Defect Reconstruction of an Infected Diabetic Foot Using Split- and Full-thickness Skin Grafts With Adjuvant Negative Pressure Wound Therapy: A Case Report and Review of the Literature

Patients that present with leg or foot ulcers are not only a major cause of surgical admissions worldwide, but also a significant cause of morbidity, mortality, and disability.¹ Acute and chronic wounds can be a serious challenge for the surgeon, requiring conservative and operative treatment. Since chronic wounds are the result of impaired healing, the focus must be to overcome this. To promote wound healing, skin transplantation is frequently conducted by the surgeon; this form of treatment is regarded as a supportive procedure that assists in the epithelialization of the wound surface and provides mechanical stability.² In order to achieve successful tissue healing and decreased patient morbidity, certain criteria must be met. These include wound closure, an acceptable aesthetic result, and minimal physical and/or psychological impairment for the patient.² By placing skin grafts on a wound surface, the central areas are covered with keratinocytes sooner. Any alteration or interference to normal wound healing can result in the development of chronic wounds. This presents major concerns for the patient as well as the surgeon, since this may lead to serious complications including local or systemic infection and patient morbidity.

When presented with chronic wounds, the surgeon’s goal is to close the wound, resulting in increased infection resistance and decreased loss of body fluid and proteins. Therefore, procedures such as skin grafting must be considered as an option. Among other alternatives, the surgeon may consider secondary wound healing, primary or secondary wound closure, local flap transfer, distant flap transfer, free (microvascular) flaps, and amputation.²

In order to successfully obtain proper wound closure, a comprehensive approach is needed. This includes the careful consideration of the various surgical techniques available and the critical patient factors present. It is important that a clear understanding of key concepts such as wound healing, graft design, and patient risk assessment is evaluated.³ 

The process of cutaneous wound healing is complex and requires a coordinated response by immune cells, hematopoietic cells, and resident cells of the skin.⁴ A skin graft is a unit of skin taken from one part of the body and used to repair a defect elsewhere. It includes the entire epidermis and part of the dermis of variable thickness. Skin grafts that incorporate all of the dermis are termed full-thickness skin grafts (FTSG or Wolfe-Krause grafts). If only a portion of the dermis is included, the term split-thickness skin graft is used (STSG or Thiersch graft). Skin grafts offer the surgeon a quick, easy method of wound closure. Split-thickness skin grafts are the most common method of wound closure in defects too large to be closed primarily.⁵

The thickness of the skin graft determines the amount of dermis tissue that is transplanted with the overlying keratinocytes. The dermal component is mainly responsible for determining the mechanical (ie, resistance to pressure and shear forces, graft shrinkage), functional (sensibility), and aesthetic properties of the graft.⁶ Generally, a thicker graft means better mechanical, functional, and aesthetic properties; however, a thicker graft has a higher fail rate than thinner grafts. Since skin grafts lack their own blood supply, this process is dependant entirely on the wound bed. In comparison to FTSGs, STSGs have fewer metabolic requirements and thus can be used to resurface wounds that offer less than ideal conditions.² Unfortunately, they are more fragile than FTSGs and can produce a less desirable aesthetic outcome.⁶

Soft tissue defects can be classified as either acute or chronic defects. Acute soft tissue injuries are typically a result of high-speed accidents, falls from great heights, burns, or projectile wounds. Due to their diagnostic and therapeutic complexity, acute soft tissue injuries must be regarded separately with 2 variations most often seen: (1) soft-tissue-only defects and (2) combined soft tissue, tendon, and/or bone exposure.² Chronic soft tissue defects are most often due to vascular insufficiency (ie, arterial and/or venous), metabolic disorders (eg, diabetes), chronic infection (eg, osteomyelitis), irradiation, scarring after multiple surgeries, and neurologic deficits.²

The International Diabetes Federation has estimated that, globally, 382 million people were affected by diabetes mellitus in 2013, with this number projected to increase to 592 million by the year 2035.⁷ This trend will result in an increase in the total number of foot ulcer cases, which occur in up to 4% of patients with diabetes mellitus.⁸ In this patient population, ulcerations contribute to the greatest cause of nontraumatic minor and major amputations of the lower limb, with patients with a diabetic foot ulcer (DFU) having a 25 times higher risk than the general population.⁹ Diabetic Charcot foot syndrome is a serious and potentially limb-threatening lower extremity complication of diabetes. Now considered an inflammatory syndrome, diabetic Charcot foot is characterized by varying degrees of bone and joint disorganization secondary to underlying neuropathy, trauma, and perturbations of bone metabolism.¹⁰

