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Biomedical subjects

H van Crevel

Publications and source records attributed to H van Crevel.

At least 55 records · Page 3Linked to original sources
PubMed1988

Prediction of delayed cerebral ischemia, rebleeding, and outcome after aneurysmal subarachnoid hemorrhage.

Using logistic regression, we analyzed the predictive value of a number of entry variables with respect to the outcome variables delayed cerebral ischemia, rebleeding, and poor outcome (death or severe disability) in patients with aneurysmal subarachnoid hemorrhage. The entry variables were clinical condition on admission (grades on the Glasgow Coma Scale, Hunt and Hess system), the amount of subarachnoid and intraventricular blood and the presence of hydrocephalus on the admission computed tomogram, and antifibrinolytic treatment with tranexamic acid. We used data from a prospectively studied population of 176 patients admitted within 72 hours after subarachnoid hemorrhage. The risk of delayed cerebral ischemia was best predicted by the amount of subarachnoid blood, intraventricular blood, and antifibrinolytic treatment irrespective of clinical condition and hydrocephalus. The site of delayed cerebral ischemia was not related to the location of the subarachnoid hemorrhage. Antifibrinolytic treatment was the only entry variable (negatively) predicting the risk of rebleeding. Death or severe disability after 3 months was best predicted by the amount of subarachnoid blood and the initial clinical condition reflected by the grade on the Glasgow Coma Scale.

Blood↗
PubMed1987

Rerupture of intracranial aneurysms: a clinicoanatomic study.

In a series of 176 prospectively studied patients who survived for at least 24 hours after aneurysmal subarachnoid hemorrhage, 39 had at least one computerized tomography (CT)-proven rebleed within 4 weeks after the first rupture. There were peaks in the incidence of rebleeding at the end of the 2nd and 3rd weeks. Sudden loss of consciousness occurred in 35 patients, preceded in one-third of them by headache. A sudden increase in headache was a symptom of rebleeding in only one patient. Loss of brain-stem reflexes was recorded in 13 patients, respiratory arrest in six, and both symptoms in eight patients. Apnea was temporary in 11 patients. Rebleeding occurred as gross intraventricular hemorrhage in 20 patients, as a space-occupying hematoma in four, as both types of hemorrhage in three, and as a purely subarachnoid hemorrhage in 12. The location of the rebleed could not be inferred from the clinical features. Rebleeding was fatal in 51% of cases (two of 12 patients with a purely subarachnoid hemorrhage, and 18 of the other 27 patients (p less than 0.005)). The risk of rebleeding could not be predicted from the patients' clinical condition on admission or from the amount of subarachnoid blood identified on the initial CT scan. The risk of further rebleeding was significantly increased in survivors of a first rebleed (47%: p less than 0.01). Only seven (18%) of the 39 patients with rebleeding had survived at 3 months after the initial hemorrhage.

Adolescent↗
PubMed1986

Decision analysis of the management of incidental intracranial saccular aneurysms.

We used decision analysis to approach the dilemma "surgery or not?" in patients with incidental intracranial saccular aneurysms. To decide if a patient should undergo surgery, the following factors are of primary importance: age and general health of the patient, chance of rupture of the aneurysm, surgical mortality and morbidity, and patient preference for immediate and long-term risks. In a fictitious patient (a woman of 45 with migraine, otherwise healthy), surgery was the option with the greatest expected utility. Sensitivity analysis showed the influence of different factors. Other patients are also discussed, and "break-even" points for age versus surgical results are given.

Decision Making↗
PubMed1985

Acute hydrocephalus after aneurysmal subarachnoid hemorrhage.

