Head Trauma pathophysiology, evaluation and Treatment Martin Young DVM , MS, DACVIM Mike Higginbotham, DVM, DACVIM

Blackwater Falls

Overview Common causes Pathophysiology Presenting signs

Common Causes Hit by automobile Falls Kicks Penetrating wounds Bites Stairs Kicks Penetrating wounds Bites

Types of Brain Injury Primary injury – initial insult. Function of trauma and forces. Linear, rotational Coup vs counter coup www.mdusd.k12.ca.us

Primary Injury Concussion Contusion Tissue laceration Brief loss of consciousness Contusion Bruising of parenchyma and secondary edema Tissue laceration Physical disruption of the parenchyma Intra-axial and extra-axial hematomas

Types of Brain Injury Secondary injury Edema cascade of biochemical pathways initiated which lead to further brain injury and increased intracranial pressure (ICP). Edema Vasogenic and cytotoxic vicious cycle of tissue damage

Secondary Injury Occurs minutes to hours after initial insult Series of events that perpetuate and initiate cellular damage Driven primarily by cerebral ischemia Hypotension, hypoxia, and  perfusion

Secondary Injury Hypotension, hypoxia, and  perfusion ATP depletion Na+ and Ca++ influx Cytotoxic edema Depolarization Other cascades Glutamate

Secondary Injury Platt & Olby. BSAVA Manual of Canine and Feline Neurology

Intracranial Pressure Dynamics Pressure autoregulation MABP Chemical autoregulation PaCO2 Intracranial compliance Monroe-Kelly Doctrine CPP = MABP – ICP Pressure Volume

Fractures

“Tippy”

Intracranial Bleeding Epidural Subdural / subarachnoid Parenchymal

Intracranial Bleeding Subdural / Subarachnoid

“Piper”

T2 image FLAIR 17

Herniation

Head Trauma Assessment

Looking for head trauma 25% of trauma patients have head trauma MGCS – only evaluates BS function PTE is a common cause of epilepsy 6.8% 36% of head trauma patients had seizures DWI - hemorrhage detected by 30 min MRI is useful for prognostication

Step 1: Can’t accurately assess the mentation of a shocky patient! Focus on ABC’s Correct hypoxia and hypotension first, will help the brain as well as the rest of the patient and will allow you to better assess your patients neurological status Baseline labwork: PCV, TS, CBC, Chem, Urinalysis, and Wt. Can’t accurately assess the mentation of a shocky patient!

Postures and respiration Postures: decerebrate vs decerebellate vs schiff sherrington Respiration: Cheyne-Stokes – deep cerebral and rostral BS –rapid breathing followed by apnea Central hyperventilation – 25/min – regardless of CO2 content – midbrain to Pons Irregular gasping – caudal BS - terminal

Head Trauma -signs- Gait and Posture Mental status Vestibular signs Paresis, circling, paralysis Normal, opisthotonus, decerebrate rigidity Mental status Bright, depressed, stuporous, comatose Vestibular signs Pupils Size, symmetry, response to light Decerebrate rigidity

Step 2: Part 1 complete. Patient is normovolemic and normotensive and we have established appropriate oxygenation and ventilation Assess the rest of the patient: Nervous system, vertebral fractures/ luxation, lungs, abdomen, musculoskeletal Additional Diagnostics: Radiographs: skull, abdomen, thorax Additional bloodwork if indicated MRI/CT, electrodiagnostics

Modified Glasgow Coma Scale Published in a 2001 JVIM article by Dr. Simon Platt Evaluates the patient using 3 criteria and assigns a severity score from 1-6 to each: Level of Mentation Motor Function Brainstem Reflexes Score assigned from 3-18; higher the score, better prognosis

Basic Levels of Mentation Bright, alert, responsive Obtunded Dull, depressed but responsive to all manner stimuli Semi-coma responsive to stimuli Stuporous responsive only to noxious stimuli Comatose unconscious, non-responsive to any stimuli

