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MICA (P) 031/04/2010

contents1 MRSA — DO WE KNOW THE DISEASE BURDEN IN SINGAPORE?

4 A CASE OF DENGUE HEMORRHAGIC FEVER WITH ENCEPHALOPATHY

7 MANAGEMENT OF PATIENTS SCHEDULED FOR CT SCANS

12 RADIOLOGY QUIZ

13 ECG QUIZ

From The Editor

Dr Leong Khai PangEDITOR

Medical Digest

You wouldn’t expect a free-of-charge medical magazine to supply the key tobeing an über-doctor, would you? Read on.

Beginners do not capture the likeness of objects they want to portray. Later, theirdrawings 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 Barcelonaand 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 expertstages. Expertise is shown by consistently superior performance to that of theexpert’s peers, concrete results and measurable outcomes (Ericsson KA, PrietulaMJ, Cokely ET. Harv Bus Rev 2007; 85:114-21, 193).

Training and practice bring us to the expert level. “It is probably self-evident toinitiate that growth in expertise is dependent upon experience. What is not soevident is that experience in itself is not sufficient ... For all but the few effortlessself-learners, changes in expertise need reflection and deliberation,” says AdvancedConsulting in Family Medicine (Radcliffe Publishing Ltd, UK 2009). Consequently,it is hard for us to become better after we have completed training becausemedical practice primarily consists of personal interactions between the patientand the doctor, usually with no external critique or audit.

Can there be skill levels above the expert? What if the medical problem wandersinto 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 worlddiscloser develops new ways things could be, defines the issues, opens newworlds and creates new domains …operates more on the margins of a domain,paying attention to other domains as well, and to anomalies and marginal practicesthat hold promises for a new vision of the domain.”

In my view, precision, economy and preternatural ability (seemingly) are a fewtraits 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 unusualdiagnosis, but it is appropriate (it’s easy to do so and be wrong). He or she doesnot over-investigate or over-treat. Analogously, Yasujiro Ozu did not need dollyshots, fades, dissolves, voice-overs or special effects to make the greatest moviesever made. We make decisions with logic and also through intuition (perhapssomething very difficult to teach). The über-doctor knows the limits of each anduses them in the right proportion. On 10 September 2011, Djokovic beat Federerin the semi-finals of the US Open. After saving two match points, everything hungon one shot. Djokovic said, “The forehand return, I cannot explain to you becauseI don't know how it happened. I read his serve and I was on the ball and I hadto hit it hard, and it got in, luckily for me.” These doctors exist; we have colleagueswho make correct diagnoses that we could never make, and avoid problems thatwe could never see coming. What we need is not longer lists of differentialdiagnoses, but more incisive decision-making; not more investigations, but moreresoluteness; and not more knowledge, but deeper understanding.

We can be better doctors. May we always be growing and learning and thinking.

Jul.Aug.Sep. 2011

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Tan Tock Seng Hospital shall not be

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EDITORDr Leong Khai Pang

MEMBERSDr Jackie Tan

Dr Jaideepraj Rao

Dr Lee Cheng Chuan

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Dr David Foo

Dr Gregory Kaw

Dr Nikol le Tan

Dr Ernest Kwek

Ms Lim Wan Peng

EDITORIALASSIST ANT

Ms Michelle Lee

DESIGNERMs Zaonah Yusof

Review

MRSA – do we know the disease burden

in Singapore?

EPIDEMIOLOGYHow prevalent is MRSA in our localpublic hospitals? In a study conductedin Singapore General Hospital in 2007during an outbreak, MRSA wasdetected in 13% of patients admittedto the intensive care unit (ICU). Inaddition, 13.8% was found MRSA-positive at exit from ICU care.4 Theauthors concluded that at least 21%of the patients had evidence of MRSApresence in their body during theepisode of ICU stay, although theycould only indentify active infection in1.8%. Interestingly and ratheralarmingly, 20.2% of healthcareworkers were found colonized withMRSA during the study period.5 TheNational University Hospital inSingapore detected MRSA soon afterthe new hospital became fullyoperational in the late 1980s. A fewyears after operation, MRSA wasaccountable for 34-46% of all clinicalisolates of Staphylococcus aureus. Ina retrospective study of a year’ssurveillance data from 1998 to 1999,the MRSA incidence rate in the ICUs

1:M E D I C A L D I G E S T

Methicillin-resistant Staphylococcus aureus (MRSA) today is no longer a name unfamiliar to many. But when it wasfirst introduced into Singapore in the early 80s, it caused quite a stir in the medical community.1 Staphylococcusaureus commonly colonizes the exterior of our body, including the mucosal areas that come into contact with externalenvironment. Given the right opportunity, it invades to cause illnesses ranging from mild superficial skin infectionto deep seated infection in almost any anatomical site of the human body. The mortality rate of bloodstream infectionby Staphylococcus aureus can reach as high as 30% despite appropriate treatment. Because Staphylococcus aureusfrequently colonizes the exterior of human body, it is important to distinguish carrier state (colonization) from clinicaldisease (infection).

