Surgical Management of Traumatic Brain Injury

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CHAPTER 335 Surgical Management of Traumatic Brain Injury

Approximately 1.5 million head injuries occur every year in the United States, with 250,000 patients requiring hospitalization and 52,000 dying of the injury.1 At least 5.3 million Americans, 2% of the U.S. population, are currently living with disabilities resulting from traumatic brain injury (TBI).2,3 Furthermore, TBI is the leading cause of death and disability in children and adults 1 to 44 years of age.1 When compared with most severe medical conditions, TBI has a predilection for the young. This magnifies the economic impact of TBI as one considers the cost of long-term care coupled with the loss of productivity from an active sector of the workforce. Even with this growing appreciation of the consequences of TBI, the number of injuries continues to climb. Hospitalization rates for TBI have increased from 79 per 100,000 in 2002 to 87.9 per 100,000 in 2003.1 In “newly mechanized” countries such as Vietnam, Columbia, China, and Brazil, the numbers are much higher, and greater effort toward prevention of TBI is needed.

Management of TBI presents extensive challenges for neurosurgeons worldwide. The complexity of the injury, which is usually associated with trauma to other organ systems, makes decisions about medical or surgical management critical to patient outcome. Gennarelli and coworkers showed that the overall mortality is 3 times higher in trauma patients with head injury than in those without intracranial trauma.4 Their study also showed that among head-injured patients, the cause of death was attributed to brain injury in 67.8%, to extracranial injuries in 6.6%, and to both cranial and extracranial trauma in 25.6%. The severity of the head injury still remains the strongest predictor of overall outcome in multiply traumatized individuals.46 In the past, many neurosurgeons regarded surgery for posttraumatic intracranial hematoma (ICH) to be unrewarding. This pessimism was based on the belief that outcome is determined principally by the magnitude of the initial injury and that it frequently remains poor despite optimal surgery. In fact, in the Traumatic Coma Data Bank series, only 37% of comatose patients underwent surgery for the removal of ICH.7 Although the mortality rate after severe head injury remains as high as 30% to 35% in some series, it has fallen to as low 20% in centers that treat brain injury frequently and aggressively.

The most dangerous consequence of severe TBI is the development of ICH, also known as “mass lesion,” which accounts for approximately 70% of the causes of clinical deterioration. One publication reported the incidence of ICH to be 25% to 45% in patients with severe TBI, 3% to 12% in those with moderate TBI, and 1 in 500 in those with mild TBI.8 Consequently, prompt and aggressive identification of ICH is of paramount importance during the evaluation of a patient with severe TBI. At least 25% of patients with mass lesions will clinically deteriorate in the initial 2 to 3 days after injury.9 This is especially true for contusions, notoriously known to blossom, as opposed to epidural hematoma (EDH) and subdural hematoma (SDH). The most commonly encountered ICHs are SDH, EDH, intraparenchymal hematoma and contusions, and posterior fossa hematoma. Surgery plays a vital role in the management of patients with severe TBI and concomitant ICH. Additionally, other complications of TBI that may warrant surgical intervention include depressed skull fractures, sinus injuries, and intractable intracranial hypertension requiring decompressive craniectomy. In general, the decision to operate is based on (1) findings on computed tomography (CT), (2) clinical neurological status, (3) clinical deterioration, and (4) extent of extracranial injury. High-volume lesions (>50 cc) customarily undergo surgery, whereas small lesions (<25 cc) are usually managed with conservative therapy. Once the indications for surgery have been met, early and urgent surgical intervention is suggested to prevent further neurological decline, minimize perilesional edema, improve the local metabolic environment, and attenuate evolving ischemic changes. Interestingly, blood constituents were shown to worsen focal ischemia in a study comparing equal volumes of hematoma with an inert fluid used to generate experimental intracerebral mass lesions.10 However, the ischemia was not improved after removal of the hematoma. Mass lesions can also alter cerebral metabolism, and their removal has been shown to improve jugular venous saturation indices.11

