Page 1

consult The Australian Medical Magazine for Specialists and GPs Summer 2011/2012

Vitamin D Vitamin D: An Update

NSAID-Induced Intestinal Injury Non-Steroidal Anti-Inflammatory Drug Induced Intestinal Injury

Multiple Sclerosis

Focus on Multiple Sclerosis Part III: Diagnosis

The Art of Psychiatry The Art of Psychiatry

The Running Shoe

Excellent Science or Excellent Marketing?

Acute Liver Failure

Acute fulminant liver failure due to reactivation of hepatitis B


medical director


t lhas been a busy 6 months for Virtual Medical Centre and this summer issue of CONSULT Magazine, while coming a little later than usual, has a strong focus on applied articles which I’m sure will be both intellectually interesting and practically useful. Following positive feedback about the last issue of CONSULT Magazine we are continuing with an online publication format. It seems the convenience of being able to read the magazine how and where you choose is a valuable feature which probably contributed to the rise in readership we observed for the last issue. Of course, the extremely high quality of the articles published in CONSULT 6 would also have been a contributing factor. The great strength of Virtual Medical Centre is having active Editorial Advisory Board members who are prepared to share their knowledge with their peers. If you have a clinical experience you think needs to be discussed or have a topic that you feel particularly passionate about, please share it with us so that we can share it with the wider medical community in Australia. You don’t need to be an EAB member either so if you would like to get involved in making the next issue of CONSULT Magazine even better than the last please send me an email at adean@ If you would like to join our EAB, or want to offer feedback about Virtual Medical Centre and CONSULT Magazine, please email me (adean@ Thank you for your support, both for our magazine and the www.virtualmedicalcentre. com website. Andrew Dean MBChB MRCP(UK) FRACP Medical Director Virtual Medical Centre

consult Magazine

NSAID-induced intestinal injury 4

Non-Steroidal Anti-Inflammatory Drug Induced Intestinal Injury

Associate Professor Andrew Keegan

Vitamin D 8

Vitamin D: An Update

Tina Aspres

Multiple Sclerosis


greetings from the

12 Focus on Multiple Sclerosis Part III: Diagnosis Dr Jeremy F Hallpike

THE ART of psychiatry 15 The Art of Psychiatry Dr Pia Brous

The Running Shoe

18 The Running Shoe - Excellent Science or Excellent Marketing?

Trent Salkavich and Emily Smith

Acute Liver Failure

21 Acute fulminant liver failure due to reactivation of hepatitis B

Associate Professor Adel Ekladious

We acknowledge the important contribution of the Medical Directors: • Dr Peter Bremner • Dr Andrew Dean • Dr Nick de Felice • Dr Clay Golledge • Dr Roger Goucke • Professor Jeffrey Hamdorf • Professor Graeme Hankey • Dr Andrew McQuillan

• Dr Brendan McQuillan • Dr Donald Ormonde • Dr Paul Snelling • Associate Professor Rob Will • Dr Garry Wilson • Dr Steve Wilson • Dr Joe Kosterich (Medical Spokesperson)

Published by Virtual Medical Pty Ltd MANAGING EDITOR: Dr Michael Banazis ( SUB EDITOR: Jennifer Browne CONTRIBUTION COORDINATOR: Sylvia Möllenbeck ( ADVERTISING SALES: Aman Madan ( LAYOUT DESIGNER: Sylvia Möllenbeck SUBSCRIPTIONS: CIRCULATION: 10,000 copies Virtual Medical Centre PO Box 1173, Osborne Park, Western Australia, 6017 Ph: Perth (08) 9388 0344 Fax: (08) 9388 0611 Email: Website: MEDICAL DIRECTOR: Dr Andrew Dean MANAGING DIRECTOR: Wayne Hughes GENERAL MANAGER: Thomas Maher COPYRIGHT WARNING: All editorial copy and some advertisements in this magazine are subject to copyright and cannot be reproduced in any form without the written permisson of the editor. Offenders will be prosecuted. DISCLAIMER: Virtual Medical Pty Ltd (‘the publishers’), and its directors, employees and related entities do not make any warranty whatsoever as to the accuracy or reliability of any information, estimates, opinions, conclusions or recommendations contained in this publication and, to the maximum extent permitted by law, the publisher disclaims all liability and responsibility for any direct or indirect loss or damage which may be suffered by any person or entity through relying on anything contained in, or omitted from, this publication whether as a result of negligence on the part of the publisher or not.



Non-Steroidal Anti-Inflammatory Drug Induced Intestinal Injury NSAID-induced gastroduodenal effects are well known, but less so than those more distally in the gastrointestinal tract. There may be inflammation and ulceration with perforation and/or stricture formation involving the intestine. Adjunct Associate Professor Andrew Keegan MB BS BSc(Med) PhD FRACP AGAF FAMA, Consultant Gastroentrologist, Nepean Hospital, Kingswood, NSW, Sydney Medical School, Nepean University of Sydney.


ver recent decades, much attention has been given to the gastroduodenal complications associated with the consumption of non-steroidal antiinflammatory agents (NSAIDs). Dyspepsia is not unusual and, more importantly, ulceration of the stomach and proximal duodenum are well known complications, with the latter responsible for significant numbers of hospital admissions. It has, however, become apparent that these agents are also capable of inducing significant injury to the more distal GI tract, with affected patients presenting with the consequences of ulceration, blood loss, perforation and or stricture formation.1 The small bowel, especially the ileum and less often the colon (mostly proximal), may be involved. Over recent years, these complications have become more evident, possibly due to changes in NSAID preparations and the advent of capsule endoscopy and deep balloon assisted enteroscopy, which have facilitated diagnosis.2,3 Antisecretory agents (H2 receptor antagonists and proton pump inhibitors) may mitigate against NSAIDinduced gastroduodenal disease, but not from the injury to the more distal small bowel and colon. The elderly are at greatest risk.4 It is likely that NSAID-induced intestinal mucosal injury is related to the duration of therapy and not to dose.4 Long-term exposure to these drugs increases mucosal permeability and induces inflammation


in 65% of patients. Approximately two thirds of NSAID users have evidence of intestinal inflammation by leukocyte scintigraphy.1 Moreover, large and small bowel perforation and bleeding are twice as likely in NSAID users.1 At post mortem, small intestinal ulceration is more common in those who have taken NSAIDs.5 Double balloon enteroscopy has shown the prevalence of small bowel mucosal injury to be greater in NSAID users than in controls. It should, however, be noted that small bowel mucosal erosions are common in healthy individuals, as shown at capsule endoscopy.2 The reduction in prostaglandin synthesis through cyclo-oxygenase (COX) inhibition contributes to intestinal injury.

Figure 1: Capsule Endoscopy view of NSAID- induced small bowel stricture

Selective COX-2 inhibitors may also induce intestinal mucosal injury, possibly as readily as non-selective NSAIDs, particularly in the elderly and those with a history of previous distal GI events. However, the use of COX-2 inhibitors does appear to be associated with a lesser risk of small bowel mucosal injury than non-selective NSAIDs in combination with a proton pump inhibitor.2

Mechanism The introduction of slow and sustained release formulations as well as enteric NSAID preparations aimed at reducing

Figure 2: Patency capsule– retained within the small bowel due to NSAID-induced stricture

Summer 2011/2012 | Consult Magazine


gastroduodenal complications may, as a consequence, increase more distal gastrointestinal injury. Mucosal damage requires the presence of significant concentrations of NSAID, which is more likely with such preparations, especially when the agent is subject to enterohepatic circulation.1,6 Proposed mechanisms of injury involve increased mucosal permeability related to inhibition of prostaglandin production and altered blood flow. The resultant inflammation and epithelial disruption (ulceration) is followed by fibrosis and at times stricture formation.7

Clinical presentation Most distal GI NSAID-induced damage remains subclinical, but when that is not the case, the presentation is non-specific. When clinically apparent, the features of NSAID-induced disease are non-specific.

