The development of scientifically based management protocols for the treatment of TBI holds considerable promise for further improvement in outcome. The guideline movement in neurosurgery began in 1995 when the first edition of the Guidelines for the Manage-ment of Severe Traumatic Brain Injury was published as a joint effort of the Brain Trauma Foundation and the American Association of Neurological Surgeons (Brain Trauma Foundation 2000b). These Guidelines are composed of 14 topics, ranging from trauma systems and prehospital resuscitation to monitoring and treat-ment of intracranial hypertension and other intensive care treatments. It is important to understand that all Brain Trauma Foundation Guidelines per se are not practical clinical tools but rather summaries and reviews of scientific evidence. They must be embedded into a comprehensive, multidisciplinary treatment protocol that comprises all different aspects of patient care as well as geographical and infrastructure-related characteristics of a particular trauma center. In this chapter, we refer to four recently published, evidence-based documents covering the prehospital and in-hos-pital surgical and medical management of patients with severe TBI and their prognosis (Brain Trauma Foun-dation 2000a, 2000b, 2000c, in press). These docu-ments can be accessed via the Internet at http://
www.braintrauma.org.
Management of Severe TBI
Prehospital Management
The prehospital management of patients with severe TBI is outlined in Guidelines for Prehospital Management of Trau-matic Brain Injury (Brain Trauma Foundation 2000c). Rapid and physiologic resuscitation is the first priority in these patients. After stabilization of airway, breathing, and circula-tion, the GCS score should be determined by direct verbal or physical interaction with the patient. Patients with a GCS score between 9 and 13 should be transported to a trauma center, and patients with a GCS score lower than 9 should be brought to a trauma center with 24-hour computed tomog-raphy (CT) scanning capability, 24-hour operating room availability, and prompt neurosurgical care.
Comatose patients with a GCS score lower than 9 should be intubated. Patients who respond to nail-bed pres-sure or axillary pinch with abnormal extension, are flaccid, or have asymmetric and/or dilated pupils are presumed to have high ICP and should be hyperventilated at a rate of 20 beats per minute. All patients should have their oxygenation and blood pressure assessed at least every 5 minutes. Their oxy-gen saturation should be maintained above 90%, and their systolic blood pressure should be kept above 90 mm Hg. In the prehospital phase, hypoxia and arterial hypotension have been shown to be the most significant secondary insults. A single hypotensive episode has been shown to be associated with increased morbidity and a doubling of mortality (Ches-nut et al. 1993; Fearnside et al. 1993).
Typical Emergency Department Workup of Patients with TBI
A typical initial neurotrauma evaluation with possible critical findings is summarized in Table 3–2. The goals
of emergency department (ED) management are to determine the severity of the primary TBI, identify patients at risk for deterioration, prevent secondary brain damage, and identify associated injuries. ED patients with TBI or suspected TBI must be followed closely for neurological deterioration. A complete trauma workup should be initiated if there is any suspi-cion of associated injuries. Nausea and/or vomiting, progressive headaches, restlessness, pupillary asymme-try, seizures, and increasing lethargy should be inter-preted as signs of neurodeterioration, and a head CT scan should be obtained immediately. Blood alcohol level determination and urine toxicology screening should be considered in all patients presenting with TBI. Routine blood tests, including coagulation param-eters, should be obtained in patients with moderate and severe TBI and in patients with associated injuries. Tet-anus toxoid must be administered if there are any asso-ciated open wounds. Immobilization of the cervical spine using a hard collar is mandatory in all patients with TBI. Any complaint of neck pain should also lead to a radiographical assessment of the cervical spine, regard-less of a patient’s GCS score. All patients with moderate or severe TBI should undergo cervical spine imaging.
