Head Trauma and Subdural Hematoma Part II: Emergency Management of Severe, Moderate, and Minor Head Trauma
Head Trauma and Subdural Hematoma
Part II: Emergency Management of Severe, Moderate, and Minor Head Trauma
Authors: Danica N. Barron, MD, Alameda County Medical Center-Highland General Hospital, Department of Emergency Medicine, Oakland, CA; M. Andrew Levitt, DO, Associate Clinical Professor, University of California, San Francisco, Department of Medicine; Director of Research, Alameda County Medical Center-Highland General Hospital, Department of Emergency Medicine; R. Carter Clements, MD, Assistant Clinical Professor, University of California, San Francisco, Department of Medicine; Assistant Chief, Alameda County Medical Center-Highland General Hospital, Department of Emergency Medicine.
Peer Reviewers: David Kramer, MD, FACEP, Program Director, Associate Professor, Department of Emergency Medicine, York Hospital, Penn State University; David P. Sklar, MD, Professor and Chair, Department of Emergency Medicine, University of New Mexico School of Medicine, Albuquerque, NM.
The extensive spectrum of injuries, complications, and approaches to managing patients with traumatic brain insults demands a customized strategy to evaluation and treatment. Although patients with very low Glasgow Coma Scale (GCS) scores tend to have poor outcomes, early management directed optimizing cerebral perfusion and intracranial pressures, oxygenation, systemic blood pressure, and establishing control of the airway can reduce morbidity and mortality. The role of a number of experimental techniques such as hypothermia and other pharmacological interventions continues to be investigated.
While severely ill patients always require aggressive, detailed evaluation and monitoring, individuals with minor and moderate traumatic brain injury (TBI) benefit from selective approaches based on risk stratification. In these individuals, especially those with minor head injury, the value of routine neuroimaging is uncertain, with some experts suggesting historical factors such as loss of consciousness (LOC) and post-traumatic amnesia (PTA) are good predictors for computed tomography (CT) head scanning, and others arguing that they are poorly predictive of intracerebral injury.
With these issues in focus, the purpose of this review, the second part of a two-part series, is to provide a systematic approach to diagnosis and evaluation of TBI. Syndrome-specific treatments based on patient risk stratification are emphasized, and criteria that suggest the need for extended observation, hospital admission, and neuroimaging are discussed in detail.— The Editor
Severe Head Trauma
Severe TBI is classified as a single, isolated head trauma producing a GCS score of 3-8. In general, the lower the initial GCS score, the more dismal the outcome. In one prospective study, a positive predictive value of 77% for a poor outcome (dead, vegetative, or severely disabled) was measured in patients with GCS scores of 3-5; in patients with GCS scores of 6-8, the positive predictive value for a poor outcome was 26%.1 Nevertheless, early, aggressive management of these patients is important and may produce marked reduction in morbidity and mortality, especially in patients who harbor surgical lesions or whose sensorium may be clouded by drugs or alcohol.
Prehospital Considerations. The challenge in managing patients with TBI in the prehospital and emergency department (ED) settings is resuscitating and identifying patients with severe TBI. Patients with TBI may have compromised cerebral blood flow (CBF) and are at risk for further ischemic insults due to hypoxia and hypotension. Onset of coma immediately postinjury signifies severe primary TBI, whereas deterioration to coma in a previously awake patient implies a possible expanding intracranial hematoma. Improved prehospital airway management may benefit TBI patients, as approximately 30% of TBI patients are reported to be hypoxemic on presentation to the ED.2,3 TBI is not an isolated injury, and more than 50% of serious TBI patients have multiple extracranial injuries, placing them at risk for significant hemorrhage and hypotension.2-4 Therefore, administration of ample intravenous fluids is critical to restore and maintain adequate CBF. The patient should be immobilized by placement on a backboard with the neck in a hard cervical collar, and if possible, elevation of the head 30 degrees to optimize cerebral perfusion pressure (CPP) in case of increased intracranial pressure (ICP). Of course, swift transport of the patient to an appropriate facility is key to optimal management of TBI patients and should not be delayed.
Airway and Oxygenation. Indications for intubation of severe TBI patients include inability to maintain and protect the airway, inadequate ventilation, hemodynamic instability, and excessive combativeness or movement precluding appropriate imaging. In TBI patients, hypoxia can take many forms. For our purposes it will be defined as apnea, cyanosis, PaO2 of less than 60 mmHg in the field, or PaO2 of less than 60 mmHg by arterial blood gas. Hypoxia is particularly detrimental to the TBI patient and should be avoided.5 Precautions for cervical spine injuries should be made during intubation in a patient with an uncleared cervical spine, as 6-8% of serious TBI patients may have concomitant cervical spine injury.6 In addition, a recent study demonstrated that as many as 3.6% of patients with seemingly milder TBI (GCS score of 13 or 14) harbor cervical fractures or dislocations.7 Therefore, traction on the neck should be avoided and the jaw-thrust maneuver is preferred to enhance ventilation. Many authorities believe that intubation is indicated in patients with GCS scores of less than 9, based on the assumption that GCS scores predict the ability to protect the patient’s airway. Nevertheless, patients with higher GCS scores can vomit and aspirate; signs of difficulty maintaining an airway (and requiring intubation) include snoring, excessive secretions in the oropharynx, breathing with the cheeks puffed out on expiration, and sluggish eye or motor response to noxious stimuli. Severe TBI patients frequently have abnormal breathing patterns, such as Cheyne-Stokes breathing, which may be caused by brainstem dysfunction. Tachypnea and hyperventilation may be an early indication of increasing ICP. Intubation may be accomplished by either the nasal or the oral route. Coughing and gagging during intubation may cause an increase in ICP; therefore, oral intubation is preferred as it permits chemical paralysis of the patient. Suspicion of basilar skull fracture, as indicated by "raccoon’s eyes" (discoloration or bruising around one or both eyes), cerebrospinal fluid (CSF) rhinorrhea, or hemotympanum, is an absolute contraindication to nasal intubation.
