France – Très présents pour décorer nos intérieurs durant les fêtes de fin d’année, le houx, le gui ou encore le poinsettia sont des plantes toxiques en cas d’ingestion. Cette mise en garde de l’Agence nationale de sécurité sanitaire de l’alimentation, de l’environnement et du travail (Anses) vaut aussi bien pour les hommes et pour les animaux [1].
L’ingestion de baies ou de feuilles par les enfants ou les animaux peut s’avérer toxique et provoquer des symptômes plus ou moins graves en fonction des quantités consommées, rappelle l’Agence.
Le houx responsable de 60 à 80 appels chaque année
Les petites branches et feuilles de houx (Ilex aquifolium) sont souvent utilisées pour fabriquer des couronnes ou décorer les gâteaux de Noël. Mais attention aux enfants qui attirés par les petites baies rouges qui ornent la base des feuilles les attrapent ou les ramassent et sont susceptibles de les porter à la bouche. Les chiffres sont loin d’être anecdotique : « chaque année, les Centres antipoison reçoivent entre 60 et 80 appels pour des enfants de moins de 15 ans qui ont accidentellement mis à la bouche des baies de houx ». Près de 40% des cas surviennent au moment des fêtes de fin d’année entre décembre et janvier.
En pratique, dans la grande majorité des cas, les enfants mettent à la bouche ou ingèrent une ou deux baies, ne provoquant pas de symptômes graves ou uniquement des troubles digestifs mineurs (nausées, vomissements, douleurs abdominales). C’est lorsqu’il ingère un plus grand nombre de baies que peuvent apparaitre des symptômes plus prononcés comme une salivation importante, des vomissements et diarrhées persistantes, voire une somnolence ou des convulsions.
Animaux domestiques : les feuilles et baies de houx sont également toxiques en cas d’ingestion par les animaux de compagnie (chien, chat…). Ils peuvent présenter des signes digestifs (diarrhée, vomissements…) voire neurologiques (somnolence, coma…) en cas d’ingestion d’une quantité importante de baies.
Le gui, toxique pour les Hommes et parfois mortel pour les animaux
Considéré comme sacré par les Celtes qui lui attribuaient des vertus médicales et miraculeuses, le gui (Viscum album) est lui aussi très présents dans les intérieurs et les jardins au moment des fêtes. Contrairement au houx, ce sont ses feuilles et non ses baies blanches qui sont toxiques en cas d’ingestion. « Les Centres antipoison reçoivent une quarantaine d’appels par an concernant des enfants de moins de 15 ans qui ont porté à la bouche des feuilles ou baies, entre novembre et janvier pour les trois-quarts d’entre eux » rapporte l’Anses. La plupart des enfants ne présentent pas de symptôme ou des signes digestifs sans gravité (vomissements, diarrhée…), du fait d’ingestion d’un petit nombre de baies.
Cependant, là encore, l’ingestion d’un nombre élevé de baies peut entrainer des troubles cardiaques (troubles du rythme cardiaque, baisse de la pression artérielle…) ou neurologiques (somnolence…).
Animaux domestiques : les feuilles et baies de gui sont également toxiques, voire mortelles, si elles sont consommées par nos animaux de compagnie, mais aussi pour les herbivores des pâturages comme les vaches, les moutons ou encore les chevaux.
Poinsettia : des troubles digestifs sans gravité chez l’enfant
Enfin, le Poinsettia (Euphorbia pulcherrima) ou “étoile de Noël”, dont les feuilles se parent de couleurs rouges ou plus claires à la fin de l’année, est un cadeau classique pendant les fêtes. La mise à la bouche d’une feuille peut provoquer des troubles digestifs sans gravité chez l’enfant.
Animaux domestiques : le mâchonnement de plusieurs feuilles ou de tiges peut avoir des conséquences plus importantes : troubles digestifs, salivation excessive….
Que faire en cas d’ingestion ?
