Vital signs, including blood pressure, heart rate, respiratory rate, temperature, and oxygen saturation, should be obtained to aid in this initial assessment. Īn assessment utilizing the ABCDE (airway, breathing, circulation, disability, exposure) approach should be performed upon initial presentation to assess the severity of intoxication/overdose quickly. Furthermore, severe symptoms, characterized as delirium/psychosis, seizures, coma, and death, manifested at doses of 1 gram or more. One retrospective study observed that moderate symptoms, characterized as agitation, confusion, hallucinations, and ECG disturbances, occurred at doses of 0.3 grams. Studies have shown that diphenhydramine toxicity is dose-dependent. The drug undergoes metabolism to much smaller degrees in the pulmonary and renal system and is, thus, minimally removed by hemodialysis. Most of the diphenhydramine that is hepatically metabolized undergoes N-demethylation via CYP2D6, with minor demethylation occurring via CYP1A2, CYP2C9, AND CYP2C19. It is extensively metabolized by the liver via cytochrome P450 enzymes. For adult patients, the Vd is approximately 17 L/kg (range: 13 to 20 L/kg) and approximately 14 L/kg (range: 7 to 20 L/kg) for elderly patients. For pediatric patients, the Vd is approximately 22 L/kg (range: 15 to 28 L/kg). Diphenhydramine is lipophilic and has a relatively large volume of distribution (Vd). For adult patients, the elimination half-life is approximately 9 hours (range: 7 to 12 hours) and approximately 13.5 hours (range: 9 to 18 hours) for elderly patients (range: 9 to 18 hours). For pediatric patients, the elimination half-life is approximately 5 hours (range: 4 to 7 hours). The elimination half-life of diphenhydramine can vary between age groups. Peak serum levels of diphenhydramine are reached approximately 2 to 3 hours after oral administration. As a result, individuals are at increased risk of developing potentially fatal arrhythmias, such as torsade de pointes.ĭiphenhydramine pharmacokinetics do not appear to change in the event of intoxication/overdose. This leads to the prolongation of the QT interval and a flattening of the T-wave. These channels are responsible for the rapid component of the cardiac repolarizing current. More specifically, diphenhydramine can affect the delayed rectifier potassium ion channels of the heart as it can act as a blocker of potassium channels. ECG changes can be observed, which include the widening of the QRS-complex and tachycardia, possibly caused by the anticholinergic effects of diphenhydramine. Diphenhydramine can also have negative cardiovascular consequences in the setting of toxicity.
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