Uwomj volume 82 supplement s1 summer 2013

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UWOMJ Volume 82, Supplement S1, Summer 2013 Western University

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case report

UWOMJ summer supplement

The University of Western Ontario Medical Journal

Volume 82, Issue S1, Summer 2013

inside 1 2

A Case of Too Much Doggy Love

3

Intergenerational Trauma in Aboriginal Peoples

4 5

An Interesting Case of Preseptal Cellulitis

6

Double Miss by Ultrasound of a Cornual Ectopic Pregnancy

7

Shades of Gray – The Sex Factor Is Not Always Black and White

A Case of Symptomatic Severe Hypercalcemia in a 72-year-old Man

New-Onset Psychogenic Non-Epileptic Seizures in a Patient with Epilepsy

UWOMJ 82:S1 | Page 1 | Summer 2013

case report editorial

Summertime Summertime, in the immortal words of George Gershwin, is when “the livin’ is easy” – that is, of course, unless one happens to be a medical student.

I imagine it must have been around last December when I and my wide-eyed colleagues began in earnest to agonize over what to do with almost three months of summer break. As if on cue, successive information sessions, electronic missives and travel brochures flooded our schedules, inboxes and backseat pouches, mesmerizing us with promises of staple guns, pipette guns and water guns. Inquiries and deliberations and applications ensued, then all was lost amid the busyness of the second semester.

In the end, I spent the majority of my summer with the MedQUEST program (now rechristened MedLINCS) in Seaforth, Ontario. There, I divided my time between frantically scribbling down clinical pearls gleaned from local healthcare professionals and running an interactive camp for high school students from the region. I emerged physically exhausted, perhaps, but with a definitely reinvigorated passion for medicine and medical education – so, I snagged up this sweet job, and now here we all are.

My first great responsibility, this congenial anthology-of-sorts which you are now perusing on your electronic device of choice, is a record of just a few of the many stories of summertime experiences that yearn to be shared. Some of these concern patient encounters: these run the gamut from heartbreakingly sincere, through intellectually challenging, all the way to something altogether unexpected and humbling. Others of these are stories of academic study and research, now told in the form of findings that are equal parts enlightening and sobering. Still others are concerned with good weather and better parties – these are adequately chronicled on Facebook and the like.

The fish might not always be jumpin’ and the cotton varies in height, but this collection of writings will always be a ready reminder of summertime memories. Read on to discover what sorts of things students of the Schulich School of Medicine & Dentistry were involved with over the summer of 2013.

Anthony Chow Junior Associate Editor UWOMJ UWOMJ 82:S1 82:S1 | Page | Page 2 | Summer 2 | Summer 2013 2013

case report A Case of Too Much Doggy Love Melissa J MacPherson, PhD (Meds 2014) Faculty Reviewer: Dr John Payne, MClSc, MD, CCFP, FCFP (Department of Family Medicine)

A

nimal bites, especially bites to the head, neck and face, are common injuries in children.1 It is estimated that in the pediatric population dog bites account for 0.3% to 1.5% of all presentations for medical care.1 Children are most likely to be bitten by a familiar dog at home and are frequently bitten due to a provoked attack.1-3 Appropriate adult supervision could prevent many of these bites from occurring.

It was while I was on a rural family medicine rotation in Dresden, a small farming community of 2800 people in Southwestern Ontario, that I gained exposure to pediatric dog bite injuries. My sweet patient, an animal lover, was playing with a neighbour’s 8-week-old puppy when the injury occurred. She picked up the puppy and squeezed him too hard and the puppy bit her ear in an attempt to escape; a very natural reaction for a small animal. She presented to the local emergency department where the wound was cleaned and closed using dissolvable sutures. The local health department was contacted and informed of her dog bite injury. The following day she presented to our clinic for follow-up care in the company of her mother, her older sister and her stuffed animal – a black doggy. It was in the family medicine clinic where I had the pleasure of meeting her and her four-legged stuffed companion.

Since the puppy at fault was only 8 weeks old, he had not yet received his immunizations. Our 3-year-old patient needed to undergo rabies postexposure prophylaxis (PEP) treatment to prevent a fatal rabies infection. The unimmunized puppy lived on a farm where he theoretically could have been exposed to rabid wild animals. He was placed under quarantine and underwent testing for the rabies virus. The Center for Disease Control in the United States recommends a quarantine period of 10 days for all unimmunized dogs involved in bite injuries.4 Animals are considered to be vaccinated against the rabies virus 28 days after the initial immunization since this is when peak rabies virus antibody titer is reached.4 All dogs are required to have booster shots on a yearly basis to ensure that their immune status against the virus is maintained.4-5 Unfortunately, the puppy in our case was now in for a miserable 10 days of confinement so that he could be monitored for signs and symptoms of rabies.

Rabies is caused by infection with the rabies virus: an enveloped, single-stranded RNA virus in the Lyssavirus genus and Rhab-

doviridae family.6 The virus infects the peripheral nervous system of mammals and undergoes retrograde axonal transport to the central nervous system (CNS).7 Once the virus reaches the CNS it is universally fatal. From the CNS it spreads to multiple organs along both sensory and autonomic nerves.7 The disease has been feared globally for over 4000 years.6 It is the only virus known that has an acute case fatality rate of nearly 100%, making it among the most deadly viruses on Earth.6-7 The World Health Organization estimates that rabies results in more than 50 000 deaths annually.6,8 Most of these deaths occur in the developing world, especially in Asia and Africa, where dogs are not routinely immunized against the virus7 and PEP is not easily available or affordable for dog bite victims.6 In North America most cases of rabies occur due to bat bites.7 In the United States, there are fewer than 2 deaths annually from rabies.8 Once a patient has developed signs and symptoms of rabies, there are no effective measures to stop the progression of the disease. Timely rabies PEP is essential to preserve the life of a patient after a bite from a rabid animal.7 The incubation period of the virus in humans is typically 20 to 90 days.7 The prodromal symptoms are non-specific but may include early localized symptoms of pain, itching and paresthesia at the bite site.7 There are two presentations of the infection: encephalitic rabies and paralytic rabies.6 The encephalitic form of the disease occurs in approximately 80% of human rabies cases.7 It is characterized by episodes of excitement and hallucinations with intermittent lucidity. Patients also have episodes of autonomic dysfunction and hydrophobia (fear of water). Death usually occurs within 7 days.7 In the paralytic form of the disease, patients develop quadriparesis, flaccid muscle weakness and sphincter dysfunction.

