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LETTER TO EDITOR
Year : 2012  |  Volume : 60  |  Issue : 1  |  Page : 105-106

A fatal combo of dengue shock syndrome with acute subdural hematoma


Department of Medicine, CSMMU, Lucknow, India

Date of Submission07-Nov-2011
Date of Decision07-Nov-2011
Date of Acceptance18-Nov-2011
Date of Web Publication7-Mar-2012

Correspondence Address:
Nirdesh Jain
Department of Medicine, CSMMU, Lucknow
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.91383

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How to cite this article:
Jain N, Gutch M, Kumar V, Naik AK. A fatal combo of dengue shock syndrome with acute subdural hematoma. Neurol India 2012;60:105-6

How to cite this URL:
Jain N, Gutch M, Kumar V, Naik AK. A fatal combo of dengue shock syndrome with acute subdural hematoma. Neurol India [serial online] 2012 [cited 2019 Oct 19];60:105-6. Available from: http://www.neurologyindia.com/text.asp?2012/60/1/105/91383


Sir,

Approximately, 50-100 million cases of dengue infection occur each year throughout the world. [1] The overall mortality in dengue infection is 1-5% without treatment and less than 1% with adequate treatment; however, severe disease carries a mortality of 26%. [2],[3] Dengue shock syndrome (DSS) is the most serious presentation of dengue fever and is characterized by a large drop or absence of blood pressure. Dengue hemorrhagic fever (DHF) has a wide spectrum of bleeding manifestations including life-threatening hematemesis/melena, intracranial hemorrhages, or epidural spinal hemotoma. [4],[5] Neurological involvement in dengue is being frequently reported. [6] We report a rare case of DSS with spontaneous acute subdural hematoma (SDH).

A 22-year-old male was admitted with high-grade fever since 1 week and headache since 3 days and unconsciousness since 1 day. History of head trauma was absent. Past history revealed that he had had dengue fever last year for which hospital admission was not required and he had recovered within a week. On examination, the patient was cyanosed with cool extremities and blood pressure was not recordable. On abdominal examination, abdomen was distended; free fluid was present without having any organomegaly and bowel sounds were present. Neurological examination revealed no signs of meningeal irritations, a Glasgow Coma Scale (GCS) score of 4 (E1M2V1) and bilateral plantar reflex was non-elicitable. Investigations revealed hemoglobin 11.2 g/dl , hematocrit 44%, normal leukocyte count 7500/mm 3 , and platelet count 1.0 × 10 5 /mm 3 ; malaria antigen was negative by card test. However, dengue-specific IgM antibody was positive. Other investigations showed the following: serum bilirubin 1.7 mg/dl, serum glutamate oxaloacetate transaminase (SGOT) 120 IU/l (normal 9-45 IU/l), serum glutamate pyruvate transaminase (SGPT) 343 IU/l (normal 9-45 IU/l), prothrombin time 14.4 (normal 12-16) seconds and international normalized ratio (INR) 1.29 (0.8-1.2). Computed tomography (CT) scan brain showed massive left parietal acute SDH obliterating left lateral ventricle with midline shift [Figure 1]. Diagnosis of DSS was considered on clinical and investigational background. The patient was given fluid resuscitation and mechanical ventilation and, but the blood pressure was not picked up even after 3 hours of resuscitation. Subsequently, he was given vasopressor support. Next day, four units of platelets were transfused when his platelet count dropped to 52,000/mm 3 . Despite all life-saving measures, he died.
Figure 1: CT scan brain shows a crescent shaped extra-axial collection with increased attenuation with the effacement of the adjacent sulci and midline shift

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There was history of prior dengue infection and prior infection with heterogeneous serotypes contributes to more chances of having DHF/DSS through the production of non-protective antiviral antibodies that bind to Fc receptor of macrophages and monocytes, which may have an antibody-dependent enhancement phenomenon. [7] This results in increased cytokine production and activation of complement system, leading to increased vascular permeability, capillary fragility, and thrombocytopenia, and ultimately contributes to mortality. [8] This case further unravels the potentially fatal neurological complication of dengue infection. Therefore, a high index of suspicion needs to be maintained in patients with short duration of febrile illness with atypical neurological manifestations, especially in endemic areas of the disease.


 » Acknowledgement Top


We owe thanks to patient attendants for their cooperation and faith on us. We also like to give gratitude to our head of department for their constant support and encouragement.

 
 » References Top

1.WHO. World Health Organization Report of the Internal Consultation, 18-20 Oct 1999. Geneva: WHO; 2000.  Back to cited text no. 1
    
2.Ranjit S, Kissoon N. Dengue hemorrhagic fever and shock syndromes. Pediatr Crit Care Med 2011;12:90-100.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.WHO. Dengue Guidelines for Diagnosis, Treatment, Prevention and Control. 10-11. Geneva: WHO; 2009.  Back to cited text no. 3
    
4.Kumar J, Kumar A, Gupta S, Jain D. Dengue haemorrhagic fever: An unusual cause of intracranial haemorrhage. BMJ Case Rep 2009;2009:bcr.2006100909.  Back to cited text no. 4
    
5.Verma SP, Himanshu D, Tripathi A K, Vaish AK, Jain N. An atypical case of dengue haemorrhagic fever presenting as quadriparesis due to compressive myelopathy. BMJ Case Reports 2011.   Back to cited text no. 5
    
6.Murthy JM. Neurological complications of dengue infection. Neurol India 2010;58:581-4.  Back to cited text no. 6
[PUBMED]  Medknow Journal  
7.Halstead SB. Pathogenesis of dengue: Challenges to molecular biology. Science 1988;239:476-81.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Varatharaj A. Encephalitis in the clinical spectrum of dengue infection. Neurol India 2010;58:585-91  Back to cited text no. 8
    


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This article has been cited by
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[Pubmed] | [DOI]



 

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