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Public Forums and Continuing Medical Education (CME) Programmes @ TTSH

Public Forum: Health for Life – Unleash Your True Potential with Weight Loss Surgery Public forum: What’s New in Breast Health? Department of General Surgery 22 October 2011 9am - 11am Annex Building, Level 4, L4-N-M007 (Rotary), TTSH To register, call Mr. Dennis Yeoh at 635 8266 Free -

Department of General Surgery

29 October 2011 1:30pm - 4pm

Theatrette, TTSH, Level 1

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Medical digest
MICA (P) 031/04/2010

Annual Pathology Seminar - Lymph Node Pathology Unravelled

Department of Pathology

3-4 November 2011 Theatrette, TTSH, Level 1

Local participants SGD$150 Overseas participants USD$150

Jul.Aug.Sep. 2011

* Pre-registration is required for all Public Forums and CME Programmes. **Please keep a lookout for the latest event updates on our website at www.ttsh.com.sg

Important T TSH contact numbers
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F rom The Editor

Jul.Aug.Sep. 2011

You wouldn’t expect a free-of-charge medical magazine to supply the key to being an über-doctor, would you? Read on. Beginners do not capture the likeness of objects they want to portray. Later, their drawings start to look like the real thing. As the artists further mature, paradoxically, the resemblance is again tenuous. Picasso’s works, in the museums in Barcelona and Paris, showed that even he had to go through the three stages in turn. Usually, we talk of three levels of expertise: novice, competent and expert. Guidelines and rules are meant for people that straddle the competent and expert stages. Expertise is shown by consistently superior performance to that of the expert’s peers, concrete results and measurable outcomes (Ericsson KA, Prietula MJ, Cokely ET. Harv Bus Rev 2007; 85:114-21, 193). Training and practice bring us to the expert level. “It is probably self-evident to initiate that growth in expertise is dependent upon experience. What is not so evident is that experience in itself is not sufficient ... For all but the few effortless self-learners, changes in expertise need reflection and deliberation,” says Advanced Consulting in Family Medicine (Radcliffe Publishing Ltd, UK 2009). Consequently, it is hard for us to become better after we have completed training because medical practice primarily consists of personal interactions between the patient and the doctor, usually with no external critique or audit. Can there be skill levels above the expert? What if the medical problem wanders into areas of great uncertainty and risk (Innes AD, Campion PD, Griffiths FE. Complex consultations and the 'edge of chaos'. Br J Gen Pract 2005; 55:47-52)? How does the doctor diagnose and treatment an illness not in the radar? Some writers propose two extra levels: the master and the visionary (http://doc.utwente.nl/58083/1/levels_of_expertise.pdf). I quote: “The …‘visionary’ consciously strives to extend the domain in which he/she works. The world discloser develops new ways things could be, defines the issues, opens new worlds and creates new domains …operates more on the margins of a domain, paying attention to other domains as well, and to anomalies and marginal practices that hold promises for a new vision of the domain.” In my view, precision, economy and preternatural ability (seemingly) are a few traits of the crack medical practitioner. He or she is right most of the time, regardless of the complexity of the case. He or she may propose an unusual diagnosis, but it is appropriate (it’s easy to do so and be wrong). He or she does not over-investigate or over-treat. Analogously, Yasujiro Ozu did not need dolly shots, fades, dissolves, voice-overs or special effects to make the greatest movies ever made. We make decisions with logic and also through intuition (perhaps something very difficult to teach). The über-doctor knows the limits of each and uses them in the right proportion. On 10 September 2011, Djokovic beat Federer in the semi-finals of the US Open. After saving two match points, everything hung on one shot. Djokovic said, “The forehand return, I cannot explain to you because I don't know how it happened. I read his serve and I was on the ball and I had to hit it hard, and it got in, luckily for me.” These doctors exist; we have colleagues who make correct diagnoses that we could never make, and avoid problems that we could never see coming. What we need is not longer lists of differential diagnoses, but more incisive decision-making; not more investigations, but more resoluteness; and not more knowledge, but deeper understanding. We can be better doctors. May we always be growing and learning and thinking.

Dr Leong Khai Pang

Dr Jackie Tan Dr Jaideepraj Rao Dr Lee Cheng Chuan Dr Khian Chong Yaw Dr David Foo Dr Gregory Kaw Dr Nikolle Tan Dr Ernest Kwek Ms Lim Wan Peng

Ms Michelle Lee

Ms Zaonah Yusof

We value your feedback. Please email your questions, comments or suggestions to: med_digest@ttsh.com.sg Please also contact us for notification of change of postal address or for requests of additional copies.

While every endeavour is made to ensure that information herein is accurate at the time of publication, Tan Tock Seng Hospital shall not be held liable for any inaccuracies. The opinions expressed in this publication do not necessarily reflect those of Tan Tock Seng Hospital. The contents of this publication may not be reproduced without written

permission from the publisher.

