Answer: D

Despite the number of patients who come in taking Digoxin, it is important to remember that this medication comes with a large range of side effects. Bradycardia (along with any of the other SLUDGE Toxidrome symptoms) is a common effect due to the Parasympathetic activity of Digoxin. (Note: This is also the reason it works as a second-line agent for rate control of Atrial Fibrillation.) Yellow, halo-like vision changes (think Van Gogh’s ‘Starry Night’) are a more rare, but classic finding. The “scooped” ST segment is also a classic finding, commonly seen on ECGs – I recommend looking this up if you are not familiar with the appearance of this finding. Gynecomastia is an idiopathic and rare side effect of Digoxin. Finally, Hyperkalemia (Not Hypokalemia) occurs due to Digoxin’s primary effect on the Na-K ATPase Pump, blocking Na from leaving and K from entering the cell. It is also important to know that Hypokalemia can increase Digoxin’s toxicity by enhancing its binding to the Na-K ATPase Pump.

References:

Kanji S, MacLean RD. Cardiac glycoside toxicity: more than 200 years and counting. Crit Care Clin. 2012 Oct; 28(4):527-35.

Smith TW. Digitalis. Mechanisms of action and clinical use. N Engl J Med. 1988 Feb 11; 318(6):358-65.

Answer: E

Succimer is the agent of choice for asymptomatic, mild Lead poisoning (45-70 mcg/dL in children, 70-100 mcg/dL in adults) because it is available PO and has a low side effect profile. Penicillamine is used predominately for the treatment of Wilson’s Disease (Copper chelation) and is no longer used in Lead toxicity due to its significant side effect profile. For severe toxicity with signs of encephalopathy, Dimercaprol (previously known as BAL; British Anti-Lewisite) is given IM followed by Calcium EDTA via continuous infusion to combine to chelate Lead from the brain and body, respectively.

Dosages are as follows:
Succimer: 10 mg/kg PO Q 8H x 5 days, followed by 10 mg/kg Q 12H for 14 days
Dimercaprol: 4 mg/kg IM Q 4H x 5 days
Calcium EDTA: 1500 mg/m2 IV Q 24H via continuous infusion x 5 days (started 4 hours after Dimercaprol)

References:

Gracia RC, Snodgrass WR. Lead toxicity and chelation therapy. Am J Health Syst Pharm. 2007 Jan 1; 64(1):45-53.

Mann KV, Travers JD. Succimer, an oral lead chelator. Clin Pharm. 1991 Dec; 10(12):914-22.

Patrick L. Lead toxicity, a review of the literature. Part 1: Exposure, evaluation, and treatment. Altern Med Rev. 2006 Mar; 11(1):2-22.

Answer: C.

Methemoglobinemia causes cyanosis due to the oxidation of the Iron molecule in Hemoglobin, thereby reducing its Oxygen carrying capacity. Boric Acid (commonly found in a variety of products, but classically, pesticides) is well-known to cause a “boiled lobster” skin rash. Carbon Monoxide causes normal appearing or pink-colored skin due to its ability to increase Hemoglobin’s affinity for Oxygen, resulting in hyper-Oxygenated red blood cells. Hypercarotinemia, classically seen among anorexic and bulimic teenagers replacing high calorie foods with low calorie carrots, results in excessive beta-carotene, a yellow-pigmented vitamin which mimics jaundice. Note: Hypercarotinemia, as opposed to hyperbilirubinemia, does not result in scleral icterus. Niacin (occasionally used to increase HDL in hypercholesterolemia) is well-known to cause prostaglandin-mediated flushing, which may be mitigated by pre-treating with Aspirin before each dose.

References:

Wright RO et al. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med. 1999 Nov;34(5):646-56.

Schillinger BM et al. Boric Acid Poisoning. J Am Acad Dermatol. 1982 Nov;7(5):667-73.

Piantadosi CA. Carbon monoxide poisoning. N Engl J Med. 2002 Oct 3;347(14):1054-5.

Mazzone A, Dal Canton A. Image in clinical medicine. Hypercarotenemia. N Engl J Med. 2002 Mar 14;346(11):821.

Hochholzer W. The facts behind niacin. Ther Adv Cardiovasc Dis. 2011 Oct;5(5):227-40.

Answer: B.

