Raffaella Butera

Carbon Monoxide Cardiotoxicity

Cardiac dysfunction including arrhythmias and myocardial ischemia have often been reported in carbon monoxide poisoning; scattered punctiform hemorrhages throughout the heart have been documented in autopsy samples. An appropriate diagnostic approach is crucial to assess carbon monoxide cardiac damage. This evaluation may be confounded by several factors, including the absence of overt symptoms and of specific ischemic changes in the electrocardiogram. In experimental studies, laboratory animals can develop cardiac changes similar to those seen in humans and therefore proved to be useful models to study the effects and the mechanisms of cardiac damage due to carbon monoxide. These investigations, as well as others performed in vitro, provide support for a direct action of carbon monoxide on the heart, in addition to systemic hypoxia produced by carboxyhemoglobin formation. This review focuses on the diagnostic aspects of carbon monoxide cardiotoxicity. Experimental results obtained in animals and in vitro models are also discussed.

Diagnostic Accuracy of Urinary Amanitin in Suspected Mushroom Poisoning: A Pilot Study

Background. Amatoxin‐containing species are responsible for the most severe cases of mushroom poisoning, with high mortality rate. Therefore, this poisoning should be ruled out in all patients presenting gastrointestinal symptoms after wild mushroom ingestion. Objective. To determine sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic efficacy (DE) of urinary amanitin analysis in cases of suspected mushroom poisoning. Methods. All cases of mushroom ingestion referred to a Poison Center during a one‐month period were analyzed. Amanitin measurements were performed by ELISA method (functional least detectable dose 1.5 ng/ml; cut‐off value not clearly established). Gastrointestinal symptoms latency and initial clinical assessment were considered alternative diagnostic tools. Definitive diagnosis was used as the reference standard. Results. Among 61 patients included in the study, amatoxin poisoning was diagnosed in 10 cases. Urine samples were collected 5.5 to 92 hours after mushroom ingestion. Urinary amanitin DE was 91.8%, 93.4%, and 80.3%, based on the cut‐off value considered (1.5, 5.0, and 10.0 ng/ml, respectively). Symptoms latency longer than 6 hours and initial clinical assessment DE were 70.5% and 67.2%, respectively. To identify amatoxin poisoning, initial clinical assessment resulted more sensitive and urinary amanitin analysis more specific. Conclusions. Urinary amanitin analysis is a valuable diagnostic tool and may significantly contribute to the management of suspected mushroom poisoning. At present, the best diagnostic accuracy can be obtained taking advantage of both the high sensitivity and negative predictive value of the clinical assessment performed by an experienced toxicologist, and the high specificity and positive predictive value that characterize urinary amanitin analysis.

Cardiac damage in pediatric carbon monoxide poisoning

Background: Cardiovascular disorders including myocardial ischemia and heart failure have been described in both laboratory animals and humans following carbon monoxide poisoning. Carbon monoxide cardiotoxicity may be clinically occult and often remains undiagnosed because of the lack of overt symptoms and specific ischemic changes in the electrocardiogram. Routine myocardial necrosis markers have low diagnostic efficiency, particularly in patients with concomitant skeletal muscle necrosis or multiple organ failure complicating carbon monoxide poisoning. Carbon monoxide-induced cardiotoxicity has been investigated rarely in children. Case Report: This paper describes carbon monoxide poisoning in a 12-year-old child who suffered from occult cardiac damage despite mild symptoms and low carboxyhemoglobin concentrations. Myocardial and mitral valve dysfunctions were observed, suggesting an ischemia-like syndrome. Cardiac damage was completely reversible within 1 month. Conclusion: This case report supports that a prolonged carbon monoxide exposure can cause cardiac damage in children even in the absence of specific symptoms, cerebral failure and high carboxyhemoglobin concentrations.

Mild ciguatera poisoning: Case reports with neurophysiological evaluations.

Ciguatera poisoning causes mainly gastrointestinal and neurological effects of variable severity. However, symptoms of peripheral neuropathy with paresthesias and paradoxical disturbance of thermal sensation are the hallmark. Electrophysiological studies are often normal, except in severe cases. We report four people who developed mild ciguatera poisoning after barracuda ingestion. Electrophysiological studies documented normocalcemic latent tetany. These findings are consistent with ciguatoxins mechanism of toxicity, which involves inactivation of voltage‐gated Na+ channels and eventually increases nerve membrane excitability.

