You are the junior resident working in the Critical Care and Trauma unit of the ED. You think to yourself that it’s a quiet day….then…EMS brings in a patient.
The patient is a 67 year-old woman with history of type 2 diabetes, hypertension, and congestive heart failure, who is brought in by EMS for altered mental status. The patient was acting like her usual self when all of a sudden she developed abdominal cramping and loose stools. Her husband found her slumped over the toilet. She awoke with a headache and asked her husband to call an ambulance.
In the ED the patient appears somnolent and complains of abdominal pain (pointing to epigastrium) and nausea. She denies chest pain and shortness of breath. The paramedic informs you that en route she was vomiting and developed severe bradycardia, which resolved without intervention.
Past surgical history: Cataract surgery two months ago complicated by persistent ptosis
Medications: glipizide, hydralazine, gabapentin, aspirin, pyridostigmine, prednisone, valsartan, carvedilol
Social history: Denies tobacco, alcohol, illicit drugs
Allergies: No food or drug allergies
What is her complete exam? Vitals General: Waxing and waning mental status, mild diaphoresis EKG: Sinus bradycardia; normal axis/intervals. T wave inversions in III, aVF, V1-V6. Minimal ST elevation in V1 and V2. Minimal ST depressions in V5 and V6. You place the patient on a cardiac monitor, elevate the head of the bed, and place transcutaneous pacer pads. Your nurses insert an IV in the right antecubital fossa. Your attending yells out to the nurses to have epinephrine and atropine at bedside. The patient is bradycardic and hypertensive, confused and lethargic, but your attending and the team decide she is stable enough for now. Based on the ECG, bradycardia, and critical nature of the patient’s presentation, you call a STEMI code. Despite atypical lead pattern for a right-sided infarct, you are concerned for an acute occlusion of the right coronary artery causing ischemia of the sinoatrial node. The cardiology team evaluates the patient and ECG; however, they do not believe the patient is having a myocardial infarction. They explain it’s unlikely an MI given the patient is not complaining of chest pain and think the bradycardia may be due to vomiting and a vagal reaction. STEMI code is cancelled. Lab Results Na: 137 mmol/L K: 5.2 mmol/L Cl: 107 mmol/L Co2: 15 mmol/L Bun: 55 mg/dL Cr: 1.94 mg/dL Gluc: 341 mg/dL Ast: 35 U/L Alt: 28 U/L Alk Phos: 42 U/L T.Bili: 0.4 mg/dL T Prot: 6 g/dL Alb: 3.7 g/dL Ca: 9.8 mg/dL Lactate: 1.9 mmol/L VBG: pH: 7.339 pCO2: 31.7mmHg sO2:98% HCO3: 18 mmol/L BE: -8.1 mmol/L Troponin: 0.007 ng/dL Portable chest radiograph (AP): Probable left retrocardiac opacity, cannot exclude infiltrate With the patient initially stabilized, you decide she needs a CT of her head given her AMS, bradycardia, and elevated BP, thinking perhaps there could be an intracranial lesion causing increased ICP that could explain all 3 of these findings. A CT of the abdomen is also ordered, given the severe abdominal cramping and diarrhea. The nurses place the patient on the portable monitor, and you’re about to head out when your attending hands you a box of atropine and epinephrine. You smile to yourself and say, “Clever!” Off to CT you go! You’re just outside of CT now, beep..beep, beep…….beep, weird those beeps are more spaced out now….oh no, the patient starts to retch…beep………………..beep You look at the monitor, HR: 50s…40s…30s…. the patient is becoming even more lethargic… The nurse runs. The attending arrives. You ask, “Is that asystole real?” 30s…40s….60s! Yay, it’s a miracle! The patient responded to atropine, it must have been a sinus pause and not asystole! ”Ok quick. Take her to CT before this happens again. Oh, and take this.” This time he gives you a pre-filled syringe of atropine. You sheepishly say, “Thanks.” For a quick video on how to open the atropine and epinephrine boxes and how to load this medications, watch this video: You make it back from CT. Your senior resident and attending are looking at the images, discussing the case. The heart rate suddenly drops to the 20’s. Yay, you make up for your box blunder! Is this pneumonia? Gastritis? Can these explain bradycardia and asystole as well as her other symptoms? What else is on your differential? Beta-Blocker toxicity? Some sort of head injury without bleeding? Drug use? MI? Cardiogenic shock? Myasthenic crisis? Myxedema coma? Digitalis toxicity? Lyme Disease? Peritoneal irritation causing vagal reaction? You discuss with your attending how to best maintain stabilization of her medical condition. Your attending does not want to take any unnecessary risks. The patient went into sinus pause with intermittent episodes of unstable bradycardia on top of it. She has survived, but your attending tells you next time we might not be so lucky…So it’s time to place a transvenous pacemaker! Your attending walks you through the procedure. You float the pacer in and watch the monitor… After careful maneuvering of the electrode you note capture at 1.8ma! Success! http://lifeinthefastlane.com/ccc/temporary-transvenous-cardiac-pacing/ “OK! Our patient had AMS after a fall this morning. Her initial