1. Description of the problem
TBI is an isolated head injury or head injury associated with polytrauma. The impact in severe head injury is due to either focal injury (contusion, hemorrhage) or diffuse axonal injury. Secondary brain injury occurs over subsequent hours and includes surgical mass lesions, cerebral edema, hypotension, hypoxia, hyper/hypocarbia, hyper/hypoglycemia, anemia, fever, electrolyte abnormalities, coagulopathies, and infection. This leads to free radical damage, amino acid excitotoxicity, lipid peroxidation, calcium-mediated damage, neuroinflammation, ischemia, and neuronal death.
Glasgow Coma Scale score of 8 or less, INTUBATE ! (See Table I)
1. ABCs (airway, breathing, circulation)
2. Assess GCS score.
3. Obtain CT scan. The immediate priority after patient stabilization is identification of any lesion/fracture on CT brain. Surgical management in a timely fashion of acute subdural hematoma, epidural hematoma, intracerebral hematoma if indicated. The decision to operate is based on patient’s clinical condition, pupillary size and reaction, GCS at scene, age, functional status, comorbid conditions, and ongoing resuscitation status
4. Transfer to Neuroscience ICU center. If GCS ≤ 8, place intracranial pressure (ICP) monitor. Coagulopathy (which frequently accompanies severe head injury, as the body’s richest source of tissue plasminogen activator [tPA] is in the brain) should be corrected first. Continue ICP measurements for as long as ICP-lowering treatment is required (including sedation, paralysis, CSF drainage, osmotherapy [eg, mannitol and hypertonic saline, hypothermia, mild hyperventilation]).
5. Barbiturate-induced coma and decompressive hemicraniectomy: last resort for intracranial hypertension refractory to medical management
2. Emergency Management
1. ATLS trauma evaluation (Airway, Breathing, Circulation, fluid resuscitation, evaluate laboratory values)
2. Assess GCS. Rapid neurological assessment, including checking for pupillary response, corneal, cough, gag, motor exam, reflexes, rectal tone). Adjust exam based on level of consciousness.
3. Look for signs of basilar skull fractures (raccoon eyes, Battle’s sign, cerebrospinal fluid leak [otorrhea or rhinorrhea])
4. Spine precautions
5. Assess for signs of herniation or worsening level of consciousness to evaluate for increasing ICP.
6. Stat CT scan of the brain and secondary survey for concomitant injuries.
Investigation of the CT brain may show intracranial mass lesions, including subdural hematoma, epidural hematoma, or intracerebral hematoma. If the size of the mass lesion warrants prevention of mass effect and midline shift, the patient is taken emergently to the operating room for evacuation. Evacuation of the hematoma may be accompanied by removal of the bone flap (craniectomy) and placement of an ICP monitor (ie, ventriculostomy, intraparenchymal fiberoptic catheter, epidural transducer, subdural catheter, or subdural bolt).
If no intracranial mass lesion found and patient continues to have a GCS score of 8 or less, consider elevated ICP secondary to global or focal swelling, which requires immediate treatment. This includes placement of an ICP monitor after correcting coagulopathy and osmotherapy.
In a patient with a low GCS score, evaluate:
1. anatomic features of injury
2. blunt versus penetrating injury
3. closed versus open skull injury
4. focal versus diffuse injury
5. hemorrhagic versus nonhemorrhagic injury
Evaluate with a stat CT of the brain.
How do I know this is what the patient has?
The diagnosis is based upon clinical findings and radiological findings. A CT brain is required if any of the following are present: GCS score <15, suspected open or depressed skull fracture, sign of fracture at the skull base (raccoon eyes, Battle’s sign, hemotympanum, cerebrospinal fluid leakage from the ears or nose), post-traumatic seizure, focal neurological deficit, vomiting, amnesia of events.
