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Subdural hematoma

A subdural hematoma (SDH) is a type of traumatic brain injury involving the accumulation of blood in the subdural space, the area between the dura mater (the outermost protective membrane of the brain) and the arachnoid mater, typically resulting from the tearing of bridging veins due to head trauma.^[1]^[2] This condition can increase intracranial pressure, potentially leading to brain compression, herniation, or death if untreated, and it represents one of the most common intracranial mass lesions following head injury.^[2] Subdural hematomas are classified by their onset and appearance on imaging into acute (developing within 72 hours, often hyperdense on CT), subacute (3–21 days, isodense), and chronic (beyond 3 weeks, hypodense), with chronic forms more prevalent in older adults due to brain atrophy that stretches bridging veins, making them susceptible to even minor trauma.^[2] Primary causes include high-impact accidents, falls, assaults, or nonaccidental trauma in children (such as shaken baby syndrome), while risk factors encompass anticoagulation therapy, chronic alcohol use, coagulopathies, and extremes of age.^[1]^[2] Epidemiologically, acute SDHs occur in 5–25% of severe head injuries, with an overall incidence of chronic SDHs ranging from 1.7 to 20.6 per 100,000 people annually, showing a male predominance (3:1 ratio) and peaking in incidence during the fifth to seventh decades of life.^[2] Symptoms depend on the hematoma's size, location, and rapidity of onset; acute cases often present dramatically with severe headache, vomiting, confusion, seizures, hemiparesis, or rapid deterioration to coma, sometimes preceded by a lucid interval in up to 38% of patients.^[2] In contrast, chronic SDHs may mimic neurodegenerative conditions like dementia, featuring insidious headache, cognitive decline, gait instability, or subtle personality changes, particularly in the elderly.^[1] Infants may exhibit nonspecific signs such as irritability, lethargy, bulging fontanelles, or increasing head circumference.^[1] Diagnosis relies on clinical history, neurological examination, and neuroimaging, with noncontrast head CT as the initial modality of choice to assess hematoma density, midline shift, and associated injuries, supplemented by MRI for equivocal cases or to evaluate chronicity.^[2] Management prioritizes airway stabilization, blood pressure control, and reversal of coagulopathies, with treatment escalating based on clinical severity: small, asymptomatic hematomas may resolve with conservative measures like bed rest and serial imaging, while symptomatic or large SDHs (>1 cm or causing >5 mm midline shift) typically require surgical intervention, such as burr hole drainage for chronic cases or craniotomy for acute ones with parenchymal involvement. Emerging adjunctive therapies, such as middle meningeal artery embolization, show promise in reducing recurrence for chronic cases (as of 2025).^[2]^[3] Prognosis varies markedly; acute SDHs carry high mortality (up to 50–90% in comatose patients), influenced by age, Glasgow Coma Scale score, and pupillary response, whereas chronic SDHs have favorable outcomes in 80% of surgically treated cases, often allowing return to pre-injury function, though survivors may require rehabilitation for residual neurological deficits.^[2]

Background

Definition and Types

A subdural hematoma (SDH) is defined as an accumulation of blood in the subdural space, the potential space located between the dura mater and the arachnoid mater, the outermost and middle layers of the meninges that envelop the brain.^[4] This collection typically arises from the rupture of bridging veins that traverse the subdural space, often due to head trauma that causes shearing forces across these fragile vessels.^[4] On neuroimaging, such as computed tomography (CT), SDH characteristically appears as a crescent-shaped hyperdense collection that conforms to the contour of the brain and can cross cranial suture lines, distinguishing it from the lens-shaped (biconvex) appearance of epidural hematomas, which are confined by dural attachments at the sutures, and the diffuse, sulcal distribution of subarachnoid hemorrhage, which involves the cerebrospinal fluid spaces.^[5]^[4] SDHs are primarily classified based on their temporal evolution and clinical presentation following injury: acute SDH develops symptoms within 72 hours and appears hyperdense on CT due to fresh blood; subacute SDH manifests between 3 and 21 days post-injury and shows isodense characteristics on CT; chronic SDH emerges after 21 days and is hypodense on CT as the blood degrades and liquefies over time.^[6]^[7] Although most SDHs are traumatic, non-traumatic or spontaneous variants can occur due to underlying vascular anomalies, such as ruptured aneurysms or arteriovenous malformations, coagulopathy from anticoagulant use or clotting disorders, or severe hypertension leading to vessel rupture without evident trauma.^[8]^[9]

