Facebook
Twitter
LinkedIn
Email
 |
Checking for direct PDF access through Ovid | |
Excerpt
Case report. After an uneventful pregnancy a female and a male twin were delivered vaginally from a 22-year-old Caucasian second gravida in the 35th week of gestation. The birth weights were 1985 and 2390 g, and the APGAR scores were 5/7/9 and 6/8/9, respectively. The children initially presented with grunting, cyanosis and intercostal retractions. Because of respiratory insufficiency both newborns were artificially ventilated, and the chest radiographs showed linear shadowing compatible with congenital pneumonia. Antibiotic therapy with piperacillin (100 mg/kg/d) and cefotaxime (100 mg/kg/d) was started. White blood cell count and C-reactive protein values were normal. Respirator-assisted ventilation was stopped 13 and 16 h after birth, respectively.
On the 6th day of antibiotic treatment, vancomycin was administered, by error as a single 1-min dose intravenously to both babies. The dosages were 38 and 35 mg/kg, respectively. After a few minutes both newborns developed a flushed face and trunk and peripheral cyanosis. Capillary refill time was prolonged. Apnea and hypoxemia (oxygen saturation between 60 and 64%, measured by transcutanous pulse oximetry) were noted. Repeated bradycardia (40 to 60 beats/min) appeared and systolic blood pressure dropped 10 mm Hg. Oxygen was delivered immediately to both infants. Blood gas analyses showed metabolic acidosis, characterized by a blood pH of 7.29 and 7.24 and a base excess of −10.5 and −10.9 mmol/l, respectively. After 30 min clinical signs and symptoms of RMS as well as the metabolic acidosis disappeared. The next morning, 9 h after administration, the vancomycin serum concentrations were 32 and 34.5 mg/l, respectively.
Funduscopic examination on Day 19 after the event revealed no retinal damage. Ototoxicity was ruled out by regular otoacoustic emissions registered on the same day. Repeated blood cell counts demonstrated no abnormalities. Clinically no renal dysfunction was obvious; especially no edema was observed. Serum creatinine values were normal for both infants. The glomerular filtration rate, estimated with the Schwartz formula,12 was also normal in both infants (29.4 ml/min/1.73 m2 in the male twin and 34.6 ml/min/1.73 m2 in the female patient on Day 9). No proteinuria was present before the vancomycin administration. Semiquantitative urinary dipstick analysis showed no proteinuria, but an urinary protein electrophoresis revealed tubular proteinuria. Proteinuria was paralleled by an elevated activity of the tubular enzyme N-acetyl-beta-D-glucosaminidase (NAG) in the urine for 16 days. Two days after vancomycin administration NAG was 38.2 U/mmol creatinine and 46 U/mmol creatinine, respectively (normal range, <20 U/mmol creatinine). One week later proteinuria resolved completely and NAG excretion returned to normal values.
Discussion. The presented cases focus attention on the infusion speed and the large dosage of vancomycin administered. Vancomycin was erroneously administered as a rapid intravenous injection.9 The rapid administration is considered by most authors to be the most likely cause of the RMS, although RMS can be observed when vancomycin is administered for longer than 60 min.
