Toxicology Flashcards
<div><b>Indications For Dialysis in Lithium Poisoned Patients</b></div>
<div>Severely symptomatic patients </div>
<div>Unable to tolerate fluid hydration </div>
<div>Renal impairment </div>
<div>Acute toxicity: Levels above 4 mEq/L </div>
<div>Chronic toxicity: Levels above 2.5 mEq/L</div>
<div><b>List the ECG changes potentially seen in lithium toxicity</b></div>
<div><b>Think about it as looking at an ECG from P to T waves</b></div>
<div><br></br></div>
<div>Bradycardia </div>
<div>AV blockade </div>
<div>QT prolongation<br></br></div>
<div>ST changes </div>
<div>Ischemic changes<br></br></div>
<div>Flattened or inverted T-waves </div>
<div>+</div>
<div>Brugada pattern</div>
<div></div>
“<div><span>List risk factors for toxicity in the setting of chronic lithium use</span></div>”
<div><i>Renal causes:</i><br></br> Nephrogenic DI </div>
<div> Renal impairment </div>
<div><i>Hypo</i>:<br></br> volemia</div>
<div> Na</div>
<div><i>Acute illness </i></div>
<div><i>Drugs:</i><br></br> Diuretic<br></br> NSAIDS<br></br> ACE/ARB </div>
<div><i>Dementia /Increased age</i></div>
<div><b>List disease states caused by Lithium</b></div>
Nephrogenic DI<div>Hypothyroidism</div><div>Hyperthyroidism</div><div>SILENT</div>
What is SILENT
“<div><span>syndrome of irreversible lithium-effectuated neurotoxicity</span></div><div><div><span>Persistent cerebellar and brainstem dysfunction, dementia, and extrapyramidal signs even after lithium use has been discontinued for more than 2 months</span></div></div>”
List three deadly clinical manifestations of clonidine toxicity
<div>Apnea/hypoventilation</div>
<div>Hypotension</div>
<div>Bradycardia</div>
Substances Causing Wide Anion-Gap Acidoses
“<b>A CAT PILES MUD</b><br></br><b><br></br></b><div><b>A: A</b>lcoholic ketoacidosis<br></br><b>C: C</b>yanide,<b>c</b>arbon monoxide (CO),<b>c</b>olchicine<div><b>A: A</b>cetaminophen (large ingestions)<br></br><b>T: T</b>oluene<br></br><b>P: P</b>araldehyde,<b>P</b>henformin</div><div><b>I: I</b>soniazid,<b>i</b>ron,<b>i</b>buprofen</div><div><b>L: L</b>actic acidosis<br></br><b>E: E</b>thylene glycol<br></br><b>S: S</b>alicylates<br></br><b>M: M</b>ethanol,<b>m</b>etformin</div><div><b>U: U</b>remia<br></br><b>D: D</b>iabetic ketoacidosis</div></div>”
Potentially Lethal Toxins Where Early Activated <br></br>Charcoal Administration May Be Indicated
<b>THE KILLER CS</b><br></br>Cyanide<br></br>Colchicine<br></br>Calcium channel blockers<br></br>Cyclic antidepressants<br></br>Cardio glycosides<br></br>Cyclopeptide mushrooms <br></br>(Amanita phalloides)<br></br>Cocaine<br></br>Cicutoxin (water hemlock)<br></br>Salicylates
Substances That Do NotBind to Activated Charcoal
<b>SAPHIL</b><div><b>S</b>olvents</div><div><b>A</b>lcohols, Acids, Alkalis</div><div><b>P</b>esticides</div><div><b>H</b>ydrocarbons, Heavy metals</div><div><b>I</b>ron</div><div><b>L</b>ithium</div>
Dialyzable Toxins
<b>STUMBLED</b><br></br>Salicylates<br></br>Theophylline<br></br>Uremia<br></br>Metformin/methanol<br></br>Barbiturates<br></br>Lithium<br></br>Ethylene glycol<br></br>Depakote (valproic acid—in massive overdose)
Substances Amenable to Multiple-Dose <br></br>Activated Charcoal
ABCDQ<br></br>Aminophylline/theophylline<br></br>Barbiturates<br></br>Carbamazepine/concretion forming drugs (eg, salicylates)<br></br>Dapsone<br></br>Quinine
Nalaxone dose in Clonidine Toxicity
<div>Escalating doses of naloxone of 0.1 mg, 0.4 mg, 2 mg, and 10 mg</div>
What is indicated in refractory Bradycardia in Clonidine Toxicity
Atropine
Clonidine withdrawal S/S
Htn<div>Anxiety</div><div>Tachycardia</div><div>Sweating</div>
GCS
“<img></img>”
Usual Bedside Tests
Blood Sugar (Accucheck)<div>ECG</div><div>Urine Preg test</div>
””“<u>Must have lab tests</u>”” in acute toxicity”
<div>Venous gas</div>
<div>Electrolytes</div>
<div>Bun</div>
<div>Cr</div>
<div>Tylenol level</div>
<div>Salicylate level</div>
<div>ETOH</div>
Universal Antidote
“Glucose<div>Oxygen</div><div>Thiamine</div><div>Nalaxone</div><div>"”Flumazenil”” in certain conditions esp children</div>”
Goal of Nalaxone
“<span>Reversal of </span><u><span>respiratory</span></u><span> depression</span>”
Factors of persistent neurological sequelae after CO poisoning
<div>significant loss of consciousness or coma</div>
<div>persistent neurological dysfunction (e.g. confusion or seizures)</div>
<div>abnormal cerebellar examination</div>
<div>metabolic acidosis</div>
<div>myocardial ischaemia</div>
<div>age >55 years</div>
<div>pregnancy</div>
Antidotes
“<img></img>”
“<img></img>”
TCA overdose<div>S in I</div><div>R in aVR</div>
ECG Findings in TCA overdose
S in lead I and aVL<div>R in aVR</div><div>Wide QRS</div><div>Rt axis deviation</div><div>Sinus tachycardia</div><div><br></br></div><div><br></br></div>
Mechanisms of TCA toxidromes
