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Acute Subdural Hematoma in a Patient with Dengue – Case Report and Review of Literature
Case Report
ACUTE SUBDURAL HEMATOMA IN A PATIENT WITH DENGUE – CASE REPORT AND REVIEW OF LITERATURE Shyam Sunder* and Rajendra Prasad** *Associate Consultant,**Senior Consultant, Department of Neurosurgery, Indraprastha Apollo Hospitals, Sarita Vihar, New Delhi 110 076,India. Correspondence to: Dr. Rajendra Prasad , 268/Sec15A, Noida 201301, India. e-mail: [email protected] Aim and Objective: Dengue fever is the most important arboviral infection in the world, with an estimated 100 million cases per year and 2.5 billion people at risk. Intra-cranial hemorrhage is a rare complication of dengue virus infection. We present a case report of a young male diagnosed to have dengue infection with low platelet count who presented to us with intracranial bleed.TheCTScan brain plain picture resembled that of an (Fig 1) intracerebral hematoma. He was worked up to look for other causes of intracerebral bleed,CT Angiogram donedid not suggest any feature of vascular malformation but the clot appeared to be extradural. (Fig 2 a,b). He underwent surgery and the clot was found to be subdural in location. He was transfused platelet on cell separator, pre and postoperatively. He showed neurological improvement after surgery and was discharged without any neurological squeale. We review the literature of neurological involvement in dengue fever. Clinical Presentation: A 29 years old, right handed male presented with fever of one week duration, headache, vomiting and altered sensorium since a day. On examination he had bradycardia, pulse56/min. Pupils were equal and reacting. He was opening eyes to call, producing incomprehensible sound and localizing briskly with right upper limb. He had left upper motor neuron facial palsy with left hemiparesis of grade 3. Left plantar was extensor in response. During investigation he was found to have thrombocytopenia. Dengue serology was reactive. His liver function was slightly deranged. He was evaluated with CT angiogram of brain showed right parietal extra-cerebral collection and ruled out the possibility of vascular malformation. Intervention: He underwent right parietal craniotomy and evacuation of the subdural hematoma. Conclusion: Intracranial hemorrhage is a rare complication of dengue fever. Other causes of encephalopathy are cerebral edema, hyponatremia, cerebral anoxia, fulminant hepatic failure with portosystemic encephalopathy, microcapillary hemorrhage. We report a rare case of acute subdural hematoma as a presenting feature of dengue fever. Key words: Dengue Fever, Acute Subdural Hematoma, Complications of Dengue
INTRODUCTION DENGUE fever also known as break bone fever, named by Dr. Benjamin Rush in Philadelphia, 1780; a reference to the symptom of aching joints. Other names given have been Dandy fever, Seven-day fever, Duengero - from the Spanish duengo and Ki denga pepo - Swahili: “it is a sudden overtaking by a spirit”. Outbreaks are occurring with[1,2] greater frequency in tropical countries with several epidemics in Delhi. This may be a result of increasing population density in cities, as well as other factors (such as open water storage for cities, irrigation canals, rain-filled tyres, and plastic bottles), which provide breeding grounds for mosquitoes and allow the mosquito population to flourish. Dengue, a flavivirus in the family 125
Arboviridae, has four known serotypes (varieties recognized as distinct by the immune system). The most severe form of the disease is dengue hemorrhagic fever, which is characterized by thrombocytopenia, bleeding, and shock. The hemorrhagic form continues to be the leading viral hemorrhagic fever in the world. The case fatality rate in patients with dengue shock syndrome can be as high as 44%. For decades, two distinct[1-4] hypotheses to explain the mechanism of dengue hemorrhagic fever(DHF) have been debated—secondary infection or viral virulence. However, a combination of both now seems to be the plausible explanation. Dengue has a second, natural host in monkeys and tree-hold breeding mosquitoes; but this natural forest cycle is not yet understood. The hemorrhagic dengue variant seems to be Apollo Medicine, Vol. 5, No. 2, June 2008
Case Report
Fig.1.
Preoperative CT Scan Brain showing right parietal intracranial hematoma
Fig.2(b). CT Angiogram of Brain did not show any vascular malformation.
