Actualización en el manejo de intoxicación sistémica por anestésicos locales / Local anesthetics systemic toxicity: update in management

Systemic toxicity by local anesthetics an adverse reaction that occurs when local anesthetics (AL) reach significant systemic levels, primarily affects the central and cardiovascular nervous system, and while it is an infrequent event, it can be potentially fatal. The main determinant of the toxicity is the plasma concentration of LA, especially the free fraction. The most serious symptoms are seizures and cardiac arrest, which can occur with the administration of any LA. Bupivacaine is the most cardiotoxic of the commonly used LAs, followed in decreasing order by levobupivacaine, ropivacaine and lidocaine.

La intoxicación sistémica por anestésicos locales (ISAL), una reacción adversa que ocurre cuando los anestésicos locales (AL) alcanzan niveles sistémicos significativos, afecta principalmente al sistema nervioso central y cardiovascular, y si bien, es un evento infrecuente, puede ser potencialmente fatal. El principal determinante de la ISAL es la concentración plasmática de AL, en especial la fracción libre. Los síntomas más graves son las convulsiones y paro cardíaco, los cuales pueden ocurrir con la administración de cualquier AL. La bupivacaína es el más cardiotóxico de los AL comúnmente utilizados, seguido en orden decreciente por levobupivacaína, ropivacaína y lidocaína.

Intoxicación por etilenglicol, fisiopatología y enfrentamiento clínico / Ethylene glycol poisonin: an update

Toxic alcohols can produce severe poisoning with multiple organic involvement and even death. The most common form is ethylene glycol. The diagnosis can be extremely difficult if there is no history of its consumption. Its clinical presentation can simulate other conditions. Ethylene glycol poisoning is characterized by an initial rise in plasma osmolal gap that decreases during the evolution, while alcohol is metabolized to acids. This last condition causes a metabolic acidosis with elevated anion gap. The clinical manifestations are diffuse neurological involvement initially, followed by hemodynamic alterations due to myocardial damage associated with hypocalcemia and acidemia. Subsequently, severe tubular renal damage appears, which may require renal replacement therapy, and finally, focal neurological alterations. To treat this poisoning, it is necessary to inhibit the transformation of alcohol into acids, increase the metabolism of the latter or withdraw them directly with hemodialysis.

Caracterização biológica do extrato de cerdas de Lonomia descimoni (Lepidópteros, Saturniidae) e eficácia da soroterapia no envenenamento experimental / Biological characterization of Lonomia descimoni bristle extract (Lepidoptera, Saturniidae) and effectiveness of serotherapy in experimental poisoning

Nas Américas são descritas ao menos 12 espécies de lagartas do gênero Lonomia. Destas, existem relatos de envenenamentos graves por contato com lagartas L. obliqua e L. achelous, caracterizados por síndrome hemorrágica, com coagulopatia de consumo, insuficiência renal aguda e, em alguns casos, hemorragia intracraniana e morte. No Brasil, o Instituto Butantan desenvolveu um antiveneno utilizando como antígeno o extrato de cerdas de lagartas L. obliqua. No entanto, esse antiveneno tem sido utilizado em outros países da América do Sul, como Peru, Guiana Francesa, Venezuela e Colômbia, no tratamento do envenenamento causado por Lonomia de outras espécies. Na Colômbia, estudos realizados com as espécies L. orientoandensis e L. casanarensis demonstraram que ambas possuem toxinas com atividades potencialmente capazes de causar acidentes característicos do lonomismo. Além destas lagartas, a L. descimoni ainda não teve suas toxinas caracterizadas quanto às suas atividades biológicas, ou a sua neutralização pelo soro antilonômico produzido no Brasil, sendo este o objetivo desse trabalho. Foram avaliadas as atividades coagulante, fosfolipásica, hialuronidásica e desfibrinogenante, sempre comparando-se com as mesmas atividades presentes no extrato obtido de lagartas L. obliqua. Foi também determinado o reconhecimento imunológico e o poder neutralizante do soro antilonômico. Os resultados demonstraram que o extrato de L. descimoni possui ação coagulante, fosfolipásica e hialuronidásica, porém significantemente menos intensas que as observadas no extrato de L. obliqua. Além disso, o extrato de L. descimoni não possui atividade fibrinolítica. Quanto à ação desfibrinogenante, o extrato de L. descimoni foi capaz de induzir envenenamento experimental, com queda nos níveis de fibrinogênio e com hemoglobinúria apenas quando foi injetado pela via intravenosa nos ratos. O extrato de L. obliqua causa esses mesmos efeitos quanto injetados nos animais pela via intradérmica. O soro antilonômico reconheceu as toxinas presentes no extrato de L. descimoni e neutralizou a atividade coagulante desse extrato. Nossos resultados indicam que as lagartas Lonomia descimoni possuem toxinas com atividades mais fracas que as da L. obliqua, porém com potencial de causar envenenamento. Ademais, o soro antilonomico foi capaz de reconhecer e neutralizar as proteínas presentes no extrato de L. descimoni.

