Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Axonal pathology is increasingly identified by beta-amyloid precursor protein (betaAPP) immunohistochemistry in the brains of patients who may or may not have a history of trauma. The presence of betaAPP-IR(+) has been variously interpreted as either that diffuse traumatic axonal injury (TAI) is indeed a universal finding in cases of fatal traumatic brain injury (TBI) or there are other causes of betaAPP-IR(+) axons which under certain circumstances may be sufficient to mimic TBI and therefore make the medico-legal interpretation of certain cases very difficult. To address some of the uncertainties we have undertaken a detailed analysis of the amount and distribution of betaAPP immunohistochemistry in 63 cases of fatal TBI, 17 cases of patients dying after cardiac arrest, 12 cases dying in association with status epilepticus, 3 cases of carbon monoxide (CO) poisoning, 13 cases of hypoglycaemia and in 60 controls. Three patterns of betaAPP-IR(+) were identified. First, diffuse multi-focal, second, corresponding to the outline of an infarct or haematoma, and thirdly a mixture of the two. The first pattern was seen in cases of the lesser grades of TAI, CO poisoning, and hypoglycaemia, the second pattern in cases in which there was evidence of raised intracranial pressure and the third in cases of severe TAI. It is concluded that the proper interpretation of cases requires the examination of a sufficient number of blocks ( [Formula: see text] ), processing using standardised protocols including betaAPP immunohistochemistry and in some cases the mapping of any IR(+) on anatomical line diagrams. betaAPP carried out on a small number of randomly taken blocks is likely to lead to misinterpretation of the clinico-pathological correlations and possibly to a miscarriage of justice.
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PMID:Trials and tribulations of using beta-amyloid precursor protein immunohistochemistry to evaluate traumatic brain injury in adults. 1554 68

Severe malaria is a common reason for admission to paediatric wards in hospitals across sub-Saharan Africa. Despite over 100 years of research, mortality remains high. Deaths are associated with severe metabolic acidosis, shock, severe anaemia, hypoglycaemia, impaired consciousness, raised intracranial pressure, and status epilepticus. Most inpatient deaths occur within 24 h of admission to hospital, before the beneficial effects of treatment with antimalarial drugs are achieved. This review covers the priority areas for research in the care of children with severe malaria, addressing each of the main risk factors associated with death, in a bid to reduce the inpatient mortality.
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PMID:Research priorities in the management of severe Plasmodium falciparum malaria in children. 1649 57

Staphylococcus aureus causes an impressive spectrum of disease in tropics and subtropics. Scanty data are available regarding disseminated staphylococcal disease (DSD) in children, especially on their critical care needs. It is important to recognize and prioritize patients who may benefit most from Pediatric Critical Care. The objective of this article is to review the, critical care needs, management and outcome of patients with DSD and to identify clinical indicators for need of critical care. The study setting is a Pediatric Intensive Care Unit of an urban tertiary care teaching hospital in a developing economy. Fifty-three patients (age, 1 month to 12 years) with DSD, admitted to PICU during June 1994 to June 1999, form the subjects for the study. DSD was defined as involvement of at least two distant organs with presence of Gram-positive cocci in clusters and/or growth of S. aureus from at least one normally sterile body fluid. Data regarding demographic and clinical picture, microbiological profile, indication for PICU admission, monitoring needs, medical and surgical management and outcome was retrieved from the case records. Critical care problems included septic shock (28/53), pericardial effusion (21/53, cardiac tamponade in six), raised intracranial pressure (5 patients) and refractory status epilepticus (1 patient). The majority developed septic shock after first few doses of parenteral antimicrobials. They required an impressive amount of fluid [100 (56) ml/kg] during initial 6 h of resuscitation, and 90% had myocardial dysfunction requiring inotropic support. Tracheal intubation was needed in 18 (34%) and ventilatory support in 17 (32%) patients. About 60% patients had metabolic abnormalities. Soft tissue disease was associated with high risk of septic shock (RR, 1.77; P < 0.05). Presence of both septic shock and need for ventilation was associated with high mortality (RR, 20.5; P < 0.001). Patients with suspected DSD need intensive cardio-respiratory monitoring during initial 48-72 h of therapy; and those who develops shock, respiratory failure, pericardial effusion and necrotizing soft tissue disease should be prioritized for PICU admission.
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PMID:A 5-year PICU experience of disseminated staphylococcal disease, part 2: management, critical care needs and outcome. 1749 23

