Subarachnoid haemorrhage
(SAH)
Definition
Subarachnoid haemorrhage is bleeding into the subarachnoid space around the brain. Trauma is the most common cause of SAH. We will not discuss traumatic SAH in this chapter. We will discuss spontaneous SAH, 80% of which are due to intracranial saccular aneurysms.
Epidemiology
. 3% of all strokes but 5% of stroke deaths.
. Incidence 6–15 per 100 000 person-years in the USA, with higher risk among African-Americans. Worldwide, higher incidence reported in Japan and Scandinavia.
. Females have the higher incidence (60% of patients are female).
. Risk factors: tobacco use, oral contraceptives, alcohol, and stimulants.
. Other disease associated with aneurysms: polycystic kidney disease, Marfan’s syndrome, Ehlers-Danlos syndrome, coarctation of the aorta, fibromuscular dysplasia.
. Location: 30% anterior communicating, 25% posterior communicating, 20% MCAs, 10% basilar, 5% vertebral, and 25% have multiple aneurysms.
Presentation
. ‘‘The worst headache of my life’’.
. ‘‘Thunder-clap a headache’’.
. A headache is sometimes associated with focal neurologic symptoms.
Diagnosis
As this condition is potentially life-threatening, diagnostic evaluation should be done emergently.
DIAGNOSIS OF SUBARACHNOID HEMORRHAGE
. CT of the head without contrast.
If head CT is normal, but you have a high clinical suspicion for SAH, you must do a lumbar puncture, because CT can miss small or subtle SAHs, especially if more than 72 hours have passed since the ictus.
. Lumbar puncture.
Don’t forget to personally examine the fluid for xanthochromia.
Compare the colour to the water. Measure red blood cells in the first and last tube collected. Also, it is often helpful to personally deliver the tubes of CSF to the lab to make sure that they are processed quickly.
DIAGNOSIS OF INTRACRANIAL ANEURYSMS
. Digital subtraction angiography (DSA): the gold standard.
. CT angiography: quite good, but depends on CT equipment.
Difficult to see aneurysms near bones.
. MRA: fair test for screening for unruptured aneurysms>5mm.
CAUSES OF SAH OTHER THAN AN INTRACRANIAL ANEURYSM
. Perimesencephalic SAH: blood limited to anterior to midbrain (or pons). The angiogram is normal. The cause of bleed is unknown (venous?). It carries a good prognosis and benign course.
. Arteriovenous malformation (AVM): it classically causes intraparenchymal haemorrhage, but it can lead to SAH. DSA will help in diagnosis.
. Arterial dissection (vertebral artery usually): arterial dissection that extends from the extracranial to the intracranial portion of an artery or is limited to the intracranial artery can lead to SAH. This can occur spontaneously or post-traumatic. DSA and MRI can be helpful in visualizing the abnormality.
. Arteriovenous fistula: can be seen only with careful DSA.
. Pituitary apoplexy: MRI is helpful in making the diagnosis.
. Cocaine: can lead to SAH, ICH, or cerebral ischemia.
. Trauma: detailed history or external head examination may suggest trauma as the primary cause.
. Vasculitis: difficult to diagnose, since DSA is neither sensitive nor specific and brain biopsy is specific but insensitive Ruptured aneurysms: management
GOALS
. Prevention of rebleeding.
. Treatment of an aneurysm itself: clip or coil.
. Prevention and treatment of complications: hydrocephalus, seizure, vasospasm, hyponatremia, infections, and DVTs.
. Rehabilitation.
PREVENTION OF REBLEEDING
Rebleeding is maximal in the first 24 hours after SAH (4%). It carries a high mortality.
The following measures are often performed, but without much evidence:
. Blood pressure control may be important before definitive treatment to reduce rebleeding.
. Bed rest in ICU with monitoring.
. Anti-fibrinolytic drugs (epsilon amino caproic acid, tanxemic acid) reduce rebleeding but promote ischemic complications.
Consequently, these drugs are rarely used.
TREATMENT OF AN ANEURYSM I T S E L F
It should be done as early as possible, especially in patients with mild to moderate clinical deficits, since the goal is to prevent rebleeding.
Surgical clipping
Craniotomy and placement of metal clip take an aneurysm out of the arterial circulation.
. It is believed to be the best way to prevent aneurismal bleeding long-term.
. But it carries morbidity, and some aneurysms are not amenable to clipping due to location, shape, etc.
Endovascular Coiling
Coiling has become the alternative treatment. When you fill an aneurysm with coils, it thromboses and effectively takes an aneurysm out of the arterial circulation.
. Subsequent rebleed rate is not as low as with surgical clipping, but pretty close.
. This procedure may not be as durable as clipping. Long-term data are not available. Also, complete obliteration of an aneurysm is not always achieved initially and may require repeat intervention.
. Some aneurysms are not amenable to coiling due to distal location or shape.
Clipping or coiling?
That is the big question.
. It appears that endovascular coiling carries lower morbidity than surgical clipping.
. ISAT was a randomized multi-centre trial comparing the two methods: 23.7% of coiled vs. 30.6% of clipped patients were dependent or dead at 1 year (absolute risk reduction of a bad outcome: 6.9%).
For this trial, the patients were required to be good candidates for both procedures (+/-60% were treated outside the trial). 88% of patients had mild SAH (World Federation of
Neurological Surgeons grade 1 or 2).
