Current issues of ACP Journal Club are published in Annals of Internal Medicine


Amount of blood in aneurysmal subarachnoid hemorrhage

ACP J Club. 1993 Nov-Dec;119:84. doi:10.7326/ACPJC-1993-119-3-084

Source Citation

Brouwers PJ, Dippel DW, Vermeulen M, et al. Amount of blood on computed tomography as an independent predictor after aneurysm rupture. Stroke. 1993 Jun;24:809-14.



To compare and combine 3 clinical scales and quantity of blood measured on computed tomography (CT) scans in predicting outcome for patients hospitalized with aneurysmal subarachnoid hemorrhage (SAH).


Inception cohort of consecutive patients followed 3 months after hospital discharge.


3 neurology centers in the Netherlands and 2 neurosurgery centers in Great Britain.


471 patients hospitalized within 72 hours of the first signs and symptoms of SAH who had confirmation of SAH on initial CT scan or in cerebrospinal fluid. Moribund patients were excluded.

Assessment of prognostic factors

The quantity of intraventricular and cisternal blood on CT scans was graded for each of the 4 ventricles and 10 basal cisterns and fissures on a scale of 0 (no blood) to 3 (completely filled). Age, gender, blood pressure, cardiovascular disease, loss of consciousness at ictus, Glasgow Coma Scale score, World Federation of Neurological Societies score, and Hunt and Hess classification were recorded.

Main outcome measures

Cerebral infarction, rebleeding, and poor outcome (defined as death, persistent vegetative state, or severe disability). Good outcome was defined as moderate disability or good recovery.

Main results

Of 471 patients, 155 had cerebral infarctions, 106 rebled, and 247 had poor outcomes 3 months after hospital discharge. Using stepwise logistic regression, predictors of poor outcome were Glasgow Coma Scale scores < 14 (odds ratio [OR] 1.28, 95% Cl 1.15 to 1.43), fluid restriction (OR 2.52, Cl 1.60 to 3.99), age > 52 years (OR 2.60, Cl 1.73 to 3.91), loss of consciousness at ictus (OR 1.72, CI 1.14 to 2.64), and quantity of subarachnoid blood (score > 14)(OR 2.01, Cl 1.29 to 3.13). Predictors of delayed cerebral infarction were quantity of subarachnoid blood (score < 14) (OR 1.79, Cl 1.21 to 2.64) and treatment with tranexamic acid (OR 1.59, Cl 1.07 to 2.37). Rebleeding was less frequent after treatment with tranexamic acid (OR 0.43, Cl 0.27 to 0.68) but more frequent for age > 52 years (OR 1.92, Cl 1.21 to 3.03), loss of consciousness at ictus (OR 1.70, Cl 1.08 to 2.68), and admission to a neurosurgery service (OR 0.57, Cl 0.34 to 0.93).


The quantity of subarchnoid blood on the initial CT scan was an independent predictor of delayed cerebral infarction after subarachnoid hemorrhage. Antithrombolytic therapy was also associated with delayed cerebral infarction.

Source of funding: Not stated.

For article reprint: Dr. P.J. Brouwers, Department of Neurology, Medisch Spectrum Twente, Postbus 50000, 7500 KA Enschede, the Netherlands. FAX 31-53-873-072.


Management of patients with SAH has improved dramatically in the past 15 years. A major cause of death in these patients was rebleeding; this can now be prevented by obliterating the aneurysm soon after the initial hemorrhage (an advance permitted by improved surgical and radiologic techniques). The remaining serious problem is delayed cerebral ischemia, occurring as a consequence of cerebral vasospasm. The mechanisms of vasospasm are not well understood; however, the consequence of cerebral infarction often leads to disability or death. Delayed ischemia is more frequent if fluid restriction is used to treat hyponatremia or if antithrombolytic treatment is administered (although the latter decreases rebleeding of unsecured aneurysms) (1).

Fisher and colleagues (2) posited a relation between thickness of cisternal blood in SAH and delayed cerebral ischemia in a 1980 case series. Since then, physicians interested in SAH have generally accepted their qualitative observation. The results of this study by Brouwers and colleagues confirm that a large amount of subarachnoid blood on CT scan represents a risk for delayed cerebral infarction independent of antithrombolytic therapy or fluid restriction; their work also shows the dangers of these latter modalities. The authors also showed that age > 52 years, loss of consciousness at ictus, any abnormality on the Glasgow Coma Scale, any neurologic abnormality worse than headache, or an isolated cranial nerve palsy is associated with poor outcome.

This study was begun in 1977; the management of SAH patients has changed profoundly since it started. These findings do, however, support current recommendations for early aneurysm obliteration, volume expansion, and avoidance of antithrombolytic agents.

Thomas P. Bleck, MD
University of Virginia Charlottesville, Virginia, USA