Skip to main content

Gastrointestinal decontamination in the acutely poisoned patient

Abstract

Objective

To define the role of gastrointestinal (GI) decontamination of the poisoned patient.

Data Sources

A computer-based PubMed/MEDLINE search of the literature on GI decontamination in the poisoned patient with cross referencing of sources.

Study Selection and Data Extraction

Clinical, animal and in vitro studies were reviewed for clinical relevance to GI decontamination of the poisoned patient.

Data Synthesis

The literature suggests that previously, widely used, aggressive approaches including the use of ipecac syrup, gastric lavage, and cathartics are now rarely recommended. Whole bowel irrigation is still often recommended for slow-release drugs, metals, and patients who "pack" or "stuff" foreign bodies filled with drugs of abuse, but with little quality data to support it. Activated charcoal (AC), single or multiple doses, was also a previous mainstay of GI decontamination, but the utility of AC is now recognized to be limited and more time dependent than previously practiced. These recommendations have resulted in several treatment guidelines that are mostly based on retrospective analysis, animal studies or small case series, and rarely based on randomized clinical trials.

Conclusions

The current literature supports limited use of GI decontamination of the poisoned patient.

Introduction

In the United States, the American Association of Poison Control Centers (AAPCC) reported about 2.4 million poisoning exposures a year in 2006, while the Institute of Medicine in 2001 estimated more than 4 million poisoning episodes with 300,000 hospitalizations and 24,173 poisoning-related deaths [1–3]. This article will review the current recommendations, guidelines and data on gastrointestinal (GI) decontamination in the poisoned patient.

Gastrointestinal decontamination of the poisoned patient has evolved significantly over the last 2 1/2 decades from a very invasive to a less aggressive approach. This less aggressive approach to GI decontamination followed a series of position statements published jointly by the American Academy of Clinical Toxicology (AACT) and the European Association of Poison Centres and Clinical Toxicologists (EAPCCT) in the late 1990s into the early 2000s [4–9]. Despite the publication of these guidelines and several outstanding reviews [10–12], data suggest that few clinicians have read the guidelines and many have poor knowledge about the use of GI decontamination [13]. In addition, uniform advice on this topic has not been demonstrated from poison information centers [14].

Criteria for selection and assessment of literature

An extensive PubMed/MEDLINE search for gastrointestinal decontamination, activated charcoal (AC), multiple dose activated charcoal (MDAC), ipecac, ipecac syrup, gastric emptying (GE), gastric lavage (GL), whole bowel irrigation (WBI), body packers, body stuffers and poisoning treatments was done from about 1980 to present. Specific drugs including acetaminophen, anticonvulsants, N-acetylcysteine, theophylline, salicylic acid/aspirin, digoxin, yellow oleander and isoniazid were searched for relevant studies related to AC and poisoning. Human clinical trials with randomized GI decontamination treatments and outcome data were given the highest priority in the review.

Gastrointestinal decontamination/ipecac

In the late 1970s and early 1980s, the use of ipecac syrup to induce vomiting after oral poisoning was widespread both at home and in the hospital [15]. Earlier work had suggested it was safer than the parenterally dosed apomorphine [16]. Ipecac contains alkaloids from the plants cephalis acuminata and cephalis ipecacuanha. The active compounds of these plants include emetine and cepheline, which cause emesis by local gastric irritation and stimulation of the chemotrigger zone of the brain. The most common side effects from ipecac include multiple episodes of vomiting persisting longer than 60 min, aspiration pneumonia, bronchospasm, Mallory-Weiss tears of the esophagus, bradycardia and barotrauma to the mediastinum.

In a simulated overdose study of acetaminophen, ten healthy subjects ingested 3 g of acetaminophen followed by no intervention, ipecac or 50 g AC-sorbitol solution at 1 h with acetaminophen levels being repeatedly drawn [17]. Both treatments significantly (P ≤ 0.05) reduced serum acetaminophen levels compared to control, but no differences between ipecac or AC treatments were seen. Using a simulated salicylate model, 12 adult volunteers took 24 81-mg aspirin tablets and were randomly treated as controls or with ipecac, AC plus magnesium sulfate or ipecac plus AC plus magnesium sulfate [18]. Total urinary salicylate excretion found 96.3% ± 7.5% of the salicylate in the control, 70.3% ± 11.8% after ipecac and 56.4%± 12% after AC plus magnesium sulfate. Only eight of ten patients who received ipecac plus AC plus magnesium sulfate were able to retain the AC, making analysis of this group impossible. The use of AC alone significantly reduced the recovered salicylate compared to both control (P < 0.01) and ipecac groups (P < 0.01), while ipecac treatment significantly reduced (P < 0.01) recovered salicylate levels compared to control [18].

In a series of four randomized trials, GE with ipecac for alert patients or GL for obtunded patients was followed by AC and compared to AC alone [19–22]. No improvement in outcomes was seen when GE approaches plus AC treated patients were compared to AC treatment alone. Three out of four of the studies reported higher complication rates with GE procedures, with aspiration pneumonia being the most predominant [19–21]. Aspiration pneumonia was more common after combined GE and AC treatment than with AC alone [20, 21]. An unblinded trial of children less than 6 years old who presented with mild to moderate acute oral ingestions were randomized to ipecac followed by AC versus AC alone [23]. There was no significant difference in clinical outcomes reported in the 70 patients randomized, but it took significantly longer to receive the AC when ipecac was given (2.6± 0.1 h vs. 0.9± 0.1 h, P < 0.05). As a result, those receiving ipecac spent significantly longer time in the emergency department (ED) (4.1± 0.2 h vs. 3.4± 0.2 h, P < 0.05). Home use of ipecac also has failed to reduce ED use or to improve outcomes in a cohort comparison [24].

The combined position statement of the AACT and EAPCCT concluded that there was no evidence from clinical studies that ipecac improves the outcome of poisoned patients and its routine administration in the ED should be abandoned [4]. This was followed by a guideline released by the AAPCC that suggested ipecac should only be used at home if there would be a delay of 1 h or more before a patient could get to an ED and then only if it could be administered within 30-90 min after the ingestion [25]. The American Academy of Pediatrics recommended removing all ipecac from the home setting and that ipecac should not be used routinely as a home treatment for pediatric poisonings [26]. A dramatic reduction in the use of ipecac in the poisoned patient has resulted. In 1985, 14.99% (132,947) of human poison exposures reported to the AAPCC received ipecac, but by 2009 only 0.02% (658) received ipecac [27].

Gastrointestinal decontamination/gastric lavage

The use of GL for patients with oral poisons who were obtunded or with altered mental status was a standard approach until the 1990s. Matthew et al. [28] in 1966 noted that data from as early as 1942 had questioned the efficacy of GL, but after studying 259 patients who had ingested a poison, he concluded that when GL was performed within 4 h after ingestion, significant recovery of barbiturates in the lavage fluid could still be demonstrated.

As noted before, various GE procedures were studied in acute poisoning cases in the five previously mentioned studies that also included ipecac treatment arms [19–23]. Specifically, GL used for obtunded patients in three of the trials [19, 21, 22] was compared to AC treatment alone. Two of the studies found no significant improvement in clinical outcome with GL compared to AC [21, 22]. One study [19] noted that obtunded, poisoned patients who had GL plus AC within 1 h of ingestion had significantly (P < 0.05) less deterioration compared to AC treatment alone. The use of GL plus AC was associated with a significantly (P = 0.0001) increased incidence of aspiration pneumonia in one study compared to AC alone in symptomatic patients (8.5% vs. 0.0%) [21]. In a review of four studies that evaluated GL versus AC in acetaminophen overdoses, no strong evidence was found for the routine use of GL [29].

A study of volunteers who had a 34-French orogastric tube placed after acetaminophen ingestion reported that GL within 1 h resulted in a significant reduction in acetaminophen bioavailability [30]. Another study of patients who presented within 4 h of acetaminophen ingestion were randomized to no intervention, GL, AC or treatment with ipecac [31]. A significant reduction in serum acetaminophen levels was seen with ipecac, GL or AC treatments compared to no treatment [31]. Use of AC within 4 h of ingestions resulted in the greatest decrease in acetaminophen levels, greater than those seen with both the GL (P = 0.013) and the ipecac syrup treatment groups (P = 0.027). Despite those acetaminophen serum reductions, no clinical outcome differences between the groups were reported [31]. A review of two small trials of volunteers with simulated aspirin/non-steroidal anti-inflammatory drug overdoses found no advantage to GL over AC alone [32].

In a study of patients with tricyclic antidepressant overdoses, treatment was randomized to AC, saline GL followed by AC or AC followed by saline GL followed by AC [33]. All three approaches had similar clinical outcomes with no advantage to GL. A systematic review of controlled trials of GL in acute organophosphorus pesticide poisoning found no "high-quality" evidence to support the use of GL in treating these poisonings [34].

One theoretical concern with the use of GL is the potential of flushing drugs out of the stomach into the small intestines. A systematic review of this topic failed to find published data that supported this concern [35]. The major complications with GL include perforation of the esophagus and stomach, pulmonary aspiration and aspiration pneumonia. In an observational study of 14 consecutive GLs performed in four hospitals in Sri Lanka, Eddleston et al. observed five aspirations and two major cardiac events during the procedure [36]. A recent study from India of 98 pesticide-poisoned patients found aspiration pneumonia in 2.2-13.2% of the patients depending on whether the lavage occurred in the academic or referral hospital [37]. A drop in arterial saturations was seen in 13.3%, and laryngospasm, tachycardia, electrolyte imbalance or tube stuck in throat was each at 2.2% [37]. Although these may be higher complication rates than expected in modern health care facilities, it draws a warning about the potential risk of GL [36].