Maintaining brain perfusion is the guiding principle in managing comatose patients with severe TBI. The cor-nerstones of resuscitation of the patient with severe head injury are as follows:
• Primary survey with cervical spine control and brief neurological assessment
• Resuscitation (airway, breathing, circulation)
• Secondary survey with complete neurological ex-amination and determination of the GCS score (see Table 3–2)
In-Hospital Management of Severe TBI
Computed Tomography Scan Assessment
As soon as possible after resuscitation, all stable patients with severe TBI should undergo a CT scan of the head. The CT scan can demonstrate a life-threat-ening mass lesion that requires surgical evacuation, evidence of raised ICP, and the degree of intracranial injury.
Approximately 10% of initial head CT scans in pa-tients with severe TBI do not show any abnormalities (Lo-bato et al. 1986; van Dongen et al. 1983). The absence of abnormalities on CT scan at admission does not preclude increased ICP. Significant new lesions and increased ICP may develop in 40% of patients with an initially normal head CT scan.
T A B L E 3 – 1 . Secondary insults that adversely affect outcome from traumatic brain injury (TBI)
Secondary insults in TBI Main cause Systolic blood pressure <90 mm
Hg
Blood loss, sepsis, cardiac failure, spinal cord injury, brainstem injury
Arterial O2 saturation <90%, PaO2
<60 mm Hg, apnea, cyanosis
Hypoventilation, thoracic injury, aspiration Sustained PaCO2 <25 mm Hg Induced or spontaneous
hyperventilation
ICP >20–25 mm Hg Mass lesion, brain swelling Note. ICP=intracranial pressure; PaO2=partial pressure of oxygen, ar-terial; PaCO2=partial pressure of carbon dioxide.
Intracranial Pressure Monitoring and Treatment of Elevated Intracranial Pressure
Comatose TBI patients (GCS score of 3 to 8) with abnor-mal CT scans should undergo ICP monitoring. ICP monitoring helps in the earlier detection of intracranial mass lesions, limits the indiscriminate use of therapies that can be potentially harmful to control ICP, and helps in determining prognosis. There is substantial evidence that ICP monitoring may improve outcome. Elevated ICP is present in the majority of patients with severe head injury (Luerssen 1997). We prefer intraventricular devices using a fluid-coupled catheter with an external strain gauge for ICP monitoring. The ventricular cathe-ter can be placed in the operating room or under scathe-terile conditions in the ED or intensive care unit. It has the advantage of not only measuring ICP but also allowing therapeutic cerebrospinal fluid drainage.
Cerebral perfusion pressure (CPP) is defined as the mean arterial blood pressure minus ICP. This physiologic vari-able defines the pressure gradient driving cerebral blood flow and metabolite delivery and is therefore closely re-lated to cerebral ischemia. A threshold CPP of 60 mm Hg for adults is currently recommended. Increased ICP or compromised CPP should be treated vigorously. The ICP management of the typical TBI patient at our institution is outlined in Table 3–3. Hyperventilation should not be used routinely in these patients because of the risk of further compromising cerebral perfusion. We use hyperventilation only for brief periods when there is acute neurological de-terioration or intracranial hypertension is refractory to other treatment interventions. Glucocorticoids have not been shown to improve outcome from severe TBI.
Mannitol is effective for the control of raised ICP after severe TBI. Limited data suggest that intermittent boluses may be more effective than continuous infusion. Effective doses range from 0.25 to 1.00 g/kg body weight.
Studies have shown that not feeding patients with se-vere TBI by the first week after injury increases mortality.
Therefore, it is our practice to initiate tube feedings within the first days after TBI.