Na channels blockade (QRS prolongation)<div>K channels blockade (QT prolongation)</div><div>Antihistamine (hypotension, sedation)</div><div>Anticholinergic toxidrome</div><div>Serotonin syndrome</div><div>GABA blockade (seizure)</div><div>Alpha-1 blockade (hypotension)</div>
Whatis the leading cause of in-hospital death from TCA overdose
“Refractory Hypotension due to:<div>Profound alpha antagonism</div><div>Decrease myocardial contractility leading to decrease cardiac output</div>”
How do you ‘set up a sodium bicarb infusion
Add 2 amps to 1 L of D5W and infuse at ~150-250 cc/hr
Target Serum ph in alkalinization
Ph 7.45 - 7.55
Indications of Na bicarb in TCA overdose
QRS widening<div>Refractory hypotension</div><div>Ventricular Dysrrhthmia</div>
Antiarrhythmic medication of choice in TCA
Lidocaine
Hunter Criteria
“<img></img>”
Agents causing serotonin syndrome
“<img></img><div><span><br></br></span></div><div><span><b>S</b>aints <b>S</b>ell <b>D</b>rugs <b>T</b>hat <b>M</b>ake <b>M</b>e <b>T</b>rip <b>O</b>nthe<b>T</b>ram <b>L</b>ine</span><div><span>St. John’s Wart</span></div><div><span>SSRI/SNRI</span></div><div><span>Dextromethorphan</span></div><div><span>TCA</span></div><div><span>Meperidine</span></div><div>MAOI</div><div>Triptans</div><div>Ondensterone</div><div>Tramadol</div><div>Linzolid</div><div><span><br></br></span></div></div>”
Pathognominic dysrhythmia associated with digoxin toxicity
“<span><b>Paroxysmal Atrial tachycardia (PAT) with block</b></span><div><b><i>Bidirectional VT</i></b><br></br></div>”
ECG findings in Digoxin Toxicity
PAT with AV block (most common)<div>Frequent PVCs (Bigeminy & trigeminy)</div><div>Slow AF</div><div>Any type of AV Block</div><div>VTs including plymorphic and bidirectional VT</div>
<div>Indications of DigiFab in Acute digoxin overdose</div>
<ul> <li>Cardiac arrest</li> <li>life threatening cardia dysrhythmia</li> <li>ingested dose >10mg (adult) or >4mg (child)</li> <li>serum digoxin level >15 mmol/L at any time</li> <li>serum potassium >5.5 mmol/L</li></ul>
“<img></img>”
Paroxysmal atrial tachycardia with AV block<div>Digitoxicity</div>
Is it indicated to replace Ca in cases of Digitoxicity
“No, will result in ““stone heart”””
How much DigiBind to use
Acute: Start with 5-10 vials<div>Chronic: Start with 3-5 vials</div><div>Cardiac arrest: Start with 10 vials</div>
[K] in digitoxicity
Hyper K in acute<div>Hupo K in chronic</div>
<div>List three plants that have the potential to cause digitalis toxicity</div>
“<div>Common oleander </div> <div>yellow oleander </div> <div>Lily of the valley </div> <div>Red squill </div> <div>Foxglove </div> <div>dog’s bane </div> <div>Milkweed</div>”
What is the main route of Digoxin elimination
Kidneys
What is The definition of hepatotoxicity after paracetamol overdose
<div>serum AST concentration ≥1000 IU/L.</div>
Tylenol toxic doses
<div>In adults and adolescents, hepatic toxicity may occur following ingestion of >7.5.</div>
<div>In children the toxic dose is 140 mg/kg</div>
NAC should also be started immediately or empirically when
<div>Patients present 8 hours or more after ingestion</div>
<div>Serum Acetaminophen level is not available within an 8-hour time window</div>
<div>There is uncertainty as to the timing of the overdose</div>
<div>When do you start NAC in chronic ingestion?</div>
“<div><i>Chronic ingestion = any ingestion(intentional, unintentional supratherapeutic) > 8hr period </i></div> <div><br></br></div><div>Toxic level > 7.5 grams (adult) </div> <div>Symptomatic regardless of APAP level </div> <div>Elevated AST (> 2x upper limit normal or above 120 IU/L) </div> <div>Elevated APAP > 30 mcg / ml </div> <div>**Controversial: all high risk pts (etoh and liver dx) w/ elevated AST **</div>”
<div>What individuals are at increased risk for hepatocellular toxicity from chronic ingestion of APAP:</div>
<div>ETOH use </div>
<div>Isoniazid use </div>
<div>Malnutrition </div>
<div>Dehydration</div>
<div>List three differences between oral and IV NAC</div>
“oral:<div>more n/v,</div><div>takes longer,</div><div>less anaphylactoid rxns</div><div><br></br></div><div>OR</div><div><br></br></div><div>IV regimen is quicker than oral (20 hrs vs 72 hrs) <br></br>IV produces more anaphylactoid reactions compared to oral<br></br><br></br><span>Also acceptable:</span><br></br><span>(1) dosing errors are more likely with IV NAC</span><br></br><span>(2) possibly too much IV fluid for kids: potentially leading to hyponatremia and seizures</span><br></br><span>(2) The oral route frequently causes nausea and vomiting whereas the IV route does not</span><br></br></div>”
<div>Rumack-Matthew Nomogram is not useful in:</div>
<div>Chronic Overdose > 8 hrs</div>
<div>Delayed release tabs</div>
<div>Unknown time of ingestion<br></br></div>
<div>Co-ingestion (anticholinergics, ETOH)</div>
<div>glutathione deficiency<br></br></div>
<div>Chronic liver diseases</div>
