Mercuric chloride poisoning: symptoms, analysis, therapies, and autoptic findings. A review of the literature.

Among mercury-related intoxications, the re-emerging of mercuric chloride poisoning has been recently described in literature. Only sparse data, reporting the clinical symptoms, the anatomo-pathological findings, the analytical procedures or the treatment have been published and no exhaustive analysis of all these factors exists in literature. The classic symptoms associated with toxicity of mercuric chloride is a combination of renal, gastrointestinal (GI) and central nervous system (CNS) damages, eventually leading to death. Fatalities related to exposure to mercuric chloride have been reported since the nineteenth century. To date, there have been 45 published cases in the medical literature in which the intoxication or the death is attributed to mercuric chloride. In this review, we will describe the modern medical treatments, with particular attenztion to the developments of the lasts two decades, in order to provide an exhaustive description of the clinical symptoms, the post-mortem findings, and the analytical procedures to act out when mercuric chloride intoxication occurs. The analysis of the data obtained permitted us to accurately describe all the organs and apparatus involved in mercuric chloride intoxication. The target organs were the kidneys, the GI tract and the CNS. A description of the analytical procedures for the determination of mercuric chloride in biological materials, to carry out in vivo and in post-mortem samples has also been described.

First case of acute respiratory distress syndrome and alimentary tract hemorrhage following mass ingestion of methylisothiazolinone.

The frequency of methylisothiazolinone (MIT)-related health concerns regarding allergic contact dermatitis with a spongiotic reaction pattern and restrictive lung function indicating peripheral airway dysfunction caused by the use of humidifier disinfectant is increasingly rising. There is a limited number of evidences supporting the environmentally acute and mass exposure to MIT resulting in acute respiratory distress syndrome (ARDS). Here, we report the first case of ARDS and alimentary tract hemorrhage following mass ingestion of methylisothiazolinone.

Pediatric Exposures to Veterinary Pharmaceuticals.

OBJECTIVE: To describe the epidemiology of veterinary pharmaceutical-related exposures to children based on calls to a regional poison control center. METHODS: A retrospective analysis of pediatric (≤19 years of age) exposures to pharmaceutical products intended for animal use, managed by a regional poison control center from 1999 through 2013, was conducted. Case narratives were reviewed and coded for exposure-related circumstances and intended species. Descriptive statistics were generated. RESULTS: From 1999 through 2013, the Central Ohio Poison Center received 1431 calls that related to a veterinary pharmaceutical exposure for children ≤19 years of age. Most of the pediatric calls (87.6%) involved children ≤5 years of age. Exploratory behavior was the most common exposure-related circumstance (61.4%) and ingestion accounted for the exposure route in 93% of cases. Substances commonly associated with exposures included: veterinary drugs without human equivalent (17.3%), antimicrobial agents (14.8%), and antiparasitics (14.6%). Based on substance and quantity, the majority of exposures (96.9%) were not expected to result in long-term or lasting health effects and were managed at home (94.1%). A total of 80 cases (5.6%) were referred to a health care facility, and 2 cases resulted in a moderate health effect. CONCLUSIONS: Children ≤5 years of age are most at risk for veterinary pharmaceutical-related exposures. Although most exposures do not result in a serious medical outcome, efforts to increase public awareness, appropriate product dispensing procedures, and attention to home storage practices may reduce the risk of veterinary pharmaceutical exposures to young children.

Bilateral putaminal necrosis and bronopol toxicity.

Among alcohols, methanol intoxication is the most frequently associated with cerebral toxicity, causing retinal damage and putaminal necrosis. This consequence is believed to be due to the transformation of methanol into formic acid. We describe the case of a patient who presented with acute impairment of consciousness and tetraparesis after she had been drinking several bottles of a topical antiseptic solution (Lysoform Medical) containing 2-bromo-2-nitro-1,3-propandiol (bronopol) among excipients, in order to lose weight during previous months. Moreover, she had been on a strict slimming diet. Soon after admission, a severe respiratory and metabolic impairment became rapidly evident, requiring an intensive care unit admission. Cerebral MRI showed the presence of bilateral putaminal necrosis. She recovered in 10 days, surprisingly, without any evident clinical neurological signs. Methanol, also bronopol, when diluted in aqueous solution, at warm temperature and/or higher pH, may release formaldehyde, which is converted into formic acid, a basal ganglia toxic compound.

