Neuropatia óptica tóxica por inalação de metanol / Optic neuropathy toxic after methanol inhalation

Resumo A intoxicação por metanol é um evento considerado raro, principalmente quando feita por via inalatória. Retratou-se neste presente estudo um relato de caso de um paciente que desenvolveu neurite óptica tóxica após exposição ao metanol e ácido acético por via inalatória em seu ambiente de trabalho. Foi descrito sobre as terapias obtidas na literatura, bem como as manifestações clínicas e o manejo a este paciente.

Abstract The methanol toxicity is considered rare event , especially when taken by inhalation . It was portrayed in the present study a case report of a patient who developed toxic optic neuritis after exposure to methanol and acetic acid by inhalation in the workplace . It was described for the therapies from the literature as well as the clinical manifestations and management in this patient.

The role of hemodialysis in treatment of acute acetic acid poisonings.

INTRODUCTION: The aim of this study is to show the importance of hemodialysis as an active method in treatment of acute acetic acid poisonings. Its main role is to support the renal function during the state of the intoxication when patients develop acute renal failure. METHODS: We analyzed data from a 10-year period, a total of 71 patients who ingested acetic acid, either intentionally or accidentally. Patients with a need of hemodialysis (HD) treatment underwent 3- to 4-hour HD sessions every day or every second day, according to clinical assessment, as needed, until recovery of kidney function. RESULTS: In the period between 2006 and 2015 at the university clinic for toxicology and urgent internal medicine, we hospitalized 6,106 patients with different kinds of intoxication, of which 1.162% ingested concentrated acetic acid; 47 patients were female and 24 were male. The minimal age of patients was 18 and the maximal 74 years. A total of 28 (39.43%) of the patients developed acute renal failure and in 10 patients (14.08%) we used hemodialysis as a part of the treatment. The maximum number of performed sessions in one patient was five and the minimal number of performed sessions in one patents was only one session. The use of heparin led to fatal bleeding in 4 patients. The mortality rate was 7% and most of the cases resulted in fatalities during the first 96 hours after ingestion. CONCLUSIONS: Acetic acid poisonings are one of the most dangerous intoxications seen in clinical toxicology. The use of hemodialysis in some of the patients who develop acute renal failure can be of great importance and it should be put into official treatment protocols due to its great number of advantages in renal function support.

Sudden death due to forced ingestion of vinegar.

Vinegar is a clear colorless liquid that commercially consists of 5% acetic acid. It has numerous benefits in everyday use, including culinary, medical, and cleaning. The ingestion of concentrated acetic acid is strongly discouraged and may have detrimental consequences, such as acute pancreatitis, disseminated intravascular coagulopathy, gastric and hepatic complications, upper airway obstruction, or death. We report the first case in the literature of a 5-year-old boy who experienced a sudden death due to ingestion of distilled white vinegar. The manner was homicide. There was evidence of nonfatal blunt force impacts of the head, trunk, and extremities. A pungent aromatic odor of the viscera, gastric/small bowel contents, and cranial cavity was noted at autopsy. A dusky gray discoloration of the gastric mucosa, small bowel, and pancreas was observed. Forensic pathologists should consider ingestion of vinegar when confronted with a compelling history as well as an aromatic odor suggesting vinegar and dusky gray discoloration of the gastric mucosa and small bowel. While vinegar is a common household item and has several advantages, it may prove fatal if ingested in large quantities.

[Metabolic and organ protective properties of various infusion solutions and the choice of starting therapy in the pre-admission stage of acetic acid poisoning].

MATERIALS AND METHODS: We conducted an open prospective study in 60 patients (30 men and 30 women) with acetic acid poisoning. A randomization was performed on the groups, taking into account the tactics of infusion therapy: group I--15 patients who did not receive an infusion therapy at a pre-admission stage; group II--15 patients who received the infiusion therapy with solution of sodium chloride 0.9%; group III--15 patients who received the infusion therapy with modified gelatin (Gelofusinwn), group IV-15 patients who received the infusion therapy with reamberinum. RESULTS: We found that the most favorable results were noted in patients of group IV in the early posttraumatic period.

