Topic Editor: Grant E. Fraser, M.D., FRACGP, FACRRM, ASTEM
Review Date: 10/17/2012
Definition
Subarachnoid hemorrhage (SAH) is a condition where intracranial hemorrhage occurs in the subarachnoid space between the pia mater and arachnoid membranes.
This topic covers information on spontaneous subarachnoid hemorrhage. Half of SAH cases are due to trauma.
Description
- SAH accounts for approximately 5% of all strokes and affects 30,000 Americans annually
- Ruptured aneurysm is the cause of 85% of atraumatic SAH's. Non-aneurysmal perimesencephalic hemorrhage and rare variable conditions lead to 10% and 5% of cases respectively
- Risk factors for SAH are similar to that of other causes of stroke with genetic factors playing a role in minority of the cases
- Patients with SAH typically present with a sudden onset of severe headache, which may be the only presenting symptom. Many patients have nausea, vomiting, photophobia, neurologic deficits, neck stiffness, seizures, meningismus, or altered level of consciousness
- Non-contrast Head CT, performed on a modern generation scanner usually makes the diagnosis of SAH. Such scans are highly sensitive, especially when the CT is obtained shortly after the onset of symptoms (one study showing 100% sensitivity within 6 hours with 5th generation or later CT scan)
Epidemiology
Incidence/Prevalence
- The incidence of SAH in most populations is 6-8/100,000/year
- SAH accounts for about 5% of all strokes
- African Americans > Caucasians (2.1:1)
Age
- Average age at onset: 50-55 years
Gender
- Predominant sex: Female > Male (1.6:1)
Genetics
- Patients with first-degree relatives with SAH are at higher risk
- It is necessary to note that only 2% of SAH cases have a strong genetic predisposition
- Increased risk is present in those with autosomal dominant polycystic kidney disease, Ehlers–Danlos Type IV, and familial intracranial aneurysms
Risk factors
- Alcohol use
- Autosomal dominant polycystic kidney disease (ADPKD)
- Cocaine use
- Ehlers-Danlos syndrome
- Facial hemangioma/PHACES syndrome
- Family history of cerebral aneurysms
- Hypertension
- Marfan's syndrome
- Neurofibromatosis type I
- Pseudoxanthoma elasticum
- Smoking
Etiology
This topic covers only spontaneous SAH which accounts for 50% of cases. The other 50% are traumatic.
- Intracranial saccular aneurysm rupture (leading cause of non-traumatic SAH and accounts for approximately 85% of cases)
- Non-aneurysmal perimesencephalic hemorrhage (10%)
- Other causes (5%)
- Amyloid angiopathy
- Arteriovenous malformations
- Intracranial neoplasm
- Mycotic (septic) aneurysm due to syphilis or endocarditis
- Pituitary apoplexy
- Vertebral or carotid artery dissection
- Severe closed head injury (50% of cases of SAH)
History
- SAH should be considered in cases with history consistent with this diagnosis
- The majority of patients present with a sudden onset of worst ever in life thunderclap headache which results in the patients going from no head pain to severe head pain instantaneously
- A proportion of patients will have loss of consciousness or seizures; quite often at the onset of headache
- Most patients have photophobia, neck stiffness, some have back pain or bilateral leg pain, which are symptoms of meningeal irritation, and can be delayed by several hours
- Patients with higher grade hemorrhage will often suffer from an altered level of consciousness or coma
- A detailed history for the etiology of the potential SAH should attempt to identify whether there has been head trauma, chronic hypertension, alcohol or drug use (especially stimulants), history of AVM, family history of SAH, and any current use of anticoagulants
- Nausea and/or vomiting from increased ICP and meningeal irritation
- Visual changes
- Other focal neurological deficits
Physical findings on examination
- Many patients with SAH will be uncomfortable, have neck stiffness, photophobia, and pain
- In the event of a high grade SAH, the patient may have altered level of consciousness, localizing neurologic signs, seizures or almost any manifestation of focal mass effect or general mass effect on the brain
- Focal neurologic signs (occur at the same time as the headache in 33% of patients) such as