These features are listed in Table 1. Small bowel disease Small bowel injury caused by NSAID exposure may be limited to tiny erosions with little consequence, or to larger lesions associated with significant blood loss and even perforation.8 Since the latter part of last century, there have been increasing published reports of NSAID-related diaphragm-like small bowel strictures. These strictures manifest as thin concentric diaphragms of mucosa which often leave a lumen of only 3–4 mm in diameter. These are felt to be pathognomonic for NSAID-induced bowel pathology, are often multiple and mostly occur more distally in the small bowel.1 They can, however, also occur in the colon.1 The mucosa of the diaphragm may appear normal or be ulcerated at the luminal apex. Data from capsule endoscopy studies suggest a 2%

Feature • • • • • • • •

Small bowel obstruction Ulceration Perforation/Acute abdomen haemorrhage Iron deficiency/anaemia Protein losing enteropathy/hypoalbuminaemia Watery diarrhoea with or without overt blood Weight loss Abdominal pain

Table 1: Clinical features of NSAID-induced intestinal disease

Consult Magazine | Summer 2011/2012

prevalence of diaphragm disease in those taking NSAIDs.9 The mucosa between strictures is often normal. Histopathological examination of diaphragm strictures reveals chronic non-specific inflammation with submucosal fibrosis and thickened muscularis mucosae. There may or may not be associated ulceration.10 Colonic disease NSAIDs may induce colitis clinically similar to inflammatory bowel disease. Furthermore, they can exacerbate established inflammatory bowel disease, lead to complicated diverticular disease (perforation or haemorrhage) and possibly play a role in the development of lymphocytic and collagenous colitis. Colonic NSAID-induced diaphragm disease is unusual but mostly (90%) in the right colon. Diclofenac seems more frequently implicated but each of this class of agents can be responsible.11

Investigation Small bowel barium radiology is neither sensitive nor specific enough for diaphragm disease or NSAID-induced mucosal damage.12 Similarly, computed tomography (CT) scanning will often not identify this pathology. A patency capsule study may identify the presence of a small bowel stricture, not apparent on radiology. This involves the patient taking a tagged radio opaque device of the same dimensions as a capsule endoscope that



degrades within several days. A stricture is likely to be present if the patency capsule is retained, as confirmed by radiology or scanning with an appropriate detector. The device degrades and subsequently passes the stricture. Wireless capsule endoscopy will identify NSAID-induced mucosal injury and diaphragm strictures.13

The capsule endoscope may be retained, unable to pass tight strictures. The chance of the capsule endoscope being retained by a diaphragm stricture can be assessed with a patency capsule study. Balloon assisted deep enteroscopy can be used to identify NSAID mucosal injury and strictures, and also allows for biopsies to be obtained and therapeutic intervention, such as balloon dilatation of strictures.14 Endoscopically, NSAIDinduced inflammation and mucosal injury are nonspecific. The differential diagnosis includes inflammatory bowel disease, infection (viral or bacterial), vasculitis, radiation enteritis and vascular disease. The diagnosis relies heavily on a comprehensive history in combination with endoscopic and histopathological findings. Improvement is expected on withdrawal of the offending medication, apart from diaphragm strictures which could continue causing bowel obstruction for years after withdrawal of the NSAID.

NSAID. Symptoms and pathological finding should resolve. Endoscopic resolution of mucosal injury supports the diagnosis but persistence of ulceration suggests the need to consider another diagnosis or ongoing NSAID consumption. Diaphragm-like strictures are unlikely to resolve and may require surgical intervention (resection), as might bleeding and perforation. At surgery, the strictures may not be visually apparent on the serosal surface of the intestine, or palpable.15 Intraoperative enteroscopy can be useful in identifying the diaphragmatic strictures to allow balloon dilatation. Deep balloon assisted enteroscopy with endoscopic balloon dilatation of diaphragm strictures is an alternative.16 It has been suggested that misoprostol may be protective of the intestinal mucosa, taken together with NSAIDs. However, this medication can induce problematic side effects and there is no robust evidence for CM its efficacy in this circumstance.17

Management Management requires the withdrawal of the offending

References 1. Bjarnason I, Hayllar J, MacPherson AJ, Russell AS. Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans. Gastroenterology. 1993;104(6):1832-47. [Abstract] 2. Goldstein JL, Eisen GM, Lewis B, et al. Video capsule endoscopy to prospectively assess small bowel injury with celecoxib, naproxen plus omeprazole, and placebo. Clin Gastroenterol Hepatol. 2005;3(2):133-41. [Abstract] 3. Matsumoto T, Kudo T, Esaki M, et al. Prevalence of non-steroidal anti-inflammatory druginduced enteropathy determined by doubleballoon endoscopy: A Japanese multicenter study. Scand J Gastroenterol. 2008;43(4):490-6. [Abstract] 4. Gibson GR, Whitacre EB, Ricotti CA. Colitis induced by nonsteroidal anti-inflammatory drugs: Report of four cases and review of the literature. Arch Intern Med. 1992;152(3):62532. [Abstract] 5. Allison MC, Howatson AG, Torrance CJ, et al. Gastrointestinal damage associated with the use of nonsteroidal antiinflammatory drugs. N Engl J Med. 1992;327(11):749-54. [Abstract | Full text] 6. Reuter BK, Davies NM, Wallace JL. Nonsteroidal anti-inflammatory drug


enteropathy in rats: Role of permeability, bacteria, and enterohepatic circulation. Gastroenterology. 1997;112(1):109-17. [Abstract] 7. Huber T, Ruchti C, Halter F. Nonsteroidal antiinflammatory drug-induced colonic strictures: a case report. Gastroenterology. 1991;100(4):1119-22. [Abstract] 8. Langman MJ, Morgan L, Worrall A. Use of anti-inflammatory drugs by patients admitted with small or large bowel perforations and haemorrhage. Br Med J (Clin Res Ed). 1985;290(6465):347-9. [Abstract | Full text] 9. Maiden L, Thjodleifsson B, Seigal A, et al. Longterm effects of nonsteroidal anti-inflammatory drugs and cyclooxygenase-2 selective agents on the small bowel: A cross-sectional capsule enteroscopy study. Clin Gastroenterol Hepatol. 2007;5(9):1040-5. [Abstract | Full text] 10. Lang J, Price AB, Levi AJ, et al. Diaphragm disease: Pathology of disease of the small intestine induced by non-steroidal anti-inflammatory drugs. J Clin Pathol. 1988;41(5):516-26. [Abstract | Full text] 11. Smith JA, Pineau BC. Endoscopic therapy of NSAID-induced colonic diaphragm disease: Two cases and a review of published reports. Gastrointest Endosc. 2000;52(1):120-5. [Abstract]

12. Chernolesskiy A, Lanzon-Miller S, Hill F, et al. Subacute small bowel obstruction due to diaphragm disease. Clin Med. 2010;10(3):2968. [Abstract | Full text] 13. Graham DY, Opekun AR, Willingham FF, Qureshi WA. Visible small-intestinal mucosal injury in chronic NSAID users. Clin Gastroenterol Hepatol. 2005;3(1):55-9. [Abstract] 14. Hayashi Y, Yamamoto H, Kita H, et al. Nonsteroidal anti-inflammatory drug-induced small bowel injuries identified by doubleballoon endoscopy. World J Gastroenterol. 2005;11(31):4861-4. [Abstract | Full text] 15. Abrahamian GA, Polhamus CD, Muskat P, Karulf RE. Diaphragm-like strictures of the ileum associated with NSAID use: A rare complication. South Med J. 1998;91(4):395-7. [Abstract] 16. Hershfield NB. Endoscopic demonstration of non-steroidal anti-inflammatory druginduced small intestinal strictures. Gastrointest Endosc. 1992;38(3):388-90. [Abstract] 17. Watanabe T, Sugimori S, Kameda N, et al. Small bowel injury by low-dose enteric-coated aspirin and treatment with misoprostol: A pilot study. Clin Gastroenterol Hepatol. 2008;6(11):1279-82. [Abstract]

Summer 2011/2012 | Consult Magazine

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Years above denote TGA approval. PBS Information: RCC and GIST. Authority required. Refer to PBS Schedule for full authority information. Pancreatic NET. This indication is not listed on the PBS.

BEFORE PRESCRIBING, REFER TO THE FULL PRODUCT INFORMATION AVAILABLE AT WWW.PFIZER.COM.AU MINIMUM PRODUCT INFORMATION. SUTENT® (sunitinib 12.5 mg, 25 mg and 50 mg as malate) Capsules. Indications: Advanced renal cell carcinoma (RCC); gastrointestinal stromal tumour (GIST) after failure of imatinib mesylate treatment due to resistance or intolerance; unresectable, well-differentiated pancreatic neuroendocrine tumours (pancreatic NET). Contraindications: Hypersensitivity to sunitinib malate or excipients. Precautions: Haemorrhage, neutropenia, thrombocytopenia, decreased left ventricular ejection fraction, pre-existing cardiac conditions, prolonged QTc interval, hypertension, thyroid dysfunction, pancreatitis, hepatotoxicity, impaired wound healing, osteonecrosis of the jaw, tumour lysis syndrome, pregnancy, lactation, CYP3A4 inhibitors or inducers. See full PI for details. Adverse Effects: More common – fatigue, diarrhoea, nausea, vomiting, hypertension, bleeding, mucositis, skin abnormalities including hand-foot syndrome and change in hair & skin colour, altered taste. See full PI for details. Dosage and Administration: For RCC and GIST, 50 mg daily for 4 weeks followed by 2 weeks off (6 week cycle). For pancreatic NET, 37.5 mg daily. See full PI for details. PBS dispensed price, January 2012: SUTENT 12.5 mg: $1834.20; SUTENT 25 mg: $3521.76; SUTENT 50 mg: $6897.44. Reference. 1. SUTENT Approved Product Information. Pfizer Australia Pty Limited, ABN 50 008 422 348. Medical Information: 1800 675 229. SUTENT® is a registered trademark of Pfizer. Copyright © 2012. All rights reserved. P5700 01/12 PON0195/VMC

