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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After describing the various methods for measuring the intracranial pressure, the causes of the rise of pressure within the skull and the possibilities for compensation are discussed. The elasticity of the brain tissue, which can be determined by pressure/volume stress, plays a crucial role in compensating for pressure. A reciprocal influence exists between intracranial pressure, cerebral circulation and brain oedema, as well as between intracerebral pressure and peripheral circulation. The treament of raised intracranial pressure is possibly by CSF drainage, hyperventilation and hypothermia, as well as by drugs such as steroids and diuretics.
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PMID:[Increased intracranial pressure. Methods of measurement, pathophysiology and treatment (author's transl)]. 70 17

The clinical course of 42 children with intracranial pressure monitoring was reviewed. Intracranial hypertension was documented in a variety of diagnostic categories. Therapy was titrated to maintain a baseline intracranial pressure of less than 15 torr (mm Hg), and to decrease the frequency of spontaneous and reactive pressure waves. Ventricular drainage, controlled hyperventilation, intravenous glycerol osmotherapy, therapeutic hypothermia, and barbiturate loading were employed as needed to achieve those goals. Survival was significantly related to average and peak intracranial pressure levels and to the degree of serum hyperosmolality that developed during therapy.
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PMID:Intracranial pressure: monitoring and normalization therapy in children. 85 Jun

Degeneration of hippocampal CA1 neurons occurs following transient complete ischemia produced by raised intracranial pressure. Both systemic injection of MK-801 and profound cerebral hypothermia produced by cisternal infusion of room temperature (22-25 degrees C) fluids protect vulnerable CA1 neurons from degeneration. Hypothermia appears to decrease hippocampal extracellular levels of glutamate during and after ischemia but provides only relative protection from ischemia as CA1 degeneration does occur with prolonged (30 min) periods of ischemia. Elevated intracranial pressure appears to produce ischemic degeneration in the hippocampus via an NMDA receptor mediated excitotoxic process which is highly temperature dependent.
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PMID:Degeneration of hippocampal CA1 neurons following transient ischemia due to raised intracranial pressure: evidence for a temperature-dependent excitotoxic process. 197 Sep 44

Sixty-four infants and children showing signs of decerebrate rigidity admitted to a paediatric unit have been studied. Cases of head injury, myelomeningocoele, and tumours were excluded from the series. The aetiological factors causing decerebration in the remainder fell into four main groups: infections, hypoxia, metabolic disease, and intracranial haemorrhage. Increased intracranial pressure was diagnosed in 87%. Defects in homeostasis occurred in 75%, respiratory abnormalities were present in 66%, cardiovascular in 33%, hypothermia in 30%, and hyponatraemia in 17%. Early recognition and treatment of raised intracranial pressure and defects in homeostasis are of the utmost importance if morbidity and mortality are to be minimized. There was a 31% mortality from the acute illness: 30% of the survivors were normal at follow-up examination; the remainder showed varying degrees of handicap. The severity of decerebration showed no correlation with aetiology or prognosis. The study shows that a wide range of disorders can lead to the clinical picture of decerebration in the young child, and that the prognosis is probably much better than in adults showing the same symptoms and signs.
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PMID:Patterns of decerebration in infants and children: defects in homeostasis and sequelae. 471 5

Intracranial hypertension leading to brain stem herniation is a major cause of death in fulminant hepatic failure (FHF). Mannitol, barbiturates, and hyperventilation have been used to treat brain swelling, but most patients are either refractory to medical management or cannot be treated because of concurrent medical problems or side effects. In this study, we examined whether allogeneic hepatocellular transplantation may prevent development of intracranial hypertension in pigs with experimentally induced liver failure. Of the two preparations tested--total hepatectomy (n = 47), and liver devascularization (n = 16)--only pigs with liver ischemia developed brain edema provided, however, that animals were maintained normothermic throughout the postoperative period. This model was then used in transplantation studies, in which six pigs received intrasplenic injection of allogeneic hepatocytes (2.5 x 10(9) cells/pig) and 3 days later acute liver failure was induced. In both models (anhepatic state, liver devascularization), pigs allowed to become hypothermic had significantly longer survival compared to those maintained normothermic. Normothermic pigs with liver ischemia had, at all time points studied, ICP greater than 20 mmHg. Pigs that received hepatocellular transplants had ICP below 15 mmHg until death; at the same time, cerebral perfusion pressure (CPP) in transplanted pigs was consistently higher than in controls (45 +/- 11 mmHg vs. 16 +/- 18 mmHg; p < 0.05). Spleens of transplanted pigs contained clusters of viable hepatocytes (hematoxylin-eosin, CAM 5.2). It was concluded that removal of the liver does not result in intracranial hypertension; hypothermia prolongs survival time in both anhepatic pigs and pigs with liver devascularization, and intrasplenic transplantation of allogeneic hepatocytes prevents development of intracranial hypertension in pigs with acute ischemic liver failure.
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PMID:Transplantation of hepatocytes for prevention of intracranial hypertension in pigs with ischemic liver failure. 971 Mar 4

