when holding

with two fingers. Hold the position for 10-30 seconds to fatigue and tear the periodontal ligament. It is important to note that the periodontal ligament is very effective in resisting intense, short forces. It is only by the exertion of prolonged force (i.e. 10-30 seconds) that the ligament will become weakened. Heavy stresses only serve to put pressure on the alveolar bone and tooth which can result in the fracture of one of these structures, so it is important not to use too much force. After holding for 10 to 30 seconds, reposition the instrument about 1/8 of the way around the tooth and repeat the above step. Continue this procedure 360 degrees around the tooth, each time moving the elevator apically as much as possible. Depending on the level of disease and the size of the tooth, a few to several rotations of the tooth may be necessary. The key point to successful elevation is PATIENCE. Only by slow, consistent elevation will the root loosen without breaking. It is always easier to extract an intact root than to remove fractured root tips.

Step 7: EXTRACT THE TOOTH: Removing the tooth should only be attempted after the tooth is very mobile and loose. This is accomplished by grasping the tooth with the extraction forceps and gently pulling the tooth from the socket. Do NOT apply undue pressure as this may result in root fracture. In many cases, especially with premolars, the roots are round in shape and will respond favorably to gentle twisting and holding of the tooth while applying traction. This should not be performed if there are root abnormalities (significant curves, weakening) seen on the preoperative radiograph. It is helpful to think of the extraction forceps as an extension of your fingers. Undue pressure should not be applied. If the tooth does not come out easily, more elevation is necessary. Start elevation again until the tooth is loose enough to be easily removed from the alveolus.

Step 8: AVELOPLASTY This step is performed to remove diseased tissue or bone, as well as rough boney edges that could irritate the gingiva and delay healing. Diseased tissue can be removed by hand with a curette. Bone removal and smoothing is best performed with a carbide, or preferably a coarse diamond bur on a water-cooled high-speed air driven hand-piece. Alternatively, ronguers or bone files may be used if a high-speed dental unit is unavailable. Next, the alveolus should be gently flushed with a 0.12% chlorhexidine solution to decrease bacterial contamination. After the alveolus is cleaned, it may be packed with an osseopromotive substance.

Step 9: CLOSURE OF THE EXTRACTION SITE: This is a controversial subject among veterinary dentists, and thus some texts recommend suturing only in large extractions, other authors (including this one) recommend suturing almost all extraction sites. Closure of the extraction site promotes hemostasis and improve post-operative discomfort and aesthetics. It is always indicated in cases of larger teeth (e.g. canines, carnassials), or any time that a gingival flap is created to allow for easier extraction. This is best accomplished with size 3/0 to 5/0 absorbable sutures on a reverse cutting needle. Closure is performed with a simple interrupted pattern with sutures placed 2 to 3 mm apart. It is further recommended to utilize one additional throw over manufacturerâ&#x20AC;&#x2122;s recommendations to counteract tongue action. In regards to flap closure, there are several key points associated with successful healing. The first and most important is that there must be no tension on the incision line. If there is any tension on the suture line, it will not heal. Tension can be removed by extending the gingival incision along the arcade (called an envelope flap) or by creating vertical releasing incisions and fenestrating the periosteum. The periosteum is a very thin fibrous tissue which attaches the buccal mucosa to the underlying bone. Since it is fibrotic, it is inflexible and will interfere with the ability to close the defect without tension. The buccal mucosa is very flexible and therefore will stretch to cover large defects. If there is no tension, the flap should stay in position without sutures. If at all possible, the suture line should not be made over a void. If sufficient tissue is present, consider removing some on the attached side to make the suture line over bone. Always suture from the unattached (flap side) to the attached tissue, because this avoids tearing the flap as the needle dulls. Finally, ensure that all tissue edges have been thoroughly debrided as intact epithelial tissues will not heal.

EXTRACTION OF MULTI ROOTED TEETH: Section all multi-rooted teeth into single rooted pieces. The roots of almost all multi-rooted teeth are divergent and this will cause the root tips to break off if extractions are attempted in one piece. Root fracture can occur even if a tooth is relatively mobile to start with. With mobile teeth, the sectioning step alone often allows for simple extraction. The best tool for sectioning teeth is a bur on a high-speed air driven hand piece. Besides being the quickest and most efficient tool for the job, it also has air and water coolant that will avoid overheating the tooth. Many different styles of burs are available, however this author prefers a cross-cut taper fissure bur (699 for cats and small dogs, 701 for medium dogs and 702 for large breeds). The best way to section the teeth is to start at the furcation and work towards the crown of the tooth. This method is used for two major reasons. First, it avoids the possibility of missing the furcation and cutting down into a root, which subsequently weakens the root and increases the risk of root fracture. In addition, this method avoids the possibility of cutting through the tooth and inadvertently damaging the gingiva or alveolar bone.

After the tooth has been properly sectioned, follow the above steps for each single rooted piece. In some cases, the individual tooth pieces can be carefully elevated against each other to gain purchase.

SURGICAL EXTRACTIONS The more difficult extractions are best performed via a surgical approach. This includes canine and carnassial (maxillary fourth premolar and mandibular first molar) teeth, as well as teeth with root malformations or pathology, and finally retained roots. A surgical approach allows the practitioner to remove a small amount of buccal cortical bone, promoting an easier extraction process. A surgical extraction is initiated by creating a gingival flap. This can be a horizontal flap along the arcade (an envelope flap) or a flap with vertical releasing incisions (a full flap). An envelope flap is created by releasing the gingival attachment with a periosteal elevator along the arcade including one to several teeth on either side of the tooth or teeth to be extracted. The gingiva along the arcade is released to or below the level of the mucogingival junction (MGJ) and the flap is connected by incising the gingiva in the interdental spaces. The advantage to this flap is that the blood supply is not interrupted and there is less suturing. The more commonly used flap includes one or more vertical releasing incisions. This method allows for a much larger flap to be created, which (if handled properly) will increase the defects which can be covered. The vertical incisions are created at the line angle of the target tooth, or one tooth mesial and distal to the target tooth. The incisions should be made slightly apically divergent (wider at the base than at the gingival margin). Furthermore, it is important that the incisions be created full thickness, in one motion (rather than slow and choppy). A full thickness incision is created by incising all the way to the bone, and the periosteum is thus kept with the flap. Once created, the entire flap is gently reflected with a periosteal elevator. Care must be taken not to tear the flap, especially at the muco-gingival junction. Following the flap elevation, a small amount of buccal bone should be removed (approximately 1/3 to Â˝ of the root length depending on the situation) to the depth of the root. This should only be performed on the buccal side. Next, the teeth should be sectioned if multirooted and the teeth then extracted as described above. After the roots are removed the alveolar bone should be smoothed and the defect closed. Closure is initiated with a procedure called fenestrating the periosteum. The periosteum is a very thin fibrous tissue which attaches the buccal mucosa to the underlying bone. Since the periosteum is fibrotic, it is inflexible and will interfere with the ability to close the defect without tension. The buccal mucosa however, is very flexible and will stretch to cover large defects. Consequently, incising the periosteum takes advantage of this attribute. The fenestration should be performed at the base of the flap, and must be very shallow as the periosteum is very thin. This step requires careful attention, as to not cut through or cut off the entire flap.

After fenestration, the flap should stay in desired position without sutures. If this is not the case, then tension is still present and further release is necessary prior to closure. Once the release is accomplished, the flap is sutured normally.

INTRODUCTION Periodontal disease is the number one medical condition in small animal veterinary medicine. We will begin this presentation with an overview of the pathogenesis as well as local and systemic effects of periodontal disease. This will give attendees the ability to improve client compliance with dental recommendations. In addition, a firm grasp of the disease process will improve practitioner understanding of proper treatment modalities. Due to the plethora of new and concerning information about this condition, treatment and prevention is the subject of significant research. This focus has resulted in numerous new products and procedures to prevent and treat periodontal disease and this presentation is designed as an introduction to these new and future therapies.

PERIODONTAL DISEASE OVERVIEW Periodontal disease is the number one health problem in small animal patients. By two years of age, 70% of cats and 80% of dogs have some form of periodontal disease. However, there are generally little to no outward clinical signs, and therefore therapy typically comes very late in the disease. Consequently, periodontal disease may also the most undertreated disease in our patients. Additionally, unchecked periodontal disease has numerous local as well as systemic consequences. Pathogenesis: Periodontal disease is generally described in two stages, gingivitis and periodontitis. Gingivitis is the initial, reversible stage in which the inflammation is confined to the gingiva. The gingival inflammation is created by plaque bacteria and may be reversed with a thorough dental prophylaxis and consistent homecare. Periodontitis is the later stage of the disease process and is defined as an inflammatory disease of the deeper supporting structures of the tooth (periodontal ligament and alveolar bone) caused by microorganisms. The inflammation results in the progressive destruction of the periodontal tissues, leading to attachment loss. This can be seen as gingival recession, periodontal pocket formation, or both. Mild to moderate periodontal pockets may be reduced or eliminated by proper plaque and calculus removal. However, periodontal bone loss is irreversible (without regenerative surgery). Although bone loss is irreversible, it is possible to arrest its progression. However, it is more difficult to maintain periodontally diseased teeth in comparison to healthy teeth.

Additionally, periodontal attachment loss may be present with or without active inflammation. Periodontal disease is initiated by oral bacteria which adhere to the teeth in a substance called plaque. Plaque is a biofilm, which is made up almost entirely of oral bacteria, contained in a matrix composed of salivary glycoproteins and extracellular polysaccharides. Calculus (or tartar) is basically plaque which has secondarily become calcified by the minerals in saliva. It is important to note that rough tooth surfaces will greatly increase the speed of plauq and calculus formation. Therefore any Plaque and calculus may contain up to 100,000,000,000 bacteria per gram. Bacteria within a biofilm do not act like free living or â&#x20AC;&#x153;planktonicâ&#x20AC;? bacteria; and in fact are 1,000 to 1,500 times more resistant to antibiotics than are planktonic bacteria. Plaque on the tooth surface is known as supragingival plaque. Once it extends under the free gingival margin and into the area known as the gingival sulcus (between the gingiva and the teeth or alveolar bone), it is called subgingival plaque. Supragingival plaque likely affects the pathogenicity of the subgingival plaque in the early stages of periodontal disease. However, once the periodontal pocket forms, the effect of the supragingival plaque and calculus is minimal. Therefore, control of supragingival plaque alone is ineffective in controlling the progression of periodontal disease. Initial plaque bacteria consists of predominately non-motile, gram-positive, aerobic facultative rods and cocci. Gingivitis is initiated by an increase in the overall number of bacteria, which is primarily motile gram negative rods and anaerobes. The specific plaque hypothesis is based on the fact that these few species are seen in virtually all cases of chronic periodontal disease. The bacteria in the subgingival plaque secrete toxins as well as metabolic products. Also produced are cytotoxins and bacterial endotoxins which can invade tissues on their own, and in turn cause inflammation to the gingival and periodontal tissues. This inflammation causes damage to the gingival tissues and initially results in gingivitis. Eventually, the inflammation can lead to periodontitis, i.e. the destruction of the attachment between the periodontal tissues and the teeth. In addition to directly stimulating inflammation, the bacterial metabolic byproducts also elicit an inflammatory response from the animal. White blood cells and other inflammatory mediators migrate out of the periodontal soft tissues and into the periodontal space due to increased vascular permeability and increased space between the crevecular epithelial cells. White blood cells fight the infection by phagocytizing bacteria, but may also release enzymes to destroy the bacterial invaders either by design or after their death. When released into the sulcus, these enzymes will cause further inflammation of the delicate gingival and periodontal tissues. In fact, the progression of periodontal disease is determined by the virulence of the bacteria combined with the host response. It is the host response that often damages the periodontal tissues. However, patients with deficient immune systems typically have more severe periodontal disease than those individuals in good health.

The inflammation produced by the combination of the subgingival bacteria and the host response damages the soft tissue attachment of the tooth, and decreases the bony support via osteoclastic activity. This causes the periodontal attachment of the tooth to move apically. The end stage of periodontal disease is tooth loss; however the disease has created significant problems prior to tooth exfoliation. Clinical Features: It is important to be familiar with normal features in order to identify abnormal findings. Normal gingival tissues are coral pink in color (allowing for normal pigmentation), and have a thin, knife-like edge, with a smooth and regular texture. In addition, there should be no demonstrable plaque or calculus on the dentition. The first obvious clinical sign of gingivitis is erythema of the gingiva. However, it is now known that the FIRST evidence of gingivitis is bleeding during brushing, probing, or after chewing hard/rough toys. Therefore it is important to realize that normal appearing teeth/gums can actually be infected. If the first stages of gingivitis are not treated, it will progress into edema, spontaneous bleeding, and halitosis. Halitosis is an important marker of periodontal disease in that it is often what the clients first perceive as periodontal disease. It is unfortunate that many clients still feel that halitosis (or doggy breath) is normal. Halitosis in veterinary patients is almost always secondary to periodontal disease and if noticeable by clients is generally seen in conjuction with ADVANCED periodontal disease. The development of halitosis in pets is almost always due to periodontal disease. As previously stated, periodontal disease is caused by an increase in anaerobic bacteria. Certain strains of tehse bacteria will digest protein as their energy source (generally provided by the host). Some amino acis contain sulfur and this metabolism creates products called volatile sulfur compounds (VSCs). One of these is hydrogen sulfide, which creates the â&#x20AC;&#x153;rotten egg smellâ&#x20AC;?. VSCs are proinflammatory and actually contribute to periodontal inflammation and attachment loss. Therefore, not only are the VSCs produced by periodontal disease, they also directly increase the level of periodontal disease. Consequently, control of halitosis should be part of the treatment. Gingivitis is typically associated with calculus on the involved dentition, but is primarily elicited by PLAQUE and thus can be seen in the absence of calculus. Alternatively, widespread supragingival calculus may be present with little to no gingivitis. It is critical to remember that calculus itself is essentially non-pathogenic. Therefore, the degree of gingival inflammation should be used to judge the need for professional therapy. As gingivitis progresses to periodontitis, the oral inflammatory changes intensify. The hallmark clinical feature of established periodontitis is attachment loss. In other words, the periodontal attachment to the tooth migrates apically. As periodontitis progresses, alveolar bone is also lost. On oral exam, there are two different presentations of attachment loss. In some cases, the apical migration results in gingival recession while the sulcal depth remains the same. Consequently, tooth roots become exposed and the disease process is easily identified on conscious exam. In other cases, the gingiva remains at the same height

while the area of attachment moves apically, thus creating a periodontal pocket. This form is typically diagnosed only under general anesthesia with a periodontal probe. It is important to note that both presentations of attachment loss can occur in the same patient, as well as the same tooth. As attachment loss progresses, alveolar bone loss continues, until tooth exfoliation in most cases. After tooth exfoliation occurs, the area generally returns to an uninfected state, but the bone loss is permanent. Severe local consequences: The most common of these local consequences is an oral-nasal fistula (ONF). ONFs are typically seen in older, small breed dogs; however they can occur in any breed as well as felines. ONFs are created by the progression of periodontal disease up the palatal surface of the maxillary canines however; any maxillary tooth is a candidate. This results in a communication between the oral and nasal cavities, creating an infection (sinusitis). Clinical signs include chronic nasal discharge, sneezing, and occasionally anorexia and halitosis. Definitive diagnosis of an oronasal fistula often requires general anesthesia. The diagnosis is made by introducing a periodontal probe into the periodontal space on the palatal surface of the tooth. Interestingly, this condition can occur even when the remainder of the patientâ&#x20AC;&#x2122;s periodontal tissues is relatively healthy (including other surfaces of the affected tooth). Appropriate treatment of an ONF requires extraction of the tooth and closure of the defect with a mucogingival flap. However, if a deep periodontal pocket is discovered prior to development of a fistula, periodontal surgery with guided tissue regeneration can be performed to save the tooth. Another potential severe consequence of periodontal disease can be seen in multi-rooted teeth, and is called a class II perio-endo abscess. This occurs when the periodontal loss progresses apically and gains access to the endodontic system, thereby causing endodontic disease via bacterial contamination. The endodontic infection subsequently spreads though the tooth via the common pulp chamber and causes periapical ramifications on the other roots. This condition is also most common in older small and toy breed dogs, however, this author has personally treated a case in a Labrador Retriever. The most common site for a class II perio-endo lesion to occur in small animal patients is the distal root of the mandibular first molars. The third potential local consequence of severe periodontal disease is a pathologic fracture. These fractures typically occur in the mandible (especially the area of the canines and first molars), due to chronic periodontal loss, which weakens the bone in affected areas. This condition is again, most commonly seen in small breed dogs, mostly because their teeth (especially the mandibular first molar) are larger in proportion to their jaws as in comparison to large breed dogs. Pathologic fractures occur most commonly as a result of mild trauma, or during dental extraction procedures. Although this is typically considered a disease of older patients, this author has personally treated three cases in dogs less than three years of age. Pathologic fractures carry a guarded prognosis for several reasons including: lack of remaining bone, low oxygen tension in the area, and difficulty in rigidly fixating the caudal

mandible. There are numerous options for fixation, but the use of wires, pins or plates is generally required. Regardless of the method of fixation, the periodontally diseased root (s) MUST be extracted. Awareness of the risk of pathologic fractures can help the practitioner to avoid problems in at risk patients during dental procedures. If one root of an affected multi-rooted tooth is periodontally healthy, there is an even greater chance of mandibular fracture due to the increased force needed to extract the healthy root. An alternate form of treatment for these cases is to section the tooth, extract the periodontally diseased root, and perform root canal therapy on the periodontally healthy root. In cases where periodontitis involving a mandibular canine or first molar is identified during a routine prophy, it is best to inform the owners of the possibility of a jaw fracture prior to attempting extraction of the offending tooth. The fourth local consequence of severe periodontal disease results from inflammation close to the orbit which could potentially lead to blindness. The proximity of the tooth root apices of the maxillary molars and fourth premolars, places the delicate optic tissues in jeopardy. In cats, the apices of the maxillary canines lie in this area and can create similar issues. The fifth local consequence is described in recent studies which have linked chronic periodontal disease to oral cancer. The association in this case is likely due to the chronic inflammatory state that exists with periodontitis. The final significant local consequence of periodontal disease is chronic osteomylitis, which is an area of dead, infected bone. Dental disease is the number one cause of oral osteomylitis. Furthermore, once an area of bone is necrotic, it does not respond effectively to antibiotic therapy. Therefore, definitive therapy generally requires aggressive surgical debridement. In some cases, the bacterial infection may also result in a septicemia. In one case treated by this Periodontal Therapyauthor, the patient presented with an entire hemi-mandible which was necrotic secondary to osteomylitis. In this case, the patient required a complete hemimandibulectomy. Severe systemic manifestations: Systemic ramifications of periodontal disease are also well documented. The inflammation of the gingiva and periodontal tissues that allows the bodyâ&#x20AC;&#x2122;s defenses to attack the invaders also allows these bacteria to gain access to the body. Recent animal studies suggest the possibility that these bacteria negatively affect the kidneys and liver, leading to decrease in function of these vital organs over time. Furthermore, it has also been suggested that these bacteria can become attached to previously damaged heart valves (IE valvular dysplasias) and cause endocarditis, which in turn can result in intermittent infections, and potentially thromboembolic disease. Other studies have linked oral bacteremias to cerebral and myocardial infarctions and other histological changes. Additional human studies have linked periodontal disease to an increased incidence of chronic respiratory disease (COPD) as well as pneumonia. There are many studies that strongly link periodontal disease to an increase in insulin resistance, resulting in poor control of diabetes mellitus as well as increased

severity of diabetic complications (wound healing, microvascular disease). Additionally, it has been shown that diabetes is also a risk factor for periodontal disease. Periodontal disease and diabetes are currently viewed as having a bidirectional interrelationship where one worsens the other.

PERIODONTAL THERAPY “New” methods and products for periodontal disease treatment and prevention can be grouped into three different treatment areas: 1) Control the infection (pathogen control) 2) Decrease the amount inflammation and/or bone destruction by the host (host modulation) 3) Re-grow lost bone (guided tissue regeneration) 4) Extraction (the ultimate pathogen control)

PATHOGEN CONTROL It is well known that periodontal disease is initiated by plaque bacteria. Therefore, the basis for periodontal therapy is, and likely always will, be plaque control. This is best achieved by a combination of thorough professional therapy and home care. A. Complete dental prophylaxis including the following steps: 1. Pre-surgical exam a. Decreases “suprises” under anesthesia 2. Proper and balanced anesthesia 3. Supragingival scaling a. Generally with a ultrasonic scaler b. Remember when 2-mm are worn away need to replace 4. SUBgingival scaling a. Generaly with a curette or SUBGINGIVAL tip b. Hand instruments MUST be sharp (www.dogbeachvet.com) 5. Polishing 6. Sulcal lavage 7. Oral exam and charting a. Niemiec color coded probes can help

8. Dental radiology a. Vetdentalrad.com for interpretation help

B. Homecare On the professional side there is now several barrier sealant available with evidence of decreasing periodontal disease. It is especially valuable post-surgery. This is because dental disease recurs so quickly and most homecare methods need to be suspended for 2 weeks during healing. Therefore, this barrier (which is ideally combined with the homecare version) provides a “bridge” between the professional therapy and homecare. As far as homecare is concerned, tooth brushing is still the gold standard. Educate your clients early about the benefits and compliance will increase. Antiseptics such as chlorhexidine and zinc ascorbate can be good adjunct therapy. As far as “passive” methods of homecare are concerned, only most products have only been proven to decrease plaque and calculus. This may or may not indicate true effectiveness against periodontal disease. This is because the decrease may be at the incisal edge to middle of the tooth. The ideal test to determine effectiveness of a product is gingivitis reduction. However, a label for gingivitis is no longer allowed and therefore the only evidence is that which supports a decrease in plaque and calculus accumulation. Rawhide chews as well as other chew treats have also been shown to be effective in this way. However, many products do not have published peer reviewed studies. Finally, added CHX has not been shown to increase effectiveness. However, one aspect of periodontal disease which CAN be evaluated and reported is halitosis control. Since halitosis is almost always due to periodontal disease, reduction in halitosis should be related to a decrease in periodontal disease. One of the downfalls of all chew based plaque control mechanisms is that they only work on the chewing teeth. Therefore, the canines and incisors (as well as small premolars) are not effectively cleaned. This may be ameliorated by brushing the front teeth, but this again required client compliance. There is a new chew with a plaque control agent called demopinol. The mechanism of action of this product is to decrease the ability of plaque to form, and is therefore not a true antiseptic. By delivering the product around the mouth, it has the ability to be a chew based treat that helps the entire dentition.

C. Periodontal Surgery The other “new” form of pathogen control should be periodontal surgery. As discussed in the last article, pockets greater than 3-mm are pathologic and in need of therapy. All pockets between 3 and 6-mm should be treated with closed root planing and ideally the administration of a sustained release local antimicrobial. Pockets greater than 6-mm or

furcation level II and III require periodontal flap surgery to effectively clean the root surface and allow for reattachment and infection control. These procedures can be learned by a general practitioner and require minimal investment in equipment. If this is not an option, these teeth should be extracted.

BONE REGENERATION Regenerating bone lost via periodontal disease is another weapon in the fight against periodontal disease. The technique of guided tissue regeneration (GTR) has been around for decades, but recent advances in barriers and bone grafting has markedly improved the success rates. Regardless, there are only a handful of conditions which carry a good prognosis for bone regeneration. The best prognosis is seen with 3-walled periodontal pockets (typically seen on the palatal aspect of the maxillary canine and distal aspect of the distal root of the mandibular first molar) and class II furcation lesions. Since these are quite common in small breed dogs, there are a large number of patients who would benefit from these procedures. The theory of GTR is that the down growth of faster healing soft tissue must be prevented to allow the slower growing bone and periodontal ligament to repopulate the periodontally induced bony defect. GTR involves creating a periodontal flap and performing open root planning to create a clean root surface for healing. After this is accomplished, the defect is filled with bone augmentation and a barrier membrane placed. There are numerous products currently utilized on the human side, however currently the products of choice for most veterinary dentists are cancellous freeze-dried demineralized bone for the graft and demineralized laminar bone sheets as the membrane.

Suggested readings: Veterinary Periodontology (Niemiec BA Ed) Wiley Blackwell, Ames. 2013. DeBowes L: Problems with the gingiva. In: Small Animal Dental, Oral and Maxillofacial Disease--A Color Handbook, (Niemiec BA ed) Manson Publishing Ltd, London 2010 Dental Extractions made Easier, (Niemiec BA Editor) Practical Veterinary Publishing, San Diego CA For educational videos of periodontal disease please visit www.dogbeachdentistry.com For hands on training in periodontal therapy and extractions please visit www.vetdentaltraining.com

Orthodontic (bite) problems Orthodontic problems are not unusual in dogs, but are fairly uncommon in cats. They may be purely cosmetic or can result in trauma to the lips, gums, palate, or teeth. By far, the most common cause of malocclusions is hereditary. Additional genetic causes include tongue size as well as lip and cheek tension. These patients often do not show any overt clinical signs other than the jaws or teeth being out of alignment. Depending on the type and severity of the problem, oral trauma may be present and can result in bleeding, oral pain, gum disease, tooth death and even nasal infection. Therapy for malocclusions is relative to type and severity of the disease process. Options include:    

No therapy (if purely cosmetic). Extraction of the offending tooth or teeth. Orthodontic correction using appliances. Lowering the tooth and then protecting the root canal (Coronal amputation and vital pulp therapy)

Strictly cosmetic correction is certainly possible; however it may not in the patient’s best interest. The pain associated with orthodontic adjustment, and the numerous anesthetics required, often makes orthodontic therapy a disservice to the otherwise healthy patient

Persistent deciduous teeth Persistent deciduous teeth are very common, especially in small and toy breed dogs. However, they can occur in any breed as well as cats. They create both orthodontic and periodontal problems if not treated promptly. It used to be believed that the persistent deciduous caused the permanent tooth to become malocclused. Studies have shown, however, that it is the permanent tooth erupting incorrectly that causes the deciduous to be persistent. It has been reported that orthodontic problems begin within two weeks of the permanent canines starting to erupt. This is due to the deciduous tooth being in the place that the adult wishes to occupy.

The periodontal issues occur due to a disruption of the normal maturation of the periodontium. When there is a persistent deciduous tooth, one area of the periodontium is not attaching to the permanent, therefore the periodontal attachment in that location will not be normal. It has been reported that the damage begins within 48 hours of the permanent teeth starting to erupt! Therefore, the adult tooth does not need to be completely erupted for these problems to occur, and they should be extracted as early as possible, do not wait until six months of age to perform the extractions along with neutering. In fact, we recommend that the owners of breeds prone to retain their teeth be instructed to watch for eruption of the permanent teeth and to present the patient for therapy as soon as this occurs.

Rotated and Crowded Teeth Rotated and crowded teeth can occur alone, in which case the malocclusion is classified as class 1, or in combination with other malocclusions. Rotated and/or crowded conditions can occur in a single tooth, in multiple teeth, or in any combination of teeth (incisors, canines, premolars and molars). It is not uncommon to find crowded mandibular incisors in brachycephalic breeds. Another common finding in many breeds, but especially in brachycephalics, is maxillary third premolars crowded with maxillary fourth premolars or the mandibular fourth premolars crowded with first molars. The maxillary third and mandibular fourth premolars are usually also rotated in this condition. Other common conditions include incisors crowded together but also against the canine teeth. Finally, impaction of the distal shoulder of the maxillary third premolar into the furcation of the mesiobuccal and mesiopalatal roots of the fourth premolar is often seen in brachycephalic breeds. Dogs with small jaws commonly have incisor crowding. This has been assumed to be an inherited condition. Often the second incisor on both sides on the mandible will be displaced out of the normal curve. Also, third incisors can be crowded with canines and maxillary premolars can be crowded together. Commonly recommended treatments for some of the most frequently found crowding situations include extraction of the lateral incisors to protect the canines, extraction of the maxillary third premolars to save the maxillary fourth premolars, or extraction of one or more of the more crowded mandibular incisors. Rotation and crowding can cause pain from chronic tooth on tooth contact. This might be compared to the pain that humans experience from a caries that has been overfilled by their dentist, resulting in trauma to the opposing tooth during mastication. It is a condition that generally does not result in clinical signs of pain or anorexia; however, it can be quite painful. The chronic trauma resulting from tooth on tooth contact can lead to tooth non vitality. Non vital teeth must be either extracted or receive endodontic therapy. Periodontal disease is commonly an eventual result of rotated and crowded teeth. Although human studies have shown that, with good home care, teeth can be maintained with some attached gingival lacking, a complete collar of attached gingiva around each tooth is ideal for ongoing periodontal health. This is often lacking for the rotated/crowded tooth. With these normal gingival attachments absent, the tooth is more prone to periodontal disease. On the

maxilla, rotation situates the tooth in an abnormal position relative to the mucosa of the hard palate, often creating a pseudopocket that can trap food and debris. This can further complicate the lack of attached gingiva that is also a result of its rotation. Furthermore, crowding can result in a lack of interdental papilla, a part of the normal gingival collar between two teeth. Without this protective collar, both teeth are susceptible to periodontal disease. Teeth affected by rotation and crowding have lowered defenses to periodontal disease because of their ability to trap food, plaque, and calculus resulting in early onset of infection and inflammation.

Fractured teeth The two main types of crown fracture seen in veterinary medicine are complicated and uncomplicated. Both types require therapy; however treatment for each is often different. The tooth crown is made up of 3 layers. The innermost layer is the pulp chamber (an extension of the root canal). It is filled with blood vessels and nerves that originate from the maxillary or mandibular artery and nerve. The outermost layer is called enamel. It is 97 % inorganic material. It has no sensory ability; however it also has no ability to regenerate if lost. Between the pulp chamber and the enamel is dentin. Dentin makes up the majority of tooth structure in mature patients. Dentin is a living structure in that it has the ability to respond to stresses and has sensory ability. This sensory ability is due to the fact that there are dentinal tubules which run at right angles to the root canal system ending at the dentinal-enamel junction (DEJ). There are 45,000 tubules per mm2 in coronal dentin. This means that a defect 1 cm in diameter will result in the exposure of 1,000,000 odontoblasts. The hydrodynamic mechanism of dentin hypersensitivity is the currently accepted explanation for pain associated with dentin exposure. Dentin exposure changes the fluid dynamics within the tubules. This change in fluid velocity is translated into electrical signals by the sensory fibers located within the tubules or subjacent odontoblast layer. These signals result in the sensation of pain (or sensitivity) within the tooth. It is rare for veterinary patients to show this discomfort, but occasionally anorexia will be the presenting complaint. Finally, the exposed dentinal tubules may act as a conduit for bacterial infection of the pulp, thus initiating endodontic disease. Over time, the tooth will respond to this exposure by laying down a layer of reparative dentin. There is no study that documents the time for an effective layer to be placed in veterinary patients. One human study found that reparative dentin is seldom found prior to 30 days following exposure of dentinal tubules and completion of formation is generally around 130 days. It is not known however, if this layer of reparative dentin is effective in decreasing tooth sensitivity. All teeth with direct pulp exposure (complicated crown fractures) should be treated with endodontic or exodontic therapy; ignoring them is NOT an option. Prior to tooth necrosis, the viable nerve is excruciatingly painful. Following tooth death, the root canal system will act as a bacterial super-highway creating not only local infection, but also a bacteraemia which has been linked to more serious systemic diseases (see the article on periodontal

disease for further information). The owners of these patients will be reluctant to pursue therapy as â&#x20AC;&#x153;It does not seem to bother the dogâ&#x20AC;?. Fractured and/or infected teeth do bother the pet and they will act better following therapy. Veterinary patients are known for being stoic, and therefore lack of outward signs of oral pain should not be misinterpreted as a benign state. Therefore, you must be a patient advocate and recommend therapy. Uncomplicated crown fractures are also a very common finding on oral exam, particularly in large breed dogs. These fractures will result in direct dentinal exposure. The exposed dentinal tubules will create significant pain for the patient. The currently accepted means by which this sensitivity is created is via the theory of fluid dynamics. In addition, some of these teeth will become non-vital due to the traumatic incident, pulpal inflammation, or direct pulpal invasion via the dentinal tubules. For these reasons, it is recommended that these teeth be radiographed to ensure vitality. If the teeth are non-vital (evidenced by periapical rarefaction or a widened root canal) endodontic or exodontic therapy is required. If the teeth appear vital, the application of a bonded composite is recommended to decrease sensitivity (please see the article on composite bonding later in the issue for further information). Intrinsically stained teeth: Endodontic disease is also manifested by intrinsic staining. This can appear as pink, purple, yellow, or grey. A study by Hale showed that only 40% of intrinsically stained teeth had radiographic signs of endodontic disease, however 92.7% are non-vital. Non-vital teeth lose their natural defence ability and are often infected via the bloodstream, which is known as anachorisis. Therefore, do not rely on radiographic appearance to determine vitality; all teeth should be definitively treated via root canal therapy or extraction. Caries: True bacterial caries are rare in dogs and almost unheard of in cats. They are most common on the occlussal surface of the upper first molars, but can be seen on any tooth. In addition, the most common breed is a German Shepherd dog. Early lesions can mimic wear, and are best diagnosed by tactile feel of the defect with a sharp explorer. If it is sticky, like wax, it is likely a caries lesion. These lesions can progress into the endodontic system resulting in pain and infection (see fracture teeth above). Treatment options are restoration (composite or amalgam) or crown therapy (+/- endodontic therapy); or extraction.

Enamel hypocalcification (hypoplasia) Enamel is a very thin (<1mm) material on the surface of tooth crowns. It is formed and deposited on the dentin by the enamel forming organ which consists of cells called ameloblasts. Enamel is only formed prior to tooth eruption and cannot be naturally repaired after eruption into the mouth. Hypoplasia/hypocalcification results from disruption of the normal enamel development. Ameloblasts are very sensitive and minor injuries can result in enamel malformation. The most common acquired cause of enamel hypocalcification of one or several teeth is trauma to the unerupted tooth. This may be due to any external trauma, but is most often

associated with the extraction of a deciduous tooth. In traumatic cases, one or several adjacent teeth may be affected. Additional causes of this pattern are infection or inflammation from a deciduous tooth. A severe systemic infectious or nutritional problem may also result in improper enamel production. In these cases, most or all of the teeth are affected, but only a small part of the crown, usually a horizontal circumferential strip. Canine distemper was a common cause of this condition in the past. Finally, enamel hypoplasia may result from a hereditary condition known as amelogenesis imperfecta. This condition is created by a decrease in the amount of enamel matrix applied to the teeth during. In these cases, nearly all teeth are involved on all surfaces. Areas of enamel hypocalcification will generally appear stained a tan to dark brown (rarely black) color, and may appear pitted and rough. The tooth surface is hard however, as opposed to the soft/sticky surface of a caries lesion. The areas of weakened enamel are easily exfoliated which will expose the underlying dentin, resulting in staining. Dentin exposure will result in significant discomfort for the patient (see uncomplicated crown fractures above). The roughness of the teeth will also result in increased plaque and calculus retention, which in turn leads to early onset of periodontal disease. For all of these reasons, prompt therapy of these teeth is critical to the health of the patient. Treatment is aimed at removing sensitivity, avoiding endodontic infection by occluding the dentinal tubules, and smoothing the tooth to decrease plaque accumulation. The most efficient and effective way to accomplish these goals is placement of a bonded composite restoration. If the damage is severe and the client is interested in a permanent correction, crown therapy can be performed. Alternatively, extraction may be performed; however this is not the recommended course of therapy if the root structure is normal with no evidence of endodontic infection. Feline Tooth resorption: TRs are a very common malady. Reports vary as to their incidence, but approximately 60% of cats over 6 years of age have at least one, and those that have one typically have more. These lesions are caused by odontoclasts which are cells that are responsible for the normal remodelling of tooth structure. These cells are activated and do not down regulate, resulting in tooth destruction. There are currently two recognized forms of resorptive lesions, type 1 and type 2. Clinically, they appear very similar, as dental defects that are first noted at the gingival margin. However, advanced cases will show significant tooth destruction and may appear to be a fractured tooth. The best diagnostic tool for differentiating between types is dental radiology. With type 1 lesions, there is no replacement of the lost root structure by bone, whereas with type 2 there is generally marked replacement of the lost tooth structure.

Type 1 TRs are typically associated with inflammation such as L/P stomatitis or periodontal disease. In these cases, it is thought that the soft tissue inflammation has activated the odontoclasts. The inciting cause of class 1 lesions is a cemental defect. Odontoclasts move in and destroy the dentin, leading to secondary enamel loss and a resorption lacuna. The weakened crown will eventually fracture, and in these cases the root canal system stays intact resulting in continued pain and infection for the patient. Type 2 lesions are generally seen in otherwise healthy mouths; however the lesions will create local gingivitis. The etiology of type 2 TRs remains unproven. The two major current theories are abfraction injuries from eating hard food and excess vitamin D in the diet. Type 2 TRs show histological evidence of simultaneous repair of the defect by osteoblasts at the same time that tooth is being resorbed by odontoclasts. Historically, restoration was a recommended therapy, however due to the progressive nature of the disease; extraction is now the treatment of choice. Extractions can be very difficult in these cases due to tooth weakening and ankylosis. Additionally, in some cases, there is little to no tooth structure remaining. In cases with significant weakening and or ankylosis, performing the extractions via a surgical approach is recommended to speed the procedure and decrease the incidence of fractured and retained roots (see extraction article). Recently, crown amputation has been suggested as an acceptable treatment option for advanced type 2 lesions as it results in significantly less trauma and faster healing than complete extraction. This procedure, although widely accepted, is still controversial. Most veterinary dentists employ this technique, however in widely varying frequency. Veterinary dentists typically employ this treatment option only when there is significant or complete root replacement by bone. Unfortunately, the majority of general practitioners use this technique far too often. Crown amputation should only be performed on teeth with radiographically confirmed advanced type 2 TRs which show no peri-apical or periodontal bone loss. Crown amputation should not be performed on teeth with: type 1 TRs, radiographic or clinical evidence of endodontic or periodontal pathology, inflammation, or infection; or in patients with L/P stomatitis. Those practitioners without dental radiology capability SHOULD NOT perform crown amputation. In these cases, the teeth should either be fully extracted or the patient referred to a facility with dental radiology.

