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 14-year-old girl with postinfectious chronic hepatitis developed a life threatening autoimmune multisystemic illness with arthralgias, intracranial hypertension, Coomb's positive hemolytic anemia and hemorrhagic diathesis (due to antiplatelet and antifactor X antibodies). Mannitol and immunosuppressive therapy abolished acute symptoms. During the first year of follow-up, two attempts of decreasing prednisone below 15 mg/day caused recurrence of the hemolytic anemia and appearance of low titer antinuclear antibodies, while doses above 15 mg/day caused an increase in transaminase levels. Daily prednisone dose was therefore fixed at 15 mg. The patient was well and, although signs of mild hemolysis persisted, there was no anemia. Transaminases were found greatly elevated on two occasions. An autoimmune multisystemic steroid sensitive disease was seemingly initiated by a postinfectious steroid irresponsive chronic hepatitis.
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PMID:Multisystemic disease with intracranial hypertension and autoimmune cytopenia in chronic active hepatitis. 395 17

Mannitol is an osmotic diuretic with properties that suit it to a variety of clinical situations. Despite the paucity of controlled studies that precisely define optimal use, a consensus based on published work and clinical experience may be reached. Mannitol can be used prophylactically, as a diagnostic aid, or as therapy for the oliguric state. The diuretic properties of mannitol are also useful in patients with refractory edema or intoxications by aspirin, barbiturates, or bromide. As an extracellular solute, the drug may ameliorate intracranial hypertension or symptoms of dialysis dysequilibrium. The renal and systemic effects of this versatile agent are discussed.
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PMID:Mannitol. 678 63

Mannitol is an osmotic diuretic used in acute oliguric renal failure, acute cerebral edema, and acute glaucoma. It is metabolically inert and is excreted through the kidneys. So once renal function is impaired, mannitol accumulates and the movement of water into the intravascular space with resultant cellular dehydration. Two patients suffered reversible acute oliguric renal failure following mannitol infusion given as treatment for intracranial hypertension. Both patients experienced nausea and vomiting and became increasingly lethargic with edema of general body. Congestive heart failure occurred. Laboratory data showed severe dilutional hyponatremia with hyperosmolality. We successfully treated them with extracorporeal ultrafiltration method (ECUM) and hemodialysis (HD). Some discussions were presented about acute renal failure following mannitol infusion.
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PMID:[Acute renal failure following mannitol infusion]. 837 73

Hemodynamic changes immediately after the administration of mannitol were investigated in monkeys (Macaca Fuscata) using transcranial Doppler ultrasound (TC2-64) and were compared with those after CO2 loading. The CO2 loading group was hyperventilated to an end-tidal PCO2 of 36.5 +/- 2.21 and hypoventilated to an end-tidal PCO2 of 46.3 +/- 2.69. Mean flow velocity in the middle cerebral artery (MCA-FV), Pulsatility index (PI) and blood flow in the internal carotid artery (IC-BF) studies were performed twice before and after hypercapnea. In the Mannitol group, Mannitol (2 g/kg) was infused at a rate 20 to 30 ml/min. MCA-FV, PI, IC-BF and intracranial pressure (ICP) studies were performed twice before administration and 10 minutes after administration of Mannitol. In the Mannitol group (n = 8), MCA-FV and IC-BF and ICP increased significantly after administration of Mannitol (p < 0.005, p < 0.005, p < 0.025), but there was no significant difference in the PI. In the CO2 loading group (n = 15), MCA-FV and IC-BF increased significantly (both p < 0.005) and PI decreased significantly (p < 0.005). These results indicated that, in the presence of normal autoregulation without intracranial hypertension, there was no change in the resistance of the peripheral cerebral vessels, while a decrease in viscosity after administration of Mannitol caused an increase in cerebral blood flow. Hence, according to Poiseuille's law, peripheral vasoconstriction occurred in the early period after administration of Mannitol. This change was considered to be due to autoregulation of the cerebral vessels.
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PMID:[Effect of rapid mannitol infusion on middle cerebral artery blood flow velocity and pulsatility index--a transcranial Doppler ultrasonography study in monkeys]. 839 85

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

The causes of death and neurological sequelae in African children with cerebral malaria are obscure. Intracranial pressure (ICP) was monitored and cerebral perfusion pressure (CPP) calculated in 23 Kenyan children with cerebral malaria. Four children had severe intracranial hypertension (ICP > 40 mm Hg, CPP < 40 mm Hg): two died, one with an ICP of 158 mm Hg and signs of transtentorial herniation, the other one with an ICP of 42 mm Hg and cardiorespiratory arrest. The other two survived with severe neurological sequelae. Nine had intermediate intracranial hypertension (ICP > 20 mm Hg, CPP < 50 mm Hg) and 10 had mild intracranial hypertension (maximum ICP 10-20 mm Hg); all survived without severe sequelae. Mannitol controlled the ICP in children with intermediate intracranial hypertension, but it did not prevent the development of intractable intracranial hypertension in children with severe intracranial hypertension. Intracranial hypertension is a feature of Kenyan children with cerebral malaria and severe intracranial hypertension is associated with a poor outcome.
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PMID:Intracranial hypertension in Africans with cerebral malaria. 913 62

