4,358 research outputs found

    The little finger ulnar palmar digital artery perforator flap: anatomical basis

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    PURPOSE: The aim of this study was to explore the cutaneous vascularization of the hypothenar region and investigate the anatomical basis for perforator propeller flaps for coverage of the flexor aspect of the little finger. METHODS: The area between the pisiform and the base of the little finger was studied in 14 hands of fresh cadavers injected with red latex. An oval flap 1.5 cm large was raised along the axis between these two points. Perforators going into the flap were dissected up to their origin from the ulnar palmar digital artery of the little finger, and their distance from the proximal edge of the A1 pulley was recorded. RESULTS: The mean number of perforator arteries entering the flap was 5.8 (range 4-8). A constant sizeable perforator was identified within 0.7 cm from the proximal margin of the A1 pulley in all 14 specimens. In the majority of cases (64 %), the most distal perforator was located at this level. Dissection of the flap was carried out suprafascially on the most distal perforator and 180° rotation allowed the flap to reach the flexor surface of the fifth finger. The donor site was closed primarily. CONCLUSION: Distal perforators of the ulnar palmar digital artery of the little finger are constantly found. Our anatomical findings support the possibility of raising a propeller perforator flap from the hypothenar region for coverage of the flexor aspect of the little finger. Its clinical application could provide a quick and straightforward single-stage option with a negligible donor-site morbidity for reconstruction of such defects

    Imatinib dose escalation versus sunitinib as a second line treatment in KIT exon 11 mutated GIST: a retrospective analysis

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    We retrospectively reviewed data from 123 patients (KIT exon 11 mutated) who received sunitinib or dose-escalated imatinib as second line.All patients progressed on imatinib (400 mg/die) and received a second line treatment with imatinib (800 mg/die) or sunitinib (50 mg/die 4 weeks on/2 off or 37.5 mg/day). Deletion versus other KIT 11 mutation was recorded, correlated with clinical benefits.64% received imatinib, 36% sunitinib. KIT exon 11 mutation was available in 94 patients. With a median follow-up of 61 months, median time to progression (TTP) in patients receiving sunitinib and imatinib was 10 (95% CI 9.7-10.9) and 5 months (95% CI 3.6-6.7) respectively (P = 0.012). No difference was found in overall survival (OS) (P = 0.883). In imatinib arm, KIT exon 11 deletions was associated with a shorter TTP (7 vs 17 months; P = 0.02), with a trend in OS (54 vs 71 months P = 0.063). No difference was found in patients treated with sunitinib (P = 0.370).A second line with sunitinib was associated with an improved TTP in KIT exon 11 mutated patients progressing on imatinib 400 mg/die. Deletions in exon 11 seemed to be correlated with worse outcome in patients receiving imatinib-based second line
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