(5.4)--viralhepatitis_casepresentations.pdf

Case reportOpen AccessAcute hepatitis a virus infection presenting with multiorgandysfunction:a case reportAbdul Rasheed*and Shahzad SaeedAddress:Combined Military Hospital,Rawalpindi,PakistanEmail:AR*-;SS-saeed_*Corresponding authorReceived:2 June 2009Accepted:22 July 2009Published:30 July 2009Cases Journal 2009,2:8124doi:10.4076/1757-1626-2-8124This article is available from:http:/ 2009 Rasheed et al.;licensee Cases Network Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License(http:/creativecommons.org/licenses/by/3.0),which permits unrestricted use,distribution,and reproduction in any medium,provided the original work is properly cited.AbstractIntroduction:Acute hepatitis due to hepatitis a virus is usually a benign self-limiting diseaseconferring lifelong immunity.However,few cases have been reported in literature with fulminanthepatitis.We report this extremely rare case with multiorgan dysfunction including liver failure,hepatic encephalopathy,renal failure,pleural effusion,pericardial effusion and hematologicdysfunction as a sequale of this infection in an otherwise healthy male at the age of 18.Case presentation:An 18 years old Pakistani male presented with two days history of fever,cough,headache and vomiting.His condition gradually deteriorated and on day 7 developed multiorgandysfunction.Initially Immunoglobulin M anti hepatitis a virus was borderline 1.40 but repeated titersone week later confirmed the diagnosis of acute hepatitis a virus infection.Conclusion:This original case report highlights the importance of focusing first uncommonmanifestations of common illnesses while diagnosing difficult cases.Moreover this case also addsknowledge to the limited available data regarding complications and predictors of prognosis.IntroductionHepatitis A virus has plagued mankind for centuries bycausing acute hepatitis associated with significant morbi-dity and occasional mortality.HAV is a 7.5-kb positive-strand RNA virus of the Picornaviridae family and the onlymember of the genus Hepatovirus 1.All four genotypesbelong to a single serotype.HAV is spread via the fecal-oralroute.The incubation period averages 30 days(range 15 to49 days).The prevalence of HAV infection varies amongcountries in Asia 2.Countries with high endemicity forHAV infection include Pakistan,India,China,Nepal,Bangladesh,Myanmar and the Philippines.Most people inthese countries are exposed during childhood.HAVinfection usually results in an acute,self-limiting illnessand only rarely leads to fulminant hepatic failure 3.Inyoung children,the disease is often asymptomatic,whereas in older children and adults there might bea range of clinical manifestations from mild,anictericinfection to fulminant hepatic failure.The risk offulminant hepatitis is high in patients having an under-lying chronic liver disease and are aged more than 40 years4.This case report describes a young person from ahighly HAV endemic area with serologically confirmedacute HAV infection with multiorgan involvement.Page 1 of 3(page number not for citation purposes)Case presentationAn 18 years old Pakistani male presented with about twodays history of intermittent fever with chills,nonproduc-tive cough,generalized headache,nausea and nonbiliousvomiting.He vomited thrice on day 1 and five times onthe next day.Vomitus contained food particles andwas devoid of blood.Clinical examination was unremark-able except raised temperature ranging from 37.22C(310.4 kelvin)to 39.44C(312.6 kelvin)with relativebradycardia(pulse ranging from 56/minute to 84/minute).Initial investigations revealed raised serum alanineaminotransferase(2043u/l),low normal platelet count(165 109/l)and total white cell count(4.2 109/l)withnormal differential count and morphology.Other investi-gations including haemoglobin,malarial parasite slides,bilirubin,alkalinephosphatase,aspartateaminotransferase,albumin,urea,creatinine,electrolytes,plasma glucose,widal test,DIC