[Preparedness on Assaults with Highly Toxic Substances in Public Space]. / Vorbereitung auf Anschläge mit hochtoxischen Substanzen im öffentlichen Raum.

The use of chemical substances in terrorist scenarios is to be feared everywhere, especially in the western world, after the events that have become known in recent years. In order to protect civilian populations in an emergency, it is essential that the poisoning pattern (toxidrome) is recognized as quickly and reliably as possible through further training of the relevant agents and the provision of necessary rescue equipment (antidotes) in prepared facilities. In the event of a chemical attack with terrorist motivation, doctors from the Public Health Service (PHS) will foreseeably play a key role in communicating with decision-makers and the public a spart of a competency network.

Psychiatric comorbidity and personality structure in patients with polyvalent addiction.

BACKGROUND: This study focuses on the systematic psychiatric evaluation of polydrug-using opiate-dependent patients, using the standard DSM-IV diagnostic interviews and a new psychodynamic instrument operationalizing personality organization (Structured Interview of Personality Organization, STIPO). SAMPLING AND METHOD: 50 patients were interviewed with the Structured Clinical Interview for DSM-IV Disorders (SCID) I and II and the STIPO by two independent researchers at a detoxification treatment unit. RESULTS: According to the SCID I and II, all patients had at least one axis I disorder, 90% at least one axis II disorder. A correspondence was found between STIPO and SCID results, in that more pathology in the SCID coincided with more severity in the STIPO. According to the STIPO, 100% of the patients were located at the level of borderline personality organization, indicating identity pathology according to Kernberg's model. CONCLUSION: Given the fact that comorbid psychiatric disorders compromise the outcome of detoxification and dehabituation treatments, it is highly relevant to diagnose these disorders and to assess underlying personality pathology. While the evidence of psychosocial treatments in addiction therapy is still weak, the integration of syndrome-tailored treatment modules may help improve the treatment of patients with this chronically relapsing condition. LIMITATION: small sample size.

Intravenous application of an anticalin dramatically lowers plasma digoxin levels and reduces its toxic effects in rats.

Lipocalins tailored with high affinity for prescribed ligands, so-called anticalins, constitute promising candidates as antidotes. Here, we present an animal study to investigate both pharmacokinetic and clinical effects of an anticalin specific for the digitalis compound digoxin. Intravenous digoxin (2.5-50 µg/kg/min) was administered to rats until first changes in the ECG occurred (dose finding study) or a priori for 30 min (kinetic study). The anticalin DigA16(H86N), dubbed DigiCal, was administered intravenously at absolute doses of 1, 5, 10 and 20 mg, while the control group received isotonic saline. Hemodynamic changes, several ECG parameters and digoxin concentration in plasma were monitored at given time intervals. After DigiCal administration free digoxin concentration in plasma ultrafiltrate declined dramatically within 1 min to the presumably non-toxic range. There was also a significant and DigiCal dose-dependent effect on longer survival, less ECG alterations, arrhythmia, and improved hemodynamics. Infusion of a lower digoxin dose (2.5 µg/kg/min) resulted in a more sustained reduction of free digoxin in plasma after DigiCal administration compared to a higher digoxin dose (25 µg/kg/min), whereas ECG and hemodynamic parameters did not markedly differ, reflecting the known relative insensitivity of rats towards digoxin toxicity. Notably, we observed a re-increase of free digoxin in plasma some time after bolus administration of DigiCal, which was presumably due to toxin redistribution from tissue in combination with the relatively fast renal clearance of the rather small protein antidote. We conclude that anticalins with appropriately engineered drug-binding activities and, possibly, prolonged plasma half-life offer prospects for next-generation antidotal therapy.

Risk assessment of moderate to severe alcohol withdrawal--predictors for seizures and delirium tremens in the course of withdrawal.

