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Physostigmine was once a widely used antidote for the treatment of antimuscarinic toxicity. However, reports describing the association of physostigmine with asystole and seizures in severe tricyclic antidepressant poisoning resulted in a decrease in use. Recent literature has demonstrated that physostigmine is a safe and effective antidote for the treatment of antimuscarinic toxicity. There are only two previously published articles regarding the use of physostigmine administered as a continuous intravenous infusion for persistent antimuscarinic toxicity. We present a case of physostigmine continuous infusion for the treatment of antimuscarinic symptoms in a polydrug overdose due to the ingestion of diphenhydramine along with bupropion, citalopram, acetaminophen, and naproxen.A 13-year-old female presented with hyperthermia, myoclonus and rigidity, hallucinations, severe agitation, and antimuscarinic toxicity including inability to sweat after a polydrug overdose. Several doses of lorazepam were administered followed by physostigmine which produced resolution of hallucinations and attenuation of the antimuscarinic symptoms including perspiration, temperature improvement, and decreased agitation. After periods of improvement and recurrence of antimuscarinic effects, a continuous infusion of physostigmine was administered at 2 mg/h and continued for almost 8 h to maintain attenuation of symptoms. GABAergic agents including lorazepam and phenobarbital were used later in the hospital course for presumed symptoms of serotonergic and adrenergic toxicity after resolution of antimuscarinic effects. The patient did not experience any adverse effects of physostigmine administration.Physostigmine administered as a continuous infusion may be a reasonable treatment option for severe and recurrent symptoms related to antimuscarinic toxicity.

Many countries have specific legislation, such as the Controlled Substances Act (1970) in the United States and the Misuse of Drugs Act (1971) in the United Kingdom to control recreational drugs. There is a growing market and supply of "novel" recreational drugs, which include the misuse of pharmaceutical compounds and research chemicals. These are often not covered under current legislation, despite the fact that they often have both similar chemical structures and/or clinical effects to controlled recreational drugs.A male patient presented to an emergency department with delayed onset of severe agitation, hallucinations, and tonic-clonic seizures following the use of Bromo-dragonFLY and an unknown white powder. He settled following IV benzodiazepines and supportive care, and was discharged with no evidence of long-term sequelae. Analysis of the white powder by gas chromatography/mass spectrometry (GC/MS), ultraviolet/visible spectrophotometry (UV/VIS) and thin layer chromatography (TLC) showed the presence of Bromo-dragonFLY (1-(8-bromobenzo[1,2-b;4,5-b']difuran-4-yl)-2-aminopropane); serum analysis by GC/MS and liquid chromatography with tandem mass spectrometry (LC/MS/MS) confirmed that a combination of Bromo-dragonFLY (0.95 ng/mL), ketamine (20 ng/mL) and cannabis had been used by the patient. No other recreational drugs were detected in an extensive toxicological screen of serum and urine samples.This is the first confirmed case to be reported of toxicity with delayed onset of severe agitation, hallucinations and tonic-clonic seizures associated with recreational use of Bromo-dragonFLY (1-(8-bromobenzo[1,2-b;4,5-b']difuran-4-yl)-2-aminopropane) in combination with ketamine and cannabis. In our view, this case provides further support for the need for a systematic approach to toxicological screening of patients with recreational drug toxicity, to identify emerging drugs and provide evidence for legislative authorities to assist in revising the legal status of emerging recreational drugs.

A 19-year-old male with an unremarkable medical history presented with his father, who requested an evaluation of a pathology specimen from a reported "lump" under the skin in the middle of the son's lower abdomen. The lump had been excised by a surgeon approximately 3 months prior, per parental request. Upon gross inspection, the specimen appeared to contain small metallic droplets. The patient denied self-injection of any metals, including mercury, despite the results of a 24-hour urine heavy-metal screen (without chelation) that revealed an elevated concentration of mercury (87.6 microg/g creatinine; reference range for nonexposed adults:4 microg/g creatinine). Confirmatory analysis of the tissue sample included gross and microscopic examination, electron microscopy using secondary and backscattered electron imaging modes, and energy dispersive x-ray spectrum analysis of isolated tissue particles. Grossly, the tissue had small silver spherules suggestive of elemental mercury; these droplets were identified histologically with associated foreign body reaction. Numerous smooth, round-to-oval particles scattered randomly throughout the tissue were identified ultrastructurally, which produced an x-ray energy spectrum corresponding to mercury.Elemental mercury is liquid at room temperature and may be injected into the body for recreational, psychiatric, and other purposes. Isolated cases of mercury injection following accidents with broken thermometers have been reported, as well as cases of elevated metallothionein concentration following human gingival amalgam tattoos.In cases of surreptitious injection, histology and ultrastructural evidence may be used to confirm the presence of mercury.

Ingestion of fireworks has been infrequently reported in the medical literature. We describe a case of acute barium poisoning following firework ingestion.A 35-year-old male with a history of severe mental retardation presented with vomiting and diarrhea following ingestion of 16 small fireworks ("color snakes" and "black snakes"). His condition rapidly deteriorated and he developed obtundation, wide complex dysrhythmias, and respiratory failure. Approximately 12 hours following ingestion, his serum potassium level was 1.5 mmol/L with a serum barium level of 20,200 microg/mL (reference range200 microg/L). The patient eventually recovered with ventilatory support and potassium supplementation.Although firework ingestion is uncommon, clinicians should be prepared for potentially severe complications. In the case of barium poisoning, treatment consists of potassium supplementation, along with respiratory and hemodynamic support.

Glucometry is widely used to confirm or exclude hypoglycemia in patients with suggestive clinical findings. Nonglucose sugars may be detected by certain types of glucometers, causing false elevation of the glucometer analysis of the blood sugar. Since these other sugars are not functionally glucose and may even induce excess insulin release, clinical hypoglycemia may be missed. We report a 79-year-old man on enteral feeds containing maltodextrin, a glucose polymer, who had persistently high glucometer-measured blood glucose despite normal blood glucose measured by formal laboratory analysis. Excess insulin administration, based on the erroneous glucometer reading, may have caused unrecognized fatal clinical hypoglycemia. This has been reported following intravenous administration of related nonglucose sugars but not with enteral maltodextrin. Further study is required to confirm the effects of maltodextrin on glucometry. False elevation of blood glucose measured on certain point-of-care glucometers can occur following the oral administration of maltodextrin.

