Fat grafting to the hand in patients with Raynaud phenomenon: a novel therapeutic modality.

BACKGROUND: Raynaud phenomenon causes progressively decreasing blood flow to the extremities, resulting from an imbalance between vasoconstriction and vasodilation. Treatment options include biofeedback, phosphodiesterase inhibitors, calcium channel inhibitors, botulinum toxin injection, or surgical sympathectomy. The authors propose fat grafting to the hands as a method to delay progression of the disease. METHODS: Indications included symptomatic Raynaud phenomenon with failure of previous management. Fat is harvested from abdominal depots. Approximately 30 ml of decanted fat is injected by means of blunt cannulae: 10 to 15 ml in the dorsum of the hand, 2 to 3 ml in the snuffbox, 1 to 2 ml in each dorsal webspace, 3 to 4 ml along the superficial palmar arch, 1 to 2 ml in volar webspaces 2 to 4, and 2 to 3 ml in the first webspace. Patients underwent preoperative and postoperative laser speckle imaging study to assess changes in perfusion. RESULTS: A total of 13 patients were treated (21 hands). Twelve patients had undergone prior botulinum toxin injection, and 11 patients had prior sympathectomies. Findings included reduced pain (average reduction, 6.86 of 10 to 2.38 of 10), fewer cold attacks, improved skin and soft-tissue texture, decrease in ulcerations, and patient-reported improved function. Three patients had no changes. Increased blood flow per imaging was noted in five of 11 hands tested. Six patients had decreased readings on laser imaging. None of the laser speckle imaging changes were statistically significant, and they did not correlate clinically. There were no major complications. CONCLUSIONS: Preliminary results of fat grafting to the hands of patients with Raynaud phenomenon revealed improved symptomatology with evidence suggestive of measurably increased perfusion in some cases. Fat grafting may benefit the management of this patient population. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.

CASE REPORT Idiopathic Tumoral Calcinosis of the Nontraumatic Thumb.

We report a case of idiopathic tumoral calcinosis localized to the thumb without prior trauma or surgery. Initial physical examination and imaging studies were suggestive of more common etiologies of thumb pain. After treatment failure, a biopsy specimen revealed calcium phosphate salt deposition in the soft tissue around the metacarpophalangeal joint, which was treated by excision of the tumoral calcinosis masses. Tumoral calcinosis can occur idiopathically in the hand and digits and should be considered when other more common pathologies of thumb pain have been ruled out.

Guided surgical debridement: staining tissues with methylene blue.

Precise surgical debridement of wounds is required to achieve wound closure. The authors describe their experience with a technique using topical methylene blue to facilitate precise surgical debridement. In this technique, methylene blue dye is applied topically to the wound surface at the onset of surgery. The stained wound site is then wiped to remove dye from the surface of normal epithelium; eschar, nonviable tissue, and granulation tissue remain stained. The methylene blue-stained tissue is surgically removed, and the newly debrided surface of the wound is assessed for adequate vascularity and biopsied to verify presence of bacteriologic balance before closure. The authors have used this technique in more than 200 wound debridements during the past year, including acute surgical or traumatic wounds, acute and subacute burn wounds, chronic granulating wounds, partially epithelialized wounds, sinus tracts, and fistulae. No adverse reactions have been noted, even on patients undergoing multiple applications through serial operations. Topical application of methylene blue to wounds with mixed tissue content helps to distinguish between viable and nonviable tissue and between epithelialized and nonepithelialized areas, facilitating more precise and complete wound debridement.

Omental free-tissue transfer for coverage of complex upper extremity and hand defects--the forgotten flap.