MGCS: Levels of Mentation 6 - BAR or intermittent periods BAR 5 – obtunded – clouded consciousness 4 – semi-coma - responsive to visual stimuli 3 – semi-coma - responsive to auditory stimuli 2 – stuporous – responsive to vigorous stimulation 1 - comatose

LOA

Brain Stem Reflexes 6 - Normal PLR and oculocephalic reflex (OcR) 5 - Slow PLR, normal to slow OcR 4 - Bilateral unresponsive miosis, normal to slow OcR 3 - Pinpoint pupils, reduced to absent OcR 2 - Unilateral, unresponsive mydriasis, reduced to absent OcR 1 - Bilateral, fixed dilated pupils

Pupil Chart De Lahunta - Vet Neuroanatomy

Oculocephalic Reflex AKA - conjugate eye movements Pathway between the vestibular system and the extraocular muscles to coordinate eye movements Pathway travels through the central brainstem in the medial longitudinal fasciculus before connecting with CN III, IV and VI and exiting the brainstem Loss of oculocephalic reflex = Poor Prognosis Denotes severe brainstem damage

MGCS: Motor Assessment 6 - Normal gait, normal spinal reflexes 5 - Hemiparesis, tetraparesis 4 - Recumbent, intermittent extensor rigidity 3 - Recumbent, constant extensor rigidity 2 - Recumbent, constant extensor rigidity w/ opisthotonus (decerebrate rigidity) 1 - Recumbent, hypotonia of muscles, depressed/absent spinal reflexes

MGCS Score Now, have your MGCS score, what does it mean? Score 15-18: Good prognosis Score 9-14: Guarded prognosis Score 3-8: Grave prognosis A linear association between score during first 48 hours and patient overall prognosis Score = 8 in the JVIM paper resulted in 50% mortality

Cushing Reflex KEY: Decreased mentation, high systemic MAP, low heart rate - suspect high ICP Increased ICP results in decreased CBF which regionally increases CO2 concentration High CO2 sensed by vasomotor center in the brain and triggers a massive sympathetic discharge resulting in a peripheral vasoconstriction Result is a rise in MAP to maintain CPP Activates baroreceptors creating the reflex bradycardia

Forebrain Can have fewer signs Seizures Menace deficit Behavior changes Sensory/proprioceptive deficits (contralateral) Large circles to the lesion Altered homeostasis (temperatue, heart rate, blood pressure)

Imaging Radiographs Unlikely to reveal additional clinically useful information but may show depressed skull fractures Presence of a skull fracture has not been shown to be a negative prognosticator Often, CT or MRI warranted to assess for severity of injury, hemorrhage, and herniation

Head Trauma Treatment

Treating the Head Trauma Patient Therapeutic Options: Mannitol/hypertonic saline Fluids Anticonvulsants Antibiotics Steroids? Oxygen Nutrition Analgesia Patient care

Mannitol: MOA Osmotic diuretic: decreases vasogenic cerebral edema and decreases ICP Reflex cerebral vasoconstriction as a result of decreased blood viscosity Free-radical scavenger Improves microvascular flow; shrinks RBCs by 15% and improves deformation and cell wall flexibility hence improving tissue oxygenation

Hypertonic saline MOA Osmotic draw: pulls fluid from interstitial and intracellular space Improves: MAP, CBP and CBF Volume expansion: not used in dehydration or hypernatremia. Can cause vago-reflex – may need atropine

Mannitol/hypertonic saline Indications: Clinical indication of increased ICP Progressive decline in neurological status Cushing’s reflex Dose: mannitol 1 to 1.5 g/kg IV over 20 minutes Hypertonic saline 3-5 ml/kg over 10 minutes Effect Mannitol max effect in 20 min last 2-5 hrs repeat q6-8 Hypertonic saline max effect in minutes, last 1 hour

Mannitol/hypertonic saline Do not give if dehydrated/volume depleted Monitor electrolytes Monitor weight/hydration No hypertonic saline if hypernatremic

