D. Hasan

Detection of subarachnoid haemorrhage on early CT: is lumbar puncture still needed after a negative scan?

Computed tomography may be normal in up to 5% of patients who are investigated within one or two days after subarachnoid haemorrhage. This study investigated the need for further diagnostic evaluation after a normal CT scan was found very early (within 12 hours) in patients suspected of subarachnoid haemorrhage. A consecutive series of 175 patients with sudden headache and a normal neurological examination who had first CT within 12 hours after the onset of headache were investigated. The patients with normal CT underwent lumbar puncture, but not earlier than 12 hours after the event. Computed tomography showed subarachnoid blood in 117 patients, and was normal in 58. Spectrophotometric analysis of CSF gave evidence for a subarachnoid haemorrhage in two of these 58 patients (3%; 95% confidence interval (95% CI) 0.4-12%); a ruptured aneurysm was found in both. Thus CT was normal in two of 119 patients with a definite subarachnoid haemorrhage (2%; 95% CI 0.2-6%). It is concluded that in patients with sudden headache but normal CT a deferred lumbar puncture is necessary to rule out subarachnoid haemorrhage, even if CT is performed within 12 hours after the onset of symptoms.

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.

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.

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.

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.

Amount of blood on computed tomography as an independent predictor after aneurysm rupture.

Background and Purpose After admission to the hospital of patients with aneurysmal subarachnoid hemorrhage, we assessed the predictive value of the extent of the hemorrhage on computed tomography in addition to that of clinical grading scales for poor outcome, infarction, and rebleeding. Methods We studied 471 consecutive patients with aneurysmal subarachnoid hemorrhage and used logistic regression with step-wise forward selection of variables. Results On admission, poor outcome was predicted by a low Glasgow Coma Scale score (odds ratio, 0.8; 95% confidence interval, 0.7-0.9); treatment with fluid restriction (2.5; 1.6-4.0); age over 52 (2.6; 1.7-3.9); loss of consciousness at ictus (1.7; 1.1-2.6); or a large amount of subarachnoid blood (2.0; 1.3-3.1). Delayed infarction was predicted by a large amount of subarachnoid blood (1.8; 1.2-2.6) or treatment with tranexamic acid (1.6; 1.1-2.4). Rebleeding was predicted by treatment with tranexamic acid (0.4; 0.3-0.7; protective effect); age over 52 (1.9; 1.2-3.0); loss of consciousness at ictus (1.7; 1.1-2.7); or admission to a neurosurgery service (0.6; 0.3-0.9; protective effect). Comparison of the observed and predicted outcome events showed that inclusion of the amount of subarachnoid blood into a predictive model added little to the prediction of poor outcome in general, but much to the prediction of delayed cerebral ischemia. Conclusions The total amount of subarachnoid blood on the initial computed tomogram has independent predictive power for the occurrence of delayed cerebral ischemia.

Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage A meta-analysis

Impact of cardiac complications after aneurysmal subarachnoid hemorrhage (SAH) remains controversial. We performed a meta-analysis to assess whether EKG changes, myocardial damage, or echocardiographic wall motion abnormalities (WMAs) are related to death, poor outcome (death or dependency), or delayed cerebral ischemia (DCI) after SAH. Methods: Articles on cardiac abnormalities after aneurysmal SAH that met predefined criteria and were published between 1960 and 2007 were retrieved. We assessed the quality of reports and extracted data on patient characteristics, cardiac abnormalities, and outcome measurements. Poor outcome was defined as death or dependence by the Glasgow Outcome Scale (dichotomized at ≤3) or the modified Rankin scale (dichotomized at >3). If studies used another dichotomy or another outcome scale, we used the numbers of patients with poor outcome provided by the authors. We calculated pooled relative risks (RRs) with corresponding 95% confidence intervals for the relation between cardiac abnormalities and outcome measurements. Results: We included 25 studies (16 prospective) with a total of 2,690 patients (mean age 53 years; 35% men). Mortality was associated with WMAs (RR 1.9), elevated troponin (RR 2.0) and brain natriuretic peptide (BNP) levels (RR 11.1), tachycardia (RR 3.9), Q waves (RR 2.9), ST-segment depression (RR 2.1), T-wave abnormalities (RR 1.8), and bradycardia (RR 0.6). Poor outcome was associated with elevated troponin (RR 2.3) and creatine kinase MB (CK-MB) levels (RR 2.3) and ST-segment depression (RR 2.4). Occurrence of DCI was associated with WMAs (RR 2.1), elevated troponin (RR 3.2), CK-MB (RR 2.9), and BNP levels (RR 4.5), and ST-segment depression (RR 2.4). All RRs were significant. Conclusion: Markers for cardiac damage and dysfunction are associated with an increased risk of death, poor outcome, and delayed cerebral ischemia after subarachnoid hemorrhage. Future research should establish whether these cardiac abnormalities are independent prognosticators and should be directed toward pathophysiologic mechanisms and potential treatment options.

