Subdural Hematoma

• Bridging vein rupture and initial hemorrhage: The bridging veins traverse the subdural space from the cerebral cortex to the dural sinuses. These veins are anchored to the dura mater distally but only loosely attached to the arachnoid membrane proximally, creating a precarious anatomical arrangement. Head trauma causes sudden acceleration-deceleration forces or rotational shearing that stretches and tears these bridging veins, resulting in venous bleeding into the subdural space. Unlike epidural hemorrhage from arterial sources, subdural bleeding typically occurs at lower pressures but is continuous and progressive. In elderly patients with cortical atrophy, the bridging veins are stretched further due to increased subdural space, rendering them more susceptible to rupture from minor trauma (sometimes so trivial that patients cannot recall the injury).

• Evolution from acute to subacute hematoma: The acute phase (0-3 days) is characterized by active bleeding from the disrupted bridging vein, with venous bleeding continuing at lower pressure than arterial sources. The expanding hematoma exerts mass effect, displacing brain parenchyma and increasing intracranial pressure (ICP). The hematoma becomes increasingly viscous as clotting occurs. The clot density on CT imaging is hyperattenuating during this phase due to the presence of oxyhemoglobin. By 3-20 days (subacute phase), the hematoma begins undergoing fibrinolysis and retraction, with fluid accumulation at the periphery due to osmotic forces and breakdown of the clot's protein matrix. This explains the heterogeneous appearance on imaging during the subacute period, with both fresh clot and serum components.

• Chronic subdural hematoma formation and neomembrane development: After 20 days, the hematoma becomes chronic with formation of a granulation tissue membrane at the dural-hematoma interface. This neomembrane represents proliferation of fibroblasts, capillaries, and inflammatory cells responding to the hematoma. Critically, these newly formed capillaries are abnormal—they lack proper pericyte coverage and possess a defective blood-brain barrier, rendering them fragile and prone to microhemorrhage. Additionally, the chronic hematoma develops an osmotic gradient; the retained breakdown products and proteins create an osmotic pull that draws fluid inward from the surrounding tissues, causing the hematoma to expand and increase mass effect over time. This is why chronic SDHs can paradoxically enlarge weeks to months after the initial injury, sometimes with minimal trauma. The hematoma becomes isodense or hypodense on CT as hemoglobin breaks down to bilirubin and hemosiderin.

• Mechanisms driving mass effect and increased intracranial pressure: The expanding hematoma acts as a space-occupying lesion within the fixed cranial vault, invoking the Monro-Kellie doctrine. The volume of blood and fluid compresses adjacent brain tissue, shifts the brain across the midline (evidenced by midline shift on neuroimaging), and increases intracranial pressure. Increased ICP reduces cerebral perfusion pressure (CPP = MAP - ICP), which falls below the autoregulation threshold, causing cerebral ischemia. The mass effect can also cause transtentorial herniation, displacing the medial temporal lobe (uncus) across the tentorial edge, compressing the brainstem and ipsilateral oculomotor nerve (CN III).

• Anticoagulation and antiplatelet effects on pathophysiology: Patients on warfarin, direct oral anticoagulants (DOACs), or antiplatelet agents (aspirin, clopidogrel) experience impaired hemostasis that prolongs bleeding from the initial bridging vein rupture and increases the risk of hematoma expansion. Warfarin inhibits vitamin K-dependent factors II, VII, IX, and X, impairing the extrinsic and common coagulation pathways. DOACs directly inhibit factor Xa or thrombin, disrupting the amplification phase of coagulation. These patients may present with larger initial hematoma volumes and experience higher rates of hematoma expansion and worse outcomes.

• Head trauma (major cause): Subdural hematoma results from traumatic injury causing bridging vein rupture. The severity of required trauma varies dramatically with age and coagulation status. In younger patients, SDH typically requires moderate to severe head trauma (motor vehicle collisions, assaults, falls from height). However, in elderly patients with cerebral atrophy and those on anticoagulation, minor head trauma (ground-level fall, striking head on furniture, minor motor vehicle collision) suffices to cause significant bleeding. This discordance between minimal trauma and significant injury represents a classic board trap—elderly patients may present with classic SDH symptoms weeks after a fall they barely remember, leading to delayed diagnosis if the trauma history is not specifically elicited.