Si l’enfant a mis à la bouche des feuilles ou des baies de houx, de gui, ou d’autres plantes d’ornement : nettoyez-lui la bouche avec un linge mouillé, ne le faites pas boire et appelez un Centre antipoison.
En cas d’intoxication de votre animal, appelez un Centre antipoison vétérinaire.
Dans tous les cas, conservez l’étiquette ou une photographie de la plante pour en faciliter l’identification.
Recently, I posted a case that involved an older woman who presented to me for the first time and had been on a long-term benzodiazepine. Although she was not happy with me when I began the discussion about deprescribing her sleep medication, I chose to educate her on risks of this medication and begin a slow taper.
This case seemed to resonate with many readers, as evidenced by the fact that over 100 of you elected to write a comment. Collectively, this level of interest highlights the high-wire act that is clinical practice when the patient and treating healthcare professional (HCP) fail to see eye-to-eye. As one savvy physician noted, “You just can’t condense a case like this into choosing between four check boxes.” Thank goodness this is never the case in clinical practice.
The confrontation with this patient escalated quickly when I brought up the subject of her long-term use of alprazolam. Thus, my first goal was to at least attempt to deescalate the emotions involved. Has there ever been a situation in which a clinical decision was improved by fear, anger, or frustration in either the patient or the professional?
Some of you pointed out that the therapeutic alliance was broken the moment that the patient started making threats. I would argue that is not true and that this patient encounter can be salvaged. Doing so, however, would require a step back on the part of the HCP and some open and clarifying questions as to what happened during her previous efforts to discontinue alprazolam.
I guessed that her previous attempts featured more abrupt discontinuation and no attempt to couple the weaning of alprazolam with other tools to promote better sleep hygiene. Addressing these previous episodes with empathy not only will assist me in my attempt to develop patient trust, but it will also likely help me to chart a precise therapeutic plan with my new patient. Most important, it enlisted her to play a large role in establishing this plan, investing her in the plan of care and increasing the likelihood of adherence.
Therefore, I respectfully disagree with the concept of firing or discharging this patient from practice that was suggested by some readers. I think that we can work together to improve her overall well-being. Just look at that nice example with the aspirin! She heard my concerns about the potential downside of her daily baby aspirin and was willing to discontinue it.
As for her threats to write letters to my superiors and the medical board, I would be happy to defend practicing evidence-based medicine in an empathic way. But the scenario does provide a good reminder to always document counseling and shared decision-making in these encounters.
Several readers were absolutely right in stating that this patient may have multiple reasons for insomnia, such as pain and anxiety. Those reasons need to be better elucidated and treated. But I also believe in the data that benzodiazepines truly are harmful for older adults. So to assume that everything will be fine over the next several years as she approaches 80 years of age on chronic treatment with alprazolam is dangerous.
Having this conversation at the very first visit is an important and necessary step in trying to reduce her dependence on alprazolam. But it is not going to be the only time we discuss the management of insomnia. She should be reassured that I would like to continue the alprazolam for the next couple of visits as we pursue a tapering dose.
In addition, I would strongly recommend talk therapy to provide her with tools to combat chronic insomnia. And I would make sure to emphasize that all of this effort is designed to help her live longer and happier.
Will this be successful? My experience is yes, more often than not. Regardless, the effort is worth it, no matter who is screaming.
Charles P. Vega, MD, is a clinical professor of family medicine at UC Irvine and also serves as the UCI School of Medicine assistant dean for culture and community education. He focuses on medical education with an intent to resolve health disparities.
Cases of poisoning — intentional and unintentional — from ingestion of alcohol-based hand sanitizer have soared during the COVID-19 pandemic.
In the United Kingdom alone, alcohol-based hand sanitizer poisonings reported to the National Poisons Information Service (NPIS) jumped 157% — from 155 between January 1 and September 16, 2019, to 398 between January 1 and September 14, 2020, new research shows.
