Pharmacology: Pharmacodynamics: Mode of Action: Vancomycin is bactericidal for most organisms and bacteriostatic for enterococci. Vancomycin inhibits bacterial cell wall synthesis at a site different from that of penicillin and cephalosporin by binding tightly to the D-alanyl-D-alanine portion of cell wall precursors and interfering with bacterial growth. This leads to activation of bacterial autolysins that destroy the cell wall by lysis. Vancomycin also may alter the permeability of bacterial cytoplasmic membranes and may selectively inhibit ribonucleic acid (RNA) synthesis. Vancomycin does not compete with penicillin for binding sites.
Pharmacokinetics: Vancomycin is widely distributed to most tissues and body fluids; adequate therapeutic concentrations in serum and in pleural, pericardial, peritoneal, ascitic, and synovial fluids; high concentrations in urine; inadequate concentrations in bile; does not readily cross normal blood-brain barrier into cerebrospinal fluid (CSF); however, penetrates into CSF when meninges are inflamed and may achieve therapeutic concentrations. Vancomycin crosses the placenta.
Vancomycin has moderate binding with plasma protein in healthy adults and low in adults with infections. Normal renal function for adults is approximately 6 hours (range, 4 to 11 hours), newborn infants is approximately 6 to 10 hours, older infants is approximately 4 hours and children is approximately 2 to 3 hours.
Vancomycin is approximately 75 to 90% or more excreted by passive glomerular filtration unchanged in urine within 24 hours; slowly eliminated by unknown route and mechanism in anephric patients. Small, into moderate amounts may be excreted in bile. Vancomycin not appreciably removed from the blood by hemodialysis or peritoneal dialysis.