Emergent care for Traumatic Brain Injury

and seizure control

Megan Stout Steele, DVM, DACVIM (N)Animal Specialty Group

4641 Colorado BlvdLos Angeles Ca 90039

818-244-7977

Outline

•  Pathophysiology of traumatic brain injury (TBI)

•  Initial assessments & care•  Diagnostic imaging•  Medical vs surgical management•  Prognosis •  Emergent seizure management

Traumatic Brain Injury

•  Morbidity & Mortality•  Numerous causes •  Primary vs secondary injury

Pathophysiology of TBI

•  Primary injury•  Direct parenchymal damage

•  Secondary injury•  Ischemia, edema, necrosis

Pathophysiology Cont’d•  Secondary injury

•  numerous pathways activated•  excessive excitatory

neurotransmitters •  cytotoxic edema, ↑ Ca++ levels

•  generation of reactive oxygen species

•  pro-inflammatory cytokines

•  complement, kinin, coagulation cascades

Cerebral Perfusion Pressure

•  CPP = MABP - ICP •  CPP is the primary determinant of brain

oxygenation and nutritional support

•  Monroe-Kellie Doctrine •  Calvaria is a fixed space•  ICV ↑, ICP↑,

•  Critical volume => herniation

Cushings Reflex

•  As ICV increases -> ICP will also increase

•  To try and maintain CPP, hypertension occurs

•  Baroreceptors stimulated •  parasympathetic response•  reflex bradycardia

Presentation

•  History•  witnessed trauma

•  External signs of trauma •  scleral hemorrhage, blood from eyes, nose, mouth,

palpable fractures

•  Initial assessment •  ADDRESS SHOCK

ABCs always come 1st

•  Concern that aggressive fluid therapy will exacerbate cerebral edema•  Contraindicated!

•  Persistent hypotension -> sustains ↑ ICP and ↑ mortality rates

•  Systolic BP > 90mmHg needs to be met and maintained.

Initial Diagnostics

•  TPR•  Blood Pressures•  Blood gas/stat electrolytes/BG•  Thoracic/abdominal radiographs

Treatments

•  Combating ↑ ICP•  Hypertonic Saline (7.5% NaCl)

•  4ml/kg IV Bolus

•  Rapid volume expansion, short duration

•  Mannitol •  0.5-1.5g/kg IV over 15-20min

•  Decreases blood viscosity (minutes), osmotic diuretic (hours)

Treatments Cont’d

•  Hyperoxygenation•  Oxygen cage, mask, flow by

•  15-30 degree Head Elevation•  no neck leads, jug sticks/jug catheters

Treatments Cont’d

•  Pain management•  Buprenorphine•  Avoid full mu agonists, butorphanol, NSAIDs

•  GI protectants•  H2 antagonists•  PPIs

•  Sucralfate

Treatments Cont’d

•  Anticonvulsants (if seizure)

•  Supportive care

•  Future treatments•  hypothermia•  glycemic control

Modified Glasgow Coma Scale

•  18 pt scale based on motor, brainstem, and consciousness scores.

•  Baseline for monitoring improvement/deterioration

•  Help prognosticate

Motor ActivityNormal Hemi/tetraparesisRecumbent/intermittent rigidityRecumbent/constant extensor rididityRecument/constant extensor rigidity & opisthotonusRecumbent/hypotnoic muscles, reduced to absent reflexes

MCGS Score654321

Brainstem ReflexesNormal PLR & oculocephalicSlow PLR, normal to decreased oculocephalicMiosis OU, normal to decreased oculocephalic Pinpoint pupils, decreased to absent oculocephalicUnilateral, unresponsive mydriasis, reduced to absent oculocephalicBilateral, unresponsive mydriasis, reduced to absent oculocephalic

MCGS Score654321

Level of ConsciousnessOccasional alertness, responsive to environmentDepression/delirium, responsive but inappropriateObtunded, responsive to visual stimuliObtunded, responsive to auditory stimuli Stuporous, responsive to noxious stimuliComatose

MCGS Score654321

MGCS scores

Score Category Actual MGCS Prognosis

I 3-8 Grave

II 9-14 Guarded

III 15-18 Good

Monitoring Pupils

•  Good

•  Bad

Predictors of Negative Outcomes

•  MGCs <8 •  Persistent hyperglycemia•  Corticosteroid administration

Imaging Modalities

•  Radiographs•  Good for displaced fractures

•  Hard to read and get well positioned skull radiographs without heavy sedation

•  CT•  quick, doesn’t require GA

•  hemorrhage is hyperattenuating

•  MRI •  best intraparenchymal detail, requires GA

When to Image

•  Severe neurologic deficits at presentation

•  After cardiovascular stabilization

•  Worsening neurologic status with time despite appropriate therapies

Surgical Indications

•  Compressed/open skull fractures

•  Compressive hematomas

•  Significant midline shift

Outcomes

• Companion animals can be functional pets with significant losses of cerebral tissue

