In contrast with a treatable epidural hematoma (EDH), an acute subdural hematoma (ASDH) carries a high risk of morbidity and mortality, even with timely decompression.

The difference in outcome between EDH and ASDH arises from two discrete but related etiologies. First, the force of trauma or impact necessary to cause an ASDH is significantly greater than that required for an EDH. The typical scenario for an ASDH involves an acceleration-deceleration shear injury (e.g., a motor vehicle accident, fall, or whiplash injury) during which the brain’s inertia continues to move the brain after the body and skull have stopped moving. This phenomenon results in significant shear vectors affecting the brain parenchyma and its tethered and vulnerable venous system. Diffuse axonal injury is common among patients suffering from ASDH.

Second, with ASDH, there is an increased likelihood of injury to the underlying brain parenchyma. Thus, the ASDH has two potential sources of hematoma formation: the brain parenchyma and the parasagittal bridging veins. A laceration of the brain resulting in an expanding hematoma is the more ominous of the two because it implies significant parenchymal injury.

A distinction must be made between a chronic subdural hematoma and an acute subdural hematoma. An ASDH is defined as a bleed occurring within the subdural space that occurred within 72 hours prior to the patient’s presentation. Bleeds in patients who present after 72 hours of injury are considered either subacute or chronic, depending on their timing and the computed tomography (CT) findings. The mechanisms and rates of hematoma expansion for acute and chronic SDHs and their corresponding outcomes are different. This chapter primarily deals with ASDHs.

An ASDH occurs after a traumatic event involving acceleration-deceleration forces, rather than the blunt trauma and skull fracture that are typically associated with EDH. Due to the impact of trauma, the patient is often in a comatose state with a Glasgow coma scale (GCS) score ≤8, necessitating the dispatch of emergency personnel and rapid transport of the patient to a trauma center.

In contrast with EDH, there is often no lucid interval for a patient with ASDH. The signs and symptoms of transtentorial or uncal herniation may be present and are dependent on the extent of the enlarging hematoma. However, the absence of these findings does not necessarily imply a good prognosis because brain parenchymal contusion and/or laceration can still lead to significant morbidity and mortality.

Some patients may remain conscious after their injury, but their condition subsequently deteriorates as the hematoma enlarges with or without signs of herniation. For patients who remain conscious after an accident with an associated high propensity for ASDH formation, it is important that the physician maintains a high index of suspicion for hematoma expansion and neurologic deterioration.

As is the case for all patients with a potential traumatic brain injury (TBI), it is imperative to obtain a head CT scan without contrast in order to adequately detect an expanding hematoma. On noncontrast CT, an expanding ASDH will appear as an intensely white, crescent-shaped mass situated between the brain parenchyma and the inner table of the skull. ASDH is most commonly unilateral, but some patients may harbor bilateral ASDHs.

An ASDH, by definition, is located between the dura mater and subarachnoid mater; thus, the expanding hematoma is not limited by the sutures of the calvarium, but rather by the dural sinuses. This property allows the ASDH to outline the entire brain hemisphere. It may be helpful to identify the volume of blood but the amount of midline shift is the key determinant for the need to proceed with surgical decompression. A small hematoma may require evaluation if the underlying brain edema is exacerbating the midline shift, leading to a depressed level of consciousness; this is not an uncommon phenomena among pediatric patients suffering from ASDH.

Finally, the frontal and temporal lobes should be examined to exclude concurrent parenchymal injuries or contusions.

Skull fractures around the dural venous sinuses should be carefully studied.

The following guidelines are not definitive, but should be considered in the decision-making process for surgical management of ASDH:

• ASDHs with thickness >10 mm or midline shift >5 mm on CT scan
• ASDHs with a thickness <10 mm and midline shift <5 mm on CT may need to be surgically treated under the following conditions:
  • GCS drops by ≥2 between injury and admission.
  • Pupils are asymmetric or fixed and dilated.
  • Intracranial pressure is >20 mmHg.
• All patients with GCS <9 should have intracranial pressure (ICP) monitoring implants.