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Make the Everyday Matter




Vitamin D: An Update Ms Tina Aspres

Vitamin D deficiency is considered to be at pandemic proportions by some, so have we gone too far in our adherence to the “sun smart” message and how much sun exposure should we be getting? Tina Aspres B.Pharm, Diploma Cosmetic Science, Dermal Research Laboratories (Director), 17 Goulburn St, Liverpool 2170 NSW, Author “All About Kids’ Skin” ABC Books 2008, Editorial Advisory Board Member: Virtual Skin Centre,


ith estimates that at least 1 billion people worldwide are vitamin D deficient, it seems that there is currently a vitamin D “pandemic”1 and Australia is no exception. One would assume that with an unenviable reputation as the “skin cancer capital of the world”, the abundance of sunlight would mean most Australians would have adequate vitamin D levels but, surprisingly, this is not the case.2 Perhaps our current acceptable level of optimum vitamin D is set too high, resulting in a high number of false positive deficiency states. Are we being too “sun smart” and overprotecting ourselves, minimising vitamin D synthesis in the skin? This brief review will outline the current state of knowledge regarding vitamin D, the notion that we all need more controlled sun exposure and the available options for systemic supplementation.

Epidemiology of vitamin D deficiency Much of the epidemiology of vitamin D deficiency has been reviewed.3 It has been estimated that 1 billion people worldwide have vitamin D deficiency or insufficiency. According to several studies, 40–100% of US and European elderly men and women still living in the community (not in nursing homes) are deficient in vitamin D. More than 50% of postmenopausal women taking medication for osteoporosis had suboptimal levels of 25-hydroxy-vitamin D (25OHD). Even in the sunniest areas, vitamin D deficiency is common when


most of the skin is shielded from the sun. In studies in Saudi Arabia, the United Arab Emirates, Australia, Turkey, India, and Lebanon, 30–50% of children and adults had suboptimal levels of 25-hydroxyvitamin D.1

three important functions:5 1. Enhancing absorption of calcium and phosphate from the small intestine; 2. Inhibiting parathyroid hormone synthesis and secretion; and 3. Mineralising the bone matrix.

Where does vitamin D come from?

Causes of vitamin D deficiency

The main source of vitamin D comes from exposure of the skin to ultraviolet radiation (sunlight). Ultraviolet radiation is required to convert 7- dehydrocholesterol to cholecalciferol (vitamin D3); the first step in active vitamin D synthesis. Cholecalciferol (vitamin D3) may also be obtained from the diet; however, dietary sources alone are insufficient to achieve adequate levels of active vitamin D.4 Active vitamin D is synthesised after hydroxylation in the liver and then the kidney.19

There are many listed causes of vitamin D deficiency. The causes of vitamin D deficiency can be divided into three groups:

Function of vitamin D Via the vitamin D receptor, calcitriol has

1. Reduced synthesis of cholecalciferol in the skin Reduced sunlight exposure and reduced synthesis of cholecalciferol from a given ultraviolet radiation exposure appears to be the main cause of vitamin D deficiency. Furthermore, some research shows that vitamin D levels may be reduced by up to 20 nmol/L during the winter months compared to summer.6 Other contributing

Dietary sources of vitamin D


Fatty fish

Salmon, tuna, mackerel, herring, canned sardines

Meat/beef liver Egg yolk Fortified foods

Margarine, orange juice, milk and soy drinks

Cod liver oil Table 1: Dietary sources of vitamin D19

Summer 2011/2012 | Consult Magazine

Signs and symptoms of vitamin D deficiency include myalgia and proximal muscle weakness, but vitamin D deficiency for the majority of individuals is asymptomatic, being diagnosed on routine blood screening using the 25-hydroxy-vitamin D radioimmunoassay.8 Stages of vitamin D deficiency can be defined as in table 2.

How much vitamin D is enough?

factors include latitude, season, time of day of exposure, amount of time spent outdoors, cloud cover and sunscreen use.7 The elderly, institutionalised and chronically hospitalised are at risk of developing vitamin D deficiency due to the reduced sunlight exposure received. The problem is compounded in the elderly where their ability to synthesise cholecalciferol from sun exposure decreases. Individuals who are veiled for religious purposes are also at risk, as are nightshift workers who spend much of the day sleeping.7 Dark-skinned individuals (Fitzpatrick skin type V and VI) are at risk as they synthesise less cholecalciferol from sun exposure than do people with lighter skin types (Fitzpatrick skin types I–IV).7 Immunosuppressed individuals8 and those who suffer genetic disorders increasing the risk of developing cutaneous malignancy2 tend to be very strict in protecting their skin from ultraviolet radiation exposure, thereby increasing the risk of becoming vitamin D deficient.2 2. Disorders of malabsorption Disorders affecting the small bowel can lead to vitamin D deficiency, particularly coeliac disease, inflammatory bowel disease and small bowel resection.5 3. Enhanced degradation Hyperparathyroidism and some medications such as anticonvulsants and rifampicin increase the metabolism of vitamin D, which may contribute to or exacerbate vitamin D deficiency.8

This is controversial. The optimal range of 25-hydroxy-vitamin D is sill debated, with values anywhere between 50 and 110 nmol/L being advocated.8 The question that must always be considered is what level of vitamin D is an adequate level for each individual’s needs and situation.

Who benefits most from vitamin D supplementation?

Evidence suggests that those who benefit most from vitamin D supplementation are high-risk individuals with decreased bone mineral density. In randomised controlled trials, vitamin D and calcium reduce the risk of falls and hip and other non-vertebral fractures in older people.9

Severity of vitamin D deficiency

Epidemiological studies have found an association between low levels of vitamin D and multiple sclerosis,10 diabetes,11 depression,12 Crohn’s disease13 and cardiovascular disease.14 However, further clinical studies showing possible benefits of vitamin D in these disorders are required.

How much sun is required to maintain normal levels of vitamin D?

There is no simple answer to this question. Factors such as skin colour, age, season, where one resides, time of day, past history of cutaneous malignancy and concurrent immunosuppressive therapy all influence the amount of time one needs to be exposed to ultraviolet radiation to achieve adequate vitamin D levels.2 There needs to be a balance between getting an adequate dose of vitamin D from sun exposure as well as being “sun smart”. The correct “dose” of ultraviolet radiation needs to be considered on a caseby-case basis and customised as required. As a guide, it appears that 10–15 minutes of sunlight exposure on most days of the week (outside the peak ultraviolet radiation hours of 10.00 am – 2.00 pm) is sufficient for most people to achieve adequate vitamin D levels.2 Appropriate sun exposure to ultraviolet radiation will produce about 3,000 international units (IU) of vitamin D.15 A safer approach in attaining adequate sun exposure to maintain ideal vitamin

Serum 25-hidroxy-vitamin D (nmol/L)







Table 2: Stages of vitamin D deficiency5

Recommended sun exposure on arms and legs for adequate vitamin D synthesis Duration of sun exposure in minutes (before 10 am and after 2 pm)

Capital city

Summer (December–January)

Winter (July–August)


















Brisbane Table 3: Recommended sun

Consult Magazine | Summer 2011/2012




Vitamin D deficiency: Diagnosis


D levels is to ensure strict sun protective measures are in place whenever the ultraviolet index (UVI) is ≥ 3. The UVI rates the danger of ultraviolet radiation intensity on a daily basis at ground level via a numerical scale. A rating of 0–2 is low, 3–5 medium, 6–7 high, 8–10 very high and 11+ extreme.16

medical practice) could raise levels of 25-hydroxy-vitamin D to higher than 374 nmol/L, resulting in hypercalcaemia and hyperphosphataemia.17 The daily requirement for vitamin D is around 800–1,000 IU.8 Estimated average dietary intake of vitamin D in adult Australians is 80–120 IU.19

What doses of vitamin D supplementation are required?