Dr Leong Khai Pang EDITOR Medical Digest





MRSA – do we know the disease burden

in Singapore?
Methicillin-resistant Staphylococcus aureus (MRSA) today is no longer a name unfamiliar to many. But when it was first introduced into Singapore in the early 80s, it caused quite a stir in the medical community.1 Staphylococcus aureus commonly colonizes the exterior of our body, including the mucosal areas that come into contact with external environment. Given the right opportunity, it invades to cause illnesses ranging from mild superficial skin infection to deep seated infection in almost any anatomical site of the human body. The mortality rate of bloodstream infection by Staphylococcus aureus can reach as high as 30% despite appropriate treatment. Because Staphylococcus aureus frequently colonizes the exterior of human body, it is important to distinguish carrier state (colonization) from clinical disease (infection). How did MRSA come about? MRSA essentially is the product of microbial evolution under the pressure of antimicrobial agents, specifically semi-synthetic beta-lactamase-resistant penicillins such as methicillin and cloxacillin. MRSA requires the presence of mec-genes that alter the penicillin-binding protein 2a on the cell-wall that render the semisynthetic beta-lactamase-resistant penicillins ineffective. The treatment of choice is vancomycin which was expensive when it was first introduced and is associated with drug toxicity. However, it is vital to note that microbes never cease to evolve; instead, they strive to survive in the hardiest of environment. Following the wider use of vancomycin, new resistant strains such as vancomycin-intermediate Staphylococcus aureus (VISA) and heteroresistant VISA have emerged. Of note, this widely accepted hospital-bound or nosocomial organism is now also identified in the community. For epidemiological purposes, we classify the likely sources of acquisition of the infection into community-associated MRSA and hospital-associated MRSA. MRSA today has evolved into multiple clones with varying degrees of antimicrobial susceptibility.2,3 EPIDEMIOLOGY How prevalent is MRSA in our local public hospitals? In a study conducted in Singapore General Hospital in 2007 during an outbreak, MRSA was detected in 13% of patients admitted to the intensive care unit (ICU). In addition, 13.8% was found MRSApositive at exit from ICU care.4 The authors concluded that at least 21% of the patients had evidence of MRSA presence in their body during the episode of ICU stay, although they could only indentify active infection in 1.8%. Interestingly and rather alarmingly, 20.2% of healthcare workers were found colonized with MRSA during the study period.5 The National University Hospital in Singapore detected MRSA soon after the new hospital became fully operational in the late 1980s. A few years after operation, MRSA was accountable for 34-46% of all clinical isolates of Staphylococcus aureus. In a retrospective study of a year’s surveillance data from 1998 to 1999, the MRSA incidence rate in the ICUs




alarming. The key findings were that cases were 10.2 times more likely to die during their hospital stay, 4.6 times to have longer hospitalization, and to incur 4.0 times higher hospitalization costs than non-infected controls. The MRSA-infected survivors had 1.3 times higher outpatient costs and poorer self-reported health-related quality of life. This study demonstrated that in the local setting, MRSA infection was independently associated with inhospital mortality, greater length of stay, higher hospitalization and postdischarge healthcare costs, and lower health-related quality of life at the time of discharge. The authors further quantified that each MRSA infection resulted in median excess inhospitalization costs of more than US$13,000.00, which was largely borne by the local health system. The reasons behind the dearth of information about MSRA disease burden are likely to be many. The plausible reasons include the difficulty in distinguishing between disease versus colonisation, the failure of the surveillance and reporting system to capture primary illness without acknowledging the etiologic agent (e.g. documenting nosocomial pneumonia instead of MRSA pneumonia) and last, but not the least, the complacency of our healthcare system leading to poor resource allocation towards research and knowledge creation. THE NEED TO ACT NOW In October 2008, Annals Academy of Medicine Singapore commissioned a special edition on “Recurring Infectious Disease Themes: Pandemic Influenza and Antimicrobial Drug Resistance (Part II)”. The control of nosocomial spread of MRSA was discussed in two papers.11,12 Both papers emphasized the importance of infection-control intervention. To achieve the ambitious goal of reducing the inpatient prevalence of MRSA colonization to below 1% requires massive infusions of infrastructural, scientific and human resources to have a chance of success. Implementing infection control initiatives successfully over the next few years will save lives in the future. What is grossly lacking at the moment is our understanding of disease burden

was 4.6 per 1000 patient days compared with the general wards with a rate of 1.4 per 1000 patient days.6 How prevalent is MRSA in our community settings? In contrast to hospital-associated MRSA (HAMRSA), community-associated MRSA tends to be more susceptible to a wider range of antibiotics and causes a different spectrum of clinical illnesses. Nonetheless, the disease carries significant morbidity and mortality.7 Reports on cases and case series in Singapore are sparse and are likely to be incomplete.8,9 Overall, there is a complete lack of information on MRSA carrier rate outside of hospital settings in Singapore including step-down care facilities and the non-healthcare communities. DISEASE BURDEN IN SINGAPORE Disease burden is the impact of a health problem in an area measured by financial cost, mortality, morbidity, or other indicators. It is often quantified in terms of quality-adjusted life years (QALY) or disability-adjusted life years (DALYs) which combine the burden due to both death and morbidity into one index. This allows for the comparison of the disease burden due

to various risk factors or diseases. It also makes it possible to predict the possible impact of health interventions. Apart from creating knowledge, disease burden measurement can be applied to formulation of health policies, prioritizing allocation of resources across health intervention and assessing performance. Information on the disease burden of MRSA infection is grossly lacking in Singapore and the region. The one and only recent report is by Pada et al who published the first local study examining the economic and clinical impact of nosocomial MRSA infections in two tertiary hospitals: National University Hospital and Singapore General Hospital.10 The study was designed to follow up matched cases and controls (at a 1:2 ratio) prospectively over 6 months in each hospital. The entire study period for both hospitals was between September 2007 and March 2008 with different start and end dates. The demographic profile, pre-existing medical conditions and treatment were comparable between the cases and controls except a tendency towards higher APACHE II score among the cases. The results were, however,




due to MRSA infections and quantum of health resources needed to achieve a pre-determined goal. CONCLUSION World Health Day marks the founding of the World Health Organization (WHO). It is celebrated each year on April 7, with a theme selected each year that highlights priority public health issues for WHO that affect the international community. The focus this year is on combating antimicrobial resistance. We ought to have a serious relook at microbe evolution and human science in antimicrobial development.

Staphylococcus aureus became resistant to penicillin shortly after the introduction of penicillin, and not long after the introduction of the semisynthetic penicillins methicillin and cloxacillin. It is no surprise that vancomycin will one day reach its “shelf-life” with MRSA. Indeed, we are already seeing an increasing minimal inhibitory concentration MIC level against vancomycin. Apart from MRSA, the multi-drug resistant gram negatives such as Acinetobacter, Klebsiella, etc are becoming a greater challenge in treatment, prevention and control. Can the human science stays ahead of the microbes? Will humans one day return to pre-antibiotics era?

Associate Professor Leo Yee-Sin is the Head and senior consultant of the Department of Infectious Diseases, Tan Tock Seng Hospital.

