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Subarachnoid Hemorrhage & Cerebral Aneurysm

SAH High-yield Verified · Sep 2026

A subarachnoid hemorrhage is bleeding into the space between the arachnoid membrane and the pia mater around the brain, most often (about 85% of nontraumatic cases) from rupture of an intracranial aneurysm — a weak, ballooning spot on a brain artery.

A cerebral aneurysm is a weak, ballooned spot on a brain artery; most never cause symptoms until they grow or rupture. When one bursts, blood fills the subarachnoid space: sudden severe headache, vomiting, stiff neck, sometimes loss of consciousness. The nurse’s job is recognition and speed, then surveillance — rebleeding before the aneurysm is secured, new deficits during the delayed-ischemia window, sodium and volume changes, and safe enteral nimodipine.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 How an aneurysm forms and ruptures

[ANEU] "A cerebral aneurysm (or brain aneurysm) is a weak spot on an artery in the brain that balloons and fills with blood." Saccular (berry) aneurysms "are the most common type and happen most often in adults"; "Approximately 85% occur within the anterior circulation, most commonly at arterial junctions or bifurcations along the circle of Willis." NINDS sizes them small (under 11 mm), large (11–25 mm) and giant (over 25 mm).

Why there. "Hemodynamic stress is the initiating factor for intracranial aneurysm (IA) formation" — aneurysms sit where "excessive hemodynamic stresses are exerted on arterial walls." Inflammation then weakens the wall; saccular aneurysms show "a thin or absent tunica media and an absent or severely fragmented internal elastic lamina." StatPearls keeps the hedge: the mechanisms "are not fully understood."

Rupture. "Most nontraumatic causes of SAH (~ 85%) are caused by the rupture of an intracranial aneurysm." Blood enters the subarachnoid space, which holds cerebrospinal fluid and the brain’s surface vessels. "The sudden surge in central sympathetic stimulation associated with aSAH results in hypertension." Blood tracking down the spinal canal "irritates surrounding nerves causing neck pain and stiffness." "Most aneurysms do not show symptoms until they become very large or rupture."

Hemodynamic stress and inflammation weaken an artery at a branch point into a berry aneurysm, which is usually silent until it grows (pressing on nerves) or ruptures into the subarachnoid space.

02 Recognizing and confirming the bleed

[SAH] "A typical presenting symptom is a thunderclap headache" — NINDS: "Some people describe it as the worst headache of their life." What makes a headache thunderclap "is how rapidly they reach their peak intensity, not the headache intensity itself"; thunderclap headache "is considered a medical emergency." "A headache is frequently associated with nausea, vomiting (often projectile), nuchal rigidity, and photophobia." Some patients report a warning (sentinel) headache days to weeks before — a small leak.

CT first, LP if needed. "A head CT scan without contrast is the initial test for a suspected ruptured cerebral aneurysm causing SAH." CT is most sensitive within about 6 hours and loses sensitivity over days (figures differ by source). "Persistent clinical suspicion despite a negative CT warrants lumbar puncture. Classic findings include elevated opening pressure and a red blood cell count that fails to diminish from tube 1 to tube 4. Xanthochromia, characterized by pink or yellow discoloration of cerebrospinal fluid due to hemoglobin breakdown products, strongly supports SAH." Imaging must come first — "brain imaging is required before performing a lumbar puncture (LP)."

Find the aneurysm and grade the patient. CT angiography locates it; digital subtraction angiography "serves as the gold standard for detecting aneurysmal SAH." Severity is graded with the Glasgow Coma Scale, Hunt and Hess, WFNS and (modified) Fisher scales — "A higher score (grade) correlates to a lower survival rate," and the Fisher scale estimates blood on CT to predict vasospasm.

Thunderclap headache is an emergency: noncontrast CT first, lumbar puncture only if the CT is negative and suspicion persists, then angiography to find the aneurysm, grading, and early securing.

03 After the bleed: rebleeding, hydrocephalus, delayed ischemia, sodium

Rebleeding — the first danger. "The significant concerns after an aSAH are rebleeding, hydrocephalus, and vasospasm. The most immediate problem is rebleeding." StatPearls: "The most significant risk of rebleeding and mortality is within the first 6 hours of the initial hemorrhage," "About 9% to 17% of patients risk rebleeding in the first 72 hours," but "once the IA is secured, the risk of rebleeding is about 1%." Securing — "surgical clipping or endovascular coiling" — "should be performed as early as feasible" (StatPearls).