Severe renal function impairment in adult patients acutely poisoned with concentrated acetic acid.

Acetic acid is a widely used organic acid with corrosive properties that depend on its concentration. If acetic acid is ingested in concentrations above 30 % it may severely damage the upper gastrointestinal tract and cause intravascular haemolysis, which can result in severe kidney and liver disorders and disseminated intravascular coagulation. In this retrospective study, we analysed acetic acid ingestion data collected at the University Clinic for Toxicology of Skopje, Macedonia from 1 January 2002 to 31 December 2011. The analysis included systemic complications, kidney damage, and the outcomes in particular. Over the ten years, 84 patients were reported at the Clinic to have ingested highly concentrated acetic acid. Twenty-eight developed kidney disorders, while the remaining 56 had no complications. Fatal outcome was reported for 11 patients, seven of whom had systemic complications and four severe gastrointestinal complications.

[The aggregation capacity of thrombocytes, lymphocytic thrombocytic adhesion and content of D-dimers in patients with acute acetic acid intoxication].

In patients with acute acetic acid intoxication the diminution of degree and velocity of thrombocytes aggregation against the background of their amount attenuation in peripheral blood is established. The significant augmentation of amount of lymphocytic thrombocytic complexes and -dimers concentration in blood is revealed. The most marked alterations are determined on first and second days in patients with severe degree of intoxication.

[Prognostic value of platelet aggreagation capacity and lymphocyte-platelet adhesion in patients suffering acute poisoning with acetic acid].

The patients experiencing severe acute poisoning with acetic acid were divided into 2 groups with and without exotoxic shock to study platelet aggregation capacity and lymphocyte-platelet adhesion. The data obtained were used to develop exotoxic shock probability coefficient for patients with acute poisoning.

[Efficacy of reamberin in patients with acetic acid poisoning].

Efficacy of reamberin infusion therapy was estimated in 38 patients with severe acetic acid intoxication. Reamberin was shown to have positive effect on certain end-points of the treatment, viz. caused a 2-fold decrease in duration of exotoxic shock (which allowed to use smaller volumes of infusion solutions), 3-fold decrease in the frequency of pneumonia, 5-fold reduction in the frequency of delirium and acute renal insufficiency in the early post-traumatic period. The use of reamberin allowed to reduce duration of patients' stay in intensive therapy and resuscitation wards by 1.2 times and mortality rate by 18.5%.

Balloon dilatation for corrosive esophageal strictures in children: radiologic and clinical outcomes.

OBJECTIVE: We retrospectively evaluated the effectiveness of the esophageal balloon dilatation (EBD) in children with a corrosive esophageal stricture. MATERIALS AND METHODS: The study subjects included 14 patients (M:F = 8:6, age range: 17-85 months) who underwent an EBD due to a corrosive esophageal stricture. The causative agents for the condition were glacial acetic acid (n = 9) and lye (n = 5). RESULTS: A total of 52 EBD sessions were performed in 14 patients (range 1-8 sessions). During the mean 15-month follow-up period (range 1-79 months), 12 patients (86%) underwent additional EBD due to recurrent esophageal stricture. Dysphagia improved after each EBD session and oral feeding was possible between EBD sessions. Long-term success (defined as dysphagia relief for at least 12 months after the last EBD) was achieved in two patients (14%). Temporary success of EBD (defined as dysphagia relief for at least one month after the EBD session) was achieved in 17 out of 52 sessions (33%). A submucosal tear of the esophagus was observed in two (4%) sessions of EBD. CONCLUSION: Only a limited number of children with corrosive esophageal strictures were considered cured by EBD. However, the outcome of repeated EBD was sufficient to allow the children to eat per os prior to surgical management.

[Lymphocyte-platelet adhesion and the content of D-dimers in patients with acute acetic acid poisoning].

