Biomedical subjects

D Hasan

Publications and source records attributed to D Hasan.

32 records · Page 2Linked to original sources

PubMed1991

Outcome in patients with subarachnoid haemorrhage and negative angiography according to pattern of haemorrhage on computed tomography.

15% of patients with spontaneous subarachnoid haemorrhage have normal cerebral angiograms; they fare better than patients with demonstrated aneurysms, though rebleeding and cerebral ischaemia can still occur. In patients with a normal angiogram and accumulation of blood in the cisterns around the midbrain--"perimesencephalic nonaneurysmal haemorrhage"--outcome is excellent. To test the hypothesis that rebleeding and disability in angiogram-negative subarachnoid haemorrhage might be limited to those with other patterns of haemorrhage on initial computed tomography (CT), complications and long-term outcome were studied in 113 patients with angiogram-negative subarachnoid haemorrhage, admitted between January, 1983, and July, 1990. All patients were investigated with third-generation CT scans within 72 h of the event, and with cerebral angiography. The mean follow-up period was 45 (range 6-96) months. None of 77 patients with a perimesencephalic pattern of haemorrhage on CT died or was left disabled as a result of the haemorrhage (0% [95% confidence interval 0-5%]). Among the other 36 patients, who had a blood distribution on CT indistinguishable from that in proven aneurysmal bleeds, 4 had rebleeds and 9 died or were left disabled as result of the haemorrhage (25% [14-43%]). Thus, two distinct subsets of patients with angiogram-negative subarachnoid haemorrhage should be recognised. Patients with a perimesencephalic pattern of haemorrhage have an excellent prognosis. Rebleeding, cerebral ischaemia, and residual disability occur exclusively in patients with aneurysmal patterns of haemorrhage on initial CT. Repeated angiography in search of an occult aneurysm is justified only in the patients with aneurysmal patterns.

Acute Disease↗

PubMed1991

The clinical course of perimesencephalic nonaneurysmal subarachnoid hemorrhage.

We studied the early clinical course of 65 patients with perimesencephalic (nonaneurysmal) subarachnoid hemorrhage. None of the patients rebled; none had delayed cerebral ischemia; and only 3 patients (5%) developed clinical signs of acute hydrocephalus, 2 requiring ventricular shunting. Hyponatremia and electrocardiographic changes were found in the same proportions as in patients with aneurysmal rupture. All patients had a good outcome after 3 months. To control for the influence of the relatively small amount of cisternal blood in perimesencephalic hemorrhage on the absence of delayed cerebral ischemia, we compared these 65 patients with 49 patients who had aneurysmal subarachnoid hemorrhage. This control group with aneurysms was selected according to a similar amount of cisternal blood, a comparable level of consciousness on admission, and absence of other factors known to increase the risk for delayed cerebral ischemia. We found that 4 of the 49 patients with aneurysmal hemorrhage developed delayed cerebral ischemia (Fisher's exact test, p = 0.03); therefore the relatively small amount of blood does not account for the absence of delayed cerebral ischemia in perimesencephalic hemorrhage. Patients with a perimesencephalic pattern of hemorrhage and a normal angiogram should be considered to have a distinct subset of subarachnoid hemorrhage and should be excluded from future treatment trials of patients with subarachnoid hemorrhage.

Adult↗

PubMed1991

Single photon emission computed tomography in patients with acute hydrocephalus or with cerebral ischaemia after subarachnoid haemorrhage.

Using single photon emission computed tomography (SPECT), cerebral blood flow was studied in eight patients with gradual deterioration in the level of consciousness after subarachnoid haemorrhage. Four had cerebral ischaemia and four had acute hydrocephalus. In patients with cerebral ischaemia, single photon emission computed tomography scanning showed multiple regions with decreased uptake of technetium-99M labelled d,l-hexamethyl-propylene amine oxime (99mTcHM-PAO) mainly in watershed areas. In patients with acute hydrocephalus, decreased uptake was seen mainly in the basal parts of the brain: around the third ventricle, around the temporal horns of the lateral ventricles, and in the basal part of the frontal lobe. After serial lumbar puncture, there was improvement of the uptake of 99mTc HM-PAO in these basal areas in three (convincingly in two and slightly in the other) of the four patients accompanied by clinical improvement in these three patients. These results suggest that patients with acute hydrocephalus and impaired consciousness after SAH, in contrast to patients with cerebral ischaemia, have decreased cerebral blood flow predominantly in the basal parts of the brain.

