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

Although experimental and pathological studies suggest an important role for ischemia in the majority of fatal cases of traumatic brain injury, ischemia has been a rare finding in most clinical studies of cerebral blood flow (CBF) in head-injured patients. The hypothesis of the present study was that cerebral ischemia occurs in the first few hours after injury, but that CBF measurements have not been performed early enough. Early measurements of CBF (by the 133Xe intravenous method) and arteriovenous oxygen difference (AVDO2) were obtained in 186 adult head-injured patients with a Glasgow Coma Scale score of 8 or less, and were correlated with neurological status and outcome. During the first 6 hours after injury, CBF was low (22.5 +/- 5.2 ml/100 gm/min) but increased significantly during the first 24 hours. The AVDO2 followed the opposite course; the decline of AVDO2 was most profound in patients with low motor scores, suggesting relative hyperemia after 24 hours. A significant correlation between motor score and CBF was found in the first 8 hours after injury (Spearman coefficient = 0.69, p less than 0.001), but as early as 12 hours postinjury this correlation was lost. A similar pattern was found for the relationship between CBF and outcome. Cerebral blood flow below the threshold for infarction (CBF less than or equal to 18 ml/100 gm/min) was found in one-third of the studies obtained within 6 hours, the incidence rapidly decreasing thereafter. A low CBF after 24 hours was not generally associated with a high AVDO2, and was probably a reflection of low oxidative metabolism rather than frank ischemia. In 24 patients, a CBF of 18 ml/100 gm/min or less was found at some point after injury; the mortality rate was significantly higher in this subgroup, and survivors did worse. In some cases, ischemia was successfully treated by reducing hyperventilation or inducing arterial hypertension. These results support the above hypothesis, and suggest that early ischemia after traumatic brain injury may be an important factor determining neurological outcome. Moreover, these data indicate that early hyperventilation or lowering of blood pressure to prevent brain edema may be harmful.
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PMID:Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. 191 89

Anesthetic management during 85 STA-MCA anastomoses with or without encephalo-myosynangiosis for 64 patients with Moyamoya disease was evaluated retrospectively. Anesthetic agents included nitrous oxide-NLA (GONLA), nitrous oxide-halothane (GOF), nitrous oxide-enflurane (GOE), and their combinations. Slight hypercarbia (40 mmHg less than PaCO2 less than 50 mmHg) was essential to avoid cerebral ischemia. Several procedures to control heart rate by beta blockade or to control hypertension by nitroglycerin were required, because tachycardia and hypertension interfered with fine surgical procedure. During microsurgery HR of GONLA anesthetized patients was significantly lower. Postoperatively the patients anesthetized by GOE showed significantly lower PaCO2 compared with the GONLA anesthetized patients. So we recommend GONLA for anastomosis in patients with Moyamoya disease.
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PMID:[Anesthetic management of revascularization for moyamoya disease]. 192 Jul 89

We determined whether the rate of metabolic recovery and electrophysiological deficit after incomplete cerebral ischemia is related to intracellular pH (pHi) achieved at the end of ischemia in a dose-dependent manner. End-ischemic pHi was varied by employing two ischemic durations, 12 and 30 min, and by setting preischemic plasma glucose to approximately 80 or 400 mg/dl. Incomplete global ischemia was produced in anesthetized dogs by transient intracranial hypertension followed by 4 h of reperfusion, and pHi, ATP, and phosphocreatine (PCr) were measured with 31P magnetic resonance spectroscopy. Cerebral blood flow was reduced to approximately 6 ml.min-1.100 g-1 during ischemia. End-ischemic pHi was greater than 5.7 in all animals from various treatment groups except for four of seven dogs treated with 30-min hyperglycemic ischemia. When end-ischemic pHi remained greater than 5.7, there was nearly complete recovery of ATP, PCr, pHi, intracellular bicarbonate concentration [( HCO3-]i), and O2 consumption. Partial recovery of somatosensory-evoked potentials (SEP) occurred in most of these animals. In the 30-min hyperglycemic animals in which pHi fell below 5.5, ATP, PCr, and O2 consumption recovered by only one-half over 60 min of reperfusion and then declined to near-zero levels without SEP recovery. In addition, pHi remained less than 6.0, and [HCO3-]i remained less than 2 mM throughout reperfusion. We conclude that there is an apparent in vivo pHi threshold of approximately 5.5-5.7 during incomplete cerebral ischemia that is associated with an inability to significantly restore pHi and [HCO3-]i and with secondary deterioration of high-energy phosphate levels.
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PMID:Dependence of cerebral energy phosphate and evoked potential recovery on end-ischemic pH. 199 96

