Head Trauma

CHAPTER 6

Head Trauma

I. Cranio-Cerebral Trauma

A. Overview

1. In persons up to 44 years old, trauma and injuries are the leading cause of death.

a. Traumatic brain injury (TBI) is responsible for 30% of trauma-related deaths.

2. Eighty percent of head injury cases are first seen by a general physician in the emergency room.

a. Seventy-five percent of TBI cases are mild in nature.

3. Less than 20% of TBI patients ever require neurosurgical intervention.

4. Men are more likely than women to suffer TBI (4:1).

5. Patients older than 75 years of age have the highest mortality from TBI.

B. Definitions

1. Concussion: violent shaking or jarring of the brain with resulting transient functional impairment

2. Contusion: bruising of the brain without interruption of its architecture

3. Coup injury: head is struck while immobilized; the focus of the injury is at the site of impact.

4. Contre-coup injury: focus of injury is opposite the site of impact due to the head not being immobilized (i.e., it was in motion, accelerating or decelerating).

5. Severe TBI: traumatic head injury leading to loss of consciousness, with a Glasgow Coma Scale (GCS) score of less than 9

C. Mechanisms of brain injury: About 1.7 million persons in the United States suffer a TBI every year.

1. Falls (35%)

2. Gunshot wound/assault to the head (10%)

3. Injury to the skull by objects (17%)

4. Motor vehicle accident (17%)

5. Sports-related injuries

6. Cranium distorted by forceps at birth

II. Approach to the Patient With Head Injury

A. Overview

1. As with all trauma, patients with head injury must be evaluated for airway and breathing compromise and circulatory distress. The “ABCs” must be intact. A full trauma survey should ideally be completed within the first minutes of arrival to a care center.

2. GCS and pupillary responses should be assessed repeatedly, especially during the first few hours, to establish neurological stability.

3. In some cases of mild and in all cases of moderate to severe head trauma, a head CT scan should be completed as soon as feasible.

4. Spine imaging should be considered if the patient shows any signs of new autonomic instability, motor weakness, or a sensory level.

5. Volume status should be ascertained and resuscitated as needed.

6. Oxygen saturation should remain above 90% at all times.

7. Currently, there is no evidence for adjunct steroid therapy in traumatic central nervous system (CNS) injury, and steroid therapy is not recommended.

8. Assess for skull fracture

a. The fracture size and type can give a rough estimate of the force that caused the trauma.

b. Skull fractures can also confer the extent of cerebral injury.

c. The skull fracture site can lead to ingress of bacteria or air or egress of cerebrospinal fluid (CSF).

9. In patients with severe TBI with minimal neurological examination, an intracranial pressure monitor should be considered.

a. Cerebral perfusion pressure is recommended at 50 to 70 mmHg

b. Adjunct monitoring (cerebral oximetry and microdialysis) are currently being studied, but are not currently recommended in all TBI patients.

B. Minor head injury

1. Most head injuries are minor, and patients generally have not lost consciousness or are rapidly regaining consciousness; 90% of concussion do not involve loss of consciousness.

2. Little need for neurologic consultation for these injuries

3. Hospitalization is generally not required, provided that a family member is able to report changes

a. 1-in-1000 chance of developing intracranial hemorrhage if without fracture and mentally clear

b. 1 in 30 if with fractures and mentally clear

4. Family or caregivers should monitor for the following:

a. Posttraumatic syndrome: headaches, giddiness, fatigability, insomnia, and nervousness

b. Delayed fainting after head injury: a vasodepressor syncopal attack, related to pain and emotional upset—must be distinguished from a “lucid interval of epidural bleed”

c. Transient traumatic paraplegia, blindness, and migrainous phenomena: both legs become temporarily weak, with bilateral Babinski sign, occasional sphincteric incontinence; symptoms disappear after a few hours.

d. Delayed hemiplegia or coma: usually young adults after relatively minor athletic or road injury; massive hemiplegia, hemianesthesia, hemianopsia, aphasia—represents either dissecting aneurysm of internal carotid, late evolving epidural or subdural hematoma, intracranial hemorrhage (ICH), or preexisting arteriovenous malformation (AVM); with fracture of large bones and pulmonary symptoms 24 to 72 hours later, traumatic fat embolism should be considered.