Amantadine hydrochloride is an antiviral medication used as therapy for parkinsonism and as a cognitive enhancer. We report 2 cases of massive, acute ingestion of amantadine hydrochloride confirmed with serial serum levels.A 47-year-old woman presented to the emergency department (ED) 30 minutes after ingesting 10 g of amantadine (150 mg/kg) by her report. Initial ECG revealed a sinus rhythm with rate of 93 bpm, and a QRS of 84 msec. While in the ED, the patient sustained a pulseless cardiac arrest and the monitor revealed ventricular tachycardia. She was successfully defibrillated. Postdefibrillation ECG showed a sinus rhythm (rate = 82 bpm), QRS of 236 msec, and QTc of 567 msec. The serum potassium was 1.0 mEq/L (1.0 mmol/L). The patient was given 300 ml (300 cc) 3% sodium chloride IV over 10 minutes. Ten minutes after completion of the hypertonic saline infusion, the patient's ECG abnormalities resolved and the QRS was 88 msec. Her potassium was repleted over the next 11 hours postpresentation, and she also received an IV bolus of 4 g of magnesium sulfate immediately after the cardiac arrest. No further hypotension, dysrhythmia, conduction delay, or ectopy was noted during the patient's hospital stay. The second case involved a 33-year-old female patient who presented 1 hour after ingesting 100 tablets of amantadine hydrochloride (100 mg/tab). Initial ECG revealed sinus tachycardia with a QRS of 113 msec, an R wave in lead aVR of 4-5 mm and a QTc of 526 msec. Her serum potassium was 3.0 mEq/L (3.0 mmol/L), her serum calcium was 9.4 mg/dl (2.35 mmol/L), and serum magnesium was 2.1 mg/dl (0.86 mmol/L) on labs drawn at initial presentation. The patient was intubated for airway protection, and her potassium was repleted and corrected over the next 9 hours. Her ECG abnormalities improved 8 hours after initial presentation and normalized at approximately 14 hours postingestion. The patient was discharged home 11 days after her ingestion.Acute amantadine toxicity manifests with life-threatening cardiotoxicity. Concurrent, often profound, hypokalemia may complicate the administration of sodium bicarbonate in the management of cardiac dysrhythmias.

Recurrences of clinical or laboratory manifestations of North American pit viper envenomation may happen despite control of the envenomation syndrome by prompt and adequate antivenom therapy. Recurrences of coagulopathy in victims of Eastern diamondback rattlesnake envenomation are generally regarded as benign. The vast majority suffer no actual bleeding despite florid coagulation laboratory abnormalities due to selective defibrinogenation.We report what we believe to be the first fatality following successful control of the envenomation syndrome following ovine antivenom treatment resulting from envenomation by a bite from the Eastern diamondback rattlesnake. This case raises the question of whether such recurrences are in fact benign, causal, or coincidental. This patient sustained significant brain hemorrhage and death ensued due to generalized cerebral edema. Defibrinogenation occurred 4 days after treatment with ovine antivenom.Coagulation abnormalities following Eastern diamondback rattlesnake envenomation are due to selective defibrinogenation. This is separate from disseminated intravascular coagulation (DIC). Thrombin generation, thus hemostasis, are generally considered normal. This case may cause reexamination of this belief.

Gasoline, ingested intentionally or accidentally, is toxic. The majority of reported cases of gasoline intoxication involve oral ingestion or inhalation. Data are scarce on complications and outcomes following hydrocarbon poisoning by intravenous injection.Following a suicide attempt by intravenous self-injection of 10 ml of gasoline, a 26-year-old medical student was admitted to the intensive care unit (ICU) with hemoptysis, symptoms of acute respiratory failure, chest pain, and severe abdominal cramps. Gas exchange was severely impaired and a chest x-ray indicated chemical pneumonitis. Initial treatment consisted of mechanical ventilation, supportive hyperventilation, administration of nitrogen oxide (NO), and prednisone. Unfortunately, the patient developed multi-organ dysfunction syndrome (MODS) complicated by life-threatening severe vasoplegia within 24 hours after gasoline injection. High doses of vasopressors along with massive amounts of parenteral fluids were necessary. Despite fluid replacement, renal function worsened and required hemofiltration on 5 sequential days. After 12 days of intensive care management, the patient recovered completely and was discharged to a psychiatric care facility.Intravenous gasoline injection causes major injury to the lungs, the organ bearing the first capillary bed encountered. Treatment of gasoline poisoning is symptomatic because no specific antidote is available. Early and aggressive supportive care may be conducive to a favorable outcome with minimal residual pulmonary sequelae.

Most hospitals lack a sufficient supply of atropine to treat, simultaneously, patients poisoned with multiple organophosphorous compound (OC) or nerve agent. The presence of a ubiquitous alternate antidote would prove useful if mass poisoning occurred. Our objective was to evaluate the effect of ophthalmic homatropine (Isopto Homatropine 5%) on survivability in a rat model of significant, acute OC poisoning.Sprague-Dawley rats were randomized to one of five pre-treatment groups (N = 10 per group). Prior to experimentation, animals were pre-treated with intramuscular (IM) injections of either atropine 5 mg/kg, atropine 10 mg/kg, homatropine 10 mg/kg, or homatropine 20 mg/kg. The control group received 0.3 mL normal saline IM. Five minutes later, 25 mg/kg of dichlorvos was subcutaneously administered. Mortality rates were compared using Fisher's Exact test. Kaplan-Meier survival curves with Logrank analysis was also performed. If alive at 120 minutes, survival was assumed, and the study was terminated.All rats pre-treated with normal saline, atropine 5 mg/kg, and homatropine 10 mg/kg died. Survival in the homatropine (20 mg/kg) and atropine (10 mg/kg) groups was 30% and 40% respectively. Times to death ranged between 4 and 12 minutes. Overall comparison of time to death revealed a statistically significant improvement for groups pre-treated with homatropine (20 mg/kg) and atropine (10 mg/kg).Pre-treatment with homatropine (20 mg/kg) was comparable with atropine (10 mg/kg) in preventing lethality in this rat model of acute OC poisoning.