Free omental tissue transfer is a versatile reconstructive option for trunk, head and neck, and extremity reconstruction. Its utility is due to the length and caliber of the vascular pedicle and the malleability and surface area of the flap. We report our experience with omental free flap coverage of complex upper-extremity defects. A retrospective analysis of eight omental free-tissue transfers in seven patients with complex upper-extremity defects between 1999 and 2008 was performed. Indications, operative technique, and outcome were evaluated. Patient age ranged from 12 to 59 years with five male and two female patients. Indications included tissue defects due to crush-degloving injuries, pitbull mauling, or necrotizing soft tissue infection. All patients had prior operations including: revascularization, debridement, tendon repair, skin grafts, and/or fixation of associated fractures. One patient sustained severe bilateral crush-degloving injuries requiring free omental hemiflap coverage of both hands. The mean defect size was 291 cm(2) with all patients achieving complete wound coverage. No flap loss or major complications were noted. Laparoscopic-assisted omental free flap harvest was performed in conjunction with the general surgery team in three cases. Mean follow-up was 2 years. The omental free flap is a valuable, often overlooked reconstructive option. The long vascular pedicle and large amount of pliable, well-vascularized tissue allow the flap to be aggressively contoured to meet the needs of complex three-dimensional defects. In addition, laparoscopic-assisted harvest may aid with flap dissection and may result in reduced donor-site morbidity.

Signals that initiate, augment, and provide directionality for human keratinocyte motility.

Human keratinocytes (HK) migration plays a critical role in the re-epithelialization of acute skin wounds. Although extracellular matrices (ECM) and growth factors (GF) are the two major pro-motility signals, their functional relationship remains unclear. We investigated how ECM and GF regulate HK motility under defined conditions: (1) in the absence of GF and ECM and (2) with or without GF with cells apposed to a known pro-motility ECM. Our results show that HK migrate on selected ECM even in the total absence of GF. This suggests that certain ECM alone are able to "initiate" HK migration. Unlike ECM, however, GF alone cannot initiate HK migration. HK cannot properly migrate when plated in the presence of GF, regardless of the concentration, without an ECM substratum. The role of GF, instead, is to augment ECM-initiated motility and provide directionality. To gain insights into the mechanism of action by ECM and GF, we compared, side-by-side, the roles of three major mitogen-activated protein kinase cascades, extracellular-signal-regulated kinase (ERK)1/2, p38, and c-Jun N-terminal kinase (JNK). Our data show that ERK1/2 is involved in mediating collagen's initiation signal and GF's augmentation signal. p38 is specific for GF's augmentation signal. JNK is uninvolved in HK motility. Constitutively activated p38 and ERK1/2 alone could not initiate HK migration. Co-expression of both constitutively activated p38 and ERK1/2, however, could partially mimic the pro-motility effects of collagen and GF. This study reveals for the first time the specific functions of ECM and GF in cell motility.

Inflammatory mediators in wound healing.

This article provides much evidence that the inflammatory process has direct effects on normal and abnormal wound healing. As better understanding develops for the mechanism for these outcomes, targeted proinflammatory and anti-inflammatory interventions are likely to be successful. When inflammation is maintained as a regulated and orchestrated response, effective and normal wound healing is likely to result.

Migration of human keratinocytes in plasma and serum and wound re-epithelialisation.

When skin is wounded, human keratinocytes at the wound edge stop differentiating and start migrating to resurface the wound. How this change takes place is unclear. Because keratinocytes at the wound edge are for the first time surrounded by serum rather than plasma, serum could contain some migration-promoting factor or factors that is absent in plasma. We did standard computer-assisted in-vitro migration assays of human keratinocytes in the presence of either human plasma or serum. We also did a semiquantitative western blot analysis to determine if p38 mitogen-activated protein kinase (p38MAPK) was activated by either serum or plasma. Our results showed that keratinocytes migrating on collagen in the presence of serum produced migration indices in the range of 28, whereas those in the presence of plasma were about 12--the same level as control assays without either serum or plasma. We also showed that induced keratinocyte polarisation, activation of p38MAPK, and production of matrix metalloprotease 9 are possible mechanisms for promotion of re-epithelialisation of skin wounds by human serum.