Subdural Hemorrhage

Subdural hemorrhage (SDH) is bleeding into the space between the dural and arachnoid meningeal layers surrounding the brain. The most common mechanism triggering the bleeding event is trauma (e.g., closed head injury) causing a tearing injury to the extracerebral “bridging” veins, but rupture of small arteries within this space or intracranial hypotension may also be causative. Acute SDH presents, immediately following head trauma, with an altered level of consciousness that may span from a momentary loss of consciousness to coma, which makes it a potentially life-threatening condition. Chronic SDH may also occur, presenting with a more gradual neurologic deterioration. Diagnosis is based on clinical suspicion following head trauma and confirmed with neuroimaging (e.g., noncontrast head CT). Management includes stabilization, stopping (possibly reversing) all anticoagulants, monitoring in a neurologic ICU, and neurosurgical intervention.

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Overview

Definition

Subdural hematoma (SDH) is bleeding, usually caused by head trauma, into the space between the dural and arachnoid meningeal layers surrounding the brain, creating a space called the subdural space.

Subarachnoid hemorrhage

Meninges and meningeal spaces:
The image depicts the 3 layers (dura mater, arachnoid mater, and pia mater) surrounding the brain and spinal cord. The meninges serve as mechanical protection of the CNS. The meninges also support the cerebral and spinal blood vessels and allow for passage of the CSF. The subarachnoid space is filled with CSF. Only the subarachnoid space is a true space present in physiologic conditions, whereas the epidural and subdural spaces form only because of pathologic processes. The subdural space opens if the arachnoid mater separates from the dura mater, most commonly because of trauma and pathologic processes.

Image by Lecturio.

Epidemiology

  • Prevalence:
    • Found in approximately 10% of cases of head trauma necessitating hospitalization
    • Found in approximately 20% of cases of severe traumatic brain injuries (TBIs)
  • More common in older individuals 
  • More common in persons on antiplatelet/anticoagulant therapies

Etiology

Head trauma: 

  • Most common cause of SDH
  • Causes injury to vascular structures that course between the dural and arachnoid meningeal layers surrounding the brain.
  • Most commonly exerts forces in the anteroposterior direction →  injury to bridging veins to the superior sagittal sinus
  • Examples:
    • Motor vehicle accident
    • Falls
    • Assaults

Anticoagulation or coagulopathy:

  • Increase risk of prolonged or excessive bleeding
  • Examples (drugs):
    • Antiplatelet agents:
      • Aspirin
      • Clopidogrel
      • Prasugrel
    • Vitamin K antagonists: warfarin
    • Factor X inhibitors:
      • Rivaroxaban
      • Apixaban
      • Edoxaban
    • Heparinoids:
      • Unfractionated heparin (UFH)
      • Low-molecular-weight heparin (LMWH)
    • Thrombolytics:
      • Tissue plasminogen activator (tPA)
      • Urokinase
  • Examples (disease states):
    • Chronic liver disease
    • Thrombocytopenia
    • Hemophilia

Cerebral atrophy:

  • Predisposes to vascular injury by allowing for excessive movement inside the cranial vault in the event of trauma.
  • Primarily causes chronic SDH
  • Examples:
    • Previous TBI
    • Previous cerebrovascular accident with parenchymal necrosis
    • Chronic alcoholism

Intracerebral hemorrhage:

  • Direct extension of an intraparenchymal bleed through the cortical surface and into the subdural space
  • More likely to occur in the absence of trauma
  • Examples:
    • Intraparenchymal hypertensive bleed
    • Intraparenchymal hemorrhagic conversion of ischemic stroke

Ruptured aneurysm of the cerebral vasculature:

  • Direct extension of an intracerebral bleed through the subarachnoid and into the subdural space 
  • More likely to occur in the absence of trauma
  • Examples:
    • Subarachnoid hemorrhage (SAH; usually the result of a ruptured saccular aneurysm)
    • Carotid artery (or a branch thereof) aneurysm

Malformations of the cerebral vasculature:

  • Direct extension from the site of bleeding into the subdural space
  • More likely to occur in the absence of trauma
  • Example: Arteriovenous fistula

Brain tumor:

  • Primary or metastatic tumors that involve the dura may cause bleeding into the subdural space.
  • More likely to occur in the absence of trauma
  • Examples:
    • Meningioma (primary)
    • Breast cancer (metastatic)
    • Lung cancer (metastatic)
    • Prostate cancer (metastatic)

Intracranial hypotension:

  • Inadequate CSF volume may create a vacuum effect within the cranial vault → transmitted to the meningeal layers → predisposes to tearing of the bridging veins
  • May occur with or without trauma
  • Examples:
    • Dural leak after epidural procedure
      • Epidural steroid injection
      • Epidural anesthesia prior to fetal delivery
    • CSF loss from trauma

Pathophysiology

Acute subdural hematoma

  • Trauma leading to tearing of the bridging veins:
    • Bridging veins drain blood from the cerebral surface into the dural sinuses.
    • Bridging veins traverse the space between the arachnoid and dural meningeal layers.
    • Tearing allows blood to collect between these layers.
    • Bleeding is typically blocked by rising intracranial pressure (ICP) or direct compression by the forming thrombus.
    • Observed most commonly in the temporoparietal region.
  • Trauma leading to arterial rupture:
    • Small arteries (< 1 mm diameter) supply blood to the superficial cerebral cortex.
    • These arteries traverse the space between the arachnoid and dural meningeal layers.
    • Rupture allows blood to collect between these layers.
    • Bleeding is typically blocked by rising ICP or direct compression by the forming thrombus.
    • Observed most commonly in the temporoparietal region. 
  • Intracranial hypotension (low CSF pressure):
    • Caused by low CSF volume, usually from a leak:
      • Spontaneous (seen in connective tissue disorders, such as Ehlers-Danlos or Marfan syndrome)
      • Iatrogenic (e.g., lumbar puncture, epidural anesthesia)
    • Low CSF pressure decreases buoyancy of the brain → traction on the meningeal support structures
    • Traction translated to bridging veins/small cortical arteries → can cause tearing/rupture of these vessels
    • A vacuum effect is produced by the low ICP, causing vasodilation and further propensity to bleed. 

Chronic subdural hematoma

  • Forms from an acute SDH that has thrombosed:
    • Fibroblasts elaborate collagen over the dural layer, stabilizing the outer surface of the thrombus.
    • Thinner membrane develops over the inner surface of the clot → complete encapsulation 
    • Process takes approximately 2 weeks 
  • Liquefaction of the thrombus:
    • In > 50% of cases of acute SDH, the above-mentioned membranes calcify, while the thrombus contained therein undergoes liquefaction into a hygroma (fluid-filled sac).
    • Hygroma is protein-rich → potential osmotic draw of fluid into the cavity and expansion of the hygroma

Acute-on-chronic SDH

  • Recurrent trauma may cause bleeding into an otherwise stable (i.e., thrombosed) SDH or hygroma → enlargement and further intracranial pathologies 
  • Expansion of a hygroma due to osmotic forces → enlargement and further intracranial pathologies 

Clinical Presentation

Head trauma is the most common etiology of SDH, most often minor trauma (e.g., ground-level fall) in an elderly individual. 

Onset of symptoms

  • Acute SDH:
    • Presents immediately: up to 72 hours after the event
    • Initial presentation: coma in ½ of cases
    • Remainder may have a “lucid interval” between injury and onset of progressive neurologic decline.
  • Subacute SDH presents 3–14 days after the event.
  • Chronic SDH presents ≥ 15 days after the event.
  • In the absence of trauma, SDH may be difficult to categorize.

Neurologic symptoms

  • Nature of neurologic symptoms/signs depend largely on the following characteristics of the hematoma:
    • Location 
    • Size 
    • Rate of growth 
    • Acuity 
  • Common symptoms:
    • Altered level of consciousness
      • Minor trauma may cause only a momentary loss of consciousness.
      • Severe trauma victims with SDH may present in a coma.
      • Subacute or chronic SDH may present with gradual deterioration in level of consciousness.
    • Headache
    • Light-headedness/dizziness
    • Neck pain/stiffness
    • Visual changes
    • Nausea/vomiting
    • Balance/gait disturbance
    • Dysphagia
  • Common signs:
    • Nuchal rigidity
    • Cranial nerve palsies
    • Ataxia
    • Seizures

Diagnosis

The diagnosis of SDH should be suspected in any elderly person presenting with head trauma, altered mental status, decreased level of consciousness, or neurologic symptoms/signs. CT of the head should be performed emergently when an acute SDH is suspected.