For mild vitamin D insufficiency (25–50 nmol/L) and moderate deficiency (12.5– 25 nmol/L), oral supplementation with 1,000–5,000 IU daily for 6–12 weeks is recommended.2 Vitamin D is stored in fat and muscle hence there is a lag time before optimal concentrations appear in serum. Consequently, the result of therapy should be assessed after 3–4 months of treatment. Once ideal levels have been attained, a maintenance dose of 1,000–2,000 IU may be required.2 For severe vitamin D deficiency of less than 12.5 nmol/L, 1,000,000 IU of cholecalciferol delivered intramuscularly (megadose therapy) may be more suitable to replenish stores quickly and effectively.2 While most oral vitamin D3 supplements available in Australia contain a sufficiently high concentration of cholecalciferol to prevent deficiency, most multivitamin tablets do not (32–200 IU).8 The risk of vitamin D toxicity is very rare. However, a dose of more than 50,000 IU/day (extremely unlikely in normal References 1. Holick MF, Chen TC. Vitamin D deficiency: A worldwide problem with health consequences. Am J Clin Nutr. 2008;87(4):1080S-6S. [Abstract | Full text] 2. Working group of the Australian and New Zealand Bone and Mineral Society, Endocrine Society of Australia and Osteoporosis Australia. Vitamin D and adult bone health in Australia and New Zealand: A position statement. Med J Aust. 2005;182(6):281-5. [Abstract | Full text] 3. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-81. [Abstract] 4. Chen TC, Chimeh F, Lu Z, et al. Factors that influence the cutaneous synthesis and dietary sources of vitamin D. Arch Biochem Biophys. 2007;460(2):213-7. [Abstract | Full text] 5. Nowson CA, Diamond TH, Pasco JA, et al. Vitamin D in Australia. Issues and recommendations. Aust Fam Physician. 2004;33(3):133-8. [Abstract | Full text] 6. Pasco JA, Henry MJ, Nicholson GC, et al. Vitamin D status of women in the Geelong Osteoporosis Study: Association with diet and casual exposure to sunlight. Med J Aust. 2001;175(8):401-5. [Abstract] 7. Prentice A. Vitamin D deficiency: a global


Based on current research, the prevalence of vitamin D deficiency in Australia is much higher than originally thought, despite an abundance of sunlight. Vitamin D deficiency is a major health concern worldwide. Much remains unknown about the possible links to disorders other than those affecting bone and muscle. In


order to effectively deal with the problem, the job of the physician and pharmacist is to dispel myths and replace them with facts. The population as a whole needs to be educated about the importance of vitamin D. In parallel with this, patients may require re-education about practising sun-safe exposure to UVB radiation that allows them to receive sufficient sunlight to maintain a reasonable level of vitamin D without the risk of sunburn. Modifying dietary intake of vitamin D and supplementation should also be proposed to individuals at high risk of deficiency. Of further importance, prospective studies to determine optimal serum levels of 25OHD CM need to be undertaken.

RDI Vitamin D

Infants 0–12 months

200 IU/day

Children 1–18 yo

200 IU/day

19–50 yo

200 IU/day

51–70 yo

400 IU/day

> 70 yo

600 IU/day

Elderly and institutionalised

1,000 IU/day

Sun avoidance

1,000 IU/day

Pregnancy and lactation

200 IU/day

Table 4: RDI vitamin D for healthy bones18 perspective. Nutr Rev. 2008;66(10 Suppl 2):S153-64. [Abstract | Full text] 8. Joshi D, Center JR, Eisman JA. Vitamin D deficiency in adults. Aust Prescr. 2010;33(4):103-6. [Full text] 9. Bischoff-Ferrari HA, Willett WC, Wong JB, et al. Prevention of nonvertebral fractures with oral vitamin D and dose dependency: A metaanalysis of randomized controlled trials. Arch Intern Med. 2009;169(6):551-61. [Abstract | Full text] 10. Hanwell HE, Banwell B. Assessment of evidence for a protective role of vitamin D in multiple sclerosis. Biochim Biophys Acta. 2011;1812(2):202-12. [Abstract] 11. Borges MC, Martini LA, Rogero MM. Current perspectives on vitamin D, immune system, and chronic diseases. Nutrition. 2011;27(4):399-404. [Abstract] 12. Ganji V, Milone C, Cody MM, et al. Serum vitamin D concentrations are related to depression in young adult US population: The Third National Health and Nutrition Examination Survey. Int Arch Med. 2010;3:29. [Abstract | Full text] 13. Maruotti N, Cantatore FP. Vitamin D and the immune system. J Rheumatol. 2010;37(3):491-

5. [Abstract] 14. Virtanen JK, Nurmi T, Voutilainen S, et al. Association of serum 25-hydroxyvitamin D with the risk of death in a general older population in Finland. Eur J Nutr. 2011;50(5):305-12. [Abstract] 15. Holick MF. Resurrection of vitamin D deficiency and rickets. J Clin Invest. 2006;116(8):2062-72. [Abstract | Full text] 16. UV and sun protection services [online]. Melbourne, VIC: Australian Government Bureau of Meteorology; 2011. Available from: URL link 17. Koutkia P, Chen TC, Holick MF. Vitamin D intoxication associated with an overthe-counter supplement. N Engl J Med. 2001;345(1):66-7. [Abstract] 18. Food and Nutrition Board. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington DC : National Academies Press; 1997. [Book] 19. Nowson CA, Margerison C. Vitamin D intake and vitamin D status of Australians. Med J Aust. 2002;177(3):149-52. [Abstract | Full text]

Summer 2011/2012 | Consult Magazine

Compliance and effective monitoring… …two essential components for optimising oral anticoagulation therapy

Compliance and monitoring - inter-related factors in oral anticoagulation The importance of compliance • C ompliance rate with long-term medication in general has been estimated at between 50% and 60%1 • Evidence shows that INR monitoring improves the quality of oral anticoagulation between 50% and 85%2

Warfarin – a particular case in point • T hese are increasingly prescribed as lifelong therapy for patients with mechanical heart valves, atrial fibrillation or thrombophilic disorders, effectively preventing arterial embolism in a wide range of conditions3 • Maintaining INR within its therapeutic range is effectively achieved through monitoring • Patients on warfarin who have had a heart valve replacement there was a 32% difference in survival at 15 years between patients with low and high variability in anticoagulation control4

s stem R The obvious choice is partnering VKA and y s S IN k® Xcompliance test e h o CoaguChek® XS Systems for gimproved o t C y u ade s Coa smart wa ver been m ment st ne References: - the itoring has herapy adju 1. DiMatteo MR. Formulary 1995; 30: 596–8, 601–2, 605. ate t mon INR r immedi fo easy

2. Heneghan C, Alonso-Coello P, Garcia-Alamino JM, Perera R, Meats E, Glasziou P. Self-monitoring of oral anticoagulation: a systematic review and meta-analysis. Lancet 2006;367:404-411. 3. Ansell J et al. Int J Cardiol 2005; 99: 37–45. 4. Butchart EG et al. J Thorac Cardiovasc Surg 2002; 123: 715-23.

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Focus on Multiple Sclerosis Part III: Diagnosis

Dr Jeremy F Hallpike

150 years after the recognition of MS as a clinico-pathological entity, still no disease-specific laboratory test has been devised. In this article, Dr Hallpike explains the diagnostic role of MRI and other investigations and stresses the importance of making this diagnosis correctly. Dr Jeremy F Hallpike, MB(Lond.) MD(Lond.) FRCP(Lond.) FRACP; Emeritus Neurologist, Royal Adelaide Hospital, Editorial Advisory Board Member: Virtual Neuro Centre,


t is notable that 150 years after its recognition as a clinico-pathological entity by J-M Charcot, the preeminent pioneer of clinical neurology, no MS-specific laboratory test has so far been devised. The diagnosis of multiple sclerosis (MS) continues to rely heavily on clinical history taking and examination. The quintessential diagnostic features of MS are evidence of dissemination in space, that is, multifocal localisation within the central nervous system (CNS), and dissemination in time, namely recurrence or progression. Magnetic resonance imaging (MRI) and evoked potentials (e.g. visually evoked potentials, VEPs,

or responses, VERs) contribute to the “multifocal” and “progression” metrics that continue to underpin the diagnosis. Although the diagnosis of MS is reasonably straightforward in most cases, pitfalls still exist. The purpose of this article is to briefly survey recent developments in diagnosis and what this label often means for the patient.