Significant limitations exist in calculating the power needed to show treatment differences in clinical trials related to GE and the treatment of actual poisoned patients. Patients take different combinations of drugs, different amounts, at different times and have different co-morbidities, which all confound the potential ability of a treatment like GE from altering the clinical course. These limitations must be considered when interpreting the results of treatments like GE in studies using actual poisoned patients.

In a review, Bond [38] notes that GL with AC should be considered for symptomatic patients who present within 1 h, who have ingested agents that slow gastrointestinal motility, who have ingested sustained-release medication or who have ingested massive/life-threatening amounts of a medication. This recommendation is in contrast to the 1997 AACT/EPCCT guidelines, which state that GL should not be used for routine poisonings, as there is no certainty that it improves clinical outcomes. Further, the guidelines suggest GL should only be considered in a potentially life-threatening ingestion and then only if it can be undertaken within 60 min of ingestion [5]. Of the over 2.4 million AAPCC reported poisonings in 2009, only 6,093 (0.25%) of the total patients and only 238 (0.02%) of those patients ≤ 5 years of age underwent GL [27].

Gastrointestinal decontamination/cathartics

Non-absorbable sugars such as sorbitol and salts including magnesium citrate and sodium sulfate have been used as adjuncts to AC to hasten the elimination of the poison-charcoal complex. One experimental trial reported reduced systemic absorption of aspirin, but not pentobarbital, chlorpheniramine or chloroquine when AC was given with sodium sulfate [39]. Activated charcoal alone or in combination with sodium sulfate were thought to be effective, and both approaches reduced the absorption of drugs compared to sodium sulfate alone [39]. Using healthy volunteers in a simulation of an aspirin overdose, AC was more effective than water alone in reducing salicylate absorption as measured by the area under the concentration curve (AUC) (428.24± 218.64 μg/ml·h vs. 846.54± 292.95 μg/ml·h, P < 0.01) [40]. Activated charcoal with sodium sulfate had no added effect in reducing aspirin absorption and did not significantly reduce the AUC compared to water alone (618.61± 324.71 μg/ml·h vs. 846.54± 292.95 μg/ml·h, NS) [40]. The authors concluded that adding sodium sulfate to AC did not improve the efficacy of AC.

A survey of EDs in 1991 found that the combination product of AC plus sorbitol was frequently the only AC product stocked in EDs [41]. Even when it was not the only available preparation, 49% of EDs reported giving repeat doses of AC and sorbitol routinely when the MDAC approach was used [42]. Cathartic use is associated with diarrhea, and when multiple doses of cathartics are given, significant free water loss and dehydration can occur. Three cases of severe hypernatremia were reported with magnesium citrate cathartic use in the management of overdoses [43].

The 1997 AACT/EAPCCT position statement notes that cathartics alone have no role in the management of the poisoned patient [6]. Further, the routine use of a cathartic in combination with AC was not endorsed [6]. The 2009 AAPCC report found that 22,034 (0.89%) of calls regarding poisoned patients were treated with cathartics, and most were used with AC [27].

Gastrointestinal decontamination/whole bowel irrigation (WBI)

Many substances are not fully bound by AC. These include slow-release medications, electrolytes and metals. In an attempt to reduce GI drug transit time, polyethylene glycol (PEG) electrolyte solution with rates of 0.5 to 2.0 l/h have been given to poisoned patients to reduce transit time of the toxic material, to get the poison beyond the GI areas of drug absorption and eventually to be eliminated. The goal of WBI is to remove the substance from the GI tract prior to it being absorbed.

Both simulated overdose or nontoxic exposure studies and clinical overdose cases have questioned the efficacy of WBI particularly in combination with MDAC [41, 44–47]. In vitro data have demonstrated adsorption of PEG by AC, which in turn reduced the adsorption of salicylic acid by AC [48]. These investigators questioned the use of AC and WBI together in treating overdoses [48]. No randomized controlled trials have been reported evaluating the efficacy of WBI.

Using enteric-coated aspirin, ten adult volunteers received AC combined with sorbitol, water alone (control) or WBI. Both WBI and the AC with sorbitol significantly (P < 0.001) reduced absorption as determined by the salicylic acid AUC. Whole bowel irrigation demonstrated the greatest reduction in salicylic acid AUC compared to AC (P < 0.05) and was associated with fewer adverse effects [49]. In another study, nine healthy patients received sustained-release preparations of carbamazepine, theophylline and verapamil followed 1 h later by AC, AC with WBI or water (control) [50]. Activated charcoal reduced the absorption as measured by the serum AUC by 62%-75% for all three drugs compared to control, but the addition of WBI to the AC actually significantly (P < 0.01) reduced the efficacy of the AC with carbamazepine (AC, 62% reduction in AUC vs. WBI/AC, 41% reduction in AUC). Similarly, the AUC for theophylline with WBI/AC resulted in less reduction in AUC compared to AC alone (65% vs. 75% reduction in AUC, P < 0.001) [50]. In contrast the combination of WBI/AC resulted in a greater reduction of verapamil absorption (85% reduction in AUC) compared to AC alone (63% reduction in AUC, P < 0.001) [50]. A study of anesthetized dogs given sustained-release theophylline and treated with either AC, WBI followed by AC or AC followed by WBI failed to demonstrate further reductions in theophylline absorption when WBI was added to the treatment [51].

The most common complication with WBI is pulmonary aspiration. Contraindications for its use include compromised airway, hemodynamic instability, seizures, and the lack of bowel sounds or a suspected or documented bowel obstruction [52].

Though many of the simulated poison studies have not demonstrated a benefit of WBI with or without AC, several case reports note improved outcomes using WBI for unusual exposures including slow-release medications such as theophylline, mercuric oxide, lead, strontium ferrite, potassium capsules and even lead bullets [53–58]. These case reports obviously lack controls or even historic controls, drawing into question whether improved outcomes were really demonstrated.

The 1997 AACT/EAPCCT position statement recommended that WBI not be used routinely in the management of the poisoned patient. Based only on volunteer studies and without randomized clinical studies, the paper recommends that WBI be considered for potentially toxic ingestions of sustained-release or enteric-coated drugs. Because of the lack of data, WBI remains a "theoretical" option for iron, lead or zinc poisonings, or for packets of illicit drugs [59]. A follow-up position paper in 2004 concluded "no new evidence" existed that would require a revision of the previous statement on WBI [60]. It would appear that WBI has a very limited role in the treatment of the poisoned patient. Only 2,108 (0.09%) of total patients and 130 (0.01%) of those patients ≤ 5 years old received WBI out of the more than 2.4 million total poisoned patients reported in 2009 to the AAPCC [27].

Gastrointestinal decontamination/special consideration/body packers/body stuffers

Body packers or "mules" are people who smuggle illicit drugs (mostly cocaine or opium/heroin) concealed in the mouth, rectum, vagina, ear, foreskin or gastrointestinal tract. The drugs are often packaged in capsules, condoms, balloons or plastic bags. Drugs in most of the anatomical body cavities or orifices can be manually removed except when they have been ingested. Once in the GI tract, decontamination or removal can be challenging, and perforations of the drug container can be fatal. A variation of the concept of the body packer is the "body stuffer" who ingests drugs in aluminum foil or plastic bags often hastily to avoid police seizure of the drug/evidence. A further variation of "body stuffing" is "parachuting" in which the illicit drug (often methamphetamine or cocaine) is swallowed in a plastic baggie that has been punctured multiple times to allow a slow-release of the drug [61]. Adults are usually involved in cases of body packing/stuffing, but disturbing reports of pediatric body packers have surfaced [62].

A recent review of approaches to GI decontamination in these patients noted no randomized clinical trials exist, leaving only case studies and series available to guide our approach [63]. One European series from Paris and Frankfurt included approximately 4,660 body packers. The vast majority of the body packers were asymptomatic. About 1.4% of the body packers (n = 64) had life-threatening symptoms of cocaine overdose after rupture or leakage of a container. Forty-four of these body packers died before surgical intervention to remove the packets could be performed, while 20 underwent emergency laparotomy for the removal of the containers and all of these patients survived [64]. Urgent surgery is routinely recommended for symptomatic patients with obstruction, bowel perforation or evidence of drug packet rupture [63–66].

Although surgery has been considered definitive in these cases, a report noted two cases where, despite careful surgical inspection and palpation of the entire GI tract, additional drug packets were identified after surgery by CT scans [67]. Plain abdominal radiographs are reported to have sensitivity for finding drug packets of between 85-90% [68–70]. Contrast-enhanced abdominal radiography has been reported to increase sensitivity to 96% [68, 71]. Although no large studies have been done with abdominal CT scanning, its use has been widely reported with CT window manipulation, identifying packets that would not have been seen on routine windows [68, 72]. Unfortunately, at least two cases of drug packets missed by CT scanning have been reported [67, 73].

With little data, conservative non-surgical measures are routinely used in the majority of patients who are asymptomatic. These approaches include endoscopy for packets thought to be retained in the stomach, light solid diets, oral fluids, AC and most commonly WBI to clear the GI tract of the drug packets [68]. Oil-based laxatives have been recommended in the past, but are now discouraged because of their potential effect on latex products used to package some drugs [68, 74]. The packets can often be collected after sorting through stool in a way that preserves them as evidence [61, 75–77]. Although not formally tested, the value of a systematic surgical protocol for treating body packers that defines conservative therapy, monitoring approaches, as well as when to use surgery has been emphasized [78, 79].