<div>Malnutrition</div>
<div>HIV infection</div>
<div>Cystic fibrosis</div>
<div>When can you stop NAC?</div>
<ol> <li>INR <1.3</li> <li>AST or ALT WNL</li> <li>Non-Detectable acetaminophen level in the blood</li></ol>
<div>Describe criteria for transfer to a transplant centre</div>
<div>Kings College criteria, as per MDCalc, </div>
<ol> <li>Arterial pH < 7.30 </li> <li>INR > 6.5 (PT > 100 sec) </li> <li>Creatinine 300 µmol/L </li> <li>Grade III or IV hepatic encephalopathy</li></ol>
<div>Dosing of NAC:</div>
<div>Oral:</div>
<div>Loading dose: 140 mg/kg, then</div>
<div>70 mg/kg q4hrs for 17 additional doses.</div>
<div></div>
<div>IV:</div>
<div>Loading dose: 150 mg/kg iv, then</div>
<div>Continuous infusion og 50mg/kg over 4 hrs, then</div>
<div>Continuous infusion of 100 mg/kg over the next 16 hrs</div>
List 6 classes of medications that can cause an anticholinergic toxidrome
<div>Antihistamines, </div>
<div>Antiparkinson agents, </div>
<div>antipsychotics</div>
<div>Antidepressants</div>
<div>mydriatics</div>
<div>antispasmodics</div>
<div>muscle relaxants</div>
Causes of acidosis in toxic alcohols
Methanol: formic acid<div>Ethylene glycole: glycolic acid</div><div>Isopropanol: acetone (not an acid) result in ketonuria wout metabolic acidosis</div>
End-organ effect of txic etoh
” <div><span>Alcohol</span></div> <div><span>End Organ</span></div> <div>Methanol:</div> <div>Eyes: Blindness, GIT: Pancreatitis</div> <div>Ethylene glycol:</div> <div>Kidney: oxalic acid crystals: ARF</div> <div>Isopropanol:</div> <div>Hemorrhagic gastritis</div> “
Causes of Double Gap
<ol> <li>Ketoacidosis (diabetic, alcoholic).</li> <li>Alcohols (Ethylene glycol, methanol)</li> <li>Failures (renal, multiorgan)</li></ol>
<div>Which vitamins are important in the treatment of ethylene glycol poisoning?</div>
“<div>Pyridoxine 100 mg and thiamine 100 mg IV/IM drive the conversion of ethylene glycol to nontoxic metabolic’s.</div><div><br></br></div><div>Calcium replacement may also be necessary</div><div><br></br></div><div>For methanol, folate 50 mg IVq4h to drive conversion of formic acid to Co2 and H2O<br></br></div>”
<div>Ketosis is present in</div>
<ol> <li>diabetic ketoacidosis, </li> <li>alcoholic ketoacidosis, </li> <li>starvation ketosis, </li> <li>salicylism, and </li> <li>cyanide and acetone ingestion</li></ol>
<div>Advantages of Fomepizole over Ethanol:</div>
<div>More accurate dosing</div>
<div>Higher affinity to dehydrogenase</div>
<div><br></br></div>
<div>Less risk for:<br></br></div>
<div>Hypoglycemia</div>
<div>Electrolyte disturbances</div>
<div>CNS depression</div>
List 6 indications for hemodialysis in salicylate poisoning
<div>Clinical deterioration despite supportive care and urinary alkalinization</div>
<div>Salicylate level rising despite adequate therapy<br></br></div>
<div>Renal insufficiency or failure</div>
<div>Severe A/B disturbance</div>
<div>Altered mental status, or seizures</div>
<div>ARDS</div>
<div><br></br></div>
<div>How is ASA toxicity managed?</div>
<div>1. Start urinary alkalinization </div>
<div>2. Correct hypovolemia: Urine output 2-3 mL/kg/hr </div>
<div>3. Keep [K] >4.5, correct any hypomagnesemia </div>
<div>4. Give glucose for any CNS changes</div>
<div>What is the primary cause of mortality in ASA toxicity?</div>
“<div><span>cerebral toxicity and metabolic acidosis</span></div>”
<div>Which β blockers have intrinsic sympathomimetic activity?</div>
<div>Why is this important?</div>
“Pindolol<div>Acebutolol</div><div>Carteolol</div><div>Sotalol</div><div><br></br></div><div><div>can lead to some unusual manifestations such as v<span>entricular dysrhythmias and sinus tachycardia instead of bradycardia</span></div></div><div><br></br></div><div>Sotalol causes Torsades</div><div>Acebutolol causes prolonged QT and VT</div>”
<div>Why is propranolol the most lethal βB?</div>
“<div>Lipophilic nature which allows it to penetrate the CNS, causing <span>obtundation</span>, <span>respiratory depression</span>and <span>seizures</span>.</div>”
<div>HIET</div>
“<ul> <li><span>Insulin</span> and <span>glucose</span>.</li><li>Bolus 1 g/kg dextrose and run infusion at 0.5 g/kg/h.</li><li>Insulin starts at 1 U/kg and infuse at 0.5U/kg/h.</li><li>Increase in 1 hour if no hemodynamic response.</li></ul>”
<div>Which β blockers can be dialysed?</div>
“<div><span>SANTA</span> can’t pee….. </div> <ul> <li>Sotalol </li> <li>Atenolol</li> <li>Nadolol </li> <li>Timolol </li> <li>Acebutolol</li></ul>”
Indications of Deferoxamine
Fe level > 500 mcg/dL<div>Repeated vomiting, <br></br>toxic appearance, <br></br>lethargy, <br></br>hypotension, <br></br>shock</div><div>Metabolic acidosis</div><div>Hemochromatosis<br></br></div>
<div>What lab abnormalities are associated with HF burns?</div>
“HypoCa<div>HypoMg</div><div>HeperK</div><div>Metabolic acidosis</div><div><br></br></div><div><u>ECG findings:</u></div><div>prolonged QT</div><div>peaked T wave</div>”