Treatment of Seizures
Posttraumatic seizures (PTSs) are divided into early (less than 7 days after trauma) and late (more than 7 days after trauma) seizures. In recent TBI studies that followed high-risk patients up to 36 months, the incidence of early PTSs varied between 4% and 25%, and the incidence of late PTSs varied between 9% and 42% in untreated patients. Prophylactic use of phenytoin, carbamazepine, or phenobarbital is not recommended for preventing late PTSs. Anticonvulsants may be used to prevent early PTSs T A B L E 3 – 2 . Initial assessment and clinical
examination of patients with TBI Resuscitation
Oxygenation/ventilation
Critical findings: Apnea, cyanosis, SaO2 <90%
Intubation if hypoxemic despite supplemental O2, keep PaCO2 at 35 mm Hg
Blood pressure
Critical finding: Systolic blood pressure <90 mm Hg Fluid resuscitation
Primary survey Spinal stability
Critical findings: Pain, step-off, external signs of trauma to neck, mechanism
Immobilization with cervical collar, spine precautions, X rays
Postresuscitation GCS score Critical finding: GCS score <9
Consider intubation, normoventilation, head CT Motor examination, pupillary diameter, light reflex, direct
orbital trauma
Critical findings: Flaccidity or motor posturing and asymmetric or fixed and dilated pupils suggest cerebral herniation
Short-term hyperventilation ± mannitol if herniation suspected
Placement of lines, urinary and gastric catheters, cervical spine, chest and pelvis X rays
Secondary survey
Detailed neurological examination
Critical findings: GCS score <9, cerebral herniation syndrome
Short-term hyperventilation ± mannitol if herniation suspected
Visual inspection, external signs of cranial trauma Critical findings: Raccoon’s eyes, Battle’s sign,
cerebrospinal fluid from ears and/or nose,
hematotympanum, facial fractures, proptosis, direct orbital trauma, skull base fractures
Consider special computed tomographic imaging of skull base, ear, nose, and throat/oral and maxillofacial surgery service involvement, prophylactic antibiotics Note. CT=computed tomography; GCS=Glasgow Coma Scale;
SaO2=arterial oxygen saturation.
in patients at high risk for seizures after TBI. Phenytoin and carbamazepine are effective in this setting. However, the available evidence does not indicate that prevention of early PTSs improves outcome after TBI. Routine seizure prophylaxis for more than 1 week after TBI is therefore not recommended. If late PTSs occur, patients should be managed in accordance with standard approaches to patients with new-onset seizures.
Surgical Management of Acute TBI
The decision regarding whether an intracranial lesion requires surgical evacuation can be difficult and is based on a patient’s GCS score, pupillary examination, comorbidi-ties, CT scan findings, age, and—in delayed decisions—
ICP. Neurological deterioration over time is also an impor-tant factor influencing the decision to operate. The surgi-cal management of TBI has recently been addressed by the Guidelines for the Surgical Management of Traumatic Brain Injury (Brain Trauma Foundation, in press).
This discussion of the surgical management of acute TBI has been organized according to the traditional litera-ture-based classification of posttraumatic mass lesions––
namely, epidural hematoma (EDH), acute subdural hema-toma (SDH), intraparenchymal lesions (e.g., contusion, in-tracerebral hematoma), acute posterior fossa mass lesions, and depressed fractures of the skull. In many patients with severe or moderate TBI, two or more of these lesions may
coexist. For this reason, the formulation of an optimal neu-rosurgical treatment plan requires individual management, more so than in other areas of TBI management.
Epidural Hematoma
An EDH is characterized as a biconvex, extraaxial, hyper-dense mass on a head CT scan (Figure 3–1). The incidence of surgical and nonsurgical EDH among TBI patients is approximately 3%. Among patients in coma, up to 9% har-bor an EDH requiring craniotomy. The peak incidence of EDH is in the second decade, and the mean age of patients with EDH is between 20 and 30 years. Traffic-related acci-dents, falls, and assaults account for the majority of all EDHs. EDHs usually result from injury to the middle meningeal artery but can also be due to bleeding from the middle meningeal vein, the diploic veins, or the venous sinuses. In patients with EDH, one-third to one-half are comatose on admission or immediately before surgery.
The classically described “lucid interval” (i.e., a period dur-ing which a patient who was initially unconscious wakes up before secondarily deteriorating) is seen in approximately one-half of patients undergoing surgery for EDH.