Apparently, the antibodies attach to the virus’s outer envelope, then signal the larger macrophages. When a macrophage responds to the antibody signal and arrives on the viral scene, it engulfs the virus. However, the virus then takes control of the macrophage and replicates inside the macrophage instead of being destroyed by it. The virus is then carried throughout the body via the macrophage transports. Physical reactions triggered by this involvement of the immune system include fevers from 104-107ºF, convulsions, shock, and death. Symptoms are characterized by sudden onset of high fever, weakness and prostration, severe headaches, retro-orbital pain, joint and muscle pain (myalgia), nausea, vomiting, and rash. The fever rises rapidly to as high as 104ºF, and may be accompanied by bradycardia. The petechiae rash appears 3-4 days after the onset of fever, and usually appears on the trunk first, before spreading peripherally. Symptoms usually persist for 7 days, hence one of the common names for the disease: seven-day fever. Fig. 2(a). CT Angiogram of brain showing the clot with displaced vessels
able to replicate in the human body only in macrophages. It is possible that the virus-antibody interactions actually help hemorrhagic viral replication by promoting cell infection. This is via specific macrophage receptors-the Fc portion of the antibody molecule, or possibly via a protease-sensitive receptor. Apollo Medicine, Vol. 5, No. 2, June 2008
The symptoms of hemorrhagic dengue are initially indistinguishable from dengue fever, but progress to clouding of sensorium, shock, and systemic bleeding (gastrointestinal haemorrhage, etc.). The mortality rate for hemorrhagic dengue is 5% but can be as high as 45%[5,6]. Various atypical manifestations of dengue virus infection, including involvement of the central nervous system, cardiac disturbances and elevated levels of aminotransferases, with reactive hepatitis, have been
126
Case Report
reported during recent years. Encephalopathy is a rare complication of the dengue virus infection and may occur due to intracranial hemorrhage, cerebral edema, hyponatremia, cerebral anoxia, fulminant hepatic failure with portosystemic encephalopathy, microcapillary hemorrhage or release of toxic products.
three days was also positive. His liver function was slightly deranged, serum bilirubin- 1.35 mg/dL, SGOT-681U/L, SGPT-385U/L, ALP-206U/L and SGGPT-233U/L. CT angiogram brain ruled out the possibility of vascular malformation. (Fig. 2a,b)
Diagnosis is made by blood test for the presence of the virus or antibodies, or by serologic testing. Lab results may indicate that fibrinogen and clotting factors V, VII, IX, and X are reduced. Dengue does not produce long-term complications. This case report is unique because intracranial hemorrhage is a rare complication of dengue and only 4 case reports are their in literature.
His platelet count was corrected day before surgery(1,80000/cumm). He underwent craniotomy and evacuation of subdural hematoma. Post-operative CT scan brain done revealed complete evacuation of hematoma (Fig 3). During surgery no active bleeders were identified. His platelets were monitored daily. His liver function improved gradually. He was discharged on ninth postoperative day without any neurological sequelae.
