Brett Roth

Carisoprodol-Induced Myoclonic Encephalopathy

CASE REPORT A 39-year-old man ingested 35 g carisoprodol. He developed agitation, tachycardia, myoclonus, and coma. The blood carisoprodol was 71 micrograms/mL; the meprobamate was 26 micrograms/mL. DISCUSSION Carisoprodol overdose is thought to induce simple central nervous system depression. This case demonstrates a severe overdose with symptoms more consistent with myoclonic encephalopathy. A review of cases presenting to the San Francisco Division of the California Poison Control System during 1997 suggests that carisoprodol is more commonly associated with agitation and bizarre movement disorders than the current literature suggests. The pharmacology and potential mechanisms of toxicity are discussed. CONCLUSION Agitation, hypertonia, and a myoclonic encephalopathy may be seen with significant carisoprodol intoxication.

Serotonin Syndrome with Elevated Paroxetine Concentrations

OBJECTIVE To describe a case of serotonin syndrome due to paroxetine and ethanol. CASE SUMMARY A 57-year-old white man was brought to the emergency department one day after ingesting paroxetine 3600 mg and a pint of hard liquor. He denied the use of any other drug or herbal products and regular use of alcohol. Upon arrival to the hospital, vital signs were blood pressure 188/103 mm Hg, heart rate 114 beats/min, respiratory rate 28 breaths/min, temperature 36.8 °C, and O2 saturation 96% on room air. Findings on physical examination included dilated pupils, facial flushing, diaphoresis, shivering, myoclonic jerks, tremors, and hyperreflexia. A tentative diagnosis of serotonin syndrome was made. Initially, cyproheptadine 8 mg was administered orally with no observable effect. An additional 12 mg was given in 3 doses over 24 hours. Symptoms abated slowly over the next 6 days, during which a thorough evaluation failed to reveal any other potential causes for the patients condition. Serum paroxetine concentrations at 27.5 and 40 hours after ingestion were 1800 and 1600 ng/mL, respectively (normal 20–200 ng/mL). DISCUSSION Serotonin syndrome is rarely reported in patients taking only one serotonergic medication. Although serum paroxetine concentrations have not been shown to correlate with efficacy or toxicity, our patients serum paroxetine concentration was 9 times the upper end of the therapeutic range. Cyproheptadine, which has been suggested as a therapy, did not appear beneficial in this patient. Use of the Naranjo probability scale indicated a probable relationship between the serotonin syndrome and the overdose of paroxetine taken by this patient. CONCLUSIONS More studies are needed to better assess the role of cyproheptadine and other serotonin antagonists in the management of the serotonin syndrome. Regardless of the use of cyproheptadine or other agents, attention should be paid to fluid status, decontamination, and management of hyperthermia, agitation, and seizures.

Prolonged delirium with psychotic features from omega conotoxin toxicity.

To the Editor: Patients with neuropathic pain constitute a considerable proportion of the population of patients with chronic pain for which there are less than optimal treatment options. The scientific literature provides information on omega conotoxin efficacy and safety in the management of chronic pain conditions ⇓. A synthetic version, ziconotide, is a first line intrathecal (IT) alternative agent to opioids in the management of cancer pain ⇓. We describe a case of prolonged delirium with psychotic features in a patient with peripheral neuropathy on a gradual escalating dose of ziconotide. A 37-year-old man with a history of idiopathic small fiber peripheral neuropathy unresponsive to usual treatment with opiate analgesics was started on IT ziconotide for better pain control 1 year before he presented to our center with a 3-day history of confusion, hallucination, and tremor. These symptoms started a day after his home was sprayed with insecticide. He had associated symptoms of loss of appetite, …

The Relationship between Occupational Exposure to Lead and Hearing Loss in a Cross-Sectional Survey of Iranian Workers.

Objectives Ototoxic effect of exposure to lead has been reported by many researchers. This study was undertaken with a view to investigate the relationship between blood lead level (BLL) and hearing loss in workers in a lead-acid battery manufacturing plant in Tehran, Iran. Methods In a cross-sectional study, 609 male workers were recruited from different locations in the factory. Association between BLL and hearing loss in different frequencies were measured. Relationships were analyzed by logistic regressions. Statistical significance was defined as p-value <0.05. Results Six hundred nine male workers with mean age 40 ± 7 years and mean noise exposure level of 80 (75–85) dB were evaluated. BLLs were categorized into four quartiles, and hearing loss in each quartile was compared to the first one. In our regression models, BLL was associated significantly with high frequency hearing loss, adjusted odds ratios for the comparison of the fourth, third, and second quartiles to the first one are respectively: 3.98 (95% CI: 1.63–9.71, p < 0.00), 3.05 (95% CI: 1.28–7.26, p < 0.01), and 2.89 (95% CI: 1.11–7.51, p < 0.03). Conclusion This study showed a dose–response relationship between BLL and hearing loss, after adjusting for potential confounders (age, body mass index, work duration, smoking, and occupational noise exposure) in logistic regressions. It is concluded that periodic hearing assessment by pure tone audiometry in workers exposed to lead should be recommended. However, additional studies are required to clarify the mechanisms of lead ototoxicity.

