Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 7-yr-old boy undergoing treatment for respiratory failure after near-drowning developed a pneumomediastinum. Intracranial hypertension refractory to previously successful therapy led to placement of a mediastinal tube, after which intracranial pressure decreased and was easier to control. A pneumomediastinum may cause intracranial hypertension by interfering with venous drainage from the cranium.
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PMID:Increased intracranial pressure: an indication to decompress a tension pneumomediastinum. 671 17

Treatment of arterial hypertension in severe hypertensive encephalopathy does not always result in clinical improvement in the patient's central nervous system. In order to elucidate further the status of the brain, the authors have measured intracranial pressure (ICP) and arterial pressure in three cases of severe hypertensive encephalopathy. ICP was elevated in two of the three cases with peak values ranging from 32-70 mm Hg. In these 2 patients, therapy to lower ICP, including hyperventilation, steroids, barbiturates, and furosemide was begun early in the course. Cerebral perfusion pressure (CPP), defined as the difference between mean arterial pressure and ICP, was kept over 50 mm Hg to maintain adequate cerebral blood flow (CBF). These 2 patients survived. In the third case, measures to control ICP were instituted late in the course and the patient died of brain herniation. Intracranial hypertension is a complication of hypertensive encephalopathy and may contribute to cerebral injury. In cases of severe hypertensive encephalopathy, both ICP and arterial pressure should be monitored continuously. Judicious therapy aimed at lowering both ICP and arterial pressure, while maintaining an adequate CPP, should be employed.
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PMID:Intracranial pressure monitoring in severe hypertensive encephalopathy. 679 Feb 26

Increased intracranial pressure due to brain oedema was produced in albino rabbits by combining a cryogenic lesion in the left hemisphere with the intraperitoneal administration of 6-aminonicotinamide (cytotoxic agent). The most effective reduction in ICP (74%) was achieved when furosemide and mannitol were used in combination. When either mannitol or furosemide was employed alone, the average ICP reduction was approximately 53%. Peak ICP reduction occurred at 45 minutes with furosemide, 30 minutes with mannitol and furosemide combined, and at 60 minutes with a combination of mannitol and acetazolamide. Also studied simultaneously in these animals were investigated elastance (Em), brain water content, hemispheric water volume content, electrolytes, EEG, and gross pathology. Following therapy there was a statistically significance reduction of water content in the left hemisphere (cryogenic lesion) by all therapeutic modalities except with furosemide alone. In the right hemisphere the water content was reduced by furosemide and the furosemide-mannitol combination but not by the association of mannitol with acetazolamide. A significant decrease of brain sodium was noted only for the combination of mannitol and furosemide. This study indicates that effective reduction of cytotoxic-cryogenic brain oedema and intracranial hypertension can be obtained with a variety of diuretic agents. From the standpoint of tissue dehydration, restoration of tissue electrolyte balance, and rate of ICP reduction, the combination of furosemide-mannitol appears to offer advantages over furosemide alone, or acetazolamide-mannitol.
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PMID:Intracranial hypertension and brain oedema in albino rabbits. Part 2: Effects of acute therapy with diuretics. 679 66

The aggressive treatment of major craniocerebral trauma has received recent attention. Barbiturate administration has been beneficial in some cases of sustained, uncontrolled intracranial hypertension. One major disadvantage of pentobarbital narcosis is the long half-life of the drug (15 to 48 hours). We have used Althesin, an intravenous steroid anesthetic (alfaxalone and alfadolone acetate; Glaxo Laboratories Ltd., Greenford, Middlesex, England), in eight seriously head-injured patients. Althesin combines the theoretical advantages of pentobarbital in the management of head trauma with almost immediate reversibility (serum half-life, 1.6 minutes). Raised intracranial pressure and clinical outcome seem to be influenced favorably and the side effects are negligible when the drug is administered by continuous intravenous infusion over several days. Further study of this compound in the management of head trauma seems warranted.
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PMID:Althesin in the management of head injuries: a preliminary report. 682 25

We report two cases of children, 7 and 14 yr old, in whom prolonged infusion of thiopental sodium (TS) was used to control intracranial hypertension previously unresponsive to conventional therapy. Intracranial hypertension followed removal of a large tumor in 1 case, and trauma in the other. TS was administered at a rate of up to 7 mg/kg . h for 8 days in 1 patient, and up to 12 mg/kg . h for 10 days in the other. Both children regained consciousness and made significant recovery of neurological function. The advantage and the side-effects of the prolonged use of TS for intracranial hypertension are discussed.
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PMID:Long-term barbiturate infusion to reduce intracranial pressure. 685 8