- 3rd-nerve palsy (posterior communicating artery aneurysm)
- 6th-nerve palsy (increased intracranial pressure [ICP])
- Bilateral leg weakness and/or abulia [lack of motivation to perform a task] (anterior communicating artery aneurysm)
- Hemiparesis and/or aphasia and/or visuospatial neglect (MCA aneurysm)
- Retinal hemorrhage (Terson's syndrome) may occurs in around 25% of cases of spontaneous SAH
Blood test findings
- Blood testing is typically has no specificity in determining whether the patient has SAH; however, in such patients, it is reasonable to do a CBC and Basic metabolic panel in cases of proven SAH
- Clotting profile (Coags): For evaluation of possible coagulopathy when SAH is present
- It is essential to obtain Renal function rapidly as intravenous contrast agents are commonly needed to evaluate such patients
- It should also be noted that the cardiac marker troponin is elevated in 10%-40% of spontaneous SAH's
Radiographic findings
- Non-contrast head CT is indicated in all cases of suspected SAH. It is highly preferable that a fifth generation or later scanner is utilized, and the scan be obtained as soon as possible after patient presentation
- Findings consistent with SAH on CT are hyperdensity consistent with blood in the basal cisterns major fissures and sulci. The most common site of ruptured aneurysm is the anterior communicating artery
- CT angiography of the brain is commonly employed when subarachnoid hemorrhage is present. This further evaluation often localizes the source of the subarachnoid bleeding, which then guides recommended treatment
- It is vital to note that CT angiography is not a first line test given that up to 3% of the population have asymptomatic aneurysms which fails to address the issue of whether a SAH is present or not
- Magnetic resonance angiography (MRA): Less sensitive for hemorrhage and has a lower sensitivity in detecting small aneurysms than CT angiography
- Chest X-ray should be performed in patients with diminished level of consciousness or proven subarachnoid hemorrhage as pulmonary complications such as aspiration or pulmonary edema are often present
Other diagnostic test findings
- It is important to note that only 6% of sudden onset severe headache are due to SAH. Current data show that 5th generation scanners miss less than 1% of SAH. In one study published in 2011, there were no cases of missed SAH, when CT with a 5th generation or newer scanner was performed within 6 hours of onset of symptoms
- It is important to have a discussion with the patient and consider how worrisome their history is for SAH. In the event the CT scan returns normal the risk of missing SAH on a 5th generation scanner does increase gradually from the time of onset of symptoms, with another recent study showing that even accounting for patients who have SAH that are several days old, modern generation CT scanners miss virtually no SAH's; however, the gold standard remains evaluation of spinal fluid, and cases of positive CSF are certainly documented, despite normal CT
- Old data from early generation scanners reported 5-10% missed rates on CT; the best information is that this percent is much lower with modern generation CT scanners
- In the event a lumbar puncture is indicated, one needs to consider whether to perform it early or late; there are advantages and disadvantages to each approach. Early lumbar puncture should not be performed sooner than 2 hours from the onset of symptoms to make sure that the CSF has adequately circulated, and a negative result is not erroneous. In the event that an early lumbar puncture is performed and it is traumatic; the expectation is a dramatically dropping red blood cell count in each successive tube. It is crucial to take enough fluid such that the last tube is clear. Some authorities have reported levels as low as a few hundred RBC's /mm3 being consistent with SAH
- Delayed LP of
12 hours from onset of symptoms is recommended by some experts. This eliminates the issue of traumatic LP, as xanthochromia is expected if there has been an SAH regardless of whether the LP is traumatic or not. In such cases a xanthochromia index on the CSF is required - ECG: Perform ECG in all patients of SAH on admission due to the risk of myocardial ischemia, or myocardial infarction (rare). ECG abnormalities detected can include:
