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INTERESTING CASE ROUNDS Alyssa Morris Emergency Medicine R3 Objectives DDX for toxin induced seizures DDX for toxin induced status epilepticus Indications for pyridoxine Review methylxanthine toxicity Review MDAC CASE 19M took an unknown ingestion and had a seizure. What is your quick ddx for drugs that cause seizure? DDX Drug induced Seizure OTIS CAMPBELL C- camphor, cocaine A- anticholinergic, O- organophosphates T- TCA I- Isoniazid, insulin S- sympathomimetics amphetamines, anticholinergic, antidepressants M- Methylxanthines P- PCP B- Benzo w/d E- EtOH w/d L- Lithium, lidocaine L- lead, lindane DDx-Toxin induced Status INH Insulin/hypoglycemic agents TCA Theophylline Wellbutrin CO Pyridoxine Indications INH Ethylene glycol Gyromitra Mushrooms Methylxanthines* CASE 19M who ingested 112 caffeine tablets (100mg/tab) who was brought in by friend for intractable nausea and vomiting • Total ingestion >11g (175mg/kg) O/E: P=131,BP= 164/67, T= 37.6, 02= 98%, agitated, vomiting ++ CASE Labs: • APAP/ASA – • CK 14 • Na 140, K 2.2, Cl 101, CO2 17, AG: 22 • Lactate 8.8 • pH 7.23 • Caffeine level 429mmol/L ECG: Sinus tach, no dysrhythmias CASE CONT Continued to be tachy, ++ vomitting, no seizure and no dysrhythmias Course in ED: • zofran 12mg • Maxeran 10g (still vomiting) • Stemitil 10mg (still vomiting) • MDAC • Central line to replace K+ • Zantac 50mg • Ativan 2mg IV x 2 CASE CONT Labs in am • CK- 2280 • PO4 0.29 • K- 3.1 • Caffeine level 295mmol/L • Lactate 3.9 Still vomiting and agitated CAFFEINE Methylxanthine Similar to theophylline Cause release of endogenous catecholamines Stimulates B1 and B2 R Structural analogue of Adenosine NE and epinephrine release Inhibit phosphodiesterase (degrades cAMP) Effects like adrenergic stimulation PHARMACOKINETICS Routes: oral, IV, SC, IM, rectal Oral almost 100% bioavailability Peak concentration 30-60min Diffuses readily into total body water and all tissues Readily crosses BBB Metabolized by Cytochrome P450 system Active metabollite is theophylline TOXICOKINETICS Range of toxicity varies greatly No definite conclusions from serum levels can be drawn Lethal dose estimated: 150-200mg/kg or 5-10g Death associated serum levels >80mm0l/L Fatalities <200mmol/L Survivial >400mmol/L OUR PT: 175mg/kg, serum 429mmol/L CLINCIAL EFFECTS Occur as a result of: 1 2 3 Adenosine antagonism Release of endogenous catecholamines Phosphodiesterase inhibiton Toxicity affects: GI system Cardiovascular system CNS MSK GI Nausea and protracted emesis • Severe and difficult to control despite use of multiple anti-emetics Increase in gastric acid secretion and smooth muscle relaxation • Gastritis and esophagitis (more common with chronic use) Transiently elevated liver enzymes CARDIOVASCULAR Tachydysrhythmias Sinus tach SVT MAT Afib PVCs VT MI Peripheral vasodilation (wide pulse pressure) Hypertension or hypotension PULMONARY Stimulates CNS respiratory centre Increased RR Resp Alkalosis Respiratory failure Acute lung injury CNS H/A Tremor Anxiety Irritability Agitation Hallucinations Insomnia Seizures* MSK Increases intracellular Ca++ Smooth muscle relaxation Tremor Fasiculations Myoclonus Rhabdomyolysis METABOLIC HypoK Shift into cells from B2 stimulation HypoMg HypoPO4 HypoNa Hyperglycemia AGMA (lactate) MANAGEMENT Basics: IV, monitored bed Labs to follow extended electrolytes Lactate CK +/- Serum caffeine level CXR, ECGs TREATMENT MDAC* Emesis Zofran, maxeran Dysrhythmias Benzos Esmolol Lidocaine Rhabdo Fluids and monitor u/o TREATMENT Electrolytes Replace, but careful b/c will become hyperK when shift back out of cell Hypotension Fluids Not dopamine Seizures Benzos Phenobarb Pyridoxine MDAC Definition: more than 2 sequential doses of AC • In many cases, the number of doses administered is substantially greater MDAC serves 2 purposes: 1 Prevent ongoing absorption of a drug that persists in the GIT 1 Enhance elimination by either disrupting enterohepatic recirculation or by enteroenteric recirculation General Indications GI decontamination for drug or poison ingestion associated with significant risk of toxicity, where supportive care/antidote alone is insufficient to ensure a satisfactory outcome The toxin must be able to bind to AC Must believe that a significant amount of agent is unabsorbed and is amenable to removal AACT Position Statement Position statement states use MDAC only for ingestions of Carbamazepine Dapsone Phenobarbital Quinine Theophylline /Methylxanthines Other Drugs Shown to increase elimination of: Digoxin Phenobarbital Carbamazepine Phenylbutazone Dapsone Nadolol Theophylline Salicylate Quinine Cyclosporine Propoxyphene Nortriptyline Amitriptyline Contraindications Any contraindication to single-dose activated charcoal • AC known not to adsorb • Airway protective reflexes are absent or expected to be lost and pt is not intubated • GI perf (esp caustic ingestion) • Increases severity of injury (hydrocarbons) • Endoscopy for dx/mx anticipated Presence of ileus Administration Initial dose • 1g/kg or 10:1 ratio of ACT:toxin, whichever is > Repeat dose • 0.25-0.5mg/kg every 1-6hrs Procedure • Can be administered with cathartic for the 1st dose only • If pt vomits, repeat the dose • Can use oral, NG or OG route *Sxn tube before removal to reduce aspiration risk SUMMARY DDX for toxin induced seizures OTIS CAMPBELL Refractory seizures in toxic ingestion Think about pyridoxine Caffeine is a methylxanthine Adrenergic stimulation Can get refractory seizures MDAC is indicated