Conservative Management

Only a third of patients who sustain severe head injuries are candidates for craniotomy, and hence a majority of patients are managed by nonsurgical means. The strategy for nonsurgical management of TBI is focused on prevention of secondary injury after TBI. Medical interventions are targeted at controlling intracranial pressure (ICP), ensuring adequate blood flow and oxygen delivery, correcting and then maintaining a healthy metabolic environment, and minimizing edema. Improvements in early resuscitation, diagnosis, neurophysiologic monitoring, and emergency surgical treatment of head injury victims may be reaching a plateau in terms of further reducing mortality and morbidity. Refinements in neurocritical care combined with technologic advancements in diagnostic and monitoring devices continue to offer new avenues for enhancing outcome. This subject is covered fully in Chapter 334.

About two thirds of patients with severe head injury have no significant mass lesion on the initial CT scan. At least 25% of patients with mass lesions will clinically deteriorate in the initial 2 to 3 days after injury.9 This is especially true for contusions, notoriously known to “blossom,” especially when occult or overt coagulopathy is present. At least 80% of patients with severe TBI have high ICP, and in the majority who die, high ICP is the cause of death.1215 For this reason, ICP monitoring and ICP-directed intensive care therapy are advocated for all patients older than 40 years whose Glasgow Coma Scale (GCS) score remains 8 or lower at 6 or more hours after injury. In patients younger than 40 years, ICP monitoring can be based on the status of the basal cisterns as demonstrated on good-quality CT. Effaced cisterns are associated with high ICP in more than 70% of patients and mandate ICP monitoring. In patients younger than 40 with patent cisterns, normal findings on CT, and the absence of hypoxic or ischemic episodes, ICP monitoring can be deferred and repeat CT performed in 6 to 12 hours.14 Among the most difficult neurotrauma patients to manage are those whose GCS scores are between 8 and 14 and who have mass lesions of intermediate size. Frequently, they are restless, combative, uncooperative, or intoxicated, thus making GCS assessment very difficult. In such circumstances, it is usually best to intubate, sedate, and ventilate the patient in an intensive care setting and carry out ICP monitoring. Appropriate management of these moderate TBIs and medium-sized hematomas is the biggest difference that clinicians can make. If ICP is persistently greater than 20 to 25 mm Hg, surgical evacuation is indicated even for small mass lesions because associated brain swelling is extremely common.

The Medical College of Virginia first proposed a “staircase” of therapeutic steps to optimally treat elevated ICP (Fig. 335-1). The early, aggressive management of ICP by surgical or medical means is directed primarily at optimizing cerebral blood flow (CBF) and preventing cerebral ischemia and the consequent irreversible neurological deficits and mortality (Fig. 335-2A). Nonsurgical management is detailed in the third edition of the “Guidelines for the Management of Severe Traumatic Brain Injury.”16 Uncal herniation with midbrain compression and Duret’s hemorrhages of the brainstem are the usual postmortem findings in patients who succumb to untreatable intracranial hypertension (Fig. 335-2B and C). Management decisions in individual patients must take into account a number of factors, such as extracranial injuries, the age of the patient, preexisting conditions, and the presence of associated intracerebral contusions or hemisphere swelling. In patients with intraparenchymal lesions, such as contusions and intracerebral hematomas, management decisions are more complex and difficult given the risk for coagulopathy and bleeding. Some recent studies have provided guidelines for the management of SDH and extradural hematoma in the relatively uncommon situation of a fully conscious patient. Nonoperative management should be considered only if the patient is fully conscious, the extra-axial mass lesion is the single dominant lesion (i.e., there are no multiple contusions or potentially significant contralateral mass lesions that may be preventing midline shift), and there are no features of a mass effect, such as a midline shift greater than 3 mm, or basal cistern effacement.17 If these criteria are met in a conscious patient with an acute subdural hematoma (aSDH) less than 10 mm at its thickest point, conservative treatment has been shown to be successful in most cases.18 Similarly, deep-seated tentorial or interhemispheric SDHs (Fig. 335-3) and small extradural hematomas in a stable, conscious patient frequently do not require surgical evacuation. However, when doubt exists and consciousness is depressed, the neurosurgeon should always monitor ICP or remove mass lesions in such patients.