The technique of rapid sequence intubation (RSI) has emerged as the most efficacious and safe means for providing airway control in patients with serious TBI.8-10 Prior to induction of sedation and paralysis for intubation, however, it is important to document a brief neurological examination. Nevertheless, the neurological examination should never delay stabilization of airway, breathing, and circulation. Selection of inducing and paralyzing agents is based on onset of action as well as their effect on the hemodynamics and ICP of the patient. Traditionally, induction has been accomplished by sodium thiopental (3-5 mg/kg IV), but newer agents, such as etomidate (0.2-0.4 mg/kg IV) have fewer effects on cardiovascular parameters and may be preferred.10 As with barbiturates and propofol, etomidate decreases ICP; however, etomidate has the added benefit of maintaining mean arterial pressure (MAP) and, therefore, CPP.11 Note, however, that etomidate does not have analgesic properties and does not blunt the sympathetic response to endotracheal intubation. Therefore, the addition of fentanyl (50-100 mcg IV) may be used to attenuate the sympathetic surge. Some clinicians use lidocaine (1.5-2.0 mg/kg IV) prior to the administration of the paralyzing agent to ease ICP increases during airway stimulation, although no studies have proven this effect.11 Recent data show that esmolol blunts the heart rate and blood pressure response to instrumentation, although it is not widely used yet.12 For paralysis, succinylcholine (1-2 mg/kg IV) is popular, although it has been shown to increase ICP and CBF and cause abnormal potassium release. Some clinicians give a small dose of a succinylcholine (0.01 mg/kg IV) or a nondepolarizing agent prior to full paralysis to prevent fasciculations and untoward effects on intracranial dynamics. Succinylcholine is contraindicated in patients with renal failure, crush injury, personal or family history of malignant hypertension, and burn victims beyond 76 hours postinjury. Nevertheless, succinylcholine can be given intramuscularly (2 mg/kg IV), which is clearly advantageous in a large, combative patient with no intravenous access. Rocuronium (0.9-1.2 mg/kg IV) is a nondepolarizing agent with a time to onset similar to that of succinylcholine without deleterious effects on ICP.13 Although it has not yet been prospectively studied, it is popular in many trauma facilities.14 Once intubated, the patient should be placed on 100% O2, titrating the fraction of inspired O2 after transfer of the patient to the ICU or another facility. The use of positive end expiratory pressure (PEEP) does not necessarily have an adverse effect on ICP,15 and a minimum of 5 cm H2O PEEP is recommended to avoid atelectasis.16
Blood Pressure. Hemodynamic stability (circulation) is a principle in the approach to any trauma patient and ranks just behind stabilization of airway and breathing as part of Advanced Trauma Life Support (ATLS) resuscitation. As described before, it is especially important in TBI patients. Delivery of intravenous fluids should be based on evaluation of volume status, with the goal of maximizing cerebral perfusion. Early hypotension, defined as a single observation of a systolic blood pressure of less than 90 mmHg, is associated with increased morbidity or mortality.5,17 Assessment of hemodynamics is based not only on vital signs, but also on skin perfusion, urine output, arterial blood gases, lactate or base deficit, changes in hemoglobin, and ongoing fluid requirements. Significant hypotension rarely is due to brain injury except as a terminal event; therefore, other causes should be sought. Hemorrhage is the most common cause of hypotension in trauma patients, the most frequent sites being the chest, abdomen, and pelvis. Nevertheless, scalp lacerations can bleed profusely and should not be overlooked. Hypotension also may be caused by spinal shock from a concomitant spinal cord injury. Cord injuries may be difficult to diagnose acutely, and high index of suspicion should be kept. Spinal shock is distinguished from hypovolemic hypotension by its unresponsiveness to fluid administration. The presence of bradycardia and hypertension is an ominous sign (Cushing response) and may indicate elevated ICP progressing to herniation. Severe TBI also may precipitate cardiac arrhythmias that can compromise blood pressure. In particular, deep T waves in the anterior leads associated with subarachnoid hematoma (SAH) or elevated ICP can deteriorate to QRS widening and ventricular tachycardia.
The TBI patient produces an additional challenge in that decreases in cerebral perfusion may be due to lower MAP, elevated ICP, or a combination of the two. Fluid should not be withheld in the hypotensive hypovolemic patient for fear of exacerbating cerebral edema and increasing ICP. In patients with evidence of circulatory shock, standard guidelines indicate rapid intravenous infusion of 2-3 L of crystalloid solution (0.9% normal saline or lactated Ringer’s solution), followed by blood if shock persists.18 The goal is to maintain the systolic blood pressure above 90 mmHg in an attempt to keep CPP greater than 70 mmHg.5 Secondary insults may be avoided in up to 74% of patients by aggressively treating with fluids.18 Evidence has shown that maintenance of hematocrit at greater than 30% is important for adequate oxygen-carrying capacity of intravascular fluids.19 In patients with no evidence of shock, crystalloid also may be used for maintenance requirements. Optimization of fluid administration is less clear in cases of brain edema. Total osmolarity is the determining factor of water movement into the brain parenchyma due to the tight junctions in an intact blood-brain barrier (BBB). Although large volumes of infused crystalloid may cause systemic edema, total osmolarity changes little and generally does not result in brain edema. Nevertheless, it is possible that ischemia can compromise the integrity of the BBB enough to permit swelling of brain parenchyma in the setting of significant crystalloid infusion. Hypotonic solutions, on the other hand, certainly will affect water movement into the brain, causing cerebral edema, and should be avoided.20,21
Concerns over elevated ICP and brain edema have sparked interest in other resuscitation fluids, namely hypertonic saline (7.5% saline). In a subset of patients, hypertonic salt solutions appear to be beneficial by improving hemodynamic parameters.22 Hypertonic saline has a positive inotropic effect via restoration of blood pressure and cardiac output.23,24 Hypertonic saline also can cause osmotic shifts in the brain, moving water from brain tissue into the systemic vascular compartment, decreasing ICP. The addition of dextran to hypertonic saline prolongs the effect and may be useful in therapy-resistant elevated ICP.25 Higher concentrated hypertonic saline (23.4%) may even assist in the management of patients with intractable ICP by reducing ICP and improving CPP.26 Nevertheless, more clinical studies are required to determine the indications, as well as the optimal time and volume of hypertonic saline. Pressor therapy is recommended as an adjunct to fluid resuscitation, with preference given to dopamine and norepinephrine. Phenylephrine increases systemic vascular resistance, but reflex bradycardia causes a decreased cardiac output, worsening CBF.27 Careful monitoring is indicated, as induced hypertension may increase or decrease ICP depending on the brain’s ability to autoregulate.28
