Oxymorphone Induced Thrombotic Microangiopathy Mimicking Atypical Haemolytic Uremic Syndrome.

BACKGROUND: Atypical Haemolytic Uremic Syndrome (aHUS) is a rare life threatening entity characterized by thrombocytopenia, haemolytic anaemia and renal dysfunction. It is a thrombotic microangiopathy related to genetic mutations in the alternate complement pathway and has a distinct pathophysiology which makes it harder to distinguish from other microangiopathies. We present a case of a 25-year-old male patient with history of polysubstance abuse who presented with chest pain and dyspnoea. He admitted to using injectable oxymorphone (Opana) two weeks before presentation. Patient's vital signs were stable except for tachycardia and high blood pressure. On physical examination, epigastric tenderness and mild splenomegaly was appreciated. Urine Drug Screen was positive for oxycodone and opiates. Laboratory work up revealed haemolytic anaemia, thrombocytopenia and acute kidney injury. Extensive evaluation resulted in our impression of the disease being atypical haemolytic-uremic syndrome. He was managed with dialysis, intravenous steroids and plasmapheresis with improvement in his hematologic parameters.

Successful treatment of intravenously abused oral Opana ER-induced thrombotic microangiopathy without plasma exchange.

In January 2013, the Centers for Disease Control and Prevention reported an illness associated with intravenous (IV) abuse of oral Opana ER (oxymorphone) in Tennessee. The clinical presentation of this syndrome was reported to resemble that of thrombotic thrombocytopenic purpura in the 15 patients reported; 12 were treated with plasma exchange. We report a similar case series of 15 patients with 18 episodes of thrombotic microangiopathy associated with recent IV abuse of oral Opana ER. In our series, we demonstrate that therapeutic plasma exchange is unnecessary; supportive care and treatment of underlying infections and renal dysfunction (without use of plasma exchange) resulted in clinical improvement in all patients. Thus, it appears that plasma exchange with associated costs and risks can be safely omitted in patients with thrombotic microangiopathy resulting from IV abuse of oral Opana ER.

Validation of blood and liver oxymorphone analysis using LC-MS-MS: concentrations in 30 fatal overdoses.

A sensitive liquid chromatography-tandem mass spectrometry method was developed and validated for the quantitation of oxymorphone (OM) in human whole blood and liver. Sample preparation was done by solid-phase extraction, using deuterated OM as the internal standard. Separation was achieved using a Waters Aquity UPLC HSS T3 column. Analysis utilized positive electrospray ionization and multiple reaction monitoring. As part of the validation, studies were conducted to determine potential interference, selectivity, ion suppression/enhancement and carryover. Calibration model, limit of detection (LOD), lower limit of quantitation (LLOQ), precision and accuracy were also established. The linear range of the method was 2-500 ng/mL in blood and 5-500 ng/g in the liver. The LOD and LLOQ were 2 ng/mL for blood and 5 ng/g for the liver. Blood and/or liver specimens from 30 cases were analyzed. OM concentrations ranged from 23 to 554 ng/mL ( , n = 26) in blood and 48 to 1740 ng/g ( , n = 30) in the liver.

Bilateral globus pallidus lesions.

Following a hypoxic-ischemic insult, the globus pallidus is selectively spared from ischemic injury in contrast to the caudate and putamen. The known causes for hemorrhagic and necrotic lesions selective for injuring the globus pallidus are varied but few. The most widely known etiology is in fatal cases of carbon monoxide poisoning. Additionally reported associations include fatalities involving 3,4-methylenedioxymethamphetamine; cocaine; opiates; and cyanide poisoning. These bilateral globus palladus necrotic lesions have been reported to occur in 5-10% of opiate addicts. In this article, we present a striking photo of selective symmetrical bilateral globus pallidus necrosis following cocaine and opiate abuse.

An overdose death involving the insufflation of extended-release oxymorphone tablets.

Two cases are reported involving the abuse of extended-release oxymorphone hydrochloride tablets (Opana® ER) in combination with alprazolam (Xanax®). Two juvenile females were discovered unresponsive and hypoxic by a male acquaintance. The trio had reportedly crushed and snorted Opana ER tablets and consumed Xanax for recreational purposes. Emergency personnel were able to stabilize one female. The second female was pronounced dead at the scene. Blood and urine samples from the surviving female were collected at the trauma center between 48 and 96 h post incident. Toxicology results showed the presence of oxymorphone, doxylamine, dextromethorphan, alprazolam, α-hydroxyalprazolam, oxazepam, and temazepam in her urine. No drugs were detected in her blood. Toxicology on the deceased female revealed the presence of 0.13 mg/L oxymorphone and 0.04 mg/L alprazolam in her blood. Gastric contents contained 0.25 and 0.93 mg/L of oxymorphone and alprazolam, respectively. Oxymorphone, alprazolam, and α-hydroxyalprazolam were present in her urine. Quantitative results were achieved by gas chromatography-mass spectrometry monitoring selected ions for the oxime-oxymorphone-trimethylsilyl derivative, alprazolam, and the α-hydroxyalprazolam tert-butyldimethylsilyl derivative. The established linearity ranges for the opiate and benzodiazepine methods were 0.050-3.000 and 0.025-1.000 mg/L, respectively. The cause of death was reported as multiple drug toxicity, and the manner of death was accidental.

Case report: Oxymorphone-involved fatalities: a report of two cases.

There has been an increased awareness of illicit opiate abusers using the narcotic oxymorphone (Opana) by inhalation. Many laboratory screening techniques currently in use cannot detect oxymorphone in blood or urine. Consequently, biological specimens containing low to moderate concentrations of oxymorphone will likely go undetected. The circumstances, pathology findings, and toxicology results of two fatalities involving oxymorphone are presented. An opiate confirmation gas chromatography-mass spectrometry (GC-MS) procedure, described in detail was able to detected, confirm, and quantify oxymorphone in both subjects. The blood concentrations were 0.05 mg/L (50 microg/L) and 0.12 mg/L (120 microg/L).