Indications for the Evacuation of Intracranial Hematomas

Until recently, the role of surgery in the management of TBI was often based on subjective criteria or previous experience of the surgeon. Most would agree that surgical evacuation is always indicated for a mass lesion when there is a decline in the patient’s level of consciousness, the development of new focal signs, and severe and worsening headache, nausea, or vomiting. In unconscious, noncommunicating, or sedated and ventilated patients, surgical evacuation is always indicated when there is a decline in neurological status (this may be revealed only by the development of new “brainstem” signs) and a sustained increase in ICP (e.g., >25 mm Hg). CT should be done urgently to evaluate progression of the ICH and brain swelling, and blood gas analysis should be performed to exclude the onset of hypoxemia, if appropriate. An increase in the size of an ICH on CT is also an indication for surgical removal.19

In 2006, a joint venture of the Congress of Neurological Surgeons and the Brain Trauma Foundation published the “Guidelines for the Surgical Management of Traumatic Brain Injury.”20 The publication is the product of an extensive review of the literature dating from 1975 to 2001. The authors applied the principles of “evidence-based medicine” throughout the evaluation process, but the paucity of well-designed, randomized controlled trials for surgical lesions prohibited classification of the literature with the “level of evidence” categories now customary in constructing guidelines. Instead, the results are presented as “literature-based recommendations.” Five primary complications of TBI warranting surgical consideration were identified: acute epidural hematomas (aEDHs), aSDHs, traumatic parenchymal lesions, posterior fossa mass lesions, and depressed cranial fractures. Worthy of special consideration are temporal lobe hematomas (Fig. 335-4), which are especially treacherous and dangerous. They may cause brainstem compression at low ICP with little midline shift, and the threshold to operate should thus be much lower. Finally, in patients who require operative intervention, urgent and rapid evacuation of the mass lesion ensures the best outcome because ischemic brain damage is dependent on the duration of ischemia. The specific recommendations in the aforementioned document are presented in the following sections.

Intraparenchymal Hemorrhage and Contusions

Evaluation of Relevant Findings on Computed Tomography

Preoperative Preparation

Frequently, surgery in the setting of TBI is done under emergency conditions, but nevertheless, every effort should be made to continue resuscitative efforts and optimize a patient’s neurophysiologic status while preparing for surgery—all of which may need to be accomplished in less than 10 minutes. Certain goals have been found to correlate with improved outcome in the setting of severe TBI and are outlined in the third edition of the “Guidelines for the Management of Severe Traumatic Brain Injury.”16 These goals include maintaining mean arterial pressure greater than 70 mm Hg (>90 mm Hg until cerebral perfusion pressure [CPP] can be measured), CPP higher than 60 mm Hg, euthermia, eucapnia, oxygen saturation greater than 93%, PaO2 of 95 to 100 mm Hg, ICP higher than 20 mm Hg, and a serum sodium concentration of 135 to 145 mEq. All patients with severe head injury should be intubated to protect the airway, ensure adequate oxygenation, and control PaCO2 at the appropriate level. Prophylactic hyperventilation or the use of mannitol is no longer recommended unless the patient exhibits focal neurological signs (contralateral weakness, ipsilateral anisocoria or “blown pupils,” decerebrate or decorticate posturing). If this is the case, the patient is best hyperventilated to a PaCO2 of 30 to 32 mm Hg and given 1 g/kg of mannitol immediately while being taken to the operating room.