CASE HISTORY
DISCUSSION
A 29 years young male presented with fever of one weeks duration, with headache, vomiting and altered sensorium for a day. On examination he had pulse-56/min. The pupils were equal and reacting. He was opening eyes to call, producing incomprehensible sound and localizing briskly with right upper limb. He had left upper motor neuron facial palsy with left hemiparesis of grade 3. Left plantar was extensor in response. During investigations he was found to have low platelet count of 77,000/cumm. Dengue serology was reactive(Pan Bio INDX), reactive sample value > 11 pan bio units. Repeat serology after
Dengue fever is a self-limiting but severe influenzalike illness. In southeast Asia, this is a disease predominantly of children and characterised by increased vascular permeability, plasma leakage, haemorrhagic manifestations, and thrombocytopenia. Epidemiological evidence suggests that DHF is most likely when infection with one dengue serotype is followed by a secondary infection with a different serotype. The relationship between hemorrhagic dengue fever (HDF) and neurological disturbances was first described in
Fig.3 Postoperative CT Scan Brain showing complete evacuation of hematoma. 127
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Case Report
1976, and since then several publications have added to the information available on this disease. Encephalopathy in HDF is an atypical manifestation and may appear in various forms, including depressed sensorium, convulsions, behavioral disorders, meningeal involvement and focal signs of the virus in the central nervous system. Pathophysiology of neurological involvement may include the following factors: direct tissue lesion caused by the virus, capillary hemorrhage, disseminated intravascular coagulation, metabolic disorder (hyponatremia and metabolic acidosis), fulminant hepatic failure and cerebral edema caused by the increase in vascular permeability. A combination of (a) biphasic pattern of fever, (b) hemoconcentration, (c) platelet count less than 50,000/ mm3 and (d) elevated ALT had a sensitivity of 79.2%, specificity of 64.7% with a positive predictive value of 70% and a negative predictive value of 75% in predicting spontaneous bleeding in dengue. Neurological findings reported in association with dengue include mononeuropathies, polyneuropathies, Guillain-Barré syndrome and transverse myelitis. Whilst few doubt that dengue infection can be associated with clouding of consciousness, until now it was not clear whether this represents CNS invasion by the virus, a nonspecific complication of severe dengue disease, or even coincident infection with another, unidentified arbovirus[5]. In one study 4% of patients with suspected CNS infections admitted to a referral centre were infected with dengue virus, although these accounted for only 1% of all dengue admissions to referral hospitals[7,8]. Complications of severe dengue implicated as possible causes of dengue encephalopathy include hypotension, cerebral oedema, microvascular or frank haemorrhage, hyponatraemia and fulminant hepatic failure-which may be part of a Reye-like syndrome. Liver function tests may be[1,5] abnormal in 90% of dengue infected patients. Intracranial haemorrhage[9] has been postulated as a cause of coma in dengue fever patients in addition to bleeding from other sites. Very few case report of intracranial [5] hemorrhage as a presenting feature of dengue has been described.
were similar to Japanese encephalitis. Many areas that are endemic for dengue viruses are also endemic for Japanese encephalitis virus. Antibodies to the two viruses are crossreactive, and encephalopathic patients with anti-flavivirus antibody in the CSF were assumed to have Japanese encephalitis. However diagnostic tests that separate these two viruses have now been adapted for field use, and neurological manifestations of dengue infection are likely to be recognised more often. In a study in Thailand, four of 44 patients with suspected Japanese encephalitis were shown to have dengue infection by IgM capture ELISA[11]. In a series of six cases of encephalopathy, Lum et al. [1996] identified the dengue virus in the cerebrospinal fluid of five patients using isolation techniques or PCR and hybridization in situ. The DENV-3 virus strain was isolated in four cases and serotype 2 (DENV-2) in one case, suggesting the neurovirulent property of dengue virus, particularly DENV-3, as one of the etiopathogenic factors responsible for affecting the nervous system[12]. A case report of pontine hemorrhage associated with HDF has been described[13]. We could not find any case report of spontaneous acute subdural hematoma associated with HDF. CONCLUSION Encephalopathy is a rare manifestation of HDF. It should, however, be investigated in endemic areas and during epidemics of dengue, since early diagnosis is essential for its management. Hemorrhagic complications and circulatory collapse are determinant factors in the prognosis and are the principal causes of death in these patients. Intracranial complications such as subdural and intracerebral hematomas should be kept in mind and should be investigated with CT-Scan brain in these endemic areas. REFERENCES
DEN-3 has been associated with neurological presentations most frequently.Whether this represents a higher transmission rate, easier isolation, or different virulence is not known[10]. The neurological manifestations of dengue infection Apollo Medicine, Vol. 5, No. 2, June 2008
128
1. Solomon T, Dung NM, Vaughn DW, et al. Neurological Manifestations of dengue infection. The Lancet 2000;355:1053-1059. 2. José G Rigau-Pérez, Gary G Clark, Duane J Gubler, Paul Reiter, Eduard J Sanders, A Vance Vorndam. Dengue and dengue haemorrhagic fever. The Lancet 1998; 352: 971-977. 3. Kho LK, Sumarmo H, Wulur EC, et al. Dengue Hemorrhagic Fever Accompanied by Encephalopathy in Jakarta. Southeast Asian J Trop Med Public Health 1981;12:83-86. 4. Thakare J, Walhecar B, Banerjee K. Hemorrhagic Manifestations and Encephalopathy in Cases of Dengue
Case Report in India. Southeast Asian J Trop Med Public Health 1996;27:471-475. 5. Pancharoen C, Thisyakorn U. Neurological Manifestations in Dengue Patients. Southeast Asian J Trop Med Public Health 2001;32:341-435. 6. Nogueira RMR, Filippis AMB, Coelho JMO, et al. Dengue virus infection of the central nervous systems (CNS): a case report from Brazil. South. Asian J Trop Med Public Health 2002;33: 68-71. 7. Miagostovich MP, Ramos RG, Nicol AF, et al. Retrospective study on dengue fatal cases. Clinical Neuropath 1997;16: 204-208. 8. Secretaria de Estado de Saúde do Rio de Janeiro (SES/ RJ). Quadro demonstrativo de casos notificados de dengue no estado do Rio de Janeiro de 1986-2002. Rio de Janeiro, Brasil; 2002.
