Carbon Monoxide Toxicity.

Carbon monoxide accounts for thousands of deaths worldwide each year. Clinical effects can be diverse and include headache, dizziness, nausea, vomiting, syncope, seizures, coma, dysrhythmias, and cardiac ischemia, and severe toxicity generally affects the nervous and cardiovascular systems. Because of its complex pathophysiology, effects of toxicity can be acute or delayed. The diagnosis can be elusive, as carboxyhemoglobin levels do not always correlate with the degree of poisoning. Even when the diagnosis is certain, appropriate therapy is widely debated. Normobaric oxygen is the standard therapy, and the efficacy of hyperbaric oxygen is unclear.

Extremely high urine arsenic level after remote seafood ingestion.

Urine testing for heavy metal concentrations is increasingly performed in the outpatient setting as a part of laboratory evaluation for neuropathy. Abnormal urine arsenic levels due to dietary intake of organic arsenic can lead to unnecessary chelation therapy. A 54-year-old man underwent a 24-hour urine collection for heavy metal concentrations in evaluation of paresthesia of the right foot. The total arsenic level was 8880 µg/d with concentrations of 4749 µg/L and 3769 µg/g creatinine. He was urgently referred to the toxicology clinic for consideration of chelation therapy. History revealed consumption of 2 lobster tails 5 days before the testing. Speciation was then performed on the original urine specimen and revealed an organic arsenic concentration of 4332 µg/L. No inorganic or methylated arsenic was detected. Repeat testing after abstaining from seafood demonstrated a total arsenic level of 50 µg/d with concentrations of 30 µg/L and 21 µg/g creatinine. Our patient demonstrates the highest level of arsenobetaine reported in the literature, and this level is higher than expected for a person who had not consumed seafood for 5 days before testing. The high levels may be due to consumption of food that he did not recognize as containing arsenobetaine or that his clearance of arsenobetaine from the ingested lobster is slower than published ranges. This case demonstrates the importance of speciation when measuring urine arsenic levels to avoid unnecessary chelation therapy.

Serotonin syndrome associated with MDPV use: a case report.

Serotonin syndrome is associated with use of certain street drugs, including methamphetamine, cocaine, and ecstasy. We describe a case of a woman who developed clinical findings consistent with serotonin syndrome after insufflation of 3,4-methylenedioxypyrovalerone (MDPV), a synthetic amphetamine. MDPV belongs to a group of substances called phenylethylamines, which are ß-ketone analogs of other drugs of abuse, such as amphetamines and 3,4-methylenedioxymethamphetamine. She also received fentanyl initially during her hospitalization, which has also been associated with serotonin syndrome. In addition to benzodiazepines and supportive care, she was treated with cyproheptadine for 8 days, with slow resolution of her symptoms.

Conservative management of elemental mercury retained in the appendix.

INTRODUCTION: Few cases of mercury sequestration in the appendix appear in the literature. Based on these, both prophylactic appendectomy and non-surgical management have been recommended. We report a case in which a patient with mercury retained in the appendix was managed conservatively without developing mercurialism or appendicitis. CASE REPORT: A 43-year-old man ingested approximately one tablespoon of elemental mercury after an argument with his wife. An initial abdominal radiograph showed mercury in the pylorus of the stomach and a follow-up x-ray at 72 hours showed mercury localized to the appendix. The patient was treated as an outpatient and examined several times over a 37-day period. He never developed signs of appendicitis. On a follow-up examination 7 months after the ingestion, he was radiographically free of mercury. Periodically throughout his clinical course, blood mercury levels were obtained. Only one, 6 days after ingestion, showed an elevated mercury level of 68 mcg/L (reference range <10 mcg/L). Despite this, the patient never developed signs or symptoms of mercury poisoning. CONCLUSION: Patients in whom elemental mercury is retained in the appendix, who are without symptoms and have normal gastric mucosa, may be conservatively managed without surgery.

Toxicity associated with carbon monoxide.

Carbon monoxide is an insidious poison that accounts for thousands of deaths each year in North America. Clinical effects maybe diverse and include headache, dizziness, nausea, vomiting,syn-cope, seizures, coma, dysrhythmias, and cardiac ischemia. Children, pregnant women, and patients who have underlying cardiovascular disease are particularly at risk for adverse out-comes. Treatment consists of oxygen therapy, supportive care, and, in selected cases, hyperbaric oxygen therapy.

Carbon monoxide poisoning.

CO is an ubiquitous poison with many sources of exposure. CO poisoning produces diverse signs and symptoms that are often subtle and may be easily misdiagnosed. Failure to diagnose CO poisoning may result insignificant morbidity and mortality and permit continued exposure to a dangerous environment. Treatment of CO poisoning begins with inhalation of supplemental oxygen and aggressive supportive care. HBOT accelerates dissociation of CO from hemoglobin and may also prevent DNS. Absolute indications forHBOT for CO poisoning remain controversial, although most authors would agree that HBOT is indicated in patients who are comatose or neurologically abnormal, have a history of LOC with their exposure, or have cardiac dysfunction. Pregnancy with an elevated CO-Hgb level(>15%-20%) is also widely, considered an indication for treatment.HBOT may be considered in patients who have persistent symptoms despite NBO, metabolic acidosis, abnormalities on neuropsychometric testing, or significantly elevated levels. The ideal regimen of oxygen therapy has yet to be determined, and significant controversy exists regarding HBOTtreatment protocols. Often the local medical toxicologist, poison control center, or hyperbaric unit may assist the treating physician with decisions regarding therapy.

