Subarachnoid hemorrhage

Introduction

Subarachnoid hemorrhage (SAH) is a serious neurological condition characterized by bleeding into the subarachnoid space of the brain. It is associated with high morbidity and mortality, requiring prompt diagnosis and management. Understanding its anatomy, causes, and clinical presentation is crucial for effective treatment.

Anatomy and Physiology Relevant to Subarachnoid Hemorrhage

Subarachnoid Space

The subarachnoid space is the area between the arachnoid mater and pia mater that surrounds the brain and spinal cord. It contains cerebrospinal fluid (CSF), which cushions the brain, provides nutrients, and removes waste. This space also serves as a conduit for cerebral blood vessels, which are susceptible to rupture in SAH.

• Definition and boundaries: Located between arachnoid mater and pia mater.
• Cerebrospinal fluid circulation: CSF flows from the ventricles through the subarachnoid space, absorbing shock and maintaining intracranial pressure.

Cerebral Vasculature

The cerebral vasculature plays a key role in SAH, as most spontaneous hemorrhages are caused by ruptured aneurysms. Understanding the anatomy of major cerebral arteries is essential for diagnosis and treatment planning.

• Circle of Willis anatomy: A ring-like arterial structure at the base of the brain connecting anterior and posterior circulations, common site for aneurysm formation.
• Major arteries prone to aneurysm formation: Includes anterior communicating artery, posterior communicating artery, and middle cerebral artery branches.

Etiology and Risk Factors

Spontaneous Causes

Spontaneous subarachnoid hemorrhage occurs without preceding trauma and is the most common type. It is primarily caused by vascular abnormalities.

• Aneurysmal rupture: The most frequent cause of spontaneous SAH, usually involving saccular aneurysms in the Circle of Willis.
• Arteriovenous malformations: Abnormal connections between arteries and veins that may rupture, leading to hemorrhage.
• Idiopathic cases: Rare instances where no clear vascular abnormality is identified.

Secondary Causes

Secondary SAH results from identifiable external or systemic factors that precipitate bleeding.

• Traumatic SAH: Resulting from head injuries, often associated with skull fractures or contusions.
• Coagulopathies: Bleeding disorders or anticoagulant therapy increasing the risk of hemorrhage.
• Vasculitis or infection-related causes: Inflammation of cerebral vessels or infectious processes weakening vessel walls.

Risk Factors

Several factors increase the likelihood of developing SAH, particularly spontaneous cases.

• Hypertension: Chronic high blood pressure can weaken arterial walls.
• Smoking: Contributes to vascular damage and aneurysm formation.
• Genetic predisposition: Family history and genetic syndromes like polycystic kidney disease increase risk.
• Age and sex considerations: Risk rises with age and is slightly higher in females.

Pathophysiology

Subarachnoid hemorrhage disrupts normal cerebral function through multiple mechanisms, leading to neurological deficits and systemic complications.

• Mechanism of vessel rupture: Weakening of arterial walls or aneurysm formation leads to sudden vessel breakage.
• Intracranial pressure changes: Bleeding into the subarachnoid space increases pressure, reducing cerebral perfusion.
• Ischemia and cerebral vasospasm: Secondary narrowing of cerebral arteries can cause delayed brain ischemia.
• Inflammatory cascade and secondary injury: Blood products trigger inflammation, oxidative stress, and neuronal damage.

Clinical Presentation

Typical Symptoms

Patients with subarachnoid hemorrhage often present with sudden and severe symptoms that require immediate medical attention.

• Sudden severe headache: Often described as a “thunderclap headache,” reaching maximum intensity within seconds to minutes.
• Nausea and vomiting: Common accompanying symptoms due to increased intracranial pressure.
• Neck stiffness: Resulting from meningeal irritation caused by blood in the subarachnoid space.
• Altered level of consciousness: Ranging from mild confusion to deep coma depending on severity.

Neurological Signs

Physical examination may reveal focal or generalized neurological deficits depending on the location and extent of bleeding.

