eMedicine Specialties > Neurology > Neurological Emergencies

Subarachnoid Hemorrhage: Follow-up

Author: George I Jallo, MD, Associate Professor of Neurosurgery, Pediatrics and Oncology, Director, Clinical Pediatric Neurosurgery, Department of Neurosurgery, Johns Hopkins University School of Medicine
Coauthor(s): Tibor Becske, MD, Assistant Professor, Department of Neurology, New York University Medical Center
Contributor Information and Disclosures

Updated: Dec 21, 2009

Follow-up

Further Inpatient Care

Inpatient or subacute rehabilitation (ie, physical, occupational, and speech therapy) is often appropriate.

Further Outpatient Care

• Neurosurgery clinic follow-up in 4-6 weeks
• Outpatient physical therapy/occupational/speech therapy as needed

Transfer

• Rehabilitation

Complications

• Hydrocephalus
  • Subarachnoid hemorrhage can cause HCP by 2 mechanisms—obstruction of CSF pathways (ie, acute, obstructive, noncommunicating type) and blockage of arachnoid granulations by blood breakdown products (ie, delayed, nonobstructive, communicating type).
    • Acute HCP may present immediately or within the first 7 days after SAH.
    • Delayed HCP has a more insidious and indolent presentation.
  • Acute (ie, obstructive) HCP is caused by compromise of CSF circulation pathways by interfering with CSF outflow through the sylvian aqueduct, fourth ventricular outlet, basal cisterns, and subarachnoid space. CSF production and absorption rates are unaltered. The presence of intraventricular blood is the strongest determinant for the development of acute HCP due to either blockage of CSF pathways by blood clot or diminished CSF outflow as a result of significantly elevated CSF viscosity.
  • Other factors increasing the risk of developing acute (obstructive) HCP include bilateral ambient cisternal blood, increased age, vasospasm, and use of antifibrinolytic drugs. HCP results in increased ICP and ventricular dilatation, decreased basal blood flow, and decreased level of consciousness. It is associated with lower preoperative grade and poorer prognosis.
• Rebleeding
  • The incidence of this dreadful complication is greatest in the first 2 weeks. The peak is within 24-48 hours following initial SAH (approximately 6%), with a rate of 1.5% per day for the next 12-13 days. The cumulative 2-week incidence is 20-30% in unoperated patients. The rebleeds in the first days ("blow out" hemorrhages) are thought to be related to the unstable nature of the aneurysmal thrombus as opposed to lysis of the clot sitting over the rupture site. Clinical factors that increase the likelihood of rebleeding include hypertension, anxiety⁷ , agitation, and seizures. Rebleeding is the cause of 7% of deaths in aneurysmal SAH.
  • After the first 30 days, rebleed rate decreases to 1.5% per year for the first 10 years. In another study, rebleeding was reported at a rate of 3% per year after 6 months, with a 67% mortality rate at 20 years. Initially, the high complication rate related to early clipping of the aneurysms was thought to outweigh the risk of rebleeding, and a philosophy of delayed surgery was generally accepted. With the improvement of surgical technique, especially since the routine use of microneurosurgical techniques, a major change in this thinking has occurred in favor of early surgery for patients with aneurysms of favorable grade.
• Delayed ischemia
  • Presently, delayed ischemia is the most common cause of death and disability following aneurysmal SAH. It has to some degree "compensated for" the improved rebleed rate related to early surgical clipping. An estimated 10-20% of patients with aneurysmal SAH suffer delayed cerebral ischemia, resulting in permanent disability or death. This complication alone accounts for 14-32% of deaths and permanent disability in large studies, while the direct effect of aneurysm rupture accounts for 25% and rebleeding for 17.6%.
  • Incidence of angiographic vasospasm is 30-70%; of these patients, 20% become symptomatic. Vasospasm is believed to be induced in areas of thick subarachnoid clot. The putative agent responsible for vasospasm is oxyhemoglobin, but its true etiology and pathogenesis remain to be elucidated. Vasospasm has its onset on day 3 after SAH, is maximal about days 6-8, and usually resolves around day 12. The actual distribution of risk of clinical vasospasm differs according to whether the patient has had a prior SAH. In patients with no prior SAH, most frequent time of onset is between days 10 and 17, with only a 4.2% incidence on day 3. In patients with previous SAH, incidence of vasospasm is 38.7% in the first 3 days and only 20% between days 10 and 17.
  • Overall, close to 50% of patients develop vasospasm in the peak period. Correlation between the initial CT scan and the incidence of vasospasm is well established. When the CT scan fails to demonstrate blood or shows only a thin layer, vasospasm is unlikely. If the CT shows significant blood clot of 5 x 3 mm or larger size, severe angiographic spasm and clinical deficits follow in nearly all cases.
• Intracerebral hemorrhage (ICH): Radiologically, ICH from aneurysmal rupture can look identical to hypertensive hemorrhage. The mechanism of ICH is direct rupture of aneurysm into the brain; it accounts for about 40% of cases of ICH. It commonly results from internal cerebral artery (ICA), pericallosal, and anterior cerebral artery (ACA) aneurysms. Secondary rupture of subarachnoid hematoma into the brain parenchyma most commonly arises from MCA aneurysms. Overall incidence of ICH from ACA is 44%; MCA 26%; ICA 21%; and pericallosal 10%.
• Intraventricular hemorrhage (IVH): Found in 13-28% of clinical cases of ruptured aneurysms and in 37-54% of autopsy cases, IVH is a significant predictor of poor neurological grade and outcome. Patients with IVH are at higher risk of developing HCP. In one study of 91 patients, it was associated with an overall mortality rate of 64%. Key prognostic indicator is the degree of ventricular dilatation. Sources of IVH are ACA (40%), ICA (25%), MCA (21%), and vertebrobasilar artery (VBA, 14%).
• Subdural hematoma (SDH): SDH is rare following aneurysmal SAH, with reported incidence of 1.3-2.8% in clinical series and as high as 20% in autopsy series. The mechanisms of SDH involve tearing of arachnoid adherent to the dome of the aneurysm at the time of rupture, direct tearing of arachnoid by a jet of blood, and disruption of arachnoid by ICH, with secondary decompression of ICH into the subdural space.
• Seizures⁸ : Seizures occur in 13-24% of patients with SAH, commonly in the first 24 hours after the bleed. Some studies argue that anticonvulsant therapy can be limited safely to the immediate perioperative period in patients with no parenchymal clot, ischemic infarct, or postoperative hematoma.
• Increased ICP: Elevations in ICP are due to mass effect of blood (subarachnoid, ICH, IVH, or SDH) or acute HCP. Once ICP reaches mean arterial pressure (MAP), cerebral perfusion pressure becomes 0 and cerebral blood flow stops, resulting in loss of consciousness and death.
• Myocardial infarction: Although rare, myocardial infarction is a reported complication of SAH.⁹