Hydrocephalus. Blood blocks CSF flow and inflames the arachnoid granulations. "Hydrocephalus often occurs within the first three days post hemorrhage," when StatPearls describes placing an external ventricular drain to relieve pressure.

Delayed cerebral ischemia (DCI). NINDS: DCI "can happen between 3 and 14 days after bleeding and causes major neurological damage and death." It was thought to be vasospasm, "but it’s much more complicated and deadly." "Approximately 60% of patients with aSAH have radiographic vasospasm"; about 39% have clinical signs. "Symptomatic vasospasm and delayed cerebral ischemia are manifested clinically by neurologic decline, including the onset of focal neurologic abnormalities."

[CSW] Sodium and volume. Hyponatremia after SAH may be cerebral salt wasting or SIADH. "The main distinguishing factor is the patient's volume status: in CSW, the patient is hypovolemic, whereas in SIADH, the patient is either euvolemic or hypervolemic." "CSW is managed with fluid and sodium replacement, whereas SIADH requires fluid restriction" — and fluid-restricting a patient with CSW "would worsen their condition by further exacerbating the hypovolemia."

After SAH, rebleeding threatens first (until the aneurysm is secured), hydrocephalus within days, and delayed cerebral ischemia around days 3–14; hyponatremia is treated by volume status — salt and fluid for cerebral salt wasting, restriction for SIADH.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

High blood pressure — among "the most consistently observed risk factors" modifiable Cigarette smoking modifiable Family history of aneurysm Cocaine or amphetamines — "can increase blood pressure and lead to aneurysms" modifiable Heavy alcohol use modifiable Female sex, especially after menopause — NINDS: "Aneurysms are more common in women than in men. The risk also seems to increase after menopause." Inherited conditions — autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome and other connective tissue disorders, coarctation of the aorta Rupture risk — NINDS: "Aneurysms that grow, even if they are small, are the biggest risk for rupture (followed by size)"; a prior rupture or sentinel bleed raises risk

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Sudden, severe thunderclap headache — “the worst headache of my life” Report immediately
Why: Blood suddenly fills the subarachnoid space. NINDS: "If you experience a sudden, severe headache, especially with any other symptoms, call 911 and seek immediate medical attention."
Nausea and vomiting (often projectile), stiff neck, photophobia Report immediately
Why: Raised pressure and blood irritating the meninges — "As the blood moves further down the spinal cord, it irritates surrounding nerves causing neck pain and stiffness."
Brief or prolonged loss of consciousness; seizure; cardiac arrest Report immediately
Why: NINDS lists "A brief or prolonged loss of consciousness" and "Cardiac arrest (the heart stops beating)" with rupture. "Seizures occur in less than 10% of patients, while sudden death develops in 10% to 15%."
Unruptured aneurysm pressing on nerves — pain above and behind the eye, pupil dilation, vision change or double vision, one-sided facial weakness Hold & notify
Why: NINDS: "Large, growing aneurysms may press on the brain tissue and nerves." A third cranial nerve palsy is one such sign.
Sudden severe “sentinel” headache days to weeks before a major bleed Report immediately
Why: A small warning leak — "But only a small number of people have a sentinel headache before a rupture."
New focal deficit, new pupil change, confusion or falling level of consciousness after SAH (rebleed, hydrocephalus, delayed ischemia) late Report immediately
Why: "A development of neurologic deficits should be evaluated with an urgent head CT scan (to identify rebleeding, cerebral infarction, hydrocephalus), angiography (to identify symptomatic vasospasm), and/or EEG (to detect subclinical seizures)."
Nausea, headache, lethargy, confusion with low sodium; low BP, fast pulse, dry mucosa, high urine output late Hold & notify
Why: Cerebral salt wasting — natriuresis and hypovolemia; "Symptoms usually occur within days to weeks following the inciting cerebral event."
Hyponatremia with seizures or coma Report immediately
Why: Severe hyponatremia — "in severe cases, seizures or coma."
Blood pressure above the ordered limits before the aneurysm is secured Hold & notify
Why: Sympathetic surge; elevated systolic pressure is a rebleeding risk factor, so BP is kept within ordered parameters "until the IA is secured."