Although stroke, defined as a focal neurological deficit lasting more than 24 hr, is uncommon in the perioperative period, its associated mortality and long-term disability are high. No large-scale data are available to identify the importance of recognized risk factors for stroke in the perioperative period. A review of the literature shows that the incidence and mechanism of its occurrence are influenced by the presence of cardiovascular disease and the type of surgery. The most common cause of perioperative stroke is embolism. In non-cardiac surgery, the incidence of perioperative stroke is higher among the elderly. Properly administered, controlled hypotension is associated with minimal risk of stroke. Cerebral vasospasm may be the cause of focal cerebral ischaemia in eclamptic patients, and the aggressive treatment of hypertension may exacerbate the neurological damage. The risk of stroke associated with carotid endarterectomy is closely related to the preoperative neurological presentation, and the experience of the surgical/anaesthetic team. Symptomatic cerebrovascular disease, acute stroke, asymptomatic carotid lesions, preoperative assessment of risk, local and general anaesthesia, cerebral protection and monitoring during carotid endarterectomy are discussed with reference to reducing the risk of perioperative stroke. Adequate monitoring and protection have minimized the risk of ischaemia from carotid clamping, and the major mechanism of stroke is embolization.
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PMID:Perioperative stroke. Part I: General surgery, carotid artery disease, and carotid endarterectomy. 174 34

Risk factors for acute cerebral ischemia in geriatrics were assessed in two groups of 100 patients by comparing anamnestic data (based on a personal questionnaire) to laboratory data. The first group included patients affected by ischemic ictus not more than 45 days prior to the start of the study; the second group comprised geriatric subjects whose clinical characteristics were considered "normal for their age". The study took into account both the quality and quantity of findings. It was observed that risk factors play a more important role in women. Arterial hypertension, cardiopathies, cerebrovascular symptomatology, drug therapy, hyperfibrinogenemia and the number of red blood cells were the most important risk factors, followed by hematocrit, hemoglobin, total cholesterol and ATS ratio. The importance of the familiar factor for women and the lack of a role for HDL cholesterol in men were underlined.
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PMID:[Risk factors of acute cerebral ischemia in geriatrics. Personal observations]. 204 17

A consecutive series of 145 patients with acute aneurysmal subarachnoid hemorrhage (SAH) were operated on within 7 days of SAH and were prospectively evaluated over a 4-year period to determine if the timing of aneurysm surgery influenced the development of delayed cerebral ischemia. All patients were managed with a standardized policy of urgent surgical clipping and treatment with aggressive prophylactic postoperative volume expansion. Patients with delayed ischemic symptoms were additionally treated with induced hypertension. Forty-nine patients underwent surgery on Day 0 or 1 (Group 1) post-SAH, 60 patients on Day 2 or 3 (Group 2), and 36 patients on Days 4 through 7 (Group 3). Postoperative delayed cerebral ischemia developed in 16% of (Group 1) patients, in 22% of Group 2 patients, and in 28% of Group 3 patients. Cerebral infarction resulting from delayed cerebral ischemia developed in only 4% of Group 1 patients, 10% of Group 2 patients, and 11% of Group 3 patients. A bad clinical outcome as a result of delayed cerebral ischemia occurred in one Group 1 patient (2%), two Group 2 patients (3%), and one Group 3 patient (3%). Preoperative grade was not significantly correlated with the incidence or severity of delayed cerebral ischemia at any time interval except that patients in modified Hunt and Hess Grade I or II who underwent surgery on Day 0 or 1 after SAH had no strokes or bad outcomes from delayed cerebral ischemia. This study demonstrates that there is no rationale for delaying aneurysm surgery based on the time interval between SAH and patient evaluation.
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PMID:Relationship between the timing of aneurysm surgery and the development of delayed cerebral ischemia. 204 19