Maintain Oxygenation Evaluate mucous membrane and tongue color, respiratory rate, pattern and thoracic auscultation Arterial Blood Gas: PaO2 > 90 mmHg Pulse Oximetry: Maintain SpO2 > 95% Provide supplemental oxygen Flow-by or mask oxygenation or tent O2 cage does not allow frequent patient assessment Nasal O2 - avoid sneeze induction which increases ICP Intubation / Ventilation

No Corticosteroids Are contra-indicated in both veterinary and human medicine for the treatment of head trauma. All studies show either no improvement or a worsening of the outcome Commonly associated with iatrogenic hyperglycemia and worse prognosis Does not help with cytotoxic edema only vasogenic edema Promote anaerobic metabolism – increase lactate Increase glutamate levels and neuronal death.

Hyperglycemia and Head Trauma Hyperglycemia > 200 mg/dL has been associated with increased mortality in severely brain injured people JAVMA, 2001 paper positively correlated degree of hyperglycemia with severity of brain injury Paper failed to correspond to overall patient prognosis but parallels human papers which correlated higher BG with lower GCS score Current guideline: Avoid iatrogenic elevation of blood glucose

Analgesia Ideal Analgesic Options: Agent that provides pain relief without inducing respiratory depression or hypotension Options: Opioids – fentanyl Benzodiazepines (reduce anxiety, muscle relaxation) Alpha-2 agonists NSAIDS Gabapentin

Fluid Resuscitation Goal is to restore normovolemia and normotension Fluid Choices: Crystalloids - 90 ml/kg/hr Colloids e.g. hetastarch - 10-20 mL/kg to effect Hypertonic saline - 4-5 mL/kg over 3-5 minutes Blood products if indicated No one fluid proven to be better than another, important point is to give to effect, don’t want to create hypertension! Ideal MAP = 70 - 90 mmHg, remember, CPP = MAP – ICP! (Minimum CPP 70 mmHg)

Monitoring Serial neurological exams necessary as the patient will change, better or worse every 1-2h depending on patient Continuous BP, ECG and O2 monitoring recommended Serial ABG indicated if patient having difficulty breathing appropriately to determine if ventilation is needed Monitor electrolytes, PCV/TS and weight twice daily

Supportive Care Circulatory support Oxygenation Analgesia Padded bedding Rotate patients Elevation of the head 15-30° above the heart Lubricated eyes to prevent ulceration Nutrition Anticonvulsants if indicated Avoid jugular compression

BAER test Not just an auditory test Can be a useful assessment of brainstem function

BAER Tracings Normal Brainstem damage

Electroencephalogram

Sequella Behavior changes Post traumatic epilepsy (weeks to years) Persistent deficits Ventricular anomalies

Post trauma

Conclusions With time and good supportive care, many head trauma patients can do quite well Most important aspect in management is maintaining good MAP and oxygenation

References Dewey, CW. Emergency Management of the Head Trauma Patient. Veterinary Clinics of North America: Common Neurological Problems. 2000: 207-25. Syring RS. Hyperglycemia in dogs and cats with head trauma: 122 cases (1997-1999). JAVMA. 2001; 218(7): 1124-29. Syring RS. Assessment and treatment of CNS abnormalities in the emergency patient. Vet Clin Small Anim. 2005; 35: 343-358. Platt SR. The Prognostic Value of the Modified Glasgow Coma Scale in Head Trauma Dogs. JVIM. 2001; 15: 581-84. Armitage-Chan EA. Anesthetic management of the head trauma patient. JVECC. 2007; 17(1):5-14. Kalita J. Current Status of osmotherapy in intracerebral hemorrhage. Neurology India. 2003; 51(1): 104-9. Oliver and Lorenz. Handbook of Veterinary Neuroanatomy. DeLahunta A. Veterinary Neuroanatomy and clinical neurology. Saunders Elsevier. 2009.