An unenhanced CT brain should be ordered in patients presenting after trauma or with new neurologic deficit. The emergent conditions to rule out include hematomas, subarachnoid blood, intracerebral hemorrhage, hemorrhagic contusion, intraventricular hemorrhage, hydrocephalus, cerebral swelling, skull fractures, ischemic infarction, pneumocephalus, midline shift. In terms of subdural and epidural hematomas, surgical lesions are usually 1 cm or greater in length. Subarachnoid blood is revealed by high-density spread over the convexity and filling of sulci or basal cisterns. When the history of trauma is unclear, an arteriogram may be indicated to rule out a ruptured aneurysm. Intracerebral hemorrhage is defined as increased density in the brain parenchyma, and hemorrhagic contusion is described as inhomogeneous high-density areas within the brain parenchyma adjacent to bony prominences. Intraventricular hemorrhage is present in approximately 10% of severe TBI cases and is associated with a poor outcome. Intraventricular tPA has been reportedly used for treatment at some centers.
Urgent follow-up CT brain is performed for neurological deterioration, persistent vomiting, worsening headache, seizures, or unexplained ICP rise. For stable patients with severe TBI, follow-up CT brains are typically obtained within 24 hours after initial CT brain to rule out delayed epidural hematoma, subdural hematoma, or traumatic contusions. A follow-up CT brain is usually obtained between day 3 to 5, and again between day 10 to 14. For patients with mild to moderate head injury with an abnormal initial CT brain, the CT brain is repeated prior to discharge. In stable patients with mild head injury and normal initial CT brain, a follow-up CT brain is not required.
Consider causes of increased ICP, which include masses/hematomas, foreign bodies, edema, hydrocephalus, venous sinus thrombosis, hypoventilation, abdominal compartment syndrome. However, other causes of altered level of consciousness include seizures, status epilepticus, drug overdose, toxins, alcoholism, alcohol withdrawal, aneurysm rupture, stroke, central nervous system infections, concussion (mild TBI), metabolic disorders or derangements, and hypo- or hyperthermia.
Specific confirmatory tests:
1. CT brain
2. Basic labs, including complete blood count (monitor platelets), basic metabolic panel, liver function panel
3. Coagulation screen, including PTT and INR
4. Urine toxicology screen
5 . Drug toxicology screen
6. Cervical spine films. Spinal injury precautions are continued until the cervical spine is cleared.
7. Thoracolumbosacral films
8. If a CT brain cannot be obtained, a skull X-ray may identify skull fracture, pineal shift, pneumocephalus, or air-fluid levels in the air sinuses.
9. MRI is usually not appropriate for acute head injuries. MRI may be helpful later once the patient is stabilized, to evaluate for brainstem injuries, white matter changes, etc.
4. Specific Treatment
Protocol for Increased ICP Management
1. Airway, Breathing, Circulation. ATLS protocol. Periprocedural antibiotics for intubation have been shown to reduce the incidence of pneumonia in a single study. There is no support for prolonged antibiotic use in intubated TBI patients. Also, early tracheostomy or extubation has not been shown to affect the rates of pneumonia.
2. Elevate head of bed to 30-45 degrees, keep head in neutral position, avoid compression of veins of neck. Elevating the head of bed reduces ICP and mean arterial pressure and therefore increases cerebral perfusion pressure. The effects are immediate. Obtain stat CT brain. Surgery if appropriate.
3. Maintain normocapnia (PCO2 goal 35-50 mmHg), and normalize physiological parameters. Hyperventilation is recommended as a temporizing agent in the reduction of elevated ICP; however, hyperventilation should be avoided during the first 24 hours after injury, given that cerebral blood flow is critically reduced during this period. Prolonged hyperventilation can lead to ischemia. Maintain cerebral perfusion pressures with intravenous fluids and pressors. The actual values of a target blood pressure goal remain unclear. However, hypotension, defined as systolic blood pressure of <90 mmHg, must be avoided or corrected in TBI patients. Although hypotension and hypoxia increase morbidity and mortality from severe TBI, clinical studies have failed to provide supporting data that correcting hypotension and hypoxia improves outcomes. Attempts at maintaining CPP >70 mmHg should be avoided due to increased risk of adult respiratory distress syndrome. CPP <50 mm Hg should be avoided. CPP target should lie within 50-70 mmHg. Evidence supports a level 3 recommendation for use of jugular venous saturation and brain tissue oxygen monitoring (in addition to ICP monitoring) in the treatment of severe TBI patients. Jugular venous saturations <50% are associated with worse outcomes, and low values of brain tissue oxygenation of <10 mmHg with duration >30 minutes are associated with higher rates of mortality.
