Soft Tissue Reconstruction After Revascularization.

Diabetic foot ulcer represents the primary cause of hospital admissions, amputations, and mortality in diabetic patients. The development of diabetic foot ulcers is influenced by peripheral neuropathy, infection, and ischemia, with diabetes contributing to peripheral artery disease. Free tissue transfer combined with revascularisation of the lower extremity provides the potential opportunity for limb salvage in individuals with lower extremity defects due to critical limb ischemia and diabetic foot.

Refractory Pseudomonas aeruginosa infections treated with phage PASA16: A compassionate use case series.

BACKGROUND: A growing number of compassionate phage therapy cases were reported in the last decade, with a limited number of clinical trials conducted and few unsuccessful clinical trials reported. There is only a little evidence on the role of phages in refractory infections. Our objective here was to present the largest compassionate-use single-organism/phage case series in 16 patients with non-resolving Pseudomonas aeruginosa infections. METHODS: We summarized clinical phage microbiology susceptibility data, administration protocol, clinical data, and outcomes of all cases treated with PASA16 phage. In all intravenous phage administrations, PASA16 phage was manufactured and provided pro bono by Adaptive Phage Therapeutics. PASA16 was administered intravenously, locally to infection site, or by topical use to 16 patients, with data available for 15 patients, mainly with osteoarticular and foreign-device-associated infections. FINDINGS: A few minor side effects were noted, including elevated liver function enzymes and a transient reduction in white blood cell count. Good clinical outcome was documented in 13 out of 15 patients (86.6%). Two clinical failures were reported. The minimum therapy duration was 8 days with a once- to twice-daily regimen. CONCLUSIONS: PASA16 with antibiotics was found to be relatively successful in patients for whom traditional treatment approaches have failed previously. Such pre-phase-1 cohorts can outline potential clinical protocols and facilitate the design of future trials. FUNDING: The study was funded in part by The Israeli Science Foundation IPMP (ISF_1349/20), Rosetrees Trust (A2232), United States-Israel Binational Science Foundation (2017123), and the Milgrom Family Support Program.

Use of Recanalized Vessels for Diabetic Foot Reconstruction: Pushing the Boundaries of Reconstruction in a Vasculopathic Lower Extremity.

BACKGROUND: Free flap after lower extremity revascularization may enable limb salvage in defects after critical limb ischemia. This study examined the outcomes of reconstruction of ischemic diabetic foot according to the severity of the vessel occlusion and assessed whether recanalized vessels may serve as a reliable recipient vessel. METHODS: A total of 62 patients who underwent diabetic foot reconstruction with free flaps after successful percutaneous transluminal angioplasty (PTA) from February of 2010 to February of 2016 were identified and divided into three groups: group 1, nonoccluded vessels as recipient ( n = 11); group 2, recanalized artery after PTA for partially occluded artery ( n = 30); and group 3, recanalized artery after PTA for completely occluded artery ( n = 21). RESULTS: Flap survival was statistically higher in group 2 (90%) compared with group 3 (67%) ( P < 0.05). Subsequent major amputation was significantly lower in groups 1 and 2 [0/7 and 1/30 (3.3%)] compared with group 3 [5/21 (23.8%)] ( P < 0.05). The patient survival and limb salvage rate was 90.9% at 1 and 3 years in group 1, 89.8% at 1 year and 86.3% at 3 and 5 years in group 2, and 76.2% at 1, 3, and 5 years in group 3. This difference was not statistically significant ( P = 0.485). CONCLUSIONS: The use of recanalized vessels after PTA can be safe for partially occluded arteries but requires caution for completely occluded arteries. Using completely occluded vessels after PTA can be attempted when other options are not available and achieves a 76% chance of limb salvage. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, III.

Facial Nerve Repair following Acute Nerve Injury.

