Hemorrhagic Encephalopathy Research Articles

Research progress of hemorrhagic shock and encephalopathy syndrome

Hemorrhagic shock and encephalopathy syndrome (HSES)is a devastating disease in infants which was first proposed by Levin in 1983.The main clinical manifestations of HSES are associated with acute onset of high fever, diarrhea, rapidly followed by convulsions, unconsciousness, bleeding tendency, shock and multiorgan dysfunction.The pathological manifestations include punctate bleeding, necrosis or inflammatory changes in multiple organs.The etiology of this syndrome is unknown, and the prognosis is poor.Despite intensive treatment, the fatality rate is still high and the survival is often associated with severe neurological sequelae.At present, there is no effective treatment for this disease, and mainly early symptomatic and supportive treatment can be obtained. Key words: Hemorrhagic shock and encephalopathy syndrome; Research progress; Child

Neurological complications of alcoholism

Nervous system lesions associated with chronic alcohol intoxication are common in clinical practice. They lead to aggravated alcoholic disease, its more frequent recurrences, and intensified pathological craving for alcohol. Neurological pathology in turn occurs with frequent exacerbations. The interaction of diseases, age, and medical pathomorphism modifies the clinical presentation and course of the major pathology, as well as comorbidity, the nature and severity of complications, worsens quality of life in a patient, and makes the diagnostic and treatment process difficult. The paper discusses the classification, clinical variants, biochemical and molecular biological aspects of various complications of alcoholic disease. It considers its most common form, in particular alcoholic polyneuropathy, as well as its rarer variants, such as hemorrhagic encephalopathy with a subacute course (Gayet–Wernicke encephalopathy).

Severe myocardial injury in an infant with hemorrhagic shock and encephalopathy syndrome

Hemorrhagic shock and encephalopathy syndrome is a severe disease that affects previously healthy infants and associated with significant mortality and neurologic morbidity. It is characterized by sudden onset of shock, convulsion and coma, bleeding due to severe coagulopathy, fever, diarrhea, metabolic acidosis, and hepatorenal dysfunction. We report a 3-month-old boy with hemorrhagic shock and encephalopathy syndrome, who had clinical and laboratory findings consistent with myocardial injury. Severe myocardial injury was demonstrated by elevation of cardaic troponin I and MB fraction of total kinase in this patient.

Acute hemorrhagic encephalopathy - diagnostic challenges in a pediatric case

Background Acute hemorrhagic encephalomyelitis (AHEM) is considered a rare form of Acute disseminated encephalomyelitis (ADEM), due to acute cerebral vasculitis. The symptomatology consists in similar neurological findings, (meningismus, headache, seizures, multifocal neurologic signs, asymmetrical neurological deficits and coma) with rapid onset of encephalopathy and biphasic evolution. Although previous respiratory disease was registered days before this condition, establishing etiology is quite a challenge, viruses being incriminated.

The Protective Effect of Glibenclamide in a Model of Hemorrhagic Encephalopathy of Prematurity

We studied a model of hemorrhagic encephalopathy of prematurity (EP) that closely recapitulates findings in humans with hemorrhagic EP. This model involves tandem insults of 20 min intrauterine ischemia (IUI) plus an episode of elevated venous pressure induced by intraperitoneal glycerol on post-natal day (P) 0. We examined Sur1 expression, which is upregulated after focal ischemia but has not been studied after brief global ischemia including IUI. We found that 20 min IUI resulted in robust upregulation of Sur1 in periventricular microvessels and tissues. We studied tandem insult pups from untreated or vehicle-treated dams (TI-CTR), and tandem insult pups from dams administered a low-dose, non-hypoglycemogenic infusion of the Sur1 blocker, glibenclamide, for 1 week after IUI (TI-GLIB). Compared to pups from the TI-CTR group, pups from the TI-GLIB group had significantly fewer and less severe hemorrhages on P1, performed significantly better on the beam walk and accelerating Rotarod on P35 and in tests of thigmotaxis and rapid learning on P35–49, and had significantly greater body and brain weights at P52. We conclude that low-dose glibenclamide administered to the mother at the end of pregnancy protects pups subjected to IUI from post-natal events of elevated venous pressure and its consequences.

The application values of cerebrospinal fluid cytological examination by slide centrifugation for diagnosis of central nervous system infectious diseases

According to the analysis of cerebrospnial fluid (CSF) cytological examination (by slide centrifugation) results of 15 940 central nervous system infectious cases, this cytologic examination method shows definite diagnostic values as follows: 1) better etiological diagnostic value for central nervous system infectious diseases, such as purulent, viral, tuberculous, fungus and parasitic encephalitis meningitis and meningoencephalitis; 2) better differential diagnostic value for acute infectious toxic encephalopathy, meningeal carcinomatosis and central nervous system non infectious diseases such as tumorous, leukemic and hemorrhagic meningoencephalitis and encephalopathy; 3) better clinical value for severity monitoring and prognostic judgement of central nervous system infectious diseases.

