2d:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/0fma7nlq6immz.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/1chr5wkk3j58k.js","/_next/static/immutable/chunks/37kmmh_zm4dov.js","/_next/static/immutable/chunks/311zvdjfxff-f.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js"],"default"] 2e:T765b,

Summary Table

Domain	Details
Risk Factors	Smoking, hypertension, heavy alcohol use, cocaine/sympathomimetic use, family history of aneurysm (first-degree relative), autosomal dominant polycystic kidney disease (ADPKD), Ehlers-Danlos syndrome type IV, fibromuscular dysplasia, female sex, age 40-60
Etiology	Ruptured saccular (berry) aneurysm (~85% of nontraumatic SAH). Less common: arteriovenous malformation (AVM), perimesencephalic hemorrhage, mycotic aneurysm, coagulopathy
Patient Presentation	Sudden "worst headache of my life" (thunderclap headache), reaching peak intensity within seconds. May be accompanied by nausea, vomiting, loss of consciousness, or seizure at onset
Classic Physical Exam	Nuchal rigidity, photophobia, Kernig and Brudzinski signs (meningismus). CN III palsy with "blown pupil" (posterior communicating artery aneurysm). Fundoscopy may show subhyaloid (preretinal) hemorrhage (Terson syndrome). Altered mental status ranging from confusion to coma
Key Diagnostic Results	Non-contrast CT head: hyperdense blood in subarachnoid space (basal cisterns, Sylvian fissure). Lumbar puncture (if CT negative): xanthochromia and elevated RBCs that do not clear across tubes. CT angiography or digital subtraction angiography (DSA): identifies aneurysm location
Management	Secure aneurysm early (endovascular coiling or surgical clipping within 24 hours). Nimodipine 60 mg PO every 4 hours for 21 days. Blood pressure control (SBP < 160 mmHg before aneurysm is secured). External ventricular drain (EVD) for hydrocephalus. Maintain euvolemia
Keywords	"Thunderclap headache," "worst headache of my life," "sentinel headache," xanthochromia, berry aneurysm, nimodipine, vasospasm, rebleeding, "blood in the basal cisterns"

1. Pathophysiology

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.

2. Classification and Clinical Manifestation

Hunt and Hess Grading Scale (Clinical Severity)

Grade	Clinical Description	Approximate Mortality
I	Asymptomatic, or mild headache with slight nuchal rigidity	~1%
II	Moderate to severe headache, nuchal rigidity, cranial nerve palsy only (no other focal deficits)	~5%
III	Drowsiness, confusion, or mild focal neurological deficit	~19%
IV	Stupor, moderate to severe hemiparesis, early decerebrate posturing	~42%
V	Deep coma, decerebrate rigidity, moribund appearance	~77%

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.

Grade	CT Findings	Vasospasm Risk
1	No blood detected on CT	Low
2	Diffuse thin layer of subarachnoid blood (< 1 mm thick)	Low
3	Localized thick clot or diffuse layer > 1 mm thick	High (~96%)
4	Diffuse or no subarachnoid blood, but intraventricular hemorrhage (IVH) or intraparenchymal extension present	Moderate

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

Aneurysm Location	Associated Clinical Finding
Anterior communicating artery (AComm)	Personality changes, abulia (lack of will), bilateral leg weakness (ACA territory). May cause visual field defects if optic chiasm is compressed
Posterior communicating artery (PComm)	Ipsilateral CN III palsy: ptosis, "down and out" eye, fixed dilated pupil. This is the classic neurosurgical emergency presentation
Middle cerebral artery (MCA)	Contralateral hemiparesis, aphasia (if dominant hemisphere), hemispatial neglect
Basilar tip	Cranial nerve palsies, brainstem signs, altered consciousness
PICA (posterior inferior cerebellar artery)	Severe headache with ataxia, vertigo, lower cranial nerve deficits

3. Diagnostic Workup

Test	Role	Key Findings	Timing/Notes
Non-contrast CT head	Best initial test	Hyperdense blood in basal cisterns, Sylvian fissures, interhemispheric fissure	Sensitivity >95% within 6 hours; declines to ~50% by day 5
Lumbar puncture	Required if CT is negative and clinical suspicion remains high	Xanthochromia (yellow CSF supernatant), elevated RBCs that do not clear across successive tubes, elevated opening pressure	Perform at least 6-12 hours after symptom onset to allow xanthochromia to develop
CT angiography (CTA)	Identifies the source (aneurysm)	Vascular outpouching at an arterial bifurcation	Rapid, noninvasive; first-line for aneurysm localization
Digital subtraction angiography (DSA)	Gold standard/most accurate test for aneurysm detection	Defines aneurysm morphology, size, neck width, and relationship to parent vessel	Invasive; used when CTA is inconclusive or for procedural planning

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:

Feature	Traumatic Tap	True SAH
RBC trend across tubes	Decreasing (clears)	Constant (does not clear)
Xanthochromia	Absent	Present
CSF appearance	Bloody then clears	Uniformly bloody or xanthochromic

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.