C. Moderate to severe head injury

1. Monitor for increased intracranial pressure (ICP), cerebral contusions (with serial CT scans), lacerations, subarachnoid hemorrhage (SAH), zones of infarction, and scattered ICHs, and consider MRI with diffusion tensor imaging to assess for diffuse axonal injury.

2. Severe head injury: first step is to clear the airway and ensure adequate ventilation; perform careful search for other injuries; Glasgow Coma Score provides a means of evaluating state of consciousness; control factors that raise ICP, such as hypoxia, hypercarbia, hyperthermia, awkward head positions, and high mean airway pressure.

3. NB: brady-arrhythmia may be sufficient to damage brain.

4. Brain death evaluation should ideally be delayed for at least 24–48 hours post TBI and assessments for anoxia, drug or alcohol intoxication and hypotension should be made.

5. Traumatic delirium: when stupor gives way to a confusional state, may last for weeks; associated with aggressive behavior or uncooperativeness

6. Traumatic dementia: once the patient improves, he or she is slow in thinking and unstable in emotion, with faulty judgment.

7. Small groups are in a vegetative state: normal vital signs but do not speak and are capable only of primitive reflexes; this signals arousal without awareness. If this is persistent, it may become persistent vegetative state.

8. After moderate to severe head injury, several conditions should be monitored for:

a. A concussion followed by a lucid interval and serious cerebral damage: initial and temporary loss of consciousness is generally due to concussion. If there is later deterioration, it is potentially because of delayed expansion of subdural hematoma, worsening brain edema, or epidural clot.

b. Acute epidural hemorrhage: generally caused by a temporal or parietal fracture with laceration of the middle meningeal artery or vein; less often a tear in dural venous sinus; meningeal vessels may be torn without a fracture.

i. CT: lens-shaped clot with a smooth inner margin

ii. Treatment: burr hole excision of epidural hematoma (EDH); emergent craniotomy or drainage may be necessary if patient becomes unstable or if bleed is uncontrollable (prognosis is poor if patient develops bilateral Babinski sign and decerebrate posturing).

c. Acute subdural hematoma (SDH)

i. May be unilateral or bilateral.

ii. Sometimes characterized by a lucid interval followed by a sudden deterioration.

iii. More often, patient is stuporous from the time of injury, and mental status progressively worsens.

iv. SDH is frequently combined with epidural hematoma.

v. CT detects in more than 90% of cases; less acute hematomas may be isodense to the cortex and present only as a ventricular shift.

vi. Treatment: burr hole excision of SDH after stabilization and liquification of clot material; craniotomy for more emergent expansion of bleed with neurological worsening.

d. Chronic subdural hematoma:

i. Generally due to traumatic injury that was trivial or forgotten

ii. Period of weeks passes before onset of headaches, giddiness, slowness of thinking, confusion, apathy, drowsiness, or seizures

iii. CSF may be clear, bloody, acellular to xanthochromic

iv. Subdural hygroma (collection of blood and CSF in subdural space) may form in the potential space created by the SDH

e. Cerebral contusion

i. Areas of brain parenchyma that suffer direct and indirect mechanical trauma due to impact—coup and coup contre-coup.

ii. These can cause parenchymal shifts and increased ICP.

iii. CT: appear as edematous areas of cortex and subcortical white matter admixed with areas of higher density (representing leaked blood); main concern is tendency of contused areas to swell or to develop hematomas, giving rise to delayed clinical deterioration; swelling may be precipitated by excessive administration of IV fluids.

D. Penetrating wounds of the head

1. Bullets and fragments: air is compressed in front of the bullet so that it has an explosive effect upon entering tissue.

2. If brain is penetrated at the lower brainstem level, death is instantaneous from respiratory or cardiac arrest.

3. If vital centers are untouched, immediate problems are bleeding, increased ICP, swelling.

4. Treatment:

a. Rapid and radical debridement

b. Control ICP with mannitol or hypertonic saline.

c. Prevent systemic complications; epilepsy is the most troublesome sequelae (more than one-half of patients).

d. Consider surgical decompression if there are compressive blood products causing neurological deficit.