The use of mild hypothermia in the management of blunt head trauma has been shown to significantly improve clinical outcomes. The use of moderate controlled hypothermia in the patient with severely raised intracranial pressure (ICP) secondary to fulminant hepatic failure (FHF) has similar potential benefits, but is not a widely accepted practice. We report a case where the use of hypothermia in the management of severely raised ICP both before and after liver transplantation was thought to effect a beneficial outcome.
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PMID:Induced hypothermia in the management of cerebral oedema secondary to fulminant liver failure. 1061 47

Mild hypothermia prevents the development of brain edema in rats with acute liver failure resulting from hepatic devascularization. Mechanistic studies performed in this model suggest that the protective effect of hypothermia results from the inhibition of blood-brain transfer of ammonia, an action which could result (at least in part) from an effect on cerebral blood flow. Hypothermia-induced reductions of brain ammonia are associated with normalization of extracellular brain glutamate concentrations in rats with acute liver failure. Studies in humans suggest that mild hypothermia is beneficial in the management of severely raised intracranial pressure, both before and after liver transplantation in patients with acute liver failure due to acetaminophen overdose. Mild hypothermia offers a potentially useful bridge therapy in patients with acute liver failure who are awaiting liver transplantation.
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PMID:Mild hypothermia prevents cerebral edema in acute liver failure. 1129 86

Increased intracranial pressure in patients with acute liver failure remains a major cause of mortality. Treatment options are limited, and without urgent liver transplantation, mortality rates of up to 90% are common in those who fulfill criteria for poor prognosis. Several studies in animal models of acute liver failure set the stage for the clinical application of moderate hypothermia in humans. Few patients are treated with hypothermia for increased intracranial pressure. However, data indicate that moderate hypothermia is a safe and effective method of treatment for increased intracranial pressure that is unresponsive to other medical therapies, and that this treatment can be used as a successful bridge to liver transplantation. Recent data also suggest that increases in intracranial pressure can be prevented during the dissection and reperfusion phases of liver transplantation for acute liver failure if patients are kept hypothermic during the surgical procedure. This article focuses on the use of moderate hypothermia for the treatment of increased intracranial pressure in patients with acute liver failure.
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PMID:Hypothermia for the management of intracranial hypertension in acute liver failure. 1157 23

Diffusion-weighted imaging (DWI) can diagnose early stage not only of the arterial infarction but also of venous infarction. We successfully diagnosed a case as acute venous infarction by DWI. The patient, an infant of one year and ten months, presented disturbance of consciousness and left hemiparesis two weeks after dehydration and infections. Computed tomographic scan revealed a cerebral hemorrhage in the right parietal lobe. Cerebral angiography revealed no contrast filling of the posterior side of superior sagittal sinus, straight sinus and transverse sinus. DWI demonstrated a large hyperintensity lesion around the hematoma, suggesting venous infarction in the early stage. We thought that venous infarction was caused by secondary extension of thrombus to cerebral cortical veins and deep cerebral veins. External decompression and postoperative hypothermia therapy were performed because of rapidly deteriorating intracranial hypertension. Intracranial hypertension was, however, uncontrollable. The patient died four days after the onset. Diagnosis of the venous infarction by DWI was discussed along with other recent reports. Diffusion hyperintensity was displayed in almost all subjects with acute venous infarction. DWI pattern of venous infarction is more heterogeneous than that of arterial one because pathway from venous obstruction to infarction is complicated.
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PMID:[Diagnosis of acute phase of venous infarction by diffusion-weighted image: case report and review of the literature]. 1172 10

Increased intracranial pressure (ICP) is a pathological state common to a variety of neurological diseases, all of which are characterized by the addition of volume to the skull contents. Elevated ICP may lead to brain damage or death by two principle mechanisms: 1) global hypoxic-ischemic injury, as a consequence of reduced cerebral perfusion pressure (CPP) and cerebral blood flow; and 2) mechanical distortion and compression of brain tissue as a result of intracranial mass effect and ICP compartmentalization. All ICP therapies have as a goal, reduction of intracranial volume. In unmonitored patients with acute neurological deterioration, head elevation, hyperventilation, and mannitol (1g/kg) can rapidly lower ICP. Fluid-coupled ventricular catheters and fiberoptic transducers are the most accurate and reliable instruments for measuring ICP. In monitored patients, the treatment of critically raised ICP should proceed in an orderly step-wise fashion: 1) consideration of neuroimaging to exclude a new surgically operable lesion; 2) intravenous sedation to attain a quiet motionless state; 3) manipulation of blood pressure to keep CPP >70 and <120; 4) mannitol infusion; 5) moderate hyperventilation (P(CO2) 26 to 30 mmHg); and 6) high-dose pentobarbital therapy. Application of moderate hypothermia (32 to 33 degrees C) shows promise as a newer method for treating refractory ICP. Placement of an ICP monitor is the critical first step in management of ICP. Treatment is best done using a stepwise protocol, with careful attention to sedation and CPP control prior to using mannitol and hyperventilation.
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PMID:Diagnosis and management of increased intracranial pressure. 1188 75


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