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

2. Blackwater Falls

3. Overview
Common causes
Pathophysiology
Presenting signs

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

5. Types of Brain Injury
Primary injury – initial insult. Function of trauma and forces.
Linear, rotational
Coup vs counter coup

6. 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

7. 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

8. 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

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

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

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

12. Fractures

13. “Tippy”

14. Intracranial Bleeding
Epidural
Subdural / subarachnoid
Parenchymal

15. Intracranial Bleeding
Subdural / Subarachnoid

16. “Piper”

17. T2 image
FLAIR 17

18. Herniation

19. Head Trauma
Assessment

20. 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

21. 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!

22. 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

23. 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

24. 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

25. 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

26. 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

27. 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

28. LOA

29. 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

30. Pupil Chart
De Lahunta - Vet Neuroanatomy

31. 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

32. 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

33. 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

34. 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

35. 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)

36. 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

37. Head Trauma
Treatment

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

39. 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

40. 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

41. 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

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

43. 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

44. 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.

45. 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

46. 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

47. Fluid Resuscitation Goal is to restore normovolemia and normotension
Fluid Choices:
Crystalloids - 90 ml/kg/hr
Colloids e.g. hetastarch mL/kg to effect
Hypertonic saline 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 = mmHg, remember, CPP = MAP – ICP! (Minimum CPP 70 mmHg)

48. 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

49. 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

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

51. BAER Tracings
Normal
Brainstem damage

52. Electroencephalogram

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

54. Post trauma

55. 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

57. References
Dewey, CW. Emergency Management of the Head Trauma Patient. Veterinary Clinics of North America: Common Neurological Problems :
Syring RS. Hyperglycemia in dogs and cats with head trauma: 122 cases ( ). JAVMA. 2001; 218(7):
Syring RS. Assessment and treatment of CNS abnormalities in the emergency patient. Vet Clin Small Anim. 2005; 35:
Platt SR. The Prognostic Value of the Modified Glasgow Coma Scale in Head Trauma Dogs. JVIM. 2001; 15:
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):
Oliver and Lorenz. Handbook of Veterinary Neuroanatomy.
DeLahunta A. Veterinary Neuroanatomy and clinical neurology. Saunders Elsevier