How did MRSA come about? MRSA essentially is the product of microbial evolution under the pressure of antimicrobialagents, specifically semi-synthetic beta-lactamase-resistant penicillins such as methicillin and cloxacillin. MRSArequires the presence of mec-genes that alter the penicillin-binding protein 2a on the cell-wall that render the semi-synthetic beta-lactamase-resistant penicillins ineffective. The treatment of choice is vancomycin which was expensivewhen it was first introduced and is associated with drug toxicity. However, it is vital to note that microbes nevercease 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 haveemerged. 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-associatedMRSA and hospital-associated MRSA. MRSA today has evolved into multiple clones with varying degrees ofantimicrobial susceptibility.2,3

was 4.6 per 1000 patient dayscompared with the general wards witha rate of 1.4 per 1000 patient days.6

How prevalent is MRSA in ourcommunity settings? In contrast tohospital-associated MRSA (HA-MRSA), community-associated MRSAtends to be more susceptible to awider range of antibiotics and causesa different spectrum of clinical illnesses.Nonetheless, the disease carriessignificant morbidity and mortality.7

Reports on cases and case series inSingapore are sparse and are likely tobe incomplete.8,9 Overall, there is acomplete lack of information on MRSAcarrier rate outside of hospital settingsin Singapore including step-down carefacilities and the non-healthcarecommunities.

DISEASE BURDEN IN SINGAPOREDisease burden is the impact of ahealth problem in an area measuredby financial cost, mortality, morbidity,or other indicators. It is often quantifiedin terms of quality-adjusted life years(QALY) or disability-adjusted life years(DALYs) which combine the burdendue to both death and morbidity intoone index. This allows for thecomparison of the disease burden due

to various risk factors or diseases. Italso makes it possible to predict thepossible impact of health interventions.Apart from creating knowledge,disease burden measurement can beapplied to formulation of healthpolicies, prioritizing allocation ofresources across health interventionand assess ing per formance.

Information on the disease burden ofMRSA infection is grossly lacking inSingapore and the region. The oneand only recent report is by Pada etal who published the first local studyexamining the economic and clinicalimpact of nosocomial MRSA infectionsin two tertiary hospitals: NationalUniversity Hospital and SingaporeGeneral Hospital.10 The study wasdesigned to follow up matched casesand controls (at a 1:2 rat io)prospectively over 6 months in eachhospital. The entire study period forboth hospi ta ls was betweenSeptember 2007 and March 2008 withdifferent start and end dates. Thedemographic profile, pre-existingmedical conditions and treatment werecomparable between the cases andcontrols except a tendency towardshigher APACHE II score among thecases. The results were, however,

alarming. The key findings were thatcases were 10.2 times more likely todie during their hospital stay, 4.6 timesto have longer hospitalization, and toincur 4.0 times higher hospitalizationcosts than non-infected controls. TheMRSA-infected survivors had 1.3 timeshigher outpatient costs and poorerself-reported health-related quality oflife. This study demonstrated that inthe local setting, MRSA infection wasindependently associated with in-hospital mortality, greater length ofstay, higher hospitalization and post-discharge healthcare costs, and lowerhealth-related quality of life at the timeof discharge. The authors furtherquantified that each MRSA infectionresulted in median excess in-hospitalization costs of more thanUS$13,000.00, which was largelyborne by the local health system.

The reasons behind the dearth ofinformation about MSRA diseaseburden are likely to be many. Theplausible reasons include the difficultyin distinguishing between diseaseversus colonisation, the failure of thesurveillance and reporting system tocapture primary illness withoutacknowledging the etiologic agent (e.g.documenting nosocomial pneumoniainstead of MRSA pneumonia) and last,but not the least, the complacency ofour healthcare system leading to poorresource allocation towards researchand knowledge creation.

THE NEED TO ACT NOWIn October 2008, Annals Academy ofMedicine Singapore commissioned aspecial edition on “Recurring InfectiousDisease Themes: Pandemic Influenzaand Antimicrobial Drug Resistance(Part II)”. The control of nosocomialspread of MRSA was discussed in twopapers.11,12 Both papers emphasizedthe importance of infection-controlintervention. To achieve the ambitiousgoal of reducing the inpatientprevalence of MRSA colonization tobelow 1% requires massive infusionsof infrastructural, scientific and humanresources to have a chance of success.Implementing infection controlinitiatives successfully over the nextfew years will save lives in the future.What is grossly lacking at the momentis our understanding of disease burden

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due to MRSA infections and quantumof health resources needed to achievea pre-determined goal.

CONCLUSIONWorld Health Day marks the foundingof the World Health Organization(WHO). It is celebrated each year onApril 7, with a theme selected eachyear that highlights priority public healthissues for WHO that affect theinternational community. The focus thisyear is on combating antimicrobialresistance.

We ought to have a serious relook atmicrobe evolution and human sciencein ant imicrobial development.