9. Souza LJ, Alves GJ, Nogueira SA, et al. Aminotransferase and Acute Hepatitis in Patients with Dengue Fever: Analysis of 1,585 Cases. BJID 2004;8:156-163. 10. Lanciotti RS, Calisher CH, Gubler DJ, et al. Rapid detection and typing of dengue viruses from clinical samples by using reverse transcriptase-polymerase chain reaction. J Clin Microbiol 1992;30: 545-551. 11. Kuno G, Gomez I, Gubler DJ. Detecting artificial antidengue IgM immune complexes using an enzyme - linked immunosorbent assay. Am J Trop Med Hyg 1987;36:153159. 12. Lum LC, Lam SK, Choy YS, et al. Dengue Encephalitis: a True Entity? Am J Trop Med Hyg 1996;54:256-259. 13. Wafa SR, Jamsari S, Karis BM. A case report: intracranial haemorrhage in a patient with probable dengue fever. Med J Malaysia. 1999; 54(2): 273-276.
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ACUTE SUBDURAL HEMATOMA IN A PATIENT WITH DENGUE – CASE REPORT AND REVIEW OF LITERATURE Shyam Sunder* and Rajendra Prasad** *Associate Consultant,**Senior Consultant, Department of Neurosurgery, Indraprastha Apollo Hospitals, Sarita Vihar, New Delhi 110 076,India. Correspondence to: Dr. Rajendra Prasad , 268/Sec15A, Noida 201301, India. e-mail: [email protected] Aim and Objective: Dengue fever is the most important arboviral infection in the world, with an estimated 100 million cases per year and 2.5 billion people at risk. Intra-cranial hemorrhage is a rare complication of dengue virus infection. We present a case report of a young male diagnosed to have dengue infection with low platelet count who presented to us with intracranial bleed.TheCTScan brain plain picture resembled that of an (Fig 1) intracerebral hematoma. He was worked up to look for other causes of intracerebral bleed,CT Angiogram donedid not suggest any feature of vascular malformation but the clot appeared to be extradural. (Fig 2 a,b). He underwent surgery and the clot was found to be subdural in location. He was transfused platelet on cell separator, pre and postoperatively. He showed neurological improvement after surgery and was discharged without any neurological squeale. We review the literature of neurological involvement in dengue fever. Clinical Presentation: A 29 years old, right handed male presented with fever of one week duration, headache, vomiting and altered sensorium since a day. On examination he had bradycardia, pulse56/min. Pupils were equal and reacting. He was opening eyes to call, producing incomprehensible sound and localizing briskly with right upper limb. He had left upper motor neuron facial palsy with left hemiparesis of grade 3. Left plantar was extensor in response. During investigation he was found to have thrombocytopenia. Dengue serology was reactive. His liver function was slightly deranged. He was evaluated with CT angiogram of brain showed right parietal extra-cerebral collection and ruled out the possibility of vascular malformation. Intervention: He underwent right parietal craniotomy and evacuation of the subdural hematoma. Conclusion: Intracranial hemorrhage is a rare complication of dengue fever. Other causes of encephalopathy are cerebral edema, hyponatremia, cerebral anoxia, fulminant hepatic failure with portosystemic encephalopathy, microcapillary hemorrhage. We report a rare case of acute subdural hematoma as a presenting feature of dengue fever. Key words: Dengue Fever, Acute Subdural Hematoma, Complications of Dengue
INTRODUCTION DENGUE fever also known as break bone fever, named by Dr. Benjamin Rush in Philadelphia, 1780; a reference to the symptom of aching joints. Other names given have been Dandy fever, Seven-day fever, Duengero - from the Spanish duengo and Ki denga pepo - Swahili: “it is a sudden overtaking by a spirit”. Outbreaks are occurring with[1,2] greater frequency in tropical countries with several epidemics in Delhi. This may be a result of increasing population density in cities, as well as other factors (such as open water storage for cities, irrigation canals, rain-filled tyres, and plastic bottles), which provide breeding grounds for mosquitoes and allow the mosquito population to flourish. Dengue, a flavivirus in the family 125