Childhood Victims of Snakebites: 2000–2013

BACKGROUND: Snakebites are not a reportable condition (to state health departments), and 1 major assessment of US children with snakebites was published 50 years ago. Increasing urbanization, population shifts south and west, newer antivenom therapy, and the importation of exotic snakes may have changed snakebites. Poison control centers are often consulted on treatment and collect surveillance data. METHODS: Generic codes for venomous, nonvenomous, and unknown snakebites were used to characterize victims aged ≤18 years reported to US poison control centers between 2000 and 2013. Data included demographic characteristics, snake types, and outcomes. RESULTS: Callers reported 18 721 pediatric snakebites (annual mean, 1337). Two-thirds were male (n = 12 688 [68%]), with a mean age of 10.7 years. One-half of the snakebites were venomous (n = 9183 [49%]), with copperheads (n = 3602 [39%]) and rattlesnakes (n = 2859 [31%]) the most frequently identified. Reported copperhead bites increased 137% and unknown crotalids (venomous) increased 107%. Exotic (nonnative) exposures were reported in 2% of cases. All 50 states reported snakebites, but one-quarter occurred in Texas and Florida. Rates for total snakebites and venomous snakebites were highest in West Virginia, Oklahoma, and Louisiana. One-fifth required ICU admission. Limited data for 28% of bites for antivenom treatment suggests increasing use. Four victims died. CONCLUSIONS: The epidemiology of pediatric snakebites is changing. One-half of the reported exposures were venomous, and copperhead bites and exotic species are being reported more frequently. Although snakebite-related deaths are rare, ICU admission is common. Antivenom treatment is incompletely reported, but its use is increasing.

Prospective evaluation of pain, swelling, and disability from copperhead envenomation

Abstract Context: In light of the existing controversy regarding antivenin treatment for copperhead envenomation, a more detailed analysis of the disability from this species is needed. Objective: Our objective was to prospectively determine the duration of pain, swelling, and functional disability, i.e., residual venom effects, in patients with copperhead envenomation. Methods: Patients with venomous snakebite reported to the North Texas Poison Center between April 2009 and November 2011 were assessed. Patients with confirmed envenomations were contacted by a specialist in poison information. Day zero was the day of the bite and verbal phone consent for study enrollment was obtained at that time. The patient (or their guardian) was contacted by phone daily thereafter, and asked to rate their pain, edema/swelling, and disability using the modified DASH and LEFS scales. Patients were followed to resolution of all symptoms or return to baseline. Results: About 104 cases of venomous snakebite were followed; of which 17 were excluded due to being a dry bites (5) or for having insufficient data during follow-up (11) or due to coagulopathy (1). Overall, residual venom effects from copperhead bites for most patients last between 7 and 13 days. Median time to complete pain resolution was 7 days (mean = 10.7 days). Median length of time to resolution of swelling was 10 days (mean = 13 days) and median length of time to resolution of functional disability was 9 days (mean = 12.2 days). Discussion: Residual venom effects from copperhead envenomation in this study had a slightly shorter duration than some other studies. Data are skewed due to outliers where residual venom effects lasted for up to 89 days. Initial reoccurrence of some symptoms may be seen. Antivenom (AV) is currently being used for a large percentage of patients with copperhead envenomation. Finally, no differences in duration of venom effects were seen based on age or location of bite. Conclusion: Our study suggests that residual venom effects from copperhead species persist for between 10 and 13 days but may persist for months. Future studies are necessary to identify risk factors for severe/prolonged injury and to define the benefit of AV in patients with copperhead envenomation.

Good Outcomes Despite High Urinary Arsenic Concentrations from Overdose with Crabgrass Killer

IntroductionMonosodium methylarsonate (MSMA) is a selective pre-emergent contact herbicide considered to be significantlyless toxic than inorganic arsenic. Animal studies extrapo-lated to humans have estimated a low order of toxicity [1],but little information is available regarding overdose inhumans. Previous reports have described oral exposureswith less concentrated formulations of MSMA herbicides[2] or via dermal absorption [3]. Because of the limitedinformation in the current literature, concern exists regard-ing exposures to concentrated forms of organic arsenic. Wedescribe exposures to a common crabgrass killer containing47% MSMA.Index CasesCase 1 A 16-year-old female with a past medical history ofdepression (not on any medications) presented afterintentional ingestion of crabgrass killer. The patient hadan argument with her grandmother and locked herself in thegarage where she drank up to 240 cc of Bonide® crabgrasskiller that contained 47% MSMA. She vomited and wastaken to the emergency department (ED) approximately 1 hafter the exposure. In the ED, the patient was agitated. Shecomplained of abdominal pain and generalized weakness.Her vital signs were: blood pressure 134/78 mmHg, heartrate 126 beats per minute, respirations 16 breaths perminute, and oxygen saturation 100% on room air. Shereceived a bolus of 3 l of normal saline (NS) and was thenstarted on NS at 500 ml/h. The patient was endotracheallyintubated for gastric lavage and for transportation to thelocal childrens hospital. Gastric lavage was done at thediscretion of the treating physician, and no material wasretrieved. On arrival to the childrens hospital, her vitalsigns and physical exam were normal; she was able tofollow commands. Electrolytes and complete blood count(CBC) were unremarkable. A single dose of 192 mg ofBritish anti-Lewisite (BAL) IM was administered approx-imately 12 h after the ingestion; extubation occurred severalhours after arrival. Urine was collected in a Foley catheterfor a 24-h heavy metal measurement. Dimercaptosuccinicacid (DMSA) was then initiated at 500 mg every 8 h bymouth for 5 days followed by 500 mg every 12 h for14 days.In the hospital, the patient complained of generalizedabdominal pain, weakness, and parasthesias. She did nothave any more vomiting and never had diarrhea; mildhyperreflexia was noted on exam. She was able to eat afterbeing extubated, and paresthesias and abdominal painimproved during her hospitalization. Initially, she haddifficulty walking, but by day 5, she was walking withoutassistance and was discharged to a psychiatric institution.There, she was continued on DMSA for the remainder ofher 19 days of treatment. After discharge, the results of herheavy metal screen returned and are noted in Table 1.Six weeks later, the patient was followed up in thetoxicology clinic where she complained of mild paresthe-sias in her hands and feet that developed after beingtransferred to the psychiatric hospital. The episodes lastedfor minutes at a time, occurred in the morning, and never