More needs to be done to protect those at risk of unintentional and intentional swallowing of alcohol-based hand sanitizer, including children, people with dementia/confusion, and those with mental health issues, according to Georgia Richards, DPhil student, Centre for Evidence-Based Medicine, Nuffield Department of Primary Care Health Sciences, University of Oxford, England.
“If providers are supplying alcohol-based hand sanitizers in the community to reduce the spread of SARS-CoV-2, the contents should be supplied in lockable and automated dispensers to reduce contamination and improve safety,” Richards told Medscape Medical News.
The study was published online December 1 in BMJ Evidence-Based Medicine.
European, US Poisoning Rates Soar
In the paper Richards describes two deaths that occurred in hospitals in England.
In one case, a 30-year-old woman, detained in a psychiatric unit who received the antidepressant venlafaxine was found dead in her hospital bed with a container of hand-sanitizing gel beside her.
“The gel was readily accessible to patients on the ward from a communal dispenser, and patients were allowed to fill cups or other containers with it to keep in their rooms,” Richards reports.
A post-mortem analysis found a high level of alcohol in her blood (214 mg of alcohol in 100 mL of blood). The medical cause of death was listed as “ingestion of alcohol and venlafaxine.” The coroner concluded that the combination of these substances suppressed the patient’s breathing, leading to her death.
The other case involved a 76-year-old man who unintentionally swallowed an unknown quantity of alcohol-based hand-sanitizing foam attached to the foot of his hospital bed.
The patient had a history of agitation and depression and was treated with antidepressants. He had become increasingly confused over the preceding 9 months, possibly because of vascular dementia.
His blood ethanol concentration was 463 mg/dL (100 mmol/L) initially and 354 mg/ dL (77mmol/L) 10 hours later. He was admitted to the intensive care unit, where he received lorazepam and haloperidol and treated with ventilation, with a plan to allow the alcohol to be naturally metabolized.
The patient developed complications and died 6 days later. The primary causes of death were bronchopneumonia and acute alcohol toxicity, secondary to acute delirium and coronary artery disease.
Since COVID-19 started, alcohol-based hand sanitizers are among the most sought-after commodities around the world. The volume of these products — now found in homes, hospitals, schools, workplaces, and elsewhere — “may be a cause for concern,” Richards writes.
Yet, warnings about the toxicity and lethality of intentional or unintentional ingestion of these products have not been widely disseminated, she notes.
To reduce the risk of harm, Richards suggests educating the public and healthcare professionals, improving warning labels on products, and increasing the awareness and reporting of such exposures to public health authorities.
“While governments and public health authorities have successfully heightened our awareness of, and need for, better hand hygiene during the COVID-19 outbreak, they must also make the public aware of the potential harms and encourage the reporting of such harms to poisons information centers,” she notes.
Increases in alcohol-based hand sanitizer poisoning during the pandemic have also been reported in the United States.
The American Association of Poison Control Centers (AAPCC) reports that data from the National Poison Data System (NPDS) show 32,892 hand sanitizer exposure cases reported to the 55 US poison control centers from January 1 through November 15, 2020 — an increase of 73% compared with the same time period during the previous year.
An Increase in Self-Harm
Weighing in on this issue, Robert Bassett, DO, associate medical director of The Poison Control Center at Children’s Hospital of Philadelphia, Pennsylvania, told Medscape Medical News that “cleaning agents and disinfectants have been around for eons and their potential for toxicity hasn’t changed.”
“Now with COVID, and this hyper-vigilance when it comes to cleanliness, there is increased access and the exposure risk has gone up,” he said.
“One of the sad casualties of an overstressed healthcare system and a globally depressed environment is worsening behavioral health emergencies and, as part of that, the risk of self-harm goes up,” Bassett added.
“The consensus is that there has been an exacerbation of behavioral health emergencies and behavioral health needs since COVID started and hand sanitizers are readily accessible to someone who may be looking to self-harm,” he said.