• Age and cerebral atrophy: Advanced age is a major independent risk factor. Patients aged >70 years comprise the majority of SDH cases. Cerebral atrophy with aging enlarges the subdural space, stretching bridging veins and increasing their vulnerability to rupture. This anatomical vulnerability explains why elderly patients can sustain significant SDH from trauma insufficient to cause SDH in younger patients. The risk increases exponentially after age 65.

• Anticoagulation and antiplatelet therapy: Chronic anticoagulation with warfarin, dabigatran, rivaroxaban, apixaban, or edoxaban significantly increases SDH risk and severity. Similarly, long-term aspirin or clopidogrel use increases SDH incidence. The combination of anticoagulation and antiplatelet therapy confers compounded risk. Patients on these agents may have hematoma volumes 2-3 times larger than non-anticoagulated patients and higher rates of hematoma expansion (20-30% risk of expansion in anticoagulated patients versus 5-10% in non-anticoagulated).

• Chronic liver disease and coagulopathy: Cirrhosis and advanced liver disease impair synthesis of clotting factors (II, V, VII, IX, X, fibrinogen), reduce platelet production, and increase portal hypertension-related platelet consumption. These patients have profoundly impaired hemostasis and are at high risk for spontaneous or trauma-related SDH with massive volumes.

• Bleeding disorders and thrombocytopenia: Hemophilia, von Willebrand disease, and severe thrombocytopenia (<50,000/μL) increase SDH risk, particularly for expansion and rebleeding. Patients with these conditions may develop SDH from minimal trauma.

• Chronic alcoholism: Alcohol causes multiple pathogenic mechanisms: (1) direct hepatotoxicity leading to coagulopathy, (2) nutritional deficiencies (particularly thiamine and vitamin K), (3) thrombocytopenia from bone marrow suppression, and (4) increased fall risk from intoxication and peripheral neuropathy. Chronic alcoholism is one of the most common risk factors for SDH overall.

• Recurrent falls: Patients with gait disturbance, Parkinson's disease, normal pressure hydrocephalus, orthostatic hypotension, or syncope-prone conditions experience recurrent head trauma, cumulatively increasing SDH risk.

• Headache: Headache is the most frequent symptom, occurring in 40-80% of patients depending on SDH chronicity and acuity. In acute SDH, headache is typically severe and sudden-onset (mimicking thunderclap headache in sentinel bleeds), reflecting acute elevation of intracranial pressure and meningeal irritation from blood. In chronic SDH, headache is often mild to moderate, progressive, and nonspecific, potentially misleading clinicians into attributing it to tension headache or medication effect. The headache may be localized ipsilateral to the hematoma or diffuse.

• Altered mental status and dementia-like symptoms: Confusion, memory impairment, personality change, apathy, and behavioral abnormalities represent the hallmark of subacute and chronic SDH, particularly in elderly patients. This reflects both the mass effect of the hematoma compressing frontal lobes (causing personality change and apathy) and increased intracranial pressure impairing global cerebral function. Chronic SDH masquerades as dementia so reliably that any elderly patient presenting with acute cognitive decline should have SDH excluded with neuroimaging. Fluctuating consciousness and delirium-like presentations are particularly characteristic of chronic SDH.

• Motor weakness and focal neurological deficits: Hemiparesis, hemiplegia, or monoparesis can occur from direct mass effect compressing motor cortex or pyramidal tracts, or from increased ICP causing cerebral ischemia. The weakness may be contralateral to the hematoma (from compression) or ipsilateral (from transtentorial herniation causing contralateral brainstem compression). Subtle motor findings such as pronator drift may be the only neurological abnormality in mild cases.

• Gait disturbance: Unsteady gait, ataxia, or veering toward the side of the lesion may occur from cerebellar compression (if the hematoma is infratentorial), pyramidal tract dysfunction, or general effects of increased ICP on balance. Gait abnormality is particularly common in chronic SDH and may progress subtly over weeks.

• Seizures: Seizures occur in 5-10% of acute SDH cases and up to 15% of chronic SDH cases. They result from cortical irritation by blood, mass effect, or cortical ischemia from elevated ICP. Seizures may be the presenting symptom and can occur weeks into the illness.

