Head Trauma - Dogwood Veterinary Emergency & Specialty Center

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Transcript Head Trauma - Dogwood Veterinary Emergency & Specialty Center

Martin Young DVM , MS, DACVIM
Mike Higginbotham, DVM, DACVIM
Blackwater Falls
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Common causes
Pathophysiology
Presenting signs
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Hit by automobile
Falls
Stairs
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Kicks
Penetrating
wounds
Bites
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Primary injury – initial insult. Function of
trauma and forces.
Linear, rotational
Coup vs counter coup
www.mdusd.k12.ca.us
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Concussion
Brief loss of consciousness
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Contusion
Bruising of parenchyma and secondary edema
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Tissue laceration
Physical disruption of the parenchyma
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Intra-axial and extra-axial hematomas
• Secondary injury
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
• 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
• Hypotension, hypoxia, and  perfusion
• ATP depletion
• Na+ and Ca++ influx
• Cytotoxic edema
Other cascades
Depolarization
Glutamate
Platt & Olby. BSAVA Manual of Canine and Feline Neurology
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Pressure autoregulation
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Chemical autoregulation
PaCO2
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Intracranial compliance
Monroe-Kelly Doctrine
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CPP = MABP – ICP
Pressure
MABP
Volume
• Epidural
• Subdural /
subarachnoid
• Parenchymal
Subdural / Subarachnoid
T2 image
FLAIR
Herniation
Head Trauma
Assessment
Looking for head trauma
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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:
• 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
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Gait and Posture
Paresis, circling, paralysis
Normal, opisthotonus, decerebrate rigidity
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Mental status
Bright, depressed, stuporous, comatose
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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
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6 - Normal PLR and oculocephalic reflex (OcR)
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5 - Slow PLR, normal to slow OcR
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4 - Bilateral unresponsive miosis, normal to slow OcR
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3 - Pinpoint pupils, reduced to absent OcR
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2 - Unilateral, unresponsive mydriasis, reduced to absent OcR
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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
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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?
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Oxygen
Nutrition
Analgesia
Patient care
Mannitol: MOA
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Osmotic diuretic: decreases vasogenic cerebral edema and
decreases ICP
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Reflex cerebral vasoconstriction as a result of decreased blood
viscosity
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Free-radical scavenger
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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
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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
 Agent that provides pain relief without inducing respiratory
depression or hypotension
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Opioids – fentanyl
Benzodiazepines (reduce anxiety, muscle relaxation)
Alpha-2 agonists
NSAIDS
Gabapentin
Fluid Resuscitation
• Goal is to restore normovolemia and normotension
• Fluid Choices:
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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
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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
• Not just an auditory test
• Can be a useful assessment of brainstem
function
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
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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.