AIMS: To develop a prediction model for withdrawal seizures (WS) and delirium tremens (DT) during moderate to severe alcohol withdrawal syndrome (AWS) in a large cohort of inpatients treated for AWS (n = 827). METHODS: Re-analysis of a cohort study population treated between 2000 and 2009. All patients received a score-guided and symptom-triggered therapy for AWS. Multivariable binary logistic regression models with stepwise variable selection procedures were conducted providing odds ratio (OR) estimates. RESULTS: In the multivariable regression, significant predictors of WS during AWS therapy were a delayed climax of withdrawal severity since admission [OR/10 h: 1.23; 95% confidence interval (CI): 1.1-1.4; P < 0.001)], prevalence of structural brain lesions in the patient's history (OR 6.5; 95% CI: 3.0-14.1; P < 0.001) and WS as the cause of admittance (OR 2.6; 95% CI: 1.4-4.8; P = 0.002). Significant predictors at admission for the occurrence of DT were lower serum potassium (OR/1 mmol/l 0.33; 95% CI: 0.17-0.65; P = 0.001), a lower platelet count (OR/100.000 0.42; 95% CI: 0.26-0.69; P = 0.001) and prevalence of structural brain lesions (OR 5.8; 95% CI: 2.6-12.9; P < 0.001). CONCLUSION: In this large retrospective cohort, some easily determinable parameters at admission may be useful to predict a complicated course of alcohol withdrawal regarding the occurrence of WS or DT. Using the provided nomograms, clinicians can estimate the percentage likelihood of patients to develop either WS or DT during their course of withdrawal. Prevalence of structural brain lesions in the patient's history does strongly warrant a careful observation of patients.

Carbamazepine and valproate as adjuncts in the treatment of alcohol withdrawal syndrome: a retrospective cohort study.

AIMS: To compare the clinical course, incidence of withdrawal seizures (WS) or delirium tremens (DT) and side effects during treatment of alcohol withdrawal in patients treated with either carbamazepine (CBZ) or valproate (VPA) as an adjunct to clomethiazole and clonidine therapy. METHODS: Retrospective analysis of charts of two cohorts of inpatients treated during 2000-2009: CBZ 374 patients, VPA 453 patients. RESULTS: At baseline, those treated with VPA and those treated with CBZ were similar except for a trend to younger age and a higher incidence of previous WS in the CBZ group. The median duration of pharmacological treatment (91 vs. 76 h; P < 0.001) and the length of stay (8 vs. 6 days; P < 0.001) as well as the need for intensive care treatment (7 vs. 2%; P = 0.001) were significantly higher in the CBZ than the VPA group. Additionally, withdrawal-related complications such as WS occurred more often in the CBZ group (9.6 vs. 5.5%; not significant after adjusting for potential confounders); the incidence of DT in the CBZ group was insignificantly higher (6.6 vs. 4.4%; P = 0.52). Admittance with seizures and older age were predictors of WS and DT, respectively. Adverse drug reactions, mainly affecting the central nervous system, were significantly more frequent with CBZ than VPA (7.6 vs. 2%; P < 0.001). CONCLUSION: During alcohol withdrawal, VPA may offer some benefits compared with CBZ due to favorable tolerability, possibly less incidence of WS and a shorter duration of pharmacological treatment.

Mushroom Poisoning.

BACKGROUND: Poisonous mushrooms are eaten by mushroom hunters out of ignorance, after misidentification as edible mushrooms, or as a psychoactive drug. Mushroom poisoning commonly leads to consultation with a poison information center and to hospitalization. METHODS: This review is based on pertinent publications about the syndromes, toxins, and diagnostic modalities that are presented here, which were retrieved by a selective search in PubMed. It is additionally based on the authors' longstanding experience in the diagnosis and treatment of mushroom intoxication, expert consultation in suspected cases, macroscopic identification of wild mushrooms, and analytic techniques. RESULTS: A distinction is usually drawn between mushroom poisoning with a short latency of less than six hours, presenting with a gastrointestinal syndrome whose course is usually relatively harmless, and cases with a longer latency of six to 24 hours or more, whose course can be life-threatening (e.g., phalloides, gyromitra, orellanus, and rhabdomyolysis syndrome). The DRG diagnosis data for Germany over the period 2000-2018 include a total of 4412 hospitalizations and 22 deaths due to the toxic effects of mushroom consumption. 90% of the fatalities were due to the death cap mushroom (amatoxins). Gastrointestinal syndromes due to mushroom consumption can be caused not only by poisonous mushrooms, but also by the eating of microbially spoiled, raw, or inadequately cooked mushrooms, or by excessively copious or frequent mushroom consumption. CONCLUSION: There are few analytic techniques available other than the qualitative demonstration of amatoxins. Thus, the diagnosis is generally made on the basis of the clinical manifestations and their latency, along with meticulous history-taking, assisted by a mushroom expert, about the type(s) of mushroom that were consumed and the manner of their preparation.