Missing teeth There are several reasons that teeth may be missing. These reasons include: congenitally missing, previously extracted, fractured (or extracted) with retained roots, or impacted. The first two scenarios do not require therapy, where as the latter two may necessitate intervention. Therefore, dental radiographs are indicated in all cases of “missing teeth”. If dental radiographs reveal retained roots and evidence of inflammation or infection (clinical or radiographic), the teeth should be surgically extracted. If they are “quiet”, the owners should be informed and given the option of having the teeth surgically extracted.

Impacted teeth are defined as any tooth that has not erupted by its normal time. This is generally considered to be the time when the surrounding or contralateral teeth have already erupted. The most common cause of impaction is the presence of an overlying structure that interferes with normal eruption. These structures may be bone, soft tissue, or even tooth/teeth that interfere with the normal eruption path. The most common interference is an area of thick and firm gingiva called an operculum. Impactions occur most commonly in the maxillary cuspid and premolar teeth (especially PM1). They also occur most often in toy and small breeds as well as brachycephalic dogs. These patients generally have no overt clinical signs other than a missing tooth in a young animal. Alternatively, there may be a persistent deciduous tooth present. On occasion, an unerupted tooth may lead to the development of a dentigerous cyst. The incidence of this is unknown in veterinary medicine; however pathologic changes were noted in 32.9% of cases in one human study. Consequently, the presenting complaint or oral examination finding may be a swelling in the area of a â&#x20AC;&#x153;missingâ&#x20AC;? tooth. A dentigerous cyst is a fluid filled structure which develops from the enamel forming organ, of an unerupted tooth. Small dentigerous cysts are generally asymptomatic, and often go undiagnosed without dental radiology. If clinical, these cysts will generally be seen as swellings in the area of a missing tooth in a young patient. Dentigerous cysts can become quite large and disfiguring, requiring major surgical correction. In addition, these cysts may become infected, resulting in acute swelling and pain. These cases are often misdiagnosed as abscesses. Finally, dentigerous cysts have reportedly to undergone neoplastic transformation. Dental radiographs are generally diagnostic, revealing a unilocular radiolucent area that is associated with the crown of an unerupted tooth. An aspirate obtained for fluid analysis and cytology will be supportive of a cyst. Definitive diagnosis can be achieved with histopathologic analysis of the cystic lining. Prognosis for these lesions is excellent if diagnosis and treatment are achieved relatively early in the disease course. Surgical removal of the offending tooth and careful debridement of the cystic lining will prove curative. It is important to avoid leaving any of the cystic lining behind, as this could allow the cyst to reform. Early surgical intervention will result in the least invasive surgery possible.

Oral neoplasia The oral cavity is the fourth most common place to encounter neoplastic growths. The most common oral growths are the epulids (fibromatous and ossifying). These are benign overgrowths of the periodontal ligament (harmatomas). These can grow very large, but are not aggressive. Acanthomatous Ameiloblastomas (epulids) are locally aggressive. They do not metastasize and are mildly aggressive locally. They respond well to local excision with Â˝ cm margins and enjoy a 90% control rate with radiation therapy.

Benign tumors are exceedingly rare in cats. By far the most common malignant oral tumor in cats is a squamous cell sarcoma. Fibrosarcomas are a distant second. Both of these tumors are typically seen in older cats, are locally aggressive, and are late to metastasize. The only therapeutic option at this point is early, aggressive surgery (2 cm surgical margins). The above tumors are also seen in dogs. Their behaviour and therapy is similar to cats, however these tumors respond better to radiation therapy in dogs. In dogs, the most common malignant tumor is a melanoma which is typically seen in older dark pigmented dogs. Melanomas are not only locally aggressive; they also metasitizes very early in the course of the disease. A combination of aggressive surgery, radiation therapy, and chemotherapy is the best way to treat this disease process. In addition, a vaccine has been recently released that shows promise as an adjunct therapy for this disease process.

Eosinophillic Granuloma Complex The true etiology of these conditions is unknown; however a local accumulation of eosinophils is thought to initiate the inflammation and necrosis. The accumulation may result from a local (food) or systemic allergies; although these lesions have been seen in cases where allergic disease has been ruled out. Additional causes include a response to irritation, such as chronic grooming or traumatic malocclusion. There may also be a genetic predisposition. Indolent Ulcers are the most common oral manifestation, and they will present as brownishred lesions on the upper lip or around the maxillary canine teeth. Linear granulomas can be single or multiple; the most common sites are the lips, gingiva, palate and tongue. They are generally non-painful, but can become secondarily infected. The typical presentation is a raised, lobulated yellow-pink mass; however, they can also appear ulcerative causing severe damage to the oral mucosa and underlying bone. This may lead to severe periodontal loss, pathologic fractures, or oronasal fistulas.

Caudal Stomatitis This is another relatively recent disease process in cats that is frustrating us at present. The best description is a severe immune mediated reaction to dental tissues, but we really donâ&#x20AC;&#x2122;t know. Some feel that this may actually be a group of disease processes that look the same clinically which is why they can be very frustrating to treat. The history will generally include anorexia, drooling, gagging, and pain during mastication. Physical exam will typically include a thin pet with unkempt fur. The oral exam will reveal severe stomatitis usually over all teeth. The inflammation will most commonly be worse on cheek teeth than canines and incisors. However, faucitis is the key clinical finding. Severe hyperplastic inflammation to the gingiva can result from periodontal disease, however faucitis will not be present.

Medical Therapy: Most medical therapies will work for a while, however in general resistance will start within a year or less. In addition, most therapies have side effects worse than the disease process in and of itself. In general, medical therapy is very frustrating to the practitioner and client. Corticosteroids are the mainstay of most medical therapy today. It is generally very effective at first and is relatively inexpensive for the client. In my experience, injectable (depomedrol 5-10 mg IM) is much more effective than oral preparations in my experience. However, they will typically loose effectiveness after a year or so requiring higher and higher doses at shorter increments. This generally results in significant deleterious effects. About 10% of stomatitis cases we treat are already diabetic!!! Antibiotics are safer than steroids but much less effective, especially in long term therapy. They are generally disappointing in their success. Metronidazole and clindamycin are the mainstays of therapy; however Clavamox and amoxicillin can be used as well. Metronidazole may be the antibiotic of choice due to its anti-inflammatory effect. Other immune suppressive such as Imuran, Cytoxan, Gold Salts, Cyclosporine have been used. However, they are all very expensive with numerous adverse side effects (mylosuppression). Surgical Therapy: Extraction is currently the ONLY effective long term treatment for this disease process in cats. In our experience, the sooner this is done, the better that cats do both post-operatively as well as long term. For extractions to be successful, the teeth must be COMPLETELY removed. Therefore postoperative radiographic confirmation of complete extraction of the tooth roots is recommended. Following the insurance of complete removal of the teeth, perform aveloplasty to remove the periodontal ligament and smooth rough bony edges. This is typically performed do this with a rough diamond bur. Studies report a 60% success rate when all teeth caudal to the canines are extracted, however our experience has not been as good. However, whole mouth extractions have a success rate of approximately 90-95% for clinical remission. Slight faucitis may remain, but pets are comfortable. In addition, the rare cases that donâ&#x20AC;&#x2122;t completely respond are generally much more responsive to medical therapy. If there is NO inflammation to the canines or incisors (which is rare), then the owner is given the option of leaving the canines. However, if these are inflamed, all teeth should be extracted. If the teeth are ankylosed, complete root pulverization may be necessary.

Canine Atopic Dermatitis (CAD) is a genetically predisposed inflammatory and pruritic allergic skin disease with characteristic (but not pathognomonic!) clinical features. It is associated with IgE antibodies to environmental (most commonly) or food allergens. CAD is a clinical diagnosis, meaning you don't need any specific allergy tests to be sure your patient is atopic, all you need â&#x20AC;&#x201C; good anamnesis, thorough clinical examination and, in some cases, elimination of other similarly looking pruritic dermatoses. Typical atopic patient is a young (6 months to 3 years) dog with chronic year-round (less commonly seasonal) pruritus, which can include scratching, licking, rubbing, chewing, scooting, and/or head shaking. At the beginning pruritus may be alesional or associated with primary skin lesions such as erythema and occasionally papules, but continuous inflammation, self-trauma, bacterial and yeast infections will lead to secondary skin lesions such as excoriations, alopecia, scaling, crusting, lichenification and hyperpigmentation. Face (eyelids, lips and chin), concave surface of pinna and ear canal, axillae, groin, perineal area and distal extremities are most commonly affected, but breed-associated variations of atopic body sites have also been identified. If your patient had already received antipruritic treatment the owner may report good answer to local and systemic glucocorticosteroids, oclaticinib. Very often atopic dogs were already treated against skin parasites, bacterial and yeast infections, but the responce was absent or short and/or insufficient. Main differential diagnoses for atopic dermatitis are parasitoses (fleas and flea allergy dermatitis, otodectosis, sarcoptosis, demodicosis, cheyletiellosis, lice infestation, trombiculiasis, pelodera dermatitis), and skin infections (staphylococcal pyoderma, Malassezia dermatitis) secondary to other than CAD dermatoses. Basic diagnostic tests, which may be required to rule out most common differentials are flea combing, skin scraping, hair plucking and cytological examination of skin and ear samples.

Parasites, especially Sarcoptes scabiei var. canis and fleas, can be difficult to find and antiparasitic trial treatment may be necessary to rule them out. When other pruritic dermatoses are excluded and your definitive diagnosis is CAD, next step would be to rule out food allergy, which can be clinically indistinguishable from environmental allergy. It can be done with 6-8 weeks of elimination diet trial with food ingredients the dog has never been exposed before. Food allergy is confirmed if there is an improvement on elimination diet, a relapse during provocation (re-challenge with an original diet) and improvement again with reinstitution of the elimination diet.

Many skin diseases have (proven or suspected) hereditary nature. Usually it reflected in certain breed(s) predisposition. Genetic skin diseases (genodermatoses) may be congenital (present at birth or soon after) or not (animal will become clinically affected later in life). Some genodermatoses that are caused by mutation in one gene only (monogenic, also called mendelian) are possible to diagnose with a DNA test. And not only to diagnose a disease in a sick animal but also to find out clinically healthy carriers of a mutation before including them in a breeding program. Required sample material for a genetic test – EDTA blood sample (best choice!), cheek swabs, hair or tissue samples, semen. It can be shipped to the diagnostic laboratory at room temperature. As vast majority of dermatoses, for which genetic testing is offered, are inherited with autosomal recessive trait, most common test results are «clear» (N/N or homozygous wildtype), «carrier» (N/n or heterozygous), and «affected» (n/n, or homozygous mutant). In case of dominant mode of inheritance the heterozygous animal (N/n) will be affected. Affected (if an animal was tested early in life and the disease is not congenital, it could be clinically healthy yet) should not be used for breeding. Carriers may be excluded from breeding or used wisely (not in a pair with another carrier). Theoretically, DNA test should have 100% sensitivity and 100% specificity, but false-positive and false-negative results are possible (sample mix-ups, contamination, wrong breed tested etc). Causative mutations have been identified for quite a number of genodermatoses and each year we have new discoveries. There is the list of genodermatoses (and some systemic diseases with skin involvement) currently available for DNA testing (note, that they are mainly canine diseases, except last one): • • • •

Anhidrotic ectodermal dysplasia (German Shepherd dog) Ectodermal dysplasia (Chinese crested, Mexican hairless dog, Peruvian hairless dog) Ectodermal dysplasia/skin fragility syndrome (Chesapeake Bay retriever) Epidermolysis bullosa dystrophic (Golden retriever)

• • •

• • • • • • • • • • • • • • •

Epidermolysis bullosa junctional (German pointer) Epidermolytic hyperkeratosis, aka ichthyosis (Norfolk terrier) Hereditary sensory neuropathy, aka acral mutilation (English Cocker Spaniel, French Spaniel, English Springer Spaniel, English Pointer, German Shorthaired Pointer) Ichthyosis (Golden retriever, American bulldog, Great dane, Jack Russell terrier) Keratoconjunctivitis sicca and ichthyosiform dermatosis (Cavalier King Charles spaniel) Excessive mucin (hyaluronosis) and predisposition to perodic fever, aka autoinflammatory disease (Sharpei) Footpad hyperkeratosis (Irish terrier, Kromfohrlander) Congenital hypothyroidism with goiter (many terrier breeds) Color linked follicular dysplasia (only for originally non-diluted colors, e.g. Large munsterlander) Dermoid sinus (Rhodesian ridgeback, Thai ridgeback) Dermatomyositis, only risk assessment (Collies, Shelties) Lethal acral dermatitis (Bullterrier) Musladin-Lueke syndrome (Beagle) Nasal parakeratosis (Labrador retriever) Oculocutaneous albinism (Doberman) Pituitary dwarfism (German shepherd dog, Saarloos wolfhound, Karelian Beardog, Czechoslovakian Wolfdog) Renal cystadenocarcinoma and nodular dermatofibrosis (German Shepherd dog) Hairlessness with short life expectancy (Birman cats)

Good way to be updated with currently known mutations – to check the list on Online Mendelian Inheritance in Animals website (www.omnia.org). Easy to find appropriate laboratory using search provided by the University of Pennsylvania's School of Veterinary Medicine http://research.vet.upenn.edu go to “available tests“, then to “tests available at labs worldwide“.

Allergen immunotherapy (AIT) is the only causative treatment for canine atopic dermatitis. Traditionally, allergen extract was administered subcutaneously in slowly increasing amount and concentration over an induction period of several weeks to months until a maintenance therapy was reached. More recently rush immunotherapy (RIT) was described, where the induction period is abbreviated to one day with injections administered every 30 minutes. The patient is sent home on maintenance therapy, typically one injection every three to four weeks. The time to maximal improvement is abbreviated and there is less chance of confusing doses with RIT. Adverse effects such as increased anaphylactoid reactions seen in humans undergoing RIT are rare in dogs. The newest type of immunotherapy is intralymphatic AIT, where allergens are injected (in much smaller amounts) into the lymphnode. In the published studies using intralymphatic AIT in dogs, the therapy was safe, but not as long lasting as in humans and the success rate does not seem to be higher than that of conventional AIT, although direct comparisons are lacking. For years, glucocorticoids, fatty acids and antihistamines were the mainstay of symptomatic therapy for CAD. Cyclosporine, a calcineurin inhibitor, was evaluated in a number of studies and proved to be as efficacious as prednisolone, although it took a few weeks for optimal improvement. It is given at 5 mg/kg daily and in more than half of the patients the drug can be tapered to every other day or even (in a quarter of dogs) to twice weekly. Concurrent fatty acid administration allows further dose reduction. Adverse effects included vomiting and diarrhoea and rarely gingival hyperplasia and a papillomatous eruptions. Long term tolerance with cyclosporine seems to be good. A couple of years ago, oclacitinib, a selective Janus kinase 1 inhibitor, was approved for the treatment of CAD at a dose of 0.4-0.6 mg/kg twice daily for the first two weeks and then once daily. In a number of studies, it was shown to be as rapidly effective as prednisolone with success rates comparable to glucocorticoids and cyclosporine. Oclacitinib is well tolerated. As with cyclosporine and prednisolone, patients on long-term therapy need to be monitored for infections. More recently an increased risk of adult-onset histocytomas has been reported with oclacitinib. The newest drug approved for the treatment of atopic dermatitis is lokivetmab, a monoclonal anti-IL-31-antibody, inactivating the pruritogenic cytokine IL-31. In a couple of larger studies published recently, the success rate of lokivetmab is comparable to that of prednisolone, cyclosporine or oclacitinib and the pruritus is improved as rapidly as with prednisolone or oclacitinib. In the USA, the dose recommended is 2 mg/kg subcutaneously, in Europe 1 mg/kg subcutaneously is approved for treatment, pruritus relief lasts approximately four weeks with that dose. Adverse effects are rare and minor such as

lethargy, depression, vomiting and diarrhoea. So far, there is no evidence for immunosuppression and lokivetmab is one of the preferred treatments in patients where immunosuppression is contraindicated, such as for example atopic dogs with demodicosis. Antibody formation against the caninised monoclonal antibody is rare and in short-term studies was shown to occur in less than 3% of the patients. In the USA, the drug is used for approximately three years now without any evidence of mid-term adverse effects, long-term adverse effects are not known at this point.

There are several indications for skin biopsies in small animal practice. When neoplastic or immune-mediated skin disease is suspected, a biopsy is the diagnostic tool of choice. Thus, any cutaneous nodules, in which a fine needle aspirate has not identified the disease or revealed mast cells, should be biopsied for diagnosis or (in case of mast cells) for staging of the disease. Any severe and crusting skin disease in an older dog (particularly if it affects the inner pinnae, lips or planum nasale) where for example pemphigus foliaceus or lupus erythematosus is suspected should be biopsied. When treatment for a suspected skin disease is very expensive or associated with potentially severe adverse effects, a biopsy may be indicated to confirm the diagnosis. When a practitioner sees a very unusual skin disease and no differential diagnoses come to mind, a biopsy can also be very helpful to dictate further proceedings. Most skin biopsies will be obtained using local anaesthesia and an 8mm punch biopsy. Biopsies obtained from the face and feet usually require general anaesthesia. In cats and smaller dogs with lesions on the planum nasale, philtrum, around the eyes or foot pads, 6mm or rarely 4mm punch biopsies are used. Excision biopsies using a scalpel blade are performed with larger or deeper lesions. For best diagnostic value, primary lesions should be biopsied. Thus, erythema, papules, pustules and nodules are more likely to yield a diagnosis than erosions and ulcers. A range of lesions should be biopsied and immediately be placed in formalin. In animals with alopecia, the centre as well as the periphery of the alopecic area should be biopsied, as the most prominent (and thus most diagnostic) changes are found in the centre with follicular dysplasias and endocrine alopecias and at the advancing border of the lesion with alopecia areata or dermatophytosis. It is also sensible to mark the direction of the hair growth with a waterproof marker on the skin surface to allow the pathology technician to ideally orient the biopsy for sectioning. This will avoid â&#x20AC;&#x153;doughnut cutsâ&#x20AC;? and allows the pathologist to evaluate all portions of the hair follicle. Specimens should be sent to a dermatopathologist or a pathologist with an interest in skin, together with the results of the physical examination, salient features of the history and a list of differential diagnoses. If the pathology report is not satisfactory, then a phone call and discussion of the case with the pathologist may result in the decision to conduct special stains or obtain recuts to reach a final diagnosis.

Pruritus in cats is often multifactorial and successful therapy requires managing all the triggers. It is most commonly associated with feline inflammatory reaction patterns. Herpesvirus can mimic these and trial therapy with famciclovir can be considered in suspicious cases. Cytology and culture should be used to identify bacterial and Malassezia infections, although they are less common than in dogs. Managing secondary infections can nevertheless considerably improve pruritus and lesions. All itchy cats should be on rigorous flea control. Flumethrin containing collars can be used to help deter mosquitos, and fipronil or (potentially) isoxazolines can be used for trombiculids. Many pruritic cats have a behaviour component. Behavioural therapy, feline pheromones and/or mood-modifying drugs should be considered in cats with anxiety and in multi-cat households. Allergen specific immunotherapy (ASIT) is widely used, although much less is known than in dogs. Both subcutaneous (SCIT) and sublingual (SLIT) aqueous and alum-precipitated ASIT vaccines are used. One-day fast-track SCIT induction protocols are also used. ASIT appears to be a relatively benign treatment that may be efficacious in some cases of presumed atopic dermatitis. Glucocorticoids can be administered by injection, orally and topically. Long-acting injections avoid having to pill cats but are more likely to cause adverse effects. Oral prednisolone or methylprednisolone are given at 1-2mg/kg per day for 7-14 days to remission and then tapered. Some cats respond better to triamcinolone or dexamethasone, which are 7-10x as potent. Treatment is daily to remission and twice weekly for maintenance. Injectable dexamethasone can be given orally in cats. Side effects include diabetes mellitus, bacterial cystitis, iatrogenic hyperadrenocorticism, hypertension and congestive heart failure. Ciclosporin can be well tolerated and effective at 7mg/kg once daily in food. Once in remission the dose and/or frequency can be reduced. Side effects include anorexia, hypersalivation, nausea and vomiting. Ciclosporin is an insulin-antagonist, but it can be successful in cats with steroid-associated diabetes mellitus. The risk of toxoplasmosis is low, but avoiding raw meat and hunting is recommended. It is not recommended during vaccination, when other treatment may be needed.

Oclacitinib is not licensed for cats but can control pruritus at 0.6-1.0mg/kg every 12 hours to remission after which the dose and/or frequency can be tapered. Short term adverse effects are uncommon but long term safety is not known. There is less evidence for essential fatty acids and high EFA diets, but they may ameliorate inflammation or pruritus in some cats. They are safe but may lead to weight gain. Antihistamines have been used in cats with variable efficacy, although there may be a synergistic response with glucocorticoids or EFAs. Tricyclic antidepressants such as amitriptyline may have mixed antihistamine and anti-anxiety effects. Palmitoylethanolamide (PEA; 10 mg/kg once daily for 30 days) reduced itch and alopecia in 15 cats with eosinophilic plaque and granuloma. Systemic PEA and topical adelmidrol may be effective and appear to be well tolerated. Interferon omega (1-2.5MU/kg SC 1-3 times weekly to remission and then monthly for maintenance) may be effective and well tolerated in eosinophilic skin diseases. Chlorambucil (0.1-0.2mg/kg/day) can be effective in cats with recalcitrant skin disease. It is usually well tolerated but can cause GIT upsets, bone marrow suppression and hepatopathy.

Prompt diagnosis and treatment is important for success in otitis media. The clinical signs can be subtle, and include head tilt, head shaking, head pain, and loss of hearing. The ear drum may be ruptured and be intact but appear opaque, inflamed and/or bulging. Debris, polyps or tumours may be seen behind the ear drum. Other problems can include facial nerve paresis, parasympathetic nose (unilateral or bilateral xeromycteria), vestibular syndrome (head tilt, nystagmus and ataxia) and deafness. These are emergencies â&#x20AC;&#x201C; prompt therapy is required to prevent permanent neurological deficits. Otoscopy and diagnostic imaging should be used to assess the extent and severity of changes in the ear drum and middle ear. CT scans image the bony structures, soft-tissue inflammation, and fluid exudates in exquisite detail (including whether the ear drum is ruptured or bulging). Radiographs are less sensitive and less detailed. MRI scans may be preferable in dogs with neurological deficits but it is harder to detect changes in the ear canals and middle ear. Myringotomy may be necessary to inspect the middle ear, collect samples and flush the middle ear. Material for cytology and culture should be collected from the middle ear in all cases, but antimicrobial therapy is not indicated unless there is evidence of infection. Middle ear infections most commonly follow severe otitis externa, particularly with Gramnegative bacteria and/or chronic disease. Ascending infections from the pharynx are less common. There is usually a flocculent, bloody and or purulent fluid in the middle ear. Severe infections may involve osteomyelitis, and adjacent soft-tissues and neurological structures. The middle ear should be thoroughly flushed, which may have to be repeated. Systemic antimicrobials should be administered until clinical resolution. This may take 4-6 weeks. High doses should be used as most drugs penetrate poorly into the middle ear, especially in chronic disease. Antimicrobials can be directly instilled after flushing. It is likely that these persist in the middle ear, so this can be repeated under sedation and local anaesthesia 1-2 times weekly. Using large volumes of aqueous antibiotic solutions topically may allow some to penetrate into the middle ear. Primary secretory otitis media is associated with abnormal Eustachian tube function that allows mucus to build up in the middle ear. Most cases are sterile but secondary infections may ascend from the pharynx or follow rupture of the ear drum. The fluid appears mucoid to milky. Systemic and topical glucocorticoids will reduce inflammation, swelling and mucus

production in the middle ear and surrounding structures, which may help to open the Eustachian tube. Mucolytics can facilitate drainage of mucus. Multiple procedures are often required to obtain long term resolution. Tympanostomy tubes have been used for drainage and relieving pressure, but can be difficult to place and maintain. Dogs are mostly resolved after 4-6 months of flushing and medical treatment, although some require treatment for 618 months. Cholesteatomas involve transformation of the middle ear lining into a keratinizing stratified squamous epithelium. This material slowly builds up, resulting in otitis media and destruction of adjacent tissues. Keratinaceous debris in the middle ear is highly suggestive. Early lesions can be aggressively flushed/curetted and treated with glucocorticoids. Material can be removed using a ventral bulla osteotomy. A total ear canal ablation/lateral bulla osteotomy is necessary in severe cases.

Pruritic cats unfortunately do not present with a label on what exactly is wrong with them. In fact, they seem to hide the real reason or feeling extremely well. To investigate a pruritic cat â&#x20AC;&#x201C; this is a challenge in a busy practice, needing systemic approach and broad-spectrum knowledge. Among referred dermatology cases, it seems to be a tendency that cats are presented with a â&#x20AC;&#x153;diagnosisâ&#x20AC;? of clinical manifestation of their pruritus/hypersensitivity (e.g. eosinophilic granuloma complex), rather than true etiological diagnosis. I can see the temptation to manage the signs only, but keep in mind that the relapsing clinical pattern is an excellent starting point for you, needing further work-up. It is worthwhile to remember that pruritus is often noticed by the owner only or even after when there are apparent skin lesions (e.g. excoriations on the neck) or completely vice versa - no itch is reported at all, but the feline patient is presented for investigations of symmetrical alopecia with macroscopically non-inflamed skin. Stay focused here, as this is just another way how cats trick us and this finesse may be one reason why symmetrical alopecia is still mis-approached as endocrine disease in cats. In addition, psychogenic excessive grooming and following alopecia can look identical. However, in majority of the feline cases, symmetrical alopecia is due to self-trauma caused by underlying hypersensitivity disorder and/or ectoparasites. Despite of the numerous clinical patterns of feline pruritus, there is still limited number of common and some less common primary causes. This lecture will walk you through the feline dermatology consultation step by step aiming to de-mystify the issues and presentations of feline pruritus. The correct primary diagnosis is allowing successful management...at least in most of the cases!

Otitis externa is common presentation in cases of hypersensitivity disorders in dogs. It has been estimated that up to 55% of atopic dogs have otitis externa additional to other dermatological signs. Approximately in 3% of atopic dogs, otitis externa is the only clinical sign of their hypersensitivity disorder. The etiopathology of otitis externa is well-presented and discussed in the literature, however, in the practice, we are still seeing many relapsing, chronic and therefore frustrating otitis cases. In order to manage otitis externa successfully, we have to identify and then adequately address all the predisposing, primary, secondary and perpetuating factors of each single case. This means that besides treating the actual infection itself, we need to manage other signs and the primary cause too (e.g. chronic inflammation, atopic dermatitis). During the lecture, we will discuss different scenarios when treating canine otitis externa cases. We will cover common pitfalls of diagnosing otitis externa, multiple aspects of treatment, including pros and cons of topical treatment and ear cleansing (e.g. stenotic ear canal, non-compliance, over-cleaning etc) together with indications and issues with systemic treatment in the cases of otitis externa. We will present typical scenarios to highlight how the change in our diagnostics and/ or treatment plan will bring a positive outcome. As a treat, tips for long term management of allergic otitis externa are discussed. Throughout the lecture, we will emphasize and work through the scenarios in a logical problem-based manner comparing the troublesome cases and pathology with normal function and anatomy. This is a lecture about secret life of canine ears!

Cardiac diseases can be classified as congenital or acquired. Evaluating cardiac size and shape on radiographs can be challenging and often required echocardiography as additional diagnostic step. When interpreting cardiac radiology the first question we need to answer is if the cardiac silhouette is enlarged or not. If there is a cardiomegaly it is necessary to further characterize if the cardiomyopathy is left sided, right sided or generalized. How do we assess if there is cardiomegaly? Expert radiologists can judge the cardiac size with a subjective evaluation, based on their experience. Students, residents and non-expert radiologists often need to measure the heart size to conclude if it is pathologic or not. The best way is to calculate the Vertebral Heart Score (VHS) by Buchanan, correlating the cardiac long and short axes on a latero-lateral projection with the size of the thoracic vertebrae. When seeing the cardiac silhouette on a DV or VD view, it can be useful to consider the heart as a clock and use the heart-clock analogy to roughly identify the region of the cardiac chambers and large vessels (aorta and pulmonary vessels). When assessing cardiac pathology is essential to evaluate the pulmonary vasculature as well, in order to achieve a more accurate picture of the cardiovascular dysfunction. Peripheral pulmonary arteries and veins should have roughly the same diameter. In case of change in size of pulmonary arteries, veins or both arteries and veins, a cardiovascular dysfunction should be suspected. An enlarged cardiac silhouette on a thoracic radiograph does not necessarily mean true cardiomegaly. The cardiac silhouette visible on the radiographs is in fact composed by the pericardium and the heart, thus any fluid or tissue in the pericardial space will also contribute to an overall enlargement of the cardiac silhouette. Additionally, in obese

patients, accumulation of fat around the pericardium can be misleading and, due to border effacement with the heart, can mimic cardiomegaly. Atrial enlargement is usually the result of volume overload leading to increased diameter of its lumen. Ventricular enlargement can be secondary to concentric or eccentric hypertrophy of the cardiac walls. In the first case this occurs at the expense of a decreasing ventricular volume while in the second case leads to an increasing ventricular lumen. In case of ventricular concentric hypertrophy, radiographic signs of cardiomegaly can be absent. Cardiac radiography should be used as screening method to evaluate cardiac changes in size and shape, to assess radiographic signs of cardiac failure and response to therapy.

Thoracic radiography is one of the most commonly performed imaging diagnostic modality in veterinary medicine but its interpretation process is considered mostly challenging. Often not enough time is spent in evaluating the radiographic study acquired. Since we are dealing with a two-dimensional interpretation of a three-dimensional object, we should acquire at least two orthogonal projections and sometimes even three. A careful evaluation of the study acquired should highlight possible technical errors (es. wrong exposure, oblique radiographs, wrong respiratory phase) and then, as second step, we should proceed to the systematic interpretation process. Moreover, if the patient referred for thoracic radiographs is in respiratory distress, the least stressful projection (i.e., dorso-ventral view) should be acquired to have an overall thoracic overview. In these cases only one single projection can help the radiologist and clinician and a complete study can be performed after stabilization of the patient.

The systematic thoracic interpretation process can be divided in four steps: 1)

evaluation of the extra thoracic region (rib cage and thoracic wall)

evaluation of the pleuro-pulmonary surface

evaluation of the pulmonary parenchyma

evaluation of the mediastinal compartment

Conventional radiography is a good diagnostic tool to highlight possibile thoracic cage lesions (es. rib tumor) and pleural effusion or pneumothorax. The lung parenchyma is normally diffusely aerated and appear radiographically radiolucent (i.e black). A clear radiographic contrast exists between the radiolucent lungs and the soft tissue opacity of the lung interstitium and vessels. In pathological condition, on a thoracic radiograph, it is possible to detect an increase in opacity of the lung tissue, which needs to be further characterised by the radiologist in order to produce a list of differential diagnoses. Four different patterns of increased lung opacity have been described in order to classify different disease processes: 1)

Interstitial

Bronchial

Alveolar

Vascular

Often, there will be a combination of the lung infiltrate (broncho-alveolar, bronchointerstitial, etc) and it is very important to evaluate not only the type of lung patterns but also its distribution and features. An accurate description of what we see will help us in producing a correct list of differential diagnoses, which of course will be associated with the clinical examination of the patient. Itâ&#x20AC;&#x2122;s very important to have a systematic approach of the thoracic structures in order to avoid undetected lesions, which could be essential for the clinical work up of the patient. The first diagnostic step is to define, if present, the type of pathologic lung pattern and the second one is to describe it by using the radiographic signs relative to the lesion/s (number, shape, volume, margins, opacity and location). The goal of the radiographic interpretation is to produce a differential diagnoses list compatible with the lesions previously described.

Primary purpose in radiographic imaging is to identify pathologic processes in a body. This requires knowledge and recognition of normal anatomy, and normal radiographic anatomy. Good quality radiographs are necessary to recognize correct anatomical structures, especially within an abdominal cavity where many of the organs are of soft tissue and fluid opacity with little contrast. It is important to acknowledge if radiography is the correct imaging modality with the question in mind to get closer to a final diagnosis, in other words if the suspected pathology will be visible with radiographs and what will it look like. A radiographic image is composed of map of X-rays that have either passed through the body/object or have been variably attenuated by anatomical structures. The degree of attenuation depends on atomic number, physical density and volume of the tissue as well as the energy of the X-rays. The higher the X-ray energy (kV), the more likely it is to pass through. Conversely the higher the atomic number, the more likely it is to absorb the X-ray (bones). The differential absorption of the X-rays by various tissues allows radiographic image to be made. This results in five different basic radiographic opacities, giving contrast between certain anatomic structures. Different anatomic structures are visible on radiographs when they are outlined and contrasted in whole or as part by tissues of different density such as the kidneys are outlined by retroperitoneal fat, the cardiac silhouette is outlined by the gas containing lungs and bones are outlined by surrounding soft tissues. Conversely, if the anatomic structures have similar density, instead of being outlined, they may get summated and superimposed with each other in a radiographic image. This causes challenges, especially when imaging body regions with minimal outlining and contrasting other tissues, such as the abdominal cavity where majority of the organs are of soft tissue and fluid opacity (with the exception of gas in the gastrointestinal tract). Optimal radiographic technique, patient preparation and positioning are therefore very important when obtaining good quality diagnostic radiographs from the abdominal cavity.

5 basic radiographic opacities (in decreasing density and opacity) â&#x20AC;˘

Metal

• • • •

Bone Soft tissue and fluid Fat Air

In radiology the image visibility is at best when the radiographic density (blackness), contrast and sharpness are optimal for the area of interest/body part being imaged. Contrast between the different anatomical structures in a radiographic image depends on differences both the density and the thickness of the structures. The greater the difference in either density or thickness of two separate and adjacent structures results in greater contrast between the structures within the image. For accurate location of structures and to overcome blurring from summation of soft tissue and fluid structures in the image, in minimum two (preferably three) views are required for standardized and appropriate abdominal imaging protocol (both laterals and a VD/DV). The right lateral is the best view for diagnosing gastric dilatation and volvulus, whilst the left lateral is the best view for evaluation of the gastric pyloric and proximal duodenal region and detecting of free abdominal gas. Sometimes even additional horizontal view may also be helpful, especially when detecting small amounts of free peritoneal gas. Besides of optimizing the imaging protocol, adequate patient preparation is a key to good quality radiographs. Things to remember to take into consideration in patient preparation is the contents of the stomach (fasting 12h), intestines (defecation) and urinary bladder (urination), and how this may interfere with the visibility of different abdominal structures and interpretation of the images. The more contents there are in the gastrointestinal tract and urinary bladder, the more superimposing will result, reducing visibility of other intraabdominal structures. Another important thing with good quality radiographs is optimal and standardized patient positioning. Often times sedation and/or anesthesia may be helpful in obtaining and keeping optimal patient positioning, as well as to reduce motion blur from both voluntary and involuntary (respiratory motion) patient movement. Standardized and symmetrical patient positioning is useful in better recognizing the different anatomical structures within a body cavity. The anatomical variation in a body is wide, and therefore knowledge and experience in radiographic anatomy is important for radiographic image interpretation. Comparison with another patient with similar body conformation, body condition, age and species, and/or comparison with images in textbooks is always recommendable and beneficial.

How to approach diagnostic radiographs? There are several ways how to approach diagnostic radiographs; systematically, by intuition and experience, or combination of all. Before you have gained enough experience to differentiate between normal and abnormal, a systematic approach can be very useful and helpful in detecting differences between normal and abnormal, and thus help in the process. A systematic approach is helpful as a guideline to always remember to look through all structures included in the image in a systematic and standardized order and method. The

start of a systematic approach can be from outside in in a body cavity, from cranial to caudal etc.. Alternatively a systematic organ by organ approach can be used. The systematic approach is also helpful in remembering to look the entire image and everything in it, and not to get too excited from the first detected radiographically visible abnormality. Learning specific roentgen signs is part of systematic approach, to always remember to look for size, shape, number, location, margination and opacity of each visible structure in the image. A systematic approach of abdominal radiographs includes evaluation of all the radiographically visible abdominal organs (liver, stomach, intestines, spleen, kidneys, urinary bladder, prostate/uterus), recognition of any abnormally visible structures (gall bladder, lymph nodes, adrenal glands), evaluation of gastrointestinal gas pattern, included skeletal structures, caudal thorax/lungs and lumbar muscles (cat). Full assessment includes also evaluation of image quality and estimating presence of image artifacts as well as combining the radiographic findings with clinical history. Learn where the organs are typically located and what are the roentgen signs for normal healthy patient. Learn also how to recognize roentgen signs for various pathologic processes in the above listed abdominal organs. After you have performed a systematic (or intuitive) through evaluation of the radiographs, it is good to go back to the initial question â&#x20AC;&#x201C; how are the radiographic findings and patient history related, or are they? Did you find what you were expecting to see in the radiographs? Did you find enough evidence to support your preliminary diagnostic suspicions? Or did you find something else? What is the clinical importance of the radiographic findings? Try to be as objective as possible, open to broaden your spectrum and change the original hypothesis of what is wrong with the patient. Finally, make a list of most likely differential diagnoses in a probability order. Alternatively, if a list of differential diagnosis cannot be made based on the radiographs, plan what to do next? How to get closer to a reliable final diagnosis? Would additional imaging (follow up, contrast studies, other diagnostic modalities such as ultrasound, CT, MRI) be helpful? Or is it time to start performing more invasive procedures such as endoscopic exam, tissue sampling, explorative surgery etc.? Besides learning the normal anatomical variants and radiographic appearance of pathologic processes, it is equally important to learn typical sources of error in radiology, such as imaging technique and patient related errors. Using standardized patient positioning, views and imaging protocols helps to reduce the amount of imaging technique related errors (scattering, magnification, summation/border effacement, image blurring, location, size and shape of organs). Location, shape and even size of organs may also vary from directly patient related errors such as in patients with different body types (diaphragm, liver, spleen, gastric axis) and respiratory phase (diaphragm, liver, gastric axis). The assessment of serosal detail is significantly associated with patient age and body condition, and should be evaluated as such. The amount of abdominal and retroperitoneal fat and gastrointestinal gas contents vary between patients, which may improve or decrease visibility of adjacent organs. Besides giving contrast and outlining the gastrointestinal structures (margination), the luminal gas contents (opacity) can be helpful besides evaluating the roentgen signs (location, size, shape), but also to evaluate if the gas contents can move freely within the gastric lumen (function).