Locations: 51% were anterior cerebral or anterior communicating artery (ACA/Acoma) and 33% were ICA or posterior communicating artery (PcomA) aneurysms. Only 14% were MCA aneurysms and 2.7% were posterior circulation aneurysms.
. Based on ISAT, the preferred treatment of ruptured ACA, ICA, anterior or posterior communicating artery aneurysms is coiling. The preferred modality for treatment of ruptured posterior circulation aneurysm (i.e., basilar artery aneurysm) in many centres is coiling. For distal MCA aneurysms, some may be difficult to approach by coiling and need to be clipped.
PREVENTION AND TREATMENT OF COMPLICATIONS
As with other strokes, general medical complications such as DVT, pneumonia, and other infection are common. SAH has particular complications that we will address here: hydrocephalus, seizure, cerebral vasospasm and delayed ischemic deficits.
Hydrocephalus
Hydrocephalus occurs in [1]20% of patients with SAH. This may be already present at the time of presentation with SAH.
Diagnosis
. Clinical signs include a decrease in the level of consciousness, agitation, hypertension, and bradycardia. However, these signs are not specific.
. CT of the head without contrast: enlargement of ventricles.
Treatment
. External drainage of CSF via an intraventricular catheter (ventriculostomy or external ventricular drain).
. Ventriculostomy must be monitored for the amount of CSF drained and for infection.
. If hydrocephalus is persistent, CSF drainage can be converted to internal drainage by placement of ventriculoperitoneal, ventriculoatrial, or lumbar-peritoneal shunt by a neurosurgeon.
Seizure
A seizure may increase blood pressure and may increase rebleeding risk.
Prevention
. Without good evidence for efficacy, the current practice is to routinely administer antiepileptic agents to prevent seizures.
. Phenytoin 300mg per day and adjusted to maintain the level of 10–20 mg/mL.
Diagnosis
. A non-convulsive seizure may go unrecognized. Bedside EEG may help if SAH itself or sedative drugs affect assessment.
Treatment
. Phenytoin is most commonly used and is available in intravenous and oral formulations. Among other anticonvulsants, valproic acid and phenobarbital are available in IV formulation.
Cerebral vasospasm and delayed ischemic deficits
. Onset usually 3–5 days after SAH, maximal at 5–10 days.
. +/-30% of SAH patients develop vasospasm, and 15–20% go on to have ischemic strokes.
Prevention
. Calcium channel blockers: nimodipine (Nimotop) 60mg PO every 4 hours 3 weeks, but adjust dose downwards if blood pressure falls so low that adequate CPP is endangered. This should be started early after diagnosis of SAH to prevent vasospasm.
. Magnesium: phase II data suggest that magnesium sulfate started within 4 days after SAH and given continuously until 14 days after aneurysm treatment may reduce delayed ischemic deficits.87 The dose used was magnesium sulfate 64 mmol/L per day with aim of magnesium level of 1.0–2.0 mmol/L.
Diagnosis
. TCD: Velocity trend with daily or sequential measurements is more useful than a one-time snapshot of velocities. So get a baseline and follow daily. Lindegaard ratio is the velocity ratio of MCAto extracranial ICA. Increasing flow velocity may indicate either vasospasm or overall increased blood flow.
Increasing Lindegaard ratio may be a more reliable sign of MCA vasospasm.
. CTA: CT angiography requires iodine contrast injection but may be combined with CT perfusion to diagnose vasospasm and ischemia.
. Angiography: more invasive, but can also be linked to treatment with angioplasty or intra-arterial papaverine.
. Clinical symptoms and signs: similar to an ischemic stroke, though in addition may have bilateral frontal lobe dysfunction in the case of anterior communicating artery vasospasm.
You want to diagnose and treat vasospasm before these symptoms and signs develop.
Treatment
. Hypertension-hypervolemia-hemodilution (HHH): commonly used. Combination of pressors and volume expanders such as albumin, synthetic starches, colloid, blood.
. Direct endovascular treatment can be performed with balloon angioplasty or drug infusion of papaverine or nicardipine.
Prognosis
Mortality: in a population-based study, 3% died before reaching medical attention and one-third died in the first month. A quarter of the deaths are attributable to initial bleed directly, another quarter to vasospasm, and another quarter to rebleeding.
. Morbidity: one-third had the neurologic deficit.
. Rebleeding risk: with an unclipped aneurysm, 6% rebleed within the first 3 days, and 12% in the first 2 weeks. Hypertension increases the chance of rebleeding.
Admission sequence
Since these patients are usually admitted to Neurosurgery, we are not providing sample admission orders, but do provide the usual sequence of events upon admitting a patient with SAH.
. Establish a diagnosis of SAH with CT or lumbar puncture as soon as possible.
. Neurosurgery consult, admission to ICU.
If necessary, transfer emergently to an appropriate hospital that has adequate neurosurgical, neurointerventional (coiling), and neurocritical care capability.
Consider ventriculostomy if hydrocephalus is present.
. Determine the location of the ruptured aneurysm with CT angiogram or digital subtraction angiography (do in the first day).
. Definitive aneurysm treatment (coiling or clipping).
. Nimodipine per nasogastric tube.
. Watch for vasospasm (first 2 weeks).