The clinical diagnosis of MS For many years the gold standard and clearest application of the principles of dissemination in space and time were the Schumacher criteria,1 based on history and clinical examination. Satisfying the Schumacher criteria equated to “clinically definite multiple sclerosis” while the subsequent Rose classification recognised three diagnostic categories: “clinically definite”, fulfilling the Schumacher criteria, “probable multiple sclerosis” and “possible multiple sclerosis”.2

Incorporating investigations The Poser criteria New diagnostic criteria for MS were set out at a workshop in 1982 which extended the Schumacher criteria by admitting neuroimaging (including MRI), evoked response testing, increased production of immunoglobulin G (IgG) and the presence of oligoclonal bands (OB) in cerebrospinal fluid (CSF).3 As


with the Rose classification, fulfilling the Schumacher criteria equated to “clinically definite”. A “laboratory-supported definite” category was introduced in which paraclinical evidence (imaging or evoked potentials) of multiplicity of lesions was accepted in the presence of raised IgG/OBs in CSF (a “positive” CSF). A “laboratory-supported probable” category was introduced for two attacks with a “positive” CSF. These two new laboratorysupported diagnostic categories advanced the earlier criteria and increased the availability of more accurately classified patients, for example for clinical trials and epidemiological studies. The McDonald criteria MRI has now become the investigation of choice for paraclinical evidence of MS and its utility has been extended through gadolinium (Gd)-enhancement (detects breakdown of the blood–brain barrier, BBB) and is employed to detect MS lesions ≤ 6 weeks old. MRI is firmly embedded in protocols used for evaluating immunosuppressive drug treatments in relapsing–remitting MS.4 More specific criteria for the incorporation of MRI into a revised diagnostic algorithm for MS were introduced in 2001 which included a reduction of diagnostic outcomes to “definite”, “possible” and “not MS” (see Table 1).5 This scheme embodies the principles of dissemination of lesions in time and space. What is also implicit is how to

Summer 2011/2012 | Consult Magazine

Further information for MS diagnosis

2 or more attacks; objective signs of 2 or more CNS lesions

No further information required (former “clinically definite”)

2 or more attacks; objective signs of 1 lesion

Dissemination in space, shown by MRI or 2 or more MRI lesions plus positive CSF or await further clinical attack at different site

1 attack; objective signs of 2 or more lesions

Dissemination in time, shown by MRI or second clinical attack

1 attack; objective signs of 1 lesion (monosymptomatic presentation, clinically isolated syndrome)

Dissemination in space, shown by MRI or MRI lesions plus positive CSF and dissemination in time shown by second clinical attack or MRI

Insidious neurological progression suggestive of MS

Positive CSF and dissemination in space shown by MRI or positive CSF and abnormal VER plus MRI brain lesions and dissemination in time by MRI or continued progression for 1 year

Table 1: Diagnostic criteria5

recognise “relapses” and “remissions”, the significance of abnormalities which are not typical of MS, and the importance of an overriding caveat, carried forward from the Schumacher and Poser criteria, that “there should be no better explanation than MS for the clinical picture”.5 Small revisions of the McDonald criteria were made by the International Panel in 2005 including relaxation of the requirement for a “positive” CSF for diagnosing chronic progressive myelopathy in the presence of typical brain MRI changes.6

The clinically isolated syndrome This typically describes commonly encountered monosymptomatic onsets suggestive of MS; for example, optic neuritis, diplopia, a hemisensory loss, and with objective signs referable to only a single lesion. The McDonald criteria for diagnosis of MS may not be immediately fulfilled, and confirmation relies on a second clinical attack implicating a new CNS site or MRI evidence of dissemination in space and time (Table 1). Such presentations which are suggestive of MS at the time but lack diagnostic certainty are now grouped under clinically isolated syndrome (CIS) rather than the earlier “probable” or “possible” labels. While there is trial evidence that early initiation of treatment with interferon beta-1b at the CIS stage is beneficial, the advantage over delaying treatment until the diagnosis is definite, or definitely required, is small.7 Initiating disease-specific treatment at the CIS stage can imply a degree of certainty about diagnosis and prognosis which turns out to be unjustified in some cases.

and subclinical cranial MRI changes consistent with MS. Application of these diagnostic “rules” is particularly important to avoid confusing spinal cord neoplasms with MS, particularly as fluctuation in the clinical course may occur under both scenarios. Clinical overlap occurs between insidiously or “primary progressive from onset” (PPMS) and “progressive–relapsing or fluctuating from onset” (PRMS).8 PPMS and PRMS as a group are distinguished from relapsing–remitting MS (RRMS) and from secondary progressive MS (SPMS) where progression follows an initial RRMS phase.9,10 Another source of diagnostic difficulty is progressive visual loss following suspicion of optic neuritis, but which is actually due to a compressive lesion such as a meningioma or pituitary tumour. An asymptomatic visual field

defect in the apparently normal eye, and subsequent appropriate imaging, often allows correction of the diagnosis.

An illustrative case history A 42-year-old female had temporary tingling in the left leg and lower trunk, persistent hot sensations in that leg and transient episodes of tingling in both legs evoked at times by neck flexion (Lhermitte symptoms) and by strenuous exercise (Uhthoff ’s phenomenon). There was no incapacity. Over time she noticed she was becoming unsteady with a sense of a delay in “getting her legs to move”. Examination then showed impairment of heel-to-toe walking, a doubtful right extensor plantar response, and reduced appreciation of pin prick on the left leg. An MRI of her brain at that time was resoundingly abnormal

Progression from onset The most frequently encountered clinical example in this category is a progressive myelopathy. Reference to the revised McDonald criteria indicates that diagnosis of MS with this presentation requires both a “positive” CSF (where two or more spinal cord MRI lesions are not apparent)

Figure 1: This proton-density axial MRI taken through the cerebrum shows multiple foci of increased signal intensity varying in size in both cerebral hemispheres with a predominantly peri-ventricular distribution. A lower cut in this sequence also showed a hyperintense lesion in the left cerebellar hemisphere.

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Clinical presentation


(Figure 1). CSF examination showed a normal total protein, an IgG 0.11 g/L (R 0.01–0.03), IgG/albumin ratio of 22% (R 0–12) and presence of oligoclonal bands. An antinuclear factor (ANF) screen was negative and the serum B12 was normal. The latency of full-field pattern-reversal VEPs from the left eye (VA 6/5 unaided) was prolonged. The right eye was normal. Initial symptoms had suggested a thoracic level spinal cord localisation. Spontaneous improvement was observed with ongoing Lhermitte and Uhthoff symptoms, supporting the likelihood of underlying MS, but no “definite” diagnosis was made. Increasing unsteadiness and leg symptoms led to a definitive evaluation: clinical findings then being consistent with a spinal cord lesion with subtle Brown–Séquard features plus a cerebellar system localisation. A diagnosis of MS was strongly suggested at that stage on clinical References 1. Schumacher GA, Beebe G, Kibler RF, et al. Problems of experimental trials of therapy in multiple sclerosis: Report by the panel on the evaluation of experimental trials of therapy in multiple sclerosis. Ann NY Acad Sci. 1965;122: 552-68. [Abstract] 2. Rose AS, Ellison GW, Myers LW, Tourtellotte WW. Criteria for the clinical diagnosis of multiple sclerosis. Neurology. 1976;26(6 PT 2):20-2. [Abstract] 3. Poser CM, Paty DW, Scheinberg L, McDonald WI et al. New diagnostic criteria for multiple sclerosis. In: Poser CM, Paty DW, Scheinberg L, et al (eds). The Diagnosis of Mutiple Sclerosis. New York, NY: Thieme-Stratton; 1984:225-9. [Book] 4. Paty DW, Li DK. Interferon beta-1b is effective


grounds as “CIS converted to secondary progressive”. The florid accompanying MRI changes (Figure 1), “positive” CSF and MStypical VEP abnormality contributed to the diagnostic–prognostic profile.

Some of the implications of the diagnosis

Under all circumstances the diagnosis of MS is a personally serious event. Initially, the person concerned will probably be told that the prognosis is very variable and that many persons with MS (PwMS) will continue to lead productive and independent lives for many years or never come to be seriously affected. However, at the minimum this label brings with it uncertainty about the future: MS is a chronic neurological illness and it carries a wheelchair image. A spouse or partner is faced with the prospect of becoming a carer and family plans must be reconsidered. in relapsing-remitting multiple sclerosis: MRI analysis results of a multicenter, randomized, double-blind, placebo-controlled trial. Neurology. 1993;43(4):662-7. [Abstract | Full text] 5. McDonald WI, Compston A, Edan G, et al. Recommended diagnostic criteria for multiple sclerosis: Guidelines from the International Panel on the diagnosis of multiple sclerosis. Ann Neurol. 2001;50(1):121-7. [Abstract | Full text] 6. Polman CH, Reingold SC, Edan G, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions of the “McDonald Criteria”. Ann Neurol. 2005;58(6):840-6. [Abstract | Full text] 7. Pittock SJ. Interferon beta in multiple sclerosis: How much BENEFIT? Lancet.

