CNS Trauma Flashcards
List the common pathologies secondary to flipping over backwards
- Fracture (petrous temporal bone, squamous temporal and parietal bones, basilar bones)
- Haemorrhage into retropharyngeal space and guttural pouch (laceration of vessels and/or rupture of rectus capitus ventralis muscle)
- Cerebral contusion secondary to acceleration-deceleration forces
List the common pathologies secondary to impact on the dorsal surface of the head
- Fracture (frontal or parietal bones)
- Cerebral cortical injury
- Spinal cord injury/cervical vertebral damage
- Damage to CN XII where it exits the hypoglossal foramen
- Stretching of the optic nerves and subsequent blindness.
Define primary versus secondary traumatic brain injury
Primary: immediate mechanical disruption of brain tissue characterised by damage to neuronal cell bodies, dendritic arborisations, axons, glial cells and brain vasculature (often irreversibly). Can be focal, multifocal or diffuse.
Secondary: A cascade of molecular, cellular and biochemical events that can occur for days-months after injury, causing delayed tissue damage. Hypoxia, ischaemia, brain swelling, altered intracranial pressure (disruption to cerebral autoregulation results in increased intracranial pressure therefore reduced cerebral perfusion/blood flow), breakdown of the BBB and impaired energy metabolism.
Define the Cushing’s Reflex
A hypothalamic response to brain ischaemia that results from acute increased intracranial pressure. You get hypertension and secondary baroreceptor-mediated bradycardia. Continued elevation of intracranial pressure and reduction of cerebral blood flow results in increased sympathetic discharge with subsequent myocardial ischaemia and development of cardiac arrhythmias - “brain-heart syndrome”.
List the signs of brainstem injury
- Coma, depression (damage to the RAS)
- Strabismus, anisocoria, loss of PLR (due to damage to CNIII)
- Apneustic or erratic breathing (poor prognosis)
- Bilaterally dilated pupils/unresponsive to light (indicates an irreversible brainstem lesion)
- Decorticate posture (rigid extension of the neck, back and limbs)
To differentiate caudal brainstem from rostral cervical spine assess mentation and function of CNX and CNXII (mentation abnormal and tongue weakness and/or lack of vagal input with brainstem only)
List the signs of cerebral injury
- Seizures (usually generalised)
- Impaired vision and menace (contralateral to the lesion; PLR should be intact)
- Decreased facial sensation contralateral to the lesion (parietal cortex)
- Altered behaviour (circling, head pressing, hyperexcitability, aggression)
List the signs of cerebellar injury/disease
- Ataxia
- Inability to regulate rate, range and force of movement
- Jerky/awkward initiation of movement
- Intention tremors
- Truncal sway
- Hypertonia causing a spastic gait
- Signs can be bilateral or unilateral depending on focal or diffuse disease.
- Vestibular signs if flocculonodular lobe or vastigial nucleus involved (dysequilibrium, nystagmus with fast phase way from the lesion, head and body tilt toward the lesion).
- Paradoxic vestibular disease (head tilt away from the lesion and nystagmus with fast phase toward the lesion) if cerebellar peduncle is involved.
List the treatment for TBI
- Optimise cerebral blood flow (optimise MAP and ensure intracranial pressure is not increased)
- If increased intracranial pressure: hyperventilation (risk is reduction of cerebral blood flow may cause ischaemia), hyperosmolar agents (hypertonic saline, mannitol), barbiturates, head elevation, CSF drainage? - only if obstruction to outflow, decompressive surgery?
- Crystalloid fluid therapy (slightly less than maintenance)
- Keep blood glucose concentration between 7.5-8mmol/L.
- Hypothermia
- Anti-inflammatories (NSAIDs, steroids? controversial; DMSO? controversial; vitamin E and C? possibly don’t reach therapeutic concentrations in time for acute disease)
- Control seizures to reduce secondary injury
- Avoid ketamine due to increases in cerebral blood flow and intracranial pressure.
- Barbiturates if intracranial pressure elevation is refractory to other treatments (decreases cerebral metabolism so protects against ischaemia but also cause hypotension)
List the mechanisms of action of hypertonic saline and mannitol
Hypertonic saline: produces an osmotic gradient b/w the intravascular and interstitial-intracellular compartments leading to shrinkage of brain tissue, therefore decreasing intracranial pressure. It also augments volume resuscitation and increases circulating volume, MAP and cerebral perfusion pressure. In addition in restores neuronal membrane potential maintains BBB integrity and modulates the inflammatory response by reducing adhesion of leukocytes to the endothelium. Contraindicated with dehydration, intracerebral haemorrhage, hypernatraemia, renal failure, HYPP and hypothermia. Need to monitor CVP and Na/K concentrations.
Mannitol: induces changes in blood rheology and increases cardiac output, leading to improved cerebral perfusion pressure and cerebral oxygenation. The effects of this are cerebral artery vasoconstriction and subsequent reduction in cerebral blood volume and intracranial pressure. Multiple doses may be associated with renal and CNS effects including intravascular dehydration, hypotension and reduction of cerebral blood flow. Concurrent use with furosemide may prolong the effects and diminish the potential for rebound intracranial pressure elevation.
List common vertebral fracture sites in adults and foals
Foals: C1-C3 and T15-T18; axial dens fracture with atlantoaxial subluxation (usually disruption of the physis of the dens and separation of the odontoid process)
Occipital-atlantoaxial region, C5-T1 and caudal thoracic. May be more common in young horses due to late closure of cervical vertebral growth plates (4-5yrs)
Are ataxia and loss of proprioception and motor function or loss of deep pain associated with more severe injury and why?
Spinal cord damage is typically worse in large myelinated motor and proprioceptive fibres compared with smaller non-myelinated nociceptive fibres hence you see ataxia and loss of both proprioceptive and motor function before you see loss of deep pain.
List the 3 phases of spinal cord injury and repair in a temporal manner
- Vascular and biochemical changes within the spinal cord (first 48 hours)
- Effects of inflammatory cells (peaks approximately 4 hours after injury)
- Axonal regeneration and lesion repair (from about 1 week after injury
Why do you sometimes see impaired ventilation, bradycardia and hypotension with spinal cord injury
Lesions cranial to C5 can affect the respiratory centre or cranial to T2, the origin of the sympathetic outflow for the thoracolumbar spinal cord.
Discuss the use of anti-inflammatories with SCI
Corticosteroids: thought to primarily help with free radical scavenging but may also decrease catecholamines and glutamate and decrease apoptosis-related cell death and spread of morphologic damage, preventing loss of axonal conduction and reflex activity. May also preserve vascular membrane integrity and stabilise white matter neural cell membranes. May help reduce fibrin and oedema and reduce Na/K imbalance secondary to oedema and necrosis. No longer used in humans. Evidence of positive effect is lacking…
DMSO: increases brain and SC blood flow, decreases brain and SC oedema, increases vasodilating PGE1, decreases platelet aggregation, decreases PGE2 and PGF2, protects cell membranes and traps hydroxyl radicals. Exact mechanisms is unknown. Evidence lacking and use is controversial.
Vit E and Se: beneficial for antioxidant effects although may not be of benefit in acute injury due to time taken to reach therapeutic concentrations.
List management strategies for recumbent horses
- Massage/therapeutic ultrasound and or hydrotherapy of affected limbs/muscle groups for 10-15min 2+ times daily to encourage blood flow
- Flexion and extension of all limbs to maintain range of motion
- Turning at least every 3-4 hours to reduce compartment syndromes/pressure necrosis.