Arboviridae, has four known serotypes (varieties recognized as distinct by the immune system). The most severe form of the disease is dengue hemorrhagic fever, which is characterized by thrombocytopenia, bleeding, and shock. The hemorrhagic form continues to be the leading viral hemorrhagic fever in the world. The case fatality rate in patients with dengue shock syndrome can be as high as 44%. For decades, two distinct[1-4] hypotheses to explain the mechanism of dengue hemorrhagic fever(DHF) have been debated—secondary infection or viral virulence. However, a combination of both now seems to be the plausible explanation. Dengue has a second, natural host in monkeys and tree-hold breeding mosquitoes; but this natural forest cycle is not yet understood. The hemorrhagic dengue variant seems to be Apollo Medicine, Vol. 5, No. 2, June 2008
Case Report
Fig.1.
Preoperative CT Scan Brain showing right parietal intracranial hematoma
Fig.2(b). CT Angiogram of Brain did not show any vascular malformation.
Apparently, the antibodies attach to the virus’s outer envelope, then signal the larger macrophages. When a macrophage responds to the antibody signal and arrives on the viral scene, it engulfs the virus. However, the virus then takes control of the macrophage and replicates inside the macrophage instead of being destroyed by it. The virus is then carried throughout the body via the macrophage transports. Physical reactions triggered by this involvement of the immune system include fevers from 104-107ºF, convulsions, shock, and death. Symptoms are characterized by sudden onset of high fever, weakness and prostration, severe headaches, retro-orbital pain, joint and muscle pain (myalgia), nausea, vomiting, and rash. The fever rises rapidly to as high as 104ºF, and may be accompanied by bradycardia. The petechiae rash appears 3-4 days after the onset of fever, and usually appears on the trunk first, before spreading peripherally. Symptoms usually persist for 7 days, hence one of the common names for the disease: seven-day fever. Fig. 2(a). CT Angiogram of brain showing the clot with displaced vessels
able to replicate in the human body only in macrophages. It is possible that the virus-antibody interactions actually help hemorrhagic viral replication by promoting cell infection. This is via specific macrophage receptors-the Fc portion of the antibody molecule, or possibly via a protease-sensitive receptor. Apollo Medicine, Vol. 5, No. 2, June 2008
The symptoms of hemorrhagic dengue are initially indistinguishable from dengue fever, but progress to clouding of sensorium, shock, and systemic bleeding (gastrointestinal haemorrhage, etc.). The mortality rate for hemorrhagic dengue is 5% but can be as high as 45%[5,6]. Various atypical manifestations of dengue virus infection, including involvement of the central nervous system, cardiac disturbances and elevated levels of aminotransferases, with reactive hepatitis, have been
126
Case Report
reported during recent years. Encephalopathy is a rare complication of the dengue virus infection and may occur due to intracranial hemorrhage, cerebral edema, hyponatremia, cerebral anoxia, fulminant hepatic failure with portosystemic encephalopathy, microcapillary hemorrhage or release of toxic products.
three days was also positive. His liver function was slightly deranged, serum bilirubin- 1.35 mg/dL, SGOT-681U/L, SGPT-385U/L, ALP-206U/L and SGGPT-233U/L. CT angiogram brain ruled out the possibility of vascular malformation. (Fig. 2a,b)
Diagnosis is made by blood test for the presence of the virus or antibodies, or by serologic testing. Lab results may indicate that fibrinogen and clotting factors V, VII, IX, and X are reduced. Dengue does not produce long-term complications. This case report is unique because intracranial hemorrhage is a rare complication of dengue and only 4 case reports are their in literature.