Sodium polystyrene sulfonate

The use of sodium polystyrene sulfonate (SPS) has been recommended in the treatment of lithium overdoses to prevent further absorption and potentially increase lithium elimination [80]. The use of SPS for the treatment of hyperkalemia has been clinically widespread since its approval by the FDA in 1958. Recently, the efficacy and safety of SPS for hyperkalemia have been questioned [81].

In vitro binding of lithium to SPS has been demonstrated [82]. Mice studies have shown significant reduction in lithium levels after oral lithium is followed by SPS. These reductions have been shown after multiple doses of SPS and with delays up to 90 min after the oral dosing of lithium, while treatment with AC has shown no effect [83–86]. Human subjects exposed to 900 mg lithium were treated 30 min later with 0, 20 or 40 g of SPS. Reduced absorption and increased clearance of lithium were demonstrated with SPS [87]. Two additional human volunteer studies have confirmed reduced lithium serum AUC, lower peak levels and delayed time to peak lithium levels when SPS is given after oral lithium [88, 89]. A retrospective cohort study of patients with lithium toxicity treated with oral SPS suggested more than a 50% reduction in lithium serum half-life. No clinical outcome improvement was reported. Constipation and mild hypokalemia were noted as side effects of treatment in this study [90].

Hypokalemia is an expected complication of the use of SPS for lithium overdose, but more troubling are reports suggesting GI necrosis in uremic patients treated with SPS [91, 92]. The use of sorbitol to prevent fecal impaction and to increase GI motility as an osmotic cathartic with the SPS powder or as a pre-mixed product has been suggested to be related to the development of GI necrosis [81]. Cases of calcium polystyrene sulfonate without sorbitol-associated GI necrosis exist and bring into question the importance of sorbitol to the mechanism [93, 94]. The incidence of this severe side effect is not currently known, and to date no cases of GI necrosis have been reported as a result of using SPS for the treatment of lithium-overdosed patients.

Gastrointestinal decontamination/activated charcoal

A dramatic early demonstration of AC occurred when Tovery, before the 1831 French Academy, took a lethal dose of strychnine mixed with charcoal. He suffered no ill effects [10, 95, 96]. Activated charcoal is a highly adsorbent material produced by grinding carbon material into a fine powder, superheating the carbon source to very high temperatures, followed by injecting or "activating" the charcoal with steam to maximize the surface area. By the 1980s, AC was generally recognized as a major treatment for most orally poisoned patients [95].

In addition to preventing drug absorption, AC can disrupt drug recycling in an enterohepatic loop and results in "drug back diffusion" out of the body into the GI tract. This "gut dialysis," where drugs move from systemic body compartments to the GI tract, explains how drugs given intravenously can have increased elimination with oral AC. Many trials have documented increased clearance with oral AC in both human and animal models after intravenous (IV) phenobarbital, phenytoin, digoxin, acetaminophen and theophylline (Table 1). These proposed AC mechanisms go beyond traditional GI decontamination and actually invoke a process that increases elimination. Multiple human and animal studies have suggested that MDAC is potentially an important treatment approach for many toxins including some IV poisonings, slow release compounds, pill bezoars or massive poisonings. In the early 2000s, some review articles were still supportive of the use of AC and MDAC (usually without GE), but others began to question this practice [38, 97]. Table 1 offers in-depth examples of the type of data on AC and MDAC focusing on aspirin, acetaminophen, N-acetylcysteine, anticonvulsants, yellow oleander, isoniazid and theophylline as examples. This table gives the reader details on the extent and limitations of the clinical and animal data supporting the use of AC. A meta-analysis that included 64 controlled trials using AC in a variety of drug exposures in healthy volunteers found that AC was most effective when given within 1 h of the ingestion, but significant reductions in drug levels could still be seen even if given as long as 4 h after drug intake [98].

Table 1 Studies and reports evaluating the effects of activated charcoal on selected drugs

Reduction in drug absorption also was significantly correlated with the AC/drug ratio (P = 0.02). Significant reductions in drug absorption at an AC to drug ratio of 10:1 were demonstrated, and little further reduction beyond the 100:1 ratio could be found. It was noted that drugs with a large volume of distributions demonstrated greater reductions in absorption with AC [98]. In vitro and in vivo studies have suggested that an AC to drug ratio of at least 10:1 for aspirin and acetaminophen should be obtained to insure maximal efficacy [99]. This recommendation on the AC to drug ratio is consistent with the findings of the above meta-analysis and has been generalized to all drugs with little additional clinical evidence [99].

Trials in actual poisoned patients with single dose AC or MDAC have shown mixed results. A randomized trial of ten patients who overdosed on phenobarbital reported a profound reduction in serum phenobarbital half-life, but no change in time on mechanical ventilation or the time in the hospital between those receiving a single dose of AC or MDAC [100]. In contrast, 12 patients with confirmed carbamazepine poisonings were randomized to receive MDAC or a single dose of AC [101]. Though peak carbamazepine levels were similar, the duration of coma was significantly decreased (P = 0.02) as were the hours on mechanical ventilation (P = 0.001) and the length of hospital stay (P = 0.00001) with MDAC. The serum half-life of carbamazepine was also significantly (P = 0.004) reduced by more than 50% with MDAC compared to a single dose of AC.

Merigian and Blaho [102] reported a prospective, randomized, controlled trial of AC compared to control (no treatment) after oral drug overdoses in patients who were able to take oral AC. Specific exposures were excluded, including ingestions of > 140 mg/kg acetaminophen, crack cocaine, mushrooms, volatiles, caustics, heavy metals, lithium and iron [102]. No GE was performed. Almost 1,500 patients were entered into the study and no difference in outcome parameters was seen between the two groups. In contrast, de Silva [103], randomized 401 patients who had ingested yellow oleander to MDAC or a single dose of AC. There were fewer deaths (2.5% vs. 8%, P = 0.025) for those treated with MDAC compared to a single dose of AC in this study. In a larger randomized trial that included 4,629 overdosed patients, Eddleston reported that there were no differences in mortality between control, single-dose AC and MDAC treatment in patients overdosed on various toxins (51% pesticides and 36% yellow oleander) [104]. A randomized trial of AC compared to control in 327 patients presenting with oral overdoses reported no significant reduction in hospital length stay or other patient outcomes with AC [105].

Compliance has been variable with AC even when ordered. In the previously mentioned large randomized controlled trials of control, AC and MDAC [104], a single dose of AC was only given 83% of the time, and only 66% of five doses of MDAC were actually given [106]. The major reasons for not receiving the AC doses were patient refusal and active vomiting. A descriptive study in pediatric poisonings found only 55% of children were given AC within 1 h of presentation to ED, and only 7.8% actually got their AC within 1 h of their poisoning because of delays in arriving to and delays within the ED [107]. Karim et al. [108] found that the median time to arrival after overdose was 136 min, and only 15 out of 63 patients received AC within 1 h of poisoning. A study in rural Australia reported the time from ingestion to ambulance arrival averaged 1 h 23 min, and the time to hospital averaged 2 h and 15 min [109]. They concluded that poisonings with long transport times would have to get AC in the ambulance if they were to have any chance of receiving AC within 1 h.

Many metals and electrolytes do not bind to AC, such as iron, lead, potassium and lithium [110]. The lack of significant binding of these agents to AC eliminates its potential usefulness in treating potassium, lithium, iron, lead and other heavy metal exposures.

Although AC is generally well tolerated, a number of complications have been reported with its use (Table 2). Many of these complications have been reported as case reports, and some are associated with MDAC, often as a result of the cathartic in the combined product. In a study of 575 poisoned patients treated with AC, adverse events occurred in 41 cases (7.1%) with nausea/vomiting found in 36, bronchoaspiration in 6 and pneumonia in 2 [111]. Spontaneous vomiting before AC, pre-hospital AC administration, repeated doses of AC and the need for specific clinical measures to treat intoxicated patients (e.g., intubation) were all associated with a significantly increased risk for an adverse event. A retrospective study in which 878 poisoned patients were treated with MDAC found that 5 (0.6%, 95% CI 0.1-1.1%) patients had clinically significant aspiration and none had GI obstruction [112]. No patients died. Mild hypernatremia (> 145 mEq/l) was seen in 53 patients (6.0%, 95% CI, 4.4-7.6%), with 5 of these patients having sodium levels greater than 155 meg/l. Hypermagnesemia (> 2.5 mg/dl) was seen in 27 patients (3.1%, 95% CI, 2.0-4.2%), and 3 patients had peak values greater than 3.75 mg/dl. These electrolyte abnormalities were usually associated with cathartic use, but not exclusively. One patient had a corneal abrasion that resolved without complication and was associated with AC getting into their eyes [112].

Table 2 Complications and Adverse Reactions to Activated Charcoal

In evaluating 50 intubated patients with evidence of new pulmonary infiltrates on chest X-ray within the first 48 h of hospitalization after AC treatment, only 2 (4%) had initial negative radiographs and then developed a new infiltrate after AC. This suggests an infrequent association of AC to aspiration pneumonia [113]. Severe cases of pulmonary aspiration of AC resulting in prolonged respiratory failure, death, empyema and bronchiolitis obliterans have been reported, but these are isolated case reports [114–117].