Nitrous oxide is a commonly abused inhalant drug. It is known to precipitate vitamin B12 deficiency when used chronically and acutely, especially in people having marginal vitamin B12 reserve.We are presenting a case of nitrous oxide "whippit" abuse in a thirty-three-year-old male with bizarre behavior and delusions. The patient had low normal levels of vitamin B12 (202 pg/ml), but he had markedly high methylmalonyl CoA (1078 nmol/L) and homocysteine (48.4 mcmol/L). Treatment with intramuscular cobalamin led to a resolution of his psychosis.This case report highlights the need to consider vitamin B12 deficiency in patients who arrive at a hospital with psychiatric manifestations and who report having a history of nitrous oxide exposure or abuse in the recent or remote past. A review of the literature on the neuropsychological manifestations of vitamin B12 deficiency is provided.

Texas poison centers identified carisoprodol as a skeletal muscle relaxant that is subject to abuse, and this investigation explores the abuse reported by Texas poison centers.This study used data from six Texas poison centers to describe the epidemiology of carisoprodol abuse and drug identification (ID) calls from 1998 to 2003.Drug ID and abuse calls were 217% higher in 2003 than in 1998. Although eastern and central Texas contains 43% of the state's population, this region reported 77% of all drug ID calls and 64% of abuse calls. For male patients, 51% of the calls were abuse calls and 37% were other human carisoprodol exposure calls. Patients from 13 to 19 years of age accounted for 17% of abuse calls and 9% of other human exposure calls. Among those human exposure calls with a known medical outcome, a higher percentage of abuse calls involved minor effects while a greater proportion of other human exposure calls involved outcomes that ranged from moderate effects to death.Carisoprodol abuse is increasing in Texas and is substantially more common in the eastern part of the state. Carisoprodol abuse is much more likely, than other types of adverse carisoprodol exposures, to involve males and adolescents; and it less likely to involve adverse medical outcomes.

Medication errors may produce severe toxicity resulting in hospitalization. This can be compounded if the physician obtains the wrong concentration from a reference manual and a pharmacy miscalculates the conversion. We report a child presenting with ileus, hypothermia and lethargy after receiving supratherapeutic dosing of phenytoin after a concentration miscalculation.A one-month-old infant presented to the Emergency Department with progressive worsening of abdominal distension, diminished activity, and a one day history of difficulty feeding secondary to a decreased level of consciousness. The past medical history was significant for neonatal Group B Strep meningitis with seizures. Among the child's discharge medications was a prescription for phenytoin (30 mg/5 mL) 2.5 cc by mouth three times daily. On exam, the child was hypothermic with pink mottled skin, poor responsiveness, prolonged capillary refill, abdominal distension with hypoactive bowel sounds, and a dysconjugate gaze. The Initial phenytoin serum concentration was 91.8 mcg/mL. She was admitted to the PICU and was started on ampicillin and cefotaxime for R/O sepsis. Phenytoin was withheld and subsequent serum concentrations revealed an extremely slow elimination (mcg/mL vs. time pair coordinates were 78.2/13.3h; 74.3/62.3h; 43.7/109.6h; 10.8/160.9h) reflecting zero-order kinetics. Post discontinuing antibiotics, phenytoin levels decreased at rates expected. She was discharged after resolution of symptoms. The MD who had written the phenytoin prescription had based it on the Harriet Lane Handbook, 2000 Ed. The 30 mg/5 mL formulation has been unavailable in the US for several years. A community pharmacy substituted the 125 mg/5 mL formulation, but miscalculated the dosage to be 1.6 cc (40 mg) tid.Abdominal distension and ileus may be presenting symptoms in children at toxic phenytoin levels. Ampicillin and cefotaxime may effect the elimination rate of phenytoin at such levels. We report one of the highest phenytoin levels recorded after therapeutic misadventure. Physicians must be aware of inaccuracies in reference manuals that may result in dosing errors.

Tretinoin (Vesanoid) is an all-trans-retinoic acid, and is related to retinol (Vitamin A). To date, there have been several case reports on overdose with its isomer isotretinoin, but none involving overdose of tretinoin. We report the first known case of a patient who ingested a massive overdose of tretinoin.A 31-year-old man ingested 1000 mg of tretinoin (100 pills of Vesanoid 10 mg) in a suicide attempt. He developed nonbloody diarrhea, but otherwise had no complaints. Clinical examination was normal. The patient was treated with activated charcoal and was hydrated. The patient's blood results did not show any deterioration on the third consecutive day. He was discharged well on the third day, but was subsequently lost to follow-up.Although there has been no reported experience with acute tretinoin overdose in humans, our patient took a dose approximately 3 times the recommended maximum tolerated daily dose in patients with myelodysplastic syndrome or solid tumors (195 mg/m2 per day). Overdose with other retinoids such as isotretinoin have been associated with only minor symptoms that resolved quickly. Our patient had diarrhea, which also resolved quickly with symptomatic treatment and hydration.We believe this to be the first case report of an acute oral overdose of tretinoin. The patient developed diarrhea, but was otherwise asymptomatic.

Quetiapine, a second-generation antipsychotic, acts at multiple brain neurotransmitter receptors and has the potential for serious complications. Although seizures have been described in the literature, delayed seizure onset has not been reported. We report the first case of delayed seizures after a significant quetiapine overdose.A 27-year-old female presented to the emergency department following an overdose of approximately 30 g of quetiapine. Twenty-four hours after arrival, the patient had 2 seizures. The patient was then intubated and remained in the ICU for four days. EEG was negative for epileptiform activity. The serum quetiapine levels (MedTox, St. Paul, MN) were 8.67 mg/L on hospital day one and 3.28 mg/L on hospital day three.Quetiapine poisoning, with serum levels, associated with seizures has been reported in one prior case. Our case report represents late-onset seizures with serum levels above therapeutic range (1 mg/L). The serum concentrations of quetiapine in this case were consistent with those in postmortem case reports.

