Surgical Management of Traumatic Acute Subdural Hematoma in Adults: A Review

I. Cerebral blood flow (CBF) changes

In patients with ASDH, it has been demonstrated that Cerebral blood flow (CBF) markedly decreases immediately after injury.^21,22) Since the early CBF reduction occurs under the condition of normal or restored systemic blood pressure and arterial oxygenation, existence of nonsystemic causes are suggested. This CBF reduction is proposed as resulting from cerebral perfusion pressure (CPP) decrease due to ICP increase. Dysautoregulation,²³⁾ cerebral vasospasm,²⁴⁾ and reduced metabolic demand²⁵⁾ due to primary brain injury may be also accounted for CBF reduction. Such secondary ischemia is a target of ICP- or CPP-oriented treatment in cases with ASDH.

Subsequent to CBF reduction, hyperemia/hyperperfusion frequently occurs in the cortex located beneath an evacuated ASDH, and prolongs to be associated with unfavorable outcomes.²⁶⁾ Hyperemia/hyperper-fusion may induce reperfusion injury initiated by oxygen free radicals, for example. Such hyperemia/hyperperfusion often occurs in the elderly.²⁷⁾ ICP- and/ or CPP-oriented management may not be suitable for hyperemia/hyperperfusion. The optimal treatment of hyperemia/hyperperfusion has not been established yet. Recently, early induction of hypothermia before craniotomy has been reported to have a potential to improve outcome in cases with evacuated traumatic intracranial hematomas.²⁸⁾ Since hypothermia has been known to reduce reperfusion injury in animal models,²⁹⁾ early induction of hypothermia before hematoma removal may have a potential to protect brain from reperfusion injury induced by hyperemia/hyperperfusion in cases with ASDH.

II. Coagulopathy

It has been known that various degree of coagulopathy frequently occurs in patients with isolated blunt TBI,^30,31) as 22.7% upon emergency room (ER) arrival.³²⁾ Brain tissue injury stimulates tissue factor pathway of coagulation, resulting in systemic bleeding tendency shortly after TBI.³³⁾ Coagulopathy may influence hemostasis, delayed expansion, or occurrence of intracranial hematoma, leading to unfavorable outcomes. Recently, a high serum D-dimer level has been demonstrated to be associated with a poor outcome in patients with traumatic intracranial hematoma.³⁴⁾ The role of D-dimer has not been fully understood; there may be a certain potential to affect outcome in TBI including ASDH.

III. Delayed deterioration

Delayed deterioration, so-called “talk-and-deteriorate”, often occurs in elderly patients with TBI including ASDH. The brain atrophies with age, and more intracranial spaces are created to compensate blood accumulation and brain swelling before symptoms appear. Delayed deterioration occurs within 6 hours after trauma in majority of cases being caused by expansion of ASDH, delayed traumatic intracerebral hematoma (DTICH), progression of contusional hematoma, and edema.^11,16) Since such deterioration is often rapid and critical, early detection and surgical intervention have been strongly recommended prior to inevitable deterioration.

As another entity of delayed deterioration, delayed posttraumatic acute subdural hematoma (DASH) has been recently recognized in elderly patients on anticoagulants following mild TBI. The patients initially have normal neurological examinations and normal CT, developing an ASDH with rapid deterioration from 9 hours to 3 days after the head injury. It has been suggested that elderly patients on anticoagulants should be admitted for observation.³⁵⁾

Contralateral acute epidural hematoma following removal of ASDH is a rare but devastating intraand post-operative complication.^36,37) The frequency of this occurrence has been reported as 6–30% in surgically treated ASDH. The mechanisms have not been fully understood. Initial decompressive craniectomy on the contralateral side has been attributed to release of a tamponade effect, usually produced by increased ICP and by post-traumatic arterial hypotension. Therefore, immediate postoperative CT scan has been recommended to evaluate this rare, but, potentially lethal complication in patients with ASDH and a contralateral skull fracture.³⁶⁾ Gradual decompression with an initial burr-hole craniotomy followed by a decompressive craniectomy has been suggested to avoid this complication; however, its efficacy has not been established.³⁷⁾

IV. Prehospital oral anticoagulant and antiplatelet

As the population ages, it is increasingly common for elderly patients to encounter with TBI including ASDH. Many of them are being treated in the outpatient setting with anticoagulant or antiplatelet prior to injury. In cases with TBI, prehospital treatment with antiplatelet and anticoagulant has been associated with an increased risk of intracranial hematoma enlargement or delayed hematoma, leading to risk for increased morbidity and mortality.

