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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report two cases of traumatic cerebral vascular disease which were treated successfully with barbiturate. The first case sustained blunt trauma to the bilateral vertebral arteries, resulting in complete occlusion of both arteries. After ligation of the injured vertebral arteries, multiple cerebral infarction appeared. Cerebral angiography revealed dissection and stenosis of the bilateral internal carotid arteries. We treated this case with barbiturate (Thiamylal) in combination with administration of heparin. The second case sustained cerebral contusion and traumatic subarachnoidal hemorrhage as a result of a motor cycle accident. This patient deteriorated and cerebral angiography showed diffuse cerebral arterial vasospasms. When this was treated with induced hypertension, he developed recurrent subarachnoid hemorrhage. In order to protect the brain from ischemia without elevating blood pressure, we employed barbiturate therapy and the patient recovered without major neurological deficit. The condition of severe head injury with cerebral ischemia is complicated. Therefore it has been hard for neurosurgeons to cure the patient with this condition. But we treated it with barbiturate successfully. Barbiturate therapy in severe head injury with cerebral ischemia may decrease the mortality in that group of patients considered difficult to treat with the usual therapeutic modalities.
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PMID:[Barbiturate therapy in traumatic cerebral vascular disease: report of two cases]. 261 99

The effects and indications of barbiturate therapy for brain protection, and prevention and reduction of the intracranial hypertension were investigated using an ultrashort acting barbiturate, thiamylal, in sixteen cases with intracranial lesions. Final outcome of the treatment revealed 8 good recoveries which were actively administered thiamylal during operation or immediately after. On the other hand, four cases, whose intracranial pressures (ICPS) of over 40 mmHg could not be controlled suffered brain death. Barbiturate therapy was not effective for brain protection of primary damaged lesions. It is concluded that barbiturate therapy may provide a satisfactory reduction of the intracranial hypertension in cases during the early postoperative stage or of under 40 mmHg initial ICP.
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PMID:[Barbiturate therapy in 16 cases with intracranial lesion with special reference to the indication and limitation]. 361 59

In 12 patients with life-threatening neurological deficits from vasospasm refractory to other measures, high dose barbiturate therapy was used in an attempt to prevent permanent changes in the brain. In each case angiography was performed and intracranial pressure was measured. Dexamethasone, a low molecular weight dextran, and mannitol were administered. If intracranial pressure (ICP) was elevated, drainage of cerebrospinal fluid and hyperventilation were used. Arterial pressure was maintained at not less than 140/90 preoperatively and 180/100 postoperatively. Barbiturate therapy was continued until vasospasm decreased angiographically and ICP was normal. Eleven of the 12 patients perished. One had a fatal rebleed. One died of an iatrogenic hemothorax. Four died from uncontrollable intracranial hypertension. One improved slightly and then died from a cardiac arrhythmia. One died of increased ICP when her ventriculostomy malfunctioned. One improved and was responding purposefully to pain, only to die suddenly with a low ICP. Two patients became awake and responsive to verbal commands; 1 of these died from Klebsiella meningitis and the other died from an intracerebral hematoma. In the 3 patients in whom hypothermia was also used, profound alterations in acid-base and fluid electrolyte balance occurred. These discouraging results are most likely a reflection of the severity of the patients' condition at the beginning of therapy. There may be some benefit of barbiturates in the management of vasospasm, and the potential effectiveness of barbiturates may be more obvious if therapy is started at an earlier stage. However, until further evidence of the usefulness of this modality becomes manifest, it should be limited to patients with life-threatening impairments unresponsive to all other measures.
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PMID:Treatment of ischemic deficits from cerebral vasospasm with high dose barbiturate therapy. 616 7

A modification of the Syva EMIT-tox Serum Barbiturate Assay was developed to provide a rapid and practical method for quantitating serum barbiturates. Standard curves for eight selected barbiturates were run using specific sets of standards for each. Correlation coefficients, slopes, and y-intercepts for the curves of best fit were determined by the least-squares method. Between-run and within-run precision analysis indicated acceptable reproducibility for barbiturate concentrations in high therapeutic to toxic serum levels. A case report describing the use of this method for the determination of serum pentobarbital concentrations during therapy for intracranial hypertension is presented. The modified EMIT assay may be useful for monitoring barbiturate blood levels in overdose, and when used for therapy of ischemic brain damage.
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PMID:Quantitation of barbiturates by a modification of the EMIT-tox serum barbiturate assay. 636 20