Intracranial hypertension is caused by various pathologic processes. From oncologic point of view, they are 1) intracranial space-occupying lesions, especially malignant tumors, 2) leptomeningeal tumors, 3) hemorrhage in the brain tumors, 4) intracranial hemorrhage due to hemorrhagic diathesis related to the malignant tumors, and 5) cerebral thrombosis or embolism due to increased blood coagulability secondary to malignancy. In the increase of intracranial pressure, brain edema or disturbance of cerebrospinal fluid (CSF) circulation due to the presence of brain tumors play more important role than the tumor bulk itself. CT scan is useful for demonstrating the process causing the intracranial hypertension. Therapeutic measures in all patients with increased intracranial pressure are initiated promptly to restore the cardiopulmonary dysfunction if any. Hyperventilation and intravenous infusion of hyperosmolar agents such as mannitol and glycerol have an immediate effect in reducing intracranial pressure when brain edema plays role in increasing it. Steroids are also very effective in reducing brain edema; the effect is less immediate but long lasting. CSF drainage or shunt operation is necessary when dilated ventricular system plays role in the intracranial hypertension. The radical treatment of the intracranial hypertension is a removal of the tumor causing it; however, if not indicated, the second choice is the internal or external decompressions. Postoperative radiotherapy and chemotherapy are also indicated for the malignant brain tumors.
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PMID:[Intracranial hypertension]. 688 68

Fourteen patients with benign intracranial hypertension who failed to respond to medical treatment, were treated with optic nerve decompression to prevent the sequelae of chronic unrelieved papilloedema. The mechanism by which optic nerve decompression protects the optic nerve is uncertain. These patients were reviewed to evaluate the efficacy of the procedure in the treatment of benign intracranial hypertension and to assess its mechanism of action. Preoperatively all patients had papilloedema, 11 patients had visual obscurations and 6 patients had evidence of visual failure. Postoperatively, visual obscurations and papilloedema resolved in all patients, and 5 of 6 patients had no further deterioration of visual function. Six patients had symptoms of raised intracranial pressure preoperatively and in 3 the symptoms resolved after surgery. Three patients had unilateral optic nerve decompression and papilloedema resolved in both eyes. In 1 patient intracranial pressure monitoring revealed raised pressure preoperatively with no significant change in the first 24 hours after surgery. We conclude that optic nerve decompression is effective in the treatment of benign intracranial hypertension, has its effect locally, and in some patients may lower the intracranial pressure.
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PMID:Optic nerve decompression in benign intracranial hypertension. 692 85

Levels of arginine vasopressin have been measured in the blood and cerebrospinal fluid of patients with benign intracranial hypertension and raised intracranial pressure, patients with other neurological diseases and in normal control subjects. There was no difference in blood levels in each of the 3 groups (mean +/- SEM, 2.8 +/- 0.5, 2.5 +/- 0.25, 2.53 +/- 0.4 pg/ml). However, levels of arginine vasopressin in the cerebrospinal fluid in patients with benign intracranial hypertension and other neurological diseases were higher (mean +/- SEM, 0.64 +/- 0.005, 0.61 +/- 0.04 pg/ml), than in the control group (0.49 +/- 0.06), but not different from each other. The origin of arginine vasopressin in cerebrospinal fluid is uncertain and a number of possibilities are discussed.
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PMID:Arginine vasopressin levels in cerebrospinal fluid in neurological disease. 709 2

High dose barbiturates were used to treat intracranial hypertension in 15 patients with nontraumatic brain lesions; (3 hypertensive hemorrhage, 4 subarachnoid hemorrhage, 5 infarction, 2 global anoxia-ischemia and 2 encephalitis). All had persistently raised intracranial pressure (ICP) while being treated with aggressive conventional therapy. The addition of barbiturates caused an initial lowering of ICP in 11 patients, but only 5 of these had sustained ICP reductions. Survival of the 5 patients with persistently lowered ICP and death of the remaining 10 may indicate an improvement in outcome attributable to the addition of high dose barbiturates to conventional therapy in non-traumatic brain swelling. Because of the resources required for their prolonged use, randomized studied in patients with intracranial hypertension are required to determine the effect of barbiturates on outcome.
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PMID:High dose barbiturates in non-traumatic brain swelling: ICP reduction and effect on outcome. 714 92

Increased intracranial pressure coexistent with cerebrospinal fluid (CSF) rhinorrhoea was encountered in five out of 46 patients with a persistent CSF leak. In four patients, hypertension was due to malabsorption of CSF. One patient had a post-traumatic intracerebral cyst. The various degrees of intracranial hypertension, their effects on the clinical course and modes of treatment are demonstrated by the cases reported. Many failures in repairing the fistulous tracts may not stem from lack of technique, but could be the result of treatment of only one of the two concomitant conditions.
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PMID:Increased intracranial pressure in post-traumatic rhinorrhoea. 715 54


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