SAH Flashcards

1
Q

What is the most common initial symptom of a ruptured intracranial aneurysm?
A) Gradual onset headache
B) Sudden severe headache
C) Vision loss
D) Progressive weakness

A

Answer: B) Sudden severe headache
Rationale: The hallmark of aneurysmal rupture is a sudden, severe headache, often described as “the worst headache of my life.” This sudden onset is the most important characteristic, distinguishing it from other types of headaches.

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2
Q

Which of the following symptoms is most indicative of an expanding posterior communicating artery aneurysm?
A) Visual field defects
B) Third cranial nerve palsy with pupillary dilation
C) Neck stiffness
D) Occipital headache

A

Answer: B) Third cranial nerve palsy with pupillary dilation
Rationale: An expanding posterior communicating artery aneurysm can compress the third cranial nerve, leading to pupillary dilation, loss of ipsilateral light reflex, and focal pain above or behind the eye.

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3
Q

Why do some patients experience a transient loss of consciousness at the moment of aneurysmal rupture?
A) Sudden increase in intracranial pressure
B) Brainstem infarction
C) Severe hypotension
D) Cerebral edema

A

Answer: A) Sudden increase in intracranial pressure
Rationale: The rapid increase in intracranial pressure (ICP) due to aneurysmal rupture and subarachnoid hemorrhage (SAH) can cause transient loss of consciousness in nearly half of patients.

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4
Q

Which of the following aneurysm locations is most commonly associated with hemiparesis and aphasia due to mass effect?
A) Posterior inferior cerebellar artery (PICA)
B) Middle cerebral artery (MCA) bifurcation
C) Cavernous sinus
D) Supraclinoid carotid artery

A

Answer: B) Middle cerebral artery (MCA) bifurcation
Rationale: Aneurysms at the MCA bifurcation can rupture and cause a hematoma large enough to exert mass effect, leading to hemiparesis, aphasia, and mental slowness.

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5
Q

What is a key distinguishing feature between a thunderclap migraine and a subarachnoid hemorrhage (SAH)?
A) Neck stiffness
B) Presence of focal neurologic deficits
C) Sudden, severe headache
D) Vomiting

A

Answer: B) Presence of focal neurologic deficits
Rationale: While both thunderclap migraine and SAH can present with a sudden, severe headache, SAH is more likely to be accompanied by focal neurologic deficits, such as cranial nerve palsies, hemiparesis, or aphasia. A definitive workup is necessary to rule out SAH before diagnosing thunderclap migraine.

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6
Q

According to the Hunt-Hess scale, what grade is assigned to a patient with a severe headache, normal mental status, and possible cranial nerve deficit?
A) Grade 1
B) Grade 2
C) Grade 3
D) Grade 4

A

Answer: B) Grade 2
Rationale: The Hunt-Hess scale classifies Grade 2 as a patient with a severe headache, normal mental status, and possible cranial nerve deficit. Grade 1 only includes mild headache with no deficits, while higher grades involve confusion, motor deficits, or coma.

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7
Q

Which finding differentiates a Hunt-Hess Grade 3 subarachnoid hemorrhage from Grade 2?
A) Presence of mild motor deficit or confusion
B) Severe headache
C) Cranial nerve involvement
D) Normal mental status

A

Answer: A) Presence of mild motor deficit or confusion
Rationale: Hunt-Hess Grade 3 includes patients who are somnolent or confused and may have mild motor deficits. Grade 2 patients have severe headaches but maintain normal mental status.

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8
Q

A patient with a GCS score of 3-6 and flaccid motor function would be classified as what grade in both the Hunt-Hess and WFNS scales?
A) Grade 3
B) Grade 4
C) Grade 5
D) Grade 2

A

Answer: C) Grade 5
Rationale: Both scales classify the most severe cases (coma, flaccidity, or reflex posturing) as Grade 5. The WFNS assigns this based on a GCS of 3-6, while Hunt-Hess considers coma and severe neurological impairment.

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9
Q

Which of the following best describes the primary clinical utility of the Hunt-Hess and WFNS grading scales?
A) Predicting aneurysm rupture risk
B) Assessing patient prognosis and mortality risk
C) Determining the cause of SAH
D) Guiding surgical intervention timing

A

Answer: B) Assessing patient prognosis and mortality risk
Rationale: Both grading systems are used to predict the outcome of SAH patients, with higher grades associated with increased mortality and worse functional outcomes. They help guide clinical decision-making regarding treatment intensity.

