Cases reported "Shock, Hemorrhagic"

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1/9. Hemorrhagic shock and encephalopathy syndrome: neurologic features.

    Hemorrhagic shock and encephalopathy syndrome (HSES) is a severe disease that affects previously healthy infants of less than 1 year of age and is associated with significant mortality and neurologic morbidity. It is characterized by sudden onset of shock, convulsions and coma, bleeding due to severe coagulopathy, fever, diarrhea, metabolic acidosis, and hepatorenal dysfunction. central nervous system involvement with recurrent seizures and brain edema is the most common cause of high mortality and neurological morbidity. In this report, we describe four patients of HSES and review the initial and follow-up neurological features, electroencephalography findings, and the results of neuroradiological examinations of this catastrophic illness.
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2/9. Hemorrhagic shock and encephalopathy syndrome: Report of two cases.

    Two young children with a history of diarrhea, for one and two days respectively, were admitted to our hospital due to high fever and conscious disturbance. disseminated intravascular coagulation, abnormal hepatic and renal functions, and metabolic acidosis were noted as well. Both patients developed shock soon after arrival and expired within one day after admission. Their serum ammonia levels were normal, and their blood and cerebrospinal fluid cultures also brought negative results. Hemorrhagic shock and encephalopathy syndrome was diagnosed by their clinical manifestation and laboratory data. We also discussed their related problems.
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3/9. Haemorrhagic shock and encephalopathy.

    Two infants are described with a fulminant disorder characterised by profound circulatory collaps and shock, generalised convulsions and unremitting coma, bleeding due to severe DIC, fever, diarrhoea, metabolic acidosis and renal and hepatic failure. Both infants died shortly after onset of the symptoms. autopsy mainly revealed haemorrhages in different organs, anoxaemic lesions in the brain and a normal structure of liver and pancreas. No causative agent could be demonstrated. We believe that both patients suffered from haemorrhagic shock and encephalopathy, a mostly fatal disorder which has recently been described. Although the clinical and biochemical features are very distinctive, this syndrome is probably heterogeneous and its differentiation from some other disorders may be difficult. Its pathogenesis is unknown but there are some indications that intravascular activity of trypsin may play a role. During a study of the two families we obtained abnormal results of immunologic tests in most members: the interpretation of this finding remains conjectural. Haemorrhagic shock and encephalopathy may occur more frequently than the restricted literature on this subject suggests. Future studies will have to deal with the question of identity and pathogenesis.
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4/9. Epidemic hemorrhagic fever in Hubei Province, The People's Republic of china: a clinical and serological study.

    Between July 1975 and April 1980, 71 patients were admitted to the Second Attached Hospital of Hubei Provincial Medical College in Wuchang with the diagnosis of epidemic hemorrhagic fever (EHF). The clinical course among these patients was similar to that described for patients with Korean hemorrhagic fever, and hemorrhagic fever with renal syndrome of the U.S.S.R. The overall mortality was 11.2 percent. Sera obtained from some of these patients as well as from patients admitted to the First Attached Hospital of Hubei Provincial Medical College were tested against an antigen associated with Korean hemorrhagic fever and showed exceedingly high antibody titers. We conclude that EHF in Central china represents the same or a closely related disease process as Korean hemorrhagic fever.
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5/9. Haemorrhagic shock and encephalopathy: a new syndrome with a high mortality in young children.

    In the past year, ten infants have been admitted to hospital with a new or previously unrecognised disorder, characterised by an acute onset of encephalopathy, fever, shock, watery diarrhoea, severe disseminated intravascular coagulation, and renal and hepatic dysfunction. Seven of the infants died. No specific causative agent has been identified, but preliminary studies suggest that the pathophysiology of the disease may involve release of proteolytic enzymes (such as trypsin) into the circulation, with destruction of the microcirculation.
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6/9. dengue fever in the united states. A report of a cluster of imported cases and review of the clinical, epidemiologic, and public health aspects of the disease.