These patients are deceased within 2 weeks.7 Dogs infected by the rabies virus excrete the virus in the saliva.4 A bite is an effective method of inoculating a victim with the virus. In an animal, signs of infection include lethargy, fever, vomiting, anorexia, cerebral dysfunction, cranial nerve dysfunction, ataxia, weakness, paralysis, seizures, abnormal behaviour, aggression and self-mutilation.4 On her first visit to the clinic, day 0, our 3-year-old patient received a shot of HyperRAB human anti-rabies immunoglobulin near the site of her bite and a shot of Imovax rabies vaccine at a site distant from her bite. The HyperRAB, a pooled immunoglobulin prepared from human donors with circulating anti-rabies anti-

UWOMJ 82:S1 | Page 3 | Summer 2013

case report bodies, provides passive immunity against the rabies virus for up to 3 weeks following administration.8 Timely treatment with HyperRAB provides passive immunity to rabies before active immunity is acquired from vaccination with Imovax.8 Our patient received a second shot of Imovax vaccine on day 3 and a third shot on day 7 postexposure. Once the puppy had been quarantined for 10 days and was still alive and healthy and had tested negative for the rabies virus, our patient did not require the fourth injection of Imovax vaccine normally administered on day 14. A fifth dose of vaccine is administered on day 28 in patients who are immunosuppressed.6,8 The side effects associated with HyperRAB and Imovax include local reactions at the site of injection such as erythema, itching and swelling, as well as systemic reactions such as headache, nausea, abdominal pain, myalgia, dizziness and fever.8-9 These are similar to side effects seen with other vaccines. Patients bitten by an animal should also receive a tetanus shot if their immunization status is not up-to-date.1 Our 3-year-old patient had received all of her scheduled tetanus vaccinations. If she were under 3 years of age, she would have required a tetanus vaccine on day 0.

Our patient was one of the estimated 15 million people worldwide who receive PEP annually.9 The wound on her ear healed well and will not result in any disfigurement. At our last encounter, she told me that despite being bitten by a puppy she was not afraid of doggies. She then showed me how to gently pat doggies using her well-loved stuffed black dog. She had been practising.

references 1. Sabhaney V, Goldman RD. Child health update. Manage2.

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ment of dog bites in children. Can Fam Physician. 2012 Oct;58(10):1094-6.

Raghavan M. Fatal dog attacks in Canada, 1990-2007. Can Vet J. 2008 Jun;49(6):577-81.

Eppley BL, Schleich AR. Facial dog bite injuries in children: treatment and outcome assessment. J Craniofac Surg. 2013 Mar;24(2):384-6.

Centers for Disease Control and Prevention [Internet]. Atlanta: Centers for Disease Control and Prevention; c2004. Rabies Resource Page; [reviewed 2013 Mar 15; updated 2013 Sep 24; cited 2013 May 29]. Available from: www.cdc.gov/rabies Ontario Veterinary Medicine Association. A Dog Owner’s Handbook [Internet]. Milton (ON): Ontario Veterniary Medicine Association; 2013 [cited 2013 May 29]. Available from: publications.ovma.org/i/115942 Both L, Banyard AC, van Dolleweerd C, Horton DL, Ma JK, Fooks AR. Passive immunity in the prevention of rabies. Lancet Infect Dis. 2012 May;12(5):397-407.

Jackson AC. Current and future approaches to the therapy of human rabies. Antiviral Res. 2013 Jul;99(1):61-7.

Bailey AM, Holder MC, Baker SN, Weant KA. Rabies prophylaxis in the emergency department. Adv Emerg Nurs J. 2013 Apr-Jun;35(2):110-9; quiz 20-1.

Warrell MJ. Current rabies vaccines and prophylaxis schedules: preventing rabies before and after exposure. Travel Med Infect Dis. 2012 Jan;10(1):1-15.

UWOMJ 82:S1 | Page 4 | Summer 2013

case report A Case of Symptomatic Severe Hypercalcemia in a 72-Year-Old Man Cassandra Lin (Meds 2014), Tamara Chu (Meds 2014), Nathalie Sela (Meds 2014) Faculty Reviewer: Dr Noureen Huda, MBBS, FRCPC (Department of Medicine, Division of General Internal Medicine)

case presentation A 72-year-old gentleman was referred to the internal medicine clinic with a one-month history of cognitive and functional decline. Further history revealed progressive confusion, recurrent falls, abdominal pain associated with constipation, an unintentional 30-pound weight loss, and nocturnal sweats for the past two years.

His past medical history and family history were non-contributory.

Physical exam was remarkable for tenderness in the coccyx region but was otherwise normal. His initial screening blood work showed a serum calcium level of 3.37 mmol/L (normal range 2.15-2.55). This suggested that his symptoms were likely a result of the elevated calcium and he was admitted to the inpatient internal medicine service for urgent treatment and further investigations.

Upon admission he was immediately started on intravenous normal saline 250 mL/h to help excrete the calcium and was given a single dose of intravenous pamidronate 90 mg to inhibit further calcium release. Further inpatient investigations were performed to assess etiology, and revealed an albumin level of 20 g/L (normal 3552) and corrected calcium level of 3.69 mmol/L. The serum PTH level was 0.5 pmol/L (normal 1.6-6.9), suggesting that the parathyroid gland was responding appropriately to the elevated serum calcium. The CBC demonstrated pancytopenia with a hemoglobin of 99 g/L (normal 135-170), leukoctyes of 3.8 × 109 /L (normal 4-10), and thrombocytes of 92 × 109 /L (normal 150-400). His hematocrit was 0.24 L/L (normal 0.4-0.5) and the reticulocyte count was normal at 43 × 109 /L, suggesting that the bone marrow (BM) was not able to respond appropriately to the anemia. Moreover, the near-normal MCV of 97.3 fL (normal 79-97) favored an intrinsic BM disease. Amongst other blood tests, the creatinine was elevated at 169 µmol/L (normal 62-120). We did not have a previous creatinine for comparison. The symptomatic hypercalcemia, normocytic anemia, renal failure, and deep coccyx bony pain was suspicious for multiple myeloma and we proceeded with further diagnostic workup.

Peripheral blood smear demonstrated rouleaux formation of red blood cells, ESR was 116 mm/h (normal 0-10), and protein level was 110 g/L (normal 64-83). Serum protein electrophoresis was performed to find the source of elevated protein and this demonstrated an abnormally elevated IgG lambda monoclonal protein.

Urine protein electrophoresis was also performed and demonstrated the elevated monoclonal protein, along with free lambda light chains. As expected, serum IgG immunoglobulin was elevated at

72.3 g/L (normal 6-13) and the other immunoglobulins were low, suggesting immune dysfunction secondary to suppressed plasma cell function. The presence of free light chains in the urine suggested that renal failure was secondary to tubular damage from cast nephropathy. The skeletal survey did not show any lytic lesions consistent with myeloma except degenerative changes in the vertebrae, which may be the cause for our patient’s bony pain.