Careers may be disadvantaged as a result of evident physical disability due to the progressive nature of MS. PwMS employed in positions of responsibility, for example a pilot or an investment manager, can expect to come under special scrutiny because of concerns about whether MS could impair judgement. The PwMS are particularly at risk of new neurological features or deterioration being put down to MS when a second diagnosis has come into play. For example, increasing paraparesis in someone with MS but who also develops a disc lesion or compressive cervical spondylosis may be attributed to the MS even though the latter causes can be relieved by surgery. These are aspects of what this diagnosis means which serve to emphasise the care and process required in CM making and following it.11

2007;370(9585):363-4. [Abstract] 8. Weinshenker BG. Progressive forms of MS: Classification streamlined or consensus overturned? Lancet. 2000;355(9199):162-3. [Abstract] 9. Hallpike JF. Focus on progressive multiple sclerosis part 1: The problem of cerebral atrophy. Consult Magazine. Autumn 2008:157. [Full text] 10. Andersen O. Natural history of multiple sclerosis. In: Raine CS, McFarland HF, Hohlfeld R (eds). Multiple Sclerosis: A Comprehensive Text. Oxford: Saunders Elsevier; 2008: 100-20. [Book] 11. Rudick RA, Schiffer RB, Schwetz KM, Herndon RM. Multiple sclerosis. The problem of incorrect diagnosis. Arch Neurol. 1986;43(6):578-83. [Abstract]

Summer 2011/2012 | Consult Magazine


The Art of

Psychiatry Dr Pia Brous

Medicine has always been an art and a science. Psychiatry is an interdisciplinary subspecialty. Science, social sciences, the humanities and the arts have all contributed. Creative arts has a role in mental health education. Dr Pia Brous, MB,BS, BMed Sci., FRANZCP, Certif. Child Psychiatry. Consultant Child and Adolescent Psychiatrist, Phoenics Health, 24/20 Commercial Road, Melbourne; and Project Manager, Dax Centre, Kenneth Myer Building, University of Melbourne, Genetics Lane, off Royal Parade, Melbourne, 3010, brous@; Editorial Advisory Board member Virtual Medical Centre


outh Mental Health In Australia

Youth mental health is an important contemporary issue in Australia. In 2010, Professor Pat McGorry, a psychiatrist, became the Australian of the Year. Mental health is now a political and media issue. These are hopeful signs. However the need is great. A recent report states that 24.3% of Australian youth aged 12–25 years suffer significant mental health disorders. However, only 25% receive any treatment, significantly less than those receiving treatment across all age groups (35%).1 Over 75% of mental health disorders emerge before 25 years. In 2009, the cost of youth mental illness was estimated as $10.6 billion. In the 2011 Budget, the Australian Government allocated $2.2 billion to mental health over 5 years:3 $492 million for mental health programs for children and youth;2 and $11 million to promote health and wellbeing for 3–4 year olds.7 The Great Smoky Mountain studies in USA showed that 20% of 4,500 children suffered a serious mental disorder;4 25– 33% of these were significantly impaired as a result.5 Many disorders were present well before adolescence. Earlier detection and intervention are clearly very important.

The Cunningham Dax Collection A busy Child and Adolescent Psychiatry practice can only meet a little of the need; and the earlier the presentation the better. Given this, in 2009 I joined the Educational

staff of the Cunningham Dax Collection, (now the Dax Centre), part-time, to teach mental health to students through the medium of art. The Cunningham Dax Collection comprises 15,000 creative works by people with the experience of mental illness or trauma. These were collected by the late Dr Cunningham Dax between the 1950’s and 1980’s. It is one of the three largest such collections in the world; the others being the Prinzhorn Collection in Heidelberg, Germany; and the Musee de l’Art Brut in Lausanne, Switzerland. Dr Dax was Psychiatrist Superintendent at Netherne Hospital in the UK before emigrating to Australia in the early 1950’s to reform the Victorian mental health system He was cognizant of new awarenesses in the twentieth century: of the therapeutic value of art; and the recognition that the creative works of those with mental illnesses could offer insights into their inner experiences.6 Concurrently there was a growing appreciation of the artistic merits of these works by artists and the wider community. Dr Dax introduced clinical art programs as treatment components in mainstream psychiatry. He initially collected works to educate mental health staff. Then he realised another application; the education of the general public about mental illness. The Cunningham Dax Collection has been a unit of the Mental Health Research Institute for 20 years, until late 2011. The artworks were created in a range of media: works on paper; paintings;

Consult Magazine | Summer 2011/2012

ceramics; sculptures and embroidery. About two-thirds were created in the psychiatric institutions; one-third were donated by individuals in the community. Initially most creators were adults; only a few were adolescents.

Artworks by young people in the Collection

More recent collections have been created by children and adolescents. These include survivors of the Tsunami in Sri Lanka; evacuees from the wars in Kosovo and East Timor who came for a time to the Safe Haven in Australia; and children and adolescents treated in psychotherapy with the late Margaret Ericksen, a psychoanalytic child psychotherapist from Melbourne. These collections present opportunities to explore many fascinating issues. These include: the inner emotional world of children; the graphic development of children’s art; the child’s experience of the family and outside world; the significance of play for the child; and the sheer beauty of the art of children, to name but a few. Each collection also presents unique issues. The Tsunami collection could raise awareness of the impact of a natural disaster, the resultant trauma and grief. The Safe Haven collection could explore the traumatic impacts of the political and social environments and of war upon children. The extensive Margaret Ericksen collection of 2,000 Works, displays issues of all the developmental,



The Tsunami Collection at the Dax Centre On December 26, 2004, an earthquake in the Indian Ocean devastated coastal populations in many countries. In Sri Lanka alone, it caused 35,000 deaths and left hundreds of thousands homeless. In July 2005, two final-year medical students from Melbourne University, Hannah Magree and Claire Stewart, spent their 5 week semester break on the southwest coast of Sri Lanka, assisting in the camps of survivors from three villages: Akurala; Ambalangoda and Godagama.

The main aim was to provide relief for these children who had experienced a tumultuous and distressing 6 months. Each day began by spreading mats on the grass and handing out materials. As trust developed, the children were encouraged to draw pictures about the Tsunami and its impact on their lives. Seventy-six works were subsequently gifted to the Dax Centre. The children were pleased that their artworks were going overseas to tell their

With sponsorship from the Dax Centre, they initiated “fun days” with the children who were encouraged to paint and draw.

Artist: Maduwega Asha Kumari, b. 1994 No title gouache and graphite pencil on paper

reactive emotional, and mental disorders of childhood; the nature of psychotherapy and psychoanalytical thinking; and the role of the creative arts in the assessment and treatment of troubled children.

The Dax Centre The Cunningham Dax Collection is now part of the Dax Centre; an independent incorporated entity, located in the new Parkville Neurosciences Facility at the University of Melbourne. The Dax Centre will foster an understanding of the mind, mental illness, the emotional world, the arts and creativity. It houses an active curatorial unit and exhibitions programs; professional development and public programs; and educational programs, amongst others. Its activities are guided by an ethical frame; and new ethical challenges are References 1. Access Economics Pty Ltd: The Economic Impact of Youth Mental Illness and the cost effectiveness of Early Intervention. December, 2009. 2. NCOSS Report: 2011 Federal Budget: Analysis of Health Measures. May, 2011. Available from URL


story. For many children, these artworks articulated experiences often too painful to put into words.

Artist: Nilande, b. 1996 No title gouache and felt pen on paper

Artist: Ayomi Kayaratna, b. 1990 No title gouache and graphite pencil on paper

Artist: R Umesh Chanuka No title gouache, oil pastel and graphite pencil on paper

explored ongoingly. The newer children’s collections have required rigorous ethical consultations, given the unique issues each raises. The educational programs have been evaluated. In 2006, the Centre for Program Evaluation of the University of Melbourne surveyed 10,000 visitors of the Centre. These included the general public; medical practitioners; health professionals; medical students; tertiary students; and VCE Psychology and Art students. 90–92% agreed that they had a better understanding of mental illness; more sympathy for the sufferers; and a greater appreciation of their creativity, after their visit.6

A day in the life of a project manager at the Dax Centre The






3. Orygen Youth Health News: Winter 2011. Available from URL 4. Costello EJ, et al. The Great Smoky Mountains Study of Youth: Goals, Designs. Methods and the Prevalence of DSM III R Disorders. Arch. Gen. Psych.53(12):pp.1129-1136. [Abstract] 5. Costello EJ, et al. The Great Smoky Mountains Study of Youth: Functional Impairment and

interdisciplinary and innovative setting is considerable. It provides an opportunity to share insights about mental health to young people earlier rather than later. I wish all Australian school children could leave their secondary education with some grounding in mental health. Art is a “safe” medium to discuss difficult issues; and has been a springboard for me to explore other projects: the new collections of the art of children and adolescents; and also the value of film for education in mental health.

Conclusion Medicine has been described as an art and a science. At the Dax Centre, the arts can illuminate contemporary and important CM issues of mental health. Serious Emotional Disturbance. Arch. Gen. Psych. 53(12):pp. 1137-1149. [Abstract] 6. The Dax Centre. Publication of the Mental Health Research Institute; 2011. 7. Roxon N, Macklin J, Butler M. 2011. National Mental Health Reform – Ministerial Statement. Canberra: CanPrint Communications; 2011. Available from: URL

Summer 2011/2012 | Consult Magazine

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The Running Shoe

- Excellent Science or Excellent Marketing?