Diagnostics

Test In this disorder Normal
Noncontrast head CT The first test. Sensitivity is highest within about 6 hours and falls over days (StatPearls chapters give different figures). Blood in the subarachnoid space —
Lumbar puncture (if CT negative and suspicion persists) Only after brain imaging. Xanthochromia needs hours to develop — StatPearls chapters differ on the ideal timing. Elevated opening pressure; red cells that do not clear from tube 1 to tube 4; xanthochromia —
CT angiography · digital subtraction angiography DSA is the gold standard; patients with contrast allergy or kidney disease "need pre-procedure treatment to decrease the risk of an adverse reaction." Location and size of the aneurysm —
Grading scales — GCS, Hunt and Hess (I–V), WFNS, Fisher Hunt and Hess: grade 1 mild headache with slight nuchal rigidity … grade 5 "coma with decerebrate posturing." WFNS 3 or more (or enlarged ventricles) prompts a ventriculostomy per StatPearls. Higher grade = worse prognosis —
Transcranial Doppler "A TCD is able to detect changes in velocity prior to the clinical sequelae of vasospasm"; angiography is required to diagnose and treat it. Rising velocities suggest vasospasm —
Serum sodium, urine sodium, volume status Correct sodium slowly (StatPearls gives limits of under 8 and no more than 10 mEq/L in 24 hours) to avoid osmotic demyelination; monitor sodium and neuro status frequently. CSW: hyponatremia, very high urine sodium, polyuria, hypovolemia; SIADH: euvolemic —

Complications

Black-box warning — most severe: ■ Rebleeding before the aneurysm is secured Report immediately
"The most immediate problem is rebleeding." Risk is highest in the first hours and "Rebleeding carries a mortality rate of up to 50%" (another StatPearls passage says up to 78%).
Risk factors: "elevated systolic blood pressure, poor Hunt-Hess grades, intracerebral or intraventricular hematomas, aneurysms > 10 mm in size, and aneurysms in the posterior circulation." Keep BP within ordered limits; StatPearls describes stopping antithrombotics and reversing anticoagulation until repair.
Black-box warning — most severe: ■ Delayed cerebral ischemia / vasospasm (about days 3–14) Report immediately
NINDS: DCI "is one of the biggest causes of complications and death after a ruptured aneurysm." It shows as new focal deficits or confusion.
Report any neurologic decline for urgent CT. Magnesium, statins and clazosentan have not proven beneficial; oral nimodipine is standard.
Warning: Hydrocephalus and raised intracranial pressure Report immediately
"Hydrocephalus often occurs within the first three days post hemorrhage"; it is present "in up to 30% of patients with intraventricular hemorrhage."
Treated with an external ventricular drain and, later, a shunt if needed.
Warning: Seizures Report immediately
Seizures occur at rupture and later; continuous EEG can detect nonconvulsive seizures "particularly for patients with poor-grade SAH who develop unexplained neurologic deterioration."
Warning: Hyponatremia — cerebral salt wasting or SIADH Hold & notify
"Some clinicians estimate that CSW accounts for up to one-quarter of cases of severe hyponatremia following aneurysmal subarachnoid hemorrhage."
Treat by volume status. "Accurate diagnosis is crucial, as mismanagement—particularly inappropriate fluid restriction—can worsen hypovolemia and increase the risk of morbidity and mortality." Hyponatremia in CSW "may persist for weeks to months."
Caution: Other complications Hold & notify
Neurogenic pulmonary edema, cardiac complications, gastrointestinal bleeding, deep vein thrombosis, and Terson syndrome (bleeding in the eye — consult ophthalmology).
Caution: Long-term effects
"Long-term complications of SAH include neurocognitive dysfunction, epilepsy, and other focal neurologic deficits"; "nearly half of survivors experience significant cognitive dysfunction."

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Calcium Channel Blockers First-line
Cardiovascular · amlodipine

[NIM] Nimodipine — enteral only, 21 days. Indicated "for the improvement of neurological outcome by reducing the incidence and severity of ischemic deficits" after aneurysmal SAH, Hunt and Hess grades I–V. Label: "The recommended oral dose is 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days," starting "as soon as possible within 96 hours of the onset of subarachnoid hemorrhage" (reduced in cirrhosis). Boxed warning: "DO NOT ADMINISTER NIMODIPINE INTRAVENOUSLY OR BY OTHER PARENTERAL ROUTES." Give 1 hour before or 2 hours after meals; avoid grapefruit juice. "Blood pressure should be carefully monitored" — hypotension is the most frequent adverse effect; a dose reduction for hypotension is the prescriber’s decision. Strong CYP3A4 inducers (carbamazepine, phenobarbital, phenytoin, rifampin, St. John’s wort) "should generally be avoided." StatPearls: nimodipine reduces DCI and improves outcome "without affecting vasospasm." Before securing, StatPearls names nicardipine and clevidipine infusions (and intermittent labetalol or hydralazine) for BP control.
Anticonvulsants
Nervous · phenytoin