The risk factors for emesis after AC in poisoned patients were found to be prior vomiting before AC and the use of a nasogastric tube for AC administration. In a study of 275 children, 56 (20.4%) had vomiting after administration of AC [118]. Case reports of charcoal bezoars or inspissated charcoal being associated with small bowel obstruction exist after treatment with AC, but these events are also likely rare [119–122]. Acute appendicitis, charcoal stercolith associated with intestinal perforation and charcoal peritoneum has all been reported with AC treatment [123–126].

The last major practical issue in the decision to use charcoal for decontamination of a poisoned patient revolves around time of ingestion. The AACT/EAPCCT 1997 guidelines recommend that single dose AC should not be routinely administered to poisoned patients and suggest its effectiveness decreases with time after ingestion [7]. If charcoal is to be administered, the greatest benefit is seen within 1 h after ingestion of poison. There is no convincing clinical evidence that AC improves clinical outcome [7]. These 1997 recommendations were reaffirmed in 2005 with the observation that "no new evidence" was found to suggest a revision in the guidelines was needed [8]. When considering MDAC, the position paper from AACT/EAPCCT suggests that MDAC should only be considered in patients with protected or intact airways. MDAC should not be used with repeat doses of cathartics, and it should only be considered if a patient has ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine or theophylline [9]. In 1995, 7.7% of all poisoned patients and 3.56% of all those patients ≤ 5 years old recorded by the AAPCC were treated with AC, but by 2009 the percentage had decreased to 3.4% of all poisoned patients and only 1.48% of patients ≤ 5 years old [27].

Conclusion

Gastrointestinal decontamination with ipecac, GL, AC and cathartics are now used less often in the hospital setting in the poisoned patient. Whole bowel irrigation for the ingestion of slow-release medications and asymptomatic foreign body drug containers (body packers/stuffers) is recommended with little quality clinical data. Current recommendations for the use of AC and MDAC are limited in the treatment of the poisoned patient. The use of AC appears to be most efficacious when given within an hour of ingestion. The use of SPS as a binder of lithium is based on limited data. The current recommendations for GI decontamination of the poisoned patient are based on a few clinical trials, small case series, retrospective analysis and animal data. The previous aggressive approach to GI decontamination is increasingly being replaced by less emphasis on active GI decontamination and more emphasis on supportive care.

Abbreviations

AACT:

American Academy of Clinical Toxicology

AC:

activated charcoal

AUC:

area under the concentration curve

EAPCCT:

European Association of Poison Centres and Clinical Toxicologists

ED:

emergency department

GE:

gastric emptying

GI:

gastrointestinal

GL:

gastric lavage

MDAC:

multiple dose activated charcoal

NS:

not statistically significant

PEG:

polyethylene glycol

SPS:

sodium polystyrene

WBI:

whole bowel irrigation.

References

  1. Frithsen IL, Simpson WM Jr: Recognition and management of acute medication poisoning. Am Fam Physician 2010, 81: 316–323.

    PubMed  Google Scholar 

  2. Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE: 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol (Phila) 2007, 45: 815–917. 10.1080/15563650701754763

    Article  Google Scholar 

  3. Prevention IoMCoP, Control: Forging a poison prevention and control system. National Academies Press; 2004.

    Google Scholar 

  4. Position Statement: Ipecac Syrup Clinical Toxicology 1997, 35: 699–709.

  5. Position Statement: Gastric Lavage Clinical Toxicology 1997, 35: 711–719.

  6. Barceloux D, McGuigan M, Hartigan-Go K: Position statement: cathartics. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997, 35: 743–752.

    Article  CAS  PubMed  Google Scholar 

  7. Chyka PA, Seger D: Position statement: single-dose activated charcoal. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997, 35: 721–741.

    Article  CAS  PubMed  Google Scholar 

  8. Chyka PA, Seger D, Krenzelok EP, Vale JA: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005, 43: 61–87.

    Article  CAS  Google Scholar 

  9. Position Statement and Practice Guidelines on the Use of Multi-Dose Activated Charcoal in the Treatment of Acute Poisoning Clinical Toxicology 1999, 37: 731–751.

  10. Olson KR: Activated charcoal for acute poisoning: one toxicologist's journey. J Med Toxicol 2010, 6: 190–198. 10.1007/s13181-010-0046-1

    Article  PubMed Central  PubMed  Google Scholar 

  11. Bailey B: To Decontaminate or Not to Decontaminate? The Balance Between Potential Risks and Foreseeable Benefits. Clinical Pediatric Emergency Medicine 2008, 9: 17–23. 10.1016/j.cpem.2007.11.001

    Article  Google Scholar 

  12. Smith SW: Drugs and pharmaceuticals: management of intoxication and antidotes. EXS 2010, 100: 397–460.

    CAS  PubMed  Google Scholar 

  13. Wood DM, Greene SL, Jones AL, Dargan PI: Gut decontamination of acutely poisoned patients: what do doctors really know about it? Emerg Med J 2007, 24: 774–775. 10.1136/emj.2007.049544

    Article  PubMed Central  PubMed  Google Scholar 

  14. Juurlink DN, Szalai JP, McGuigan MA: Discrepant advice from poison centres and their medical directors. Can J Clin Pharmacol 2002, 9: 101–105.

    PubMed  Google Scholar 

  15. King WD: Syrup of ipecac: a drug review. Clin Toxicol 1980, 17: 353–358. 10.3109/15563658008989984

    Article  CAS  PubMed  Google Scholar 

  16. MacLean WC Jr: A comparison of ipecac syrup and apomorphine in the immediate treatment of ingestion of poisons. J Pediatr 1973, 82: 121–124. 10.1016/S0022-3476(73)80029-0

    Article  PubMed  Google Scholar 

  17. McNamara RM, Aaron CK, Gemborys M, Davidheiser S: Efficacy of charcoal cathartic versus ipecac in reducing serum acetaminophen in a simulated overdose. Ann Emerg Med 1989, 18: 934–938. 10.1016/S0196-0644(89)80456-1

    Article  CAS  PubMed  Google Scholar 

  18. Curtis RA, Barone J, Giacona N: Efficacy of ipecac and activated charcoal/cathartic. Prevention of salicylate absorption in a simulated overdose. Arch Intern Med 1984, 144: 48–52. 10.1001/archinte.144.1.48

    Article  CAS  PubMed  Google Scholar 

  19. Kulig K, Bar-Or D, Cantrill SV, Rosen P, Rumack BH: Management of acutely poisoned patients without gastric emptying. Ann Emerg Med 1985, 14: 562–567. 10.1016/S0196-0644(85)80780-0

    Article  CAS  PubMed  Google Scholar 

  20. Albertson TE, Derlet RW, Foulke GE, Minguillon MC, Tharratt SR: Superiority of activated charcoal alone compared with ipecac and activated charcoal in the treatment of acute toxic ingestions. Ann Emerg Med 1989, 18: 56–59. 10.1016/S0196-0644(89)80314-2

    Article  CAS  PubMed  Google Scholar 

  21. Merigian KS, Woodard M, Hedges JR, Roberts JR, Stuebing R, Rashkin MC: Prospective evaluation of gastric emptying in the self-poisoned patient. Am J Emerg Med 1990, 8: 479–483. 10.1016/0735-6757(90)90146-Q

    Article  CAS  PubMed  Google Scholar 

  22. Pond SM, Lewis-Driver DJ, Williams GM, Green AC, Stevenson NW: Gastric emptying in acute overdose: a prospective randomised controlled trial. Med J Aust 1995, 163: 345–349.

    CAS  PubMed  Google Scholar 

  23. Kornberg AE, Dolgin J: Pediatric ingestions: charcoal alone versus ipecac and charcoal. Ann Emerg Med 1991, 20: 648–651. 10.1016/S0196-0644(05)82385-6

    Article  CAS  PubMed  Google Scholar 

  24. Bond GR: Home syrup of ipecac use does not reduce emergency department use or improve outcome. Pediatrics 2003, 112: 1061–1064. 10.1542/peds.112.5.1061

    Article  CAS  PubMed  Google Scholar 

  25. Manoguerra AS, Cobaugh DJ, Panel TMotGftMoPC: Guideline on the Use of Ipecac Syrup in the Out-of-Hospital Management of Ingested Poisons*. Clinical Toxicology 2005, 43: 1–10.

    Article  PubMed  Google Scholar 

  26. Poison treatment in the home. American Academy of Pediatrics Committee on Injury, Violence, and Poison Prevention Pediatrics 2003, 112: 1182–1185.

