18 TRAUMATIC BRAIN INJURY
J. Paul Elliott M.D., Sanjay Misra M.D.

1. Is traumatic brain injury (TBI) a common problem?

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Yes. In the United States, 1 in 12 deaths is due to injury. One third of traumatic deaths are associated with TBI. Of deaths resulting from motor vehicle accidents, 60% are due to brain injury. Even more common is minor TBI, which accounts for 75% of admissions for head trauma.

2. What is a concussion?

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The relatively common occurrence of transient loss of neurologic function without macroscopic brain abnormality. Concussion is on one end of a spectrum that extends to coma. The Glasgow Coma Scale (GCS) score is used to categorize brain injuries as follows: mild, 14-15; moderate, 9-13; and severe, ≤ 8.

3. How is the GCS score derived?

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The GCS is a means of identifying change in neurologic status. Its principal strengths are ease of use and reproducibility among observers. It is a 15-point scale; 15 is the best score, and 3 is the worst. The score is derived from the addition of the three individual components: best eye-opening response (1-4 points), best verbal response (1-5 points), and best motor response (1-6 points). The GCS is insensitive to pupillary response and focality. A patient with a perfect score of 15 may have hemiparesis and a life-threatening lesion.

4. When should a neurosurgeon be consulted?

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For patients with loss of consciousness and subsequent neurologic abnormality or abnormality on computed tomography (CT) scan. These patients usually but not always have a GCS score ≤ 13.

5. How does one initially assess the brain-injured patient?

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Just like any trauma patient. The first steps are assessment of the ABCs (airway, breathing, circulation) and rapid physiologic resuscitation. The neurologic examination is crucial. The initial examination includes (1) level of consciousness, (2) pupillary examination, and (3) motor examination. Repetition of the neurologic examination is also crucial. If deterioration is missed and appropriate treatment is not initiated quickly, irreversible brain injury may result. Finally, watch for concurrent cervical spine injury.

6. What takes priority in a hypotensive patient with TBI?

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Hypotension in patients with head injury frequently accompanies other injuries. Do not assume that hypotension is due to the brain injury alone. Hypotension resulting from brain injury is a terminal event.

7. What is the significance of anisocoria in a patient with a decreased level of consciousness?

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Anisocoria (unequal pupils) is a true neurologic emergency. Commonly a mass lesion (e.g., subdural or epidural hematoma, contusion, or diffuse swelling of one hemisphere) leads to uncal herniation and stretching of the ipsilateral third nerve. Time is crucial. Give mannitol, get a CT scan, and proceed with surgical decompression (if possible).

8. What if the larger pupil is reactive?

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If the larger pupil is reactive, the third cranial nerve is functioning. Think of Horner’s syndrome (miosis, ptosis, and anhydrosis) on the other side. This syndrome may be due to injury to the sympathetic nerves traveling with the carotid artery in the neck. Consider evaluation (angiography) for a carotid dissection.

9. Are terms such as semicomatose nonsense?

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Yes. Patients are alert (like medical students and surgeons), lethargic (like internists, in whom arousal is maintained by verbal interaction), obtunded (like hospital administrators, who require constant mechanical stimulation to maintain arousal), or comatose (like most deans, in whom neither verbal nor mechanical stimulation elicits arousal). Change in level of consciousness is often the first sign of increasing intracranial pressure (ICP); it is also the most poorly documented part of the neurologic examination. Document all findings!

10. How is motor response tested?

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Ascertain the ability to follow commands by asking the patient to hold up fingers and move his or her arms and legs. If the patient does not follow commands (he or she may be a dean), test response to painful central stimulus. Localization of painful stimulus is confirmed by the patient’s hand reaching toward a sternal rub. The patient may be in even bigger trouble if in response to pain he or she exhibits flexor posturing (decorticate), extensor posturing (decerebrate), or no response. Flexor posturing indicates a high brainstem injury, and extensor posturing is associated with low brainstem dysfunction. The patient with no motor response may have a cervical spine injury.