Seizures after SAH. Seizures occur in fewer than 10%; StatPearls lists "seizure prophylaxis" among ICU interventions for poor-grade patients (an older-guideline relay) and seizure prophylaxis after discharge. Interaction: the enzyme-inducing anticonvulsants carbamazepine, phenobarbital and phenytoin can markedly lower nimodipine levels and efficacy — the nimodipine label advises avoiding the combination.
Opioid Analgesics High-alert
Nervous · morphine

Headache — after acetaminophen, with a sedation watch. Acetaminophen is first-line; "NSAIDs like aspirin should be avoided until the aneurysm is secured." Opioids "may provide pain relief as well as a degree of sedation and serve to decrease anxiety," but "Patients response to pain medications must be monitored closely to avoid oversedation and an inability to accurately assess the patients’ neurological status." No doses here — see the class page.

Beyond medications

  • Secure the aneurysm early — "surgical clipping or endovascular coiling is the only effective treatment" for a ruptured aneurysm (StatPearls). Clipping is open brain surgery and "aneurysms that are completely clipped do not come back"; coiling "is less invasive," but coiled aneurysms "can sometimes come back" and may need repeat treatment (NINDS).
  • External ventricular drain or shunt for hydrocephalus (StatPearls; NINDS).
  • Intermittent pneumatic compression on ICU admission; pharmacologic VTE prophylaxis is usually started 24–48 hours after surgery (StatPearls).
  • Intubation and ventilation for poor-grade patients who cannot protect their airway.
  • Unruptured aneurysm — "Not all cerebral aneurysms need treatment." Very small ones may be watched while aggressively treating high blood pressure and quitting smoking or drugs such as cocaine (NINDS); StatPearls notes most experts intervene at 7 mm or larger.
  • Rehabilitation — "Physical, speech, and occupational therapy can help people who have had a rupture improve function"; tobacco and alcohol counseling; serial imaging to confirm the aneurysm stays closed.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment
For a sudden severe headache, assess level of consciousness, pupils, neck stiffness, vomiting and focal deficits — and activate the emergency response.
Why: Thunderclap headache "is considered a medical emergency"; SAH needs rapid CT at a neuro-capable center.
Perform serial neurologic exams (GCS, pupils, motor strength, speech) — StatPearls: patients "should be carefully examined every one to two hours, especially during the high-risk period for delayed cerebral ischemia" (about days 3–14).
Why: Delayed ischemia shows as "neurologic decline, including the onset of focal neurologic abnormalities."
Monitor BP (arterial line if placed), heart rate, sodium, intake and output, and daily volume status.
Why: BP control before securing; hyponatremia and hypovolemia from cerebral salt wasting; nimodipine hypotension.
Assess sedation after every opioid dose.
Why: Oversedation can mask a worsening neurologic exam.
Interventions
Report any new focal deficit, seizure, confusion or drop in consciousness immediately.
Why: Needs "an urgent head CT scan" for rebleeding, infarction or hydrocephalus, angiography for vasospasm, or EEG for seizures.
Keep BP within ordered parameters until the aneurysm is secured; give acetaminophen first and no NSAIDs or aspirin.
Why: High systolic pressure is a rebleeding risk factor; NSAIDs "should be avoided until the aneurysm is secured."
[NIM] Give nimodipine only by mouth or feeding tube, every 4 hours, 1 hour before or 2 hours after feeds; for tube use, extract the capsule contents and transfer them to an oral syringe that cannot take a needle, labeled “Not for IV Use”, then give via the tube and flush with saline.
Why: IV or parenteral injection of capsule contents has caused death and life-threatening cardiovascular events (boxed warning).
[NIM] Check BP before each dose and report hypotension; do not change the dose on your own.
Why: Hypotension is the most frequent adverse effect; dose reduction is a prescriber decision.
[CSW] Do not fluid-restrict a hyponatremic patient without an order; if hypovolemic, expect saline and sodium replacement with frequent sodium checks.
Why: In cerebral salt wasting, restriction "would worsen their condition by further exacerbating the hypovolemia."
Patient and family teaching
Call 911 for a sudden, severe headache, especially with vomiting, stiff neck, fainting or stroke signs.
Why: NINDS: "call 911 and seek immediate medical attention."
Explain the risk of rebleeding and the purpose of clipping or coiling; coiled aneurysms need follow-up imaging.
Why: Families "should be aware of the chance of rebleed"; coiled aneurysms "can sometimes come back."
For an unruptured aneurysm under observation: control blood pressure, quit smoking, avoid cocaine, and know the rupture symptoms.
Why: NINDS advises aggressively treating rupture risk factors; StatPearls: advise "on all the complications that can occur if it ruptures."
Nimodipine: complete all 21 days, avoid grapefruit juice, and report signs of low blood pressure.
Why: Label regimen; decreased blood pressure is the most frequent adverse reaction, and grapefruit juice can prolong the blood-pressure-lowering effect for days.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    Day 6 (inside the about 3–14-day delayed-ischemia window): new confusion and right-arm weakness, lower BP with tachycardia, sodium falling to 128, high urine output and dry mucosa; a nimodipine dose is due.