Value of radiography in abdominal imaging? Radiographs are used for further diagnostics in various clinical conditions, but most importantly in determining the need for surgical emergency in patients with suspected gastrointestinal (luminal foreign material and obstruction, gastric dilatation and volvulus, perforation of a hollow viscous organ) and urogenital emergencies (number and appearance of fetuses, radiopaque uroliths +/- urinary obstruction). Radiographs can also be used in the assessment of gastrointestinal hernias, visualizing presence/absence of urinary bladder in trauma patients, and differentiating abdominal enlargement due to true intra-abdominal mass, organomegaly or free peritoneal effusion. Sometimes it may however, be necessary to do further imaging (contrast radiographs or changing into other type of diagnostic modality such as ultrasound or CT). It is important to learn to recognize which diagnostic imaging modality is most useful and diagnostic for the patient, based on the clinical history and your clinical assessment. For example radiographs and ultrasound have very different strengths and weaknesses and may thus complement each other well. In general ultrasound is more sensitive for any parenchymal abnormalities, better as for initial investigation of most urogenital disorders, early diagnosis for pregnancy, and evaluation of abdominal organs and viscera in patients with peritoneal effusion. However, in patients with large amount of gastrointestinal or peritoneal gas, the value of ultrasound is often limited. In very large patients, however, the penetration of the ultrasound may be insufficient, and CT may be needed for more detailed evaluation of abdominal organs. Despite better detectability of radiolucent intestinal contents and foreign material with ultrasound according to some recent publications (Sharma et al, 2011, Tyrrell et al, 2006), I personally consider radiographs as primary diagnostic modality for vomiting patients with suspicion of intestinal obstruction. It should be kept in mind that presence of gastrointestinal foreign material does not equal with clinically significant obstruction and is not always necessarily a surgical emergency/condition. Some studies have even proven radiographs to be continuously more accurate in the assessment for need of surgical exploration (Shanaman et al 2013, Drost et al 2016) when compared with ultrasound and CT. Due to limited contrast between the abdominal soft tissue organs, contrast studies may sometimes be needed to better visualize and differentiate the soft tissue structures from each other and to evaluate gastrointestinal contents and function more in detail, to evaluate the urinary tract (excretion and perfusion) and to search for presence of gastric or urinary perforation (trauma or disease) or obstruction. Most commonly used contrast procedures in abdominal imaging include gastrointestinal and urogenital positive contrast studies, including oral barium studies (gastrointestinal tract), intravenous urography (iodine), retrograde urethrocystography (diluted iodine) and colonography (barium). Occasionally negative or double contrast studies may also be needed. The diagnostic usefulness of the contrast studies, especially gastrointestinal, depends highly on the technical quality and may sometimes be limited due to inadequate technique or patient preparation (insufficient volume of contrast, inadequate fasting/cleansing enema prior the study, certain drugs affecting gastrointestinal motility, insufficient number of views, failure of follow up 12-24h post po barium study). Due to potential nephrotoxicity of iodine based contrast media, routine laboratory analyses are recommended prior intravenous contrast studies. It should also be kept in mind that contrast media will also interfere in the assessment of urinalysis.

Literature: 1)

Thrall DE, Robertson ID, Atlas of Normal radiographic anatomy & anatomic variants in the dog and cat, 2nd edit, 2011

Holloway A, McConnel JF, BSAVA Manual of canine and feline radiography and radiology, A foundation manual, 2013

OÂ´Brien R, Barr F, BSAVA Manual of canine and feline abdominal imaging, 2009

Schwartz T, Johnson V, BSAVA Manual of canine and feline thoracic imaging, 2008

Sharma A, Thompson MS, Scrivani PV, et al. Comparison of radiography and ultrasonography for diagnosing small-intestinal mechanical obstruction in vomiting dogs, Vet Radiol Ultrasound 2011

Tyrrell D, Beck C. Survey of the use of radiography vs. ultrasonography in the investigation of gastrointestinal foreign bodies in small animals, Vet Radiol Ultrasound 2006.

Shanaman M, et al, Comparison between survey radiography, B-mode ultrasonography, contrast-enhanced ultrasonography and contrast-enhanced multidetector computed tomography findings in dogs with acute abdominal signs, Vet Rad Us 2013

Drost T, et al, Comparison of computed tomography and abdominal radiography for detection of canine mechanical intestinal obstruction, Vet Rad Us, 2016

Hess RS, Saunders HM, Van Winkle TJ, et al. Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases (1986â&#x20AC;&#x201C;1995), JAVMA 1998

INTRODUCTION Anesthesia, definable as the loss of feeling or sensation, is used in veterinary medicine to produce immobilization, analgesia and muscle relaxation in a safe and reversible manner. For some minor procedures, for example blood sampling, simple restraint may be all that is required. For more invasive and painful procedures, or when dealing with potentially dangerous species, general anesthesia must be used. In exotic animals we deal with several thousand different species of 3 different classes, with considerable anatomical, physiological and pharmacological differences, some general guidelines are applicable throughout.

PRE-ANESTHETIC ASSESSMENT & STABILIZATION A full history should be taken, assessing not only the animal's current and previous health status, but also paying attention to housing and feeding, since many animals ailments relate to sub-optimal environmental conditions or nutritional factors. Accurate identification of species (birds, reptiles) is also essential; this may influence the choice of drugs administered and also the required hospitalization facilities. Pre-operative hematology and biochemistry should be routinely considered, but may not be possible due to animal size or difficulties associated with conscious venipuncture. For elective procedures (e.g. neutering), underweight, dehydrated or debilitated animals should be nursed until their condition improves. In reptiles for non-elective surgery attempts to correct dehydration must be started prior to anesthesia. Even the most moribund egg-bound reptile will usually benefit from stabilization for at least 24 hrs before embarking on surgery. Fasting should be carried out before all elective surgery in order to reduce the chances of regurgitation or in reptiles to reduce compression of lung(s) associated with large meals. In general 1-2 feeding cycles should be skipped (e.g. 2 hours in small birds, some hours in small mamals, 2-4 weeks for a large constrictor, 1-2 days for an iguana).

AN INTRODUCTION TO AVIAN SURGERY Avian surgery requires adherence to three main principles: hemostasis, precision, and speed. Close attention to hemostasis is required to minimize blood loss. Remember that the allowable blood loss in 30g parakeet is only 0.3ml of blood. Surgical precision in dissection is required to minimize soft tissue damage. At the same time, speed results in minimizing anesthetic time. Combining these three principles and becoming accustomed to working with very small structures takes time and practice.

AN INTRODUCTION TO REPTILE SURGERY In general, performing surgery on a reptile patient should be approached with the same principles as those used for domestic animals. However, there are some specific anatomical and physiological considerations, as well as unique aspects of patient preparation, positioning and equipment with which the reptile clinician should be familiar. Surgical coeliotomy provides access to most of the major internal organs, and therefore is useful for a range of surgical procedures including exploration, biopsy and surgical corrections. The technique is simplest to perform in the uncompartmentalized coelom of most lizards, more difficult in snakes with diffuse fat bodies and fascial planes, and most difficult in chelonians and crocodilians due to their bony integument and/or compartmentalized coelomic cavities.

Blood Collection Sample Size Birds: The volume of blood to be safely collected in birds is dependent upon species, and may vary from 5ml/100g (pheasant) to 16.3ml/100g (racing pigeon). A good rule of thumb is to collect 1ml/100g, or 1% of the body weight.

Reptiles: Reptiles have a lower total blood volume than a similarly sized mammal, 5% to 8% of their body weight, and 10% of this volume may be safely collected from healthy reptiles (e.g. 0.5 to 0.8 ml/100g).

Venipuncture site Birds: Jugular vein: The jugular vein is preferable for smaller species as well as collection of larger blood volume. The right jugular vein is usually larger than the left. In many species, there is a featherless tract of skin (apterium) overlying the jugular vein; therefore, lightly wetting the feathers with alcohol in this area will aid in the visualization of the vein. To collect blood from the jugular vein, the bird is properly restrained with the head and neck extended. This site is often preferred in smaller birds, but is also a frequently used in bigger animals.

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Ulnar (basilic) vein: The basilic vein is found crossing the ventral surface of the humeroradioulnar joint (elbow). Hematoma formation can be a common result of venipuncture on this site. Stabilization of the wing during blood collection is necessary to avoid tearing of the vein and is often difficult on the conscious patient. This site is often preferred in medium to large birds.

Reptiles: Venipuncture is usually a blind technique in reptiles, with few exceptions. Optimal patient positioning may aid visualization of the blood vessel (e.g. positioning a turtle with the head down to aid visualization of the jugular vein). Lymphatic contamination/hemodilution may occur in most of the venipuncture sites in reptiles. The jugular vein (chelonians) and the heart (snakes) are considered best to reduce contamination of the blood sample.

Companion exotic mammals: Blood collection in companion exotic mammals is very similar to dogs and cats, thus only unique venipuncture sites will be described in details on this section.

Rabbits: Common venipuncture sites include marginal ear vein, central ear artery, jugular vein, cephalic vein and lateral saphenous vein. Alcohol can be used to part the fur and allow visualization of the vessels. In the conscious rabbit the author prefers to collect blood from the lateral saphenous vein with an assistant supporting the rabbit against the assistant's body with a hand positioned alongside the ventral abdomen and thorax of the rabbit leaving the limbs loose. The collector will then hold the hindlimb at the base with the non-dominant hand (with that also holding off the vein) and collect the blood with the dominant hand.

Guinea pigs and chinchillas: Common venipuncture sites include jugular vein, cephalic vein and lateral saphenous vein. Tranquilization and/or anesthesia are usually necessary.

Hedgehog: Common venipuncture sites include jugular vein, cephalic vein femoral, and lateral saphenous vein. Tranquilization and/or anesthesia are usually necessary.

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Respiratory disease is commonly seen in exotic species, regardless of the animal being avian, reptile or small mammal. In contrast, cardiovascular diseases have long been considered rare in exotic species other than parrots and ferrets. However, with the growing demand of exotic pet owners to provide high quality of care for their animal as well as the advanced diagnostic opportunities, cardiovascular disease is nowadays more frequently recognized in other exotic species. Nevertheless, disease aetiology, susceptibility and clinical presentation may vary among the different species due to differences in their anatomy and physiology. For example, in rabbits, rhinitis is commonly bacterial in origin and secondary to acquired dental disease, whereas in larger psittacines, upper respiratory disease commonly involves aspergillosis infections that may arise secondary to hypovitaminosis A. Poor husbandry and nutrition often play a role, not only in respiratory disease (e.g. exposure to dust, toxins or allergens) but also in cardiovascular (e.g. atherosclerosis). Respiratory cases may occasionally be easy to recognize as obvious signs of upper and/or respiratory disease such as nasal discharge, sneezing, sinus swelling (in birds), stridor, cyanosis and/or dyspnoea. However, due to the large â&#x20AC;&#x153;reserve capacityâ&#x20AC;? of the lungs, such clinical signs may not be obvious until disease is advanced. Instead, patients may present with non-specific clinical signs including anorexia, weight loss, or general malaise. Similar non-specific signs are commonly seen in patients presenting with cardiovascular disease. In addition, hind limb weakness, falling of the perch and syncopes (especially in bradycardic animals) or signs of left- and/or right-sided heart failure, including thoracic effusions, lung oedema, hepatosplenomegaly, generalized oedema and/or ascites, can be noted. In both cardiac and respiratory patients, auscultation is essential and may reveal murmurs, arrhythmias, crackles, muffled lung or heart sounds sounds and/or increased bronchovesicular sounds. In the smaller species, the use of a pediatric or infant stethoscope is recommended to increase diagnostic accuracy. In reptiles, auscultation can be hindered due to the presence of scales. Dampening the sounds using a wet cloth and/or using an electronic stethoscope will often help to filter out sounds. Further diagnostic testing is almost always needed to obtain a diagnosis. To confirm presence of cardiovascular disease, an echocardiogram, thoracic radiographs,

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electrocardiography and/or blood pressure measurement will often be most helpful, whereas radiography, computed tomography (especially in birds) and endoscopy are the mainstays of diagnosing respiratory disease. Dependent on the suspected underlying cause, additional tests can be performed including testing for heartworm (Dirofilaria immitis) in ferrets or PCR for Chlamydia psittaci in birds. In general, therapeutic intervention for cardiac disease will follow similar guidelines as those applied in dogs and cats. Aside from treating the potential underlying cause, therapeutic intervention is aimed at alleviating signs of congestive heart failure by 1) improving oxygenation by placing the animal in an incubator with supplemental oxygen; 2) reducing preload by giving diuretics (e.g. furosemide, thiazide, spironolactone); and 3) reducing afterload by giving angiotensin-converting enzyme (ACE) inhibitors which induce vasodilatation and decrease water and salt retention (thus also reducing the preload). In case of significant pleural effusion or ascites, thoracocentesis/abdominocentesis is recommended to alleviate the dyspnea associated with it. Once the animal has been stabilized, digoxin and/or pimobendan can be added to the treatment regimen to enhance inotropy. For patients with respiratory disease, treatment often comprises alleviation of the clinical signs (e.g. oxygen suppletion, bronchodilators, mucolytics/expectorants), correction of underlying husbandry and nutritional issues, removal of obstructions (if any) by e.g. flushing (sinuses, nasal cavity) and/or endoscopy, and eliminating the underlying cause which will generally include topical and/or systemic administration of an antimicrobial agent (e.g. antibiotic, antimycotic). Key to treating any exotic with respiratory distress and/or cardiac failure is to minimize stress and maximize the patientâ&#x20AC;&#x2122;s comfort level and condition as these patients may otherwise rapidly deteriorate and succumb to the disease.

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Various disorders may affect the plumage of birds, resulting in poor feather quality, colour changes, malformations, loss of feathers and/ or improper moulting. In addition, birds â&#x20AC;&#x201C; in particular parrots â&#x20AC;&#x201C; are presented commonly with signs of feather damaging behaviour (also referred to as feather plucking or feather picking), which can have a variety of medical and behavioural causes that result in the parrot pulling, biting and/or fraying its own feathers. When confronted with a parrot with feather abnormalities, one should consider that, aside from a primary skin and feather disorder, a more serious, generalized or systemic disorder or a behavioural issue may be present. The list of potential aetiologies is long and includes a variety of infectious, toxic, nutritional, neoplastic, immune-mediated, metabolic, endocrine, behavioural, traumatic and management-related conditions. In order to be able to effectively treat the bird and resolve the problem, it is thus of utmost importance to identify the underlying cause for the feather abnormalities. For this purpose, a full diagnostic work-up is warranted. As a first step, a thorough and comprehensive history needs to be obtained, which includes information on the presenting complaint (e.g. duration, initial appearance, progression, [responses to] previous treatments and presence of pruritus or self-inflicted trauma), husbandry, diet, living conditions, general condition and behaviour of the bird. Next, a full physical examination should be performed, in which attention should not only be paid to the overall condition of the skin, feathers and feather follicles, but also to identifying signs of a potential underlying generalized illness. If specific dermatologic lesions (e.g. nodules, papules, plaques, ulcers and/or exudate) and/or feather abnormalities are present, these should be examined closely and classified according to their type, localization and distribution. Dependent on the findings during the physical examination, diagnostic work-up may furthermore include a complete blood count and plasma biochemistry, faecal cytology including wet mount, diagnostic imaging (ultrasound, radiographs, CT imaging or MRI) and/or endoscopy to identify or exclude presence of a systemic illness or organ dysfunction. In addition, specific tests may be performed to identify presence of a specific pathogen, such as PCR on whole blood to screen for presence of circovirus, the virus causing Psittacine Beak and Feather Disease (PBFD). Other diagnostic procedures that may be used in the medical work-up of a patient with (localized) feather abnormalities and/or skin lesions include (superficial or deep) skin scrapings, fine needle aspirates, tape strip samples, impression smears, feather digest and/or feather pulp cytology, culture and sensitivity tests and/or

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histopathological examination of skin and/or feather biopsies. When diagnostic work-up fails to identify an underlying medical condition for the feather abnormalities, self-inflicted trauma due to a psychogenic cause (e.g. ‘stress’, ‘boredom’, ‘anxiety’, ‘frustration’) may be suspected, which subsequently requires the conduction of an extensive behavioural assessment to identify the triggering events and design an appropriate behavioural modification plan.

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Skin abnormalities are a common presenting sign in small mammals, whether as a primary condition or as a secondary manifestation of systemic disease. Amongst the primary skin diseases diagnosed in small mammals, infectious diseases, including parasitic (except in chinchillas), bacterial, viral (particularly in rabbits) and/or fungal infections, are frequently encountered. In addition, non-infectious diseases can be seen, which includes a variety of neoplastic, immune mediated, endocrine, and/or husbandry- and/or environmentallyrelated conditions (e.g. barbering, urinary scald, pododermatitis, hypovitaminosis A). However, it is reasonable to assume that many of the dermatologic conditions described in dogs and cats and not yet diagnosed in small mammals can also occur in these species. Similar to dogs and cats, a systematic approach is recommended to achieve a diagnosis and formulate an appropriate treatment plan. Occasionally, the diagnosis will be immediately obvious from its typical clinical presentation (including any species, breed, sex or age predispositions), but in general a more detailed history, clinical examination, and/or additional diagnostic testing will be required to obtain a definitive diagnosis. Important questions include those pertaining to the diet, husbandry (e.g. floor substrate) and other aspects of the living environment (e.g. social structure, climate, sanitation). In addition, it is important to identify whether pruritus or signs of general illness are present and whether any other animals (or people) are affected. Following the history, a thorough physical and dermatologic examination is performed, during which a detailed assessment is made of the type, distribution, and configuration of the skin lesions that are present. Dependent on the complaint, diagnostic sampling can include collection of hair and/or skin samples (e.g. impression smears, acetate tape impressions, skin scrapings, fine needle aspirate biopsies, trichograms, bacterial and/or fungal cultures, skin biopsies). In addition, a hematologic and/or biochemical exam, hormone analysis, radiography or ultrasound can be performed to identify underlying and/or concurrent systemic disease (e.g. thymoma, osteomyelitis, cystic ovarian disease, hyperadrenocorticism, lymphoma). Commonly, some form of restraint or sedation/anaesthesia is required to enable good quality diagnostic samples to be obtained. Treatment of skin disease in small mammals is largely consistent with guidelines describe for other companion animals. However, caution is warranted with the use of antibiotics in the herbivorous small mammals, because of the risk of life-threatening diarrhoea due to dysbacteriosis following oral administration of penicillins, cephalosporins, macrolides, and lincosamides. Similarly, fipronil has been reported as toxic for rabbits. Topical medications

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also warrant special attention, as toxicity and hypothermia may respectively arise from ingestion during grooming, and shampooing and dipping.

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Presentation supported by KARL STORZ

Part 1: Diagnosis The diagnosis of acute pancreatitis (AP) in dogs and cats in routine praxis is based on the combination of clinical signs, laboratory test results, and findings of imaging procedures. Clinical signs suggestive for AP are non-specific but sudden in onset and can include depression, abdominal pain and vomiting. Clinical severity reaches from mild to signs of severe illness such as tachycardia, tachypnea, prolonged capillary reďŹ ll time, hypothermia, and dry mucous membranes as hallmarks of hypovolemia and shock. A comorbidity of AP is diabetic ketoacidosis. AP can lead to systemic inflammatory response syndrome resulting in multi organ failure with acute kidney failure, lung injury, disseminated intravasal coagulation, and arrhythmia. Independent of severity, AP is mostly reversible but can result in acute death or chronic pancreatitis. Laboratory tests such as hematology, clinical chemistry, and urinalysis are used to rule in/out important differential diagnoses of AP, and to assess the extension of multi organ failure. There have been several AP serum test validated such as immunoassays for pancreatic lipase of dogs (cPL) and cats (fPL) and colorimetric lipase activity assays utilizing 1,2-o-dilauryl-racglycero-3-glutaric acid-(6'-methylresorufin) ester (DGGR). A recent study in dogs comparing three immunoassays and one DGGE method reported tests sensitivities of 73.9-100% and specificities of 64-83.8% with good to excellent level of agreement between all tests. However, results of any of the tests alone are considered insufficient to establish a diagnosis

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of AP. (Cridge et al. 2018) Three recent studies comparing Spec fPL and DGGR lipase in cats with signs of AP revealed for both tests substantial agreement of results and fair agreement with ultrasonographic results, but limited agreement with histological pancreatic inflammation (Opplinger et al. 2013, 2014, 2016) In case of abdominal effusions, the determination of lipase activity in the fluid can also aid the diagnosis of AP in dogs. (Guija de Arespacochaga et al. 2006, Chartier et al. 2014) In diagnostic imaging, abdominal ultrasound is mainly used to visualize changes in and around the canine and feline pancreas in clinical practice. Its sensitivity is, however, limited. A common feature of necrotizing AP is an enlarged hyperechoic pancreas and peripancreatic necrosis. Ultrasonography does not allow distinguishing between inflammation, necrosis or neoplasia. (Hecht et al.2007, Saunders et al. 2002, Larson 2016) Fine needle aspiration for cytology is rather safe and can aid the diagnosis. (Cordner et al. 2015) There have been attempts to use contrast enhanced ultrasound (Lim et al. 2014; Rademacher et al 2016), contrast enhanced computed tomography (Adrian et al. 2015), and endosonography (Schweighauser et al 2009). They should allow a better differentiation between inflammation and neoplasia, and improved assessment of their extent. However, their current use is limited due to accessibility, high costs, and the need for general anesthesia. For severity assessment scoring systems have been used in human medicine and introduced into veterinary medicine. Indicators of poor prognosis in canine AP are the presence of cardiac and respiratory abnormalities, altered oncotic/hydrostatic pressure, anorexia for â&#x2030;Ľ3 days, decreased platelet count, azotemia and hyponatremia. (Mansfield et al 2008, Sato et al 2017, Marchetti et al. 2017) Negative prognostic factors in feline AP are dyspnea, high fPL concentration, hyperkalemia, and hypocalcemia. (Stockhaus et al 2013; Diaz & Carreira 2015)

Part 2: Treatment The treatment of canine and feline acute pancreatitis (AP) is tailored to the clinical severity and addresses etiopathogenetic mechanisms and consequences of AP which include (1) dietary and medical risk factors, (2) vomiting and abdominal pain, (3) disturbed pancreatic microcirculation, (4) local complications, and (5) systemic inflammatory response syndrome (SIRS) with multi organ dysfunction syndrome (MODS). (Bazelle & Watson 2014; Jensen & Chan 2014; Phillip et al. 2014; Mansfield & Beth 2015; Armstrong & Craig 2015) For addressing dietary and medical risk factors fasting should not exceed 3 days and feeding of small amounts of a low fat diet (< 15% DM fat content) should start as soon as vomiting is controlled. Since lipemia is considered a risk factor for AP in dogs a low fat diet should be fed for 4-6 weeks to patients with hypertriglyceridemia and continued if hypertriglyceridemia reoccurs. Drugs with AP as possible side effect (e.g. phenobarbital, potassium bromide) should be discontinued. Antibiotics are rarely indicated. There has been no report of septic pancreatitis in dogs and cats so far. Antiemetic and analgesic therapy is important to address clinical illness and considered a vital component to manage AP. Maropitant seems to be the best option since it has also

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effects on relieving visceral pain. (Boscan et al 2011) The addition of ondansetron has shown some benefit. Cats do not show pain as obvious as dogs but both species respond favorable to pain medication. Dependent on the severity of pain buprenorphine, butorphanol, methadone, fentanyl and tramadol are used. In dogs, the Glasgow pain score is useful for choosing the appropriate pain medication. In case of refractory pain ketamine or lidocaine continuous rate infusions are indicated. Morphine should be avoided. Gastric acid suppression with famotidine or omeprazole is only required for signs of gastric mucosal injury (hematemesis, melena, or hematochezia). Improving pancreatic microcirculation is vital in moderate to severe AP for improving clinical outcome. In AP, pancreatic micocirculation is disturbed due to increased vascular permeability caused by inflammatory cytokines and microthrombi. Crystalloid fluids (lactated Ringerâ&#x20AC;&#x2122;s solution) should be administered and in hypoalbuminemia be combined with colloids. Plasma infusion might be of benefit in disseminated intravasal coagulation in patients with SIRS. To treat local complications minimal invasive or surgical interventions are indicated when there is marked acute fluid collection in the pancreatic parenchyma or post-hepatic biliary obstruction since both cause intensive pain. Ultrasound guided percutaneous drainage of fluids from the pancreas or bile from the extended gallbladder can lead to pain relief. Surgically placed choledochal tube stents have been described to decompress the extrahepatic portion of the biliary tract in dogs with AP induced posthepatic biliary obstruction. Using endoscopy for biliary stent placement might overcome the disadvantages of open surgery in AP. To avoid SIRS with MODS early pain medication and fluid resuscitation are corner stones. Affected patients need to be transferred to intensive care and treated according the diagnosed organ failure(s). Corticosteroids are not anymore considered risk drugs. They counteract all pathways of inflammation and dogs with AP might even suffer from criticalillness related corticoid insufficiency. Therefore, the judicious use of low-dose hydrocortisone can be considered in severe AP being refractory to conventional treatment.

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Cats Cobalamin (cbl) transport and absorption in cats is similar to the mechanisms previously described for dogs (see previous section). In cats, however, Intrinsic Factor (IF), is exclusively produced by the exocrine pancreas. Documented diseases causing cbl deficiency in cats are chronic enteropathies (CE), Exocrine Pancreatic Insufficiency (EPI), small intestinal lymphoma, pancreatitis, hepatic lipidosis and cholangitis/cholangiehepatits. Hypocobalaminemia has further been reported in a case report of a cat suspected of having congenital disorder of cbl absorption, and in cats with hyperthyroidism. The mechanism behind cbl deficiency in hyperthyroidism has not been described, but a recent study suggests that it is not a functional deficiency. A clear correlation between low serum cbl concentrations and increased serum MMA concentrations have been shown in cats, but HCY is not a useful marker of cbl deficiency in cats (see previous section on cbl deficiency in dogs). Cats with malabsorption have a markedly reduced half-life of cbl compared to healthy cats, thus their demand for cbl increases. Positive effects of cbl supplementation in cbl deficient cats are well documented. Cobalamin supplementation has been proven to increase body weight and decrease clinical disease activity. Further, in cats with EPI, cbl supplementation improved the response to treatment with pancreatic enzymes. As in dogs, EPI has to be excluded or confirmed in cats with cbl deficiency. Many cats with cbl deficiency have rather unspecific clinical signs. Weight loss and vomiting were more common clinical signs in two studies than diarrhea. Other common presenting clinical signs in cats with hypocobalaminemia are anorexia and lethargy. It is important to include serum cobalamin in the diagnostic plan of cats exhibiting weight loss, anorexia and lethargy despite a lack of diarrhea and/or vomiting. Both successful oral and parenteral cbl supplementation has been described. Recurrence of hypocobalaminemia was very common after weekly cbl injections during 6 weeks in one study, emphasizing the need for re-evaluation of serum cbl concentrations after end of supplementation.

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Selected references: 1)

3) 4) 5)

Kempf, J., et al. Effects of 6 Weeks of Parenteral Cobalamin Supplementation on Clinical and Biochemical Variables in Cats with Gastrointestinal Disease. JVIM 2017, 31, 1664-1672. Ruaux, C.G., et al. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. JVIM 2005, 19, 155-160. Toresson, L., et al. Oral cobalamin supplementation in cats with hypocobalaminaemia: A retrospective study. JFMS 2017, 19,1302-1306 Simpson, K.W., et al. Subnormal concentrations of serum cobalamin (vitamin B12) in cats with gastrointestinal disease. JVIM 2001, 15, 26-32. Xenoulis, P.G., et al. Feline Exocrine Pancreatic Insufficiency: A Retrospective Study of 150 Cases. JVIM 2016, 30, 1790-1797.

Dogs Cobalamin (cbl) is a water-soluble vitamin found in proteins of animal origin. It is a vital cofactor for DNA and protein synthesis. Consequently, all cells in the body need cbl. Transport and absorption of cbl is complex, involving several carrier proteins and an Intrinsic Factor (IF), mainly produced by the exocrine pancreas in dogs. Cobalamin binds to IF in the duodenum. This complex is transported to the cubam-receptors in the ileum, where cbl is absorbed. Documented diseases causing cbl deficiency in dogs are either affecting IF production, as seen in Exocrine Pancreatic Insuffisciency (EPI), associated with defect cubam-receptors (in congenital cbl deficiency), or mucosal damage, causing decreased expression of the cubam-receptors (in chronic enteropathies (CE) and/or intestinal lymphoma). Intestinal dysbiosis could further result in cbl deficiency, as some anaerobes are capable of adhering to the cbl-IF complex, making it unavailable for absorption. The most common reasons for cbl deficiency in dogs are CE and EPI. If cbl deficiency is diagnosed, the function of the exocrine pancreas has to be assessed for further work-up, diagnosis and treatment. In dogs with CE, it has been suggested that a poor response to treatment of the underlying condition occurs if cbl deficiency is not corrected. Cbl deficiency is further a proven negative prognostic factor in dogs with CE, EPI or chronic diarrhea. Congenital cbl deficiency is a rare condition, reported in Shar Peis, Giant Schnauzers, Beagles, Australian Shepherds and Border Collies. Affected dogs usually present at an early age with lethargy, failure to thrive, anorexia, a poor body condition score, vomiting and diarrhea, and sometimes seizures, although Shar Peis usually present later in life with mainly GI signs. To diagnose cbl deficiency in humans, both low serum cbl concentrations and increased levels of biomarkers of cbl deficiency are required, since serum cbl concentration may not reflect the intracellular levels of cbl correctly. The intracellular biomarkers methylmalonic

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acid (MMA) and homocysteine (HCY) have also been studied in dogs with cbl deficiency. An association between MMA and serum cbl concentrations has been shown, as well as a correlation between HCY and serum cbl concentrations in breeds affected with familial cbl deficiency. At present, it is not proven if these biomarkers should belong to the standard diagnostic profile in cbl deficiency. The traditional supplementation protocol involves multiple parenteral injections. Recent studies have shown that oral cbl supplementation also is effective in treating cbl deficient dogs with CE or EPI, as previously shown in people. An alternative intestinal uptake of cbl, independent of IF or an intact ileum, has been shown in humans. Successful oral supplementation of dogs with EPI suggests that dogs too have an alternative absorptive pathway of cbl.

Selected references: 1)

2) 3) 4)

Berghoff, N., Suchodolski, J.S., Steiner, J.M., 2012. Association between serum cobalamin and methylmalonic acid concentrations in dogs. Veterinary journal 191, 306-311. Grutzner, N., et al. Serum homocysteine and methylmalonic acid concentrations in Chinese Shar-Pei dogs with cobalamin deficiency. Vet J 2013, 197, 420-426 Ruaux, C.G. Cobalamin in companion animals: diagnostic marker, deficiency states and therapeutic implications. Vet J 2013, 196, 145-152. Toresson, L., et al. Comparison of efficacy of oral and parenteral cobalamin supplementation in normalising low cobalamin concentrations in dogs: A randomised controlled study. Vet J 2018, 232, 27-32. Vidal-Alaball, J., et al. Oral vitamin B12 versus intramuscular vitamin B12 for vitamin B12 deficiency. The Cochrane database of systematic reviews 2005 (3):CD004655. doi, CD004655.

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Acute hemorrhagic diarrhea (AHD) is a common reason for dogs to be presented to primary care veterinarians, and the first goal when presented with such a patient is to differentiate gastrointestinal bleeding (e.g., due to coagulopathies or GI ulceration) from hemorrhagic enteritis. This can usually be achieved by determination of the packed cell volume (PCV), since dogs with acute hemorrhagic enteritis typically have severe fluid loss into the intestinal tract and often have significantly increased PCV on presentation. There are numerous potential causes for hemorrhagic enteritis. However, in most cases the underlying cause cannot be identified using routine diagnostic tests. For these cases of sudden onset of severe hemorrhagic diarrhea of unknown cause the term “hemorrhagic gastroenteritis” (HGE) was established in the 1970s and defined as a specific syndrome. In a more recent prospective study, endoscopic and histologic mucosal changes as well as the presence of bacterial species in the intestines of 10 dogs with AHD were evaluated. In these dogs dense layers of large rod-shaped bacteria identified as C. perfringens type A strains were intimately associated with the epithelial necrosis in both the small and large intestines. However, no lesions were identified in the stomach. Two conclusions can be drawn from this study: 1) C. perfringens are responsible for the epithelial necrosis, and 2) the stomach is not primarily involved in the disease process. The syndrome was renamed as “acute hemorrhagic diarrhea syndrome” (AHDS), and a search for clostridial toxins capable of damaging the mucosa in these dogs was initiated. In 2015, a novel toxin designated as NetF was detected in a C. perfringens type A strain isolated from a dog with fatal hemorrhagic enteritis. By performing in vitro studies, it was confirmed that NetF is highly cytotoxic for an equine ovarian cell line. In addition, several studies showed that the prevalence of C. perfringens encoding the netF gene was significantly higher in dogs with AHDS compared to control dogs. Thus, currently it is believed that an overgrowth of C. perfringens type A strains associated with an increased production of NetF toxins potentially in combination with other clostridial toxins (e.g., Clostridium perfringens enterotoxin - CPE) is the underlying cause for AHDS in dogs. AHDS is a very dynamic disease. C. perfringens strains that encode the netF and cpe gene decrease significantly over the first days and after day seven nearly every dog is below the detection limit of the PCR assay. Because of this rapid decline of toxigenic C. perfringens strains, many dogs with AHDS are already negative for PCR testing at presentation -

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especially if dogs are not tested during the acute phase of the disease. Therefore, the diagnosis of AHDS is still based on typical clinical course of the disease and by excluding other known causes of AHD. A serum biochemistry profile, including serum bile acids and acute pancreatitis. Furthermore, to rule out hypoadrenocorticism, a serum baseline cortisol concentration should be determined, followed by an ACTH stimulation test if the test result canine parvovirus) should be performed to rule out nematodes, protozoan parasites and parvovirosis in suspicious cases. An abdominal ultrasound and/or radiographic examination is indicated to rule out a foreign body, focal intestinal disease, or pancreatitis and should be performed in older dogs and dogs not adequately responding to symptomatic therapy. Diagnosing a bacterial infection causing hemorrhagic enteritis is challenging, since potentially enteropathogenic bacteria can also be found in healthy dogs. Positive test results on diarrhea panels (e.g., fecal culture for enteropathogens, PCR testing for bacterial genes encoding for toxins) are not an indication for antibiotic treatment per se. AHDS is characterized by its rapid self-limiting course with symptomatic treatment. Thus, antimicrobials should only be administered to patients that manifest systemic signs of illness after rehydration and pain management. With adequate fluid therapy (i.e., administration of crystalloids; volumes are depending on the level of dehydration, maintenance requirements, and ongoing losses) a rapid improvement of clinical signs can typically be observed during the first 48 hours without antibiotic treatment. Dogs that do not adequately respond to fluid therapy after 4 hours (i.e., alert mental status, heart and respiratory rate dropping into normal range, adequate production of urine) should be categorized as â&#x20AC;&#x153;complicated AHDSâ&#x20AC;? patients. Complicated AHDS patients should be evaluated for other underlying causes (e.g., acute pancreatitis, viral enteritis) and systemic infection with pathogenic bacteria should be considered. Antibiotic therapy is also indicated in patients that are immunocompromised (e.g., patients treated with immunosuppressive dosages of a corticosteroid or another immunosuppressant), show evidence of hepatic dysfunction, have a portosystemic shunt flow or a patient that fulfills the criteria listed in Table 1. Additional symptomatic treatment includes antiemetic therapy in every patient that appears nauseated or is actively vomiting (e.g., maropitant 1 mg/kg q24h SQ/IV) and analgesics in every dog with suspected abdominal pain (e.g., buprenorphine 0.01 mg/kg q6-8h IV). Trickle feeding with an oral glutamine solution or low-fat (liquid) diet is important for local nutrition of enterocytes and can improve regeneration of the intestinal mucosa. High-dose probiotic therapy potentially helps to displace C. perfringens strains from the gastrointestinal tract in dogs with AHDS. In summary, there is strong evidence that the clostridial NetF toxin causes intestinal epithelial necrosis in dogs with AHDS. Most dogs with acute hemorrhagic diarrhea present with severe dehydration and show rapid clinical improvement with adequate fluid therapy. Septic complications are uncommon, and prognosis is good, even without antibiotic therapy. However, close patient monitoring is essential to identify dogs requiring antibiotic treatment.

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Table1: Criteria for antibiotic use in dogs with AHDS Physical examination finding at presentation Hyperthermia (°C)

>39.5° C

Physical examination findings after rehydration and pain management Tachycardia (beats/min)

> 140 (small breed dogs) > 120 (large breed dogs)

Tachypnea (breaths/min)

> 40

Hematologic and serum biochemical changes Neutrophilia (cells/l)

> 20 000

Neutropenia (cells/l)

< 3 000

Band neutrophils (cells/l)

> 1500

Hypoglycemia (mmol/l)

< 3.5

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Exocrine pancreatic insufficiency (EPI) in dogs and cats is easily diagnosed by species specific assay of serum trypsin-like immunoreactivity (cTLI, fTLI) at a trusted laboratory. Concurrent assay of serum cobalamin, folate and pancreatic lipase (cPL, fPL) is almost always indicated. Clinical signs and response to treatment are notoriously unreliable ways to make the diagnosis because clinical signs, especially in cats, are highly variable and nonspecific. Also, while treatment always requires oral pancreatic enzyme supplements, other therapies are often required for an optimal response, especially in cats. Most, but not all, affected dogs are relatively young, while most, but not all, affected cats are relatively old. Treatment is almost always required for life, and so omitting specific testing at the start a workup in a patient with gastrointestinal signs is usually a false economy. In both dogs and cats several years of survival with a good quality of life is anticipated once a successful management strategy has been established. Many patients respond well and rapidly (within days) to supplementation of the food with raw pancreas or dried pancreatic enzymes. Others are mildly to severely deficient in cobalamin (less commonly folate) and require appropriate supplementation; even with initial good response to pancreatic enzymes and initial normal serum cobalamin concentrations, nearly all patient will develop cobalamin deficiency insidiously over 1 to 3 years, and so annual testing or preventative supplementation is warranted. Fat malabsorption in these patients predisposes to fat soluble vitamin deficiency too, especially of tocopherol (vitamin E). Rare patients develop vitamin K responsive bleeding problems, but this is not common enough to warrant routine screening or supplementation. Recent evidence suggests that abnormalities in vitamin A status may develop too, but supplementation is not currently recommended. Most if not all patients with EPI have small intestinal dysbiosis too. This has historically been treated with antibiotic treatment (usually tylosin) for 4 to 6 weeks, but probably is most effectively treated long term by dietary change. Unfortunately finding a suitable diet is a trial and error process, what is successful varies from patient to patient. This variability probably reflects the variability of the endogenous microbiota, and differing responses to diets with different non-fermentable and fermentable components. Prebiotic additives in some diets

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may also be beneficial. In general diets with low non-fermentable / insoluble fiber contents are probably preferred in dogs with EPI, a formula utilized in many veterinary â&#x20AC;&#x153;gastrointestinalâ&#x20AC;? diets. In cats, high protein low carbohydrate diets are often effective. In both species hydrolyzed diets may be tried if other diets are ineffective. On-line support groups such as EPI4DOGS.COM may help owners find suggestions for other dietary trials. Drugs that block gastric acid production are rarely if ever helpful. In cases that fail to respond to the above measures a trial of prednisone or prednisolone (cats) is warranted, especially if serum folate is subnormal (this should be rectified as well). This enhances the function of the enterocytes and helps to treat concurrent mucosal enteropathy. Long term therapy is rarely required and the drug can usually be withdrawn after 8 to 12 weeks.