Neuroimaging

Noncontrast head CT:

  • Imaging method of choice:
    • For acute head trauma
    • For acute loss of consciousness
    • For suspected SDH (and other intracranial bleeds)
  • Acute SDH appears as a high-density crescent-shaped collection of blood along the convexity of the affected hemisphere.
    • Fresh blood appears with high intensity on CT.
    • Easily distinguishable from the surrounding anatomy 
  • Subacute and chronic SDH appear as an isodense or hypodense crescentic collection of blood with associated deformation of cerebral contours.
    • The hematoma loses its intensity as thrombosis and clot remodeling/resolution progress.
    • Subacute/chronic blood collection is more difficult to distinguish from the surrounding anatomy.
  • Unilateral SDH creates an obvious distortion of cerebral contours. 
  • Bilateral SDH may create symmetric distortion of cerebral contours and be less obvious. 

Head MRI:

  • Fluid-attenuated inversion recovery (FLAIR) sequencing 
  • Less widely used and not as readily available as CT
  • Sensitivity is superior to that of noncontrast CT in the detection of intracranial hemorrhage.
  • Acute, subacute, and chronic subdural blood appear hyperintense in CSF. 
    • May detect small SDHs that may be missed on noncontrast CT
    • May detect dural lesions (e.g., dural tears, neoplasm) missed on noncontrast CT
  • May reveal the presence and extent of associated intraparenchymal injuries

Angiography:

  • Noninvasive MRA or CTA: 
    • May be indicated for evaluation of nontraumatic or idiopathic SDH
    • May reveal small intracranial aneurysms or other vascular lesions
  • Conventional angiography may be considered if a vascular lesion is suspected but not detected by noninvasive angiography.

Contraindicated procedures

Lumbar puncture: 

  • Contraindicated when SDH is suspected
  • Increased ICP due to expanding hematoma increases risk of herniation.
Subdural hemorrhage

Subdural hemorrhage:
Note the convexity of the hematoma and associated midline shift (with distortion of cerebral anatomy and obliteration of the lateral ventricle).

Image: “This CT scan is an example of Subdural haemorrhage caused by trauma. Single arrow marked the spread of the subdural haematoma. Double arrow marked the midline shift” by Glitzy queen00. License: Public Domain

Management

Acute SDH, especially that presenting with neurologic compromise or coma, is an emergent neurologic situation often requiring surgical intervention. Failure to promptly stabilize, diagnose, evaluate, and intervene could result in hemorrhagic expansion, parenchymal brain injury, elevated ICP, brain herniation, and death.

Stabilization

  • Individual should be evaluated and stabilized using advanced trauma life support/advanced cardiac life support (ATLS/ACLS) protocols.
  • Life-threatening injuries should be addressed.
  • Immediate discontinuation (and possible reversal) of antiplatelets/anticoagulants
  • Efforts to achieve/maintain hemodynamic instability
  • Noncontrast head CT as soon as possible
  • Emergent neurosurgical consultation: 
    • Surgical clinical decision making 
    • Placement of ICP monitoring device

Stratification

Clinical decision tools used to determine operative or nonoperative management include:

  • GCS score
  • Head CT findings:
    • Clot thickness
    • Degree of midline shift
    • Presence of associated brain lesion
  • Neurologic examination
  • Presence of pupillary palsy
  • Acuity of SDH
  • Presence of comorbidities 
  • Severity of associated trauma
  • Age

Nonoperative management

  • May be appropriate for:
    • Clinically stable individuals (GCS score > 9)
    • Small hematomas (< 10 mm thickness on CT)
    • Absence of brain herniation signs by clinical and/or radiographic evaluation: 
      • Absent or minimal midline shift on CT (< 5 mm)
      • Absence of direct visualization of herniation on CT
      • Absence of physical examination findings of elevated ICP (e.g., papilledema)
      • Absence of elevated ICP on neuromonitoring
  • Should be monitored in a neurologic ICU
  • Should have continuous ICP monitoring
  • Serial head CT should be performed every 6–8 hours for 36 hours.
  • Hematoma may resolve through resorption over weeks.