Disseminated intravascular coagulation is a menacing complication due to acute acetic acid poisoning. However, many key mechanisms of this condition remain to be not clearly understood. The authors have studied lymphocyte-platelet adhesion and D-dimer concentrations in the blood. The most pronounced changes were observed in patients with severe poisoning in the first 24 hours, which were characterized by a significant increase in the number of lymphocyte-platelet complexes and D-dimer concentrations in the blood. A statistically significant correlation was established between the parameters being studied.

Chemical colitis.

Chemical colitis can occur as a result of accidental contamination of endoscopes or by intentional or accidental administration of enemas containing various chemicals. Most cases have occurred after accidental contamination of endoscopes with glutaraldehyde and/or hydrogen peroxide. There have been multiple case reports of chemical colitis resulting from unintentional administration of caustic chemicals. Intentional administration of corrosive enemas has been implicated in sexual practices, bowel cleansing, or in suicide attempts. Patients present with nonspecific symptoms including abdominal pain, rectal bleeding, and/or diarrhea. As chemical colitis remains rare, the literature consists of scattered case reports and small series. Agents implicated in chemical colitis that are covered in this review include alcohol, radiocontrast agents, glutaraldehyde, formalin, ergotamine, hydrofluoric acid, sulfuric acid, acetic acid, ammonia, soap, sodium hydroxide, hydrogen peroxide, herbal medicines, chloro-m-xylenol, and potassium permanganate. Clinical, endoscopic, and histologic features are outlined for each agent in addition to the existing literature. Given the nonspecific presentation of many cases of chemically induced colitis, the diagnosis can be challenging if the pertinent history is not obtained. Most patients demonstrate the resolution of chemical-induced colitis after conservative or medical therapy. Depending on the depth and extent of injury, patients rarely require colectomy for ischemic colitis and/or peritonitis. Other postingestion complications include colonic strictures and rectovaginal fistulae. The benefits of medical therapy compared with conservative therapy are not known, as comparative clinical management trials have not been performed.

CT imaging of gastric and hepatic complications after ingestion of glacial acetic acid.

OBJECTIVE: To document the computed tomographic (CT) image features of gastric and hepatic complications after ingestion of glacial acetic acid. MATERIALS AND METHODS: There were 5 patients (2 men and 3 women; age range, 2-84 years) who had ingested glacial acetic acid to commit suicide or accidentally. Their abdominal and chest CT scans were retrospectively reviewed to detect and evaluate visceral organ injury. Clinical and laboratory data were also reviewed. RESULTS: Diffuse edematous wall thickening of esophagus and stomach was observed in all patients. Three patients showed nonenhancing, wedge-shaped low densities in the liver on portal venous phase abdominal CT scans. These 3 patients also showed laboratory findings to indicate hepatic failure, hemolysis, metabolic acidosis, and disseminated intravascular coagulation. Two of these patients died despite vigorous supportive treatment. CONCLUSIONS: Wedge-shaped low densities can be seen in the liver on CT scans after ingestion of glacial acetic acid. They may represent hepatic necrosis caused by the direct effect of toxic materials absorbed into portal circulation.

Ingestion of caustic substances: a 15-year experience.

