Perdarahan Subaraknoid

01Pathophysiology

Subarachnoid hemorrhage refers to bleeding into the subarachnoid space, the compartment between the arachnoid mater and the pia mater where cerebrospinal fluid (CSF) circulates. The most common nontraumatic cause is the rupture of a saccular (berry) aneurysm, which accounts for approximately 85% of spontaneous cases.

Berry aneurysms develop at arterial bifurcation points within the Circle of Willis. These locations are structurally vulnerable because they lack a full muscular media and internal elastic lamina, making the arterial wall prone to progressive outpouching under hemodynamic stress. The most common aneurysm locations are the anterior communicating artery (AComm, ~30%), the posterior communicating artery (PComm, ~25%), and the middle cerebral artery (MCA) bifurcation (~20%). Understanding these locations matters because each has a characteristic clinical pattern. For example, a PComm aneurysm classically compresses cranial nerve III, producing an ipsilateral "down and out" eye with a fixed, dilated pupil.

When an aneurysm ruptures, arterial blood floods the subarachnoid space at systemic pressure. This produces several consequences.

The sudden rise in intracranial pressure (ICP) explains the instantaneous, explosive headache and why patients may lose consciousness at onset. The ICP can transiently approach mean arterial pressure, causing a brief period of global cerebral hypoperfusion.

Blood in the subarachnoid space triggers a chemical meningitis. Hemoglobin breakdown products irritate the meninges, producing the classic triad of nuchal rigidity, photophobia, and positive Kernig/Brudzinski signs. This is meningismus without infection, and it typically develops over 6 to 12 hours as the blood degrades.

Blood also impairs CSF reabsorption at the arachnoid granulations. When the granulations become clogged with blood products, CSF accumulates and produces communicating (non-obstructive) hydrocephalus. This is a common early complication and the reason patients may develop progressive lethargy and declining mental status in the first few days.

The most feared delayed complication is cerebral vasospasm, which leads to delayed cerebral ischemia (DCI). The mechanism involves oxyhemoglobin and its breakdown products (bilirubin oxidation products, endothelin-1) acting on smooth muscle cells in cerebral arteries, causing prolonged constriction. Vasospasm typically occurs between days 3 and 14 after the initial bleed, with a peak around days 7 to 10. This is the primary rationale for nimodipine prophylaxis.

Rebleeding is the other critical early complication. Before the aneurysm is secured, the clot sealing the rupture site is fragile and can dislodge. The risk of rebleeding is highest in the first 24 hours, with a peak around 2 to 12 hours. Rebleeding carries a mortality rate exceeding 70%, which is why early aneurysm treatment (within 24 hours) is the standard of care.

02Classification and Clinical Manifestation

Hunt and Hess Grading Scale (Clinical Severity)

Grades I through III are generally considered "good grade" SAH with favorable surgical outcomes. Grades IV and V are "poor grade" and carry substantially higher morbidity and mortality.

Fisher Scale (CT-Based Classification)

The Fisher scale uses the appearance of blood on the initial non-contrast CT to predict the risk of subsequent vasospasm. This is a radiological classification, not a clinical one.

Fisher Grade 3 carries the highest risk of vasospasm. This is a commonly tested point: thick, localized subarachnoid clot burden is the strongest CT predictor of delayed vasospasm.

Clinical Manifestation by Aneurysm Location

03Diagnostic Workup

The diagnostic workup for SAH follows a strict, stepwise approach. If a patient presents with a sudden-onset thunderclap headache, the first test is always a non-contrast CT of the head. Contrast is not needed and is not useful for detecting acute blood, which appears hyperdense (white) on CT. The classic distribution of blood is within the basal cisterns, the Sylvian fissures, and the interhemispheric fissure.

If the CT is performed within 6 hours of symptom onset, its sensitivity exceeds 95%, approaching nearly 100% with modern multidetector scanners. However, sensitivity drops significantly after 24 hours as the blood isodenses with brain parenchyma. This is why timing matters.

If the CT is negative but clinical suspicion remains high, the next step is a lumbar puncture (LP). This is not optional. A negative CT does not rule out SAH. The LP is looking for two things: elevated RBCs that do not diminish from tube 1 to tube 4 (distinguishing true SAH from a traumatic tap) and, more importantly, xanthochromia. Xanthochromia is the yellowish discoloration of CSF caused by the enzymatic breakdown of hemoglobin into bilirubin. It takes approximately 6 to 12 hours to develop after the hemorrhage, so if the LP is performed too early, it may be falsely negative.

The distinction between a traumatic tap and true SAH is a tested concept:

Once SAH is confirmed, the next step is to identify the source. CT angiography (CTA) is the standard first-line vascular imaging study. It is fast, widely available, and has excellent sensitivity for aneurysms larger than 3 mm. If CTA is negative or equivocal, digital subtraction angiography (DSA) is performed. DSA is the gold standard for aneurysm detection because it provides the highest spatial resolution and can detect small aneurysms that CTA may miss. If the initial DSA is negative, it should be repeated in 1 to 2 weeks, because vasospasm in the acute phase can obscure the aneurysm.

04Management and Treatment

Immediate priorities. Upon recognition of SAH, secure the airway if the patient has a depressed level of consciousness (GCS $\le \backslash leq$ 8 mandates intubation). Elevate the head of bed to 30 degrees to promote venous drainage and reduce ICP. Place the patient in a quiet, low-stimulation environment.