Serpents exotiques en Europe: Un cas de morsure par Mocassin du Mexique (Agkistrodon bilineatus)

INTRODUCTION In the last years exotic snakebite envenomations are increasingly reported. These cases are difficult to manage because of the limited experience of European physicians in the treatment of bites from such venomous snakes; moreover, specific antivenoms are unevenly stocked and they are difficult to find in case of a medical emergency. OBSERVATION A 39-year-old herpetologist was bitten in his right hand by a mexican moccasin (Agkistrodon bilineatus) at the workplace, and presented in the Emergency Department 19 hours later. At admission, clinical evaluation showed local necrosis, swelling involving the entire limb up to the trunk, and severe pain. The specific antidote, not stocked in Italy, was sought abroad; its finding and routeing up to spot delivery required 12 hours. The antivenom, given 32 hours after the bite with no adverse reactions, was only partially effective. The clinical course was characterized by extensive edema with rhabdomyolysis. The necrotic wound at the bite site required after several days surgical debridement, and eventually skin graft. At 3 months follow-up, motor impairment of his right hand fingers with functional disability was still present. COMMENTS The envenomation by Agkistrodon bilineatus has some clinical aspects in common with that by European viper species, although crotalid venom usually causes more severe manifestations. The antivenom supply from a foreign country may delay its administration. A specific legislation aimed to simplify antidotes importing procedures for professional snake handlers may improve antivenoms availability and allow their timely use, as soon as clinically indicated.Resume Introduction Durant ces dernieres annees, les cas rapportes d’envenimation par serpents exotiques ont augmente. Leur prise en charge est delicate a cause, d’une part, de la faible experience des medecins europeens face a ce type d’intoxication, d’autre part, des difficultes de localisation des antivenins specifiques. Observation Un herpetologiste de 49 ans est admis aux urgences 19 heures apres avoir ete mordu a la main droite par un Mocassin du Mexique (Agkistrodon bilineatus) de son reptilarium. A son arrivee, on observe une necrose locale, un œdeme du membre superieur s’etendant jusqu’au creux axillaire et une douleur d’aggravation progressive. Douze heures sont necessaires a la localisation et a la delivrance en urgence de l’antivenin specifique, obtenu a partir de l’etranger car non disponible en Italie. L’antidote, administre 32 heures apres la morsure, a une efficacite partielle et n’entraine pas d’effets secondaires. L’evolution clinique est caracterisee par un œdeme massif et par une rhabdomyolyse. La necrose locale provoque une perte de substance necessitant une greffe cutanee. A 3 mois persiste un deficit moteur partiel de la main. Commentaires L’envenimation par morsure de Agkistrodon bilineatus presente des analogies avec celle imputable aux viperes europeennes, bien que le venin des crotalides soit habituellement responsable de manifestations plus graves. Le temps necessaire a l’approvisionnement en urgence de l’antivenin a partir d’un pays etranger peut entrainer des retards dans l’administration. La creation d’une legislation ad hoc visant a simplifier, pour les eleveurs specialises et/ou les reptilariums, les procedures d’approvisionnement et de stockage des antivenins specifiques pourraient permettre un traitement en temps utile.

Widespread nickel dermatitis from inhalation

Keywords: nickel; allergic contact dermatitis; occupational; electroplating; disulfiram; systemic contact dermatitis; inhalation; airborne

Neonatal Toxicity Following Maternal Citalopram Treatment

Late gestational exposure to citalopram, may be associated with a neonatal toxicity syndrome with immediate onset at birth or soon after birth and sometimes may be mistaken for neonatal withdrawal syndrome. A 3860 g infant was delivered at 40 weeks gestation. The mother had been taking citalopram 20 mg/day until the day of delivery. Fifteen minutes after birth, the baby became hypertonic. Neonatal serotonin toxicity due to citalopram seems the most likely mechanism, though an important differential diagnosis is a citalopram withdrawal syndrome. We suggest the hypothesis that neonatal withdrawal syndrome may follow citalopram serotonin toxicity.

Review : Carbon Monoxide Poisoning in Fire Victims

During fires, the effects of heat and noxious effluents are cumulative in caus ing injury to the victims. Carbon monoxide (CO), which is invariably present as a toxic component of fire emissions, often acts synergistically with cyanide released by various materials. Clinical findings are variable, depending on the extent of external burns, upper airway and lung damage, and toxic exposure. Neuropsychiatric symptoms and respiratory distress are common manifesta tions. Life-threatening complications, such as pulmonary oedema, may sud denly develop up to several days after the smoke exposure. Therapeutic mea sures include general supportive care as well as the treatment of bums and associated systemic toxicity. Arterial blood gases, carboxyhaemoglobin and cyanide levels should be monitored. Patients exposed to significant concentra tions of CO require hyperbaric oxygen therapy. Suspected cyanide poisoning must be treated without the waiting for laboratory confirmation. Untimely or incorrect intervention may compromise the chances of survival and seriously affect the future health status of fire victims.

Normocytic Normochromic Anaemia and Asymptomatic Neutropenia in a 40-Day-Old Infant Breastfed by an Epileptic Mother Treated With Lamotrigine: Infant's Adverse Drug Reaction: Letters to the Editor

the course went probably this way. In a study in which complete recovery was the endpoint, two HBO sessions were shown to have worse outcomes than one session in patients with initial coma. Our case suggests the contrary. Repeated HBO therapy could have allowed the oedema to resolve, as in delayed encephalopathy. Despite an uneventful recovery in the early period of treatment, HBO therapy may need to be repeated in severe cases that might cause subsequent brain oedema.