Ecological risk assessment of urban creek sediments contaminated by untreated domestic wastewater: potential contribution of antimicrobials and a musk fragrance.

Despite the fact that some hydrophobic pharmaceuticals and personal care products (PPCPs) have been found to accumulate in river sediments, little is known about the contribution of these compounds to the toxicity of the whole sediment. We sampled river sediments from two urban creeks with an unsewered drainage area to investigate the toxicity for a benthic organism, Chironomus yoshimatsui. The concentrations of selected hydrophobic PPCPs, triclosan (TCS), triclocarban (TCC) and galaxolide (HHCB) were analysed using gas chromatographic mass spectroscopy or liquid chromatographic mass spectroscopy and were found to lie within the range 50 to 200 ng g(-1). The toxicity of the three individual contaminants for the chironomid was also determined. The toxicity of TCC was found to be the strongest, with an NOEC value of 2.5 microg g(-1). Combining the toxicity and measured environmental concentration, the ecological risk was assessed and the contribution of these contaminants to the whole sediment toxicity estimated, assuming additivity. The hazard quotient of all three compounds, determined without assessment factor, ranged between 0.01 and 0.1. The combined contribution of the three compounds to total sediment toxicity was as high as 8.2%, but other unknown factors may also make an important contribution.

Acute dapsone overdose: the effects of continuous veno-venous haemofiltration on the elimination of dapsone.

A 15-year-old girl presented after intentional ingestion of dapsone (7.2 g) and small quantities of azathioprine, methotrexate and prednisolone. The resulting methaemoglobinaemia and lactic acidosis persisted despite treatment with methylene blue, multiple-dose activated charcoal and ascorbic acid. Continuous veno-venous haemofiltration for 75 hours was used to treat the dapsone overdose. The patient's serum dapsone concentrations were measured during and after continuous veno-venous haemofiltration. The rate of elimination of dapsone was over three times higher during, compared to after, continuous veno-venous haemofiltration. Continuous renal replacement therapy successfully reduced toxic dapsone concentrations in this patient with a good outcome.

Case files of the medical toxicology fellowship at Banner Good Samaritan Medical Center in Phoenix, AZ: methemoglobinemia following dapsone exposure.

Acquired methemoglobinemia is a common, potentially fatal syndrome that can occur as a result of exposure to numerous xenobiotics. A case report of a 14-month-old female who developed methemoglobinemia following a dapsone ingestion. The child was treated with numerous boluses of methylene blue and ultimately required a continuous infusion of methylene blue. The common causes of methemoglobinemia, as well as the underlying pathophysiology, diagnosis, and treatment strategies are discussed.

Acute antimicrobial pesticide-related illnesses among workers in health-care facilities - California, Louisiana, Michigan, and Texas, 2002-2007.

Antimicrobial pesticides (e.g., sterilizers, disinfectants, and sanitizers) are chemicals used to destroy or suppress the growth of harmful microorganisms on inanimate objects and surfaces. Health-care facilities use antimicrobial pesticides to prevent pathogen transmission from contaminated environmental surfaces. Occupational exposures to antimicrobial pesticides are known to cause adverse health effects. To assess the nature and frequency of such exposures in health-care settings, CDC analyzed data from pesticide poisoning surveillance programs in California, Louisiana, Michigan, and Texas (the only four states that regularly collect data on antimicrobial pesticide-related illness) for the period 2002-2007. This report summarizes the results of that analysis, which identified 401 cases of work-related illness associated with antimicrobial pesticide exposures in health-care facilities. Most cases were identified through workers compensation systems (61%) and occurred among females (82%) and persons aged 25-54 years (73%). The most frequent occupations reported were janitors/housekeepers (24%) and nursing/medical assistants (16%). The reported mechanism of injury usually was splashes/spills (51%). The eyes were the most common organ/system affected (55%); only 15% of the 265 persons who had exposures while handling antimicrobial pesticides reported using eye protection. Reported symptoms were mostly mild and temporary. One fatality due to acute asthma and subsequent cardiopulmonary collapse was identified. Health-care facilities should educate workers about antimicrobial pesticide hazards, promote the use of personal protective equipment (PPE) as appropriate, and implement effective risk communication strategies for antimicrobial pesticide use to prevent bystander exposure. Improved design of handling equipment might prevent handler and bystander exposure.

Dapsone induced methemoglobinemia : Intermittent vs continuous intravenous methylene blue therapy.