  2. 2
    Analyze cues

    A new focal deficit after SAH may be delayed cerebral ischemia, rebleeding or hydrocephalus — it needs an urgent head CT. Hyponatremia with hypovolemic signs fits cerebral salt wasting, not SIADH. Low BP also affects the nimodipine dose, whose main adverse effect is hypotension.

  3. 3
    Prioritize

    The new neurologic deficit is the emergency — notify the provider immediately for urgent evaluation and CT.

  4. 4
    Generate solutions

    Report the deficit, BP, sodium and fluid balance together; ask how to handle the 0800 nimodipine dose given the low BP; do not start fluid restriction; expect saline and sodium replacement with frequent sodium and neuro checks.

  5. 5
    Take action

    SBAR: Day 6 post-coiling SAH; new drowsiness, disorientation and right-arm weakness since 0700; BP 104/60, HR 110; Na 128 from 136; urine output 3.6 L, dry mucosa. Requesting immediate evaluation and head CT, and direction on the nimodipine dose. The provider orders an urgent CT and isotonic saline.

  6. 6
    Evaluate

    Continue frequent neuro exams, trend sodium (avoiding an overly rapid rise), BP and urine output, and report any further decline immediately.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Neurosurgical ICU · day 6 after aneurysmal SAH, 0800

A 54-year-old woman who smokes and has hypertension arrived 6 days ago with a sudden “worst headache of my life” and vomiting. CT showed SAH; an anterior communicating artery aneurysm was coiled on day 1. She is on oral nimodipine every 4 hours via nasogastric tube.