  27. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Giffin SL: 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 27th Annual Report. Clin Toxicol (Phila) 2010, 48: 979–1178. 10.3109/15563650.2010.543906

    Article  Google Scholar 

  28. Matthew H, Mackintosh TF, Tompsett SL, Cameron JC: Gastric aspiration and lavage in acute poisoning. Br Med J 1966, 1: 1333–1337. 10.1136/bmj.1.5499.1333

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  29. Teece S, Hogg K: Best evidence topic reports. Gastric lavage in paracetamol poisoning. Emerg Med J 2004, 21: 75–76. 10.1136/emj.2003.011890

    Article  PubMed Central  PubMed  Google Scholar 

  30. Grierson R, Green R, Sitar DS, Tenenbein M: Gastric lavage for liquid poisons. Ann Emerg Med 2000, 35: 435–439.

    Article  CAS  PubMed  Google Scholar 

  31. Underhill TJ, Greene MK, Dove AF: A comparison of the efficacy of gastric lavage, ipecacuanha and activated charcoal in the emergency management of paracetamol overdose. Arch Emerg Med 1990, 7: 148–154.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  32. Teece S, Crawford I: Best evidence topic report. Gastric lavage in aspirin and non-steroidal anti-inflammatory drug overdose. Emerg Med J 2004, 21: 591–592. 10.1136/emj.2004.017988

    Article  PubMed Central  PubMed  Google Scholar 

  33. Bosse GM, Barefoot JA, Pfeifer MP, Rodgers GC: Comparison of three methods of gut decontamination in tricyclic antidepressant overdose. J Emerg Med 1995, 13: 203–209. 10.1016/0736-4679(94)00153-7

    Article  CAS  PubMed  Google Scholar 

  34. Li Y, Tse ML, Gawarammana I, Buckley N, Eddleston M: Systematic review of controlled clinical trials of gastric lavage in acute organophosphorus pesticide poisoning. Clin Toxicol (Phila) 2009, 47: 179–192. 10.1080/15563650701846262

    Article  CAS  Google Scholar 

  35. Eddleston M, Juszczak E, Buckley N: Does gastric lavage really push poisons beyond the pylorus? A systematic review of the evidence. Ann Emerg Med 2003, 42: 359–364. 10.1016/S0196-0644(03)00440-2

    Article  PubMed  Google Scholar 

  36. Eddleston M, Haggalla S, Reginald K, Sudarshan K, Senthilkumaran M, Karalliedde L, Ariaratnam A, Sheriff MH, Warrell DA, Buckley NA: The hazards of gastric lavage for intentional self-poisoning in a resource poor location. Clin Toxicol (Phila) 2007, 45: 136–143. 10.1080/15563650601006009

    Article  Google Scholar 

  37. Bhardwaj UB, Subramaniyan A, Bhalla A, Sharma N, Singh S: Safety of gastric lavage using nasogastric ryle's tube inpesticide poisoning. Health (London) 2011, 3: 401–405.

    CAS  Google Scholar 

  38. Bond GR: The role of activated charcoal and gastric emptying in gastrointestinal decontamination: a state-of-the-art review. Ann Emerg Med 2002, 39: 273–286. 10.1067/mem.2002.122058

    Article  PubMed  Google Scholar 

  39. Chin L, Picchioni AL, Gillespie T: Saline cathartics and saline cathartics plus activated charcoal as antidotal treatments. Clin Toxicol 1981, 18: 865–871. 10.3109/15563658108990311

    Article  CAS  PubMed  Google Scholar 

  40. Sketris IS, Mowry JB, Czajka PA, Anderson WH, Stafford DT: Saline catharsis: effect on aspirin bioavailability in combination with activated charcoal. J Clin Pharmacol 1982, 22: 59–64.

    Article  CAS  PubMed  Google Scholar 

  41. Olsen KM, Ma FH, Ackerman BH, Stull RE: Low-volume whole bowel irrigation and salicylate absorption: a comparison with ipecac-charcoal. Pharmacotherapy 1993, 13: 229–232.

    CAS  PubMed  Google Scholar 

  42. Wax PM, Wang RY, Hoffman RS, Mercurio M, Howland MA, Goldfrank LR: Prevalence of sorbitol in multiple-dose activated charcoal regimens in emergency departments. Ann Emerg Med 1993, 22: 1807–1812. 10.1016/S0196-0644(05)80406-8

    Article  CAS  PubMed  Google Scholar 

  43. Caldwell JW, Nava AJ, de Haas DD: Hypernatremia associated with cathartics in overdose management. West J Med 1987, 147: 593–596.

    PubMed Central  CAS  PubMed  Google Scholar 

  44. Mayer AL, Sitar DS, Tenenbein M: Multiple-dose charcoal and whole-bowel irrigation do not increase clearance of absorbed salicylate. Arch Intern Med 1992, 152: 393–396. 10.1001/archinte.152.2.393

    Article  CAS  PubMed  Google Scholar 

  45. Lurie Y, Bentur Y, Levy Y, Baum E, Krivoy N: Limited efficacy of gastrointestinal decontamination in severe slow-release carbamazepine overdose. Ann Pharmacother 2007, 41: 1539–1543. 10.1345/aph.1K162

    Article  CAS  PubMed  Google Scholar 

  46. Hoffman RS, Chiang WK, Howland MA, Weisman RS, Goldfrank LR: Theophylline desorption from activated charcoal caused by whole bowel irrigation solution. J Toxicol Clin Toxicol 1991, 29: 191–201. 10.3109/15563659109038611

    Article  CAS  PubMed  Google Scholar 

  47. Graudins A, Peden G, Dowsett RP: Massive overdose with controlled-release carbamazepine resulting in delayed peak serum concentrations and life-threatening toxicity. Emerg Med (Fremantle) 2002, 14: 89–94. 10.1046/j.1442-2026.2002.00290.x

    Article  Google Scholar 

  48. Kirshenbaum LA, Sitar DS, Tenenbein M: Interaction between whole-bowel irrigation solution and activated charcoal: implications for the treatment of toxic ingestions. Ann Emerg Med 1990, 19: 1129–1132. 10.1016/S0196-0644(05)81516-1

    Article  CAS  PubMed  Google Scholar 

  49. Kirshenbaum LA, Mathews SC, Sitar DS, Tenenbein M: Whole-bowel irrigation versus activated charcoal in sorbitol for the ingestion of modified-release pharmaceuticals. Clin Pharmacol Ther 1989, 46: 264–271. 10.1038/clpt.1989.137

    Article  CAS  PubMed  Google Scholar 

  50. Lapatto-Reiniluoto O, Kivisto KT, Neuvonen PJ: Activated charcoal alone and followed by whole-bowel irrigation in preventing the absorption of sustained-release drugs. Clin Pharmacol Ther 2001, 70: 255–260. 10.1067/mcp.2001.118184

    Article  CAS  PubMed  Google Scholar 

  51. Burkhart KK, Wuerz RC, Donovan JW: Whole-bowel irrigation as adjunctive treatment for sustained-release theophylline overdose. Ann Emerg Med 1992, 21: 1316–1320. 10.1016/S0196-0644(05)81894-3

    Article  CAS  PubMed  Google Scholar 

  52. Bryant SM, Naples J: Morbidity associated with whole bowel irrigation. Pediatr Emerg Care 2007, 23: 846.

    Article  PubMed  Google Scholar 

  53. Ly BT, Williams SR, Clark RF: Mercuric oxide poisoning treated with whole-bowel irrigation and chelation therapy. Ann Emerg Med 2002, 39: 312–315. 10.1067/mem.2002.119508

    Article  PubMed  Google Scholar 

  54. Janss GJ: Acute theophylline overdose treated with whole bowel irrigation. S D J Med 1990, 43: 7–8.

    CAS  PubMed  Google Scholar 

  55. Roberge RJ, Martin TG: Whole bowel irrigation in an acute oral lead intoxication. Am J Emerg Med 1992, 10: 577–583.

    Article  CAS  PubMed  Google Scholar 

  56. Kirrane BM, Nelson LS, Hoffman RS: Massive strontium ferrite ingestion without acute toxicity. Basic Clin Pharmacol Toxicol 2006, 99: 358–359. 10.1111/j.1742-7843.2006.pto_566.x

    Article  CAS  PubMed  Google Scholar 

  57. Hojer J, Forsberg S: Successful whole bowel irrigation in self-poisoning with potassium capsules. Clin Toxicol (Phila) 2008, 46: 1102–1103. 10.1080/15563650802415165

    Article  Google Scholar 

  58. Schwarz KA, Alsop JA: Pediatric ingestion of seven lead bullets successfully treated with outpatient whole bowel irrigation. Clinical Toxicology 2008, 46: 919–919.

    Article  PubMed  Google Scholar 

  59. Tenenbein M: Position statement: whole bowel irrigation. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 1997, 35: 753–762.

    Article  CAS  PubMed  Google Scholar 

  60. Position Paper: Whole Bowel Irrigation # Clinical Toxicology 2004, 42: 843–854.

  61. Hendrickson RG, Horowitz BZ, Norton RL, Notenboom H: "Parachuting" meth: a novel delivery method for methamphetamine and delayed-onset toxicity from "body stuffing". Clin Toxicol (Phila) 2006, 44: 379–382. 10.1080/15563650600671746

    Article  CAS  Google Scholar 

  62. Traub SJ, Kohn GL, Hoffman RS, Nelson LS: Pediatric "body packing". Arch Pediatr Adolesc Med 2003, 157: 174–177.

    Article  PubMed  Google Scholar 

  63. Booker RJ, Smith JE, Rodger MP: Packers, pushers and stuffers--managing patients with concealed drugs in UK emergency departments: a clinical and medicolegal review. Emerg Med J 2009, 26: 316–320. 10.1136/emj.2008.057695

    Article  CAS  PubMed  Google Scholar 

  64. Schaper A, Hofmann R, Bargain P, Desel H, Ebbecke M, Langer C: Surgical treatment in cocaine body packers and body pushers. Int J Colorectal Dis 2007, 22: 1531–1535. 10.1007/s00384-007-0324-9

    Article  PubMed  Google Scholar 

  65. Schaper A, Hofmann R, Ebbecke M, Desel H, Langer C: [Cocaine-body-packing. Infrequent indication for laparotomy]. Chirurg 2003, 74: 626–631. 10.1007/s00104-002-0603-5