Epidemiology

Subdural hematoma (SDH) exhibits varying incidence rates depending on acuity and demographic factors, with chronic SDH (cSDH) being more common in older populations. The global annual incidence of cSDH ranges from 1.7 to 20.6 cases per 100,000 individuals, while acute SDH occurs in approximately 10% to 20% of traumatic brain injury cases.^[10]^[11]^[12] In elderly populations over 65 years, cSDH incidence rises to as high as 58 per 100,000, and exceeds 127 per 100,000 in those over 80 years, reflecting greater vulnerability due to age-related changes.^[13] Overall SDH rates reach about 52 per 100,000 persons per year, with non-traumatic, non-acute forms at 17 per 100,000 in adults.^[14] Males predominate with a 3:1 ratio compared to females across age groups, attributed to higher exposure to risk factors like trauma.^[2] Prevalence trends for SDH are increasing worldwide, driven primarily by aging populations and rising use of anticoagulants, which amplify hemorrhage risk in the elderly.^[7] In the United States, annual cSDH cases are estimated at 30,000 to 60,000, with projections reaching 60,000 by 2030 based on demographic shifts.^[15]^[13] Recent studies from 2023 to 2025 confirm this upward trajectory, particularly in elderly cohorts, though the COVID-19 pandemic temporarily altered patterns with reduced trauma-related cases during lockdowns.^[10]^[16] Geographic variations highlight higher SDH incidence in low- and middle-income countries, where road traffic accidents contribute disproportionately to acute cases, alongside elevated rates in regions with prevalent alcohol use that predisposes to falls and chronic forms.^[17]^[18] In contrast, high-income settings see more cSDH linked to anticoagulation and falls in aging demographics.^[19]

Etiology

Causes

The primary cause of subdural hematoma (SDH) is head trauma, which leads to the rupture of bridging veins that drain blood from the cerebral cortex into the dural sinuses.^[4] These veins are particularly vulnerable to shearing forces during acceleration-deceleration injuries, such as those occurring in motor vehicle accidents or falls, where the brain moves relative to the skull, stretching and tearing the vessels.^[2] Even mild trauma can precipitate SDH in at-risk populations, such as the elderly, where a simple fall from standing height may suffice due to increased vulnerability from brain atrophy.^[4] Traumatic SDH encompasses various subtypes depending on the inciting event, including falls, assaults, sports injuries, and vehicular trauma, with falls being particularly common in the elderly.^[2] In children, it often results from non-accidental injury, such as shaken baby syndrome, where violent shaking causes rotational forces that rupture bridging veins without significant external impact.^[4] Non-traumatic causes are less common but include coagulopathies, such as hemophilia or anticoagulant use, which impair clotting and allow bleeding to accumulate after minor or spontaneous vessel disruption. Non-traumatic causes are rare in acute SDH but can account for up to 50% of chronic cases without evident trauma history.^[2]^[20] Other origins involve vascular malformations like aneurysms or arteriovenous malformations, iatrogenic factors such as post-spinal anesthesia or lumbar puncture, and spontaneous occurrences related to severe hypertension.^[2] Chronic SDH was first recognized in non-traumatic cases in the 19th century, with Rudolf Virchow describing it as a form of chronic hemorrhagic inflammation in 1857, though trauma is the precipitating event in the vast majority of acute cases.^[20]^[2]

Risk Factors

Advanced age is a primary demographic risk factor for subdural hematoma, particularly in individuals over 65 years, where age-related brain atrophy widens the subdural space, facilitating hematoma formation after minor trauma.^[4] In the elderly, this atrophy contributes to a higher incidence, with chronic subdural hematomas becoming more prevalent due to the increased potential for bridging vein rupture.^[21] Infants under 1 year also face elevated risk owing to their thin cranial bones, larger head-to-body ratio, and underdeveloped subdural spaces, resulting in an incidence of approximately 1 in 4,761 live births in some populations.^[4] Medical conditions that impair coagulation or increase fall risk significantly predispose individuals to subdural hematoma. Anticoagulant and antiplatelet therapies, such as warfarin and aspirin, elevate the risk by 2- to 5-fold compared to non-users, with vitamin K antagonists specifically associated with about a 3-fold increase relative to antiplatelet agents alone.^[22]^[23] Chronic alcohol abuse further heightens susceptibility through induced coagulopathy, brain atrophy, and propensity for falls, with daily alcohol use linked to a 150% increased odds of intracranial hemorrhage following head trauma in older adults.^[21]^[24] Conditions like dementia and cerebral atrophy exacerbate these vulnerabilities by promoting instability and enlarging the subdural space, often compounding the effects of age.^[25] Other predisposing factors include cerebrospinal fluid (CSF) leaks, often following neurosurgery, which can lead to intracranial hypotension and subsequent hematoma development in up to 25.9% of non-geriatric chronic cases.^[26] Arachnoid cysts represent another risk, as they may rupture or cause mass effect, increasing subdural hematoma incidence, particularly after trivial head injury in younger patients.^[27] Prior craniotomy or shunt procedures similarly heighten risk by altering intracranial dynamics.^[21] Emerging evidence from 2023–2024 studies highlights COVID-19-related coagulopathy as a novel factor, with the virus's prothrombotic and hemorrhagic effects contributing to spontaneous subdural hematomas even in non-traumatized individuals.^[28]^[29] Quantitatively, chronic alcohol abuse is associated with a marked rise in subdural hematoma incidence, while anticoagulant use accounts for approximately 40% of chronic cases among the elderly.^[30] These factors often interact with trauma as the inciting event, underscoring the importance of vulnerability in pathogenesis.