Anticonvulsant hypersensitivity syndrome is a severe idiosyncratic reaction to antiepileptic drugs. We report a case of a woman with lamotrigine-associated hepatitis who recovered spontaneously with supportive treatment.A 43-year-old woman was being treated with oxcarbazepine for depression and was started on lamotrigine 2 weeks prior to her presentation. The patient then developed nausea and a generalized pruritic macular rash, and was found to have elevated liver enzymes, which peaked at AST, 6079 IU/L; ALT, 6900 IU/L; total bilirubin, 3.9 mg/dL(66.7 micromol/L); alkaline phosphatase, 149 IU/L; international normalized ration (INR), 1.9. The patient showed no signs of encephalopathy and her clinical examination was essentially normal except for very mild jaundice and a diffuse erythematous pruritic macular rash. The patient was hydrated and managed with supportive care. On the third day of hospitalization, her liver enzymes had improved substantially and she was discharged. At follow-up 1 month later the patient's liver enzymes were within the normal range.We hypothesize that lamotrigine was directly responsible for the patient's rash and liver impairment given the time sequence of drug introduction and resolution of symptoms and liver enzyme abnormality once the drug was withdrawn. The patient suffered severe transaminitis when lamotrigine was added to oxcarbazepine, which resolved after termination of the medication and supportive management. We recommend monitoring the hepatic function in patients who have just been initiated on lamotrigine, especially if they develop jaundice.

Lithium toxicity is associated with electrocardiogram (ECG) changes, but changes suggestive of an ST segment elevation myocardial infarction have not been reported.A 46-year-old incarcerated man suffering from diabetes, hypertension, and schizoaffective/bipolar disorder was treated with lithium 1,200 mg twice daily. Two days prior to presentation the patient became confused, ataxic, and anorexic in jail. Lithium level was 4.69 mmol/L. He was transferred to the emergency department. On arrival, vital signs were normal. The ECG showed a normal sinus rhythm. ST segments were elevated in the anterior leads with downward concavity. T waves were biphasic. Since these changes suggested cardiac ischemia and the patient was unable to respond to questions about chest pain, cardiac enzymes and an emergent echocardiogram were done. Troponin I was less than 0.1 microg/L. Echocardiogram was normal, without wall motion abnormalities. Treatment was with hemodialysis and whole-bowel irrigation. Postdialysis lithium level was 1.30 mmol/L. Over the next several days, electrocardiogram normalized. His speech gradually became coherent. After a 1-week hospitalization, he returned to jail.Lithium intoxication can cause transient ST segment elevations suggesting an acute myocardial infarction. In the absence of a clear history, echocardiogram and cardiac enzymes can be used to rule out a myocardial infarction.

The use of 3,4-methylenedioxymethamphetamine (MDMA, known as "ecstasy"), a synthetic amphetamine and "club drug," has been associated with acute, transient urinary retention. We report a case of neurogenic bladder and chronic urinary retention associated with MDMA abuse.A 21-year-old male presented to the emergency department (ED) because he had abdominal pain and difficulty urinating. He had experienced difficulty in initiating urination over the past 1.5 months, with periods of 24 to 36 hours between voids and large volumes of urine. The patient had a chronic pattern of MDMA use, taking 4 tablets/day for 3 months. Two weeks before coming to the ED, he had been admitted to an inpatient drug rehabilitation center. During the time since that admission, the patient had visited EDs repeatedly for insertion and removal of Foley catheters to relieve the urinary retention until he could be admitted to a urologic service. Cystometrogram was abnormal, finding no sensation of bladder fullness after instillation of 350 mL of saline and inability to generate a voluntary voiding pressure. Cystoscopy revealed no outlet obstruction. The findings were consistent with neurogenic bladder. The patient was given prescriptions for bethanecol and phenazopyridine, and told to continue a 10-day course of sulfamethoxazole/trimethoprim for urinary tract infection. He was discharged with a Foley catheter in place. Symptoms of urinary retention persisted at 1-year follow-up, despite self-catheterization and complete cessation of MDMA use.Chronic MDMA use may lead to neurogenic bladder and chronic urinary retention.

Copper toxicity has previously been reported from the wood preservative, copper naphthenate. Serum copper levels may be elevated by estrogen. Reported here is a case of a woman who was initially diagnosed with elevated serum copper levels from copper naphthenate exposure. She was later found to have a normal RBC copper level with resolution of her elevated serum copper level following discontinuation of estrogen.A previously healthy 44-year-old Caucasian female was referred for toxicology consultation due to persistently elevated serum copper levels following copper naphthenate applied in her home. She had initial nausea, nasal congestion and headache from the fumes but then remained asymptomatic. No evidence of underlying systemic disease or organ injury was found. Despite this and no further exposure, her serum copper remained elevated by 30% above normal over 9 months, peaking at 2301 microg/L (36 micromol/L). Review of the literature confirmed that oral contraceptive use will routinely elevate serum copper levels to the extent noted in this case. Her RBC copper level was normal. Cessation of the oral contraceptive for 2 months returned the serum copper levels to normal.This patient's elevations in serum copper were probably unrelated to her chemical exposure to copper naphthenate. Serum levels of copper were falsely elevated as a result of concomitant estrogen use, and were returned to normal when estrogen was discontinued.

Tiagabine (TGB) is a novel antiepileptic that decreases GABA uptake. The literature contains one report of an adult with epilepsy who ingested up to 1 gram of TGB and developed status epilepticus. We reported on a pediatric patient who ingested significantly less TGB but still developed tonic-clonic seizures.A previously healthy, 13 kg, two-year-old girl developed generalized tonic-clonic seizure activity at home approximately 1 hour after ingesting 90 mg of her grandmother's TGB (forty five 2 mg tablets). At the hospital she had two 5 minute seizures at 1.5 and 3.5 hours post ingestion. Her serum TGB levels were 530 and 130 ng/ml approximately 5 and 11 hours post-ingestion (5-70 ng/ml trough levels with most probable range for seizure control). She was discharged 27 hours post ingestion, and she was in good condition.An overdose of TGB, a novel anti-epileptic, can cause convulsive seizures.

In 1999, a new synthetic tryptamine, 5-MeO-DIPT, became known as a street drug, with the street name of "Foxy" or "Foxy Methoxy". By February 2003, the DEA reported law enforcement seizures and/or reports of abuse in 12 states. We report a case along with an analysis of poison center data on this new drug of abuse.A 19-year-old male was brought to the emergency department following ingestion of a larger than his usual dose of Foxy. Upon arrival, he had hallucinations, hypertension, tachycardia, mydriasis, and catalepsy. Symptoms resolved within two hours after administration of lorazepam and he recovered uneventfully.The AAPCC TESS database contained 41 exposures to "Foxy" between April, 2002 and June, 2003; 26 had moderate or major effects, indicating this drug has significant toxic potential. Given the expanding use of this and other club drugs, the spectrum of toxicity from this new agent will continue to be elucidated.