Prehospital antiplatelet has been associated with significantly increased mortality and unfavorable outcome in TBI patients,^38–40) or with higher rates of neurosurgical interventions as well as more episodes of rebleeding.⁴¹⁾ Although several reports suggest no association of prehospital antiplatelet with increased mortality or unfavorable outcome,^42,43) the available data suggest that patients on antiplatelet therapy may have a higher risk of mortality and morbidity after TBI, especially in cases with intracranial hematoma including ASDH.⁴⁴⁾ Issues of withdrawal and/or reversal of antiplatelet are still controversial. It has been demonstrated that platelet transfusion had no impact on rate of intracranial hematoma progression, neurological decline, or neurological outcomes in patients with TBI. Discontinuation of antiplatelet markedly increases risk of thromboembolism, especially in patients with coronary heart disease. The risk of coronary thrombosis after withdrawal of antiplatelet is greater than the risk of surgical bleeding.⁴⁵⁾ In contrast, the risk of stroke seems relatively low as approximately 2% within 30 days after discontinuation of antiplatelet.⁴⁶⁾ Thus, whether to withdraw or reverse antiplatelet in TBI may be decisions that depend on a variety of circumstances, such as extent of hematoma, necessity of surgical treatment, or indication for prehospital use of antiplatelet agent.⁴⁴⁾

Prehospital use of warfarin, seems to be a trend toward increased mortality in elderly patients regardless of injury severity.⁴⁷⁾ The admitted prothrombin time-international normalized ratio (PT-INR) is directly correlated with mortality.⁴⁸⁾ Specific replacement therapy, including vitamin K, fresh frozen plasma, or VII factor, facilitates successful clot evacuation without bleeding complications.⁴⁹⁾ As antiplatelet agent, withdrawal and reversal of anticoagulant increases the risk of thromboembolism. Whether to withdraw or reverse may depend on a variety of circumstances.

I. Indications

Theoretically, intracranial hypertension due to ASDH may lead to transtentorial cerebral herniation and secondary ischemic injury of the brain. The purpose of surgery is to release from herniation and to reduce secondary ischemic injury minimally. Thus, ASDH causing significant mass effect, which may be effectively reduced by surgery, is supposed to be an indication for surgery.⁵⁰⁾ In general, initial surgical indication may be based on the patients GCS score, pupillary examination, and CT findings. Neurological deterioration⁵⁰⁾ and/or increase in ICP may also be an important factor in delayed decision.⁵¹⁾

In a study analyzing CT findings in initially non-surgically treated patients, it has been demonstrated that an midline shift greater than 5 mm in patients with a GCS score of lower than 15 on the initial CT was significantly related to the failure of nonsurgical treatment.³⁹⁾ In another study, significant differences in clot thickness and hematoma volume have also been demonstrated between the operative and the nonoperative groups in patients with GCS scores 13–15. In addition, all patients with an initial hematoma thickness greater than 10 mm required surgery.⁵²⁾ On the basis of the above literature review, a clot thickness greater than 10 mm, or a midline shift greater than 5 mm are suggested as critical parameters for surgery to remove ASDH, regardless of the GCS scores.⁵¹⁾

As an indication for elective surgery, ICP monitoring may be important to make decision for surgery. Servadei et al.²⁾ developed a protocol to select comatose patients for nonoperative management. The criteria used to select comatose patients for nonoperative management were clinical stability or improvement during the time from injury to evaluation at the hospital, hematoma thickness less than 10 mm and midline shift less than 5 mm on the initial CT, and ICP monitoring. Surgery was performed if the ICP exceeded 20 mmHg. Under this protocol, 15 of 65 comatose patients were treated nonoperatively, and 2 patients were identified as elective surgery based on increasing ICP and intracranial hematoma development. Since this protocol worked successfully, the authors concluded that nonoperative treatment can be safely used for a defined group of comatose patients with ASDH.