Staphylococcus aureus becameresistant to penicillin shortly after theintroduction of penicillin, and not longafter the introduction of the semi-synthetic penicillins methicillin andcloxacillin. It is no surprise thatvancomycin will one day reach its“shelf-life” with MRSA. Indeed, we arealready seeing an increasing minimalinhibitory concentration MIC levelagainst vancomycin. Apart from MRSA,the multi-drug resistant gram negativessuch as Acinetobacter, Klebsiella, etcare becoming a greater challenge intreatment, prevention and control. Canthe human science stays ahead of themicrobes? Will humans one day returnto pre-antibiotics era?

Associate Professor Leo Yee-Sin is theHead and senior consultant of theDepartment of Infectious Diseases, TanTock Seng Hospital.

References1. 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 community-

associated 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.

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Case Report

A case of dengue hemorrhagic fever

with encephalopathyDengue is the most common cause of arthropod-transmitted disease worldwide. It has a broad spectrum of clinicalmanifestations, and a wide range of severity including uncomplicated dengue fever, dengue hemorrhagic fever, anddengue shock syndrome. Encephalopathy although rare has been well reported and is thought to result from themultisystem derangement that occurs in severe dengue infection; with liver failure, shock, and coagulopathy causingcerebral insult. However, there is increasing evidence for dengue viral neurotropism, suggesting that, in a proportionof cases, there may be an element of direct viral encephalitis. Understanding the pathophysiology of dengueencephalopathy is crucial toward developing a more effective management strategy.1 We report a case of dengueencephalopathy in Singapore and review the literature on dengue encephalopathy and encephalitis.

Dengue is a viral infection transmittedin mainly urban areas by Aedes aegyptiand Aedes albopictus. The denguevirus is a Flavivirus that is responsiblefor an endemic disease throughouttropical and subtropical countriesespecially in the Caribbean Basin,Southeast Asia, Pacific Islands, andSouth America. Human are the mainnatural reservoir and the primary factorin dissemination of the virus. After anincubation period of 2 to 7 days,dengue classically begins with abruptonset of fever, chills and headache. Atransient macular rash may also beobserved which usually resolvesspontaneously. Dengue may becomplicated by a variety of problemsincluding dengue encephalopathy. Inview of this, dengue fever and denguehaemorrhagic fever are causes ofsignificantly raised health burden. InSingapore, the national burden isestimated to be similar to that forbacterial meningitis, or for sexuallytransmitted diseases apart fromHIV/AIDS.2 In Singapore in 2009, atotal of 4,497 cases of dengue werenotified to the ministry including eightfatal cases.3

CASE REPORTA 50-year-old male hotel managerpresented to Tan Tock Seng HospitalEmergency Department on 15November 2004 with 4 days’ historyof fever, mild cough, loss of appetite,gum bleeding and body ache, highh a e m a t o c r i t ( 5 0 . 5 % ) a n dthrombocytopenia (platelet 100 x 109

/L). He had no past medical history ofnote. He was oriented to time, place

and person. On review the followingday in clinic, his platelet count haddropped to 40 x 109 /L and he wasadmitted. Investigations revealeddengue polymerase chain reaction(PCR) was positive on the day ofadmission. He was diagnosed to haveDHF based on presence of fever,h e m o r r h a g i c t e n d e n c i e s ,thrombocytopenia of less than 100x109/L and high hematocrit. On day 4of hospitalisation (day 9 of illness), hedeveloped chills, rigors, drowsiness,lethargy, was slow to respond tocommands and was not oriented in

time and place. His lower and upperlimb power was grade 3/5. He wastransferred to the high dependencyunit (HDU) on the same day. The patientwas treated with ceftriaxone (2g 12-hourly) and acyclovir empirically.Computed tomography (CT) of thebrain detected subtle right temporalloss of gray-white differentiation ofunknown significance. Magneticresonance imaging (MRI) of the brainshowed a few foci of non-specific T2signal prolongation in the subcorticaland juxtacortical white matter of theposterior parietal lobe, though not

M E D I C A L D I G E S T

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sugges t i ve o f encepha l i t i s .Cerebrospinal fluid (CSF) was clearand colorless with a white blood cellcount of 5 cells/ul, glucose 3.6 mmol/L,and total protein: 87 mg/dL. Herpessimplex virus (HSV) and dengue viruswere not detected in CSF by PCR.Central nervous system investigationsexcluded 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 5of fever that subsequently decreasedand normalised at day 25 on followu p i n c l i n i c . H i s i n i t i a lthrombocytopaenia also recovered bydischarge. After 9 days of fever, hedeveloped problems with orientationand responsiveness which took 5 daysto recover. He was discharged 16 daysafter onset of illness.

