254. Head Trauma in Adults and Children

General

TBI: Traumatic Brain Injury – impairment in brain function due to result of force. Either temporary or permanent. Mild: GCS 14-15, Moderate 9-13, Severe < 8.

Cranium is fixed volume made up of brain, CSF and blood. ICP < 15 in adults, children its less with infants being 1.5-6. Cerebral blood flow usually maintained if CPP < 60. CPP: Cerebral Perfusion Pressure Рcerebral blow flow measured. CPP = MAP (DBP + (SBP-DBP)/3 РICP

Cushing reflex: rapid rise in ICP causing triad: bradycardia, HTN, and irregular respirations. more common in children than adults.

GCS: 15 point scale used to assess TBI. Motor score correlates just as well as full GCS.

Mild TBI

“Concussion.” GCS 13-15 with either LOC, amnesia, dazed/confused period, or focal neuro deficit that may/may not be temporary. Can have normal CT and due to metabolic injury have significant symptoms/effects. CT positive in 15% though < 1% requiring NSGY intervention. Cognitive symptoms (most consistent abnormalities with mild TBI): attention difficulty, concentration, amnesia, orientation, altered reaction time, calculation issues. Physical symptoms: headache, dizziness, insomnia, fatigue, uneven gait, nausea/vomiting, blurred vision, olfactory nerve abnormality most common CN affected. Behavioral symptoms: depression irritability, anxiety, sleep disturbance. Symptoms can occur immediately afterward or delayed for days/weeks. No pharmacological treatment. “Brain rest”, NSAIDs, hydration. Complete resolution in 80% by 6 weeks. Most common lingering symptoms: headache, difficulty concentrating, memory difficulties.

New Orleans Criteria and Canadian CT are 100% sensitive on finding NSGY interventional findings on CT. LOC/amnesia is required as starting point before considering studies though. New Orleans more sensitive at ANY CT finding.

Sports: Most common concussion sports are football, ice hockey, soccer, lacrosse. SCAT3 (Sports Concussion Assessment Tool) for ages > 13 (ChildSCAT3 for 5-12). Takes 15-20 minutes to complete. No return to play after concussion that day. Requires stepwise approach to go return to play – at minimum 1 week to get through steps asymptomatic.

Second Impact Syndrome: rapid edema and and death if second injury before first injury has fully resolved. Rare. First cases didn’t really have a ‘second’ impact.

Post-concussive syndrome: persistent symptoms for months/years. 20-40% have symptoms at 3 months, 15% at 1 year. Usually associated with previous migraine history, depression/anxiety. If symptoms persist for more than 3 weeks, need to see concussion clinic/specialist.

Moderate / Severe TBI

3 goals: prevent further secondary brain injury, identify treatable mass lesions, and identify other life-threatening injuries.

Prevent secondary brain injury: correct/treat hypoxia/hypotension (2x mortality, single incident of either one increases mortality 150%, keep SBP >90, MAP > 80), anemia, hyperglycemia, hyperthermia.

Induction agents for intubation: Etomidate 0.3mg/kg Рrapid onset (45 seconds), short acting (3-5min), favorably hemodynamically stable, reduces ICP. Adrenal suppression with continuous use.  Propofol 1-3mg/kg Рanti seizure properties, boluses can cause hypotension.

Decorticate posturing: “to the core” – arms flexed/legs extended. Injury above midbrain.

Decerebrate posturing: arms extended and internal rotated wrists – more caudal injury, worse prognosis.

Elevated ICP treatment: Oxygen saturation > 95%, PaCO2 35-40, elevated head of bed to 30 degrees (reverse trendelberg in spinal precautions), keep neck straight. Mannitol: reduces ICP quickly and last 6 hours. .25mg-1g/kg. No dose-dependent effect. Net intravascular volume loss – acts as diuretic. Hypertonic saline: less studied than mannitol – no preferred benefit over mannitol. 23.4% 30mL though needs central line to give. Hyperventilation: no longer recommended unless very temporizing before surgery. Steroids not recommended. Seizure prophylaxis: NSGY dependent, Fosphenytoin or Keppra. Definitely give in penetrating trauma.

Skull Fractures

Linear skull fractures with overlying laceration are open fractures requiring NSGY consult. Vancomycin + Ceftriaxone 2g. Linear skull fractures along dural sinus or middle meningeal artery – watch for signs of epidural hematoma formation.

Skull fracture open/depressed with sinus can cause intracranial air (pneumocephalus) – needs IV abs with Vancomycin/Rocephin.

