We review a case of a 22-year-old healthy man who underwent a 5-h maxillofacial surgery while continuously supine with foam pads placed prophylactically over elevated heels. Immediately after surgery, Stage 1 pressure injuries appeared on the left lateral heel and right lateral ankle, despite the absence of local pressure to these areas. Both lesions eventually resolved. Eight months later, a Doppler evaluation was performed of the patient's lower extremities, the peroneal artery and its tributaries were marked, and the intraoperative positioning was simulated to determine if a wedge at the back of the calf could have obstructed blood flow in these vessels. In this position, the feet naturally abducted so that the lateral calcaneal and posterior malleolar arteries became positioned immediately underneath the wedge. We propose a vascular mechanism of pressure injury development, postulating that some heel pressure injuries are not the result of localized pressure but rather angiosomal ischemia, based on the observation that the anatomical pattern of these lesions frequently follow the distribution of a named vessel. We hypothesize that in this case, intraoperative positioning along with permissive hypotension may have occluded arterial or venous flow to the relevant angiosomes, causing an ischemia reperfusion injury to the downstream tissues.
Split thickness skin graft (STSG) is a versatile procedure performed for the treatment of wounds resulting from varying pathology. This remains very useful because of its ability for quick healing and low complication rate. The surface of the foot and ankle is an area frequently affected by severe skin and soft tissue structure infections (SSTIs) whose treatment results in wounds. These infections and resultant surgical wounds are commonly seen patients with diabetes. The objective of the present study was to retrospectively evaluate initial healing and immediate post-operative outcomes following STSG application in a diabetic population when negative pressure wound therapy (NPWT) was used as a bolster. Ten patients were identified, including 11 surgical wounds, who underwent STSG bolstered with NPWT from January 2016 to October 2018. Mean follow-up was 13 months (range 1-33 months) with an average time to heal of 17 days (range 14-30 days) for 11 surgical wounds averaging 57 cm2 (range 6.3 - 91 cm2). Consistent improved outcomes have been demonstrated when compared to alternative bolstering techniques available in the literature making a STSG bolstered with NPWT a powerful tool in the reconstruction of diabetic foot wounds resulting from the treatment of infection. Levels of Evidence: Level IV
Open surgical decompression of the tarsal tunnel is the standard surgical approach for compression of the tibial nerve within the tarsal tunnel. Complications associated with this approach can be significant and periods of non-weight bearing are required. An alternative approach allowing for minimal soft tissue trauma and reduced time to ambulation is therefore desirable. Endoscopic tarsal tunnel decompression may provide such an alternative. The authors performed a systematic review of electronic databases and other relevant sources to identify material regarding the safety of endoscopic tarsal tunnel decompression. Only articles that included clear information concerning the safety of endoscopic tarsal tunnel decompression with a follow-up of at least 12 months were included. Three studies were identified involving 37 feet, with a weighted mean follow-up of 27 months. There were no permanent complications relating to iatrogenic nerve injury, deep infection, or prolonged wound healing problems documented despite initiating ambulation within one week of surgery. Two patients (5.6%) developed recurrence more than 2 years postoperative and one (2.7%) showed no improvement. Endoscopic tarsal tunnel decompression is a safe procedure with a low rate of recurrence or failure and allows for near-immediate ambulation. However, additional prospective investigations comparing open and endoscopic approaches to tarsal tunnel decompression are warranted.
Wounds continue to pose significant challenges to clinicians. Data based on randomized controlled trials from the US Wound Registry showed that less than 50% of wounds heal in an unpredictable period of time. Chronic wounds are difficult to heal, with multiple barriers to healing that include inadequate nutrient flow, an inflammatory-coagulation vicious cycle, redox imbalance, and anatomical, physiological, and biochemical dysfunction in the endothelium. In clinical practice, wounds that fail to heal within an appropriate time are at higher risk for deterioration as well as development of infection that further complicates the pathology. Wounds complicated by deep abscess and osteomyelitis often result in amputation. Higher level amputations, below the knee and above the knee, are associated with increased morbidity and mortality rates. However, the most consequential barrier to healing is the prolonged inflammatory phase, which prevents progression to the proliferation phase of wound healing. Diabetic foot ulcers are especially difficult to heal because of angiopathy, hypoxia and ischemia, AGEs, and other factors related to impaired hemodynamics. Restoration of physiological levels of blood flow to DFUs will concomitantly bring about normalization of laminar SS on the endothelium. These multifaceted healing mechanisms, specifically related to the effects of vascular SS on the endothelium, are reviewed here. Such mechanisms involve anti-inflammation, anticoagulation, antioxidation, vasodilation, and angiogenesis. A concluding inference is made that if normalized SS could be produced in the vasculature serving chronic wounds, the sequential healing processes would be enhanced.
Anatomic constraints of the foot make it vulnerable to infection when the primary defense, the soft-tissue envelope is compromised due to vicinity of tendons, joints and bone to the skin. Reconstructive efforts in the presence of osteomyelitis compounds the clinical picture. Treatment of midfoot osteomyelitis can have devastating outcomes with loss of biomechanic integrity of the foot, and often loss of part of the foot which at that level results in significant functional deficits. When primary closure is not an option due to potential loss of structural and ultimately biomechanic integrity; soft tissue defects in the presence of exposed tendon, joint or bone with intact vasculotome require expeditious and predictable coverage options. Local muscle flaps belong to the same armamentarium as local random flaps and free flaps considering their unique intricacies. The abductor hallucis muscle flap has been employed for covering soft tissue defects of different etiologies encompassing from the medial hindfoot and ankle to the medial plantar forefoot often with concomitant osteomyelitis of the underlying bone. In this case report, we describe a technique of a proximally based abductor hallucis flap for a patient with traumatic Lisfranc dislocation that developed surgical site infection complicated by osteomyelitis of the tarsometatarsal joint.
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