His platelet count was corrected day before surgery(1,80000/cumm). He underwent craniotomy and evacuation of subdural hematoma. Post-operative CT scan brain done revealed complete evacuation of hematoma (Fig 3). During surgery no active bleeders were identified. His platelets were monitored daily. His liver function improved gradually. He was discharged on ninth postoperative day without any neurological sequelae.
CASE HISTORY
DISCUSSION
A 29 years young male presented with fever of one weeks duration, with headache, vomiting and altered sensorium for a day. On examination he had pulse-56/min. The pupils were equal and reacting. He was opening eyes to call, producing incomprehensible sound and localizing briskly with right upper limb. He had left upper motor neuron facial palsy with left hemiparesis of grade 3. Left plantar was extensor in response. During investigations he was found to have low platelet count of 77,000/cumm. Dengue serology was reactive(Pan Bio INDX), reactive sample value > 11 pan bio units. Repeat serology after
Dengue fever is a self-limiting but severe influenzalike illness. In southeast Asia, this is a disease predominantly of children and characterised by increased vascular permeability, plasma leakage, haemorrhagic manifestations, and thrombocytopenia. Epidemiological evidence suggests that DHF is most likely when infection with one dengue serotype is followed by a secondary infection with a different serotype. The relationship between hemorrhagic dengue fever (HDF) and neurological disturbances was first described in
Fig.3 Postoperative CT Scan Brain showing complete evacuation of hematoma. 127
Apollo Medicine, Vol. 5, No. 2, June 2008
Case Report
1976, and since then several publications have added to the information available on this disease. Encephalopathy in HDF is an atypical manifestation and may appear in various forms, including depressed sensorium, convulsions, behavioral disorders, meningeal involvement and focal signs of the virus in the central nervous system. Pathophysiology of neurological involvement may include the following factors: direct tissue lesion caused by the virus, capillary hemorrhage, disseminated intravascular coagulation, metabolic disorder (hyponatremia and metabolic acidosis), fulminant hepatic failure and cerebral edema caused by the increase in vascular permeability. A combination of (a) biphasic pattern of fever, (b) hemoconcentration, (c) platelet count less than 50,000/ mm3 and (d) elevated ALT had a sensitivity of 79.2%, specificity of 64.7% with a positive predictive value of 70% and a negative predictive value of 75% in predicting spontaneous bleeding in dengue. Neurological findings reported in association with dengue include mononeuropathies, polyneuropathies, Guillain-Barré syndrome and transverse myelitis. Whilst few doubt that dengue infection can be associated with clouding of consciousness, until now it was not clear whether this represents CNS invasion by the virus, a nonspecific complication of severe dengue disease, or even coincident infection with another, unidentified arbovirus[5]. In one study 4% of patients with suspected CNS infections admitted to a referral centre were infected with dengue virus, although these accounted for only 1% of all dengue admissions to referral hospitals[7,8]. Complications of severe dengue implicated as possible causes of dengue encephalopathy include hypotension, cerebral oedema, microvascular or frank haemorrhage, hyponatraemia and fulminant hepatic failure-which may be part of a Reye-like syndrome. Liver function tests may be[1,5] abnormal in 90% of dengue infected patients. Intracranial haemorrhage[9] has been postulated as a cause of coma in dengue fever patients in addition to bleeding from other sites. Very few case report of intracranial [5] hemorrhage as a presenting feature of dengue has been described.