In patients with diabetes, open foot wounds resulting from ulcerations are slow to heal, often become infected, and present as a major comorbidity that can lead to limb amputation. Therefore, in order to close (and heal) these wounds quickly, surgeons have recognized skin grafts (STSG and FTSG) as a quick and viable method for wound closure in this population.¹¹ 

A 43-year-old woman was admitted to the University Hospital Rebro (Zagreb, Croatia) due to an infected wound on her left foot. The patient had a history of reactive arthritis and was prescribed corticosteroid therapy when the disease was in its active phase. She also was diagnosed with type 2 diabetes mellitus 6 months prior to hospitalization for which she was taking oral antidiabetic medication.

Seven days prior to admission, the patient cut her left foot after stepping on a sharp rock. Over the course of 1-week post injury, the swelling and redness progressively worsened, and a purulent secretion from the wound gradually developed. She did not consult her primary care physician before presenting to the hospital. 

At initial presentation to the University Hospital Rebro emergency department, she complained of pain and a purulent secretion from the wound site. She was febrile (axillary temperature: 38.6°C), and the laboratory results showed increased inflammatory markers with leukocyte count of 13.82 x 10⁹/L, a neutrophil of 82.7%, and a C-reactive protein (CRP) of 116.44 mg/L. Physical examination revealed a large laceration with macerated skin on the plantar side of her left foot. There was redness and edema of the entire foot and ankle with a purulent secretion draining from the wound site. X-rays revealed a loss of normal morphology of the tarsal bones with necrosis and erosion of the articular surfaces. There were destructive changes present in the soft tissues with localized areas of gas collection. Based on the clinical, radiologic, and laboratory findings, surgical intervention was determined the best treatment method. 

Intraoperatively, there was a presence of necrotic tissue in the dermal and subdermal layers, with the presence of a purulent plantar fascia. Necrectomy and debridement of devitalized tissues were performed. Swabs for aerobic and anaerobic microorganisms were taken as well as a muscle biopsy for which pathohistological analysis (PHA) was ordered. The wound also was treated chemically with hydrogen peroxide (H₂O₂) and 0.9% sodium chloride solution (NaCl). A rubber drainage tube was inserted beneath the plantar fascia and the wound was covered with a petroleum jelly gauze and wet bandage of 10% NaCl. Tetanus immunoglobulin of human origin and a tetanus vaccine was administered to the patient immediately following the procedure. A course of intravenous antibiotics (200 mg ciprofloxacin twice daily and 600 mg clindamycin 3 times daily) were stared postoperatively on the hospital ward. 

On postoperative day 1, the PHA results showed areas of acute and chronic inflammation of the sample tissue with areas of necrosis and an infiltration of leukocytes and fibrin. Blood samples were repeated, which showed increased levels of leucocytes and CRP (10.83 x 10⁹/L and 30.4 mg/L, respectively).

On postop day 4, the intraoperative microbiological swabs tested positive for Enterobacter species, Enterococcus faecalis, and Serratia species. The antibiotic therapy was adjusted according to the antibiogram results. Clindamycin was stopped and 200 mg ampicillin twice daily was added. The previously ordinated ciprofloxacin was continued. Negative pressure wound therapy (NPWT) was applied at intermittent pressures of -60 mm Hg to -100 mm Hg. 

On postop day 7, an examination of the wound revealed areas of necrosis, and the patient underwent wound debridement. Intraoperatively, the fibrin layers were removed surgically as well as any necrotic epidermal or subdermal tissue. Once again, NPWT was applied at intermittent pressures of -60 mm Hg to -100 mm Hg. 

On postop day 10, NPWT was removed, and the wound was chemically treated with H₂O₂ and 0.9% NaCl solutions. After the wound was treated, NPWT was applied once again.