Impact of Medical Treatment on the Outcome of Patients After Aneurysmal Subarachnoid Hemorrhage

BACKGROUND AND PURPOSE The rationale behind early aneurysm surgery in patients with subarachnoid hemorrhage (SAH) is the prevention of rebleeding as early as possible after SAH. In addition, by clipping the aneurysm as early as possible, one can apply treatment for cerebral ischemia more vigorously (induced hypertension) without the risk of rebleeding. Hypervolemic hemodilution is now a well-accepted treatment for delayed cerebral ischemia. We compared the prospectively collected clinical data and outcome of patients admitted to the intensive care unit in the period 1977 to 1982 with those of patients admitted in the period 1989 to 1992 to measure the effect of the change in medical management procedures on patients admitted in our hospital with SAH. METHODS We studied 348 patients admitted within 72 hours after aneurysmal SAH. Patients with negative angiography results and those in whom death appeared imminent on admission were excluded. The first group (group A) consisted of 176 consecutive patients admitted from 1977 through 1982. Maximum daily fluid intake was 1.5 to 2 L. Hyponatremia was treated with fluid restriction (<1 L/24 h). Antihypertensive treatment with diuretic agents was given if diastolic blood pressure was >110 mm Hg. Patients in the second group (172 consecutive patients; group B) were admitted from 1989 through 1992. Daily fluid intake was at least 3 L, unless cardiac failure occurred. Diuretic agents and antihypertensive medications were avoided. Cerebral ischemia was treated with vigorous plasma volume expansion under intermittent monitoring of pulmonary wedge pressure, cardiac output, and arterial blood pressure, aiming for a hematocrit of 0.29 to 0.33. Aneurysm surgery was planned for day 12. RESULTS Patients admitted in group B had less favorable characteristics for the development of cerebral ischemia and for good outcome when compared with patients in group A. Despite this, we found a significant decrease in the frequency of delayed cerebral ischemia in patients of group B treated with tranexamic acid (P=0.00005 by log rank test) and significantly improved outcomes among patients with delayed cerebral ischemia (P=0.006 by chi2 test) and among patients with deterioration from hydrocephalus (P=0.001 by chi2 test). This resulted in a significant improvement of the overall outcome of patients in group B when compared with those in group A (P=0.006 by chi2 test). The major cause of death in group B was rebleeding (P=0.011 by chi2 test). CONCLUSIONS We conclude that the outcome in our patients with aneurysmal SAH was improved but that rebleeding remains a major cause of death. Patient outcome can be further improved if we can increase the efficacy of preventive measures against rebleeding by performing early aneurysm surgery.

Definition of initial grading, specific events, and overall outcome in patients with aneurysmal subarachnoid hemorrhage. A survey.

Background and Purpose Scientific communication in medicine can be effective only if reports are based on unequivocal criteria for clinical conditions or specific diagnoses. Methods We reviewed all articles about subarachnoid hemorrhage published in nine neurosurgical or neurological journals from 1985 through 1992 and assessed the presence and the precision of definitions used for reporting the initial grade, the specific complications of rebleeding, delayed cerebral ischemia, and hydrocephalus, and the overall outcome. We identified 184 articles reporting direct observations in at least 10 patients on one or more of these conditions. Results Of 161 articles reporting the initial condition, only 19% used an unequivocal grading system (World Federation of Neurological Surgeons Scale or Glasgow Coma Scale); this proportion did not increase after 1988, when the World Federation of Neurological Surgeons Scale was introduced. The specific outcome events of rebleeding, ischemia, and hydrocephalus (283 instances) were sufficiently defined in only 31% of instances, incompletely in 22%, and not at all in 47%. The proportions were similar when the results were analyzed according to the type of complication, the year of publication, or per study. The four exclusively neurosurgical journals featured suitable definitions for any of the three outcome events in 20% of 209 instances, whereas the five mainly neurological journals published fewer articles about subarachnoid hemorrhage (74 instances of outcome events) but more often with precise criteria (65%). Overall outcome was adequately reported in 63% of all articles, with an increase over the years (54% in 1985 through 1988, 71% in 1989 through 1992). Conclusions Reports about subarachnoid hemorrhage require closer scrutiny before publication to ascertain whether the conclusions about specific outcome events are based on unequivocal criteria.

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.