Laboratory Studies. During the resuscitative phase, certain laboratory tests are performed to guide further management of the TBI patient. Hypoxia and hypoglycemia should be excluded by pulse oximetry and rapid glucose test stick, respectively. As with other trauma patients, initial laboratory tests include: complete blood count, serum chemistry panel, and serum lactate. Alcohol frequently is a confounding factor in the assessment of TBI patients, and a blood ethanol level (BAL) also should be included in the initial draw. Note, however, that the actual blood ethanol level does not necessarily correlate with the level of consciousness. Alcohol is metabolized at a rate of 0.020-0.030 g/dL per hour.29 Therefore, BAL may help the clinician estimate the speed at which the mental status should improve if the decreased level of consciousness was related primarily to inebriation. In some cases, continued absorption of alcohol from the stomach can confound this assumption and repeat BAL levels may be helpful. Serum or urine drug screens also may be useful for identification of other agents that may cloud sensorium. Repeat laboratory tests are required to determine ongoing blood loss and gauge success of the resuscitation. Metabolic acidosis associated with adequate oxygenation implies reduced tissue perfusion, even though vital signs may not be markedly abnormal. TBI also may induce a hyperadrenergic state leading to temporary hypokalemia. Early hyperglycemia is a common component of the stress response and also may correlate with severity of head injury and poor prognosis.30 TBI patients also are at risk of developing hypomagnesemia and hypophosphatemia and, to a lesser degree, hypocalcemia.31 Finally, coagulation studies may be of value in early management of TBI. If clotting studies are normal at admission, the TBI patient has a 31% risk of developing delayed injury, as compared to 85% of patients in whom either prothrombin time, partial thromboplastin time, or platelet count were abnormal.32
Hyperventilation. For many years, aggressive hyperventilation (arterial pCO2 < 25 mmHg) has been a cornerstone in the management of patients with severe TBI. Forty percent of severe TBI patients develop brain edema and swelling post injury. High or uncontrolled ICP is the most common cause of morbidity and mortality post injury.33-36 However, concern has arisen that hyperventilation, by decreasing CBF (and therefore ICP) via cerebral vasoconstriction, may exacerbate cerebral ischemia. Hyperventilation reduces CBF values by a measure of 3% change per torr of pCO2; however, hyperventilation does not produce a consistent decrease in ICP.37 Further, cerebral vascular response to hypocapnia is altered in those with more severe injuries (subdural hematomas and diffuse contusions), and there is substantial variability in perfusion. The actual value of CBF at which irreversible ischemia occurs has not yet been determined, but positron emission tomography data suggest that such damage is likely to occur when CBF drops below 15-20 mL/100g/min. The most recent guidelines from The Brain Trauma Foundation advocate that the use of prophylactic hyperventilation (paCO2 < 35 mmHg) therapy during the first 24 hours after severe TBI should be avoided.38 In cases of acute neurological deterioration, brief periods of hyperventilation to less than 30 mmHg may be necessary. The onset of action appears to be within 30 seconds, and peaks within eight minutes. In most patients, hyperventilation lowers the ICP by 25%; if the patient does not rapidly respond, the prognosis for survival is generally poor.39-41 Prolongation of hyperventilation decreases its effectiveness and is of limited value outside of acute intermittent therapy. Further, prolonged hyperventilation might even be deleterious based on poorer outcomes at three and six months.42 Hyperventilation beyond 25 mmHg appears to cause profound vasoconstriction and global ischemia and should be avoided.38
Osmotic Agents. An additional option for decreasing ICP in the acute phase includes the administration of an osmotic diuretic, notably mannitol. The benefit of mannitol on ICP, CPP, CBF, and brain metabolism is widely accepted, though controversy exists over the exact mechanism. Mannitol probably lowers ICP by two effects: 1) deceasing blood viscosity by expanding plasma and lowering hematocrit;43,44 and 2) formation of an osmotic gradient across the BBB, allowing brain water to move down this gradient into the intravascular space and be diuresed by the kidneys.45,46 Sources of the brain water include neurons, glial cells, brain extracellular fluid, and possibly CSF. The plasma expanding effect of mannitol appears to be immediate and is best accomplished with bolus administration. The osmotic effect of mannitol is delayed for 15-30 minutes while gradients are established between plasma and cells.47 The maximal effect of mannitol on ICP occurs within 30-60 minutes and lasts 90 minutes to six hours or longer, depending on clinical conditions.45,46,48-50
Empiric administration of mannitol to TBI patients prior to CT scanning or ICP monitoring is controversial. If a patient develops signs of transtentorial herniation (deepening coma, focal neurological signs, anisocoria) or progressive neurological deterioration not explained by extracranial complications, a presumptive diagnosis of increased ICP is made and mannitol administration is appropriate.51 In stable TBI patients, mannitol should be deferred until results of a CT scan and neurosurgical consultation are available. Optimal mannitol dosages and regimens have been debated. Effective lowering of ICP has been found using doses ranging from 0.25 to 1.0 g/kg IV. Data from clinical studies suggest that doses on the lower end of this range are as effective as higher doses.50,52 Mannitol usually is administered 0.25-0.5 g/kg IV every 4-6 hours to maintain ICP within normal limits.46,50
Mannitol is known to cause an "opening" of the BBB through which both mannitol and small molecules from the circulation may pass into the brain.53-55 After numerous doses, mannitol may accumulate in the brain, causing a reverse osmotic shift and increased brain osmolarity. Accumulation of mannitol in the brain is most marked when mannitol has been present continuously in the circulation, such as during continuous mannitol infusion.52,56 Thus, mannitol should be administered as repeated boluses, instead of a continuous infusion. Usage of mannitol also necessitates frequent assessment of serum chemistries and osmolarity, usually obtained every four hours. Mannitol is excreted entirely in the urine. Administration of mannitol in large quantities may cause acute renal failure via acute tubular necrosis, particularly if serum osmolarity exceeds 320 Osm.51 Concurrent administration of other potentially nephrotoxic drugs, or the presence of sepsis or preexisting renal disease, increases susceptibility to renal failure. Adjunctive use of diuretics (such as furosemide), along with the mannitol boluses, has been advocated, presumably to decrease total body water and reduce brain water content. Furosemide is thought to augment the effect of mannitol by producing an analogous gradient in the kidney; however, few data exist to support this effect.57,58 Other osmotically active agents have been studied in TBI patients, notably buffered glycerol 30% sodium ascorbate 20% solution (GLIAS). Data suggest that this hyperosmolar solution may be similar to mannitol but has a prolonged effect.59
Sedative and Hypnotic Agents. Many patients with severe TBI initially are combative or agitated. Straining and resisting against physical restraints or the ventilator may cause detrimental ICP increases. Parenteral benzodiazepines assist in reducing agitation and anxiety, limiting ICP increases. They stimulate the activity of inhibitory neurons by acting on brain GABA receptors. Midazolam is a popular choice for managing agitation in the ED, though lorazepam has the added benefit of a longer duration of action and is a more powerful antiepileptic. Benzodiazepines do not decrease ICP and have minimal effect on hemodynamics. TBI patients, even those who are comatose, perceive pain, as is manifested by increases in ICP, blood pressure, and heart rate.60 Management of pain in TBI patients should not be neglected. Opiate agents may be administered as boluses or drips; fentanyl is preferred in the emergent setting, as it has less effect on blood pressure and is titrated more easily due to its shorter half-life.61 The effects of opiates and benzodiazepines may be reversed by naloxone and flumazenil, respectively; however, this may precipitate dangerous increases in ICP, and severe agitation and should be avoided.62 Administration of flumazenil also may cause seizures. Alternately, sedative/hypnotic agents should be tapered slowly and then discontinued as is appropriate to prevent rebound phenomenon.