Lab findings of NMS
Increased:<div>CK</div><div>WBC</div><div>BUN/Cr</div><div>LFT</div><div>Metabolic acidosis</div>
Toxins That Cause Hypoglycemia
“<img></img><div><br></br></div><div>Acetaminophen</div><div>ASA Alcohol</div><div>Sulfonylureas (Gliburide)</div><div>Insulin</div><div>BB</div>”
Medications causing NMS other than antipsychotics
Metoclopromide<div>Li</div><div>Antidepressants</div><div>Withdrawal of Antiparkinson medication</div>
<div>Common drugs causing nystagmus</div>
<div>Barbiturates</div>
<div>Carbamazepine,</div>
<div>PCP</div>
<div>Phenytoin</div>
<div>Lithium</div>
<div>Toxins which are radiopaque on X-Ray</div>
“<span>CHIPES</span><div></div><div><img></img><span><br></br></span></div>”
<div>Indications for Whole Bowel Irrigation:</div>
<ol> <li>Ingestion of certain drugs: (Li, CCB)</li> <li>Extended release preparations </li> <li>Illicit drug packets </li> <li>Metals (iron / lead)</li></ol>
<div>List 5 Dialyzable Drug<br></br>Properties</div>
<div>Low<br></br>molecular weight </div>
<br></br><div>Low protein<br></br>binding</div><br></br><div>Low volume<br></br>of distribution </div><br></br><div>Low plasma clearance <br></br></div><br></br><div>Low<br></br>dialysate drug concentrations </div><br></br><div>High water<br></br>solubility</div>
<div>List the “One Pill Can Kill” Drugs</div>
“<div><span>MISCAST: </span></div> <div></div> <div>Methadone (and opiates) </div> <div>Iron / Insulin</div> <div>Sulfonylureas </div> <div>CCBs clonidine </div> <div>ASA</div> <div>Suboxone </div> <div>TCA’s</div>”
Indications of intralipid
LA (Bupivacaine)<div>CCB (Verapamil)</div><div>BB (Propranolol)</div><div>Antidepressants (TCA, bupropion)</div><div>Organophosphate</div>
Brady + HTN
Clonidine
Brady + Hypotension + Narrow QRS
Centrally acting alpha agonist (Clonidine)<div>BB</div><div>CCB</div><div>Cardiac Glycosides (Digoxin)</div><div>Sedative/hypnotics (benzo, barbiturates)</div><div>Opioids</div><div>Organophosphates</div><div><br></br></div>
Brady + Hypotension + Wide QRS
<div>Class 1a drugs (procainamide)</div>
Class 1b drugs (lidocaine)<div>Class 1c drugs (flecainide)<br></br><div>BB (propranolol, acebutolol, metoprolol)</div><div>CCB</div><div>Digoxin</div><div>Hyper K</div><div><br></br></div></div>
Tachy + HTN
Sympathomimetics (amphet, cocaine)<div>Anticholinergics (diphenhydramine, atropine)</div>
Tachy + Hypotension
MAO<div>Alpha 1 aNTAgonists (prazosin, terazosin)</div><div>Phenothiazines (promethazine)</div><div>Diuretics</div><div>Nitrates</div><div>Theophylline</div><div>Caffein</div>
Tachy + Hypotension + Wide QRS
TCA (amitriptyline)<div>M. Relaxants (cyclobenzaprine)</div><div>Anticholinergics (diphenhydramine)</div><div>Cocaine</div>
<div>Special note on decontamination:</div>
<div>PPE </div>
<div>Remove Clothing and place in plastic bags </div>
<div>BRUSH OFF DRY CHEMICALS before hydrotherapy </div>
<div>Use gentle irrigation with low pressure water</div>
Most predictive test for cyanide toxicity
Profound lactic acidosis<div>(lactate > 10 mmol/L)</div>
Indications for HBO
CNS: AMS, focal deficit, Coma<div>CVS: Syncope, Myocardial ischemia, dysrrhythmia</div><div>COHb > 25%</div><div>Pregnant</div>
Goal for CO poisoning treatment
To prevent delayed neuropsychiatric sequelae
Rapidly Lethal Toxins
<ul> <li>Cyanide</li> <li>Paraquat (herbicidal causing oxygen free radical concentrated in the lungs causing ARDS and resp failure)</li> <li>Carbon monoxide</li> <li>Hydrogen Sulfide</li> <li>Sarin</li> <li>VX gas</li> <li>Fentanyl</li> <li>Arsenic </li> <li>Strychnine</li> <li>Botulinum toxins</li></ul>
Most comon digitoxicity dysrrhythmia is?
PVCs
Most common ECG finding in Digoxin use (toxicity or not)
ST depression with Dali Mustache
Criteria for increased toxicity of a hydrocarbon
High volatility<div>Low viscosity</div><div>Low surface tension</div><div>Halogenated</div>
Effect of Hydrocarbons on the heart
Increase sensitivity of myocardium to catecholamines<div>Hypoxia secondary to lung injury</div>
Indications of gastric lavage in Hydrocarbon toxicity
<b>CHAMP</b><div>Camphor</div><div>Halogenated HC (Carb tetrachloride, PVC)</div><div>Aromatic HC (Benzen, toluene)</div><div>Metals HC (leaded gas)</div><div>Pesticides</div>
What to avoid when treating HC toxicity dysrrhythmia
Epinephrine<div>Defebrillation</div>
Toxicity of H2S is due to
Blockade of cytochrome oxidase leading to anaerobic metabolism and lactic acidosis
H2S antidote
Amyl nitrate<div>Na nitrate</div><div><br></br></div><div>(no Na thiosulfate)</div>
INH toxicity
Decrease B6 (required for GABA synthesis)<div>Decrease seizure threshold</div><div>Metabolic acidosis</div>
INH toxicity antidote
Pyridoxine (B6):<div>Known amount, dose is gram for gram</div><div>If unknown amount, dose is 5 grams</div>
How INH toxicity present?