BM biopsy revealed more than 60% infiltration of plasma cells and the flow cytometry markers were indicative of both monoclonal plasma cells and lambda light chains. These investigations suggested immune suppression and BM infiltration from an elevated monoclonal protein. Coupled with the clinical presentation of anemia, hypercalcemia, and renal failure, this confirmed a diagnosis of IgG multiple myeloma (MM).

initial presentation, epidemiology, and pathogenesis of mm Hypercalcemia is a frequent problem among hospitalized patients with an estimated prevalence of 15%.1 The majority of cases are caused by primary hyperparathyroidism or malignancy.2 MM, a consequence of the latter, is a malignancy of plasma cells resulting in clonal proliferation of immunoglobulins. It causes extreme abnormal bone remodeling with over 80% of myeloma patients having bone disease,3 73% presenting with anemia at diagnosis,4 and 30% having renal insufficiency.5 It accounts for 1% of all cancers and roughly 10% of all haematological malignancies.6 It is thought that almost all MM patients start off with asymptomatic monoclonal gammopathy of undetermined significance (MGUS), which then progresses to MM at a rate of 1% each year.6 Sometimes there is an intermediate stage known as smouldering MM (SMM), which progresses to MM at a rate of 10% each year for the first five years.7

diagnosis and treatment of mm Diagnosis of MM is based on serum and/or urine identification of monoclonal immunoglobulins or the presence of heavy or light chains, evidence of proliferation of plasma cells on BM, and inspection of lytic bone lesions.6 These diagnostic criteria can differentiate between MGUS, SMM, and MM. Symptomatic MM requires >10% infiltration of clonal plasma cells on BM biopsy and evidence of end-organ damage, commonly known as the CRAB criteria: hypercalcemia, renal insufficiency, anemia, and bone lesions.6 Symptomatic MM requires immediate treatment. Standard

UWOMJ 82:S1 | Page 5 | Summer 2013

case report treatment for healthy patients younger than 65 years includes induction therapy followed by autologous stem cell transplantation.

Patients older than 65 years with significant comorbidities should receive chemotherapy. Two therapies are recommended in this clinical setting based on level 1A evidence: (1) melphalan/prednisone/thalidomine (MPT) and (2) bortezomib/melphalan/prednisone (VMP).8-9

references 1. French S, Subauste J, Geraci S. Calcium abnormalities in hospitalized patients. South Med J. 2012 Apr;105(4):231-7.

2. Hussain N, Khan M, Natarajan A, Mohammedabdul M, Musta-

3.

case conclusion Clinically, our patient responded well to IV fluids and pamidronate. The corrected calcium improved to 2.47 mmol/L and this coincided with an improvement in his mentation and abdominal symptoms. The hematology service was consulted for definitive management of MM. Given that our patient likely had lambda light chain cast nephropathy as the cause of renal failure, the hematologist suggested a pulse cycle of dexamethasone 40mg IV for 4 days on, 4 days off, and repeated once. These cycles were a part of a chemotherapy regime consisting of oral melphalan and intravenous bortezomib. Given our patient’s advanced age, he was not a candidate for BM transplant. He was discharged with a normal serum calcium, full recovery from symptoms, and a prescription including instructions for the oral 4 mg pulse dexamethasone cycle. The hematology service took over further care and chemotherapy on an outpatient basis.

Our patient’s follow-up includes bloodwork, serum and urine protein electrophoresis, creatinine, and calcium levels every 2-3 months. Furthermore, new onset of bone pain warrants thorough investigations to detect new bone lesions.7 Considering MM patients are living longer nowadays and suffering from resulting bone disease, it is important for future therapies to target novel mediators of bone destruction.10

4.

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fa U, Yedulla K, Mirrakhimov AE. A case of multiple myeloma coexisting with primary hyperparathyroidism and review of the literature. Case Rep Oncol Med. 2013;2013:420565.

Roodman GD. Pathogenesis of myeloma bone disease. Blood Cells Mol Dis. 2004 Mar-Apr;32(2):290-2.

Palumbo A, Anderson K. Multiple myeloma. N Engl J Med. 2011 Mar 17;364(11):1046-60.

Dimopoulos MA, Roussou M, Gkotzamanidou M, Nikitas N, Psimenou E, Mparmparoussi D, Matsouka C, Spyropoulou-Vlachou M, Terpos E, Kastritis E. The role of novel agents on the reversibility of renal impairment in newly diagnosed symptomatic patients with multiple myeloma. Leukemia. 2013 Feb;27(2):423-9.

Moreau P, San Miguel J, Ludwig H, Schouten H, Mohty M, Dimopoulos M, Dreyling M. Multiple myeloma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.

Ann Oncol. 2013 Aug 16.

Kyle RA, Rajkumar SV. Criteria for diagnosis, staging, risk stratification and response assessment of multiple myeloma.

Leukemia. 2009 Jan;23(1):3-9.

Fayers PM, Palumbo A, Hulin C, Waage A, Wijermans P, Beksac M, Bringhen S, Mary JY, Gimsing P, Termorshuizen F, Haznedar R, Caravita T, Moreau P, Turesson I, Musto P, Benboubker L, Schaafsma M, Sonneveld P, Facon T. Thalidomide for previously untreated elderly patients with multiple myeloma: meta-analysis of 1685 individual patient data from 6 randomized clinical trials. Blood. 2011 Aug 4;118(5):1239-47.

Mateos MV, Richardson PG, Schlag R, Khuageva NK, Dimopoulos MA, Shpilberg O, Kropff M, Spicka I, Petrucci MT, Palumbo A, Samoilova OS, Dmoszynska A, Abdulkadyrov KM, Schots R, Jiang B, Esseltine DL, Liu K, Cakana A, van de Velde H, San Miguel JF. Bortezomib plus melphalan and prednisone compared with melphalan and prednisone in previously untreated multiple myeloma: updated follow-up and impact of subsequent therapy in the phase III VISTA trial. J Clin Oncol.

2010 May 1;28(13):2259-66.

Galson DL, Silbermann R, Roodman GD. Mechanisms of multiple myeloma bone disease. Bonekey Rep. 2012;1:135.

UWOMJ 82:S1 | Page 6 | Summer 2013

case report Intergenerational Trauma in Aboriginal Peoples The Importance of Understanding Historical Context as a Health Professional Peter Cordell (Meds 2016) Faculty Reviewer: Dr Tara Somerville, MD

background information

cultural safety

Aboriginal peoples (First Nations, Inuit, and Metis peoples) represent approximately 4% of the Canadian population1 and 1.7% of the population in the region served by the Southwest Local Health Integration Network (LHIN).2 In fact, Aboriginal peoples are the fastest growing population in Canada,2 with an average age that is significantly younger than that of the non-Aboriginal population.1 However, Aboriginals face higher rates of chronic disease and a variety of challenges accessing care and therefore deserve particular attention.2 Although many efforts are underway to improve health outcomes in Aboriginals, their health outcomes are still disproportionately poor in comparison to those of non-Aboriginal Canadians.3 Awareness of this disparity is not only important to health professionals practicing in Northern Ontario, but also to those in the Southwest LHIN region, due to the number of Aboriginal people residing in this region.2 In London alone there are 4590 persons identified as First Nations people, another 1345 identified as Métis, and 80 identified as Inuit.4

Cultural safety involves health professionals’ recognition that they bring their own culture and attitudes to the relationship with the patient and need to be respectful of the patient’s nationality, culture, age, sex, political and religious beliefs, and sexual orientation.5 In order to achieve cultural safety, health professionals must learn to move beyond the concept of cultural awareness – being aware that a difference exists—to analyzing power imbalances, institutional discrimination, colonization, and colonial relationships as they apply to health care.5 Recognition of the health disparity between Aboriginals and non-Aboriginals is critical for practitioners to adjust screening and treatment practices accordingly. However, this awareness can be harmful if it leads to the impression that Aboriginal people are inherently sick.6 Such an impression puts health professionals at risk of blaming Aboriginal people for their health status.3

case presentation A 19-year-old male from an Ontario First Nations community presented for an appointment with his family physician at the local health centre complaining of arm pain. The patient had visited the local emergency room the day prior, but had been quickly released as his injuries were not the result of a fracture.