II. Timing of surgery

Theoretically, time from injury to surgery may be an important factor to rescue brain from secondary ischemia due to compression and/or intracranial hypertension by ASDH. In general, prompt evacuation of ASDH has been recommended in patients with indications for surgery.^50,51) This recommendation may be supported by the following studies. Seelig et al. demonstrated a 30% mortality in patients with ASDH operated within 4 hours after injury and a 90% mortality in those more than 4 hours after injury. It has also been demonstrated that the duration from injury to surgery was significantly shorter in patients with a functional recovery than with a fatal outcome, suggesting the importance of prompt evacuation of subdural hematoma.^5,53) It has also been reported that there were trends indicating that earlier surgery improved outcome, although the time from injury to operative evacuation of ASDH with regard to outcome morbidity and mortality were not statistically significant even when examined at hourly intervals.⁶⁾ However, the relationship between the time from injury to surgery and the outcome may be difficult to study, because patients operated in sooner time may have more severe injuries than those with delayed surgery.⁵¹⁾ Actually, most studies focusing on the time between injury and surgery have failed to demonstrate a correlation with outcome.^{1,2,10,12,18,54)}

On the other hand, time from TBI to surgery may not be as important as time from clinical deterioration to surgery. Haselberger et al. reported relationship between the time interval from onset of coma to surgery and outcome. They demonstrated that the outcome of patients operated within 2 hours after clinical deterioration is significantly better than those operated longer than 2 hours.⁵⁵⁾ These results suggest that prompt evacuation of ASDH is indicated even after deterioration, including delayed deterioration such as talk and deteriorate.^50,51) The therapeutic time window has not been established, however, prompt surgery within 2 to 4 hours after clinical deterioration have a better outcome than those who undergo delayed surgery.⁵¹⁾

In situations of elective surgery, timing of ICP increase beyond the threshold is suggested as the timing of surgery. (See “Indications” paragraph 3 for details.)

III. Surgical technique

Commonly used surgical techniques for the evacuation of ASDH include cranioplastic craniotomy, large decompressive craniectomy, trephination/craniostomy, or combination of these procedures. In reality, surgical techniques are not specified in most papers, and the effectiveness of surgical procedures is not addressed. For example, some institutes use decompressive craniectomies in all ASDH,¹²⁾ whereas other institutes use cranioplastic craniotomies,⁶⁾ or various procedures are used on different occasions.^10,17,55) The choice of surgical procedures may depend on the surgeon's expertise, training, neurological status of patients, duration from deterioration, pre-operative radiological findings, degree of intraoperative brain swelling, and availability of operating theater. In principle, the purpose of surgery is to release brain from intracranial hypertension to suppress secondary injury minimally. Thus, large craniotomy with hematoma evacuation may be principle.⁵⁰⁾ When intra- and/or post-operative brain swelling is strongly expected, decompressive craniectomy may be suitable. It is supported by a recent publication which has demonstrated that decompressive craniectomy significantly improve outcome in patients with refractory intracranial hypertension due to extensive contusion, compared to routine craniotomy.⁵⁶⁾ However, as it has been known that bony decompression result in apparent exacerbation of edema,⁵⁷⁾ the superiority of decompressive craniectomy to craniotomy is still controversial.^58–60)

As an alternative strategy, emergency trephination has been widely accepted as an initial procedure for ASDH presented with impending herniation.^61–63) Trephination is a quick and easy technique to reduce ICP by evacuating hematoma. However, hematoma evacuation may often result in partially, ICP reduction may be often temporary, and hemostasis may not be obtained occasionally. Thus, emergency trephination should be followed by craniotomy or craniectomy. In recent years, trephination has been also applied as a minimum invasive procedure for elderly or patients with certain risks for craniotomy or craniectomy. As another aspect of trephination, hematoma irrigation with trephination therapy (HITT) has been also applied.⁶⁴⁾ The concept of this procedure is to evacuate subdural hematoma as much as possible, and to handle parenchymal injury under physiological condition, in order to reduce unfavorable effect of decompressive craniectomy, such as exacerbation of edema. The above-mentioned initial trephination strategies seem to have relatively good outcome, however, the superiority to other procedures are still controversial.