Acute Disease↗

PubMed1991

Treatment of acute hydrocephalus after subarachnoid hemorrhage with serial lumbar puncture.

Computed tomography demonstrated acute hydrocephalus less than or equal to 72 hours after subarachnoid hemorrhage in 24 (23%) of 104 patients. Of these 24 patients, six (25%) had no impairment of consciousness. In nine (11%) of the remaining 80 patients, acute hydrocephalus developed within 1 week after subarachnoid hemorrhage. With the exception of three patients, all 104 patients received antifibrinolytic treatment. Delayed clinical deterioration from acute hydrocephalus occurred in seven (29%) of the 24 patients with acute hydrocephalus on admission and in six (8%) of the remaining 80 patients. Serial lumbar puncture was performed in 17 patients. Twelve (71%) of the 17 patients treated with serial lumbar puncture, including 10 (77%) of the 13 patients with delayed deterioration from acute hydrocephalus after admission, achieved improvement in the level of consciousness. Four of these 17 patients (4% of all 104 patients) required an internal shunt. No patient deteriorated from coning following serial lumbar puncture. The rebleeding rate within 12 days after subarachnoid hemorrhage in hydrocephalic patients with serial lumbar puncture was not higher than the rate in those without hydrocephalus (two [12%] of 17 versus nine [13%] of 71). Neither meningitis nor ventriculitis was observed. We conclude that if neither a hematoma with a mass effect nor an obstructive element exists, cerebrospinal fluid drainage with serial lumbar puncture is a good alternative to ventricular drainage in patients with acute hydrocephalus after subarachnoid hemorrhage.

Acute Disease↗

PubMed1990

Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage.

The association between hyponatremia and cerebral ischemia was investigated in a consecutive series of 208 patients with subarachnoid hemorrhage who had a daily fluid intake of at least 3 L and in whom fluid restriction, to correct hyponatremia, was not applied. Hyponatremia occurred in 70 (34%) of the 208 patients. The occurrence of cerebral ischemia in patients with hyponatremia, 17 (24%) of 70 patients, was significantly higher than in patients without hyponatremia, 17 (12%) of 138 patients (chi 2 = 4.028, p = 0.045). Cerebral ischemia was not more often fatal in hyponatremic patients than in patients without hyponatremia. We conclude that patients with hyponatremia are at increased risk of developing cerebral ischemia even if fluid restriction is not applied.

Brain Ischemia↗

PubMed1989

Xanthochromia.

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Diagnosis, Differential↗

PubMed1989

Xanthochromia after subarachnoid haemorrhage needs no revisitation.

Recently it was contended that it is bloodstained cerebrospinal fluid (CSF) that is important in the diagnosis of subarachnoid haemorrhage (SAH) and not xanthochromia, and also that a normal CT scan and the absence of xanthochromia in the CSF do not exclude a ruptured intracranial aneurysm. The CSF findings were therefore reviewed of 111 patients with a proven SAH. All patients had xanthochromia of the CSF. Lumbar punctures were performed between 12 hours and one week after the ictus. Xanthochromia was still present in all (41) patients after 1 week, in all (32) patients after 2 weeks, in 20 of 22 patients after three weeks and in 10 of 14 patients after four weeks. In six years we identified only 12 patients with sudden headache, normal CT, bloodstained CSF, and no xanthochromia. Angiography was carried out in three and was negative. All 12 patients survived without disability and were not re-admitted with a SAH (mean follow up 4 years). It is concluded that it is still xanthochromia that is important in the diagnosis of SAH and not bloodstained CSF. Furthermore a normal CT scan and the absence of xanthochromia do exclude a ruptured aneurysm, provided xanthochromia is investigated by spectrophotometry and lumbar puncture is carried out between 12 hours and 2 weeks after the ictus.

Humans↗

PubMed1989

Effect of fluid intake and antihypertensive treatment on cerebral ischemia after subarachnoid hemorrhage.