Status epilepticus
Toxic dose of Iron
30-40 mg/kg
Indications of deferoxamine
Fe level > 500 mcg/dl<div>Unstable vital signs</div><div>Repetitive vomiting</div><div>AMS/Coma</div><div>Seizures</div>
SE of deferoxamine
Hypotension<div>ARDS</div><div>Increase yersinia sepsis</div>
What confirms Iron overdose after giving deferoxamine
Vin Urine
Blood film of lead posoining
Hypochromic microcytic anemia<div>basophilic stippling of the RBC</div>
<div>How is lead toxicity diagnosed?</div>
<ul> <li>Blood lead level</li> <li>Anemia w/ basophilic stippling on smear </li> <li>Radio-opaque lead in stomach </li> <li>Radiographs of wrists and knees may show “lead lines”</li></ul>
Precipitating substances of hypertensive crisis in MAOI tox
Tyramine containing substances:<div>Amphetamines</div><div>Cheese</div><div>Wine</div><div>Fava beans</div>
Causes of methemoglobinemia
Nitrites<div>Nitrates</div><div>Benzocaine</div><div>Dapsone</div><div>Pyridium</div>
Methemoglobinemia antidote
Methylene blue (reduces Fe+3 to Fe+2)<div>Contraindicated in GSPD def</div>
Bad prognostic sign of Mushroom poisoning
Delayed onset of symptoms of N/V/D (>6hrs)<div>Ends with liver failure and renal failure</div>
Antidote for sulfonylurea OD
Dextrose<div>Octreotide</div>
What are the nicotinic effect of organophosphate poisoning
Muscle weakness<div>Fasciculation</div><div>Respiratory failure</div>
Hyperthermia + Rhubdomyolysis
NMS<div>PCP</div><div>Sympathomimetics</div><div>Opiate wirhdrawal</div><div>ETOH withdrawal</div><div>Seizures</div>
Classical eye sign of PCP
Rotatory nystagmus
Miosis by toxins
<b>COPS</b><div><br></br></div><div>Cholinergics, clonidine</div><div>Opioids, organophosphates</div><div>Phenothiazines, pilocarpine, pontine bleed</div><div>Sedative/hyonotics</div>
Skin findings by toxins
Red: Anticholinergics, CO<div>Blue skin: MetHbemia</div><div>Blistering: Barbiturates, CO, spider bites, snake envenomations</div>
Common toxins by odour
Bitter almonds: Cyanide<div>Rotten eggs: Hydrogen sulfide</div><div>Garlic: Arsenic, organoph</div><div>Fruity: DKA, isopropanol</div>
Radiopaque Drugs
<b>COINS</b><div><br></br></div><div>Chloral hydrate, cocaine packets</div><div>Opiate packets</div><div>Iron & heavy metals (Pb, As, Hg)</div><div>Neuroleptic agents</div><div>Sustained release products</div>
<div>List 10 Toxins That Cause Delirium</div>
<div>1. Prescription medications (e.g., opioids, sedative-hypnotics, antipsychotics, etc…) </div>
<div>2. Non-prescription medications (e.g., OTC antihistamines) </div>
<div>3. Drugs of abuse (e.g., ethanol, heroin, hallucinogens, etc…) </div>
<div>4. Withdrawal states (e.g., ethanol, benzodiazepines) </div>
<div>5. Medication side effects (e.g.,serotonin syndrome, etc…) </div>
<div>6. Poisons </div>
<div> a. Toxic alcohols </div>
<div> b. Inhaled toxins (e.g., carbon monoxide) </div>
<div> c. Plant-derived toxins (e.g.,Salvia)</div>
<div>Indications for gastric lavage</div>
<div>❏ Lethal ingestion </div>
<div>❏ Early ingestion (drugs not in GI transit) </div>
<div>❏ No known antidote </div>
<div>❏ Not amenable to other decontamination strategies </div>
<div>❏ FACT (Fe, ASA, Colchicine, TCA)</div>
<div>Hypoglycemia induced Toxins</div>
<div>❏ Beta blockers (especially in peds) </div>
<div>❏ Isoniazid (INH) </div>
<div>❏ Salicylates </div>
<div>❏ Sulfonylureas </div>
<div>❏ Insulin </div>
<div>❏ Ethanol</div>
<div>How does co-ingestion of diphenhydramine (Benadryl) impact Tylenol OD</div>
<div>Co-ingestion with anticholinergics will impact gut motility, and can impact both your absorption times (i.e. interfering with nomogram interpretation) and may be associated with ongoing hepatocellular toxicity despite NAC 20hr IV protocol</div>
<div>What are the indications for dialysis in acetaminophen overdose?</div>
<ol> <li>Highly elevated serum acetaminophen concentration (>1000 mg/L) at 4 hours post-ingestion </li> <li>Hepatorenal syndrome (Cr > 300) </li> <li>Metabolic acidosis with pH < 7.30 </li> <li>Encephalopathy </li> <li>Elevated lactate (>3.5 mmol/L)</li></ol>
Indications for Emergent Hemodialysis <br></br>Following Acute Acetaminophen Ingestion
Highly elevated serum acetaminophen concentration (>1000 mg/L) at 4 hours post-ingestion<br></br>Hepatorenal syndrome<br></br>Metabolic acidosis with pH <7.30<br></br>Encephalopathy<br></br>Elevated lactate (>3.5 mmol/L)
Indications of Physostigmine in Anticholinergic Toxicity
<div>Delirium / Coma / Seizure </div>
<div>Risk of harming themselves or staff </div>
<div>Requiring ongoing physical restraint, or </div>
<div>Interfering with effective treatment (eg, pulling out IV lines)</div>
“<div><span>Contraindications of Physostigmine</span></div>”
<div>TCA overdose </div>
<div>Widened QRS >100 </div>
<div>AV blocks </div>
<div>Bradycardia </div>
<div>Narrow angle Glaucoma</div>
<div>Unknown co-ingestions</div>
Other than Na bicarb, what can be used in TCA toxicity related wide QRS
Hypertonic Saline
What are the indications of Hypertonic Saline in TCA toxicity?
