7.1  Intracranial Injuries

7.1.1  Statistics: Intracranial Injuries

in CF Fractures

Depending on the size and extent of the osseous injuries to the craniofacial area, there are associated intracranial injuries in about 20–30% of the cases (Manson et al. 1987; Neidhardt 2002). In the present series, 56% of all patients were found to have at least a dural tear, whereas in only 17% a dural injury was suspected before surgery. On imaging studies, additional cerebral contusions were seen in 42%, brain oedema in 11% and intracranial hemorrhages in 25%.

Frequency of intracranial injuries in craniofacial fractures (Neidhardt 2002/MKG-Luzern)

7.1.2  Principles of Neurotraumatology

(Rengachary and Ellenbogen 2004)

The basic management principles for patients with traumatic brain injury (TBI) apply equally to those who happen to sustain a craniofacial injury.

Head injuries are probably the most common condition neurosurgeons have to deal with. Even though

1Contributed by Karl Kothbauer, Kantonsspital Luzern (CH), Neurosurgical Department, Luzern, Switzerland­

it is commonly believed that mortality from head injury has significantly declined over the past five decades due to a major improvement in immediate medical care, TBI continues to be a major cause of mortality and morbidity, particularly in the young and it will remain so in the foreseeable future.

The treatment goal is orientated in two directions. Firstly, to repair the immediate effects of the primary injury and facilitate healing. This is mostly achieved with surgical intervention. Secondly, to prevent the development or at least minimize the effects of secondary injury.

This is attempted with medical treatment, such as adequate oxygenation and maintenance of ­cardiovascular, cerebrovascular, fluid, and electrolyte homeostasis. Depending upon circumstances, this also requires surgical intervention, such as drainage of cerebrospinal fluid (CSF) or decompressive craniectomy.

• Classification of head injuries

Neurosurgeons and neuroscientists use different aspects of TBI for its classification:

Severity of injury, mechanism of injury, morphology with focal or diffuse lesions, as well as course of time in primary and secondary injuries

• Severity

Since its inception in 1974, the Glasgow Coma Scale (GCS) has gained worldwide acceptance in describing the level of consciousness of patients after trauma and in nontraumatic conditions affecting consciousness (Tables 7.1 and 7.2).

Thescaleissimple,language-,andculture-­independent and provides a high interobserver reliability. It is used to categorize the severity of head injury into three groups (Teasdale and Jennett 1974).

Only patients with severe head injuries are unconscious (i.e., GCS 8 or smaller).

• Mechanism

Closed head injuries are all injuries without an open communication between the outside and the brain and/ or CSF spaces. Stab and gunshot wounds are referred to as penetrating injuries. Obviously overlap and combinations exist. The majority of craniofacial injuries therefore fall into the category of open head injury.

• Morphology

Initial imaging studies enable structural brain injuries to be anatomically distinguished between diffuse and

Table 7.1  Glasgow Coma Scale

focal brain injuries. Again overlap exists, as every TBI, however mild, with a history of brief loss of consciousness and a memory gap is by definition a mild type of diffuse brain injury and usually one that shows no focal signs of injury on computed tomography (CT) imaging. Extracerebral hematomas, circumscribed brain contusions, traumatic subarachnoid hemorrhage, skull, or skull base fractures are focal injuries that may occur in any severity category as defined by GCS.

• Time course

The initial physical impact causes a primary injury which may affect the brain and soft tissues with lacerations, fractures, contusions, etc.

A massive wave of secondary injuries may occur in patients with severe head injuries in the days following the initial trauma. This may result in elevated intracranial pressure (ICP) and consequently in relative impairment of brain tissue oxygenation and disruption of cerebrovascular autoregulation. The secondary injury forms the basis of all surgical and intensive care measures used for patients with severe head injuries.

• Patient assessment

As far as possible, a neurological examination is required for each patient with TBI, in addition to assessing the GCS. This includes pupillary size, symmetry, and response to light, eye movements, oculocephalic testing, motor power and testing of sensory function. Certainly note must be taken of additional injuries, such as spinal injuries, thorax, and abdominal injuries, peripheral fractures and craniofacial injuries.

• Diagnostic imaging

Cranial CT (CCT) is the modality of choice to evaluate all cranial injuries. For the neurosurgeon, the standard X-rays have become increasingly irrelevant in the light of excellent high-resolution and readily available CCT. Magnetic resonance imaging (MRI) may reveal additional information that may not be apparent on CCT, such as multiple small lesions in patients with normal CT scans. However, at present, MRI is not routinely used for head-injury patients. Other modalities such as cerebral angiography are used in rare cases of vascular injury at the skull base or after penetrating head injuries.

7.1.3  Management of Mild Head Injuries

(GCS 14-15)

Mild head injuries make up 80% of all head injuries, e.g., traumas with brief loss of consciousness and amnesia.

