Epidemiology of head injury
A traumatic brain injury (TBI) is defined as a blow or jolt to the head or a penetrating head injury that disrupts the function of the brain. TBI is one of the most serious, life-threatening conditions in trauma victims. It is a leading cause of disability and death in children and adults. An estimated 1.5 million people sustain TBIs every year in the United States. Of these, more than 50,000 die annually as a result of TBI, and another 80,000 become impaired or disabled for life. TBI is a leading cause of disability in the United States, affecting approximately 5.3 million people. TBI-related disability has a devastating effect on the lives of the injured individuals and their families and results in a tremendous cost to hospital systems and society in terms of the rehabilitation and chronic care of these individuals.
Head injury occurs most often in adolescents, young adults, and people older than 75 years. In all age groups, males are affected two times more often than females and are more likely to sustain severe head injury. The leading causes of TBI are falls, motor vehicle crashes, and assaults. Blasts are a leading cause of TBI among active duty military personnel in war zones. On April 28, 2008, the 110th United States Congress passed a bill to provide for the expansion and improvement of TBI programs (Public Law 110-206), such as research funding for therapeutic interventions and development of practice guidelines for rehabilitation.
Head injury guidelines
In 1995, recognizing the need to standardize care to improve the outcome for head-injured patients, the Brain Trauma Foundation approved guidelines for the initial resuscitation of the patient with severe head injury and the treatment of intracranial hypertension. A task force was formed in 1998 to review and update the scientific evidence for the guidelines. These evidence-based guidelines for the management of severe TBI were published in 2000 , and then updated in 2007 ( Box 19.1 ). This extensive review of the literature recommends only three standards based on Class I evidence and several guidelines based on Class II evidence. Adherence to these guidelines has remained variable across the trauma centers. However, studies have shown a causal relationship between adherence to the guidelines and improved outcomes. In a study with 22 New York State trauma centers, increased guideline adherence for intracranial pressure monitoring and cerebral perfusion pressure management resulted in significant reductions in mortality over 9 years.
Standards Based on Class I Evidence
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If intracranial pressure (ICP) is normal, avoid prolonged hyperventilation therapy (Paco 2 < 25 mmHg).
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The use of steroids is not recommended for improving outcome or reducing ICP.
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Prophylactic use of anticonvulsants does not prevent late post-traumatic seizures.
Guidelines Based on Class II Evidence
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All regions should have an organized trauma care system.
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Avoid or immediately correct hypotension (systolic blood pressure < 90 mmHg) and hypoxia (Sao 2 < 90% or Pao 2 < 60 mmHg).
- •
Indications for ICP monitoring include Glasgow Coma Scale score of 3–8 with abnormal computed tomography findings or two or more of the following adverse features: age > 40 years, motor posturing, and systolic blood pressure < 90 mmHg.
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Initiate treatment for ICP at an upper threshold above 20 mmHg.
- •
The cerebral perfusion pressure (CPP) value to target lies within the range of 50–70 mmHg. Aggressive attempts to maintain CPP above 70 mmHg should be avoided because of the risk of acute respiratory distress syndrome.
- •
Avoid using prophylactic hyperventilation (PaCO 2 ≤ 25 mmHg) therapy during the first 24 hours after severe traumatic brain injury (TBI).
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Mannitol is effective for controlling raised ICP after severe TBI, in doses ranging from 0.25 to 1 g/kg.
- •
High-dose barbiturate therapy may be considered in hemodynamically stable, salvageable patients who have severe TBI and whose intracranial hypertension is refractory to maximal medical and surgical ICP-lowering therapy.
- •
Provide nutritional support (140% of resting energy expenditure in patients without respiratory paralysis and 100% of resting energy expenditure in patients with it), using enteral or parenteral formulas containing at least 15% of calories as protein by day 7 after injury.