Zigadenus (commonly known as "death camas" or "mountain camas") is a common plant in the lily family found throughout the United States. Its onion-like roots can be mistaken for an edible plant. Ingestion may cause hemodynamic instability which has successfully been treated with atropine. It has been suggested that vasopressors may be an effective therapy for this ingestion. We report the successful use of dopamine as therapy in Zigadenus ingestion.A 45 year-old, previously healthy male presented to the ED with complaints of severe nausea and vomiting after ingesting two "wild onion" bulbs. He was noted to have marked hypotension and bradycardia in the ED, which initially responded to treatment with IV fluids and atropine. The plant was identified as a species of Zigadenus. After a second drop in heart rate and blood pressure in the ICU, hypotension and bradycardia were treated successfully with a dopamine infusion.Zigadenus ingestion presents with vomiting, hypotension and bradycardia. The hemodynamic instability responded well to atropine for 1-2 hours. Dopamine infusion was used to stabilize both heart rate and blood pressure. With supportive care, poisoned individuals become relatively asymptomatic within 24 hours of their ingestion. Patients may be discharged once asymptomatic, typically the day after ingestion, and do not have any known long term sequelae.Zigadenus poisoning causes vomiting, hypotension and bradycardia. The hemodynamic instability may be treated with atropine administration and dopamine infusion.

Extracts of the bark of the central African tree Pausinystalia yohimbe contain yohimbine, an indole alkaloid, which is used to treat erectile dysfunction. The reported side effects of over-the-counter preparations of yohimbine include gastrointestinal upset, anxiety, increased blood pressure, headache, agitation, rash, tachycardia, and frequent urination. In this report, we describe a severe case of intractable priapism associated with the ingestion of yohimbe extract. Management required insertion of a proximal cavernosal spongiosum shunt (Quackles shunt) in the operating room.

Unintentional ingestions of dilute (7.5%) cleaning solutions containing ammonium chloride typically do not cause serious harm. We present a case of an intentional ingestion of a dilute ammonium chloride solution resulting in significant morbidity.A 60-year-old woman with bipolar disorder presented one hour after an intentional ingestion of approximately 15 fluid ounces (500 mL) of an algae and odor humidifier treatment containing a total of 2.25% ethyl ammonium chloride. Initial complaints included nausea with a single episode of nonbilious, nonbloody emesis, mild shortness of breath, and chest and epigastric pain. Physical exam was remarkable for bilateral wheezing and epigastric tenderness. An emergent endoscopy demonstrated a Grade 2b caustic injury in the esophagus and a Grade 3b injury in the stomach. Due to persistent cough, copious oral secretions, and worsening hoarseness, the patient was intubated and admitted to the ICU. Her course was complicated by mild hypotension, nonanion gap metabolic acidosis, and oliguria treated successfully with intravenous (IV) fluids. She also developed bilateral pneumonias later in the hospital course. Bedside bronchoscopy showed laryngeal edema and mucosal injury to the segmental level. The patient underwent tracheostomy on hospital day 6. An upper GI swallow study revealed poor esophageal motility in the mid- to lower third of the esophagus. The patient gradually tolerated oral fluids and on hospital day 20 had her tracheostomy tube removed. The patient was subsequently transferred to the psychiatric ward on hospital day 22.Intentional ingestions of dilute ammonium chloride solutions can cause serious injury to the gastrointestinal tract and pulmonary systems, which can result in a complicated and prolonged hospitalization.

The management of life-threatening beta-blocker toxicity and its associated low cardiac output state is clinically challenging. Previous case reports and case series describe the use of hyperinsulinemia/euglycemia therapy in mono-ingestions of calcium channel blockers and mixed ingestions, including calcium channel and beta-blockers. In this case report we describe the use of high-dose insulin (10 IU/kg per hour) in a case of massive metoprolol ingestion (5 g) in which hypotension was unresponsive to conventional therapies. Although the metoprolol concentrations measured in plasma were approximately 100–200 times therapeutic concentrations, the pharmacokinetics appeared to be similar to therapeutic metoprolol dosing.

Concurrent abuse of alcohol and cocaine results in the formation of cocaethylene, a powerful cocaine metabolite. Cocaethylene potentiates the direct cardiotoxic and indirect neurotoxic effects of cocaine or alcohol alone.A 44-year-old female with history of cocaine and alcohol abuse presented with massive stroke in the emergency department. CT scan revealed extensive left internal carotid artery dissection extending into the left middle and anterior cerebral arteries resulting in a massive left hemispheric infarct, requiring urgent decompressive craniectomy. The patient had a stormy hospital course with multiple episodes of torsades de pointes in the first 4 days requiring aggressive management. She survived all events and was discharged to a nursing home with residual right hemiplegia and aphasia.The combination of ethanol and cocaine has been associated with a significant increase in the incidence of neurological and cardiac emergencies including cerebral infarction, intracranial hemorrhage, myocardial infarction, cardiomyopathy, and cardiac arrhythmias. The alteration of cocaine pharmacokinetics and the formation of cocaethylene have been implicated, at least partially, in the increased toxicity of this drug combination.

Clonidine is frequently prescribed to children. Clonidine overdose in children has resulted in major clinical effects and deaths.A 3.5-year-old male with a history of a seizure disorder and night terrors presented following difficulty walking, excessive sleeping, agitation when awake, and possible seizure activity. Chronic medications were valproic acid (VPA) and clonidine. On presentation, he alternated between poor responsiveness and agitation, with initial vitals: blood pressure, BP 144/76 mmHg; heart rate, 65 bpm; respiratory rate, 18 bpm; temperature 99.5 degrees F; and pulse oximetry 96% on room air. VPA level was 35 microg/mL. A toxicology consult the next day noted a dry mouth, 2-mm pupils, intermittent gasping, and central nervous system (CNS) depression, with a diagnostic impression of clonidine overdose. The caregiver had been giving 1 mL (0.1 mg) qd of a pharmacy-compounded clonidine suspension by a provided syringe. The pharmacy procedure record agreed with the physicians order. The amount dispensed was a 30-day supply but the bottle was empty on day 19, leading us to suspect a possible accelerated dosing error. The concentration in the bottle thus could not be confirmed. The child slowly returned to his baseline state over 48 hours. A serum clonidine level drawn approximately 18 hours after his last dose later returned at 300 ng/mL (reference range = 0.5-4.5 ng/mL).Compounding and liquid dosing errors are common in children and may result in massive overdoses. There was an accelerated dosing error, but whether a compounding or suspension error or even an acute overdose occurred as well is unknown.Particular care should be taken with medications that have low therapeutic indices, that are extemporaneously compounded, and are prepared as liquids, where medication errors are more likely.