Increased risk for hypothyroidism after anticholinesterase pesticide poisoning: a nationwide population-based study.

PURPOSE: Previous animal studies have reported that acute anticholinesterase pesticide (organophosphate and carbamate) poisoning may affect thyroid hormones. However, there is no human study investigating the association between hypothyroidism and anticholinesterase pesticide poisoning, and therefore, we conducted a retrospective nationwide population-based cohort study to delineate this issue. METHODS: We identified 10,372 anticholinesterase pesticide poisoning subjects and matched 31,116 non-anticholinesterase pesticide poisoning subjects between 2003 and 2012 from the Nationwide Poisoning Database and the Longitudinal Health Insurance Database 2000, respectively, in a 1:3 ratio by index date, age, and sex for this study. We compared the cumulative incidence of hypothyroidism between the two cohorts by following up until 2013. Independent predictors for hypothyroidism were also investigated. RESULTS: In total, 75 (0.72%) anticholinesterase pesticide poisoning subjects and 184 (0.59%) non-anticholinesterase pesticide poisoning subjects were diagnosed with hypothyroidism during the follow-up. Cox proportional hazard regression analysis showed that anticholinesterase pesticide poisoning subjects had higher risk for hypothyroidism than did non-anticholinesterase pesticide poisoning subjects (adjusted hazard ratio: 1.47, 95% confidence interval: 1.11-1.95) after adjusting for age, sex, hypertension, malignancy, liver disease, renal disease, atrial fibrillation or flutter, thyroiditis, goiter, other endocrine disorders, and mental disorder. Stratified analysis showed that anticholinesterase pesticide poisoning subjects had higher risk for hypothyroidism than did non-anticholinesterase pesticide poisoning subjects in terms of the age subgroup of 40-64 years, female sex, past history of goiter, follow-up of <1 month, and anticholinesterase pesticide poisoning subjects without atropine treatment (incidence rate ratio [IRR]: 1.66, 95% confidence interval: 1.20-2.30). Female sex, malignancy, renal disease, thyroiditis, goiter, mental disorder, and anticholinesterase pesticide poisoning without atropine treatment were independent predictors for hypothyroidism. CONCLUSIONS: Anticholinesterase pesticide poisoning is associated with increased risk for hypothyroidism. Early evaluation of thyroid function in anticholinesterase pesticide poisoning subjects is suggested, especially in subjects without atropine treatment, aged 40-64 years, female sex, and past history of goiter.

Antioxidants as a Potential Preventive and Therapeutic Strategy for Cadmium.