This research had no specific funding. Richards is the editorial registrar of BMJ Evidence Based Medicine and is developing a website to track preventable deaths. Bassett has disclosed no relevant financial relationships.
BMJ Evid Based Med. Published online December 1, 2020. Full text
Marijuana use was associated with a higher prevalence of recurrent myocardial infarction (MI) and a greater risk of bleeding or stroke after percutaneous coronary intervention (PCI) in separate studies.
Rhushik Bhuva, MD, presented the recurrent-MI results from a national US study, and Sang Gune K. Yoo, MD, presented the PCI study, which used data from a Michigan cohort. The studies were presented at the virtual American Heart Association (AHA) Scientific Sessions 2020.
Both studies “add to our accumulating knowledge of the cardiovascular risks of marijuana,” Ersilia M. DeFilippis, MD, a cardiology fellow at Columbia University Irvine Medical Center, New York City, who was not involved with this research, told theheart.org | Medscape Cardiology.
DeFilippis and the two study authors say clinicians and patients need to be more aware of cardiovascular risks from smoking marijuana, and they call for more patient screening, counseling, and research.
Need for Screening, Counseling
Marijuana is a Schedule 1 controlled substance in the United States, which makes it illegal to conduct rigorous controlled trials of marijuana products. Existing knowledge is therefore based on observational studies, DeFilippis noted.
She was lead author of a review of marijuana use by patients with cardiovascular disease. The review was published in January 2020 in the Journal of the American College of Cardiology. An AHA scientific statement about marijuana and cardiovascular health was published in Circulation in August 2020.
Both documents drew attention to risks from marijuana use in patients with cardiovascular disease.
Until more data are available, “I think it’s absolutely critical” that cardiologists and general providers screen patients for marijuana use, “either at the time of their MI or ideally prior to that, when they are making a cardiovascular risk assessment,” said DeFilippis.
That is also the time to “counsel patients, especially those who have had an MI, about risks associated with continuing to use marijuana.”
Importantly, providers and patients need to be aware that “cannabinoids, through the cytochrome P450 system, can interact with well-known cardiovascular medications, which we know provide benefit in the post-MI period,” she added. “For example, marijuana can interfere with beta blockers, statins, antiarrhythmics, and certain anticoagulants.”
Bhuva, a cardiology fellow with the Wright Center for Community Health, Scranton, Pennsylvania, said that it is “concerning” that “recurrent heart attacks and cardiac interventions [were] higher among cannabis users, even though they were younger and had fewer risk factors for heart disease.
“Spreading awareness regarding the potential risk of recurrent heart attacks in middle-aged, African American and male cannabis users and screening them at an earlier age for potential risk factors of future heart attacks should be encouraged among clinicians,” he urged in a statement from the AHA.
Yoo, an internal medicine resident at the University of Michigan, Ann Arbor, pointed out that in their study of patients who underwent PCI after MI or because they had coronary artery disease, those who smoked or vaped marijuana were younger and were more likely to be male. They were less likely to have traditional cardiovascular risk factors except for smoking tobacco, which was highly prevalent.
After propensity matching, patients who used marijuana had a 1.5-fold increased risk of in-hospital bleeding and an 11-fold higher risk for in-hospital stroke following PCI.
However, the absolute number of strokes in PCI was small, and the confidence interval was wide (indicating a large uncertainty), Yoo pointed out to theheart.org | Medscape Cardiology.
These risks “should not deter patients from undergoing these [lifesaving] procedures,” he said; however, clinicians should be aware of these risks with marijuana use and should screen and counsel patients about this.
Hospitalized Patients With Prior MI
Bhuva and colleagues identified patients from the National Inpatient Sample who were hospitalized in the United States from 2007 to 2014 and who had had a prior MI and had undergone revascularization with PCI or coronary artery bypass grafting (CABG).
There were about 8 million hospital stays per year. The database did not specify the type of marijuana that patients used.