DISCUSSIONWe report a patient with dengueh a e m o r r h a g i c f e v e r a n dencephalopathy. Unusually, this wasassociated with a persistent feverdespite platelet recovery. Thisextended fever was associated withhis change in mental status. Herecovered after 4 days during whichhe was given ceftriaxone and acyclovirbefore bacterial cultures and HSV testcame back negative. CSF for dengue

was negative by PCR. An alternativetest that may be used is dengue IgMin CSF which may be useful with 64%positive in one case series.4

The mechanism of encephalopathymay resu l t f rom int racran ia lhemorrhage, cerebral edema,

hyponatremia, cerebral anoxia,fulminant hepatic fai lure withportosysemic encephalopathy,microcapillary hemorrhage or releaseof toxic products.5 In our patient,encephalopathy did not appear to besecondary to any of these. There wasno evidence of hepatic encephalopathy

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

Day of illness4 5 6 7 8 9 10 11 13 16At Admitted ConfusionED /PCR started Confusion

positive /HDU resolved Discharged

Temperature (°C) 39.6 38.7 38.9 39.4 38.2 38.4 36.8 36.8 36.6 36.2

WBC (x109 ) 3 3.4 4.1 7.5 9.3 13.2 8.2 7.3 5.6

HB (g/L) 17.6 18 17 16.8 15.2 16 14.9 15.2 15

HCT (%) 50.5 50.5 48.6 48.4 43.5 46.6 44 43 44

PLT (x109) 100 40 23 32 76 136 159 217 375

ALB (g/L) 38 30 33 39

GL (g/L) 28 26 32 36

ALP (U/L) 50 79 104 82 73

ALT (U/L) 161 141 139 105 81

AST (U/L) 503 449 382 201 98

GGT (U/L) 192 223 234 207 168

BIL (μmol/L) 19 14 16 11 15

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

M E D I C A L D I G E S T

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with transaminases trending downwardprior to onset of mental state alterationand no derangement of liver syntheticfunction. There was a history of chronicalcohol intake but no previousadmissions for intoxication and all liverfunction tests were normal at followup two weeks after hospitalization.Renal function remained normal, withurea 3-6 mmol/L over the course ofthe illness. No candidates for likelydrug-induced mental state changewere identified. Whilst few doubt thatdengue infection can be associatedwith clouding of consciousness, untilnow it was not clear whether thisrepresents central nervous system(CNS) invasion by the virus, a non-specific complication of severe denguedisease, or even coincident infectionwith another, unidentified arbovirus orother agent. Most published dataconsist of case-reports or reviews ofpatients admitted to dengue wardswith classical features of dengueinfection. Published cases fromSingapore include one report ofdengue with hepatic encephalopathyand one of hippocampal encephalitis.6,7

CSF tests can confirm dengueencephalitis but may not always beavailable, and sensitivity and specificityare unknown. In the single publishedprospective case-control study ofdengue encephalopathy in Vietnamese

children, out of 27 clinically definedcases of dengue encephalopathy, 16of 22 available CSF samples testedpositive for dengue IgM, and only onesample was positive by RT-PCR.4 Inanother case series from Brazil, out of18 cases of dengue encephalopathy,7 of 13 that had a lumbar puncturewere positive for dengue RNA by PCR.8

A pediatric case series from India had62 cases of dengue encephalopathy,21 of 29 available CSF samples were

PCR positive.9 NS1 antigen testing inCSF has been proposed as anotheroption, with 13 NS1 positive out of apanel of 26 CSF samples from denguepatients with encephalopathy andeither IgM or PCR positive in CSF fromBrazil.10 Dengue encephalopathycarried a mortality rate of 47% in onecase series.5 Our patient recoveredcompletely but he should serve as areminder of severe organ involvementin adult dengue infection.

References1. 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 Surveil lance 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 immunosorbentassay. J Virol Methods 2011 Jul [Epub ahead of print].

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

M E D I C A L D I G E S T

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CONTRAST MEDIABefore sending a patient for a CT scan,the physician has to assess thesuitability of administering iodinatedcontrast agents. While the use of aniodinated contrast agent is notmandatory, it makes specific organs,blood vessels or tissues more visibleto better illustrate disease or injury.Iodinated contrast agents can beadmin is tered ora l ly, recta l ly,intravenously or intra-arterially,depending on the site of imaging (table1).

These agents can be divided into high-osmolar (HOCM), low-osmolar (LOCM)or iso-osmolar contrast media (table2). HOCMs are the first-generation ofcontrast agents. They are ionicmonomers with osmolalities rangingfrom 1400 to 1800 mOsm/kg (normalplasma osmolality is 280 to 300mOsm/kg). Due to their high osmolality,the i r p ropens i ty o f caus ingnephrotoxicity is also the highest.LOCMs are second-generation agentswith osmolality ranging from 500 to850 mOsm/kg. Iso-osmolar contrastmedia are the newest non-ioniccontrast agents with osmolalitiescomparable to normal plasma. Theyare the least nephrotoxic among allagents. Apart from osmolality, theseagents also vary in their iodinec o n c e n t r a t i o n s a n d t h e i rphysicochemical properties such asviscosity.