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In general, only healthy cats should be vaccinated. Thus, in cats with acute diseases or short term immunosuppressive vaccination should be postponed. In some situations, however, postponing vaccination would imply a significant risk, such as when entering a shelter environment with high infectious pressure, and in theses specific situations vaccination might be necessary despite acute illness. In addition, some cats suffer life-long from a chronic disease and thus, vaccination cannot be postponed until recovery. Immunosuppression can be caused by a variety of conditions, including feline immunodeficiency virus (FIV) or feline leukemia virus (FeLV) infection, tumors, tumor chemotherapy or radiation, glucocorticoids, cyclosporine, or other immunosuppressive drugs. Some important points have to be considered when vaccinating immunocompromised cats, including (1) the safety of modified-live virus vaccines and the concern that vaccines might regain their pathogenicity if the immune system is not working properly, (2) the question whether vaccines work at all in immunocompromised cats and whether duration of immunity after vaccination is shortened compared to that in healthy cats, (3) the concern that in some of these conditions, e.g., in cats with FIV infection or

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chronic kidney disease, vaccination and resulting immune stimulation might lead to a progression of the disease. In adult FIV-infected cats that had been vaccinated previously and are kept strictly indoors, the risk of being infected with other pathogens is likely lower than the possible harmful effect of vaccination. Thus, booster vaccinations in adult indoor-only cats, that have received previous vaccinations, are not recommended. Protection after vaccination in a cat with progressive FeLV infection is not considered complete and long-lasting. Thus, either more frequent vaccinations (e.g. every 6 months) or measurement of antibodies to assure sufficient protection are recommended. In cats with tumors, protection rate is not comparable to those of healthy cats. Antibody measurement to confirm protection or more frequent boosters (e.g. once yearly) should be considered. In cats with tumor-associated severe neutropenia vaccination should be postponed until tumor chemotherapy improved the condition. Cats with diabetes mellitus should be vaccinated according to the guidelines for healthy cats, but vaccination should be postponed in an uncontrolled diabetic case. Chronic kidney disease can lead to an increased risk for infections but studies suggest a risk association between chronic kidney disease and frequent vaccination in cats. Ideally, antibody levels should be determined and only cats lacking protective antibodies should be vaccinated. Otherwise, booster vaccination is not recommended if the cat has been vaccinated previously and is kept strictly indoors. In cats receiving glucocorticoid therapy, veterinarians should wait > 3 months after discontinuation of glucocorticoid therapy before vaccinating cats that have received highdose systemic steroids for > 2 weeks. If continuous long-term glucocorticoid therapy is necessary, vaccinations schedules should be maintained. Booster vaccination can be given to cats receiving cyclosporine, but novel vaccinations should be applied before cyclosporine treatment is initiated. In cats in which tumor chemotherapy is considered, vaccination should precede the initiation of chemotherapy by > 2 weeks or should be repeated > 3 months after discontinuation of chemotherapy.

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Point of care tests based on enzyme-linked immunosorbent assays (ELISA) or other similar immunomigration-type techniques are available for detection of various infections. In addition, in-house PCR tests for detection of viral, bacterial, or parasitic DNA or RNA are currently under development. Most in-house tests are either based on detection of antibodies that detect pathogen proteins (antigens) or on detection of antigen that detect specific antibodies against a specific pathogen and therefore, contain purified monoclonal antibodies or a specific antigen that bind antigen or antibodies, respectively. A second enzyme-linked antibody serves as signal. Color reaction is preceded by a reaction catalyzed by the enzyme. In-house tests for detection of canine parvovirus (CPV) antigen in feces are highly specific. However, the tests are not capable to differentiate between field and vaccine virus; thus, positive results after vaccination are common. The sensitivity of these tests is very poor. A current study showed a sensitivity of less than 50%. False negative test results can lead to misdiagnosis of CPV infection that can result in inadequate treatment and spread of the virus. The SNAP®4Dx® detects antibodies against Ehrlichia (E.) canis, Borrelia species (spp.), and Anaplasma (A.) phagocytophilum, and antigen of Dirofilaria (D.) immitis. The detection of Borrelia spp. antibodies is based on C6 technology. The SNAP®4Dx® shows a high sensitivity (82%) and specificity (99%) compared to the western blot. Therefore, and because of its simple handling, the SNAP®4Dx® is a very good test for use in practice. An additional benefit is the capability to differentiate between infected and vaccinated dogs, and the fast decrease of C6 antibodies (within about 3 weeks) during treatment. The SNAP®4Dx® also detects antibodies against A. phagocytophilum. Antibodies are still absent in the early course of infection (up to 30 days after infection), but clinical signs (if they occur) usually occur before antibodies can be detected. Thus, the detection of antibodies is not suitable for the diagnosis of an acute clinical manifestation of the disease anaplasmosis. Furthermore, the SNAP®4Dx® detects antibodies against E. canis. The test is highly sensitive and specific. However, in rare cases clinical signs occur before presence of antibodies. The 4th pathogen, that can be detected with the SNAP®4Dx®, is D. immitis. Special proteins of the uterus of adult worms are detected as antigen. The test shows a sensitivity of almost 100%, if at least 2 female adult worms are present. However, antigen tests will only become positive after 5 to 6 months of infection.

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In-house tests that detect feline leukemia virus (FeLV) antigen (and thus diagnose progressive FeLV infection) and feline immunodeficiency virus (FIV) antibodies are commonly used. In addition, point of care tests for detection of FeLV antibodies and inhouse PCR tests for detection of FeLV provirus are currently under development. Those would allow not only to detect progressive, but also regressive, and abortive infections. Currently available in-clinic FeLV and FIV tests are highly sensitive and specific. Several recent studies documented an excellent performance of patient-side FIV/FeLV test kits. Since the consequences of a positive test result are potentially clinically important, confirmatory testing is still recommended in case of a positive test, especially in asymptomatic or indoor only cats for which the likelihood of a false positive result is high.

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In this lecture, Drs. Hartmann and Lappin will discuss two of the most serious potential vaccine side-effects in cats, feline injection site sarcoma and chronic kidney disease (CKD). The potential link between vaccination and CKD in cats was first suggested when it was shown that feline vaccines for which the viruses were grown on cell cultures induced antibodies that cross-react with feline renal tissues (Lappin et al., 2005). Subsequently, it was shown that cats that were hypersensitized with a lysate of a commonly used cell line developed lymphocytic-plasmacytic interstitial nephritis (Lappin et al., 2006). The immunodominant cell line antigen recognized by parenterally vaccinated cats is alphaenolase, which is present in all mammalian cells (Whittemore et al, 2010). In people, antienolase antibodies are markers for immune-mediated disease, including nephritis. Cats develop both post-vaccination and naturally-occurring anti-enolase antibodies and so it can be difficult to determine whether vaccinations is directly associated with CKD in cats. However recently, an epidemiological study associated CKD to vaccination in cats (Elliott et al, 2016). One of the best ways to avoid this potential association is to only administer vaccines that are currently needed and to use vaccines not grown on cells or that are delivered by the intranasal route.

References

Lappin MR, Jensen WA, Jensen TD, Basaraba RJ, Brown CA, Radecki SV. Investigation of the induction of antibodies against Crandell Rees feline kidney cell lysates and feline renal cell lysates after parenteral administration of vaccines

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2) 3) 4) 5)

against feline viral rhinotracheitis, calicivirus, and panleukopenia in cats. Am J Vet Res 2005;66:506-511. Lappin MR, Basaraba RJ, Jensen WA. Interstitial nephritis in cats inoculated with Crandell Rees feline kidney cell lysates. J Feline Med Surg. 2006;8:353-356. Whittemore JC, Hawley JR, Jensen WA, Lappin MR. Antibodies against Crandell Rees feline kidney (CRFK) cell line antigens, alpha-enolase, and annexin A2 in vaccinated and CRFK hyperinoculated cats. Vet Intern Med. 2010;24:306-313. Finch NC, Syme HM, Elliott J. Risk factors for development of chronic kidney Disease in cats. J Vet Intern Med. 2016;30:602-610.

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Presentation is supported by FECAVA

The use of antiviral drugs is still uncommon in veterinary medicine, and the number of controlled studies of the efficacy of these drugs is limited. Unlike with antibacterial therapy, complete elimination of infectious agents is usually not achieved, mainly because viruses are inhibited only during their replicative cycle and are not susceptible during latency. Diagnosis of viral infections is often made after the replicative phase of the virus; thus, antiviral drugs are mainly used to treat chronic viral infections and to prevent reactivation of latent infections. Antiviral drugs also affect the function of host cell machinery, so they have considerable potential for toxicity. Antiviral drugs are widely used in human medicine for treatment of human immunodeficiency virus (HIV), herpesvirus, and other viral infections. Much less is known about these medications in cats and dogs, and there are few diseases of cats and dogs for which efficacy has been proven. There are important differences between human and animal virus infections, so it should never be assumed that an antiviral agent used in people can be used in animals unless there is proof of safety and efficacy. With the exception of feline interferon (IFN)-Ď&#x2030;, no antiviral drugs are licensed for use in dogs and cats. Antiviral drugs can be assigned to different drug classes based on the stage(s) of virus replication they interfere with. Potential targets in the retroviral replication process for antiviral drugs include binding of virus to specific cell surface receptors, entry into the cell and uncoating of the virus, reverse transcription of viral genome, integration of proviral DNA into host genome, viral protein processing, virion assembly and maturation, and virion release. Combinations of antiviral drugs with different mechanisms of action and combinations that include immunomodulatory drugs are increasingly being used to treat human viral infections, especially HIV infection, with an associated decrease in toxicity and reduction in selection for resistant mutants, but data on combination treatment in cats and dogs is limited. Most antiviral drugs available for treatment of feline and canine viral infections are nucleoside analogues with greatest activity against retroviruses and herpesviruses. The retroviral enzyme reverse transcriptase transcribes viral RNA into proviral DNA, which is subsequently integrated into the host cellâ&#x20AC;&#x2122;s genome. Reverse transcriptase inhibitors can be

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divided into 3 categories, nucleoside reverse transcriptase inhibitors (NRTIs), nucleotide reverse transcriptase inhibitors (NtRTIs), and non-nucleoside reverse transcriptase inhibitors (NNRTIs). Of these, NRTIs are the most commonly used. NRTIs are analogues of mammalian 2´-deoxynucleosides, and inhibit the polymerase function of the retroviral reverse transcriptase enzyme. Nucleosides are building blocks for the formation of DNA or RNA that are composed of a nitrogenous base and a 5-carbon sugar (ribose or deoxyribose). Like natural nucleosides, NRTIs must first be converted to a 5´-triphosphate form (nucleotide) through phosphorylation. In this form, they compete with host nucleotides and are incorporated into the elongating proviral DNA strand, thus functioning as competitive substrate inhibitors. However, NRTIs lack a 3´-hydroxyl group on the deoxyribose moiety, and this leads to strand termination as the subsequent nucleotide cannot form the next 5´-3´ phosphodiester bond necessary to extend the DNA strand. This leads to inhibition of virus replication.

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Immunomodulators are also referred to as biologic response modifiers. Their use for treatment of infectious diseases has the potential to be beneficial when compromise of the immune system impairs effective antimicrobial drug treatment. Some of the immunomodulators not only affect the immune system, but also possess true antiviral activity (e.g. interferons, acemannan). In a broader sense, immunomodulators also include drugs that are used to dampen an excessive host inflammatory response, such as glucocorticoids, e.g. used to treat cats with feline infectious peritonitis (FIP). In addition, specific antibodies directed against cytokines, such as against feline tumor necrosis factorfor treatment of cats with FIP. Probiotics also have immunomodulatory activity and have been used to treat virus, e.g. feline herpesvirus-1 (FHV-1), infections. Specific neutralizing antibodies (passive immunization), such as against FHV-1, feline calicivirus (FCV), feline panleukopenia virus (FPV), canine parvovirus (CPV), canine distemper virus (CDV), and infectious canine hepatitis (ICH) virus, have also been used for treatment with variable results. Vaccines, such as intranasal vaccines, also have been used as therapeutic immunomodulators. Treatment of canine and feline viral infections with immunomodulators has frequently yielded disappointing results, and data from large, prospective, controlled clinical trials are lacking. The use of human recombinant cytokines beyond 1 or 2 weeks of treatment has been associated with the development of anti-cytokine antibodies, which can cross-react with endogenous cytokines. In the absence of data from randomized, placebo-controlled clinical trials to support their use, immunomodulators should be used with caution, because they might actually have the potential to accelerate disease. This can occur for viruses that are dependent on rapidly dividing cells for replication, such as parvoviruses, or those that replicate in activated lymphocytes, such as feline immunodeficiency virus (FIV). Promotion of an inflammatory response might also have detrimental effects if immune-mediated processes play an important role in the pathogenesis of disease, such as for FIP. Interferons (IFNs) also belong to the group of immunomodulators, but also have direct antiviral activity. IFNs bind to specific cell surface receptors and stimulate expression of

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proteins that can interfere with various stages of viral replication. Commercially available recombinant IFNs that are mostly used in cats and dogs include human IFN-α and feline IFNω. IFN-ω is licensed for use in cats and dogs in Europe, Asia, and Australia. No severe adverse effects of IFN-ω treatment have been reported in cats and dogs. IFN-ω has been used for treatment of viral infections in cats and dogs with variable success. It has been proven to improve clinical signs and reduce mortality in dogs with CPV infection. Some studies demonstrated clinical improvement in cats with FIV or feline leukemia virus (FeLV) infection, but there was no change in viremia and most cytokine concentrations during treatment which raised questions if the clinical improvement observed resulted from an effect of IFN-ω on secondary infections rather than on the retrovirus infection itself. So far, prove of efficacy is lacking for many virus infections.

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Clinical syndromes induced by infectious agents are common in small animal practice. The combination of signalment, history, and physical examination findings is used to develop a list of differential diagnoses ranking the most likely infectious agents involved. If infectious disease agents are likely, documenting that the infectious agent is still present using cytology, culture, antigen assays, and molecular diagnostic tests like polymerase chain reaction assay is the best way to make a definitive diagnosis. Antibody detection is commonly used to aid in the diagnosis of specific infectious diseases but can be inferior to organism demonstration for three reasons: (1) Antibodies can persist long after an infectious disease has resolved, (2) positive antibody test results do not confirm clinical disease induced by the infectious agent, and (3) in peracute infections, results of serum antibody tests can be negative if the humoral immune responses have not had time to develop. In this lecture, Dr. Lappin will emphasize the key issues associated with antibody assays, antigen assays, and PCR assays. As PCR assays are becoming more routinely available around the world and in clinic PCR assays are now available in some countries, these techniques will be emphasized. PCR assays can be designed that have very high analytical sensitivity and specificity. The assays are most commonly positive in the acute stages of illness and so are best used in cases that have clinical signs that develop primary to production of antibodies; Ehrlichia canis infection is an example that will be presented. PCR assays are also very beneficial for cases that do not have currently available antibody or antigen tests; Mycoplasma haemofelis associated anemia is an example that will be presented. As these assays are very sensitive, results can be positive event though an animal is just a carrier and not sick due to the infection. Feline herpesvirus 1 infection is a great example of this potential problem that will be presented during the lecture.

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Recently, most countries around the world have been attempting to develop protocols encouraging veterinarians to use antibiotics more judiciously. Antimicrobial Guidelines Working Group of the International Society for Companion Animal Infectious Diseases (ISCAID) has now published guidelines for the treatment of urinary tract infections, respiratory infections and superficial pyoderma. This group has members that are internal medicine specialists, microbiologists, or pharmacologists. The published guidelines are on the website for the group (www.iscaid.org). In each document, the committee members strive to emphasize the clinical findings that suggest a bacterial infection, detail the optimal diagnostic plan, and then discuss empirical and culture proven treatments. For example, for acute (less than 10 days) feline bacterial upper respiratory tract infections, the committee suggests that few diagnostic procedures are needed and that if treatment is indicated, the veterinarian should chose empirically between doxycycline and amoxicillin. If the cat does not respond favorably within 10 days, a further diagnostic workup should be performed to rule out other treatable diseases like nasopharyngeal polyps and foreign bodies before prescribing other antibiotics. In this lecture, Dr. Lappin will cover key points concerning the antibiotic treatment of respiratory, urinary, and vector borne diseases.

References Lappin MR, Blondeau J, Boothe D, Breitschwerdt EB, Guardabassi L, Lloyd DH, Papich MG, Rankin SC, Sykes JE, Turnidge J, Weese JS. Antimicrobial use Guidelines for Treatment of Respiratory Tract Disease in Dogs and Cats: Antimicrobial Guidelines Working Group of the International Society for Companion Animal Infectious Diseases. J Vet Intern Med. 2017 Feb 10. doi: 10.1111/jvim.14627. [Epub ahead of print]

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There are multiple pathogenic protozoal diseases in dogs and cats around the world. In this lecture, Dr. Lappin will update the attendees on the most common infections and suggest optimal treatment protocols. Toxoplasma gondii is one of the most common protozoal infections but rarely results in clinical signs of disease. However, when clinical signs are suspected to be from toxoplasmosis, I prescribe clindamycin or azithromycin most frequently. Fever, muscle pain and uveitis has usually responded favorably to clindamycin, but CNS signs and pneumonia may respond better to azithromycin. Recently, it was shown that dogs or cats with Isospora infections should be administered ponazuril (or related compound) at 50 mg/kg, PO, daily for 3 days. This drug class is cidal and so preferred to sulfa and other drugs previously used. During the lecture, the drugs used to treat the enteric protozoans Giardia, Tritrichomonas foetus, and Cryptosporidium spp. will be reviewed. For Giardia, fenbendazole, febantel (labeled for Giardia in some countries), or metronidazole are prescribed most frequently. Newer alternatives include secnidazole and nitazoxanide which will be discussed. The use of probiotics concurrently may be beneficial for management of diarrhea associated with these agents. Ronidazole is still the best T. foetus drug, but there may be up to 35% resistant strains; alternative drugs like quinolones will be discussed. Most cats with suspected C. felis as a co-factor to diarrhea respond to oral administration of azithromycin. Babesia canis (vogeli and others) may respond to imidocarb injections, but B. gibsoni seems to respond best to the combination of azithromycin and atovaquone (or related drug). This protocol has also be used to save about 60% of the cats in the United States that are clinically ill due to Cytauxzoon felis infections.

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Does every patient with azotaemia and impaired urine concentration have renal failure? If not, why not? Urea and creatinine are probably the most commonly measured clinical parameters in small animal practice. To correctly assess what the results mean requires a basic understanding of what the kidney does in health and disease and the impact of non-renal disease on renal function. During this case-based lecture we will review the important factors that influence the kidneyâ&#x20AC;&#x2122;s ability to function to enhance understanding of why patients with azotaemia and poorly concentrated urine do not necessarily have renal disease.

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At what level does an increased ALT or ALP unequivocally indicate liver disease? When are bile acids useful and when are they not? What does a positive PLI really mean? Do the results mean the same in dogs and cats – if not, why not? Liver and pancreatic enzymes and other diagnostic parameters used to assess the hepatobiliary system are commonly measured by veterinarians on unwell patients, prior to anaesthesia or as a general metabolic profile for geriatric animals. Yet deciding exactly what the results mean and what they confirm or rule out can be difficult. During this lecture, I will discuss my top tips for interpreting clin path results related to the liver and pancreas. The learning outcomes for this lecture will include: • • • •

To understand how to interpret liver enzymes and what mild, moderate and marked increases mean To appreciate when bile acids useful and when are they not To learn what a positive PLI really means in dogs and cats To understand why liver and pancreatic clinical pathology results differ in dogs vs cats

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The definition of fever of unknown origin (FUO), as established in human medicine, describes any fever lasting for more than 3 weeks with no obvious or identifiable cause after repeated examinations on ambulant or in-hospital basis. More than 200 different causes have been described in humans so far. Self understandably, such fever is debilitating to the patient and results in significant costs. In small animal medicine, the definition established by Katharine Lunn is most commonly used â&#x20AC;&#x201C; any fever that does not disappear spontaneously within 1 â&#x20AC;&#x201C; 3 days and its cause cannot be disclosed regardless of thorough workup (history, clinical examination, hematology, biochemistry, urinalysis and diagnostic radiography) can be considered to be FUO. This lecture will present a logical, strongly clinic-based approach to a patient with FUO. Usefulness of routine diagnostic tests, like radiography as well indications for specific tests, like advanced imaging and infectious disease screening will be discussed. Treatment options for patients with undisclosed causes of FUO, their advantages and disadvantages will be assessed.

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OVERVIEW Urinary tract infections (UTIs) are common, especially in canines and older cats. UTIs are rare in young cats (< 1%). Relapsing/persistent infections are of concern. PATHOPHYSIOLOGY Most acute UTIs (cystitis) occur in healthy animals with anatomically/functionally healthy urinary tract due to ascending fecal bacteria. These bind to surface receptors of urothelium, invade it and replicate within cytosol to build resistant intracellular bacterial communities (IBCs). CLINICAL SIGNS Typical signs are pollakiuria, stranguria, dysuria and changes in physical appearance of urine. Vaginal or preputial discharge suggest a different cause (e.g. neoplasia, pyometra, urethral stones). Panting, anorexia, fever, vomiting or back pain suggest a pyelonephritis. Prostatitis can lead to paraparesis. PU/PD is frequent in E. coli infections, due to the ADH antagonism. CAUSATIVE AGENTS Acute cystitis is most commonly caused by E. coli. Common isolates also include Staphylococcus spp., Streptococcus spp., Proteus spp and Klebsiella spp., In relapsing/persistent infections, resistant isolates like Enterobacter spp. occur. DIAGNOSTIC APPROACH History, careful clinical examination, urine strip and sediment are a minimal database. Definitive evidence of UTI is a positive urinary culture (cystocenthesis preferred). Up to 18.5% of patients with sterile urine are positive when the bladder mucosa or urolith are cultured. Antimicrobial sensitivity testing is recommended, but does not guarantee therapeutic success. Diagnostic imaging should be done in all relapsing cases. THERAPY Typical clinical signs accompanied by a minimal database results are sufficient evidence of an acute UTI and antibiotic treatment without urinary culture is adequate for first-time infections in young and adult dogs.

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UNCOMPLICATED CYSTITIS Penicillins (amoxicillin, 11 – 15 mg/kg, three times daily; amoxicillin-clavulanate, 12.5 – 25 mg/kg, twice to three times daily) or potentiated sulfonamides (trimethoprimsulfamethoxazole, 15 -30 mg/kg, twice daily) can be recommended. TMS has been associated with immune-mediated side effects especially if used for > 5 days. Duration of therapy is usually set to 7 – 14 days. Antimicrobial must be applied after a walk, to increase the contact time with the urothelium. PYELONEPHRITIS Treatment of pyelonephritis can be difficult. In small animals, E. coli is the most common and fluoroquinolones can be recommended. Treatment duration is usually set to 6 – 8 weeks. In Gram-positive infections, often accompanied with struvite nephrolithiasis, beta-lactams are usually good choice. PROSTATITIS Following antimicrobials penetrate well the prostatic tissue: sulfonamides, chloramphenicol and fluoroquinolones. Fluoroquinolones are usually the best therapeutic option as they possess excellent activity against E. coli, are bactericidal with post-antibiotic effect. Treatment duration should last 3 to 6 weeks. Castration is recommended to reduce the likelihood of relapse. APPROACH TO RELAPSING INFECTIONS Non-antimicrobial strategies include use of probiotics, cranberries or forskolin (efficiency controversial). Prophylactic antibiotic therapy is often the only option. Amoxicillin (20 mg/kg, once daily for Gram + bacteria), nitrofurantoin (4 mg/kg, once daily for Gram – bacteria) are good choices. The drug should be applied after the last walk. Novel therapies like E. coli vaccines are investigated.

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Intervertebral disk disease (IVDD) is the most frequent disease diagnosed in canine spine. Disk degeneration predisposes patient for disk herniation: extrusion or protrusion. For a long time it has been thought that two different types of disk degeneration exist in dogs: chondroid (in chondrodystrophic) and fibroid (in nonchondrodystrophic) breeds. Recent research has shown that in both types of breeds might exists the same type of degeneration: the chondroid degeneration. Nevertheless, the chondroid metaplasia in chondrodystrophic breeds is more complete (all disks degenerate, disk calcification frequent), quick (disk degeneration observed in juvenile animals already) and predisposing animals for disk extrusion. In contrary, chondroid metaplasia in nonchondrodystrophic animals usually affects just several disks within the spine, starts later in life (around 5 years), is associated with secondary spondylosis and is predisposing animals for disk protrusion. New information concerning inheritance of disk degeneration in chondrodystrophic breeds became available. In 2009 an FGF4-retrogene insertion in dog chromosome 18 (FGF4-18) causing short-legged phenotype known as chondrodysplasia (CDPA) was discovered. In 2017 a second FGF4-retrogene insertion in dog chromosome 12 causing a short-legged phenotype and abnormal premature degeneration of intervertebral discs known as chondrodysdrophy (CDDY) was described. Preliminary available data indicate that Dachshunds will be homozygous for both of these risk factors. It has been postulated that extremely small, low and long phenotypes should be avoided in breeding as they predispose dogs for intervertebral disk disease. Recently new types of disk herniation have been described. Acute noncompressive nucleus pulposus extrusion is characterized by sudden extrusion of nucleus pulposus causing spinal cord contusion without compression. Disease has peracute onset during play or trauma, is frequently asymmetrical in clinical appearance and is not associated with pain. Diagnosis is based on MRI examination and therapy includes supportive care. The other type of disk herniation described recently is acute compressive hydrated nucleus pulposus extrusion. It is characterized by gelatinous and hydrated nucleus pulposus

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extrusion and spinal cord compression which can be identified on MRI. Disease has predilection for cervical region although also thoracolumbar vertebral column can be affected. Although it has been advocated that this type of extrusion might be treated conservatively with good results, in cases with severe clinical signs and considerable spinal cord compression surgery is indicated. Over 80% of dogs with disk herniation have a significant inflammatory reaction in the epidural space at the site of extrusion. It seems that the higher the inflammatory response in IVDD the more negative might be the outcome. Further research might reveal new and additional treatment strategies in this frequent and serious disease of cats and dogs.

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Patients with diseases of spine and/or spinal cord can be divided in two groups: the ones with neurological deficits and the ones without. Presence of neurological deficits indicates spinal cord or cauda equina involvement. Since spinal cord or nerve roots/nerves cannot be visualized on x-rays it is questionable if performing x-rays before referral in paralyzed patients is at all justified. It is very important that clinician has a clear understanding of the list of the differential diagnoses. If patient is presented with a clear and localized pain and a discospondylitis or a bone tumor is suspected x-ray might be diagnostic. Patient with history of trauma, can be x-rayed in order to assess the bony changes. Although x-rays might provide initial information in cases with intervertebral disk disease, degenerative lumbosacral stenosis and cervical spondylomyelopathy, these diseases cannot be diagnosed on x-rays. Value of x-rays in these conditions is limited and might be misleading. Narrowing of intervertebral disk does not confirm disk herniation or spinal cord compression. Although disk calcification is a clear sign of disk degeneration it does not indicate disk herniation. Disk calcifications are frequent in chondrodystrophic breeds and in most cases are asymptomatic. The same goes with degenerative lumbosacral stenosis and cervical spondylomyelopathy. Spondylosis in the lumbosacral area is a frequent sign of disk degeneration, nevertheless it can be frequently seen in dogs without any clinical signs. Caudal cervical vertebrae can be totally normal in cases with cervical spondylomyelopathy and clearly misshaped vertebras can be seen in Dobermans without signs of CSM. Ischaemic myelopathy, syringomyelia, spinal cord tumors, meningomyelitis, acute noncompressive nucleus pulposus extrusion, steroid-responsive meningitis-arteritis, subarachnoid diverticulum and degenerative myelopathy can not be seen and diagnosed on x-rays. Vertebral anomalies in brachycephalic breeds, diffuse idiopathic skeletal hyperostosis (DISH) and spondylosis deformans in giant breeds as well as transitional vertebra are frequent but usually asymptomatic findings. Vertebral anomalies are seen in more than 90% of French bulldogs and in more than 70% of Pugs but just around 1% of French bulldogs and only 4% of Pugs were diagnosed with a thoracic vertebral malformation as the cause of their clinical signs.

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Prevalence of lumbosacral transitional vertebra has been reported to be around 3% in medium and large breed dogs. Lumbosacral transitional vertebra may predispose German Shepherd dogs for the development of degenerative lumbosacral stenosis. Interestingly, a congenital predisposition for early degeneration of the lumbosacral intervertebral disc has been suspected in German Shepherd breed. Spondylosis deformans is acquired disease secondary to disk degeneration or damage. Finding of spondylosis deformans on plain radiographs is usually an accidental finding having no clinical relevance. In cases where bony spurs ascend dorsally and impinge on the exiting spinal nerve roots, the possibility of pain and neurologic abnormalities must be considered. Diffuse idiopathic skeletal hyperostosis is characterized in dogs by the new bone formation along the ventral longitudinal ligament and is not associated with the degenerative changes within the intervertebral disk. The etiology of DISH is suspected to be genetic.

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Chiari-like malformation (CM) has been defined as a multifactorial condition causing overcrowding of the caudal cranial fossa and craniocervical junction (CCJ). Syringomyelia (SM) is characterized by fluid-filled cavities within the spinal cord and occurs commonly in the cervical spinal cord. The disease is commonly encountered in Cavalier King Charles Spaniels and Griffox Bruxellois dogs, and in some toy breed dogs, such as Chihuahuas. Morphometric studies suggest that SM-affected dogs have a smaller caudal cranial fossa and relative caudal cranial fossa overcrowding, although other studies have challenged these results. It has further been suggested that cranial venous outflow is impaired in SM-affected dogs, which might also contribute to the pathogenesis of SM. Recently, in addition to CM, other CCJ abnormalities, such as dorsal spinal cord compression at the first 2 cervical vertebrae, caudal position of the medulla oblongata, and atlantooccipital overlapping, have been reported to be associated with SM. Although not all SM-affected dogs show clinical signs, SM is an important predisposing factor for the presence of clinical signs. Many of the clinical signs in dogs with CM and SM, like persistent scratching episodes (ears, and shoulders) with or without skin contact, facial rubbing, spinal pain and vocalization (without an obvious cause) are interpreted as signs of neuropathic pain. Additionally, ataxia can be witnessed. The presence of clinical signs are more likely, if the syrinx is large, asymmetrical and extends into the dorsal horn of the spinal cord. In humans, type I Chiari malformation (a human counterpart of canine CM), is also associated with neuropathic pain, and it has been suggested that various CCJ abnormalities especially if occurring concomitantly, are associated with the presence of clinical signs in dogs, too. Neuropathic pain is caused by a disease or a lesion that causes damage or dysfunction of the somatosensory system. Neuropathic pain can manifest as evoked (stimulus dependent hypersensitivity) or spontaneous pain, and the sigs can be either intermittent or continuous in nature. Humans with SM describe often suboccipital headache, neck pain, continuous burning and discomfort in the shoulders, neck, the chest or the upper limbs. Additionally, hyperalgesia (excessively painful response to a mildly painful stimulus), allodynia (a painful

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response to a non-painful stimulus) and radicular pain have been described. Neuropathic pain is considered to be caused by sensitization of the central nervous system causing amplification of the nociceptive input by release of excitatory neurotransmitters, increased expression of voltage gated sodium channels and alterations of NMDA- and AMPAreceptors. Treatment of neuropathic pain can be challenging. In people, antiepileptic medications such as gabapentin and pregabalin alone or in combination with antidepressive medication is commonly recommended. Extrapolating from human studies, the use of gabapentin (1020mg/kg TID) or pregabalin (4mg/kg BID) has been suggested in dogs. If not responsive to antiepileptic medication, tricyclic antidepressant amitriptyline (3-4mg/kg BID) or NMDAantagonist amantadine (3-5mg/kg SID-BID) can be prescribed. Surgery is commonly used in treating people with CM and SM, and it has been described in dogs, too. Though majority of the dogs improve after surgery, resolution of the syrinx is uncommon and in many dogs the clinical signs recur in a median of one year after surgery.

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Epileptic seizures can be a symptom of variable causes: reactive seizures caused by systemic metabolic disorders, structural epilepsy caused by structural forebrain disorders and idiopathic epilepsy. In reactive seizures, the treatment focuses on correcting the underlining metabolic disorder, and in structural epilepsy correcting the underlining disorder (if possible) in addition to administering antiepileptic medication (AEM). Currently, The International Veterinary Epilepsy Task Force suggests initiating a long-term AEM, when the seizure frequency is less than 1 per 3 months, if a cluster seizure (more than 1 seizure occurring during 24h) or status epilepticus (a seizure lasting more than 5 min) occurs. Additionally, if the postictal signs are severe and last >24h it is recommended to start the AEM. When choosing an AEM it is important to consider the efficacy of the AEM, possible adverse effects, safety, drug interactions, frequency of administration, legal regulations, concurrent other diseases (like hepatic disease) and owner related factors, like financial restraints. In all cases the dose should be tailored individually based on seizure control, adverse effects and drug concentration results (if applicable). Ideally, monotherapy is used. An additional AEM is administered if seizure control is poor (with serum drug concentration in the reference range), or the adverse effects of the first AEM are intolerable. Phenobarbital is an effective AEM. The most common adverse effects are dose dependent and include sedation, ataxia, polyphagia, polydipsia and polyuria and it has the risk of causing hepatic injury. The recommended oral starting dose in dogs is 2.5-3mg/kg BID in dogs and 1-2mg/kg BID in cats. The therapeutic range of phenobarbital in serum is 15hepatotoxicity in dogs. As cats are more sensitive to the sedative effect of phenobarbital, a serum concentration of 10Imepitoin is recommended to be used as monotherapy in dogs suffering from single generalized epileptic seizures. Adverse reactions are commonly transient and include for example polyphagia, polyuria, polydipsia, hyperactivity and somnolence. The recommended dose is 10-30mg/kg BID in dogs, and a dose of 30mg/kg BID has been suggested in cats.

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Potassium bromide (KBr) has been reported to be less efficacious and tolerable than phenobarbital. Common, dose dependent adverse effects are sedation ataxia, polydipsia, polyuria and polyphagia, and it may increase the risk for pancreatitis. A recommended dose for KBr is 20mg/kg BID when used as monotherapy and 15mg/kg BID when used as an addon drug. Potassium bromide is not recommended to be used in cats. Levetiracetam can be used in both dogs and cats as an add-on drug, and a dose of 20mg/kg TID-QID in dogs and 20mg/kg TID in cats has been recommended. Status epilepticus is a life-threatening condition. During status epilepticus the treatment targets to stop epileptic activity and to correct the physiological disturbances caused by prolonged epileptic activity. Additionally, serum biochemistry, CBC and blood gases should be analyzed to rule out metabolic causes. To stop epileptic activity, diazepam (0.5-2.0mg/kg iv,in,pr, can be repeated twice) or midazolam (0.1-0.3mg/kg iv,in,pr) can be used. Additional, longer acting AEM, like phenobarbital or levetiracetam should be used, and a loading dose for phenobarbital (16-24mg/kg during 24h divided in 4mg/kg doses) and levetiracetam (3060mg/kg iv) have been suggested.

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In the diagnostics of epilepsy it is important to establish whether the behavioral event is truly a seizure before attempting to identify the underlying cause. This evaluation is usually based on the data obtained from the owners or based on the assessment of home-made videos. Still, it may be difficult even for a specialist to determine whether paroxysmal behavior represents a seizure or a non-epileptic event. Video-EEG and observation of simultaneous EEG changes and the actual behavioral event would be the only way to definitely differentiate epileptic versus non-epileptic behavioral paroxysms. The clinical manifestation of a seizure depends on the brain area involved in the epileptic activity and may contain motor, behavioral and autonomic signs. In case of a generalized tonic-clonic seizure with lost consciousness it is rather easy to recognize this as an epileptic event. Instead, in case of focal seizures it may be more difficult to determine whether the event is epileptic or not. An epileptic seizure can be suspected based on the sudden onset and offset, typical pattern of each event, presence of involuntary motor activity, decreased consciousness, or autonomic signs such as salivation, urination or defecation. In most cases there is increased muscle tone accompanying motor movements or collapse which helps to differentiate epileptic seizures from other forms of collapse. Recognition of pre-ictal or post-ictal signs may also help to determine the epileptic nature of the event. Additionally, it is important to observe the length of the episodes, possible behavioral abnormalities between the episodes, or familial history of seizures. Several other diseases may present with paroxysmal abnormal activity and should be considered when evaluating whether a paroxysmal event is a manifestation of seizure activity or not. These include neuromuscular collapse (e.g. myasthenia gravis), cardiovascular disease causing syncope, sleep disorders (REM sleep disorders and narcolepsy/cataplexy), obsessive compulsive disorders and paroxysmal movement disorders. Paroxysmal movement disorders or paroxysmal dyskinesias (PD) are a group of conditions characterized by episodes of disturbed movement that are self-limiting. The duration of episodes varies from seconds to hours with the beginning and end of movement disturbance being abrupt. There are no autonomic signs during the episodes, consciousness is not impaired and abnormal post-ictal behavior is not observed. A recent report suggests the

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following classification of PDs in veterinary medicine: PDs with genetic, dietary, secondary, and unidentified causes. For the majority of PDs, no specific biological marker exits that would definitely identify the condition. Breed-specific features can aid in achieving a definite diagnosis. These include genetic testing in episodic falling syndrome in Cavalier King Charles Spaniels, and serological testing for gluten-specific antibodies in Canine epileptoid cramping syndrome in Border Terriers. Brain MRI scan and CSF analysis are used to exclude secondary PDs (caused by an intracranial disease) although the diagnostic value of this in dogs with video footage and historical data supporting PD, without neurological deficits, is low. Finally, it is important to bear in mind that a similar clinical manifestation does not always mean similar etiology. For example, ‘fly-catching syndrome’ seems to be an epileptic disorder in some patients and in others represents an obsessive-compulsive disorder. The same seems to be true in patients with ‘idiopathic head-bobbing’.