• Focal neurological deficits: Weakness, sensory loss, or cranial nerve abnormalities.
• Seizures: May occur due to cortical irritation from hemorrhage.
• Signs of raised intracranial pressure: Papilledema, bradycardia, or hypertension.

Grading Scales

Clinical grading scales help assess severity and guide management decisions.

• Hunt and Hess scale: Grades SAH from I (minimal headache, mild nuchal rigidity) to V (deep coma, moribund).
• World Federation of Neurological Surgeons (WFNS) scale: Combines Glasgow Coma Scale and focal neurological deficits to stratify risk.

Diagnostic Evaluation

Imaging

Imaging studies are essential for confirming the diagnosis, identifying the source of bleeding, and planning treatment.

• Non-contrast CT scan: First-line investigation, highly sensitive within the first 24 hours.
• CT angiography (CTA): Helps visualize aneurysms and vascular malformations.
• Magnetic resonance imaging (MRI): Useful for subacute or chronic cases and for detecting complications.
• Digital subtraction angiography (DSA): Gold standard for detailed vascular mapping, used for planning interventions.

Laboratory Tests

Laboratory evaluation supports diagnosis and identifies underlying risk factors.

• Complete blood count and coagulation profile: Detects anemia, thrombocytopenia, or coagulopathy.
• Cerebrospinal fluid analysis: Performed via lumbar puncture if CT scan is negative but suspicion remains high; detects xanthochromia.

Management

Initial Stabilization

Immediate stabilization focuses on preventing further neurological damage and managing life-threatening complications.

• Airway, breathing, circulation (ABC): Ensure adequate oxygenation and hemodynamic stability.
• Blood pressure management: Maintain optimal pressure to reduce risk of rebleeding while preserving cerebral perfusion.
• Pain control and sedation: Alleviates headache and agitation, reducing sympathetic stress.

Definitive Treatment

Definitive interventions aim to secure the source of bleeding and prevent recurrence.

• Surgical clipping of aneurysm: Open neurosurgical procedure to place a clip across the aneurysm neck.
• Endovascular coiling: Minimally invasive technique to occlude aneurysms using detachable coils.
• Management of vasospasm: Pharmacologic therapy with nimodipine and hemodynamic augmentation to prevent delayed ischemia.

Supportive Care

Supportive measures reduce secondary injury and optimize recovery.

• Intracranial pressure monitoring: Guides therapy in patients with elevated pressure.
• Seizure prophylaxis: Prevents seizure-related complications in high-risk patients.
• Fluid and electrolyte management: Maintains hemodynamic stability and prevents hyponatremia or dehydration.

Complications

Complications of subarachnoid hemorrhage can significantly affect morbidity and mortality.

• Cerebral vasospasm and delayed ischemic neurologic deficit: Narrowing of arteries days after SAH leading to secondary ischemia.
• Hydrocephalus: Accumulation of CSF due to impaired absorption, sometimes requiring shunt placement.
• Rebleeding: Early recurrence of hemorrhage, often associated with high mortality.
• Seizures: Resulting from cortical irritation or structural damage.
• Cardiopulmonary complications: Arrhythmias, pulmonary edema, or myocardial injury due to sympathetic surge.

Prognosis and Outcomes

The prognosis of subarachnoid hemorrhage depends on the severity of the initial bleed, patient factors, and timeliness of treatment. Early intervention can significantly improve survival and functional recovery.

• Factors affecting mortality and morbidity: Age, neurological grade at presentation, aneurysm size, and rebleeding risk.
• Long-term neurological outcomes: Cognitive deficits, motor weakness, and emotional disturbances may persist in survivors.
• Rehabilitation and recovery: Multidisciplinary approach including physical therapy, occupational therapy, and neurocognitive rehabilitation is essential for functional improvement.

Prevention

Preventive strategies focus on reducing risk factors and early detection of vascular abnormalities in high-risk populations.

• Screening for high-risk patients: Imaging in patients with family history or genetic syndromes like polycystic kidney disease.
• Lifestyle modifications: Smoking cessation, regular exercise, and a healthy diet to maintain vascular health.
• Blood pressure control: Effective management of hypertension to reduce aneurysm formation and rupture risk.

References

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