There is paucity of data evaluating intracranial pressure (ICP) rise and its management in acute viral encephalitis (AVE). Noteworthy is the current prevalence of unselective and broad utilization of ICP lowering therapies in clinical practice. Trends in current management of ICP in AVE emanate from data extrapolated from results of studies done on cerebral malaria, bacterial meningitis, stroke, and brain trauma patients. In this article we review (1) clinical correlates of raised ICP, (2) pathology, (3) imaging data, (4) monitoring, and, (5) treatment, of raised ICP in AVE. ICP monitoring is a useful adjunct to management of raised ICP in adults, becoming especially important in Herpes encephalitis and encephalitis with status epilepticus. In children it substantially influences clinical management and continuous monitoring of mean blood pressure (MBP) and ICP can aid in early diagnosis and treatment when cerebral perfusion pressure (CPP) falls below critical levels. Current evidence suggests that the pathomechanisms that contribute to the development of raised intracranial pressure vary in viral encephalitides of different etiology, and different forms of cerebral edema result at different times in the course of the illness, thus creating a need for studies to investigate the usefulness of various edema-specific ICP lowering modalities in AVE.
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PMID:Raised intracranial pressure in acute viral encephalitis. 1937 1

Coma and other states of impaired consciousness represent a medical emergency. The potential causes are numerous, and the critical window for diagnosis and effective intervention is often short. The common causes of non-traumatic coma include central nervous system infections, metabolic encephalopathy (hepatic, uremic, diabetic ketoacidosis etc.), intracranial bleed, stroke and status epilepticus. The basic principles of management include 1) Rapid assessment and stabilization, 2) Focussed clinical evaluation to assess depth of coma, localization of lesion in the central nervous system and possible clues to etiology, and 3) Treatment including general and specific measures. Commonly associated problems such as raised intracranial pressure and seizures must be recognized and managed to prevent secondary neurologic injury.
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PMID:Approach to the child with coma. 2140 16

Cerebral venous thrombosis is a rare but potentially severe condition in children. We present the case of a teenager with corticodependent nephrotic syndrome diagnosed at five months of age and treated with cyclosporine A. In the context of recurrence of nephrotic syndrome he presented with headache, vomiting and severe intracranial hypertension. While the raised intracranial pressure and the status epilepticus were controlled, the brain imaging revealed venous thrombosis of all venous sinus, with absence of venous drainage. He was submitted to local thrombolysis with recombinant tissue plasminogen activator, with recanalization of the venous sinuses. The outcome was favourable, without neurological deficits. In this case, the early radiologic intervention was crucial, enabling a full neurological recovery, in a teenager whose initial prognosis was very poor.
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PMID:[Endovascular thrombolysis for massive cerebral venous thrombosis in a teenager with nephrotic syndrome]. 2162 91

A previously healthy 29-year-old man was admitted to a tertiary referral center with acute left hemiparesis followed shortly by de novo convulsive status epilepticus. This was in the context of a 2-month history of flu-like symptoms, severe headaches, and retinopathy recently diagnosed as acute multifocal placoid pigment epitheliopathy. Neuroimaging demonstrated bilateral, multiple territory cerebral infarction. Despite intravenous methylprednisolone and craniotomy for the management of raised intracranial pressure, the patient deteriorated and died 14 days later. At autopsy, multiple infarcts of varying ages within a 10-day period were seen in association with a segmental giant cell vasculopathy of meningeal arteries.
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PMID:Fatal ischemic stroke complicating acute multifocal placoid pigment epitheliopathy: histopathological findings. 2378 29

CNS infections in children are medical emergency and are associated with high mortality and morbidity. For diagnosis, a high index of suspicion is required. Clinical assessment should be supplemented by laboratory investigations including CSF Gram stain and cultures, blood culture, PCR on CSF, serological tests, and imaging. Commonly associated life threatening complications include coma, seizure, raised intracranial pressure (ICP), focal deficits, shock, respiratory failure, and fluid and electrolyte abnormalities. Immediate management should first address control of airway, breathing and circulation; protocolized management of raised ICP and status epilepticus; maintaining adequate intravascular volume; and close monitoring for early detection of complications. Appropriate antimicrobial agents should be administered promptly according to the suspected pathogen. Clinical evaluation, laboratory workup, specific antimicrobial therapy, supportive treatment, and management of associated complications should go hand in hand in a protocolized way for better outcome.
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PMID:Principles of Management of Central Nervous System Infections. 2933 66


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