Approach to Head Injury

Question 1

Impairment of brain function as a result of mechanical force

• may cause permanent or temporary impairment
• may or may not cause structural damage to brain
• associated with diminished or altered state of consciousness

Answer 1

TBI

Question 2

Trauma induced alteration of mental status which may or may not involve loss of counsciousness

• Rapid onset of short-lived impairment that resolves spontaneously
• clinical symptoms reflect functional disturbance rather than structural injury
• imaging usually normal

Answer 2

Concussion

Question 3

How are TBI severity’s ranked?

Answer 3

mild= GCS 14-15 (about 80% of head injuries)
moderate= GCS 9-13 (about 10% of head injuries
severe= GCS 3-8 (mortality approx. 40%) - only about 10% of these patients make even a moderate recovery

Question 4

Glasgow Coma Scale for Eye opening

Answer 4

• 4 = spontaneous
• 3 = to voice
• 2 = to pain
• 1 = none

Question 5

Glasgow Coma Scale for Verbal Response

Answer 5

• 5 = normal conservation
• 4 = disoriented conversation
• 3 = words, but not coherent
• 2 = no words, only sounds
• 1 = none

Question 6

Glasgow Coma Scale Motor Response

Answer 6

• 6 = normal
• 5 = localized to pain
• 4 = withdraw to pain
• 3= decorticate posture (rigidity, clenched fists, legs held straight out, and arms bent inward toward the body with the wrists and fingers bend and held on the chest; mummy pose)
• 2 = decerebrate (an abnormal posture that can include rigidity, arms and legs held straight out, toes pointed downward, head and neck arched backwards)
• 1 = none

Question 7

Direct tissue damage from traumatic mechanism (contusion, shearing, hemorrhage)

Answer 7

Primary injury

Question 8

• Tissue damage (min to hours after the primary injury)
  -Ion shifts, free radical production, etc leading to inflammation, cytotoxic edema and cell death
• elevated ICP causes direct compressive damage and leads to ischemia, vascular compression, herniation
• additional insults (systemic hypotension, hypoxemia) will also lead to worse clincial outcomes

Answer 8

Secondary Injury

Question 9

what are the 3 goals in approach to head injury?

Answer 9

• 1. identify life-threatening injuries
• 2. identify treatable mass lesions (i.e bleeding)
• 3. prevent further brain injury
     -minimize or prevent hypoxemia, anemia, hypotension, hyperglycemia, hyperthermia (things that will increase metabolic demand)

Question 10

• Pupil size and reaction is a function of the Autonomic Nervous System
• parasympathetic innervation of the oculomotor nerve controls constriction of the pupil
• exits from the brainstem-any compression/swelling wil result in a dilated, non-reactive pupil

Answer 10

Pupillary response

Question 11

the pupilary response could be fixed in what ways?

Answer 11

• single fixed and dilated pupil in unresponsive pt may indicate uncal herniation- will be same side lesion
• bilateral fixed and dilated pupils suggest increased ICP with poor brain perfusion, bilateral uncal herniation, drug effects, or severe hypoxia
• bilateral pinpoint suggests opiate use or pontine lesion

Question 12

what are signs of a severe TBI?

Answer 12

• fixed or dilated pupils (uni or bilateral), decorticate (flexion) or decerebrate (extension) posturing, bradycardia, hypertension, respiratory depression)
• periorbital ecchymosis (raccoon eyes) battle signs, hemotympanum, CSF otorrhea, CSF rhinorrhea

Question 13

If aggressive management is warranted for a head injury, what should be considered?

Answer 13

• Get patient to CT scan ASAP
• If GCS < 8 (or if uncooperative, combative) = intubation
  -Etomidate, propofol for induction and succinylcholine/rocuronium are appropriate (agents that are long acting may mask neurologic changes (i.e, seizure) an those that can cause hypotension should be avoided
• Aggressive fluid resuscitation to prevent hypotension and secondary brain injury
• single episode of hypotension/hypoxemia is associated with 150% increase in mortality

Question 14

• Bleeding into the brain tissue
• usually a component of cerebral contusion
• disruption of the intraparechymal capillaries as the result of a contusion
• an intraparenchymal hemorrhage that displaces surrounding brain tissue appears as frankly hyperdense area on CT scanning with a hypodense (edematous) periphery

Answer 14

intracerebral hemorrhage

Question 15

• These patients are twice as likely to die, remain in a persistent vegetative state or experience severe disability
• can be missed on early T

Answer 15

Subarachnoid hemorrhage

Question 16

• caused by laceration of meningeal arteries (often in association with skull fractures)
• arterial bleeding in epidural space (between the skull and dura mater)
• lenticular (lens-shaped) hematomas that appear hyperdense on CT scanning
• classic presentation is LOC followed by lucid interval with subsequent rapid neurologic demise (can lead to herniation within hours
• early recognition and decompression is key- full recovery is likely evauated prior to herniation or development of neuro deficits

Answer 16

Epidural hemorrhage

Question 17

• Trauma tears cerebral veins bridging the space between the brain and cerebral venous sinus
• slower venous bleeding into subdural space between the arachnoid and dura
• blood surrounds the brain, forming crescent-shaped hyperdense areas on CT (acute)
• common in elderly and alcoholics, even with trivial trauma (pts may be asymptomica or have progressive focal neurological deficits over days/weeks)
• need to have high suspicion even for near falls or other minor injuries

Answer 17

Subdural hematoma

Question 18

Indications for surgical drainage?

Answer 18

• epidural hematoma if > 30ml
• acute subdural hematoma if > 10mm in thickness or if > 5mm of midline shift
• also if GCS has decreased 2 points or more since admission or ICP measurements are > 20mmHg
• intracerebral hemorrhage if evidence of mass effect

Question 19

• osmotic agent that can reduce ICP and improve cerebral blood flow, CPP, and metabolism
  -immediate plasma expanding effects that reduce blood viscosity and increase cerebral blood flow to improve oxygen delivery
  -after 30 minutes the diuretic effects help to reduce cerebral edema and decrease ICP
• reduces ICP within 30 minutes and effect lasts up to 6-8 hours
• used in the cases of acute neurologic deterioration while prepping definitive management
• administered by repetitive boluses

Answer 19

Mannitol