Sustaining continuous ambulatory peritoneal dialysis after herniotomy.

Controversy still exists as to whether peritoneal dialysis (PD) treatment can be safely continued after herniotomy. Many nephrologists withhold PD treatment for several weeks after herniotomy for fear of dialysate leakage and hernia recurrence. Here, we report on 9 patients (2 women, 7 men) in whom herniotomy was performed for umbilical (n = 3), inguinal (n = 5), or cicatricial hernia (n = 2), or for open processus vaginalis (n = 2). Surgery was performed according to the Lichtenstein method with insertion of a polypropylene mesh and ligation of the hernia sac. In all patients, PD treatment was paused for the day of surgery and for 1-3 days postoperatively, depending on residual renal function. Over the next several days, low-volume (1.0-1.5 L), high-frequency (6 per day) exchanges were started. The patient's original PD regimen was gradually reinstated over the next 2-4 weeks. All patients recovered rapidly, with no uremia or dialysis-related complications. Particularly, no leakage and no hernia recurrence could be observed 3 months thereafter. None of the patients had to be hemodialyzed intercurrently. In conclusion, continuing a modified regimen of CAPD treatment after herniotomy seems to be safe, with excellent patient comfort.

[Sternocostoclavicular hyperostosis]. / Die sternokostoklavikuläre Hyperostose.

HISTORY AND CLINICAL FINDINGS: A 35-year-old previously healthy man developed a painful swelling in the area of the left sternoclavicular joint (SCJ), restricting movement. There had been no history of trauma. INVESTIGATIONS: A moderately increased erythrocyte sedimentation rate was the only abnormal finding among the usual laboratory tests. Radiologically there were marked hyperostotic changes in the area of the left upper thoracic cage with synostosis of the SCJ. Biopsy of the left clavicle showed non-specific chronic sclerosing osteomyelitis. TREATMENT AND COURSE: Over the next 6 years the SCJ became completely ankylosed and there were now extensive fibroses, some presternal and some in the upper mediastinum with thrombosis of the left subclavian, axillary and jugular veins causing inflow occlusion (Paget-von-Schroetter-syndrome). Lymph nodes in the region of the mandible, jugular veins bilaterally and mediastinum were noted for the first time, remaining unchanged in size over six months. CONCLUSION: Sternoclavicular hyperostosis is an important condition in the differential diagnosis of inflammatory or malignant processes of this joint.

Propafenone in a usual dose produces severe side-effects: the impact of genetically determined metabolic status on drug therapy.

We report the case of an elderly lady presenting with dizziness, a head injury resulting from a fall and bradycardia. Propafenone 150 mg t.i.d. had been prescribed for atrial fibrillation with tachyarrhythmia, induced by hyperthyroidism, 18 months earlier. A toxic concentration of parent propafenone, and no 5-hydroxy metabolite, was detected in a plasma sample. Symptoms disappeared after the discontinuation of propafenone. The poor metaboliser (PM) phenotype of sparteine/debrisoquine was assumed and subsequently confirmed by phenotyping (sparteine test) and genotyping (allele-specific polymerase chain reaction). The PM phenotype is common in European populations, with a prevalence of about 7%. If drugs with narrow therapeutic ranges undergo genetically polymorphic metabolism, toxicity may arise even with recommended doses. Individualization of doses is required to avoid adverse effects.

Free radicals and pathogenesis during ischemia and reperfusion of the cat small intestine.

BACKGROUND/AIM: In spite of the interest in free radicals as mediators of ischemic damage, most information on these species in biological systems is derived from indirect measurements. Our aim was to obtain more direct information concerning sources of free radical production during ischemia and reperfusion. METHODS: We have performed simultaneous measurement of radical generation, purine metabolites, reduced glutathione, neutrophil infiltration and morphological appearance in the cat small intestine in vivo during 60 minutes of ischemia followed by 60 minutes of reperfusion. RESULTS: Radical formation increased abruptly on reperfusion and remained elevated in untreated animals. Inhibition by a monoclonal antibody (IB4) against the neutrophil and by allopurinol treatment was paralleled by improvement of biochemical and morphological parameters. The radicals detected during reperfusion could be divided into one component arising directly from the neutrophils, one due to the xanthine oxidase reaction, and one unknown source. CONCLUSIONS: Neutrophils are a major source of radical production during reperfusion after ischemia. Radicals formed in the xanthine oxidase reaction seem to function as a primer for the neutrophils. The nonsignificant linear correlation between radical formation and morphological appearance suggests that factors other than free radicals are important for the development of intestinal damage after a period of ischemia.