Should activated charcoal be given after tramadol overdose?

Hamid Khosrojerdi,Reza Afshari,Omid Mehrpour

doi:10.1186/2008-2231-21-46

Abstract

Letter to the editor The efficacy of oral activated charcoal (AC) for the adsorption of drugs and poisons has been widely described in the literature [1]. AC can prevent systemic absorption of drugs if administrated within 1–2 h of ingestion and possibly longer after ingestion of sustained-release preparations or drugs that delay gastric emptying, such as opioids or antimuscarinic drugs. Since routine use of AC is discouraged [1], it is important to consider the risks and benefits of AC on a drug-by-drug basis. This brings us to the question of whether AC should be administrated to patients with tramadol overdose? Balancing the hazards of tramadol poisoning versus the potential risks of charcoal administration is important for answering this question. In general, AC is considered to be a benign type of management, but some risks are associated with its use. Many patients vomit while some aspirate gastric contents into the lungs, causing pneumonitis [2-4]. Significant predictive factors for aspiration pneumonitis after drug overdose include a Glasgow Coma Scale score of <15, emesis, seizure, and ingestion of tricyclic antidepressants [2]. The mortality for patients with aspiration pneumonitis has been reported to be 8.5% compared with 0.4% for those without aspiration pneumonitis, with patients with aspiration pneumonia having a significantly longer hospitalization [2]. In recent years, tramadol poisoning has become one of the most common causes of admissions to emergency departments in Iran [5-11]. Important complications of tramadol poisoning include seizures as well as depression of the central nervous system (CNS) and respiratory system. It has been reported that 15% to 35% of hospital referred patients with tramadol poisoning experience

Highlights

Obesity has reached epidemic proportions and is still escalating at an alarming rate worldwide
Obesity is associated with chronic activation of low-grade inflammation [3], which is implicated in the pathogenesis of obesity-associated diseases including insulin resistance, type-2 diabetes (T2D) [4, 5] and cardiovascular disease [6, 7]
A numerous of studies has been shown that shortchain fatty acids (SCFAs) inhibit inflammation with focus on butyrate and to a lesser extent on acetate and Propionic Acid (PA), [16]

Summary

Introduction

Obesity has reached epidemic proportions and is still escalating at an alarming rate worldwide. In Palestine the prevalence of obesity has been shown to be approximately 4. The etiology of obesity and low-grade inflammation is complex and involves intrinsic and extrinsic factors. The colonization of germ-free mice with microbiota derived from obese mice results in significantly greater adiposity than colonization with microbiota from lean mice [12]. Prebiotic diets such as fructans [13] are associated with general better health, including the decrease in body weight, fat mass and the severity of T2D [14,15,16]. The factors that influence the composition and metabolism of intestinal

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