Fetal risk through maternal Amanita phalloides poisoning at the end of pregnancy.

There is a paucity of knowledge about prenatal and perinatal risks through maternal amatoxin poisoning. No symptoms of amatoxin intoxication, except for a slight temporary increase in liver enzymes activity, occurred in a term newborn after delivery despite an Amanita phalloides intoxication of the mother 2 days before. Considering previous reports, severe fetal intoxication may not occur during the entire pregnancy.

Does a specific dental amalgam syndrome exist? A comparative study.

OBJECTIVE: The aim of this article was to investigate whether there is evidence for a specific syndrome of health problems attributed to dental amalgam. MATERIAL AND METHODS: A secondary and retrospective analysis of two different databases was performed: (a) 90 patients (47% female, mean (SD) age 34 (6) years) of a clinical trial to remove amalgam fillings who attribute their health complaints to dental amalgam, and (b) 116 patients (62% female, mean (SD) age 37 (8) years) from an outpatient unit for environmental medicine who attribute their symptoms to environmental sources other than amalgam. RESULTS: The samples differed in age, sex, and educational level. No statistically significant differences between either of the groups were found in overall psychological distress, intensity of the symptoms, or in numbers of self-reported symptoms in the Symptom Check List after controlling for age, sex, and education (Mean Global Severity Index 0.62 versus 0.63). Patients from the amalgam group showed mean values for private and public self-consciousness similar to the population norm, while patients from the comparison group had statistically significantly decreased mean values. While the amalgam group more frequently reported mental symptoms, patients from the comparison group had a higher prevalence of somatic symptoms. CONCLUSIONS: The results showed some differences in symptomatology, while general psychological distress was similar in both groups, indicating no strong evidence for an amalgam-specific syndrome.

[Caustic injuries of the eye, skin and the gastrointestinal tract]. / Expositionen mit Atzstoffen.

Caustic injuries of the eye usually occur accidentally and can result in minor eye irritations to total loss of vision. All chemical exposures to the eye require immediate decontamination by copious irrigation with an aqueous solution for at least 15-30 minutes up to two hours in single cases of massive exposure. Tap water is readily available, safe, and effective and, thus, the preferred irrigation fluid. Warmed lactated Ringer's solution is theoretically preferable to normal saline as an ocular irrigant because it has a more physiologic pH and osmolarity. Immediate ophthalmologic referral is recommended for all but the most trivial chemical burns to the eye. Specific treatments for decontamination depend on the underlying agent. Chemical burns of the skin usually occur accidentally. Initial treatment consists of copious water lavage commencing at the scene and removal of particles. While most caustic injuries are treated symptomatically, exposures to hydrofluoric acid (HFA) frequently necessitate specific topic, subcutaneous, intralesional, intravenous or intraarterial injections of calcium gluconate to bind fluoride ions until analgesia. A burn from HFA that involves more than 5% of total body-surface area, or more than 1% of total body-surface area if the concentration of HFA is greater than 50%, requires admission to an ICU for electrocardiographic monitoring and serial measurements of calcium levels, since life-threatening arrhythmias and hypocalcemia can occur. Caustic injuries of the gastrointestinal tract can occur due to inadvertent ingestion of mislabelled fluids or as a suicidal attempt. Ingestion of alkalis is generally thought to result in more severe injuries than ingestion of acids. The oropharynx needs to be first examined by laryngoscopy. A supraglottic or epiglottic burn with erythema and edema formation may be a harbinger of airway obstruction and should be seen as an indication of early endotracheal intubation or tracheostomy. Endoscopy should be performed preferably within 12 hours and generally not later than 24 hours and can serve as a prognostic tool to manage patients appropriately. The risk of procedure related perforation is generally accepted to be negligible. Existing data fail to support the routine use of steroids and antibiotics to prevent esophageal stricture formation and may mask signs of peritonitis. Esophageal strictures, stenosis or gastric outlet obstruction are formidably long-term complications. There is a 1000- to 3000-fold increase in the incidence of esophageal carcinoma after lye-ingestion with a latent period between the time of ingestion and the development of carcinoma as long as 60 years. Endoscopic dilatation or insertion of intraluminal stents should not be performed within the first 6 weeks. Patients with grade 3b injuries may underwent prompt surgical resection in single cases, even if no perforation is confirmed. Perforation, evolution of a mediastinitis or peritonitis with multi-organ failure are devastating complications with extremely high mortality and warrants immediate surgical treatment.

