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Emergency and Acute Medicine - Subdural Hematoma
Subdural hematoma (SDH) is bleeding between the dura and arachnoid mater, most commonly due to tearing of bridging veins. It is classified based on timing into acute (within 3 days), subacute (3 days to 3 weeks), and chronic (after 3 weeks). On CT imaging, SDH typically appears as a crescent-shaped collection that crosses suture lines but does not cross the midline, often with irregular inner margins. Acute SDH is most commonly caused by acceleration–deceleration forces that stretch and tear parasagittal bridging veins, though bleeding may also arise from cortical arteries, dural lacerations, or venous sinuses. Nontraumatic causes include aneurysm rupture, arteriovenous malformations, coagulopathy, hypertension, and substance abuse. Chronic SDH develops from repeated small venous bleeds and becomes encapsulated over time.
Acute SDH is the most common intracranial hematoma, accounting for 66–70% of cases and frequently associated with blunt head trauma, particularly motor vehicle accidents, falls, and assaults. There is a bimodal age distribution, affecting young adults and the elderly, with higher risk in older patients, those with brain atrophy, alcohol use, or seizure disorders. Chronic SDH is more common in older adults and infants, often with minimal or no clear history of trauma. Coagulopathy significantly increases the risk and severity of bleeding, particularly with elevated INR levels.
Clinically, acute SDH often presents with headache and altered mental status, and up to half of patients may be unconscious at presentation. It is frequently misdiagnosed as intoxication or stroke. Focal neurologic deficits such as hemiparesis or hemiplegia are common, and pupillary abnormalities may indicate ipsilateral mass effect. Seizures can occur early. Subacute and chronic SDH present more insidiously, with symptoms such as headache, nausea, vomiting, seizures, fluctuating mental status, gait instability, and progressive neurologic deficits. In children, especially infants, symptoms may include irritability, lethargy, vomiting, seizures, or bulging fontanelles.
Diagnosis relies on urgent neuroimaging, with noncontrast CT scan as the first-line modality. Acute SDH appears as a hyperdense crescent-shaped lesion over the cerebral convexity, often associated with other intracranial injuries. Mixed densities may suggest ongoing bleeding. Chronic SDH may appear hypodense on CT after several weeks, and MRI is more sensitive in subacute or chronic stages when lesions may be isodense. The volume of hematoma and degree of midline shift are important prognostic indicators.
Management focuses on rapid stabilization and prevention of secondary brain injury. Airway protection is critical, with rapid-sequence intubation indicated for patients with a Glasgow Coma Scale (GCS) score less than 9 or signs of increased intracranial pressure. Oxygenation should be maintained with saturation above 95%, and hypotension must be avoided, as even a single episode significantly worsens outcomes. Controlled ventilation is used to maintain normocapnia, and routine hyperventilation is no longer recommended except in impending herniation. Head elevation to 20–30° can help reduce intracranial pressure once hemodynamically stable.
Early neurosurgical consultation is essential. Surgical evacuation, often via burr holes or craniotomy, is indicated in patients with significant hematomas, neurologic deficits, or clinical deterioration. Early intervention within 4 hours in comatose patients improves survival. Small, stable hematomas without mass effect may be managed conservatively with close neurologic monitoring, although a subset will require delayed surgery. Intracranial pressure management includes sedation, neuromuscular blockade if intubated, and osmotic therapy such as mannitol once euvolemia is achieved. Blood pressure control, correction of coagulopathy, and management of seizures are also critical components of care.
All patients with acute SDH require admission to an intensive care unit or operating room under neurosurgical care. Subacute cases are admitted for monitoring, while selected chronic SDH patients may be managed as outpatients with appropriate follow-up. Prognosis depends on several key factors, including initial GCS score, time to treatment, pupillary abnormalities, hematoma size, and degree of midline shift. A major pitfall is delayed recognition, especially in elderly patients or those with subtle symptoms, where SDH may mimic other conditions such as stroke, dementia, or intoxication.