Results of the Corticosteroid Randomization After Significant Head Injury (CRASH) trial, which studied the effect of early administration of methylprednisolone on outcome after head injury in 10,008 adults, were published in 2005. This was an international randomized, placebo-controlled trial on the effect of early administration of 48-hour infusion of methylprednisolone on the risk of death and disability after head injury. The CRASH trial revealed a higher risk of death within 2 weeks of injury in the group receiving corticosteroids than in the group receiving placebo, as well as a higher risk of death or severe disability. The trial investigators concluded that “corticosteroids should not be used routinely in the treatment of head injury.”
Evidence-based guidelines for prehospital management of TBI , and for pediatric brain injury have also been published, and in March 2006, surgical management guidelines were published. However, unlike the writers of the severe TBI management guidelines, , the writers of the surgical management guidelines report no controlled clinical trials in the literature to support different forms of surgical management or surgical versus conservative therapy. As with the other published guidelines for the management of severe TBI, they state that “this is a document in evolution,” and revisions will be made as new knowledge is gained.
Head injury guidelines
In 1995, recognizing the need to standardize care to improve the outcome for head-injured patients, the Brain Trauma Foundation approved guidelines for the initial resuscitation of the patient with severe head injury and the treatment of intracranial hypertension. A task force was formed in 1998 to review and update the scientific evidence for the guidelines. These evidence-based guidelines for the management of severe TBI were published in 2000 , and then updated in 2007 ( Box 19.1 ). This extensive review of the literature recommends only three standards based on Class I evidence and several guidelines based on Class II evidence. Adherence to these guidelines has remained variable across the trauma centers. However, studies have shown a causal relationship between adherence to the guidelines and improved outcomes. In a study with 22 New York State trauma centers, increased guideline adherence for intracranial pressure monitoring and cerebral perfusion pressure management resulted in significant reductions in mortality over 9 years.
Standards Based on Class I Evidence
- •
If intracranial pressure (ICP) is normal, avoid prolonged hyperventilation therapy (Paco 2 < 25 mmHg).
- •
The use of steroids is not recommended for improving outcome or reducing ICP.
- •
Prophylactic use of anticonvulsants does not prevent late post-traumatic seizures.
Guidelines Based on Class II Evidence
- •
All regions should have an organized trauma care system.
- •
Avoid or immediately correct hypotension (systolic blood pressure < 90 mmHg) and hypoxia (Sao 2 < 90% or Pao 2 < 60 mmHg).
- •
Indications for ICP monitoring include Glasgow Coma Scale score of 3–8 with abnormal computed tomography findings or two or more of the following adverse features: age > 40 years, motor posturing, and systolic blood pressure < 90 mmHg.
- •
Initiate treatment for ICP at an upper threshold above 20 mmHg.
- •
The cerebral perfusion pressure (CPP) value to target lies within the range of 50–70 mmHg. Aggressive attempts to maintain CPP above 70 mmHg should be avoided because of the risk of acute respiratory distress syndrome.
- •
Avoid using prophylactic hyperventilation (PaCO 2 ≤ 25 mmHg) therapy during the first 24 hours after severe traumatic brain injury (TBI).
- •
Mannitol is effective for controlling raised ICP after severe TBI, in doses ranging from 0.25 to 1 g/kg.
- •
High-dose barbiturate therapy may be considered in hemodynamically stable, salvageable patients who have severe TBI and whose intracranial hypertension is refractory to maximal medical and surgical ICP-lowering therapy.
- •
Provide nutritional support (140% of resting energy expenditure in patients without respiratory paralysis and 100% of resting energy expenditure in patients with it), using enteral or parenteral formulas containing at least 15% of calories as protein by day 7 after injury.
Results of the Corticosteroid Randomization After Significant Head Injury (CRASH) trial, which studied the effect of early administration of methylprednisolone on outcome after head injury in 10,008 adults, were published in 2005. This was an international randomized, placebo-controlled trial on the effect of early administration of 48-hour infusion of methylprednisolone on the risk of death and disability after head injury. The CRASH trial revealed a higher risk of death within 2 weeks of injury in the group receiving corticosteroids than in the group receiving placebo, as well as a higher risk of death or severe disability. The trial investigators concluded that “corticosteroids should not be used routinely in the treatment of head injury.”