SCREENINGScreening is necessary to minimizethe occurrence of adverse reactionsto contrast media. It includesdetermining if the patient:

Pharmaceutical Update

Management of patients

scheduled for CT scansComputed tomography (CT) was invented for medical purposes in 1972. Unlike conventional X-ray imaging, CTscanning 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 ofpatients who are scheduled for a CT scan.

Route of contrast administration Examples of imaging studies

Oral Computed tomography of the abdomen, and pelvis

Rectal Computed tomography colonoscopy

Intravenous Computed tomography of head and bodyDigital subtraction angiographyIntravenous urographyVenography

Intra-arterial AngiocardiographyCoronary angiographyPulmonary angiographyAortographyVisceral and peripheral arteriagraphyDigital subtraction angiographyCentral nervous system angiography

Table 1. Routes of contrast administration and sites of imaging

M E D I C A L D I G E S T

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Compound Name Type Iodine content Osmolality Level(mg/mL) (mOsm/kg)

Ionic Diatrizoate (Hypaque 50) Monomer 300 1550 High osmolarMetrizoate (Isopaque 370) Monomer 370 2100 High osmolarIoxaglate (Hexabrix) Dimer 320 580 Low osmolar

Non-ionic Iopamidol (Isovue 370) Monomer 370 796 Low osmolarIohexol (Omnipaque 350) Monomer 350 884 Low osmolarIoxilan (Oxilan 350) Monomer 350 695 Low osmolarIopromide (Ultravist 370) Monomer 370 774 Low osmolarIodixanol (Visipaque 320) Dimer 320 290 Iso-osmolar

Table 2: Examples of contrast media

• had any previous allergic reactionsto iodinated contrast media;

• has any severe allergies or reactionsto 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-containingmedications; or

• is pregnant or breast-feeding.

These factors will help decide if aniodinated contrast agent can beadministered safely.1

ACUTE ADVERSE REACTIONS OFCONTRAST MEDIAObtaining a complete history isessential since a prior adverse reactionis a highly reliable predictor of arecurrent episode.2 Contrast-inducedadverse reactions can be generallyclassi f ied as id iosyncrat ic orchemotoxic. Idiosyncratic reactions areunpredictable, anaphylactoid in natureand independent of the contrast doseadministered. On the other hand,chemotoxic reactions are morepredictable since they are dependenton the dose, chemical toxicity andphysiological character ist ics.3

Acute reactions can be divided intomild, moderate or severe. Mild reactionsinclude nausea and vomit ing,headache, fever and chills, rash,pruritus, flushing and facial edema.They are usually bearable, self-limitingand transient. Moderate reactionsinclude urticaria, bronchospasm andmoderate hypotension that usuallycease with appropriate therapy. Severereactions include convulsions, severebronchospasm, pulmonary edema or

cardiovascular collapse. Thesereactions, though rare, can be life-threatening.2

Apart from a previous history of adversereactions to contrast media, pre-existing drug allergies or medicalconditions such as asthma, hay fever,eczema also increase the risk of acontrast-induced reaction.4 Forexample, urticaria occurs morefrequently in patients with activeallergies and bronchospasm occursmore readily in patients with activeasthma.2

P R E V E N T I O N O F A C U T ECONTRAST MEDIA REACTIONSP r e - m e d i c a t i o n w i t h o r a lcorticosteroidsTo reduce the probability of occurrenceof an adverse reaction in high-riskgroups, various studies have concludedthe safer use of non-ionic, low-osmolaras compared to ionic contrastmedia.5-7 The Royal College ofRadiologists has also adopted thisrecommendation.3,8 In addition to non-ionic, low osmolar agents, the practiceof using prophylactic corticosteroidsas a pre-medication to reduce the riskof a reaction seems to have becomepopular. This happened even thoughonly a few studies have demonstratedthe benefits of corticosteroids whenused in addition to non-ionic contrastagents.

In 2002, a repeat survey targeting theradiology departments was carriedout in UK. It revealed that, comparedto 1994, there was an increase inusage of prophylactic corticosteroidsin high-risk patients, especiallyasthmatic patients on treatment. Thesurvey showed that the most common

choice of corticosteroid was oralprednisolone. The most commonregimen was either prednisolone 20mg or 40 mg once daily for 2 daysincluding the day of contrastadministration. Some departmentshad a regimen that involvedprophylaxis over 3 days while somecontinued the prophylaxis till a dayafter contrast use. The survey foundthat within UK, there was noconsensus regarding the need, doseand duration of steroid prophylaxis.The dose of oral prednisolone rangedbetween 5 mg to 180 mg a day.9

In Europe, a wide variety of regimenswith different dosages was alsoobserved. In some rad io logydepartments, corticosteroids are usedin combination with H1 or H2antihistamines. The majority surveyedused oral prednisolone 30 mg, varyingfrom once to thrice before thecontrast. Although the frequency ofsteroid administration differed, therewas better consensus regarding theneed to give oral corticosteroids atleast 11 hours before the contrastmedium to ensure effectiveness.10