References 1. Allen DM. Methicillin-resistant Staphylococcus aureus – where are we now? Singapore Med J 1991; 32:17-9. 2. Hsu LY, Koh YL, Chlebicka NL, Tan TY,Krishnan P, Lin RTP, etal. Establishment of ST30 as the predominant clonal type among communityassociated methicillin-resistant staphylococcus aureus Isolates in Singapore. J Clin Microbiol 2006; 44:1090–3. 3. Hsu LY, Chlebicka NL, Koh YL,Tan TY, Krishnan P, Lin RTP, et al. Evolving EMRSA-15 epidemic in Singapore hospitals. J Med Microbiol 2007; 56:376–9. 4. Kurup A, Chlebicka N, Tan KY, Chen E, Oon L, Ling TA, Ling ML, Hong JL. Active surveillance testing and decontamination strategies in intensive care units to reduce methicillin-resistant Staphylococcus aureus infections. Am J Infect Control 2010; 38:361-7. 5. Chan KS, Ling ML, Hsu LY, Tan AL. Methicillin-Resistant Staphylococcus aureus throat colonization among healthcare workers during an outbreak in Singapore General Hospital. Infect Control Hosp Epidemiol 2009; 30:95-7. 6. Tambyah PA, Kumarasinghe G Methicillin-resistant Staphylococcus aureus Control at the National University Hospital, Singapore: A historical perspective. Ann Acad Med Singapore 2008; 37:855-60. 7. Chua AP, Lee KH. Fatal bacteraemic pneumonia due to community-acquired methicillin- resistant Staphylococcus aureus. Singapore Med J 2006; 47:546-8. 8. Wijaya L, Hsu LY, Kurup A. Community-associated Methicillin-resistant Staphylococcus aureus: Overview and Local Situation. Ann Acad Med Singapore 2006; 35:479-86. 9. Hsu L Y, Koh T H, Tan T Y, Ito T, Ma X X, Lin R T, et al. Emergence of community-associated methicillin-resistant Staphylococcus aureus in Singapore: a further six cases. Singapore Med J 2006; 47:20-6. 10. Pada SK, Ding Y, Ling ML, Hsu LY, Earnest A, Lee TE, et al. Economic and clinical impact of nosocomial methicillin-resistant Staphylococcus aureus infections in Singapore: a matched case-control study. J Hosp Infect 2011; 78:36-40. 11. Pereira LA, Fisher DA. Methicillin-resistant Staphylococcus aureus Control in Singapore – Moving Forward. Ann Acad Med Singapore 2008; 37:891-6. 12. Tambyah PA, Kumarasinghe G. Methicillin-resistant Staphylococcus aureus Control at the National University Hospital, Singapore: A Historical Perspective. Ann Acad Med Singapore 2008; 37:855-60.




Case Report

A case of dengue hemorrhagic fever

with encephalopathy
Dengue is the most common cause of arthropod-transmitted disease worldwide. It has a broad spectrum of clinical manifestations, and a wide range of severity including uncomplicated dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. Encephalopathy although rare has been well reported and is thought to result from the multisystem derangement that occurs in severe dengue infection; with liver failure, shock, and coagulopathy causing cerebral insult. However, there is increasing evidence for dengue viral neurotropism, suggesting that, in a proportion of cases, there may be an element of direct viral encephalitis. Understanding the pathophysiology of dengue encephalopathy is crucial toward developing a more effective management strategy.1 We report a case of dengue encephalopathy in Singapore and review the literature on dengue encephalopathy and encephalitis. Dengue is a viral infection transmitted in mainly urban areas by Aedes aegypti and Aedes albopictus. The dengue virus is a Flavivirus that is responsible for an endemic disease throughout tropical and subtropical countries especially in the Caribbean Basin, Southeast Asia, Pacific Islands, and South America. Human are the main natural reservoir and the primary factor in dissemination of the virus. After an incubation period of 2 to 7 days, dengue classically begins with abrupt onset of fever, chills and headache. A transient macular rash may also be observed which usually resolves spontaneously. Dengue may be complicated by a variety of problems including dengue encephalopathy. In view of this, dengue fever and dengue haemorrhagic fever are causes of significantly raised health burden. In Singapore, the national burden is estimated to be similar to that for bacterial meningitis, or for sexually transmitted diseases apart from HIV/AIDS.2 In Singapore in 2009, a total of 4,497 cases of dengue were notified to the ministry including eight fatal cases.3 CASE REPORT A 50-year-old male hotel manager presented to Tan Tock Seng Hospital Emergency Department on 15 November 2004 with 4 days’ history of fever, mild cough, loss of appetite, gum bleeding and body ache, high haematocrit (50.5%) and thrombocytopenia (platelet 100 x 109 /L). He had no past medical history of note. He was oriented to time, place

and person. On review the following day in clinic, his platelet count had dropped to 40 x 109 /L and he was admitted. Investigations revealed dengue polymerase chain reaction (PCR) was positive on the day of admission. He was diagnosed to have DHF based on presence of fever, hemorrhagic tendencies, thrombocytopenia of less than 100 x109/L and high hematocrit. On day 4 of hospitalisation (day 9 of illness), he developed chills, rigors, drowsiness, lethargy, was slow to respond to commands and was not oriented in

time and place. His lower and upper limb power was grade 3/5. He was transferred to the high dependency unit (HDU) on the same day. The patient was treated with ceftriaxone (2g 12hourly) and acyclovir empirically. Computed tomography (CT) of the brain detected subtle right temporal loss of gray-white differentiation of unknown significance. Magnetic resonance imaging (MRI) of the brain showed a few foci of non-specific T2 signal prolongation in the subcortical and juxtacortical white matter of the posterior parietal lobe, though not




Table 1: Relevant laboratory results in relation to day of illness


Admitted /PCR positive




Day of illness 9 10
Confusion started /HDU


Confusion resolved


Temperature (°C) WBC (x109 ) HB (g/L) HCT (%) PLT (x109) ALB (g/L) GL (g/L) ALP (U/L) ALT (U/L) AST (U/L) GGT (U/L) BIL (μmol/L)