Finally, preoperative assessment must always rule out coagulopathic states. This is especially important in view of the increase in TBI among the growing elderly population. The frequent use of anticoagulant and antiplatelet drugs, often for marginal indications, can generate dangerous operative conditions. Qualitative platelet disorders have been described in those with chronic alcoholism and chronic aspirin ingestion. The recent development plus use of recombinant factor VIIa (rFVIIa) has provided a new option in the management strategy for these patients. rFVIIa is thought to induce hemostasis within 10 minutes of administration and has been used successfully to decrease hematoma expansion in patients with hypertensive hemorrhage and trauma.25,26 Recently, rFVIIa was shown to decrease the time needed to normalize coagulopathic trauma patients and allow earlier surgical intervention.27 By decreasing the time to invention it is hoped that outcomes can be improved as well. However, rFVIIa is very expensive, has been linked to increased thromboembolic complications, and has a relatively short half-life of 2 to 3 hours. Research is still ongoing to determine the optimal dose of rFVIIa in patients with TBI. However, in coagulopathic patients requiring urgent normalization for emergency surgery, such as those with herniation, it is suggested that 20 to 40 mg of rFVIIa, 5 to 10 mg of vitamin K intravenously, platelets, and fresh frozen plasma (FFP) be administered as determined by preoperative laboratory work. Because of its short half-life, rFVIIa may need to be redosed if further normalization is necessary based on the partial thromboplastin time (PTT) and international normalization ratio (INR). Finally, in addition to its hemostatic actions, rFVIIa was unexpectedly shown to be neuroprotective by reducing hippocampal neuronal degeneration, as well as the extent of traumatic axonal injury, in an animal model of TBI.28

Before or during preparation for craniotomy, the following checklist should be completed:

Figure 335-5 shows how a patient is positioned for a craniotomy. In general, the head is placed on a horseshoe or “doughnut” headrest, turned to the opposite side while avoiding any constriction of the neck veins, and elevated above the level of the heart. A sandbag placed beneath the ipsilateral shoulder makes turning the head easier and also relaxes the tissues in the neck. The pressure points should be padded carefully. Unless deterioration is rapid, the scalp should be shaved and prepared as for any other neurosurgical procedure.

Strict attention to anesthetic techniques is vital to avoid hypercapnia and further elevation of ICP. All inhaled anesthetics have a potential cerebral vasodilator effect and may therefore increase ICP. They also lower cerebral metabolism, with the exception of nitrous oxide (N2O). Thus, a beneficial dissociation of CBF and the cerebral metabolic rate of oxygen (CMRO2) may occur with their use.2931 N2O was used widely in the past to maintain anesthesia, and its rapid action allows easy control of the depth of anesthesia. However, because there is evidence that N2O may increase ICP as a result of vasodilation and because the interaction of N2O with volatile and intravenous anesthetics is complex, N2O should be avoided in surgery after acute central nervous system trauma. Similarly, the use of volatile agents (halothane, enflurane, sevoflurane, desflurane, and isoflurane) has had its drawbacks. Use of halothane for surgery on intracranial lesions has decreased in recent years, although it may be safe in low concentrations (≈0.5%), because it can also increase ICP and uncouples CBF and CMRO2 in a dose-dependent manner, thereby producing cerebral vasodilation and a decline in CMRO2.31 Enflurane, like halothane, is a cerebral metabolic depressant but has weaker vasodilatory properties. Because of its potential effects on ICP and the risk of inducing seizures, high concentrations of enflurane should be avoided in neurosurgical patients. Sevoflurane and desflurane have cerebrovascular effects similar to those of enflurane and should also be avoided. Isoflurane is not as lipid soluble as other volatile agents. Because of its depressive effect on cerebral metabolism, isoflurane may be neuroprotective and is a more desirable anesthetic for neurosurgical procedures among the inhaled anesthetic agents. Isoflurane also produces a moderate increase in CBF and a pronounced beneficial decrease in cerebral metabolism.