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Classification of epileptic seizures and epilepsy and the definition of the corresponding terminology are ongoing processes, and the International League Against Epilepsy (ILAE) has published several reports revising the terminology in human medicine. In 2015, the International Veterinary Epilepsy Task Force (IVETF) published consensus statements on the key areas in the field of veterinary epilepsy corresponding to reports of the ILAE. An epileptic seizure is a manifestation of excessive, synchronous, usually self-limiting activity of neurons in the brain. Seizure types can be divided into self-limited and continuous seizures. Seizures are further classified as focal, generalized, and focal seizures evolving into generalized epileptic seizures. In focal seizures the abnormal electrical activity arises in a localized group of neurons or network within one hemisphere. Focal seizures are characterized by lateralized and/or regional signs. Thus, focal seizures can present with focal motor phenomena including facial twitches or repeated rhythmic jerks of one extremity, with parasympathetic and epigastric components including hypersalivation or vomiting, or with episodic change in behavior including restlessness or abnormal attention seeking. Generalized seizures are characterized by involvement of both sides of the body, thus involving both cerebral hemispheres. Generalized seizures may occur alone or evolve from a focal seizure. Epilepsy can also be classified based on the etiology. In idiopathic epilepsy (IE; epilepsy per se) there is no underlying brain abnormality and IVETF has further divided it into three subclasses, namely idiopathic â&#x20AC;&#x201C; genetic (a causative gene for epilepsy has been identified/confirmed genetic background), idiopathic â&#x20AC;&#x201C;suspected genetic (a genetic influence supported by a high breed prevalence (>2 %), genealogical analysis and/or familial accumulation of epileptic individuals), and idiopathic â&#x20AC;&#x201C; unknown cause. Structural epilepsy is a result of an identifiable structural lesion of the brain, including vascular, inflammatory/infectious, traumatic, anomalous, neoplastic and degenerative diseases, and it is important to notice that these can also be inherited (genetic) diseases. Reactive seizures occur as a response of normal brain to an extracranial disturbance (metabolic conditions like

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hypoglycemia or electrolyte abnormalities, or toxins), and should not be considered as epilepsy. In human medicine, single-gene epilepsies, including recessive and dominant Mendelian epilepsy genes, represent the minority of genetic epilepsies. Instead of monogenic epilepsies, most genetic epilepsies are thought to have polygenic inheritance determined by multiple genes with or without environmental influences. To date, two monogenic idiopathic epilepsies have been recognized in veterinary medicine, namely benign familial juvenile epilepsy in Lagotto Romagnolo dogs (LGI2) and juvenile myoclonic epilepsy in Rhodesian Ridgeback dogs (DIRAS1). Additionally, ADAM 23 has been reported to be a risk gene for IE in several dog breeds including Belgian Shepherd dogs. Neurobehavioral comorbidities, such as psychiatric, cognitive, and social deficits, are evident in children and adults with epilepsy. Different epilepsy syndromes recognized in human medicine may pose different risk for comorbidities. To date only few studies have investigated the existence of neurobehavioral comorbidities in dogs with epilepsy. Researchers have reported increased anxiety and ADHD-like behavior, and recently also cognitive dysfunction in dogs with IE.

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Pain can be described as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain evoking stimuli share the features that they are, or may soon become, injurious to body tissue. Pain can be classified into nociceptive and neurogenic pain. Nociceptive pain represent the normal response to noxious insult or injury of tissues, and is further divided into somatic and visceral pain. Somatic pain is detected by the nerves located in the skin, muscles, and joints. Somatic pain is often well localized and experienced as a sharp pain, a dull ache, or a burning sensation. Visceral pain is detected by nociceptors in the body's internal organs. Sensory nerves in the internal organs are not as widespread as they are in the body's muscles and skin, making visceral pain feel dull and hard to localize. Neurogenic pain is defined as pain due to dysfunction of the peripheral or central nervous system. This type of pain is often described as shooting pain Recognizing pain Animals are not able to verbally describe if they are in pain, nor where the pain is coming from. As clinicians we need to be able to recognise not only the presence of pain in our patients, but also how pain is expressed depending on its underlying aetiology. We also need to be aware that different species (and individuals) express pain in different ways. Possible behavioural effects of pain          

Decreased appetite Altered sleep Alterations in gait including changes in locomotion Alterations in facial expression “squinting of the eyes” Abnormal posture Reluctance to move Aversion to gentle palpation Changes in grooming activity Self-mutilation including excessive licking or scratching Vocalisation

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

Aggression

Back pain and neck pain, contributed to damage of the nervous system, represent a neurogenic pain characterised by a shooting experience. The pain may be very intense, appear unprovoked or may be triggered by small postural changes. Common behavioural effects of spinal pain: dog    



Common behavioural effects of spinal pain: cat

Vocalisation (changing position, when lifted, collar is put on, unprovoked) Changes in posture (arched back, lowered head, torticollis) Prefers to lie sternally Change in activity level (reluctant to play, go for walks, to jump up in the car/furniture) Avoids shaking its body

    

Changes in posture (arched back) Changes in activity level (reluctant to go outside, to jump) Changes in litter box use (may soil outside the litter box) Constipation Spends less time grooming/excessive grooming

Differentials to spinal pain: •

•

Orthopaedic pain is in general somatic pain. The most common presentation of orthopaedic pain is lameness. The most common cause of lameness is orthopaedic but neurologic causes should always be considered (indicating entrapment or compression of a nerve or nerve root). Examples of orthopaedic pain that may be mistaken for back pain are a cranial cruciate ligament rupture and polyarthritis. Abdominal pain is visceral pain, often expressed as loss of appetite, decreased activity and abnormal posture (“guarding” the abdomen, leaning forward in a “praying” position). Examples of abdominal pain that may be mistaken for back pain are pancreatitis, a splenic tumour and pyelonephritis. Neuromuscular pain; neuropathy, myopathy and synaptic disease may be mistaken for back pain. Pain may be intense as with vascular lesions such as femoral thrombus (more common in cats than dogs) or the patient may present with a stilted “stiff” gait as with a polymyositis.

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X-rays and computed tomography (CT) studies are created by using external radiation to produce images of the body, making this technique useful for diagnosing lesions in the bone. X-rays and CT examinations are however less useful when soft tissues, including the spinal cord, needs examining. Magnetic resonance imaging (MRI), using the body´s natural magnetic properties to produce detailed images of any part of the body, is the preferred diagnostic modality for most spinal cord disorders. The spine can be affected by various disorders e.g. vascular insults and inflammatory disease. The signalment and history of the patient are important in helping to make a list of differentials. Age, breed, associated spinal pain, clinical course, presence of fever are especially helpful in ranking these differentials as more or less likely. Vascular disorders •

•

Fibrocartilaginous emboli are characterized by a peracute onset of asymmetric neurological signs and are fairly common in dogs (rare in cats). Although pain upon spinal manipulation is not found most dogs seem agitated upon presentation, progression of neurological deficits may be seen the first 24 hours, after that improvement is expected. Ischemic myelopathy may present as a consequence of external injury (more often in cats). Severe abdominal compression, such as could occur if a car tire ran over the cat can cause a prolonged vasospasm of the lumbar arteries and cause an ischemic myelopathy.

Inflammatory disorders • • •

•

Immune-mediated or infectious disorders may affect the spinal cord. Infectious aetiologies are far more uncommon than autoimmune. Steroid responsive meningo-arteritis is a fairly common immune-mediated disorder affecting mainly young, large breed dogs. Severe spinal, mostly neck, pain is the most common sign, fever may be seen acutely and in more chronic cases neurological signs may present. Spinal involvement may be seen alone or in conjunction with brain lesions in immune-mediated meningoencephalomyelitis.

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Anomalies affecting the spine •

• •

Congenital vertebral anomalies are common especially in screw-tailed breeds and although the majority are incidental some are clinically important. Congenital vertebral anomalies are best appreciated on X-rays/CT examination. MRI is however needed to verify their clinical importance. Congenital subarachnoid diverticulaes. Sporadic reports in several dog breeds, may be more common in Pugs. Syringohydromyelia, develops as a consequence of disturbed flow of cerebrospinal fluid. Described in many breeds in association with an underdeveloped caudal cranial fossa.

Neoplastic disorders •

The central nervous system can be affected by neoplasia either directly or indirectly (by interfering with the spinal cord e.g. vertebral tumour). The majority have a slow onset of progressive signs including spinal pain, paresis and ataxia.

Degenerative disorders •

•

Intervertebral disc disease (IVDD) is the most common cause of spinal cord lesions in dogs, less common in cats. Depending on the underlying disk pathology (Hansen type I or type II) the clinical presentation may vary greatly, e.g. acute onset of paraplegia and loss of pain perception with disc extrusions, or chronic spinal pain with a disc protrusion. X-rays are not sensitive enough to diagnose IVDD and should never be the used to plan your surgical treatment of IVDD. Degenerative myelopathy is a chronic slowly progressive disorder with a genetic predisposition. Pelvic limb involvement without obvious signs of spinal pain may progress to include faecal and urinary incontinence and thoracic limbs late in the clinical course.

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In 1622 Richard Bannister wrote “If one feele the eye by rubbing upon the eie-lids that the eye be growne more solid and hard than naturally it should be…..the humour settled in the hollow nerves be growne to any or solid substance, it is not possible to be cured.” (Quoted in Sorsby A; 1963; A Modern Ophthalmology). Quite obviously digital tonometry was around in those days for the human patient, albeit that the digit was the clinician`s finger, but fundamentally the diagnosis and prognosis for glaucoma remain approximately the same when those words are applied to our canine and feline patients in this, the 21st. century. Little did he know it, but Bannister had identified the failure of axoplasmic flow in his observation that the “hollow nerves be growne to any or solid substance”. In glaucoma it is increased intraocular pressure (IOP) that causes the axon shut down responsible for retinal ganglion cell (RGC) death by apoptosis and hence the loss of sight. In our patients glaucoma is generally accepted as being a pathological process of varied aetiology in which there is a sustained rise in IOP beyond normal physiological limits. If one thinks about the normal eye as a bathroom sink with the taps running and plughole open, then in a glaucoma situation the taps are still running but the plughole is either partially or totally blocked. In this bathroom sink analogy the sink would fill and then overflow, but in glaucoma with the eye being an enclosed sphere there can be no overflow, so the internal pressure builds up. For the sink it is the plughole that is the cause of the problem and for our patients it is a defect within the aqueous outflow pathways that is the reason for the rise in IOP. These defects are several, some known but others speculative and as such glaucoma may present to the clinician in several ways, but basically as an acute onset problem or it may be much slower in onset. Acute onset glaucomas are sudden, painful and blinding, whereas the more slower glaucomas may be pain free and not observed until the effect on

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sight is noticed. The cause of sight loss is the same in all glaucomas and that is the immediate or slowly progressive degeneration of the RGC`s. As clinicians we classify the glaucomas we see as either being inherited or acquired. Inherited glaucoma is further described as either angle closure (narrow angle)(PACG) or open angle disease (POAG). In the former goniodysgenesis with pectinate ligament abnormality is the predisposing factor and there is sudden closure of the aqueous drainage pathway to deny drainage and cause the disease. In POAG the ciliary cleft remains patent until the end stage of the disease. Defective mucometalloprotease (MMP) activity in the formation of extracellular matrix involving the trabecular meshwork, the lens zonule and possibly the lamina cribrosa has been shown to be the cause. For the acquired or secondary glaucomas the causes are several and include trauma, uveitis, neoplasia, lens luxation, the pigment dispersal syndrome and cataract related problems. Early diagnosis and effective hypotensive therapy are essential if RGC degeneration is to be prevented, but although this advice is easily written in practice it is beset with problems. Acute onset glaucoma may be readily diagnosed, but restoring normal function to the aqueous outflow pathways is not readily achievable. It is not easy to generalise for the unknown factor in treatment is the amount of residual drainage that is possible through the defective ciliary cleft and associated structures. There are clues in the history and from the diagnostic work-up, but the drug induced suppression of aqueous production does nothing to restore normal drainage. The possibility of increasing uveo-scleral drainage is dependent on an ability to access the ciliary cleft and the permeability of the trabecular meshwork. To date the beneficial results of angle bypass surgery are not sustained for the long term. A quick and easy method of determining the facility of aqueous outflow would be useful in assessing the value of medical therapy, the various cyclo-destructive techniques and the necessity of angle bypass surgery. Again generalising within this picture of the varied aetiologies involved in the obstruction to aqueous drainage, it is the slow glaucomas for which IOP can be reduced, but late diagnosis means irreversible RGC degeneration. It has been shown in some, but not all human studies in the treatment of open angle glaucoma where early diagnosis is possible that the early use of angle bypass surgery can lead to a rebound thickening of the nerve fibre layer, indicating an RGC recovery which is accompanied by a maintenance of visual status. In breeds like the Norwegian Elkhound and the Petit Basset Griffon Vendeen the early treatment of POAG should be attended by a good prognosis simply because predisposed dogs can be identified by a DNA test. On the other hand PACG will remain a problem until more effective surgical drainage procedures are available. For the acquired glaucomas adequate treatment of the initial problem is required : for example uveitic complications leading to synechial occlusion of the drainage pathways should be prevented and the emergency removal of the anteriorly luxated lens may prevent permanent collapse of the ciliary cleft. Is the treatment of glaucoma possible? The answer is a qualified yes and it requires early diagnosis, effective hypotensive therapy and the development of effective RGC protection.

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Worldwide there are probably some 400 + genetically determined diseases in what is a highly inbred population of pedigree dogs. In the in the United Kingdom 32 types of inherited ocular disease are seen in 59 breeds, with another 49 breeds under investigation for these diseases. Contrary to popular belief the mutations responsible for these diseases have not been created by dog breeders for they are to be found as part of the canine genome, but it is the concentration of breeding within certain lines which has led to the dominance of these mutations in those lines and the emergence of disease. There has been strong selection for certain anatomical features, some of which are directly responsible for disease, whilst the selection of desirable features which have no adverse effects in themselves has unfortunately resulted in the co-selection of disease mutations. Thus we see conformational abnormalities such as euryblepharon resulting in conjunctival and corneal disease whilst the search for temperament or the set of ears may unwittingly co-select cataract or a serious retinal disease. As veterinary surgeons we should have a strong voice in effecting those changes to breed standards which have resulted in conformational predisposition to disease. Even today you may see examples of poor conformation at dog shows at which dogs considered to be the finest examples of their breed and therefore potential breeding stock are being celebrated. One man`s desire is another`s welfare case. The diagnosis of conformational abnormality is simple and straight forward, but there can be difficulties in the interpretation and the significance of some clinical findings which involve the globe and its internal structures. For example, when does the small globe become microphthalmia and what is the significance of the retinal folds seen in Collie breeds as opposed to those neuroretinal folds described as retinal dysplasia in many other breeds ? When is an opacity of the lens an hereditary cataract and what makes a retinal degeneration an inherited retinopathy? When is glaucoma a primary or a secondary disease? Our ability to make decisions about the true nature of findings revealed during the examination of the eye relies upon the fact that the lesion seen has all the characteristics of lesions described in the same or other breeds as inherited. The appearance of the lesion, its pattern, its position, the possibility of change and the age at which it has made its appearance are all significant. The prevalence of the lesion within the breed indicates inheritance, but of course the disease mutation may already be known, an inheritance pattern may have been described and a DNA test may exist. The diagnosis relies upon the skill of the clinician in finding and interpreting the lesion in terms of inheritance, but some clinical findings may be misleading or remain open to speculation. All retinal degeneration within the tapetal fundus is

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characterised by increased tapetal reflectivity, but only some degeneration is inherited and the rest may be the result of other acquired disease processes. The same can be said for pigmentation within the retina and both the appearance of melanin and its disappearance can occur in both hereditary and acquired disease. Similarly cataract can be genetically determined or acquired as the result of other diseases and here pattern and the position of the opacity are most important in differentiation. For example the posterior polar subcapsular cataract make its classical appearance in many breeds, but it must be differentiated from those polar capsular opacities which are due to remnant hyaloid attachment to the lens. In the Siberian husky the hereditary cataract occupies the posterior cortical part of the lens and seldom involves the anterior cortex : however any lens opacity is considered to be inherited in the American Cocker Spaniel and unilateral involvement is possible, putting this breed at odds with the rest of the cataract breeds. The control of inherited ocular disease in our pedigree dog population relies upon an awareness that disease is always possible, largely as a result of intense breeding practices, and the necessity of routine ophthalmic examinations, positively encouraged by kennel club and breed society regulations. Awareness and the examination of meaningful numbers of each breed accrues the data necessary to effect improvement. It is the random finding of the lesion that could be inherited which should stimulate widespread examination of the breed to establish the line or lines that are involved and hence dictate future breeding.

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INTRODUCTION The conjunctiva is a mucous membrane that covers the inner surface of the eyelids (palpebral conjunctiva), the inner and outer surfaces of the third eyelid and the anterior part of the sclera (bulbar conjunctiva). Because it is the most exposed mucous membrane in the body, and as it is very rich in lymphocytes, inflammations of the conjunctiva are very common. However, it should be remembered that the conjunctiva is very often secondarily inflamed with almost all other ocular and periocular diseases, including keratitis, orbital disease, blepharitis, keratoconjunctivitis sicca (KCS), dacryocystitis, and sometimes uveitis and glaucoma. Therefore conjunctivitis should be seen as a potential sign of numerous, diverse, and often blinding ocular diseases and occasionally as a sign of systemic and potentially fatal. As a result, every eye in which conjunctival inflammation is identified should undergo thorough ophthalmic examination to determine if the patient has primary conjunctivitis or conjunctival inflammation as a sign of more serious ocular or systemic disease.

DIAGNOSIS Clinical signs of conjunctivitis include conjunctival hyperemia, chemosis (conjunctival edema) and ocular discharge (typically mucoid). The conjunctiva may become swollen or thickened, and hyperplastic lymphatic follicles may be seen, especially on the inner surface of the third eyelid. Conjunctival or subconjunctival hemorrhage, conjunctival hemorrhage and eyelid pruritis may also be seen. The "red eye" caused by conjunctival hyperemia may sometimes be confused with that caused by uveitis or glaucoma. The clinician should carefully observe the congested blood vessels to determine if they are superficial conjunctival vessels associated with conjunctivitis or deeper vessels associated with uveitis or glaucoma. Conjunctivitis is not associated with changes in intraocular pressure, pupil size and reaction, aqueous flare, funduscopic signs or visual deficits that may be seen in glaucoma and uveitis. Clinical approach Common causes of conjunctivitis vary by species. Feline and ruminant conjunctivitis is frequently infectious, canine conjunctivitis is almost exclusively noninfectious, and horses are more likely to have conjunctival inflammation as a sign of keratitis or uveitis. As the

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name of this talk indicates, these etiologic differences are especially important in the pathogenesis, workup and treatment of conjunctivitis in the dog and the cat. In dogs, with the notable exception of canine distemper, inflammation of the conjunctiva is usually secondary to due to its irritation by another adnexal disease. Tear film deficiencies such as KCS, exposure in brachicephalic breeds and irritation due to entropion, ectropion or trichiasis are common causes. Therefore, when presented with a case of canine conjunctivitis, the practitioner should concentrate on identifying the primary cause of the inflammation, by measuring tear production, carefully examining the eyelid and eyelash anatomy, etc. Once the primary cause has been diagnosed and successfully treated, most cases will resolve spontaneously, or with topical symptomatic treatment. In cats, on the other hand, conjunctivitis is usually caused by primary infectious pathogens of the cornea. Feline herpes (FeHV-1) infections are the most common cause, though infections with Chlamydophila are also frequently diagnosed. Therefore, when presented with a case of feline conjunctivitis, most of the diagnostic and therapeutic effort should be aimed at these primary pathogens. Bacterial Culturing Bacterial culturing is not a commonly used diagnostic procedure in determining the cause of conjunctivitis for a number of reasons. First, very few bacteria are the primary cause of conjunctivitis, especially in small animals. Rather, most primary causes of conjunctivitis result in increased numbers of bacteria from the normal flora. Second, most true primary conjunctival pathogens (e.g., Chlamydophila, Mycoplasma) require special collection and culture conditions. Therefore, cultures are performed rarely and usually after initial antibiotic therapy has failed. However, failure of conjunctivitis to respond to antibiotics is more commonly the result of failure to determine the underlying primary etiologic factors rather than incorrect choice of antibiotic. Conjunctival Scrapings Unlike culture, scrapings and biopsies are often extremely useful for better defining cause of conjunctivitis and for guiding therapy. Scrapings are useful to determine potential malignancy of cells associated with conjunctival masses, and identify allergic reactions and inclusions bodies

GENERAL TREATMENT CONSIDERATIONS FOR CONJUNCTIVITIS After determination and treatment of specific causative factors of conjunctivitis (e.g., KCS treatment ), the following general therapeutic agents can be employed. Antibiotics Topical ophthalmic antibiotics are frequently prescribed for patients with conjunctivitis. This approach is appropriate, however, only for treating a primary bacterial conjunctivitis (which is relatively rare) or if the goal is simply to limit overgrowth of the normal conjunctival flora while the primary cause of conjunctivitis is simultaneously addressed by another therapy. Reflexive use of an antibiotic whenever conjunctival inflammation is seen and without further testing or thought as to the primary cause of

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conjunctival inflammation is unlikely to be successful in the long term. Unfortunately, temporary â&#x20AC;&#x153;responseâ&#x20AC;? to antibiotic therapy can entrench such prescribing patterns. For example, conjunctivitis caused by KCS will improve while but not because the patient is treated with an antibiotic. Corticosteroids Corticosteroids are commonly used to treat conjunctivitis, often in conjunction with antibiotics. However, as with antibiotics, use of corticosteroids is not always indicated. They should be used in noninfectious disorders and only after correction of the primary cause. Their major role is in those conjunctivitides, such as pannus, in which an immune-mediated cause is suspected. By contrast, they are contraindicated in most feline conjunctivitis because most cases are infectious in nature. Cleansing Agents Removal of accumulated ocular discharge is important to prevent blepharitis, periocular dermatitis, and eyelid or conjunctival adhesions, and to improve patient comfort and penetration of ophthalmic medications. Therefore cleaning, flushing, and warm-packing of ocular structures through closed eyelids is a useful adjunct in the early therapy of many conjunctival disorders. Many commercial cleansing solutions are available. Cleansing may be followed by application of a bland protective ointment Topical Mast Cell Stabilizers and Antihistamines Sodium cromoglycate, lodoxamide, and other mast cellâ&#x20AC;&#x201C;stabilizing agents have been used topically to treat allergic and eosinophilic conjunctivitis. However, anecdotal reports of the efficacy of these products vary, and controlled studies on their safety or efficacy in veterinary patients are lacking. Just like antibiotics and corticosteroids, these drugs should not be used unless and until other more common causes of conjunctivitis have been eliminated.

SPECIFIC CAUSES Chlamydial Conjunctivitis In cats, chlamydial conjunctivitis initially may be unilateral but typically spreads to the other eye within 7 days of primary infection. Mild rhinitis, fever, and submandibular lymphadenopathy are typically seen coincident with ocular signs in primary exposure but often resolve more promptly and completely than the conjunctival signs, which can be very persistent. Chemosis is a predominant feature. With chronicity, membranous or follicular conjunctivitis can be notable. Chlamydial conjunctivitis is diagnosed from its clinical signs, a history of exposure, occasional demonstration of characteristic intracytoplasmic elementary bodies in scrapings of epithelial cells or PCR testing. The major differential diagnosis is conjunctivitis resulting from feline herpesvirus type 1. Recent information shows that cats may harbor C. felis in nonocular sites. This finding, along with controlled studies has led to the recommendation that systemic antibiotics (typically 10 mg/kg doxycycline orally once daily for at least 3 weeks) be used in addition to or instead of topical ophthalmic ointments. Feline Viral Conjunctivitis FHV-1 is considered the most common cause of conjunctivitis (and keratitis) in cats. Critical to the interpretation of diagnostic test results for FHV-1 and the management of cats

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infected with this organism is knowledge that FHV-1 establishes a lifelong latent or carrier state in most cats infected. Serologic studies suggest that at least 95% of cats have been exposed to the virus, and lifelong latency within the trigeminal ganglia of carrier cats occurs in at least 80% of cats. At least half of these cats assume epidemiologic importance owing to later reactivation and shedding of virus. Such episodes of reactivation may be stimulated by stress such as rehousing or intercurrent illness. Administration of corticosteroids is a very reliable method of reactivating latent virus under experimental conditions, and this possibility should be considered whenever one is tempted to administer a topical or systemic steroids in cats. Antiviral agents should be considered when clinical signs are severe, persistent, or recurrent, and especially when there is corneal involvement (with or without ulceration). Some important general concepts about antiviral agents assist with selection and expectations of this class of drugs. Antiviral agents in common use are virostatic; therefore,they require frequent dosing or topical application. Given owner and veterinary limitations as to therapeutic frequency, antiviral agents should be applied at least 5 times daily, especially in the early stages of disease. However, consideration must be given to the stress this induces in some animals and medication should be discontinued (not reduced in frequency) if the risks of viral reactivation caused by stress of application are likely to exceed any benefits of the antiviral medication. Therapy with any antiviral drugs should be continued for at least 1 week beyond resolution of ocular lesions, which typically occurs within 2 to 3 weeks. The superior potency and corneal penetration of trifluridine suggest that it should be the first choice for topical therapy. Unfortunately, however, cats often show marked aversion to application of this drug, suggesting that it is irritating.Idoxuridine may be a more practical choice in veterinary patients owing to its high clinical efficacy, lower cost, and reduced irritancy. Cidofovir is a relatively new antiviral drug that is highly effective when applied topically twice daily as a compounded 0.5% solution. Oral famcyclovir (90 mg/kg, Q12H) is another efficacious option. Keraotconjunctivitis Sicca Deficiency of the aqueous layer of the precorneal tear film is a common disorder in dogs (less so in cats) that leads to KCS. It must be differentiated from dryness caused by deficiencies in the mucin or lipid tearfilm layers. There are many potential causes for KCS, including drug induced (sulfa derivatives), facial nerve paralysis, cherry eye excision and senile gland atrophy. However, KCS in dogs is most often immune mediated. Indeed, in some dogs with KCS, circulating autoantibodies to the lacrimal glands, salivary glands, and gland of the third eyelid are present. Spaniels, English bulldogs, West Highland white terriers, and brachycephalic dogs are susceptible. The signs of KCS depend on whether the condition is bilateral or unilateral, acute or chronic, and temporaryor permanent. They include mucoid and mucopurulent dicharge, blepharospasm, corneal ulceration, vascularization and pigmentation, and signs of bacterial conjunvitivitis. The diagnosis of KCS is suggested by the history (repeated bouts of conjunctivitis that recur when topical medication is stopped), clinical signs, and STT values.

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STT values less than 15 mm/min are suspicious for KCS, especially in susceptible breeds or in patients that should have epiphora (e.g., due to conjunctivitis). In the majority of patients consistent medical therapy adequately controls the disease, but in select cases surgery may be of benefit. The main aim of medical therapy is to stimulate natural tear production. Topical cyclosporine forms the cornerstone of KCS therapy. A common regimen is to begin with topical cyclosporine ophthalmic ointment every 12 hours. A month or more may be required before an effect may be seen. If tear production (STT value) consistently exceeds 20 mm/min (uncommon), tear stimulant therapy may be reduced to once a day. Tacrolimus 0.02% may also be used with similar efficacy, while topical or oral pilocarpine may provide neurogenic stimulation of tear production. Supplemental treatment includes replacement of tear with artificial tear products while waiting for tear stimulant therapy to begin to work. Inflammation may be controlled with topical steroids , though these are usually not used for the long term, and it is mandatory to perform fluorescein staining of the cornea before their use. Infection is controlled with antibiotics, and eyes should be cleaned prior to treatment. Application of any medication to a dry eye and caked with discharge is almost invariably ineffective. Cleaning of the eyes and periocular tissues is usually best accomplished with a sterile eye wash and gentle wiping of the eyes with soft gauze or tissue. Cases that do not respond to medical treatment should be referred for parotid duct transposition surgery.

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TRAUMATIC PROLAPSE Owners of pets with traumatic prolapse of the globe will want to know whether the eye can be salvaged. This question actually has two components, as in some cases vision may be salvaged, while in other cases the eye will be blinded, but the globe can be salvaged cosmetically. Criteria that will help you answer these questions include: 1)

2) 3) 4) 5)

What is the skull conformation? Traumatic prolapse is common in brachycephalic dog breeds, due to the shallow orbit and poor lid closure. Therefore, in these breeds minimal trauma may cause prolapse. However, frequently there will be no additional injuries to the eye, skull or body. On the other hand, in cats and in mesocephalic and dolichocephalic dogs, the eye is situated in a deep orbit and is protected by tight lid closure. In these animals, traumatic prolapse is frequently accompanied by other intraocular or bodily injuries, and the prognosis is poorer. Duration of prolapse. Depending on the duration of the prolapse, animals may present with corneal ulceration, necrosis or perforation. Intraocular injury. Hyphema is a bad prognostic indicator, implying trauma to the uvea or globe rupture. An ultrasound examination may reveal intraocular injuries. Pupils. Pupillary light reaction (PLR) is an important sign. If the pupil can not be seen (due to hyphema), the consensual PLR should be checked. Strabismus and extraocular muscles. Since ciliary arteries, which supply blood to the anterior segment of the eye, are carried in the extraocular muscles, rupture of too many muscles will result in ocular ischemia.

Overall prognosis for vision is rather poor, with only 20% of dogs reportedly remaining visual. However, prognosis for cosmetic salvage is better. Unless prognostic indicators are very poor, you should attempt globe replacement at presentation. Treatment. Owners who telephone regarding traumatic ocular prolapse should be instructed to keep the cornea moist, using water, moist gauze, vaseline, ophthalmic lubricants, etc. Upon presentation, conduct the prognostic tests described. The cornea should be washed, cleaned and lubricated. After the patient has been stabilized and anesthetized, the lids should be rolled/pulled out over the equator, using muscle/strabismus hooks, forceps, etc. The globe is pushed back into the orbit using gentle pressure. A lateral canthotomy may be required to facilitate replacement. Temporary tarsorrhaphy is performed to maintain lid closure. Depending on

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the size of the animal, 2-4 horizontal mattress sutures, using 2-0 to 4-0 non-absorbable monofilament material are used, with stents for tension relief. Make sure that the suture passes through the lid margin (meibomian gland openings) and not through the palpebral conjunctiva. EXOPHTHALMOS â&#x20AC;&#x201C; WHAT IS PUSHING THIS EYE? WHAT SHOULD I DO? A.

Retrobulbar cellulitis/abscess

Clinical signs & diagnosis of retrobulbar abscess

The disease is characterized by acute onset and by severe pain. The pain is caused when the condyle of the mandible presses on the abscess whenever the animal opens its mouth. This leads to refusal to eat and great resistance to opening the mouth for examination. It is often necessary to sedate the animal in order to open its mouth. Once the mouth has been opened, it is often possible to see a red swelling, or even an open draining tract, in the oral mucosa, behind the last upper molar tooth. If no gross lesion is visible in the oral cavity, it is possible to use imaging techniques, such as ultrasound or CT that may also demonstrate foreign bodies, or allow to perform guided fine needle aspirations for cytological diagnosis. 2.

Treatment of retrobulbar abscess

Treatment of a retrobulbar abscess requires general anesthesia. This is because the patient must be intubated to avoid aspiration of exudate when the abscess is drained. Make an incision in the mucosa behind the last upper molar, and slowly inset a pair of curved hemostats to blindly explore the orbit and open pockets of exudate. If a pocket of exudate is encountered, copious amounts of exudate will flow out. This can be collected for cytology, and culture & sensitivity. In cases of retrobulbar cellulitis, no massive drainage of exudate will be seen. However, the very act of establishing a draining tract is usually sufficient to achieve a cure. After creating a draining tract, flush the orbit with saline and antibiotics. The wound is not sutured. Systemic antibiotics are administered for 10-14 days, and the animal fed soft food. Dramatic, and most rewarding, improvement is usually observed within 1-2 days.

Retrobulbar tumor

Clinical signs & diagnosis

As noted, retrobulbar tumors share a number of signs with retrobulbar abscesses. However, in contrast to retrobulbar abscesses, retrobulbar tumors are usually very slowly progressive, and non painful. Furthermore, patients with retrobulbar tumors are 10-11 years old, on average, significantly older than patients with retrobulbar abscesses. A retrobulbar tumor can cause deformation of the posterior part of the globe which can be visualized ophthalmoscopically, or using an ultrasound. However, ultimate localization relies on ultrasonography, CT or MRI imaging. The final diagnosis is usually made by guided fine needle aspiration and cytology.

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Treatment and prognosis

Solitary tumors discovered in early stages may be removed surgically. In such cases, the best surgical approach is usually oribitotmy, and it may be possible to preserve the globe and vision. Advanced cases may require radical orbitectomy, combined with radiation therapy and/or chemotherapy. However, most tumors are discovered in advanced stages, and due to their malignant nature they carry a very poor prognosis. One retrospective study reported a mean survival time of 1 month in cats and 10 months in dogs, with 35% of patients euthanized at the time of diagnosis.

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Presentation is supported by FECAVA

Elbow Dysplasia (ED) is a developmental multifactorial disease with genetic predisposition and secondary environmental influences, eventually leading to osteoarthritis. The risk factors include body weight (overnutrition), feeding pattern, diet (high fat/energy intake), rapid growth and explosive excessive exercise. ED can be grouped into 4 subgroups: ununited anconeal process [UAP], osteochondrosis [OC/OCDD], medial coronoid disease [MCD] and elbow incongruity [INC]. In UAP, the anconeal process is not fused with the ulna at 16-20 weeks of age. OCD of the medial humeral condyle develops as a result of a dislodged cartilage flap due to disturbed enchondral ossification. MCD is the most common manifestation of ED and consists of pathologic changes of the articular cartilage and subchondral bone of the medial coronoid process. All these conditions can be caused by or get worsened by incongruity of the elbow joint [INC]. This INC can be caused by a relative short radius or a relative short ulna .This is called radius-ulna-incongruity, or humero-ulnar incongruity with an oval shaped trochlear notch. Elbow Dysplasia can effect one or both front limbs and several forms of ED can be present in one limb. The kinematics are significantly different between the sound and the dysplastic elbow .In dysplastic elbows, there is humero-ulnar instability during motion and reduced contact area. This results in areas of increased weight load and overstress.

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Diagnosis of ED has 2 purposes. First as a screening tool to select ED free breeding stock and secondly to diagnose the disease as early as possible in individual patients presented for forelimb lameness in order to improve the prognostic outcome with early treatment. (IEWG Gielen 2016) The diagnosis of ED in lame dogs is a combination of clinical symptoms, orthopedic examination, diagnostic imaging, and arthroscopy as a minimal invasive tool combining diagnosis and treatment. Radiography is still the standard technique for the diagnosis of ED . It should consist of 2 MLprojections (40 ⁰ flexed and 100-120⁰ neutral) to evaluate the medial coronoid process, incongruity and presence of osteophytosis, as well as a 15⁰ cranio-caudal oblique view to evaluate the medial humeral condyle. Especially in MCD, the radiographic changes can be minimal and indistinct. The sensitivity and specificity of radiography for the diagnosis of MCD is 98% and 64%, even with high quality images.This means that we still have 36% false positives. Trochlea notch sclerosis was identified in 87%, periosteal reactions on the anconeal process in 70%,osteophytosis of the lateral epicondyle in 56%, as well as blunt medial coronoid process. CT, MRI and arthroscopy clearly have a higher sensitivity and specificity, especially for diagnosing MCD and RUI .However, they are expensive tools and usually only available at referral centers. In case of absencent radiographic signs of ED but pain localization in the elbow, advanced imaging with CT and/or arthroscopy is strongly advised, because early treatment of the disease improves outcome. In cases where forelimb pain cannot be localized, scintigraphy is the next step. Treatment of the individual conditions is advised as early as possible. All intraarticular manipulations are preferably done by arthroscopy as minimal invasive tool. In case of arthrothomy a medial approach to the elbow by an intermuscular incision should be used. For OC/OCD, removal of the flap with minimal curettage of the defected bed and perpendicular cartilage edges ,is the treatment of choice. In extended lesions, additional treatment options such as bi-oblique proximal ulnar osteotomy, microfracturing or even OATS (osteochondral autograft transfer system) should be considered. Concerning the treatment of MCP, there is a consensus in removing the fragment with arthroscopy as a gold standard, but not in further additional optimal treatments, such as: proximal (bi-oblique) or distal ulnar osteotomy, sub/total coronoid ostectomy, biceps ulnar release procedure (BURP), proximal abduction ulna osteotomy (PAUL), sliding humeral osteotomy (SHO) or canine uni-compartiemental elbow (CUE). Ununited anconeal process has a breed disposition. It affects large breeds dogs such as German shephards, Great Danes, Saint Bernards and others. The pathogenesis has not been proved, but it is expected to be based on radio-ulnar or humero-ulnar incongruity. The diagnosis is best made by medio-lateral radiographs with in flexion. Especially in GSD, combined UAP and MCD can be present.Therefore, additional joint exploration (medial compartment) ,preferably with arthroscopy, is advised. Alternatively, a caudo-medial approach, combining removal of the AP and evaluation of the medial coronoid process ,is

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described. (Meyer-Lindenberg et al 2002) The risk for development of advanced osteoarthritis is the highest with UAP,therefore treatment should be started as early as possible in order to improve the outcome. Conservative treatment is only advised in adult dogs with stable UAP or chronic cases with advanced osteoarthritis. The surgical treatment options include removal of the fragment, proximal ulnar osteotomy (PUO), screw fixation or a combination of PUO with screw fixation.