The family physician assessed the patient’s injuries, which appeared to be the reason for his appointment. However, further discussion revealed that the individual’s partner was physically violent and that the trend was escalating. On examination, the physician noted several abrasions, a cigarette burn, and a contusion on the patient’s back. After treating the injuries, the individual’s current living situation and safety were discussed. The individual described his willingness to end this abusive relationship and an action plan was created. Later in the appointment, as the patient felt more comfortable, he explained that he had considered suicide. His immediate risk of suicide was assessed and the reasons behind his suicidal ideation were explored.

The individual had an extensive history of witnessing and experiencing domestic violence in his childhood, as did his partner.

The challenge, the physician described, is that in order to enter a healthy relationship, one must know what that looks like, whereas in this case, both individuals understood relationships in the context of abuse and violence as this was their environment as children.

abuse and intergenerational trauma Sources of intergenerational trauma due to colonization include residential schools, forced relocation, involuntary sterilization, forced adoption, religious conversion, and enfranchisement.1 For example, residential school survivors experienced trauma through the abuse and violence that took place in the schools.7 Testimony from former students reveals the extremely harsh and hazardous living conditions at the schools, including hunger and malnutrition, poor heating and sanitation, inadequate clothing, and exposure to contagious diseases.8 Furthermore, many students suffered sexual, physical, and emotional abuse by the teachers and staff responsible for their care.8 The lack of proper treatment and conditions in the schools contributed to the deaths of thousands of children.8 This experience enacts its intergenerational effects through the relationship between trauma and future family violence and abuse.

Domestic violence and abuse are almost always linked to trauma.7 It is estimated that 3.2 million American children witness incidents of domestic violence annually.9-10 When children grow up witnessing violence and abuse, they are far more likely to be violent themselves or to enter into abusive relationships.7 In fact, child witnesses have been found to display inappropriate attitudes about violence as a means of resolving conflict and indicate a greater willingness to use violence themselves.9,11,12,13 In the long-term, the future parenting and relationship skills of children are at stake.14 Thus, trauma is both one of the primary causes as well as a principal outcome of domestic violence and abuse.7 This creates a challenging cycle to break due to its intergenerational effects.7

UWOMJ 82:S1 | Page 7 | Summer 2013

case report In 1999 Statistics Canada found that 25% of Aboriginal women and 13% of Aboriginal men reported experiencing violence from a current or previous partner over the past five years7 – the national average was 8% and 7% in Canadian women and men, respectively, over the same period7. Subsequently, in 2009 Statistics Canada found that Aboriginal women were 3 times as likely as non-Aboriginal women to experience spousal abuse.15 This is especially alarming given that reports are much less frequent than the violence itself.14 The critical point to understand is that the current statistics on domestic violence and abuse in Aboriginals is intimately related to the intergenerational trauma sustained through colonization.

This is demonstrated through the abuse cycle initiated by residential school survivors that have experienced violence and abuse.

discussion

3.

4.

5.

6.

It is extremely important to understand the inequities and statistics regarding various illnesses and diseases in Aboriginal peoples. However, when risk factors are removed from their historical, social, and economic contexts, there is a potential to encourage or reinforce the development of negative stereotypes.1 Health professionals must recognize that colonization is a root cause of the negative health outcomes in Aboriginals.3 This recognition helps prevent the blaming of Aboriginal patients for their health-related behaviours.3 The experience of many Aboriginal People with the mainstream health care system has been negative, often due to cultural differences.5 Frequently, cultural differences and the inability of health professionals to appropriately address these in a culturally safe manner have contributed to high rates of noncompliance and reluctance to visit mainstream health facilities.5 Consequently, this has left Aboriginal patients with feelings of fear, disrespect and alienation.5 Cultural safety conversely entails respectful communication, empowers the patient, and improves quality of care.5 Due to the inherent power imbalance present in the health-professional-to-patient relationship,1 it is the responsibility of the health professional to pursue training in cultural safety as it pertains to Aboriginal peoples. This knowledge is especially important given the health inequity faced by Aboriginals, as well as the aforementioned population demographics for the Southwest LHIN region.

In conclusion, it is critical for health professionals to be aware of the difference in health outcomes in Aboriginal peoples, while being sure not to stereotype Aboriginal patients based on these statistics.3 Health professionals must work together with Aboriginal communities to provide community-directed and culturally safe solutions that disrupt the cycle of abuse stemming from colonization.

7.

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references 1. Wilson D, et al. Health professionals working with First Nations, Inuit, and Metis consensus guideline. J Obstet Gynaecol Can. 2013 Jun;35(6):13-41.

2. South West LHIN. South West LHIN IHSP 2010-2013: Appendix J: Aboriginal population profile [Internet]. London (ON): South West LHIN; 2009 Nov 30 [cited 2013 Aug 31]. Available from: http://www.southwestlhin.on.ca/uploadedFiles/Pub-

lic_Community/Integrated_Health_Service_Plan/2009_IHSP/ Appendix%20J%20-%20Aboriginal%20Profile%20FINAL.pdf Baker AC, Giles AR. Cultural Safety: A framework for interactions between Aboriginal patients and Canadian family medicine practitioners. J Aborig Health. 2012 Nov;9(1):15-21.

Statistics Canada. 2006 Aboriginal population profile for London [Internet]. Ottawa: Statistics Canada; 2010 Mar 24 [cited 2013 Aug 30]. Available from: http://www.statcan.gc.ca/ pub/89-638-x/2009001/article/10828-eng.htm.

National Aboriginal Health Organization. Cultural competency and safety: a guide for health care administrators, providers and educators. Ottawa: National Aboriginal Health Organization; 2008 Jul [cited 2013 Aug 20]. Available from: http://www.naho. ca/documents/naho/publications/culturalCompetency.pdf Elliot CT & de Leeuw SN. Our aboriginal relations: When family doctors and aboriginal patients meet. Can Fam Physician.

2009 Apr;55(4):443-4.

Bopp M, Bopp J, Lane P Jr. Aboriginal domestic violence in Canada [Internet]. Ottawa: Aboriginal Healing Foundation; 2003 [cited 2013 Aug 20]. Available from: http://site.ebrary.com. proxy2.lib.uwo.ca/lib/uwo/docDetail.action?docID=10082945 Troniak S. Addressing the legacy of residential schools [Internet]. Ottawa: Library of Parliament; 2011[cited 2013 Sep 6].

Available from: http://www.parl.gc.ca/Content/LOP/ResearchPublications/2011-76-e.pdf Stiles MM. Witnessing domestic violence: the effects on children. Am Fam Physician. 2002 Dec;66(11):2052-67.

Roberts AR. Battered women and their families: intervention strategies and treatment programs. New York: Simon & Schuster; 1984.