Ph > 7.55 with failure of Na bicarb to shorten the QRS
<div>List 3 meds to avoid in TCA overdoses</div>
Physostigmine<div>Class 1a anti arrhythmic meds (procainamide)</div><div>Class 1c anti arrhythmic meds (flecainide)</div><div>Phenytoin</div>
<div>What rhythm is NOT associated with Dig toxicity</div>
<div>Afib with rapid ventricular response due to AV block</div>
What medications/procedures to be avoided in treating Digitoxicity?
Ca<div>Salbutamol</div><div>Epinephrine</div><div>Defibrillation</div><div>Pacing</div>
Temporizing measures while awaiting for DigiBind
Atropin for shock and bradycardia then pacing (avoid if possible)<div>Lidocaine & Phenytoin for tachydysrrhythmia</div><div>Maintain K (3.5-4)</div>
Dose of MDAC
1g/kg every 2-4 hrs for 4 doses
Rx of metHbemia
O2 therapy/HBO<div>Methylene blue (if MetHb >25%)</div><div>Vit. C</div><div>Exchange transfusion</div>
Leading cause of mortality in cocaine/sympathomimetic OD
Severe hyperthermia<div>Dysrrhythmia</div><div>Intractable seizures</div><div>HTN leading to ICH, aortic dissection, MI</div>
DDX of aggitation + hyperthermia
SS<div>NMS</div><div>Sympathomimetic OD</div><div>Anticholinergic OD</div><div>Malignant hyperthermia</div><div>ASA</div><div>T4 OD</div><div>ETOH withdrawal</div>
Principles of Mx of Stim-induced hyperthermia
Rapid cooling<div>Iv fluids</div><div>Sedation</div><div>Paralysis + intubation</div>
What is a consequence of a long-term toluene abuse?
Cortical atrophy and dementia
“<span>What signs/characteristics could you look for to help determine if the patient is truly in alcohol withdrawal instead of drug-seeking?</span>”
“<span>A</span><strong>tongue tremor</strong><span>is a possible finding in alcohol withdrawalthat is impossible to feign and could help confirm the patient truly has withdrawal (see link below for video).</span><div><span>The general tremor of alcohol withdrawal has a few key characteristics:</span></div><div><span>it is an</span><strong>intention tremor</strong><span>(thus there is no tremor at rest),</span></div><div><span>it is</span><strong>constant</strong><span>, and</span></div><div><span>it</span><strong>does not fatigue</strong><span>.</span></div>”
Pupils in Toxicology
“<img></img>”
“TCA OD,<span>What are your next five management steps?</span>”
- Obtain IV access<br></br>2. Administer sodium bicarbonate 1 amp immediately (or 1-2 mEq/kg/IV bolus). Continue bolus q3-5 mins until QRS narrows.<br></br>3. Set up a sodium bicarbonate infusion (FYI: Setting up a sodium bicarb infusion: Add 2 amps to 1 L of D5W and infuse at ~150\200 cc/hr)<br></br>4. ICU Consult<br></br>5. Consider calling poison center<br></br>6. Consider decontamination
“<span>List 6 lab tests you must order in toxicology</span>”
Best answers:<br></br>1. electrolytes<br></br>2. venous gas<br></br>3. Tylenol/acetaminophen level<br></br>4. salicylate level<br></br>5. Creatinine<br></br><br></br>Also acceptable: CBC, BUN, Cr, alcohol level, blood glucose, lactate, serum osmolality, magnesium<br></br><br></br>NOT ACCEPTABLE: random urine drug screen
“In TCA,<span>What key ECG and laboratory parameters must you monitor and what are your endpoints?</span>”
“<div>ECG: QRS narrowing to <120 ms<br></br><br></br>Serum pH: The patient’s pH should be maintained between 7.45 and 7.55.</div><br></br>”
“<span>Generally speaking, list 2 circumstances in which you would start NAC even before receiving any lab values.</span>”
- Patient presents 8 hours or more after ingestion<br></br>2. Serum acetaminophen level is not available within an 8 hour window<br></br>3. There is uncertainty re: the timing of the overdose<br></br>4. Massive overdose
General non-toxicological DDX of toxidromes:
- DKA<br></br>2. Meningitis<br></br>3. Encephalopathy<br></br>4. Sepsis - any source (Pneumonia, UTI, intra-abdominal infection)<br></br>5. Peripheral vertigo/ vestibular neuritis/ meniere’s disease<br></br>6. Intracranial mass<br></br>7. Intracranial hemorrhage<br></br>8. Posterior circulation CVA<br></br>9. Gastroenteritis<br></br>10. Hyponatremia<br></br>11. Thyroid storm
“In ASA posoning,<span>what history and physical findings support the diagnosis of salicylate poisoning?</span>”
- Tinnitus<br></br>2. Confusion<br></br>3. Tachypnea<br></br>4. Hyperthermia<br></br>5. Increased ASA use on Hx<br></br>6. Tachycardia<br></br>7. GI upset
“ASA,<span>List your next 4 management priorities, including two treatments that you will need to consider.</span>”
- High acuity monitored bed<br></br>2. IV access<br></br>3. IV fluid bolus<br></br>4. Start sodium bicarbonate infusion<br></br>5. Consider dialysis<br></br>6. Consider decontamination/Whole bowel irrigation<br></br>7. Consider starting potassium supplementation
“<span>Assuming the patient has taken a massive dose of Verapamil, name 5 different treatments/medications you could treat him with?</span>”
