Acute lead arsenate poisoning in beef cattle in Uruguay.

We describe and illustrate lesions in an outbreak of lead arsenate poisoning in beef cattle that ingested pesticide residues stored in an abandoned building of a former orange orchard. Of 70 exposed cattle, 14 had diarrhea, paresis, ataxia, recumbency, and/or seizures. Ten of the affected animals died after a clinical course of 12-18 h. Pathologic findings in 3 steers included extensive necrohemorrhagic, ulcerative rumenitis, omasitis, and abomasitis; lymphocytolysis in lymphoid organs; and nephrosis. Hepatic arsenic and lead levels in cases 1-3 were 20, 24, and 31 ppm, and 8.3, 25, and 9.4 ppm, respectively. Lesions in the forestomachs and lymphoid tissues have been rarely reported in cases of lead arsenate poisoning. In southern South America, these lesions are indistinguishable from those produced by Baccharis coridifolia, a toxic plant that contains macrocyclic trichothecenes, thus these conditions should be considered in the differential diagnosis of necrotizing lesions in alimentary and lymphoid organs.

[Arsenic poisoning]. / Forgiftning med arsen.

BACKGROUND: Arsenic poisoning has been discussed frequently in Norway during the past year on the background of a suspected crime case. There seem to be several uncertainties regarding this issue, also in the medical profession. MATERIAL AND METHODS: We have searched the literature and made a review based upon the present knowledge about arsenic and arsenic poisoning. RESULTS: Arsenic can be found in numerous chemical compounds with different properties. Inorganic arsenic compounds, like arsenic trioxide, are reactive and can cause damage to the body. Organic arsenic compounds, which are found in high concentrations in fish and shellfish, are not considered toxic. Ingestion of inorganic arsenic affects cellular energy production; lethal poisonings can occur. Common clinical features after acute intoxication with arsenic are dysphagia, nausea, vomiting, abdominal pain, diarrhoea, intense thirst, and muscle cramps. Clinical features of chronic poisoning are hyperkeratosis in the palms and foot soles, pigmentation and conjunctivitis. INTERPRETATION: Arsenic poisoning is a rare condition; its clinical features are uncharacteristic and the diagnosis must be confirmed by analysis of blood, urine and hair.

Arsenic in a child's world.

Ten-year-old Tim P. presented at a local emergency room complaining of bloody diarrhea. Despite treatment, his diarrhea continued with additional symptoms of nausea, raspy voice, headaches, abdominal pain, tingling of the feet and hands, lethargy, and eczema. Do you recognize the health risks and clinical aspects of arsenic, and could you assist Tim and his family?

Suicide by ingestion of a CCA wood preservative.

Chromated-copper-arsenate (CCA) is a compound used worldwide for wood preservation. Occupational hazards from chronic exposure to CCA are well known, but acute ingestion of CCA wood preservative is very rare. We describe a case of suicide by ingestion of a CCA wood preservative. A 33-year-old man attempted suicide by ingesting an unknown liquid, later identified as a CCA wood preservative, 75 min before his arrival in the emergency department. He was in severe respiratory distress, drooling, tachycardic, and hypotensive. There was an orange color on the palms of both hands. Severe, green colored burns of the buccal mucosa were observed. He was intubated shortly after arrival. The larynx was edematous, but a 7-mm endotracheal tube was successfully introduced. Blood tests revealed partially compensated metabolic acidosis. The patient deteriorated rapidly; the systolic blood pressure dropped to 70 mmHg, and he passed bloody diarrhea. He developed multiple premature atrial contractions and supraventricular tachycardia, and later in the intensive care unit, refractory ventricular tachycardia and ventricular fibrillation. The patient was declared dead 212 h after his arrival. Unfortunately, postmortem blood levels of heavy metals and autopsy were not performed because of refusal by the family for religious reasons.

Bovine arsenic toxicosis from ingestion of ashed copper-chrome-arsenate treated timber.

Arsenic toxicosis is reported in a variety of animal species. It occurs most commonly in cattle and ranks second only to lead as a cause of heavy metal poisoning. We describe a case of arsenic toxicosis attributable to ingestion of ashes from burned posts treated with an arsenic-containing preservative. Burning of the posts concentrated the arsenic and rendered lethal a product normally used around livestock. Lack of normal salt supplementation to the herd was conducive to pica-like behavior and ingestion of toxic ashes. Rapid diagnosis led to removal of the arsenic source and limited losses to 4 cows.

Lead arsenate poisoning in a herd of beef cattle.