Epidemiological studies provide a growing number of evidences that chronic exposure to relatively low levels of cadmium (Cd), nowadays taking place in industrialized countries, may cause health hazard. Thus, growing interest has been focused on effective ways of protection from adverse effects of exposure to this heavy metal. Because numerous effects to Cd's toxic action result from its prooxidative properties, it seems reasonable that special attention should be directed to agents that can prevent or reduce this metal-induced oxidative stress and its consequences in tissues, organs and systems at risk of toxicity, including liver, kidneys, testes, ears, eyes, cardiovascular system and nervous system as well as bone tissue. This review discusses a wide range of natural (plant and animal origin) and synthetic antioxidants together with many plant extracts (e.g. black and green tea, Aronia melanocarpa, Allium sativum, Allium cepa, Ocimum sanctum, Phoenix dactylifera, Physalis peruviana, Zingiber officinale) that have been shown to prevent from Cd toxicity. Moreover, some attention has been focused on the fact that substances not possessing antioxidative potential may also prevent Cd-induced oxidative stress and its consequences. So far, most of the data on the protective effects of the natural and synthetic antioxidants and plant extracts come from studies in animals' models; however, numerous of them seem to be promising preventive/therapeutic strategies for Cd toxicity in humans. Further investigation of prophylactic and therapeutic use of antioxidants in populations exposed to Cd environmentally and occupationally is warranted, given that therapeutically effective chelation therapy for this toxic metal is currently lacking.

Orchiectomy attenuates oxidative stress induced by aluminum in rats.

The aim of this work was to study whether the increase in antioxidant defenses associated with orchiectomy may account for the reduced susceptibility to aluminum (Al) in male kidney and also to examine whether the reduced antioxidant defenses are associated with androgen levels in orchiectomized (ORX) rats treated with testosterone propionate (TP). Rats were divided into nine groups, namely, intact males (without treatment, treated with sodium lactate, and treated with Al), sham males, ORX males (without treatment, treated with sodium lactate, treated with TP, treated with Al, and treated with TP and Al). Al groups were chronically treated with aluminum lactate for 12 weeks (0.575 mg Al/100 g of body weight, intraperitoneally, three times per week). We reported that ORX rats treated with Al had significantly less lipid peroxidation and an increased level of reduced glutathione (GSH) and GSH/oxidized glutathione ratio in the kidney when compared with intact and TP-treated ORX rats. The activity of superoxide dismutase, catalase, and glutathione peroxidase in ORX rats was much greater than in intact or TP-administered ORX rats. Castration reduced the glomerular alterations caused by Al as well as the number of necrotic tubular cells and nuclear abnormalities. However, we observed a slight alteration in brush border, dilation of proximal tubules, mononuclear infiltrates, and interstitial fibrosis. Castrated males treated with TP showed that this intervention cancels the protective effect of the ORX. This finding suggests that androgens contribute to the development of renal alterations and proteinuria in rats treated with Al. Our results showed that ORX rats are protected against the induction of oxidative stress by Al, but the morphological damage to the kidney tissue induced by the cation was only reduced. Male intact rats treated with Al had more severe glomerulosclerosis, tubular damage, and proteinuria than ORX rats.

Death following intentional ingestion of e-liquid.

CONTEXT: Electronic cigarette (e-cigarette) use is growing within the United States, resulting in both intentional and unintentional exposures to concentrated liquid nicotine or "e-liquid." Nicotine has been culpable for severe poisoning and deaths in the past. However, sources of nicotine have traditionally been from cigarettes, cigars, or pesticides. Fatalities due to liquid nicotine are rare, and fatalities following ingestion of e-liquid are even scarcer. CASE: We present a case of a 24-year-old woman who intentionally ingested up to 3000 mg of liquid nicotine intended for e-cigarette use. She was found in pulseless electrical activity and had return of spontaneous circulation (ROSC) after undergoing approximately 10 min of cardiopulmonary resuscitation with a blood pressure of 74/53 mmHg and a pulse rate of 106 beats/min. Despite aggressive supportive care, she ultimately died after she was found to have multiple acute infarcts, consistent with severe anoxic brain injury, on magnetic resonance imaging. The patient's toxicologic testing, obtained shortly after ROSC, was notable for plasma nicotine and cotinine levels each >1000 ng/mL. DISCUSSION: This fatality highlights the potential toxicity associated with suicidal ingestion of liquid nicotine.