We prospectively studied 244 consecutive patients with subarachnoid hemorrhage who were admitted within 72 hours to the same institution between November 1977 and May 1987 and who were not treated with antifibrinolytics. From November 1977 through December 1982 (the first study period), daily fluid intake was 1.5-2.1 and fluid restriction was applied when hyponatremia developed; antihypertensives were administered to all patients with high blood pressure. From January 1983 through April 1987 (the second study period), daily fluid intake was at least 3 l, fluid restriction was not applied, and antihypertensives were administered only when patients were receiving this treatment before admission; calcium antagonists were not administered. Entry variables of the patients admitted during the two study periods were not significantly different, although patients admitted during the second study period were at slightly increased risks of developing cerebral ischemia and of having a poor outcome. Despite this, cerebral ischemia occurred less frequently among patients admitted during the second study period than among those admitted during the first (16 [10%] of 155 patients vs. 19 [21%] of 89 patients; p = 0.030). Overall mortality decreased from 46% to 36% while mortality among patients with cerebral ischemia decreased from 60% to 31% (difference not significant). Rebleeding and acute hydrocephalus occurred with the same frequency among patients admitted during both study periods. We conclude that the combination of increased fluid intake and the avoidance of antihypertensives helps prevent cerebral ischemia after subarachnoid hemorrhage.

Antihypertensive Agents↗

PubMed1989

Short-term tranexamic acid treatment in aneurysmal subarachnoid hemorrhage.

Antifibrinolytic treatment for 4 weeks after a subarachnoid hemorrhage has been shown to have no effect on outcome since a reduction in the rate of rebleeding was offset by an increase in ischemic events. To determine if a shorter course (4 days) of antifibrinolytic treatment before the expected onset of ischemic complications might reduce the rate of rebleeding yet avoid ischemic complications, we prospectively studied a series of 119 patients with subarachnoid hemorrhage; 479 patients with subarachnoid hemorrhage from our previous randomized double-blind study (238 treated with placebo, 241 with long-term tranexamic acid) served as historical control groups. At 3 months' follow-up, the outcome of patients treated with short-term tranexamic acid was not different from that of patients treated with long-term tranexamic acid. The rate of rebleeding (24 of 119, 20%) was near that with placebo (56 of 238, 24%). In contrast, the rate of cerebral infarction (33 of 119, 28%) was almost identical to that after long-term tranexamic acid (59 of 241, 24%), although mortality from cerebral infarction was reduced. Compared with historical control groups, treatment with tranexamic acid for 4 days fails to reduce the incidence of rebleeding but still increases the rate of cerebral infarction.

Cerebral Angiography↗

PubMed1989

Management problems in acute hydrocephalus after subarachnoid hemorrhage.

In a consecutive series of 473 patients admitted within 72 hours after a subarachnoid hemorrhage, 91 (19%) had hydrocephalus on the initial computed tomogram. Consciousness was unimpaired in 25 of the 91 (28%). In 11 more patients acute hydrocephalus developed within 1 week after subarachnoid hemorrhage. Thirty-eight (8%) of all 473 patients subsequently showed clinical deterioration because of acute hydrocephalus; 11 of these 38 had fluctuations in the level of consciousness. Of the 66 patients with acute hydrocephalus and impaired consciousness on admission, 26 (39%) spontaneously improved within 24 hours. Ventricular drainage was performed in 32 (31%) of the 102 patients with acute hydrocephalus (7% of all 473 patients). Consciousness improved after ventricular drainage in 25 (78%) of the 32 patients. Ventriculitis developed in 12 of the 24 patients with external drainage, mainly after greater than 3 days of drainage, and in none of the eight patients with an internal shunt. Among the 340 patients with aneurysmal subarachnoid hemorrhage and no long-term tranexamic acid treatment, the frequency of rebleeding in patients with ventricular drainage (43% of 23) was significantly higher than in hydrocephalic patients without drainage (15% of 52 patients; chi 2 = 5.009, p = 0.025) and patients without acute hydrocephalus (20% of 265 patients; chi 2 = 5.521, p = 0.019). We conclude that spontaneous improvement occurs in half of the patients with acute hydrocephalus and impaired consciousness on admission, which is usually apparent within 24 hours, and that the outcome of patients who need ventricular drainage will improve if rebleeding and infection after insertion of the ventricular drain can be prevented.

Acute Disease↗

PubMed1989

Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage.

In this study with randomized controls, we administered fludrocortisone acetate to 46 of 91 patients with subarachnoid hemorrhage in an attempt to prevent excessive natriuresis and plasma volume depletion. Fludrocortisone significantly reduced the frequency of a negative sodium balance during the first 6 days (from 63% to 38%, p = 0.041). A negative sodium balance was significantly correlated with decreased plasma volume during both the first 6 days (p = 0.014) and during the entire 12-day study period (p = 0.004). Although fludrocortisone treatment tended to diminish the decrease in plasma volume, the difference was not significant (p = 0.188). More patients in the control group developed cerebral ischemia (31% vs. 22%) and, consequently, more control patients were treated with plasma volume expanders (24% vs. 15%), which may have masked the effects of fludrocortisone on plasma volume. Fludrocortisone therefore reduces natriuresis and remains of possible therapeutic benefit in the prevention of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

Clinical Trials as Topic↗

PubMed1989

Serial electrocardiographic recording in aneurysmal subarachnoid hemorrhage.