    Article  CAS  PubMed  Google Scholar 

  66. A Case Report of Opium Body Packer; Review of the Treatment Protocols and Mechanisms of Poisoning Toxicology Mechanisms and Methods 2007, 17: 205–214. 10.1080/15376510600992574

  67. Olmedo R, Nelson L, Chu J, Hoffman RS: Is surgical decontamination definitive treatment of "body-packers"? Am J Emerg Med 2001, 19: 593–596. 10.1053/ajem.2001.21720

    Article  CAS  PubMed  Google Scholar 

  68. Traub SJ, Hoffman RS, Nelson LS: Body packing--the internal concealment of illicit drugs. N Engl J Med 2003, 349: 2519–2526. 10.1056/NEJMra022719

    Article  CAS  PubMed  Google Scholar 

  69. Hergan K, Kofler K, Oser W: Drug smuggling by body packing: what radiologists should know about it. Eur Radiol 2004, 14: 736–742. 10.1007/s00330-003-2091-5

    Article  PubMed  Google Scholar 

  70. Beerman R, Nunez D Jr, Wetli CV: Radiographic evaluation of the cocaine smuggler. Gastrointest Radiol 1986, 11: 351–354. 10.1007/BF02035108

    Article  CAS  PubMed  Google Scholar 

  71. Marc B, Baud FJ, Aelion MJ, Gherardi R, Diamant-Berger O, Blery M, Bismuth C: The cocaine body-packer syndrome: evaluation of a method of contrast study of the bowel. J Forensic Sci 1990, 35: 345–355.

    Article  CAS  PubMed  Google Scholar 

  72. Sengupta A, Page P: Window manipulation in diagnosis of body packing using computed tomography. Emerg Radiol 2008, 15: 203–205. 10.1007/s10140-007-0652-7

    Article  PubMed  Google Scholar 

  73. Hahn IH, Hoffman RS, Nelson LS: Contrast CT scan fails to detect the last heroin packet. J Emerg Med 2004, 27: 279–283. 10.1016/j.jemermed.2004.04.012

    Article  PubMed  Google Scholar 

  74. White N, Taylor K, Lyszkowski A, Tullett J, Morris C: Dangers of lubricants used with condoms. Nature 1988, 335: 19.

    Article  CAS  PubMed  Google Scholar 

  75. Aldrighetti L, Paganelli M, Giacomelli M, Villa G, Ferla G: Conservative management of cocaine-packet ingestion: experience in Milan, the main Italian smuggling center of South American cocaine. Panminerva Med 1996, 38: 111–116.

    CAS  PubMed  Google Scholar 

  76. Beckley I, Ansari NA, Khwaja HA, Mohsen Y: Clinical management of cocaine body packers: the Hillingdon experience. Can J Surg 2009, 52: 417–421.

    PubMed Central  PubMed  Google Scholar 

  77. Hoffman RS, Smilkstein MJ, Goldfrank LR: Whole bowel irrigation and the cocaine body-packer: a new approach to a common problem. Am J Emerg Med 1990, 8: 523–527.

    Article  CAS  PubMed  Google Scholar 

  78. Veyrie N, Servajean S, Aissat A, Corigliano N, Angelakov C, Bouillot JL: Value of a systematic operative protocol for cocaine body packers. World J Surg 2008, 32: 1432–1437. 10.1007/s00268-007-9432-5

    Article  PubMed  Google Scholar 

  79. Mandava N, Chang RS, Wang JH, Bertocchi M, Yrad J, Allamaneni S, Aboian E, Lall MH, Mariano R, Richards N: Establishment of a definitive protocol for the diagnosis and management of body packers (drug mules). Emerg Med J 2011, 28: 98–101. 10.1136/emj.2008.059717

    Article  PubMed  Google Scholar 

  80. Roberge RJ, Martin TG, Schneider SM: Use of sodium polystyrene sulfonate in a lithium overdose. Ann Emerg Med 1993, 22: 1911–1915. 10.1016/S0196-0644(05)80422-6

    Article  CAS  PubMed  Google Scholar 

  81. Sterns RH, Rojas M, Bernstein P, Chennupati S: Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective? J Am Soc Nephrol 2010, 21: 733–735. 10.1681/ASN.2010010079

    Article  CAS  PubMed  Google Scholar 

  82. Watling SM, Gehrke JC, Gehrke CW, Zumwalt R, Pribble J: In vitro binding of lithium using the cation exchange resin sodium polystyrene sulfonate. Am J Emerg Med 1995, 13: 294–296. 10.1016/0735-6757(95)90202-3

    Article  CAS  PubMed  Google Scholar 

  83. Linakis JG, Hull KM, Lacouture PG, Lockhart GR, Lewander WJ, Maher TJ: Enhancement of lithium elimination by multiple-dose sodium polystyrene sulfonate. Acad Emerg Med 1997, 4: 175–178. 10.1111/j.1553-2712.1997.tb03736.x

    Article  CAS  PubMed  Google Scholar 

  84. Linakis JG, Hull KM, Lee CM, Maher TJ, Lewander WJ, Lacouture PG: Effect of delayed treatment with sodium polystyrene sulfonate on serum lithium concentrations in mice. Acad Emerg Med 1995, 2: 681–685. 10.1111/j.1553-2712.1995.tb03618.x

    Article  CAS  PubMed  Google Scholar 

  85. Linakis JG, Lacouture PG, Eisenberg MS, Maher TJ, Lewander WJ, Driscoll JL, Woolf AD: Administration of activated charcoal or sodium polystyrene sulfonate (Kayexalate) as gastric decontamination for lithium intoxication: an animal model. Pharmacol Toxicol 1989, 65: 387–389. 10.1111/j.1600-0773.1989.tb01194.x

    Article  CAS  PubMed  Google Scholar 

  86. Linakis JG, Eisenberg MS, Lacouture PG, Maher TJ, Lewander WJ, Driscoll JL, Woolf A: Multiple-dose sodium polystyrene sulfonate in lithium intoxication: an animal model. Pharmacol Toxicol 1992, 70: 38–40. 10.1111/j.1600-0773.1992.tb00422.x

    Article  CAS  PubMed  Google Scholar 

  87. Gehrke JC, Watling SM, Gehrke CW, Zumwalt R: In-vivo binding of lithium using the cation exchange resin sodium polystyrene sulfonate. Am J Emerg Med 1996, 14: 37–38. 10.1016/S0735-6757(96)90010-8

    Article  CAS  PubMed  Google Scholar 

  88. Belanger DR, Tierney MG, Dickinson G: Effect of sodium polystyrene sulfonate on lithium bioavailability. Ann Emerg Med 1992, 21: 1312–1315. 10.1016/S0196-0644(05)81893-1

    Article  CAS  PubMed  Google Scholar 

  89. Tomaszewski C, Musso C, Pearson JR, Kulig K, Marx JA: Lithium absorption prevented by sodium polystyrene sulfonate in volunteers. Ann Emerg Med 1992, 21: 1308–1311. 10.1016/S0196-0644(05)81892-X

    Article  CAS  PubMed  Google Scholar 

  90. Ghannoum M, Lavergne V, Yue CS, Ayoub P, Perreault MM, Roy L: Successful treatment of lithium toxicity with sodium polystyrene sulfonate: a retrospective cohort study. Clin Toxicol (Phila) 2010, 48: 34–41. 10.3109/15563650903344785

    Article  CAS  Google Scholar 

  91. Rashid A, Hamilton SR: Necrosis of the gastrointestinal tract in uremic patients as a result of sodium polystyrene sulfonate (Kayexalate) in sorbitol: an underrecognized condition. Am J Surg Pathol 1997, 21: 60–69. 10.1097/00000478-199701000-00007

    Article  CAS  PubMed  Google Scholar 

  92. McGowan CE, Saha S, Chu G, Resnick MB, Moss SF: Intestinal necrosis due to sodium polystyrene sulfonate (Kayexalate) in sorbitol. South Med J 2009, 102: 493–497. 10.1097/SMJ.0b013e31819e8978

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  93. Joo M, Bae WK, Kim NH, Han SR: Colonic mucosal necrosis following administration of calcium polystryrene sulfonate (Kalimate) in a uremic patient. J Korean Med Sci 2009, 24: 1207–1211. 10.3346/jkms.2009.24.6.1207

    Article  PubMed Central  PubMed  Google Scholar 

  94. Goutorbe P, Montcriol A, Lacroix G, Bordes J, Meaudre E, Souraud JB: Intestinal Necrosis Associated with Orally Administered Calcium Polystyrene Sulfonate Without Sorbitol (February). Ann Pharmacother 2011.

    Google Scholar 

  95. Derlet RW, Albertson TE: Activated charcoal--past, present and future. West J Med 1986, 145: 493–496.

    PubMed Central  CAS  PubMed  Google Scholar 

  96. Greene S, Harris C, Singer J: Gastrointestinal decontamination of the poisoned patient. Pediatr Emerg Care 2008, 24: 176–186. quiz 187–179 10.1097/PEC.0b013e318166a092

    Article  PubMed  Google Scholar 

  97. Burns MM: Activated charcoal as the sole intervention for treatment after childhood poisoning. Curr Opin Pediatr 2000, 12: 166–171. 10.1097/00008480-200004000-00015

    Article  CAS  PubMed  Google Scholar 

  98. Jurgens G, Hoegberg LC, Graudal NA: The effect of activated charcoal on drug exposure in healthy volunteers: a meta-analysis. Clin Pharmacol Ther 2009, 85: 501–505. 10.1038/clpt.2008.278

    Article  CAS  PubMed  Google Scholar 

  99. Gude AB, Hoegberg LC, Angelo HR, Christensen HR: Dose-dependent adsorptive capacity of activated charcoal for gastrointestinal decontamination of a simulated paracetamol overdose in human volunteers. Basic Clin Pharmacol Toxicol 2010, 106: 406–410.