Approximately 10-15% of patients admitted with severe TBI ultimately will manifest intractably elevated ICP, which has a mortality of 84-100%.36,63,64 Since the 1930s, high-dose barbiturates have been demonstrated to lower ICP;65 however, known complications have limited their application to the most extreme of circumstances. The most common complication of barbiturates is hypotension, occurring in almost 58% of patients.65 Barbiturate therapy rarely is initiated in the ED but may be considered in hemodynamically stable patients if other ICP-lowering regimens have been unsuccessful. Studies suggest that barbiturates lower ICP and exert their cerebral protective effects through several distinct mechanisms: changes in vascular tone, inhibition of free radical mediated cell membrane lipid peroxidation, and suppression of cerebral metabolism.66,67 Barbiturates appear to affect coupling of CBF and metabolism, lowering metabolic requirements, decreasing cerebral blood flow and related cerebral blood volume, and improving ICP and global cerebral perfusion.68
Pentobarbital is the most commonly studied barbiturate. All barbiturates will suppress metabolism; however, not much is known about their comparative efficacy except with reference to their particular pharmacological properties. The pentobarbital loading dose is 10 mg/kg IV over 30 minutes, followed by 1.0-1.5 mg/kg/hour IV for the induction of coma. Pentobarbital levels are checked periodically and adjusted to maintain 3.0 mg/dL.68,69 Studies have demonstrated that barbiturates could be used to decrease ICP in the event of intractably elevated ICP. Patients with uncontrollable ICP despite administration of barbiturates had a higher mortality.35,69,70 Prophylactic use of barbiturate, however, has not proven to improve neurological function after TBI and may even worsen the patient’s condition.71 Other new hypnotic agents, notably propofol, have similar central nervous system depressant effects. Propofol has the additional advantage of a shorter duration of action, and patients recover from the sedative effects minutes after stopping the infusion. As a result, patients who require frequent neurological checks may be evaluated more easily.72 Like barbiturates, however, propofol causes hemodynamic depression and is not recommended for hemodynamically unstable patients.62,73
Steroids. Numerous studies have failed to demonstrate the benefit of high-dose glucocorticoids on ICP or outcome in patients with severe head injury (presenting with GCS score of 8 or less).74-78 Although principally used in the management of cerebral edema secondary to brain tumors, steroids were administered readily in the 1970s and early 1980s for treatment of cerebral edema related to head injury. Data from experimental models suggested that steroids were useful in the restoration of altered vascular permeability in brain edema, reduction of CSF production, and blunting of free radical production. Steroids lessen vasogenic edema surrounding cerebral neoplasms; however, they do not appear to affect cytotoxic edema associated with TBI caused by secondary brain injury. Despite lack of evidence to suggest their benefit, many hospitals continue to administer steroids to TBI patients.79 Problems associated with the administration of steroids include increased risk of infection, alterations in fluid and electrolyte balance, and suppression of the hypothalamus-pituitary-adrenal cortex axis. Therefore, the use of steroids is no longer recommended for attenuation of ICP in patients with severe TBI.80 However, in patients with concurrent spinal cord injury, current literature supports the use of steroids.81
Seizure Prophylaxis. Posttraumatic seizures (PTS) are characterized as early PTS and late PTS, occurring within seven days of injury and after seven days of injury, respectively.82 Prevention of both early and late PTS is desirable; however, anticonvulsant therapy is associated with neurobehavioral and other side effects, including rashes, Steven-Johnson syndrome, hematological abnormalities, and ataxia.83 Approximately 4-25% of all TBI patients suffer from early PTS, and risk of development of PTS appears to depend on the severity of the injury.84 These risk factors include the following: GCS score of less than 10, cortical contusion, depressed skull fracture, subdural hematoma, epidural hematoma, intracerebral hematoma, penetrating head wound, and seizure within 24 hours of injury.85 (See Table 1.)
| Table 1. Indications for Seizure Prophylaxis |
| GCS score < 10 |
| Cortical contusion |
| Depressed skull fracture |
| Acute subdural hematoma |
| Acute epidural hematoma |
| Acute intracerebral hematoma |
| Penetrating head wound |
| Seizure within 24 hours of injury |
| Prior history of seizures |
| Adapted from: Anonymous. The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Role of antiseizure prophylaxis following head injury. J Neurotrauma 2000;17:549-553. |
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Patients with prior history of seizures also may be considered to be at high risk for developing PTS. Early PTS do not appear to cause chronic epilepsy; however, early seizures may worsen secondary brain injury by increasing metabolic demands in the brain and systemic tissues and precipitating hypercarbia, hypoxia, and release of excitatory neurotransmitters.83 Further, breath holding, tonic-clonic movements, and hypertension during the seizure may increase ICP.86
Late PTS also are common in TBI patients, the occurrence of seizures exceeding 12 times the population risk within the first year of TBI.87 As with early TBI, the risk of late PTS also depends on the severity of injury. The incidence of epilepsy in patients with neurological deficits with the dura mater intact is 7-39%. In patients with penetration of dura mater and neurological abnormalities, the incidence range increases to 20-57%. Although the time frame between TBI and onset of seizures varies, up to 57% of TBI patients will develop seizures within one year of injury.88 Eighteen percent of patients with penetrating TBI may not have their first seizure until five years or more following injury.89 The development of seizures is characterized by alterations in membrane potential and synchronization of neurons in the focus. Following TBI, biochemical injury to neurons may induce a number of changes, ranging from loss of neurons and replacement with glial cells to changes in neuronal membranes. The actual mechanism inducing posttraumatic epileptogenesis remains unknown; however, it likely is related to trauma-induced release of excitatory neurotransmitters.85
In the early management of TBI, the approach to seizures is similar to that in the nontrauma patient. Actively seizing patients should receive intravenous benzodiazepines as first-line agents. Diazepam (5 mg IV push) or lorazepam (2-4 mg IV push) every five minutes may be used until the seizure stops or a maximum of 20 mg of diazepam or 8-10 mg of lorazepam is approached. If benzodiazepines are unsuccessful in aborting the seizure, barbiturates may be initiated. For the prevention of further seizures, phenytoin (10-20 mg/kg IV) is loaded as soon as possible at a rate no faster than 50 mg/min.90 Fosphenytoin, a newer synthetic, water-soluble, pro-drug form of phenytoin, can be administered more quickly (15-20 "phenytoin equivalents" per kg IV or IM at 100-150 mg/min). In patients who are paralyzed, manifestations of seizure activity may be difficult to ascertain; therefore, prophylactic therapy may be considered in paralyzed TBI patients in the acute phase. Continuous EEG monitoring facilitates ongoing evaluation of seizure activity in paralyzed patients and should be started in the ED or ICU. Phenytoin also should be administered prophylactically in high-risk TBI patients. A recent study demonstrated that treatment with phenytoin was associated with a 73% decrease in early PTS (< 7 days) as compared with placebo. No significant benefit, however, was observed between day 8 and year 2 of the study.91 Therefore, prophylactic phenytoin does not appear to prevent late PTS and should be discontinued after day 7 following TBI.82 The approach to management of late PTS is the same as that of new onset seizure. Administration of phenytoin may cause cardiac arrhythmias and rate-related transient hypotension.86 This hypotension is best avoided as it is remarkably recalcitrant to fluid or pressor therapy.