More recently, the American Collegeof Radiology (ACR) proposed twofrequently used regimens:• PO prednisolone 50 mg at 13

hours, 7 hours and 1 hour inc o m b i n a t i o n w i t hdiphenhydramine 50 mg eitherintravenously, intramuscularly ororally an hour before contrastmedia injection

• PO methylprednisolone 32 mg at12 hours and 2 hours beforecontrast media in ject ion ±diphenhydramine 50 mg as inoption 1.1

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Pre-medication with intravenouscorticosteroidsBased on the postulated time neededfor oral corticosteroids to work (11hours), they are not favoured duringan emergency. It then seemsreasonable to use IV corticosteroidsinstead. Studies have shown that IVcorticosteroids may be able to preventan acute reaction if it is administeredat least 4 to 6 hours before the contrastmedia, although the onset of itsprophylactic effect may have begunabout an hour after IV administration.T h e A C R s u g g e s t s I Vmethylprednisolone 40 mg or IVhydrocortisone 200 mg every 4 hourlytill contrast injection, in combinationwith IV diphenhydramine 50mg an hourprior to contrast injection.1 A lowerdose of hydrocortisone 100 mg canalso be considered.2,6

Current ly, the mechanism ofcorticosteroid prophylaxis is not fullyunderstood, hence the minimum leadtime for corticosteroid use is unknown.However, it is postulated to be not lessthan 6 hours in view of time neededfor the body to produce sufficientspecific enzyme inhibitors to manifestthe effect.10

Even with the use of non-ionic, lowosmolar contrast agents andprophylactic corticosteroids, anadverse reaction can still occur.Therefore, resuscitation drugs shouldalways be available and patient shouldbe observed for 20 to 30 minutes afterthe contrast administration.

C O N T R A S T - I N D U C E DNEPHROTOXICITYContrast-induced nephrotoxicity (CIN)is a sudden deterioration of the renalstatus after the administration of acontrast media when all other possibleetiologies have been ruled out.However, the true prevalence of CINis not established due to the lack ofstandard diagnostic criteria. Thus, itis dependent on the definition beingadopted.11 The most common, widelyaccepted definition of CIN is anincrease in baseline serum creatinine(SCr) by ≥25% or an absolute increaseof ≥0.5 mg/dL (44 mcmol/L) 48 to 72hours following contrast media

exposure.12,13 Other variations in thedefinition of CIN include an increasein SCr by greater than 25% if baselineSCr is less than 1.5 mg/dL (132umol/L), or an increase of SCr greaterthan 1.0 mg/dL if baseline SCr is morethan 1.5mg/dL within 72 hours aftercontrast media administration.14

However, as SCr can be influencedsignificantly by the patient’s gender,muscle mass, nutritional status andage, the use of this parameter alonelimits the accuracy of the renal function,resulting in controversial viewpointsover its clinical significance.12 Inaddition, there is also no consensuson the threshold of SCr beyond whichiodinated contrast media should notbe used.11

P A T H O P H Y S I O L O G Y O FC O N T R A S T - I N D U C E DNEPHROTOXICITYCIN may occur with any type ofcontrast media, with HOCM having ahigher prevalence.15 The exactpathophysiology of CIN is not fullyunderstood although several attemptshave been made to explain it. Onepossibility is the result of renalhemodynamic changes. Renalvasoconstriction occurs because ofthe contrast-induced the release ofendothelin and adenosine or the highosmolality of the contrast mediun.Renal vasoconstriction can causereduction in renal blood flow and thehigh osmolality of contrast mediaincreases blood viscosity, increasingintra-renal pressure. The end result ishypoperfusion of renal cells, leadingto cell injury.11,16

Another explanation for CIN is thedirect tubular toxicity of the contrastmedium, due to its cytotoxic effectand generation of free oxygen radicals.

RISK FACTORS FOR CONTRAST-INDUCED NEPHROTOXICITYThe risk of CIN is inversely proportionalto the baseline renal function. Renalinsufficiency, typically defined as SCrof more than 1.5mg/dL (132 umol/L)or glomerular filtration rate (GRF) ofless than 60 ml/min/1.73m2, is one ofthe main risk factors for CIN.13,17

Apart from renal insufficiency, other

non-modifiable risk factors includediabetes mellitus (DM) with diabeticnephropathy, cardiovascular disease(eg. advanced heart failure or any othercauses reduced renal perfusion),history of percutaneous coronaryintervention (PCI) as this promotes thedevelopment of an atheroemboli, agegreater than 60 years, multiplemye loma, hyper tens ion andhyperuricemia. Modifiable risk factorsinclude dehydration, use of diuretics,angiotensin-converting enzymeinhibitors, non-steroidal ant i-inf lammatory drugs (NSAIDs),nephrotoxic antibiotics (such asaminoglycosides), high doses ofcontrast media, hypotension, anemiaand blood loss.11,18 However, studieshave shown that the highest risk ofCIN lies in patients who have both pre-existing renal insufficiency and DM.13