On postop day 11, detailed microbiological swab results were obtained, which showed the initial infection was caused by E cloacae and S rubidaea. As per the results, the antibiotic therapy was adjusted accordingly. Ampicillin was stopped, and ciprofloxacin was altered to oral administration at 500 mg twice daily. In addition, NPWT was continued at the same intermittent as before.

For the next 13 days, NPWT was replaced every 4 days and the wound was chemically treated with H₂O₂ and 0.9% NaCl solutions.

On postop day 24, due to the progression of the infection and the presence of gangrene in the second digit of the left foot, a transmetatarsal amputation of the toe was performed. Bacterial swabs of the wound were taken and were still positive for S rubidaea. Antibiotic therapy was continued; NWPT was discontinued. 

For the next 21 days, the patient remained on antibiotic therapy (ciprofloxacin 500 mg 2x/day). The wound was treated chemically with H₂O₂ and 0.9% NaCl solutions twice daily and covered with sterile gauze. Minor debridement of necrotic wound edges was performed twice during this period. The patient’s blood glucose was monitored 3 times daily and oral sitagliptin and metformin combination therapy (50 mg/500 mg 2x/day) were used in order to maintain normal values. The wound surface remained clean for the duration; there were no signs of purulent secretions and no local redness, and the patient was afebrile.

On postop day 45, after careful preparation of the wound bed with chemical treatments, the patient underwent wound debridement and a FTSG was transplanted over the wound site in order to close the defect.

In the first 3 days following the procedure, the foot remained bandaged in order not to disturb the graft. On day 4 post graft, the graft site was washed using 0.9% NaCl solution and sterile gauze was applied. This regiment was continued for the following 3 weeks. During this period, there was no sign of graft failure. The patient started light physiotherapy 1 week post procedure. 

Sixty-five days after the initial operation (20 days after FTSG application), slight discoloration of the graft edges appeared; this was monitored for the following 4 days. 

Seventy days after the initial operation, due to the slight presence of necrosis around the graft site, the patient underwent a partial necrectomy and wound reconstruction using a STSG. Offloading included the use of crutches and a boot.

Once the skin grafts had successfully taken, a computed tomography scan of the left foot was conducted and showed neuroarthropathic bone and joint changes with osteomyelitis of the tarsal bones. There were significant morphological changes in the sense of a thin bone cortex beginning at the level of the distal tibia and involving all of the bones of the foot. She was discharged soon after with regular check-ups in the outpatient clinic.

Due to the patient’s history and clinical and radiographic findings, a final diagnosis of Charcot foot syndrome was made. At 10 months post initial operation, the patient is doing well. The wound site healed successfully with 100% graft take, and she is completely satisfied with the aesthetic result of her procedure (Figure). 

The number of individuals suffering from diabetes mellitus is continually increasing; therefore, clinicians can expect the number of patients who present with foot ulcers to increase. Lower limb ulcerations are the leading cause of hospitalization in patients with diabetes mellitus and are a great cause of morbidity in this population.^7-9,12 

The development of DFUs is multifactorial, generally due to peripheral vascular disease, peripheral neuropathy, and immunopathy affecting about 15% of the diabetic population at some point during their life.^13,14 This triad not only leads to pedal ulcerations but also increases the susceptibility to soft tissue and osseous infections, which can ultimately lead to amputation, loss of limb, and life. In addition, it can lead to Charcot foot syndrome, a serious and potentially limb-threatening lower extremity complication of diabetes characterized by varying degrees of bone and joint disorganization secondary to underlying neuropathy, trauma, and changes in bone metabolism. In this patient population, who has any degree of soft tissue injury, the restoration of an intact skin barrier is of utmost importance, thus preventing a portal of entry for infection. Ideally, this is accomplished in a manner that minimizes wound contraction to maintain function and minimize cosmetic disfigurement.¹⁰

The ability of the skin to repair itself after injury is vital to human survival and is disrupted by a spectrum of disorders. The process of cutaneous wound healing is complex, requiring a coordinated response by immune cells, hematopoietic cells, and resident cells of the skin.⁴ In chronic wounds, successful wound closure requires a comprehensive approach that includes the careful consideration of suitable surgical techniques and critical patient factors. The surgeon must have a clear understanding of key concepts such as wound healing, graft design, and patient risk assessment as this is imperative to a favorable outcome.³

A skin graft is a unit of skin taken from one part of the body and used to repair a defect elsewhere. The use of STSGs is the most commonly performed procedure used to close defects unable to be closed by simple wound-edge approximation. ⁵ Skin grafts are further classified according to origin and thickness and can be autograft, allograft (homograft), xenograft (heterograft), and isograft (syngenic) depending on the sources. Split-thickness skin grafts are subdivided into thin, medium, and thick (Table).

