Context. Although extracorporeal membrane oxygenation (ECMO) was used in many patients following its introduction in 1972, most hospitals had abandoned this experimental treatment for adult patients. Recently, improvements in the ECMO circuitry rendered it more biocompatible. The surprisingly low mortality in patients with severe acute respiratory distress syndrome who were treated with ECMO in the influenza A/H1N1 pandemic of 2009 resurrected interest in ECMO in many intensive care units around the world.

Objectives.

This article reviews the different techniques of ECMO, the indications, contraindications and complications of its use, its role in poisoned patients and the ethics of its use. Methods. We searched Pubmed, Toxnet, Cochrane database and Embase from 1966 to September 2012 using the search terms (''extracorporeal membrane oxygenation'', 'extracorporeal life support', 'ECMO', 'ECLS', 'assist-device', and 'intox*' or 'poison*'). These searches identified 242 papers of which 116 described ECMO in conditions other than intoxications or were reviews. In total 46 publications selected for this manuscript were case reports or case series involving poisoned patients. ECMO techniques. Two types of ECMO are used: veno-venous ECMO (VV-ECMO) or veno-arterial ECMO (VA-ECMO). VV-ECMO is used for patients with severe ARDS to secure adequate oxygenation of the organs while protecting the lungs from harmful ventilation pressures or prolonged inspiratory fraction of oxygen. VA-ECMO can be used whenever the patient remains in shock despite adequate fluid resuscitation and is refractory to administration of inotropes and vasopressors. Indications. The organ support that can be applied with ECMO makes it especially useful in patients with severe poisoning as the clinical impact of the intoxication is often temporary; ECMO can be used as a 'bridge to recovery'. Contraindications. Absolute contraindications are uncontrolled coagulopathy and severe intracranial bleeding, which precludes the use of anticoagulation therapy. Relative contraindications to ECMO include advanced age, severe irreversible brain injury, untreatable metastatic cancer, severe organ dysfunction (some suggest a Sequential Organ Failure Assessment (SOFA) score > 15), and high pressure positive pressure ventilation for more than 7 days. Complications. The most common complication of ECMO is either bleeding at the cannulation site (in VV-ECMO) or bleeding at the surgical entry site (in VA-ECMO). Overall bleeding complications currently occur in 10-36% patients, and intracranial haemorrhage is seen in up to 6% of patients. ECMO should be reserved, therefore, for the most severely ill poisoned patients with a high risk of death. ECMO in poisoned patients. There are no randomised trials of ECMO in poisoned patients with refractory shock or who have ARDS caused by an intoxication. VV-ECMO can be considered in patients with type l and ll respiratory failure. In patients with life-threatening haemodynamic instability, VA-ECMO can be considered when shock persists despite volume administration, inotropes and vasoconstrictors, and (sometimes) intra-aortic balloon counterpulsation. Typical examples include poisoning due to calcium channel antagonists, beta-blockers, tricyclic antidepressants, chloroquine and colchicine. Ethics of ECMO use. It is only ethical to use such a costly intervention (£19,252 and US$ 31,000 per quality-adjusted life year) if the treatment has a real purpose such as a 'bridge to recovery', a 'bridge to transplant', or a 'bridge to permanent assist device' (in the case of persistent cardiac failure).

Conclusions.

In the last decade, ECMO equipment has improved considerably, rendering it more biocompatible, and it has been used more frequently as an assist device for patients needing oxygenation as well as circulatory support. ECMO is considered a good salvage therapy for patients who are severely poisoned with ARDS or refractory circulatory shock.

Context. Poison control centers (PCCs) and emergency departments (EDs) rely upon telephone communication to collaborate. PCCs and EDs each create electronic records for the same patient during the course of collaboration, but those electronic records are not shared.

Objective.

The purpose of this study was to describe the current, telephone based process of PCC-ED communication as the basis for potential process improvement. Materials and methods. This study was conducted at one PCC and two tertiary care EDs. We developed workflow diagrams to depict clinician descriptions of the current process, descriptions obtained through interviews of key informants. We also analyzed transcripts of phone calls between emergency departments and the poison control center, corresponding to a random sample of 120 PCC cases occurring January 1-December 31, 2011.

Results.

Collaboration between the ED and PCC takes place during multiple telephone calls, and the process is unsupported by shared documentation. The process occurs in three phases: notification, collaborative care, and ongoing consultation. In the ED, multiple care providers may communicate with the PCC, but only one ED care provider communicates with the poison control center specialist at a time. Handoffs occur for both ED and PCC. Collaborative care planning is common and most cases involve some type of request for information, whether vital signs, laboratory results, or verification that a treatment was administered. We found evidence of inefficiencies and safety vulnerabilities, including the inability of PCC specialists to reach ED care providers, telephone calls routed through multiple ED staff members in an attempt to reach the appropriate care provider, and exchange of clinical information with non-clinical staff. In 55% of cases, the patient was discharged prior to any synchronous telephone communication between the ED care provider and a PCC specialist. Ambiguous communication of information was observed in 22% of cases. In 12% of cases, a PCC specialist was unable to obtain requested information from the ED. Discussion and conclusion. Inefficiencies and vulnerabilities occur in telephone-based PCC-ED communication. Prudence begs consideration of alternative processes and models of ED-PCC communication and information sharing, including a process that supports collaboration with health information exchange.

Context. N-acetylcysteine (NAC) is acknowledged as an effective antidote for paracetamol overdose. However, adverse effects to NAC are common and may be a point of concern for the patient and the treating physician.

Objective.

