An interdisciplinary clinical advancement program within a patient-centered care model.

Restructuring in health care does not have to compromise the pursuit of clinical excellence and quality patient care. The clinical advancement program (CAP) at the Hospital for Special Care is a newly developed multidisciplinary reward and recognition program for clinical staff. The program is integrated into the hospital's structure of service line management and, unlike traditional advancement programs, is open to all levels of care providers: professional personnel, technical staff, and aides. This article describes the basic features of the CAP model and how its was developed by a multidisciplinary task force.

[Bepridil and torsades de pointes: are the precautions of use respected?]. / Bepridil et torsades de pointes: les précautions d'emploi sont-elles respectées?

The torsades de pointes with bepridil are serious side-effects, known right from 1982, and for which definite therapeutic recommendations were decreed in 1984 then in 1991. The observations of 7 new cases drove us to discuss about the respect for these recommendations. From the study of these 7 middle-aged patients (+/- esm) 76.9 +/- 2.4, we have noticed that they all combined 3 risk-factors at least with an average (+/- esm) 3.71 +/- 0.29 (range 3-5). The non-respect for the methods of prescription of bepridil leads to serious trouble in the rate of heartbeat and can threaten vital prognosis. So, it is advisable for the practicians to be warmly and precisely informed and prescribe another anti-angina-pectoris treatment in high risk-patients.

Unmasking the significant enzyme-inducing effects of phenytoin on serum carbamazepine concentrations during phenytoin withdrawal.

OBJECTIVE: We report on two patients who appeared to exhibit profound induction of carbamazepine metabolism during cotherapy with phenytoin. Gradual withdrawal of phenytoin confirmed this impression. DESIGN: Two case studies. RESULTS: Two patients receiving carbamazepine and phenytoin as combination anticonvulsant therapy were admitted for comprehensive rehabilitation. A 23-year-old man had therapeutic serum phenytoin concentrations, but his serum carbamazepine concentrations were so low that they were nonquantifiable. Doubling the daily carbamazepine dosage did not yield quantifiable serum concentrations. When the daily phenytoin dosage was tapered from 500 to 200 mg, the carbamazepine concentration rose to 10.0 micrograms/mL. No further changes in serum carbamazepine concentrations were observed when the phenytoin was discontinued. A 49-year-old man was receiving large daily dosage of phenytoin (600 mg) and carbamazepine (2300 mg). In the process of tapering and discontinuing phenytoin, the patient became lethargic and confused. These signs and symptoms suggested carbamazepine toxicity. The patient was eventually stabilized on a carbamazepine dosage of 1200 mg/d, which produced a serum concentration of 8.4 micrograms/mL. When this patient had been receiving concurrent phenytoin therapy, approximately twice as much carbamazepine (2300 mg) was required to maintain a similar serum concentration. CONCLUSIONS: Phenytoin is a potent inducer of carbamazepine metabolism. Whenever phenytoin dosages are tapered and discontinued in patients receiving these medications concomitantly, frequent serum carbamazepine monitoring is recommended during the ensuing deinduction phase.