Lead arsenate poisoning was diagnosed in 2 beef heifers and was suspected in 6 other cattle from the same herd that had died previously and were not examined. Clinical signs in affected cattle included staggering, dehydration, hemorrhage, acidemia, and shock. Diagnosis was by arsenic and lead analysis of urine samples and kidney and liver tissue digests. Both examined heifers died within 4 days of onset of clinical signs. These cattle had been moved from an area with poor grazing conditions to a pasture with abundant forage. This pasture had an open shed that contained an open sack of lead arsenate insecticide. Old stores of this inorganic insecticide may still exist on farms or ranches, and are a hazard to livestock.

Pediatric arsenic ingestion.

Acute arsenic toxicity is rare, and there have been no pediatric cases of acute arsenic poisoning in the recent literature. We report a pediatric case of acute arsenic ingestion treated initially with British antilewisite (BAL) and D-penicillamine (DP), and later with dimercaptosuccinic acid (DMSA). A 22-month-old girl ingested 1 oz 2.27% sodium arsenate and developed immediate vomiting and diarrhea. The patient presented to a community emergency department with the following vital signs: blood pressure 96/72 mm Hg, pulse 160 beats/min, respirations 22 breaths/min. She was pale and lethargic. Gastric lavage was performed, and abdominal X-ray was normal. She continued to have gastrointestinal symptoms and received 3 mg/kg BAL. Sinus tachycardia persisted, with heart rate increasing to 200 beats/min. In 12 hours, she was asymptomatic and was started on oral DP. On day 1, 24-hour urine arsenic was 4,880 micrograms/L. She remained asymptomatic and was discharged on day 6 on oral DP. She did well except for a rash that could have been a side effect of DP. On day 8, when the day 5 24-hour urine arsenic level was returned at 650 micrograms/L, the patient was readmitted and started on DMSA. After 4 days on DMSA, the 24-hour urine arsenic level was 96 micrograms/L. White blood cell count and renal and hepatic function remained normal. The excretion half-life was approximately 2.5 days, which is at least 2 to 3 times faster than the spontaneous excretion half-life expected in adults. Long-term follow-up was unavailable.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical observations and medical outcome in 149 cases of arsenate ant killer ingestion.

One hundred forty-nine (149) consecutive cases of arsenate-containing ant killer reported to the Minnesota Regional Poison Center over 4 1/2 months were retrospectively reviewed with a follow-up (1 week to 3 months) completed in 132 (89%) of the population studied. One hundred and forty eight (99%) of the ingestions were accidental. The majority of cases involved children 3 years of age and younger. Only three patients accidentally ingesting the product were symptomatic (mild episodes of vomiting and diarrhea which cleared in all patients within 12 hours). No patient was referred to a medical center for treatment and no patient reached on follow-up reported any additional ill effects as a result of the exposure. In addition to the 149 patients in this series, we describe two representative patients who accidentally ingested similar amounts of sodium arsenate-containing ant killer, resulting in urine arsenic of 3500 micrograms/24 h and 5819 micrograms/24 h. They required no chelation treatment and had no evident sequelae during 4-6 months of medical follow-up. This experience supports poison center directed home management for the majority of single, acute, and accidental ingestions of small quantities (< 5 mL) of arsenate-containing ant killers as a safe alternative to medical center referral and adverse reactions to chelation.

Effect of some arsenic antagonists on the toxicity, distribution and excretion of arsenite and arsenate in rats.

1. Arsenite and arsenate poisoned rats were treated with either BAL (2,3-dimercapto-1-propanol), penicillamine (PA) (beta-beta dimethyl cystein) or selenium (Se) (as sodium selenite). 2. The minimal dose of each antagonist that treated arsenic-induced lethality (causing 100% survival) was the same for both arsenite and arsenate. 3. Arsenic mobilization from the tissues (blood, kidney, liver, lungs, spleen, muscles, brain, heart) and its excretion in urine and feces were higher in arsenite-intoxicated animals than in arsenate-intoxicated ones. 4. The effect of each antagonist, when injected alone, on the urinary and fecal excretion of endogenous metals (Cu, Zn, Fe, Ca and Mg) was also examined. 5. The results indicated marked differences in the relative ability of BAL, PA and Se to increase the excretion of the metals.

N-acetylcysteine in the treatment of human arsenic poisoning.

