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Subarachnoid Hemorrhage Overview and Management
Aug 28, 2024
Subarachnoid Hemorrhage Overview
Definition
Subarachnoid hemorrhage (SAH)
: Hemorrhage of cerebral vessels (primarily from the Circle of Willis) into the
subarachnoid space
.
Can also involve
intraventricular hemorrhage
if vessels rupture into the ventricles.
Causes
Traumatic SAH (Most Common)
Blunt force trauma
: E.g., hit on the head.
Penetrating trauma
: E.g., stab wound.
Non-Traumatic SAH (Less Common)
Aneurysmal:
Saccular (Berry) Aneurysm
: Asymmetric ballooning of the vessel.
Giant Saccular Aneurysm
: >2.5 cm.
Fusiform Aneurysm
: Symmetrical dilation of vessels.
Pseudoaneurysm
: Vessel dissection that resembles an aneurysm.
Mycotic Aneurysm
: Infected aneurysm.
Risk Factors for Aneurysm Formation
Hypertension
: Increases stress on vessel walls.
Sympathomimetics
: Drugs like cocaine and methamphetamine increase sympathetic activity.
Smoking and Alcohol
: Contributes to vessel wall stress.
Oral Contraceptives/Pregnancy
: Hormonal influences on vascular integrity.
Connective Tissue Disorders
:
Marfan Syndrome
: Deficiency in fibrillin.
Ehlers-Danlos Syndrome
: Deficiency in collagen.
Polycystic Kidney Disease
: Defect in polycystin proteins.
Fibromuscular Dysplasia
: Abnormal growth of smooth muscle in vessels.
Triggers for Aneurysm Rupture
Acute rise in blood pressure
.
Painful stimuli
or
anger
can also trigger rupture.
Locations of Aneurysms within the Circle of Willis
Anterior Communicating Artery
: ~30% of saccular aneurysms.
Posterior Communicating Artery
: ~25%.
Middle Cerebral Artery (MCA) bifurcation
: ~20%.
Internal Carotid Artery (ICA) terminus
: ~7.5%.
Basilar Tip
: ~7%.
Anterior Cerebral Artery
: ~4%.
Posterior Inferior Cerebellar Artery (PICA)
: ~3.5%.
Clinical Features of SAH
Thunderclap headache
: Sudden onset, often described as the worst headache ever.
Meningeal signs
: Photophobia, neck stiffness, positive Kernig's and Brudzinski's signs.
Increased intracranial pressure (ICP)
: Symptoms include nausea, vomiting, cranial nerve deficits, and Cushing's triad (hypertension, bradycardia, irregular respirations).
Focal neurological deficits
: Possible stroke-like symptoms depending on the affected vessel.
Diagnosis
Non-contrast CT scan
: Initial test to identify SAH.
Look for blood in the
sulci
and
cisterns
.
Assess for
intraventricular hemorrhage (IVH)
and hydrocephalus.
Modified Fischer Score
: Helps assess the risk of vasospasm and delayed cerebral ischemia.
CT Angiogram (CTA)
: To identify the ruptured aneurysm.
Digital Subtraction Angiogram
: Gold standard for visualizing blood vessels.
Lumbar Puncture
: Can confirm SAH if CT is inconclusive (look for xanthochromia).
Treatment
Initial Care
Airway, Breathing, Circulation (ABCs)
: Secure airway due to potential ICP increase.
Ventilation
: Options include Continuous Mechanical Ventilation (CMV) or Adaptive Support Ventilation (ASV).
Blood Pressure Control
Target systolic BP <160 mmHg to prevent rebleeding.
Medications: Nicardipine, Labetalol, Hydralazine, Enalapril.
External Ventricular Drain (EVD)
Indicated in high Hunt-Hess score, presence of IVH, or hydrocephalus to monitor and reduce ICP.
Aneurysm Management
Coiling or Clipping
within 24 hours to prevent rebleeding.
Choice depends on various factors: age of the patient, neck size of the aneurysm, hemodynamic stability, and aneurysm location.
Complications Management
Rebleeding
: High mortality (70%); stabilize with antifibrinolytics (Aminocaproic acid, TXA) and replace fibrinogen.
Vasospasm
: Delayed cerebral ischemia may occur around days 4-14.
Monitor with daily Transcranial Dopplers (TCDs) for blood flow velocity and Lindegaard ratio.
Treatment: Nimodipine, induced hypertension, intra-arterial dilators.
Seizures
: Treat with antiepileptic medications.
Pyrexia
: Manage with cooling measures and medications that prevent shivering.
Cerebral Salt Wasting
: Treat with Florinef (Fludrocortisone) and sodium/water replacement.
Stress Cardiomyopathy
: Address hypotension with vasopressors.
Neurogenic Pulmonary Edema
: Manage hypoxia with increased PEEP and oxygenation.
Conclusion
Understand pathophysiology, risk factors, clinical features, and management strategies for subarachnoid hemorrhage to improve patient outcomes.
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