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IEWG Proceeding 2017 IEWG Proceeding 2016 Review on canine elbow dysplasia: pathogenesis, diagnosis, prevalence and genetic aspects. Janutta V , Distl O. Dtsch Tierarztl Wochenschr. 2008 May;115(5):172-81 Genetic variances, trends and mode of inheritance for hip and elbow dysplasia in Finnish dog populations, Mäki, K, Groen, A F, Liinamo, A E, Ojala, M, Animal Science 2002 Estimates of genetic parameters for hip and elbow dysplasia in Finnish Rottweilers , Mäki K, Liinamo A.E., Ojala M., Journal of Animal Science, Volume 78, Issue 5, 1 May 2000, Phenotypic and genetic evaluation of elbow dysplasia in Dutch Labrador Retrievers, Golden Retrievers, and Bernese Mountain dogs I.C.M. Lavrijsen a, H.C.M. Heuven a, G. Voorhout b, B.P. Meij a, L.F.H. Theyse a, P.A.J. Leegwater a,H.A.W. Hazewinkel Vet J. 2012 Aug;193(2):48692 Breed Susceptibility for Developmental Orthopedic Diseases in Dogs, LaFond E., Breur G.J., Austin C.C., J Am Anim Hosp Assoc 2002;38:467–477 Heritabilities and genetic trends for elbow score as recorded by the New Zealand Veterinary Association Elbow Dysplasia Scheme (1992–2013) in four breeds of dog, Soo, M., LopezVillalobos, N., Worth, A., New Zealand Veterinary Journal 2018 Diet, Exercise, and Weight as Risk Factors in Hip Dysplasia and Elbow Arthrosis in Labrador Retrievers, Marie H. Sallander, Hedhammar A., Trogen M., J. Nutr. July 2006 vol. 136 Assessment of medial coronoid disease in 180 canine lame elbow joints: A sensitivity and specificity comparison of radiographic, computed tomographic and arthroscopic findings, Villamonte-Chevalier, A.van Bree, H., Broeckx, B. J.G. Dingemanse, W, Soler, M., Van Ryssen, B., Gielen, I., BMC Veterinary Research 2015 Sensitivity of radiographic evaluation of radio-ulnar incongruence in the dog in vitro, Mason, David R., Schulz, Kurt S., Samii, Valerie F., Fujita, Yukihiro, Hornof, William J., Herrgesell, Eric J., Long, Craig D., Morgan, Joe P., Kass, Phillip H., Veterinary Surgery 2002 Radiographic, computed tomographic, and arthroscopic evaluation of experimental radioulnar incongruence in the dog, Wagner, Kahrma, Griffon, Dominique J., Thomas, Micheal W., Schaeffer, David J., Schulz, Kurt, Samii, Valerie F., Necas, Alois, Veterinary Surgery 2007 Sensitivity and specificity of arthroscopic estimation of positive and negative radio-ulnar incongruence in dogs, Werner, Hinnerk, Winkels, P., Grevel, V., Oechtering, G., Böttcher, P., VCOT 2009 Erosion of the medial compartment of the canine elbow: occurrence, diagnosis and currently available treatment options, Coppieters, E., Gielen, I., Verhoeven, G., Van Vynckt, D., Van Ryssen, B., VCOT 2015 Etiology and Pathogenesis of Osteochondrosis, Ytrehus B, Carlson C.S., Ekman S., Vet Pathol 44:429–448 (2007) Autogenous osteochondral grafting for treatment of stifle osteochondrosis in dogs, Cook, James L., Hudson, Caleb C., Kuroki, Keiichi, Vet Surg 2008

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Early Clinical Experience with Osteochondral Autograft Transfer for Treatment of Osteochondritis Dissecans of the Medial Humeral , Condyle in Dogs, Fitzpatrick N., Yeadon R, Smith TJ., Vet Surg 38:246 2009 Histomorphometry of fragmented medial coronoid process in dogs: A comparison of affected and normal coronoid processes, Danielson, K.C., Fitzpatrick, N., Muir, P., Manley, P.A., Veterinary Surgery 35:6, 2006 Delayed endochondral ossification in early medial coronoid disease, Lau S.F., Hazewinkel H.A.W., , Grinwis G.C.M., Wolschrijn C.F., Siebelt M., Vernooij J.C.M., Voorhout G., Tryfonidou M.A., Thesis Univerity of Utrecht 2013 Relationship between axial radioulnar incongruence with cartilage damage in dogs with medial coronoid disease Eljack, H., Böttcher, P. Veterinary Surgery 44:2 2015 In vivo fluoroscopic kinematography of dynamic radio-ulnar incongruence in dogs, Rohwedder, Thomas, Fischer, M., Böttcher, P., Open veterinary journal 7:2017 In-vivo kinematics of the elbow, Böttcher, P., Schmidt Th., Fischer M., www.fluokin.de Does Radiographic Arthrosis Correlate With Cartilage Pathology in Labrador Retrievers Affected by Medial Coronoid Process Disease? Farrell, M., Heller, J., Solano M., Fitzpatrick, N., Sparrow, T., Kowaleski, M. Veterinary Surgery 43: 2015 Sensitivity and specificity of arthroscopic estimation of positive and negative radio-ulnar incongruence in dogs, Werner, H., Winkels, P., Grevel, V., Oechtering, G., Böttcher, P. VCOT 22:2009 Arthroscopic Biceps Ulnar Release Procedure (BURP): Technique Description and In Vitro Assessment of the Association of Visual Control and Surgeon Experience to Regional Damage and Tenotomy Completeness, Wilson, D., Goh, C.S S, Palmer, R. H. Veterinary Surgery 43: 2014 Canine elbow dysplasia: Aetiopathogenesis and current treatment recommendations, Michelsen, J., Veterinary Journal 196: 2013 Working algorithm for treatment decision making for developmental disease of the medial compartment of the elbow in dogs, Fitzpatrick, N. Yeadon, R. Veterinary Surgery 2:2009 Subtotal coronoid ostectomy for treatment of medial coronoid disease in 263 dogs, Fitzpatrick N.,Smith, TJ., Evans, RB., O'Riordan, J., Yeadon, R. Veterinary Surgery 38: 2009 Accelerated Cartilage Loss Following Subtotalcoronoid ostectomy ACVS proceeding 2011 Estimation of Joint Incongruence in Dysplastic Canine Elbows Before and After Dynamic Proximal Ulnar Osteotomy, Böttcher, P., Bräuer, S., Werner, H. Veterinary Surgery 42:2013

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Disorders of the shoulder joint are a common cause of front limb lameness in immature as well as adult dogs. In the last few years, they have been diagnosed with increased frequency. Diagnosis and therapy of specific disorders, especially those concerning soft tissues, can be challenging. This lecture will discuss a variety of shoulder problems including osteochondritis dissecans (OCD), glenoid fragmentation, biceps tendon problems, supraspinatus tendon injury, infraspinatus contracture and shoulder instability. Beside a thorough orthopedic and neurological examination, intra-articular anesthesia can be very helpful to identify the shoulder as origin of pain. (van Vynckt et al VCOT 2013) In cases of obscure lameness, scintigraphy can provide the necessary localization. It has a high sensitivity but low specifity. Further diagnostic imaging, such as radiography, ultrasound, CT, MRI or arthroscopy is usually needed. (Samoy et al 2008) Radiographs are usually diagnostic with conditions affecting the bones but not for conditions originating from the soft tissues. Arthrography increases the diagnostic value of radiography and ultrasound with a highfrequency linear transducer can accurately identify the tendon/muscle structure and its possible disorders. (Kunkel JAAHA 2008) Most shoulder disorders are related to soft tissues, such as the rotator cuff muscles and tendons. These need different imaging modalities such as ultrasound, CT and/or MRI. (Kramer et al 2001, Cook CR. 2016, Fransson et al 2005) Osteochondrositis dissecans (OCD) Osteochondrosis (OC) is caused by a disturbance in endochondral ossification. This results in thickened cartilage, which is then susceptible to fissures and the development of a cartilage flap (OCD)(Ytrehus 2007). This condition is usually seen in large breed immature dogs, but has also been described in small breed dogs (LaFond etal 2002, Ohlert etal 2016, Bruggemann Vet Rec 2013). The diagnosis can usually be made with a clinical examination and radiographs. The treatment of choice entails the removal of the flap, preferably by using minimal invasive arthroscopy. (Tobias and Johnston, 2012, Beale et al 2003) The outcome is very good in >90% of the patients if they are properly rested postoperative (van Ryssen et al Vet rec 1993, Olivier ESVOT 2010) Glenoid fragmentation Glenoid fragmentation is the separation of the caudal edge of the cavitas glenoidale. This can be the result of a traumatic injury or due to incomplete ossification of a secondary ossification center. The condition is often asymptomatic and a coincidental finding,however,

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if the fragment is mobile,it will usually cause pain. The clinical signs are pain with manipulation of the shoulder, forelimb lameness and in chronic cases, muscle atrophy. The diagnosis can be made radiographically. However the evaluation of fragment mobility, as well as possible secondary changes (kissing lesion on the humeral head) are performed by arthroscopy. The treatment options are conservative management with NSAID’s, rest and rehabilitation. If the patient does not respond, surgical treatment with removal of the fragment and debridement of the erosions, if present, are recommended. The preferable surgical treatment is arthroscopy due to the clear diagnosis of fragment mobility, less patient morbidity and higher precision therapy. (Beale WSAVA 2013, Kunkel 2008)

Most shoulder disorders in adult dogs are conditions affecting the soft tissues(rotator cuff muscles and tendons). Supraspinatus tendinopathy Supraspinatus tendinopathy (ST) is a common cause of front limb lameness in performance as well as active companion dogs. It can be acute or chronic. The diagnosis can be challenging. Besides the orthopaedic examination, diagnostic imaging with radiographs for calcifying tendinopathy and ultrasound, as well as MRI for non-calcifying tendinopathy, is the most effective. (LaFuente 2009, Spall 2016, Mistieri 2012). Usually the lameness is of variable degree, waxing and waning and it is exercise dependant. 76% of dogs fail to respond to rest and NSAID’s and 42% to rehabilitation therapy (Canapp S., 2016).This is due to the fact that in chronic cases there is no inflammatory disease, but myxomatous degeneration (LaFuente 2009) The treatment options include rest, NSAID’s, rehabilitation, extracorporal shockwave therapy and regenerative medicine with PRP and/or stem cells. According to the literature, 62% of the cases with ST have additional disorders such as medial shoulder instability, bicipital tenosynovitis or elbow pathology. This can influence the prognosis and needs to be addressed as well. (Canapp S. 2016) In cases of insufficient response to conservative treatment, surgical therapy is recommended. This includes debridement of the thickened calcified tendon. Infraspinatus myopathy Infraspinatus myopathy is a less common disease.It is usually seen in adult working dogs due to trauma of the infraspinatus muscle. Muscles only have minor regenerative abilities, therefore fibrosis and contracture will develop secondary to muscle disrupture. The history is usually bi-phasic with an acute painful and a chronic non-painful phase. Patients show a typical gait abnormality with adduction of the elbow, outward rotation of the antebrachium and a carpal flip. In acute cases with a low chance of healing, treatment includes rest, NSAID’s and physiotherapy. Tenotomy of the infraspinatus muscle is the treatment of choice in chronic cases. The prognosis after tenotomy is excellent. (Zink and van Dyke 2013, Tobias and Johnston, 2012) Biceps tendinopathy

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The pathologies of the biceps tendon include tenosynovitis, partial or complete rupture, avulsion or luxation. Historically, tenosynovitis is often overdiagnosed. With improvement in diagnostic imaging, (Ultrasound and MRI) more refined diagnosis can be made. Tenosynovitis can be primary, as a result of overuse or trauma, or it can be secondary due to other intraarticular diseases such as OCD, joint mouse entrapment in the bicipital tendon sheath or shoulder instability. Originally it was thought to be an inflammatory process, however histological examinations have regularily shown degenerative changes. (Gilley et al 2002) Therapy includes treatment of the primary lesion, if present, or in cases of primary disease, rest, pain relief, rehabilitation and intraarticular injections with PRP or Cortison. Bicipital tendon rupture can be caused by an acute single trauma or by repetitive strain injury, causing degeneration and weakening of the tendon. Also, joint mouse entrapment can cause chronic changes in the tendon causing it to rupture. The diagnosis can be made with an orthopedic examination, radiographs, ultrasound, MRI as well as arthroscopy. Arthroscopy is a minimal invasive tool combining diagnosis and therapy. Shoulder instability Shoulder instability (SI) is defined as the inability to maintain the humeral head in the cavitas glenoidale. It is thought to be a common cause of shoulder lameness (Bardet et al 1998). Elbow dysplasia must be ruled out as a differential diagnosis. The diagnosis of SI is difficult and controversial. The instability is mainly medial, but can also be lateral or multidirectional. (Franklin etal 2013) Joint stability is created by passive stabilizers like the medial glenohumeral ligament, and active stabilizers such as the rotator cuff muscles (MarcellinLittle 2007) .The diagnosis is as difficult and controversial as the therapy. Clinical examination should show a weight bearing lameness and localization of pain in the shoulder joint. Abduction angles can be measured with goniometry. Angles of >50â ° and a > 20â ° difference between both sides suggest a pathologic condition and should be suspicious for medial shoulder instability. (Cook et al 2005, Cogar et al 2008) However, other forelimb conditions can also cause increased abduction angles due to muscle atrophy and loss of active restraint of the shoulder joint. Radiographs and ultrasound are of little help in diagnosing MSI. While MRI gives information about the rotator cuff muscles, arthroscopy allows for evaluation and treatment of all intraarticular structures such as the biceps tendon, glenohumeral ligaments, subscapularis tendon and the articular surfaces. Decision making concerning treatment is complicated by difficulty in assessing all potential anatomical structures, possibility of multiple changes and the lack of evidence based studies proving certain treatment options superior to others. Conservative treatment with rest, NSAIDâ&#x20AC;&#x2122;s and rehabilitation can be done. It is successful in up to 69% of cases(Cook et al 2005). In cases of insufficient response or relapse, surgical treatment is advised. The goal is immediate functional shoulder stability. This can be achieved by arthrothomy or arthroscopy. It is important to combine this with controlled activity, rehabilitation and external protection such as DogLeggs. Surgical techniques include radiofrequency induced capsulorrhaphy, arthroscopic or open primary repair using bone anchors, arthroscopically assisted or open prosthetic ligament placement, subscapular imbrication, biceps tendon transposition or shoulder arthrodesis.

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Sidaway K, McLaughlin RM, Elder SH, et al. Role of the tendons of the biceps brachii and infraspinatus muscles and the medial glenohumeral ligament in the maintenance of passive shoulder joint stability in dogs. Am J Vet Res. 2004;65:1216–1222.

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Franklin SP , Devitt CM, Ogawa J, Ridge P, Cook JL., Outcomes associated with treatments for medial, lateral, and multidirectional shoulder instability in dogs. Vet Surg. 2013 May;42(4):361-4 Marcellin-Little DJ , Levine D, Canapp SO Jr., The canine shoulder: selected disorders and their management with physical therapy. Clin Tech Small Anim Pract. 2007 Nov;22(4):171-82 Pettitt RA, Clements DN, Guilliard MJ. Stabilisation of medial shoulder instability by imbrication of the subscapularis muscle tendon of insertion. J Small Anim Pract. 2007;48(11):626–631.

41. 42.

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Fitch RB, Breshears L, Staats A, et al. Clinical evaluation of a prosthetic medial glenohumeral ligament repair in the dog (ten cases). Vet Comp Orthop Traumatol. 2001;14:222–228.

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Kramer M, Gerwing M, Sheppard C, et al: Ultrasonography for the diagnosis of diseases of the tendon and tendon sheath of the biceps brachii muscle. Vet Surg 30:64, 2001

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Kunkel KA, Rochat MC. A review of lameness attributable to the shoulder in the dog: part two.J Am Anim Hosp Assoc. 2008 Jul-Aug;44(4):163-70 Cogar, SM., Cook, CR., Curry, SL., Grandis, A., Cook, JL., Prospective evaluation of techniques for differentiating shoulder pathology as a source of forelimb lameness in medium and large breed dogs, VetSurg 2008, 372) 132-141

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Canine hip dysplasia (CHD) is a progressive disease, which develops during postnatal skeletal growth. A definitive diagnosis can be made radiographically when secondary signs of osteoarthritis due to joint incongruity become evident. At this point it is too late to prevent osteoarthritis. However, if joint incongruity is diagnosed before the start of degenerative joint changes, osteoarthritis can be prevented. The development of hip dysplasia can be diagnosed during the growth period; the more severe the hip dysplasia, the earlier the diagnosis can be made based on the early clinical and radiographic signs of the disease. Predictive clinical and radiographic signs are related to joint morphology and congruity and to the detection and measurement of passive joint laxity (Ortolani sign, subluxation and distraction index) and of the slope and shape of the dorsal acetabular rim. Early diagnosis and proper treatment can arrest and reverse the progression of disease and change its pathogenesis. Triple pelvic osteotomy (TPO) or, more recently developed DPO (Double pelvic Osteotomy can be performed in puppies with femoral head subluxation due to increased dorsal acetabular rim slope.6, 11, 12, 13, 14 In puppies without signs of osteoarthritis, these techniques modify the direction of the forces inside the joint, leading to a redirection of the femoral head inside the acetabulum. During the residual growth period, the femoral head and the acetabulum regain their joint congruity through uniform cartilage loading, thus preventing or limiting osteoarthritis. The juvenile pubic symphysiodesis (JPS) described by Mathews and colleagues in 1996 is a technique intended to modify the slope of the acetabular roofs in a more ventral direction during skeletal growth in puppies with signs that indicate the start of hip dysplasia. Limiting the circumferential growth of the pelvic canal by arresting the pubic symphysis results in bilateral acetabular rotation, which improves femoral head coverage by the acetabular roofs. In the residual growth period, joint congruity is improved, thus allowing more favourable joint biomechanics and preventing or limiting osteoarthritis.2

Protocol for preoperative evaluation and patient assessment To be consistent, the protocol for preoperative evaluation and patient assessment must be performed in a systematic manner. A thorough examination of the hips, consisting of Fig.1 â&#x20AC;&#x201C; Measurement of angles of orthopaedic examination and several reduction and of subluxation with the radiographic views, is necessary to Slocum Electronic Goniometer ď&#x192;Ł. obtain reliable and predictive results

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from the selected treatments5. Clinical and radiographic findings should be compared with each other and contrasting data should be further scrutinized. Incomplete evaluations, such as examination of only a standard ventrodorsal radiographic view, lead to unreliable results. Ortolani Sign: In the anaesthetized or deeply sedated dog, the stability of the femoral head in the acetabulum, the amount of joint laxity and the features of femoral head subluxation, if present, are evaluated. Measurement and evaluation of the angles at which subluxation and reduction occur are recommended to obtain reference values, which are very useful for planning treatment when indicated. To measure these angles precisely, we use the Canine Electronic Goniometer designed for by Slocum for this purpose. The angle of reduction is indicative of joint capsule laxity. The angle of subluxation is indicative of the dorsal acetabular rim (DAR) slope and of acetabular filling: the DAR slope is the inclination of the weight-bearing dorsal part of the acetabulum. To be perfectly functional, the DAR slope should be almost perpendicular to the direction of the weight-bearing forces; in normal dogs the slope is less than 7.5° from a line perpendicular to the long axis of the pelvis. As the DAR slope increases, so does the angle of subluxation. Filling of the acetabulum with osteophytes and thickening of the round ligament can also increase the angle of subluxation. Static radiographic hip study: Using orthogonal views, lateral, ventrodorsal and anteroposterior, a three dimensional study of the hip can be done to evaluate the bone morphology of both the pelvis and femur. Because correct positioning and muscle relaxation are essential to carry out this study, the dog must be anaesthetized. In the standard ventrodorsal view joint incongruity is evaluated and signs of osteoarthritis are identified by examining the craniolateral acetabular rim, the dorsal acetabular rim and the femoral head Fig.2 – Positioning for the DAR radiographic view.

and neck. In the standard frog view any filling of the acetabular fossa caused by a permanently displaced femoral head or hypertrophied round ligament will widen the articular rim. The lateral view is useful to evaluate the lumbosacral joint thereby differentiating other skeletal problems. The dorsal acetabular rim view, described by B. Slocum in 1990, is the most informative view to evaluate the integrity and slope of the dorsal acetabular rim, to evaluate the functional laxity and to select the best treatment. With this view, it is possible to see and evaluate most of the weight-bearing portion of the acetabulum in cross section. In the dysplastic dog, the lateral aspect of the DAR is blunted and rounded because of erosion and its slope is increased to 20° or more; the femoral head moves dorsally and laterally along the inclined plane of the sloped DAR. By combining the DAR study to passive joint laxity measurement the functional joint laxity is evaluated. Distraction view: With a distraction device to push the femoral heads apart, a dynamic evaluation of passive joint laxity is carried out. In a study conducted by R. Badertscher at the University of Georgia in 1977, the half-axial position was used to improve the radiographic visualization of subluxation in dogs with hip dysplasia; the results were similar to those

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described later by Smith in 1990. We have used the procedure described by Badertscher since 1994 because it is simple, rapid and provides reliable; the only modification we made Fig. 3 – Distraction device and positioning for the distraction radiographic view.

has been improvement of the device used to distract the hips. The dog is positioned ventrodorsally with the femurs slightly extended at approximately 95°-105° to the table surface and the tibiae parallel to the plane of the table surface. For this purpose, we developed an S-shaped teflon table-device that is 2 cm thick, 5 to 12 cm wide and 50 cm long; the S-shape provides good adaption to the pubic area. The device has a hinged base to keep it in contact with, and parallel to, the table, and is placed on the ventral surface of the pelvis. Pressure applied to the medial aspects of the proximal femurs through the hand-held tibiae results in the fulcrum to subluxate the femoral heads from the acetabula. To calculate the passive joint laxity, the distraction index (DI) described in by G. Smith and colleagues at the University of Pennsylvania in 1990 was used.

Case selection for prophylactic treatment When hip dysplasia is detected at an early age, it is possible to alter the progression of the disease with appropriate treatment before the onset of osteoarthritis, which would prevent a favourable outcome. The success of preventive treatment is measured by its ability to prevent osteoarthritis in clinical cases with pathological joint conditions. The time-window to correct developing hip dysplasia by surgical treatments is limited and is lost once cartilage damage, DAR microfractures and acetabular filling have occurred.6,9, 14 With the most commonly used techniques aimed at altering the course of developing hip dysplasia in the growing dog, the best results are obtained when lameness and other signs of disease have not yet occurred. Case selection for prophylactic treatment is accomplished according to the following criteria: Double Pelvic Osteotomy (DPO): DPO replaced TPO (Triple Pelvic Osteotomy) because of better outcome, much less morbidity and less complications. DPO is are indicated in dogs 5 to 8 months old (better age 5-6 months) with no or minimal signs of osteoarthritis and joint subluxation, an angle of reduction between 20° and 40°, an angle of subluxation between 10° and 20° and a DAR slope between 10° and 20° with its lateral border preserved. The degree of acetabular rotation, i.e. the degree of torsion of the canine pelvic osteotomy plate, is determined according to the DAR slope, whereby excessive correction that would limit abduction of the leg must be avoided and to the angle of subluxation. After correction, the DAR slope should be 0° to -5° and the angle of subluxation under 0° to 5°. With the indications described above, the most successful degree of correction is 25° to 30° for DPO ; with this correction, the DAR does not impinge upon the femoral neck and the gait is not altered. When the angles of reduction and subluxation are very close (less than 15°), acetabular filling and blunting of the dorsolateral acetabular rim are present, indicating loss

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of dorsal coverage; in these cases, DPO is contraindicated.6,9, 14 When properly performed and with the right indications, DPO can reverse CHD, prevent the development of osteoarthritis and provide full joint function.9 When performed in less than ideal candidates with mild osteoarthritis, DPO will not prevent further development of osteoarthritis and for that reason it is not indicated.6, 9, 14 Juvenile Pubic Symphysiodesis: JPS is performed at an early age and the most favourable results are achieved in 3.5- to 4-month-old puppies. Indications for pubic symphysiodesis are signs that predict the future development of CHD: a positive Ortolani sign with an angle of reduction of 20° to 40°, an angle of subluxation of 0° to 15°, DI from 0.4 to 0.8 and DAR angles of 7° to 12°.10 The procedure is not effective in puppies with more severe findings or with established osteoarthritis and clinical signs; the degenerative process cannot be stopped by a slow-effect procedure such as pubic symphysiodesis. While the acetabular roofs are slowly moving ventrally, the femoral heads slip laterally along the sloped and rounded lateral acetabular border, leading to further erosion of this area. In contrast, when performed in selected cases with the appropriate indications and post-operative restriction of physical activity (limiting playing and jumping, promoting swimming), pubic symphysiodesis is effective in improving joint congruity and preventing or limiting the development of osteoarthritis.

Contraindications for prophylactic treatment The disadvantages of preventive surgeries are related to incorrect case selection, such as performing DPO or pubic symphysiodesis in dogs with osteoarthritis. These techniques are contraindicated in such cases because they will not prevent the progression of osteoarthritis. In these cases, elective surgeries such as total hip replacement should be suggested instead. In severe early CHD, cementless total hip replacement like “Zurich” model can be applied successfully in patients as young as 5-6 months.10 JPS is a surgical procedure that modifies the canine phenotype without leaving radiographic evidence of the operation. For this reason, pubic symphysiodesis has a strong ethical implication that must be discussed thoroughly with puppy owners to gain their understanding and compliance. We strongly recommended that puppies undergoing pubic symphysiodesis be neutered at the same time. We believe that the life-long benefits provided by successful pubic symphysiodesis would justify this procedure, provided that the ethical aspects are well understood.

Conclusions The predictive value of early diagnosis and treatment of CHD can be substantiated by monitoring cases that receive conservative treatment. Early and reliable diagnosis of CHD allows timely surgery that is intended to modify joint morphology, restore joint congruity and prevent or limit osteoarthritis.

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References 1) 2) 3) 4) 5)

9) 10)

11) 12)

13)

14)

15)

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Badertscher RR: The half-axial position: improved radiographic visualization of subluxation in canine hip dysplasia. MS Thesys, Athens, Georgia, 1977 Dueland RT, Adams WM, Fialkowski JP et al.: Effect of pubic symphysiodesis in dysplstic puppies. Vet Surg 30:201-217, 2001 Mathews KG, Stover SM, Kass PH: Effect of pubic symphysiodesis on acetabular rotation and pelvic development in guinea pigs. Am J Vet Res 57:1427-1433, 1996 Slocum B, Devine TM: Dorsal acetabular rim radiographic view for the evaluation of the canine hip. J Am An Hosp Assoc 26: 289, 1990 Slocum B & Devine Slocum T: Hip: Diagnostic Tests, in Bojrab MJ, Ellison GW, Slocum B (editors): Current Techniques in Small Animal Surgery, (4th Ed.). Baltimore, Williams & Wilkins, 1998, pp 1127-1145 Slocum B & Devine Slocum T: Pelvic Osteotomy, in Bojrab MJ, Ellison GW, Slocum B, (editors): Current Techniques in Small Animal Surgery, (4th Ed.). Baltimore, Williams & Wilkins, 1998, pp 1159-1165 Slocum B & Devine Slocum T: DARthroplasty, in Bojrab MJ, Ellison GW, Slocum B, (editors): Current Techniques in Small Animal Surgery, (4th Ed.). Baltimore, Williams & Wilkins, 1998, pp 1168-1170 Smith GK, Biery DN, Gregor TP: New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog. J Am Vet Med Ass 196: 59-70, 1990 Vezzoni A. Complications in Triple Pelvic Osteotomy. Proceedings 11th ECVS Annual Scientific Meeting, Vienna 2002: 289-294 Vezzoni A, Dravelli G, Vezzoni L, De Lorenzi M, Corbari A, Cirla A, Nassauto C, Tranquillo V; Comparison of conservative management and juvenile pubic symphysiodesis in the early treatment of canine hip dysplasia. VCOT 2008; 21: 267-279 Haudiquet P H: Other strategies for HD - DPO vs TPO. Proceedings of 14th ESVOT Congress, Munich, 10th-14th September 2008 12. Haudiquet PH, Guillon JF: Radiographic evaluation of double pelvic osteotomy versus triple pelvic osteotomy in the dog: an in vitro experimental study. Proceedings of 13th ESVOT Congress, Munich, 7th-10th September 2006 13. Vezzoni A, Boiocchi S, Vezzoni L, Bohorquez Vanelli A, Corbari A, De Lorenzi M: Double Pelvic Osteotomy (DPO) as tretament option for hip dysplasia in growing dogs: preliminary results. Poster presentation, VOS, 2009 14. Vezzoni A, Boiocchi S, Vezzoni L, Bohorquez Vanelli A, Bronzo V: Double Pelvic Osteotomy (DPO) for the treatment of hip dysplasia in young dogs. Accepted for publication VCOT 2010 15. Vezzoni A, Peck J. Surgical Treatment of Hip Dysplasia. Chapter 59: 992-1018. In Textbook of Small Animal Surgery. Edited by Johnston S and Tobias K. Elsiever Saunders 2017 16. B. Broeckx, A. Vezzoni, E. Bogaerts, M. Bertal, E. Stock, D. Deforce, L. Peelman. J. Saunders. Comparison of three methods to quantify laxity in the canine hip joint. VCOT 2017 30 6

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INTRODUCTION Patellar luxation is one of the most common orthopedic problems in the dog. Medial patellar luxation is more common (80%) than lateral patellar luxation (20%). Small breed are usually affected by medial patellar luxation, but large breed dogs like Labrador, Rottweiler, Boxer, Bullmastiff, Pitbulls can be affected too. Other large and giant breeds (Newfoundland, Great Dane, St. Bernard, Caucasian shepherd dogs and other are more predisposed to lateral patellar luxation. While in small breed dogs minor degrees of patellar luxation can be tolerated for years of even for ever, in large and giant breed dogs patellar luxation most of the times results in invalidating conditions. In small dogs minor degrees (1째 and 2째) of patellar luxation cause erosion of joint cartilage and predispose to cruciate tears, while major degrees (3째 and 4째) results in severe debilitating conditions. Surgical treatment of patellar luxation is a very common procedure but has a high percentage (20% or more) of failure and recurrence. Understanding the underlying predisposing factors for patellar luxation in each patient and addressing them with custom made treatments can help in improving the success of the surgical treatment. PHYSICAL EXAMINATION Physical examination of the dog lying on his side is performed with the following method, repeating the procedure on the opposite side: -

the clinician holds the hock with one hand and palpate the patella with the other hand; keeping the hip and the knee fully extended, he checks the stability of the patella inside the femoral trochlea; keeping the hip extended and the knee extended, he inward rotates the hock and checks for medial patella luxation; keeping the hip fully flexed and the knee flexed, he outward rotates the hock and checks for lateral patella luxation; he repeats the procedure three to four times and if the patella luxates he checks if it returns in place extending the knee and keeping the hock straight.

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CLASSIFICATION OF PATELLAR LUXATION Patella luxation is classified in 4 degrees accroding to Putman’s and Singleton’s description in 1968: Grade 1, the patella can be manually luxated, but returns to normal position when released; Grade 2, the patella luxates during stifle flexion or ambulation and remains luxated until stifle extension or manual reduction. Grade 3, the patella is luxated most of the time, it can be reduced manually, but reluxates spontaneously; Grade 4, the patella is permanently luxated and can not be manually reduced.

SKELETAL ABNORMALITIES ASSOCIATED WITH MEDIAL PATELLAR LUXATION A variety of anatomic abnormalities can be present in the patient with medial patellar luxation with varying degrees of severity and combinations. These include coxa vara, a diminished angle of inclination of the femoral neck; genu varum, a bowlegged stance in which the knees are abnormally separated, distal femoral varus in which the distal femur bows toward midline, external torsion of the distal femur, hypoplasia of the medial femoral condyle, a shallow trochlear sulcus, proximal tibial varus or valgus in which the proximal tibia bows toward midline or away from midline respectively, external tibial torsion, and medial displacement of the tibial tubercle, internal rotation of the tibia at the knee joint level. Patella “alta” is associated with medial patellar luxation.

SKELETAL ABNORMALITIES ASSOCIATED WITH LATERAL PATELLAR LUXATION A different variety of anatomic abnormalities can be present in the patient with lateral patellar luxation with varying degrees of severity and combinations. These include coxa valga, an increased angle of inclination of the femoral neck; genu valgum, a knock kneed stance in which the knees are abnormally close, distal femoral valgus in which the distal femur bows toward lateral, internal torsion of the distal femur, hypoplasia of the lateral femoral condyle, a shallow trochlear sulcus, proximal tibial valgus in which the proximal tibia bows toward midline or away from midline respectively, internal tibial torsion and lateral displacement of the tibial tubercle, external rotation of the tibia at the knee joint level. Patella “baja” is associated with lateral patellar luxation.

DIFFERENT SURGICAL TREATMENTS FOR PATELLAR LUXATION Several surgical procedures are used to treat patellar luxation, alone or in combination: opposite joint capsule capsulorrhaphy, ipsilateral retinacular and joint capsule desmotomy, ipsilateral pes anserinus release for MPL, transposition or release of the rectus femoris origin for MPL, throcleoplasty, wedge or en-block, patelloplasty, patellar lowering or rising (patella

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alta or baja), distal femoral osteotomy for varus-valgus and torsion, tibial tuberosity transposition (TTT), proximal tibial osteotomy for varus-valgus and torsion, femoral throclea prosthesis, total knee prosthesis. The surgical treatment should be personalized, according to the individual underlaying conditions. Typically, the surgical treatment for patellar luxation is called “a la carte”, according to age of the patient, body size and weight, degree of luxaytion, medial versus lateral, severity of skeletal alterations, chronicity and degree of cartilage degeneration.

CONSERVATIVE TREATMENT Conservative management of patellar luxation is usually indicated in toy and small breed dogs and cats with 1° degree patellar luxation. Conservative management can also be considered in 2° degree patellar luxation in toy and small dogs without clinical signs and not intended for sport activities, as a temporary solution. In medium to large breed dogs conservative management is rarely indicated; it can be considered only in 1° degree patellar luxation without underlying skeletal alteration, when patellar luxation is usually traumatic.

CASE SELECTION FOR SURGICAL TREATMENT Patients with patellar luxation, both for medial and for lateral luxation could be summarized into four groups: For each group the following surgical treatments are usually indicated: 1. Growing dogs with open physis (3-5 months of age), with minimal skeletal alterations, 2° and 3° degrees: -

deepening throcleoplasty & patelloplasty overlapping capsulorrhaphy (retinacular desmotomy only if required) aims: to stabilize the patella and realign the quadriceps mechanism, promoting a spontaneous skeletal realignment to be re-evaluated at skeletal maturity for further procedures in case of recurrence

2. Growing dogs with open physis (3-5 months of age), with severe skeletal alterations, 4° degree: -

corrective osteotomies (varus-valgus-detorsion) of distal femur and/or proximal tibia, saving the physis no Tibial Tuberosity Transposition (resulting in patella baja) deepening throcleoplasty & patelloplasty overlapping capsulorrhaphy opposite side retinacular desmotomy to release tension

3. Young dogs with closed physis and adult dogs, with minimal skeletal alterations, 1° and 2° (3°) degrees:

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deepening throcleoplasty & patelloplasty lateral or medial TTT, compromise for more complex detorsional tibia osteotomy overlapping capsulorrhaphy opposite side retinacular desmotomy to release tension (3° degree) 10-15% recurrence risk simple solution, compromise vs more safe, but more complex and expensive surgeries

4. Young dogs with closed physis and adult dogs, with severe skeletal alterations, 3° and 4° degrees: -

> 8 -10° to normal values corrective osteotomies (varus-valgus-detorsion) of femur and/or tibia deepening throcleoplasty overlapping capsulorrhaphy opposite side retinacular desmotomy to release tension < 5% recurrence risk

RECURRENCE Recurrence of patellar luxation is the most undesirable complication after surgical treatment of patellar luxation. The reported incidence is from 8 to 29% and it’s more common in large breed dogs. In case of recurrence, the first question to be answered is WHY it recurred, performing a critical re-evaluation of the underlying limb deformities, if they were properly addressed or if some mistakes or surgical complication did occur. Concurrent cruciate ligament rupture could be a predisposing factor for recurrence. Then a more personalized planning should be done, addressing the limb deformities and other alterations overlooked in the first surgery.