Skin grafts completely lack their own blood supply and therefore rely entirely on the blood supply of the recipient bed. Thus, they are limited by the vascularity of the area they are resurfacing. Because they are relatively thin, STSGs have fewer metabolic requirements compared with FTSGs. This makes them the ideal material for resurfacing wounds that offer less than ideal conditions. Unfortunately, they also are more fragile than FTSGs and can produce a worse aesthetic outcome.

Split-thickness skin grafts are useful when a large surface area needs to be covered. Since STSG donor sites can heal spontaneously, they can be reharvested. This is opposed to flaps and FTSGs, which have a limited supply, particularly if multiple types of tissue are needed (eg, flaps bearing bone, periosteum, fasciocutaneous, and muscle components).⁶ For both chronic and acute wounds, STSGs offer a rapid and effective way to provide closure and healing.¹¹ Historically, this technique has a significant role in burn wounds and plastic surgery reconstruction but also has been implemented successfully for the treatment of chronic DFUs.^15-17 There is a wide variety of wound care products and synthetic grafts available to the surgeon today, but STSGs remain the gold standard and are considered a first-line treatment for lower extremity wounds associated with diabetes.¹² The availability of STSGs and FTSGs gives the surgeon a wide spectrum of treatment options but also requires great expertise in this field.

McCartan and Dinh¹⁸ observed that when STSGs were used as the primary closure technique on DFUs, 78% were successful at closing 90% of the wound by 8 weeks. Audrain et al¹⁹ evaluated the outcome of FTSGs in order to repair lower limb defects. They conducted a retrospective review of 50 consecutive patients who underwent FTSGs to cover defects below the knee. They concluded that the graft take was good in 44 patients (88%), moderate in 5 patients (10%), and poor in 1 patient (2%) at day 30. Complications such as infections and ulcerations were infrequent.¹⁹ They found no significant association between the graft size and graft take and concluded that the FTSG is an effective method for repairing defects of the lower limb. The aftercare of FTSGs also was found acceptable, with 86% of patients requiring ≤ 5 visits for secondary care.¹⁹

Due to the complexity of the disease, patients with diabetes who present with leg ulcers frequently have some other forms of comorbidity or associated conditions. It is because of this that surgeons must be aware of and avoid any possible complications that may result. Anderson et al¹² retrospectively reviewed 107 patients with diabetes who received a STSG for the treatment of a nonhealing DFU or leg ulcer. Their goal was to describe healing times based on patient characteristics, comorbidities, or complications. They observed a very low (2.8%) complication rate and an average wound healing time of 5.1 weeks for all patients who received a STSG for the treatment of a DFU or leg ulcer. None of the patient characteristics or comorbidities in this study appeared to affect STSG healing times. They did observe an average increase in healing time among patients with complications (12.0 weeks) compared with those without complications (4.9 weeks). The patients with decreased graft take also had prolonged healing times. These findings¹² emphasize the importance of patient screening and preparation in order to minimize any mechanical or biological barriers that may affect STSGs and wound healing. They concluded that autologous STSGs are a safe and reliable alternative for the treatment of nonhealing diabetic foot and leg wounds. 

Despite success using STSGs in procedures and wound care, there remain relatively few studies addressing its use in diabetic lower extremity wounds. Recently, Ramanujam et al²⁰ retrospectively reviewed 83 patients with diabetes who were treated with STSGs for diabetic foot and ankle wounds and reported a median time to healing of 6.9 weeks among those patients without complications. Puttirutvong et al²¹ compared the healing rates of meshed versus non-meshed STSGs in 42 patients and found no significant difference. The mean healing time for the meshed group was 19.84 and 20.36 days for the non-meshed group. This result is similar to STSG healing times in the non-diabetic patient population, which was found to be between 2 and 4 weeks.²¹ Due to the nature of the disease, impaired healing in patients with diabetes can be attributed to multiple factors, including impaired macro- and microcirculation, peripheral neuropathy, endothelial dysfunction, and poor glycemic control.^22-25 Ramanujam et al²⁰ showed that patients with diabetes and without comorbidities had no significant difference in healing times compared with those without diabetes for STSG; however, compared with patients with diabetes and comorbidities, there was a significant difference. Overall, the healing time was found to be 1.99 weeks longer in those with diabetes.²⁰ 

