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LETTER TO EDITOR |
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Year : 2012 | Volume
: 60
| Issue : 1 | Page : 105-106 |
A fatal combo of dengue shock syndrome with acute subdural hematoma
Nirdesh Jain, Manish Gutch, Vivek Kumar, Ajit K Naik
Department of Medicine, CSMMU, Lucknow, India
Date of Submission | 07-Nov-2011 |
Date of Decision | 07-Nov-2011 |
Date of Acceptance | 18-Nov-2011 |
Date of Web Publication | 7-Mar-2012 |
Correspondence Address: Nirdesh Jain Department of Medicine, CSMMU, Lucknow India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.91383
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 |
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 | |  |
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 | |  |
1. | WHO. World Health Organization Report of the Internal Consultation, 18-20 Oct 1999. Geneva: WHO; 2000.  |
2. | Ranjit S, Kissoon N. Dengue hemorrhagic fever and shock syndromes. Pediatr Crit Care Med 2011;12:90-100.  [PUBMED] [FULLTEXT] |
3. | WHO. Dengue Guidelines for Diagnosis, Treatment, Prevention and Control. 10-11. Geneva: WHO; 2009.  |
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.  |
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.  |
6. | Murthy JM. Neurological complications of dengue infection. Neurol India 2010;58:581-4.  [PUBMED] |
7. | Halstead SB. Pathogenesis of dengue: Challenges to molecular biology. Science 1988;239:476-81.  [PUBMED] [FULLTEXT] |
8. | Varatharaj A. Encephalitis in the clinical spectrum of dengue infection. Neurol India 2010;58:585-91  |
[Figure 1]
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