Aneurysmal subarachnoid hemorrhage

FACTS HPI PHYSICAL EXAM IMAGING Table 1: Electrolyte Targets in Vasospasm Figure 1: Saccular aneurysms and locations Sentinel Bleed workup without SAH Specific Aneurysms Cavernous Sinus Carotid Aneurysms Mycotic Aneurysms Opthalmic Aneurysms Acomm Aneurysms Intradural ICA Aneurysms Basilar Apex Aneurysms P-comm Aneurysms Infundibulum vs Aneurysms Associated Syndromes PCKD Marfan Syndrome Subarachnoid hemorrhage mimic Takotsubo cardiomyopathy (neurogenic stress cardiomyopathy)

FACTS

peak age 55-60 yo --> although 20% between 15-45 yrs

10-15% die before getting care

Risk of re-rupture is greatest in first 24 hours

HPI

Smoker

Etoh use

Family Hx of ruptured aneurysms

Known syndromes or connective tissue diseases (PCKD, Marfan, EDS)

seizures - this matters, because not all SAH are started on AEDs

Drug use (specifically, cocaine)

Neurologic baseline - pertinent in old people to know baseline level of confusion because confusion alone is a HH3 and indication for EVD

recent myelography (very rare mimic - see below)

Is this a previously coiled aneurysm? If so, know the Raymond grade.

Raymond–Roy Occlusion Classification

Labs: ensure Cr reasonable for CTA/DSA and CBC/Coags ready for EVD

PHYSICAL EXAM

Neck pain or lumbar back pain (more pertinent if sentinel bleed, from runoff gravity)

More important in the un-ruptured setting

vision exam (compressive optic neuropathy from Opth A --> nasal quadrantopsia)

CN III exam

facial pain evaluation

IMAGING

CTH non-con

impossible to use this to diagnose aneurysm location, however there are some patterns:

Acomm = anterior interhemispheric fissures or gyrus rectus

MCA / Pcomm = unilateral sylvian fissure

Basilar apex / SCA = prepontine pr peduncular cistern

Lower posterior fossa (PICA/VA dissection) = predominantly within ventricles

CTA H&N:

look for the neck wideness (narrower <5mm = better for coiling)

CT C-spine - should be included on CTA H&N, but this is necessary to clear a C-collar which is often placed when a person is found down after rupture

MRA will not be more useful than CTA, however can be done if patient has a real and serious allergy to contrast or whatever contraindication. Pretty poor sensitivity for aneurysms < 3mm in diameter

MRI Brain with and without contrast:

FLAIR is best sequence for acute SAH detection

A/P

I. Acute management

HOB > 30

Clear C-collar ASAP with CT C-spine or MRI C-spine: many of these patients are found down and treated as traumas. C-collars can reduce jugular venous outflow if applied correctly and tightly.

Ventriculostomy as indicated: EVD at 20AMB, cannot drain too aggressively, you actually want the high ICP to "tamponade" the bleeding, SBP CAP at 140

Ask CCM to place a Left radial a-line while you do the EVD to get ready for DSA

II. Secure the aneurysm

DSA vs. OR

After securing aneurysm, EVD to 5 or 10, CAP liberalized3

III. Managing Spasm / Neuro ICU admission orders

Euvolemia: avoid hypotension, check IOs at 4am and 4pm, place foley if needed

SAH precautions: minimize stimulations

HA management: can be very intractable, steroids often the only thing that help if not other contraindications

HOB > 30 degrees

Nimotop 30q2 or 60q4 (more frequent = to avoid periodic dips in BP)

TCDs to monitor MCA, ACA, ICA velocities and Lindegaard ratio if available at your institution

Angio negative SAH: repeat DSA or MRI Brain and pan-spine in about a week

Spasm watch (Days 4-14)

White (Vascular, Functional, Tumor)

HHH Therapy: Hypervolemia, Hypertension, Hemodilution

Euvolemia: (Hypervolemia/Hypertension)

Daily TCDs

Electrolyte repletion: preserve cerebral perfusion, maintain vascular tone, and reduce the risk and severity of vasospasm

Na+
K+: low K+ causes hyperexcitability of vascular smooth muscle
Mg2+: has direct vasodilatory effects (acts as Ca2+ channel blocker)

