AN APPROACH TO NEUROLOGICAL EMERGENCIES IN DOGS

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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.

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AN APPROACH TO NEUROLOGICAL EMERGENCIES IN DOGS

  1. 1. WELCOME
  2. 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. 3. Objectives  Brief discussion on Triage  Lesion localization  Types of Neuro. Emergencies common in SA  Diag. / Diff. Diag.  Therapeutic Management
  4. 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. 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. 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. 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. 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. 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. 10. DIAGNOSTIC APPROACHES
  11. 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. 12. LESION LOCALISATION LIMB C1 – C5 C6 – T2 T3 – L3 L4 – S3 WR F ++ + ++ ++ H ++ ++ ++ - CP F - - ++ ++ H - -- - - HL-WR-FL-CP-WR
  13. 13. Left sided Head tilt and facial paralysis in 6 yr old Boxer with Otitis Media/Interna Photo Courtesy: Platt and Gourosi, 2012
  14. 14. 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
  15. 15. 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
  16. 16.  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
  17. 17. 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
  18. 18. 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
  19. 19. 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)
  20. 20. 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
  21. 21. 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
  22. 22. 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
  23. 23. 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!
  24. 24. 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)
  25. 25. 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
  26. 26.  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]).
  27. 27. 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.
  28. 28. Portable EEG readings
  29. 29. 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.
  30. 30. 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
  31. 31. 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
  32. 32. 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!)
  33. 33. 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
  34. 34. 3. TRAUMATIC BRAIN INJURY (TBI) HEAD TRAUMA:  Bites  Accidents  High rise fall  Kicks  Gunshots
  35. 35. Pathophysiology of TBI  Cranio-cerbral Trauma will always lead to: Secondary brain lesions.  HYPOXIA! 1. Extracranial causes 2. Intracranial causes
  36. 36. Extracranial causes  Hypovolaemic shock  Anemia  Lung contusions  Hypoglycemia  Electrolyte imbalance  SIRS (IL-1, 6, 8 and TNF)
  37. 37. 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
  38. 38. 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)
  39. 39. 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.
  40. 40. 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?
  41. 41. CUSHING REFLEX MAP BRADYCARDIA
  42. 42. 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% +.
  43. 43. 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)
  44. 44. 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.
  45. 45. 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
  46. 46. 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.
  47. 47. 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
  48. 48. 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
  49. 49. 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.
  50. 50. Picture Courtesy: Platt and Gourosi,
  51. 51. Decerebrate posture with head trauma due to road accident Picture Courtesy: Platt and Gourosi,
  52. 52. Decrebellate posture due to rostral cerebellar artery infarction Picture Courtesy: Platt and Gourosi,
  53. 53. 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)
  54. 54. 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)
  55. 55. 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
  56. 56. 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.
  57. 57. References  Andrić, N., N. Popović, P. Stepanović, Francuski, Jelena and D. Đurđević, 2010. 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.  Macintire D K, Drobratz K J, Haskins S C and Saxon W D (2006). Manual of Small Animal Emergency and Critical Care Medicine (1st edn), Blackwell Publishing Professional, Iowa: 5-6.
  58. 58.  Moore, Sarah A., 2014. Seizures and epilepsy in cats. Veterinary Medicine: Research & Reports; 5:41.  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
  59. 59. THANK YOU

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