Bilateral putaminal necrosis and bronopol toxicity.

Among alcohols, methanol intoxication is the most frequently associated with cerebral toxicity, causing retinal damage and putaminal necrosis. This consequence is believed to be due to the transformation of methanol into formic acid. We describe the case of a patient who presented with acute impairment of consciousness and tetraparesis after she had been drinking several bottles of a topical antiseptic solution (Lysoform Medical) containing 2-bromo-2-nitro-1,3-propandiol (bronopol) among excipients, in order to lose weight during previous months. Moreover, she had been on a strict slimming diet. Soon after admission, a severe respiratory and metabolic impairment became rapidly evident, requiring an intensive care unit admission. Cerebral MRI showed the presence of bilateral putaminal necrosis. She recovered in 10 days, surprisingly, without any evident clinical neurological signs. Methanol, also bronopol, when diluted in aqueous solution, at warm temperature and/or higher pH, may release formaldehyde, which is converted into formic acid, a basal ganglia toxic compound.

Deliberate fingolimod overdose presenting with delayed hypotension and bradycardia responsive to atropine.

INTRODUCTION: Fingolimod is an immunomodulating agent used in multiple sclerosis (MS). It is a sphingosine-1-phosphate (S1P) receptor agonist prescribed for relapsing forms of MS to delay onset of physical disability. As fingolimod is known to cause first-dose bradycardia, telemetry is recommended for the first 6 h post-dose. We present the first reported case of deliberate fingolimod overdose requiring atropine administration for bradycardia and hemodynamic instability. CASE REPORT: A 33-year-old woman ingested 14 mg of fingolimod and 2 g of phenoxymethylpenicillin. After presenting to the emergency department 19 h later, she was initially hemodynamically stable (heart rate (HR) 60, blood pressure (BP) 113/89 mmHg). Two hours later, she then developed bradycardia (HR 48) and hypotension (87/57 mmHg). Despite intravenous fluids, stabilisation was only achieved after administration of atropine (300 µg). She was then admitted to the intensive care unit (ICU) for further monitoring where another episode of bradycardia and hypotension required atropine. She was monitored in the ICU for 48 h and then discharged on day 5 with no further episodes. DISCUSSION: Fingolimod is known to cause bradycardia in the first 6 h post first therapeutic dose. Following intentional overdose, onset of bradycardia occurred at 21 h post-ingestion and was associated with hypotension. Atropine was successful in treating bradycardia and associated hypotension.

Acute renal failure, neuropathy, and myopathy after ingestion of dipropylene glycol fog solution.

Dipropylene glycol is used in several industrial products including cosmetics, emulsifiers, solvents, and as a fog solution for dance club special effects. Animal studies have suggested that dipropylene glycol has minimal toxicity. We report a case of a 32-year-old man who ingested more than 500 mL of dipropylene glycol-containing Fantasia fog solution (High Energy Lighting, Houston, TX) and subsequently developed acute renal failure, polyneuropathy, and myopathy.

A fatality involving 1,3-propanediol and its implications in measurement of other glycols.

The decomposed body of a 45-year-old female was found, face down, in a mobile home, along with a suicide note and two antifreeze containers. Analysis of the body fluid collected from the decedent showed the presence of 58 mg/dL ethanol, but suspected ethylene glycol was not found in the sample. However, an unusually large peak of internal standard, 1,3-propanediol, was found in the sample. Gas chromatography-mass spectrometry analysis confirmed the presence of 1,3-propanediol in the sample. Using gas chromatography-flame-ionization detection, the concentration of 1,3-propanediol was determined to be 445 mg/dL. To our knowledge, this is the first report involving 1,3-propanediol as the cause of death. The study also highlights the importance for the close scrutiny of data, as 1,3-propanediol is a frequently used internal standard for the assay of glycols.

Acute felbamate overdose with crystalluria.