OBJECTIVE: The study compares the decline in blood methemoglobin (MetHb) level in children of dapsone intoxication treated with intermittent and continuous methylene blue therapy. METHODS: Eleven children with history of accidental dapsone ingestion and suggestive clinical features of dapsone intoxication were studied. Patients were randomized into two groups: Gr I (n=5) received intermittent methylene blue therapy, while Gr II (N=6) as continuous infusion. The dose of methylene blue was same in both groups. MetHb level in blood was assessed by spectrophotometer at admission and thereafter 12hrly up to 72 hrs. The decline in MetHb was statistically analyzed with student t-test. RESULTS: Six patients had history of seizure and altered sensorium. Severe anemia was observed in 2 patients. The mean levels of MetHb in Gr II was statistically significant after 12, 24, 36, 48 and 72 hrs of methylene blue therapy as compared to Gr I. CONCLUSION: Continuous I.V methylene blue therapy causes significant decline in MetHb level and is more effective in treatment of methemoglobinemia as compared to intermittent regimen.

Between a rock and a hard place: disclosing medical errors.

BACKGROUND: Healthcare-related errors cause patient morbidity and mortality. Despite fear of reprimand, laboratory personnel have a professional obligation to rapidly report major medical errors when they are identified. Well-defined protocols regarding how and when to disclose a suspected error by a colleague do not exist. PATIENT: We describe a woman with a well documented allergy to sulfamethoxazole who was treated with sulfadiazine that led to toxic epidermal necrolysis. After the patient's death, the laboratory medicine resident was asked by one of the patient's physicians to measure serum sulfadiazine, but only if the results were not reported in the patient's electronic medical record. The case was brought to the attention of a laboratory medicine faculty member and the hospital risk management team. ISSUES: Laboratorians are patient fiduciaries and are responsible for reporting errors. Most medical associations have codes of ethics that address disclosure of incompetence and errors, although the AACC's Guide to Ethics does not. New types of error, risk management, and root-cause analyses help to shift the focus to system errors and away from individuals' errors. This can lead to a healthcare environment that encourages truth and disclosure rather than fear and reprimand. Disposition: The individuals involved in the presented case fulfilled their fiduciary duty to the patient by reporting this incident. An extensive investigation showed that, in fact, no medical errors or misconducts had occurred in the care of the patient.

Unintentional ingestion of 60% hydrogen peroxide by a six-year-old child.

Ingestion of industrial-strength hydrogen peroxide is rare. Fatal outcomes have been reported with solutions of 35%. We report a six-year-old boy who unintentionally ingested an unknown quantity of hydrogen peroxide with a concentration of 60%. Upon admission to our Pediatric Intensive Care Unit he was intubated and received ventilatory assistance for 48h. Upper gastrointestinal endoscopy was performed soon after admission and laparoscopy was performed 24h later. Recovery was satisfactory, and the patient was discharged on day 18 with no evidence of pathological sequelae.

Pollution-induced community tolerance of soil microbial communities caused by the antibiotic sulfachloropyridazine.

Little is known about the environmental hazards linked to the treatment of farm animals with antibiotics and subsequent spreading of manure, especially regarding soil microbial communities. In this investigation, pollution-induced community tolerance (PICT) of bacteria from soils artificially spiked with the sulfonamide sulfachloropyridazine (SCP) was investigated. Tolerance of the bacterial communities after 3 weeks' exposure to SCP was determined by analyzing the sensitivity of 31 microbial metabolic processes in microtiter plates. Bacterial suspensions extracted from soils containing higher concentrations of SCP showed an increased tolerance of their metabolic activities to this antibiotic. An increase in tolerance by 10% was found at 7.3 mg/kg dw SCP. The PICT effect could be demonstrated by both a shift in the tolerance of the average of all metabolic activities and a shift of the physiological process sensitivity distributions made up from the single metabolic processes. The PICT effect was accompanied by smaller changes in the community-level physiological profile (CLPP). To conclude, PICT has been shown to be a versatile and illustrative method for the detection of the effects of antibacterial agents on soil microorganisms.

Metrondazole-induced neurotoxicity.

A 50 year old male with history of prolonged intake of metronidazole for treatment of liver abscess developed acute ataxia, disorientation, distal symmetrical sensory and proximal motor neuropathy. Patients being treated with metronidazole particularly those on high doses for prolonged period should be monitored for neurotoxicity.

A study on the toxicity of intravitreal levofloxacin in rabbits.

