Bilateral exudative pleural effusions following intravenous ethchlorvynol administration.

A 26-year-old man had bilateral alveolar infiltrates and exudative pleural effusions following self-administration of intravenous ethchlorvynol (ECV). The effusions and pulmonary edema resolved by 72 h with supportive therapy only. As no other etiology was established, we concluded that the pathogenesis of the pleural fluid was the transvisceral pleural leak of the increased extravascular lung water induced by ECV. Current experimental and clinical evidence support the concept that pleural effusions probably develop in most states of permeability pulmonary edema.

Placidyl abuse: a dimorphic picture.

Eleven patients with documented intoxication with ethchlorvynol were evaluated for clinical and laboratory manifestations. All of the 7 patients who ingested the drug were severity neurologically depressed; 3 were hemodynamically unstable and 1 developed pulmonary edema documented to be noncardiogenic 40 h after admission. All of the remaining patients (including 1 who also ingested a small amount) presented with pulmonary edema in the absence of neurological changes, soon after injection of 2--3 capsules iv; hemodynamic measurements in one of these demonstrated a noncardiogenic etiology. The clinical manifestations in these 2 groups of patients seem to be clearly separable, depending on the dose and route of administration.

Adult respiratory distress syndrome after Placidyl abuse.

A case of intravenous Placidyl injection is described which resulted in pulmonary pathophysiology consistent with adult respiratory distress syndrome (ARDS). Concise documentation of pulmonary and hemodynamic function demonstrated the dramatic response to PEEP therapy. Previously reported cases, mechanisms, and similarity to heroin-induced ARDS are discussed.

Comparative trial of a new hypnotic (Finorgal) with nitrazepam and triclofos sodium.

Thirty patients complaining of insomnia were studied in a double-blind trial with crossover of Finorgal, nitrazepam and triclofos sodium. Finorgal given as a hypnotic produced similar results to nitrazepam and triclofos sodium in terms of induction of sleep, duration and quality of sleep, dream recall and morning 'hangover'. Reported side-effects were not serious and occurred less frequently in association with Finorgal treatment than with nitrazepam or triclofos sodium. Laboratory investigations gave no indication of the development of any drug toxicity during the three-week period of the trial.

Comparison of a new hypnotic (Finorgal) with placebo in a double-blind trial.

The hypnotic effects of Finorgal (ethchlorvynol with diphenhydramine) were compared with those of placebo in a double-blind study with crossover of treatments in thirty-five hospital in-patients. During the four-week period of Finorgal treatment there was a significant reduction in the mean time elapsing between the administration of the hypnotic and the onset of sleep, and a significant increase in the duration of sleep, compared with the four weeks of placebo treatment. There was also a significant increase in the proportion of nights when the patients felt they had slept well, and in the incidence of morning 'hangover' and nocturnal confusion during the Finorgal treatment periods. Patients had to be actively woken in the morning significantly more often following Finorgal administration. In patients experiencing pain in the night there was a significant reduction in the occurrence of pain during the nights when Finorgal had been given.

Pulmonary tissue concentrations of ethchlorvynol after intravenous injection.

Noncardiogenic pulmonary edema has been reported to follow the intravenous use of ethchlorvynol (Placidyl) in both human clinical and animal experimental situations. In a further attempt to define ethchlorvynol-pulmonary tissue inter-relations, we measured ethchlorvynol concentrations in venous and arterial blood and lung and liver tissue of dogs after intravenous injection of 15 to 25 mg of the drug per kg of body weight. In 10 dogs, the mean +/- SEM lung concentrations 1, 3, and 5 min after injection were 70 +/- 20, 50 +/- 13, and 24 +/- 9 mug per g of tissue, respectively. Simultaneous mean +/- SEM venous contrations were 75 +/- 40, 29+/-5, and 22 +/- 5 mug per ml of blood, respectively. During minutes 1 and 3, the liver concentrations were lower than those found in the lung. In an additional 3 dogs, injection of ethchlorvynol into the portal vein led to higher concentrations (at all sample times) in the liver when compared to the lung. In vitro lung slice studies using ethchlorvynol labeled with iodine-131 revealed no active energy-dependent uptake. Intravenously administered ethchlorvynol rapidly fluxes into and out of lung tissue, apparently following the laws of diffusion.

Ethchlorvynol (Placidyl)-induced pulmonary edema.

Two patients experienced severe nonhemodynamic pulmonary edema following the intravenous injection of 25 and 40 mg/kg of body weight of ethchlorvynol (Placidyl). The pulmonary edema cleared rapidly. Injection of Placidyl (12 to 80 mg/kg of body weight) intravenously into dogs caused acute, severe, nonhemodynamic pulmonary edema (as evidenced by markedly elevated lung weights and microscopic evidence of intra-alveolar edema), hypotension with a relative bradycardia, and a decreased cardiac output. Injection of polyethylene glycol, the vehicle in which ethchlorvynol is diluted, did not reproduce the syndrome.