Intravenous anesthetics also cause a decrease in CBF and CMRO2 because of their depressant effect on cerebral metabolism. In recent years, propofol has become the “mainstay” of most anesthetic and sedation regimens for patients with TBI. Propofol’s metabolic effect on cerebral metabolism is similar to that of barbiturates and it may decrease ICP.32 This drug is very useful in neurosurgical patients for sedation and as an anesthetic, provided that hypotension is prevented. Barbiturates (thiopental, pentobarbital) produce a potent dose-dependent reduction in CBF, CMRO2, and ICP, as well as a burst suppression pattern on electroencephalography (at about a 40% decrease in CBF). Barbiturates also attenuate the cerebral vasodilation produced by volatile anesthetics.33 Etomidate has metabolic effects similar to those of barbiturates, and both may be used for “cerebral protection” and to control brain swelling intraoperatively after TBI.34 Benzodiazepine derivatives (e.g., midazolam) are also useful as induction or supplemental drugs during anesthesia in neurosurgical patients with TBI. A newer agent currently under intense scrutiny for use in neurosurgery is dexmedetomidine. It is an α2-agonist that has been promoted as a sedative that does not cause respiratory depression. Although its full utility in neuroanesthetic practice is still being investigated, it is primarily used in operative settings requiring patient interaction and very rapid onset/offset times (e.g., functional cases and awake craniotomies). At the current time, its role in TBI appears to best be suited to the intensive care unit in patients requiring mild sedation yet frequent neurological assessment. More studies are needed to establish the cost-effectiveness and utility of dexmedetomidine versus older agents, such as propofol.

Narcotic analgesics (morphine, fentanyl, sufentanil) have modest depressive effects on CBF and CMRO2, and in most circumstances they have only a minimal effect on ICP. They should generally be avoided or used in small amounts during anesthesia for acute central nervous system trauma because of their long duration of action and the availability of other agents.35

The use of nondepolarizing muscle relaxants (tubocurarine, pancuronium, atracurium, vecuronium) changes CBF and ICP only minimally if respiration is well controlled. If succinylcholine is used, a small dose of a nondepolarizing muscle relaxant should be given before its administration to prevent a rise in ICP with fasciculation.36


A ventriculostomy catheter serves two basic purposes. It is the “gold standard” method for measuring ICP, and it provides drainage of cerebrospinal fluid (CSF) to lower ICP. The procedure can be done at the bedside under local anesthesia and is usually a quick and effective method of reducing raised ICP. Before placement, however, coagulopathy must be excluded by checking the prothrombin time (PT), PTT, and platelets, and rapid correction may be needed.

After shaving the scalp and sterile surgical preparation, the patient’s head is placed supine. A small incision (<3 cm) is made in the midpupillary line, 4 cm from the midline and 2 cm in front of the coronal suture on the right side (Fig. 335-6A). The incision is carried down to the underlying bone, and the periosteum is elevated. If the coronal suture cannot be felt easily under the scalp, a distance of approximately 10 cm is measured upward and posteriorly from the superior orbital margin in the midpupillary plane. Next, a twist drill is used to make an opening in the skull perpendicular to the plane of the skull. The twist drill hole is cleaned of any bony fragments with a small curet, and the underlying dura is pierced with a blunt stylet. A ventriculostomy catheter is placed with use of the standard landmarks while keeping the trajectory of the cannula in the coronal plane of the coronal suture and aiming at the medial canthus of the ipsilateral eye (Fig. 335-6B and C). A distinct “popping” sensation is usually felt as one reaches the frontal horn of the lateral ventricle. This should occur when the tip of the ventricular catheter is 7 to 10 cm from the surface of the skull, which usually means that it is at the opening of the foramen of Monro of the ipsilateral frontal horn. Return of CSF should be apparent; if not, another pass should be made. The catheter should not be advanced more than 10 cm from the skull because of the risk for damage to the diencephalic structures. The ventriculostomy catheter is tunneled for a few centimeters in the subgaleal space (Fig. 335-6D) and brought out through a separate stab incision. It is then secured firmly to the skin with sutures and connected to the pressure transducer system.