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10
Q

What is the approximate incidence of aneurysmal rerupture in the first month following SAH if untreated?
A) 10%
B) 20%
C) 30%
D) 50%

A

Answer: C) 30%
Rationale: The incidence of rerupture is about 30% in the first month, with the highest risk occurring in the first 7 days. Early treatment significantly reduces this risk.

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11
Q

Which of the following is the most common early clinical manifestation of subacute hydrocephalus following SAH?
A) Hemiparesis
B) Progressive drowsiness and slowed mentation
C) Severe headache
D) Seizures

A

Answer: B) Progressive drowsiness and slowed mentation
Rationale: Subacute hydrocephalus develops over days to weeks and presents with progressive drowsiness, cognitive slowing, and incontinence. It can be mistaken for cerebral vasospasm but is differentiated using imaging studies.

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12
Q

Which of the following is the major cause of delayed morbidity and mortality in SAH patients?
A) Hydrocephalus
B) Vasospasm leading to delayed cerebral ischemia
C) Hyponatremia
D) Seizures

A

Answer: B) Vasospasm leading to delayed cerebral ischemia
Rationale: Vasospasm is the leading cause of delayed morbidity and death, affecting ~30% of patients. It typically occurs 4-14 days after SAH and can result in ischemia and infarction.

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13
Q

What is the primary imaging modality used to monitor cerebral vasospasm in SAH patients?
A) EEG
B) Transcranial Doppler ultrasound
C) CT scan
D) PET scan

A

Answer: B) Transcranial Doppler ultrasound
Rationale: TCD ultrasound is frequently used to monitor blood flow velocity in major cerebral arteries. Increased velocity indicates vasospasm. CT angiography and conventional angiography are also useful but more invasive.

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14
Q

Which of the following best describes the mechanism of vasospasm in SAH?
A) Direct pressure from hematoma on cerebral arteries
B) Inflammatory response to subarachnoid blood breakdown products
C) Compression of the brainstem
D) Overproduction of cerebrospinal fluid

A

Answer: B) Inflammatory response to subarachnoid blood breakdown products
Rationale: Vasospasm occurs due to direct effects of clotted blood and its breakdown products on cerebral arteries, leading to their narrowing and potential infarction.

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15
Q

Which of the following is a common early symptom of delayed cerebral ischemia due to vasospasm?
A) Progressive mental decline
B) Sudden loss of consciousness
C) Severe occipital headache
D) Seizures

A

Answer: A) Progressive mental decline
Rationale: DCI is often preceded by a decline in mental status. Focal neurological symptoms can follow if infarction occurs due to severe vasospasm.

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16
Q

What is the primary cause of hyponatremia in SAH patients?
A) Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
B) Cerebral salt-wasting syndrome
C) Renal failure
D) Fluid overload

A

Answer: B) Cerebral salt-wasting syndrome
Rationale: Hyponatremia in SAH is due to cerebral salt-wasting syndrome, which involves natriuresis and volume depletion, exacerbated by brain natriuretic peptide. It is distinct from SIADH, which typically occurs with euvolemia.

17
Q

Which of the following is the most appropriate management for hyponatremia in SAH patients?
A) Free water restriction
B) Administration of isotonic or hypertonic saline
C) Diuretics
D) Immediate dialysis

A

Answer: B) Administration of isotonic or hypertonic saline
Rationale: Hyponatremia in SAH should not be treated with water restriction, as this can worsen cerebral ischemia. Instead, isotonic or hypertonic saline is used to maintain adequate intravascular volume.

18
Q

What is the hallmark finding in cerebrospinal fluid (CSF) that suggests an aneurysmal rupture?
A) Increased protein concentration
B) Xanthochromia
C) Elevated white blood cell count
D) Decreased glucose levels

A

Answer: B) Xanthochromia
Rationale: Xanthochromia, a yellow discoloration of the CSF, results from hemoglobin breakdown into bilirubin and is a key indicator of subarachnoid hemorrhage (SAH). It appears 6–12 hours after bleeding, peaks at 48 hours, and can last 1–4 weeks.

19
Q

If an SAH is suspected but a noncontrast CT scan is negative, what is the next best step in diagnosis?
A) MRI
B) Cerebral angiography
C) Lumbar puncture
D) Transcranial Doppler ultrasound

A

Answer: C) Lumbar puncture
Rationale: A noncontrast CT scan detects SAH in >95% of cases within the first 72 hours. If CT is negative and suspicion remains high, a lumbar puncture is performed to detect xanthochromia or red blood cells in the CSF, confirming the diagnosis.