OBJECTIVE: The objective of this study was to analyze the circumstance, demographic features, clinical findings, and complications of caustic ingestion in relation to the type and amount of caustic substance. STUDY DESIGN: The authors conducted a retrospective cohort study in a tertiary medical center. METHODS: The authors reviewed medical records from 1988 to 2003 of patients with a history of caustic ingestion and clinical signs of injury to the aerodigestive tract. Parameters examined included age at presentation, gender, demographic status, nature of the caustic substance ingested, amount of substance, circumstance of the event, diagnostic tools, degree of injury, and anatomic distribution of the injury, early and late complications, and requirement for ventilatory support. RESULTS: A total of 50 cases of caustic ingestion were identified (age range, 5 months-71 years). A biphasic distribution of the patients was noted; half were children under 5 years old and the remainder was adults. The most common caustic agent ingested was alkaline (42%) followed by acidic (32%) and chlorine bleach (26%). The most frequent cause for ingestion was accidental (67%) as opposed to attempt suicide (33%). All cases of attempted suicide occurred in adults. Most of them reported ingestion of large amounts of caustic substance. In the pediatric group, an association between the caustic agent and ethnicity was observed. Among Jewish children, alkaline cleaning agents were the most common cause (82%). Acetic acid was the most common substance ingested by the Arab children (100%). The findings of rigid esophagoscopy in 36 patients were as follows: first-degree esophageal injury in 16 (44%), second-degree in 6 (17%), third-degree in 7 (19%), fourth-degree in 6 (17%), and one (3%) was normal. Mucosal injury to the esophagus was worse in the acidic ingestion group as compared with the alkaline substance ingestion group with marginally statistically significant difference in the median degree of injury between the three types of ingested substances (P = .054). Mucosal injury to the esophagus was worse among patients who attempted suicide as compared with accidental ingestion with a statistically significant difference in the median degree of injury between the two reasons for ingestion (P = .002). CONCLUSION: Severity of injury from caustic ingestion damages depend on the type of ingested substance, which varies depending on ethnicity. Ingestion of caustic agents by children involves specific substances according to the season, cultural and religious festivals, and ethnicity. The majority of adult cases are intentional with more serious injuries and a higher rate of complications. In our series, ingestion of acidic substances and ingestion associated with suicide attempt had the most severe consequences.

[Detection of acetic acid in cadavers by gas chromatography].

A simple technique of sample preparation for gas chromatographic test for acetic acid in cadaveric material has been developed. The background concentration of natural content of acetates in the stomach, liver and kidneys are determined. The error of the method is no more than 10% with standard deviation +/- 0.04-0.13.

Massive noninflammatory periportal liver necrosis following concentrated acetic acid ingestion.

In a fatal occurrence of massive liver necrosis following ingestion of concentrated (90%) acetic acid, the patient showed evidence of hemolysis, disseminated intravascular coagulation, and liver dysfunction at only 45 minutes after exposure. With refractory to vigorous supportive care, the patient s condition deteriorated until death occurred 39 hours after ingestion, despite some improvement of coagulopathy. Autopsy revealed corrosive injuries in the upper gastrointestinal tract and massive hepatic necrosis in a periportal distribution without significant inflammation. A direct effect of the noxious agent on hepatocytes involving the portal circulation is suggested.

[Combined suicide by drinking acetic acid with subsequent hanging]. / Kombinierte Suizide durch Einnahme von Essigsäure mit nachfolgendem Erhängen.

Three late emigrants of German origin from Russia (1 man, 2 women) drank 70- and 86% acetic acid respectively before hanging themselves. In one of the suicides the hanging noose was running across the face. None of the cases presented showed any perioral chemical burns. At autopsy an intense odor of acetic acid was noticeable. The mucosa of the upper digestive tract showed a whitish, grey, brown or black discoloration and was partially detached. In two cases intravascular clotting of blood was discernible in the area affected by the acid; in one case the vessels were imbibed with haemoglobin due to haemolysis. Highly concentrated acetic acid is generally available in the successor states of the former USSR and its use in suicides is thus not uncommon. The legal regulations applying in Germany to the sale of acetic acid and the toxicological data are briefly described.

[Acute oliguric kidney failure secondary to acetic acid poisoning]. / Fracaso renal agudo oligúrico, secundario a intoxicación por ácido acético.

A case of acute oliguric renal failure secondary to poisoning by acetic acid (AA) is described. The patient presents caustic damage in the mucous digestive, myoglobinuria, thrombopaenia, elevation of the enzymes of damage tissular and acute hepatic affectation. To the entrance, the patient show a good hemodynamic state and the hematologic study discarded the hemolysis presence, what allowed to establish the direct action of the AA on the kidney like cause of the oliguric failure renal next to the tubular toxic effect of the myoglobin. The oral ingesta of AA is an unusual fact and its relationship with the acute renal failure it has not been communicated previously in our country.