screening,urinalysis and chest radiographwere within normal limits.He was provisionally diagnosedas a case of anicteric hepatitis with differential diagnosesof malaria and enteric fever due to their high prevalence inthe area.He was managed with antimalarial(artemether),third generation cephalosporin(Ceftriaxone)and suppor-tive parenteral fluids.Samples for blood cultures,viral(including hepatitis and dengue)screening,typhi dot,serology for brucella,leptospira,rickettsia and toxoplasmawere sent to laboratory.On day 3,he developed dizziness and unsteadiness of gaitand asterixis while fever with relative bradycardia,head-ache and vomiting continued.CT scan head revealed noabnormality.IgM anti HAV was borderline 1.40(cut off1.20).Repeated investigations showed rising serumalanine aminotransferase 3690u/l,prothrombin time30 seconds(control 12 seconds),PTTK 46 seconds(control 32 seconds),fibrinogen 130 mg/dl,D-dimers200400,serum albumin 28 g/l,urea 13 mmol/l,creatinine 266 umol/l,sodium 133 mmol/l potassium4.8 mmol/l,creatinine kinase 1112 u/l with CK-MB 6.1%,LDH 6130 u/l,AST 66 u/l,haemoglobin 12.8 g/l,totalwhite cell count 11 109/l,platelets 116 109/l,pus cells(8-10/HPF)&red blood cells(5-7/HPF)seen onurinalysis.Other investigations including ECG,bilirubin,alkaline phosphatase,hepatitis B surface antigen,serologyfor hepatitis E,C,dengue,brucella,leptospira,rickettsia,toxoplasma and typhoid were normal.Antimalarial(artemether)was stopped when repeated malarial parasiteslides were found negative.Vitamin K was added totreatment but his clinical and laboratory parameterscontinued to deteriorate.On day 7,fever settled but his blood pressure rose to170/110 mmHgandbecame oliguric with 24hour urinaryoutput falling to 150 ml while investigations revealedurea 14.1 mmol/l,creatinine 1204 umol/l,sodium127 mmol/l,potassium 4.4 mmol/l,serum alanineaminotransferase 2149 u/l,bilirubin 77 umol/l,alkalinephosphatase 367u/l,prothrombin time 16 seconds,PTTK39 seconds and fibrinogen 180 mg/dl.Ultrasonographyshowed bilateral pleural effusion(mild)and renalparenchymal disease with increased echogenicity nor-mal sized kidneys(Right 11.2 cm,Left 11.6 cm).Echocardiography showed minimal amount of pericar-dial effusion with no evidence of tamponade.He wasmanaged with frusemide and haemodialyzed thriceon day 7,8 and 10 via dual lumen catheter in rightsubclavian vein.On day 10,he started showing signs of improvement withbetter control of blood pressure,urinary output improvingto 900 ml/24 hours and significant improvement in thelevels of serum urea/creatinine as well as the liver functiontests etc.Repeated IgM anti hepatitis A virus was positive,while rest of the investigations including blood cultures,serum cryoglobulins,aldolase,rheumatoid factor,com-plement levels,autoimmune and vasculitic screeningrevealed no abnormality.Dual lumen catheter wasremoved post dialysis on day 10.On day 16,investigations revealed normal serum albu-min,coagulation profile,cardiac enzymes,electrolytes andblood counts while levels of serum urea 11.2 mmol/l,creatinine 246 umol/l,alanine aminotransferase 127 u/l,bilirubin 38 mmol/l,alkaline phosphatase 594 u/l wereshowing gradual improvement.Follow up on day 23 revealed completely normal clinicaland laboratory parameters including renal,hepatic,cardiac,pleural and hematological functions.Monthlyfollow up during last five months has not shown anyevidence of relapse.DiscussionHAV infection usually results in an acute,self-limitingillness conferring lifelong immunity and only rarely leadsto fulminant hepatic failure.Fulminant hepatic failureoccurs more commonly in patients with underlying liverdisease;particularly chronic hepatitis B and C infection,advanced age and addiction of intravenous drugs 3-6.This case is very unusual as there was no pre-existinghepatic or non hepatic illness or other risk factors.Few cases of acute renal failure and nephrotic syndromehave been reported in the literature in association withHAV infection 7-10.Acute