• Speech abnormalities and language deficits: Aphasia (if left hemisphere dominant hematoma), dysarthria, or speech slowness may reflect mass effect on language areas or general effects of increased ICP on cognition. Fluent or expressive aphasia depends on hematoma location.

• Loss of consciousness: In acute SDH with large volume and significant mass effect, patients may present comatose or in profound altered consciousness. This represents a neurosurgical emergency. The Glasgow Coma Scale (GCS) score at presentation strongly predicts outcomes—GCS ≤8 indicates severe injury with high mortality (40-60% without surgical intervention).

• Physical exam findings—pupillary abnormalities: Ipsilateral pupillary dilation (blown pupil) represents uncal herniation with compression of the ipsilateral oculomotor nerve (CN III), indicating massive midline shift and imminent brainstem herniation. This is a neurosurgical emergency requiring emergent decompression. The finding is ipsilateral to the hematoma side.

• Physical exam findings—brainstem signs: Decerebrate or decorticate posturing indicates brainstem compression from herniation. Oculomotor nerve palsy (ptosis, "down and out" eye from CN III palsy concurrent with CN VI involvement), absent pupillary light reflex, absent corneal reflexes, and absent gag reflex indicate transtentorial herniation. These findings demand emergent neurosurgical consultation.

• Important clinical variants—"talk and die" syndrome: Some acute SDH patients present with relatively minor symptoms, are discharged from the emergency department, and subsequently deteriorate dramatically or die within hours to days. This occurs when initial hematoma volume is relatively small but the bleeding continues, or when rapid hematoma expansion occurs. Patients with mechanism for significant trauma should be observed and rescanned even if initially asymptomatic or minimally symptomatic.

• Important clinical variants—chronic SDH with minimal symptoms: The opposite presentation occurs in chronic SDH: patients may have enormous hematoma volumes with relatively preserved consciousness because the slow accumulation allows compensatory increase in cerebrospinal fluid reabsorption and brain volume reduction through parenchymal collapse. Symptoms progress insidiously over weeks to months, leading to delayed diagnosis.

• Clinical history and mechanism assessment: A detailed history of head trauma (even trivial trauma) is essential, as elderly patients often cannot recall minor head injuries. Specific questioning about falls, assaults, motor vehicle collisions, or head strikes should be performed. Timing of symptom onset relative to trauma should be documented. A history of anticoagulation, antiplatelet therapy, bleeding disorders, liver disease, or chronic alcoholism should be elicited, as these are critical risk factors. Cognitive decline, personality change, or progressive weakness in an elderly patient should prompt inquiry about remote head trauma.

• Physical examination pearls: Beyond the neurological exam findings mentioned above, general examination should assess for signs of head trauma (scalp lacerations, bruising, hematomas). Assessment of gait, cognition (miniature cognitive assessment), and motor/sensory function should be systematic. Comparison to baseline mental status (from family or prior medical records) is invaluable in chronic SDH cases. Fundoscopic examination may reveal papilledema (suggesting elevated ICP), though this finding is inconstant.

• Non-contrast head CT (gold standard imaging): Non-contrast CT of the head is the imaging modality of choice for diagnosis and assessment of SDH. CT is rapid, widely available, and highly sensitive for acute and subacute bleeding. Acute SDH appears as a hyperdense (white) collection between the skull and brain parenchyma with a crescent or lens-shaped appearance (though SDH may appear crescentic only on axial imaging; on coronal imaging it may show convexity). The hyperdensity reflects oxyhemoglobin. Subacute SDH (3-20 days) appears isodense to the brain parenchyma (similar density to gray matter), making it potentially occult on standard window settings; this is a critical diagnostic trap—the hematoma may be invisible unless windowing is specifically adjusted. Chronic SDH appears hypodense (darker than brain), reflecting hemoglobin breakdown. The midline shift (deviation of the septum pellucidum or other midline structures >5 mm) indicates mass effect and increased ICP. The subdural space thickness can be measured; hematomas causing significant symptoms typically measure >10-15 mm. Acute SDH with midline shift >5 mm or thickness >10 mm generally requires urgent surgical evacuation.

• CT with IV contrast: Contrast is generally not needed for acute SDH diagnosis but may be useful in chronic SDH to identify the dural membrane (which enhances with contrast), assess for subdural empyema (if infection is suspected), or evaluate for associated injuries.