PREVENTION OF CONTRAST-INDUCED NEPHROTOXICITYFor patients who are at risk of CIN,prevention is crucial. The attendingphysician should ensure that a CTscan with contrast is absolutelynecessary before proceeding. If is ofutmost importance to ensure that thepatient is well-hydrated. The ACRand the Consensus Panel for CINrecommend all patients receivingcontrast media to be sufficientlyhydrated. Ideally, hydration shouldstart 6 to 12 hours before contrastmedia administration and continuefor 4 to 12 hours beyond.11 TheEuropean Society of UrogenitalRadiology (ESUR) guidelines oncontrast media resonate with ACRon the importance of hydration. Itrecommends at least 100ml per hourof f lu id hydrat ion , o ra l l y o rintravenously, starting 4 hours beforeand lasting 24 hours after thecontrast administration in non-fluid-restricted patients. Apart fromhydration, low or iso-osmolarcontrast media are preferred. Inaddit ion, ESUR guideline alsorecommends that all nephrotoxicagents (e.g. NSAIDs) to be withheldtemporarily for at least 48 hoursbefore the scan.18 Agents such asN-acetylcysteine may also beconsidered for use to diminish thenephrotoxic effects of the contrast.

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EVIDENCE FOR N-ACETYLCYSTEINEIn 2000, Tepel et al first presented thenovel finding that oral N-acetylcysteine(brand name F lu imuci l ) canprophylactically reduce the risk of acuterenal failure in patients who have pre-existing chronic renal insufficiency(defined as SCr concentration above1.2 mg/dL (106 umol/L) or creatinineclearance of less than 50 ml/min). Thestudy dose of 600 mg oral N-acetylcysteine twice a day on the daybefore and on the day of theadministration of the contrast mediaresulted in a reduction of SCr by 0.4mg/dL (35 umol/L) after 48 hours whenused with hydration. Only 1 of the 41(2%) patients in the N-acetylcysteinegroup had an increase of at least 0.5mg/dL in SCr at 48 hours compared to9 of 42 (21%) patients in the controlgroup (p=0.01). Both the treatment andcontrol arms were hydrated with 0.45%sodium chloride at a rate of 1 mL/kgbody weight for 12 hours before andafter contrast administration. It waspostulated that the ability of N-acetylcysteine to prevent CIN is due toits vasodilatory effects which canovercome contrast-induced renalvasoconstriction and also its antioxidantproperty which allows it to scavengeoxygen-derived free radicals that cancause direct tubular damage.7,20

More recently, Marenzi et al have alsoreiterated the benefi ts of N-a c e t y l c y s t e i n e . T h e s t u d ydemonstrated the possibility that N-acetylcysteine has a dose-dependentprotective effect which is particularlycrucial for procedures such as primaryangioplasty where the volume ofcontrast required is typically higher. Itreported that an intravenous bolus of1200 mg N-acetylcysteine prior toprimary angioplasty followed by oral1200 mg N-acetylcysteine twice a dayfor 48 hours after the procedurereduced the risk of CIN more thanusing 600 mg of N-acetylcysteine inthe same manner.21

Doses higher than Tepel’s initialsuggestion were also proven to bebeneficial in situations wherepretreatment with oral N-acetylcysteineone day before is not feasible. A studyreported reductions in SCr when

patients were administered 900 mg ofN-acetylcysteine intravenously an hourbefore the emergency CT scanfol lowed by another 900 mgintravenously after the scan.22

Despite the multiple studies that supportTepel’s initial findings, several studieshave yielded contradictory results.23Therefore, the benefits of N-acetylcysteine in preventing CIN arehighly controversial. The ACR guidelineonly recommends the use of N-acetylcysteine as a supplementalmanagement in patients who are atrisk of acute renal failure with contrastadministration. It still holds that themost important and probably the onlywell-proven method of preventing CINis by hydration, either orally orintravenously with 0.9% sodiumchloride at 100 mL/hr in adults,beginning 6 to 12 hours before andcontinuing 4 to 12 hours after theadministration of contrast media.

METFORMIN AND CONTRAST–INDUCED NEPHROTOXICITYMetformin is an oral anti-hyperglycemicagent that belongs to the biguanidegroup. It is indicated for the treatmentof non-insulin-dependent DM. Itsmechanisms of action involvedecreasing the hepatic glucoseproduction and enhancing peripheralglucose uptake by up-regulating theperipheral tissues’ sensitivity to insulin.

Hence, by itself, metformin rarelycauses hypoglycemia.Instead, one of the most significant andpotentially fatal adverse effects ofmetformin is lactic acidosis, a medicalemergency caused by an accumulationof lactic acid in the body. As metforminis eliminated unchanged via the kidneys,its excretion will be hindered if renaltoxicity occurs. As the presence ofmetformin stimulates the production oflact ic acid in the intest ines,accumulation of metformin in the bodycan increase serum lactic acid levelsleading to lactic acidosis.