4. Management and Treatment

Phase	Intervention	Details
Immediate stabilization	Airway, breathing, circulation (ABCs)	Intubation if GCS $\leq$ 8. Head of bed elevated 30 degrees
Blood pressure control	Antihypertensives before aneurysm is secured	Target SBP < 160 mmHg. Agents: nicardipine or labetalol IV drip. Avoid nitroprusside (raises ICP)
Pain and agitation control	Analgesics, anxiolytics	Short-acting opioids (e.g., fentanyl). Avoid aspirin and NSAIDs. Stool softeners to prevent Valsalva straining
Vasospasm prophylaxis	Nimodipine	60 mg PO (or via NG tube) every 4 hours for 21 days
Aneurysm securing	Endovascular coiling or surgical clipping	Within 24 hours. Coiling generally preferred (ISAT trial), especially for posterior circulation. Clipping preferred for MCA aneurysms and when hematoma evacuation is needed
Hydrocephalus management	External ventricular drain (EVD)	For acute symptomatic hydrocephalus. May need VP shunt if chronic
Post-securing hemodynamics	Maintain euvolemia and adequate cerebral perfusion	Isotonic crystalloids. Induced hypertension if clinical vasospasm develops
Seizure management	Short-term prophylaxis (controversial)	Levetiracetam or phenytoin for acute period only. Prolonged prophylaxis is NOT recommended
Vasospasm treatment	Induced hypertension, intraarterial vasodilators, balloon angioplasty	Transcranial Doppler monitoring to detect elevated flow velocities

Immediate priorities. Upon recognition of SAH, secure the airway if the patient has a depressed level of consciousness (GCS $\leq$ 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:

Feature	SIADH	Cerebral Salt Wasting (CSW)
Volume status	Euvolemic	Hypovolemic
Urine sodium	High (> 40 mEq/L)	High (> 40 mEq/L)
Urine output	Decreased/normal	Increased (polyuria)
Treatment	Fluid restriction	Isotonic or hypertonic saline replacement

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.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Meningitis	Both present with headache, nuchal rigidity, photophobia, and positive Kernig/Brudzinski signs. CSF may show elevated WBCs in both	SAH: sudden onset (seconds to minutes), thunderclap quality. Meningitis: gradual onset (hours to days) with fever. CSF in meningitis shows WBC predominance with positive Gram stain/culture. CSF in SAH shows RBCs and xanthochromia
Intracerebral hemorrhage (ICH)	Both cause sudden headache and neurological deficits. Both show blood on CT	ICH: blood is intraparenchymal, not in the subarachnoid space. ICH typically presents with prominent focal neurological deficits (hemiplegia, aphasia). SAH blood is in the basal cisterns and sulci. SAH headache is typically more prominent than focal deficits
Migraine with aura	Severe headache, photophobia, nausea, vomiting	Migraine: recurrent episodes with a history pattern, gradual buildup over minutes, associated aura. SAH: first or worst headache, maximal at onset (within seconds), no prior similar episodes. Any "first and worst" headache must be worked up for SAH
Cerebral venous sinus thrombosis (CVST)	Headache, may have focal deficits, can show hemorrhage on CT	CVST: headache is progressive over days, not thunderclap. Risk factors include oral contraceptives, pregnancy, and hypercoagulable states. CT/MRV shows venous thrombosis. Hemorrhage in CVST is typically lobar, not subarachnoid
Hypertensive emergency	Severe headache with elevated blood pressure	Hypertensive emergency: headache develops in the context of severely elevated BP (typically > 180/120), with evidence of end-organ damage (AKI, papilledema). CT head is normal or shows posterior reversible encephalopathy (PRES). No subarachnoid blood
Pheochromocytoma crisis	Sudden severe headache, hypertension, diaphoresis	Pheochromocytoma: episodic symptoms (paroxysmal headache, sweating, palpitations, hypertension). Elevated plasma free metanephrines. No blood on CT head
Sentinel headache (warning leak)	Sudden headache that resolves, actually a small SAH	Not a true differential but a missed diagnosis trap. Up to 50% of SAH patients report a "warning headache" days to weeks before the major bleed. If a patient describes a prior sudden severe headache that self-resolved and now presents with a second thunderclap headache, the first event was likely a sentinel bleed

6. Traps 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.

1e:["$","$L2d",null,{"article":{"id":"50ef03e2-8429-44c4-a5a2-4ea75e61cfa9","title":"Perdarahan Subaraknoid","content":"$2e","category":"Neurologi","created_at":"2026-08-07T06:25:24.047679+00:00","status":"published","subcategory":null},"questionCount":1,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]