The aim of the present study was to further analyse possible risk factors of anaphylactoid adverse effects to intravenous NAC in order to identify individual patients or groups of patients at particular risk. Methods. This study is an observational case series of adverse effects to NAC administered according to the standard guidelines in patients who presented with paracetamol overdose between March 1999 and September 2011.

Results.

A total of 1218 admissions for paracetamol overdose receiving intravenous NAC were recorded in 950 patients. Anaphylactoid adverse effects occurred in 18.6%. The proportion of cases with adverse effects gradually declined from 25.9% in cases with undetectable p-paracetamol to 6.3% in cases with p-paracetamol above 1.5 mmol/L (226 μg/mL) (Spearman Rank R-test: p < 0.00001). The proportion of cases with adverse effects was significantly higher in cases of non-Danish origin than that of Danish origin (28.5% vs. 15.1%; Chi-square: p < 0.00001). In patients with repeated exposure to NAC, the rate of adverse effects on re-exposure was significantly higher in patients with a previous reaction to NAC compared to those without a previous reaction (Rate Ratio 6.2; 95% CI 2.9-17.1).

Conclusion.

The development of anaphylactoid adverse effects to intravenous NAC was strongly associated with a low p-paracetamol, non-Danish origin and a history of previous reaction to NAC. These adverse effects are common, but usually mild and easily manageable. The incidence of adverse effects may be reduced by pre-treating selected patients with antihistamines, in particular those with a previous reaction to NAC.

Background.

Previous reports describe false-positive urine immunoassay screens for phencyclidine (PCP) associated with use of tramadol, dextromethorphan, or diphenhydramine. The likelihood of these false positives is unknown.

Objective.

We sought to find the relative frequency of false-positive PCP screens associated with these medications and to look for any other medications with similar associations. Methods. In an IRB-approved study, we retrospectively reviewed charts of all ED encounters with positive urine screens for PCP in our hospital from 2007 through 2011, inclusive. Urine samples were tested for drugs of abuse using the Siemens Syva EMIT II Immunoassay. Our laboratory routinely confirmed all positive screens using GC-MS with results classified as either "confirmed" (true positive) or "failed to confirm" (false positive). We recorded all medications mentioned in the chart as current medications or medications given before the urine sample. We used Fisher's exact test to compare frequencies of tramadol, dextromethorphan, diphenhydramine, and other medications between the two groups.

Results.

Tramadol, dextromethorphan, alprazolam, clonazepam, and carvedilol were significantly more frequent among the false-positive group, but the latter three were also associated with polysubstance abuse. Diphenhydramine was more frequently recorded among the false-positive group, but this was not statistically significant.

Conclusion.

False-positive urine screens for PCP are associated with tramadol and dextromethorphan and may also occur with diphenhydramine. Positive PCP screens associated with alprazolam, clonazepam, and carvedilol were also associated with polysubstance abuse.

Objective.

In Germany, increasing prescription rates of angiotensin II antagonists resulted in rising enquiries to Poisons Information Centres (PICs) during the last decade. Therefore, we aimed to assess their acute toxicity for deriving triage recommendations.

Methods:

An observational case series with data collected retrospectively from eight PICs in Austria, Germany and Switzerland. Inclusion criteria were monoexposure, defined dose, and documented follow-up.

Results.

In total, 206 cases of exposures to angiotensin II antagonists were included (candesartan, 94; eprosartan, 3; irbesartan, 20; losartan, 26; olmesartan, 16; telmisartan, 18; and valsartan, 29). The median dose expressed as a multiple of their maximum daily dose for adults adjusted to body weight (MDDw) was 2.3 in children and 6.8 in adults. Patients involved were 150 children with a median age of 2 years and a median body weight of 13 kg and 56 adults with a median age of 47 years and a median body weight of 70 kg. Most children remained asymptomatic (82.7%), 16.7% developed minor symptoms. Only once, a low blood pressure of 60/40 mm Hg required intravenous fluids after ingestion of a 8.75-fold MDDw of candesartan by a 2.5-year-old toddler. Among adults, 53.6% remained asymptomatic while almost half of the patients suffered from minor (37.5%) or moderate (8.9%) symptoms.

Conclusion.

As no or only minor symptoms were observed after ingestion of less than a fivefold MDDw in both children and adults, only symptomatic patients and those who have ingested a fivefold MDDw or higher dose should be referred for medical assessment.

Context. Erythromelalgia is a rare disorder characterized by reddening, severe burning pain, and swelling of the extremities. Food poisoning by Clitocybe acromelalga, a poisonous mushroom, is known to induce erythromelalgia; however, its treatment protocol remains unclear. We describe here three cases of erythromelalgia following the consumption of C. acromelalga with varying clinical courses. Case details. Of the three patients, the first patient presented 22 days after the onset of erythromelalgia; although he was treated with aspirin, numbness in the limbs persisted as sequela. Patient 2 presented at 3 days after the symptomatic onset and was immediately treated with high-dose intravenous nicotinic acid, with a dramatic symptomatic improvement. Patient 3, who had milder symptoms, spontaneously recovered within a week without any treatment. Discussion. The clinical manifestations and varying clinical courses associated with C. acromelalga toxicity are discussed here, with the pathogenesis of this mycotoxin and a potential treatment. Detailed interviews of such patients are important, particularly because of the remarkably slow course of this mycotoxin as compared with common food poisonings. Treatment with intravenous nicotinic acid was associated with improvement in one patient. We believe that this painful disorder might thus be treatable, although the mechanism underlying the treatment remains unclear.