Background Acute facial nerve iatrogenic or traumatic injury warrants rapid management with the goal of reestablishing nerve continuity within 72 hours. However, reconstructive efforts should be performed up to 12 months from the time of injury since facial musculature may still be viable and thus facial tone and function may be salvaged. Methods Data of all patients who underwent facial nerve repair following iatrogenic or traumatic injury were retrospectively collected and assessed. Paralysis etiology, demographics, operative data, postoperative course, and outcome were examined. Results Twenty patients underwent facial nerve repair during the years 2004 to 2019. Data were available for 16 of them. Iatrogenic injury was the common category ( n = 13, 81%) with parotidectomy due to primary parotid gland malignancy being the common surgery ( n = 7, 44%). Nerve repair was most commonly performed during the first 72 hours of injury ( n = 12, 75%) and most of the patients underwent nerve graft repair ( n = 15, 94%). Outcome was available for 12 patients, all of which remained with some degree of facial paresis. Six patients suffered from complete facial paralysis (50%) and three underwent secondary facial reanimation (25%). There were no major operative or postoperative complications. Conclusion Iatrogenic and traumatic facial nerve injuries are common etiologies of acquired facial paralysis. In such cases, immediate repair should be performed. For patients presenting with facial paralysis following previous surgery or trauma, nerve repair should be considered up to at least 6 months of injury. Longstanding paralysis is best treated with standard facial reanimation procedures.

[BREAST CANCER-RELATED LYMPHEDEMA: INCIDENCE AND RISK FACTORS, PREVENTIVE MEASURES AND TREATMENTS].

INTRODUCTION: Lymphedema is a pathological condition in which intercellular protein-rich fluid accumulates and leads over time to inflammation, adipose tissue hypertrophy and fibrosis. Secondary lymphedema is caused by injury or blockage of the lymphatic system and the main cause in the Western world is the treatment of a variety of cancers, the main one being breast cancer. Chronic arm edema after breast cancer surgery is a common problem with an estimated incidence of 1 in 5 patients after breast cancer treatment. In this article we review the main risk factors, approaches to reducing the risk of developing lymphedema after treatment for breast cancer and existing treatment protocols for lymphedema including the surgical innovations in this field and our experience in these innovative surgical approaches. To date, 26 physiological surgeries have been performed at the Tel Aviv Medical Center using the microsurgical approach for treating lymphedema. These surgeries had no significant complications and the improvement was observed to be greater in the group of patients with secondary lymphedema. Lymphovenous anastomosis and vascularized lymph node transfer offer promising solutions for the treatment of breast cancer related lymphedema. The introduction of additional techniques and the refinement of these procedures will probably continue to improve the results in the future.

COMMD10 is critical for Kupffer cell survival and controls Ly6Chi monocyte differentiation and inflammation in the injured liver.

Liver-resident macrophages Kupffer cells (KCs) and infiltrating Ly6Chi monocytes both contribute to liver tissue regeneration in various pathologies but also to disease progression upon disruption of orderly consecutive regeneration cascades. Little is known about molecular pathways that regulate their differentiation, maintenance, or inflammatory behavior during injury. Here, we show that copper metabolism MURR1 domain (COMMD)10-deficient KCs adopt liver-specific identity. Strikingly, COMMD10 deficiency in KCs and in other tissue-resident macrophages impedes their homeostatic survival, leading to their continuous replacement by Ly6Chi monocytes. While COMMD10 deficiency in KCs mildly worsens acetaminophen-induced liver injury (AILI), its deficiency in Ly6Chi monocytes results in exacerbated and sustained hepatic damage. Monocytes display unleashed inflammasome activation and a reduced type I interferon response and acquire "neutrophil-like" and lipid-associated macrophage differentiation fates. Collectively, COMMD10 appears indispensable for KC and other tissue-resident macrophage survival and is an important regulator of Ly6Chi monocyte fate decisions and reparative behavior in the diseased liver.

Propeller Flaps in the Posterior Trunk.