Pathophysiology

Acute Subdural Hematoma

Acute subdural hematoma (ASDH) arises from immediate venous bleeding due to laceration of bridging veins, which traverse the subdural space between the arachnoid and dura mater. This typically occurs following high-energy head trauma, where acceleration-deceleration forces stretch and tear these fragile veins, leading to rapid accumulation of blood in the subdural compartment. The resulting hematoma exerts a mass effect on the underlying brain tissue, causing swift elevation of intracranial pressure (ICP) and potential transtentorial herniation within hours of injury.^[4]^[31] The physiological response involves formation of a hyperdense clot on computed tomography imaging, reflecting the acute, non-liquefied nature of the hemorrhage. ASDH is frequently associated with underlying brain contusions or lacerations in up to 50-70% of cases, contributing to secondary injury through direct parenchymal damage. Additionally, the expanding hematoma compresses cortical arteries, inducing cerebral ischemia by reducing cerebral blood flow and exacerbating neuronal dysfunction.^[2]^[32]^[33] Progression of ASDH is characterized by ongoing bleeding from the ruptured veins, which can expand the hematoma volume rapidly; volumes exceeding 30 mL often produce significant mass effect and clinical symptoms. Coagulopathy, triggered by the traumatic brain injury itself, further exacerbates this expansion by promoting a systemic bleeding tendency and impairing hemostasis. The rise in ICP follows principles of intracranial compliance, approximated by the relationship ΔICP ≈ k × ΔVolume, where k represents the brain's compliance constant, illustrating how even modest volume increases in the constrained cranial space lead to disproportionate pressure surges.^[4]^[33]^[34] ASDH frequently accompanies severe traumatic brain injury and is present in approximately 60% of cases with a GCS score of 8 or less, often indicating profound neurological impairment at onset. Symptom onset, such as altered consciousness, typically occurs rapidly and is detailed further in clinical presentation sections.^[35]^[36]

Chronic Subdural Hematoma

Chronic subdural hematoma (CSDH) typically arises from an initial minor bleed, often following low-impact trauma, which disrupts the dural border cell layer and triggers the separation of dural layers. This leads to the formation of a neomembrane through fibroblast proliferation and vascularization, particularly in the outer membrane, encapsulating the hematoma.^[37] Repeated micro-hemorrhages occur from the fragile neovessels within this membrane, which are prone to leakage due to immature endothelial junctions. Additionally, osmotic forces from high concentrations of serum proteins that extravasate into the hematoma draw in extracellular fluid, progressively enlarging the collection over weeks to months.^[38] In elderly patients, brain atrophy exacerbates this process by increasing the potential space for expansion.^[39] The inflammatory cascade plays a central role in CSDH evolution, initiating with the release of proinflammatory cytokines such as interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) from macrophages and neutrophils infiltrating the hematoma. These cytokines enhance vascular permeability and promote angiogenesis, leading to the development of leaky, immature vessels that contribute to further bleeding and fibrosis via transforming growth factor-beta (TGF-β) signaling. Recent studies from 2023 to 2025 emphasize a dual trauma-inflammation model, where initial mechanical injury synergizes with sustained local inflammation to drive persistent hematoma growth and membrane maturation.^[40] VEGF levels in CSDH fluid can be markedly elevated—up to 28 times higher than in serum—correlating with neovascularization and increased recurrence risk.^[37] As CSDH progresses, the hematoma undergoes liquefaction through fibrinolysis, resulting in a hypodense appearance on imaging due to the breakdown of blood components into fluid rich in degradation products. This phase is characterized by a slow expansion rate, estimated at 1-2 mL per day from recurrent microbleeds and exudation, allowing insidious accumulation without acute symptoms. In some cases, cerebrospinal fluid (CSF) hypovolemia contributes to expansion by creating a pressure gradient that facilitates fluid ingress into the subdural space. The condition is particularly prevalent in the elderly population, where even minimal or no recalled trauma suffices to initiate the process, owing to age-related vascular fragility and impaired hemostasis. Recurrence, occurring in up to 20-30% of cases, is closely tied to the persistence of the outer neomembrane, which continues to harbor angiogenic and inflammatory activity post-evacuation.^[41]^[37]^[40]