20
Q

What CT finding is most predictive of symptomatic vasospasm following SAH?
A) Presence of hydrocephalus
B) Blood clot >5 × 3 mm in basal cisterns
C) Diffuse brain atrophy
D) White matter hyperintensities

A

Answer: B) Blood clot >5 × 3 mm in basal cisterns
Rationale: The presence of large subarachnoid clots (>5 × 3 mm in the basal cisterns) or >1 mm thick layers of blood in cerebral fissures is associated with a higher incidence of symptomatic vasospasm, particularly in the MCA and ACA territories.

21
Q

What is the primary imaging modality used to identify and define the anatomy of a ruptured aneurysm?
A) MRI
B) Four-vessel conventional angiography
C) Transcranial Doppler ultrasound
D) Chest X-ray

A

Answer: B) Four-vessel conventional angiography
Rationale: Four-vessel conventional angiography (both carotid and vertebral arteries) is the gold standard for locating the ruptured aneurysm, evaluating its anatomy, and identifying other unruptured aneurysms. In some cases, endovascular treatment can be performed at the time of the angiogram.

22
Q

Which of the following electrocardiographic (ECG) findings is commonly associated with SAH?
A) ST-segment elevation with reciprocal changes
B) Deeply inverted, symmetric T waves
C) Mobitz type II second-degree AV block
D) Sinus bradycardia with delta waves

A

Answer: B) Deeply inverted, symmetric T waves
Rationale: SAH can cause ST-segment and T-wave changes that mimic cardiac ischemia, including deeply inverted, symmetric T waves, prolonged QT intervals, and a widened QRS complex. These changes are due to catecholamine surge and sympathetic nervous system injury, which can also lead to reversible cardiomyopathy.

23
Q

Which of the following statements about vasospasm in SAH is true?
A) It peaks within the first 24 hours
B) Nimodipine improves outcomes by directly reversing vasospasm
C) Induced hypertension can improve cerebral perfusion
D) It is primarily caused by thromboembolism rather than vessel constriction

A

Answer: C) Induced hypertension can improve cerebral perfusion
Rationale: Vasospasm and DCI typically occur 3–14 days after SAH. Induced hypertension can increase cerebral perfusion and improve symptoms. Nimodipine helps prevent ischemic injury but does not directly reverse vasospasm.

24
Q

What is the most appropriate initial blood pressure target before aneurysm repair in an alert SAH patient?
A) SBP <120 mmHg
B) SBP <140 mmHg
C) SBP <160 mmHg
D) No specific BP target

A

Answer: C) SBP <160 mmHg
Rationale: In alert SAH patients, systolic BP should be kept below 160 mmHg using nicardipine, labetalol, or esmolol to reduce rebleeding risk while maintaining adequate cerebral perfusion.

25
What is the preferred treatment for symptomatic cerebral vasospasm if medical therapy fails? A) Subcutaneous heparin B) Intra-arterial vasodilators or angioplasty C) Surgical decompression D) Corticosteroids
Answer: B) Intra-arterial vasodilators or angioplasty Rationale: Intra-arterial vasodilators (e.g., verapamil, nicardipine) and percutaneous transluminal angioplasty are used when vasospasm persists despite medical therapy. Papaverine is avoided due to neurotoxicity.
26
What is the main goal of using nimodipine in SAH management? A) Directly dilating cerebral arteries B) Lowering blood pressure to prevent rebleeding C) Preventing ischemic injury D) Treating hydrocephalus
Answer: C) Preventing ischemic injury Rationale: Nimodipine (60 mg PO every 4 hours) improves functional outcomes by preventing ischemic injury, though it does not directly relieve vasospasm.
27
Why is free-water restriction contraindicated in SAH patients at risk for delayed cerebral ischemia? A) It increases the risk of seizures B) It leads to hypernatremia, which worsens vasospasm C) It can cause hypovolemia and hypotension, worsening cerebral ischemia D) It is associated with increased ICP
Answer: C) It can cause hypovolemia and hypotension, worsening cerebral ischemia Rationale: Hypovolemia and hypotension can worsen cerebral ischemia. Euvolemia is the goal, often requiring IV saline and oral salt supplementation to prevent hyponatremia.
28
In SAH patients, when is systemic anticoagulation contraindicated for deep vein thrombosis (DVT) or pulmonary embolism (PE)? A) Immediately after aneurysm repair B) If the aneurysm is ruptured and untreated C) In patients with chronic hydrocephalus D) If ICP monitoring is in place
Answer: B) If the aneurysm is ruptured and untreated Rationale: Systemic anticoagulation is contraindicated in patients with an untreated, ruptured aneurysm due to high risk of rebleeding. If DVT or PE occurs early post-craniotomy, an IVC filter may be used instead.