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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.

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.