During carotid surgery a monitoring device that will identify patients with inadequate cerebral perfusion and impending cerebral damage after carotid clamping is desirable. Such patients may benefit from cerebral protective measures, which should be applied selectively as their use can also lead to complications. METHODS. In order to evaluate the reliability of somatosensory evoked responses as a means of detecting patients with insufficient collateral perfusion after carotid cross clamping, a prospective study involving 482 operations for reconstruction of supraaortic vessels was performed. Somatosensory evoked potentials (SEPs) were recorded from a cervical (C2-Fz) and a parietal (C3'/C4'-Fz) electrode above the ipsilateral hemisphere following stimulation of the contralateral median nerve. RESULTS. In 22 procedures (4.6%) complete flattening of the cortical SEP occurred after carotid cross clamping. In 7 of 9 cases in which no indwelling shunt was used despite electrical silence neurological deficits were found postoperatively. The SEP amplitude was restored in 12 of the remaining 13 patients with complete loss of the SEP after shunt insertion. Only 3 of these patients demonstrated neurological impairment. During 460 operations evoked potentials were always present. Nevertheless, 5 neurological sequelae were noticed despite unchanged SEP after carotid artery clamping. All deficits, however, were caused by embolization and were unrelated to reduced blood flow after carotid cross clamping. CONCLUSIONS. Our results confirm the reliability of SEP monitoring for the detection of significant cerebral ischemia after carotid clamping. In absence of the cortical SEP immediate shunt placement is necessary to avoid neurological deficits. On the other hand, the risks attendant on indiscriminate cerebral support (embolism after shunt placement, cardiac ischemia due to induced hypertension) can be avoided in the presence of cortical potentials. This allows protection of the heart and the brain by anesthetic management and enables the surgeon to perform endarterectomy with no hurry, to avoid technical failure. SEP data may also be helpful in decision making on reoperation to look for sources of embolization. In conclusion, advanced monitoring by somatosensory evoked responses may help to improve the outcome of carotid surgery.
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PMID:[Somatosensory evoked potentials in carotid surgery]. 204 7

Cerebral vasospasm occurs, following subarachnoid haemorrhage, in the majority of patients and is accompanied by cerebral ischaemia in 30%. The objectives of this article are to review (1) the effects of subarachnoid haemorrhage and vasospasm on cerebral blood flow (CBF); (2) the effects of induced hypotension and hypocapnia on CBF in these patients; (3) current therapy for cerebral ischaemia from vasospasm. The medical literature was searched using Index Medicus; for the period 1983-90 this search was done on a computer with the CD-ROM version of Index Medicus, Silver Platter. Papers were selected on the basis of validity and applicability to clinical practice; animal studies are included when human data is lacking. Cerebral vasospasm may decrease cerebral blood flow, disturb autoregulation and place the patient at risk for delayed cerebral ischaemia. Intraoperative induced hypotension and hypocapnia can decrease CBF further, although effects of either on outcome have not been evaluated. Calcium antagonists are effective for both the prevention and the treatment of delayed cerebral ischaemia. Of the mechanical treatments, systemic-arterial hypertension has the firmest scientific foundation, although this is frequently combined with haemodilution and blood volume expansion. There is a need for randomized clinical trials to assess the efficacy of these latter treatments.
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PMID:Haemodynamic considerations in the management of patients with subarachnoid haemorrhage. 206 13

To detect the functional reversibility and hemodynamic process in cerebral ischemia, the EEG topography cased on % time and amplitude was applied. % time and amplitude were obtained by the wave-form recognition method/EEGs were recorded under the resting state and during drug-induced conditions in 18 patients with steno-occlusion of main cerebral artery. The type of ischemic attack was TIA in 2 patients, RIND in 4, minor stroke in 7 and major stroke in 5. Six of 11 patients showed the improvement of EEG under induced hypertension. Four of those 6 patients were operated on ECIC bypass surgery, and all of them showed the improvement of clinical and EEG findings postoperatively. Twelve patients showed the deterioration of EEG under induced hypotension. Eight of them were operated on ECIC bypass surgery, and none of them suffered from reattack of cerebral ischemia postoperatively. Those preoperative EEG changes were observed mainly on the EEG topography of % time. And, the analysis of the EEG topography of % time under drug-induced conditions was available to study the pathophysiology of cerebral ischemia for selecting the suitable treatment.
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PMID:Clinical application of EEG topography in cerebral ischemia: detection of functional reversibility and hemodynamics. 209 4

Ischemic cerebral edema frequently develops after aneurysm surgery and may lead to severe intracranial hypertension. Of prime importance are reducing the level of ICP and preserving oligemic areas from becoming infarcted. Besides correction of factors known to worsen intracranial hypertension, several therapeutics may be of value: external CSF drainage, perfusion of mannitol, induced arterial hypertension and use of anesthetic agents with cerebral vasoconstricting capability. Hyperventilation is not recommended. Arterial hypotension and hypovolemia certainly contribute to aggravate cerebral ischemia and must be corrected. Cerebral ischemia may be reduced by two specific approaches: by improving cerebral oxygen transport in ischemic areas using arterial hypertension and calcium blockers rather than hemodilution or hypervolemia; by reducing cerebral metabolic rates with heavy anesthesia under the cover of a complete cardiovascular monitoring. In view of the large heterogenicity in cerebral lesions and physiopathological stages, a therapeutical trial appears suitable in each individual case. Criteria allowing to know if any therapeutic, used alone or in association, is beneficial include increase in blood flow in ischemic areas, reduction of ICP level and normalizing of indices like CSF or venous jugular blood lactate.
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PMID:[Treatment of ischemic cerebral edema with intracranial hypertension after neurosurgery of intracranial aneurysms]. 212 75


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