Severe TBI Management — Lecture Notes

Management

• Focal = contact injury
• causing laceration, contusion, intracranial hemorrhage
• Diffuse = acceleration/deceleration injury, anoxic
• leading to brain swelling, diffuse axonal injury

• Primary = injury at the time of trauma/mechanical
• Secondary = delayed non-mechanical damage, result of a complication from the initial trauma
• Cerebral edema,
• Intracranial HTN
• Neurotransmitter changes
• Inflammation
• Hypoperfusion/hyperperfusion
• Ischemia

• Primary = Injury prevention
• Irreversible damage

+Necrotic death neurons, astrocytes, oligodendrocytes, neuronal interconnection disruptions (DAI)

• Secondary = Therapeutic/supportive measures
• Penumbra – area of viable but threatened brain tissue around damaged tissue
• Salvageable with support

• Skull Fracture
• ICH
• EDH
• SDH
• SAH
• IPH

Extra-axial

• Coup–Contrecoup
• Diffuse Axonal Injury (DAI)

• Flat bones v skull base
• Linear v comminuted
• Degree of depression
• Degree of communication (dura, parenchyma)
• Basilar w/ middle ear, nasopharynx, sinuses
• Greater risk of post-traumatic seizures
• Open – increased CNS infection risk

• Laceration of dural veins/arteries between dura & skull
• i. e temporal fracture & middle meningeal artery
• Arterial injury – higher pressure – faster neurologic deterioration
• "Lucid interval"

• Tearing of bridging veins
• Accumulation of blood w/in arachnoid membrane

& dura

• Hematoma does not develop as rapidly, but leads to mass lesions
• Mortality of 60–80% (higher than EDH)

• Accumulation of blood between arachnoid & pia mater
• Adjacent to site injury/impact
• Portend worse outcome
• Outside of trauma associated w/ aneurysmal rupture
• "Worst headache of life"
• Vasospasm

(IPH)

• Frequently evolve
• Increasing cerebral edema, mass effect
• Delayed IPH in 20% of TBI
• Typically w/in 72h

• Contusion both initial site & opposite side of the insult,
• Movement of the brain within skull
• Energy leads to rupture of micro vessels
• Extravasation of blood & inability of these vessels to perfuse tissues

• Disruption of neuronal interconnections – shear/stretch injury
• CT normal in 50-80%
• Poor prognosis
• Grades:
• Grade 1: Mild diffuse external injury w/ microscopic white matter changes of the cerebral cortex, corpus callosum, brain stem
• Grade 2: Moderate DAI w/ focal corpus callosum lesions
• Grade 3: Grade 2 & additional brain stem lesions

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• EDH
• Coma (GCS score < 9) with anisocoria
• EDH > 30 cm3 (regardless of GCS)
• SDH
• Thickness > 10 mm OR midline shift > 5 mm (regardless of GCS)
• Comatose (GCS < 9) & SDH < 10mm thick & midline shift < 5mm should undergo surgical evacuation if:
• GCS decreased ≥ 2 between time of injury & admission
• Presents with asymmetric or fixed & dilated pupils
• ICP > 20 mm Hg
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• IPH
• Progressive neuro deterioration, refractory intracranial HTN, or mass effect (CT)
• GCS 6-8 w/ frontal or temporal contusions > 20 cm 3 w/ midline shift > 5 mm and/or cisternal compression
• Any lesion > 50 cm 3
• Skull fractures
• Open, depressed > than thickness of cranium (to prevent infection)
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aka

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• TBI = loss of cerebral autoregulation
• Disrupted:
• blood flow/perfusion
• O2 delivery
• Brain perfusion & oxygenation #1
• Hypotension & Hypoxia = INCREASE mortality with every episode

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• Edema
• Electrolyte disturbances, hypoglycemia
• Infection
• Seizure

• Hyperthermia

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• Cerebral perfusion pressure (CPP) = MAP - ICP
• Represents cerebral blood flow & oxygen delivery
• Goal 50-70mm Hg
• TOO low - inability to meet metabolic demands – worse
• utcome
• TOO high - cerebral edema
• ICP < 22mmHg
• Monro-Kellie Doctrine = total volume fixed (brain,

CSF, intracranial blood)

• If 1 increases the volume of the others must decrease

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• Severe TBI (GCS 3-8 after resuscitation) & abnormal CT
• Or in severe TBI with normal CT if ≥ 2 of the following:
• Age > 40 years,
• Unilateral or bilateral motor posturing
• SBP <90 mm Hg
• Internal monitors – invasive, introduced into specific anatomical locations (i. e intraparenchymal, intraventricular)
• EVD is gold standard
• External monitors – accuracy? (TCD, TMD, ONSD)

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• Treat pain & agitation
• Propofol reduces cerebral oxygen consumption – possible neuroprotective effect (acute setting)
• No evidence improved outcome
• High dose therapy can worsen mortality
• Barbiturates – only in high ICP refractory to max medical/ surgical treatment
• Elevation head of bed (30-45°)
• Displaces CSF
• Venous outflow

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• Hyperosmolar therapy
• Na goal 145-160 mEq/L - oncotic gradient
• Hypertonic Saline
• Oncotic gradient & volume expansion
• Onset minutes (can last hours)
• Mannitol
• Osmotic diuresis
• o.25-1g/kg, onset minutes (can last 6h)
• AVOID in hypotensive

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• Hyperventilation
• Hypocarbia resulting in cerebral vasoconstriction
• Acutely reduces cerebral volume – reduced ICP (temporizing therapy, bridge to emergent surgery ONLY)
• Long term – vasoconstriction = reduced perfusion
• Hypercarbia – vasodilation & increased ICP

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• Decompressive Craniectomy (DC) = consider for laterefractory ICP elevation but not early-refractory ICP elevation
• Diffuse Traumatic Brain Injury (DECRA) trial - secondary DC for early-refractory ICP elevation (w/in 72h)
• No mortality benefit, poorer function outcomes (6m)
• Randomized Evaluation of Surgery with Craniectomy for

Uncontrolled Elevation of Intracranial Pressure (RESCUEicp) trialsecondary DC for late-refractory ICP elevation

• Mortality benefit
• BUT HIGHER rates of vegetative state & severe disability

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• Blood pressure
• SBP ≥100 mm Hg (50 to 69 years)
• SBP ≥110 mm Hg (15 to 49 or > 70 years)
• Oxygenation/Ventilation
• Normal pH, normocarbia (35-40)
• PaO2 80-200 mmHg (some suggest 120 mmHg as max)
• Higher PEEP - increased intrathoracic pressure & impair venous return – can increased ICP & reduced CPP
• Data mixed on whether clinically sig effect, must balance pt needs

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• Temperature = Fever in 40-70% (pyrogens, disruption hypothalamic set point, infx)
• Increase brain metabolic demand – cerebral ischemia/injury
• Goal = normothermia
• Avoid shivering – counter acts benefit via O2 reduction to brain tissue
• Buspirone, meperidine
• Dexmedetomidine
• Magnesium?
• Euglycemia

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• Avoidance coagulopathy
• INR < 1.5, plt >100, Hgb>7
• CRASH 3 (RCT TXA 2g within 3h of injury)
• Mild to moderate TBI (GCS>8) - reduction in head-injury-related
• Severe TBI no difference
• Earlier treatment more effective
• No difference in VTE or seizures
• VTE ppx
• ASAP
• LMWH or SQH

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• Seizure ppx
• Phenytoin (or levetiracetam) recommended to decrease incidence of early PTS (w/in 7d of injury) (when benefit felt to outweigh the complication risk of meds)
• Early PTS not associated w/ worse outcomes