Clinical Presentation

Acute Presentation

Acute subdural hematoma typically presents with rapid neurological deterioration following head trauma, often due to rupture of bridging veins. Symptoms emerge within hours of injury and include severe headache, vomiting, and altered consciousness ranging from confusion to coma. Additionally, seizures occur in approximately 20-30% of cases, reflecting the acute mass effect on the brain.^[4]^[42] Key clinical signs include Cushing's triad, characterized by systemic hypertension, bradycardia, and irregular respirations, indicating elevated intracranial pressure. Other findings encompass ipsilateral pupillary dilation, hemiparesis, and a low Glasgow Coma Scale (GCS) score, often below 8 in severe instances. These manifestations underscore the emergency nature of the condition, necessitating immediate intervention.^[4] The onset is generally acute, occurring shortly after trauma, though a lucid interval—wherein the patient initially appears to recover before declining— is observed in up to 38% of cases. This transient improvement can delay recognition and heighten the risk of rapid decompensation.^[4]^[2] In infants, acute subdural hematoma often manifests as irritability, a bulging fontanelle, and altered consciousness, frequently in the context of abusive head trauma associated with polytrauma such as fractures. Seizures are particularly common in this population, affecting 40-70% of affected infants.^[43]

Chronic Presentation

Chronic subdural hematoma (CSDH) typically manifests with subtle, progressive symptoms that develop over weeks to months following minor or even unnoticed head trauma. The most common initial symptom is a gradual onset headache, often more severe in the morning due to increased intracranial pressure during recumbency, affecting up to 80% of patients.^[44] Accompanying features include cognitive decline such as memory disturbance and disorientation, personality changes like irritability or apathy, and fluctuating levels of consciousness that may wax and wane over time.^[45] These symptoms arise from the slow accumulation of liquefied blood and inflammatory membranes exerting mass effect on the brain, often without acute decompensation.^[46] Neurological signs in CSDH are generally mild and insidious, reflecting localized compression rather than widespread injury. Patients may exhibit mild hemiparesis, gait instability, or aphasia, depending on the hematoma's location and size.^[47] Seizures occur in approximately 10% of cases, typically as focal or generalized events stemming from cortical irritation.^[48] Bilateral hematomas, seen in 9-22% of patients, can lead to more symmetric symptoms like bilateral weakness or altered mental status, complicating the clinical picture.^[46] In elderly individuals, CSDH often presents as a mimic of neurodegenerative conditions, with symptoms such as urinary incontinence, decreased activity, and rapidly progressing senility overshadowing the headache.^[49] The insidious onset, usually more than three weeks after minor trauma, contributes to delayed recognition, with about 40% of cases initially misdiagnosed as dementia or other degenerative diseases due to overlapping nonspecific features.^[50] This diagnostic challenge is heightened in older adults, where brain atrophy facilitates hematoma formation and symptom subtlety.^[44]

Diagnosis

Clinical Evaluation

The clinical evaluation of suspected subdural hematoma begins with a thorough history to identify potential etiologies and risk factors. Clinicians should inquire about recent head trauma, which may be trivial or absent in up to 50% of chronic cases, particularly in elderly patients.^[47] Additional history should cover anticoagulant or antiplatelet medication use, as these increase bleeding risk, and chronic alcohol intake, which is associated with coagulopathy and falls.^[4] Assessment of the patient's baseline mental status and any preceding symptoms, such as gradual cognitive decline or gait instability, is essential to contextualize acute changes.^[51] The physical examination focuses on neurological status to detect signs of mass effect or herniation. The Glasgow Coma Scale (GCS) is used to quantify level of consciousness, with scores below 15 indicating potential urgency for further investigation.^[47] Pupillary response should be evaluated bilaterally for asymmetry or non-reactivity, which may signal ipsilateral hematoma expansion and transtentorial herniation.^[4] Focal neurological deficits, such as contralateral hemiparesis or hemisensory loss, hyperreflexia, or Babinski signs, are assessed through motor and sensory testing. Vital signs are monitored for Cushing's triad (hypertension, bradycardia, irregular respirations) suggestive of elevated intracranial pressure (ICP). Fundoscopic examination may reveal papilledema in cases of subacute or chronic progression.^[51] Red flags warranting immediate concern include worsening headache, persistent vomiting, new-onset seizures, or rapid neurological deterioration, as these indicate expanding hematoma and ICP elevation.^[47] In elderly patients, unexplained falls, acute confusion, or subtle personality changes should raise suspicion, given the higher incidence and atypical presentation in this group.^[4] Initial laboratory evaluation includes a coagulation profile, such as prothrombin time (PT) and international normalized ratio (INR), to identify reversible coagulopathy, particularly in patients on antithrombotics. A complete blood count (CBC) assesses for thrombocytopenia or anemia from blood loss. The 2024 clinical practice guidelines for chronic subdural hematoma emphasize rapid triage with these labs alongside clinical assessment to guide reversal of coagulopathy if needed.^[52]^[53]

