Acute Subdural Hematoma

Authors:

Manish KC,

Junaid Siddiquie, MD, MRCP

Introduction

• Extravasation of blood into the subdural space between the dura and arachnoid membranes

• Most common neurosurgical emergency associated with high morbidity and mortality

• A potentially life-threatening condition requiring urgent surgical evacuation for good clinical outcomes

Epidemiology

• mostly traumatic but can be spontaneous

• 50-90% death rate in acute traumatic SDH

• Incidence of traumatic SDH: 11-49%

• After surgical evacuation, recurrent rates as high as 20% in some cases

• Most commonly seen in MVAs in the younger population and from falls in the older age group

• May have a lucid interval in 12-38% of patients

• 35-80% present with GCS ≤8 with a mortality of 55-70%

• Death in patients with GCS 3-15: 30-60%

Etiology

• Rupture of the bridging veins

• Mostly traumatic but can be spontaneous

• Spontaneous causes of acute SDH: anticoagulants/antiplatelet use, intracranial aneurysmal rupture

• Less common causes: AVMs rupture, cocaine abuse, vascular meningiomas, dural metastases, etc

Figure 1: Acute Subdural Hematoma on CT Brain

Types

• Parafalcine and tentorial
• Seen in younger patients with mild traumatic brain injury
• Managed nonoperatively

• Posterior fossa
• Rare
• Poor outcome
• 50% death rate
• Coagulopathy present
• Associated with low GCS score and occipital fracture

• Non-traumatic
• Seen in ruptured intracranial aneurysms, cancers, anticoagulants use, AIDS, bleeding disorders

Pathophysiology

• Cerebral blood flow changes
• Reduces significantly instantly after injury due to a decrease in CPP and an increase in ICP
• Cerebral vasoconstriction and defect in autoregulation after brain trauma also contribute to a decrease in CBF
• Hyperemia/hyperperfusion occurs followed by reperfusion injury by oxygen-derived free radicals that are associated with poor clinical outcome

• Coagulopathy
• Occur following traumatic brain injury
• Trigger coagulation pathway increases the likelihood of bleeding
• Affects hemostasis, intracerebral hematoma formation, and expansion that lead to poor clinical outcomes

• Delayed deterioration
• Also known as talk and deteriorate
• Seen in the elderly
• Seen within 6 hours after trauma
• Atrophied brains in the elderly allow more intracranial space to accumulate blood and cerebral edema before clinical deterioration occurs
• Early identification and evacuation of hematoma are important to avoid this phenomenon

Clinical Features

• Headache

• Altered mental status

• Nausea/vomiting

• Lethargy

• Motor weakness

• Seizures

• Stupor

• Coma

Differential Diagnosis

• Epidural hematoma

• Subarachnoid hemorrhage

• Meningitis

• Encephalitis

• Intracerebral hemorrhage

Diagnosis

• Non-contrast CT scan of Head: easily available, Crescent shaped mass, sensitivity nearly 100%

• MRI is superior to CT in identifying small SDH, tentorial, and interhemispheric SDH

• Additional findings like midline shift, brain herniation, associated brain injuries can be seen in brain imaging

• Digital subtraction angiography in non-traumatic acute SDH for suspected rupture of a cerebral aneurysm

Treatment

• Emergent resuscitation

• Neurosurgical consultation

• Maintenance of airway, breathing, and circulation

• Maintain Pao2> 60mm Hg and MAP> 65mm Hg

• Intubate patient, if unable to maintain the airway

• Rapid sequence intubation to facilitate endotracheal intubation

• Adequate intravenous access

• Reversal of anticoagulation to avoid hematoma expansion

• Intracranial pressure monitoring and treatment
• Elevate head of bed to 300

• Intracranial pressure Treatment
• ICP treatment only recommended if the patient is a surgical candidate and on the way to surgical intervention
• Brief Hyperventilation to maintain PaCO2 of 32-36 mm Hg (max 4 hours)
• Osmolar therapy with Mannitol 1 to 1.5g/kg and/or 30 to 120ml of 23.4% Hypertonic saline (on the way to surgical suite)

• Seizure prophylaxis: Phenytoin/fosphenytoin or Levetiracetam

• Blood pressure and cerebral perfusion pressure management
• Maintain CPP above 60 mm Hg in adults and 40-65mm Hg in children

• Analgesia
• Fentanyl- 25 to 200 mcg/hr
• Remi-fentanyl- 0.5 to 2 mcg/kg/min

• Sedation
• Propofol- 5mcg/kg/min followed by increase in 5-10mcg/kg/min until adequate sedation is achieved

• Temperature control
• Maintain normothermia by acetaminophen

• Glucose control
• Maintain blood glucose level 120-180 mg/dl
• Avoid hyperglycemia using insulin sliding scales

• Stress ulcer prophylaxis
• PPIs preferred over H2 blockers, sucralfate

Indications for emergent surgery

• A rapid decline in neurological status Mydriasis: unilateral or bilateral Extensor posture Midline shift in CT Head > 5mmHematoma size in CT Head > 10mm

• Neurosurgical evacuation under general anesthesia

Complications

• Brain herniation

• Coma

• Death

Prognosis

• Prognosis depends upon age, neurological condition, radiological appearance, the timing of neurosurgery, associated brain injuries, extracranial injuries, and postoperative care

• 25-50% of cases are comatose after the trauma

• 12-38% of cases undergo gradual neurological deterioration followed by coma a few hours after the trauma

• Overall bad prognosis in serious trauma to the brain parenchyma, associated brain edema and/or herniation

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