0700 exam — alert, oriented ×3, moves all limbs equally, speech clear
0800 exam — drowsy, oriented to person only; new weakness of the right arm; pupils equal and reactive
Vital signs — BP 104/60 (previous 128/74) · HR 110 · T 37.4 °C
Labs — Na 128 mmol/L (day 3: 136)
Fluids — urine output 3.6 L in 24 h; mucous membranes dry
Nimodipine — next dose due at 0800
Q1 Multiple choice
A patient in the emergency department reports the sudden onset of “the worst headache of my life” with vomiting. Which test does the nurse anticipate first?
  1. A. Lumbar puncture
  2. B. Noncontrast head CT
  3. C. Electroencephalogram
  4. D. MRI of the cervical spine
Reveal answer & rationale
Answer: B
"A head CT scan without contrast is the initial test for a suspected ruptured cerebral aneurysm causing SAH" (B). A lumbar puncture (A) follows only if the CT is negative and suspicion persists — and "brain imaging is required before performing a lumbar puncture." EEG (C) looks for seizures, not blood; a spine MRI (D) does not diagnose SAH.
Q2 Select all that apply
Which actions are correct when giving nimodipine to a patient with a nasogastric tube? Select all that apply.
  1. A. Transfer the capsule contents to an oral syringe labeled “Not for IV Use”
  2. B. Give it every 4 hours, 1 hour before or 2 hours after feeds
  3. C. Inject the capsule contents into the IV line if the tube is blocked
  4. D. Check blood pressure before the dose and report hypotension
  5. E. Mix it with grapefruit juice to improve the taste
Reveal answer & rationale
Answer: A, B, D
The label directs transfer to an oral syringe that cannot take a needle, labeled “Not for IV Use” (A), dosing every 4 hours away from meals (B), and careful BP monitoring because hypotension is the most frequent adverse effect (D). IV injection (C) has caused deaths — boxed warning. Grapefruit juice (E) must be avoided.
Q3 Multiple choice
On day 6 after SAH, the patient becomes drowsy with new right-arm weakness. What should the nurse do first?
  1. A. Document the finding and recheck in 4 hours
  2. B. Notify the provider immediately for urgent evaluation and head CT
  3. C. Give a PRN opioid for restlessness
  4. D. Restrict fluids because the sodium is low
Reveal answer & rationale
Answer: B
A new deficit "should be evaluated with an urgent head CT scan" for rebleeding, infarction or hydrocephalus, and delayed ischemia can occur about days 3–14 (B). Waiting (A) loses time. An opioid (C) could cause oversedation that masks the neuro exam. Fluid restriction (D) can worsen hypovolemia if this is cerebral salt wasting.
Q4 Multiple choice
The patient’s sodium is 128 mmol/L with low BP, tachycardia, dry mucous membranes and a high urine output. Which treatment does the nurse anticipate?
  1. A. Fluid restriction
  2. B. Isotonic saline and sodium replacement
  3. C. A loop diuretic
  4. D. Withholding all IV fluids
Reveal answer & rationale
Answer: B
Hypovolemia points to cerebral salt wasting, which "is managed with fluid and sodium replacement" (B). Fluid restriction (A) treats SIADH, and applied to CSW "would worsen their condition." A diuretic (C) or withholding fluids (D) would deepen the hypovolemia.
Q5 Select all that apply
Before the aneurysm is secured, which interventions help reduce the risk of rebleeding? Select all that apply.
  1. A. Keep blood pressure within the ordered parameters
  2. B. Give acetaminophen rather than NSAIDs for headache
  3. C. Prepare the patient for early clipping or coiling
  4. D. Give aspirin for the headache
  5. E. Start magnesium to prevent vasospasm
Reveal answer & rationale
Answer: A, B, C
Elevated systolic pressure is a rebleeding risk factor, so BP is controlled until the aneurysm is secured (A); acetaminophen is first-line and "NSAIDs like aspirin should be avoided until the aneurysm is secured" (B, and D is wrong); securing early is "the only effective treatment" and drops rebleeding risk to about 1% (C). "magnesium cannot be recommended for routine administration in aSAH" (E).

Common questions

What causes subarachnoid hemorrhage & cerebral aneurysm?
Common causes and risk factors include high blood pressure — among "the most consistently observed risk factors", cigarette smoking, family history of aneurysm, cocaine or amphetamines — "can increase blood pressure and lead to aneurysms", heavy alcohol use, and others.
Why can’t nimodipine be given IV?
The US labels carry a boxed warning: "DO NOT ADMINISTER NIMODIPINE INTRAVENOUSLY OR BY OTHER PARENTERAL ROUTES" — injecting capsule contents has caused cardiac arrest, cardiovascular collapse, hypotension and bradycardia. Give it only by mouth or feeding tube, using an oral syringe labeled “Not for IV Use.”
Does nimodipine stop vasospasm?
Not directly. StatPearls: oral nimodipine is "the only treatment with consistent, high-quality evidence for decreasing DCI," but early studies showed it improved outcomes "without affecting vasospasm." NINDS calls it "a minimally successful treatment for vasospasm."
When is the vasospasm/delayed ischemia risk highest?
NINDS: delayed cerebral ischemia "can happen between 3 and 14 days after bleeding." StatPearls chapters describe a "4 to 14-day" window and vasospasm that starts around days 3–5 and peaks around day 7.
How is cerebral salt wasting different from SIADH?
Both cause low sodium; the key difference is volume status. In cerebral salt wasting the patient is hypovolemic and needs fluid and sodium; in SIADH the patient is euvolemic (or hypervolemic) and needs fluid restriction. Restricting fluid in CSW is harmful.
Do all brain aneurysms need surgery?
No. NINDS: "Not all cerebral aneurysms need treatment." Very small unruptured aneurysms may be monitored while blood pressure and smoking are aggressively addressed; ruptured aneurysms are clipped or coiled as early as feasible.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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