References 1)

2) 3)

Koch DA, St Grundmann, Savoldelli D, L’Eplattenier H, Montavon PM The diagnosis of Patellar luxation in small animals. (German) Schweiz Arch Tierheilkd 1998;140(9):371-4 Arthus G, Langley-Hobbs S. Complications associated with corrective surgery for patellar luxation in 109 dogs. Veterinary Surgery 35:559-566, 2006 Brinker, Piermattie, Flo. Handbook of Small Animal Orthopedics & Fracture Treatment 2nd edition Philadelphia WB Saunders Co. 1990;377-397

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Part 1 There is no set definition of neonatology in puppies and kittens. Most consider the first two to three weeks of life being the neonatal period. In humans, there are volumes of books with tables, graphs, and guidelines such as the “Denver scores” which one can refer to for assessment of growth and development in a pediatric patient. Unfortunately, we can only rely on very few tables, our own experience and the breeders’ observations and thus may not be completely aware of the diversity present in the many different breeds of dogs and cats. In this session, we will be dealing with normal neonatal development and some of the more common problems associated with the “delay” in development. Because of the unusual or non-specific clinical signs, it is of great importance to obtain a comprehensive history not only of the patient himself, but also of the littermates, parents and other relatives. The history should include number of ill animals, the method by which they were raised, their normal environment, behavior of each puppy or kitten within the litter, body weight curves, duration and type of clinical signs, and medications given. The queen's or the bitch's history should include vaccination dates, estrous cycle (intervals and duration), breeding practices, medications or supplements given during pregnancy, and problems during pregnancy or birth. Has the disorder with which the patient is being presented, been seen in previous litters or in any of the relatives? In certain cases, clients are advised to bring the whole litter or at least one healthy littermate including the mother, so that the patient can be compared with its littermate(s). The physical examination of the neonate can be challenging. Usually, one cannot expect cooperation from the youngest of our patients, especially those that are already aware of their surroundings. They are so distracted by the new environment that something as simple as a menace reflex is difficult to elicit. While everyone knows how to perform a physical

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examination, this presentation will focus on some of the differences to adults and are illustrated with some examples. The list is not complete, but comparison with the some of the developmental landmarks may be helpful in determining other abnormalities. Diagnostic approaches are similar to those in adult animals. However, sample volumes are much smaller due to the size of the patient; radiographic imaging is more difficult due to the lack of fat in the patient, which normally provides contrast; and the results of bloodwork and imaging are difficult to interpret without normal values for the specific age group and breed. The development of select organ systems will also be highlighted to aid in the detection of abnormalities as early in life as possible before disease progression and clinical signs have obscured the original cause. Finally, differences in organ development and function between neonatal and adult patients should be kept in mind when choosing and administering medications, as they may not have the same effect on the two age groups due to the incomplete development of organ systems in the neonate. In summary, the study of pediatric development and diseases can be difficult as alluded to earlier, but it is an interesting and rewarding challenge.

Part 2 The most common reason for presenting neonatal patients to the veterinary clinic are diarrhea, respiratory disease, stunted growth, and fading/death. Neonatal patients are not just small versions of the adult animals. Their immune system and metabolic processes are not fully developed. Unlike adults, puppies and kittens are not able to respond to stressful situations. Therefore, neonatal patients are more susceptible to infectious diseases, and illness will be more pronounced due to limited reserves and decreased ability to respond to dehydration, hypothermia, and hypoglycemia. For these reasons, clinical signs need to be recognized early and a working diagnosis should be made as soon as possible, so that treatment can be initiated to reduce both severity and duration of illness. Diarrhea is among the most common clinical signs observed in both neonatal and pediatric patients. The younger the patient, the more quickly these signs will lead to dehydration and hypoglycemia. A thorough history will reveal nutritional deficits. A fecal sample should be examined for pathogens. Diagnosing metabolic and genetic disorders takes somewhat more time and requires specialized assays. While specific treatment depends on the inciting cause, dehydration, hypoglycemia, and hypothermia must be addressed immediately. In kittens, upper respiratory diseases are more common, while lower respiratory diseases predominate in puppies. Clinical signs include nasal and ocular discharge, sneezing, coughing, lethargy, weakness, and anorexia. A physical examination should include careful auscultation of lung fields, trachea, and heart to allow localization of the most prominent clinical signs. If an accurate diagnosis is needed, samples can be submitted for specialized viral cultures (e.g. distemper in dogs, rhinotracheitis in kittens). Microbiology cultures and antibacterial sensitivity assays should be performed either by obtaining nasal swabs, tracheal washes, or ocular swabs if primary or secondary bacterial infections are suspected. Treatment may involve antibiotics, fluids, and high-quality nutrition.

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A variety of environmental, congenital, and genetic disorders may result in stunted growth. A detailed history may reveal inappropriate nutrition, poor environmental conditions, or inadequate preventative healthcare. The history should also include that of the parents, the littermates, related animals, and if any animals of the same breed have shown any of the same clinical signs. A careful physical examination may reveal facial dysmorphia, short limbs, or cataracts. Comparison to littermates and review of weight charts may reveal the extent and onset of growth retardation. Diagnostics may need to be extensive in the case of congenital or genetic diseases. A diagnosis is essential to determine the extent of treatment and if therapy is even possible. A detailed history, if available, and a thorough physical examination using most senses (smell, observation, palpation, and auscultation) are the most essential tools and with experience, provide the basis for choosing the right diagnostic approach. Therapy may need to be directed towards treating the most detrimental clinical signs first before specific therapy can be initiated. Most importantly, it is important not to give up on the youngest of our patients, as they can be incredibly resilient.

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Encourage the owner to do breeding management: Poor/no breeding management is the most common reason for infertility in the bitch. Proper breeding management includes vaginal cytology, vaginoscopy and progesterone (P4) determination. Due to the combination of the methods, P4 analysis can be reduced to a necessary minimum, usually 2-3 determinations. Ovulation should be verified before sending for mating/insemination as the optimum time for fertilisation of oocytes is 1-3/2-4 days after ovulation. Do diagnostics in case of abortion: The majority of abortions is infectious, why bacterial culture, possibly viral and parasitological diagnosis should be performed in any case of abortion. Fetusses as well as fetal membranes and possibly vaginal discharge of the dam should be assessed. Necropsies on pups – either by an experienced pathologist or yourself for immediate sample collection should be performed. Paired serum samples of the dam with 2 weeks apart should be collected in case of suspicion of canine herpes virus related abortion/puppy death. In any case, tissues/animals sent for analysis should never be frozen, only cooled (+4°C). Do caesarean section immediately in case of black-green vaginal discharge before birth of the first pup: This green-black discharge indicates separation of the placenta why the hemosiderin from the placental margins becomes visible. Fetal hypoxia is the consequence of placental separation, resulting in puppy death if not treated quickly. Never use oxytocin before the birth of the first puppy: Use of oxytocin before the first pup is born is medical malpractice as you cannot rule out for sure that the birth way is free. Rule out obstruction before using oxytocin during labour: In case of one or more puppies have been born and then labour ceases/dystocia occurs, various reasons for dystocia, including obstruction, are possible. Oxytocin is contraindicated in case of obstruction why xrays should be take before oxytocin application. When you are willing to evaluate if a puppy fits through the birth canal, a single laterolateral x-ray is not suitable to rule out obstruction; the ventrodorsal level needs to be taken additionally for proper evaluation of the situation. Be careful with oxytocin – use low dose (1-2 IU/dog) only and repeat only once per puppy with 30 minutes apart: Some textbooks recommend 10-20 IU oxytocin/dog. These high dosages will result in uterine spasm or even uterine rupture only, nowadays very low

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dosages are used only. Two oxytocin injections 30 minutes apart with/without glucose and/or calcium provision should be sufficient for delivery of a puppy. If this is not successful, other injections will only delay your further procedure. Donâ&#x20AC;&#x2122;t do c-section too early, but when necessary. Prepare as much as possible before sedation/anaesthesia of the bitch when performing csection: Several things, including preparation of the surgical theatre, equipment for resuscitation of the pups, clipping and washing of the bitch, should be prepared before anaesthesizing the bitch. Preoxygenation is recommended and improves survival/recovery of the puppies. Avoid single stitches â&#x20AC;&#x201C; perform intracutaneous sutures following c-section, especially in case of surviving puppies: This has been proven to be superior when puppies suckle as it results in less irritation of the abdominal would.

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Various gynecological and andrological cases are presented in small animal clinics, not only in referral clinics. The diagnostic work-up and treatment options of selected diseases are presented here. Pyometra: Pyometra is common in intact middle-aged and older bitches, mainly in diestrus. E. coli is the most common pathogen related to pyometra. The disease can be associated with (sub-)clinical cystitis and cystic endometrial hyperplasia (CEH). Clinical signs can include vaginal discharge (open cervix only) and more or less disturbed general condition, polyuria/polydipsia, fever. Left sheft in white blood cells are common as well as increased kidney parameters due to endotoxemia. Leucopenia is the most predictive value for peritonitis and sepsis. Medical treatment in case of undisturbed/only slightly disturbed general condition can be initiated after exclusion of ovarian cysts/tumour and CEH when the bitch should be used for breeding later. A recent protocol administering aglepristone on days 0, 2, 5 and 8 seems to be more effective compared to the classical protocol (day 0, 1 and 6). Standard treatment is ovariohysterectomy (OHE). Antibiotics effective against gram-negative bacteria/E. coli should be used based on general condition. Ovarian cysts/tumour: Bitches presented with prolonged estrus (> 6 weeks) are suspicious of estrogen producing ovarian cysts or ovarian tumour (esp. Granulosa cell tumour). Other clinical signs include bilateral alopecia, behavioural changes and unspecific symptoms. Vaginal cytology is suitable to detect estrogenic influence, ultrasound of the ovaries necessary to verify either tumorous appearance or fluid filled ovarian cysts. Concomitant pyometra is not uncommon due to hormonal imbalance. Blood sampling for cell count and analysis of organe parameters should be included as prolonged estrogen exposure results in pancytopenia and panmyelophthisis. If this is present, appropriate measures are crucial (blood transfusion, prednisolone 1 mg/kg or CSF). Radiographs and ultrasound of the abdomen to search for metastasis should be done in case of ovarian tumour suspicion. OHE

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is the treatment of choice for ovarian tumours that did not metastasize. In case of ovarian cysts (without uterine changes), hormonal treatment with GnRH agonist injections or hCG can be initiated, but is often not successful resulting in OHE. Ovarian remnant syndrome (ORS): Presence of estrus signs, such as vulva oedema, bloody vaginal discharge, interest of males in the bitch, as well as pseudopregnancy in a previously neutered bitch indicate presence of ORS. Easiest diagnosis at the time when estrus is suspected or slightly thereafter is performed using vaginal cytology (estrus smear). At the time of suspected ovarian quiescence (=anoestrus), blood sampling for LH or AMH can verify gonadal tissue (LH low/AMH present in intact bitch). Ultrasound should be used to identify the location of the ovarian remnant and surgical removal is recommended. Benign hyperplasia of the prostate (BPH): BPH is common in older intact male dogs and often associated with the development of intraprostatic cysts. BPH and cysts predispose for prostatitis and prostate abscessation. Clinical signs include defecation and urination problems. Diagnosis is performed by digital palpation of the prostate and ultrasound. Blood analysis for CPSE (canine prostate specific arginine esterase) can be included to confirm diagnosis; however, there is still no laboratory marker for identification of the prostate carcinoma. X-ray can be used for diagnosis of BPH (less good as ultrasound) and prostate carcinoma, including search for metastasis into local lymph nodes or the pelvis. Treatment of choice is withdrawal of androgens â&#x20AC;&#x201C; either medically with antiandrogens, progestins or GnRH-agonists or surgically (castration). Choosing GnRH-agonist implants as treatment option, the delay in reaching basal testosterone concentrations (4-6 weeks) must be taken into consideration. This is why in severe cases initial treatment with antiandrogens or progestins followed by a GnRH-agonist implant at a later time should be selected. As BPH is so common, preventive geriatric examination should always include prostate examination and owner education about clinical symptoms to allow early identification. Cryptorchidism is the failure of one or both testes to descend from the abdomen through the inguinal ring into the scrotum. It is associated with infertility (bilateral) and increased risk for tumour formation and feminization. Normally testes should be descended at 6 weeks of age; however, cryptorchidism should first be diagnosed at the age of 6 months as until then (rarely) delayed testicular descent can occur. There is agreement about the fact that it is a genetic defect, with epigenetic and environmental factors being involved and that both parents serve as carriers.. In case of no testes is visible and previous castration should be ruled out, blood sampling for AMH or LH could be performed or a GnRH stimulation test. Exclusion from breeding should be aimed for, revealing treatment ethically critical. Medical treatment with GnRH agonists or hCG at an early age has not been proven to be efficient. Surgically, orchidopexy (with vasectomy) or castration of the cryptorchid testis/both testes can be performed.

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Are you? Good. But you can be better. You can be a surgical oncologist!

To operate tumours better, it is essential to know their biology, and therefore be an oncologist before being a surgeon. Concretely, it means that the tumour type should always be determined, so that the biological behaviour of the tumour can be understood. This, in turn, makes it possible to determine the â&#x20AC;&#x153;doseâ&#x20AC;? of surgery required. The most complex surgeries can then be planned based of advanced imaging (CT, MRI). Practically, the possibility to apply the required surgical dose can be limited by the possibilities to reconstruct resulting tissue defects, as well as by the severity of the functional deficits that the resection would cause. To some degree, the ability to reconstruct tissue defects are surgeon-dependant and, from a technical point of view, the most efficient way to be able to operate tumours better is often to become better at reconstructive surgery. Lastly, the surgical oncologist must at all times avoid the contamination of healthy tissues with neoplastic cells.

Before surgery Knowing tumour biology No tumour should ever be resected without the surgeon knowing what type of neoplasia they are facing. At the very least, fine-needle aspirates of the tumour should allow to have a

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broad idea of the tumour type. Depending on this type and on the localisation of the tumour, it can be sufficient to determine the surgical dose required for treatment. Every time determining the tumour type more precisely or knowing the tumour grade would have a significant impact on the surgical dose to apply, an incisional biopsy should be considered. The tumour type and grade, together with the clinical data, allow to know its expected behaviour, from which the surgical dose required for treatment can be determined. This dose is tailored to each individual case, which requires a knowledge of oncology which goes far beyond oncologic surgery technique. This knowledge is critical to determine the optimal course of action for each patient, depending on the characteristics of the tumour, on the current possibilities of veterinary oncology, as well as on the constraints and expectations of the owners. At times, knowing that a procedure is possible in spite of not being able to perform it allows a veterinarian to refer and offer the patient a chance to have the best treatment. Conversely, the mere fact that a surgical procedure is technically possible does not necessarily make it the right thing to do for a particular patient. Stage the tumour Once the type and sometimes grade of the tumour are known, the necessity of staging the tumour can be determined. The TNM staging includes the evaluation of the local extension of the tumour itself (T) and the screening for signs of metastasis in the locoregional lymph nodes (N) and key distant sites (M). The most appropriate distant sites to screen depend on the type of the tumour and most commonly include the lungs, liver and spleen. From a biological viewpoint, all three T, N and M staging are important, but from a surgical technique perspective, the T staging is most relevant. It is most often carried out by advanced imaging: computed tomodensitometry (CT) or magnetic resonance imaging (MRI). It is based on this T staging that it can be assessed whether a tumour can be resected surgically with the required margins determined previously and, if so, what functional and cosmetic consequences can be expected from such a resection. These consequences, together with the anticipated recovery time, must be weighed against the hoped benefits from the surgery with regards to quality of life and life expectancy. Generally, it is more ethically acceptable to put a patient through a heavy surgery with a significant recovery time when the procedure has reasonable chances of being curative or provide tumour control for a long period of time (curative intent) rather than when the life expectancy is thought to be short regardless of treatment. In this latter case, only surgeries with short recovery times, aimed at rapidly improve the patientâ&#x20AC;&#x2122;s quality of life should be considered (palliative intent). All these considerations must be discussed with the owners and a decision to operate or not, and the choice of the type of surgical procedure can be made, knowing clearly what the intent of the treatment will be (curative or palliative).

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Surgical technique Biopsies Surgical biopsies can be incisional or excisional. An incisional biopsy consists in the resection of a small portion of the tumour in view of its pathological examination. An excisional biopsy consists in the excision of the entire mass, often marginally, in the same view. An excisional biopsy should only be performed when knowing the precise nature and grade of the tumour would not change significantly the dose of surgery applied, either for biological or practical reasons. The excessive resort to excisional biopsies is a major cause for treatment failure in surgical oncology. In doubt, fine-needle aspirates or an incisional biopsy should be carried out in order to determine with confidence the extent of the surgical resection required to meet its objectives. In general, it is preferable to take biopsies at the junction between the tumour and the surrounding healthy tissues, so that the pathologist can assess the patterns of the tumoral invasion. In addition, many tumours have an inflammatory, infected or necrotic centre, which hinders the pathological diagnosis. However, some tumours must nonetheless be biopsied in their centre because the intense reaction their cause in surrounding tissues complicate diagnoses made from peripheral samples. It is particularly true for aggressive bone tumours, such as osteosarcomas. In any case, it is critical not to jeopardise later local treatments (surgery, radiotherapy) by a lack of anticipation and planning of the biopsies. Indeed, all biopsy tracts must be resected en-bloc with the tumour at the time of treatment, which can be made difficult or impossible by insufficiently planned biopsy approaches. In addition, the use of electrocautery should be proscribed when taking small biopsy samples, as it creates a particular artefact (cautery artefact) which can prevent reaching a pathological diagnosis. If cautery is required, it can be applied once the samples have been collected. Fine-needle aspirates of the locoregional lymph nodes must frequently be taken, regardless of their presentation and size, as these criteria are not reliable indicators of their possible neoplastic infiltration. However, tumours do not necessarily drain in the closest lymph node and can even drain contralaterally. Therefore, ideally a lymphatic mapping should be performed to determine the position of the sentinel lymph node, which is the first lymph node on the draining route of the tumour. Evaluation of this sentinel lymph node is consequently the most sensitive indicator of any lymphatic metastasis (N staging). In practice, such a mapping is only uncommonly carried out and, in its absence, it can only be recommended to excise for biopsy any lymph nodes which could be the sentinel lymph node, as long as it does not prolong the surgical time and morbidity unreasonably. Tumour resection The most important point, when resecting a tumour is contemplated, it to consider the consequences of the surgery and its potential complications against its anticipated benefits. In other words, the treatment should never be worse that the disease! Surgeons can easily be tempted to perform invasive, technically challenging procedures, which turn out to be of little, if any, benefit for the patient. Conversely, a veterinarian should not deter owners from

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seeking surgical treatment when the required procedure may seem heavy but is known to be well-tolerated (e.g. amputations, maxillectomies, mandibulectomies), just because this veterinarian cannot perform such a procedure themselves. Referral to a specialist surgeon or, better, a surgical oncologist should be offered. It is primordial to make the patientâ&#x20AC;&#x2122;s wellbeing the highest priority, before the wishes of its owners. The discussion with the owners of a pet with cancer should allow the veterinarian to understand their wishes and hopes, and determine whether they are compatible with medical possibilities. Setting clear expectations for the owners is the best way to avoid misunderstandings and later disagreements. Knowing the type and behaviour of the tumour to treat is essential to plan its resection. The determination of the â&#x20AC;&#x153;doseâ&#x20AC;? of surgery to administer relies on it. The first attempt at surgical resection is the best chance of a cure that the patient will ever have, and it should not be wasted by lack of, or inappropriate, planning. Whenever possible, the wide resection of a tumour should be sought. The concern that the resulting tissue defect will not be amenable to closure should not lead to compromise in the oncologic resection. Depending on the tumour type and size, lateral margins of 1 to 3 cm are most commonly sought, but wider margins can be indicated for the most locally aggressive tumours, such as feline injection-site sarcomas for which 5-cm lateral margins have been recommended. In depth, depending on the tumour type and size, a minimum of 1 or 2 fascial plane(s) should be resected en-bloc with the tumour. Alternatively, if an adjuvant treatment is anticipated (radiotherapy especially), the surgical resection can be more conservative. Taking intraoperative pictures and leaving metallic vascular clips at the periphery of the surgical site will assist the radiation oncologist in the treatment planning. Tumours must be manipulated a minima and as delicately as possible to minimise the risk of dissemination of neoplastic cells. Ideally, a tumour should be resected by only manipulating the healthy surrounding tissues resected en-bloc with it, and it should not be approached or seen directly. Any biopsy tracts should be resected en-bloc with the tumour. When possible, major veins draining the resected tissues should be ligated as early as possible during the procedure, before the associated arteries, to limit the risks of sending macro-emboli of neoplastic cells in the systemic circulation when mobilising the tumour. Tumours should be handled like infected tissues would be: any tissues, instruments, gloves, gowns and drapes having potentially been in contact with tumour cells should be changed. The same instruments should not be used to biopsy or resect two separate masses. Similarly, when the surgical wound is closed, it is important to remember that any distant tissues used for or approached during reconstruction (e.g. skin flaps) have to be considered contaminated with tumour, which can have dramatic consequences if revision surgery or an adjuvant treatment is later considered (radiotherapy especially). The use of extensive skin flaps must be proscribed until the status of the surgical margins is known as free of cancer cells, to avoid distant seeding of the tumour. The enlargement of the potentially contaminated field when using a skin flap can render greatly more difficult, if not impossible,

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adjuvant radiotherapy. A solution to the use of skin flaps without contamination consists in elevating any flaps required for reconstruction before resecting the tumour. This strategy however requires solid planning before execution. Postoperative care must also be anticipated at the time of surgery. Feeding tubes must be considered in every patient which may not rapidly get back to normal feeding habits. Likewise, placement of a wound-soaking catheter should be considered after any extensive resection, to regularly inject local anaesthetics in the wound and potentiate postoperative analgesia. Even if the tumour was biopsied before excision, it is submitted for pathology. It is orientated (with sutures, for example) and its margins are inked. Larger excision pieces are sliced on a portion of their thickness to ensure their good fixation in 10% formalin, which only penetrates approximately 1-cm deep in tissues.

After surgery Non-specifically, postoperative care of the cancer patient includes wound care, analgesia, nutritional support and medical treatments. Depending on tumour types, potential paraneoplastic syndromes can need managing (hyper- or hypocalcaemia, hypo- or hyperglycaemia, etc.). Similarly, care specific to the type of surgery performed may be required (chest drains for thoracic tumours, physiotherapy for spinal tumour patients or amputees, etc.). When adjuvant treatments are required, they must be started as early as possible. In most cases, chemotherapy can safely be started 7 to 10 days after surgery. Most chemotherapy agents negatively impact on wound healing experimentally, but this has little clinical relevance. Conversely, radiotherapy is clearly deleterious to all stages of wound healing, and adjuvant radiotherapy should only be started once wound healing is well-advanced, that is 2 to 3 weeks postoperatively.

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All surgeons have complications, often more than they would care to admit. It is however said that it is in the face of complications that surgeons show their value. I would agree and believe this is because managing complications requires not only the know the “how”, but also to understand the “why” and have a deep understanding of the biologic grounds of surgical principles. In other words, it requires to be an achieved surgical biologist, not a mere technician. It is obviously impossible to discuss in detail how to all possible complications. The list of potential complications is long and unfortunate or inadequate surgeons add to it every day. It is however possible to take some perspective to try to figure out the common features of their management and help defining how surgeons should react when facing them. 1. Anticipate them An ounce of prevention is worth a pound of cure, or more appropriately, a stitch in time saves nine. This applies to complications as to anything else. Learning to recognise which patients, which diseases and which surgeries are associated with higher risks of complications helps limiting this risk. First of all, by staying away from lost battles. Good surgeons know how to operate, better surgeons know when to operate and the best surgeons know when not to operate. A fair number of postoperative complications results from bad surgical indications. It is obviously always to find so with hindsight, but it remains true objectively. Fighting lost battles is in nobody’s interest: not the patient’s, not its owners’, not the veterinary team’s. Knowing the risk factors for each disease and each procedure helps anticipating how likely and how severe potential complications are. This allows steering away from surgery if the risks outweigh the expected benefits, or at the very least helps advising clients clearly about the risks carried. Generally, a good number of complications are associated with the poor general condition of the patient or with concurrent diseases and their treatments (e.g. haemostatic disorders, endocrine diseases). Albuminaemia, for instance, is a universal risk factor for surgical patients. When the plasmatic level of albumin is below 20 g/L, the risk of postoperative

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complication increases as wound healing deteriorates. It is particularly critical in gastrointestinal surgery in which wound dehiscence translate in septic peritonitis. Fundamentally, avoiding complications lies in respecting the patient’s biology and physiology. This is the object of respecting Halsted’s very few and simple rules of atraumatic surgery. In addition, good knowledge of the pathophysiology of the treated disease and of the effects the surgical procedure has on it is essential to understand the roots of complications and how to prevent them. 2. Detect them. Acknowledge them. Detecting complications early is essential to limiting their severity and successfully treating them. Here again, the best way to detect complications early is to anticipate them, know which complications are most likely and actively monitor specific parameters associated with them. Unfortunately, some complications are uncommon or never experienced before and are therefore harder, if possible, to anticipate. It is therefore important to have a baseline surveillance protocol for all surgical patients. The heavier the surgery and the more important the organs operated on, the greater the risk of severe complications and the closer the monitoring should be. The systematic postoperative monitoring of surgical patients should have 3 axes: assessment of the general condition of the patient (vital functions and systemic parameters), of the function of the operated system (digestive signs after gastrointestinal surgery, neurologic function after neurosurgery, locomotion after orthopaedic surgery, etc.) and of the surgical wound. The last obstacles to the early detection of complications sadly are surgeons themselves. Mark M. Ravitch, paediatric surgeon observed that “the last man to see the necessity for reoperation is the one having performed the operation”. Surgeons tend to be ostriches and be the last to admit that a patient they operated on may be complicating. If this only was deleterious for their ego, this would be of little consequence, but patients unfortunately are the ones ultimately paying the price for this delayed acknowledgement of complications. Detecting severe complications, such as septic peritonitis, early is a major determinant of patient survival. Being self-aware and realising this natural tendency helps fight it. Being humble and realising that all surgeons have complications help accepting them. In fact, it takes a good surgeon to be relaxed and remain reasonably self-confident in the face of complications, provided their number of complications remain within normal limits, obviously. In fact, to the educated observer (junior colleagues, support staff, etc.), a wellmanaged complication is probably the best benchmark of the value of a surgeon. 3. Treat them. When a complication has developed, it is important to try to determine its cause. In the vast majority of cases, it lies in the disrespect of biology. Going against biology will invariably fail. Yet it is easy to ignore and persist. If a wound has broken down a couple of times already, it is futile to try and close it again grossly the same way with larger-gauge, tighter sutures. The successful approach will involve understanding the reasons for the repeated dehiscence and chose a closure method aiming at addressing them.

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From experience, regardless of a surgeonâ&#x20AC;&#x2122;s skills and expertise, when facing a complication seemingly difficult to treat, it is essential to get back to the fundamentals of surgery, especially if the complication is rare and unexpected. Complications are unfortunately unfrequently and only superficially covered in most textbooks and finding guidance as to how to address very specific ones is not easy. Surgeons must therefore often find the solution themselves and this requires going back to basics. Thinking again in terms of biology and find where the surgical treatment has gone against it. Reviewing essential points including the patientâ&#x20AC;&#x2122;s general condition and concurrent diseases, the pathophysiology of the treated disease, the consequences of the surgery performed, the vascularisation of the operated organs and surgical approach, etc. The practical implications of the conclusions of this review are sometimes hard to accept or implement, as they can be heavy, disappointing or hardly possible, but they must be objectively determined. At the very least, it allows discussing options and expectable results with owners and setting clear and acceptable objectives and limits in treatment. Nothing is costlier than a complication, both in terms of finances and morale, especially if it drags on. It is therefore essential, here again, not to embark on fighting lost battles. It is however more difficult to recognise these lost battles when it comes to complications. Any guilt the surgeon may feel, consciously or not, makes this even harder and in surgeons will more easily embark on treatments they may otherwise deem unreasonable when it comes to treating their complications. Lastly, knowing our limits help both preventing and treating complications, by not embarking on surgeries beyond our abilities, in terms of biology, technique or facilities, and by knowing when to seek help. It is difficult to pass over or refer a complication, but it should be done if it is in the patientâ&#x20AC;&#x2122;s best interest. The issue is almost invariably only in our minds: good surgeons will know that complications happen, having their own, and will not wrongly estimate colleagues seeking help or referring them.

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Wounds are a common encounter in veterinary medicine. The body has a strong drive to heal them and will do so unless intrinsic or extrinsic factors impede wound healing. Understanding the phases of wound healing and how to promote them is essential to effective wound care. The wound may be present on a (poly)traumatised patient. Obviously, the general assessment o of the patient takes precedence over the examination of the wound, which can wait until the animal is unstable, except if the wound is bleeding heavily. In such case, it should be compressed immediately, as aseptically as possible, to prevent a haemorrhagic shock. When a wound cannot be attended immediately, it should be protected from any additional trauma and contamination as early as possible and until the patient is sufficiently stable to undergo wound assessment. Often, the cause of the wound is known from the history, which determines the wound type. If not, the type of the wound should be established during the first inspection of the wound. This is essential, as the severity of the tissue trauma and bacterial contamination heavily varies among wound types. It allows not to be mislead by some wound types, such as puncture wounds from bites, which can appear benign superficially and yet be masking severe deep tissue damage. Initial wound care is carried out on the conscious, sedated or anaesthetised animal, depending on its severity and the overall clinical condition of the patient. Clipping around the wound is generally indicated to facilitate its cleaning. To avoid contamination of the wound by clipped hair, it can be filled by a sterile water-soluble gel or sterile swabs. Similarly, hairs on the margins of the wound can be cut with scissors covered with watersoluble gel, which keeps them on the scissor blades and avoid wound contamination. After clipping, the swabs are removed or the gel is rinsed with warm sterile isotonic fluids. The wound is then cleansed. When it is very extensive or heavily contaminated, it may be initially cleansed with warm tap water, ideally showered under moderate pressure. Tap water is hypotonic, non-sterile, and cytotoxic for fibroblasts and is not ideal to clean wounds, but in the face of massive contamination, the benefits of the mechanical cleaning provided by the use of large volumes of tap water exceed these disadvantages. Most wounds are otherwise rinsed with warm sterile isotonic fluids should be used instead of tap

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water. Adding antiseptics to rinsing fluids, in appropriate concentrations (i.e. up to 0.05% for chlorhexidine and 1% for povidone-iodine), is possible but not essential. As soon as the animal's condition allows it, the wound should be explored, which is especially important or deep and complex wounds. Wounds located over body cavities (chest, abdomen) must be explored cautiously, and the surgeon must be ready to penetrate the underlying body cavity if required, which can be done through the wound itself, or through a separate standard surgical approach to this cavity. The severity of the tissue damage will be determinant in future therapeutic decisions. The 6 hours following the creation of wound are often referred to as the â&#x20AC;&#x153;golden periodâ&#x20AC;?, during which a wound is contaminated but not infected, and can therefore potentially be closed. A corollary to this rule states that wounds older than 12 hours are classically considered infected and must initially be left open. These 'rules' are obviously only gross indications. The age of a wound is only one of several criteria which will determine the risk of infection, and whether a wound can be closed immediately or not. Among these criteria, the severity and extent of the tissue damage are probably the most important. It is more reasonable to close a 24-hour-old frank incisional wound than a 2-hour-old severely traumatic wound. No absolute rules can replace the surgeonâ&#x20AC;&#x2122;s critical clinical judgment and knowledge of biology. Surgical debridement is necessary when significant amounts of necrotic tissue and debris persist in the wound after it has been washed. It is more conventionally performed in layers, from superficial to deep. The viability of tissues is subjectively appreciated (colour, bleeding, etc.). Absence of bleeding should not be considered a reliable test of tissue non-viability as the initial vasoconstriction of the inflammatory phase can limit or prevent bleeding of viable tissues. This could lead to excessive debridement. Depending on their quantitative and qualitative importance, as well as the anticipated therapeutic decision, it is possible to resect tissues of questionable viability (expandable structures, immediate closure sought) or leave them in place (critical structures, open wound management required). In general, debridement should be conservative and only discard tissues which are known with certainty to be necrotic. Tissues of uncertain viability are left in place and examined again at the time of the next dressing change. This may postpone wound closure by 24 to 48 hours, but monitoring the evolution of these tissues before wound closure is beneficial. The wound may have to be debrided repeatedly before it can be safely closed. Other debridement techniques are possible. Wound debridement is said to be selective if it is limited to necrotic tissues, and non-selective if both necrotic and healthy tissues are removed. It can be mechanical (e.g. surgical, dressings), autolytic, enzymatic or a combination of these (e.g. maggot therapy). Several options can be considered when it comes to wound closure. Depending on the condition of the wound after it has been inspected, explored and debrided, a wound can be closed by primary closure, delayed primary closure or secondary closure (third-intention), or be left to heal by second intention.

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If a wound cannot be closed, it is dressed until it is assessed again. How often a wound requires assessment depends on its characteristics, including severity, production and phase (i.e. inflammation and debridement, proliferation, maturation). Many topicals and primary dressing layers can be applied on the wound, with various antibacterial and wound-healing promoting properties. They include hydrocolloids, hydrogels, sugar, honey, alginates, extracellular matrices, tripeptide-copper complexes, acemannan, glycerol, maltrodextrin, zinc, chitosan, platelet gels, yeast extracts, antiseptics and antiobiotics. In addition, advanced wound management techniques can be used, such as hyperbaric oxygen therapy, negative pressure wound therapy (NPWT), installation therapy or low-level laser therapy (LLLT), each with variable level of evidence of efficacy. The principle of moist wound healing is arguably the most important concept to understand and choose modern dressings. Wound healing is faster and better in a moist environment because cell proliferation and functions are facilitated. The exudate produced by the wound contains proteases, inhibitors of proteases, growth factors and cytokines in physiological concentration adapted to every stage of wound healing. This exudate is beneficial to the healing process and should, whenever possible and if the wound is not infected, be left in contact with the wound, rather than removed. Dressings that maintain the wound in a wet environment are referred to as moisture-retentive dressings. They promote autolytic debridement as white blood cells in the exudate selectively eliminate necrotic tissues, leaving healthy tissues in place. Infection rates of wounds maintained in a moist environment are inferior than those of wounds covered with non-occlusive dressings and therefore allowed to dry. The exudate is a physical barrier preventing germs from reaching the wound, as well as an immunological barrier as promoting optimal leukocyte functions. Moisture-retentive dressings also facilitate wound healing by maintaining the wound at physiological temperatures. They maintain a low tension of oxygen in contact with the wound, which lowers its pH, hinders bacterial growth, attracts leukocytes, promotes angiogenesis and collagen deposition. They are more comfortable to wear and less painful to change, since they are non-adherent. In addition, they generally need to be changed less often than other dressings, and are waterproof, which protects the wound of liquid external contaminants, such as urine. A dressing may be occlusive (impervious to gases and liquids), semi-occlusive (permeable to gas and allowing the removal of exudate in excess, but keeping the wound in a moist environment) or non-occlusive (permeable to gases and liquids in both directions). Occlusive dressings are impervious to bacteria. The amount of moisture that runs through a dressing per unit of time is measured in g/m²/h and is called moisture vapour transmission rate (MVTR). The amount of moisture going through human skin is 4 to 9 g/m²/h when the skin is healthy and 80 to 90 g/m²/h when a wound is present. Therefore, the lower the MVTR of a dressing, the more it is moisture-retentive and promoting wound healing. A dressing is considered moisture-retentive if its MVTR is less than 35 g/m²/h. On average, the MVTR (g/m²/h) of hydrocolloids, polyurethane films, polyurethane foams and swabs are 11.2, 13.7, 33.4 and 67, respectively. Moisture-retentive

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dressing however have some disadvantages, such as promoting maceration of the skin surrounding the wound if they are not cut to the shape of the wound and only covering it. The skin around the wound can also be protected from maceration by applying ointments or a protective film. These dressings are also contra-indicated for highly exudative wounds. Moisture-retentive dressings also tend to be more expensive than non-retentive dressings but, when used appropriately, need less frequent changes and shorten healing times, which minimise this extra cost to some extent.

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Becoming a better surgeon happens at many levels. Becoming a better veterinarian in general is a requisite. Good surgeons are skilled technicians, excellent surgeons are biologists, with a broad medical knowledge and understanding which feed their technical skills. Visionary, innovative, ground-breaking surgeons combine this wide medical understanding of biology with a broader extra-medical knowledge enabling them to think and create beyond the boundaries of established medicine. These aspects of a surgeonâ&#x20AC;&#x2122;s development are beyond the scope of this text, which focuses on more practical aspects. The points listed here are by no means exhaustive, but are a good basis to work on when trying to improve as a surgeon. 1. Be equipped The best surgeons can be significantly stifled when using poor quality instruments or when the appropriate instruments for the task at hand are not available. Assembling versatile sets of surgical instruments is an important part of a veterinary surgeonâ&#x20AC;&#x2122;s responsibility. It consists in finding a good compromise between limiting the number of instruments in the kit (and therefore its cost) and yet have a wide-enough variety of instruments to face any situation with sufficient comfort. Good-quality instruments are more expensive to buy, but are more reliable and last longer (provided they are used appropriately), which eventually tend to be more cost-effective. The use of such good-quality instruments invariably translates in greater safety, efficacy and comfort at surgery. A good-quality cautery unit, ideally offering bipolar cautery, is indispensable to the performance of general surgeries, adhering to the general principles of atraumatic surgery. A surgical suction unit is equally indispensable for performance of surgeries in body cavities (coeliotomies, thoracotomies) and advanced procedures (e.g. spinal surgeries). 2. Use your instruments well The range of surgical instruments on offer is virtually limitless, and each instrument has been designed for a precise purpose. Possessing the instrument specifically designed for a precise procedure will greatly facilitate that procedure, but it is naturally not practical to consider acquiring all types of instruments. However, some instruments may misleadingly appear multipurpose and their misuse will not only damage them, leading to unnecessary

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replacement costs, but also put the patient’s safety at risk. Good surgeons know how to use their instruments safely for their patients, their instruments and themselves. Respecting instruments and using them appropriately is the best way of being able to rely on them at critical times. Abusing instruments by using them outside their intended purpose will damage them and make them unreliable and therefore hazardous for the patient. 3. Select your patients One of the reasons the best surgeons have better outcomes and fewer complications does not lie in their technical skills, but in their ability to establish surgical indications appropriately. Patient selection is key. Some patients will not fare well, no matter how good the surgeon. Determining which patients are potential candidates for surgery and which are not requires a broad knowledge of surgical pathophysiology and biology, as well as clinical experience. The fact that a surgical procedure is technically possible does not necessarily make it the best option for the patient. The cost of bad patient selection is paid by the patient, undergoing procedures to little or no benefit, by its owners, financially and emotionally, and by the veterinary staff dealing with the patient, as efforts only leading to disappointing outcomes wear out the morale and confidence of veterinary teams. 4. Be obsessed with atraumatic surgery Gentle tissue handling should be every surgeon’s constant obsession at surgery. The secret of surgery, if there is any, lies in limiting tissue trauma as much as possible. Preserving vascularisation, in particular, is critical. The best surgeons have an acute sense of biology, which makes them realise that they are not fixing problems or repairing organs, but merely trying to place the patient’s body in the best possible position to do so itself. This means that the quality of a surgical procedure should not be only evaluated as per intraoperative criteria, but also as per the anticipated evolution of the patient’s body as a result of this procedure. Briefly, principles of atraumatic surgery include asepsis, gentle tissue handling (delicate dissection and debridement, prevention of ischaemia and tissue desiccation), precise haemostasis and dead-space management. 5. Know your fundamentals Average surgeons merely perform surgeries following recipes. This approach leaves them defenceless when an unexpected situation occurs. The best surgeons do not need precise descriptions of techniques. They only need to understand their purpose and, because they have a deep knowledge of surgical biology and a broad knowledge of existing techniques, they can figure out the details of the procedures themselves. In other words, because they understand the “why”, the “how” comes naturally. Taking the time to learn and review, again and again, the fundamentals of surgical science and techniques, is the best way to prepare to adapt to any unexpected situation or surgical complication. Often, the way out from an unexpected situation comes from resorting to fundamental principles or techniques normally applied to other organs or conditions. If we take a bit of perspective, it becomes obvious that surgical principles are rather few and that the vast majority of techniques are merely the application of these few principles to different organs and conditions.