Basilar Skull Fractures: most common region is temporal bone – petrous portion. Associated with torn dura causing otorrhea or rhinorrhea. CSF otorrhea/rhinorrhea, mastoid ecchymosis (Battle sign), periorbital ecchymosis (raccoon eyes), hemotympanic membrane, vertigo, decreased hearing and 7th CN palsy. Possible CSF leak – collect fluid and check for beta-transferrin (only found in CSF) – Ring sign on paper not accurate/reliable. Acute CSF leaks are at increased risk for meningitis though no abx prophylaxis needed initially. Sometimes spontaneously close – up to NSGY/ENT. Persistent > 1 week leaks require abx and surgery.

Brain Herniations

Uncal Hernation: most common type. Temporal lobe uncus displaces inferiorly through medial edge of tentorium causing compression of CNIII (parasymptomatic nerves first) – ipsilateral sluggish pupil/dilation with contralateral motor weakness. Kernohan’s notch syndrome: contralateral cerebral peduncle is forced against the opposite edge of the tentorium hiatus causing ipsilateral hemiparesis.

Central Transtentorial Hernation: initial pinpoint pupils, bilateral babinski, increased muscle tone. usually decorticate posturing as well. Expanding lesions at vertex/frontal/occipital poles with bilateral central pressure.

Cerebellotonsillar Herniation: cerebellar tonsil herniates through foramen magnum. Pinpoint pupils, flaccid paralysis, sudden death.

Upward Transtentorial Hernation: posterior fossa lesion causing pinpoint pupils, conjugate downward gaze with absence of vertical eye movements.

Cerebral Contusion

Contusion in subfrontal cortex. Associated with SAH. ICH can occur days after contusion. Usually no NSGY intervention.

Traumatic Subarachnoid Hemorrhage

Most common CT abnormality with moderate/severe TBI. CT 6-8 hours after injury more sensitive. Risk factor for early mortality.

Epidural Hematoma

Blood between skull and dura mater. Associated with middle meningeal artery. Classic presentation with head injury with LOC, followed by lucid period and then rapid decline. Strikes to lateral skull (baseball, pool stick). Biconvex hematoma in temporal region usually. Not usually crossing sutures/midline. Can lead to herniation within hours. Full recovery if hematoma evacuated prior to herniation or neuro deficits. Look for linear skull fracture along dura sinus or middle meningeal artery. Surgery for mass effect or hematoma > 30cm, or comatose.

Subdural Hematoma

Sudden accel/decel of brain parenchyma. Tearing of bridging veins. Blood between dura and arachnoid space. SDH associated with other brain injuries. Elderly and children < 2yo at risk. Subacute: is odense on CT. Chronic: hypodense. Treatment varies. NSGY intervention for >10mm or midline shift > 5mm, worsening GCS dilated/fixed pupils, elevated ICP.

Subdural Hygroma: collection of clear, xanthochromic blood tinged fluid in dura – sometimes from CSF escape from injuried vessels. Can occur immediately or in delayed manner.

Diffuse/Traumatic Axonal Injury

Disruption of axonal fibers in white matter/brain stem secondary to shear forces. Usually blunt trauma. Edema can develop rapidly. CT can be normal initially but classically CT shows punctuate hemorrhage. Treatment is preventing secondary injury. Usually present in coma with ‘normal’ CT. Time will show how severe TAI is as patient either improves from comatose state.

Penetrating Injury

GCS >8 with reactive pupils have only 25% mortality. GCS < 5 100% mortality. Prophylaxis abx needed with Ceftriaxone 2g. Stab wounds very low mortality relative to GSW. Impaled objets should be left in until surgery removes. Projectiles that cross midline or center of brain, pass through ventricles or rest in posterior fossa have high mortality.

Non-Accidental Trauma

Subdural Hematoma associated with NAT in infants. Look for concurrent retinal hemorrhages. 50% of SDH were related to NAT. Only 10% accidental.

Coagulopathy

4x poorer outcome with elevated INR. ICH with warfarin has mortality of 82%. Negative CT with coagulation is reassuring though delayed hemorrhage is reported. Not necessary to observe if clinically well appearing – rebleeding/delayed bleeding can occur at 24 hours or up to 4 weeks after. TXA for systemic hemorrhage – not recommended for isolated brain injury. Idarucizumab used for reversal of dabigatran (5g total, 2.5g x 2). Antiplatelet therapy are more likely for acute bleeding over delayed bleeding like warfarin.

Questions

 

References/Resources

Tintinalli, Seventh Edition, Chapter 254: Head Trauma in Adults/Children

Rosens, Chapter 34: Head Trauma

254. Head Trauma in Adults and Children

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