Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 8  |  Issue : 6  |  Page : 830-832  

Dengue: A rare differential of acute hepatic failure


Department of Medicine, S.N. Medical College, Agra, Uttar Pradesh, India

Date of Web Publication19-Nov-2015

Correspondence Address:
Ayush Agarwal
Department of Medicine, S.N. Medical College, Agra, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.169931

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  Abstract 

Dengue is viral illness which manifests as high grade fever, myalgia, hemorrhagic manifestation and shock. Recently, dengue has been reported with rare presentations like encephalopathy, liver failure, and renal failure. We are presenting a case of acute fulminant liver failure due to dengue in which a 19-year-old previously healthy female who presented to us in the emergency department with complaints of high grade fever for past 3 days without chills and rigors, and altered sensorium past 1 day. The patient had icterus. On laboratory evaluation, her liver function tests were deranged while neuroimaging was normal. In view of presence of coagulopathy and altered sensorium, a diagnosis of dengue related acute hepatic failure was made. The patient was provided supportive and symptomatic management to which she responded and was discharged a few days later and is on regular follow-up.

Keywords: Complicated malaria, dengue, encephalopathy, liver failure, viral hepatitis


How to cite this article:
Alam S, Singh AK, Singh B, Agarwal A. Dengue: A rare differential of acute hepatic failure. Med J DY Patil Univ 2015;8:830-2

How to cite this URL:
Alam S, Singh AK, Singh B, Agarwal A. Dengue: A rare differential of acute hepatic failure. Med J DY Patil Univ [serial online] 2015 [cited 2020 Nov 28];8:830-2. Available from: https://www.mjdrdypu.org/text.asp?2015/8/6/830/169931


  Introduction Top


Dengue is a mosquito-borne viral infection causing a severe flu-like illness and sometimes causing a potentially lethal complication called severe dengue.

Previously, the presentation of dengue infection was classified into 5 main forms: Nonspecific febrile illness, classic dengue fever (DF), dengue hemorrhagic fever (DHF), DHF with dengue shock syndrome, and unusual syndromes like encephalopathy. [1],[2] However, now dengue has been classified in three categories dengue, dengue with warning signs, and severe dengue. [1]

There are four serotypes of dengue virus and all four serotypes of dengue virus can cause DHF, but the patient with secondary infections with a different serotype is more prone for this. [2],[3]

Mild grade liver dysfunction in DHF is usual. However, its presentation as acute fulminant liver failure is unusual. [4],[5] We present the case of a young female who developed acute hepatic failure due to dengue.


  Case Report Top


A 19-year-old female, who was previously healthy, presented to us in the emergency department with complaints of high grade fever for past 3 days without chills and rigors, and altered sensorium from past 1 day. We did not find any obvious history of bleeding from any site, rash, joint pain, cough, expectoration, any drug abuse, head trauma, ear discharge, diabetes, hypertension or antitubercular therapy intake. On examination, blood pressure was 110/76 mm Hg, pulse rate 96/min, respiratory rate 18/min, pallor was absent, but icterus was present. Cardiovascular, respiratory, and per abdominal examinations were found to be within normal limits. In neurological examination, the patient's Glasgow Coma Scale (GCS) score was E 1 V 1 M 5 . Plantar reflex was bilateral extensor; deep tendon reflexes were diminished in all the four limbs and signs of meningeal irritation were absent. Fundus examination was within normal limits. Patient's investigation profile was-hemoglobin −10.7 g/dl, total leucocyte count −4800/cumm, no toxic granules, differential leucocyte count −N 69 L 29 M 01 E 01 , platelet count −67000/cumm, packed cell volume (PCV) −38.3%, mean cell hemoglobin concentration −32 g/dl, erythrocyte sedimentation rate −55 mm/h, serum glutamic oxaloacetic transaminase (SGOT) (aspartate aminotransferase [AST]) −4190.6 IU/L, serum glutamic pyruvic transaminase (SGPT) (alanine aminotransferase [ALT]) −2632.6 IU/L. Serum bilirubin −Total was 3.41 mg/dl in which direct component was 2.96 mg/dl and indirect component was 0.45 mg/dl, serum albumin was 3.2 g/dl, and serum alkaline phosphatase was 126 IU/l serum creatinine was 0.8 mg/dl, random blood sugar −126 mg/dl, blood urea −32.6 mg/dl, Na + −138 mmol/l, K −4.01 mmol/l, iCa −1.01 mmol/l, urine routine microscopy examination was within normal limits. The peripheral smear for malarial parasite (MP) was negative. MP enzyme linked immunosorbent assay (MP ELISA) for malaria was also negative and so were widal and IgM typhidot tests. HIV, hepatitis B surface antigen, anti-hepatitis C virus, anti-hepatitis E virus were all negative. NS1, IgM, IgG were all positive when tested for, in dengue serology. Leptospira serology came to be negative. Bilateral mild pleural effusion was seen on chest X-ray PA view. Ultrasonography abdomen revealed mild ascites, with gall bladder wall thickening and a normal sized liver. Electrocardiogram was normal. Magnetic resonance imaging brain did not reveal any abnormality.

After initial intensive management, we started injection paracetamol intravenous (IV) 6 hourly, injection vitamin K (Menadione Sodium Bisulfite) slow IV OD, injection pantoprazole 40 mg OD, injection L-ornithine L-aspartate IV 8 hourly, tablet rifaximin 550 mg BD, tablet ursodeoxycholic acid 300 mg BD, syrup lactulose 30 ml (through Ryle's tube). Isolyte M and 5% dextrose in normal saline were started through IV line. Patient was shifted to the intensive care unit (ICU).