During the 8-year study period, many states legalized or decriminalized medical and/or recreational marijuana, and marijuana use increased steadily, from 0.2% to 0.7%.
Fewer marijuana users had hypertension (72% vs 75%), diabetes (24% vs 33%), or dyslipidemia (51% vs 58%; all P < .001).
More marijuana users underwent a repeat MI (67% vs 41%).
On the other hand, marijuana users, who were younger and healthier than the other patients, were less likely to die during hospitalization for a recurrent MI (0.8% vs 2.5%), and their hospital costs were lower.
The researchers acknowledge that study limitations include lack of information about marijuana type (smoked, edible, medicinal, or recreational) or dose, as well as the time from marijuana use to cardiac event.
In-Hospital Outcomes After PCI
Yoo and colleagues analyzed data from patients who underwent PCI from January 1, 2013, to October 1, 2016, at Michigan’s 48 nonfederal hospitals, which are part of the Blue Cross Blue Shield Michigan Cardiovascular Consortium PCI registry.
In this cohort, 3970 patients (3.5%) had smoked or vaped marijuana in the month prior to PCI, and 109,507 patients had not done so.
The marijuana users were younger (mean age, 54 vs 66) and were more likely to be male (79% vs 67%) and to smoke cigarettes (73% vs 27%).
They were less likely to have hypertension, type 2 diabetes, dyslipidemia, cerebrovascular disease, or prior CABG and were equally likely to have had a prior MI (36%).
Compared to nonusers, marijuana users were more likely to present with NSTEMI (30% vs 23%) or STEMI (27% vs 16%) and were less likely to present with angina.
Using propensity score matching, the researchers matched 3803 marijuana users with the same number of nonusers.
In the matched cohort, patients who used marijuana had a greater risk of in-hospital bleeding (adjusted odds ratio [aOR], 1.54; 95% CI, 1.20 – 1.97; P < .001) or stroke (aOR, 11.01; 95% CI, 1.32 – 91.67; P = .026) following PCI.
Marijuana users had a lower risk for acute kidney injury (2.2% vs 2.9%; P = .007). Transfusion and mortality rates were similar in both groups.
The researchers acknowledge study limitations, including the fact that it did not include marijuana edibles, that the results may not be generalizable, and that marijuana use is now likely more common in Michigan following legalization of recreational marijuana in 2018.
Bhuva, Yoo, and DeFilippis have disclosed no relevant financial relationships.
American Heart Association (AHA) Scientific Sessions 2020: Abstracts P380 and P1916.
France – Après les fleurs et les champignons (voir encadré Champignons), l’Agence nationale de sécurité sanitairede l’alimentation, de l’environnementet du travail (Anses) met en garde contre les confusions entre les fruits du marronnier et du châtaignier, bien plus fréquentes que ce que l’on pourrait penser et à l’origine d’intoxications. L’Agence donne par ailleurs des conseils en prévention et en cas d’intoxication (voir encadré Vigilance).
Dans une étude de l’Anses sur les confusions des plantes enregistrées par les centres antipoison de 2012 à 2018, les confusions de marrons avec des châtaignes représentaient 11% des confusions, toutes saisons confondues, et étaient les plus fréquentes après les confusions de plantes à bulbes (12% des confusions).
L’Agence rappelle donc que si les châtaignes, cultivées ou sauvages, sont comestibles, les marrons d’Inde sont eux toxiques, et peuvent entraîner des troubles digestifs tels que des douleurs abdominales, des nausées, des vomissements, ou des irritations de la gorge…
Celle des châtaignes, appelée « bogue », est brune, hérissée de nombreux et longs piquants, et contient 2 à 3 châtaignes à la fois, plutôt petites, aplaties et triangulaires ;
Celle des marrons d’Inde est épaisse, verte, pourvue de petits pics espacés et courts, et contient généralement un seul marron, plus gros et arrondi.