Subdural hematoma (SDH) is bleeding between the dura and arachnoid mater, most commonly due to tearing of bridging veins. It is classified based on timing into acute (within 3 days), subacute (3 days to 3 weeks), and chronic (after 3 weeks). On CT imaging, SDH typically appears as a crescent-shaped collection that crosses suture lines but does not cross the midline, often with irregular inner margins. Acute SDH is most commonly caused by acceleration–deceleration forces that stretch and tear parasagittal bridging veins, though bleeding may also arise from cortical arteries, dural lacerations, or venous sinuses. Nontraumatic causes include aneurysm rupture, arteriovenous malformations, coagulopathy, hypertension, and substance abuse. Chronic SDH develops from repeated small venous bleeds and becomes encapsulated over time.
Acute SDH is the most common intracranial hematoma, accounting for 66–70% of cases and frequently associated with blunt head trauma, particularly motor vehicle accidents, falls, and assaults. There is a bimodal age distribution, affecting young adults and the elderly, with higher risk in older patients, those with brain atrophy, alcohol use, or seizure disorders. Chronic SDH is more common in older adults and infants, often with minimal or no clear history of trauma. Coagulopathy significantly increases the risk and severity of bleeding, particularly with elevated INR levels.
Clinically, acute SDH often presents with headache and altered mental status, and up to half of patients may be unconscious at presentation. It is frequently misdiagnosed as intoxication or stroke. Focal neurologic deficits such as hemiparesis or hemiplegia are common, and pupillary abnormalities may indicate ipsilateral mass effect. Seizures can occur early. Subacute and chronic SDH present more insidiously, with symptoms such as headache, nausea, vomiting, seizures, fluctuating mental status, gait instability, and progressive neurologic deficits. In children, especially infants, symptoms may include irritability, lethargy, vomiting, seizures, or bulging fontanelles.
Diagnosis relies on urgent neuroimaging, with noncontrast CT scan as the first-line modality. Acute SDH appears as a hyperdense crescent-shaped lesion over the cerebral convexity, often associated with other intracranial injuries. Mixed densities may suggest ongoing bleeding. Chronic SDH may appear hypodense on CT after several weeks, and MRI is more sensitive in subacute or chronic stages when lesions may be isodense. The volume of hematoma and degree of midline shift are important prognostic indicators.
Management focuses on rapid stabilization and prevention of secondary brain injury. Airway protection is critical, with rapid-sequence intubation indicated for patients with a Glasgow Coma Scale (GCS) score less than 9 or signs of increased intracranial pressure. Oxygenation should be maintained with saturation above 95%, and hypotension must be avoided, as even a single episode significantly worsens outcomes. Controlled ventilation is used to maintain normocapnia, and routine hyperventilation is no longer recommended except in impending herniation. Head elevation to 20–30° can help reduce intracranial pressure once hemodynamically stable.
Early neurosurgical consultation is essential. Surgical evacuation, often via burr holes or craniotomy, is indicated in patients with significant hematomas, neurologic deficits, or clinical deterioration. Early intervention within 4 hours in comatose patients improves survival. Small, stable hematomas without mass effect may be managed conservatively with close neurologic monitoring, although a subset will require delayed surgery. Intracranial pressure management includes sedation, neuromuscular blockade if intubated, and osmotic therapy such as mannitol once euvolemia is achieved. Blood pressure control, correction of coagulopathy, and management of seizures are also critical components of care.
All patients with acute SDH require admission to an intensive care unit or operating room under neurosurgical care. Subacute cases are admitted for monitoring, while selected chronic SDH patients may be managed as outpatients with appropriate follow-up. Prognosis depends on several key factors, including initial GCS score, time to treatment, pupillary abnormalities, hematoma size, and degree of midline shift. A major pitfall is delayed recognition, especially in elderly patients or those with subtle symptoms, where SDH may mimic other conditions such as stroke, dementia, or intoxication.
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