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WELCOME
NEUROLOGICAL EMERGENCIES IN DOGS
DOCTORAL SEMINAR – I
VMD(C)-891
DEPARTMENT OF VETERINARY CLINICAL MEDICINE
MADRAS VETERINARY COLLEGE, VEPERY,
TANUVAS, CHENNAI-07
Presented byAbhishek KalundiaDPV(M)14009VMD(C)
Objectives
Brief discussion on Triage
Lesion localization
Types of Neuro. Emergencies common in SA
Diag. / Diff. Diag.
Therapeutic Management
INTRODUCTION
Common Neurological Emergencies
Loss of consciousness / Coma
Seizures & Status Epilepticus
Paresis and paralysis.
Acute Vestibular syndrome
Traumatic Brain Injury (TBI) / Head Trauma.
Job of an Emergency Clinician – Assessment, Stabilization & Treatment.
History, PE, Lesion localization & Analysis of readily available test results.
ANAMNESIS
Presenting complaint;
The animal’s respiratory rate
And effort;
Mucous membrane colour;
Level of consciousness/seizure activity;
Ability to urinate;
Ability to walk;
Presence of external injuries and degree of haemorrhage;
Presence of obvious fractures;
Absence/ presence of abdominal distension; and
Vomiting/diarrhoea.
Primary Goal of approach
1) Is the patient in shock?
2) Is it really a neurological case?
3) Where actually is the lesion?
4) What is the prognosis?
A(irway), B(reathing), C(irculation)of the Neurological Emergency Patient
ABC Assesment Additional tests
Initial Rx
Airway Open mouth?Dyspnea – pattern?
Inspection of mouth
IntubationTracheotomy
Breathing FrequencyType Auscultation
SpO2 (90% +)Blood Gas Analysis
O2 supplementation@ 5-15 l/min
Circulation Heart ratePulse strengthColour of MMCRT
End systolic blood pressure
Fluid therapy10-30ml/kg IV Bolus(Ringers Lactate)
Neurological status
ConsciousnessPupil sizeMenace response
Complete neurological assesement
Maintain ICP (8-10mm/Hg)
Pain level Heart rateSigns of pain
Analgesia
Hemorrhage Occular bleedingPostural defectsExternal hemorrhage
PT/APTT/FDPACT
AntifibrinolyticsPressure bandage
Clinical signs of shock in Neurological Emergencies
Signs Compensated
Decompensated
Aims of therapy
Heart rate Tachycardia Tachycardia Normal (Age/breed)
Colour of MM Reddened Pale Pink, Moist
Capillary refill time
Less than 1 sec
More than 2 sec
1-2 sec
Pulse Throbbing Weak Strong, regular
Blood pressure Normal to increased
normal., increased, reduced
MAP – 60mm/HgESAP – 100m/Hg
Emergency Neurological Examination
SHOULD BE ALWAYS AFTER STABLISATION!
Neurological Assessment:
1) Motor activity / Ambulation
2) Level of consciousness / Mental Status
3) Cranial Nerve function / Brain stem function
DIAGNOSTIC APPROACHES
Pelvic Limb Reflexes – Patellar Reflex – L4-L5-L6 – Femoral Nerve Cranio Tibial Reflex – L6-S1 – Peroneal Nerve Flexor Reflex - L4-S3– Sciatic Nerve
Thoracic Limbs – Extensor CarpI Radialis Reflex – C7-T1 – Radial Nerve Triceps Reflex – C6-T2 – Radial Nerve Flexor Reflex – Radial Nerve
Crossed Ext Reflex
BCRVURPer R
LESION LOCALISATION
LIMB C1 – C5 C6 – T2 T3 – L3 L4 – S3
WR F ++ + ++ ++
H ++ ++ ++ -
CP F - - ++ ++
H - -- - -
HL-WR-FL-CP-WR
Left sided Head tilt and facial paralysis in 6 yr old Boxer with Otitis Media/Interna
Photo Courtesy: Platt and Gourosi, 2012
Left sided head and body turn (Pleurothotonus) in a 4 yr old Terrier with a left forebrain lesion caused by Granulomatous meningoencephalitis.
Photo Courtesy: Platt and Gourosi, 2012
PRINCIPLES OF THERAPY OF NEUROLOGICAL DISEASES
Seizure control
DZP @ 0.5-1mg/kg/hr CRI (short acting?)