Evidence-based guidelines for prehospital management of TBI , and for pediatric brain injury have also been published, and in March 2006, surgical management guidelines were published. However, unlike the writers of the severe TBI management guidelines, , the writers of the surgical management guidelines report no controlled clinical trials in the literature to support different forms of surgical management or surgical versus conservative therapy. As with the other published guidelines for the management of severe TBI, they state that “this is a document in evolution,” and revisions will be made as new knowledge is gained.
Classification of head injury
Classification of severe head injury is based on the Glasgow Coma Scale (GCS) ( Table 19.1 ), which defines neurologic impairment in terms of eye opening, speech, and motor function. , The total score that can be obtained is 15, and severe head injury is determined by a score of 8 or less persisting for 6 hours or more. The GCS and Glasgow Outcome Scale permit comparison between series of traumatically head-injured patients on the basis of initial clinical presentation and eventual outcome. The prognosis after head injury depends on the type of lesion sustained, the age of the patient, and the severity of the injury as defined by the GCS. In general, mortality is closely related to the initial score on the GCS. For any given lesion and score, however, the elderly have a poorer outcome than do younger patients. ,
| Feature | Point(s) |
|---|---|
| Eye Opening | |
| Spontaneously | 4 |
| To verbal command | 3 |
| To pain | 2 |
| None | 1 |
| Best Verbal Response | |
| Oriented, conversing | 5 |
| Disoriented, conversing | 4 |
| Inappropriate words | 3 |
| Incomprehensible sounds | 2 |
| No verbal response | 1 |
| Best Motor Response | |
| Obeys verbal commands | 6 |
| Localizes to pain | 5 |
| Flexion or withdrawal | 4 |
| Abnormal flexion (decorticate) | 3 |
| Extension (decerebrate) | 2 |
| No response (flaccid) | 1 |
* Total scores: mild head injury = 13–15 points; moderate = 9–12 points; severe ≤ 8 points.
Following head trauma, the primary injury results from the biomechanical effect of forces applied to the skull and brain at the time of the insult and are manifested within milliseconds. Currently, there is no treatment for the primary injury. However, primary injuries continue to evolve over the hours after impact and the cascade of injury leading to cell death may be modified. Secondary injury begins within minutes, hours, or days after the impact and represents complicating processes initiated by the primary injury, such as ischemia, brain swelling and edema, intracranial hemorrhage, intracranial hypertension, and herniation. The common denominator of secondary injury is cerebral hypoxia and ischemia ( Box 19.2 ). Factors that aggravate the initial injury include hypoxia, hypercarbia, hypotension, anemia, and hyperglycemia. These contributing factors to secondary injury are preventable. Seizures, infection, and sepsis that may occur hours to days after injury can further aggravate brain damage and must also be prevented or treated promptly.
Secondary insults complicate the course of more than 50% of head-injured patients. An outcome study using data from the Traumatic Coma Data Bank revealed that hypotension occurring after head injury is profoundly detrimental, with more than 70% of patients with hypotension experiencing significant morbidity and mortality ( Table 19.2 ). Furthermore, the combination of hypoxia and hypotension is significantly more detrimental than that of hypotension alone; more than 90% of patients who had both of these experienced a severe outcome or died. These findings confirm the importance of avoiding hypovolemic shock in head-injured patients. The management goal in head-injured patients is to initiate timely and appropriate therapy to prevent secondary brain injury. When the initial injury is not fatal, subsequent neurologic damage and systemic complications should be preventable in most patients.