• Ultimate goal is to return the patient to its previous role in society

• Often attainable with time•  and supportive care

Seizures

•  Most common neurologic problem in companion animals

•  Clinical manifestation of excessive, hypersynchronous, electrical activity in the cerebral cortex

•  Directly caused by inadequate neuronal inhibition, excessive neuronal excitation, or a combination of both

Seizure Stages•  Aura (prodrome)

•  Initial sensation of a seizure, may see a behavior change

•  Ictus•  active seizure event

•  Post-ictus•  pacing, blindness,

disorientation, increased appetite

•  Inter-ictus•  time between seizures

Seizure Types

•  Generalized•  “classic” seizure (tonic/clonic)

•  alteration in consciousness

•  ANS sigsn (salivation, urination)

•  Partial •  Focal motor signs (chewing gum fits, abnormal single

limb movements, etc)

•  Focal ANS signs

•  Abnormal behavior/psychomotor seizures

Seizure Causes

•  Intracranial Extracranial•  Idiopathic Electrolyte imbalances•  Inflammatory Toxins•  Infectious Live disease (HE)•  Immune-mediated Renal disease (RE)•  Vascular Hypoglycemia•  Neoplasia •  Trauma

Seizure Mimics

•  Syncope•  Tremors•  Vestibular•  Myoclonus•  Weakness•  Cataplexy •  Pain

Goals of Treatment

•  Stop the seizures•  Reassess status of the patient •  Consider differentials/history•  Maintenance therapy

•  Ideally consider all these goals concurrently

Stop Seizures Quickly

•  Status epilepticus (SE)•  Continuous seizure activity that lasts for 5 minutes or 2+

seizures between which there is incomplete recovery

•  Seizures that persist for > 30 minutes consistently produce brain pathology (necrosis)

•  Prolonged seizures can have secondary consequences: hypoxia, hyperthermia, hypoglycemia, acidosis, renal failure, DIC...

Stabilization & Minimum Database

•  Patient presents seizuring•  Place IVC•  Administer 0.5mg/kg IV diazepam/

midazolam •  Get TPR, baseline electrolyte status,

blood glucose, blood pressure, ecg *if on ACDs, pull blood for drug levels*

•  If another seizure occurs, give a 2nd dose of diazepam

Physical Assessment

•  Heart rate•  <80bpm consider Cushings reflex

•  Do not treat with atropine

•  Temperature•  > 104F consider external cooling

•  Blood pressure•  if > 160mmHg with bradycardia, consider Cushings

reflex

•  Assess brainstem reflexes (menace, pupil size and light responses, oculocephalic)

After the second dose of Diazepam

Emergency Anticonvulsants

•  Benzodiazepines: GABA agonists •  Diazepam/Midazolam

•  IV: 0.5-1mg/kg

•  PR: 1-2mg/kg

•  IN: 0.5mg/kg

•  CRIs: 0.5-2mg/kg/hr

•  Light sensitive, absorbed by plastic (D), phlebitis (D)

Emergency Anticonvulsants

•  Loading maintenance ACDs•  Phenobarbital - GABA agonist

•  Dogs: 16-20 mg/kg IV total dose

•  Cats: 12mg/kg IV total dose

•  1/4 total dose, IV q6hrs until loaded

•  20-30 minutes to be effective

•  Maintenance dose: 2.2mg/kg q24 hr

•  Levetiracetam - SV2A inhibitor•  Dogs/cats: 60mg/kg IV bolus

•  Maintenance dose: 20mg/kg q8 hr

Still no Response?

•  Propofol•  1-2 mg/kg IV bolus•  0.1-0.6 mg/kg/min CRI

•  Intubation

•  One on one care

•  Gas anesthetics

Discharge

•  Ideally hospitalize until 24 hrs seizure free

•  If CRI required to stop seizures, wait 24 hours before weaning•  wean 25% q4-6 hrs until off

Trauma-associated seizures?

•  In people: up to 42% TBI patients develop seizures, with 4-13% developing seizures within 3 years of their trauma

•  Post-traumatic seizures •  Immediate: within 24 hrs of injury

•  Early: >24 hrs, < 7 days of injury •  Late: >7 days after injury

Post-traumatic Seizures�Dogs

•  Late (> 7 days after injury) more common•  ~ 6.8%

•  Immediate/early: only seen in ~ 3.5% TBI/Head trauma cases

•  Post-traumatic epilepsy occurs more frequently compared to the prevalence of idiopathic epilepsy

•  No evidence to support increased risk of seizures with head trauma in cats at this time

Thanks for Coming

• QUESTIONS?

•  References available upon request