Antibiotics. Wounds resulting from penetrating injuries have a high propensity to develop infection because of the presence of contaminated foreign objects, hair, skin, and bone fragments driven into the brain. Stab wounds, in particular, are prone to developing delayed meningitis and brain abscess because these injuries may not cause neurological deficit and can be overlooked.92 The patient should be screened for small puncture wounds, especially in the anterior temporal and anterior frontal regions.93 When evaluating a patient for penetrating and perforating wounds, no attempt should be made to remove the wounding instrument in the ED. The degree of debridement necessary is under debate and likely is better accomplished in the operating theater. During World War I, the rate of intracranial infection in the preantibiotic era was reported to be 58.8%.94 More recent military and civilian series estimate an infection rate of 4-11% depending on the antibiotic regimen.95 Risk factors for the development of infection include CSF leaks, air sinus wounds, and wound dehiscence.96,97 The most frequent causative agent is Staphylcoccus; however, gram-negative bacteria and anaerobic organisms may be involved. Although there is no consensus for which antibiotic to use, current recommendations support the use of a broad-spectrum antibiotic.95
Cranial Decompression. Evacuation of hematoma and emergency craniotomy is key in the care of significant TBI-associated epidural hematoma (EDH) and subdural hematoma (SDH). SDH, in particular, is the most important cause of death in severe TBI patients, accounting for 60% of deaths.98 Thirty percent of patients with TBI have subdural bleeding, but only 0.5% of patients will have EDH.99 SDH is formed by the coagulation of blood between the arachnoid and dura, whereas EDH forms between the skull and dura. Eighty percent of cases of EDH are linked with skull fractures overlying the temporoparietal region, likely due to laceration of the middle meningeal artery or dural sinuses.99 Most EDHs are unilateral, although 40% will have associated lesions, including subarachnoid hemorrhage, contusion, or SDH. EDHs that develop from arterial bleeding form rapidly and usually are detected within hours of injury. If a non-comatose patient is diagnosed with an EDH, the mortality rate is nearly zero; however, once the patient becomes comatose, mortality increases to 20%.99 Posterior fossa bleeds (cerebellar) also have a marked increase in mortality once the patient becomes comatose. Clinical presentation of EDH classically is described as TBI precipitating a decreased level of consciousness followed by a return to normal mental status and then neurological deterioration. Medical literature often refers to such cases as examples of the "talk and deteriorate" syndrome,100-102 although only 30% of patients present with these classic symptoms.98 Of note, the "lucid interval" is not particular to EDH; 50-60% of patients with SDH also will have a similar interval.102,103 EDHs appear as hyperdense, biconvex, lenticular structures on CT scan, and the most common site is the temporal region. (See Figure 1.)
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Depending on how quickly the EDH is expanding, patients with EDH may complain of severe headache, dizziness, vomiting, and sleepiness. SDHs are formed by the shearing of bridge veins between the arachnoid and dura and tend to be more common in atrophic brains, such as those of alcoholics and the elderly. SDHs are classified according to time to presentation. Acute SDH is symptomatic within 24 hours of injury, subacute SDH is symptomatic 24 hours to two weeks after injury, and chronic SDH is symptomatic after two weeks. Lower GCS score (3-5), advanced age (65 and older), or unilateral pupillary dilatation and nonreactivity to light are associated with a markedly increased mortality rate, ranging from 54% to 100%.104 An acute SDH appears on the head CT scan as a hyperdense, crescent-shaped lesion that becomes isodense or hypodense as the hematoma ages. (See Figures 2 and 3 for an acute SDH and chronic SDH, respectively.)
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Patients tend to present with signs and symptoms of headache, nausea, vomiting, altered mental status, changes in personality, or muscle weakness. In subacute or chronic SDH, patients may not recall the event or may relate a seemingly minor incident. Signs and symptoms of chronic SDH can be understated; however, almost half the patients have some unilateral weakness or hemiparesis. Forty-five percent of chronic SDH will rebleed. The overall mortality of chronic SDH is 10%, with an increased mortality in the elderly.99 Survival from SDH appears not to be related to the size of the hematoma, but to other intracranial injuries caused by the initial impact and pressure from the hematoma. Chronic SDH may be misdiagnosed as dementia. A traumatic subarachnoid hemorrhage (SAH) is depicted in Figure 4.