11. What is the significance of periorbital ecchymosis (raccoon eyes) and ecchymosis over the mastoid (Battle’s sign)?

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In the absence of direct trauma to the eyes or mastoid regions, periorbital ecchymosis and ecchymosis over the mastoid are reliable signs of basilar skull fractures. Of patients with basilar skull fractures, 10% have cerebrospinal fluid (CSF) leaks, including rhinorrhea or otorrhea. Persistent CSF leaks are associated with meningitis.

12. Should scalp lacerations be explored in the emergency department?

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Yes-but gently. You want to know whether there is an underlying fracture. A laceration over a linear nondisplaced fracture can be cleaned and closed. If CSF or brain tissue is evident in the wound or if a depressed fracture is identified, surgical intervention is required to debride the wound and to close any dural tears. If you are worried, get a head CT scan.

13. Which patients need CT scans of the head?

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The CT scan is used partly as a triage tool with minor brain injuries and can be cost-effective compared with admission to the intensive care unit for observation. Conversely, patients with focality on examination do not proceed to the operating room without a CT scan.

14. What are the common traumatic surgical lesions?

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If the ventricles are large (ventriculomegaly), a ventriculostomy can drain excessive CSF. Epidural hematomas (from arterial bleeding), subdural hematomas (from venous bleeding), and intraparenchymal hematomas with significant mass effect should be surgically evacuated. A depressed skull fracture or foreign body (e.g., a bullet) also requires a trip to the operating room.

15. When is ICP monitoring indicated?

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When the neurologic examination becomes insensitive (when the patient is unconscious) to changes in ICP. It also may be indicated when there is known brain injury and the patient will be under general anesthesia for a surgical procedure for an extended period.

16. Describe the initial treatment of patients with a suspected increase in ICP.

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The brain, similar to every other organ, must have adequate blood flow and oxygen delivery. The ABCs come first. Systolic blood pressures < 90 mmHg and Pao2 < 60 mmHg are correlated significantly with poor outcomes in patients with TBI. Keep the systolic blood pressure > 100 mmHg and avoid hypoxia.

17. Should all patients with elevated ICP be hyperventilated?

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Decreasing the Pco2 is the most rapidly effective treatment for elevated ICP. The goal is usually a Pco2 of 30-35 mmHg. Any patient with a depressed level of consciousness and inability to protect the airway should be intubated. Before a CT scan is obtained, patients thought to have a mass lesion by neurologic examination should be hyperventilated until definitive treatment is achieved. Avoid chronic hyperventilation, which can cause ischemic brain injury.

18. In hemodynamically stable patients, how do you decrease ICP?

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Mannitol, 1 g/kg, as an IV bolus. Also be sure the cervical collar is not obstructing venous outflow through the jugular system.
KEY POINTS: INDICATIONS FOR BLOOD TRANSFUSION IN THE TRAUMA BAY

1. An unstable adult patient who does not respond to 2 L of “wide open” crystalloid infusion should receive uncrossed, O-negative packed red cells.
2. For pediatric patients, give 20 mL/kg of lactate Ringer’s by bolus; then repeat if necessary.
3. If the pediatric patient does not respond to lactate Ringer’s, proceed to transfuse 10 mL/kg uncrossed, O-negative packed red cells.
4. Do not wait for type-specific blood in the unstable patient who is not responding to crystalloid resuscitation.

19. What is the end point of diuresis?

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Serum sodium of 150 mEq/L and serum osmolarity of 320 mOsm are usually the upper limits of diuresis. Blood volume should be maintained with colloids to help form an osmotic gradient between the extravascular and the intravascular spaces. Anticipate intravascular hypovolemia, and treat with colloids and blood products as necessary.
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strong>20. What is the significance of cerebral perfusion pressure (CPP)?

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CPP is the difference between mean arterial pressure (MAP) and ICP:

CPP = MAP – ICP

CPP is important. Neurologic outcome is best in patients with CPPs in the 60s-70s. Some patients require treatment with pressors to maintain the CPP; if CPP is < 60 mmHg, you may be creating a dean.

21. Why should all children with TBI be undressed and examined thoroughly?

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Half of children suffering nonaccidental trauma (child abuse) have TBI.