On the 2 nd day in ICU, the patient started improving. The GCS of patient was E 3 V 2 M 6 . Fever was controlled only by antipyretic agent. No evidence of any bleeding manifestation was found and we continued the same treatment.

On the 3 rd day in ICU, patient's GCS improved to E 4 V 4 M 6 -patient could take orally now. One episode of hematuria occurred in the morning. Patient's prothrombin time was 19 s, control prothrombin time was 12.6 s. INR was 1.86. We infused 6 units of fresh frozen plasma prophylactically. Apart from that, we continued the same treatment.

On the 4 th day of patient's hospital stay, patient's GCS was E 4 V 4 M 6 . Patient's prothrombin time was 14.4 s, control prothrombin time was 12.6 s. INR is 1.21.

On the 6 th day, patient was fully oriented to time, place, and person. Fever had subsided even without the use of an antipyretic agent. Patient's GCS was E 4 V 5 M 6. On day 8, patient was fully oriented to time, place and person. Patient's GCS was E 4 V 5 M 6. Patient was fever free for more than 2 days, without any antipyretic drugs. Platelet and PCV were found to be in an increasing trend (platelet count on that day was 1.1 lakhs and PCV is 28.8 fl). SGOT (AST) was 78 IU/L and SGPT (ALT) was 66 IU/L. Patient was then discharged with advice for follow-up.


  Discussion Top


In our patient, the differentials to be considered include acute viral hepatitis, complicated malaria, leptospirosis, and Reye's syndrome. The presence of high grade fever, thrombocytopenia, liver enzyme derangement, pleural effusion and ascites, gall bladder wall edema (evidence of plasma leak syndrome) were all consistent with possibility of dengue. All the viral markers of acute viral hepatitis were negative. In complicated malaria, liver enzymes will not be markedly raised, moreover peripheral smear for MP was negative, and MP ELISA was also negative thereby ruling out malaria.

Jaundice is rare in Reye's syndrome. Furthermore, in Reye's syndrome, features of thrombocytopenia and plasma leakage are not seen. As a result, the diagnosis of acute liver failure with associated hepatic encephalopathy due to dengue should be considered in our patient.

Our patient previously may have had an asymptomatic dengue infection with a different serotype, leading to a more severe secondary infection on this occasion. The patient being positive for IgG antibody to dengue virus on day 4 of the illness makes this possibility highly possible. However, IgG antibody titer was not done.[Additional file 1]

Dengue is a viral illness characterized by high grade fever, hemorrhagic manifestations, and shock. However, in recent times, dengue disease has been reported with many rare manifestations, which may include liver failure, renal failure, and encephalopathy. [6] Liver enzyme elevations are usually seen in dengue. Usually, the AST levels are elevated more than ALT levels, probably due to skeletal muscle injury. Occasionally, jaundice may also be seen. [7] Very few reports of acute liver failure due to dengue have been reported globally in adults. A study has found that dengue was the most common cause of acute liver failure in pediatric population of Thailand. [8]

Dengue has been reported to be a common cause of acute liver failure, especially during epidemic periods, in the pediatric age group, in India as well. [9] However, dengue is not usually considered as a differential diagnosis in acute liver failure patients when it comes to adults.

Agarwal et al., [10] also demonstrated that a patient suspected to have developed acute hepatic failure due to dengue improved with supportive measures, as seen in our patient. In addition, they suggested that underlying liver disease may result in a more severe hepatitis with dengue.

This case illustrates the importance of awareness of infectious disease outbreaks around the world and their pattern. Acute liver failure is a rare complication of DF, and should be included in the differential of acute hepatitis in individuals who have recently been in or have travelled to an area in which dengue is endemic.

 
  References Top

1.
WHO and TDR. Dengue Guidelines for Diagnosis, Treatment Prevention and Control. ISBN 978924154787, NJM Classification: WC 528: WHO; 2009.  Back to cited text no. 1
    
2.
Gibbons RV, Vaughn DW. Dengue: An escalating problem. BMJ 2002;324:1563-6.  Back to cited text no. 2
    
3.
Guzmán MG, Kourí G. Dengue: An update. Lancet Infect Dis 2002;2:33-42.  Back to cited text no. 3
    
4.
Lum LC, Lam SK, George R, Devi S. Fulminant hepatitis in dengue infection. Southeast Asian J Trop Med Public Health 1993;24:467-71.  Back to cited text no. 4
    
5.
Alvarez ME, Ramírez-Ronda CH. Dengue and hepatic failure. Am J Med 1985;79:670-4.  Back to cited text no. 5
    
6.
World Health Organization. Clinical diagnosis. In: Dengue Haemorrhagic Fever: Diagnosis, Treatment, Prevention and Control. 2 nd ed. Geneva: World Health Organization; 1997. p. 12-23.  Back to cited text no. 6
    
7.
Nguyen TL, Nguyen TH, Tieu NT. The impact of dengue haemorrhagic fever on liver function. Res Virol 1997;148:273-7.  Back to cited text no. 7
    
8.
Poovorawan Y, Hutagalung Y, Chongsrisawat V, Boudville I, Bock HL. Dengue virus infection: A major cause of acute hepatic failure in Thai children. Ann Trop Paediatr 2006;26:17-23.  Back to cited text no. 8
    
9.
Kumar R, Tripathi P, Tripathi S, Kanodia A, Venkatesh V. Prevalence of dengue infection in north Indian children with acute hepatic failure. Ann Hepatol 2008;7:59-62.  Back to cited text no. 9
    
10.
Agarwal MP, Giri S, Sharma V, Roy U, Gharsangi K. Dengue causing fulminant hepatitis in a hepatitis B virus carrier. Biosci Trends 2011;5:44-5.  Back to cited text no. 10
    




 

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