Rhonda Dixon, DVM Section Head, Emergency and Critical Care Sugar Land Veterinary Specialty and Emergency

Transcription

1 Rhonda Dixon, DVM Section Head, Emergency and Critical Care Sugar Land Veterinary Specialty and Emergency

2 Traumatic Brain Injury Causes Pathophysiology Neurologic assessment Therapeutic Approach Status Epilepticus Introduction Key therapeutic Points Drugs to control

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4 Can occur subsequent to trauma from falls, motor vehicle accidents, crushing injuries, animal attacks or attacks from humans (inadvertent or purposeful) Should be suspected in any patient with trauma Injuries can include: Oral hemorrhage Epistaxis Aural hemorrhage Facial/skull lacerations Ocular trauma Facial/skull fractures Severe brain injury is associated with a high level of mortality in both humans and pets

5 Primary Injury Result of initial traumatic impact to the skull and the intracranial contents Occurs at time of incident Little to nothing can be done to prevent Secondary Injury Results from a cascade of events which contribute to neuronal cell death after the initial trauma Occurs minutes to days following initial trauma Common contributing factors are: Hypotension Hypoxia Hyperthermia Hypo- or hypercapnia

6 ABC s (airway, breathing, cardiovascular status) Important to focus on imminently life threatening abnormalities Most are in hypovolemic shock Traumatized, hypovolemic patients with no appreciable brain injury often have depressed mention. Can be difficult to assess neurologic status (voluntary motor or pain sensation) of patients in shock Focus on stabilizing the patient and the neuro system will benefit Obtain minimum data base (PCV, TP, BG, and vitals including blood pressure)

7 Should include Level of consciousness Pupil size and responsiveness Ocular position Breathing pattern Skeletal motor responses Complete initial assessment BEFORE any pain medications are given Reassessment every minutes

8 Most reliable empiric measure of impaired cerebral function after head injury Provides information about function of cerebral cortex and Reticular activating system (RAS) in brainstem Patients presenting in coma generally have bilateral cerebral abnormalities or severe brainstem injury--- guarded to poor prognosis. LOC can affect motor activity Decerebrate posture = opisthotonus with hyperextension of all 4 limbs and decreased LOC (cerebral damage) Decerebellate = opisthotonus and variable flexion/ extension of hind limbs, intact mental status (cerebellar injury)

9 Neuro-ophthalmologic exam evaluates brainstem reflexes Ocular and orbital trauma should be interpreted during this exam Progression to bilaterally fixed dilated unresponsive pupils---poor prognostic indicator, associated with death if not addressed with treatment.

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11 Incorporates 3 categories 1. Level of consciousness 2. Motor activity 3. Brainstem Reflexes Assigns a score of 1-6 for each category Provides a total score of 3-18 Higher scores correlate with better prognosis

12 3-8 GRAVE 9-14 GUARDED GOOD

13 Minimize increases in Intracranial Pressure Position animal with head elevated to degrees Elevate the animal at an angle using wedges or firm surfaces; not recommended to use towels to prop head due to pressure on jugular area Use caution when restraining patient Avoid jugular venipuncture and head/neck restraint Oxygen Decreased O2 delivery is a main contributor to secondary brain injury Oxygen is recommended in most if not all head trauma patients 1. Face mask 2. Flow by 3. Oxygen cage ** 4. Nasal oxygen 5. Trans-tracheal catheter

14 Oxygenation can be measured by spo2 or arterial blood gases spo2 >95%= PaO2 of at least 80 mmhg spo2 < 89% (PaO2 <60 mmhg)----should not be tolerated Maintain proper CO2 levels Plasma CO2 tension regulates cerebral blood flow vessel dilation, therefore impacts cerebral blood flow and intracranial pressure Hypercapnia leads to increased ICP Arterial Blood Gas measurement is most accurate Venous PCO mmhg, Arterial PaCO mm Hg End Tidal CO2 measurement tends to underestimate actual PaCO2 levels