Surgical indication. Clot thickness, hematoma volume, and midline shift (MLS) on the preoperative CT scan are related to outcome. Noncomatose patients without focal neu-rological deficits and with an acute EDH with a thickness of less than 15 mm, a volume less than 30 cc, and an MLS less T A B L E 3 – 3 . Treatment algorithm for patients with intracranial hypertension
In all patients with GCS score <9
Add if ICP
>20 mm Hg
Add if ICP
>25 mm Hg
Add for persistent ICP >25 mm Hg
Add for persistent ICP
>25 mm Hg and/or pu-pillary abnormalities ICP monitoring
Ventricular CSF drainage
Neuromuscular blockade:
vecuronium, atracurium
Moderate hypothermia, core temperature
34–36°C
High-dose propofol infusion Elevate head of bed
30 degrees Maintain euvolemia and
hemodynamic stability
IV sedation with midazolam or
lorazepam
Mannitol bolus infusions every 4–6 hours
Hyperventilation to PaCO2 30–35 mm Hg
Hyperventilation to PaCO2
25–30 mm Hg
PaO2 >90 mm Hg
Analgesia: fentanyl or morphine
Consider hypertonic saline bolus infusion
PaCO2 35–40 mm Hg Consider decompressive
craniectomy Systolic blood pressure
>90 mm Hg “CPP management”: Inotropic and pressor support to maintain CPP
CPP≈60 mm Hg Repeat head CT to exclude operable mass lesion
Note. CPP=cerebral perfusion pressure; CSF=cerebrospinal fluid; CT=computed tomography; GCS=Glasgow Coma Scale; ICP=intracranial pressure; PaCO2=partial pressure of carbon dioxide; PaO2=partial pressure of oxygen, arterial.
than 5 mm may be managed nonoperatively with serial CT scanning and close neurological evaluation in a neurosurgical center (Figure 3–2). The first follow-up CT scan in nonoper-ative patients should be obtained within 6–8 hours after TBI.
Temporal location of an EDH is associated with failure of nonoperative management and should lower the threshold for surgery. Patients with a GCS score lower than 9 and an EDH volume greater than 30 cc should undergo surgical evacuation of the lesion. All patients, regardless of GCS score, should undergo surgery if the volume of their EDH exceeds 30 cc. Patients with an EDH volume less than 30 cc should be considered for surgery but may be managed successfully without surgery in selected cases. Time from neurological deterioration to surgery correlates with outcome. Therefore, surgical evacuation should be done as soon as possible.
Acute Subdural Hematoma
SDHs are diagnosed on a CT scan as extracranial, hyper-dense, crescentic collections between the dura and the brain parenchyma (Figure 3–3). They can be divided into acute and chronic lesions. The incidence of acute SDH is between 12%
and 29% in patients admitted with severe TBI. The mean age is between 31 and 47 years, and the vast majority of patients are men. Most SDHs are caused by motor vehicle–
related accidents, falls, and assaults. Falls have been identified as the main cause of traumatic SDH in patients older than ages 75 and 80 years. Between 37% and 80% of patients with acute SDH present with an initial GCS score of 8 or less.
Surgical indication. Clot thickness or volume and MLS on the preoperative CT scan correlate with outcome.
Patients with SDH with a clot thickness greater than 10 mm or MLS greater than 5 mm should undergo surgical evacuation, regardless of their GCS score. Noncomatose patients with a clot thickness less than 10 mm and MLS less than 5 mm may undergo nonoperative management (Figure 3–4). Comatose patients (GCS score less than 9) with an SDH with a thickness less than 10 mm and MLS F I G U R E 3 – 1 . Computed tomographic scan of the
head of a patient with severe traumatic brain injury demonstrating a left frontal acute epidural
hematoma with significant mass effect.
F I G U R E 3 – 2 . Treatment option for epidural hematoma (EDH) in patients with a Glasgow Coma Scale score greater than 8.