39.6 3 17.6 50.5 100

38.7 3.4 18 50.5 40 38 28 50 161 503 192 19

38.9 4.1 17 48.6 23

39.4 7.5 16.8 48.4 32

38.2 9.3 15.2 43.5 76 30 26 79 141 449 223 14

38.4 13.2 16 46.6 136 33 32 104 139 382 234 16

36.8 8.2 14.9 44 159

36.8 7.3 15.2 43 217


36.2 5.6 15 44 375 39 36

82 105 201 207 11

73 81 98 168 15

WBC: white blood cells; HB: haemoglobin; HCT: haematocrit; PLT: platelets; TP: total protein; ALB: albumin; GL: globulin; ALP: alkaline phosphatase; ALT: alanine transferase; AST: aspartate aminotransferase; GGT: gamma-glutamyl-transferase; BIL: bilirubin

suggestive of encephalitis. Cerebrospinal fluid (CSF) was clear and colorless with a white blood cell count of 5 cells/ul, glucose 3.6 mmol/L, and total protein: 87 mg/dL. Herpes simplex virus (HSV) and dengue virus were not detected in CSF by PCR. Central nervous system investigations excluded any explicit brain lesion. Examining the entire course of illness, he had a maximum ALT: 161 U/L, AST: 503 U/L, and GGT: 192 U/L at day 5 of fever that subsequently decreased and normalised at day 25 on follow up in clinic. His initial thrombocytopaenia also recovered by discharge. After 9 days of fever, he developed problems with orientation and responsiveness which took 5 days to recover. He was discharged 16 days after onset of illness. DISCUSSION We report a patient with dengue haemorrhagic fever and encephalopathy. Unusually, this was associated with a persistent fever despite platelet recovery. This extended fever was associated with his change in mental status. He recovered after 4 days during which he was given ceftriaxone and acyclovir before bacterial cultures and HSV test came back negative. CSF for dengue

was negative by PCR. An alternative test that may be used is dengue IgM in CSF which may be useful with 64% positive in one case series.4 The mechanism of encephalopathy m a y re s u l t f ro m i n t r a c r a n i a l hemorrhage, cerebral edema,

hyponatremia, cerebral anoxia, fulminant hepatic failure with portosysemic encephalopathy, microcapillary hemorrhage or release of toxic products. 5 In our patient, encephalopathy did not appear to be secondary to any of these. There was no evidence of hepatic encephalopathy




with transaminases trending downward prior to onset of mental state alteration and no derangement of liver synthetic function. There was a history of chronic alcohol intake but no previous admissions for intoxication and all liver function tests were normal at follow up two weeks after hospitalization. Renal function remained normal, with urea 3-6 mmol/L over the course of the illness. No candidates for likely drug-induced mental state change were identified. Whilst few doubt that dengue infection can be associated with clouding of consciousness, until now it was not clear whether this represents central nervous system (CNS) invasion by the virus, a nonspecific complication of severe dengue disease, or even coincident infection with another, unidentified arbovirus or other agent. Most published data consist of case-reports or reviews of patients admitted to dengue wards with classical features of dengue infection. Published cases from Singapore include one report of dengue with hepatic encephalopathy and one of hippocampal encephalitis.6,7 CSF tests can confirm dengue encephalitis but may not always be available, and sensitivity and specificity are unknown. In the single published prospective case-control study of dengue encephalopathy in Vietnamese

children, out of 27 clinically defined cases of dengue encephalopathy, 16 of 22 available CSF samples tested positive for dengue IgM, and only one sample was positive by RT-PCR.4 In another case series from Brazil, out of 18 cases of dengue encephalopathy, 7 of 13 that had a lumbar puncture were positive for dengue RNA by PCR.8 A pediatric case series from India had 62 cases of dengue encephalopathy, 21 of 29 available CSF samples were

PCR positive.9 NS1 antigen testing in CSF has been proposed as another option, with 13 NS1 positive out of a panel of 26 CSF samples from dengue patients with encephalopathy and either IgM or PCR positive in CSF from Brazil. 10 Dengue encephalopathy carried a mortality rate of 47% in one case series.5 Our patient recovered completely but he should serve as a reminder of severe organ involvement in adult dengue infection.

Dr Viengsavanh Kitthiphong (middle) is a visiting fellow, Dr Victor Gan (right) is a medical officer and Associate Porfessor Leo Yee-Sin (left) is Head and senior consultant, all from the Department of Infectious Disease, Tan Tock Seng Hospital.

References 1. Varatharaj, A. Encephalitis in the clinical spectrum of dengue infection. Neurol India. 2010; 58(4):585-591. 2. Epidemiology & Disease Control Division, Ministry of Health, Singapore (2009). Singapore Burden of Disease Study 2004. Singapore, Ministry of Health. 3. Ministry of Health (2010). Communicable Disease Surveillance in Singapore 2009. Singapore, Ministry of Health. 4. Cam BV, Fonsmark L, Hue NB, Phuong NT, Poulsen A, Heegaard ED. Prospective case-control study of encephalopathy in children with dengue hemorrhagic fever. Am. J. Trop. Med. Hyg 2001 Dec;65(6):848-851. 5. Muzaffar J, Venkata Krishnamp, et al. Dengue encephalitis: why we need to identify this entity in a dengue-prone region, Singapore Med J. 2006; 47(11): 975-7. 6. Penafiel, A., Devanand, A., Tan, H.K. & Eng, P. Use of molecular adsorbent recirculating system in acute liver failure attributable to dengue hemorrhagic fever. J Intensive Care Med 2006; 21, 369-371. 7. Yeo, P.S.D., Pinheiro, L., Tong, P., Lim, P.L. & Sitoh, Y.Y. Hippocampal involvement in dengue fever. Singapore Med J 2005; 46, 647-650. 8. Domingues RB, Kuster GW, Onuki-Castro FL, Souza VA, Levi JE, Pannuti CS. Involvement of the central nervous system in patients with dengue virus infection. Journal of the Neurological Sciences. 2008 Apr 15;267(1-2):36-40. 9. Kumar R, Tripathi S, Tambe JJ, Arora V, Srivastava A, Nag VL. Dengue encephalopathy in children in Northern India: Clinical features and comparison with non dengue. Journal of the Neurological Sciences. 2008 Jun 15;269(1-2):41-48. 10. Araújo FMC, Brilhante RSN, Cavalcanti LPG, Rocha MFG, Cordeiro RA, Perdigão ACB, Miralles IS, Araújo LC, Araújo RMC, Lima EG, Sidrim JJC. Detection of the dengue non-structural 1 antigen in cerebral spinal fluid samples using a commercially available enzyme-linked immunosorbent assay. J Virol Methods 2011 Jul [Epub ahead of print].