Barbiturate therapy is a controversial mode of therapy instituted in patients with acute head injuries after conventional means of treatment to decrease intracranial hypertension have been unsuccessful. Thiopental is a fast-acting central nervous system depressant and is one of the agents used for barbiturate therapy. Baseline laboratory values and access to four IV sites, including a Swan-Ganz catheterization site, should be obtained prior to institution of barbiturate therapy. While a patient is on barbiturate therapy, it is difficult to assess his clinical status. Nursing care for a patient on barbiturate therapy is an exciting challenge. It is the nurse's responsibility to continuously assess the patient's pressure readings, laboratory values, fluid balance, and pulmonary status to accurately interpret his clinical status.
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PMID:Nursing management for barbiturate therapy in acute head injuries. 654 36

The sympatho-adrenal activity as reflected in plasma catecholamine levels was studied in rats subjected to a standardized hemorrhage. A comparison was performed between awake rats and rats anesthetized with diethylether, enflurane, barbiturate or ketamine. As expected diethylether increased sympathoadrenal activity. Enflurane induction increased adrenaline and decreased noradrenaline levels. Upon hemorrhage the sympatho-adrenal activity was depressed compared to the awake state. Barbiturate anesthesia depressed sympatho-adrenal activity. Ketamine increased noradrenaline levels and a relative hypertension was noticed during bleeding. The results focus attention on important differences in sympatho-adrenal activity between awake rats and rats anesthetized with different agents.
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PMID:Anesthetic agents and sympatho-adrenal response to hemorrhage in the rat. 659 65

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

Malignant cerebral edema following ischemic stroke is life threatening, as it can cause inadequate blood flow and perfusion leading to irreversible tissue hypoxia and metabolic crisis. Increased intracranial pressure and brain shift can cause herniation syndrome and finally brain death. Multiple randomized clinical trials have shown that preemptive decompressive hemicraniectomy effectively reduces mortality and morbidity in patients with malignant middle cerebral artery infarction. Another life-saving decompressive surgery is suboccipital craniectomy for patients with brainstem compression by edematous cerebellar infarction. In addition to decompressive surgery, cerebrospinal fluid drainage by ventriculostomy should be considered for patients with acute hydrocephalus following stroke. Medical treatment begins with sedation, analgesia, and general measures including ventilatory support, head elevation, maintaining a neutral neck position, and avoiding conditions associated with intracranial hypertension. Optimization of cerebral perfusion pressure and reduction of intracranial pressure should always be pursued simultaneously. Osmotherapy with mannitol is the standard treatment for intracranial hypertension, but hypertonic saline is also an effective alternative. Therapeutic hypothermia may also be considered for treatment of brain edema and intracranial hypertension, but its neuroprotective effects have not been demonstrated in stroke. Barbiturate coma therapy has been used to reduce metabolic demand, but has become less popular because of its systemic adverse effects. Furthermore, general medical care is critical because of the complex interactions between the brain and other organ systems. Some challenging aspects of critical care, including ventilator support, sedation and analgesia, and performing neurological examinations in the setting of a minimal stimulation protocol, are addressed in this review.
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PMID:Critical care for patients with massive ischemic stroke. 2532 73

Barbiturate coma therapy (BCT) is a choice treatment for refractory intracranial hypertension after all surgical or medical managements have failed to control the intracranial pressure (ICP). It helps to reduce cerebral blood flow, cerebral metabolic rate of oxygen consumption and ICP. However, this therapy can also cause many complications. One of the underreported, but life-threatening complications is refractory hypokalemia, which can lead to subsequent rebound hyperkalemia after sudden cessation. We report our experience of managing unusual complication of refractory hypokalemia during BCT with thiopentone in postdecompressive craniectomy patient.
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PMID:Refractory hypokalemia during barbiturate coma therapy used for treating refractory intracranial hypertension in traumatic brain injury. 2576 95

Barbiturate coma therapy (BCT) is a treatment option that is used for refractory intracranial hypertension after all other options have been exhausted. Although BCT is a brain protection treatment, it also has several side effects such as hypotension, hepatic dysfunction, renal dysfunction, respiratory complications and electrolyte imbalances. One less concerning but potentially life-threatening complication of BCT is dyskalaemia. This complication could present as severe refractory hypokalaemia during the therapy with subsequent rebound hyperkalaemia after cessation of the therapy. Judicious potassium replacement during severe refractory hypokalaemia and gradual cessation of the therapy to prevent rebound hyperkalaemia are recommended strategies to deal with this complication, based on previous case series and reports. In this case report, we show that these strategies were applicable in improving severe hypokalaemia and preventing sudden, life-threatening rebound hyperkalaemia. However, even with use of these strategies, BCT patients could still present with mild, asymptomatic hyperkalaemia.
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PMID:Life-Threatening Dyskalaemia after Barbiturate Coma Therapy: The Strategy of Management. 2889 10


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