    Article  CAS  PubMed  Google Scholar 

  100. Pond SM, Olson KR, Osterloh JD, Tong TG: Randomized study of the treatment of phenobarbital overdose with repeated doses of activated charcoal. JAMA 1984, 251: 3104–3108. 10.1001/jama.251.23.3104

    Article  CAS  PubMed  Google Scholar 

  101. Brahmi N, Kouraichi N, Thabet H, Amamou M: Influence of activated charcoal on the pharmacokinetics and the clinical features of carbamazepine poisoning. Am J Emerg Med 2006, 24: 440–443. 10.1016/j.ajem.2005.12.025

    Article  PubMed  Google Scholar 

  102. Merigian KS, Blaho KE: Single-dose oral activated charcoal in the treatment of the self-poisoned patient: a prospective, randomized, controlled trial. Am J Ther 2002, 9: 301–308. 10.1097/00045391-200207000-00007

    Article  PubMed  Google Scholar 

  103. de Silva HA, Fonseka MM, Pathmeswaran A, Alahakone DG, Ratnatilake GA, Gunatilake SB, Ranasinha CD, Lalloo DG, Aronson JK, de Silva HJ: Multiple-dose activated charcoal for treatment of yellow oleander poisoning: a single-blind, randomised, placebo-controlled trial. Lancet 2003, 361: 1935–1938. 10.1016/S0140-6736(03)13581-7

    Article  CAS  PubMed  Google Scholar 

  104. Eddleston M, Juszczak E, Buckley NA, Senarathna L, Mohamed F, Dissanayake W, Hittarage A, Azher S, Jeganathan K, Jayamanne S, et al.: Multiple-dose activated charcoal in acute self-poisoning: a randomised controlled trial. Lancet 2008, 371: 579–587. 10.1016/S0140-6736(08)60270-6

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  105. Cooper GM, Le Couteur DG, Richardson D, Buckley NA: A randomized clinical trial of activated charcoal for the routine management of oral drug overdose. QJM 2005, 98: 655–660. 10.1093/qjmed/hci102

    Article  CAS  PubMed  Google Scholar 

  106. Mohamed F, Sooriyarachchi MR, Senarathna L, Azhar S, Sheriff MH, Buckley NA, Eddleston M: Compliance for single and multiple dose regimens of superactivated charcoal: a prospective study of patients in a clinical trial. Clin Toxicol (Phila) 2007, 45: 132–135. 10.1080/15563650600981145

    Article  Google Scholar 

  107. Osterhoudt KC, Alpern ER, Durbin D, Nadel F, Henretig FM: Activated charcoal administration in a pediatric emergency department. Pediatr Emerg Care 2004, 20: 493–498. 10.1097/01.pec.0000136064.14704.d1

    Article  PubMed  Google Scholar 

  108. Karim A, Ivatts S, Dargan P, Jones A: How feasible is it to conform to the European guidelines on administration of activated charcoal within one hour of an overdose? Emerg Med J 2001, 18: 390–392. 10.1136/emj.18.5.390

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  109. Isbister GK, Dawson AH, Whyte IM: Feasibility of prehospital treatment with activated charcoal: Who could we treat, who should we treat? Emerg Med J 2003, 20: 375–378. 10.1136/emj.20.4.375

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  110. Favin FD, Klein-Schwartz W, Oderda GM, Rose SR: In vitro study of lithium carbonate adsorption by activated charcoal. J Toxicol Clin Toxicol 1988, 26: 443–450. 10.3109/15563658809038560

    Article  CAS  PubMed  Google Scholar 

  111. Amigo M, Nogue S, Miro O: [Use of activated charcoal in acute poisonings: clinical safety and factors associated with adverse reactions in 575 cases]. Med Clin (Barc) 2010, 135: 243–249. 10.1016/j.medcli.2009.10.053

    Article  Google Scholar 

  112. Dorrington CL, Johnson DW, Brant R: The frequency of complications associated with the use of multiple-dose activated charcoal. Ann Emerg Med 2003, 41: 370–377. 10.1067/mem.2003.86

    Article  PubMed  Google Scholar 

  113. Moll J, Kerns W, Tomaszewski C, Rose R: Incidence of aspiration pneumonia in intubated patients receiving activated charcoal. J Emerg Med 1999, 17: 279–283. 10.1016/S0736-4679(98)00192-9

    Article  CAS  PubMed  Google Scholar 

  114. Pollack MM, Dunbar BS, Holbrook PR, Fields AI: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981, 10: 528–529. 10.1016/S0196-0644(81)80009-1

    Article  CAS  PubMed  Google Scholar 

  115. Menzies DG, Busuttil A, Prescott LF: Fatal pulmonary aspiration of oral activated charcoal. BMJ 1988, 297: 459–460. 10.1136/bmj.297.6646.459

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  116. Justiniani FR, Hippalgaonkar R, Martinez LO: Charcoal-containing empyema complicating treatment for overdose. Chest 1985, 87: 404–405. 10.1378/chest.87.3.404

    Article  CAS  PubMed  Google Scholar 

  117. Elliott CG, Colby TV, Kelly TM, Hicks HG: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989, 96: 672–674. 10.1378/chest.96.3.672

    Article  CAS  PubMed  Google Scholar 

  118. Osterhoudt KC, Durbin D, Alpern ER, Henretig FM: Risk factors for emesis after therapeutic use of activated charcoal in acutely poisoned children. Pediatrics 2004, 113: 806–810. 10.1542/peds.113.4.806

    Article  PubMed  Google Scholar 

  119. Atkinson S, Young Y, Trotter GA: Treatment with activated charcoal complicated by gastrointestinal obstruciton requiring surgery. BMJ 1992, 305: 563. 10.1136/bmj.305.6853.563

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  120. Chan JC, Saranasuriya C, Waxman BP: Bezoar causing small bowel obstruction after repeated activated charcoal administration. Med J Aust 2005, 183: 537.

    PubMed  Google Scholar 

  121. Watson WA, Cremer KF, Chapman JA: Gastrointestinal obstruction associated with multiple-dose activated charcoal. J Emerg Med 1986, 4: 401–407. 10.1016/0736-4679(86)90219-2

    Article  CAS  PubMed  Google Scholar 

  122. Goulbourne KB, Cisek JE: Small-bowel obstruction secondary to activated charcoal and adhesions. Ann Emerg Med 1994, 24: 108–110. 10.1016/S0196-0644(94)70170-9

    Article  CAS  PubMed  Google Scholar 

  123. Eroglu A, Kucuktulu U, Erciyes N, Turgutalp H: Multiple Dose-Activated Charcoal as a Cause of Acute Appendicitis. Clinical Toxicology 2003, 41: 71–73. 10.1081/CLT-120018274

    PubMed  Google Scholar 

  124. Gomez HF, Brent JA, Munoz DCt, Mimmack RF, Ritvo J, Phillips S, McKinney P: Charcoal stercolith with intestinal perforation in a patient treated for amitriptyline ingestion. J Emerg Med 1994, 12: 57–60. 10.1016/0736-4679(94)90013-2

    Article  CAS  PubMed  Google Scholar 

  125. Green JP, McCauley W: Bowel perforation after single-dose activated charcoal. CJEM 2006, 8: 358–360.

    PubMed  Google Scholar 

  126. Mariani PJ, Pook N: Gastrointestinal tract perforation with charcoal peritoneum complicating orogastric intubation and lavage. Ann Emerg Med 1993, 22: 606–609. 10.1016/S0196-0644(05)81954-7

    Article  CAS  PubMed  Google Scholar 

  127. Rose SR, Gorman RL, Oderda GM, Klein-Schwartz W, Watson WA: Simulated acetaminophen overdose: pharmacokinetics and effectiveness of activated charcoal. Ann Emerg Med 1991, 20: 1064–1068. 10.1016/S0196-0644(05)81353-8

    Article  CAS  PubMed  Google Scholar 

  128. Spiller HA, Winter ML, Klein-Schwartz W, Bangh SA: Efficacy of activated charcoal administered more than four hours after acetaminophen overdose. J Emerg Med 2006, 30: 1–5. 10.1016/j.jemermed.2005.02.019

    Article  PubMed  Google Scholar 

  129. Spiller HA, Sawyer TS: Impact of activated charcoal after acute acetaminophen overdoses treated with N-acetylcysteine. J Emerg Med 2007, 33: 141–144. 10.1016/j.jemermed.2007.02.016

    Article  PubMed  Google Scholar 

  130. Christophersen AB, Levin D, Hoegberg LC, Angelo HR, Kampmann JP: Activated charcoal alone or after gastric lavage: a simulated large paracetamol intoxication. Br J Clin Pharmacol 2002, 53: 312–317. 10.1046/j.0306-5251.2001.01568.x

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  131. Buckley NA, Whyte IM, O'Connell DL, Dawson AH: Activated charcoal reduces the need for N-acetylcysteine treatment after acetaminophen (paracetamol) overdose. J Toxicol Clin Toxicol 1999, 37: 753–757. 10.1081/CLT-100102452

    Article  CAS  PubMed  Google Scholar 

  132. Renzi FP, Donovan JW, Martin TG, Morgan L, Harrison EF: Concomitant use of activated charcoal and N-acetylcysteine. Ann Emerg Med 1985, 14: 568–572. 10.1016/S0196-0644(85)80781-2

    Article  CAS  PubMed  Google Scholar 

  133. Ekins BR, Ford DC, Thompson MI, Bridges RR, Rollins DE, Jenkins RD: The effect of activated charcoal on N-acetylcysteine absorption in normal subjects. Am J Emerg Med 1987, 5: 483–487. 10.1016/0735-6757(87)90166-5

    Article  CAS  PubMed  Google Scholar 

  134. Wananukul W, Klaikleun S, Sriapha C, Tongpoo A: Effect of activated charcoal in reducing paracetamol absorption at a supra-therapeutic dose. J Med Assoc Thai 2010, 93: 1145–1149.