Phenobarbital @2-4mg/kg/BID PO, IV (Liver?)
Levetiracitam @ 40-60 mg/kg IV, SC, PR (9hrs)
KBr @ 22-44mg/kg (bypasses live; 250mg/ml)
Zonisamide ?
Acute Spinal Cord Injury
Methylprednisolone Na Succinate @ 30mg/kg IV – 15mg/kg in 2-6hrs (8hrs>; max 60mg/kg total dose; TBI?)
30% Polyethylene Glycol (PEG)@ 2.2mg/kg IV OD
Antiedema drugs
Brain tumors & TBI
Mannitol @ 0.5-1g/kg IV over 20 min
Furosemide @ 2.2mg/kg IV prior to Mannitol
Muscle relaxants
IVDD/IVDP
DZP
Methocarbamol @ 40 mg/kg TID/QID
Antibiotics
Nursing care
PRINCIPLES OF THERAPY OF NEUROLOGICAL DISEASES
1. SEIZURES / STATUS EPILEPTICUS
Seizures are the physical manifestation of an abnormal balance between excitatory and inhibitory tone in the CNS.
Status epilepticus Seizures more than 5-10 min Focal fits more than 20 min
Excitatory tone is mediated by the neurotransmitter Glutamate
Inhibitory tone is mediated by Gamma Aminobutyric Acid (GABA)
TYPES:
Generalised Seizure – Grand Mal/Convulsions
Partial – Simple/Complex
Pathological changes during SE
Sudden massive activation of neurons Release of Glutamate Changes in extracellular K Changes in intracellular Ca Hyperthermia Hypotension Endothelial damage - DIC Reduced O2 concentration – secondary
hypoxia – cell death
DIAGNOSTIC APROACH to SE
Anamnesis – duration/relapsing/previous disease
Diff. Diag. :
Seizures Vs Syncope (History. EEG, Holter ECG)
Cluster Seizures Vs Status Epilepticus
Stablise & IV access - Diazepam @ 1mg/kg PR
CBC, CUE, SE
MABP & BG (Blood Glucose)
CSF Vs Imaging (CT/MRI)
WHAT TO LOOK FOR!
History of Trauma - ICP
≤ 1 – 5 yr ≤ - SES (Inflamatory/ Infectious)
Young – PSS (BAT/Serum Ammonia); BG
Petechia – FCE (Platelets)
Cats - BG (Insulin overdose); Pyrethrin exp.
Nursing Bitch – Hypocalcemic Tetany
EMERGENCY STABLISATION OF PATIENT WITH SE
Status epilepticus
O2 mask/ flow by
IV access possible?
Diazepam 0.5-1mg/kg IV and RL
@ 10ml/kg/h
Hyperthermia
PCV?TP/BG/BUN/Na/BGA
Hypoglycemia ?
Hypocalcemia?
Diazepam 1mg/kg PR
Active cooling <39.5 C
D-25 1ml/kg diluted with RL
Calcium gluconate 100mg/kg iv over 20 min
NO
YES
YES
YES
Azotemia?
SE stopped?
Diazepam 0.5-1mg.kg IV
SE stopped?
Phenobarbital 5mg/kg IV
Status Epilepticus stopped?
Anesthesia
Propofol 2-6mg/kg
Isofluran 1-2%
Diazepam 1mg/kg
Max 30/mg/kg
Phenobarbital 5mg/kg PO/IV q12hr
YES
q20-30min
YES
SE stopped
EMERGENCY STABLISATION OF PATIENT WITH SE
A case of Refractory SE
2.8kg Yorkshire Terrier
Seizures episodes for past 4 weeks
1-2/24 hrs (1-4min each)
CBC, Biochem = NAD
Curr Rx – Phenobarb @ 5.4mg/kg BID PO & Valium Per Rec.
Thoracic Radiography & Abd. US = NAD
Convulsions gradually increased in 3 days!
On Presentation
Nystagmus – Horizontal/Fast phase towards left.