An Unusual Cause of Confusion: Hepatic Encephalopathy in Hereditary Haemorrhagic Telangectasia

This case report describes a 73 year old lady with a known Hereditary Haemorrhagic Encephalopathy (HHT) who presented with confusion. She had several previous self-limiting episodes over 3 months. She had known hepatic arterio-venous (AV) malformations. A urinary tract infection was detected and thought to be the cause of her confusion. However despite targeted antibiotic treatment her neurological state worsened (GCS 10/15) and she developed hepatic asterixis. Hepatic encephalopathy was confirmed with diagnostic EEG and elevated ammonia 211umol/l (

Sudden Reversible Painless Binocular Vision Loss - A New Cause: Case Report and Review of Literature (P06.256)

Objective: To describe a case of isolated cortical blindness due to Hemorrhagic Posterior Reversible Encephalopathy Syndrome (HPRES) and review of literature. Background PRES is characterized by a variety of symptoms including headache, altered mental status, vision loss and seizures. Vasogenic edema is the characteristic radiological finding, hemorrahge is rare.Isolated cortical blindness due to HPRES has not been previously reported. Design/Methods: Case report and review of literature. Results: A 55- year- old white male was brought to the emergency department after he woke up with complete blindnessand mild headache His vitals inlcuded BP of 220/110 mm Hg, HR 80 and RR 12 and afebrile.His examination revealed complete blindness with no light perception but normal light reaction. The fundoscopy was normal. Rest of the neurological examiantion incliding higher mental function, cranial nerves, speech, strength and gait were normal. The Noncontrast CT head revealed intraparenchymal hemorrhage over bilateral occipital lobe with massive edema. MRI brain revealed occipial hematoma with vasogenic edema, no diffusion restriction. MR angiogram and venogram of brain were normal.His laboratory works included normal drug screen, vasculitic panel, PT/aPTT/INR. His vision started improving in 48 hours with significant recovery in 3 weeks ( 20/60) with resolution of hematoma on MRI. Conclusions: Isolated cortical blindness is a rare clinical presentation of Hemorrhagic PRES.It is important to recognize this condition given good prognosis. The most common postulates is endothelial cell dysfunction leading to blood-brain barrier leakage, with resultant cortical and subcortical vasogenic edema. Potential etiologic factors include eclampsia, or other causes, such as conditioning regimens before transplantation, effects of graft-versus-host disease, or the results of the immunosuppressive drugs cyclosporine and tacrolimus. Our patient did not had any of these factors. Studies have demonstrated that the incidence of parenchymal or sulcal Subarachnoid hemorrhage in PRES is around 5-17%. Exact pathophysiology is unknown. Disclosure: Dr. Bollu has nothing to disclose. Dr. Lim has nothing to disclose. Dr. Uppal has nothing to disclose. Dr. Singh has nothing to disclose.

Central nervous system pathology in fatal swine-origin influenza A H1N1 virus infection in patients with and without neurological symptoms: an autopsy study of 15 cases

The first influenza pandemic of the twenty-first century was caused by a swine-origin, influenza A (H1N1) virus that contained genes from human, swine, and avian influenza A viruses [4]. It has long been recognized that a small subset of influenza patients develops neurologic complications [1]. Central nervous system (CNS) pathology in influenza virus infection is thought to be indirect and multifactorial [15] and whether H1N1 infects the brain or cerebrospinal fluid (CSF) remains controversial [2]. The current model is that H1N1 triggers a cytokine storm that disrupts the blood–brain barrier and activates glial cells. Subsequent disseminated intravascular coagulation (DIC) and liver and renal dysfunction triggered by hypercytokinemia may also contribute to CNS damage [15]. A number of clinical syndromes affecting the CNS have been described in the context of influenza infection. Although these syndromes have overlapping features and can be caused by other viruses and toxic agents, they have specific clinical, radiological, and laboratory criteria for their diagnosis and the pathogenesis and predisposing factors differ. Classical Reye’s syndrome is a non-inflammatory encephalopathy with associated hepatic microvesicular fatty change and hyperammonemia, and is usually precipitated by the use of salicylates [5]. Reye’slike syndrome occurs at a younger age and does not have the microvesicular fatty change and mitochondrial abnormality of classical Reye’s syndrome [13] and it is not associated with salicylate use. Hemorrhagic shock and encephalopathy syndrome (HSES) occurs in infants, and there is associated fever, shock, DIC, hepatic and renal dysfunction, and the brain shows edema with occasional intracranial hemorrhage [3]. Acute necrotizing encephalopathy (ANE) was first described in Japan in 1995 [8], and then subsequently in other countries [7, 16]. MRI and autopsy studies show bilateral symmetrical infarcts in the thalamus, basal ganglia, cerebellar and cerebral white matter, and brainstem tegmentum. CSF protein is typically elevated and the mortality rate is high. Some infants have complex febrile seizures at the onset, followed by delayed involvement of bilateral frontal lobes or the entire cerebral hemisphere [12]. Recently, familial and recurrent ANE has been described and is associated with mutation in the Ranbinding protein gene (RANBP2) [10]. Like earlier influenza pandemics, the recent pandemic of novel influenza A (H1N1) infection has resulted in a number of cases with neurological complications [2, 7, 16]. The purpose of the present study was to document the changes present in the brains of fatal H1N1 virus patients to determine if cases without documented neurologic A. Mukherjee and J.E.G. Peterson contributed equally to this work.