Imaging Modalities

Computed tomography (CT) scanning serves as the first-line imaging modality for suspected subdural hematoma due to its rapid acquisition, widespread availability, and high sensitivity for acute hemorrhage.^[4] On non-contrast CT, acute subdural hematomas typically appear as crescent-shaped hyperdense collections along the convexity of the brain, with Hounsfield unit (HU) values ranging from 40 to 90, reflecting the density of fresh blood.^[54] Subacute hematomas exhibit mixed densities as liquefaction occurs, while chronic ones become hypodense (0-20 HU) due to resorption and organization of the blood products.^[54] Midline shift, a critical measurement of mass effect, is routinely assessed on CT axial slices by quantifying the deviation of midline structures such as the falx cerebri from the ideal central position, aiding in urgency triage.^[4] Magnetic resonance imaging (MRI) offers superior soft tissue contrast and is particularly valuable for detecting chronic subdural hematomas, especially when CT findings are equivocal or isodense.^[55] In chronic cases, hematomas often show hyperintense signals on both T1- and T2-weighted sequences due to methemoglobin accumulation, with heterogeneous patterns reflecting repeated hemorrhages or membranes.^[56] MRI excels at identifying small or isodense collections missed on CT, providing better delineation of internal septations and associated brain parenchymal changes.^[52] Diffusion-weighted imaging (DWI) sequences can additionally detect underlying ischemia or infarction adjacent to the hematoma, which may influence management.^[57] Other modalities include cranial ultrasound, primarily in infants with open fontanelles, where it allows non-invasive bedside detection of hypoechoic or mixed echogenicity collections through the anterior fontanelle acoustic window.^[58] Digital subtraction angiography (DSA) is reserved for evaluating vascular etiologies in atypical or spontaneous subdural hematomas, such as arterial rupture or dural arteriovenous fistulas, by visualizing contrast extravasation or abnormal vascular supply.^[59] Recent advances from 2023 to 2025 include AI-enhanced CT tools for automated volume quantification of hematomas, improving accuracy in serial monitoring and treatment planning through deep learning models that analyze HU distributions.^[60] Membrane imaging biomarkers on MRI, such as enhancement patterns and thickness, have emerged as predictors of recurrence risk in chronic subdural hematomas, guiding personalized interventions.^[11]

Classification and Differential Diagnosis

Subdural hematomas (SDHs) are primarily classified based on their temporal evolution, which reflects the age of the blood collection and its imaging characteristics on computed tomography (CT). Acute SDHs develop within 72 hours of injury and appear hyperdense on non-contrast CT due to fresh blood.^[4] Subacute SDHs occur between 3 and 21 days post-injury, presenting as isodense to brain tissue as hemoglobin breakdown progresses.^[61] Chronic SDHs form beyond 21 days, appearing hypodense as liquefaction and resorption occur, often in the absence of significant trauma.^[7] Additional classification considers anatomical location and laterality. SDHs most commonly occur along the convexity of the cerebral hemispheres, particularly in frontoparietal regions, but can also involve the falx cerebri, tentorium cerebelli, or interhemispheric fissure.^[62] They may be unilateral, affecting one hemisphere, or bilateral, which is more frequent in elderly patients and infants, particularly in cases of abusive head trauma.^[63] Convexity SDHs, the most prevalent subtype, overlie the brain surface without deep extension.^[46] Severity is assessed by hematoma thickness and mass effect, guiding clinical decision-making. Thin SDHs measure less than 10 mm in maximum thickness without significant midline shift, often managed conservatively if asymptomatic.^[64] Thick SDHs exceed 10 mm or cause a midline shift greater than 5 mm, indicating substantial mass effect and higher risk of herniation.^[64] A discrepancy where midline shift exceeds hematoma thickness by more than 3 mm suggests underlying cerebral edema, worsening prognosis.^[62] Differential diagnosis of SDH requires distinguishing it from other intracranial hemorrhages and mass lesions based on location, shape, and etiology. Epidural hematomas (EDHs) arise from arterial sources like the middle meningeal artery, forming a biconvex, lens-shaped collection outside the dura, often with a lucid interval post-trauma.^[65] In contrast, SDHs result from venous bleeding, typically bridging veins, and appear crescentic, conforming to the brain's contour.^[66] Intracerebral hemorrhages involve parenchymal tissue, often hypertensive or amyloid-related, without dural involvement.^[67] Subarachnoid hemorrhages occur in cerebrospinal fluid spaces, presenting as bloody CSF from aneurysmal rupture, with linear hyperdensities along sulci rather than extracerebral collections.^[68] Non-hemorrhagic mimics include ischemic stroke (hypodense wedge on CT), tumors (enhancing masses with edema), and abscesses (ring-enhancing lesions with restricted diffusion on MRI).^[69] ^[70] Diagnostic challenges arise particularly with acute isodense SDHs on CT, which may blend with adjacent brain parenchyma due to anemia, early evolution, or clotting disorders, leading to missed diagnoses.^[71] In such cases, contrast-enhanced CT can highlight the collection, while MRI provides superior sensitivity for subtle or isodense blood products through gradient echo or susceptibility-weighted sequences.^[72] Multimodal imaging, combining CT for initial screening with MRI for confirmation, can refine differentials and detect associated injuries like diffuse axonal damage. Prognostically, thick acute SDHs (>10 mm) are associated with poor outcomes, including higher mortality and unfavorable functional recovery, due to increased intracranial pressure and brain compression.^[73] Factors such as hematoma volume exceeding 50 mL or significant midline shift further predict coma progression and reduced Glasgow Outcome Scale scores at 6 months.^[74]

