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.

Racemose neurocysticercosis.

Neurocysticercosis is one of the most common infections of the central nervous system in the developing world. Most often, neurocysticerci are found in the brain parenchyma, at the gray-white matter junction. A rare form of neurocysticercosis is the development of cysts at the basal subarachnoid region, termed racemose neurocysticercosis.

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.

Thymoma, myasthenia gravis, and other paraneoplastic syndromes.

The relationship between myasthenia gravis and thymic pathology, including thymoma, is well known. Approximately 10% to 15% of patients who have myasthenia gravis are observed to have a thymoma. Myasthenia gravis may be considered as the most common of the paraneoplastic syndromes in patients who have thymoma. This article summarizes the clinical aspects of myasthenia gravis, followed by a review of the less often recognized paraneoplastic disorders noted to occur in patients who have thymoma.

Neuroleptic malignant syndrome and serotonin syndrome.

The clinical manifestation of drug-induced abnormalities in thermoregulation occurs across a variety of drug mechanisms. The aim of this chapter is to review two of the most common drug-induced hyperthermic states, serotonin syndrome and neuroleptic malignant syndrome. Clinical features, pathophysiology, and treatment strategies will be discussed, in addition to differentiating between these two syndromes and differentiating them from other hyperthermic or febrile syndromes. Our goal is to both review the current literature and to provide a practical guide to identification and treatment of these potentially life-threatening illnesses. The diagnostic and treatment recommendations made by us, and by other authors, are likely to change with a better understanding of the pathophysiology of these syndromes.

The Pharmacology and Toxicology of Third-Generation Anticonvulsant Drugs.

Epilepsy is a neurologic disorder affecting approximately 50 million people worldwide, or about 0.7% of the population [1]. Thus, the use of anticonvulsant drugs in the treatment of epilepsy is common and widespread. There are three generations of anticonvulsant drugs, categorized by the year in which they were developed and released. The aim of this review is to discuss the pharmacokinetics, drug-drug interactions, and adverse events of the third generation of anticonvulsant drugs. Where available, overdose data will be included. The pharmacokinetic properties of third-generation anticonvulsant drugs include relatively fewer drug-drug interactions, as well as several unique and life-threatening adverse events. Overdose data are limited, so thorough review of adverse events and knowledge of drug mechanism will guide expectant management of future overdose cases. Reporting of these cases as they occur will be necessary to further clarify toxicity of these drugs.

Disparities and guideline adherence in drugs of abuse screening in intracerebral hemorrhage.

OBJECTIVE: To characterize the pattern of urine drug screening in a cohort of intracerebral hemorrhage (ICH) patients at our academic centers. METHODS: We identified cases of primary ICH occurring from 2009 to 2011 in our academic centers. Demographic data, imaging characteristics, processes of care, and short-term outcomes were ascertained. We performed logistic regression to identify predictors for screening and evaluated preguideline and postguideline reiteration screening patterns. RESULTS: We identified 610 patients with primary ICH in 2009-2011; 379 (62.1%) were initially evaluated at an outside hospital. Overall, 142/610 (23.3%) patients were screened, with 21 positive for cocaine and 3 for amphetamine. Of patients <55 years of age, only 65/140 (46.4%) were screened. Black patients <55 years of age were screened more than nonblack patients <55 years of age (38/61 [62.3%] vs 27/79 [34.2%]; p = 0.0009). In the best multivariable model, age group (p = 0.0001), black race (p = 0.4529), first Glasgow Coma Scale score (p = 0.0492), current smoking (p < 0.0001), and age group × black race (p = 0.0097) were associated with screening. Guideline reiteration in 2010 did not improve the proportion <55 years of age who were screened: 42/74 (56.8%) were screened before and 23/66 (34.9%) after (p = 0.01). CONCLUSIONS: We found disparities in drugs of abuse (DOA) screening and suboptimal guideline adherence. Systematic efforts to improve screening for DOA are warranted. Improved identification of sympathomimetic exposure may improve etiologic classification and influence decision-making and prognosis counseling.

Toxic leukoencephalopathies.

Leukoencephalopathy is a syndrome of neurologic deficits, including alteration of mental status, caused by pathologic changes in the cerebral white matter. The term, toxic leukoencephalopathy, encompasses a wide variety of exposures and clinical presentations. The diagnosis in these Frontiers in Clinical Neurotoxicology syndromes is made by careful attention to the history, clinical features, and radiologic findings. This article details three of the best-defined toxic leukoencephalopathies: delayed posthypoxic leukoencephalopathy, including delayed neurologic sequelae after carbon monoxide poisoning; heroin inhalation leukoencephalopathy; and posterior reversible encephalopathy syndrome.