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6. Embrace complications Surgeons can avoid mistakes, not complications. The more advanced and complex the surgeries, the more severe and disastrous the potential complications. Surgeons must constantly objectively keep track of their complication rates and, provided they remain in line with current standards, not be ashamed to have complications. Complications invariably give an opportunity to differentiate good surgeons from average surgeons, as dealing with them requires going back to surgical biology fundamentals to come out of a difficult situation. They are always an opportunity to learn and grow as a surgeon. They are also one of the benchmarks of a surgeon’s performance. Be humble Constant self-criticism and assessment is essential to refine surgical decision-making, techniques and skills to progress as a surgeon. This journey is never complete. Every surgeon can, and should, improve further, regardless of their degree of mastery. All it takes is enough humility to constantly self-criticise, reflect and learn, and enough passion to drive through the efforts self-improvement requires. Surgeons must remain open to constructive criticism and suggestions. They should strive to remain up to date with the current knowledge in veterinary medicine and surgery. They should use every opportunity to confront their knowledge, techniques and outcomes with colleagues for mutual benefits. Objective outcome measurements should be used as much as possible to assess a surgeon’s performance. For instance, keeping track of morbidity, complication and mortality rates, condition by condition, procedure by procedure, is a good way to objectively monitor a surgeon’s quality of care. Above all, surgeons must remain humble. Not matter how good they are (or believe they are), every surgeon is regularly humbled by a patient which fails to fare as they expected. Such cases always involve some degree of surgical arrogance, of which the surgeon may be oblivious, leading to overlooking or disregarding the biology of the patient. The embracement of each patient with its diseases and biology as a whole, the awareness of the strengths and limitations of surgery for them, and the technical skills and knowledge to perform the most appropriate procedures probably constitute the surgeon’s holy grail.

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Having to close a large or challenging wounds is common in small animal surgery, whether it be after tumour resection or in traumatised patients. Many reconstructive techniques have been reported, reviewed and described in a number of textbooks. Primary closure, combined when needed with tension-relieving techniques, remains most commonly used, thanks to the laxity of the skin of small animals. Frequently, however, the skin surrounding the wound edges needs to be undermined to free the loose skin around the wound and allow such primary closure. Whenever primary closure is not possible, skin flaps should be considered for wound reconstruction. They allow closure of the vast majority of wounds in small animals. A good understanding of their biological grounds, design and performance maximises the chances of success and allows to adapt to any given situation.

Vascular anatomy of the skin Understanding the organisation of the cutaneous vasculature is critical for skin reconstruction. In dogs and cats, the skin is vascularised by 3 plexi: the subpapillary, cutaneous and subdermal plexi. The two most superficial plexuses depend on the subdermal plexus, which is therefore the most important to preserve. This subdermal plexus lies in depth of the hypodermis. In regions of the body where a panniculus muscle is present (trunk, neck), the subdermal plexus runs immediately deeply and superficially to it. As a practical consequence, when the skin is undermined for primary closure or performance of a skin flap, it must be elevated in depth of the panniculus muscle. In areas where no such muscle is present, the skin must be elevated as close as possible from the underlying fascial or muscular plane.

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Figure 1: Vascular anatomy of the skin a: epidermis b: dermis c: panniculus muscle d: squelettal muscle 1: subpapillary plexus 2: cutaneous plexus 3: subdermal plexus 4: hypodermis Arrow: direct cutaneous artery

Skin flaps Skin flaps are either subdermal (relying on the subdermal vascular plexus) or axial (relying on a direct cutaneous artery)(Figure 2). Figure 2: Types of skin flaps

Subdermal flaps Subdermal flaps are sometimes referred to as â&#x20AC;&#x153;randomâ&#x20AC;? flaps, as they rely on the random subdermal plexus to vascularise the elevated skin. This means that these flaps can be harvested in any location and direction. However, the perfusion pressure of the elevated skin has to be estimated as an empirical statistical notion, as the potential presence and direction of direct cutaneous arteries supplying the elevated skin are unknown (Figure 3). As a consequence, these flaps can only be elevated on a limited length, and their base need to be at least as wide as their free end. As an empirical rule, subdermal flaps should only be 1.5 to 2 times longer than they are wide.

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Figure 3: Vascularisation subdermal flaps

Subdermal flaps can either be local or distant.

Local flaps include advancement (Figure 4), rotation (Figure 5), transposition (Figure 6) and interpolation flaps (Figure 7), depending on the way the excess (loose) skin is transferred to the wound. These flaps are elevated from skin adjacent to the wound. The interpolation flaps involve a staged reconstruction on the same principle than that of distant flaps (see later). It is used when the flap pans over a portion of intact skin which is preferred left untouched rather than split by a bridging incision.

Figure 4: Advancement flap

Figure 5: Rotation flap

Figure 6: Transposition flap

Figure 7: Interpolation flap

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The choice of the type of subdermal flap to use depends on the relative orientation and position of the skin in excess to be transferred and the wound to be covered.

Figure 8: Possibilities of elevation of the inguinal skin fold flap

The axillary and inguinal skin folds can be used to create a wide range of subdermal skin flaps. These skin folds are attached in 4 places, 2 (medial and lateral) on the trunk and 2 (medial and lateral) on the limb. Any 3 of these can be severed for the flap to be created, remaining attached by the 4th one (Figure 8).

Distant flaps can be used for wounds of the extremities of the limb (distal to the elbow or stifle). Ideally, part or the whole of the wound is lateral. Extensive, circumferential wounds (degloving injuries) are very good indications. With these flaps, the wound is taken to the excess skin rather than the other way round, like in other flaps. With distant flap, the reconstruction is by necessarily staged, as their principle is to give enough time for a vascularised portion of skin to heal on the wound to reconstruct, sufficiently to be secondarily detached from the trunk and survive on its neovascularisation from the wound. These flaps include hinge and pouch flaps, depending on whether a monopedicular or a bipedicular subdermal flap is elevated on the trunk. Pouch flaps (â&#x20AC;&#x153;tunnelisationâ&#x20AC;?, Figure 9) are safer both because of their double pedicle and because they immobilise the leg better. The disadvantages of these flaps are to require that the patient tolerate having the treated leg maintained against the trunk during the first phase of the reconstruction. Very heavy patients or patients with severe orthopaedic issues of the remaining limbs may not be good candidates for this technique. In any case, a degree of ankylosis is expected when the leg is released, but is usually resolves spontaneously or with minimal physiotherapy.

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To perform a distant flap, the leg to treat is brought to the trunk and a skin flap is elevated from the trunk to cover the wound. This is left to heal 7-18 days depending on the age of the dog and whether the flap is released from the trunk progressively or not. If a circumferential wound is to be covered, enough skin is harvested from the trunk to be wrapped around the released leg and cover the medial aspect of the wound. If the wound to reconstruct is large, closure of the donor site may itself require the use of skin flaps.

Figure 9: Principle of distant flaps (bipedicular â&#x20AC;&#x153;pouchâ&#x20AC;? flap depicted)

Axial pattern flaps Axial pattern flaps are determined by the area of skin vascularised by a major direct cutaneous artery (angiosome), after which it is named (Figure 10a). Many direct cutaneous arteries which can be used to perform axial flaps have been described (Figure 11). Provided this artery is preserved, such flaps are more robust and survive on greater lengths compared to equivalent subdermal flaps. They can even be islanded, i.e. entirely cut out from the donor site apart from their vascular pedicle (Figure 10b). However, axial flaps cannot be elevated in any direction: their design has to follow the description of the cutaneous area vascularised by the chosen direct cutaneous artery. The anatomical landmarks of each axial pattern flap is provided in their original description and in textbooks1-4. The most commonly used axial flaps include the caudal superficial epigastric, thoracodorsal, omocervical, deep circumflex iliac and caudal auricular flaps.

Figure 10: Vascularisation of axial flaps (a). Island flap (b)

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Figure 11: Main direct cutaneous arteries of the dog

Skin flaps, either subdermal or axial, are transposed with their own vascularisation and can survive on poorly vascular beds or over cavities.

Skin grafts Skin grafts consist of transposing free portions of skin to a wound. The transposed skin is therefore no longer perfused and relies on the development of a neovascularisation from the receiving bed for survival. The receiving bed must therefore be healthy and wellvascularised, so that sufficient neovascularisation can develop from it. Graft thickness Graft can be harvested as full-thickness (epidermis and entire dermis) or partial-thickness (epidermis and variable portions of dermis). In practice, harvesting partial-thickness grafts in dogs and cats is technically difficult without dedicated devices (dermatome). In consequence, only full-thickness grafts will be discussed here. Graft types In veterinary surgery full-thickness grafts, harvested from the ventrolateral portions of the trunk, are most commonly used. Different forms of grafts exist: meshed, unmeshed, pinch, punch and strip grafts. Pinch and punch grafts consist of a number of few-millimetre-wide portions of skin placed evenly apart in the recipient bed. Pinch grafts are harvested with a scalpel, whereas punch grafts are harvested with a punch biopsy instrument. Matching-size holes or pockets are created in the granulation tissue of the recipient bed to accommodate the grafts. The main advantages of these grafts are that they are easy to perform, allow very good drainage of

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the wound and withstand infection better than other types of graft. However, the resulting cosmetic aspect is rather poor.

Strip grafts consist of several strips of skin placed parallel in the recipient bed. Matching-size strips of granulation tissue are excised to accommodate the grafts. Like pinch and punch grafts, these grafts allow good drainage but often lead to poor cosmetic results. Meshed and unmeshed grafts use a single skin portion to cover the recipient bed. Meshed grafts are obtained by creating incisions throughout the graft. These incisions allow postoperative drainage, which favours graft adhesion and survival, and enable grafts to cover greater areas compared to unmeshed grafts of similar size. Meshed grafts can be prepared manually or with a dedicated device, which produces more even and expandable meshes, but relying more on second-intention healing and therefore possibly resulting in a poorer cosmetic result. The author almost exclusively uses meshed full-thickness free skin grafts (Figure 12). Principles of free skin-grafting techniques It is essential to understand that a free graft is transferred without any vascular supply, since it is entirely separated from the donor site. It therefore relies on the rapid development of neovascularisation from the recipient bed. Every effort must be made to minimise the time required for new vessels to grow from the recipient bed to the dermis of the graft. Therefore, in contrast with the principles of skin flaps, in which the hypodermis is elevated with the flap to preserve the flapâ&#x20AC;&#x2122;s vascular supply, for skin grafts, the hypodermis is removed from the graft as thoroughly as possible before it is placed on the recipient bed. If it were left on the graft, the hypodermis would only act as a barrier between the vascular buds of the recipient bed and the dermis to be re-vascularised. For the same reasons, the graft must be tacked as much as possible on the recipient bed, to minimise the gap that the new vessels have to cross to reach the dermis and to minimise the movements of the graft relative to the recipient bed, as any such movements prevent the development of the neovascularisation. Lastly, it is crucial to prevent accumulation of any fluid interface (seroma, blood) between the graft and the recipient bed. The graft must therefore be tacked on the recipient bed and immobilised, and drainage of any fluid which may accumulate between the graft and the recipient bed must be provided as required. This is sought both by placement of tacking sutures at the time of surgery and bandages in the postoperative period. These bandages are placed aseptically at the end of surgery and are left unchanged for 3 to 5 days, to avoid disrupting the graft in the early, critical stages of its adhesion on the recipient bed. Infection is a major cause of graft failure, as it impairs the adhesion and revascularisation of the graft. Some authors recommend applying an antibiotic ointment on the recipient bed for 1 or 2 days before surgery and on the graft after surgery.

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Figure 12: Harvesting, preparation and placement of a meshed free skin graft in a dog

At the time of surgery, the recipient bed should either be a healthy granulating wound or a fresh, well-vascularised surgical wound. For grafting limbs, the skin is most often harvested from the ventral third of the thorax or the abdomen. Considerations for donor site selection include its accessibility during surgery (depends on the position of the patient), the availability of its skin (ease of closure) and its aspect (thickness, colour and length of the hair, etc.). At surgery, the recipient bed is prepared first as required (rubbing and cleansing of any granulation tissue, trimming of wound edges, etc.) so that time is left for haemostasis to be complete and perfect before the graft is applied. Once the recipient bed is prepared, a template of it is made in a sterile material (e.g. piece of surgical drape, swab). The recipient bed is then protected with moist swabs while the graft is harvested. The template is placed on the donor site and orientated in anticipation that the direction of hair growth on the grafted skin will match that of the portion of the body on which it is grafted. The skin of the donor site in then incised around the template and elevated. If 2 surgeons are operating, one is then closing the donor site, which may require reconstruction techniques, while the other is preparing the graft. The graft preparation consists of trimming its hypodermis off as much as possible. This is achieved by placing the graft under tension over a sterile support (cardboard, instrument box, bandage roll) and excising the hypodermis with a scalpel (Figure 12). At the end of preparation, no visible hypodermis should remain and the hair follicles should be readily visible on the deep surface of the graft, which is then very thin. The graft is then meshed, either manually or mechanically. The moist swabs covering the recipient bed are removed and the latter is inspected. When haemostasis is complete, the graft can be applied. It is orientated on the recipient bed so

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that its future hair growth will match that of the surrounding skin. The edges of the graft are sutured to the edges of the wound. Tacking sutures are then placed between the edges of the meshing incisions and the underlying recipient bed. The aim is to tack the graft to the recipient bed and immobilise it as much as possible. A sterile bandage is then placed by the surgeon. It is crucial that this bandage be nonadherent and designed to be left in place for 3 to 5 days. It must therefore be sufficiently absorbent. Before placing the bandage, the surgeon may choose to apply an antibiotic ointment on the graft and surrounding skin. The bandage must be mildly compressive to tack the graft further to the recipient bed and immobilise it. It should also absorb any fluids draining from the mesh incisions. The utilisation of vacuum-assisted wound closure (VAC) for a few days after surgery is an effective means of achieving these goals, which has recently been shown to increase the surviving proportion of free skin-grafts in dogs. The bandage is first changed 3 to 5 days after surgery, under general anaesthesia or sedation, depending on the compliance of the patient. Extreme care is taken when changing the bandage not to pull the graft off the recipient bed. The aspect of the graft can be variable and appear concerning during the first week after surgery. It can be either pale or dark, before becoming pink again. Consequently, unless the graft is clearly necrotic, it should not be touched in spite of its aspect, and bandage changes must be continued every 2 to 4 days, as needed. In most cases, the aspect of the graft will improve and it takes at least partially. Free skin grafts are technically simple to perform. Their success mainly depends on their postoperative management, provided they have been done well and to cover an appropriate wound. However, as a result of the wide range and great versatility of available skin flaps in dogs and cats, free skin grafts are not that commonly resorted to, but this depends greatly on the surgeonâ&#x20AC;&#x2122;s preference. They nonetheless are a very useful option for a number of wounds, especially on the distal aspect of limbs, which cannot easily be reached with skin flaps.

Wound closure decision making Wound closure options depend on the location, age, type, severity and contamination of the wound. In small animals, the great skin elasticity allows primary or secondary closure of many wounds. If not, the wound can either be left to heal by second intention or more advanced reconstructive techniques be used to achieve wound closure. Second intention healing may seem financially attractive at first, but it is often long to complete, requires numerous dressing/bandages and regular follow-up, which may eventually cost more than a reconstructive surgery. In addition, it often leaves an epithelium of poor quality and cosmetics, and occasionally results in skin contractures. Skin flaps and grafts can be used to avoid these drawbacks. In all cases, the surgeon must opt for the technique which, in his hands, is the safest, simplest and cheapest. The technique with the greatest chances of success must be chosen

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in priority. If several techniques have equal chances of success, the simplest must be preferred. Lastly, the financial aspect may also be accounted for and the cheapest method among the most likely to be successful may also be chosen.

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Hypoxaemia refers to low levels of oxygen in the blood, whereas hypoxia means abnormally low tissue oxygenation. Maintaining an adequate content of oxygen in the arterial blood is vital in order to maintain oxygen delivery to the tissues. Normal tissue oxygenation is required for cellular metabolism and the preservation of cellular function. Since the tissues have no oxygen storage system, a continuous oxygen supply is necessary. Failure of oxygen supply to meet metabolic needs leads quickly to cellular dysfunction and cell death. Indeed, the definition of shock is inadequate oxygen delivery to the tissues. The lungs are responsible for the movement of oxygen from the atmosphere into the blood. In the blood oxygen is carried in two forms: â&#x20AC;˘ â&#x20AC;˘

A very small proportion of the total oxygen content of blood is present dissolved in plasma. This is measured as the partial pressure of oxygen (PaO2). The majority (>98%) of oxygen is carried bound to haemoglobin (Hb) and is measured as haemoglobin saturation (SpO2).

Even though the PaO2 has a very minor contribution to the total quantity of oxygen transported to the tissues, the PaO2 is essential to adequate tissue oxygenation because it determines the degree of Hb saturation (SpO2). In other words, PaO2 is the driving force for movement of oxygen into the red blood cell. Therefore, hypoxaemia is defined by the PaO2. Normoxaemia = normal PaO2 = 100 mmHg; this corresponds to SpO2 > 99%.

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Hypoxaemia can be divided into moderate and severe. Moderate hypoxaemia is PaO2 < 80 mmHg or SpO2 < 95%. Severe hypoxaemia is PaO2 < 60 mmHg or SpO2 < 90%. This lecture revises the causes, diagnosis and management of tissue hypoxia in the perioperative veterinary patient.

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Hofmeister E et al. (2005) Evaluating Veterinarians’ and Veterinary Students’ Knowledge and Clinical Use of Pulse Oximetry, Journal of Veterinary Medical Education, 32(2); 272-277. Hoad J (2013) Immediate postoperative recovery: Part 1. Veterinary Nursing Journal, 28; 44-46. https://doi.org/10.1111/vnj.12009 Jackson and Murison (2010) Influence of oxygen supplementation on hypoxaemia during recovery from anaesthesia in dogs. Veterinary Record, 166; 142-143. https://doi.org/10.1136/vr.b4765 Killner J (2014) The ups and downs of anaesthesia monitoring: Part 2. Veterinary Nursing Journal, 24; 21-23. https://doi.org/10.1080/17415349.2009.11013148 Lumb AB. Nunn’s Applied Respiratory Physiology. 6th edition. Elsevier Butterworth Heinemann 2009. McMillan M (2016) Pitfalls and common errors of anaesthetic monitoring devices part 1: Pulse oximetry. Veterinary Nursing Journal, 31; 297-302. https://doi.org/10.1080/17415349.2016.1218190 McKay WP, Noble WH (1988) Critical incidents detected by pulse oximetry during anaesthesia. Canadian Journal of Anaesthesia, 35; 265-9. Power I. and Kam P. Principles of Physiology for the Anaesthetist. 2nd edition. Hodder Arnold 2008. Sullivan L et al (2011) Comparison of tissue oxygen saturation in ovariohysterectomized dogs recovering on room air versus nasal oxygen insufflation. Journal of Veterinary Emergency and Critical Care, 21; 633-638. Webb RK et al. (1993) Which monitor? An analysis of 2000 incident reports. Anaesthesia and Intensive Care, 21; 529-42. West JB. Respiratory Physiology, the Essentials. 7th edition. Lippincott Williams &Wilkins 2005.

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Introduction Domestic cats often find themselves living in groups of unrelated individuals, being made to share important resources and being denied the opportunity to hide or retreat from situations of potential conflict. They may also be living in neighbourhoods with large feline populations and find interaction with their feline neighbours something of a challenge. Such factors can readily result in stress and tension and in some cases overt aggressive interactions between cats may occur. An understanding of feline ethology not only helps to explain how and why aggression develops in multi-cat households but also offers practical methods for dealing with it.

Social compatibility The most important consideration in multi-cat households is the issue of social compatibility and while cats may co-exist under the same roof that does not necessarily mean that they belong to the same social grouping. When investigating behaviours within a multi-cat household it is important to take into account natural feline behaviour and remember that cats do not have an inherent tolerance of feline strangers. Owners have often acquired the cats as companions for one another and when problems of inter-cat aggression begin to surface within the household they are genuinely dismayed and perplexed by the situation. Ideally cats will live with genetically related individuals so sibling groupings may stand the best chance of success but cats can also cohabit successfully with other non-related cats if they are introduced early enough and in the right way. The high proportion of neutering in the domestic cat population undoubtedly reduces hostility between strangers, and enhances the chances of feline integration, but it by no means guarantees it. In already existing multicat households it is important for owners to spend time observing their cats and looking for affiliative behaviour patterns, such as allogrooming and allorubbing, in order to establish how many social groups are living within the household. Observation is also useful as it helps to highlight some of the more passive manifestations of social tension, which have been previously overlooked. Overt aggression is certainly a possible manifestation of this situation and when there is outright physical confrontation the cats may be taken to the local veterinary practice with torn ears and puncture wounds to prove it. However, feline tension can also result in more

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subtle signs of unease and can result in chronic low grade stress which in turn contributes to obvious behavioural issues, such as indoor marking and over grooming, but may also be a significant factor in medical conditions, such as feline idiopathic cystitis.

Conclusions Inter-cat aggression within households is certainly a serious issue and one that carries the potential for significant consequences. Where physical confrontation is involved the risk of injury is high and when passive conflict is ongoing the resulting physiological stress response can have significant effects on physical health. It is a relatively common problem for cat owners and one that can be detrimental to both human-cat and cat-cat relations. As with all behavioural issues, dealing with feline aggression relies on establishing the underlying emotional motivation and understanding the influence of natural ethology on the strategies that cats select. When hostility breaks out between cats we need to ask ourselves if their living arrangements are suitable and put our desires as cat owners on the back burner while we look at things from a feline point of view.

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The neonatal period in the kitten is defined as the first 2-3 weeks of life, at which time the kitten is entirely dependent on the mother. Often though, we are faced with abandoned kittens, kittens that have lost their mother due to death or disease, or mothers that are unwilling or unable to take care of one or more of their kittens. In contrast, some neonatal kittens appear to fade and do poorly despite adequate attention by the mother. Nurses provide the first line of care when it comes to these critically ill patients. On one hand, one would want to obtain samples or perform imaging (e.g. blood, urine, radiographs, ultrasound, etc.) to make a diagnosis. On the other hand, the biggest enemies of neonatal kittens are hypothermia, hypoglycemia, and dehydration, which need to be dealt with immediately to stabilize the kitten. Neonatal kittens can become hypothermic quite rapidly, as they are unable to generate heat themselves and are dependent on the mother or outside heat sources. All external heat sources can create problems and therefore need to be monitored carefully. Warm water bottles can spring a leak, and heat lamps can be too close to the neonate resulting in burns. Irrespective of the heating method, it is of utmost importance to reheat the neonate slowly (no more than 1Â°C per hour). If heated too quickly, delayed organ failure and death may result. The risk of hypoglycemia is great because the neonate is born with very little glycogen stores, and the liver is not developed enough to respond well to hypoglycemia. A variety of clinical signs may occur in the hypoglycemic neonate including tremors, crying, irritability, increased appetite, dullness, lethargy, coma, stupor, and seizures being the most common clinical sign. Treatment consists of giving dextrose slowly IV. Higher concentrations of IV dextrose should be avoided because it may cause phlebitis. Dextrose can be given at higher concentrations directly under the tongue. The neonate is particularly susceptible to dehydration, as water makes up 82% of body weight and water turnover is about twice that of an adult. Therefore, fluid requirements are high. Much of the kidney is not fully developed during the neonatal period. This explains the low urine specific gravity during the first weeks of life (1.006-1.017). It is better to check the mucous membranes for hydration in neonatal kittens, because their skin is stretchier than in adults, so it wonâ&#x20AC;&#x2122;t make a tent as readily when dehydrated. Moist mucous membranes are present in a good state of hydration, but tacky to dry mucous membranes indicate 5-7% dehydration. At 10% dehydration, the mucous membranes are very dry and there is a noticeable decrease in skin elasticity.

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Lastly, routes of fluid and medication administration will depend on how poorly the kitten is doing. If possible, IV access should be maintained. The cephalic vein is quite small. Therefore, the jugular vein might be used. Intraosseous catheters are a great alternative, as fluids and medications can be given at the same rate as if given IV. In milder cases, fluids can be given subcutaneously but the addition of dextrose or glucose should be avoided, as it will call skin sloughing. If blood samples need to be obtained, one must not take more than 0.5 ml blood per 100 g of body weight within a weekâ&#x20AC;&#x2122;s worth of time, otherwise the kitten will become anemic. Urine can be obtained by simply stimulating the neonatal kitten to urinate using a moistened cotton ball in the anogenital region.

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Dystocia, the problem of giving birth, is a serious problem in the parturient bitch and may negatively affect dam and puppy health if not recognized in time and veterinary intervention is not sought. For early diagnosis, understanding physiological parturition is crucial. Canine pregnancy is maintained by progesterone deriving from the corpora lutea only. As in other species, parturition itself consists of 3 phases, however, detailed events inducing birth in the dog are still poorly understood. The different phases include: 1. „Preparation“ or „opening“ stage – This stage begins with the onset of synchronous uterine contractions and ends with the cervix being completely dilated. (Uterine contractions are not externally visible.) The average duration of this stage is 6-12 hours, but may be up to 36 hours in nervous/primiparous bitches. 2. “Stage of expulsion” – With complete cervical dilation, expulsion of fetuses starts, myometrial contractions are stronger and abdominal contractions visible. The average duration strongly depends on the number of pups and can typically range between 3-12 hours. 3. “Stage of secundinae” – The expulsion of placentas, typically after each pup, characterises this stage. Once after all puppies have been delivered and all placentas expelled, parturition is completed. Dystocia requiring monitoring and either medical or surgical treatment can be of maternal or fetal origin. About 75% of dystocia cases are of maternal origin; most common etiologies include primary or secondary uterine inertia (48.9%), uterine spasms, too narrow birth way due to e.g. incomplete cervical dilatation, vaginal septa, hip fractures, uterine torsion/ rupture, inguinal hernia. The remaining 25% are related to fetal origin and include relatively/absolutely too large pups, malpresentation/-position/-posture, malformations and dead pups. Clinical signs of dystocia include: • • • • • •

fetal fluids 2-3 hours ago without signs of stage II labour black/green discharge before birth of the first pup (immediate indication for section) 2-4 hours of intermittent, weak or ceasing contractions or no more active contractions for more than 2 hours (with still pups palpable in the uterus) active stage 2 labour with strong, permanent, but non-effective contractions for 20-30 minutes large amounts of bloody discharge before birth of the first pup or in between parturition signs of toxaemia with disturbed general condition.

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Rapid identification of the fact on the phone that the dog is experiencing dystocia, and at the time of presentation quick and proper veterinary diagnosis as well as intervention are crucial for optimum survival rates of the dam and the offspring. Diagnosis includes an obstetrical examination preferably by digital palpation, a transabdominal ultrasound and if necessary a radiological examination. Fetal heart rate below 150 bpm is an immediate indication for caesarean section suggesting fetal respiratory distress (hypoxia). If the fetal heart rate is not critical and no pup is stuck in the soft birth canal, x-rays (laterolateral and ventrodorsal) provide useful information about presentation etc. of the pup, also in relation to the (size of the) maternal pelvis. In case, obstruction, uterine rupture etc. can be ruled out and at least one pup was born naturally, medical treatment of dystocia can be initiated. Importantly, current recommendations about oxytocin dosages are significantly lower than in some older textbooks and as rule of thumb maximum two oxytocin treatments per pup with a 30 min break in between should not be exceeded.

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Similarly to humans, changes of the intestinal microbiota in dogs have been associated with some diseases such as chronic and acute diarrhoea. Also obesity is a common medical disorder in dogs with increasing tendency, being estimated recently that 54% of dogs are overweight in the USA. The objective of this work was the characterization of the microbiota of obese dogs and compare it with normal-weight dog microbiota. Faecal samples from 30 privately owned dogs from Finland (12 obese and 18 normal weight dogs) were taken and analyzed by Illumina sequencing method after DNA extraction. Dogs were classified based on body condition scores using a five-point scale. The results indicate that the predominant group is Firmicutes (24%), followed for Actinobacteria (19%), Fusobacteria (15.8%), Bacteroidetes (14.1%). Obese dogs were characterized to have a more diverse microbiota at class level (p<0.05), with significantly higher amounts of Verrucomicrobiae, Gammaproteobacteria and Actinobacteria (p<0.05). Clostridium perfringens was found in the 55% of the obese dogs and only in the 22% of the normal weight dogs. Methylobacterium adhaesivum was found at significantly higher levels

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(p<0.05) in the 56% of the normal weight dogs, being practically absents (0.09%) in the obese dogs. Our data indicate that there are differences in the faecal microbiota between obese and normal weight dogs at different taxonomic levels. Canine intestinal microbiota is highly diverse being required further work to clarify the role of intestinal microbiota in dog obesity.

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The aim of the study was to investigate the occurrence of methicillin-resistant (MR) staphylococci and Acinetobacter spp. in the environment of small animal clinics in Estonia and to document the most contaminated surfaces. The material was collected from 23 small animal clinics in 2017. The environmental sampling locations were categorized as human contact surfaces, animal contact surfaces and the floors of the clinics. A swab sampling technique was used on surface and the sampling booties for the floors. MRS were isolated in mannitol salt agar with oxacillin and Acinetobacter spp. with the standard microbiological method. The presence of meqA gene of MRS were confirmed by PCR. On average, 15.5 samples per clinic were collected. In total, 55 (15.3%) MRS and 28 (7.8%) Acinetobacter spp. isolates were found out of 358 samples. Eight staphylococcal species were isolated (S. aureus (4.8%)). Only one boot swab sample was MRS positive. The isolation of the environmental MRS and Acinetobacter spp. were higher on human contact surfaces (p < 0.05). According to the questionnaire results, 88% of the clinics do not use special or any disinfection of the surfaces that are in contact with humans. In conclusion, the occurrence of MRS and Acinetobacter spp. was high in the small animal clinics in Estonia. It is crucial to find ways for the prevention of nosocomial infections in

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veterinary practices and it also shows the importance of the disinfection of the human contact surfaces.

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The report describes clinical, CT, surgical and histopathological (HP) findings of a multilobular tumor of the bone on acrus zygomaticus in a dog. A 10-year-old, spayed male, fox terrier, was presented with a 10-week history of inflamed eye and increased tissue volume around the eye. Clinical examination findings were normal expect changes in the ocular region and I grade systolic heart murmur. Eye examination revealed: enophthalmic blind eye, dyscoria, iris darkening, IOP 8 mmHg and complete, mature cataract. Transverse CT show a cartilage mass like structure (30,9 x 28,7 mm, 202,4 HU) dorsal to the left zygomatic arch, with moderate bone destruction and mechanical coverage and compression to the left eye. The transformed tissue with capsule and zygomatic bone was removed. Post-operative treatment included topical ocular and systemic NSAIDs, systemic antibiotics. Recovery was successful, cosmetic result was good, eye reminded normal appearance, but unvisual with a mild phacouveitis. HP tumor was composed of variably distinct lobules surrounded by fibrous connective tissue septae. In the center of lobules variably sized deposits of mineralized bone and cartilage was noted. Between deposits and fibrous septae streams of spindle to plump cells with oval nuclei and single small to moderately sized nucleolus was noted with rare mitoses in this spindle cell population; anisocytosis and anisokaryosis. Multilobular tumor (Grade1) of the bone was approved as a low-grade malignancy chondroma rodens and multilobular chondrosarcoma among others.

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Introduction: Herpesviruses (HVs) are important pathogens in terrestrial tortoises and have also been increasingly found in aquatic turtles in recent years. They are generally associated with severe lesions of the upper digestive and respiratory tract. The purpose of this study was to determine the prevalence and types of HVs found in turtle and tortoise samples submitted from veterinary practices in Europe. Methods and Materials: We tested samples from a total of 2145 chelonians for the presence of HVs using a panherpesvirus PCR followed by strain specific PCRs and sequencing. Results: HVs were detected in 169 (7.8%) of the animals tested. In terrestrial tortoises, the two HVs most commonly found were testudinid HV (TeHV)1, which was found in 83 cases (49.1%), and TeHV3, which was found in 80 cases (47.3%). Three animals were co-infected with TeHV1 and 3. TeHV2 was found in one animal (0.6%) and TeHV4 was found in three animals (1.8%). These were the first detections of TeHV2 and 4 in tortoises in Europe. Additional herpesviruses were found in 3 out of 72 pond sliders (Trachemys sp.) tested (4.2%) and two out of 15 box turtles tested (13.3%).

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Conclusion: This study demonstrates the variability of herpesviruses found in pet turtles and tortoises presented to veterinarians and also underlines the importance of these pathogens in chelonians in general.

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Introduction: Rabbit haemorrhagic disease virus (RHDV) causes severe clinical disease and death in wild and domestic European rabbits (Oryctolagus cuniculus). A new virus type (RHDV2) has emerged in various countries in recent years, although other types (RHDV1) may also cocirculate. This study describes the detection of RHDV1 and 2 in samples from rabbits in various European countries. Methods and Materials: Samples from 684 rabbits submitted by veterinary practices and private owners were tested between January, 2015 and June 2017. Virus detection was carried out using genotype specific real-time PCRs.

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Results: RHDV1 was detected in four samples (0.6%) while RHDV2 was detected in 257 samples (37.4%). RHDV1 was detected in rabbits from Germany and The Netherlands, while RHDV2 was detected in rabbits from Germany, Great Britain, Luxembourg, The Netherlands, Spain, Switzerland, Poland, Belgium, Austria, Sweden, and Finland. Conclusion: These findings reflect the increased importance of this disease and specifically the new virus variant RHDV2 in pet rabbits, while confirming that RHDV1 remains active in Europe.

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The optimal breeding time in the bitch is estimated generally by serum progesterone measurements. The progesterone is excreted in urine as water-soluble metabolites, which can be measured by selective assays. The aims of this study were to develop urinary hormone metabolite assays and to assess the optimal breeding time in bitches noninvasively. In the study, ten urine sample series were collected through visible prooestrus and oestrus from nine bitches. The levels of oestradiol-3-glucuronide (oestrogen metabolite, E2G) and pregnanediol-3-glucuronide (progesterone metabolite, PdG) were measured by inhouse enzyme immunoassays. The concentrations were normalized by urinary creatinine level (ng/Crmg). According to the literature of serum hormone concentrations, the day of the maximum urinary E2G concentration was considered as day -2 and the LH-peak was considered occurring at day 0 following the ovulations at day 2 and the maturation of oocytes at day 4. Urinary E2G concentration started increasing about a week before the maximum concentration (day -2). The PdG concentration began to increase shortly after the ovulations (day 2). Based on the urinary hormone metabolite concentrations, the optimal breeding time began 12 (8â&#x20AC;&#x201C;14) days after the onset of prooestrus bleeding when E2G concentration was decreased and the PdG concentration started increasing. The results show that optimal breeding time can be estimated by urinary hormone assays.

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The dialyzer type has crucial impact on dog hemodialysis, preserving albumin and filtrating urea and creatinine. This study aims to compare the effect of high flux and low flux, fully-synthetic polysulfone dialyzers on Urea, creatinine and albumin in dogs undergoing hemodialysis. The study has been conducted in the Hemodialivet Center on 12 dogs from different breeds, both males and females, aged between one year and 14 years old, weighing between 21 and 25 kilograms during a period of two years. High flux, fully-synthetic polysulfone dialyzers, 1.2 sqm were used in six cases and low flux, fully-synthetic polysulfone dialyzers, 1.2 sqm were used in other six cases. We evaluated only one four hours length session for each case, in which we used a 150 ml/min blood flow. All other hemodialysis parameters were kept the same in all cases. In both groups, Urea (60 Da), creatinine (113 Da) and albumin (69.000 Da) serum concentration at the beginning and in the end of each session were determined. In low flux dialyzers group, albumin decreased with 0.2 to 0.3 mg/dl in average in all cases and in high flux dialyzers group albumin levels had no change after hemodialysis session. Urea and creatinine decreased significantly better in high flux dialyzers group. In conclusion, using high flux dialyzers in hemodialysis in dogs leads to better results regarding the decrease in urea and creatinine and offers great results in limiting the loss of serum albumin.

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Initially, the compositional development of the infant gut microbiota is strongly determined by the mother. Subsequent modifiers are derived from the proximate environment.Shift of the gut microbiota in early infancy is an important element in the development of noncommunicable diseases, emphasizing the relevance of the balance of the microbe contact. Dogs carry potentially pathogenic and tolerogenic microbes, the balance of which may be impacted by probiotics. The aim here was to characterise the transfer of microbes between dogs and infants and determine how dog-specific probiotics modify the process.We studied 34 children (<6 years) from allergic families with dog(s) and controls without a dog. Altogether 40 dogs were randomized for a 4-week period in a double-blind design to receive canine-derived lactobacilli (L. fermentum NCIMB 41636, L. plantarum NCIMB 41638 and L. rhamnosus NCIMB 41640) or placebo (cellulose). Blood and faecal samples from children and faecal samples from dogs were taken prior to and after the treatment.Distinctive gut microbiota composition was observed between infants with dogs compared to those without. Probiotic intervention had an impact on the composition of the gut microbiota in both dogs and children. Specifically, bidirectional exchange of bifidobacterial species between dogs and infants was noted. The sources of early microbe contact extent from mother-infant interaction to the environment, which can represent as targets for interventions aiming to balance the earliest and the most massive microbe contact of the child: the gut microbiota.

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