Aluminum phosphide (ALP) is a pesticide that is highly toxic. It is a mitochondrial toxin that causes death by cardiac and metabolic toxicity. The most ominous effect is cardiac toxicity, which may range from minor electrocardiographic abnormalities to severe depression of cardiac contractility secondary to toxic myocarditis. There is no documented report of the use of Intra-aortic Balloon Pump (IABP) for toxic myocarditis from ALP poisoning, although it has been used effectively for toxic myocarditis due to other toxins.We are reporting a young female who presented with ALP poisoning, in cardiogenic shock due to myocarditis. We used an IABP for cardio-circulatory support until the effects of ALP resolved. She is the only reported survivor of ALP poisoning, presenting with cardiogenic shock.Several reports describe the use of IABP for cardiogenic shock due to toxic myocarditis. There is no report in the medical literature using IABP for cardiogenic shock caused by ALP toxin-induced myocarditis. Our patient presented with cardiocirculatory shock, necessitating the use of inotropes and mechanical ventilation. As she did not improve despite ventilation and maximal doses of inotropes, IABP was used for cardio-circulatory support until the effects of ALP resolved.

Combined glucocorticoids and cyclophosphamide pulse therapy showed promising results in moderate-to-severe paraquat poisonings to reduce life-threatening respiratory complications. Its benefit has been observed when given early in the course of poisoning; however, whether its delayed administration remains beneficial is unknown.We describe a 23-year-old male who ingested 70 mL of a commercialized concentrate formulation with 20% weight/volume paraquat in a suicide attempt. Within 24 hours from paraquat ingestion, he presented most of the indicators of poor outcome, including gastritis, early renal dysfunction, dark blue urine colorimetric dithionite test, and marked plasma paraquat concentrations (0.56 microg/mL at 13 hours, and 0.41 microg/mL at 24 hours after ingestion). The patient received early gastrointestinal decontamination and aggressive supportive treatments. However, due to a rapidly progressive severe pulmonary infection, glucocorticoids and cyclophosphamide were delayed until day 14. Interestingly, our patient survived with mild respiratory sequelae despite poor initial prognosis.This observation suggests the potential benefit of immunosuppressive pulse therapy, even if administered 14 days after paraquat ingestion, and highlights the role of paraquat-induced alveolitis in the development of fibrosis.Combined glucocorticoids and cyclophosphamide should be considered in moderate-to-severe paraquat poisonings, even if delayed.

Neuroleptic malignant syndrome (NMS) is a relatively uncommon side effect that may develop after a recent increase in the therapeutic dose of an antipsychotic medication or the addition of a new agent in therapeutic doses.We report a case of NMS developing in a 36-year-old female patient 2 days following deliberate self-poisoning with 30 x 10-mg olanzapine tablets, 7 x 100-mg chlorpromazine tablets and an unknown amount of escitalopram. These were the patient's own medications. She had not been taking these for several weeks. The patient initially presented with sedation from her overdose which resolved over the next 24 hours. Following this, over the subsequent 24 hours, she became progressively confused, ataxic, hypertonic, ferbrile and tachycardic, with marked lead pipe rigidity of the limbs. Head CT, lumbar puncture and septic screen were all negative. She was treated with intravenous midazolam infusion, nasogastrically administered bromocriptine, external cooling and was mechanically ventilated. She gradually improved over a period of 10 days, with residual confusion lasting another week, and was discharged well with no deterioration from her premorbid neurologic state.To our knowledge, although there are numerous cases reported with therapeutic use, NMS has not been reported to develop following acute olanzapine overdose. Clinicians should be aware that this may be an uncommon side effect of antipsychotic medication.

There is emerging evidence of increasing use of legally available synthetic compounds as recreational drugs. While there are some changes to legislation relating to these synthetic compounds, often the emergence of the agents outpaces the effect of the legislation to curb their use, and the legal status of these agents may change as more information on their toxicity becomes known. TFMPP [1-(3-trifluoromethylphenyl) piperazine] was initially temporarily controlled under Schedule I of the Controlled Substances Act in 2002 in the US, but following further review and lack of published information on toxicity, it was removed from this control in 2004. In addition, there are very few "user reports" of effects when TFMPP is taken alone or in combination with BZP [1-benzylpiperazine].Three patients presented to our emergency department after ingesting 4 tablets thought to be 3,4-methylenedioxy-N-methylamphetamine (MDMA, street name "Ecstasy") over the course of an evening. They presented with dissociative-type symptoms, nausea, and signs consistent with sympathomimetic toxicity. All 3 improved with conservative management and observation, within 12 hours of presentation. Serum analysis demonstrated the presence of TFMPP and BZP at concentrations of 263 +/- 5.8 ng/mL (range 260-270 ng/mL) and 46.7 +/- 15.3 ng/mL (range 30-60 ng/mL), respectively. No other recreational drugs were detected in an extended toxicological screen of blood and urine samples.This is the first case series of confirmed toxicity associated with recreational use of TFMPP in combination with BZP, with clinical features not consistent with BZP toxicity. In our view, the current legal status of TFMPP should be reviewed.

We report a case of a 61-year-old woman treated for a suspected verapamil overdose with continuous calcium chloride infusion, resulting in severe hypercalcemia of 32.3 mg/dL (8.07 mmol/L) with a normal range of 8.6–10.5 mg/dL (2.15–2.63 mmol/L). Treatment with acute hemodialysis rapidly normalized the serum calcium level, but the patient later died of vasoconstrictive complications of hypercalcemia.

Human ingestion of denture cleansers leading to gastric perforation has not previously been described.A 27-year-old male ingested three denture cleanser tablets in water over two days in an attempt to cause a false negative result on a workplace urine drug screen. Seven days later he presented to an emergency department with a perforated gastric ulcer.A literature review of cases and the chemistry of the components of his ingestion was conducted to determine the possible relationship between these events. Ingestion of intact fragments of the tablets would be likely to result in significant gastric toxicity, but ingestion of dissolved tablets would be unlikely to have caused his illness.