Blood pressure control before aneurysm securing is critical. The goal is to prevent rebleeding by keeping SBP below 160 mmHg, while avoiding hypotension that could worsen cerebral ischemia. Nicardipine IV infusion is the preferred agent because it is titratable and does not increase ICP. Avoid sodium nitroprusside, which is a cerebral vasodilator and raises ICP.

Nimodipine is the cornerstone of vasospasm prophylaxis and is the most frequently tested pharmacologic intervention. The dose is 60 mg PO every 4 hours, continued for 21 days. If the patient cannot swallow, it is given via nasogastric tube. Nimodipine is a calcium channel blocker that selectively acts on cerebral vasculature. Important nuance: nimodipine improves neurological outcomes by reducing delayed cerebral ischemia, but angiographic studies show it does not reliably prevent large-vessel vasospasm. Its benefit appears to be at the microvascular level. Despite this, it remains the only pharmacologic agent with proven mortality benefit in SAH and should never be omitted.

Aneurysm securing should occur within 24 hours to prevent rebleeding. Two options exist.

Endovascular coiling involves threading a microcatheter through the femoral artery to the aneurysm and packing it with platinum coils to induce thrombosis. The International Subarachnoid Aneurysm Trial (ISAT) demonstrated that coiling had better 1-year outcomes compared to clipping for anterior circulation aneurysms amenable to either approach. Coiling is generally preferred for posterior circulation aneurysms (basilar tip, PComm), which are surgically difficult to access.

Surgical clipping involves a craniotomy and placement of a metal clip across the aneurysm neck. It is preferred for MCA aneurysms (superficial, easily accessible surgically), wide-necked aneurysms not amenable to coiling, and cases with large intraparenchymal hematomas requiring evacuation.

Hydrocephalus occurs in up to 20-30% of SAH patients. If the patient develops progressive drowsiness with CT showing enlarged ventricles, an EVD is placed emergently. Some patients require a permanent VP shunt if hydrocephalus does not resolve.

Monitoring for vasospasm begins immediately and continues through the high-risk window (days 3 to 14). Transcranial Doppler (TCD) ultrasonography is performed daily to detect rising mean flow velocities in the middle cerebral artery. Mean flow velocity > 200 cm/s or a Lindegaard ratio > 6 is highly suggestive of vasospasm. If clinical vasospasm develops (new focal deficit or decline in consciousness during the risk window), the first step is to induce hypertension with vasopressors (phenylephrine or norepinephrine) to drive flow through the narrowed vessel. If this fails, intraarterial verapamil or balloon angioplasty can be performed.

Hyponatremia is common after SAH and requires careful differentiation between two causes, because the treatment is opposite:

In the SAH patient, always presume cerebral salt wasting first, because fluid restriction (the treatment for SIADH) can worsen hypovolemia and precipitate vasospasm. This is a high-yield trap.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on SAH questions is by stopping at a negative CT. The reflex to "CT is normal, therefore no SAH" is the single most dangerous reasoning error. A negative CT does not exclude SAH, particularly when the scan is obtained more than 6 hours after symptom onset. The correct next step after a negative CT in a patient with a thunderclap headache is lumbar puncture, and the finding that clinches the diagnosis is xanthochromia, not just the presence of RBCs (which can also come from a traumatic tap).

A second common trap involves nimodipine. Students sometimes confuse it with other calcium channel blockers or assume it is given intravenously. Nimodipine is given orally (or via NG tube), never intravenously in standard practice, because IV administration has been associated with fatal hypotension due to dosing errors. The oral route is the standard. Additionally, nimodipine improves outcomes but does not reliably prevent angiographic vasospasm; its benefit is believed to be at the microvascular and neuroprotective level. Regardless, it is never omitted.

A third trap is the management of hyponatremia after SAH. The instinct may be to fluid-restrict (as in SIADH), but in the post-SAH patient, hypovolemia from cerebral salt wasting is the more dangerous scenario. Fluid restriction in a hypovolemic patient will worsen cerebral perfusion and increase the risk of vasospasm. Always assess volume status first, and when in doubt, treat with isotonic saline, not fluid restriction.

The CN III palsy question is a classic. A patient with sudden headache and a dilated, fixed pupil with ptosis and "down and out" gaze should immediately raise suspicion for a PComm aneurysm rupture. The key discriminator from a diabetic CN III palsy (which is caused by ischemia of the nerve's core fibers) is pupil involvement: a compressive lesion (aneurysm) affects the parasympathetic fibers on the outside of the nerve, producing a dilated pupil. A medical/ischemic CN III palsy (diabetes) spares the pupil. Pupil-involving CN III palsy equals aneurysm until proven otherwise.

Finally, know the timeline of complications. Rebleeding is the enemy in the first 24 hours (prevented by early aneurysm securing). Vasospasm is the enemy from days 3 to 14 (prevented by nimodipine, monitored with transcranial Doppler). Hydrocephalus can occur early or late. Getting the timeline wrong, such as worrying about vasospasm on day 1 or ignoring rebleeding risk on day 7, is a common source of errors in test questions that ask about "next best step" at a given time point.

The core competency being tested across all SAH questions is the ability to recognize the presentation (thunderclap headache), execute the correct diagnostic sequence (CT first, then LP if negative, then vascular imaging), initiate the correct acute management (nimodipine, early aneurysm securing, blood pressure control), and anticipate complications based on the timeline.