Prognosis

The prognosis of patients who have suffered a subarachnoid hemorrhage depends upon several factors, which include age, Hunt and Hess grade, smoking history, and location of the aneurysm.

• Age: Younger patients do better.
• Hunt and Hess grade
  • Grade 0 - Unruptured aneurysm
  • Grade 1 - Asymptomatic or mild headache and slight nuchal rigidity
  • Grade 1a - Fixed neurological deficit without acute meningeal/brain reaction
  • Grade 2 - Cranial nerve palsy, moderate to severe headache, nuchal rigidity
  • Grade 3 - Mild focal deficit, lethargy, or confusion
  • Grade 4 - Stupor, moderate to severe hemiparesis, early decerebrate rigidity
  • Grade 5 - Deep coma, decerebrate rigidity, moribund appearance
  • The lower the grade, the better the prognosis. Grades 1-3 generally are associated with favorable outcome; these patients are candidates for early surgery. Grades 4 and 5 carry poor prognosis; these patients need stabilization and improvement to grade 3 before surgery is undertaken. Some recommend more aggressive management for patients with poor clinical grade.
• Smoking: Patients with a history of cigarette smoking have a poorer prognosis.
• Location of aneurysm: Anterior circulation aneurysms carry a more favorable prognosis.

Patient Education

For excellent patient education resources, visit eMedicine's Headache Center. Also, see eMedicine's patient education article, Aneurysm, Brain.

Miscellaneous

Medicolegal Pitfalls

• The usual medicolegal risks of delayed diagnosis, misdiagnosis, surgical risk and complications, and medication complications are pertinent in subarachnoid hemorrhage.
• Missing SAH obviously carries major medical-legal consequences.¹⁰ In the emergency department, clinicians should err on the side of "overtapping" patients. A good history of the current headache is essential, even in known migraineurs, and if anything unusual presents (eg, worst ever headache, episode of loss of consciousness, first ever episode of diplopia), obtain a CT scan of the head and LP even if the CT scan is negative for blood. Do not forget to measure opening pressure and adequately check for xanthochromia.

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