| Outcome (% of Patients) | ||||
|---|---|---|---|---|
| Secondary Insults | Number of Patients | Good or Moderate | Severe or Vegetative | Dead |
| Total number of cases | 699 | 43 | 21 | 37 |
| Neither insult | 456 | 51 | 22 | 27 |
| Hypoxia (Pao 2 < 60 mmHg) | 78 | 45 | 22 | 33 |
| Hypotension (systemic blood pressure < 90 mmHg) | 113 | 26 | 14 | 60 |
| Both | 52 | 6 | 19 | 75 |
Primary injury or biomechanical trauma to brain parenchyma consists of concussion, contusion, laceration, and hematoma. Not all severely head-injured patients require surgery. Generalized brain injury with edema or contusion is a common finding, whether or not a surgically correctable mass lesion is present. Diffuse cerebral swelling occurs because of sudden intracerebral congestion and hyperemia. Twenty-four hours or more after the initial insult, cerebral edema develops in the extracellular spaces of the white matter. Nonoperative treatment of diffuse cerebral swelling involves hyperventilation, diuresis with mannitol and/or furosemide, and barbiturates in conjunction with intracranial pressure (ICP) monitoring. With hyperventilation of PaCO 2 < 30 mmHg, oxygen saturation in the jugular bulb (SJO 2 ), arterio-jugular differences of oxygen (AVDO 2 ) and/or CBF monitoring is recommended. Aggressive hyperventilation (PaCO 2 ≤ 25 mmHg) should be avoided because reductions in cerebral blood flow can potentially exaccerbate cerebral hypoxia and ischemia.
Depressed skull fractures and acute epidural, subdural, and intracerebral hematomas usually require craniotomy. Chronic subdural hematomas are often evacuated through burr holes. Depressed skull fractures under lacerations should be elevated and debrided within 24 hours to minimize the risk of infection. Bony fragments and penetrating objects should not be manipulated in the emergency department (ED), because they may be tamponading a lacerated vessel or dural sinus.
Traumatic epidural hematoma is an infrequent complication of head injury, usually the result of a motor vehicle accident. The initial injury tears middle meningeal vessels or dural sinuses and causes unconsciousness. When a spasm and clot occur in the vessel(s), the bleeding stops and the patient recovers, experiencing a lucid interval. Over the next several hours, the vessel bleeds and the patient rapidly deteriorates (especially with arterial bleeding). In rapidly deteriorating conditions, treatment should not be delayed to await radiologic evaluation; emergency evacuation is necessary. Venous epidural hematomas develop more slowly, and there may be time for diagnostic testing.
The clinical presentation of acute subdural hematomas ranges from minimal deficits to unconsciousness and signs of a mass lesion (hemiparesis, unilateral decerebration, and pupillary enlargement). A lucid interval may occur. The most common cause of subdural hematoma is trauma, but it may occur spontaneously and is associated with coagulopathies, aneurysms, and neoplasms. The severity of injury to the underlying brain is greater with subdural hematomas than with epidural hematomas. It is considered acute if the patient becomes symptomatic within 72 hours, subacute if symptoms appear between 3 and 15 days, and chronic with symptoms after 2 weeks. Subacute or chronic subdural hematoma is usually observed in patients older than 50 years. There may be no history of head trauma. The clinical presentation in these patients may vary from focal signs of brain dysfunction to a depressed level of consciousness or development of an organic brain syndrome. Intracranial hypertension is usually associated with acute subdural hematoma. Intensive medical therapy to correct elevated ICP and control brain edema and swelling may be required before, during, and after hematoma evacuation.
In patients with intracerebral hematomas , the clinical picture may vary from minimal neurologic deficits to deep coma. Large, solitary intracerebral hematomas should be evacuated. Lesions causing delayed neurologic deterioration from fresh hemorrhage are also evacuated but carry a poor prognosis. Depending on the extent of cerebral injury, patients with intracerebral hematomas may require intensive medical therapy to control intracranial hypertension and cerebral edema. Coup and contrecoup injuries usually cause cerebral contusion and intracerebral hemorrhage. In general, contused brain tissue is not removed; occasionally, however, contused tissue over the frontal or temporal poles may be removed to control edema formation and prevent herniation.
Emergency therapy
Perioperative management of the head-injured patient focuses on aggressive stabilization of the patient and avoidance of systemic and intracranial insults that cause secondary neuronal injury (see Box 19.2 ). Secondary brain injury complicates the course of the majority of head-injured patients, adversely influencing outcome. The need to improve care of these patients in the field and ED has been recognized with the development of guidelines, improvement of emergency response services, and better training of providers. The goals of emergency therapy in the field and ED are to prevent and treat all secondary insults and, ultimately, to improve outcome in patients with TBI.
