Patients who have survived SAH and are ultimately discharged from the hospital require close follow up to detect and treat latent complications. Communicating hydrocephalus, manifested by increasing headache, lethargy, confusion, or regression of a previously improving neurological status, may develop following discharge. Fluid and electrolyte disturbances may not become evident until after discharge and may only be suspected with a patient history of abnormal fluid intake coupled with mental status changes. Seizures following SAH occur in 10-30% of patients, with the highest incidence associated with middle cerebral artery aneurysms. Most occur within 18 months of the haemorrhage and 83% of patients have fewer than three events. The most important risk factors determining the development of a seizure disorder are poor neurological grade and focal neurological deficits. There is no evidence that seizures during the initial haemorrhage are likely to persist or recur. Hart was unable to demonstrate the benefit of prophylactic anticonvulsant therapy after acute SAH.31 Patients in our practice suffering SAH are usually placed on prophylactic anticonvulsants when they present to the hospital and are postoperatively maintained on medications for 7-10 days following surgery. Patients who undergo significant brain resection or had large intracerebral haematomas are maintained on anticonvulsants for three to six months.
An important consideration in SAH survivors is the disease's neuropsychiatric sequelae.225,226 Even patients with good Glasgow Outcome Scores will have deficits 12 months posthaemorrhage. Short term memory is reduced in 53% and long term memory is reduced in 21%. Visuospatial construction and memory, mental flexibility, and psychomotor speed remain abnormal in 28-62%. Ten per cent have dysphasic language performance and up to 50% remain unemployed.
Because latent complications may develop, our protocol is to follow patients on a monthly basis following discharge with CT scans and laboratory testing as necessary. Patients who have remained on anticonvulsants are weaned approximately three to six months postoperatively and are followed with clinic visits until they are neurologically stable for one year.
Subarachnoid haemorrhage is a complex medical event. Among the multiple aetiologies, one of the most common relates to bleeding from a cerebral aneurysm. The optimal management of this life threatening condition relies on a systematic and organised approach leading to the correct diagnosis and timely referral to a neurosurgeon capable of treating this condition. The following is a brief summary of the steps that should be initiated when SAH is suspected.
• The clinician should have a high index of suspicion that a sudden, severe, unexplained headache in any patient could represent an acute subarachnoid haemorrhage.
• A CT scan should be obtained immediately after the diagnosis is suspected.
• If the CT scan is positive, lumbar puncture is unnecessary and dangerous due to the risks of aneurysm rebleeding or transtentorial brain herniation. If the CT scan is negative, lumbar puncture may be helpful if the history of the ictal headache is not typical of subarachnoid haemorrhage, insidious in onset, or of migrainous character. If the patient relates a history typical of SAH, a cerebral arteriogram should be performed despite a negative CT scan. Up to 15% of CT scans obtained within 48 hours of SAH will be negative.
• Once the diagnosis is confirmed with a CT scan, a neurosurgeon who can ultimately treat the patient should be contacted immediately. Delays in transfer may prove fatal because of the potential for aneurysm rebleeding prior to intervention. It is often best to allow the surgeon who will be caring for the patient to arrange for the diagnostic arteriogram to be performed at the institution where the patient will undergo surgery to repair the aneurysm. Arteriography performed by institutions infrequently treating SAH may be technically inadequate and require repetition upon transfer to the neurosurgeon.
• Blood pressure must be closely monitored and controlled following SAH. Hypertension will increase the chance of catastrophic rebleeding. Blood pressure control should be initiated immediately upon diagnosis of SAH.
• Preoperative medications include prophylactic anticonvulsants, calcium channel blockade, corticosteroids, and antihypertensives as needed. We do not initiate antifibrinolytic therapy unless surgery is not considered within 48 hours of the initial SAH. Medications that can be initiated prior to transfer to a neurosurgeon include:
- dexamethasone, 4 mg IV six hourly
- nimodipine, 60 mg orally four hourly
- phenytoin, 10 mg/kg IV load, then 100 mg orally/IV three times daily.
A frequent source of diagnostic difficulty for the neurosurgeon lies in the use of excessive amounts of narcotic analgesics prior to transfer to the neurosurgical service. Although pain control facilitates blood pressure control, the ability to grade accurately the patient's level of consciousness has significant impact on the timing of surgery. Clinical grading obscured by large doses of narcotic analgesics makes surgical planning more difficult.
• Send all x ray films, MRI scans, and lab work with the patient to avoid needless repetition.
• We perform surgery or endovascular coiling to obliterate the ruptured aneurysm as soon as possible after the onset of SAH. Poor grade patients, grades 4 and 5, are treated non-operatively or neurointerventionally until their clinical condition improves.
• Postoperative care is directed towards supportive care and complication recognition and treatment. Frequent postoperative complications include brain oedema, bleeding into the operative site, fluid and electrolyte disturbances, hydrocephalus, and cerebral vasospasm.
• Cerebral vasospasm may occur at any time, with a peak incidence around the sixth to eighth day following SAH, and should be suspected for any unexplained decline in neurological status.
• CT scans are useful to detect haematomas, acute hydrocephalus, or the development of subclinical ischaemic infarcts.
• Current treatments for cerebral vasospasm include calcium channel blockers, induced hypervolaemia and systemic hypertension, transluminal angioplasty, intra-arterial vasodilator infusion, and investigational systemic medications such as tirilizad.
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