Accidental and experimental Closantel intoxication in Uruguayan sheep / Intoxicação acidental e experimental por Closantel em ovinos no Uruguai

An outbreak of Closantel intoxication in sheep in Uruguay is described. The outbreak occurred in a group of 1300 weaning lambs treated orally with a 10% solution of Closantel. One hundred forty eight lambs showed clinical signs of intoxication and 14 died. The clinical signs included mydriasis, nystagmus, and negative pupillary reflex, bilateral blindness, bump into objects, and lateral movement of the head. No macroscopic lesions were observed. The histological lesions of the retina were cytoplasmic vacuolization in ganglion cells and in cells of the inner and outer nuclear layers with different degrees of atrophy. Vacuolization and axonal degeneration were observed in the optic nerve, with multifocal areas of fibrosis and infiltration by lymphocytes and Gitter cells. To reproduce the intoxication, four sheep were given two, four and 10 times the therapeutic dose of Closantel (0.1g/kg of BW). Only the animals receiving 10 times the recommended dose showed clinical signs. The histological examination of the lesions in experimental sheep showed similar results to those described in the accidental outbreak, except for the absence of optic nerve fibrosis and inflammation, characterizing an acute phase. Axonal myelin sheaths loss, fibroblasts and collagen fibers were observed in the ultrastructural study of the optic nerve of accidental intoxicated animals. The optic nerve of experimentally intoxicated animals had vacuoles that separated the myelin sheaths of axons. To prevent outbreaks it is suggested to weigh the animals before Closantel administration to avoid errors in dose calculation.

Descreve-se um surto de intoxicação por Closantel em ovinos no Uruguai. O surto ocorreu em um lote de 1300 cordeiros que foram dosados com uma solução de Closantel 10%, por via oral. Do total, 148 apresentaram sinais clínicos de intoxicação e 14 morreram. Os sinais clínicos incluíam midríase, nistagmo, reflexo pupilar negativo, cegueira bilateral, pressão da cabeça contra objetos e desvio lateral da cabeça. Lesões macroscópicas não foram observadas. Histologicamente havia vacuolização citoplasmática das células ganglionares e nas células das camadas nuclear interna e externa. Na retina havia, também, diferentes graus de atrofia. Vacuolização e degeneração axonal foram observados no nervo óptico, com áreas multifocais de fibrose e infiltrado de linfócitos e células Gitter. Quatro ovinos receberam experimentalmente duas, quatro e 10 vezes a dose terapêutica de Closantel (0,1 g/kg de peso vivo). Apenas os animais que receberam 10 vezes a dose recomendada apresentaram sinais clínicos. O exame histológico nos ovinos experimentais mostrou resultados semelhantes aos do surto, com exceção da ausência de fibrose e infiltrado inflamatório do nervo óptico, caracterizando um quadro agudo. Foram observadas a perda da bainha de mielina dos axônios e a presença de fibroblastos e fibras colágenas no estudo ultra-estrutural do nervo óptico de animais intoxicados espontaneamente. No nervo óptico de animais intoxicados experimentalmente havia vacúolos que separavam as bainhas de mielina dos axônios. Para evitar surtos, sugere-se pesar os animais antes da administração de Closantel para evitar erros no cálculo da dose.

Intoxicação experimental pelos frutos de uva-Japão, hovenia dulcis (rhamnaceae), em bovinos / Experimental poisoning by the fruits of hovenia dulcis (rhamnaceae) in cattle