Management of patients

Pharmaceutical Update

scheduled for CT scans
Computed tomography (CT) was invented for medical purposes in 1972. Unlike conventional X-ray imaging, CT scanning produces non-superimposed, cross-sectional images of the body with higher contrast resolution. Hence, it allows better visualization of differently structured soft tissue regions, offering insight into pathology within the body. CT imaging is now widely use. In this article, we discuss the pharmacological management of special groups of patients who are scheduled for a CT scan.

CONTRAST MEDIA Before sending a patient for a CT scan, the physician has to assess the suitability of administering iodinated contrast agents. While the use of an iodinated contrast agent is not mandatory, it makes specific organs, blood vessels or tissues more visible to better illustrate disease or injury. Iodinated contrast agents can be a d m i n i s t e re d o r a l l y, re c t a l l y, intravenously or intra-arterially, depending on the site of imaging (table 1). These agents can be divided into highosmolar (HOCM), low-osmolar (LOCM) or iso-osmolar contrast media (table 2). HOCMs are the first-generation of contrast agents. They are ionic monomers with osmolalities ranging from 1400 to 1800 mOsm/kg (normal plasma osmolality is 280 to 300 mOsm/kg). Due to their high osmolality, their propensity of causing nephrotoxicity is also the highest. LOCMs are second-generation agents with osmolality ranging from 500 to 850 mOsm/kg. Iso-osmolar contrast media are the newest non-ionic contrast agents with osmolalities comparable to normal plasma. They are the least nephrotoxic among all agents. Apart from osmolality, these agents also vary in their iodine concentrations and their physicochemical properties such as viscosity. SCREENING Screening is necessary to minimize the occurrence of adverse reactions to contrast media. It includes determining if the patient:

Table 1. Routes of contrast administration and sites of imaging

Route of contrast administration Oral Rectal Intravenous

Examples of imaging studies Computed tomography of the abdomen, and pelvis Computed tomography colonoscopy Computed tomography of head and body Digital subtraction angiography Intravenous urography Venography Angiocardiography Coronary angiography Pulmonary angiography Aortography Visceral and peripheral arteriagraphy Digital subtraction angiography Central nervous system angiography





Table 2: Examples of contrast media

Compound Ionic

Name Diatrizoate (Hypaque 50) Metrizoate (Isopaque 370) Ioxaglate (Hexabrix) Iopamidol (Isovue 370) Iohexol (Omnipaque 350) Ioxilan (Oxilan 350) Iopromide (Ultravist 370) Iodixanol (Visipaque 320)

Type Monomer Monomer Dimer Monomer Monomer Monomer Monomer Dimer

Iodine content (mg/mL) 300 370 320 370 350 350 370 320

Osmolality (mOsm/kg) 1550 2100 580 796 884 695 774 290

Level High osmolar High osmolar Low osmolar Low osmolar Low osmolar Low osmolar Low osmolar Iso-osmolar


• • • •

• •

had any previous allergic reactions to iodinated contrast media; has any severe allergies or reactions to medications or food; is above 60 years of age; has a history of asthma, diabetes, kidney disease, pheochromocytoma, solitary kidney, organ transplantation or myeloma; is taking any metformin-containing medications; or is pregnant or breast-feeding.

cardiovascular collapse. These reactions, though rare, can be lifethreatening.2 Apart from a previous history of adverse reactions to contrast media, preexisting drug allergies or medical conditions such as asthma, hay fever, eczema also increase the risk of a contrast-induced reaction. 4 For example, urticaria occurs more frequently in patients with active allergies and bronchospasm occurs more readily in patients with active asthma.2 PREVENTION OF ACUTE CONTRAST MEDIA REACTIONS Pre-medication with oral corticosteroids To reduce the probability of occurrence of an adverse reaction in high-risk groups, various studies have concluded the safer use of non-ionic, low-osmolar as compared to ionic contrast media. 5 - 7 The Royal College of Radiologists has also adopted this recommendation.3,8 In addition to nonionic, low osmolar agents, the practice of using prophylactic corticosteroids as a pre-medication to reduce the risk of a reaction seems to have become popular. This happened even though only a few studies have demonstrated the benefits of corticosteroids when used in addition to non-ionic contrast agents. In 2002, a repeat survey targeting the radiology departments was carried out in UK. It revealed that, compared to 1994, there was an increase in usage of prophylactic corticosteroids in high-risk patients, especially asthmatic patients on treatment. The survey showed that the most common

These factors will help decide if an iodinated contrast agent can be administered safely.1 ACUTE ADVERSE REACTIONS OF CONTRAST MEDIA Obtaining a complete history is essential since a prior adverse reaction is a highly reliable predictor of a recurrent episode.2 Contrast-induced adverse reactions can be generally classified as idiosyncratic or chemotoxic. Idiosyncratic reactions are unpredictable, anaphylactoid in nature and independent of the contrast dose administered. On the other hand, chemotoxic reactions are more predictable since they are dependent on the dose, chemical toxicity and physiological characteristics.3 Acute reactions can be divided into mild, moderate or severe. Mild reactions include nausea and vomiting, headache, fever and chills, rash, pruritus, flushing and facial edema. They are usually bearable, self-limiting and transient. Moderate reactions include urticaria, bronchospasm and moderate hypotension that usually cease with appropriate therapy. Severe reactions include convulsions, severe bronchospasm, pulmonary edema or

choice of corticosteroid was oral prednisolone. The most common regimen was either prednisolone 20 mg or 40 mg once daily for 2 days including the day of contrast administration. Some departments h a d a re g i m e n t h a t i n v o l v e d prophylaxis over 3 days while some continued the prophylaxis till a day after contrast use. The survey found that within UK, there was no consensus regarding the need, dose and duration of steroid prophylaxis. The dose of oral prednisolone ranged between 5 mg to 180 mg a day. 9 In Europe, a wide variety of regimens with different dosages was also observed. In some radiology departments, corticosteroids are used in combination with H1 or H2 antihistamines. The majority surveyed used oral prednisolone 30 mg, varying from once to thrice before the contrast. Although the frequency of steroid administration differed, there was better consensus regarding the need to give oral corticosteroids at least 11 hours before the contrast medium to ensure effectiveness. 10 More recently, the American College of Radiology (ACR) proposed two frequently used regimens: • PO prednisolone 50 mg at 13 hours, 7 hours and 1 hour in combination with diphenhydramine 50 mg either intravenously, intramuscularly or orally an hour before contrast media injection • PO methylprednisolone 32 mg at 12 hours and 2 hours before contrast media injection ± diphenhydramine 50 mg as in option 1.1