-High dose insulin euglycemic therapy<br></br>-Glucagon<br></br>-Calcium gluconate/chloride<br></br>-Vasopressor infusion<br></br>-Lipid emulsion therapy<br></br>-IV Fluid bolus<br></br>-Consider decontamination/Whole bowel irrigation<br></br>- Consider Atropine (low evidence)
Fever+ALOC DDX:
<ul> <li>Sepsis,</li> <li>Meningitis,</li> <li>Encephalitis,</li> <li>Serotonin syondrome,</li> <li>NMS,</li> <li>anticholinergic,</li> <li>Salicylates,</li> <li>Thyroid Storm,</li> <li>Heat Stroke</li> </ul>
<p>List three classes of drugs that can impair lithium clearance</p>
<p>1.NSAIDs</p>
<p>2.ACE INHIBITORS</p>
<p>3.SSRIs</p>
<p>4.THIAZIDE DIURETICS</p>
<p>5.Nb also, topirimate</p>
<p>Besides drugs, list 3 contributors to impaired lithium clearance</p>
<p>1.Dehydration</p>
<p>2.Hyponatremia</p>
<p>3.Renal impairment</p>
<p>4.Hyperthyroid</p>
<p>List 3 likely clinical manifestations of <u><em>acute</em></u> lithium toxicity in the absence of impaired lithium clearance.</p>
“<p>Acute lithium toxicity mainly affects the <span><strong>GI tract</strong></span> as lithium (like other metal salts) is a direct irritant. It <strong><em>causes nausea, vomiting, abdominal pain and </em></strong><strong><em>diarrhoea</em></strong>.</p> <p>If Li clearance is impaired, can see:</p> <p><span><em><strong>Neurotox</strong></em></span> (sluggishness, ataxia, confusion, tremosrs, myoclonus, seizures). <br></br><span><em><strong>Cardiac</strong></em></span> (arrythmias, bradycardia, prolonged QT)</p>”
<ul> <li>List three ECG changes that are associated with Lithium toxicity</li> </ul>
<ol> <li>Transient ST depression (also accept ST segment changes)</li> <li>Inverted T waves</li> <li>Occasional patients develop sinus node dysfunction and syncope (also accept heart blocks)</li> </ol>
Key factors for acute Li toxicity
Volume depletion<br></br>NSAIDs
Universal DDx of Severe HA,N,V:
Infections:<br></br> Meningitis<br></br> Encephalitis<br></br> Sinusitis<br></br>Hge:<br></br> SAH<br></br> SDH<br></br>Tox:<br></br> CO poisoning<br></br> OD: sedative, hypnotics<br></br> W/D: ETOH<br></br>Acute angle glosire glaucoma<br></br>Metabolic:<br></br> HypoNa<br></br> DKA/HHS<br></br>Preeclampsia
What specific lab tests for CO poisoning?
CoHb conc<br></br>CK<br></br>Trop<br></br>VBG<br></br>Lactete (more reliable index of severity than COHb)
Causes of death in CO poisoning
MI<br></br>Dysrrhythmia<br></br>Non cardiogenic pulm edema<br></br>Rhubdomyolysis leading to renal failure
ECG finding of TCA
R in aVR<br></br>S in I and aVL<br></br>RAD in terminal QRS<br></br>Wide QRS > 100<br></br>RBBB<br></br>Tachycardia<br></br>Bradycardia (pre-terminal)
Indications for DigiBind
<ul> <li>Symptomatic bradydysrhythmias</li> <li>Ventricular dysrhythmias</li> <li>Any patient with acute digoxin overdose and potassium concentrations >5.0 mEq/L</li> <li>Acute ingestion of >4 mg in a healthy child (or 0.1 mg/kg)</li> <li>Acute ingestion of >10 mg in a healthy adult</li> <li>Serum concentration of ≥10 ng/mL 4 to 6 hours after ingestion</li> <li>Serum concentration of ≥15 ng/mL at any time.</li> <li>Chronic poisoning w/ significant GI sxs, altered LOC, or renal insufficiency</li> </ul>
<p>If this woman’s granddaughter had taken her digoxin acutely in a suicide attempt, how might her granddaughter’s presentation and management differ from her own?</p>
“<p>1.The granddaughter’s course is less indolent – she would likely be asymptomatic for minutes to hours after exposure and then rapidly deteriorate.</p> <p>2.Grandma would be more likely have HYPOkalemia and granddaughter would more likely have HYPERkalemia. The hypokalemia is often from concommitent diuretic use or losses from n/v/d.</p> <ul> <li>In fact, hyperkalemia is a marker of morbidity and mortality, although correcting it does not change the m or m</li> </ul> <p>3.Granddaughter will be less likely to die than grandmother.</p> <ol> <li>Gastrointestinal symptoms, such as nausea and vomiting, are usually less pronounced in chronic toxicity as compared with acute toxicity.</li> <li>Neurologic manifestations, such as lethargy, confusion, delirium, disorientation, and weakness, may be more prominent with chronic toxicity.</li> <li>Visual changes are more common with chronic toxicity and may include alterations in color vision, development of scotomata, or blindness.</li> </ol> <p>**In both cases, call your local poison center!!</p>”
CI of Mg Rx
Bradycardia<br></br>AV block<br></br>Renal failure<br></br>HyperMg
Causes of Osmolar gap and anion gap
“<img></img>”
ECG Abnormalities in Bupropiom toxicity
QRS prolongation<br></br>QT prolongation
“<span>List two potentially deadly consequences of Bupropion toxicity?</span>”
<ol><li>Refractory status epilepticus</li><li>Cardiogenic shock/hypotension/tachydysrhythmias</li></ol>
“<span>Clonazepam + Bupropion co-ingestion. Which complication is potentially less likely in this case and why?</span>”
A benzodiazepine co-ingestion reduces the change of seizures
Urin alkalinization is useful in what Toxins?