Jaffe PG, Hurley DJ, Wolfe D. Children’s observations of violence: I. Critical issues in child development and intervention planning. Can J Psychiatry. 1990 Aug;35(6):466-70.

Jaffe PG, Wolfe D, Wilson S, Zak L. Similarities in behavioural and social maladjustment among child victims and witnesses to family violence. Am J Orthopsychiatry. 1986 Jan;56(1):142-6.

Spaccarelli S, Coatsworth JD, Bowden BS. Exposure to serious family violence among incarcerated boys: its association with violent offending and potential mediating variables. Violence Vict. 1995 Fall;10(3):163-82.

National Clearinghouse on Family Violence (Canada). Aboriginal women and family violence [Internet]. Ottawa: National Clearinghouse on Family Violence; c2008 [cited 2013 Sep 2].

Available from: http://books.scholarsportal.info/viewdoc. html?id=365778 Brennan S. Violent Victimization of Aboriginal Women in the Canadian Provinces, 2009 [Internet]. Ottawa: Statistics Canada; 2011 May 17 [cited 2013 Sep 2]. Available from: http://www. statcan.gc.ca/pub/85-002-x/2011001/article/11439-eng.htm

UWOMJ 82:S1 | Page 8 | Summer 2013

case report

An interesting case of preseptal cellulitis Eddie Liu (Meds 2014) Faculty Reviewer: Dr Saira Zafar, MD, FRCPC (Department of Medicine, Division of General Internal Medicine)

case presentation A 39-year-old woman presents to the Emergency Department with swelling and erythema of her face involving the right eye. Her symptoms were preceded by a 6-day history of sore throat, fever and chills. Her medical history is significant for depression and she is on sertraline 25 mg P.O. daily. On exam the patient had diffuse erythema and swelling in the lower half of her forehead and the entire region surrounding her right eye. Her right eye was swollen shut.

Gross examination of the eye revealed no proptosis, no ophthalmoplegia and normal ocular movements. Pupils were round and equal with normal direct and consensual response. A CT scan of the head showed no involvement of the orbit and sinuses. Blood culture, urine culture and antistreptolysin O titre (ASOT) were all negative.

Interestingly, the patient’s husband was admitted to hospital a few days earlier with aggressive leg cellulitis and her child recently had strep throat and impetigo. Although no infectious organism was identified in this patient, Streptococcus pyogenes was isolated in an area of cellulitis on her husband’s leg. For this reason, she was treated for S. pyogenes with ceftriaxone 1 mg IV OD for three days followed by cefuroxime 500 mg P.O. BID for 10 days.

discussion It is important to distinguish between preseptal cellulitis and orbital cellulitis. The two conditions share similar clinical symptoms of ocular pain and eyelid swelling and erythema, but they have drastically differently clinical implications.1 Preseptal cellulitis, also known as periorbital cellulitis, is an infection of the anterior portion of the eyelid. It is generally a mild condition that rarely leads to serious complications.5 Conversely, orbital cellulitis is an infection that involves the contents of the orbit, such as the ocular muscles and fat, but not the globe.2 Orbital cellulitis can cause loss of vision and can be fatal. Clinical features that indicate orbital cellulitis include ophthalmoplegia, pain with eye movement and proptosis.7 In addition, imaging studies such as CT scans of the head can help to distinguish between the two.1 Even though preseptal cellulitis is more common than orbital cellulitis, in cases where distinction is unclear, patients should be treated as though they have orbital cellulitis due to the serious complications associated with untreated orbital cellulitis. In the case above, the patient exhibited clinical symptoms indicative of preseptal cellulitis and CT head ruled out any orbital involvement.

The treatment for preseptal cellulitis is usually empirical and depends on knowledge of the common infecting organisms and their antibiotic susceptibility.3 The most common organisms include Staphylococcus aureus, Streptococcus pneumoniae, other

streptococci and anaerobes. If orbital cellulitis is suspected, a referral to an ophthalmologist should be made for further investigations.6 In this case the infectious organism was likely to be S. pyogenes because two of the patient’s family members had recent streptococcal infections: cellulitis, strep throat and impetigo. It is interesting that her ASOT was tested negative; however the test is associated with a false negative rate of 20% - 30% and does not definitively rule out a streptococcal infection on its own.4

summary Preseptal and orbital cellulitis are two conditions that share similar clinical symptoms of swelling, erythema and ocular pain.

Although preseptal cellulitis is more common and generally a mild condition, it is important to distinguish it from orbital cellulitis, which can lead to loss of vision and death. A careful history and physical can be extremely helpful in distinguishing the two conditions and may lead to identification of the offending organism. CT scans of the head are often advisable to rule out orbital and sinus involvement. Preseptal cellulitis is a condition that can be managed by antibiotics as an outpatient. If orbital cellulitis is suspected, however, an ophthalmology referral is warranted and hospital admission is strongly recommended.

references 1. Botting AM, McIntosh D, Mahadevan M. Paediatric pre- and

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post-septal peri-orbital infections are different diseases. A retrospective review of 262 cases. Int J Pediatr Otorhinolaryngol.

2008 Mar;72(3):377-83.

Hofbauer JD, Gordon LK, Palmer J. Acute orbital cellulitis after peribulbar injection. Am J Ophthalmol. 1994 Sep;118(3):391-2.

Howe L, Jones NS. Guidelines for the management of periorbital cellulitis/abscess. Clin Otolaryngol Allied Sci. 2004 Dec;29(6):725-8.

Hahn RG, Knox LM, Forman TA. Evaluation of poststreptococcal illness. Am Fam Physician. 2005 May;71(10):1949-54.

Smith TF, O’Day D, Wright PF. Clinical implications of preseptal (periorbital) cellulitis in childhood. Pediatrics. 1978 Dec;62(6):1006-9.

Uzcátegui N, Warman R, Smith A, Howard CW. Clinical practice guidelines for the management of orbital cellulitis. J Pediatr Ophthalmol Strabismus. 1998 Mar-Apr;35(2):73-9.

Varma D, Metcalfe TW. Orbital cellulitis after peribulbar anaesthesia for cataract surgery. Eye (Lond). 2003 Jan;17(1):105-6.

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case report New-onset psychogenic non-epileptic seizures in a patient with epilepsy The importance of inpatient monitoring on an epilepsy unit to ensure appropriate diagnosis and treatment Kendra L Derry (Meds 2015) Faculty Reviewers: Dr Paul A Derry, PhD (C Psych) (Department of Psychology) & Dr Jorge G Burneo, MSPH, MD (Department of Clinical Neurological Sciences)

introduction Epileptic seizures are paroxysmal behavior patterns due to central nervous system (CNS) dysfunction.1 Psychogenic non-epileptic seizures (PNES) are disorders that can be mistaken for epilepsy.

However, unlike genuine epilepsy, PNES are not the consequence of abnormal electrical discharges in the brain. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) categorizes PNES under Somatoform Disorders: Conversion Disorder along with seizures or convulsions.2 PNES involves unconscious physical manifestation of psychosocial distress.