Hydrocephalus, defined as a bicaudate index above the 95th percentile for age, was found in 34 (20%) of 174 prospectively studied patients with subarachnoid hemorrhage (SAH) who survived the first 24 hours and who underwent computerized tomography (CT) scanning within 72 hours. The occurrence of acute hydrocephalus was related to the presence of intraventricular blood, and not to the extent of cisternal hemorrhage. The level of consciousness was depressed in 30 of the 34 patients. Characteristic clinical features were present in 19 patients, including a gradual obtundation after the initial hemorrhage in 16 patients and small nonreactive pupils in nine patients (all with a Glasgow Coma Scale score of 7 or less). In the remaining 15 patients (44%), the diagnosis could be made only by CT scanning. After 1 month, 20 of the 34 patients had died: six from rebleeding (four after shunting), 11 from cerebral infarction (eight after an initial improvement), and three from other or mixed causes. Only one of nine patients in whom a shunt was placed survived, despite rapid improvement in all immediately after shunting. The mortality rate among patients with acute hydrocephalus was significantly higher than in those without, with the higher incidence caused by cerebral infarction (11 of 34 versus 12 of 140 cases, respectively; p less than 0.001). Death from infarction could not be attributed to the extent of cisternal hemorrhage, the use of antifibrinolytic drugs, or failure to apply surgical drainage, but could often be explained by the development of hyponatremia, probably accompanied by hypovolemia.

Acute Disease↗
PubMed1984

Antifibrinolytic treatment in subarachnoid hemorrhage.

We enrolled 479 patients with subarachnoid hemorrhage in a multicenter, randomized, double-blind, placebo-controlled trial to determine whether treatment with the antifibrinolytic agent tranexamic acid improves outcome by preventing rebleeding. At three months there was no statistical difference between the outcomes in the tranexamic acid group and the control group. Of the 173 patients who died, 84 had received tranexamic acid and 89 placebo (95 per cent confidence interval for the difference in mortality rate, -6 to 11 per cent). Similarly, when analysis was restricted to patients with an angiographically demonstrated aneurysm, there was no significant difference between the groups. This absence of effect was not due to a lack of antifibrinolytic action, since the rate of rebleeding was reduced from 24 per cent in the control group to 9 per cent in the tranexamic acid-treated group (chi-square = 18.07, P less than 0.001), but resulted from a concurrent increase in the incidence of ischemic complications (15 per cent in the control group and 24 per cent in the tranexamic acid group; chi-square = 8.07, P less than 0.01). We conclude that until some method can be found to minimize ischemic complications, tranexamic acid is of no benefit in patients with subarachnoid hemorrhage.

Cerebral Angiography↗
PubMed1984

Respiratory arrest in subarachnoid hemorrhage.

Sudden loss of consciousness and cardiorespiratory disorders occurred in 43 of 254 patients with subarachnoid hemorrhage. Two patients had ventricular fibrillation, 37 had one or more episodes with a disturbance of respiratory rhythm that required assisted ventilation, and 4 died suddenly without recorded vital signs. Sixteen patients recovered after resuscitation. The outcome could not be predicted at an early stage from the anatomic type of hemorrhage on CT, the initial presence or absence of brainstem reflexes, or the type of cardiorespiratory disorder. Spontaneous respiration and responsiveness returned within 1 hour in all patients who recovered.

Arrhythmias, Cardiac↗
PubMed1984

Causes of acute deterioration in patients with a ruptured intracranial aneurysm. A prospective study with serial CT scanning.

The authors studied the acute neurological deterioration in 150 patients with aneurysmal hemorrhage. These patients were closely observed for a 4-week period or until death or operation. Forty-six patients suffered a total of 62 episodes of deterioration that developed within 5 minutes after aneurysm rupture; 59 of these episodes consisted of severe impairment of consciousness. Computerized tomography (CT) was performed within a few hours of the event. Serial scans were obtained at least weekly after admission. Rebleeding was diagnosed as the cause of 42 episodes (68%), including six patients who died rapidly without a repeat CT scan. The final diagnosis of the cause in other acute episodes was epilepsy (in six), acute onset of ischemia (in three), and ventricular fibrillation (in one). Ten unexplained events occurred in nine patients. Rebleeding could be excluded with confidence in nine of these events, because the residual clots had disappeared or markedly decreased on CT. It is concluded that a purely clinical diagnosis of rebleeding will be incorrect in about every third patient, even if these patients are under close observation.

Cerebral Hemorrhage↗
PubMed1982

Pathogenesis of raised cerebrospinal fluid pressure.

Raised cerebrospinal fluid pressure may be caused by (a) subarachnoid CSF circulation blocks (b) obstruction of CSF absorption in the arachnoid villi (c) disorders of the venous return from the superior sagittal sinus to the heart. The common factor in these mechanisms is obstructed CSF drainage. Some clinical conditions illustrating these principles are reviewed.

Arachnoid↗