The reconstruction of complex posterior trunk defects remains challenging. But now with an increased knowledge of angiosomes and the practice of perforator flaps, the posterior trunk offers a new plethora of options for reconstruction. Propeller flaps based on such perforator(s) offer an elegant solution for managing defects while achieving primary donor-site closure without significant morbidity. We will discuss the relevant anatomy and design principles for propeller flaps based on a review of the literature and our experience. Steps beginning with preoperative planning, perforator selection, and intraoperative surgical technique will be discussed, together with pearls on both avoiding and managing complications.

[FACIAL NERVE PARALYSIS - THERAPEUTIC APPROACH, FACIAL REANIMATION AND ADJUNCTIVE TREATMENT].

INTRODUCTION: Paralysis of the facial mimetic muscles causes loss of voluntary and non-voluntary muscle function, as well as facial tone. This is a devastating condition with profound functional, aesthetic and psychological consequences. Etiologies include congenital paralysis and acquired paralysis following viral infection, trauma, head and neck tumors, iatrogenic damage and more. Clinical presentation includes ocular symptoms (dry eye, epiphora, corneal irritation), nasal symptoms (nasal obstruction) and oral symptoms (drooling and speech disturbances). Reconstruction of facial nerve function is based on renewing the neural input to the paralyzed face in parallel with transferring a functioning muscle. The gold standard in long term facial paralysis reanimation includes a two-stage procedure that involves cross-face nerve grafting and later on a free gracilis muscle transfer. This method allows reconstruction of a symmetric, spontaneous and voluntary smile. In cases when cross-face nerve grafting is impossible, a free-gracilis muscle transfer is performed with neural coaptation to another cranial nerve, most commonly the motor nerve to the masseter muscle (of the trigeminal nerve). Non-microsurgical methods for facial reanimation exist, however, nowadays they are rarely performed. In addition to the surgical reconstruction, other surgical and non-surgical procedures are performed for functional and aesthetic symmetrization purposes. These include fat injection to the face, botulinum toxin injection, oculoplastic procedures and more. In this article we describe our patient population with facial nerve paralysis, common facial reanimation procedures, considerations in choosing the appropriate reconstruction procedure and the general approach for treatment of facial paralysis in our multidisciplinary facial paralysis clinic.

Incomplete Facial Paralysis: The Use of the Ipsilateral Residual Facial Nerve as a Donor Nerve for Facial Reanimation.

BACKGROUND: The reconstructive approach for incomplete facial paralysis is not yet determined. In this article, the authors present a new surgical approach for patients with incomplete facial paralysis in which residual, ineffective movement is detected preoperatively in the ipsilateral buccozygomatic territory of the paretic facial nerve. METHODS: Sixteen patients with incomplete facial paralysis were found eligible for the procedure and underwent one-stage facial reanimation performed by the senior author (E.G.). Reanimation was performed using free gracilis muscle transfer with neural coaptation to an active facial nerve branch(es) responsible for the predetected buccozygomatic residual movement. Patients were reviewed in a systematic fashion using a combined still photographic and video scoring scale for symmetry at rest and at dynamic states. RESULTS: Following surgery, improved symmetry was observed in the majority of observations of the mouth region at rest and while smiling and of the nasolabial fold region while smiling. There was no significant change in symmetry in the majority of observations of the eye region at rest and while smiling and the nasolabial fold region at rest. Video assessment of dynamic facial symmetry while smiling demonstrated improved symmetry in 91 percent of the observations (n = 191 observations). Comparison of mean scores for dynamic smile symmetry produced a statistically significant improvement of 1.68 points following surgery (p < 0.001). CONCLUSION: Based on this series, the authors recommend that use of the ipsilateral facial nerve buccozygomatic residual branch be considered as a donor nerve for facial reanimation using a free gracilis muscle transfer in patients with incomplete facial paralysis with residual preoperative movement in the midface. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.