Mushroom poisoning: A proposed new clinical classification.

Mushroom poisoning is a significant and increasing form of toxin-induced-disease. Existing classifications of mushroom poisoning do not include more recently described new syndromes of mushroom poisoning and this can impede the diagnostic process. We reviewed the literature on mushroom poisoning, concentrating on the period since the current major classification published in 1994, to identify all new syndromes of poisoning and organise them into a new integrated classification, supported by a new diagnostic algorithm. New syndromes were eligible for inclusion if there was sufficient detail about both causation and clinical descriptions. Criteria included: identity of mushrooms, clinical profile, epidemiology, and the distinctive features of poisoning in comparison with previously documented syndromes. We propose 6 major groups based on key clinical features relevant in distinguishing between poisoning syndromes. Some clinical features, notably gastrointestinal symptoms, are common to many mushroom poisoning syndromes. Group 1 - Cytotoxic mushroom poisoning. Syndromes with specific major internal organ pathology: (Subgroup 1.1; Primary hepatotoxicity); 1A, primary hepatotoxicity (amatoxins); (Subgroup 1.2; Primary nephrotoxicity); 1B, early primary nephrotoxicity (amino hexadienoic acid; AHDA); 1C, delayed primary nephrotoxicity (orellanines). Group 2 - Neurotoxic mushroom poisoning. Syndromes with primary neurotoxicity: 2A, hallucinogenic mushrooms (psilocybins and related toxins); 2B, autonomic-toxicity mushrooms (muscarines); 2C, CNS-toxicity mushrooms (ibotenic acid/muscimol); 2D, morel neurologic syndrome (Morchella spp.). Group 3 - Myotoxic mushroom poisoning. Syndromes with rhabdomyolysis as the primary feature: 3A, rapid onset (Russula spp.); 3B, delayed onset (Tricholoma spp.). Group 4 - Metabolic, endocrine and related toxicity mushroom poisoning. Syndromes with a variety of clinical presentations affecting metabolic and/or endocrine processes: 4A, GABA-blocking mushroom poisoning (gyromitrins); 4B, disulfiram-like (coprines); 4C, polyporic mushroom poisoning (polyporic acid); 4D, trichothecene mushroom poisoning (Podostroma spp.); 4E, hypoglycaemic mushroom poisoning (Trogia venenata); 4F, hyperprocalcitoninemia mushroom poisoning (Boletus satanas); 4G, pancytopenic mushroom poisoning (Ganoderma neojaponicum). Group 5 - Gastrointestinal irritant mushroom poisoning. This group includes a wide variety of mushrooms that cause gastrointestinal effects without causing other clinically significant effects. Group 6 - Miscellaneous adverse reactions to mushrooms. Syndromes which do not fit within the previous 5 groups: 6A, Shiitake mushroom dermatitis; 6B, erythromelagic mushrooms (Clitocybe acromelagia); 6C, Paxillus syndrome (Paxillus involutus); 6D, encephalopathy syndrome (Pleurocybella porrigens).

Treatment of severe intravenous phenytoin overdose with hemodialysis and hemoperfusion.

