Acute Subdural Hematoma

Introduction

• Subdural hematoma (SDH) is a type of intracranial hemorrhage characterized by bleeding that occurs between the dural and arachnoid membranes surrounding the brain (Figure 1).^1,2
• SDHs can be classified into several subtypes based on:²
  • Time course: acute, subacute, acute on chronic, and chronic
  • Etiology: traumatic, spontaneous, and other pathologies
  • Special considerations: anticoagulation-induced, bilateral, recurrent, etc.

Etiology

• Acute SDH results from head trauma about 70% of the time.¹
  • The acceleration of the brain in the lateral direction can cause injury to the bridging veins.¹
  • Minor injuries can result in acute SDH in at-risk patients, such as older patients or patients on anticoagulation.
  • Nonaccidental trauma is the typical etiology of acute SDH in infants and children. Concern for abuse should remain high.²
• Decreased intracranial pressure (ICP) or intracranial hypotension is another mechanism of acute SDH.¹
  • Decreased ICP may result from a cerebral spinal fluid (CSF) leak following a lumbar puncture, a ventriculostomy, a shunt placement, excessive drainage from a lumbar drain, or other neurosurgical procedures.¹
  • The decrease in ICP causes the brain to depress in the skull and puts stress on the bridging vessels.
  • Intracranial hypotension can also lead to engorgement of the veins and cause leakage.¹
• Any cause of arterial hemorrhage can also lead to SDH, including:
  • intracerebral hemorrhage
  • ruptured aneurysm
  • arteriovenous malformations
  • vasculopathy
• SDH can also be the result of an underlying malignancy.
• Acute on chronic subdural hematoma: Chronic subdural hematomas or chronic hygromas have a risk of acute bleeding into the subdural space.

Pathophysiology

• An acute SDH should be suspected in patients with a steadily decreasing level of consciousness and/or unilateral neurological symptoms from compression:
  • dilated pupil, focal weakness, hemiparesis, posturing, and/or focal seizure.
• Older patients are at a higher risk for SDH, and mortality increases significantly in patients older than 60 years.²
  • Cerebral atrophy results in a larger subdural space, lending more tension on the bridging veins, higher clot burden, and increased midline shift.²
  • More comorbid conditions in this population increase the risk of hospital complications.
• Venous SDHs most commonly occur in the frontoparietal region, whereas arterial SDHs are typically found in the temporoparietal region.¹

Diagnosis

• A noncontrast head computed tomography (CT) is the first choice imaging study to diagnose SDH. An acute SDH appears as a hyperattenuating mass overlying the cerebral convexity, falx cerebri, or cerebellar tentorium.² It typically has a crescent-like or half-moon appreance that crosses suture lines (Figure 2). Unilateral SDH may cause a mass effect with midline shift. Chronic SDH appears as isodense to hypodense crescent-shaped lesions that may contain pseudomembranes.

Treatment Options/Anesthetic Considerations

The management of SDH requires a multi-faceted approach (Figure 3).

Acute SDH Management

• Intubation for a Glasgow coma score (GCS) less than 8 or a decline in GCS by 2 or more points should be considered.²
• Adequate oxygenation and ventilation should be ensured.
• Systolic blood pressure should be maintained less than 140-160 mmHg to prevent hematoma expansion.^1,2
• Hypotension should be avoided and normotension should be maintained to prevent cerebral hypoperfusion in the setting of elevated ICP.
• Hypercapnia should be avoided, which could trigger an ICP crisis.
• A noncontrast head CT should be repeated to assess for stability at 4 hours if no immediate operative intervention is performed.

Reverse Any Anticoagulation or Coagulopathy (Table 1).²

Elevated ICP Management²

• Surgical evacuation and decompression are the most effective means of lowering ICP.
• Head of the bed should be elevated.
• Sources of venous obstruction (i.e. improperly placed cervical collar) should be eliminated.
• Hyperventilation is a bridging treatment before surgical evacuation.
• Caution should be taken with the placement of external ventricular drains to remove CSF, as it may worsen the condition by causing further retraction of the injured veins.
• Caution should be taken with osmotic agents, as they may cause further tension on dural vessels exacerbating the hematoma.

Seizure prophylaxis²

• Antiseizure prophylaxis with levetiracetam, lacosamide, or fosphenytoin should be considered.
  • Lesions involving the temporal lobe or tentorium can be more epileptogenic.²
  • Acute traumatic injuries should include seizure prophylaxis for 7 days.

Operative Intervention²

• Current guidelines recommend open craniotomy for an acute SDH with a maximum thickness greater than 1cm or a midline shift greater than 0.5 cm.
• Smaller lesions may still require surgical intervention if the patient is doing poorly clinically, especially if the GCS decreases by 2 or more points from the time of presentation.
• Traditional ICP management techniques are safer after hematoma evacuation.
• Some institutions will leave subdural and subgaleal drains for a few days after surgery.