• Diagnostic workup (Stiell et al. 2001)

Since only about 3% of all patients with mild head injuries are believed to deteriorate due to an intracranial lesion, which develops in the hours following the initial injury, there is considerable controversy about the pros and cons of optimal versus most cost-effective management. Risk factors from delayed deterioration have been established in various efforts to clarify this issue and put it beyond personal or institutional “policy”. These risk factors include: ambiguous accident history, high-impact trauma (e.g., man vs truck), retrograde amnesia over 30 min duration, continued GCS < 15 2 h after injury, clinical, or radiographic evidence of skull fractures, or skull base fractures, age over 60–65 or under 2 years, coagulation disorders or medical anticoagulation with vitamin K antagonists or treatment with platelet inhibitors.

There are no guidelines as to whether or not blood tests should be obtained routinely. It is probably advisable, since the patients are being checked for a possible lesion which may require emergency surgical intervention.

These risk factors characterize victims with mild head injuries who should be referred to CT scanning.

• Intervention

With or without CT scan, it is advisable to keep the patient in hospital for 24 h for neurological and medical observation. There are no strict management guidelines and without doubt in many institutions patients are discharged into the care of their families when a CT scan has documented the absence of an intracranial mass lesion.

Decrease in GCS by two points must prompt a CCT or a repeat scan if the former was normal. The presence of a mass lesion may then require surgery. If this is not the case it may be possible to discharge such a patient after approximately 24 h, similar to patients with no clinical deterioration.

• Rehabilitation

Most patients with mild head injury will not require additional care 2 weeks post injury. Protracted headaches

and mild disturbances in memory regeneration and concentration may occur.

7.1.4  Management of Moderate Head

Injuries (GCS 13-9)

About 10% of patients with TBI suffer from mild head injuries. About 10% of this group will deteriorate and loose consciousness shortly following trauma.

• Diagnostic workup

CCT is indicated for all patients in this group. An abnormal scan should be repeated after 24 h even if no surgical intervention is necessary. All patients must also have definitive imaging of the cervical spine, nowadays preferably a spiral CT, which provides optimal imaging and avoids tiring discussions about incomplete visualization of the cervicothoracic section. These patients should have a routine preoperative laboratory workup.

• Intervention

Patients with moderate head injuries are monitored in the same way as those with mild head injuries. However, it is unlikely that discharge is possible after 24 h. Even if no deterioration or further problems occur, such patients are likely to remain hospitalized for a minimum of 2–4 days.

• Rehabilitation

A significant number of patients with moderate head injuries will require at least some form of rehabilitation. This may be on an inpatient or outpatient basis.

7.1.5  Management of Severe Head

Injuries (GCS 8-3)

Patients with severe head injuries, unable to follow commands,­ require urgent and persistent attention. Cardiorespiratory stabilization is the first priority for these patients. Hypotension <90 mmHg of systolic

blood pressure is associated with subsequent ICP elevation and poor outcome. Patients in this category must be intubated early.

• Diagnostic workup

Cranial CT and CT of the cervical spine are obligatory studies. Other imaging studies must be done as appropriate since additional severe injuries are frequent, such as long-bone or pelvic fractures (30%), craniofacial injuries (20%), chest injuries (20%) or intrathoracal and intraabdominal injuries.

The neurologic examination beyond assessment of the GCS may be limited to pupillary size and response to light, blink reflex and oculocephalic maneuvres, as well as caloric vestibular testing. Bilaterally dilated and fixed pupils indicate severe transtentorial herniation and inadequate brain perfusion.

Additional imaging studies, such as MRI, may be indicated for associated spinal cord injury. Cerebral angiography may at times be important in case of severe orificial hemorrhage, which may only be controlled by endovascular techniques.

Common findings on CCT are intracranial mass lesions, such as epidural and subdural hematomas. These require craniotomy and evacuation in most instances (see below). Furthermore, brain contusions may be seen as hypodense areas or hyperdense in case of hemorrhagic contusion.

Traumatic subarachnoid hemorrhage is a frequent finding and indicates added severity of the initial injury but does not carry similar significance in and of itself as subarachnoid hemorrhage from spontaneous rupture of a cerebral aneurysm. Air inclusion indicates open fracture or skull base fracture. Today, fractures are well visualized with high-resolution spiral CT scanners.

Further findings on CT scans may be ventricular hemorrhage or diffuse cerebral edema. Hemorrhagic contusions are usually located at the base of the frontal and temporal lobes, wherever the cortex borders onto rugged bone edges of the skull base. So-called “contrecoup” contusions are frequently seen opposite to the impact site.