- ST-segment elevation or depression
- QT prolongation
- T-wave abnormalities
- Often mimics ischemia or infarction
- Symptomatic bradycardia, ventricular tachycardia, and ventricular fibrillation
General treatment items
- Once the diagnosis of SAH is made, the severity of hemorrhage and the patient's co-morbidities impact recommended treatment
- Patients who present with massive SAH, coma and increased intracranial pressure have a poor prognosis and usually require endotracheal intubation, close monitoring of blood pressure and cardiac rhythm, along with urgent consideration for neurosurgical intervention
- If specific therapy is undertaken it is critical that it occur as early as possible. Treatment for ruptured aneurysm includes either endovascular coiling or surgical clipping of the aneurysm. The ISAT trial indicated that outcomes in terms of survival free of disability at 1 year were significantly better with endovascular coiling versus surgical clipping
- It is important to serially monitor the patient's neurologic status, including both the level of mentation (usually by Glasgow Coma Scale) and general neurologic findings such as motor and sensory deficits
- It is essential to monitor blood pressure and treat severe hypertension if the mean arterial pressure exceeds 130 mmHg
- Administration of nimodipine (an oral calcium channel blocker) is indicated to decrease cerebral arterial vasospasm which can worsen neurologic outcome
- Preferred treatment for severe hypertension with subarachnoid hemorrhage is intravenous beta blockers or beta blockers with some alpha blocker activity such as labetalol
- The patient's pain should be treated, usually with a narcotic agent. Narcotics with low vasoactive effects are preferred (e.g. hydromorphone or fentanyl instead of morphine)
- Treat hydrocephalus with an external ventricular drain, lumbar drain, or permanent CSF drainage
- Increased intracranial pressure: These patients should be ventilated with a goal PaCO2 of 30-35 mmHg (moderate hyperventilation). Mannitol infusion +/- furosemide or hypertonic saline can be administered to temporarily diminish intracranial pressure
- Treating other complications:
- Hyponatremia (occurs in 10-34% of cases following SAH): Based on sodium level and the rate of drop, hypertonic saline solutions can be used (1.25%, 1.5%, 2%, or 3% saline). To determine the response monitor sodium levels and adjust the rate and composition accordingly
- Seizures: For acute treatment of seizures, benzodiazepines such as lorazepam, midazolam or diazepam are preferred. Phenytoin or fosphenytoin are preferred for seizure prophylaxis
- Monitor for cardiac arrhythmias, pulmonary edema, and aspiration
- Stool softeners may be used to prevent straining which can increase the risk of rebleeding
Medications indicated with specific doses
Acute treatment of seizures
- Lorazepam
- Midazolam
- Diazepam
- Phenytoin
- Fosphenytoin
Intracerebral vasospasmTreatment of hypertension: Short acting beta-Blockers, infusion preferred with esmolol [IV]- Esmolol [IV]
- Metoprolol [IV]
- Metoprolol [Oral]
- or Atenolol
- or Labetalol [IV] (beta blocker with alpha blocker activity)
- Labetalol [Oral]
Antiemetic Agents [preferably use non-sedating agents]- Metoclopramide
- Ondansetron (Oral)
- Ondansetron (IM/IV)
AnalgesicsDietary or Activity restrictions
- If the patient has intact cough and swallowing reflexes (should have dysphagia screening), and does not need operative intervention then normal feeding can occur. If not, then the patient should be NPO or NGT fed
- Parenteral nutrition is advised only in cases where oral feeding is not possible
Disposition
Admission criteria
- Proven SAH should be admitted to hospital and in most cases to the ICU
- Patients with unclear diagnostic results such as negative head CT with equivocal LP findings often require admission and further investigation
Discharge criteria
- Negative head CT and, if indicated, normal findings on spinal fluid
- No concerns for other serious diagnosis as the cause of the patient symptoms
- Outpatient follow-up for any continuing symptoms