Although these guidelines provide a framework for operative decision-making, it is important to consider the overall clinical picture and exam in assessment of the patient. Specifically, a poor GCS score (GCS <5), old age, and massive brain herniation (as determined by pupils’ status) predict a high mortality rate regardless of surgical intervention and medical management. Thus, even when all of the operative guidelines are met, there are scenarios that call for operative restraint and palliative management. Concurrent multifocal intracerebral contusions are associated with poor prognosis and should be considered during selection of the treatment strategy.

Conservative management may be used when the operative guidelines are not met, but this decision does not rule out the potential need for operative management in the near future. Moreover, conservative management indicates frequent neurologic evaluations, potential need for ICP monitoring, and serial CT scans for continual assessment of hematoma status, evolution of contusions, and brain edema.

Although the initial CT scan may not be very concerning in the case of a comatose patient, initial ICP measurements after implantation of the monitor may indicate a need for an emergent operative intervention and a decompressive craniectomy.

Additional diagnostic studies are necessary at presentation. The patient’s prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR) are assessed. The use of antiplatelet and anticoagulation medications should be reviewed. Correction of coagulation and platelet dysfunctions prior to surgery should be considered. In the absence of other coagulation abnormalities, I do not reverse the effect of acetylsalicylic acid (ASA) derivatives (aspirin).

The patient’s presenting neurologic status may be concerning or may continue to deteriorate after admission to the hospital. In almost any instance, it is preferential to obtain a head CT before proceeding with surgical decompression. If increasing intracranial pressure is responsible for the patient’s neurologic deterioration, appropriate measures should be instituted, including hyperventilation (PCO2 of 30-35 mmHg), administration of mannitol, and head elevation.

The patient must not be overly hyperventilated because this may lead to cerebral ischemia secondary to the excessive cerebral vasoconstriction and coexisting pressure gradients. Immediate neurosurgical evaluation and triage is crucial.

Once a decision is made to proceed with surgical decompression, the procedure should be performed as soon as possible if symptomatic mass effect is present. Two variables have been shown to correlate with outcome: 1) timing of the operation, and 2) strict control of the patient’s ICP. Numerous studies have supported the theory that the best operative outcomes for patients with ASDH occur when the procedure takes place within 4 hours of the injury.

Following completion of the incision, I reflect a myocutaneous flap anteriorly. An expanded burr hole may be placed in the temporal bone and the dura incised in a cruciate fashion to allow the hematoma to extrude out through the burr hole. This maneuver may be used for rapidly deteriorating patients.

The methods of incising the dura for an ASDH should be well thought out because the underlying brain injury may have resulted in significant brain edema, which can lead to massive brain herniation upon opening the dura.

Moreover, the edema may leave very little space between the dura and brain along the edges of the hematoma, thus causing cortical disruption when the dura is opened with scissors. The dural incision should typically follow the outline of the bone flap while leaving enough dura at the edge of the flap to allow for dural closure after evacuation of the hematoma.

If significant brain edema is present (or the extent of mass effect is out of proportion to the size of the hematoma) on the preoperative scans, numerous dural linear incisions or slits (~3 to 4 cm in length) may be made and the hematoma evacuated while the operator works between these slits. This maneuver will prevent massive cerebral herniation after a wide dural opening, which could lead to hemodynamic instability because of acute cerebral and brainstem dislocations.

Rapid decompression of the hematoma is the most effective method to relieve intracranial tension.

Any obvious small cortical bleeding veins or arteries should be controlled with bipolar electrocautery. The subdural space beyond the edges of the craniotomy should be carefully re-explored, and additional remote clots removed as described above. I attempt to remove most mobile hematoma fragments that do not reside close to the dural venous sinuses.

Smaller clots that are not well visualized or reside near the dural sinuses or other large vital bridging/cortical veins (such as the vein of Labbe) should be left alone and undisturbed. Manipulation of these clots can uncover the original source of the hematoma; these venous channels are difficult to control without their sacrifice, and they invariably lead to more bleeding if they are manipulated. Aggressive coagulation and packing of hemostatic materials will further compromise the lumen of the venous drainage systems and lead to exacerbation of cerebral swelling.