• MRI: MRI is more sensitive than CT for detecting small SDHs and can better characterize hematoma age based on signal characteristics (T1 and T2 sequences show different signal intensities depending on hemoglobin breakdown products—oxyhemoglobin, deoxyhemoglobin, methemoglobin, hemosiderin—allowing precise dating of hematomas). However, MRI is slower than CT and less practical in acute settings. MRI is reserved for subacute/chronic cases where CT findings are equivocal or for surgical planning.

• Laboratory studies: Complete blood count assesses baseline hemoglobin and platelet count. Coagulation studies (PT/INR, activated partial thromboplastin time [aPTT], fibrinogen) should be obtained in all SDH patients to assess bleeding risk and guide reversal strategies. If the patient is on warfarin, the INR should be measured (goal reversal is INR <2). If on DOACs, specific DOAC level testing (chromogenic anti-Xa assay for factor Xa inhibitors) can be considered, though clinical reversal is based on agent type. Creatinine and liver function tests assess organ function and coagulopathy severity. In chronic SDH, these labs may be entirely normal.

• Diagnostic criteria and scoring systems: SDH is diagnosed by imaging (CT or MRI) showing blood collection in the subdural space. No lab values diagnose SDH directly. The Rotterdam CT Score (developed for traumatic brain injury but applicable to SDH) predicts mortality and functional outcome based on imaging findings: midline shift, hematoma volume, subarachnoid hemorrhage presence, obliteration of the third ventricle, and injury severity classification. The Marshall Classification grades diffuse brain injury. However, the most practical bedside assessment combines hematoma thickness (>10 mm is concerning), presence of midline shift (>5 mm), and clinical presentation (GCS score, focal deficits).

• Differential diagnosis considerations: Acute SDH must be distinguished from epidural hematoma (lens-shaped rather than crescen

Immediate stabilisation (all severities)

• Airway, oxygenation, blood pressure: The Brain Trauma Foundation guidelines emphasise that a single episode of hypoxia or hypotension markedly worsens outcome; intubate for GCS ≤8 or inability to protect the airway, keep saturation adequate, and avoid systolic hypotension (BTF specifies age-stratified minimum systolic thresholds). Target cerebral perfusion pressure in the range BTF recommends (roughly 60–70 mmHg) once ICP monitoring is in place.
• Anticoagulant/antiplatelet reversal: Per the Neurocritical Care Society/SCCM antithrombotic reversal guideline, reverse before or in parallel with imaging-guided surgical planning. Vitamin K antagonist: 4-factor prothrombin complex concentrate plus IV vitamin K (PCC over FFP — faster, lower volume). Direct thrombin inhibitor (dabigatran): idarucizumab. Factor Xa inhibitor (apixaban, rivaroxaban): andexanet alfa, or 4F-PCC if unavailable. Routine platelet transfusion for aspirin/clopidogrel-associated bleeding is not supported (PATCH trial, spontaneous ICH) and may be harmful, though it is often given before craniotomy.

Medical control of intracranial pressure

• Positioning and physiology: head of bed ~30°, midline neck, normocapnia, treat fever, pain and agitation.
• Hyperosmolar therapy: mannitol or hypertonic saline creates an osmotic gradient drawing water from brain parenchyma — a temporising bridge to the operating room, not a substitute for it.
• Hyperventilation: only brief and for impending herniation; BTF advises against prolonged prophylactic hyperventilation because vasoconstriction causes ischaemia.
• Seizure prophylaxis: an antiseizure drug (levetiracetam or phenytoin) for roughly one week reduces early post-traumatic seizures per BTF; it does not prevent late epilepsy.

Definitive/surgical management

• Acute SDH: emergent craniotomy with clot evacuation for thickness >10 mm or midline shift >5 mm regardless of GCS, or for neurological deterioration/pupillary change (AANS/CNS surgical management guideline). Decompressive craniectomy for refractory swelling.
• Chronic SDH: burr-hole drainage with subdural drain placement, which lowers recurrence.
• Middle meningeal artery embolisation: an adjunct targeting the fragile neomembrane vasculature, supported by recent randomised trials for recurrence reduction.