As PNES and epileptic seizures share many features, it can be difficult to differentiate between the two.3 Diagnosis of PNES is further complicated in cases where there is a concomitant diagnosis of epilepsy. Data suggests that the prevalence of co-existing epilepsy with PNES lies between 10 and 50%.4-7 It is important to accurately diagnose PNES because treatment regimens that are appropriate for epileptic seizures (medication and possible epilepsy surgery) are inappropriate, ineffectual, costly and potentially harmful in the treatment of PNES. We present a case of new onset PNES in a patient with previously diagnosed epilepsy. This case exemplifies how an accurate diagnosis, achieved through admission to the Epilepsy Monitoring Unit (EMU), can drastically alter prognosis and management. This case also highlights the importance of a multidisciplinary approach when dealing with conversion disorders.

case presentation Ms X is a 44-year-old married woman who was admitted to the University Hospital EMU in August 2013, for re-investigation as a surgical candidate for her previously diagnosed epilepsy.

In March of 2004 Ms X experienced her first seizure. On November 7, 2006 Ms X was admitted to the EMU for investigation.

Subdural electrodes were implanted and localized the origins of the seizures to the left anterior temporal and left orbitofrontal region.

A diagnosis of left fronto-temporal epilepsy was made. At this time Ms X was offered a left temporal lobectomy plus posterior inferior frontal lobectomy. The subdural electrodes were explanted on November 30, 2006 with no complications, and the patient was discharged home December 1, 2006 with full medications. At the

time, Ms X wished to proceed with surgery and was to be scheduled for the procedure. On December 14, 2006 Ms X presented to the Emergency Room in London with a headache. It was discovered that she had developed bilateral temporal lobe abscesses. Incision and needle drainage of the left postero-temporal brain abscess was performed and ceftriaxone was administered for 6 weeks. Ms X recovered well from the infection and it was the surgeon’s opinion that her infection would not interfere with her ability to undergo surgery. However, the patient decided to defer surgery and opted for medical management.

With continued problematic seizures, Ms X recently decided she wished to pursue surgery. As is standard practice, she was re-admitted for further seizure monitoring to confirm seizure origin. In contrast to the seizure activity recorded in 2006, all events recorded during her 2013 evaluation revealed entirely normal EEGs. No epileptic seizures were recorded. Ms X did however, experience numerous PNES which were recorded via continuous EEG/video monitoring. In contrast to her seizures in 2006, her current spells are long in duration (5 to 45 min) and non-stereotyped, with asynchronous thrashing of arms and legs and retained consciousness.

The patient reported she experiences about one event per day.

Ms X’s past medical history is significant for migraines (once per week), anxiety disorder with panic attacks and an anoxthalmic left eye.

Medications at the time included 1. Atenolol 50 mg 2. Vimpat 200 mg twice daily 3. Topamax 100 mg twice daily 4. Dilantin 350mg once at nighttime Ms X has a significant psychological history. As a teenager she was in a physically abusive relationship and she was sexually assaulted. In early adulthood, her first husband and her father both unexpectedly passed away. Three years ago she suffered multiple leg fractures in a serious snowmobile accident, and underwent several surgeries and significant rehabilitation.

On admission, Ms X’s physical examination, including a detailed neurologic exam, was normal.

Psychological assessment included formal psychological testing, which indicated the diagnosis of conversion disorder.

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case report discussion

references

The absence of electrographic evidence of epileptic seizures during Ms X’s most recent admission to the EMU was an unanticipated finding. In 2006, her EEG recordings showed clear evidence of left fronto-temporal epilepsy. No PNESs were recorded at that time. Over the nine years since her diagnosis, it was presumed her epilepsy was refractory to medical therapy, as her seizures were uncontrolled by medications alone. Epilepsy surgery seemed to be the most appropriate treatment option for this patient. The importance of re-investigating her is demonstrated by the realization that her epileptic seizures are now apparently well-controlled, and that her problem is caused by new symptoms that are non-epileptic in origin. Discovering this prevented brain surgery and allowed for implementation of appropriate treatment.

The diagnosis of PNES can be difficult. Intensive video-EEG monitoring in the EMU remains the gold standard for the diagnostic evaluation of patients with conversion disorder.8 Video-EEG simultaneously records a patient’s behavior and brain electrical activity.9 When video-EEG monitoring captures a characteristic spell while the EEG background is normal before, during and after the event, a diagnosis of PNES should be considered.

Although there are no pathognomonic clinical signs that distinguish PNES from epileptic seizures, there are some risk factors and warning signs. Psychogenic seizures are characteristically longer in duration,10 with motor manifestations that tend to involve non-stereotyped, asynchronous, non-rhythmical thrashing of the extremities.11 This is in comparison to epileptic seizures which (1) tend to onset earlier in life, (2) are usually brief and stereotyped and (3) generally respond at least somewhat to medication. Additionally, retained consciousness and retrospective recall of ictal events is more indicative of PNES. Psychiatric comorbidities are also common in patients with PNES. The most common include depression, anxiety,12 post-traumatic stress disorder and personality disorders.13 A history of physical abuse is more likely in PNES (~75%) than in epilepsy (~42%).

Further, the rate of sexual abuse is higher in the PNES population (~42%) compared to the epilepsy population (19%).10 Ms X has a good prognosis. She accepts that her current spells are psychogenic in origin and she is attending counseling. Since no epileptic seizures were recorded during her admission, we assume that her epilepsy is well controlled with medications. It is not uncommon for epileptic medications to be increased and/or added to the regime to attempt to control seizures in cases similar to this one. Inappropriate treatment, however, exposes the patient to the adverse effects of antiepileptic drugs and socioeconomic hardships – patients may be unable to work or drive or have limited social activities – and adds to the burden on healthcare resources.

In summary, this case highlights the difficulty in distinguishing between epilepsy and PNES, and emphasizes the importance of both neurological and psychological evaluation for developing a correct diagnosis. It is important to appreciate that some patients with PNES also have genuine epileptic attacks that do require anticonvulsant medications.

1. Leppik I. Contemporary diagnosis and management of the 2.

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patient with epilepsy. 3rd ed. Newtown (PA): Handbooks in Health Care; 1997.

Michael B, editor. Diagnostic and statistical manual of mental disorders. 4th ed. [Internet]. Washington, DC: American Psychiatric Association; 2000 [cited 2013 Aug 22]. Available from http://online.statref.com/Document.aspx?FxId=37&SessionId=1BC2793WJJQFNMKD#H&0&ChaptersTab&APFTKtW5n3gfGFj5b7FkLg%3d%3d&&37 Lesser RP. Psychogenic seizures. Neurology. 1996 Jun;46(6):1499-507.

Benbadis SR, Allen Hauser W. An estimate of the prevalence of psychogenic non-epileptic seizures. Seizure. 2000 Jun;9(4):280-1.

Benbadis SR, Agrawal V, Tatum WO. How many patients with psychogenic nonepileptic seizures also have epilepsy? Neurology. 2001 Sep;57(5):915-7.

Reuber M, Elger CE. Psychogenic nonepileptic seizures: review and update. Epilepsy Behav. 2003 Jun;4(3):205-16.

