Freier Paraskapular-/Skapularlappen bei frakturbegleitendem Weichteildefekt an Talus oder Kalkaneus

BASIS: Fractures of the talus or calcaneus with accompanying soft tissue damage require precisely planned treatment to prevent infection of the wound over time, especially in severely injured patients. MATERIAL AND METHODS: Seven patients with fractures of the talus or calcaneus and accompanying 2nd and 3rd degree open or 3rd degree closed soft tissue injuries were followed up retrospectively. These patients were operated on between January 1999 and January 2006 with free fasciocutaneous scapular or parascapular flaps. The average age was 34 (range 16-54). Follow-up was at 6-36 months. RESULTS: Osteosynthesis was primarily in six cases, post-primarily in one, and in four cases exterior fixation was used additively. Temporary vacuum therapy was performed for a mean of 28 days (6-42). Parascapular, scapular, and Latissimus dorsi flap coverage was performed six, one, and one times, respectively. Six flaps healed without complication. One necrosis of a parascapular flap occurred and made a Latissimus dorsi flap necessary. In one case of donor-site wound dehiscense, a local rotation flap became necessary. There was no joint infection or osteomyelitis. Bony consolidation was achieved within all fractures. CONCLUSION: Traumatic soft tissue damage must be taken into account when primary or secondary internal fixation is performed and should influence the choice of implant. Free fasciocutaneous parascapular or scapular flaps are a powerful tool for preventing infection if local flaps are not sufficient to achieve stable soft tissue coverage.     

Bladder contracture following intravesical doxorubicin therapy: case report and a review of the literature

Intravesical doxorubicin rarely has been implicated as a cause of bladder contracture. We present a case of severe bladder contracture, documented radiographically and urodynamically after 8 weekly intravesical instillations of doxorubicin. The patient subsequently underwent cystectomy because of voiding dysfunction and the specimen demonstrated marked fibrosis in the bladder wall. We postulate that a benign, recurrent bladder ulceration during doxorubicin therapy may have potentiated the fibrotic response in the bladder to the doxorubicin. Objective monitoring of bladder capacity should be considered in patients treated with intravesical chemotherapy.     

Aluminum-citrate interaction in end-stage renal disease.

The influence of a sodium citrate/citric acid mixture on the gastrointestinal (GI) absorption of aluminum (Al) from an Al(OH)3 preparation was evaluated in six stable maintenance hemodialysis patients. Plasma Al concentrations were determined serially after each of the following treatment sequences (I) Al(OH)3; (II) Al(OH)3 + sodium citrate/citric acid; (III) sodium citrate/citric acid; (IV) Al(OH)3 + NaHCO3. AUC0-8 for plasma Al from 0 to 8 hours was significantly greater (p less than 0.05) for Al(OH)3 + sodium citrate/citric acid (73 +/- 23 micrograms.hr/l; mean +/- SEM) than Al(OH)3 (16 +/- 30 micrograms.hr/l); sodium citrate/citric acid (-27 +/- 14 micrograms.hr/l); or Al(OH)3 + NaHCO3 (6 +/- 22 micrograms.hr/l). The 24 hour Al level remained above baseline (p less than 0.03) following Al(OH)3 + sodium citrate/citric acid (31 +/- 12 (pre) vs 54 +/- 14 micrograms/l (post), in contradistinction to study limb: l (34 +/- 14 vs 30 +/- 12 micrograms/l); III (79 +/- 40 vs 65 +/- 35 micrograms/l); and IV (71 +/- 37 vs 66 +/- 42 micrograms/l). We conclude that the GI absorption of Al from Al(OH)3 is enhanced by citrate in patients undergoing hemodialysis and that elevations of plasma Al persist longer. The concomitant administration of citrate and Al-containing phosphate (PO4) binders should be avoided in patients with end-stage renal disease (ESRD). NaHCO3 may serve as an alternative therapy for metabolic acidosis with less risk of enhancing Al absorption.     

3H]-flunitrazepam binding after morphine treatment and under abstinence syndrome.

Chronic morphine treatment produced increases in [3H]-flunitrazepam binding in some hippocampal areas of the rat brain. The differences in binding were statistically significant in some cases. Both morphine-dependent and morphine-deprived (abstinence syndrome) animals showed an identical response in binding, which confirms a real, although small, increase in benzodiazepine binding sites in the hippocampus after morphine treatment, that is not affected by a naloxone-induced abstinence syndrome under the conditions studied. These findings support the hypothesis of a morphine-induced up-regulation of benzodiazepine binding sites in the hippocampus. A possible different response in benzodiazepine binding sites 1 and 2 could explain the different findings reported in the literature. Our data suggest that the detected increase in benzodiazepine binding would be mainly due to type 2 binding sites, since the hippocampus has a higher density of this type of benzodiazepine binding sites.