tubular necrosis was the mostcommon form of renal injury in such patients while inothers renal biopsy was suggestive of interstitial nephritis,immune complex mesangial glomerulonephritis 7,and IgA dominant glomerulonephritis.Only once IgAPage 2 of 3(page number not for citation purposes)Cases Journal 2009,2:8124http:/ glomerulonephritis was accompanied withcutaneous cryoglobulinemic vasculitis.This is a truly rare event in which a young patient at the ageof 18,experienced multiorgan dysfunction secondary tohepatitis A virus infection comprising of fulminant liverfailure,hepatic encephalopathy,acute renalfailure,pleuraleffusion,pericardial effusion and hematological dysfunc-tion within short span of time and without preexistingunderlying liver disease.ConclusionThis emphasizes the importance of focusing on commonillnesses with their uncommon manifestations whilesearching for solution of various clinical diagnosticmysteries even in the absence of poor prognostic markers.AbbreviationsAST,Aspartate transaminase;CK-MB,Myocardial fractionof creatinine kinase;DIC,Disseminated intravascularcoagulation;ECG,Electrocardiogram;HAV,Hepatitis Avirus;HPF,High power field;Ig,Immunoglobulin;LDH,Lactate dehydrogenase;PTTK,Partial thromboplastin timewith kaolin;RNA,Ribonucleic acid.ConsentWritten informed consent was obtained from the patientfor publication of this case report and accompanyingimages.A copy of the written consent is available forreview by the Editor-in-Chief of this journal.Competing interestsThe authors declare that they have no competing interests.Authors contributionsAR was a major contributor in drafting the manuscript.Heanalyzed and interpreted the patient data.He was alsoactively involved in the management of this case alongwith the coauthor.SS was head of the medical teamresponsible for the management of this case.Herevised the manuscript critically for important intellectualcontent.All authors read and approved the finalmanuscript.AcknowledgementsWe acknowledge the efforts of all doctors and paramedicsthat were involved in the management of this caseparticularly Dr.Iqbal,Dr.Raja Khalid,Dr.Zulfiqar AliKango and Dr.Shahid Ahmed.References1.Robertson BH,Jansen RW,Khanna B,Totsuka A,Nainan OV,Siegl G,Widell A,Margolis HS,Isomura S,Ito K,Ishizu T,Moritsugu Y,Lemon SM:Genetic relatedness of hepatitis A virus strainsrecovered from different geographic regions.J Gen Virol 1992,73:1365-1377.2.Gust ID:Epidemiological patterns of hepatitis A in differentparts of the world.Vaccine 1992,10:S56-58.3.Vento S,Garofano T,Renzini C,Cainelli F,Casali F,Ghironzi G,Ferraro T,Concia E:Fulminant hepatitis associated withhepatitis A virus superinfection in patients with chronichepatitis C.N Engl J Med 1998,338:286-290.4.Keeffe EB:Is hepatitis A more severe in patients with chronichepatitis B and other chronic liver diseases.Am.J.Gastroenterol1995,90:201-205.5.Brown GR,Persley K:Hepatitis A epidemic in the elderly.SouthMed J 2002,95:826-833.6.Akriviadis EA,Redeker AG:Fulminant hepatitis a in intravenousdrug users with chronic liver disease.Ann Intern Med 1989,10:838-839.7.Kim SE,Kim SJ,Kim HS,Kim HS,Nam ES,Lee SK,Shin SR,Kim HY:Two cases of acute renal failure associated with non-fulminant acute hepatitis A.Korean J Gastroenterol 2006,48:421-426.8.Vaboe AL,Leh S,Forslund T:Interstitial nephritis,acute renalfailure in a patient with non-fulminant hepatitis A infection.Clin Nephrol 2002,57:149-153.9.Zikos D,Grewal KS,Craig K,Cheng JC,Peterson DR,Fisher KA:Nephrotic syndrome and acute renal failure associatedwith hepatitis A virus infection.Am J Gastroenterol 1995,90:295-298.10.Cheema SR,Arif F,Charney D,Meisels IS:IgA-dominantglomerulonephritis associated with hepatitis A.Clin Nephrol2004,62:138-143.Do you have a case to share?Submit your case report todayRapid peer reviewFast publicationPubMed indexingInclusion in Cases DatabaseAny patient,any case,can teach Page 3 of 3(page number not for citation purposes)Cases Journal 2009,2:8124http:/