A 3-year-old child developed vomiting, ataxia, and crystalluria after ingestion of approximately 232 mg/kg of felbamate elixir. High-powered polarization microscopy of the urine revealed sharp, needle-like crystals. The analysis of the urine crystals showed unchanged felbamate (80.9%), monocarbamate felbamate (18.8%), and trace amounts of mercapturic acid conjugates of the metabolite 2-phenylpropenal (0.1%). The serum felbamate level 15 h after ingestion was 138 mg/L. Crystalluria and hematuria resolved with intravenous fluid therapy, and the child recovered within 24 h.

Felbamate overdose complicated by massive crystalluria and acute renal failure.

CASE REPORT: We report a 20-year-old woman who developed altered mental status, massive crystalluria, and acute renal failure following an intentional overdose of felbamate and sodium valproate. Peak plasma concentrations of felbamate and sodium valproate were 200 microg/mL and 470 microg/mL, respectively. Macroscopic urinary crystals formed approximately 18 hours after ingestion and were identified by gas chromatography as containing felbamate. Renal ultrasound revealed unilateral hydronephrosis. Following parenteral hydration, the crystalluria and acute renal failure resolved and the patient recovered. The frequency and significance of crystalluria in felbamate intoxication is unknown.

Propylene glycol: the safe diluent that continues to cause harm.

Propylene glycol (PG) is present in many pharmaceutical products, lotions, ointments, and cosmetics. Although considered to be a relatively safe substance, overdoses have been associated with serious adverse effects. Propylene glycol intoxication occurred in a child and caused central nervous system depression and a severe metabolic acidosis. Initial assessment revealed an elevated serum anion gap, a slight increase in measured serum osmolality, and a normal osmolal gap. The child's acidosis was due to increased concentrations of lactate and pyruvate. The possibility of serious PG intoxication should be considered in any patient with an unexplained serious metabolic acidosis.

Felbamate overdose: a case report and discussion of a new antiepileptic drug.

Felbamate was approved in July 1993 for use alone or in combination with other antiepileptic drugs for partial seizures and Lennox-Gastaut syndrome. We report an overdose of felbamate in a teenage female patient who, in a suicide gesture, ingested eight times her maximum dose and suffered only mild side effects. This first report of a felbamate overdose is presented and followed by a discussion of felbamate's effectiveness, pharmacology, adverse effects, and drug interactions.

Fatal propylene glycol toxicosis in a horse.

Toxicosis attributable to propylene glycol (1,2-propanediol) was suspected in an 8-year-old 450- to 500-kg male Quarter Horse. Clinical signs of toxicosis developed within 15 minutes of the accidental iatrogenic oral administration of 3.8 L of propylene glycol. Clinical signs of toxicosis included salivation, sweating, ataxia, and signs of pain. Additionally, at 24 hours after propylene glycol ingestion, the horse became increasingly atactic, had an abnormal breath odor, developed rapid shallow breathing, and was cyanotic. The horse died of apparent respiratory arrest 28 hours after the propylene glycol ingestion. Analysis of serum and combined urine and blood from the kidneys confirmed the presence of propylene glycol. Propylene glycol is used for the treatment and prevention of bovine ketosis, and is similar in appearance to mineral oil. The accidental administration of propylene glycol to horses may result in fatal poisoning.

Cerebral depression due to propylene glycol in a patient with chronic epilepsy--the value of the plasma osmolal gap in diagnosis.

A case of propylene glycol poisoning is described in a 39 year old woman which resulted in her admission to hospital in status epilepticus. She had had a long-standing history of uncontrollable epilepsy. The diagnosis of propylene glycol poisoning resulted directly from the finding of a high plasma osmolal gap on admission. This finding would have been missed if later samples only had been analysed. Plasma osmolality and the osmolal gap should be considered first line investigations in patients presenting with metabolic acidosis and cerebral signs and symptoms. Since her discharge from hospital a year ago the patient has had no further seizures.