O’Sullivan SS, Spillane JE, McMahon EM, Sweeney BJ, Galvin RJ, McNamara B, Cassidy EM. Clinical characteristics and outcome of patients diagnosed with psychogenic nonepileptic seizures: A 5-year review. Epilepsy & Behaviour. 2007 Aug;11(1):77-84.

Krumholz A. Nonepileptic seizures: diagnosis and management. Neurology. 1999;53(5 Suppl 2):S76-S83.

Alsaadi TM, Thieman C, Shatzel A, Farias S. Video-EEG telemetry can be a crucial tool for neurologists experienced in epilepsy when diagnosing seizure disorders. Seizure.2004 Jan;13(1):32-4.

Cragar DE, Berry D, Fakhoury TA, Cibula JE, Schmitt F. A review of diagnostic techniques in the differential diagnosis of epileptic and nonepileptic seizures. Neuropsychol Rev. 2002 Mar;12(1):31-64.

Boon PA, Williamson PD. The diagnosis of pseudoseizures.

Clin Neurol Neurosurg. 1993 Mar;95(1):1-8.

Tellez Zenteno JF, Patten SB, Jetté N, Williams J, Wiebe S. Psychiatric comorbidity in epilepsy: a population based analysis. Epilepsia. 2007 Dec;48(12): 2336-44.

Bowman, ES. Nonepileptic seizures: psychiatric framework, treatment, and outcome. Neurology.1999;53(5 Suppl 2):S84-8.

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case report Double miss by ultrasound of a cornual ectopic pregnancy Daniel Myran (Meds 2014) Faculty Reviewer: Dr Meagan O’Brien, MD, FRCSC

abstract Cornual ectopic pregnancy is a rare subtype of ectopic pregnancy that is associated with later presentation and higher likelihood of mortality. Despite advances in sonography cornual ectopic pregnancies remain a challenging diagnosis. We present a case of a left cornual pregnancy that was initially interpreted as a live intrauterine pregnancy by sonographic examination and found during repeat assessment to be a cornual pregnancy.

introduction Ectopic pregnancy, a pregnancy occurring outside the uterus, is one of the most common causes of first trimester bleeding and the most common life-threatening emergency in early pregnancy.1 Currently, 2% of pregnancies result in an ectopic pregnancy, of which 95% occur in the body of fallopian tubes.2 Interstitial ectopic pregnancies (cornual pregnancies) are a rare subtype of ectopic pregnancy, resulting when implantation occurs in the most proximal part of the fallopian tube. Cornual pregnancies occur in approximately 2 to 4 percent of ectopic pregnancies or 1 in every 2500 to 5000 pregnancies.3 Cornual pregnancies are a life-threatening condition with an associated maternal mortality rate of 2 to 2.5% compared to the overall 0.14% mortality rate for ectopic pregnancy.3,4 We report here a case of a cornual pregnancy that was twice interpreted by sonographic examination as a normal intrauterine gestation before diagnosis and treatment with an open resection.

case presentation A 33-year-old woman, gravida 6, para 3 with two previous miscarriages, presented to the emergency department with a one-week history of left lower quadrant pain that had worsened over the past 24 hours. In addition, the patient noted vaginal spotting occurring in the past 24-hour period. Her menstrual periods had been regular, lasting 5 days with a 28-day cycle. At the time of presentation she was at 10 weeks gestation age by last menstrual period. The patient was otherwise healthy with no previous pelvic surgeries, no known history of sexually transmitted infections, and no history of assisted fertilization.

Vitals of the patient at triage were as follows: blood pressure 100/73, temperature 36.2°C, heart rate 81, and respiratory rate 16.

Physical exam showed a stable, well-appearing 33 year old with scant vaginal bleeding. A solid tender mass in the left lower quadrant was palpated.

Image 1: Intact cornual ectopic pregnancy removed from patient.

investigations A transabdominal ultrasound, performed one week prior at an outside institution for routine dating, was interpreted as showing a viable intrauterine pregnancy at 10 weeks gestation. A bedside transabdominal ultrasound performed by the emergency physician on call at the time of presentation was interpreted as showing a viable intrauterine pregnancy. Given the clinical picture, formal repeat ultrasound in the radiology department was conducted on the following day. Ultrasound findings were “an empty uterus and a gestational sac and embryo with motion and cardiac activity located in the left adnexal region with a moderately prominent endometrial canal.”

The patient was taken for emergency laparotomy. A nonruptured amniotic sac measuring 5 x 5-cm with a fetus inside (pictured below) was visualized and removed. A left salpingectomy and repair of uterine cornua were performed and the incision was closed.

The patient had an uneventful postoperative course and was discharged from hospital.

discussion anatomy The anatomy of a cornual pregnancy is responsible for both its late presentation and increased mortality. Cornual pregnancies are located in the proximal portion of the fallopian tube and surrounded by the muscle of the myometrium. The surrounding myometrium allows for greater distensibility before rupture and results in presentation at later stages than in a typical ectopic pregnancy, often as late as 12 to 16 weeks.4 The cornual implantation site is also located between the uterine and ovarian arteries. Consequently, expansion and rupture of the implantation leads to increased risk of life-threatening hemorrhage.5

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case report case, transabdominal ultrasound can miss the diagnosis as the pregnancy may appear to be in an intrauterine location.

treatment

Image 2. Ultrasound image from patient left sagittal view of uterus showing gestational sac on cornua.

With the development and increasing availability of transvaginal ultrasound, the diagnosis of cornual pregnancy is more frequently being made before rupture.

Traditionally cornual ectopic pregnancies were treated with hysterectomy. The current gold standard for a cornual pregnancy is a diagnostic laparotomy followed by a cornual wedge resection. Recent surgical advances have demonstrated that operative laparoscopy is a possible alternative in a stable patient with no suspicion of rupture.8 Conservative methods of treating cornual ectopic pregnancies include systemic administration of methotrexate and laprascopy-assisted or ultrasound-guided injection of methotrexate into the gestational sac.1 Conservative methods have been demonstrated to have an up to 65% success rate with systemic treatment.9 Local injections appear to be more effective but are operator dependent.9 All conservative methotrexate-based therapy is dependent on a stable patient and early diagnosis.

conclusion

Image 3. Ultrasound image from patient showing the crown to rump length (CRL) for gestation. CRL is used to date early pregnancies; it is highly reproducible and up to 12 weeks is the best way of predicting gestational age. Our patient’s CRL showed an 11-week 2-day gestation.

risk factors

Cornual pregnancy remains a rare but significant diagnostic challenge. With increasing use of assisted reproductive technologies its incidence is expected to rise. A high index of suspicion should be maintained in any patient presenting with heavy bleeding during the first trimester. Repeat sonographic assessment is essential even in light of a “normal” intrauterine pregnancy if a patient’s symptoms are consistent with ectopic pregnancy. Diagnosis before rupture is essential to prevent mortality and potential loss of fertility.

references 1. Murray H, Baakdah H, Bardell T, Tulandi T. Diagnosis and treatment of ectopic pregnancy. CMAJ. 2005 Oct;173(8):905-12.