4. Provide adequate sedation (including propofol, fentanyl, or midazolam). Prolonged EEG to titrate sedation and exclude seizures.
5. Cerebrospinal fluid drainage by ventriculostomy vs. other ICP monitoring device if appropriate. Level 2 recommendations suggest that ICP monitoring should take place in all TBI patients with a GCS score of 3-8 and an abnormal CT brain. Level 3 recommendations suggest that an ICP monitor is indicated in patients with severe TBI patients with a normal CT scan if 2 or more of the following are present: age >40 years, unilateral or bilateral motor posturing, or systolic blood pressure <90 mmHg. A ventricular catheter connected to an external transducer is the most accurate and cost-effective means of monitoring ICP. Infections and hemorrhage associated with ICP monitoring devices are rare and should not deter their insertion. Parenchymal monitors measure ICP similarly to ventricular devices but have the potential for measurement differences due to recalibration issues. Subarachnoid, subdural, and epidural ICP monitoring devices are less accurate. Treatment should be initiated for ICP measurements >20 mmHg. Routine ventricular catheter exchange or prophylactic antibiotic use for a ventricular catheter is not recommended to reduce infection. ICP monitors should be placed under sterile conditions, but there are no data to support routine catheter exchanges or prophylactic antibiotics as a means of preventing cerebrospinal fluid infections.
6. Osmotherapy (mannitol, hypertonic saline). Check osmolality and serum sodium levels at least every three hours. Consider intravenous furosemide if patient has a positive fluid balance. Mannitol is effective in reducing ICP. Current evidence, however, has not been strong enough to make recommendations on the use, concentration and method of administration of hypertonic saline in the treatment of increased ICP. There have not been any published randomized controlled trials to determine the relative benefit of hypertonic saline versus mannitol.
7. Neuromuscular paralysis, especially if difficulty with ICP control and patient continues to cough or move on maximal sedation. Of note, paralysis has been associated with prolonged ICU stay and increased incidence of chest sepsis.
8. Prophylactic hypothermia. Evidence from randomized controlled trials did not demonstrate statistically significant reductions in mortality from TBI. However, patients treated with hypothermia were more likely to have favorable neurological outcomes; preliminary findings suggest that if cooling is maintained for >48 hours, mortality may be reduced. Target temperature associated with better outcomes range between 32-33 and 33-35 degrees Celsius. The rate of rewarming suggested is 1 degree Celsius per hour, 1 degree Celsius per day, or slower.
9. Deep vein thrombosis prophylaxis. Level 3 recommendations are for graduated compression stockings or intermittent pneumatic compression stockings, unless the patient has a lower extremity injury preventing the use of such devices. Low-molecular-weight heparin or low-dose unfractionated heparin should be used in combination with mechanical prophylaxis, but there is increased risk of intracranial hemorrhage expansion. There is currently insufficient evidence to support a preferred agent, dose, or timing of pharmacologic deep venous thrombosis prophylaxis.
10. Although there is no evidence to show that they positively affect outcome, analgesics and sedatives are used as an adjunct for ICP control. Common medications include morphine sulfate, midazolam, fentanyl, sufentanil, and propofol. To prevent ICP elevations, these medications decrease cerebral metabolic rate.
11. If all other medical and surgical treatments have failed, consider high-dose barbiturate therapy. Theoretical benefits include vasoconstriction in normal areas resulting in shunting to ischemic brain, decreased metabolic demand for oxygen, reduction of cerebral blood flow, free radical scavenging, reduced intracellular calcium, and lysosomal stabilization. Barbiturates lower ICP; however, its use has shown no clear benefit in improving outcome. Use of this therapy should be limited to critical care physicians in a setting where continuous hemodynamic monitoring can take place, particularly given the fact that hypotension occurs in approximately 50% of treated patients despite adequate blood volume and pressor therapy.
12. Decompressive hemicraniectomy involves removing a portion of the calvaria and/or large areas of contused hemorrhagic brain. Its use is controversial, as it may enhance cerebral edema formation.