Pre-medication with intravenous corticosteroids Based on the postulated time needed for oral corticosteroids to work (11 hours), they are not favoured during an emergency. It then seems reasonable to use IV corticosteroids instead. Studies have shown that IV corticosteroids may be able to prevent an acute reaction if it is administered at least 4 to 6 hours before the contrast media, although the onset of its prophylactic effect may have begun about an hour after IV administration. The ACR suggests IV methylprednisolone 40 mg or IV hydrocortisone 200 mg every 4 hourly till contrast injection, in combination with IV diphenhydramine 50mg an hour prior to contrast injection.1 A lower dose of hydrocortisone 100 mg can also be considered.2,6 C u r re n t l y, t h e m e c h a n i s m o f corticosteroid prophylaxis is not fully understood, hence the minimum lead time for corticosteroid use is unknown. However, it is postulated to be not less than 6 hours in view of time needed for the body to produce sufficient specific enzyme inhibitors to manifest the effect.10 Even with the use of non-ionic, low osmolar contrast agents and prophylactic corticosteroids, an adverse reaction can still occur. Therefore, resuscitation drugs should always be available and patient should be observed for 20 to 30 minutes after the contrast administration. CONTRAST-INDUCED NEPHROTOXICITY Contrast-induced nephrotoxicity (CIN) is a sudden deterioration of the renal status after the administration of a contrast media when all other possible etiologies have been ruled out. However, the true prevalence of CIN is not established due to the lack of standard diagnostic criteria. Thus, it is dependent on the definition being adopted.11 The most common, widely accepted definition of CIN is an increase in baseline serum creatinine (SCr) by ≥25% or an absolute increase of ≥0.5 mg/dL (44 mcmol/L) 48 to 72 hours following contrast media

exposure.12,13 Other variations in the definition of CIN include an increase in SCr by greater than 25% if baseline SCr is less than 1.5 mg/dL (132 umol/L), or an increase of SCr greater than 1.0 mg/dL if baseline SCr is more than 1.5mg/dL within 72 hours after contrast media administration. 14 However, as SCr can be influenced significantly by the patient’s gender, muscle mass, nutritional status and age, the use of this parameter alone limits the accuracy of the renal function, resulting in controversial viewpoints over its clinical significance. 12 In addition, there is also no consensus on the threshold of SCr beyond which iodinated contrast media should not be used.11 PA T H O P H Y S I O L O G Y OF CONTRAST-INDUCED NEPHROTOXICITY CIN may occur with any type of contrast media, with HOCM having a higher prevalence. 1 5 The exact pathophysiology of CIN is not fully understood although several attempts have been made to explain it. One possibility is the result of renal hemodynamic changes. Renal vasoconstriction occurs because of the contrast-induced the release of endothelin and adenosine or the high osmolality of the contrast mediun. Renal vasoconstriction can cause reduction in renal blood flow and the high osmolality of contrast media increases blood viscosity, increasing intra-renal pressure. The end result is hypoperfusion of renal cells, leading to cell injury.11,16 Another explanation for CIN is the direct tubular toxicity of the contrast medium, due to its cytotoxic effect and generation of free oxygen radicals. RISK FACTORS FOR CONTRASTI N D U C E D N E P H RO T O X I C I T Y The risk of CIN is inversely proportional to the baseline renal function. Renal insufficiency, typically defined as SCr of more than 1.5mg/dL (132 umol/L) or glomerular filtration rate (GRF) of less than 60 ml/min/1.73m2, is one of the main risk factors for CIN. 13,17 Apart from renal insufficiency, other

non-modifiable risk factors include diabetes mellitus (DM) with diabetic nephropathy, cardiovascular disease (eg. advanced heart failure or any other causes reduced renal perfusion), history of percutaneous coronary intervention (PCI) as this promotes the development of an atheroemboli, age greater than 60 years, multiple myeloma, hypertension and hyperuricemia. Modifiable risk factors include dehydration, use of diuretics, angiotensin-converting enzyme inhibitors, non-steroidal antiinflammatory drugs (NSAIDs), nephrotoxic antibiotics (such as aminoglycosides), high doses of contrast media, hypotension, anemia and blood loss.11,18 However, studies have shown that the highest risk of CIN lies in patients who have both preexisting renal insufficiency and DM.13 PREVENTION OF CONTRASTI N D U C E D N E P H RO T O X I C I T Y For patients who are at risk of CIN, prevention is crucial. The attending physician should ensure that a CT scan with contrast is absolutely necessary before proceeding. If is of utmost importance to ensure that the patient is well-hydrated. The ACR and the Consensus Panel for CIN recommend all patients receiving contrast media to be sufficiently hydrated. Ideally, hydration should start 6 to 12 hours before contrast media administration and continue for 4 to 12 hours beyond. 11 The European Society of Urogenital Radiology (ESUR) guidelines on contrast media resonate with ACR on the importance of hydration. It recommends at least 100ml per hour of fluid hydration, orally or intravenously, starting 4 hours before and lasting 24 hours after the contrast administration in non-fluidrestricted patients. Apart from hydration, low or iso-osmolar contrast media are preferred. In addition, ESUR guideline also recommends that all nephrotoxic agents (e.g. NSAIDs) to be withheld temporarily for at least 48 hours before the scan. 18 Agents such as N-acetylcysteine may also be considered for use to diminish the nephrotoxic effects of the contrast.




