C A S E R E P O R T

* Assistant Professor, Department of Medicine, C. S. M. Medical University, Lucknow - 226 003, Uttar Pradesh,** Professor, *** Ex-Senior Resident, Department of Medicine, UCMS and GTB Hospital, Shahdara, Delhi - 110 095.

Dengue Shock Syndrome – An Unusual Manifestation

SC Chaudhary*, R Avasthi**, D Mohanty***

Abstract

Dengue fever is usually a self-limiting viral disease, manifesting with myalgia, headache, retroorbital pain, vomiting, maculopapularrashes, leukopenia, and thrombocytopenia. Dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS) are more severeforms of disease associated with complications in the form of haemorrhagic manifestations, hepatomegaly, and signs of impendingcirculatory failure. The major physiological abnormality differentiating dengue fever from DHF is plasma leakage syndrome(haemoconcentration, hypoproteinaemia and/or serous effusion), and severity of disease depends on the quantum of plasmaleakage. DHF/DSS are potentially fatal conditions. Here we report a case of dengue haemorrhagic fever grade III (DSS) to highlightthe importance of suspecting and initiating early treatment in severe forms of disease associated with complications (spontaneousbacterial peritonitis and myocarditis) to prevent fatal outcome.

Key words: Dengue haemorrhagic fever, dengue shock syndrome, spontaneous bacterial peritonitis, myocarditis, bradycardia.

JIACM 2010; 11(4): 309-11

Introduction

Dengue fever is an acute viral disease caused by four

different serotypes of dengue viruses. It is endemic in

India. Delhi and surrounding areas have been regularly

affected by dengue outbreaks for the last few years. The

common manifestations of fever, rash along with

thrombocytopenia and other laboratory investigations

are usually enough to make a diagnosis. Abdominal

involvement such as mild hepatitis, cholecystitis, and

ascites are common, but spontaneous bacterial peritonitis

(SBP)1 in DSS is uncommonly reported. We hereby report

a case of DSS who had SBP along with concomitant

evidence of myocarditis2,3.

Case report

A 13-year-old female referred from a private hospital,

admitted with high-grade continuous fever associated

with chills and rigors for four days. She also had

complaints of abdominal pain, nausea, frontal headache,

periorbital pain for the same duration, and facial

puffiness for two days. There was no history of rash,

bleeding from any site, chest pain, dyspnoea on exertion,

and decreased urine output. On examination, her general

condition was poor, blood pressure 88/70 mmHg, pulse

rate 58/min regular and respiratory rate was 18/min. She

was pale, febrile (103°F) and had bilateral pedal oedema.

Abdominal examination revealed diffuse tenderness,

hepatomegaly, and ascites. Respiratory system – bilateral

decreased air entry at bases (right > left). Cardiovascular

system – heart sounds were feeble and no added sound

or murmur was appreciated. Central nervous system

examination was normal.

Investigations revealed haemoglobin of 10.7 g/dl, total

leucocyte count 4,000/mm3 (polymorphs 78%,

lymphocytes 20%, monocytes 1%, eosinophils 1%),

platelet count 58,000/mm3 and haematocrit was 50%.

Tourniquet test was positive. Blood sugar, urine

examination and kidney function tests along with

electrolytes were normal. Peripheral smear for malarial

parasite and malarial antigen were negative. In liver

function test – total serum bilirubin was 1.6 mg/dl, serum

aspartate aminotransferase (SGOT) 124 U/l, serum alanine

aminotransferase (SGPT) 50 U/l, alkaline phosphatase 206

U/l and total serum protein was 5.1 g/dl (albumin 2.8 g/

dl, globulin 2.3 g/dl). Chest radiograph showed bilateral

pleural effusion (right > left). Ultrasound showed mild

hepatomegaly, acalculus cholecystitis, moderate ascites,

and bilateral pleural effusion. Ascitic fluid was turbid in

colour, total protein was 2.1 g/dl (albumin 1.1 g/dl), serum

ascites albumin gradiant (SAAG) 1.7 g/dl, glucose 108 mg/

dl, total leucocyte count 870 cells/mm3 with 70%

polymorphs. Acid-fast bacilli stain was negative, no

organism was found on Gram’s stain, and culture was

sterile. HBsAg and anti-HCV were negative. ELISA for HIV

was non-reactive. Blood culture was sterile and serum

amylase was normal. Electrocardiography showed T-wave

310 Journal, Indian Academy of Clinical Medicine Vol. 11, No. 4 October-December, 2010

inversion in lead II, III, aVF, and V1-V4 (Fig. 1). Cardiac

enzymes were elevated (creatine kinase-MB 86 ng/ml,

SGOT 124 U/l) and repeated arterial blood gas analysis

were normal without any evidence of acidosis.

Echocardiographic study was suggestive of global left

ventricular hypokinesia with ejection fraction of 46%.

Diagnosis of DSS associated with SBP and myocarditis

was made as the patient presented during an epidemic

of dengue fever in the National Capital Region. This

patient was treated with intravenous fluids and

antibiotics including ceftriaxone, amikacin, and

metronidazole. Her clinical condition showed gradual

improvement with stabilisation of vitals. Her platelet

counts, haematocrit, and cardiac rhythm were regularly

monitored during this period and became normal

steadily. The patient became afebrile after two to three

days, electrocardiographic changes reverted to normal

within a week of admission with gradual reduction in

ascites and pleural effusion over two weeks. Cardiac

enzymes and echocardiography repeated after two

weeks were normal. The blood sample sent on day seven

of fever was positive for IgM dengue assay (MAC-ELISA).

Discussion

This patient with DHF grade III (DSS) is interesting in view

of unusual clinical features in the form of SBP and

concomitant myocarditis, characterised by global T-wave

changes, elevated cardiac enzymes and

echocardiographic evidence of transient left ventricular

dysfunction, both resolving without any ill effect.

SBP has been occasionally reported, although

gastrointestinal symptoms such as acute hepatitis, acute

cholecystitis and vague abdominal pain are extremely

common. Other associated causes like acute pancreatitis,

appendicitis, enteritis, peptic ulcer disease, and gastric

erosion can also occur1. Gall bladder wall thickness has a

significant association with severity as well as progression

of the disease4. It has been suggested that aetiology of

abdominal pain should be aggressively looked into for

appropriate management.

Cardiac manifestations in dengue fever are benign,

transient, and resolve without long-term sequelae. They

have been attributed to subclinical viral myocarditis, but

the exact mechanism is not known. Bradycardia5 is the

commonest finding, although first and second degree AV

block, poor R wave progression, ST elevation and non-

specific ST-T wave changes, partial right bundle branch

block, and rarely atrial fibrillation, have been described.

Transient LV dysfunction has been shown in two-third of

the cases by using radionuclide ventriculography, but

myocardial necrosis is not seen6.

In patients with dengue shock syndrome due to increased

vascular permeability and hypovolaemia in addition to

significant volume expansion one must evaluate and treat

the accompanying complications.

References

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2. Wiwanitkit V. Dengue myocarditis, rare but not fatal

Fig. 1: ECG showing T-wave inversion in lead II, III, aVF, and V1-V4.

Journal, Indian Academy of Clinical Medicine Vol. 11, No. 4 October-December, 2010 311

manifestation. Int J Cardiol 2006; 112: 122.

3. Gulati S, Maheshwari A. Atypical manifestations of dengue.Trop Med Int Health 2007; 12: 1087-95.

4. Setiawan MW, Samsi TK, Pool TN et al. Gall bladder wallthickening in dengue haemorrhagic fever: anultrasonographic study. J Clin Ultrasound 1995; 23: 357-62.

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