Hovenia dulcis Thunberg (uva-Japão) é uma árvore caducifolia nativa da China e de alguns lugares do Japão. Nos últimos anos essa planta foi utilizada como forma de sombreamento para aviários no Oeste e Meio-Oeste de Santa Catarina e passou a disseminar-se por toda a região. Os bovinos comem avidamente seus frutos maduros quando caem ao chão. Suspeitas de intoxicação ocorreram no outono e início de inverno e coincidiam com a maturação dos frutos. A doença foi reproduzida em 2004 por outros autores através da administração dos frutos a bovinos, em dose única de 24,5g/kg. Nos anos subsequentes não ocorreram reclamações sobre a intoxicação pelos frutos dessa planta, embora, muitos criadores afirmavam que os bovinos, na temporada de maturação, continuavam a ingerir os frutos. Experimentalmente, nove bovinos que receberam frutos da planta em doses únicas entre 30 e 50g/kg, apenas dois bovinos adoeceram gravemente e um morreu. O quadro clínico e as lesões foram semelhantes à intoxicação reproduzida em 2004, porém, a dose necessária para reproduzirmos a doença foi 100% superior à dose tóxica preconizada como letal em 2004.

Hovenia dulcis Thunberg (Japan grape) is a deciduous tree native of China and some parts of Japan. Over the last years, the tree has been used for shading in poultry farms of western and middle western Santa Catarina, spreading in the region. Cattle ingest the ripe fruits of H. dulcis fallen to the ground. The fruits were suspected to cause poisoning during fall and early winter, period of their maturation. The disease has been reproduced in 2004 by other authors with a single dose of 24.5g/kg. In the subsequent years no complaints regarding the toxicity of H. dulcis fruits have been reported, although many breeders observed that cattle continued to consume them during the ripening season. We administered the fruits at single doses of 30-50g/kg to nine calves, only two of them became seriously ill and one died. The clinical picture and lesions were similar to the poisoning reproduced in 2004, however, the dose required to reproduce the poisoning was 100% higher than the lethal dose found in 2004.

Substitution effects of a carbonated hydroxyapatite biomaterial against intoxication chloride nickel-exposed rats.

AIMS: This study aimed to investigate the potential effects of a synthetic apatite (carbonated hydroxyapatite) on the detoxification of a group of male "Wistar" rats exposed to nickel chloride. METHODS: Toxicity was evaluated by rats' bioassay of nickel chloride. Wistar rats received this metal daily by gavage for seven days (4 mg/ml nickel chloride/200 g body weight, BW). To detoxify this organism, a subcutaneous implantation of the apatite is made. RESULTS: The results revealed that exposure to nickel induced oxidative stress, disorders in the balances of ferric phosphocalcic, renal failures, liver toxicity and significant increase in nickel rates in the bones of intoxicated rats. The application of the carbonated hydroxyapatite presented in this study restored those disorders back to normal. The synthetic apatite protected the rats against the toxic effects of nickel by lowering the levels of lipid peroxidation markers and improving the activities of defense enzymes. It also amended ferric and phosphocalcic equilibriums, protected liver and kidney functions and reduced the nickel rate in the bones of the rats. Overall, the results provided strong support for the protective role of carbonated hydroxyapatite in the detoxification of rats exposed to nickel. Those beneficial effects were further confirmed by physico-chemical characterization (X-ray diffraction and infrared spectroscopy), which revealed its property of anionic and cationic substitution, thus supporting its promising candidacy for future biomedical application. CONCLUSION: The hydroxyapatite is an effective biomaterial to solve health problems, particularly detoxification against metals (nickel).

Acute kidney injury associated with smoking synthetic cannabinoid.