Limbs:
Ataxia (All 4 limbs)
Normal Spinal Reflexes
Head pressing, Circling to left
Neuroanatomic Localization – MULTIFOCAL (included the Central Vestibular System and Forebrain)
Clinical Examination
Patent Airway
CMM – Congested
Pulse – Bounding
Tachycardia (190 bpm); No murmurs
Tachypnea (40 breaths pm)
Doppler systolic BP = 180 mm Hg
Rec. Temp = 105 F
Intranasal diazepam (0.5 mg/kg) reduced motor activity sufficiently to establish vascular access and obtain blood for CBC, biochemistry, blood ammonia concentration, and serum phenobarbital concentration.
Initial laboratory results: Acidemia (Venous Ph 7.332; Normal Range, 7.360–7.440) Metabolic Acidosis (Base Excess -8 Meq/L; Normal Range,
-3±2) Hyperlactatemia (64.8 Mg/dl [7.2 Mmol/L]; Normal Range,
5.4–22.5 [0.6–2.5] and Hypoglycemia (40 Mg/dl[2.2 Mmol/L]; Normal Range, 70–
110 [3.3–6.1]).
TREATMENT APPROACH
IV bolus of 0.5 g/kg glucose over 5 minutes
Maintenance fluid therapy - crystalloidc supplemented with 5% dextrose.
Diazepam was given again (0.5 mg/kg IV) followed by a CRI @ 0.25 mg/kg/h, increasing to 0.5 mg/kg/h) which failed to eliminate all muscular activity.
Propofol then was administered (4 mg/kg IV) to achieve anesthesia followed by a CRI @ 8 mg/kg/h – muscular activity slight controlled BUT failed to show normal EEG readings.
Portable EEG readings
Seizures cont. 6 hrs!
GABAergic drugs were proving ineffective.
Ketamine then was administered (5 mg/kg IV), which resulted in a marked reduction in both amplitude and frequency of the EEG pattern in less than 1 minute!
Epileptic activity resumed in 10 minutes
Second bolus of 5 mg/kg ketamine - followed by a CRI at 5 mg/kg/h.
Why Ketamine?
Pharmacology textbooks describe ketamine as having epileptogenic potential.
Ionotropic Glutamate receptors occur in 3 subtypes: alphaamino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate, and NMDA receptors.
Ketamine = N-methyl-D-aspartic acid (NMDA) antagonist.
NMDA receptor antagonists prolonged status epilepticus in animals - NMDA receptor activation is not present in the initial phases of SE
2 INTOXICATIONS (POISONINGS)
INTOXICATIONS THAT CAN LEAD TO NEUROLOGICAL SYMPTOMS
CAUSE SEIZURES/TREMOR
CHANGES IN CONSCIUOSNESS
TETANY PARALYSIS
NEUROTIXINS CARBAMATES AMITRAZ BOTULINUM TOXINS
CARBAMATES
IVERMECTIN BARBITURATES ORGANOPHOSPHATES
LEAD BZD
LIDOCAINE EHTYLENE GLYCOL
MYCOTOXINS OPIODS
OPIODS IVERMECTIN
ORGANOPHOSPHATES
PEYRETHROIDS
GENERAL THERAPY FOR INTOXICATION
Triage (occurs on phone)
Initial stablization
Detoxification
Topical toxins – warm soap water wash.
Gastrointestinal toxins – lavage; vomiting; Act. Charcoal slurry (<2-4hrs)
Diuresis (Furosemide; Dialysis)
Symptomatic only (no Antidote!)
EMERGENCY STABLISATION OF INTOXICATED PATIENTS
Intoxication confirmed/proba
ble
Ingested?
Seizures?
Diazepam 0.5-1mg/kg IV and RL
@ 10ml/kg/h
Intake <4hrs
Elicit vomiting
Diuresis
Dialysis
Wash with warm water/soap?
Activated Charcoal 2-4g PO/lavage
Apomorphine 0.04mg/kgXylazine 0.4mg/kg3% H2O2 1-2ml/kg PO
Topical
NO
3. TRAUMATIC BRAIN INJURY (TBI)
HEAD TRAUMA:
Bites
Accidents
High rise fall
Kicks
Gunshots
Pathophysiology of TBI
Cranio-cerbral Trauma will always lead to: Secondary brain lesions.
HYPOXIA!