Treatment

Conservative Management

Conservative management is indicated for patients with subdural hematoma (SDH) who are asymptomatic or exhibit minimal neurological symptoms, particularly when the hematoma is thin (less than 10 mm in thickness) and without significant midline shift (less than 5 mm).^[75] For acute SDH, this approach is suitable in cases of mild traumatic brain injury where surgical risks outweigh benefits, as supported by a 2025 comparative effectiveness study showing similar functional outcomes between acute surgery and conservative treatment in selected centers.^[76] In chronic SDH, conservative strategies are preferred for patients with mild to moderate symptoms, such as subtle headaches or gait disturbance, avoiding intervention in up to 60% of appropriately selected cases.^[77] Key strategies in conservative management include close clinical monitoring combined with serial neuroimaging to detect hematoma expansion or neurological deterioration. Patients undergo serial computed tomography (CT) scans, typically every 24 to 48 hours initially, followed by less frequent intervals based on stability, to assess for changes in hematoma size or midline shift.^[78] If coagulopathy is present, particularly from vitamin K antagonists like warfarin, rapid reversal is essential using intravenous vitamin K (5-10 mg) alongside prothrombin complex concentrate (PCC) dosed at 25-50 units/kg to normalize the international normalized ratio (INR) within hours and prevent hematoma progression.^[79] For elevated intracranial pressure (ICP), medical measures such as hyperosmolar therapy with mannitol (0.5-1 g/kg intravenously) or brief hyperventilation may be employed temporarily to maintain cerebral perfusion, though invasive ICP monitoring is reserved for deteriorating cases.^[80] Pharmacotherapy plays a supportive role in conservative management to mitigate secondary complications. Seizure prophylaxis is recommended for the first week post-diagnosis in patients with acute or subacute SDH, using either levetiracetam (loading dose 20-60 mg/kg, maintenance 500-1000 mg twice daily) or phenytoin (loading 15-20 mg/kg, maintenance 300-400 mg daily), as both agents show comparable efficacy in preventing early post-traumatic seizures with levetiracetam offering a lower adverse event profile.^[81] Outcomes of conservative management vary by SDH type and patient selection, with success rates (avoiding surgery) ranging from 50% to 80% in selected chronic cases with mild symptoms, though 20-50% risk of progression necessitating delayed surgery.^[77]^[82] In acute SDH cohorts managed conservatively, functional recovery rates approach those of surgical groups when initial hematoma characteristics are favorable, but early intervention is critical if expansion is detected on follow-up imaging.^[83]