<b>CLAMP</b><br></br><i>Chlorpropamide<br></br>Lead<br></br>ASA<br></br>Methotrexate<br></br>Phenobab<br></br></i>
<p>Indications and Contraindications for Hemodialyis</p>
<p>Indications: <strong>I STUMBLE NASA</strong></p>
<p><em>Isopropanyl, salicylates, theophylline, uremia, methanol, barbituates, lithium, ethylene glycol, nadolol, atenolol, sotalol, acebutolol</em></p>
<p><u>Small</u> Vd,</p>
<p><u>Low</u> protein binding,</p>
<p><u>Small</u> size,</p>
<p><u>low </u>endogenous clearance,</p>
<p>water soluble</p>
<p>Indications for Liver Transplant after APAP OD</p>
<ul> <li>pH < 7.3, 2 days post resus (i.e. refractory metabolic acidosis)</li> <li>INR > 6.5 - coagulopathy</li> <li>Hepatic encephalopathy</li> </ul>
<p>Disturbances caused by salicylate toxicity & their effect</p>
<p>1.Stimulates the resp center (medula)- increase RR – Resp alkalosis</p>
<p>2.Inhibits Kreb Cycle - increase lactate – metabolic acidosis</p>
<p>3.Uncoupling of oxidative-phosphorylation - increase metabolic rate - increase temp, increase O2 consumption, increase tissue glycolysis – decrease Glu</p>
<p>4.increase Hepatic gluconeogenesis increase Glu</p>
<p>5.Direct corrosive toxicity to gut</p>
<p>6.increase Lipid metabolism - increase Ketones – thus Ketosis</p>
<p>Indications for serum alkalinization in TCA OD and Mechanism of Action</p>
<ul> <li>QRS > 120msec</li> <li>VT (2nd line = lidocaine)</li> <li>Cardiac Arrest</li> <li>Seizures</li> <li>Hypotension</li> </ul>
<p><u><strong>MOA:</strong></u></p>
<p>Uncouples tricyclic from Na channel for 10 – 15 min</p>
<p>decrease protein binding</p>
<p>Increase Na gradient</p>
<p>Increase pH</p>
<p>Management of Toxic Alcohols</p>
“<p>1.Correct Acidosis with Bicarb ± hyperventilation – prevents diffusion of toxic metabolites into target tissues</p> <p>– target pH 7.45 – 7.55</p> <p>2.Fomepizole –</p> <p> <em><span>Indications</span>: OsM Gap > 10, pH < 7.3, Bicarb <20, Urine: Oxalate Crystals</em></p> <p>3.Dialysis:</p> <p><em><span>Indications</span>: Ethylene Glycol > 8mmol, Methanol > 5mmol, Metabolic acidosis, end organ symptoms (eg. Visual/ decrease LOC) renal impairment, lyte abnormalities, unstable VS</em></p> <p>4.Adjunctive treatment:</p> <ul> <li>Thiamine 100mg IV</li> <li>Folic Acid 50mg IV</li> <li>Pyridoxine 100 mg iv</li> </ul>”
<p>What is the antidote to iron and what are its main side-effects?</p>
<ul> <li>Deferoxamine 15mg/kg/hr IV x 24 hours</li> <li>Side Effects: <ul> <li><em>decrease BP – just slow down the infusion</em></li> <li><em>Respiratory toxicity if prolonged infusion</em></li> </ul> </li> </ul>
What is the most frequent cause of treatment failure in organophosphate poisoning
Inadequate atropine. <br></br>Large doses are needed nearly 20-40 mg/day
Why is glucagon useful in rx of BB OD
Glucagon enhances myocardial contractility, heart rate and AV conduction by stimulation the production of cyclic AMP<br></br>It works on receptors other than BB receptors
What medications can cause hyperthermia
Neuroleptics<br></br>Anticholinergic <br></br>ASA<br></br>Succinylcholine<br></br>Sympathomimetics<br></br>PCP<br></br>Lithium
Organophosphate poisoning
“<img></img>”
<div><b><u>Phencyclidine (PCP) Intoxication</u></b></div>
“<div>· HTN,tachycardia, hyperthermia</div> <div>· Vertical, horizontal, or rotatory nystagmus</div> <div>· Variable pupil size</div> <div>· Combative behavior</div> <div>· Complications: rhabdomyolysis, seizures</div> <div>· BZDs, cooling, IVF, charcoal<br></br><img></img><br></br></div>”
LA toxicity
Neuro:<br></br>- Tinnitus.<br></br>- Numbness of mouth.<br></br>- Confusion, anxiety, sense impending doom, HA, drowsiness, dizziness, tremors.<br></br>-Seizures.<br></br>Cardiac:<br></br>- widening PR interval, QRS, bradycardia, VT, VF, hypoTN, asystole<br></br>- Methemoglobinemia with exposure to benzocaine, prilocaine<br></br>- Hemodynamic collapse.
Rx of LA toxicity
Intralipid (IV fat emulsion): acts as lipid sink, pulling local anesthetics from site of toxicity<br></br>- Give 20% solution 1.5cc/kg bolus then 0.25cc/kg/min over 30-60min.<br></br><br></br>Supportive:<br></br>- Benzos for seizures<br></br>- Methylene blue for methemoglobinemia
Which group of local anesthetics cause most allergic reactions?
Esters, due to production of metabolite, paraaminobenzoic acid (PABA).<br></br>Note that multi-dose bottles of amide contain preservative methylparaben which is chemically related to PABA.