Monitoring of brain tissue partial pressure of O2 (ti-pO2) is a promising new technique that allows early detection of impending cerebral ischemia in brain-injured patients. The purpose of this study was to investigate the effects of standard therapeutic interventions used in the treatment of intracranial hypertension in comatose patients on cerebral oxygenation. In the neurosurgical intensive care unit ti-pO2, arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and jugular bulb oxygen saturation (SjvO2) were prospectively studied (0.1 Hz acquisition rate) in 23 comatose patients (21 with severe traumatic brain injury, 2 with intracerebral hematoma) during various treatment modalities: elevation of CPP with dopamine (n = 35), lowering of the head (n = 22), induced arterial hypocapnia (n = 13), mannitol infusion (n = 16), and decompressive craniotomy (n = 1). Ischemic episodes ('IE' = ti-pO2 < 10 mmHg for > 15 min) within the first week after the insult were always associated with unfavorable neurological outcome. Elevation of CPP from 32 +/- 2 to 67 +/- 4 mmHg significantly improved ti-pO2 by 62% (13 +/- 2 to 21 +/- 1 mmHg) and reduced ICP indicating intact cerebral autoregulation. Further raising CPP from 68 +/- 2 to 84 +/- 2 mmHg did not alter ti-pO2. Mannitol-induced ICP reduction from 23 +/- 1 to 16 +/- 2 mmHg did not affect ti-pO2, nor did lowering of the head from 30 degrees to 0 degree. Hyperventilation from an endtidal pCO2 of 29 +/- 3 to 21 +/- 3 mmHg normalized ICP and CPP, but significantly reduced ti-pO2 from 31 +/- 2 to 14 +/- 3 mmHg. Decompressive craniotomy in a 15-year old patient with refractory intracranial hypertension instantly restored ti-pO2. Based on the present data, our understanding of many interventions previously believed to improve brain oxygenation might have to be re-evaluated. A CPP > 60 mmHg emerges as the most important factor determining sufficient brain tissue pO2. Any intervention used to further elevate CPP does not improve ti-pO2, to the contrary, hyperventilation even bears the risk of inducing brain ischemia.
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PMID:Brain tissue pO2-monitoring in comatose patients: implications for therapy. 919 72

Osmotic agents are still the most common treatment for controlling intracranial hypertension (ICH). Mannitol, glycerol, sorbitol, and hypertonic serum saline are the agents currently available. This work was designed to compare mannitol and glycerol in a similar population of brain injured patients, randomly divided into two groups of eight. The following mean day parameters were obtained: number of infusions, hydric balance, mean arterial pressure (MAP), and intracranial pressure (ICP). Cerebral perfusion pressure (CPP) was calculated. Brain computed tomographies (CT) were obtained on arrival, at follow-up whenever justified and at discharge. For comparison of both groups a modified therapeutic intensity level (mTIL) was used. Both agents induced a statistically equally effective decrease on ICP and increase on CPP evaluated at one and two hours post infusion but the mean day mTIL showed a statistically significant difference in favour of glycerol. The possible explanations of this difference are discussed. According to our results mannitol would be most indicated as a bolus to control sudden rises in ICP whereas glycerol would be most indicated as a basal treatment.
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PMID:Osmotherapy for increased intracranial pressure: comparison between mannitol and glycerol. 930 87

This report describes a sudden decrease in blood pressure after conservative treatment of acute intracranial hypertension. A 63-year-old woman with acute hydrocephalus after undergoing clipping of an aneurysm of the right supracerebellar artery developed increased intracranial pressure, necessitating surgical management. On the operating table, the patient developed Cushing's reflex. Mannitol injection combined with hyperventilation was begun immediately to reduce her intracranial pressure. Fifteen minutes later, a sudden and prolonged suppression of circulation was observed (blood pressure 65/35-85/40 mmHg, heart rate 90-100 beats/min). Postoperatively, computed tomography of the head showed compression of the brain stem. We believe that this patient's blood pressure decrease was related to a sudden reduction of intracranial pressure and that mannitol injection was principally responsible for this occurrence.
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PMID:A case of shock subsequent to treatment of intracranial hypertension by mannitol injection combined with hyperventilation. 955 70

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


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