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Acute SDH is associated with severe profound reduction in CBF adjacent to the mass.105 Forty percent of TBI patients who have a GCS score of 9 or less unexplained by ethanol or drugs will have a significant hematoma, and many of these patients will require surgery.2,106 One group of researchers observed a marked decrease in morbidity and mortality in patients with acute SDH who underwent craniotomy for evacuation of the hematoma within four hours of their injuries.107 In their series, 30% of patients who underwent surgery within four hours died and 65% had functional recovery. When surgery was delayed past four hours, the mortality rate rose to 85% and functional recovery decreased to 7%. A more recent study, however, demonstrated that controlling ICP was more important to outcome than the absolute timing of surgery. Therefore, overall brain injury may be more crucial than the SDH itself in determining outcome.108 CT scan is the swiftest and safest way to diagnose intracranial hemorrhage at present. Indications for surgery include: penetrating injury, depressed skull fracture, expanding mass lesions, and epidural hematoma. The decision for surgical intervention for SDH, focal contusion, or intracerebral hemorrhage is case-by-case and timing is individualized. Spontaneous resolution of EDH or SDH is rare;109-111 however, some neurosurgeons may choose to manage small SDHs (only a few millimeters in diameter per CT scan) nonoperatively. The need for emergency craniotomy is twofold: first, to remove the nidus increasing ICP or mass effect; and second, debridement of contaminated, open wounds in penetrating trauma. Treatment of chronic SDHs is controversial; however, surgical intervention is indicated if they become symptomatic.99 Surgical intervention also may be necessary in TBI that is associated with intracerebral hemorrhage to control intractable ICP.
Monitoring the TBI Patient
Lack of sufficient monitoring of serious TBI patients is one of the more commonly cited deficiencies in the care of these patients.90 In the ED, monitoring of patients includes vital sign and GCS score assessment, urine output, serial arterial blood gases, and oxygen saturation measurements. Of course, the frequency and complexity increases according to the severity of the injury. Placement of arterial catheters may assist with measurement of MAP and permit frequent ABGs. Patients with other injuries may necessitate placement of a central venous line and/or Swan-Ganz catheter for fluid resuscitation and evaluation of hemodynamics.
Serious TBI patients also may require monitoring of intracranial parameters, specifically ICP and CPP. Elevated ICP following TBI is common and is associated with poorer outcome; however, the benefits of ICP monitoring, per se, has never been analyzed in a prospective, randomized clinical trial. Nevertheless, clinical experience implies that ICP monitoring 1) assists the detection of intracranial mass lesions; 2) helps determine prognosis; and 3) improves outcome.112 Current indications for ICP monitoring include patients with severe head injury (GCS score 3-8) after ATLS resuscitation and an abnormal head CT scan. An abnormal head CT scan is one that demonstrates hematoma, edema, contusion, or compression of basal cisterns. ICP management also is indicated in patients with severe head injury with a normal CT scan if two or more of the following factors are present: age greater than 40 years, unilateral or bilateral motor posturing, or systolic blood pressure less than 90 mmHg. Routine ICP monitoring usually is not required in patients with mild or moderate TBI. Normal ICP is 0-10 mmHg (0-135 mmH20) and ICP treatment should be started at an upper limit of 20-25 mmHg.112,113 However, research group observed that patients with pressures as low as 18 mmHg may herniate; therefore, ICP monitoring does not substitute for frequent neurological checks.33 Recent data suggest that CPP, which reflects the pressure gradient driving CBF and metabolic delivery, is more closely indicative of ischemia. Low CPP may endanger areas of the brain with preexisting ischemia, and augmentation of CPP may enhance CBF. Therefore, therapy should be directed at both maximizing CPP and minimizing ICP.
The most popular method for ICP monitoring is ventriculostomy; the intraventricular catheter placed in the brain allows not only for measurement of intracranial pressure, but also for drainage of CSF from the brain to alleviate elevated ICP and for measurement of biochemical parameters. Information about the rate of CSF production and absorption also may be ascertained by ventriculostomy. A ventriculostomy involves the blind introduction of a plastic catheter through brain tissue into the frontal horn of the lateral ventricle. Once in position, the catheter is hooked up to a transducer and monitor. Hemorrhage and infection are the major complications of ventriculostomy. The rate of infection is proportional to duration of time the catheter is in the ventricle. Other methods of measuring ICP include the subarachnoid bolt method to insert a catheter into the subarachnoid space and the use of fiberoptic catheters; however, at this point they are not widely in use due to decreased reliability and increased expense, respectively.90
In the ED, the decision to monitor ICP is made on an individual basis. ICP monitoring is accepted as a relatively low risk, high-yield, modest cost intervention. However, placement of an ICP monitor involves coordination of ED physicians, neurosurgeons, trauma surgeons, and nursing staff so that the appropriate equipment is readily available. In some cases, ICP monitoring in the ED may be desired but not possible due to inadequate or inexperienced personnel. The procedure also takes some time to perform, and may not be feasible in the multiply traumatized patient. In this situation, an expeditious ED work-up and transfer of the patient to an appropriate ICU for definitive monitoring may be preferred.90
Moderate Head Injury
Moderate TBI is classified as a post-resuscitative GCS score of 9-12 and includes approximately 10% of all patients who sustained head trauma.99 Many authors chose to include patients with GCS scores of 13 in this category, as these patients appear to have similar complication rates.114-121 Patients in this group tend to be victims of motor vehicle accidents, and alcohol frequently is involved. A study of moderate head trauma demonstrated that in comparison to minor TBI, moderate TBI victims were twice as likely to be intoxicated.122 The pathophysiology of moderate TBI is on the same continuum as that of severe TBI and likely represents the earlier reversible changes. As a consequence, these patients deserve special mention, as prompt medical care is likely to result in the greatest improvement in overall neurological function. Patients with severe TBI, on the other hand, have significant primary brain damage that more likely is irreversible and, therefore, resuscitation is less apt to be fruitful.
The initial resuscitation of moderate TBI patients is similar to that of severe TBI victims. Special attention is paid to the airway patency, as many patients suffer from facial injuries. As mentioned before, there is no specific GCS score that mandates intubation. Patients should be monitored continuously, and hypoxia and hypotension should be treated aggressively to avoid secondary systemic insults. Patients with moderate TBI have a wide range of clinical presentations, but most are able to obey commands. Many patients will complain of headache, amnesia, nausea, and vomiting. Clinical examination usually is not able to predict which patients will necessitate surgery. A head CT scan is crucial to the timely management of moderate TBI, and 40% of patients will have an abnormal head CT scan. Ten percent of patients will deteriorate into coma.99 Repeat head CT scans are mandated if the patient’s condition worsens or fails to improve 48 hours post injury.