BACKGROUND: Phenytoin is a widely used anticonvulsant agent responsible for a number of intentional and unintentional overdoses. However, besides supportive care, specific treatment recommendations to enhance elimination of the parent compound have been discussed controversially and effectiveness of hemoperfusion is under debate. CASE REPORT: A women with a prehistory of cerebral seizures was presented following a severe iatrogenic phenytoin overdose with a peak plasma concentration of 117 mg/L. A Phenytoin overdose could be contributed to both inadequate dosing and missed repeated drug monitoring. Native phenytoin body clearance failed to relevantly lower phenytoin concentration. Thus, three sessions of a four-hour long combination of activated charcoal hemoperfusion and high-flux hemodialysis were performed resulting in considerably reduced half-life during these measures of about 7-13 hours compared to the native half-life wavering between 40-100 hours. This resulted in a substantial clinical improvement in terms of central nervous system toxicity. CONCLUSIONS: Hemodiaperfusion with activated charcoal seems to be a reasonable measure for forced lowering of highly toxic phenytoin plasma concentration and should be considered especially in circumstances following intravenous overdose (e.g. inadequate iatrogenic dosing). Its narrow therapeutic range enforces strictly adequate dosing and subsequent repeated drug monitoring of phenytoin.

Biomonitoring of mercury in patients with complaints attributed to dental amalgam, healthy amalgam bearers, and amalgam-free subjects: a diagnostic study.

OBJECTIVE: To investigate the suitability of measurements of mercury (Hg) concentration as a means of identifying patients with health complaints attributed to dental amalgam. METHODS: Hg in erythrocytes, plasma, urine, and saliva was determined in 27 patients complaining about health problems attributed to amalgam, 27 healthy volunteers with amalgam fillings, and 27 healthy amalgam-free volunteers. RESULTS: Concentrations of inorganic mercury in blood and of total mercury in urine and saliva differed significantly between individuals with amalgam fillings and amalgam-free volunteers, but not between symptomatic patients and healthy volunteers with amalgam fillings. Urine Hg levels tended to be better correlated with blood than with saliva data. Levels of organic Hg were equal in all groups. CONCLUSION: Concentrations of total and inorganic mercury in body fluids do not distinguish between asymptomatic amalgam bearers and those who suffer from a poorly defined syndrome of multiple nonspecific symptoms.

Pest controllers: a high-risk group for Multiple Chemical Sensitivity (MCS)?

INTRODUCTION: Based on the assumption that professional groups with frequent chemical exposure are at an increased risk for developing Multiple Chemical Sensitivity (MCS), a sample of 45 professional pest controllers was investigated. METHODS: The examination of the pest controllers consisted of a physical and laboratory examination with urine screening for pyrethroid metabolites, a psychiatric interview, a neuropsychological test battery, and a chemical sensitivity questionnaire. RESULTS: Persistent or serious work related health problems and chemical sensitivity were not reported. In urine, cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (Br(2)CA) was detected in 11%, 4-fluoro-3-phenoxybenzoic acid (F-PBA) in 7%. 3-phenoxybenzoic acid (3-PBA) exceeded the reference range in 9%, cis- and trans-3-(2,2-dichlorovinyl)-2,2-dimethyl-cyclopropane-1-carboxylic acid (Cl(2)CA) in 20%. Increased liver enzymes and blood count deviations were rather common. 38% had psychiatric disorders. With few exceptions, neuropsychological testing results were normal. CONCLUSIONS: The results do not support the hypothesis that work-related insecticide exposure promotes chemical sensitivity.

Testing of antidotes for organophosphorus compounds: experimental procedures and clinical reality.

According to current knowledge, inhibition of acetylcholinesterase (AChE) is a very important toxic action of organphosphorus compounds (OP). Hence, it is obvious to follow the AChE activity in order to quantify the degree of inhibition and to assess possible reactivation. Red blood cell (RBC)-AChE provides an easily accessible source to follow the AChE status also in humans. There are many reports underlining the appropriateness of RBC-AChE as a surrogate parameter that mirrors the synaptic enzyme. With this tool at hand, we can study the kinetic parameters of inhibition, spontaneous and oxime-induced reactivation, as well as aging with human RBCs under physiological conditions in vitro. Moreover, we can simulate the influence of inhibitor and reactivator on enzyme activity and can calculate what happens when both components change with time. Finally, we can correlate under controlled conditions the AChE-status in intoxicated patients with the clinical signs and symptoms and determine the time-dependent changes of the oxime and OP concentration. Data of a clinical trial performed in Munich to analyze the value of obidoxime has elucidated that obidoxime worked as expected from in vitro studies. Following a 250mg bolus, obidoxime was administered by continuous infusion at 750mg/24h aimed at maintaining a plasma concentration of 10-20microM obidoxime. This oxime concentration reactivated RBC-AChE>20% of normal in most cases of OP poisoning by diethylphosphoryl compounds within a few hours. The degree of reactivation fitted theoretical calculations very well when the obidoxime and paraoxon concentrations were fed into the model. Only in a few cases reactivation was much lower than expected. The reason for this effect is probably based on the polymorphism of paraoxonase (PON1) in that the (192)arginine phenotype does hardly hydrolyze the arising diethylphosphoryl obidoxime. While this variable may complicate a proper assessment even more, we are confident that the in vitro evaluation of all relevant kinetic data enables the prediction of probable effectiveness in humans. These studies also help to understand therapeutic failures and to define scenarios where oximes are virtually ineffective. These include poisonings with rapidly aging phosphylated AChE, late start with an effective oxime and too early discontinuation of oximes in poisonings with a persistent OP. The experience gathered with the experimental and therapeutic approaches to human poisoning by OP pesticides may be helpful when oximes have to be selected against nerve agents.

