APPROACH TO A NEUROLOGICAL EMERGENCY CASE STARTS WITH THE BASIC TRIAGE APPROACH AS IN ANY OTHER EMERGENCY CASE. A NEUROLOGICAL ASSESSMENT IS ONLY DONE AFTER THE STABILIZATION OF THE PATIENT. THERE CAN BE MANY DIFFERENT APPROACHES BUT ALL BASICALLY AIM AT FIRST CONFIRMING IF AT ALL IT IS A NEURO CASE AND IF YES, WHERE IS THE LESION..IS IT IN THE CRANIUM OR BRAINSTEM OR THE SPINAL CORD? LESION LOCALISATION WILL NOT ONLY HELP TO UNDERSTAND BETTER THE TYPE OF THERAPY TO BE CHOSEN BUT WILL ALSO HELP TO TELL ABOUT THE PROGNOSIS OF THE CASE. MOST COMMONLY WE GET STATUS EPILEPTICUS, TRAUMATIC BRAIN INJURY, POISONING, SPINAL CORD INJURIES AND ACUTE VESTIBULAR DISEASES AS THOUGHT TO LINKED WITH NEUROLOGICAL EMERGENCY SITUATIONS. AN EMERGENCY MUST BE FAMILIAR WITH WITH THE RELEVANT HISTORY OF THE PATIENT. HE SHOULD ALSO BE KEEP A TEAM READY WHO CAN HELP HIM PUT THE IV ACCESS AND SEDATIONS WHILE HE CAN COLLECT THE BLOOD FOR BASIC ROUTINE BLOOD ANALYSIS. COUNTERING THE ONGOING STAGE OF SHOCK TO BRING IT TO NORMAL, CHECKING THE SYSTEMIC BLOOD PRESSURE, RECTAL TEMPERATURE AND OXYGEN CONCENTRATION ARE FEW OF THE MOST IMPORTANT FACTORS A CLINICIAN HAS TO DO WHILE ADMINISTERING THE MEDICS. SCORING SYSTEMS LIKE MODIFIED GLASSGOW COMA SCALE AS SUGGESTED BY DR PLATT ARE REALLY HELPFUL TO GIVE A PROGNOSTIC IDEA IN CASES LIKE CRANIO-CERBRAL INJURIES. RECENT TREATMENT UPDATES ARE REALLY HELPFUL TO KEEP HAVING BETTER OPTIONS IN CASE THE ROUTINE PROTOCOL FOR STABILIZING A SEIZURE PATIENT IS NOT WORKING.

1. WELCOME

2. NEUROLOGICAL
EMERGENCIES IN DOGS
DOCTORAL SEMINAR – I
VMD(C)-891
DEPARTMENT OF VETERINARY CLINICAL MEDICINE
MADRAS VETERINARY COLLEGE, VEPERY,
TANUVAS, CHENNAI-07
Presented by
Abhishek Kalundia
DPV(M)14009VMD(C)

3. Objectives
 Brief discussion on Triage
 Lesion localization
 Types of Neuro. Emergencies common in SA
 Diag. / Diff. Diag.
 Therapeutic Management

4. 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.

5. 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.

6. 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?

7. 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
Intubation
Tracheotomy
Breathing Frequency
Type
Auscultation
SpO2 (90% +)
Blood Gas
Analysis
O2
supplementation
@ 5-15 l/min
Circulation Heart rate
Pulse strength
Colour of MM
CRT
End systolic blood
pressure
Fluid therapy
10-30ml/kg IV
Bolus
(Ringers Lactate)
Neurological
status
Consciousness
Pupil size
Menace
response
Complete
neurological
assesement
Maintain ICP
(8-10mm/Hg)
Pain level Heart rate
Signs of pain
Analgesia
Hemorrhage Occular bleeding
Postural defects
External
PT/APTT/FDP
ACT
Antifibrinolytics
Pressure
bandage

8. Clinical signs of shock in
Neurological Emergencies
Signs Compensated Decompensate
d
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/Hg
ESAP –
100m/Hg

9. 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

10. DIAGNOSTIC APPROACHES

11. 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
BCR
VUR
Per R

12. LESION LOCALISATION
LIMB C1 – C5 C6 – T2 T3 – L3 L4 – S3
WR F ++ + ++ ++
H ++ ++ ++ -
CP F - - ++ ++
H - -- - -
HL-WR-FL-CP-WR

14. Left sided Head tilt and facial paralysis in
6 yr old Boxer with Otitis Media/Interna
Photo Courtesy: Platt and Gourosi, 2012

15. 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

16. 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

17.  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

18. 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

19. 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

20. 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)

21. 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

22. 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

23. 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

24. 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!

25. 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)

26. 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

27.  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]).

28. 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.

29. Portable EEG readings

30. 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.

32. 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

33. 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 ORGANOPHOSPH
ATES
LEAD BZD
LIDOCAINE EHTYLENE
GLYCOL
MYCOTOXINS OPIODS
OPIODS IVERMECTIN
ORGANOPHOSPH
ATES
PEYRETHROIDS

34. 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!)

35. 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/kg
Xylazine 0.4mg/kg
3% H2O2 1-2ml/kg PO
Topical
NO

36. 3. TRAUMATIC BRAIN INJURY (TBI)
HEAD TRAUMA:
 Bites
 Accidents
 High rise fall
 Kicks
 Gunshots

37. Pathophysiology of TBI
 Cranio-cerbral Trauma will always lead to:
Secondary brain lesions.
 HYPOXIA!
1. Extracranial causes
2. Intracranial causes

38. Extracranial causes
 Hypovolaemic shock
 Anemia
 Lung contusions
 Hypoglycemia
 Electrolyte imbalance
 SIRS (IL-1, 6, 8 and TNF)

39. Intracranial causes
 Glutamate release into extracellular space
 Increased ICP – reduced Cerebral Perfusion Pressure (CPP)
CPP = MAP – ICP
With 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

40. 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)

41. 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.

42. 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?

43. CUSHING REFLEX
MAP
BRADYCARDIA

44. 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% +.

45. 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)

46. 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.

48. 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

50. 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.

51. 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

52. 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)
Gait
Short strides; Tendency to
collapse
Stiff and ataxic strides
Motor function Flaccid paeresis/paralysis Spastic paralysis/paeresis
Segmental reflexes Decreased to absent Normal to increased
Resting muscle tone Decreased resistance Slight resistance

53. 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.

54. Picture Courtesy: Platt and Gourosi,

55. Decerebrate posture with head trauma due to road accident
Picture Courtesy: Platt and Gourosi,

56. Decrebellate posture due to rostral cerebellar artery infarction
Picture Courtesy: Platt and Gourosi,

59. 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)

60. 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)

62. 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

63. 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.

64. References
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66. THANK YOU