With regard to patients to be given aniodinated contrast medium, the ACR andthe Consensus Panel for CIN recommendthat metformin need not be discontinuedin patients with normal renal function.However, for patients with multiplecomorbidities but normal renal function,metformin should be withheld from thetime of contrast administration for thenext 48 hours. Thereafter, metformin maybe restarted without a repeat SCrmeasurement. For patients withunderlying renal insufficiency, metforminshould be withheld from the time ofcontrast administration till SCr returns tobaseline after which metformin can besafely resumed.24

On the other hand, the ESUR guidelinesappear to be more conservative. ESURadvises that even though the SCr is

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normal, metformin should be withheldfrom the time of the study and should notbe resumed till at least 48 hours laterwhen blood test shows that SCr remainswithin the normal range. If the renalfunction is abnormal, metformin shouldbe stopped and the contrast study shouldbe delayed for 48 hours. Metformin shouldonly be resumed 48 hours after theadministration of contrast when renalfunction is unaffected. During anemergency, if contrast administration isnecessary and renal function is abnormal,metformin should be withheld immediatelyand the patient needs to be well-hydrated.Monitoring of SCr, serum lactic acid andblood pH is recommended.25,26

CONCLUSIONContrast media are commonly requiredfor various diagnostic procedures suchas CT scans and angioplasty. However,physicians should always be mindful of

special populations of patients who maynot be suitable for contrast agents. Shouldthe benefits outweigh the risks, thecontrast should be administered withprecaution.

Currently, there is still no internationalconsensus on the management ofpatients who need to receive contrastmedia. However, it has been observedthat for patients at risk of contrast-inducedadverse reactions, a non-ionic, low-osmolar contrast agent is preferred. Forpatients who are at high risk of an acutereaction, physicians may consider theuse of prophylactic corticosteroids. Inorder to reduce the occurrence ofcontrast-induced nephrotoxicity, hydrationis important for all patients and in thosewith poor renal function, N-acetylcysteinemay be considered. Lastly, for diabeticpatients treated with metformin, it isimportant to pay attention to the patient’s

existing renal function and the importanceof restarting metformin once renal functionrecovers post-procedure.

References1. 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; 60:307-

13.4. 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 non-

ionic 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: 513-819. 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;19:1803-721. Marenzi G, Assanelli E, Marana I, et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med 2006; 354:2773-8222. 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- 4124. 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.

Ms Tay Hui Lin is a pharmacist in theDepartment of Pharmacy, Tan Tock SengHospital.

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RADIOLOGY Quiz

Discussion

Necrotizing fasciitis is an infection of thedeep fascia, characterized by rapid andaggressive spread. Toxin released by theinfection causes cell death, local vascularthrombosis, and subsequent tissueinfarction and necrosis. The initiatingbacteria is typically Group A beta-hemolytic Streptococcus or less oftenStaphylococcus aureus. Concomitantinfection with anaerobic bacteria canlead to the development of subcutaneousemphysema.

The initial presentation may be similar tocellulitis, with overlying skin erythemaand tenderness. The erythema increasesin size and spreads rapidly. Underlyingnecrosis may become evident followingthe development of dusky discoloration,cool or cold skin, or putrid discharge.

Subcutaneous emphysema is manifest

on physical examination as crepitationon palpation, and may be detected onstandard radiographs. CT or MRI maybe useful for delineation of the extent ofthe infection, but should not supplantnor delay timely surgical exploration anddebridement.

Rapid initiation of antibiotics andaggressive surgical debridement arenecessary to reduce morbidity andmortality. All necrotic tissue must beremoved. Involvement of a limb bynecrotizing fasciitis frequently requiresamputation for infection control. Salvageof the limb is often impossible due toextensive tissue necrosis and non-viability. Overall morbidity and mortalityranges between 70-80%. Mortality isoften due to complications from septicshock, including ARDS and multi-systemorgan failure.

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

Question 2: Where are the abnormalities on the axial T2-weighted fat-saturated MRI image (figure 2)?

Answer 2: Abnormal fluid and air locules are seen in the subcutaneous (arrow) and deep intermuscular (arrow heads)planes. Findings are consistent with necrotizing fasciitis.

Question 1: What abnormality is seen in the lateral radiograph of the left leg (figure 1)?

Answer 1: Lucencies are seen projected over the soft tissue of the leg in keeping with gas locules.

Figure 1. Lateral radiograph of left leg. Figure 2. Axial T2-weighted fat-saturated MRI image of left leg.

ReferenceEmedic ine . "Necro t i z ing Fasc i i t i s "http://www.emedicine.com/derm/topic743.htm

Dr Ashutosh Prakash is a registrar in theDepartment of Diagnostic Radiology, TanTock Seng Hospital.

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ECG Quiz

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

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

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

M E D I C A L D I G E S T

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

Question

Answer