Articles: subarachnoid-hemorrhage.
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Ultrasound Med Biol · Jan 1995
Computerised transient hyperaemic response test--a method for the assessment of cerebral autoregulation.
A simple bedside test has been developed to assess the state of autoregulation in subarachnoid haemorrhage patients. Transcranial Doppler was used to measure blood flow velocity in the middle cerebral artery after a brief common carotid compression. Acceleration of blood flow postcompression was interpreted as evidence of intact cerebral autoregulation. ⋯ The flow velocity signal from the TCD was recorded, carotid compression and release automatically detected and the test results immediately displayed and stored in a database. The program was verified in 614 tests; 552 of them were analysed off-line using previously recorded data and 62 on-line during the examination. A significant correlation was found between the results of computerised testing and the patient's neurological state.
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Acta neurochirurgica · Jan 1995
Cerebral oedema after subarachnoid haemorrhage. Pathogenetic significance of vasopressin.
The authors report the frequency, characteristic clinical symptoms, laboratory alterations and diagnostic criteria of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after subarachnoid haemorrhage. The data on 290 patients with subarachnoid haemorrhage (SAH) during a period of years at the Division of Neurosurgery, University Medical School, Szeged, are analysed. Twenty-seven (9.3%) patients developed SIADH. ⋯ AVP plays an important role in the development of antidiuresis following water loading and disturbance of the brain water and electrolyte balance after SAH. Water retention and the higher brain water and sodium accumulation could be totally prevented by administration of a V2 antagonist. These results demonstrate that cerebral oedema generated by artificial cerebral bleeding in rats is significantly reduced following the administration of a highly specific V2 antagonist, suggesting a new approach to the treatment of SIADH.
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Acta neurochirurgica · Jan 1995
The effect of nimodipine on autoregulation of cerebral blood flow after subarachnoid haemorrhage in rat.
Disturbance of the autoregulation of the cerebral blood flow (CBF) is frequently seen following subarachnoid haemorrhage (SAH) and is possibly partly caused by cerebral ischaemia. It is well-known, that the calcium channel blocker nimodipine reduces the incidence of cerebral infarction and ischaemic dysfunction after SAH. The aim of the present study was to investigate the effect of nimodipine on autoregulation of CBF in an experimental model of SAH. ⋯ In the control rats the autoregulation was severely disturbed, no plateau was found where CBF was independent of changes in the arterial blood pressure (MABP). In rats treated with intravenous nimodipine (0.03 mg/kg body weight/h), CBF was 33.0% higher and MABP 5.3% higher compared with the controls. CBF was found constant in the MABP interval between 60 and 100 mmHg which indicates, that nimodipine improves the autoregulation of CBF after SAH.
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Journal of anesthesia · Dec 1994
Preoperative hypoxemia in conscious patients after subarachnoid hemorrhage.
We retrospectively examined partial arterial pressure of oxygen (Pao2) afer subarachnoid hemorrhage (SAH), adjusted for patient-related risk factors for hypoxemia in 51 adult patients with no disturbance of consciousness undergoing surgery for clipping of intracranial aneurysms. A control group of 174 patients undergoing other operations were used for comparison. ⋯ In three patients in the SAH group, Pao2 was less than 60 mmHg. Close monitoring of arterial oxygenation with pulse oximetry is desirable, and supplemental oxygen should be considered during transfer from the patients' room to the operating suite, even for conscious patients of SAH without cardiopulmonary disease.
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Nimodipine is a lipophilic dihydropyridine calcium antagonist which is used to reduce the incidence and severity of delayed cerebral ischaemia in patients with subarachnoid haemorrhage. This article reviews its mechanism of action, pharmacology and indications for use.