Prehospital Management
Emergency therapy should begin at the site of the accident and in the ambulance. According to the Brain Trauma Foundation’s guidelines for prehospital management of traumatic brain injury, emergency medical service (EMS) providers should be trained to follow an established algorithm for the assessment and treatment of TBI. The first priority is initiation of a basic resuscitation protocol that prioritizes the CABs (circulation, airway, and breathing), assessment, and treatment. The patient’s airway is maintained, and blood pressure is supported. The EMS provider performs an assessment for appropriate triage of the patient and all necessary therapy to stabilize the patient prior to transport. It is recommended that the severely injured patient (GCS score < 9) be taken directly to a level I trauma center “with 24 hour scanning capability, operating room, prompt neurosurgical care and the ability to monitor intracranial pressure and treat intracranial hypertension as delineated in the Guidelines for the Management of Severe Head Injury.” Optimal results for patients with intracranial hematomas require surgical evacuation within 2 to 4 hours of the injury. Therefore, direct transport to a neurosurgical center is crucial for such patients.
The prehospital management guidelines published in 2002 and 2008 are accepted as the standard for management by prehospital and ED clinicians. Currently, there are insufficient data to support any standard recommendations for prehospital assessment, treatment, transport, and destination. Subsequent to the initial publication of these guidelines, the results of several studies have questioned whether outcome is improved by following them. , These studies support the direct transfer of patients with severe TBI to a level I or level II trauma center, but controversy remains regarding whether patient outcome is improved by paramedic endotracheal intubation in the field and the mode of transport. The Ontario Prehospital Advanced Life Support (OPALS) Major Trauma Study has shown that a delay for advanced life support, especially on-scene endotracheal intubation, is associated with increased mortality among patients with suspected severe head injuries. This makes it unclear as to which elements of airway management should be revised or reserved for a controlled hospital setting, especially given regional variations in infrastructure and EMS experience.
A prospective, randomized controlled study conducted in New South Wales, Australia known as the Head Injury Retrieval Trial (HIRT) attempted to address the efficacy of advanced prehospital intervention. The goal of the study was to evaluate physician-led prehospital teams compared to paramedic-only teams. The trial results suggests a potential reduction in 30-day mortality for patients with GCS < 9 who received prehospital physician care. The study’s conclusion, however, was obscured by the significant crossover where many patients received care they were not intended to receive; that is, changes in prehospital treatment policy during the recruitment period caused a higher rate of dispatched physicians than intended. Therefore, additional studies are needed to confirm these findings.
Emergency Department Management
All patients with head injury require full diagnostic evaluation with complete history and neurologic examination. Not all patients require radiologic examination. Two comprehensive studies have resulted in the development of two slightly different sets of rules for determining whether or not a patient with minor head injury must undergo computed tomography (CT) scanning. , These are the Canadian and New Orleans CT scanning rules for minor head injury ( Box 19.3 ). An unenhanced CT scan is the radiologic procedure of choice in acute TBI. A spiral CT of the head and craniocervical junction is useful in the patients with more severe TBI and potential high cervical spine injuries. Ongoing research is being performed to determine whether or not S100B, a biomarker for blood–brain barrier permeability and CNS injury, may assist in screening patients with minor head injuries.
Canadian Rules
High risk (for neurological intervention):
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GCS score < 15 at 2 h after injury
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Suspected open or depressed skull fracture
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Any sign of basal skull fracture
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Vomiting ≥ two episodes
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Age ≥ 65 years
Medium risk (for brain injury on CT):
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Amnesia before impact > 30 min
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High-risk mechanism of injury
New Orleans Rules
Short-term memory deficits (persistent anterograde amnesia with GCS score 15)
Intoxication (drug alcohol)
Physical evidence of trauma above the clavicles
Age > 60 years
Seizure (suspected or witnessed)
Headache
Vomiting
Coagulopathy
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