Bench-to-bedside review: mechanisms and management of hyperthermia due to toxicity.

Body temperature can be severely disturbed by drugs capable of altering the balance between heat production and dissipation. If not treated aggressively, these events may become rapidly fatal. Several toxins can induce such non-infection-based temperature disturbances through different underlying mechanisms. The drugs involved in the eruption of these syndromes include sympathomimetics and monoamine oxidase inhibitors, antidopaminergic agents, anticholinergic compounds, serotonergic agents, medicaments with the capability of uncoupling oxidative phosphorylation, inhalation anesthetics, and unspecific agents causing drug fever. Besides centrally disturbed regulation disorders, hyperthermia often results as a consequence of intense skeletal muscle hypermetabolic reaction. This leads mostly to rapidly evolving muscle rigidity, extensive rhabdomyolysis, electrolyte disorders, and renal failure and may be fatal. The goal of treatment is to reduce body core temperature with both symptomatic supportive care, including active cooling, and specific treatment options.

Neuropsychological and positron emission tomography correlates in idiopathic environmental intolerances.

OBJECTIVES: It has been hypothesized that people with subjective hypersensitivity to chemicals may indeed suffer from neuronal damage due to widely distributed environmental toxins and that such deficits of diagnostic importance can be demonstrated with the help of functional neuroimaging even in single cases. In this study, a small group of well-characterized patients with idiopathic environmental intolerance were examined in order to identify such changes. METHODS: Twelve patients with idiopathic environmental intolerance were investigated neuropsychologically and underwent cerebral F-18 fluorodeoxyglucose (F-18 FDG) positron emission tomography (PET). The imaging results were compared with findings from 17 healthy controls. RESULTS: Six patients showed deficits in verbal learning and memory, three of them also had a reduced information processing speed. In the individual analyses, 11 patients showed normal cerebral glucose metabolism. In the group analysis of the patients, no areas with significantly reduced glucose metabolism could be found. CONCLUSIONS: No consistent pathological cognitive performance and functional imaging pattern was found. It appears premature to claim specific neuropsychological or neuroimaging findings characteristic of idiopathic environmental intolerance. Therefore cerebral F-18 FDG PET should not be used to corroborate or rule out suspected idiopathic environmental intolerance, a syndrome whose potential biological underpinnings still need to be clarified.

Enteral exsorption of acetaminophen after intravenous injection in rats: influence of activated charcoal on this clearance path.

The fate of acetaminophen after intravenous injection in whole bowel-irrigated rats (n = 40) and the influence of activated charcoal on the kinetics were investigated. After randomization to four groups (n = 10, each group), plasma concentration and the quantities of acetaminophen and metabolites excreted into bile, urine and intestine were determined using an in vivo model with or without orally administered activated charcoal and with or without bile duct cannulation. The cumulative amount of acetaminiphen and metabolites exsorbed into the small intestine within 3.5 hr after intravenous injection was about 20% of dose in the animals with bile duct cannulation and about 7% of dose in the animals without. Correspondingly, about 13% of dose was detected in the externalized bile. Activated charcoal did not influence the amount exsorbed into the small intestine. Terminal half-life in plasma ranged from 35 to 51 min. within the four treatment groups without statistically significant difference (P = 0.152). Correspondingly, the area under the curve did not vary much and ranged between 2.6 and 3.3 g/min./l (P = 0.392). Deposition of acetaminophen and metabolites in liver and kidney after 3.5 hr was marginal and ranged between 0.02% and 0.6% of the dose within all groups. The excretion of acetaminophen and metabolites into urine varied strikingly between 31% and 56% of the dose within all groups and correlated with diuresis. The lack of effect of activated charcoal on the elimination of acetaminophen and metabolites may be due to the small amount of the drug being exsorbed into the intestine or the reduced adsorbent capacity of activated charcoal to acetaminophen and metabolites, which also could be influenced by inadequate luminal stirring.