1. Extracranial causes
2. Intracranial causes
Extracranial causes
Hypovolaemic shock
Anemia
Lung contusions
Hypoglycemia
Electrolyte imbalance
SIRS (IL-1, 6, 8 and TNF)
Intracranial causes
Glutamate release into extracellular space
Increased ICP – reduced Cerebral Perfusion Pressure (CPP)
CPP = MAP – ICPWith normal conditions of MABPs of 80 to 120 mm Hg and ICPs of 5 to 12 mm Hg, CPP can be expected to be 70 to 85 mm Hg. With conventional limits of intact autoregulation, CBF remains normal as CPP varies between 60 and 140 mm Hg.
Normal CBF in a dog = 75.9 ± 10.4 ml/min/100g
When the case comes..
Caution - About 60% cases – concurrent systemic injuries. Life Threatening abnormalities!
It is easy to focus primarily on the most obvious presenting abnormalities.
Patient’s mentation may be artificially worsened simply by being in a state of shock.
Chest – pneumothorax, Lung contusions or Neurogenic Pulm. Edema.
Spine/limbs – Fractures & Luxations.
ABC (Airway, Breathing & Cardiovascular status)
What to do First!
Apply oxygen supply (oxygen mask or intubate if comatose)
Place intravenous line(s)
Administer IV fluids
Measure blood pressure
Perform blood sampling for at least:
PCV/TP, Urea, Glucose & BGA/Electrolytes.
Neurological Assessment
Should be performed only after Primary Assessment
Can be very subjective.
Aim:
To establish whether a TBI is present?
And if it is, then think of Cushing Reflex ?
What is the likely prognosis?
CUSHING REFLEX
MAP
BRADYCARDIA
TREATMENT
AIM:
To maintain an adequate cerebral perfusion by limiting the raise in Intracranial pressure and
Limiting Arterial Hypotension.
O2 supply and ventilation aiming at a partial pressure of CO2 in the arterial blood - 35mmHg (PaCo2) and SpO2 of 95% +.
MEDICAL TREATMENT
Fluids of choice - Hypertonic saline (4-5ml/kg) and/or Colloids (10-20ml/kg).
Mannitol - Rheological effect on Intra Vascular Fluid
Improving cerebral perfusion – INITIAL EXPANTION
And an anti-oedematous effect – SIG. CONTRACTION
0.2-1.0g/kg over 20 minutes IV X can be repeated three times/ 24 hours.
Administration of furosemide (1-4mg/kg) prior to mannitol is recommended – prevent initial rise of ICP.
Anticonvulsant treatment (ONLY IF REQUIRED)
SCORING SYSTEM
Methods have been developed that allow a score neurological abnormalities identified at presentation.
Adapted from human GCS with head trauma.
GCS – Glassgow Coma Scale.
Modified Glassgow Coma Scale
There are three components to the MGCS to be individually evaluated:
1. Level of consciousness;
2. Motor function; and
3. Size, position and movement of the eyes.
1 - severely affected; 6- mildly affected. (3-18)
A score of ≤8 = grave prognosis
Platt et. al., 2001
1. Assessment of consciousness
Mentation – normal/depressed, obtunded, stuporous or comatose.
Due to:
Diffuse lesion of the cerebral Hemispheres (forebrain) – more common – ICP high
Focal lesion affecting the ascending reticular activating system in the brainstem.
2. Assessment of Motor Function
A full assessment of motor function can only be made by assisting the animal to walk.
Voluntary motor activity (Paeresis/ Paralysis)
Posture
DIFFERENTIATION CRITERIA BETWEEN LMN AND UMN
Criterion LMN paeresis UMN Paresis
Posture
Difficulty in supporting
weight. Overflexion of
joints.
Often Normal with
abnormal limb position
(abducted, adducted or
crossed over)
GaitShort strides; Tendency
to collapseStiff and ataxic strides
Motor functionFlaccid
paeresis/paralysis
Spastic
paralysis/paeresis
Segmental reflexes Decreased to absent Normal to increased
Resting muscle tone Decreased resistance Slight resistance
Posture
Decerebrate posture – severe midbrain lesion - guarded to poor prognosis –
rigid extension of all four limbs and opisthotonus – stuporous or comatose mental
status.
Decerebellate posture - due to a rostral cerebellar lesion increase in extensor
muscle tone in all four limbs- Opisthotonus – mentation unaffected - hips may be
flexed (increased tone in the iliopsoas muscle) or extended.