Neurotoxicology: Five new things.

Neurotoxic disease can mimic many common neurologic disease states, including parkinsonism, myelopathy, neuropathy, and encephalopathy. Accurate diagnosis and appropriate treatment may result in a favorable outcome. This review highlights 5 areas of neurotoxicology for which there is an emerging understanding of disease processes or patterns of exposure, including 3 specific metal toxicities (manganism, zinc-induced copper deficiency, and cobalt-chromium neuropathy). Toxin-induced posterior reversible encephalopathy syndrome is more widely recognized and reported in association with an ever-growing list of drugs. Two new categories of street drugs, synthetic cathinones and cannabinoids, have been identified as public health threats due to their popularity, availability, and severity of toxicity.

Baclofen overdose mimicking brain death.

CONTEXT: Brain death guidelines should be used with caution in patients with drug intoxication. It is often suggested that physicians use five half-lives of a drug when observing a patient with an overdose. We report two cases of baclofen intoxication where brain death was entertained as an explanation for prolonged coma, with arousal seen days later, suggesting that routine use of a 5-half-life observation period is insufficient with baclofen intoxication. CASE PRESENTATION: A 40-year-old woman was found unresponsive by her family. Baclofen was found to be the responsible overdose. The patient had absent brain stem reflexes and was intubated and in the ICU for several days. Although EEG and Apnea test were inconclusive, the patient was thought to be brain dead and organ procurement was arranged. On hospital day 5, the patient started having purposeful movements. The patient had progressive arousal and was eventually transferred without neurologic sequelae to psychiatry. The second patient also had a massive baclofen overdose, had absence of almost all brain stem reflexes and was also intubated and in the ICU. Brain death was felt to be imminent, but the patient began to awake on hospital day 7. DISCUSSION: Our two cases suggest that baclofen intoxication may result in very prolonged and profound coma and may, in fact, mimic brain death. Conclusion. The determination of brain death in the comatose overdose patient must proceed with caution. An adequate period of time to allow drug clearance must be allowed.

Toxic leukoencephalopathies.

Leukoencephalopathy is a syndrome of neurologic deficits, including alteration of mental status, caused by pathologic changes in the cerebral white matter. The term, toxic leukoencephalopathy, encompasses a wide variety of exposures and clinical presentations. The diagnosis in these syndromes is made by careful attention to the history, clinical features, and radiologic findings. This article details three of the best-defined toxic leukoencephalopathies: delayed posthypoxic leukoencephalopathy, including delayed neurologic sequelae after carbon monoxide poisoning; heroin inhalation leukoencephalopathy; and posterior reversible encephalopathy syndrome.

Increased adolescent opioid use and complications reported to a poison control center following the 2000 JCAHO pain initiative.

CONTEXT: Adolescents are at risk to abuse opioid analgesics for many reasons, including inaccurate perception of risk and increased drug availability. In 2000, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) released pain management standards that emphasized pain control as a patient rights issue. This focus on analgesia may have increased both the prescribing and use of opioid analgesics, thereby increasing availability. OBJECTIVE: Using data from a US poison center, this study aims to compare the number of adolescent opioid cases and their outcome severity before and after the 2000 JCAHO pain initiative. METHODS: Retrospective case series of opioid exposures involving persons 12-18 years of age reported to a US poison center from 1994 to 2007. The main outcome measure was the number of adolescent opioid cases reported for 1994-2000 compared to 2001-2007. Secondary outcomes included outcome severity, number of cases involving specific opioids, and correlation between the number of cases and the amount of opioids distributed to the state. RESULTS: There were 1634 adolescent opioid-related cases with 187 cases developing medical complications. Compared with 1994-2000, the rate ratio of cases involving adolescents and opioid analgesics for the years 2001-2007 was 1.69 (95% CI: 1.53, 1.86), and these cases were 2.84 (95% CI: 2.06, 3.91) times more likely to have had medical complications. Medical complications involving methadone (p =0.001) increased after the JCAHO initiative, while complications related to codeine (p =0.001) and propoxyphene (p =0.030) decreased. There were 15 deaths in 2001-2007 and none in 1994-2000 (p =0.012). Lastly, there was a correlation between the rate of adolescent opioid cases and the amount of opioids distributed to the state (r(2) =0.90; p < 0.001). CONCLUSION: In the 7 years following the JCAHO pain standards, there was an increase in the number and severity of adolescent opioid-related poison center cases. The increase correlates with statewide availability of opioids. These data may prove useful in drug education and prevention programs targeting adolescents.