Timely antidote administration is a critical step in acute poisoning management. Awareness of poisoning patterns and the essential antidotal requirement could improve patient care with better hospital resource allocation. This study investigates the pattern and impact of antidotal administration on patient outcomes in an Egyptian tertiary poison control center, providing insights to optimize the antidote stocking of essential antidotes. A three-year cross-sectional study was conducted at Tanta University Poison Control Center from January 2021 to December 2023. Demographic data, poisoning characteristics, causative agents, and administered antidotal data were retrieved. The initial Poisoning Severity Score (PSS), total hospitalization period, and patient outcomes were also recorded. The included 447 antidote-treated poisoned patients showed near equal gender distribution and median age of 25 years. Atropine, oximes, N-acetylcysteine (NAC), and naloxone were the top administered antidotes among patients (48.3 %, 25.7 %, 19.9 %, and 11.2 %, respectively). Mortality and complications were recorded in 5.15 % and 20.8 %, respectively. Administration of atropine, oximes, NAC, and L-carnitine significantly improved all outcomes (p < 0.05). Although HBO therapy significantly improved mortality, it substantially increased intensive care unit admissions (p < 0.001). Despite folic acid administration significantly improved mortality and complication incidences (p < 0.05), its therapeutic efficiency is still questionable. Availability constraints of the digibind and botulinum antitoxin could affect patient outcomes. Administration of atropine, oximes, NAC, naloxone, and sodium bicarbonate was significantly linked to prolonged hospitalization (p < 0.001). Accordingly, the emergency department in each institution should regularly update the antidotal stock based on a review of the list of essential and commonly used antidotes.

Acute digoxin poisoning is increasingly uncommon in emergency medicine. Furthermore, controversy exists regarding indications for antidotal digoxin immune fab in acute poisoning. In healthy adults, the fab prescribing information recommends administration based on "known consumption of fatal doses of digoxin: ≥10mg," while many emergency medicine textbooks suggest fab administration be driven by clinical features or potassium concentration. A 54 kg adult, not on digoxin, presented one hour after ingesting 12.5 mg. Electrocardiogram revealed only ST depression and first degree heart block. Initial pulse was 102 beats/min, systolic blood pressure was 170 mmHg. The patient was otherwise asymptomatic. Poison center recommended immediately obtaining serum potassium and digoxin concentrations; call-back was planned for two hours. The emergency physician was instructed to have ≥10 fab vials bedside and to administer if instability ensued. Thirty-five minutes later (≈90 min post-ingestion) ventricular fibrillation cardiac arrest occurred; initial serum potassium resulted at this time at 3.3 mEq/L. Bicarbonate, insulin and glucose, amiodarone, magnesium, calcium, and 10 fab vials were administered. Cardioversion resulted in wide-complex tachycardia which became ventricular fibrillation then asystole and the patient died. Serum digoxin concentration drawn on hospital arrival resulted after death at 44 ng/mL. In this fatal case of acute digoxin poisoning, fab was not empirically recommended because the patient initially did not have significant signs or symptoms that accompanied the history of ingesting ≥10 mg digoxin. While the bedside team was given clear anticipatory guidance by the regional poison center, the patient died despite fab administration once instability occurred.

While there has been a decline in the use of digoxin in patients with heart failure and atrial fibrillation, acute and chronic digoxin toxicity remains a significant clinical problem. Digoxin's narrow therapeutic window and nonspecific signs and symptoms of toxicity create clinical challenges and uncertainty around the diagnostic criteria of toxicity and responsive treatment choices for the bedside clinician. A systematic review of published literature on digoxin toxicity (34,587 publications over 6 decades, with 114 meeting inclusion criteria) was performed to develop 33 consensus statements on diagnostic and therapeutic approaches which were then evaluated through a modified Delphi process involving a panel of experts in cardiology, nursing, emergency medicine, and medical toxicology. The results demonstrate agreement about the need to consider time of ingestion and nature of the exposure (ie, acute, acute-on-chronic, chronic) and the use of digoxin immune Fab for life-threatening exposure to decrease risk of death. While several areas of continued uncertainty were identified, this work offers formalized guidance that may help providers better manage this persistent clinical challenge.

Oleander is a prevalent tropical plant used in many parts of India for deliberate self-harm. The active ingredients act in a mechanism similar to cardiac glycosides; hence, the toxicological profile is similar to digoxin toxicity. Cardiac toxicity occurs in the form of a heart block with concomitant ventricular arrhythmia. Identifying the distinct electrocardiographic pattern for early diagnosis and initiating emergency management is imperative. Here, we present two such interesting cases of oleander intoxication, one with Nerium oleander and the other with Thevetia peruviana.

