Subarachnoid hemorrhage presents a truly volatile clinical situation to the doctor treating headache patients. Approximately 26,000 people in the United States suffer from acute subarachnoid hemorrhages each year and just over half die or become severely disabled. Approximately one quarter of all morbidity and mortality is related to subarachnoid hemorrhage rebleeding.4,12
The incidence for subarachnoid hemorrhage is strongly age related and is more common in the adult population.10 Subarachnoid hemorrhage is rare in children, has an incidence of three per 100,000 per year for those who are 25-34 years old, and then steadily increases to a rate of 37 per 100,000 per year for those over 65 years of age.9 The highest percentage of incidents are recorded between the ages of 40 and 60.3,5,9
Most subarachnoid hemorrhages are due to ruptures of berry aneurysms near the circle of Willis (75 percent), with multiple aneurysms present in approximately 20 percent of the afflicted population.1,7,12 Other etiologies for subarachnoid hemorrhage include: arteriovenous malformations (5-6 percent), other bleeding disorders (5-6 percent), and unknown etiologies (13-20 percent).1,12 The incidence of aneurysms is higher for patients with coarctation of the aorta and polycystic kidney disease.3,9 Additionally, cigarette smoking and oral contraceptives together are thought to significantly increase the risk in women for subarachnoid hemorrhage.8
Intracranial arterial ruptures bleed into the subarachnoid space, which is between the pia mater covering the cerebral cortex and the arachnoid. Most intracranial vessels lie between these two meningeal layers. Bleeding into the subarachnoid space due to arterial rupture transiently elevates intracranial pressure and distorts pain sensitive intracranial structures to produce a sudden, severe headache. As the intracranial pressure increases, cerebral perfusion may drop dramatically due to disturbance of the autoregulatory mechanism for circulation to the cortex and to reflex vasospasm that may be triggered by blood in the subarachnoid space. This may cause the patient to drop into unconsciousness at the onset of the subarachnoid hemorrhage. Additionally, blood acts as an irritant to the meninges and can cause an acute chemical meningitis to develop.1,5,6,7
Symptoms Associated with Subarachnoid Hemorrhage
The hallmark symptom of a subarachnoid hemorrhage is a severe, generalized headache of sudden onset that may drop the patient to his knees. Patients describe the headache as "the worst headache of their life" or like a "blow to the head." The patient, if aware during the examination, can usually report the exact time and onset of the headache pain. The headache associated with subarachnoid hemorrhage was shown to be severe in character 98 percent of the time in one study and bilateral 68 percent of the time. The most distinctive feature of a headache related to a subarachnoid hemorrhage in a patient who has had a chronic history of benign headaches is that the headache is "new" and is "different" than headaches previously experienced.1,2,3,5,6,7,9,10,12 Subarachnoid hemorrhage can occur at rest or during physical exertion (i.e., straining at the stool, weightlifting, sexual intercourse, etc.).3,5,8 The headache's severity remains unchanged for several days and then tends to gradually subside over the next two weeks.2,5 The patient will also exhibit nausea and vomiting, transient or prolonged loss of consciousness, meningeal irritation symptoms such as nuchal rigidity and photophobia, dizziness, and seizures.1,2,3,5,6,7,8, 9,10,12
Sentinel Headaches and Subarachnoid Hemorrhages
Sentinel headaches or "warning" headaches occur hours to weeks before the actual acute event in 30-60 percent of patients and are attributed to small prodromal hemorrhages. Symptoms can be of gradual onset and last from 24 to 48 hours. Patients with histories of benign headaches will describe the sentinel headaches as being different in quality from their usual headaches. Sentinel headaches are typically milder than headaches due to subarachnoid hemorrhage but associated symptoms are otherwise similar. Symptoms due to these minor bleeds include the previously mentioned generalized headache, nausea, neckache, lethargy, and photophobia. Associated signs include visual field deficits, extraocular eye movement abnormalities, orbital/facial pain, and localized head pain.5,8,9,10,12
Clinical Signs of Subarachnoid Hemorrhage
Subarachnoid hemorrhage, in its purest sense, manifests with the acute onset of a severe headache that may be associated with transient loss of consciousness and/or weakness of the lower extremities from which the patient recovers. Therefore, it is possible that the examination of the patient who has experienced a subarachnoid hemorrhage may be normal in the early stages of the event. This is in part due to the fact that the patient bleeds directly into the subarachnoid space and prominent neurological signs upon examination are uncommon.5,7 The patient typically appears ill and acts as if his head hurts severely. Among the first clinical signs noted in a case of subarachnoid hemorrhage are photophobia and miosis, which are early signs of meningeal irritation. Nuchal rigidity may not be present in the early stages of subarachnoid hemorrhage.7 When present, nuchal rigidity typically presents as a limitation to forward flexion of the cervical spine with intact rotation to either side.11 It is of paramount importance that the clinician recognize the presence of a new, severe, generalized headache as being highly indicative of subarachnoid hemorrhage because mortality due to the first aneurysmal hemorrhage is approximately 10 percent; however the mortality associated with the second hemorrhage, or rebleed, is more than 50 percent.7
Signs of meningeal irritation such as Brudzinski's and Kernig's sign may develop within a few hours following the onset of the headache.1,5,12 Bilateral extensor plantar responses (Babinski's signs) occur frequently and hemiparesis may be evident.1,6,12 Other clinical signs may include visual field anomalies, diplopia, oculomotor paralysis, disturbances of higher cortical function ranging from lethargy to coma, hypertension, and fever.1,2,3,5,6,7,9,12 The blood pressure may be markedly elevated in these patients and the pulse may be substantially slowed due to the increase in intracranial pressure.1,5,6 Fever is also common in the subarachnoid hemorrhage patient. Fever may occur during the first two weeks following the acute event and may rise as high as 102.2oF. A severe and fluctuating fever may reflect ischemic damage to the hypothalamus as a sequelae to the hemorrhage.1,3,5
Funduscopic examination may reveal subhyaloid hemorrhages which are pathognomonic for subarachnoid hemorrhage. Subhyaloid hemorrhages are dark red, globular swellings around the optic disc that are thought to be caused by rapid venous engorgement secondary to the rapid increase in intracranial pressure that results from the initial hemorrhage.1,3,7,9
The patient with a suspected subarachnoid hemorrhage should be immediately referred to the hospital due to the possibility for catastrophic outcome. Differential diagnoses for this condition include meningitis and hypertensive intracerebral hemorrhage. Communicating hydrocephalus has been cited as a late complication of subarachnoid hemorrhage which may lead to mental symptoms, behavioral disturbances, spasticity, seizures, and arterial hypertension.8
References
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