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    <title>IMC Journal of Medical Science</title>
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                <title><![CDATA[A case of acute liver failure in dengue hemorrhagic fever]]></title>

                                    <author><![CDATA[Rama Biswas]]></author>
                                    <author><![CDATA[Kazi Ali Hasan]]></author>
                
                <link data-url="https://imcjms.com/registration/journal_full_text/63">
    https://imcjms.com/registration/journal_full_text/63
</link>
                <pubDate>Tue, 02 Aug 2016 11:48:11 +0000</pubDate>
                <category><![CDATA[Clinical Case Report]]></category>
                <comments><![CDATA[Ibrahim Med. Coll. J. 2013; 7(2): 41-42]]></comments>
                <description>Dengue is an arboviral disease endemic in many
parts of the world. The clinical presentation of dengue viral infection ranges
from asymptomatic illness to fatal dengue shock syndrome. Although, it is known
to cause hepatic involvement, it occasionally results in acute hepatic failure.
We report a case of dengue hemorrhagic fever presenting with acute liver
failure. The case recovered completely after treatment.
Introduction
&amp;nbsp;
A 35-year-old housewife came to the emergency
with the complaints of high grade fever with chills, myalgia for 4days and
severe abdominal pain with non-bilious vomiting for 2 days. There was no
history of bleeding from any site and she was not exposed to any hepatotoxic
drugs. There was no significant past medical or surgical history. On
examination, she was febrile, dehydrated and normotensive. Abdomen was
diffusely tender and chest examination revealed reduced air entry in right
infrascapular and infra-axillary area.
On the
following day, platelet count dropped to 8. 0x109/L and haematocrit level rose to 53%. There were petechial
hemorrhages and mild gum bleeding. By the next day, she became dyspnoic and her
level of consciousness deteriorated. Her pulse rate was 140/min, blood pressure
was 100/60 mm of Hg, respiratory rate was 44/min and Glasgow coma scale was
10/15. She became icteric and developed tender hepatomegaly and moderate
ascites. The platelet count rose to 38.0x109/L and haematocrit became 42% after one unit of apheretic platelet
was transfused. The liver function tests further deteriorated: serum bilirubin
3.2 mg/dL, ALT -2150 IU/L, AST – 3050 IU/L. Prothrombin time (PT) was 32
seconds against control of 13 seconds and activated partial thromboplastin time
(APTT) was 43.8 second (normal 13-25 seconds). Serum ammonia was 70 mmol/L and
serum lactate was 108 mg/dl. She was shifted to intensive care unit and intubated
due to severe metabolic acidosis with increased oxygen requirement. Antibodies
to hepatitis A, C, and E as well as hepatitis B surface antigen were negative.
Peripheral smear for malarial parasites were negative. Dengue NS1 antigen and
dengue IgM antibody against dengue virus were positive. Computed tomography of
brain showed diffuse cerebral edema. Based on the above findings, she was
diagnosed as a case of dengue hemorrhagic fever with hepatic encephalopathy.
&amp;nbsp;
Dengue infections are caused by a flavivirus
which has four serotypes (DEN1-4). It is the commonest arbovirus and a common
cause of hemorrhagic fever in the world. The virus is transmitted by mosquitoes
of Aedes genus, mainly Aedes aegypti. Dengue virus can infect
many cell types in the body to cause diverse clinical effects. Liver involvement
appears to occur more commonly with serotypes DEN3 and DEN4.5&amp;nbsp;Although liver is not the
main target organ, direct infection of hepatocytes and Kupffers cells by dengue
virus can be observed.6
An increase in liver transaminases is observed
in the first week of dengue infection mainly in dengue hemorrhagic fever rather
than in dengue fever. This can vary from 2-3folds to more than 10 fold rise
from normal level. AST raises more than ALT which is different from other types
of hepatitis.6&amp;nbsp;Similar
pattern was observed in our patient as well.
The management in such cases includes
supportive therapy in the form of adequate and cautious fluid replacement,
timely ventilator support, prophylactic antibiotic coverage, anticerebral edema
measures and continuous monitoring of neurological status. 
&amp;nbsp;
&amp;nbsp;
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haemmorhagic fever: diagnosis, treatment, prevention and control. 2nd&amp;nbsp;edn. World Health
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dengue infection. In: Gubler DJ, Kuno G (eds). Dengue and dengue hemorrhagic
fever. Washington: Cab International; 1997.
5.&amp;nbsp; Gasperino J, et al. Fulminant hepatic
failures secondary to hemorrhagic fever in an international traveler. Liver
Int. 2007; 27: 1148-51.
7.&amp;nbsp; Sirivichayakul C, Sabcharoen A,
Chanthavanich P, Pengsaa K, Chokejindachai W, Prarinyanupharb V: Dengue
infection with unusual manifestations: a case report. J Med Assoc Thai
2000; 83: 325-329.
9.&amp;nbsp;&amp;nbsp; Malavige GN, Ranatunga PK, Velathanthiri
VGNS, Fernando S,&amp;nbsp; Karunatilaka DH,&amp;nbsp; Aaskov J,&amp;nbsp;
Seneviratne SL. Patterns of disease in Sri Lankan dengue patients. Arch
Dis Child 2006; 91: 396-400.
10.&amp;nbsp;&amp;nbsp; de
Souza LJ, Alves JG, Nogueira RMR, Neto CG, Bastos DA, et al.
Aminotransferase changes and acute hepatitis in patients with dengue fever:
analysis of 1,585 cases, Braz J Infect Dis 2004; 8: 156-63.</description>

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