EVIDENCE FOR N-ACETYLCYSTEINE In 2000, Tepel et al first presented the novel finding that oral N-acetylcysteine (brand name Fluimucil) can prophylactically reduce the risk of acute renal failure in patients who have preexisting chronic renal insufficiency (defined as SCr concentration above 1.2 mg/dL (106 umol/L) or creatinine clearance of less than 50 ml/min). The study dose of 600 mg oral Nacetylcysteine twice a day on the day before and on the day of the administration of the contrast media resulted in a reduction of SCr by 0.4 mg/dL (35 umol/L) after 48 hours when used with hydration. Only 1 of the 41 (2%) patients in the N-acetylcysteine group had an increase of at least 0.5 mg/dL in SCr at 48 hours compared to 9 of 42 (21%) patients in the control group (p=0.01). Both the treatment and control arms were hydrated with 0.45% sodium chloride at a rate of 1 mL/kg body weight for 12 hours before and after contrast administration. It was postulated that the ability of Nacetylcysteine to prevent CIN is due to its vasodilatory effects which can overcome contrast-induced renal vasoconstriction and also its antioxidant property which allows it to scavenge oxygen-derived free radicals that can cause direct tubular damage. 7,20 More recently, Marenzi et al have also reiterated the benefits of Nacetylcysteine. The study demonstrated the possibility that Nacetylcysteine has a dose-dependent protective effect which is particularly crucial for procedures such as primary angioplasty where the volume of contrast required is typically higher. It reported that an intravenous bolus of 1200 mg N-acetylcysteine prior to primary angioplasty followed by oral 1200 mg N-acetylcysteine twice a day for 48 hours after the procedure reduced the risk of CIN more than using 600 mg of N-acetylcysteine in the same manner.21 Doses higher than Tepel’s initial suggestion were also proven to be beneficial in situations where pretreatment with oral N-acetylcysteine one day before is not feasible. A study reported reductions in SCr when

patients were administered 900 mg of N-acetylcysteine intravenously an hour before the emergency CT scan followed by another 900 mg intravenously after the scan. 2 2 Despite the multiple studies that support Tepel’s initial findings, several studies have yielded contradictory results.23 Therefore, the benefits of Nacetylcysteine in preventing CIN are highly controversial. The ACR guideline only recommends the use of Nacetylcysteine as a supplemental management in patients who are at risk of acute renal failure with contrast administration. It still holds that the most important and probably the only well-proven method of preventing CIN is by hydration, either orally or intravenously with 0.9% sodium chloride at 100 mL/hr in adults, beginning 6 to 12 hours before and continuing 4 to 12 hours after the administration of contrast media. METFORMIN AND CONTRAST– I N D U C E D N E P H RO T O X I C I T Y Metformin is an oral anti-hyperglycemic agent that belongs to the biguanide group. It is indicated for the treatment of non-insulin-dependent DM. Its mechanisms of action involve decreasing the hepatic glucose production and enhancing peripheral glucose uptake by up-regulating the peripheral tissues’ sensitivity to insulin.

Hence, by itself, metformin rarely causes hypoglycemia. Instead, one of the most significant and potentially fatal adverse effects of metformin is lactic acidosis, a medical emergency caused by an accumulation of lactic acid in the body. As metformin is eliminated unchanged via the kidneys, its excretion will be hindered if renal toxicity occurs. As the presence of metformin stimulates the production of lactic acid in the intestines, accumulation of metformin in the body can increase serum lactic acid levels leading to lactic acidosis. With regard to patients to be given an iodinated contrast medium, the ACR and the Consensus Panel for CIN recommend that metformin need not be discontinued in patients with normal renal function. However, for patients with multiple comorbidities but normal renal function, metformin should be withheld from the time of contrast administration for the next 48 hours. Thereafter, metformin may be restarted without a repeat SCr measurement. For patients with underlying renal insufficiency, metformin should be withheld from the time of contrast administration till SCr returns to baseline after which metformin can be safely resumed.24 On the other hand, the ESUR guidelines appear to be more conservative. ESUR advises that even though the SCr is




normal, metformin should be withheld from the time of the study and should not be resumed till at least 48 hours later when blood test shows that SCr remains within the normal range. If the renal function is abnormal, metformin should be stopped and the contrast study should be delayed for 48 hours. Metformin should only be resumed 48 hours after the administration of contrast when renal function is unaffected. During an emergency, if contrast administration is necessary and renal function is abnormal, metformin should be withheld immediately and the patient needs to be well-hydrated. Monitoring of SCr, serum lactic acid and blood pH is recommended. 2 5 , 2 6 CONCLUSION Contrast media are commonly required for various diagnostic procedures such as CT scans and angioplasty. However, physicians should always be mindful of

special populations of patients who may not be suitable for contrast agents. Should the benefits outweigh the risks, the contrast should be administered with precaution. Currently, there is still no international consensus on the management of patients who need to receive contrast media. However, it has been observed that for patients at risk of contrast-induced adverse reactions, a non-ionic, lowosmolar contrast agent is preferred. For patients who are at high risk of an acute reaction, physicians may consider the use of prophylactic corticosteroids. In order to reduce the occurrence of contrast-induced nephrotoxicity, hydration is important for all patients and in those with poor renal function, N-acetylcysteine may be considered. Lastly, for diabetic patients treated with metformin, it is important to pay attention to the patient’s

existing renal function and the importance of restarting metformin once renal function recovers post-procedure.

Ms Tay Hui Lin is a pharmacist in the Department of Pharmacy, Tan Tock Seng Hospital.