2. Goldner TE, Lawson HW, Xia Z, Atrash HK. Surveillance for

Risk factors for cornual pregnancy are the same as those for ectopic pregnancy. These include pelvic inflammatory disease, previous pelvic surgeries including ruptured appendix, uterine abnormalities, and artificial fertilization.5

3.

4.

diagnosis Of any pregnant patient presenting to the emergency room with first trimester bleeding or pain, 6 to 16% will have an ectopic pregnancy.5 Even with a high index of suspicion and advances in sonography, including transvaginal sonography and serum beta hCG, cornual pregnancy remains the most difficult type of ectopic pregnancy to diagnose due to the low sensitivity and specificity of symptoms and imaging.3 The classic diagnostic triad of ectopic pregnancy - abdominal pain, amenorrhea, and vaginal bleeding occurs in less than 40% of patients with cornual pregnancy.5 This triad is also present in ectopic pregnancy, threatened, and incomplete abortions. Cornual pregnancies show fewer early symptoms due to the increased distensibility of the uterine wall.6 The site of implantation also makes the pregnancy difficult to differentiate from an intrauterine pregnancy on ultrasound.4,7 As was seen in our

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ectopic pregnancy — United States, 1970-1989. MMWR CDC Surveill Summ. 1993 Dec;42(6):73-85.

Radwan F, Steel M. Review Management of cornual (interstitial) pregnancy. Obstet & Gynaecol. 2007 Jan;9(4):249-55.

Wright CT. Sonographic Evaluation of Interstitial (Cornual) Ectopic Pregnancy. J Diagn Med Sonogr. 2008 Oct;24:374-9.

Kun W, Tung W. On the Look out for a rarity – interstitial / cornual pregnancy. Eur J of Emerg Med. 2001;8(2):147-50.

Molinaro TA, Barnhart KT. Ectopic Pregnancies in Unusual locations. Semin Reprod Med. 2007;25(2):123-30.

Auslender R, Arodi J, Pascal B, Abramovici H. Interstitial pregnancy: early diagnosis by ultrasonography. Am J Obstet Gynecol. 1983 Jul;146(6):717-8.

Walid MS, Heaton RL. Diagnosis and laparoscopic treatment of cornual ectopic pregnancy. Ger Med Sci. 2010 Jul;8:1-4.

Lau S, Tulandi T. Conservative medical and surgical management of interstitial ectopic pregnancy. Fertil Steril. 1999 Aug;72(2):207-15.

Bowman, ES. Nonepileptic seizures: psychiatric framework, treatment, and outcome. Neurology.1999;53(5 Suppl 2):S84-8.

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case report Shades of Gray The sex factor is not always black and white Noor Jawaid (Meds 2015) Faculty Reviewer: Dr Norman Furtado, MD, CCFP (Department of Family Medicine)

case presentation Patients with complex healthcare needs are the mainstay of medicine today. In order to simplify management, physicians classify their patients’ symptoms, risk factors and medical histories into categories. A category commonly used by healthcare practitioners and researchers alike is “sex”, since in many diseases, sex can play an important role in attributing level of risk. ML, 64 years old and SL, 66 years old, are two patients who do not fit neatly into such categories.

They are a transgendered, surgically reconstructed married couple, who are both female. I had the pleasure of meeting them on a rural family medicine rotation where they presented together, as they always do, on a follow up appointment regarding their many complicated medical issues.

One was tall with cascading platinum blonde ringlets (a wig on closer inspection), the other wore her hair in a low-slung ponytail and wide-brimmed sun hat – both found exquisitely individual ways to hide their male-patterned baldness in their current female life.

Right away, their openness and matter-of-fact manner made it easy to honestly question them about their past, present and future. ML and SL both had their gender reassignment surgeries conducted in Montreal in 1989. Opting for the same type of surgery, each had their penis and scrotum removed and a vaginal vault constructed but retained their prostate. Their surgeries went well and they now live a happy life together, spending half the year in Canada and the other half in the southern United States golfing. They are highly aware of their medical issues and actively involved in each other’s health. Each one suffers from major conditions with a few notable examples which are placed in sharp focus when discussing risk factors related to “sex” in this unique couple.

using ‘sex’ as a defining feature in research Some of their health needs are easily taken care of because they strictly involve screenings for men or women – in this case, both are applicable. For instance, despite being female, since ML and SL still have their prostates and are over the age of 50, as recommended by Canadian guidelines, they receive their prostate cancer screenings via DRE testing.1 Furthermore, SL has a positive immediate family history of prostate cancer which would usually require more vigilant monitoring, but with taking estrogen and removing her testicles, her risk becomes much lower. To add to their repertoire of annual screening, they also take part in the Ontario Breast Screening program for women over 50. Just because they now live their lives as females does not mean that they can erase the risks they were born into as males.

Other health needs, such as ML’s impaired glucose tolerance and SL’s full blown diabetes, are more difficult to keep track of. Physicians use “sex” as a useful marker to improve their estimates of risks that

apply to their patients, but what happens when the research is telling you two different things? The MONICA Augsburg Cohort Study examines sex difference in risk factors for type 2 diabetes and finds some interesting patterns.2 Systolic blood pressure, smoking and high daily alcohol intake predict diabetes development only in men whereas uric acid and physical inactivity are factors associated with women. It is a difficult decision for the family physician as to which of these factors apply to patients like ML who need to be monitored closely for the possible development of diabetes. There is a similar dilemma present regarding cardiac health risk factors: ML and SL suffer from hypertension, dyslipidemia, hypercholesterolemia and a certain love for red meat and bacon. Some of these conditions have been shown to be greater risks for women in the development of coronary heart disease, while others are more dangerous in men.3 In such cases, even meticulously conducted research has its limitations in application to unique patients like ML and SL

discussion The role of the family physician is paramount in the care of patients like ML and SL who have extra risk factors and screening needs. As discussed, research performed with males and females in mind can only provide so much information in the case of certain patients. The scenario is further convoluted when patients present with uncommon medical backgrounds with which the average physician may be unfamiliar. Information about less common procedures such as gender reassignment surgeries should be made available especially early on in the training of medical professionals.4 These patients must be cared for with great sensitivity for their unique needs and be understood in the context of each person as an individual. Patients should be treated as wholes regardless of the complexity of their medical needs – male, female or both.

references 1. Izawa J, Klotz L, Siemens D, Kassouf W, So A, Jordan J, Chetner M, Iansavichene A. Prostate cancer screening: Canadian guidelines 2011. Can Urol Assoc J. 2011 Aug; 5(4):235-40.

2. Meisinger C, Thorand B, Schneider A, Stieber J, Doring A, Lowel H. Sex Differences in Risk Factors for Incident Type 2 Diabetes Mellitus: the MONICA Augsburg Cohort Study. Arch Intern Med. 2002 Jan;162(1):82-9.

3. Roeters van Lennep J, Westerveld H, Erkelens D, van der Wall E. Risk factors for coronary heart disease: implications of gender. Cardiovasc Res. 2002;53(3):538-49.

4. Lombardi E. Enhancing transgender health care. Am J Public Health. 2001 Jun;91(6):869.

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