A 32-year-old man was brought to the emergency department 5 1/2 hours after ingesting a potentially lethal dose (900 mg) of sodium arsenate ant poison in a suicide attempt. The patient deteriorated progressively for 27 hours. After intramuscular dimercaprol and supportive measures failed to improve his condition, he was given N-acetylcysteine intravenously. The patient showed remarkable clinical improvement during the following 24 hours and was discharged from the hospital several days later.

Acute lead arsenate poisoning.

Three cases of acute lead arsenate poisoning which occurred in South Australia during a 12 month interval are described. The case reports demonstrate a number of features of the characteristic clinical syndrome which may follow ingestion of lead arsenate. The recommended management is immediate gastric lavage and subsequent chelation therapy with calcium EDTA and dimercaprol. Early gastric lavage may prevent significant lead absorption. However, arsenic acid (produced in the stomach when lead arsenate reacts with hydrochloric acid) is relatively water soluble and prompt gastric lavage is unlikely to prevent extensive arsenic absorption. It remains controversial as to whether chelation with dimercaprol prevents arsenical neuropathy.

[Portal hypertension and chronic arsenic exposure. A differential diagnostic challenge]. / Portale Hypertension und chronische Arsenexposition. Eine differentialdiagnostische Herausforderung.

We are reporting on a 62 year old female patient with portal hypertension (splenomegaly, esophageal varicosis) without signs of liver cirrhosis, who was hospitalized for sclerotherapy of her esophageal varices. Physical examination showed up palmar- and plantar hyperkeratosis and Morbus Bowen or basalioma-like skin lesions++. Anamnestic evaluation revealed, that the patient's psoriasis had been treated with arsenic for many years. This kind of treatment may have induced intraluminal proliferation and obliteration of the portal vein's endothelium, thus being the etiologic factor responsible for noncirrhotic portal hypertension in this patient.

Arsenic speciation in urine from humans intoxicated by inorganic arsenic compounds.

Trends in the urinary concentrations of the four arsenic species, pentavalent [As (V)] and trivalent [As (III)] inorganic arsenic, monomethylarsonic acid (MMAA) and dimethylarsinic acid (DMAA), were followed for several days subsequent to the acute intoxication of two human subjects by arsenic trioxide [As (III)2O3] and sodium orthoarsenate [Na2HAs(V)O4 X 7H2O], respectively, in unsuccessful suicide attempts. Total arsenic concentrations ranged from 1.6 to 18.7 mg/l. The increasing predominance of the less toxic methylated species, especially DMAA, after 3 or 4 days supports the concept of methylation as a natural detoxification mechanism as part of an overall reduction/methylation sequence involved in the biotransformation of inorganic arsenic by the human body. However, the additional possibility of oxidation of As(III) to As(V) in vivo under extreme immediate postingestion conditions is suggested by initial high urinary As(V) after arsenic trioxide intoxication. Relative proportions of As(V), As(III), MMAA and DMAA in both cases probably reflect species-dependent differences in rates of direct elimination and reactivity with tissues as well as the efficiency of methylation.

DMSA, DMPS, and DMPA--as arsenic antidotes.

meso-Dimercaptosuccinic acid (DMSA), 2,3-dimercapto-1-propanesulfonic acid, Na salt (DMPS), and N-(2,3- dimercaptopropyl )- phthalamidic acid (DMPA) are water soluble analogs of 2,3-dimercapto-1-propanol (BAL). The relative effectiveness or therapeutic index of these dimercapto compounds in protecting mice from the lethal effects of an LD99 of sodium arsenite is DMSA greater than DMPS greater than DMPA greater than BAL in the magnitude of 42:14:4:1, respectively. DMPS, DMPA, or DMSA will mobilize tissue arsenic. BAL, however, increases the arsenic content of the brain of rabbits injected with sodium arsenite. These results raise the question as to the appropriateness of BAL as the treatment for systemic arsenic poisoning. Either DMSA or DMPS, when given sc or po, will protect rabbits against the lethal systemic effects of subcutaneously administered Lewisite . DMPS and DMSA have promise as prophylactics for the prevention of the vesicant action of Lewisite . The sodium arsenite inhibition of the pyruvate dehydrogenase (PDH) complex can be prevented and reversed in vitro or in vivo by DMPS, DMSA, DMPA, or BAL. Of them all, DMPS is most potent and BAL appears to be the least potent. The usefulness of all these dimercapto compounds would be enhanced by a careful study of their metabolism and biotransformation. These dimercapto compounds are in a great many respects orphan drugs. At this stage of their development, it is very difficult for the clinician to obtain funds to study them clinically even though they appear to be useful for treatment of poisoning by any one of the heavy metals.