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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References

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