    In the united states during 1981, fourteen state health departments reported a total of 44 imported cases of dengue fever. Most originated in the Caribbean, where dengue type 4 has reached pandemic proportions. Because the mosquito vector for dengue is abundant throughout the southeast and imported cases continue to occur, the possibility exists for indigenous dengue transmission. We report a cluster of imported dengue type 1 cases in florida, discuss the clinical, epidemiologic, and public health aspects of the disease, and make recommendations as to how clinicians can assist public health officials in minimizing the risk of indigenous dengue transmission in the united states.
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7/9. Extensive white matter involvement in hemorrhagic shock and encephalopathy syndrome.

    Reported is a case of hemorrhagic shock and encephalopathy syndrome (HSE) with extensive white matter involvement. A three year old, previously healthy boy was presented with an acute onset of fever, loss of consciousness and convulsions. He had disseminated intravascular coagulation, metabolic acidosis, non-ketotic hypoglycemia and hepatorenal dysfunction. The computed tomography (CT) scan of his head on the second day of illness demonstrated symmetric, extensive low-density areas in the cerebral and cerebellar white matter. The child died on the 13th hospital day. A post-mortem histopathological examination of the liver revealed centrilobular necrosis and infiltration of fatty acid droplets. The concentrations of serum 2',5'-oligoadenylate synthetase and urinary neopterin were markedly elevated, indicating excessively activated cell-mediated immunity. This overproduction of inflammatory cytokines might play an important role in the pathogenesis of the brain lesion as well as in other clinical and laboratory manifestations. The patient had a decreased serum level of alpha l-antitrypsin, which may have been associated with the development of uncontrolled inflammation and coagulation disorder.
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8/9. Hemorrhagic shock and encephalopathy syndrome. An unusual cause of sudden death in children.

    Hemorrhagic shock and encephalopathy syndrome (HSES) is a sudden-onset symptom complex occurring in previously healthy infants and children. It was first described in 1983 in the United Kingdom in 10 infants. Subsequently, > 140 cases have been reported worldwide, although no cases have been previously reported in the forensic literature. Typically the child presents with fever, shock, encephalopathy with coma and seizures, evidence of hemorrhage, and diarrhea. Laboratory investigation reveals falling hemoglobin and platelet counts, renal impairment, evidence of disseminated intravascular coagulation, metabolic acidosis, and raised serum transaminases. Microbiological cultures are uniformly negative. The condition has a high mortality and morbidity. The etiology is unknown and may be multifactorial. However, hyperpyrexia appears to play a central role in pathogenesis. The diagnosis of HSES in the deceased child is one of exclusion and requires a careful antemortem history as well as a thorough autopsy with toxicological and microbiological investigations. A case of HSES is reported and the literature reviewed.
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9/9. Toxic shock syndrome without rash in a young child: link with syndrome of hemorrhagic shock and encephalopathy?

    A diffuse macular erythroderma and subsequent desquamation after 1 to 2 weeks are two of the five major diagnostic criteria of toxic shock syndrome (TSS). We present the case of a 15-month-old girl with TSS, but without erythroderma or desquamation. She was admitted with high fever, shock, and multiorgan involvement. Minimal or no cutaneous signs were present. Initially the diagnosis of the syndrome of hemorrhagic shock and encephalopathy was made. After 7 days, a TSS toxin 1-producing strain of staphylococcus aureus was cultured from an inguinal lymph node, where inflammation had already been noticed on admission. Moreover, the girl had no antibodies against this toxin. The serum cytokine profile during the acute phase of her illness showed high levels of tumor necrosis factor-alpha, interleukin-6 and interferon-gamma, as is seen during activation of the immune system by TSS toxin 1. Other possible causes for the patient's illness were excluded. We conclude that the patient had TSS without rash. Without the evidence implicating a TSS toxin 1-producing strain of S. aureus as the cause of her disease, a diagnosis of syndrome of hemorrhagic shock and encephalopathy would have been made. It is possible that some cases of syndrome of hemorrhagic shock and encephalopathy represent a variant of TSS in small children.
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