Based on its primary action of serotonin reuptake inhibition, venlafaxine overdose would be expected to result in serotonergic effects.A 40 year old male ingested venlafaxine without co-ingestants in a suicide attempt. The patient developed refractory ventricular fibrillation and expired approximately 9 hours post-ingestion. ECG monitoring revealed significant QRS and QTC interval prolongation prior to his demise.A literature review of venlafaxine overdose cases and investigation into its mechanism of action was conducted. The potential for sodium channel blockade and implications for therapy are discussed.

The emergency department (ED) evaluation of cocaine-associated acute coronary syndrome (CAACS) is often a diagnostic and therapeutic challenge.We are reporting on the treatment of a patient with cocaine-associated acute coronary syndrome (CAACS) who did not benefit from standard therapy, but who eventually responded positively to phentolamine, an alpha-adrenergic receptor antagonist.This report should encourage physicians to add phentolamine to their pharmacotherapeutic armamentarium in the treatment of CAACS.

Paraquat remains one of the common substances involved in intentional ingestions in Thailand. However, data on outcomes of paraquat ingestion during pregnancy is rarely available and the management is controversial.A 17-year-old female in 36 weeks of gestation attempted suicide by ingesting 1/2 a glass of Gramozonetrade mark (paraquat 27.6 % w/v) 5 hours prior to arrival to the hospital. Gastric aspiration and lavage was performed and she was given 50 g of activated charcoal and 150 g of Fuller's Earth suspension. A male infant, weighing 2,390 g with an Apgar score of 71 1010, was delivered via emergency caesarean section 7 hours after ingestion. Due to presence of paraquat in the gastric lavage fluid, the mother was placed on dexamethasone/cyclophosphamide therapy. She developed mild renal insufficiency 63 hours after the ingestion. The infant developed tachypnea immediately after birth that self-resolved. The infant developed tachypnea again on day 6 of life. A chest x-ray revealed right lower lobe infiltration that progressed to diffuse interstitial pattern; subsequent chest x-rays showed evidence of fibrosis. Both mother and infant survived and the infant was discharged and sent home with oxygen 0.5 LPM. Upon follow up at 10 months of age, he still had evidence of chronic lung disease clinically and on chest x-ray.Paraquat ingestion during the third trimester of pregnancy usually carries a very poor prognosis. Review of reported literature suggests that this case report represents only the second survival of mother and child.

This case report is about reversible cardiomyopathy associated with intrathecal baclofen withdrawal. Previous literature has reported that enteral baclofen does not adequately control intrathecal baclofen withdrawal. In our case, coronary atherosclerosis did not play a role in the development of the cardiomyopathy. However, reinstitution of intrathecal baclofen promptly resulted in improvement. One could hypothesize that myocardial stunning from sympathetic hyperactivity led to a similar cardiomyopathy reported with catecholamine excess or acute sympathomimetic poisoning.

Although it is commonly stated that the use of beta adrenergic receptor antagonists is contraindicated in patients with cocaine toxicity, actual clinical evidence of harm is lacking. This case helps to highlight the risks of beta adrenergic receptor antagonists in patients with chest pain associated with cocaine use.A 54-year-old man was brought to the emergency department (ED) complaining of chest pain after using approximately 1 gram of intranasal cocaine. Aspirin and nitroglycerin spray relieved his pain. Although he remained pain free, tachycardia persisted despite 15 mg of diazepam intravenously. Nearly two hours after presentation, a total of 5 mg of metoprolol was given for persistent tachycardia (115/minute) and an elevated troponin. Shortly thereafter, the patient complained of crushing substernal chest pain, developed pulseless electrical activity, and could not be resuscitated.The administration of beta adrenergic receptor antagonists exacerbates cocaine-induced lethality in animals. In humans given smaller doses of cocaine, beta adrenergic receptor antagonists exacerbate coronary vasoconstriction. Both effects are presumed to occur through unopposed alpha adrenergic receptor agonism. Despite these data, actual cases describing adverse effects in cocaine users given beta adrenergic receptor antagonists are uncommon. This case supports the potential lethality of a cocaine-beta adrenergic receptor antagonist interaction.

Profound metabolic acidosis in critically ill adults sometimes remains unexplained despite extensive evaluation.A 58-year-old female presented in a confused state to the emergency department; she had been confused for several days. Laboratory evaluation revealed a high anion gap metabolic acidosis and modestly elevated acetaminophen level. Lactic acid was only modestly elevated. There was no evidence of ketoacids, salicylate, methanol, or ethylene glycol. A urine sample submitted on day 1 of hospitalization revealed a markedly elevated level of 5-oxoproline.Originally described in children with an inherited defect of glutathione synthetase, 5-oxoproline is an unusual cause of metabolic acidosis. More recently this disturbance has been recognized in critically ill adults without a recognized inherited metabolic disorder. In most of these cases there has been the concomitant use of acetaminophen. Any causal relationship between acetaminophen and this disturbance is speculative.In critically ill adults with unexplained metabolic acidosis, 5-Oxoproline should be considered in the differential.

Ibuprofen is a commonly used non-steroidal anti-inflammatory drug. While the vast majority of exposures to the drug do not result in significant morbidity, we are reporting 2 fatalities that resulted from massive ibuprofen ingestion. CASE 1: A 17-year-old girl presented to the emergency department (ED) following an ibuprofen overdose; she was unresponsive with a metabolic acidosis and hypothermic. Her serum ibuprofen concentration was 352 microg/mL: the therapeutic range is 10-50 microg/mL. Despite intensive supportive care and continuous veno-venous hemofiltration, she expired. CASE 2: A 49-year-old man presents to the ED with a history of divalproex sodium and ibuprofen ingestion. He was unresponsive, hypotensive, and had a significant metabolic acidosis. His serum ibuprofen concentration was 260 microg/mL and serum valproate concentration was 560 microg/mL: the therapeutic range is 50-100 microg/mL. In spite of supportive care and hemodialysis, he expired.We will describe 2 cases of ibuprofen overdose characterized by cardiovascular collapse, acidosis, and hypothermia despite the use of vasopressors and renal replacement therapy. Although rarely reported, massive ibuprofen overdose may result in refractory multisystem organ failure and death.