The standard landmarks may be altered in patients with intracranial mass lesions because of the associated brain swelling, which results in slit-like ventricles, and because of shift of the ventricles as a result of mass-producing lesions. No more than three passes should be made to reach the ventricles before placing intraparenchymal pressure monitoring devices (e.g., the Codman or Camino transducer-tipped device).

For the placement of intraparenchymal monitoring devices, the twist drill opening is made as described earlier. After opening the dura with a blunt stylet, the transducer tip is placed directly in the brain parenchyma at a distance of 2 to 3 cm. The catheter is then tunneled under the skin. A fixation bolt may be useful for these devices (Fig. 335-6E).

Before leaving the operating room, a ventriculostomy catheter should be placed in all patients with an initial GCS score of 8 or less because raised ICP requiring treatment develops in at least 80% of these patients.12,13,37 It may also be placed under direct vision before closure of the bone flap.

Exploratory Bur Holes

In the modern CT era, neurosurgeons seldom need to use exploratory bur holes. However, every neurosurgeon should be familiar with the procedure and be prepared to proceed to a full craniotomy because CT may be may be unavailable in some instances (e.g., during military campaigns or disasters) and acute traumatic hematomas cannot be dealt with adequately through bur holes.

The patient is placed supine with the head preferably in a head holder, which also gives wide access to both sides (Fig. 335-7B). The whole head is shaved, prepared, and draped to allow access to the frontal, parietal, and temporal areas. The bur holes are typically placed on the side of localizing neurological findings—ipsilateral to a dilated pupil, contralateral to the most abnormal motor response, and ipsilateral to a skull fracture. It must be stressed that none of these signs are absolute and that if no hematoma is found on the suspected side, the other side should be explored in all cases. Initially, a bur hole is placed in the temporal region 2.5 cm above the zygomatic arch (see Fig. 335-7A). After diagnosis of either an acute subdural or extradural hematoma or no hematoma, two additional bur holes can be placed appropriately in the parietal and frontal regions. The skin incisions must be made in such a manner that if a formal craniotomy is required, they can be joined to form the skin flap (see Fig. 335-7A).

General Considerations for Supratentorial Hematomas

Craniotomy Technique

Scalp Incision

The superficial temporal artery should be palpated and marked and the vertical limb of the incision placed between the artery and the tragus. The skin incision is started at the zygomatic arch and then curved backward to the parietal eminence and upward above the auricle to reach 2 cm from the midline. It is then carried forward to the frontal region and curved across the midline just behind the hairline (Fig. 335-8A). In balding patients, the frontal part of the incision may be carried into the forehead, but it should be closed with 5-0 nylon suture for a good cosmetic result. The incision can be made with a scalpel, although use of a needle-tipped (Colorado) Bovie may minimize scalp bleeding. Hemostasis of the skin margins is achieved with Raney clips or electrocautery. Then, using a Bovie cutting diathermy device, an incision is made in the superficial temporal fascia and in the temporalis muscle down to the bone, close to the margin of the skin opening. The myocutaneous flap is then reflected inferiorly and secured. Ideally, the margins of the bony craniotomy should be approximately 15 by 12 to 15 cm in size.

Rapid Temporal Decompression

In a patient who has herniated or whose condition is deteriorating from an ICH, the temporal end of the incision is opened rapidly, for 3 to 4 cm only, and a bur hole is made. This opening is then rapidly extended with Leksell rongeurs to form a limited craniectomy about 3 cm in diameter (see Fig. 335-8A). If the hematoma is in the subdural space, the dura is opened, and the underlying hematoma is promptly evacuated (Fig. 335-8B). This procedure helps reduce ICP as early as possible and allows the craniotomy to then be completed more slowly, with better hemostasis.