Trent Salkavich

In an era where athletes are training in barefoot running shoes and it’s not uncommon for a shoe to carry a microprocessor to retain gait information, it is important for practitioners to be able to recommend the most appropriate footwear for their patients. Trent Salkavich, B App Sc (Pod); Sports Podiatrist, Director; Consultant Podiatrist to Sydney Sports Medicine Centre, Balmain Sports Medicine, Australian Defence Force; Emily Smith, B App Sc (Pod); Sports Podiatrist, Director; Consultant Podiatrist to Sydney Sports Medicine Centre, Balmain Sports Medicine, Australian Defence Force;


he shoe industry has evolved most rapidly over the previous decade and will continue to evolve as new technologies and markets are formed. We are in an era where athletes are training in barefoot running shoes and it’s not uncommon for a shoe to carry a microprocessor to play music and/or retain information for further gait evaluation post-training. This article aims to unravel the hype and assist practitioners to advise on the most appropriate footwear for their patients. The primary purpose of a shoe is to protect the foot. A shoe, however, also has the potential to change lower limb/ foot function.1 Due to the relationship between footwear and pathology, health professionals have a responsibility to


Emily Smith

consider footwear characteristics in the aetiology and treatment of various patient presentations.2 A correctly prescribed shoe can assist with healing rates, improve mobility and reduce injury risk of the lower limb.3 In the United Kingdom, foot and ankle problems account for approximately 8% of musculoskeletal consultations in primary care.4 Whilst further investigations are often required for foot and ankle pathology, the correct shoe is an easily accessible intervention for early management of symptoms.

Key shoe features A shoe can have the greatest biomechanical affect on the rearfoot (ankle and subtalar joints), midfoot (midtarsal joints) and the metatarsals at the forefoot.5 Key features of a shoe include the heel counter, density and placement of foams on the medial sole,6 shoelace system and forefoot rocker angle. These shoe prescription variables have the greatest potential to influence gait and are taken into consideration when choosing a shoe for a particular foot posture

and foot/ankle pathology. Summer footwear, which includes the use of ‘open back’ slip-on footwear, increases the incidence of Achilles and calf muscle pathology.7 Early intervention strategies such as changing attitudes to appropriate footwear can help reduce the risk of this common injury and commence early treatment for pathological patients. The sandal with adjustable rearfoot, midfoot and forefoot straps is advisable for patients wanting to wear a summer shoe. This will ensure the main anatomical foot structures are in a position of optimal functional efficiency.

Footwear prescription The gold standard of footwear prescription is the running shoe. The spectrum of functional components does not present in any other shoe category. Whether the foot requires pronatory control, pressure reduction or improved sagittal plane motion, there is a running shoe on the market that can cater for this.8 It has been generally accepted throughout the allied health and retail communities that footwear prescription comes in three categories: motion control, stability and neutral. However, recent research has challenged this prescription process.9 In my opinion, running shoes should be prescribed based on the person’s functional foot posture and injury

Summer 2011/2012 | Consult Magazine


history. If a patient does not run on a regular basis, running shoes can still be prescribed for the pathological foot. When foot pathology presents to general practice, an appropriate running shoe can be recommended for use as a first-line treatment. Advice may be for the patient to wear their appropriate running shoes for the majority of weightbearing time until further investigations, diagnosis or referrals have been implemented.

Cushioning During running the body experiences an initial peak force of between two and three times the person’s body weight.10 During the 1980s running shoes were marketed with suggestions that the primary goal was to reduce initial peak force.11 Research over a decade later revealed that shoes do not reduce the initial peak force.12 Cushioning materials are marketed very heavily in today’s running shoes. While we cannot affect the initial peak force with cushioning material alone, we can slow down the rate at which force is applied to the body10 and reduce pressure on the sole of the foot by 17–33%13 – important variables to consider when prescribing shoes for our patients.

Replacing footwear Generally, a running shoe will last

between 800 and 1,200 km.14 For the regular walker and runner, this equates to approximately 9–18 months. The materials in running shoes are not overly durable. After running just 500 km, foot pressure can increase by as much as 100%.14 The foams used in footwear manufacture are closed cell – once ruptured, they can never return to their original form. These ruptured compression lines are visible, and it is recommended to update the shoe once these lines are first noticed. Signs of a worn out shoe include firmness under foot, reduced cushioning, significant wear on the upper and/ or wear through the outsole. Some runners find it useful to alternate a second pair of running shoes, which will help improve the durability.

of the foot and ankle, specifically tendinitis and tendinopathies of the Achilles and tibialis posterior tendons.16 The forefoot is also susceptible to pressure-type pathologies such as capsulitis, bursitis and metatarsalgic symptoms. An increase in forefoot load may also lead to early degenerative arthritis, particularly of the first metatarsal head.16 It is a matter of weighing up how susceptible your

Barefoot running shoes Since the release of the Nike Free shoe in 2006 the barefoot running shoe market has been growing. A barefoot running shoe can be prescribed for the athlete wanting to improve intrinsic foot muscular strength or as an aid to assist running efficiency.15 Care has to be taken when recommending these shoes to pathological general populations. The risks associated with the use of barefoot running shoes include overuse musculoskeletal conditions

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patient is to these types of injuries and working together whilst maintaining open communication to achieve the desired outcome. There have been suggestions that barefoot running shoes contribute to a higher incidence of midfoot ground contact during gait. Midfoot ground contact (as opposed to initial heel contact or forefoot contact) has been shown to be the most efficient strike pattern whilst running.17 Barefoot running shoes can help but are not necessary to achieve this. In my opinion, a barefoot running shoe should be prescribed for the elite running athlete with sound medical history looking

References 1. Boyer KA, Andriacchi TP. Changes in running kinematics and kinetics in response to a rockered shoe intervention. Clin Biomech (Bristol, Avon). 2009;24(10):872-6. [Abstract] 2. Barton CJ, Bonanno D, Menz HB. Development and evaluation of a tool for the assessment of footwear characteristics. J Foot Ankle Res. 2009;2:10. [Abstract | Full text] 3. Butler RJ, Davis IS, Hamill J. Interaction of arch type and footwear on running mechanics. Am J Sports Med. 2006;34(12):1998-2005. [Abstract] 4. Menz HB, Jordan KP, Roddy E, Croft PR. Characteristics of primary care consultations for musculoskeletal foot and ankle problems in the UK. Rheumatology (Oxford). 2010;49(7):1391-8. [Abstract | Full text] 5. Segesser B, Stüssi E, von A Stacoff M, et al. Torsion: A new concept in construction of sports shoes. Motion excursion of the foot in athletic stress: Anatomical and biomechanical observations and their effects on construction of sports shoes [in German]. Sportverletz Sportschaden. 1989;3(4):167-82. [Abstract]


to modify gait patterns to achieve a desired outcome. Barefoot running shoes should only be worn for a minority (10–15%) of training and athletes should be monitored closely by their health professional and/or coach.

Conclusion The running shoe will certainly continue to evolve. We have a responsibility as health professionals to keep up with the new technology in order to achieve the most desirable outcomes for our patients. However, we also have a responsibility not to lose our perception in the hype and marketing surrounding running shoes. CM

6. Kersting UG, Brüggemann GP. Midsole material-related force control during heeltoe running. Res Sports Med. 2006;14(1):117. [Abstract] 7. Sella EJ. Disorders of the Achilles tendon and its insertion. Clin Podiatr Med Surg. 2005;22(1):87-99. [Abstract] 8. Bishop M, Fiolkowski P, Conrad B, et al. Athletic footwear, leg stiffness, and running kinematics. J Athl Train. 2006;41(4):387-92. [Abstract | Full text] 9. Knapik JJ, Brosch LC, Venuto M, et al. Effect on injuries of assigning shoes based on foot shape in air force basic training. Am J Prev Med. 2010;38(1 Suppl):S197-211. [Abstract] 10. Cavanagh PR, Lafortune MA. Ground reaction forces in distance running. J Biomech. 1980;13(5):397-406. [Abstract] 11. Nigg BM, Bahlsen HA, Luethi SM, Stokes S. The influence of running velocity and midsole hardness on external impact forces in heel-toe running. J Biomech. 1987;20(10):951-9. [Abstract] 12. De Wit B, De Clercq D, Aerts P. Biomechanical analysis of the stance phase during barefoot and shod running. J Biomech. 2000;33(3):269-78. [Abstract] 13. Wegener C, Burns J, Penkala S. Effect of neutral-cushioned running shoes on

plantar pressure loading and comfort in athletes with cavus feet: A crossover randomized controlled trial. Am J Sports Med. 2008;36(11):2139-46. [Abstract] 14. Verdejo R, Mills NJ. Heel-shoe interactions and the durability of EVA foam runningshoe midsoles. J Biomech. 2004;37(9):137986. [Abstract] 15. Knapik JJ, Feltwell D, Canham-Chervek M, et al. Evaluation of Injury Rates During Implementation of the Fort Drum Running Shoe Injury Prevention Program. 12-MA6558-01. Aberdeen Proving Ground, MD: US Army Center for Health Promotion and Preventive Medicine; 2001. [Abstract | Full text] 16. Snel JG, Delleman NJ, Heerkens YF, van Ingen Schenau GJ. Shock-absorbing characteristics of running shoes during actual running. In: Winter DA, Norman RW, Wells RP, et al (eds). Biomechanics IX-B. Champaign, IL: Human Kinetics Publishers; 1985: 133-7. [Book] 17. Ghani Zadeh Hesar N, Van Ginckel A, Cools A, et al. A prospective study on gait-related intrinsic risk factors for lower leg overuse injuries. Br J Sports Med. 2009;43(13):105761. [Abstract]

