Traumatic brain injury (Proceedings)

     • Primary brain injury

          o Direct parenchymal and vascular damage

          o Occurs immediately as a result of traumatic event

     • Secondary brain injury

          o Result of biochemical cascades initiated by primary injury

          o Includes ATP depletion, increases in intracellular Na+ and Ca2+ as well as extracellular excitatory neurotransmitters, production of oxygen free radicals, increased cytokine production, accumulation of nitric oxide, lactic acidosis and activation of arachidonic acid, kinin, complement, coagulation and fibrinolytic cascades

          o Results in further damage to brain tissue and resultant increases in intracranial pressure (ICP)

          o Therapy directed at minimizing secondary injury

     • Intracranial pressure dynamics

          o ICP = pressure exerted by tissues and fluid within the skull

          o Cerebral blood flow determined in large part by cerebral perfusion pressure (CPP) CPP = MAP– ICP (where MAP = mean arterial blood pressure)

          o Autoregulatory mechanisms used to maintain ICP within normal limits despite normal fluctuations in MAP, via vasoconstriction and vasodilation

          o As intracranial volume increases (e.g. from hemorrhage, edema), compensatory mechanisms shift fluid (blood, CSF) to maintain ICP constant; progressive increases beyond this capacity result in increases in ICP with subsequent decreases in CPP and ischemic injury to the brain

     • Therapeutic goals

          o Preservation of CPP by:

               • Controlling ICP

               • Maintaining adequate MAP

               • Decreasing cerebral metabolism

          o Maintenance of oxygen availability

     • Extracranial assessment and therapy

          o Airways, Breathing & Circulation (ABCs) 1st

               • Airway obstruction should be addressed ASAP – even mild hypercapnia can have a significant effect on ICP

               • Oxygen supplementation should be provided

               • Hypovolemic shock should be treated aggressively with goal of MAP 80-100 (but no more than 120mmHg)

               • Hypovolemia and hypoxemia are strongly correlated with elevated ICP and increased mortality in humans with TBI

          o Often concurrent extracranial trauma

               • Pneumothorax, pulmonary contusions

               • Traumatic cardiac arrhythmias

               • Fractures (other than skull)

          o Laboratory tests of particular importance include PCV/TP, electrolytes, blood gas analysis

     • Intracranial assessment and therapy

          o Important components of neurologic exam

               • Mentation – obtunded, stuporous, comatose, ± compulsive

               • Motor/Posture – ambulatory, recumbent, muscle tone and movements

               • Brainstem function – pupil size/symmetry, PLRs, physiologic nystagmus

          o Modified Glasgow Coma Scale in dogs based on findings above – shown to be related to survival at 48h

          o Initial neurologic status may improve following initial therapy for shock; reassess neurologic status often, as changes can occur rapidly

          o ICP monitoring ideal for dictating therapy; indirect assessment via trends in patient's neurologic exam used more often (and less accurately) in veterinary settings

          o Diagnostic imaging

               • Skull radiographs – depressed skull fractures may be seen, inadequate for more thorough evaluation of injuries

               • CT preferred in acute evaluation vs. MRI

          o Hyperosmotics

               • Mannitol – osmotic diuretic

                    • Decreases brain edema and ICP in TBI via several mechanisms

                    • 0.5-1.0g/kg IV bolus dosing more effective than CRI

                    • Effects last 2-5h

                    • Important to monitor serum osmolality and electrolytes with repeated use

               • Hypertonic saline

                    • Similar osmotic effects to mannitol

                    • Additional benefit of improved hemodynamic status – good choice for TBI in hypovolemic patients

          o Corticosteroids

               • A randomized placebo controlled study of over 10,000 human TBIpatients showed treatment with methylprednisolone resulted in a significantly increased risk of death in the steroid group vs. controls.

               • Not recommended for TBI patients

          o Furosemide

               • Not recommended specifically for TBI given IV volume depletion and risk of systemic hypotension

          o Decreasing cerebral blood volume (and therefore ICP)

               • Elevation of the head by 15-30° used to increase venous drainage (avoid jugular vein compression!)

               • Maintenance of normocapnia ideal; short term hyperventilation can be used to decrease ICP in the quickly deteriorating patient, but can ultimately result in decreases in cerebral blood flow

          o Anticonvulsants

Indicated in face of TBI induced seizures

               • Potential role of preventing seizures in first 7 days in humans

          o Analgesics

               • To be considered, especially in face of concurrent injuries

               • Can potentially interfere with neurologic assessment, however

          o Polyethylene glycol (PEG)

               • Hydrophilic polymer shown to have reparative effects with in vitro models of CNS injury

               • Potential future role in treatment of TBI

          o Surgical intervention

               • Craniectomy should be considered in open or depressed skull fractures, identification of focal intracranial hematoma or in the face of progressive neurologic deterioration despite aggressive medical management

          o Moderate hypothermia

               • Investigated in human medicine as a means of decreasing ICP and improving outcome; results have been variable and so not recommended

     • Prognosis and complications

          o Prognosis generally considered guarded to poor, but even severe cases can show marked improvement over the first few days after injury

               • Loss of brainstem reflexes poor prognostic indicator

          o Persistent neurologic deficits and/or seizures are common

          o Additional complications include aspiration pneumonia, coagulopathies, fluid and electrolyte imbalances, sepsis, meningitis, CSF leakage as well as those seen with recumbent patients – e.g. UTI, pressure sores

Suggested reading:

Emergency Management of the Head trauma Patient, Dewey, CW, The Veterinary Clinics of North America: Small Animal Practice, Common Neurologic Problems, 30(1), 2000

Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Edwards P, et al. Lancet, 2005 Jun 4-10:365(9475):1957-9.