Preeclampsia (PE), the most severe presentation of hypertensive disorders of pregnancy, is the major cause of morbidity and mortality linked to pregnancy, affecting both mother and fetus. Despite advances in prophylaxis and managing PE, delivery of the fetus remains the only causative treatment available. Focus on complex pathophysiology brought the potential for new treatment options, and more conservative options allowing reduction of feto-maternal complications and sequelae are being investigated. Endogenous digitalis-like factors, which have been linked to the pathogenesis of preeclampsia since the mid-1980s, have been shown to play a role in the pathogenesis of various cardiovascular diseases, including congestive heart failure and chronic renal disease. Elevated levels of EDLF have been described in pregnancy complicated by hypertensive disorders and are currently being investigated as a therapeutic target in the context of a possible breakthrough in managing preeclampsia. This review summarizes mechanisms implicating EDLFs in the pathogenesis of preeclampsia and evidence for their potential role in treating this doubly life-threatening disease.

We investigated whether digoxin lowered muscle Na+ ,K+ -ATPase (NKA), impaired muscle performance and exacerbated exercise K+ disturbances. Ten healthy adults ingested digoxin (0.25 mg; DIG) or placebo (CON) for 14 days and performed quadriceps strength and fatiguability, finger flexion (FF, 105%peak-workrate , 3 × 1 min, fourth bout to fatigue) and leg cycling (LC, 10 min at 33% V O 2 peak ${\rm{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ and 67% V O 2 peak ${\rm{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ , 90% V O 2 peak ${\rm{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ to fatigue) trials using a double-blind, crossover, randomised, counter-balanced design. Arterial (a) and antecubital venous (v) blood was sampled (FF, LC) and muscle biopsied (LC, rest, 67% V O 2 peak ${\rm{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ , fatigue, 3 h after exercise). In DIG, in resting muscle, [3 H]-ouabain binding site content (OB-Fab) was unchanged; however, bound-digoxin removal with Digibind revealed total ouabain binding (OB+Fab) increased (8.2%, P = 0.047), indicating 7.6% NKA-digoxin occupancy. Quadriceps muscle strength declined in DIG (-4.3%, P = 0.010) but fatiguability was unchanged. During LC, in DIG (main effects), time to fatigue and [K+ ]a were unchanged, whilst [K+ ]v was lower (P = 0.042) and [K+ ]a-v greater (P = 0.004) than in CON; with exercise (main effects), muscle OB-Fab was increased at 67% V O 2 peak ${\rm{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ (per wet-weight, P = 0.005; per protein P = 0.001) and at fatigue (per protein, P = 0.003), whilst [K+ ]a , [K+ ]v and [K+ ]a-v were each increased at fatigue (P = 0.001). During FF, in DIG (main effects), time to fatigue, [K+ ]a , [K+ ]v and [K+ ]a-v were unchanged; with exercise (main effects), plasma [K+ ]a , [K+ ]v , [K+ ]a-v and muscle K+ efflux were all increased at fatigue (P = 0.001). Thus, muscle strength declined, but functional muscle NKA content was preserved during DIG, despite elevated plasma digoxin and muscle NKA-digoxin occupancy, with K+ disturbances and fatiguability unchanged. KEY POINTS: The Na+ ,K+ -ATPase (NKA) is vital in regulating skeletal muscle extracellular potassium concentration ([K+ ]), excitability and plasma [K+ ] and thereby also in modulating fatigue during intense contractions. NKA is inhibited by digoxin, which in cardiac patients lowers muscle functional NKA content ([3 H]-ouabain binding) and exacerbates K+ disturbances during exercise. In healthy adults, we found that digoxin at clinical levels surprisingly did not reduce functional muscle NKA content, whilst digoxin removal by Digibind antibody revealed an ∼8% increased muscle total NKA content. Accordingly, digoxin did not exacerbate arterial plasma [K+ ] disturbances or worsen fatigue during intense exercise, although quadriceps muscle strength was reduced. Thus, digoxin treatment in healthy participants elevated serum digoxin, but muscle functional NKA content was preserved, whilst K+ disturbances and fatigue with intense exercise were unchanged. This resilience to digoxin NKA inhibition is consistent with the importance of NKA in preserving K+ regulation and muscle function.

We present the case of a 46-year-old male who developed refractory bradycardia with cardiogenic shock after attempting suicide by ingestion of yew leaves. Due to delayed availability of the Digoxin immune fab, a va-ECMO was established to maintain sufficient circulation. Administration of the digoxin fab resulted in recovery of spontaneous circulation. Continuous venovenous hemodiafiltration with hemoadsorption and albumin dialysis were initiated with the intention to remove immune fab-toxin complexes and as organ support in acute kidney and liver failure. Within 5 days the patient was successfully weaned from ECMO, liver support and renal replacement and discharged without physical sequelae.