Case Presentation: 82-year-old female with atrial fibrillation, non-ischemic cardiomyopathy (EF 25%), rheumatoid arthritis, bed bound at home with hospice care presents for acute encephalopathy and tachycardia. Patient’s son (the primary caregiver) reported that patient is on four drops of oral 1% atropine solution daily for bronchorrhea. Accidentally a family member who is not a primary caretaker administered four mL (equivalent to forty mg) of atropine. After approximately five hours patient was disoriented, agitated and eventually obtunded. At baseline her mental status is alert and oriented to name, place, and time. In the Emergency Department, patient’s initial vitals were blood pressure 85/50 mmHg, heart rate 130 beats per minute, respiratory rate 12 breaths per minute, temperature 96.6F, and oxygen saturation of 99% on 4 liters of oxygen via nasal cannula. Physical exam was significant for dry skin, dry mucous membranes, somnolent, non-verbal, pupils were 8 mm, symmetric, minimally reactive to light, decreased bowel sounds and mild bilateral upper extremity myoclonus. She was immediately started on parenteral hydration via intravenous normal saline bolus. Toxicology and Medical Intensive Care Unit were consulted immediately. Labs significant for elevated serum creatinine 1.24 mg/dL, lactate of 2.6 mmol/L, high sensitivity troponin of 119 ng/L, and mild hyperkalemia of 5.5 mmol/L when compared to her baseline values from one month ago. Her EKG showed sinus tachycardia without evidence of ischemic changes. She was given one milligram of physostigmine IV push every ten minutes. With every physostigmine push the interdisciplinary team evaluated for improvement in mental status and resolving tachycardia. She had regained mental status after a total of ten milligrams of intravenous physostigmine and heart rate decreased to nineties. Patient was admitted to telemetry unit.

Discussion: Atropine is a competitive antagonist of muscarinic cholinergic receptors. This medication classically produces an anticholinergic toxidrome which consists of tachycardia, hyperthermia, altered mental status, dry mucous membranes, ileus and urinary retention. Treatment for anticholinergic toxicity is primarily supportive in nature but physostigmine can be given as an antidote. This is not commonly given as it does not have long lasting effects with duration of action of only forty-five to sixty minutes. However, physostigmine was given in this case because of evidence of type II MI with elevated troponin. In addition, the patient was at risk for a major cardiac event given antimuscarinic driven persistent tachycardia in setting of non-ischemic cardiomyopathy and poor ejection fraction. The recommended dosing for physostigmine is IM/IV 0.5 milligram to 2 milligram every 10 to 30 minutes until response occurs. Post antidotal treatment, patients need further telemetry monitoring for physostigmine toxicity which includes cholinergic symptoms such as bradycardia, hypersalivation, bronchospasm etc.

Conclusions: Anticholinergic agents such as atropine are most commonly utilized in hospice patients with excess bronchorrhea, but the toxicity profile itself can lead to patient demise and distress. Therefore, health care providers prescribing medications associated with life threatening overdose toxicity should educate patients and their families about the related toxidromes. They should also instruct families to present to the Emergency Department if the symptoms associated with toxidrome occurs.