We prospectively studied serial electrocardiograms in 61 patients with aneurysmal subarachnoid hemorrhage. Electrocardiographic changes were related to the initial level of consciousness, to subsequent events, and to outcome after 3 months. All 61 patients had at least one abnormal electrocardiogram, but cardiac disease did not contribute directly to morbidity or mortality. Fast rhythm disturbances, ischemic changes, or both on the electrocardiograms were significantly correlated with poor outcome but not with specific outcome events, particularly not with rebleeding or cerebral ischemia. The Glasgow Coma Scale score on admission and the amount of cisternal and (to a lesser extent) intraventricular blood on the initial computed tomogram were also significantly correlated with poor outcome, but these factors only partially confounded the relation between electrocardiographic abnormalities and poor outcome. We conclude that in patients with aneurysmal subarachnoid hemorrhage, electrocardiographic abnormalities do not herald impending cardiac disease but indirectly reflect adverse intracranial factors. Electrocardiographic abnormalities may therefore have some independent value in predicting poor outcome.

Arrhythmias, Cardiac↗

PubMedDate not supplied

Regional cerebral blood flow and cerebrovascular risk factors in the elderly population.

Regional cerebral blood flow (rCBF) was studied in 60 elderly persons (aged 65 to 84 years) recruited from a population-based study, with single photon emission computed tomography using technetium 99m-labeled hexamethylpropylene amine oxime. We investigated whether it is only age that affects rCBF or whether other factors can be indentified that explain this relationship. Using multiple linear regression analysis, increasing age was significantly associated with rCBF decrease in parietal, temporo-parietal, and temporal cortex, but not in frontal cortex. Adjustment with several risk factors for cerebrovascular disease, including hypertension, history of myocardial infarction, factor VIIc, factor VIIIc, cholesterol and HDL cholesterol, smoking, and diabetes mellitus had no influence on these relations. Conversely, the association between age and rCBF was no longer statistically significant after adjustment with fibrinogen and indicators of carotid atherosclerosis, including intima-media wall thickness of the carotid artery and plaques in the carotid artery. Correction with local ratings of cortical atrophy did not affect the relations between age and rCBF. The results suggest that in the elderly population rCBF declines with age in posterior cortical areas and that these changes may well be explained by the presence of atherosclerosis. Reduced contractility of the vascular muscle wall with increasing age resulting from atherosclerosis may be the underlying mechanism.

Aged↗

PubMedDate not supplied

Nonaneurysmal perimesencephalic subarachnoid hemorrhage: CT and MR patterns that differ from aneurysmal rupture.

We describe a characteristic distribution of cisternal blood in 52 patients with nonaneurysmal subarachnoid hemorrhage proved by a normal angiogram. On CT, the center of the bleeding was located immediately anterior to the brainstem in all patients, which was confirmed in four patients who were studied with MR imaging. Extension to the ambient cisterns or to the basal parts of the sylvian fissures was common, but the lateral sylvian or anterior interhemispheric fissures were never completely filled with blood. Rupture into the ventricular system did not occur. MR demonstrated downward extension of the blood anterior to the brainstem as far as the medulla, but failed to detect the source of hemorrhage. Our aim was to determine whether this so-called nonaneurysmal perimesencephalic hemorrhage could be distinguished from aneurysmal subarachnoid hemorrhage on early CT scans. Two neuroradiologists were shown a consecutive series of 221 CT scans of patients with subarachnoid hemorrhage who subsequently underwent angiography. Only one patient with a basilar artery aneurysm on angiography was incorrectly labeled by both observers as having a nonaneurysmal perimesencephalic pattern of hemorrhage. The high predictive value of the perimesencephalic pattern of hemorrhage for a normal angiogram (0.95 and 0.94, respectively, for the two observers) and the excellent interobserver agreement (kappa 0.87) demonstrate that nonaneurysmal perimesencephalic hemorrhage can be distinguished on CT in the majority of patients. Recognition of this pattern of hemorrhage is important as patients with this subset of subarachnoid hemorrhage have an excellent prognosis.

Adult↗