Les marronniers sont dans les villes, les parcs, les allées et les cours d’école… tandis que les châtaigniers sont dans les bois, les forêts ou les vergers ;
Les feuilles du marronnier sont composées chacune de plusieurs « petites feuilles » (folioles) de forme ovale, qui donnent à l’ensemble de la feuille un aspect palmé, alors que les feuilles du châtaignier sont simples sans foliole et allongées.
Champignons : les intoxications ont surtout lieu en octobre
Il y a quelques semaines, l’Anses rapportait qu’en 2019, plus de 2000 cas d’intoxication ont été rapportés aux Centres antipoison, entre le 1 juillet et le 31 décembre [2]. Ces intoxications ont eu lieu principalement au mois d’octobre (57% des cas), période favorable aux champignons et à leur cueillette. La majorité des cas d’intoxication était liée à des champignons cueillis mais pour certains cas, il s’agissait d’un achat sur un marché, dans un commerce ou une consommation dans un restaurant (4%). Si les personnes s’étaient majoritairement intoxiquées au cours d’un repas, dans 3% des cas, il s’agissait de l’ingestion d’un morceau de champignon non comestible par un enfant en bas âge ou par un adulte présentant des troubles cognitifs (maladie d’Alzheimer, déficience intellectuelle etc.). Les symptômes observés étaient essentiellement digestifs: douleurs abdominales, nausées, vomissements, diarrhées. Si ces intoxications sont pour la plupart de faible gravité, 24 cas de forte gravité pouvant menacer le pronostic vital ont été recensés ainsi que 3 décès.
A maior parte dos casos de intoxicação por arsênio estão relacionados à tentativa de suicídio. Encontramos o produto em indústrias de microeletrônica, agrotóxicos, águas profundas como contaminante, carvão e em produtos para conservação de madeira. Muito associado ao consumo de frutos do mar.
Apresentação clínica
A intoxicação pode acontecer por via inalatória ou por ingestão.
Quadro clínico agudo:
Gastroenterite hemorrágica: inicia-se com quadro de náuseas, vômitos e diarreia, associado à dor abdominal de forte intensidade. O quadro diarreico pode conter sangue;
Simultaneamente ocorre a progressão para um quadro hipovolêmico com repercussão hipotensiva e oligúrica, podendo se encaminhar ao estado de choque;
Casos mais graves podem evoluir com arritmias malignas como Torsade de Pointes, hemólise e necrose tubular aguda.
Quadro clínico crônico:
Quadro abdominal inespecífico associado à fraqueza e emagrecimento;
Neuropatia periférica, diabetes e insuficiência vascular periférica;
Podem ocorrer hepatotoxicidade com evolução para quadro encefalopatia crônica. Sinais comuns como hiperceratose palmoplantar, linhas de Mees, eliminação de odor de alho no suor e lesões dermatológicas hipercrômicas;
Possui componente neoplásico eventualmente conduzindo tumores de pele, fígado, bexiga, entre outros.
Exames complementares
Dosagem urinária do elemento para confirmação definitiva da intoxicação;
Dosagem pontual de referência: > 50 microgramas/L;
Dosagem em urina de 24 horas: > 200 microgramas/L.
Tratamento
Em casos de intoxicação aguda, deve-se adotar medidas de suporte de acordo com a sintomatologia apresentada pelo paciente. Este tipo de intoxicação deve ser sempre considerada grave. Utilizar reposição volêmica generosa e uso de drogas vasoativas.
O afastamento da fonte expositora e utilização de quelantes devem ser considerados em pacientes sintomáticos (50-200 microgramas/L) e assintomáticos (> 200 microgramas/L).
Arsênio (As). Guia de intoxicações. Whitebook Clinical Decision;
Manual de Toxicologia Clínica: Orientações para assistência e vigilância das intoxicações agudas. 1º ed. São Paulo: Secretaria Municipal da Saúde, 2017;
Olson Kent R. Manual de Toxicologia Clínica. 6º ed. Artmed, 2014.