The subdural spaces along the middle and anterior cranial fossae must also be inspected to ensure adequate hematoma evacuation. This tactic will potentially help with compromised cerebrospinal fluid flow and resolve uncal herniation.

During ASDH evacuation, brain edema is most likely related to the loss of cerebrovascular autoregulation and reactivity. The intense cerebral tension may be startling to the surgeon because it can lead to massive brain herniation through the bony defect. This phenomenon results in cerebral and brainstem dislocation and associated hemodynamic instability. It can also impede proper dural closure at the completion of the operation.

It is imperative to rapidly attempt to tamper the amount of edema with the following interventions. First, the surgeon and anesthesiologist should ensure that the patient is properly positioned, the jugular venous drainage is not compromised, and the endotracheal tube is not kinked. Next, the anesthesiologist should induce the patient into a state of mild arterial hypotension while avoiding any significant risk of ischemia. As mentioned above, the cerebral vascular autoregulation is markedly impaired; this mechanism is one of the common reasons for massive intraoperative brain swelling during ASDH surgery.

A barbiturate coma may be induced while the surgeon completes a temporal or frontal lobectomy as a final decisive step. If difficult or refractory swelling is encountered, the operator must consider the potential presence of a contralateral epidural, subdural, and/or intracerebral hematoma(s) as causative factors. These pathologies should be ruled out using intraoperative Doppler ultrasonography or a postoperative CT scan. Ultimately, rapid dural and scalp closure without replacement of the bone flap is prudent.

Intraoperative bleeding or venous “ooze” is common during removal of ASDHs. Undetectable irregularities in coagulation cascades are often present after massive brain injury. As ASDHs are most commonly caused by shear injury of the parasagittal veins, recurrent intraoperative bleeding is also usually venous in origin.

For more information regarding management of intraoperative cerebral swelling, refer to the chapter on Brain Swelling.

If the operator has any suspicion of brain swelling after hematoma evacuation, the dura is loosely approximated, a duraplasty performed using a piece of pericranium and the bone flap not replaced. Upon closure of the dura, tack-up sutures are placed at the edge of the craniotomy and, if a potential space is present, in the middle of the dural flap.

Finally, many patients who undergo the operation will need ICP monitoring postoperatively; placement of an intraparenchymal monitor is reasonable. A contralateral ventriculostomy may also be considered if significant ICP issues are expected postoperatively.

Strict control of the ICP is crucial for minimizing secondary brain injury postoperatively. The rise in ICP occurs most often because of a defective autoregulatory mechanism of the cerebral blood flow. A CT scan should be performed on the first postoperative day to assess for any residual, recurrent or distant hematomas. Serial CT scans should also be obtained in a patient who suffered from an unexplained rise in ICP or who fails to improve neurologically.

Patients with TBI commonly experience seizures before and after surgical intervention. The patient should be loaded with a preferred anticonvulsant drug either prior to or immediately after surgery to prevent the occurrence of early seizures. Early seizures are defined as those occurring within one week of the insult, and they do not necessarily imply epilepsy or the need for life-long anticonvulsant therapy. Unexplained lack of neurological improvement or deterioration may indicate subclinical seizures and electroencephalographic monitoring is recommended.

Finally, extracranial complications are common in patients with acute head injuries. Pulmonary sequelae, including acute respiratory failure or infections, should be closely monitored and pre-emptively treated. The increased ICP may also lead to Cushing ulcers and should be prophylactically treated through the administration of proton pump inhibitors or histamine blockers.

• The mechanisms of brain trauma are different in EDHs and ASDHs. The underlying cerebral injury can be a limiting factor in achieving desirable outcomes after adequate removal of ASDHs. Postoperative secondary injury should be avoided via controlling ICP.
• Manipulation or removal of small clots over large parasagittal draining veins or dural sinuses should be kept to minimum.

Contributor: Jonathan Weyhenmeyer, MD

DOI: https://doi.org/10.18791/nsatlas.v8.ch01.2