PURPOSE: To investigate the retinal toxicity of different doses of intravitreal injections of levofloxacin in a rabbit model, which is the levorotatory component of ofloxacin and approximately twice as potent as ofloxacin and highly active in vitro against gram-positive and -negative bacteria, and anaerobic bacteria including many ocular pathogens. METHODS: Sixteen albino rabbits were used in this study, and divided four groups. Levofloxacin in doses of 50, 100, 250 and 500 microg was injected into the midvitreous of rabbit's left eyes. The other eye served as a control and received normal saline solution. Indirect ophthalmoscopy, electroretinography (ERG) and light microscopy were used for retinal toxicity of levofloxacin. ERGs were recorded before injection and at 1(st) day, 1(st), 2(nd) and 4(th) weeks. At the end of follow-up period, the rabbits were killed and the eyes were enucleated for histologic evaluation. RESULTS: Intravitreal injections of 50, 100, 250 and 500 microg levofloxacin did not cause any deterioration of the a-wave, b-wave or oscillatory potentials of ERG throughout the follow-up period of 4 weeks. No evidence of retinal toxicity was observed by indirect ophthalmoscopy and light microscopy in any case. CONCLUSIONS: In therapeutic doses of 500 microg or less, intravitreal levofloxacin does not have retinal toxicity in rabbit eyes and this dose was well above the MIC(90) values of ocular pathogens that cause endophthalmitis. If future studies in other species confirm our findings, intravitreal levofloxacin may be a potentially important drug in the treatment and prevention of clinical bacterial endophthalmitis.

Chlorhexidine gluconate ingestion resulting in fatal respiratory distress syndrome.

As ingestion of chlorhexidine gluconate (CHG) usually causes relatively mild symptoms, this chemical has been considered safe. An 80-y-old woman with dementia accidentally ingested approximately 200 ml of Maskin (5% CHG) in a nursing home and then presumably aspirated gastric contents. She was intubated for airway protection in the nearest hospital and referred to our critical care unit because of hypotension and rapid deterioration of consciousness. Despite intensive treatment, the patient died of acute respiratory distress syndrome (ARDS) 12 h after ingestion. The serum concentration of CHG was markedly high, although CHG reportedly has poor enteral absorption. We suspect the CHG was absorbed through the pulmonary alveoli following aspiration, not from the gastrointestinal tract. CHG has the potential for fatal ARDS when aspiration occurs following ingestion.

Intravenous chlorhexidine gluconate causing acute respiratory distress syndrome.

CASE REPORT: A 67-year-old man undergoing a colectomy for colon cancer was unintentionally administered 0.8 mg of chlorhexidine gluconate intravenously and subsequently developed acute respiratory distress syndrome. The operation was discontinued immediately. Respiratory failure progressed despite three cycles of plasma exchange beginning on day 1. Extracorporeal membrane oxygenation for 72 h beginning on day 3 was associated with dramatic improvement. The patient showed complete recovery of intellectual function and subsequently underwent a colectomy with lymph node dissection for colon cancer. CONCLUSION: For acute respiratory distress syndrome secondary to chlorhexidine gluconate intoxication, consideration should be given to the treatment of initial respiratory distress and subsequent pneumonia. The benefit of extracorporeal membrane oxygenation and plasma exchange may merit further investigation.

[Methemoglobinemia--causes, diagnosis and treatment]. / Methemoglobinemi--årsaker, diagnostikk og behandling.

BACKGROUND: Methaemoglobinaemia is an infrequent condition. It can be congenital or be induced by several toxic compounds. In methaemoglobin (metHb) the iron in the haem moiety of haemoglobin is oxidized from the ferrous (Fe2+) to the ferric state (Fe3+). This complex is dark brown and unable to transport oxygen. Combined with a leftward shift in the oxyhaemoglobin dissociation curve this leads to decreased tissue oxygenation with subsequent hypoxic features in patients. CASE REPORTS: We report two cases of dapsone-induced methaemoglobinaemia. The blood, mucosa and nail beds adopted a brown-bluish appearance which was used diagnostically. One patient was treated effectively with repeated injections of methylene blue, which reduces methaemoglobin. In the other patient, the methaemoglobin level declined with a T50 of 50 hours. Both patients had few symptoms and made an uneventful recovery. INTERPRETATION: The hypoxia in methaemoglobinaemia may be effectively treated with methylene blue. Repeated injections may be necessary.