Drugs and dosages
1. Mannitol is given as 1-g/kg bolus followed by 0.25 g/kg rapidly intravenously every 3-6 hours.
2. Lasix is given at 0.7 mg/kg to inhibit CSF production and can be synergistic to the effects of mannitol.
3. Hypertonic saline is administered as 30-60 ml of 23.4% infused over 20 minutes. This can be repeated every 3 hours based on sodium levels. Requires a central line.
4. Morphine sulfate is given as a 4-mg/hr continuous infusion; titrate as needed.
5. Midazolam is given initially as a 2-mg test dose, and then as a 2- to 4-mg/h continuous infusion. Flumazenil is given for reversal.
6. Fentanyl is given as a 2-mcg/kg test dose, and then as a 2- to 5-mcg/kg/h continuous infusion.
7. Sufentanil is given as a 10- to 30-mcg test bolus dose, and then as a 0.05- to 2-mcg/kg continuous infusion.
8. Propofol is given as a 0.5-mg/kg bolus, and then as a 20- to 75-mcg/kg/min continuous infusion; do not exceed 5 mg/kg/hr.
9. Pentobarbital is given as a 10-mg/kg bolus over 30 minutes, then given at 5 mg/kg/hr for 3 doses. Maintenance dose is given at 1 mg/kg/hr.
1. Steroids are not recommended for improving outcome or reducing ICP in TBI patients, and are in fact contraindicated. In patients with moderate to severe TBI, high-dose steroids are associated with increased mortality. This is based on the results from the CRASH study.
2. Anticonvulsants are recommended within 7 days of injury to decrease the incidence of early posttraumatic seizures. Evidence does not support the use of prophylactic anticonvulsants later than 7 days following TBI.
3. TBI patients lose sufficient nitrogen to reduce weight by 15% per week. A 30% weight loss increases mortality rate in non-TBI-injured patients. Data support feeding at least by the end of the first week following TBI, and full nutritional replacement must be implemented by day 7 post-TBI. There are no data, however, to support early feeding within 7 days following TBI. There are not sufficient data to support one method of feeding over another.
4. Hyperglycemia exacerbates hypoxic ischemic brain injury in animal studies, and has been associated with worsened outcome in some Class 3 human studies. Therefore, a goal of normoglycemia should be implemented in the management of TBI.
5. Disease monitoring, follow-up and disposition
Expected response to treatment
Response to treatment depends on the injury. Typically, one looks for an improvement in neurologic exam and improvement in GCS score. For example, there is significantly improved mortality from acute subdural hematomas when evacuated <4 hours after injury (90%) compared with >4 hours (30%).
A wrong diagnosis should be suspected in a neurologically abnormal patient with a normal CT brain, normal ICPs, and normal cerebral perfusion pressures. Consider more global, metabolic causes of encephalopathy.
Treatment for late complications of TBI is typically supportive. Follow-up comprises neurologists, primary care physicians, neuropsychologists, and psychiatrists trained to treat patients who have suffered from a TBI. Recovery is highly variable. Neurosurgical involvement is at the discretion of the individual physician based on practice.
Normal brain function is totally dependent on adequate blood flow, as the brain consumes 25% of the body’s oxygen and 20% of the cardiac output. Primary injury results from direct tissue damage from traumatic mechanism (hemorrhage, contusion, or shearing). Secondary injury is a result of delayed tissue damage, and ischemic injury from elevated ICP or hypotension.
Secondary injury can also be the result of metabolic derangement, which leads to the release of free radicals and excitotoxic neurotransmitters. Systemic causes of secondary cerebral insults include hypoxia, hypotension, electrolyte imbalance, anemia, hyperthermia, hypercarbia, hypoglycemia. Intracranial causes of secondary cerebral insults include intracranial hypertension, delayed intracerebral hemorrhage, edema, hyperemia, carotid dissection, seizures, and vasospasm.
Secondary damage from head injury usually results from intracranial hypertension, and approximately 50% of patients with an severe head injury and abnormal CT scan of the brain will have increased ICP. 13% of patients with severe head injury and normal CT scan of the brain will have increased ICP.
In the United States, trauma is the leading cause of death in ages 45 and younger. The estimated incidence of TBI is 100 per 100,000, resulting in approximately 52,000 deaths per year. Approximately 500,000 admissions for head injury occur each year in the United States. The most common causes are motor vehicle collisions (50%), falls (21%), violence (12%), sports/recreational injuries (10%), etc.