Perceived poisons.

Perceived poisoning may manifest in numerous ways; however, all cases share certain characteristics. All are fostered by the wide availability of unreliable information about chemical safety, poor understanding of scientific principles, and ineffective risk communication. Although this problem is still incompletely understood, some approaches have been demonstrated to be useful, such as education about risk, appropriate reassurance, and empathy on the part of the practitioner. Successful management may curtail the spread or exacerbation of symptoms, whereas unsuccessful treatment may cause the problems to escalate, with detrimental effects on both society and patient.

Carbon monoxide poisoning.

CO is an insidious poison with many sources of exposure. CO poisoning produces diverse signs and symptoms, which often are subtle and can be misdiagnosed easily. Failure to diagnose CO poisoning may result insignificant morbidity and mortality and allow continued exposure to a dangerous environment. In the ED, a high index of suspicion must be maintained for occult CO exposure. Headache, particularly when associated with certain environments, and flulike illness in the wintertime with symptomatic cohabitants should raise the index of suspicion in the ED significantly for occult CO poisoning. Emergency treatment of CO poisoning begins with inhalation of supplemental oxygen and aggressive supportive care. HBOT accelerates dissociation of CO from hemoglobin and may prevent DNS. Absolute indications for HBOT for CO poisoning remain controversial, although most would agree that HBOT is indicated in patients who are comatose, are neurologically abnormal, have a history of loss of consciousness with their exposure, or have cardiac dysfunction. Pregnancy with an elevated CO-Hgb level (>15-20%) also is widely considered an indication for treatment. HBOT may be considered in patients who have persistent symptoms despite NBO, metabolic acidosis, abnormalities on neuropsychometric testing, or significantly elevated levels. The ideal regimen of oxygen therapy has yet to be determined, and significant controversy exists regarding HBOT protocols. The emergency physician may be confronted with the difficult decision regarding disposition and even transfer to a hyperbaric facility. Often the local medical toxicologist, poison control center, or hyperbaric unit can assist the emergency physician with the decision-making process.

Organophosphate poisoning.

Organophosphates are commonly used as pesticides around the world. Exposures to organophosphates cause a significant number of poisonings and deaths each year. Organophosphates bind and inhibit cholinesterase enzymes. Acute toxicity manifests as a cholinergic crisis with excessive glandular secretions, altered mental status, and weakness. Several delayed syndromes have also been associated with organophosphate exposure, including a myasthenic-like syndrome, peripheral neuropathies, neuropsychiatric abnormalities, and extrapyramidal disorders. Clinical features and management of organophosphate poisoning is reviewed with emphasis on those affecting the central and peripheral nervous system.

Dimercaptosuccinic acid and Prussian Blue in the treatment of acute thallium poisoning in rats.

INTRODUCTION: Despite being banned as a pesticide, thallium still results in human and animal poisonings. Current recommended treatments include the use of the chemical Prussian Blue. Limitations in its availability may result in Prussian Blue not being obtainable in the thallium-poisoned patient. The chelator 2,3-Dimercaptosuccinic acid (DMSA) is currently FDA-approved for use in childhood lead poisoning and has been reported to be beneficial in treating other heavy metal poisonings. The objective of this study was to determine the efficacy of DMSA as a treatment for thallium poisoning by studying mortality and whole-brain concentrations in thallium poisoned rats. MATERIAL AND METHODS: Rats were gavaged with 30 mg/kg of thallium. After 24 hours they were randomized to DMSA (n = 20) 50 mg/kg twice daily for 5 days, Prussian Blue (n = 20) 50 mg/kg twice daily for 5 days, or control (n = 30). Animals were monitored twice daily for weight loss and mortality. Animals losing greater than 20% of their starting weight were euthanized and counted as a mortality. All surviving rats at 120 hours had their brains harvested and digested and underwent subsequent thallium analysis. RESULTS: The rate of survival in DMSA-treated animals compared to control was 45% vs. 21%, p = 0.07. Mean whole-brain thallium concentrations between DMSA and control rats were 3.4 vs. 3.0 microg/g, p = 0.06. Prussian Blue-treated rats had significantly improved survival (70% vs. 21%, p < 0.01) and lower whole-brain thallium concentrations (1.6 vs. 3.0 microg/g, p < 0.01 tissue) compared to controls. CONCLUSION: DMSA failed to reduce brain thallium concentrations in rats poisoned with thallium and had an indeterminate effect on mortality while Prussian Blue significantly reduces both brain thallium concentrations and mortality.