Operative management

  • May be appropriate for:
    • Clinically unstable individuals:
      • GCS score < 9
      • GCS score reduction by ≥ 2 from time of injury to time of evaluation
      • Presence of pupillary palsy
    • Large hematomas (> 10 mm thickness on CT)
    • Midline shift on CT > 5 mm, regardless of GCS score
    • ICP > 20 mm Hg
  • Should be undertaken as soon as clinically feasible for individuals meeting these criteria (within 2–4 hours after onset of neurologic deterioration)
  • Surgical techniques:
    • Craniotomy with hematoma evacuation is the most commonly performed surgical technique.
    • Burr hole trephination
    • Decompressive craniectomy 
    • Subdural evacuation port system
  • Culprit vessel identification and tamponade may be undertaken simultaneously:
    • Traditional tamponade with ligatures
    • Endovascular embolization of the middle meningeal artery 

Prognosis

  • Mortality rate: 
    • Approximately 50% in SDH requiring surgery
    • Approximately 40% if surgical intervention is prompt (2–4 hours after injury)
    • Approximately 85% if surgical intervention is delayed
    • Approximately 60%–70% in SDH presenting with coma prior to evaluation
  • Age and GCS score are the most important prognostic indicators.

Differential Diagnosis

  • Ischemic stroke: ischemic infarct of the cerebral parenchyma caused by occlusion of a cerebral artery by atherosclerotic lesions or cardioembolic emboli. Ischemic stroke presents with neurologic deficits and/or altered mental status/altered level of consciousness that depends on the size and location of infarct. Diagnosis is clinical and confirmed by neuroimaging. Management includes initial stabilization, possible cerebrovascular intervention, addressing identifiable underlying etiologies (severe hypertension, embolus), and management of cardiovascular risk factors. 
  • Other hemorrhagic cerebral conditions: Carotid/cerebral artery dissection, epidural hemorrhage, intraparenchymal hemorrhage, and subdural hemorrhage are other hemorrhagic manifestations of the cerebral vasculature that can present with neurologic deficits and/or altered mental status/altered level of consciousness. Diagnosis is clinical and confirmed by neuroimaging. Management depends on the hemorrhagic etiology and includes initial stabilization, neurosurgical/endovascular consultation, management of ICP, and monitoring in a neurologic ICU. 
  • Hypertensive encephalopathy: neurologic deficits and/or altered mental status/altered level of consciousness that present in the setting of severe hypertension. Diagnosis is based on the presence of elevated blood pressure and neurologic signs/symptoms. Neuroimaging is useful to rule out ischemic or hemorrhagic cerebrovascular accident. 

References

  1. McBride, W. (2020). Subdural hematoma in adults: etiology, clinical features, and diagnosis. Retrieved September 12, 2021, from https://www.uptodate.com/contents/subdural-hematoma-in-adults-etiology-clinical-features-and-diagnosis?search=subdural%20hemorrhage&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  2. McBride, W. (2021). Subdural hematoma in adults: prognosis and management. Retrieved September 12, 2021, from https://www.uptodate.com/contents/subdural-hematoma-in-adults-prognosis-and-management?search=subdural%20hemorrhage&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2
  3. Iliescu I. A. (2015). Current diagnosis and treatment of chronic subdural haematomas. Journal of Medicine and Life 8:278–284. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4556906/
  4. Meagher, R. (2018). Subdural hematoma workup. Retrieved September 16, 2021, from https://emedicine.medscape.com/article/1137207-workup?ecd=ppc_google_rlsa-traf_mscp_emed_md_us
  5. Yang, A. I., Balser, D. S., Mikheev, A., et al. (2012). Cerebral atrophy is associated with development of chronic subdural haematoma. Brain Injury 26:1731–1736. https://doi.org/10.3109/02699052.2012.698364 

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