•Management of severe head injuries (Markwalder and Seiler 1985)

At times, an intubated and sedated patient delivered to a trauma centre with a presumed low initial GCS may have a normal CCT. Under certain circumstances it

may be in order to wait for such a patient to awaken or antagonize medication in order to fully assess the clinical situation. Many patients may, in fact, have higher GCS scores and the initial low scores may be the result of poor reporting or simply hemodynamic instability at the scene of the accident.

In all other circumstances, patients with severe head injuries must be monitored in the setting of an intensive care unit. An ICP monitoring probe should be placed, together with a ventricular drain. The latter provides direct hydrostatic ICP measurement and access to release CSF as a measure to reduce elevated ICP. Further monitoring probes may be placed in the cerebral parenchyma as appropriate. Differential measurements are often necessary to monitor brain temperature, tissue pO2, microdialysis, and jugular pO2. The comatose and, in most cases, heavily sedated patient cannot usually be assessed clinically and thus the physiological parameters measured with these devices, combined with hemodynamic parameters obtained from invasive measurements, substitute the direct monitoring.

All patients should have a second CCT within no more than 12 h of injury or if ICP rises above 25 mm Hg. This may indicate a secondary space occupying hemorrhage, which may require surgery. In the absence of a surgical lesion increasing ICP must be treated in conjunction with the cerebral perfusion pressure (CPP). Currently the recommended CPP is 60–65 mm Hg. The mean arterial pressure (MAP) may have to be adjusted with volume or vasopressors. CPP results from the MAP minus the ICP.

Intervention to keep ICP within normal limits should be initiated when ICP consistently exceeds 20–25 mm Hg.

There are numerous strategies utilized to lower ICP and therefore to preserve CPP to avoid secondary ischemic brain damage. Positioning the patient with the head and upper body elevated by 15–30° enables free venous outflow and thus helps keep ICP and cerebral circulation within normal limits. Sedation, preferably with a short-acting substance such as propofol reduces the body’s response to stress and blunts vegetative irritation, it also limits the brain’s oxygen requirements and thus helps prevent elevated ICP. Adequate pain medication with fentanyl or remifentanil minimizes pain induced stress, vegetative arousal and subsequent hypertension.

Mannitol is very effective in reducing elevated ICP but has the disadvantage of accumulating in contused areas of the brain where the blood brain barrier is disrupted. Thus, it may actually worsen the local swelling around contusions. Therefore, it should only be used in situations of critical ICP elevation; for instance, on the way to surgery with a newly detected hematoma. Long-term use in regular intervals, such as 2–4 h, should be discouraged.

Other diuretics, such as furosemide and azetazolamide, are effective in reducing CSF production and ICP in the absence of trauma. They are, however, rarely used in the setting of severe head injury, due to their limited efficacy in the TBI setting.

Hyperventilation is a very effective short-term intervention to lower elevated ICP. The physiologic response is due to cerebral vasoconstriction, which in turn reduces cerebral blood flow (CBF) and CBV and consequently ICP. It has been shown however, that sustained hyperventilation lowers the paCO2 to around 30 mm Hg or less. This increases the incidence of significant focal cerebral ischemia and, thus, has a net deleterious effect and a negative effect on outcome. Hyperventilation is, therefore, only used in critical situations (see above, like mannitol) or under the guidance of continuous measurement of global oxygen extraction with jugular pO2 assessment and, if available, with focal tissue pO2 measurement.

The use of steroids in TBI has been abandoned since the CRASH study proved the deleterious effects of steroids on long-term TBI outcome.

Barbiturates are very effective in reducing cerebral oxygen requirements, CBF, and thus ICP. However, the side effects of shutting down the airway clearance mechanisms, immune response dysfunction, hypotension, and subsequent requirement for increased need of vasopressors often make this treatment problematic. It should only be used in acute situations where other measures are not effective in controlling ICP and preserving CPP. The use of barbiturates is often discussed even after performing a craniectomy to control ICP.

Anti-epileptic drugs are frequently used on a prophylactic basis, particularly in the United States. However, sedation is in itself prophylactic for seizures and seizures in the acute phase of severe head injury in no more than 5–15%. The use of standard anticonvulsants, such as phenytoin, is also problematic as more recent studies have shown that patients who initially received this drug demonstrated a reduced rehabilitation response at a later phase. We only used anticonvulsants in patients who had suffered seizures.

7.1.6  Neurosurgical Management

of Intracranial Hematomas

The large majority of treatment recommendations for the management of traumatic intracranial mass lesions are experience-rather than evidence-based. No-one will ever undertake a prospective trial to prove that surgical evacuation of an epidural hematoma is superior

to conservative treatment! Nevertheless, the literature permits to formulate certain guidelines for the indications of surgery, use of adjuvant medical treatment and timing of intervention.