Summer 2011/2012 | Consult Magazine

Liver Failure

due to reactivation of hepatitis B


Acute fulminant liver failure Associate Professor Adel Ekladious

Acute fulminant hepatitis is a devastating disease with a very high mortality. Recognition of the initial symptoms, which may be subtle, is of paramount importance to enabling involvement of the liver transplant unit and subsequently improving prognosis dramatically. Dr Adel Ekladious, MBcHB MD MRCP FRCP(Ireland) FRCP(Glasgow) FRACP; Clinical Associate Professor of Medicine, Director of Clinical Medicine, Redland Hospital, Brisbane;


mmunosuppression is not an uncommon cause of acute liver failure, or even fulminant hepatitis in patients who have any serological markers of chronic hepatitis B infection. We are going to present a patient who has been seen recently in our hospital. A 65-year-old gentleman of Asian descent who is a recent immigrant was admitted for exacerbation of chronic obstructive airways disease. Clinical examination on admission was unremarkable apart from signs of hyperinflation of the lungs and occasional wheeze. His oxygen saturation was 90% on room air and his arterial blood gas showed chronic respiratory acidosis compensated by chronic metabolic alkalosis. His blood tests, including liver function and kidney function, were unremarkable. He was treated with a bronchodilator and steroids for 10 days. Before discharge he was found to be deeply jaundiced and encephalopathic. CT scan did not show any evidence of stroke or space-occupying lesion and chest x-ray did not show any signs of consolidation. His ALT was 1,000 units/L, AST was 800 units/L, alkaline phosphatase was 340 units/L, bilirubin was 55 mg/dL and serum albumin was 20 g/dL. His hepatitis A and C serology were negative. Hepatitis B surface antigen was positive. Hepatitis E antigen and hepatitis E antibody were negative. Hepatitis B Core IgG was positive. Hepatitis B Core IgM was negative. His hepatitis B virus load by polymerase chain reaction was 103

IU/mL . Ultrasound of the liver showed only fatty liver and small sized liver but no splenomegaly or ascites. His serum ammonia was elevated. The patient was diagnosed with acute fulminant hepatitis due to flare-up of hepatitis B caused by the 10 day dose of steroids. He was admitted to ICU and the Liver Transplant Unit was involved. His intracranial pressure was monitored and he was treated with tenofovir. He required intubation with no PEEP. He also required a repeated dose of concentrated glucose and he received an urgent liver transplant. Acute liver failure is a syndrome characterised by acute liver injury in the form of impaired synthetic function and coagulopathy in addition to encephalopathy, in a patient who has previously had normal liver function tests or compensated liver disease. The main manifestation of acute liver failure is coagulopathy. It is divided into hyperacute, acute and subacute dependent on the interval between the development of jaundice and onset of encephalopathy. It has recently been brought to our attention that reactivation of chronic hepatitis B can occur as a side effect of infliximab or rituximab, but to our knowledge steroids are not a common cause for reactivation of chronic hepatitis B. The main causes of acute fulminant hepatitis in developing countries are hepatitis A, hepatitis B and hepatitis E. Uncommon viral causes of acute fulminant hepatitis are herpes simplex, herpes zoster, Epstein-Barr

Consult Magazine | Summer 2011/2012

virus, cytomegalovirus and human herpes 6 virus. Hepatitis A and hepatitis E are transmitted via a faecalâ&#x20AC;&#x201C;oral route. Hepatitis E is the most common cause of acute liver failure in India, Pakistan and China.1 Acute hepatitis E infection has become more common than acute hepatitis A.2 Infection with acute hepatitis E is more common in pregnant women and has a worse prognosis. Unlike hepatitis A infection, transition from acute to chronic infection with persistent hepatic inflammation can occur in immunosuppressed patients.3 Hepatitis B infection is the main cause in Asia and Sub-Saharan Africa.4 Mortality with acute hepatitis B is higher than that with acute hepatitis A



or E infection.5 Acute fulminant hepatitis associated with hepatitis B infection can occur not only from acute infection but also from reactivation of chronic hepatitis B or even occult hepatitis B (where the hepatitis B surface antigen is negative and the hepatitis B Core IgG is positive). Super infection or Core infection with hepatitis D can cause acute fulminant hepatitis. Not uncommonly, treatmentinduced immunosuppression for solid organ or haematological malignancy can cause reactivation of chronic hepatitis, but it is not common to have reactivation of chronic hepatitis in a patient with chronic obstructive airways disease treated with steroids. Acute hepatitis B usually has a longer prodroma than acute hepatitis A or acute hepatitis E. Acute hepatitis C very rarely causes acute fulminant hepatitis. Patients with acute fulminant failure should be transferred to an Intensive Care Unit with a facility for urgent liver transplant. A hepatologist should be informed and involved in the management. The broad lines of the management would include monitoring of intracranial pressure because this is the most common cause of death due to herniation. Usually the monitoring will be done by epidural References 1. Dalton HR, Bendall R, Ijaz S, Banks M. Hepatitis E: An emerging infection in developed countries. Lancet Infect Dis. 2008;8(11):698-709. [Abstract] 2. Dalton HR, Stableforth W, Hazeldine S, et al. Autochthonous hepatitis E in Southwest England: a comparison with hepatitis A. Eur J Clin Microbiol Infect Dis. 2008;27(7):57985. [Abstract] 3. Kamar N, Selves J, Mansuy JM, et al. Hepatitis E virus and chronic hepatitis in


catheter because it is less invasive in a patient who has impaired coagulation. The target for intracranial pressure is to be below 20 mmHg and the cerebral perfusion pressure would be around 50 mmHg. Fresh frozen plasma is not recommended because it can increase the intracranial pressure, except if there is an eminent bleed. Activated factor 7 is commonly used now. The patient should be prevented from becoming hypoglycaemic by being given repeated doses of concentrated glucose. Cerebral oedema is commonly treated by multiple boluses of hypertonic saline, although mannitol is still used in many ICUs. Because of the increased tendency to GI bleed, the patient will be treated with an IV H2 blocker. Hypothermia combined with close monitoring of intracranial pressure can improve cerebral blood flow.6 There is no indication for prophylactic phenytoin, which should only be given if the patient develops seizures. Patients with acute fulminant failure are at high risk of developing infection because of decreased immunity. The threshold to start antibiotics and antifungals should be very low based on the autoimmune markers, degree of encephalopathy, and if the patient develops hypotension. organ-transplant recipients. N Engl J Med. 2008;358(8):811-7. [Abstract | Full text] 4. Escorsell A, Mas A, de la Mata M. Acute liver failure in Spain: Analysis of 267 cases. Liver Transpl. 2007;13(10):1389-95. [Abstract | Full text] 5. Khuroo MS, Kamili S. Aetiology and prognostic factors in acute liver failure in India. J Viral Hepat. 2003;10(3):224-31. [Abstract] 6. Dmello D, Cruz-Flores S, Matuschak GM. Moderate hypothermia with intracranial

Patients who develop severe intracranial hypertension should be intubated and mechanically ventilated. Usually positive end expiratory pressure is not used because this can adversely affect the intracranial pressure. Metabolic disturbances are mainly hypoglycaemia, hypokalaemia, hyponatraemia and hypomagnesaemia, and these should be monitored closely. The only approved treatment is liver transplant, the prognosis of which depends on: 1. 2. 3. 4.

The patientâ&#x20AC;&#x2122;s age; The cause of acute fulminant failure; The quality of the donor. Auxiliary liver transplant, which involves placement of a graft adjacent to the patientâ&#x20AC;&#x2122;s native liver. The advantage of this is that it supports the native liver for regeneration, which will eliminate the need for chronic immunosuppression7.

Patients with chronic hepatitis, or an inactive carrier, should be screened before starting on immunosuppressive medication and treated with a prophylactic antiviral (entecavir or tenofovir) before starting on immunosuppressive CM medication. pressure monitoring as a therapeutic paradigm for the management of acute liver failure: A systematic review. Intensive Care Med. 2010;36(2):210-3. [Abstract] 7. Lodge JP, Dasgupta D, Prasad KR, et al. Emergency subtotal hepatectomy: A new concept for acetaminophen-induced acute liver failure: Temporary hepatic support by auxiliary orthotopic liver transplantation enables long-term success. Ann Surg. 2008;247(2):238-49. [Abstract]

Summer 2011/2012 | Consult Magazine

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