Surgical and Adjunctive Therapies

Surgical evacuation remains the cornerstone for managing symptomatic or large chronic subdural hematomas (cSDH), with burr-hole craniostomy serving as the first-line technique due to its efficacy and relative safety in most patients.^[84] This procedure involves creating one or two 12-14 mm burr holes under local or general anesthesia, followed by irrigation and suction to evacuate the hematoma, often yielding good clinical recovery in approximately 89% of cases.^[85] For frail or elderly patients, twist-drill craniostomy offers a minimally invasive alternative, utilizing a small (<5 mm) hole performed at the bedside under local anesthesia to drain the collection, thereby reducing operative risks while achieving comparable short-term outcomes to burr-hole methods.^[84] In contrast, craniotomy is reserved for acute subdural hematomas or chronic cases with organized, septated, or thick clots that preclude adequate drainage via smaller access points, involving a larger bone flap under general anesthesia to facilitate complete evacuation and membranectomy.^[84] Adjunctive therapies have evolved to address recurrence, a key challenge in cSDH management, with middle meningeal artery embolization (MMAE) emerging as a promising intervention based on advances from 2023 to 2025. MMAE targets the middle meningeal artery branches supplying the hematoma membrane using liquid embolics like n-butyl cyanoacrylate or Onyx, typically performed endovascularly in neurologically stable patients to devascularize the neomembrane and prevent reaccumulation.^[13] Recent randomized trials, such as EMBOLISE and STEM, demonstrate that MMAE reduces recurrence rates to as low as 6.7% at 90 days when used adjunctively with surgery, compared to 10-21% with surgery alone, with overall complication rates around 3%.^[13] The ARISE I consensus statement from 2024 endorses MMAE specifically for recurrence prevention in cSDH, recommending its integration into protocols for patients at high risk of reoperation.^[13] Endoscopic irrigation enhances visualization during evacuation, particularly for septated or multi-loculated cSDH, allowing direct removal of membranes and trabeculae through a burr-hole port with a rigid endoscope and irrigation to clear residual fluid.^[86] This technique improves clot clearance under direct vision, potentially lowering recurrence by addressing underlying septations more effectively than standard drainage alone.^[87] Postoperative protocols emphasize subdural or subgaleal drainage for 24-48 hours to minimize reaccumulation, as evidenced by reduced recurrence with this duration compared to shorter intervals.^[84] Antibiotic prophylaxis, typically with a single perioperative dose such as cefazolin, is standard to prevent surgical site infections, though prolonged systemic use beyond 24 hours does not confer additional benefit.^[88] The field has shifted toward minimally invasive approaches, with 2025 reviews highlighting lower morbidity rates—such as reduced hospital stays and complication profiles—for techniques like twist-drill, endoscopic methods, and MMAE relative to traditional craniotomy, which carries higher risks in elderly populations.^[13] This evolution prioritizes outpatient feasibility and adjunctive endovascular options to optimize recovery while curbing recurrence.^[13]

Complications

Short-Term Complications

Intraoperative complications of subdural hematoma surgery primarily include brain swelling and recurrent bleeding, which can arise due to underlying parenchymal injury or rapid decompression. Acute traumatic subdural hematomas are frequently associated with intraoperative brain swelling, potentially complicating evacuation and requiring careful management to avoid excessive pressure shifts.^[64] Recurrent bleeding during surgery may necessitate additional hemostatic measures.^[89] Delayed surgical intervention can lead to brain herniation, particularly in acute cases where mass effect progresses unchecked.^[90] Postoperative short-term complications encompass infections, seizures, and hematoma reaccumulation, typically manifesting within the first few weeks. Infections such as meningitis occur in 1-5% of patients following craniotomy or burr-hole procedures, with risk factors including prolonged operative time and cerebrospinal fluid leakage.^[91] Postoperative seizures affect 15-25% of patients after surgical evacuation, often early-onset within the first week, and are managed with prophylactic anticonvulsants to mitigate neurological impact.^[92] Hematoma reaccumulation in acute subdural cases requires reoperation in approximately 28% of instances within 14 days, influenced by factors like incomplete initial evacuation.^[93] Treatment-related short-term risks vary by adjunctive therapies. Middle meningeal artery embolization, used to reduce recurrence, carries a stroke risk of less than 2%, alongside rare instances of cranial nerve palsy or transient ischemia.^[94] Dexamethasone administration for conservative or adjunctive management can induce hyperglycemia and gastrointestinal bleeding as common side effects, particularly in elderly patients with comorbidities.^[95] Recent studies from 2023-2025 highlight variations in infection risks across surgical approaches, with endoscopic-assisted burr-hole craniostomy showing comparable overall complication profiles to traditional burr-hole due to extended manipulation.^[96]

Long-Term Complications

One of the primary long-term complications of subdural hematoma is recurrence, particularly in chronic cases, where rates range from 9% to 33% following surgical evacuation, with higher risks (up to 30%) observed without adjunctive therapies due to incomplete hematoma drainage and persistent neomembrane formation that promotes reaccumulation.^[46] Risk factors for recurrence include older age, bilateral hematomas, and residual hematoma volume greater than 50 cm³ on postoperative imaging.^[97] Incomplete evacuation leaves behind organizing membranes that can impair cerebrospinal fluid absorption and foster rebleeding from fragile vessels.^[98] Neurological sequelae are common, especially in elderly patients, with cognitive impairment persisting in approximately 45% of survivors three months post-treatment, manifesting as memory deficits, executive dysfunction, and reversible dementia-like symptoms that may not fully resolve despite intervention.^[99]^[100] Post-traumatic epilepsy develops in 10-15% of chronic subdural hematoma cases, often as late post-traumatic seizures with a high recurrence risk exceeding 60% if initial seizures occur, necessitating long-term antiepileptic management.^[101]^[48] Motor deficits, such as hemiparesis, affect up to 46% of patients at presentation and can persist in a subset, contributing to gait disturbances and reduced independence.^[102] Additional complications include hydrocephalus, arising in 5-10% of cases from compressive membranes obstructing cerebrospinal fluid pathways, which may require ventriculoperitoneal shunting and further increases recurrence risk.^[13] Psychological issues, particularly depression, emerge in up to 50% of survivors due to traumatic brain injury-related changes, including frustration from cognitive and functional losses, with elevated lifetime risk persisting for decades post-injury.^[103]^[104] Recent advancements as of 2025 highlight middle meningeal artery embolization (MMAE) as an adjunctive therapy that reduces long-term recurrence by approximately 50% through targeted occlusion of feeding vessels, decreasing reoperation rates without added procedural risks.^[105] In acute subdural hematoma survivors, persistent neurological deficits occur in about 20%, underscoring the need for multidisciplinary follow-up to address ongoing impairments.^[103]