complaints were abdominal pain and loose stools. En route with EMS, she started vomiting, then developed bradycardia and sinus pauses. She had epigastric pain and nausea with a soft non-tender abdomen. On exam, she has left eye ptosis, miosis, waxing and waning mental status, bradycardia, and mild diaphoresis. The ECG showed diffuse T wave inversions with minimal ST elevations in leads V1 and V2. Upon review of the medications, they include antihypertensives, antihyperglycemics, a steroid, a medication for neuropathic pain …. and an acetylcholinesterase inhibitor! Pyridostigmine-induced cholinergic toxicity! SLUDGE • Salivation Treatment: Atropine, Glycopyrrolate* Atropine IV: Pralidoxime (2PAM) is indicated for organophosphates https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1475922/ ) Glycopyrrolate IV: The patient was admitted to the CCU. She remained bradycardic for a few hours after which her heart rate stabilized in the 60s and 70s. She was asymptomatic. She was eventually discharged home and instructed to discontinue pyridostigmine and follow up with her ophthalmologist for alternative treatment for ptosis. At the time of discharge, it was unclear whether this toxidrome came from an intentional or accidental overdose or an adverse drug reaction from the reduced drug clearance, perhaps from AKI (creatinine was 1.94 mg/dL, with previous level 0.7 mg/dL). Written by Miguel A. Martínez-Romo, MD Special thanks to Adam Blumenberg MD, Ian deSouza MD, Mark Silverberg MD, & Sage Wiener MD Eddleston M. Insecticides: Organic Phosphorus Compounds and Carbamates. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. eds. Goldfrank’s Toxicologic Emergencies, 10e New York, NY: McGraw-Hill; 2015. Howland M. Antidotes in Depth. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. eds. Goldfrank’s Toxicologic Emergencies, 10e New York, NY: McGraw-Hill; 2015. Agency for Toxic Substances and Disease Registry (ATSDR), “Nerve Agents,” 2011. Available at http://www.atsdr.cdc.gov/MHMI/mmg166.pdf Roberts DM and Aaron CK, “Management of Acute Organophosphorus Pesticide Poisoning,” BMJ, 2007, 334(7594):629-34. [PubMed 17379909] Eddleston M, Dawson A, Karalliedde L, et al. Early management after self-poisoning with an organophosphorus or carbamate pesticide – a treatment protocol for junior doctors. Crit Care. 2004b;8(6):R391-R397. [PubMed 15566582] Reigart JR and Roberts JR, “Recognition and Management of Pesticide Poisonings,” U.S. Environmental Protection Agency, Washington, D.C., 5th edition, 1999: 34-47.
T: 96.9ºF P: 48/min BP: 223/67 mm Hg RR: 15/min SpO2: 99% Fingerstick: 295 mg/dL
HEENT: Left eye ptosis, pupils 2mm and reactive bilaterally, EOMI
CVS: Bradycardic, no murmurs, no JVD
Chest: CTAB, no w/r/r
Abd: obese, soft, non-distended, non-tender, normoactive bowel sounds
Ext: moves all equally, no peripheral edema, no rashes
WBC: 14.35 K/uL Hb: 9.9 g/dL Hct: 30.7% Plt: 276 K/uL
You reach for that box of atropine! But wait, in your clumsy nervousness you can’t open the darn box! Ahhhh! You tell the nurse, “Get the attending!”
He grabs the box of atropine from your hand, opens it up (successfully), and gives atropine through the IV. (He pushed 0.5mg of atropine, or 5ml of a 0.1mg/ml concentration.)
Abd/Pelvis CT: Questionable mildly inflamed loop of distal ileum; correlate with symptoms of nonspecific enteritis.
You inject it through the IV and her heart rate is now in the 60’s.
We later find out that the patient’s ophthalmologist prescribed for the left eye ptosis that developed after the cataract surgery.
• Lacrimation
• Urinary incontinence
• Defecation
• GI pain
• Emesis
DUMBELLS, Killer B’s
• Defecation
• Urination
• Muscle weakness, Miosis
• Bradycardia, Bronchorrhea, Bronchospasm (Killer B’s). The Killer Bees are dangerous muscarinic effects of the cholinergic toxidrome.
• Emesis
• Lacrimation
• Salvation
Nicotinic effects of cholinergics: fasciculations, weakness, and paralysis.
Bradycardia:0.5 mg every 3-5 minutes
Organophosphate or carbamate poisoning : Start at 1 mg and repeat every 3-5 minutes, doubling the dose each time if the previous dose did not achieve atropinization (the end point is clear lungs). Maintain atropinization by repeating doses as needed for >2 to 12 hours based on recurrence of symptoms.
(Note: 2PAM is an oxime that would treat the nicotinic effects of cholinergics. If the patient is having muscle weakness, particularly to the muscles of respiration, consider using 2PAM even with carbamates [such as pyridostigmine]. Also note that the use of oximes in cholinergic poisoning is controversial. For more on the controversy see:
Bradycardia, vagal reflexes: IV 0.1mg as a single dose, repeat every 2-3 minutes as needed
Reversal of muscarinic effects of cholinergic agents: IV 0.2 mg for each 1 mg of neostigmine or 5 mg of pyridostigmine
*Glycopyrrolate wouldn’t be used for most cholinergic poisonings, since it doesn’t cross the blood-brain barrier (BBB). However, pyridostigmine also does not cross the BBB, so glycopyrrolate may be used to counteract the adverse effects of pyridostigmine .
** There is no clear data on the dosing of glycopyrrolate for overdosing vs simple adverse drug events
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