Schiff-Sherrington Phenomenon – due to acute, severe lesions of the spinal
cord between T2 and L3 - pelvic limb paralysis accompanied by an extensor
rigidity of the thoracic limbs when the animal is in lateral recumbency - because
of an interruption of an ascending spinal cord tract from the lumbar
intumescence, which inhibits extensors of the forelimb.
Picture Courtesy: Platt and Gourosi, 2012
Decerebrate posture with head trauma due to road accident
Picture Courtesy: Platt and Gourosi, 2012
Decrebellate posture due to rostral cerebellar artery infarction
Picture Courtesy: Platt and Gourosi, 2012
3. Assessment of Brainstem reflexes
Pupillary size, symmetry, reactivity to light and eye movements.
Acute ocular injury - spasm of the ciliary muscles of the iris - unilateral miosis.
Chronic ocular injury to the iris, retina or periorbital structures - unilateral mydriasis.
Dilated pupil + Normal Mentation = peripheral lesion involving the oculomotor nerve (CN III)
Pupil size and responsiveness
Dynamic Equilibrium Between:
The Parasympathetic Component (PLR)
The Sympathetic Component (Emotion)
Severely depressed mental status, bilateral miotic (small pin prick) pupils are likely to indicate a diffuse forebrain injury.
Progression to mydriasis (dilation) - brain herniation.
Fixed, unresponsive and midrange pupils are usually seen with cerebellar herniation. (Trauma)
MGCS SCORE – Category and prognostic value
Score Category Actual MGCS Score
Suggested Prognosis
I 3-8 Grave
II 9-14 Guarded
III 15-18 Good
SUMMARY
Importance of Anamnesis
Basic systemic stabilisation is essential before embarking on a neurological examination.
Neurological case?
Aggressive or non - aggressive Rx?
Assessment/monitoring of the Therapy
Prognosis?
MGCS - The mainstay of the neurological examination in patients suffering TBI.
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Biochemical Changes In The Blood Serum Of Dogs Treated With Phenobarbital. Acta Veterinaria. 60(5):573
Beghi, E., 1999. The Use of Anticonvulsants in Neurological Conditions Other Than Epilepsy: A Review of the Evidence from Randomised Controlled Trials.CNS Drugs. 11(1):61.
Bichsel, Pierre and Lyman, Ronald, 2012. Canine epilepsy treatment: Phenobarbital vs. bromide. The Newsmagazine of Veterinary Medicine;43(9):15.
Browand-Stainback, Laura, L. Donald; M. Matthew, 2011. Canine and Feline Epileptic Seizures and the Lunar Cycle: 2,507 Seizures (2000-2008). Journal of the American Animal Hospital Association. 47(5):324.
Goel, R., A. Goel, M. Sharma, Y. kumar, 2010. Evidence of the antiepileptic potential of carvedilol with neuropharmacological benefits in rodents models of epilepsy and behaviour. Journal of Pharmacy Research. 3(8):1827.
Hoskins, Johnny D., 2008. New anticonvulsant drugs show promise in dogs, cats. The Newsmagazine of Veterinary Medicine. 39(3):8.
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Neurological Emergencies, BASAVA Manual, 2nd ed.
Neurology, Mercks Veterinary Manual, 10th Ed.
Penderis, J. and V. Holger, 2013. Switching between medications for the management of epilepsy in dogs. Veterinary Record: Journal of the British Veterinary Association. 173(13):323.
Platt S R, Radaelli S T and McDonnell J J (2001). The prognostic value of the modified Glasgow Coma Scale in head trauma in dogs, Journal of Veterinary Internal Medicine 15(6): 581-584.
Platt, Simon and L. Garosi, 2012. Small animal neurological emergencies, 1st ed., Manson Publishing: 20-45.
Sergi Serrano, Dez Hughes, and Kate Chandler, 2006. Use of Ketamine for the Management of Refractory Status Epilepticus in a Dog , J Vet Intern Med;20:194–197
Sigrist N E, K N Adamik, M G Doherr and D E, Spreng. 2011. Evaluation of respiratory parameters at presentation as clinical indicators of the respiratory localization in dogs and cats with respiratory distress, Journal of Veterinary Emergency and Critical Care 21(1): 13-23.
Simon R. Platt, T. Simona Radaelli, and J. John McDonnell, 2001 The Prognostic Value of the Modified Glasgow Coma Scale in Head Trauma in Dogs. J Vet Intern Me, 15:581–584.
References
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