Twice as common in men than women, it is often associated with cervical spine injury, facial fractures, abdominal and orthopedic injuries. Financial burden is estimated to be $100 billion per year. However, the incidences of fatal and nonfatal head injuries have decreased over the past 30 years due to prevention strategies, including seatbelts, DUI (driving under the influence) penalties, and improvement in trauma care centers.
Of note, 50-60% of patients with a GCS score of 8 or less have one or more other organ systems injured. 25% of these patients have surgical lesions, and 15% of patients with head trauma who do not initially exhibit signs of brain injury may deteriorate in a delayed fasion (typically patients with intracranial hematomas).
The mortality for severe TBI is 23%. Outcome has improved significantly over the past 30 years (from 50% to 23%) due to prevention and response to treatment of secondary neurological insults. 60% of TBI survivors have residual deficits, including cognitive impairment, mood changes, and behavioral problems. These factors all affect morbidity, functional status, and quality of life. Poor outcome from closed head injury is increased in patients with persistent ICP values >20 after hyperventilation, particularly within the first 24 hours of injury.
One of the most important predictors for poor outcome is a mass lesion requiring surgical evacuation. Poor prognostic factors include low GCS score on admission, nonreactive pupils, old age, comorbidity, and CT findings including midline shift. Other factors to consider include hypoxia, hypotension, serum glucose concentrations, and hemoglobin. 85% of adults remain disabled for >1 year after sustaining a severe head injury, and neuropsychological studies have shown that many continue to have persistent symptoms 1 year after injury. For patients with minor injuries, 47% have moderate to severe disabilities at 12 months.
Late complications from TBI include posttraumatic seizures, communicating hydrocephalus, posttraumatic syndrome, hypogonadotropic hypogonadism, chronic traumatic encephalopathy, and Alzheimer’s disease.
What’s the evidence?
Description of the Problem
Lu, J, Marmarou, A, Choi, S. “Mortality from traumatic brain injury”. Acta Neurochir. vol. 95. 2005. pp. 281-5.
Diagnosis, Emergency Management, and Epidemiology
Tsang, KK, Whitfield, PC. “Traumatic brain injury: review of current management strategies”. British Journal of Oral and Maxillofacial Surgery. 2011.
Chesnut, RM. “=Management of brain and spine injuries”. Crit Care Clin. vol. 20. 2004. pp. 25-55.
Rangel-Castillo, L, Gopinath, S, Robertson, CS. “Management of intracranial hypertension”. Neurol Clin. vol. 26. 2008. pp. 521-41.
Specific Treatment and Pathophysiology
Dunn, J, Smith, M. “Critical care management of head injury”. Anesthesia and Intensive Care Medicine. vol. 9. 2008. pp. 197-201. Provides TBI management strategies in a critical care setting, including fluid hydration, ICP monitoring, pressor therapy, analgesia.
Pompucci, A, De Bonis, P, Pettorini, B, Petrella, G, Di Chirico, A, Anile, C. “Decompressive craniectomy for traumatic brain injury: patient age and outcome”. Journal of Neurotrauma. vol. 24. 2007. pp. 1182-8.
Winter, CD, Adamides, AA, Lewis, PM, Rosenfeld, JV. “A review of the current management of severe traumatic brain injury”. Surgeon. vol. 3. 2005. pp. 329-37.
Guidelines for the management of severe traumatic brain injury. 2007. (TBI experts drafted a list of guidelines, based on detailed literature review of class 1, 2, and 3 data on management of patients with TBI.)
Marquez de la Plata, CD, Hart, T, Hammond, F, Frol, AB, Hudak, A. “Impact of age on long-term recovery from traumatic brain injury”. Arch Phys Med Rehab. vol. 89. 2005. pp. 896-903.
Graham, JE, Radice-Neumann, DM, Reistetter, TA, Hammond, FM, Dijkers, M, Granger, CV. “Influence of sex and age on inpatient rehabilitation outcomes among older adults with traumatic brain injury”. Arch Phys Med Rehab. vol. 91. 2010. pp. 43-50.
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- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- 4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
- What's the evidence?