Foi confirmada ontem, dia 15, em coletiva de imprensa, a segunda morte entre os 17 casos de síndrome nefroneural, possivelmente causada pela intoxicação por dietilenoglicol (DEG). Entre as duas mortes, uma delas foi um homem que estava internado em Juiz de Fora, e estava entre os quatro pacientes que tiveram os exames confirmados para DEG; a segunda entra com os outros 13 casos suspeitos, em Belo Horizonte, e a causa deve ser confirmada após a liberação do laudo.
Uma idosa que apresentou os mesmos sintomas, no interior de Minas Gerais, também evoluiu a óbito, mas o caso ainda não foi confirmado pela Polícia como a síndrome que pode ser causada pela intoxicação.
Casos de intoxicação por dietilenoglicol
Entre os 17 casos investigados para associação à intoxicação, o que sabemos:
16 homens e uma mulher;
12 pacientes de Belo Horizonte e os outros cinco residentes em: Ubá, Viçosa, São Lourenço, Nova Lima e São João Del Rei;
Todos relataram ingerir a cerveja Belorizontina, da cervejaria Backer, a partir de primeiro de novembro de 2019;
A média de dias entre início dos primeiros sintomas e a internação foi de dois a três dias;
Todos apresentaram sintomas gastrointestinais em até 72 horas associados à insuficiência renal aguda grave de rápida evolução, seguida ou não de uma ou mais alterações neurológicas: paralisia facial, borramento visual, amaurose, alteração de sensório e paralisia descendente;
Até o momento, quatro tiveram exames positivos para DEG.
Segundo o protocolo divulgado pela Secretaria de Estado de Minas Gerais (SES-MG), o antídoto que está sendo utilizado para os casos confirmados é o etanol oral ou venoso. Fora do Brasil existe um medicamento específico para estes casos, o fomepizole, mas ele não está disponível no país.
A SES-MG informa que devem ser imediatamente notificados (em até 24 horas) ao CIEVS BH (casos de Belo Horizonte) e CIEVS Minas (casos do restante do estado), pelo telefone e por e-mail.
Água do processo de produção também estava contaminada
Segundo o Ministério da Agricultura, Pecuária e Abastecimento (MAPA), além do tanque de fermentação da cervejaria Backer, o tanque de água, que resfria e depois faz parte das cervejas, utilizado em um processo anterior na produção da cerveja, também estava contaminado com o dietilenoglicol. Ainda não é possível, porém identificar a etapa em que a contaminação ocorreu.
Como a fábrica possui apenas um tanque de água, é possível que todos os lotes de cervejas estejam contaminados, por isso o MAPA ordenou o recall de todas as cervejas produzidas desde outubro e a suspensão das vendas da Backer. Além da Belorizontina, vendida como Capixaba no Espírito Santo, os rótulos da empresa são: Backer Pilsen, Cerveja Trigo, Cerveja Pale Ale, Cerveja Bronw, Medieval, Pele Vermelha, Bravo, Exterminador de Trigo, Três Lobos, Capitão Senra, Corleone, Tommy Gun, Diabolique, Pilsen Export, Backer Bohemian Pilsen, Julieta, Backer Reserva do Propietário, Fargo 46, Cabral, Belorizontina e Cacau Bomb.
A perícia contratada pela fábrica confirmou os laudos apresentados pela Polícia e pelo MAPA.
As atuais hipóteses da contaminação são sabotagem, vazamento ou uso incorreto da substância usada para resfriar a cerveja (o monoetilenoglicol). Como o monoetilenoglicol foi também encontrado durante as perícias, existe a possibilidade que ele tenha se transformado em dietilenoglicol em alguma etapa, apesar de ser uma reação que só acontece em ambientes muito ácidos.
Segundo a cervejaria, o dietilenoglicol não é utilizado na fábrica da Backer, mas o mono sim, durante o processo de resfriamento. Nesse caso, a substância não entra em contato com a cerveja – ou não deveria entrar.
maismaismedicina 