SEQUELAE OF HEAD INJURY	SYMPTOMS	TREATMENT
Posttraumatic epilepsy	Focal or generalized seizures that occur shortly after TBI. This is the most common delayed sequela of craniocerebral trauma, although the interval between injury and epilepsy varies. The interval is generally longer in children. Earlier seizures are more likely to have complete remission	Antiepileptic medications
Autonomic dysfunction syndrome in the vegetative state (“diencephalic storming”)	Extensor posturing, profuse diaphoresis, hypertension, tachycardia following TBI	Narcotics, benzodiazepines, bromocriptine, nonselective beta blockade
Posttraumatic nervous instability (postconcussion syndrome)	Following TBI, symptoms of neurasthenia, dizziness, and generalized or localized headache of variable quality. Symptoms are precipitated by straining or emotion. Intolerance to noise, emotional excitement, crowds. Patients also experience tenseness, restless, decreased concentration, and resistance in doing varieties of treatment.	Relieved by rest, quiet room, and benzodiazepines. Some antidepressants can be of use in this population.
Posttraumatic Parkinson syndrome	Controversial syndrome; most patients likely had Parkinson’s disease or postencephalitic parkinsonism brought to light by head injury (seen in boxers).	Some Parkinsonian medications can help treat underlying Parkinson’s disease in this population.
Punch-drunk encephalopathy, “dementia pugilistica”	Dysarthric speech, forgetful, slow thinking; movements are slow, stiff, uncertain; legs with shuffling, wide-based gait; often with parkinsonian syndrome and ataxia. Other symptoms include enlargement of lateral ventricles, thinning of corpus callosum, widened cavum septum pellucidum; fenestration of septal leaves; diffuse plaques and Alzheimer’s changes; no Lewy bodies.	No known treatments
Posttraumatic hydrocephalus	Adhesive basilar arachnoiditis	Shunt placement
Posttraumatic cognitive and psychiatric disorders	Long anterograde amnesia and permanent cognitive and personality changes

III. Head Trauma Related to Sports

A. The American Academy of Neurology updated the evaluation, management and treatment guidelines for the management of concussion in sports in 2013. The following is a summary of the new recommendations.

1. Greatest risk for concussion exists in

a. Football

b. Rugby

c. Soccer

d. Hockey

2. Female athletes who play soccer and basketball have a predominance for head injury.

3. Athletes with history of concussion or mild TBI have a higher risk for further concussions, especially within the first 10 days of a previous concussion.

4. Wearing a helmet during contact sports reduces but does not eliminate risk of concussion and head injury.

5. Standard symptom checklists (postconcussion symptom scale/graded symptom checklist) and the standardized assessment of concussion are highly specific and sensitive for identifying concussion if completed early after a sports-related head injury.

6. Physicians and other health care providers who are knowledgeable on sideline assessment tools should train sideline health officials.

7. If an athlete suffers symptoms of concussion, a trained health official should complete the sideline assessment tool and provide the data to the treating physician for further assessment.

8. Athletes with suspected head injury or concussion should immediately be removed from play to avoid further injury.

9. The injured athlete should not return to play until assessed by an experienced care provider with training both in the diagnosis and management of concussion and in the recognition of more severe TBI.

10. Imaging: CT imaging should be considered to assess intracranial hemorrhage in athletes who have loss of consciousness, posttraumatic amnesia, persistently altered mental status (Glasgow Coma Scale <15), focal neurologic deficit, evidence of skull fracture on examination, or signs of clinical deterioration.

11. Return to play: Athletes with concussion should not return to play or practice until the concussion has resolved as confirmed by health care professional clinical examination and assessment. Athletes with concussion should be prohibited from playing until the concussion has resolved.

12. Early postconcussive symptoms and cognitive impairments last longer in younger athletes relative to older athletes and thus these patients should be managed more conservatively than older adults.

13. Concussion resolution is also predominantly a clinical determination made on the basis of a comprehensive neurologic history, neurologic examination, and cognitive assessment. There is moderate evidence that tests such as symptom checklists, neurocognitive testing, and balance testing are helpful in monitoring recovery from concussion.

14. Cognitive restructuring may be a useful form of brief psychological counseling that consists of education, reassurance, and reattribution of symptoms, often utilizing both verbal and written information, and has been shown to diminish the development of chronic postconcussion syndrome.

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