15 Not recommended in hypovolemic patients Beneficial effects on: 1. Intracranial Pressure (ICP) 2. Cerebral Perfusion Pressure (CPP) 3. Cerebral Blood Flow (CBF) 4. Brain metabolism 5. Neurologic Outcome Reduces ICP within minutes Duration only lasts hours dose is g/kg, slow over 15min Give with filter, crystals can form at room temp. Warm to ~99 degrees F Can repeat in 2-4 hours if response seen

16 Volume resuscitation should be aggressive and rapid MAP mmhg Doppler mmhg Combination of crystalloids, Artificial Colloids, Hypertonic Saline ¼ shock doses to start Goal oriented Crystalloid Shock Dose 1. Dog 90ml/kg 2. Cat 60ml/kg Artificial Colloid Shock Dose 1. Dog ml/kg 2. Cat 5-10 ml/kg Hypertonic Saline 3-5 ml/kg over 3-5 minutes Combined administration of colloid and HTS is more effective than when given alone

17 Glucose control 1. Hyperglycemia assoc. with increased mortality or worse neurologic outcomes 2. Hyperglycemia result of sympathoadrenal response 3. Avoid iatrogenic causes of hyperglycemia (i.e. corticosteroids) 4. Insulin? Thermoregulation 1. Hypothermia used in human medicine 2. Not widely used in veterinary patients 3. Maintain normothermia or slight hypothermia degrees F Analgesia 1. Opioids are favored due to ability to reverse, lack of effects on CV system 2. Fentanyl or morphine CRI 3. Buprenorphine, Butorphanol

18 Seizure Control Seizures can occur immediately or days/weeks after Diazepam mg/kg IV Phenobarbital loading mg/kg total dose Levetiracetam mg/kg IV initially, then 20mg/kg Q 8 PO/IV GI protectants/motility Modifiers Famotidine mg/kg Q24 Omeprazole/Pantoprazole Cerenia, Ondansetron, Metoclopramide Nutrition Should be started ASAP Full caloric requirements by 7 days NG/NE tubes if patient tolerates Esophagostomy tube if undergoing anesthesia for anything else IV PPN or TPN if patient does not have gag reflex or not conscious

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20 Status epilepticus (SE): Single seizure lasting > 5 minutes OR 2+ seizures w/o recovery in between Signalment is similar to seizure disorders in general 2:1 Male to female Median age 3.3 years Large Breed more likely than small breed Majority are caused by idiopathic epilepsy Can be caused by neoplasia, inflammatory, vascular, toxin and trauma Systemic Effects Increases sympathetic tone leading to increased HR, BP, BG,T cardiac arrhythmias metabolic acidosis DIC NCPE predisposition to further seizures

21 SE is a medical emergency and needs to be treated aggressively and quickly 1. STOP the seizure! 2. PREVENT adverse systemic effects 3. INITIATE maintenance anticonvulsant therapy to prevent recurrent emergent seizures

22 Obtain vascular access Provide oxygen supplementation if needed Obtain initial database (vitals, BP, BG, electrolytes, spo2, etc) Treat hypoglycemia or hypocalcemia if needed First line therapy is a benzodiazepine given as bolus (give up to 3x) 1. Diazepam mg/kg IV 2. Midazolam mg/kg IV, mg/kg IM

23 Benzodiazepine CRI Diazepam CRI mg/kg/hour titrated Midazolam CRI mg/kg/hour titrated Start longer acting anticonvulsant therapy Phenobarbital IV dose distributes rapidly into CSF (20-30min) Loading dose up to 16mg/kg can be given to naïve animal Prefer 4-5mg/kg IV dose initially; re-evaluate patient status and level of sedation Monitor respiratory and CV depression Levetiracetam (Keppra) Renal elimination Little to no sedation mg/kg initially, then 20 mg/kg IV/PO Q8

24 2-8 mg/kg IV bolus Then can give mg/kg/ min Patient will have to be continually monitored Intubate patient if needed Use for 6 hours, then begin weaning off, or discontinue

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