Avoid

• Corticosteroids — increase mortality in TBI and worsened outcomes in chronic SDH trials.
• Lumbar puncture — herniation risk with a mass lesion.
• Hypotonic fluids and prophylactic hypothermia.

Emergencies — recognise immediately

• Uncal (transtentorial) herniation: expanding clot forces the medial temporal lobe over the tentorial edge. Signalled by an ipsilateral fixed, dilated pupil (superficial parasympathetic fibres of CN III compressed first), then contralateral hemiparesis and coma. Requires emergent hyperosmolar therapy and operative decompression.
• Cushing reflex: hypertension with widened pulse pressure, bradycardia and irregular respirations — a late brainstem response to critically elevated ICP, not a sign to "treat the blood pressure."
• Duret hemorrhages: brainstem perforator tearing from caudal displacement; usually fatal.
• Kernohan notch phenomenon: contralateral cerebral peduncle compressed against the tentorium produces hemiparesis ipsilateral to the clot — a classic false localising sign that misleads to wrong-side surgery.
• Hematoma expansion / rebleeding: continued venous ooze in an uncorrected coagulopathy; heralded by any drop in GCS. Repeat non-contrast CT.

Later disease complications

• Post-traumatic seizures and epilepsy: cortical irritation by hemosiderin; prophylaxis reduces early seizures only.
• Cerebral ischaemia and infarction: mass effect on the posterior cerebral artery at the tentorial edge causes occipital infarct; global hypoperfusion follows a falling CPP.
• Hydrocephalus: blood breakdown products impair arachnoid granulation reabsorption; ventricular enlargement with poor recovery.
• Hyponatremia (SIADH or cerebral salt wasting): distinguish by volume status — euvolemic versus hypovolemic — since treatment diverges (fluid restriction versus salt/volume repletion).
• Immobility complications: venous thromboembolism, aspiration pneumonia, pressure injury.

Treatment-related complications

• Recurrence after burr-hole drainage of chronic SDH: the fragile neomembrane capillaries rebleed; recurrent headache or deficit weeks later — subdural drain placement lowers this risk.
• Tension pneumocephalus: air trapped after evacuation acts as a mass; Mount Fuji sign on CT with deterioration — an emergency needing decompression.
• Subdural empyema, wound infection, seizures from cortical injury after craniotomy.
• Thrombotic events after reversal agents: PCC and andexanet alfa restore thrombin generation and can precipitate stroke, MI or VTE, particularly with a mechanical valve or recent thromboembolism.

• Shape and boundaries are the discriminator: SDH is a crescent-shaped (concave) collection that crosses suture lines but not the midline, because dural reflections (falx, tentorium) bound it. Epidural hematoma is lens-shaped/biconvex, stops at sutures, and can cross the midline. The stem's picture, not the history, usually settles this.
• Vessel of origin: SDH = bridging veins; epidural = middle meningeal artery with an overlying temporal bone fracture. A lucid interval is classically epidural — do not reflexively assign it to SDH.
• Single best next step is almost always non-contrast head CT — fast, sensitive for acute blood, and it excludes a mass lesion before anything else. Never lumbar puncture first.
• The elderly/alcoholic atrophy association: cortical atrophy stretches bridging veins, so trivial or unremembered trauma produces a large clot. Any older adult with subacute cognitive decline, gait change or personality change deserves imaging — chronic SDH is a reversible dementia mimic.
• The subacute isodense trap: at roughly 1–3 weeks the clot is isodense to cortex and can be nearly invisible; look for effaced sulci, a compressed ventricle, and midline shift. Bilateral isodense SDH may show no shift at all.
• Ipsilateral blown pupil = uncal herniation compressing CN III — surgical emergency, not a medication side effect. The Kernohan notch gives hemiparesis ipsilateral to the clot, the classic false localising sign.
• In an infant, SDH plus retinal hemorrhages plus posterior rib/metaphyseal fractures is abusive head trauma — the mandated next step is a skeletal survey and a child-protective services report.
• Common distractors: steroids (harmful in TBI and in chronic SDH), prophylactic hyperventilation to profound hypocapnia (causes ischaemia), and routine platelet transfusion for aspirin use (not beneficial). Warfarin reversal is 4-factor PCC plus IV vitamin K — not FFP as first choice.