CONTEXT AND OBJECTIVES: Synthetic cannabinoids are illegal drugs of abuse known to cause adverse neurologic and sympathomimetic effects. They are an emerging health risk: 11% of high school seniors reported smoking them during the previous 12 months. We describe the epidemiology of a toxicologic syndrome of acute kidney injury associated with synthetic cannabinoids, review the toxicologic and public health investigation of the cluster, and describe clinical implications of the cluster investigation. MATERIALS AND METHODS: Case series of nine patients affected by the toxicologic syndrome in Oregon and southwestern Washington during May-October 2012. Cases were defined as acute kidney injury (creatinine > 1.3 mg/dL) among persons aged 13-40 years without known renal disease who reported smoking synthetic cannabinoids. Toxicology laboratories used liquid chromatography and time-of-flight mass spectrometry to test clinical and product specimens for synthetic cannabinoids, their metabolites, and known nephrotoxins. Public health alerts informed clinicians, law enforcement, and the community about the cluster and the need to be alert for toxidromes associated with emerging drugs of abuse. RESULTS: Patients were males aged 15-27 years (median, 18 years), with intense nausea and flank or abdominal pain, and included two sets of siblings. Peak creatinine levels were 2.6-17.7 mg/dL (median, 6.6 mg/dL). All patients were hospitalized; one required dialysis; none died. No alternate causes of acute kidney injury or nephrotoxins were identified. Patients reported easily purchasing synthetic cannabinoids at convenience, tobacco, and adult bookstores. One clinical and 2 product samples contained evidence of a novel synthetic cannabinoid, XLR-11 ([1-(5-fluoropentyl)-1H-indol-3-yl](2,2,3,3-tetramethylcyclopropyl)methanone). DISCUSSION AND CONCLUSION: Whether caused by direct toxicity, genetic predisposition, or an as-yet unidentified nephrotoxin, this association between synthetic cannabinoid exposure and acute kidney injury reinforces the need for vigilance to detect new toxicologic syndromes associated with emerging drugs of abuse. Liquid chromatography and time-of-flight mass spectrometry are useful tools in determining the active ingredients in these evolving products and evaluating them for toxic contaminants.

Edaravone mitigates hexavalent chromium-induced oxidative stress and depletion of antioxidant enzymes while estrogen restores antioxidant enzymes in the rat ovary in F1 offspring.

Environmental contamination of drinking water with chromium (Cr) has been increasing in more than 30 cities in the United States. Previous studies from our group have shown that Cr affects reproductive functions in female Sprague Dawley rats. Although it is impossible to completely remove Cr from the drinking water, it is imperative to develop effective intervention strategies to inhibit Cr-induced deleterious health effects. Edaravone (EDA), a potential inhibitor of free radicals, has been clinically used to treat cancer and cardiac ischemia. This study evaluated the efficacy of EDA against Cr-induced ovarian toxicity. Results showed that maternal exposure to CrVI in rats increased follicular atresia, decreased steroidogenesis, and delayed puberty in F1 offspring. CrVI increased oxidative stress and decreased antioxidant (AOX) enzyme levels in the ovary. CrVI increased follicle atresia by increased expression of cleaved caspase 3, and decreased expression of Bcl2 and Bcl2l1 in the ovary. EDA mitigated or inhibited the effects of CrVI on follicle atresia, pubertal onset, steroid hormone levels, and AOX enzyme activity, as well as the expression of Bcl2 and Bcl2l1 in the ovary. In a second study, CrVI treatment was withdrawn, and F1 rats were injected with estradiol (E2) (10 µg in PBS/ethanol per 100 g body weight) for a period of 2 wk to evaluate whether E2 treatment will restore Cr-induced depletion of AOX enzymes. E2 restored CrVI-induced depletion of glutathione peroxidase 1, catalase, thioredoxin 2, and peroxiredoxin 3 in the ovary. This is the first study to demonstrate the protective effects of EDA against any toxicant in the ovary.

Outpatient toxicology clinic experience of patients with hip implants.