References 1. American College of Radiology (ACR) Committee on Drugs and Contrast Media. Patient Selection and Preparation Strategies. Manual on Contrast Media. Version 7, 2010. 2. American College of Radiology (ACR) Committee on Drugs and Contrast Media. Adverse Effects of Iodinated Contrast Media. Manual on Contrast Media. Version 7, 2010. 3. Thomsen HS. European Society of Urogenital Radiology (ESUR) guidelines on the safe use of iodinated contrast media. Eur J Radiol. 2006; 60:30713. 4. Morcos SK, Thomsen HS, Webb JA. Prevention of generalized reactions to contrast media: a consensus report and guidelines. Eur Radiol 2001; 11:1720–8. 5. Wolf GL, Mihkin MM, Roux SG, et al. Comparison of the rates of adverse drug reactions. Ionic agents, ionic agents combined with steroids, and nonionic agents. Investig Radiol 1991; 26:404–10. 6. Katayama M, Yamaguchi K, Kozuka T, et al. Adverse reaction to ionic and non-ionic contrast media. Final report for the Japanese committee on safety of contrast media. Radiology 1990; 175:621–8. 7. Palmer FJ. The RACR Survey of intravenous contrast media reactions. Final report. Australas Radiol 1988; 32:426–8. 8. Dawson P, Grainger RG. Guidelines for use of low osmolar contrast agents. Faculty of clinical radiology of the Royal College of Radiologists; 1992. 9. Radhakrishnan S, Manoharan S, Fleet M. Repeat survey of current practice regarding corticosteroid prophylaxis for patients at increased risk of adverse reaction to intravascular contrast agents. Clin Radiol 2005; 60: 58-63. 10. Morcos SK, Thomsen HS, Webb JAW. Contrast Media Safety Committee of the European Society of Urogenital Radiology. Prevention of generalized reactions to contrast media: a consensus report and guidelines. Eur Radiol 2001; 11:1720–8. 11. American College of Radiology (ACR) Committee on Drugs and Contrast Media. Contrast Nephroptoxicity. Manual on Contrast Media. Version 7, 2010. 12. Mehran R, Nikolsky E. Contrast-induced nephropathy: Definition, epidemiology, and patients at risk. Kidney Int 2006; 69: S11–S15. 13. Morcos SK, Thomsen HS, Webb JAW and members of contrast media safety committee of the European Society of Urogenital Radiology (ESUR). Contrast media induced nephrotoxicity: A consensus report. Eur Radiol 1999; 9:1602–13. 14. Porter GA. Contrast medium-associated nephropathy. Recognition and management. Invest Radiol 1993; 28 Suppl 4:S11–18. 15. American College of Radiology (ACR) Committee on Drugs and Contrast Media. Incidence of Adverse Effects. Manual on Contrast Media. Version 7, 2010. 16. Tumlin J, Stacu F, Adam A, et al. Pathogenesis of contrast-induced nephropathy. Am J Cardiol 2006; 98: 14-20. 17. Rudnik MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: a randomized trial. Kidney Int 1995; 47:254–61. 18. Thomsen H, Morcos S.K. Contrast media and the kidney: European society of urogenital radiology (ESUR) guidelines. Br J Radiol 2003; 76: 513-8 19. Tepel M, van der Giet M, Schwarzfeld C, et al. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med 2000; 343: 180-4. 20. Drager LF, Andrade L, Barros de Toledo JF, et al. Renal effects of N-acetylcysteine in patients at risk for contrast nephropathy: decrease in oxidant stress-mediated renal tubular injury. Nephrol Dial Transplant 2004;19:1803-7 21. Marenzi G, Assanelli E, Marana I, et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med 2006; 354:2773-82 22. Poletti PA, Saudan P, Platon A, et al. IV N-acetylcysteine and emergency CT: Use of serum creatinine and cystatin C as markers of radiocontrast nephrotoxicity. AJR. Am J Roentgenol 2007; 189: 687-92. 23. Boccalandro F, Amhad M, Smalling RW, et al. Oral acetylcysteine does not protect renal function from moderate to high doses of intravenous radiographic contrast. Catheter Cardiovasc Interv 2003; 58: 336- 41 24. American College of Radiology (ACR) Committee on Drugs and Contrast Media. Metformin. Manual on Contrast Media. Version 7, 2010. 25. Thomsen HS, Morcos SK, et al. Contrast media and metformin: Guidelines to diminish the risk of lactic acidosis in non-insulin dependent diabetics after administration of contrast media. Eur Radiol 1999; 9:738–40. 26. Greenberger PA, Halwig JM, et al. Emergency administration of radiocontrast media in high-risk patients. J Allergy Clin Immunol. 1986; 77:630-4.




A 28-year-woman with a history of type 1 diabetes mellitus presents to the hospital with pain and swelling of the left leg.

Figure 1. Lateral radiograph of left leg.

Figure 2. Axial T2-weighted fat-saturated MRI image of left leg.

Question 1: Answer 1: Question 2: Answer 2:

What abnormality is seen in the lateral radiograph of the left leg (figure 1)? Lucencies are seen projected over the soft tissue of the leg in keeping with gas locules. Where are the abnormalities on the axial T2-weighted fat-saturated MRI image (figure 2)?

Abnormal fluid and air locules are seen in the subcutaneous (arrow) and deep intermuscular (arrow heads) planes. Findings are consistent with necrotizing fasciitis.

Necrotizing fasciitis is an infection of the deep fascia, characterized by rapid and aggressive spread. Toxin released by the infection causes cell death, local vascular thrombosis, and subsequent tissue infarction and necrosis. The initiating bacteria is typically Group A betahemolytic Streptococcus or less often Staphylococcus aureus. Concomitant infection with anaerobic bacteria can lead to the development of subcutaneous emphysema. The initial presentation may be similar to cellulitis, with overlying skin erythema and tenderness. The erythema increases in size and spreads rapidly. Underlying necrosis may become evident following the development of dusky discoloration, cool or cold skin, or putrid discharge. Subcutaneous emphysema is manifest on physical examination as crepitation on palpation, and may be detected on standard radiographs. CT or MRI may be useful for delineation of the extent of the infection, but should not supplant nor delay timely surgical exploration and debridement. Rapid initiation of antibiotics and aggressive surgical debridement are necessary to reduce morbidity and mortality. All necrotic tissue must be removed. Involvement of a limb by necrotizing fasciitis frequently requires amputation for infection control. Salvage of the limb is often impossible due to extensive tissue necrosis and nonviability. Overall morbidity and mortality ranges between 70-80%. Mortality is often due to complications from septic shock, including ARDS and multi-system organ failure.

Dr Ashutosh Prakash is a registrar in the Department of Diagnostic Radiology, Tan Tock Seng Hospital.
Reference Emedicine. "Necrotizing Fasciitis" http://www.emedicine.com/derm/topic743.htm




ECG Quiz
This ECG was ordered by a doctor on call. What is the diagnosis?

The ECG shows subtle but extensive ST elevation in V1 to V6, I and aVL. There are also Q waves in the inferior leads. The ECG is consistent with the diagnosis of extensive acute anterior myocardial infarction. Rapid revascularization needs to be performed. After 5 minutes, this ECG was recorded:

Ventricular tachycardia is recorded towards the end of this 12-lead ECG! The ST elevations have gone higher and patient is at the brink of frank cardiovascular collapse.

Dr David Foo is a consultant and Head of the Department of Cardiology, Tan Tock Seng Hospital.

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