The widespread availability of medications and herbal products on the Internet has increased the potential for poisonings. We are reporting a case of mild, acute lithium toxicity occurring after the intentional misuse of a lithium-containing "dietary supplement" (Find Serenity Now) obtained over the Internet.An 18-year-old woman presented to our emergency department (ED) after ingesting 18 tablets of Find Serenity Now; each tablet contained, according to the listing, 120 mg of lithium orotate [3.83 mg of elemental lithium per 100 mg of (organic) lithium orotate compared to 18.8 mg of elemental lithium per 100 mg of (inorganic) lithium carbonate]. The patient complained of nausea and reported one episode of emesis. Her examination revealed normal vital signs. The only finding was a mild tremor without rigidity. Almost 90 minutes after the ingestion, her serum lithium level was 0.31 mEq/L, a urine drug screen was negative, and an electrocardiogram (ECG) showed a normal sinus rhythm. The patient received intravenous fluids and an anti-emetic; one hour later, her repeat serum lithium level was 0.40 mEq/L. After 3 hours of observation, nausea and tremor were resolved, and she was subsequently transferred to a psychiatric hospital for further care. Prior human and animal data have shown similar pharmacokinetics and shared clinical effects of these lithium salts.Over-the-Internet dietary supplements may contain ingredients capable of causing toxicity in overdose. Chronic lithium toxicity from ingestion of this product is also of theoretical concern.

We are presenting a case illustrating the complex metabolic and rhythm disturbances associated with acute clenbuterol intoxication.Clenbuterol is a long-acting beta2-adrenergic agonist primarily used in veterinary medicine in the United States. It has become a common drug of abuse by body builders because of its reported anabolic and lipolytic properties. In this case report, a body builder using veterinary clenbuterol developed significant electrolyte and cardiac manifestations.A 31-year-old man presented to the emergency department approximately 30 minutes after ingesting 1.5 ml (a tenfold dosing error) of Ventipulmin syrup (72.5 mcg/ml clenbuterol HCl). The product was brought to the emergency department (ED) by the patient. He reported no current use of anabolic steroids. He presented in an anxious state with complaints of palpitations and shortness of breath. Vital signs upon examination were as follows: BP, 122/77 mmHg (16.3/10.3 kPa); HR 254 bpm; RR, 22 bpm; Temperature, 97.1 degrees F (36 degrees C); and oxygen saturation, 100% on ambient air. His electrocardiogram (ECG) demonstrated supraventricular tachycardia with a ventricular rate of 254 bpm. Esmolol was recommended for rate control after the unsuccessful use of adenosine and diltiazem. Laboratory studies showed potassium, 2.1 mmol/L; magnesium, 1.3 mg/dL (0.54 mmol/L); phosphorus, 1.0 mg/dL (0.32 mmol/L); serum glucose, 209 mg/dL (11.6 mmol/L); creatinine, 0.8 mg/dL (70.7 micromol/L); AST, 20 U/L; ALT, 55 U/L; hemoglobin, 12.6 g/dL (126 g/L); CPK total, 87 U/L; and troponin I, 0.23 mug/L. The patient's urine was negative for any drugs of abuse. Clenbuterol levels were not obtained. A second ECG, 16 hours post ingestion, reflected atrial fibrillation with a ventricular rate of 125 to 147 bpm. On hospital day 3, he was electively cardioverted to sinus rhythm; heart rate and rhythm returned to normal, and he was discharged with oral metoprolol.Clenbuterol is approved for use in countries outside the U.S. as a bronchodilator for the treatment of acute asthma exacerbations in humans. Although clenbuterol is not a steroid hormone, it possesses anabolic properties that increase muscle mass. Its longer duration of action compared to other beta2-agonists (such as albuterol) make it a desired agent for body-building because of its high and prolonged serum level. The mechanism for the short and long-term cardiovascular complications of clenbuterol is complex. The anabolic effects of clenbuterol are associated with its beta2-adrenoreceptor agonist activity on striated skeletal muscles. In addition, clenbuterol promotes lipolysis through adipocyte beta3-adrenoreceptors.Considering the significant number of body-building enthusiasts, physicians will continue to encounter clenbuterol abuse in their clinical practices.

In countries such as India, the silver jewelry industry is an important cottage industry. Silver is mixed with cadmium and then used to make silver jewelry. During this process there is a formation of cadmium fumes, and the workers inhale the fumes. Cadmium is a neurotoxic and nephrotoxic heavy metal, and there are no national policies to prevent exposure to such chemicals. We will present a case of cadmium induced peripheral neuropathy, nephropathy, and decreased bone density.

Ethylene glycol is a widely used chemical that is capable of causing significant injury if ingested. Treatment for ethylene glycol poisoning typically includes basic supportive care, alcohol dehydrogenase inhibition, and hemodialysis. Recent data have suggested that hemodialysis may not be necessary for cases of ethylene glycol poisoning that can be treated with fomepizole as blocking therapy before acidosis or renal dysfunction develops.A 33-year-old man presented to the emergency department 1 hour after drinking approximately 1/2 gallon of ethylene glycol antifreeze and an unknown quantity of beer. On arrival he was mildly inebriated but otherwise displayed no other features of ethylene glycol poisoning. Fomepizole therapy was initiated and initial laboratory studies later revealed an osmol gap of 157 mOsm and an ethylene glycol concentration of 706 mg/dL. Nephrology and toxicology services were consulted. Over the next 3 days, fomepizole therapy was continued while the patient's acid-base status and renal function were closely monitored. No evidence of acid-base abnormalities or renal impairment was ever observed and the patient was discharged to psychiatric care on the fourth hospital day.This report describes the case of a patient who presented soon after a massive ingestion of ethylene glycol with very high serum concentrations. He was successfully treated using fomepizole and basic supportive care. Our patient developed neither renal insufficiency nor metabolic acidosis. His concomitant ethanol consumption, early presentation, and treatment likely contributed to his favorable outcome. This case report underscores the effectiveness of supportive care and fomepizole in the treatment of ethylene glycol poisoning.

Introduction Effective whole bowel irrigation may be difficult in the presence of drug-induced ileus. Neostigmine, which inhibits the enzymatic degradation of acetylcholine, has been suggested to improve drug-induced ileus. We present two poisoning cases in which neostigmine was used to facilitate gut decontamination complicated by ileus.