Table 1: Electrolyte Targets in Vasospasm

Electrolyte	Target Range (Post-SAH)	Rationale	Notes
Sodium (Na⁺)	140–150 mmol/L (high-normal)	Prevents hyponatremia-induced cerebral edema and hypovolemia; maintains osmotic gradient to limit ICP spikes.	Avoid rapid correction (>8–10 mmol/L/24h) to prevent osmotic demyelination. Often managed with hypertonic saline in salt-wasting.
Magnesium (Mg²⁺)	≥2.0 mg/dL (0.82 mmol/L)	Vasodilatory effect via calcium channel antagonism; neuroprotective in ischemia.	Check daily; replete IV if low—monitor for hypotension with rapid infusion.
Potassium (K⁺)	4.0–4.5 mmol/L	Stabilizes vascular and neuronal membrane potentials; prevents arrhythmia that could reduce cerebral perfusion.	Prefer central line for high-dose IV repletion; avoid hypokalemia in nimodipine therapy.
Calcium (Ca²⁺)	Ionized Ca²⁺ >1.1 mmol/L	Needed for cardiac contractility and vascular tone regulation; hypocalcemia can worsen hypotension.	Correct Mg first if refractory hypocalcemia.
Phosphate (PO₄³⁻)	≥2.5 mg/dL	Supports ATP production for neuronal and vascular smooth muscle function.	Often drops during aggressive repletion of other electrolytes—replace enterally if possible.

Figure 1: Saccular aneurysms and locations

most commonly at branch points. Fusiform aneurysms more common in vertebrobasilar system.

Sentinel Bleed workup without SAH

sometimes people have a thunderclap HA w/o clear SAH on a low-quality CT. These are managed as SAH until proven otherwise, especially if the patient has a known aneurysm

How to prove otherwise

1) MRI Brain w/wo contrast - higher definition picture to evaluate for presence of blood however this is not sensitive until 2-3 days post-bleed

+/- MRI pan-spine to evaluate for dependent blood

2) Lumbar puncture: send CSF in 4 tubes, very important to be as atraumatic as possible

if RBCs stable or downtrending from tubes 1-4 --> unlikely SAH

if RBCs uptrending or xanthochromic supernatant --> more likely SAH

if this is traumatic, its a useless test

this is not without risk, if there is an actual ruptured aneurysm can precipitate rebleeding

if a person is jaundiced, this can be false-positive

Specific Aneurysms

Cavernous Sinus Carotid Aneurysms

For unruptured, most likely symptom is a CN6 palsy (closest proximity to abducens nerve in cavernous sinus)

facial pain syndromes in the maxillary nerve distribution

Mycotic Aneurysms

Opthalmic Aneurysms

may present with chiasmal syndrome

Acomm Aneurysms

may present with chiasmal syndrome

5mm anterior, superiorly, L projecting AComm aneurysm

Intradural ICA Aneurysms

ruptured, blister appearing ventral carotid wall aneursym in a middle aged adult with seizures and hydrocephalus managed with a flow diverter extending from M1 distally to supraclinoid ICA proximally.

(top-left) CTA showing ventral anteriorly projecting tiny blister aneurysm causing a devastatingly large aneurysmal bleed w/ IVH (top-right) re-demonstrated on angiography (bottom left) and simultaneously treated with a flow diverter (bottom right)

Basilar Apex Aneurysms

may present with chiasmal syndrome

P-comm Aneurysms

10% of these aneurysms p/w non-pupil sparing CN 3 palsy

Infundibulum vs Aneurysms

infundibulum = funnel shaped initial artery segment, most commonly at Pcomm origin

Associated Syndromes

PCKD

PCKD is associated with intracranial aneurysms, cervical arterial dissections, intracranial dolichoectasia, spinal meningeal diverticula

general mechanism is abnormal collagen/proteoglycans produced --> weaken

Marfan Syndrome

Subarachnoid hemorrhage mimic

This is a very rare mimic of subarachnoid hemorrhage - if you see someone who is wide awake with what looks like a modified fisher 7 subarachnoid hemorrhage, ask them if they recently got a myelogram!

Intracranial accumulation of contrast agent after myelography | Radiology Case | Radiopaedia.org

Takotsubo cardiomyopathy (neurogenic stress cardiomyopathy)

SAH can induce cardiac dysfunction → ↓ LV function → CHF/PE