All moderate TBI patients warrant admission for observation, despite a normal CT scan. In-hospital management includes frequent neurological examinations and repeat head CT if the patient’s neurological condition worsens. The duration of hospital stay is decided on an individual basis, and 90% of patients should improve during the first 72 hours. Moderate TBI results in morbidity and mortality intermediate between those of severe and minor TBI. Only 20% of moderate TBI patients die; however, the morbidity associated with moderate TBI is substantial. One group of researchers observed that only 38% of moderate TBI patients made a good recovery at three months compared to minor TBI victims. Within the category of good recovery, nearly all patients had chronic neurological complaints; 93% had headache, 90% had memory difficulties, and 87% had problems with activities of daily living. Only 7% were asymptomatic. Two-thirds of patients who previously were employed had not returned to work.122 Emotional lability also is common. Victims of moderate TBI with these chronic neurological complaints may return to the ED for reevaluation. A repeat head CT scan may reveal a subdural hematoma necessitating surgical drainage. In patients with a negative CT scan, an MRI scan can be useful to define lesions not visualized on CT scan and may help direct future rehabilitation.123
Minor Head Trauma
Approximately 80% of all TBI are minor, and minor TBI is the second most common neurological diagnosis in the ED after migraine headache. The causes of minor TBI are the same as those of more severe TBI.124 Lesser mechanisms of injury, such as assaults, falls, and whiplash, are more common causes of minor TBI. Minor TBI traditionally has been classified as head trauma producing a GCS score of 13-15.122,125 As mentioned before, patients with GCS scores of 13 have complication rates comparable to those with moderate TBI. These patients also have a markedly higher percentage of abnormal findings on CT scans than patients with GCS scores of 14-15. Data suggest that 33.8% of patients with GCS scores of 13 will have abnormalities on head CT and 10% will require emergency surgery, either hematoma evacuation or ICP monitor insertion.114-119,124,126,127 Therefore, some authors favor the definition of minor head trauma as that producing a GCS score of 14-15,120,128 while others use only a GCS score of 15.126,129 Nevertheless, it has been suggested that the GCS score may not be the best way to assess patients with minor injuries. The GCS score originally was designed for estimating prognosis from severe TBI. The GCS score may be insensitive for detecting subtle mental changes in minor TBI patients. For example, a patient who immediately opens his or her eyes to a simple question is very different from a patient who barely does so to shouting, even though both have an eye opening score of 3.130 The first patient may be observed with repeated clinical examinations, whereas the second individual would warrant a CT scan. Further, many studies examining GCS score and the correlation with CT scan abnormalities did not address the presence and degree of ethanol intoxication. Therefore, it is questionable how useful the GCS score is in defining mild TBI. Some investigators believe that the definition should be simply, "blunt head injury but awake and alert."131 However, because of its repeated use in the literature the GCS score has been used in minor TBI populations to study and define clinical rules.
The primary neuropathology of minor TBI is diffuse axonal injury caused by shearing forces generated by rapid deceleration. These forces disrupt structures coursing the long axis of the brain, leading to axonal injury and excitatory neurotransmitter release, as previously described. The primary distribution of damage appears to be in the parasagittal deep white matter connecting cortex to brainstem. This pattern of injury likely is responsible for the eventual preponderance of cognitive and attention deficits observed in these patients. Disruption of small veins may cause small petechial hemorrhages that may cause focal or local edema.
Computed Tomography. The management of patients with minor TBI is similar to that of severe TBI, with emphasis on reduction of factors precipitating secondary injury. The most contentious point in the care of minor TBI patients is when to obtain a head CT. Data suggest that it is more cost-effective to scan minor TBI patients than to admit them for observation.132 However, obtaining a head CT scan is expensive and time-consuming. As a consequence, many investigators have directed their attention toward identifying clinical findings associated with significant intracranial lesions. It is difficult to combine the published studies to formulate a guideline for head CT scanning. Studies differ in terms of patient inclusion criteria, the definition of minor head trauma, and the decision to obtain a head CT scan. Numerous studies included only patients with LOC and/or posttraumatic amnesia, while other studies did not mandate this as a selective inclusion criteria. Many of the surgical studies included admitted patients only.7,121,133,134 Some investigators did not scan their entire sample.7,133-135 Further, many studies did not differentiate between the severity and types of CT scan abnormalities.
Retrospective data generally support the use of head CT in patients with GCS scores of 13-147,116,120,121,136 unless alcohol is involved.131 One study showed that 20-35% of patients with GCS scores of 13-14 have abnormal CT scans, and many required surgical intervention.137 Therefore, the current impetus is to identify which patients with GCS scores of 15 — who represent the vast majority of TBI patients seen in the ED (65-85%) — require head CT scan. LOC is the most frequently sought-after piece of historical information, the premise being that patients who do not have LOC are unlikely to have significant brain injury. Studies have demonstrated that a small percentage of patients with seemingly mild TBI, all of whom had transient LOC before presentation, "talk and deteriorate."138 As a consequence, many trauma centers obtain head CT scans on all patients who present with a history of LOC.136,140,141 Note however, that patients may harbor intracranial lesions even in the absence of LOC and posttraumatic amnesia.131 Two reports on minor TBI patients found that LOC was absent in 50% of all patients135 and in 67% of ethanol-intoxicated patients142 with CT evidence of craniocerebral injury. These studies put into question whether LOC should be a part of the definition or clinical decision rules for CT scanning in minor head injured patients.