•Epidural hematoma (EDH) (Bullock et al 1996, 2006a)

EDHs are frequent in the younger age groups as the dura becomes increasingly adherent to the inner table with increasing age. Typically, the epidural clot evolves in the context of a skull fracture that crosses the course of a meningeal vessel, particularly the middle meningeal artery, which ruptures and bleeds. Patients with epidural hemorrhage are the classical “talk-and-die”

patients, as their initial injury may appear mild but their deterioration may be dramatic, and the course without intervention lethal.

EDHs are evacuated via a standard craniotomy centered on the location of the clot. Bleeding is controlled using bipolar coagulation and the dura must be secured to the skull using strong tack-up sutures.

Guidelines for surgical indications have recently been defined. Hematomas larger than 30 cm3 should be evacuated regardless of GCS and in a timely fashion. Nonsurgical management with serial imaging and close neurological monitoring can be used for smaller hematomas with thickness less than 15 mm and midline shift less than 5 mm and GCS greater than 8 and no focal neurological deficits (Figs. 7.1–7.3).

•Acute subdural hematoma (SDH) (Bullock et al. 1996, 2006b)

By and large the presence of an acute SDH indicates a more serious brain injury than the presence of an epidural clot. Direct brain injury with surface contusions is a frequent source of subdural bleeding, as is rupture of bridging veins as a result of traumatic shifting of the brain on impact.

Acute SDHs are usually evacuated via a large (“trauma flap”) craniotomy with bone flap removal

Fig. 7.4  Large SDH covering the right cerebral hemisphere (arrow)

and a duroplasty to provide room for brain swelling. It is advised to place an ICP probe as well as a ventricular drainage catheter at the same time in all patients with a GCS of 8 or less.

The recently published guidelines recommend surgery for acute SDHs with a thickness of greater than 10 mm or a midline shift of greater than 5 mm regardless of GCS. Furthermore, patients with acute SDHs smaller than indicated above but with a decrease of at least 2 points of GCS between injury and hospital admission and/or pupillary asymmetry and/or an ICP exceeding 20 mm Hg should also undergo surgery as soon as possible (Figs. 7.4 and 7.5).

• Parenchymal contusions (Bullock et al. 1996, 2006c)

Surgical management of traumatic parenchymal lesions depends upon the assessment of tissue damage exerted by a focal contusion and the effect such a lesion has on the overall elevation of ICP. Due to the ­heterogeneity of parenchymal lesions, treatment recommendations vary. Parenchymal lesions causing progressive ­neurological deterioration, medically refractory ICP ­elevation or mass effect on CT should be surgically removed.

Patients with GCS 6-8, who have frontal or temporal contusions greater than 20 cm3 and midline shift of 5 mm or greater and cisternal compression, as well as any patients with lesions larger than 50 cm3, should undergo surgery.

If surgery is performed, in the majority of cases it will be a craniotomy with the removal of the contusional hemorrhage and meticulous hemostasis. Other treatment options, such as large hemispheric or bifrontal craniectomies or smaller focal decompressions, exist and their applicability depends upon the individual circumstances (Figs. 7.6–7.9).

•Depressed skull fractures (Bullock et al. 1996, 2006d)

The management of depressed skull fractures has varied over the past two decades, from an aggressive surgical to a more conservative approach. The recent guidelines again put more emphasis on surgery and state that all management options include antibiotic prophylaxis. Indications for surgery are open calvarial fractures depressed to a greater extent than the thickness of the cranium or the risk of infection. Infections are best combated with surgery. Conservative management is an option, if there is no evidence of dural penetration, significant intracranial hematoma, frontal

sinus involvement, infection, pneumocephalus, or gross wound contamination. In order to prevent infection surgery should be performed early (Fig. 7.10).

•Chronic SDH (Markwalder 1981; Markwalder and Sailer 1985)

Chronic SDHs frequently (but not exclusively) occur in the elderly and are significantly associated with oral anticoagulation, use of platelet inhibiting medication, other factors reducing normal hemostasis, and a recent history of, often only mild, head trauma. Not infrequently they start as small, nonsurgical acute or subacute hematomas and then undergo a process of evolution. This includes the accumulation

of fluid, the formation of neomembranes and thus an increase in volume, which may cause a mass effect and consequently a variety of symptoms, including headache, gait problems, ataxia, confusion, dysphasia, and hemiparesis. Once significant symptoms are present, surgical evacuation is recommended, although spontaneous remission sometimes occurs.

Surgical techniques vary from single bur-hole drainage to double bur-hole drainage to craniotomy. Most authors recommend draining the liquid during surgery and leaving a subdural drain for 24 – 48 h to complete drainage and subsequent re-expansion of the brain. Chronic SDHs are rare in the context of craniofacial injury (Fig. 7.11).