Noncomatose patients with an EDH volume less than 30 cc and a thickness less than 15 mm with less than 5 mm midline shift (MLS) can be managed nonoperatively.
F I G U R E 3 – 3 . Computed tomographic scan of the head of a patient with severe traumatic brain injury demonstrating left-sided acute subdural hematoma.
less than 5 mm can be treated nonoperatively, providing that they undergo ICP monitoring, are neurologically stable, and have no pupillary abnormalities or intracranial hypertension (i.e., ICP greater than 20 mm Hg). A fre-quently observed complication with surgical evacuation of acute SDH is acute brain swelling, sometimes so dra-matic that it is impossible to close the dura after evacua-tion of the hematoma. We use a surgical technique that avoids brain herniation by cutting multiple 2- to 3-cm slits in the dura. This allows rapid and complete removal of the blood clot and at the same time prevents the brain from protruding out of the craniotomy (Figure 3–5).
Traumatic Parenchymal Lesions
Traumatic parenchymal mass lesions occur in up to 10%
of all patients with TBI and 13% to 35% of patients with severe TBI (Figure 3–6). Most small parenchymal lesions do not require surgical evacuation. However, the devel-opment of mass effect from larger lesions may result in secondary brain injury, placing the patient at risk of fur-ther neurological deterioration, herniation, and death.
Parenchymal lesions tend to evolve, and timing of surgery affects outcome.
Surgical indication. Patients with parenchymal mass lesions and signs of progressive neurological deteriora-tion referable to the lesion, medically refractory intracra-nial hypertension, or signs of mass effect on CT scan should be treated operatively. Comatose patients with frontal or temporal contusions greater than 20 cc in vol-ume with MLS of 5 mm or more and/or cisternal com-pression on CT scan, as well as patients with any lesion greater than 50 cc in volume, should be treated opera-tively. Patients with parenchymal mass lesions who do not show evidence of neurological compromise and have
con-trolled ICP and no significant signs of mass effect on CT scan may be managed nonoperatively.
Posterior Fossa Mass Lesions
Less than 3% of patients with TBI present with posterior fossa lesions. The vast majority of these lesions are poste-rior fossa EDHs. It is important to recognize these lesions early on, because patients can undergo rapid clinical dete-rioration due to the limited size of the posterior fossa and the propensity for these lesions to produce brainstem com-pression. Patients with fourth ventricular mass effect on CT scan or with neurological dysfunction or deterioration referable to the lesion should undergo a suboccipital craniectomy as soon as possible. Patients without signifi-cant mass effect on CT scan and without signs of neurolog-ical dysfunction may be managed by close observation and serial imaging.
Depressed Skull Fractures
Depressed skull fractures complicate up to 6% of head injuries, and the presence of skull fracture is associated with a higher incidence of intracranial lesions, neurolog-ical deficit, and poorer outcome. Patients with open skull fractures depressed greater than the thickness of the skull should undergo operative intervention to prevent infec-F I G U R E 3 – 4 . Treatment option for patients with
acute subdural hematoma (SDH) with a Glasgow Coma Scale score greater than 8.
Noncomatose patients with an SDH less than 10 mm thick and with less than 5-mm midline shift (MLS) can be managed non-operatively.
F I G U R E 3 – 5 . Slit technique for evacuation of acute subdural hematoma in patients with traumatic brain injury.
The dura is incised at multiple sites to drain the subdural blood collection and prevent the brain from herniating out of the cra-nial opening.
tion. Patients with open depressed fractures should be treated with antibiotic prophylaxis.
Decompressive Craniectomy for Control of Intracranial Hypertension
Decompressive procedures, such as subtemporal pression, temporal lobectomy, and hemispheric decom-pressive craniectomy, are surgical procedures that have been used to treat patients with refractory intracranial hypertension and diffuse parenchymal injury. Decompres-sive craniectomy may be effective if it is done early after TBI in young patients who are expected to develop postop-erative brain swelling and intracranial hypertension.