CONTEXT: With regard to biological effects, the increasing number of early failure of metal-on-metal (MoM) hip arthroplasties and possible parenteral exposure to orthopedic metal alloys have caused concern for patients and providers alike. OBJECTIVE: We sought to characterize our outpatient clinical experience of patients with MoM and other forms of hip implants and associated serum/blood chromium and cobalt levels, with a focus on possible systemic sequelae. METHODS: This was an observational and retrospective chart review of consecutive patients presenting to two outpatient medical toxicology clinics from January 1, 2010-June 1, 2012 with history of hip implants. Presenting signs, symptoms, and interventions were reviewed. Available cobalt and chromium levels were summarized as median concentration with interquartile range. RESULTS: A total of 39 patients were analyzed; of the 39 patients, 26 had MoM hip implants while 13 did not. Twelve patients exhibited no symptoms and nine sought evaluation for fatigue while two other patients had been previously diagnosed with fibromyalgia. Tinnitus/hearing loss was also a frequent complaint noted in 12 patients (one presenting complaint), however there was no difference between the incidence of this symptom between the MoM and non-MoM groups. Three patients were provisionally diagnosed with demyelinating neuropathy with one patient demonstrating marked (subjective and objective) improvement after revision. Patients with MoM arthroplasties generally exhibit an approximately tenfold increase in metal ion levels than traditional arthroplasties. Finally, 20 (51.2%) patients had replacement or revision of their hip implant with subsequent decreases in metal ion levels. DISCUSSION: A majority of our patients had minor symptoms (fatigue and muscle aches) or no symptoms (n = 23 or 59%). Documented peripheral neurotoxicity is uncommon. The decision for hip revision solely for toxicologic reasons is rare and usually involves a multidisciplinary approach. CONCLUSION: Most patients seeking toxicologic referral may be minimally symptomatic and seek guidance regarding elevated blood or serum metal ions; however, solely toxicologic-based interventions are unusual. Revision was associated with a decrease in metal ion levels; however, subjective complaints did not correlate with metal ion levels.

A review of emergency cardiopulmonary bypass for severe poisoning by cardiotoxic drugs.

Cardiovascular collapse remains a leading cause of death in severe acute drug intoxication. Commonly prescribed medications such as antidysrhythmics, calcium channel antagonists, and beta adrenergic receptor antagonists can cause refractory cardiovascular collapse in massive overdose. Emergency cardiopulmonary bypass (ECPB), a modality originating in cardiac surgery, is a rescue technique that has been successfully implemented in the treatment of refractory cardiogenic shock and cardiac arrest unresponsive to traditional medical interventions. More recently a growing number of animal studies, case reports, and case series have documented its use in refractory hemodynamic collapse in poisoned patients. This article will review current ECPB techniques and explore its growing role in the treatment of severely hemodynamically compromised poisoned patients.

Clinical, high resolution computed tomography and pulmonary function in sulphur mustard victims.

We aimed to evaluate clinical, high resolution computed tomography (HRCT) and pulmonary function test (PFT) findings after 18-23 years of exposure in veterans of sulphur mustard (SM) exposure. We performed a cross-sectional study of 106 patients. Inclusion criteria were 1: documented exposure to SM as confirmed by toxicological analysis of their urine and vesicular fluid after exposure 2: single exposure to SM that cause skin blisters and subsequent transient or permanent sequel. Cigarette smoking and pre-exposure lung diseases were of exclusion criteria. After taking history and thorough respiratory examination, patients underwent high resolution computed tomography and spirometry. Clinical diagnoses were made considering the findings. More than 85% of the patients were complaining of dyspnea and cough. Obstructive pattern (56.6%) was main finding in spirometry followed by restrictive and normal patterns. HRCT revealed air trapping (65.09%) and mosaic parenchymal attenuation patterns (58.49%) as most common results. Established diagnoses mainly were chronic obstructive pulmonary disease (COPD) (54.71%), bronchiolitis obliterans (27.35%) and asthmatic bronchitis (8.49%). There were not any significant association between the clinical findings and results of PFT and HRCT imaging and also between PFT and HRCT findings (P-values were more than 0.05). Considering debilitating and progressive nature of the respiratory complications of SM exposure, attempts are needed for appropriate diagnosis and treatment.

Surto de intoxicação por sal em suínos em Santa Catarina / Outbreak of salt poisoning in pigs in Santa Catarina