Encefalopatia hemorrágica hipernatrêmica: relato de caso e revisão da literatura

Hypernatremia is a common electrolyte disorder in people with impaired thirst control mechanism or access to water, and may lead from minimal disorders until coma. Among the hypernatremia morbidities, central nervous system hemorrhage is uncommon and poorly studied. We report a case involving a patient admitted to the intensive care unit with reduced consciousness level, hypernatremia and head computed tomography scan showing bilateral parenchyma hemorrhage. A literature review of hypernatremia hemorrhagic encephalopathy was conducted.

Serial Diffusion-Weighted MRI in Hemorrhagic Shock and Encephalopathy Syndrome

This report presents a case of hemorrhagic shock and encephalopathy syndrome. In the acute stage, brain magnetic resonance imaging demonstrated symmetrical hyperintensity on diffusion-weighted images and hypointensity on the apparent diffusion coefficient maps in the subcortical white matter. Whereas the abnormal diffusion-weighted imaging signals of the white matter resolved in the subacute stage, the adjacent gray matter became hyperintense on diffusion-weighted images and hypointense on apparent diffusion coefficient maps. The evolution of diffusion-weighted imaging signals is thus considered to be one of the early findings in hemorrhagic shock and encephalopathy syndrome.

Hemorrhagic encephalopathy in dengue shock syndrome: a case report

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. Encephalopathy is a rare complication of dengue virus infection and may occur as a consequence of intracranial hemorrhage, cerebral edema, hyponatremia, cerebral anoxia, fulminant hepatic failure with portosystemic encephalopathy, microcapillary hemorrhage or release of toxic products. We report a rare case of hemorrhagic encephalopathy in dengue shock syndrome caused by type 3 dengue virus.

Chemokine expression during mouse adenovirus type 1 induced hemorrhagic encephalopathy

Chemokine expression during mouse adenovirus type 1 induced hemorrhagic encephalopathy

Fever, heatstroke, and hemorrhagic shock and encephalopathy.

Fever, heatstroke, and hemorrhagic shock and encephalopathy.

Hemorrhagic Shock and Infantile Encephalopathy

The clinical characteristics, treatment and possible causes of hemorrhagic shock and encephalopathy in infants are described and a 5-month-old patient is reported from the Section of Neurology, The Children’s Mercy Hospital, Kansas City, MO.

Abnormal Magnetic Resonance Images in Hemorrhagic Shock and Encephalopathy Syndrome

Abnormal Magnetic Resonance Images in Hemorrhagic Shock and Encephalopathy Syndrome

Haemorrhagic shock encephalopathy syndrome

Haemorrhagic shock encephalopathy syndrome

An animal model of life-threatening hyperthermia during infancy.

A mathematical model of heat balance in human infants suggests that it may be possible for severe hyperthermia to develop if an infant is unable to remove his blankets in response to overheating (thermal entrapment). This hypothesis was tested in an animal model of weanling piglets. Ten piglets were warmed in a radiant heater to rectal temperature of 41 degrees C to simulate a fever. Animals in the experimental and control groups were removed from the heater and covered with ordinary infant blankets (to a thickness of approximately 3 cm). Endogenously produced heat caused the animals to warm to 42 degrees C. At this point, the control animals were uncovered. They rapidly cooled to normal body temperature. Animals in the experimental group remained covered until they expired from hyperthermia at 43.9 +/- 0.7 degrees C (SD) after 96 +/- 43 (SD) min. These data show that lethal hyperthermia may result from thermal entrapment. This finding may help clarify the role that hyperthermia may play in illnesses such as hemorrhagic shock and encephalopathy syndrome and some cases of sudden infant death syndrome.

Hemorrhagic shock and encephalopathy syndrome

Hemorrhagic shock and encephalopathy syndrome (HSES) is a devastating symptom complex that affects previously healthy infants and is associated with significant mortality and neurologic morbidity. The syndrome was first reported less than ten years ago, and there continues to be debate regarding whether HSES actually represents a distinct clinical entity or instead is a manifestation of heat illness, occult sepsis or endotoxic shock, or perhaps toxic ingestion. Nevertheless, the signs and symptoms described as HSES present in a typical fashion in the emergency department with sudden onset of shock, encephalopathy, seizures, and coagulopathy. Even with the initiation of intensive support in the ED, the outcome is probably dismal. We describe a case of HSES and review the presentation, proposed etiologies, and management of this catastrophic illness.

Hemorrhagic Shock and Encephalopathy Syndrome of Infants and Children

Hemorrhagic Shock and Encephalopathy Syndrome of Infants and Children