were similar to Japanese encephalitis. Many areas that are endemic for dengue viruses are also endemic for Japanese encephalitis virus. Antibodies to the two viruses are crossreactive, and encephalopathic patients with anti-flavivirus antibody in the CSF were assumed to have Japanese encephalitis. However diagnostic tests that separate these two viruses have now been adapted for field use, and neurological manifestations of dengue infection are likely to be recognised more often. In a study in Thailand, four of 44 patients with suspected Japanese encephalitis were shown to have dengue infection by IgM capture ELISA[11]. In a series of six cases of encephalopathy, Lum et al. [1996] identified the dengue virus in the cerebrospinal fluid of five patients using isolation techniques or PCR and hybridization in situ. The DENV-3 virus strain was isolated in four cases and serotype 2 (DENV-2) in one case, suggesting the neurovirulent property of dengue virus, particularly DENV-3, as one of the etiopathogenic factors responsible for affecting the nervous system[12]. A case report of pontine hemorrhage associated with HDF has been described[13]. We could not find any case report of spontaneous acute subdural hematoma associated with HDF. CONCLUSION Encephalopathy is a rare manifestation of HDF. It should, however, be investigated in endemic areas and during epidemics of dengue, since early diagnosis is essential for its management. Hemorrhagic complications and circulatory collapse are determinant factors in the prognosis and are the principal causes of death in these patients. Intracranial complications such as subdural and intracerebral hematomas should be kept in mind and should be investigated with CT-Scan brain in these endemic areas. REFERENCES
DEN-3 has been associated with neurological presentations most frequently.Whether this represents a higher transmission rate, easier isolation, or different virulence is not known[10]. The neurological manifestations of dengue infection Apollo Medicine, Vol. 5, No. 2, June 2008
128
1. Solomon T, Dung NM, Vaughn DW, et al. Neurological Manifestations of dengue infection. The Lancet 2000;355:1053-1059. 2. José G Rigau-Pérez, Gary G Clark, Duane J Gubler, Paul Reiter, Eduard J Sanders, A Vance Vorndam. Dengue and dengue haemorrhagic fever. The Lancet 1998; 352: 971-977. 3. Kho LK, Sumarmo H, Wulur EC, et al. Dengue Hemorrhagic Fever Accompanied by Encephalopathy in Jakarta. Southeast Asian J Trop Med Public Health 1981;12:83-86. 4. Thakare J, Walhecar B, Banerjee K. Hemorrhagic Manifestations and Encephalopathy in Cases of Dengue
Case Report in India. Southeast Asian J Trop Med Public Health 1996;27:471-475. 5. Pancharoen C, Thisyakorn U. Neurological Manifestations in Dengue Patients. Southeast Asian J Trop Med Public Health 2001;32:341-435. 6. Nogueira RMR, Filippis AMB, Coelho JMO, et al. Dengue virus infection of the central nervous systems (CNS): a case report from Brazil. South. Asian J Trop Med Public Health 2002;33: 68-71. 7. Miagostovich MP, Ramos RG, Nicol AF, et al. Retrospective study on dengue fatal cases. Clinical Neuropath 1997;16: 204-208. 8. Secretaria de Estado de Saúde do Rio de Janeiro (SES/ RJ). Quadro demonstrativo de casos notificados de dengue no estado do Rio de Janeiro de 1986-2002. Rio de Janeiro, Brasil; 2002.
9. Souza LJ, Alves GJ, Nogueira SA, et al. Aminotransferase and Acute Hepatitis in Patients with Dengue Fever: Analysis of 1,585 Cases. BJID 2004;8:156-163. 10. Lanciotti RS, Calisher CH, Gubler DJ, et al. Rapid detection and typing of dengue viruses from clinical samples by using reverse transcriptase-polymerase chain reaction. J Clin Microbiol 1992;30: 545-551. 11. Kuno G, Gomez I, Gubler DJ. Detecting artificial antidengue IgM immune complexes using an enzyme - linked immunosorbent assay. Am J Trop Med Hyg 1987;36:153159. 12. Lum LC, Lam SK, Choy YS, et al. Dengue Encephalitis: a True Entity? Am J Trop Med Hyg 1996;54:256-259. 13. Wafa SR, Jamsari S, Karis BM. A case report: intracranial haemorrhage in a patient with probable dengue fever. Med J Malaysia. 1999; 54(2): 273-276.
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