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Emergency Board Review

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Emergency Board ReviewTriage A- airway (patent, adequate FiO2)- arterial bleeding ( pressure) B- Breathing (characterize pattern)inspiratory, expiratory, paradoxical C- Circulation D- Disability (neurologic, musculoskeletal) E- Evaluate (abdominal, urinary, general)Triage- Secondary Survey A- airway C- Cardiovascular/circulatory R- Respiratory A- Abdomen S- Spine H- Head (eyes, ears, and neck too)Triage- Secondary Survey P- Pelvis (rectal) L- Limbs (including tail) A-Arteries N- Nerves (including cranial nerves, reflexes, pain sensation)Quick Blood Gas- 6 Questions 1. Is the patient hypoxemic? PaO2 2. Is the patient hypo or hyperventilating? PaCO2 3. Is there an acid-base abnormality? 4. What it is the primary abnormality? Metabolic or respiratory 5. Is it simple, simple with compensation or mixed? 6. Why does it exist, how do you fix it?Quick facts for acid base Rules of 4  pH- 7.4 +/- .o4 PaCO2- 40 +/-4 HCO3- 24 +/-2 PaO2- 4-5 x FiO2 You can not compensate to normal pHQuick facts for acid base Most common cause of respiratory alkalosis in emergency is pain or fever induced hyperventilation Most common cause of respiratory acidosis is hypoventilation from anesthetics, upper airway obstruction, severe parenchymal disease, or neurologic diseaseQuick facts for acid base Most common cause of metabolic acidosis in emergency is lactic acidosis (shock), ketosis, other unmeasured anions (ethylene glycol), or hypochloridemia (differentiate with anion gap) Most common cause of metabolic alkalosis is vomitingSmall Animal Toxicology Basic steps Eliminate further absorbtion• Bathe or vacuum• EmesisHydrogen peroxide (3%) 1-2 ml/kgcan repeat once in 10 minDishwashing liquid 1:8 with water and give 10 ml/kg onceSmall Animal Toxicology Eliminate absorbtion - emesisApomorphine (dogs) .03mg/kg IV, .04 mg/kg IM, .08 mg/kg SC, or .3 mg/kg conjunctivalXylazine (cats) .44mg/kg IMSyrup of Ipecac- potential cardiotoxicity, muscle weakness, hemorrhagic diarrheaSmall Animal Toxicology Eliminate absorbtion Gastric lavage- light sedation maybe• 20 ml/kg of tepid water repeated until clear Activated charcoal• 1-4 g/kg with 1g/50 ml water (if not premixed)- not good with heavy metal Cathartic- often with activated charcoalSmall Animal Toxicology Eliminate absorbed toxin Diuresis for some Ion trapping Definitive antidote or competitive inhibitor- depends on toxin Supportive careSmall Animal Toxicology Acetaminophen Clinical signs• Methemoglobinemia- dark blood, dyspnea, facial and front limb swelling (cats typical or dogs with very high dose)• Hepatic necrosis- 24-48 hours later vomiting, abdominal pain, anorexia (cats and dogs)Small Animal Toxicology Acetaminophen Treatment- basic principles plus• N-acetylcysteine IV or PO (140 mg/kg first then 70 mg/kg QID for 6 doses)• Ascorbic acid for methemoglobin• Cimetidine• SupportiveSmall Animal Toxicology Methylxanthines (chocolate, caffeine, theophylline) Clinical signs- vomiting, hyperactivity, restlessness, tachycardia, tachypnea, ataxia, convulsions, cardiac arrhytmia, deathSmall Animal Toxicology Treatment• Arrhythmia- lidocaine (ventricular) or esmolol (SVT)• Tremors/seizures- diazepam, phenobarbital or pentobarbital induction• Renal excretion and can reabsorb in urinary bladderSmall Animal Toxicology Lead Clinical signs• Gi- anorexia, vomiting, pain, diarrhea• Neuro- seizures, hysteria, ataxia, blindness, tremors• Hemolytic anemia (very high nRBCbeyond expected for anemia)Small Animal Toxicology Lead Diagnosis• High nRBC, basophilic stippling with mild anemia and other signs• Radiographs• Blood levels (>0.6ppm) or liver post mortemSmall Animal Toxicology Lead Treatment• Chelation- calcium EDTA, Penicallimine, Succimer• Repeat lead levels after treatment to determine if more is needed• Supportive careSmall Animal Toxicology Cholinesterase inhibitors (organophosphates and carbamates) Clinical signs- depends if muscarinicor nicatinic• Nicotinic- striated muscle stiffness, fasciculation, tremor, weakness, paralysis• Muscarinic- smooth muscle SLUD, bradycardiaSmall Animal Toxicology Ch. Inhibitors Treatment• Atropine (.1-.2 mg/kg, 1/4 IV, ¾ SC) can be repeated, glycopyrrolate not effective b/c does not cross blood brain barrier)• 2-PAM in addition to atropine in organophosphate, may reverse binding to Achesterase• Midazolam and diphenhydramine for nicotinicSmall Animal Toxicology Pyrethrins Clinical signs• Hypersalivation, vomiting, diarrhea, ataxia, hyperexcitability, fasciculation, depression, disorientation, seizures, dyspneaSmall Animal Toxicology Pyrethrin Treatment• Diazepam for seizures• Phenobarbitol for continued seizures• Methacarbamol for muscle tremorsSmall Animal Toxicology Zinc Clinical signs• Depression, vomiting, diarrhea, hemolytic anemia, renal failure Diagnosis• Radiographs, hemolytic anemia• Zinc levls in serum, urine, or tissueSmall Animal Toxicology Treatment Supportive care Remove source Chelation with calcium EDTA or penicallimineSmall Animal Toxicology Ivermectin Clinical signs• Mydriasis, apparent blindness, aggresion, bradycardia, cyanosis, dyspnea, seizures, coma, death Treatment• NO BENZODIAZIPINE• Physostigmine?• SupportiveSmall Animal Toxicology Ethylene glycol Clinical signs• 1st12 hours- vomiting, intoxicated, stuporous, ataxic, comatose, PU/PD• 2nd12-24 hours- may be normal, may have tachycardia, or signs of pulmonary disease• 3rd>24 hours (or 12-24 in cats)- renal failureSmall Animal Toxicology E.G. Diagnosis• Crucial to diagnosis as soon as possible, therapies do not work after 4-6 hours in cat or 8-12 hours in dog• Ethylene glycol test- false positives• Clinical signs plus high osmolar gap or acidosis with high anion gap• Calcium oxalate crystalluria (occ. Early as 3 hours in cat or 6 hours in dog, often later)Small Animal Toxicology E.G. Treatment• Aggressive fluids• Competitive inhibition of alcohol dehydrogenase• Ethanol 7% IV• 4-mehtylpyrazole (better for dogs, high dose in cats early)• Hemo or peritoneal dialysisSmall Animal Toxicology Rodenticide Clinical signs• Generally act via Vitamin K antagonism• Affects factors II, VII, IX, X• Clinical


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