Chylous transport of amiodarone.

A patient receiving amiodarone for longstanding ventricular dysrhythmias presented with idiopathic chylothorax. During drainage of chylothorax for pleurodesis, serial plasma amiodarone concentrations declined while pleural fluid concentrations remained stable. Chylous transport of amiodarone and other lipid-bound drugs should be recognized to avert complications during chylothorax drainage.

A comparison of rotation and nonrotation in tetracycline pleurodesis.

Previously, we have shown rapid and complete dispersion of tetracycline hydrochloride in the pleural space following chest tube instillation. To assess the clinical relevance of this observation, we randomized patients with symptomatic pleural effusions to rotation (R) (n = 19) and nonrotation (NR) (n = 21) groups following administration of tetracycline hydrochloride, 20 mg/kg (n = 30); 300 mg of minocycline hydrochloride (n = 6); and 500 mg of doxycycline hydrochloride (n = 4) through a chest tube. Patients in the R group were maneuvered through six positions for the 2 h that the chest tube remained clamped. The NR patients remained supine for 2 h. Rotation and nonrotation groups were similar in demographics, source of pleural effusion, symptoms, and serum and pleural fluid analyses (all p = NS). A chest radiograph was scored based on pleural fluid recurrence throughout survival or up to 12 months. Survival, duration of chest tube instillation, and success of pleurodesis assessed by radiographic pleural fluid reaccumulation (73.7 vs 61.9 percent; R vs NR) were similar (p = NS). Rotational maneuvers appear to offer no benefit to the success of pleural symphysis after intrapleural instillation of tetracycline class agents.

Early inflammatory response of minocycline and tetracycline on the rabbit pleura.

The histopathologic findings were compared from 20 mg/kg intrapleural tetracycline hydrochloride (TCN) and three doses of intrapleural minocycline hydrochloride (5, 10, and 20 mg/kg) (MCN) in New Zealand white rabbits. Both TCN and MCN produced an early neutrophilic predominant pleural effusion that became mononuclear over 48 h. There was no difference in pleural fluid accumulation, number of adhesions, or histologically measured visceral and parietal pleural thickness between TCN and MCN (all p = ns). The TCN, 20 mg/kg, produced more visceral pleural plaque than MCN, 5 mg/kg (p < 0.05). Increasing MCN doses resulted in greater pleural fluid neutrophil accumulation. With higher dose MCN, greater mesothelial cell desquamation and fibroblast proliferation was evident compared to the 5 mg/kg dose. The MCN and TCN produce similar histopathologic condition in the rabbit pleura which suggests that MCN should cause a similar clinical response in humans.