Scanning all patients with GCS scores of 15 and LOC is still tedious and very costly. Nevertheless, studies have shown that the patient with mild head injury has the most to gain from early identification of an intracranial lesion. In a recent prospective analysis, such patients (GCS score of 15, positive LOC with normal cranial nerves, strength and sensation in arms and legs) were evaluated to determine which clinical findings identified patients with positive findings on head CT. Patients with amnesia for the traumatic event in the face of questionable LOC also were included. Data showed that the presence of one or more of the following factors was predictive of a positive head CT scan: headache, vomiting, age older than 60 years, drug or alcohol intoxication, deficits in short-term memory, physical evidence of trauma above the clavicles, and seizure. (See Table 2.) The combination of these findings had a sensitivity of 100%; however, the study is limited by failure to define duration of LOC for inclusion in the study and which of the identified lesions required surgical intervention.141
| Table 2. Findings Associated with Positive Head CT Scan |
| In TBI Patients with GCS score of 15 and LOC:1 |
|
Drug or alcohol intoxication Physical evidence of trauma above clavicles Age > 60 years Seizure Headache Vomiting Short-term memory deficits |
| In TBI Patients with GCS of 15 regardless of LOC:2 |
|
Clinical signs of skull fracture or skull fracture base Therapeutic coagulation or hemophilia Posttraumatic seizures Shunt-treated hydrocephalus |
|
|
| 1. Adapted from: Haydel MJ, Preston CA, Mills TJ, et al. Indications for computerized tomography in patients with minor head injury. N Engl J Med 2000 343:100-104. |
| 2. Adapted from: Ingebrigtsen T, Romner B, Kock-Jensen C. Scandinavian guidelines for initial management of minimal, mild, and moderate head injuries. J Trauma 2000;48:760-765. |
|
|
A contemporary study from Sweden identified other factors associated with increased risk of acute intracranial pathology regardless of reported LOC, including: clinical signs of depressed skull fracture or skull fracture base, anticoagulation or hemophilia, posttraumatic seizures, and shunt-treated hydrocephalus.129 (See Table 2.) More recently, Stiell and colleagues created the Canadian CT Head Rule to risk-stratify patients presenting with GCS scores of 13-15 for neurological intervention or death within seven days secondary to head injury. Patients with suspected open or depressed skull fractures also are considered to be high risk for neurological intervention, as are those with any sign of basal skull fracture, two or more episodes of vomiting, age 65 years or older, and GCS score of less than 15 two hours after injury. The neurological interventions included craniotomy, elevation of skull fracture, ICP monitoring, or intubation for head injury (revealed by head CT scan). Patients with lack of recall about a period longer than the 30 minutes prior to impact and dangerous mechanism (pedestrian struck by a motor vehicle, occupant ejected from a motor vehicle, fall from a height greater than 3 feet or the height of five stairs) were considered to be medium-risk for brain injury on CT.142 More objective predictors for identifying high-risk individuals are being evaluated, including the use of serum markers such as dopamine and epinephrine.143
In evaluating a patient with minor TBI, the physician needs to define the goals that are to be achieved. Presumptively, the primary aim should be to prevent patients who are likely to deteriorate rapidly from being discharged from the ED to home. This phenomenon, albeit devastating, is very rare (0.3%).144 The question then becomes whether a few such cases should dictate universal CT scan policy. Even if the goal is to identify all patients who will eventually require neurosurgical intervention, based on less than 1% prevalence of neurosurgical lesions in patients with GCS scores of 15, it also may be possible to omit a CT scan in these patients. If the goal is to identify all patients with an abnormal CT scan, it is unlikely that a simple algorithm will identify all patients with a positive scan. Even patients with an initial normal neurological examination and normal head CT can develop a hematoma requiring surgical intervention.145 Based on our review of current literature, most authors suggest routine CT scanning on all patients with GCS scores of 14 or less. For patients with GCS scores of 15, consideration may be given to the risk factors listed in Tables 1 and 2; however, a more specific recommendation cannot be offered at this time. Another option to contemplate is observation of the patient. One group proposed scanning patients with GCS scores of 13 and 14 if their GCS scores do not improve to 15 within two hours.142 One could extrapolate the two-hour observation time frame to GCS patients presenting with a GCS scores of 15 based on the perception that patients who deteriorate from significant hematomas tend to so within hours.144 A Danish study evaluated the outcome of 2204 patients who presented to the ED with minor TBI. Through the use of the National Danish Patient Registrar and the Danish Cause of Death Registrar they were able to determine that there was no morbidity and mortality at one-year follow-up in patients discharged from the ED without CT scanning. All four patients (0.3%) in the study who developed an intracranial complication were identified in the first hour after arrival in the ED, due to a decline in consciousness.144
Post-Concussion Syndrome. Approximately 50% of patients with mild TBI suffer from post-concussion syndrome (PCS),146 which is comprised of one or more of the following symptoms and signs: headache, dizziness, difficulty with memory or concentration, depression, vertigo, tinnitus, hearing loss, diplopia, hyperacusis, photophobia, diminished taste and smell, fatigue, anxiety, personality change, sleep disturbance, decreased libido, decreased appetite, memory dysfunction, and slowing of reaction time and information processing speed.147 These symptoms arise within the first few days following injury. Headaches have been estimated to occur in about 30-90% of patients. Of interest, patients with more mild head injury tend to have headaches more frequently and of greater duration than those patients with more severe TBI. The varieties of posttraumatic headaches include muscle contraction; occipital, supraorbital, and infraorbital neuralgia; migraine; cluster; referred pain from neck and temporomandibular joint injury; and pain secondary to scalp lacerations or local trauma. Eighty-five percent of posttraumatic headaches are due to muscle contraction of the superior trapezius or semispinalis capitis muscles precipitating occipital neuralgia. Dizziness is a common complaint following mild TBI and occurs in 53% of patients within one week of injury. Etiologies include labyrinthine concussion, benign positional vertigo due to dislodged otoliths, and perilymph fistula. Hearing loss may be caused by conduction from blood in the middle ear, disruption of the ossicular chain, or damage to the auditory nerve. Fourteen percent of patients report blurry vision. Somatic complaints also are common, with fatigue reported in up to 29% of patients.148 Twenty-three percent of these patients could not spontaneously remember any discharge instruction from their ED visit.149 Mild TBI patients also may perform less well on complicated tasks involving prolonged attention and rapid response times.
These signs and symptoms largely resolve within one month. After three months, neurological improvement is substantial, and only 30-50% of patients of the original group are limited by symptoms. By one year, 85-90% of patients will have nearly full recovery, though many may have subjective decreased mental functioning. The risk of developing seizures within five years of mild TBI (no skull fracture) is the same as that of the general population (0.8%).150 Well-motivated young patients with the mildest concussions—those without LOC—tend to be at low risk of developing significant PCS and usually recover within a few days.147 Age older than 55, female sex, and prolonged post-traumatic amnesia are associated with a higher risk of developing PCS.151 Patients with symptoms persisting after one year are classified as having persistent post concussive syndrome (PPCS). Factors predicting PPCS include female sex, low socioeconomic status, alcohol abuse, serious other illnesses, or prior mild TBI.151 Contrary to popular belief, malingerers comprise a small percentage of patients, and verdicts seldom cure patients with litigation or compensation claims.152 Treatment of PCS and PPCS is fundamentally supportive and may involve psychotherapy, psychoactive medications, neuropsychiatric testing, and neuropsychological exercises. Antidepressants, such as amitriptyline (25-40 mg PO daily), may assist with the relief of posttraumatic muscle contraction headache, irritability, fatigue, depression, and insomnia.153 TBI-related migraine headaches usually respond to migraine medications, such as amitriptyline, propranolol, calcium channel blockers, and non-steroidal anti-inflammatory drugs (NSAIDs).147
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