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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five methods of therapy for increased ICP were used in the treatment of 32 head-injured patients. The effects of steroids could not be evaluated. Withdrawal of CSF was always effective because intracranial volume was reduced and pressure must follow, but because of brain swelling and collapse of the ventricular system in this group of patients, it was not an effective permanent form of therapy. Hypertonic Mannitol reduced ICP in nearly every case irrespective of the degree of brain damage or the height of ICP. Hyperventilation was least effective in the most severely ill patients, presumably due to the non-responsiveness of the cerebral vessels to changes in PaCO2. The poorest response of ICP seemed to be with hypothermia.
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PMID:Analysis of the response to therapeutic measures to reduce intracranial pressure in head injured patients. 93 13

CBF and ICP were measured in cats following cerebral cold injury and mannitol infusion. Mannitol was found to reduce the intracranial hypertension caused by the injury. The restoration of CBF and ICP was of short duration and was followed by a reduction of CBF and elevation of ICP. A repeated restoration of CBF by a second dose of mannitol was followed by a more severe impairment of CBF. The prolonged beneficial effect of mannitol on CBF after brain injury has to be reassessed.
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PMID:Transient effect on mannitol on cerebral blood flow following brain injury. 212 73

The effect of THAM on brain oedema parameters was initially investigated in animals with cold brain lesions; THAM was then used in head injury patients, ICP, SAP and CPP were analyzed. In the experiments with rats after freezing lesion, THAM was compared to equivalent doses of Na-bicarbonate. The animals were artificially respirated and sacrificed 6 h after trauma. THAM did significantly reduce water (wet-dry weight technique) and sodium contents in both hemispheres, whereas bicarbonate was ineffective. The potassium contents were even preserved at almost normal levels. In 80 patients receiving alternatively THAM (18-36 g/100-200 ml/1-2h), mannitol (20%, 125-250 ml/20-40 min) or sorbitol (40%, 70-140 ml/20-40 min), the ICP rapidly decreased following THAM infusion. The maximal fall in ICP (33%) was equal to that with mannitol and sorbitol. The slope of ICP decrease was equal with THAM and Mannitol but steeper with sorbitol. With THAM, however, the effect on ICP lasts longer than with osmotherapy. The EEG improved more rapidly after THAM. As shown by blood plasma values, the action of THAM is not based on osmotic effects. The increases in pH and especially in base excess suggest an intracerebral buffering. The encouraging results with THAM require a randomized clinical trial after severe head injury which is presently prepared.
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PMID:A comparative analysis of THAM (Tris-buffer) in traumatic brain oedema. 212 78

Continuous measurement of CBV and CBF by means of laser-Doppler flowmetry was performed to analyze the temporal profile of cerebrovascular response to water accumulation in an infusion model of brain oedema. Using this method, the effect of mannitol on CBV was also examined to determine how mannitol improves the intracranial pressure-volume relationship. The results show that: (1) The presence of an oedema generator elicits a continuous reduction of CBV and a transient reduction of CBF. With cessation of this mechanical force of oedema production, CBV and CBF return to control levels. (2) Mannitol increases CBV and PVI. The improvement of PVI might be due to an increase in CBV as well as ICP reduction.
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PMID:Effect of mannitol on intracranial pressure-volume status and cerebral haemodynamics in brain oedema. 212 81

Investigation into the use of osmotic therapy for ICP reduction began in 1919. Mannitol is the osmotic agent currently in use. Mannitol's effectiveness in reducing ICP has been shown. Osmotic therapy using mannitol reduces ICP by mechanisms that remain unclear. Mannitol is thought to decrease brain volume by decreasing overall water content, to reduce blood volume by vasoconstriction and to reduce CSF volume by decreasing water content. Mannitol may also improve cerebral perfusion by decreasing viscosity or altering red blood cell rheology. Lastly, mannitol may exert a protective effect against biochemical injury. The most common complications of therapy are fluid and electrolyte imbalances, cardiopulmonary edema and rebound cerebral edema. Nursing care of the patient receiving mannitol requires vigilant monitoring of electrolytes and overall fluid balance, and observation for the development of cardiopulmonary complications in addition to neurologic assessment.
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PMID:Mannitol revisited. 796 23

Mannitol is effective in reducing ICP, and we recommend its use in the management of traumatic intracranial hypertension. Serum osmolalities greater than 320 mOSsm/L and hypovolemia should be avoided. Some data suggest that bolus administration is preferable to continuous infusion.
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PMID:The use of mannitol in severe head injury. Brain Trauma Foundation. 894 89

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

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.
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PMID:[The internal environment and intracranial hypertension]. 975 May 95

There are two "class 1" studies, and one "class 2" study, and a large body of "Class 3" data, which can be used to support mannitol. The evidence supporting use of mannitol for ICP control is sufficiently strong to warrant guideline status. Mannitol is effective in reducing ICP, and its use is recommended as a guideline in the management of traumatic intracranial hypertension. Serum osmolalities >320 mOsm and hypovolemia should be avoided. There is some data to suggest that bolus administration is preferable to continuous infusion.
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PMID:The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Use of mannitol. 1093 95

137Cs and 40K activity concentrations and stable elements have been measured in Clavariadelphus truncatus collected in Mexico. Iron-chelating compounds of siderophore-type was also studied in the species. 137Cs and 40K were determined in soil and mushroom samples with HpGe gamma-ray spectrometry. Macro- and micro-elemental concentrations were determined by XRF and ICP-MS. Siderophore detection was obtained with a colorimetric assay and X-ray diffraction analysis was performed using a Siemens D5000 diffractometer. 137Cs geometric mean concentration in C. truncatus was 26 times higher as compared with other Mexican edible mushroom species, while 40K showed stability. Soil-C. truncatus concentration ratio for 137Cs and other micro-elements such as Cs, Rb and Pb were also higher than other Mexican edible species. The 137Cs committed effective dose due to the ingestion of C. truncatus was 8 x 10(-6) Sv year(-1). The main crystalline structure found in C. truncatus was D-Mannitol.
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PMID:Radioactive and stable metal bioaccumulation, crystalline compound and siderophore detection in Clavariadelphus truncatus. 1746 20


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