Bone Flap

Multiple bur holes (five to seven) are placed in the parietal and frontal regions (see Fig. 335-8A) with an ACRA-CUT bit for the Midas Rex or Anspach drill systems (or an 8-mm cutting bur). The bur holes are then enlarged with a Kerrison bone punch and undermined to allow a Penfield No. 3 dissector to slide between the dura and the inner aspect of the bone flap for gentle separation of the dura from the skull. Special care is needed at this stage near the sagittal sinus. If the dura is torn during this step, it is desirable to drill extra bur holes to prevent inadvertent lacerations of the dura by the craniotome. Joining the bur holes with a craniotome completes the craniotomy opening. The bone flap is fashioned so that its medial margin is at least 1.5 to 2 cm from the midline. If greater medial exposure is needed, it can be carried out more safely with Leksell rongeurs under direct vision. Further exposure of the middle fossa is obtained with the use of Leksell rongeurs to remove parts of the lateral sphenoid wing and the temporal bone in piecemeal fashion, as low as needed, for temporal tip access. The first goal after removing the bone flap is decompression of any mass lesions that may be present.

Dural Opening

Any dural opening should be carefully planned to avoid injury to the underlying brain tissue or venous sinuses, facilitate closure, and in the case of TBI, deal with intraoperative swelling. Commonly described techniques include a C-shaped durotomy based on the sagittal sinus, a cruciate opening, and a “basal” or “reversed U-shaped” durotomy. We favor “basal durotomy” (Fig. 335-8C) because it is a technique that is particularly useful in dealing with massive intraoperative swelling.38 With this technique, a No. 15 scalpel blade is used to start the dural incision at the frontobasal eminence of the frontal lobe anterior to the pterion. A second durotomy is begun over the lowest part of the temporal lobe so that the temporal tip may be removed, if major brain swelling ensues, after any subdural clots are removed. The dura should not be cut near the midline to avoid damage to the parasagittal bridging veins. Instead, the dural flap should be based along the sinus. The incision is carried low across the middle meningeal artery toward the temporal lobe to fashion the reversed U-shaped dural opening. Care is taken to protect the underlying brain tissue with a cottonoid pad if indicated. This durotomy technique permits good access to the basal frontal and temporal lobes and prevents parasagittal herniation of the frontal lobe and occlusion of bridging veins against the dural edge. Next, smaller slit incisions may be made circumferentially around the craniotomy (although not parasagittally) to grant additional access for removing the hematoma (i.e., over the convexities). Once the hematoma is removed, the surgeon may decide to connect and complete the full extent of the durotomy, depending on the amount of swelling present or how much visualization is needed to adequately address the surgical goals.

Epidural Hematoma

In 1990, Pickard and coworkers showed that surgical management of posttraumatic EDH is one of the most “cost-effective” of all surgical procedures in terms of quality of life and years preserved.39 EDH is estimated to complicate 2.7% to 4% of TBIs, with a mortality rate of approximately 10%. However, EDH does not always occur in isolation. Associated ICHs are found in 30% to 50% of patients with surgically evacuated EDHs.20 EDHs are located primarily in the temporal (see Fig. 335-4) and temporoparietal regions and are usually caused by tears in the anterior or posterior divisions of the middle meningeal artery with an associated linear fracture of the skull. Bleeding can also originate from the middle meningeal vein, the diploic veins, or the venous sinuses. One study reported an arterial source of bleeding in only 36% of adults and 18% of children.40 The deformation of the skull is probably responsible for initiating the process of dural stripping. As the hematoma enlarges, the dura is progressively stripped from the inner table. The blood in the epidural space is usually clotted (Fig. 335-9). Sometimes, depressed skull fractures overlying the major venous sinuses are associated with EDHs. Posterior fossa EDHs, which often extend above and below the tentorium, account for approximately 5% to 10% of these lesions.41,

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