Red blood cell acetylcholinesterase and plasma butyrylcholinesterase status: important indicators for the treatment of patients poisoned by organophosphorus compounds.

Inhibition of acetylcholinesterase (AChE) is regarded as the primary toxic mechanism of organophosphorus compounds (OP). Therapeutic strategies are directed to antagonise overstimulation of muscarinic receptors with atropine and to reactivate inhibited AChE with oximes. Reactivation is crucial within the neuromuscular synapse, where atropine is ineffective, since peripheral neuromuscular block eventually leads to respiratory failure. Patients with OP intoxication have to be identified as early as possible. During an international NBC-defence exercise anesthetised pigs were poisoned with sarin, followed by treatment with atropine and oxime. Blood samples were drawn and red blood cell (RBC)-AChE activity determined with a fielded test system on-site. Within a few minutes the poisoning was verified. After administration of HI-6, RBC-AChE activity increased rapidly. Blood samples were reanalysed in our laboratory in Munich. Almost identical course of the AChE activities was recorded by both systems.The more comprehensive cholinesterase status was determined in Munich. Oxime administration can be stopped when AChE is aged completely, but has to be continued as long as poison is present in the body and reactivation is possible. To aid the on-site physician in optimising diagnosis and treatment, a fielded test system should be available to allow rapid determination of the complete cholinesterase status.

Psychiatric morbidity and toxic burden in patients with environmental illness: a controlled study.

OBJECTIVE: Patients with environmental illness experience a large number of psychological symptoms. The nature of these symptoms and their pathogenesis (toxicogenic versus psychogenic) is controversial. The objective was to (1) characterize the nature of the psychological symptoms according to well-established diagnostic criteria, and (2) to investigate the association between toxicological factors and psychological symptoms. METHODS: Toxic burden, somatic morbidity, and psychiatric morbidity were assessed in 309 outpatients with environmental illness and 59 semiconductor industry workers matched for age and gender. Psychiatric disorders were assessed by a structured psychiatric interview (SCID), and distress was assessed by the Symptom-Checklist-90-Revised (SCL-90-R). Routine and specific laboratory tests in blood and urine samples were used to assess chemical exposures. RESULTS: Overall psychiatric morbidity was significantly higher in patients than in controls according to SCID (75% versus 24%). Somatoform, mood, and anxiety disorders were significantly more frequent in patients with environmental illness. They also revealed marked stress on the SCL-90-R somatization subscale and scored significantly higher than controls on most of the other subscales. Industry workers from the control group tended to have higher urine metal concentrations than environmental illness patients and similar concentrations of solvents in blood. CONCLUSION: Our data extend previous findings of high psychiatric morbidity in patients with environmental illness. They do not support the notion of a direct causal link between chemical exposure and the psychological symptoms.

New aspects of psychiatric morbidity in idiopathic environmental intolerances.

OBJECTIVE: To understand idiopathic environmental intolerances (IEI)-formerly multiple chemical sensitivities (MCS)-it is helpful to outline its characteristic psychiatric morbidity. METHOD: We applied a standardized interview according to the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (SCID) to 305 environmental patients with and without IEI. RESULTS: Somatoform, affective and anxiety disorders were the most frequent diagnoses but only slightly differed between patients with or without IEI. In both groups, current substance-related disorders were rare. We found a clearly higher prevalence of psychotic, especially current delusional disorders, in IEI. CONCLUSION: Somatization, depression, and anxiety are frequent in IEI but nonspecific. Psychotic disorders are more common in IEI than in other types of environmental illness. It appears worthwhile to study personality and cognitive style to explain the pivotal features of IEI.