Prognosis and Prevention

Prognosis

The prognosis of subdural hematoma (SDH) varies significantly by type, patient age, initial clinical status, and treatment approach. For acute SDH, mortality rates in severe cases range from 30% to 90%, with recent studies reporting overall rates of 14-34%; good functional recovery (Glasgow Outcome Scale [GOS] scores of 4-5) is achieved in approximately 50-60% of survivors.^[106]^[36]^[107]^[108] Outcomes are notably worse in patients with a Glasgow Coma Scale (GCS) score below 6 on admission or those older than 70 years, where mortality can exceed 75%.^[36]^[109] In contrast, chronic SDH carries a more favorable short-term prognosis, particularly in elderly patients, with mortality rates of 10-17% reported in surgical cohorts.^[110] Early intervention yields good outcomes in about 80% of cases, though recurrence rates of 10-20% can negatively impact recovery and necessitate reoperation.^[111]^[112] Recent 2025 data on middle meningeal artery embolization (MMAE) as an adjunct or primary therapy for chronic SDH demonstrate improved prognosis, with mortality rates below 5%, reduced reoperation needs, and treatment failure reduced by up to 50% compared to surgery alone per 2024 NEJM trial and subsequent reviews.^[113]^[114]^[115]^[116] Key predictors of poor prognosis across SDH types include hematoma volume exceeding 50 mL, midline shift greater than 5 mm, and pupillary abnormalities, which independently correlate with higher mortality and worse functional outcomes.^[109]^[117] Long-term neurological morbidity affects 30-50% of survivors, manifesting as persistent deficits in cognition, motor function, or independence; however, non-traumatic SDH cases show substantially better recovery rates, approaching 90% with minimal sequelae when managed promptly.^[118]^[119]

Prevention

Preventing subdural hematoma primarily involves strategies to mitigate head trauma and manage modifiable risk factors, particularly in vulnerable populations such as the elderly. Fall prevention programs for older adults, including home modifications like installing grab bars and removing tripping hazards, along with balance and strength training exercises, have been shown to reduce the rate of falls by approximately 23%.^[120] These interventions are crucial since falls account for a significant portion of traumatic brain injuries leading to subdural hematomas in individuals over 65 years old, and multifactorial approaches can decrease fall-related injury risk by 20-25%.^[121] Additionally, promoting helmet use during activities such as cycling, motorcycling, and contact sports lowers the risk of traumatic brain injury, including subdural hematomas, by 65-88%.^[122] Seat belt usage in vehicles further reduces the incidence of head injuries from motor vehicle crashes, a key preventive measure endorsed by public health authorities.^[123] Medication management plays a vital role in primary prevention, especially for patients on anticoagulants or antiplatelet therapy, which increase the risk of hematoma expansion following minor trauma. Peri-procedural bridging with shorter-acting agents and patient education on fall risks while on these medications help minimize bleeding complications, as recommended in recent clinical guidelines.^[78]^[13] For individuals with chronic alcohol abuse, which elevates the odds of intracranial hemorrhage, including subdural hematomas, by up to twofold due to increased falls and impaired coagulation, cessation programs can substantially lower this risk by addressing both behavioral and physiological factors.^[24]^[124] Structured alcohol reduction interventions have been associated with decreased overall trauma incidence in at-risk populations.^[125] Secondary prevention focuses on early intervention in high-risk scenarios to avert hematoma development. Prompt diagnosis and treatment of cerebrospinal fluid (CSF) leaks, often through epidural blood patching or surgical repair, can resolve spontaneous intracranial hypotension and prevent associated subdural hematomas in most cases without requiring direct hematoma evacuation.^[126]^[127] Screening via imaging, such as CT or MRI, is advised for high-risk patients, including those post-craniotomy or with known coagulopathy, to detect early subdural collections before symptomatic progression.^[78] Public health measures, including the 2024 ARISE consensus guidelines, emphasize education on anticoagulant risks and trauma avoidance in aging populations, where subdural hematomas are increasingly prevalent.^[13] Campaigns like the CDC's STEADI initiative promote widespread fall prevention awareness through community programs and healthcare provider training, targeting societies with growing elderly demographics to reduce head trauma incidence.^[128]

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