    PubMed  Google Scholar 

  135. Montoya-Cabrera MA, Escalante-Galindo P, Nava-Juarez A, Terroba-Larios VM, Teran-Hernandez JA: [Evaluation of the efficacy of N-acetylcysteine administered alone or in combination with activated charcoal in the treatment of acetaminophen overdoses]. Gac Med Mex 1999, 135: 239–243.

    CAS  PubMed  Google Scholar 

  136. Roberts JR, Gracely EJ, Schoffstall JM: Advantage of high-surface-area charcoal for gastrointestinal decontamination in a human acetaminophen ingestion model. Acad Emerg Med 1997, 4: 167–174. 10.1111/j.1553-2712.1997.tb03735.x

    Article  CAS  PubMed  Google Scholar 

  137. Green R, Sitar DS, Tenenbein M: Effect of anticholinergic drugs on the efficacy of activated charcoal. J Toxicol Clin Toxicol 2004, 42: 267–272. 10.1081/CLT-120037426

    Article  CAS  PubMed  Google Scholar 

  138. Chyka PA, Holley JE, Mandrell TD, Sugathan P: Correlation of drug pharmacokinetics and effectiveness of multiple-dose activated charcoal therapy. Ann Emerg Med 1995, 25: 356–362. 10.1016/S0196-0644(95)70295-4

    Article  CAS  PubMed  Google Scholar 

  139. Mullins M, Froelke BR, Rivera MR: Effect of delayed activated charcoal on acetaminophen concentration after simulated overdose of oxycodone and acetaminophen. Clin Toxicol (Phila) 2009, 47: 112–115. 10.1080/15563650802093681

    Article  CAS  Google Scholar 

  140. Yeates PJ, Thomas SH: Effectiveness of delayed activated charcoal administration in simulated paracetamol (acetaminophen) overdose. Br J Clin Pharmacol 2000, 49: 11–14.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  141. Olkkola KT: Effect of charcoal-drug ratio on antidotal efficacy of oral activated charcoal in man. Br J Clin Pharmacol 1985, 19: 767–773.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  142. Danel V, Henry JA, Glucksman E: Activated charcoal, emesis, and gastric lavage in aspirin overdose. Br Med J (Clin Res Ed) 1988, 296: 1507. 10.1136/bmj.296.6635.1507

    Article  CAS  Google Scholar 

  143. Barone JA, Raia JJ, Huang YC: Evaluation of the effects of multiple-dose activated charcoal on the absorption of orally administered salicylate in a simulated toxic ingestion model. Ann Emerg Med 1988, 17: 34–37.

    Article  CAS  PubMed  Google Scholar 

  144. Kirshenbaum LA, Mathews SC, Sitar DS, Tenenbein M: Does multiple-dose charcoal therapy enhance salicylate excretion? Arch Intern Med 1990, 150: 1281–1283. 10.1001/archinte.150.6.1281

    Article  CAS  PubMed  Google Scholar 

  145. Neuvonen PJ, Elfving SM, Elonen E: Reduction of absorption of digoxin, phenytoin and aspirin by activated charcoal in man. Eur J Clin Pharmacol 1978, 13: 213–218. 10.1007/BF00609985

    Article  CAS  PubMed  Google Scholar 

  146. Kulig KW, Bar-Or D, Rumack BH: Intravenous theophylline poisoning and multiple-dose charcoal in an animal model. Ann Emerg Med 1987, 16: 842–846. 10.1016/S0196-0644(87)80519-X

    Article  CAS  PubMed  Google Scholar 

  147. Arimori K, Nakano M: Accelerated clearance of intravenously administered theophylline and phenobarbital by oral doses of activated charcoal in rats. A possibility of the intestinal dialysis. J Pharmacobiodyn 1986, 9: 437–441.

    Article  CAS  PubMed  Google Scholar 

  148. Ilkhanipour K, Yealy DM, Krenzelok EP: The comparative efficacy of various multiple-dose activated charcoal regimens. Am J Emerg Med 1992, 10: 298–300. 10.1016/0735-6757(92)90006-J

    Article  CAS  PubMed  Google Scholar 

  149. Arimori K, Nakano M: Dose-dependency in the exsorption of theophylline and the intestinal dialysis of theophylline by oral activated charcoal in rats. J Pharm Pharmacol 1988, 40: 101–105.

    Article  CAS  PubMed  Google Scholar 

  150. Albertson TE, Fisher CJ Jr, Shragg TA, Baselt RC: A prolonged severe intoxication after ingestion of phenytoin and phenobarbital. West J Med 1981, 135: 418–422.

    PubMed Central  CAS  PubMed  Google Scholar 

  151. Boldy DA, Vale JA, Prescott LF: Treatment of phenobarbitone poisoning with repeated oral administration of activated charcoal. Q J Med 1986, 61: 997–1002.

    CAS  PubMed  Google Scholar 

  152. Amitai Y, Degani Y: Treatment of phenobarbital poisoning with multiple dose activated charcoal in an infant. J Emerg Med 1990, 8: 449–450. 10.1016/0736-4679(90)90174-T

    Article  CAS  PubMed  Google Scholar 

  153. Frenia ML, Schauben JL, Wears RL, Karlix JL, Tucker CA, Kunisaki TA: Multiple-dose activated charcoal compared to urinary alkalinization for the enhancement of phenobarbital elimination. J Toxicol Clin Toxicol 1996, 34: 169–175. 10.3109/15563659609013766

    Article  CAS  PubMed  Google Scholar 

  154. Berg MJ, Berlinger WG, Goldberg MJ, Spector R, Johnson GF: Acceleration of the body clearance of phenobarbital by oral activated charcoal. N Engl J Med 1982, 307: 642–644. 10.1056/NEJM198209093071102

    Article  CAS  PubMed  Google Scholar 

  155. Howard CE, Roberts RS, Ely DS, Moye RA: Use of multiple-dose activated charcoal in phenytoin toxicity. Ann Pharmacother 1994, 28: 201–203.

    CAS  PubMed  Google Scholar 

  156. Weichbrodt GD, Elliott DP: Treatment of phenytoin toxicity with repeated doses of activated charcoal. Ann Emerg Med 1987, 16: 1387–1389. 10.1016/S0196-0644(87)80428-6

    Article  CAS  PubMed  Google Scholar 

  157. Mauro LS, Mauro VF, Brown DL, Somani P: Enhancement of phenytoin elimination by multiple-dose activated charcoal. Ann Emerg Med 1987, 16: 1132–1135. 10.1016/S0196-0644(87)80471-7

    Article  CAS  PubMed  Google Scholar 

  158. Montoya-Cabrera MA, Sauceda-Garcia JM, Escalante-Galindo P, Flores-Alvarez E, Ruiz-Gomez A: Carbamazepine poisoning in adolescent suicide attempters. Effectiveness of multiple-dose activated charcoal in enhancing carbamazepine elimination. Arch Med Res 1996, 27: 485–489.

    CAS  PubMed  Google Scholar 

  159. Vannaprasaht S, Tiamkao S, Sirivongs D, Piyavhatkul N: Acute valproic acid overdose: enhance elimination with multiple-doses activated charcoal. J Med Assoc Thai 2009, 92: 1113–1115.

    PubMed  Google Scholar 

  160. Siefkin AD, Albertson TE, Corbett MG: Isoniazid overdose: pharmacokinetics and effects of oral charcoal in treatment. Hum Toxicol 1987, 6: 497–501. 10.1177/096032718700600608

    Article  CAS  PubMed  Google Scholar 

  161. Ofoefule SI, Onuoha LC, Okonta MJ, Udeogaranya PO, Orisakwe OE: Effect of activated charcoal on isoniazid absorption in rabbits. Boll Chim Farm 2001, 140: 183–186.

    CAS  PubMed  Google Scholar 

  162. Scolding N, Ward MJ, Hutchings A, Routledge PA: Charcoal and isoniazid pharmacokinetics. Hum Toxicol 1986, 5: 285–286. 10.1177/096032718600500414

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

The authors would like to acknowledge the excellent help with Endnotes and the manuscript by Lisa Pastore.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Timothy E Albertson.

Additional information

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

All the authors participated in the literature search and evaluation of the literature. All authors participated in writing and editing of the manuscript.

Rights and permissions

Open Access This article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and permissions

About this article

Cite this article

Albertson, T.E., Owen, K.P., Sutter, M.E. et al. Gastrointestinal decontamination in the acutely poisoned patient. Int J Emerg Med 4, 65 (2011). https://doi.org/10.1186/1865-1380-4-65

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/1865-1380-4-65

Keywords