22. Should posttraumatic seizures be treated prophylactically?

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Patients with brain parenchymal abnormalities on CT scan after head injury may benefit from 1 week of antiseizure prophylaxis. Early seizures can increase the metabolic demand of the injured brain and adversely affect ICP. Of patients who have seizures within the first 7 days of injury, 10% also have late seizures. Prevention of early seizures does not reduce the incidence of late seizures, however.

23. Which coagulopathy is associated with severe brain injury?

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Disseminated intravascular coagulation. The presumed mechanism is massive release of thromboplastin from the injured brain into the circulation. The serum levels of fibrin degradation products roughly correlate with the extent of brain parenchymal injury. All severely brain-injured patients should be evaluated with prothrombin time, partial thromboplastin time, platelet counts, and fibrinogen levels.

24. What other medical complications may result from severe head injury?

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Diabetes insipidus (DI) secondary to the inadequate secretion of antidiuretic hormone is caused by injury to the pituitary or hypothalamic tracts. The kidney is unable to decrease free water loss. Usually the urine output is > 200 mL/hr, and the urine specific gravity is < 1.003. The serum sodium may rise precipitously if DI is not treated promptly. The treatment of choice in trauma is IV infusion of synthetic vasopressin (Pitressin), which has a 20-minute half-life and can be titrated to produce the appropriate urine output. Because most trauma-induced DI is self-limited, long-term 1-deamino-8-d-arginine vasopressin (DDAVP), which has a 12-hour half-life, is not necessary.

25. If a patient is awake with significant neurologic symptoms but no abnormality on CT scan, what are the likely explanations?

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A spinal cord injury or carotid or vertebral artery dissection.

26. Are gunshot wounds that cross the midline of the brain uniformly fatal?

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No (although such a wound killed Lincoln). The tract that the bullet takes is important, but so is the energy that it imparts to the brain.

27. What is the significance of concussion?

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In most studies of minor TBI, > 50% of patients have complaints of headache, fatigue, dizziness, irritability, and alterations of cognition and short-term memory. It is important to alert the patient to the likelihood of developing these symptoms. The neurobehavioral problems significantly affect patients’ lives. The symptoms usually resolve within 3-6 months after injury.

28. Can patients with minor TBIs be discharged from the emergency department?

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Patients whose examination (including short-term memory) returns to normal and who have a normal head CT scan can be discharged to home if they are accompanied by a responsible person.

29. Is brain injury permanent? Is the outcome always poor?

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No and no. Brain injury occurs in two phases. The primary injury occurs at the moment of impact. Secondary injury is preventable and treatable. Examples include hypoxia, hypotension, elevated ICP, and decreased perfusion to the brain secondary to ischemia, brain swelling, and expanding mass lesions. Rapid surgical management and avoidance of secondary injury improve outcome. Although previously it was believed that the brain was not capable of repair, it is now clear that neuronal repair and reorganization occur after injury.

References
WEB SITES

1. http://www.acssurgery.com/abstracts/acs/acs0501.htm
2. http://www.surgery.ucsf.edu/eastbaytrauma/Protocols/ER%20protocol%20pages/closedheadinjury.htm
3. http://www.ascsurgery.com/abstracts/acs/acs0612.htm

BIBLIOGRAPHY
1. Brain Trauma Foundation: Management and Prognosis of Severe Traumatic Brain Injury. New York, Brain Trauma Foundation, 2000. Available at www.braintrauma.org.
2. Mazzola CA, Adelman PD: Critical care management of head trauma in children. Crit Care Med 30:S393-S401, 2002. Medline Similar articles
3. Narayan RK, Michel ME, Ansell B, et al: Clinical trials in head injury. J Neurotrauma 19:503-557, 2002. Medline Similar articles Full article
4. Narayan RK, Wilberger JE, Povlishock JT: Neurotrauma. New York, McGraw-Hill, 1996. Medline Similar articles Full article
5. Shaw NA: The neurophysiology of concussion. Prog Neurobiol 67:281-344, 2002.