Ciguatoxin (found on warm-water, bottom-dwelling fish – including barracudas, sea bass, red snappers, grouper, and sturgeons, among others) binds to sodium channels and increases sodium channel permeability. This results in a variety of symptoms, such as diaphoresis, bradycardia, hypotension, abdominal pain, nausea, vomiting, diarrhea, metallic taste, myalgias, arthralgias, weakness, headache, ataxia, vertigo, sensation of loose and painful teeth, reversal of temperature sensation, peripheral and peri-oral paresthesias, and visual disturbances.

Flushing is a classic symptom of Scombroid toxicity. Recall that Scombroid poisoning is caused by Histamine-producing bacteria on the surface of improperly stored dark, tropical fish (e.g. tuna, mackerel, mahi-mahi, etc.). Symptoms include headache, abdominal pain, nausea, vomiting, diarrhea, peri-oral and peripheral paresthesias, dizziness, palpitations, and diffuse flushing of the skin.

References:

Lawrence DT et al. Food Poisoning. Emerg Med Clin North Am. 2007 May;25(2):357-73

Isbister GK and Kiernan MC. Neurotoxic marine poisoning. Lancet Neurol. 2005 Apr;4(4):219-28.

Answer: D.

The Rumack-Matthew Normogram is a graph of “possible” and “probably” hepatic toxicity for ingestions ranging from 4-24 hours before measurement. It has been validated in multiple patient populations and is NOT valid for chronic ingestions or ingestions outside of the above time range. The APAP level should be checked between 4 and 24 hours post-ingestion (consistent with the range of the normogram), ideally within 4-8 hours of ingestion. Levels checked within 4 hours of ingestion are unreliable and will need to be rechecked at the 4-hour mark. Studies have shown that NAC is most effective when given within 8 hours of ingestion. If an APAP level will not be available at that time, NAC should be empirically started and can be stopped if the APAP level returns below the treatment threshold. Finally, Activated Charcoal may be used for acute ingestions within one hour (if the patient is not vomiting and protecting their airway), but should not be used beyond this time period.

References:

Rumack BH, Matthew H. Acetaminophen poisoning and toxicity. Pediatrics. 1975 Jun;55(6):871-6.

Prescott LF, Illingworth RN, Critchley JA, et al. Intravenous N-acetylcysteine: the treatment of choice for paracetamol poisoning. BMJ. 1979 Nov 3;2(6198):1097-100.

Yeates PJ, Thomas SH. Effectiveness of delayed activated charcoal administration in simulated paracetamol (acetaminophen) overdose. Br J Clin Pharmacol. 2000 Jan;49(1):11-4.

Answer: B.

Ethylene Glycol toxicity is caused by the eventual conversion to Oxalic Acid, which causes renal toxicity. Methanol toxicity is caused by the eventual conversion to Formic Acid, which causes both renal and ocular toxicity. Fomepizole is an alcohol dehydrogenase inhibitor, which blocks the initial conversion of Ethylene Glycol to Glycoaldehyde and Methanol to Formaldehyde, thus decreasing the precursors to Oxalic and Formic Acid. Thiamine and Pyridoxine should both be given as 100 mg IV Q6H in suspected Ethylene Glycol poisoning. Thiamine is a cofactor involved in converting Glycolic Acid (a precursor to Oxalic Acid) to the non-toxic molecule, alpha-hydroxy-beta-ketoadipate. Pyridoxine is a cofactor involved in converting Glycolic Acid to the non-toxic molecule, Glycine. Folic Acid should be given as 1-2 mg/kg (up to 50 mg) IV Q6H in suspected Methanol poisoning. Folic Acid is a cofactor involved in converting the toxic Formic Acid to CO2 and H2O. Hydroxocobalamin is a treatment for Cyanide toxicity and has no role in toxic alcohol poisoning.

References:

Sivilotti ML, Burns MJ, McMartin KE, et al. Toxicokinetics of ethylene glycol during fomepizole therapy: implications for management. For the Methylpyrazole for Toxic Alcohols Study Group. Ann Emerg Med. 2000 Aug;36(2):114-25.

Brent J. Fomepizole for ethylene glycol and methanol poisoning. N Engl J Med. 2009 May 21;360(21):2216-23.

Lheureux P, Penaloza A, Gris M. Pyridoxine in clinical toxicology: a review. Eur J Emerg Med. 2005 Apr;12(2):78-85.