Descreve-se a ocorrência de surto de intoxicação por sal em suínos de duas propriedades, onde 70 porcos morreram. Soro de leite proveniente da salga de queijo era servido no cocho como única fonte hídrica aos animais. Não havia bebedouros nas instalações. Um dia após o fornecimento do soro, os porcos começaram a adoecer e apresentaram salivação excessiva, movimentos de pedalagem, opistótono e tremores cíclicos. Na necropsia, dois suínos apresentaram achatamento das circunvoluções do córtex telencefálico e um outro, edema no córtex telencefálico. Na histopatologia, observou-se necrose neuronal laminar difusa acentuada no córtex telencefálico, astrócitos de Alzheimer tipo II (AIIA), infiltrado multifocal perivascular de eosinófilos e linfócitos e edema perivascular. Outros achados incluíram marcação imuno-histoquímica fraca ou ausente para proteína glial fibrilar ácida (GFAP), mas intensa marcação positiva no citoplasma dos AIIA para S-100. As concentrações de sódio sérico e do líquor mensuradas nos porcos estudados foram de 140 e 156mmol/L, respectivamente.

A total of 70 pigs were affected and died due to salt poisoning in two farms in southern Brazil. The only source of drinking water available to the pigs was whey from cheese salting process. One day after receiving the whey, animals started getting sick and showed excessive salivation, opisthotonus, paddling, and cyclic tremors. At necropsy of three pigs, two of them presented flattening of gyri and the other one presented cortical telencephalon edema. Microscopically, severe diffuse neuronal necrosis in telencephalic laminar cortex, Alzheimer type II astrocytes (AIIA), eosinophilic and lymphocytic perivascular cuffing apart of perivascular edema were observed. Weak or absent anti-glial fibrillary acidic protein (GFAP) immunolabeling was associated with positive immunostaining for S-100 in AIIA cytoplasm. Concentration of sodium in serum and liquor samples from dead pigs resulted 140 and 156mmol/L, respectively.

Iron poisoning: a literature-based review of epidemiology, diagnosis, and management.

Although seen less frequently than acetaminophen or salicylate poisoning, acute iron poisoning remains a dangerous threat, particularly to pediatric patients. Multiple factors-including legal and manufacturing practices-have changed the landscape of iron poisoning over the decades. Despite these changes, diagnosis and management of iron poisoning have minimally evolved, and the current evidence for iron poisoning is yet based principally on case series, expert consensus, animal studies, and adult volunteer studies. This review article describes in detail the epidemiology of acute iron poisoning as it relates to the pediatric patient, as well as the historical and current array of literature on diagnosis and management.

Toxicology in the ICU: Part 1: general overview and approach to treatment.

Poisonings, adverse drug effects, and envenomations continue to be commonly encountered. Patients often present critically ill and warrant ICU admission. Many other patients who are initially stable have the potential for rapid deterioration and require continuous cardiopulmonary and neurologic monitoring. Given the potential for rapid deterioration, and because patients need continuous monitoring, ICU admission is frequently required. This article is the first of a three-part series to be published in CHEST; it discusses general management, laboratory tests, enhanced elimination, and emerging therapies. The second article will address the management of specific overdoses; the last will cover plants, mushrooms, envenomations, and heavy metals.

An alternative antidote therapy in amitriptyline-induced rat toxicity model: theophylline.

We planned this study in order to investigate the effects of theophylline on cardiovascular parameters in an anaesthetized rat model of amitriptyline toxicity. In the preliminary study, we tested theophylline as 1 mg/kg of bolus, followed by a 0.5-mg/kg infusion. Toxicity was induced by the infusion of 0.94 mg/kg/min of amitriptyline up to the point of a 40-45% inhibition of mean arterial pressure (MAP). The rats were randomized to two groups: a group of 5% dextrose bolus followed by 5% dextrose infusion, and another group with theophylline bolus followed by infusion. Amitriptyline caused a significant decrease in MAP and prolongation in QRS; however, it did not alter heart rate (HR). When compared to the dextrose group, theophylline administration increased MAP, shortened prolonged QRS duration, and increased HR (P < 0.05, respectively). There was no statistically significant difference in the results of arterial blood-gas analyses among the groups (P > 0.05). Bolus doses followed by a continuous infusion of theophylline were found to be effective in reversing the hypotension and QRS prolongation seen in amitriptyline toxicity. One of the possible explanations of this beneficial effect is nonselective adenosine antagonism of theophylline. Further studies are needed to reveal the exact mechanism of the observed effect.