When compared with patients without diabetes mellitus, patients with diabetes experience a 5.15 times higher risk of postoperative complications after STSG procedures, which may include wound dehiscence, infection, and the need for revisional surgery.¹¹ Patients with diabetes and comorbidities are at a significantly higher risk for delayed healing from STSG procedures compared with those without comorbidities and patients without diabetes. For patients with diabetes, the presence of any pre-existing comorbidity, history of amputation, or trauma is negatively associated with the successful outcome of STSG take. Furthermore, factors such as the duration of diabetes, hemoglobin A_1c level, chronic kidney disease, blood urea nitrogen level, and creatinine concentration represent conditions that need to be addressed when selecting patients for STSG transplant in diabetic foot wounds. Therefore, it is suggested that a complete and detailed medical and surgical approach is taken in order to maximize the STSG success.¹²

It is important that the ideal conditions for successful STSG are present in order to achieve the best possible result for the patient. These factors include red granulation tissue dominating the wound bed, no visible tendon or bone, no discernible sloughing or exudate in the wound, no residual necrotic tissue, no local signs of soft-tissue infection, no systemic signs of infection, and no severe peripheral arterial disease.²⁵ Successful incorporation of STSG requires vascularized granulation tissue and given the high prevalence of peripheral vascular disease in the diabetic population, it is important to identify the need for patient co-management with vascular surgeons.

Grafts initially survive via diffusion, called plasmatic imbibition, and subsequently inosculation, and revascularization occurs. Immediately after a skin graft is placed on the recipient bed, a fibrin network develops, providing a scaffold necessary for graft adherence. During the first 48 hours, the graft becomes engorged with plasmatic fluid by means of diffusion; a poorly vascularized bed requires a longer period of plasmatic imbibition before the graft is revascularized. The in-growth of capillary buds from the recipient bed into the open vessels on the undersurface of the graft occurs within 2 to 4 days (ie, inosculation). Revascularization is thought to be directed by angiogenic factors and can be restored within 5 to 7 days. Thin grafts of skin are revascularized more rapidly than thick grafts while lymphatic circulation, which is established by the fifth day, may aid in decompressing the increased graft interstitial fluid. Within the first week of graft placement, the thickness of the epidermis can increase 7- to 8-fold. Dermal fibroblasts proliferate at a rapid rate within the healing skin grafts following an initial decrease of about 3 days. By the seventh to eighth day, there is a marked hyperplasia of fibroblasts as the graft begins to heal. The recovery of sensation in humans can begin as early as 1 to 2 months postoperatively and may be abnormal during the first year. Full-thickness skin grafts appear to achieve better sensation than STSGs, although the rate of return of innervations is faster in STSGs. Graft failure rates are primarily attributed to infection, highlighting the importance of biofilm management and the need for initial antibiotic therapy. The prevention of shearing, seroma, and hematoma formation beneath the graft is also important to allow for the initial take and graft incorporation.¹¹

Prior to graft application, any source of bacteria and necrotic tissue should be addressed by the surgeon. Necrotic tissues in a wound should be removed since it prevents proper assessment of the wound bed and also can be a source of bacterial growth. When present, bacterial colonies have a negative effect on normal components of wound healing. Bacteria also may form biofilm on the wound surface; it is resistant to commonly used antibiotics and makes treatment difficult.^26-35 Biofilms show increased resistance to antimicrobial, immunological, predatory, and chemical treatments^28-30 and, once established, are highly resistant to removal and eradication.³⁶ The reason acute wounds progress through stages of healing, while chronic wounds appear to stall in the inflammatory stage, is most likely due to the persistent bacterial colonization,³⁷ leading to persistent inflammatory responses with abnormal cytokine and matrix metalloproteinase levels. ^38,39 James et al⁴⁰ reported the presence of biofilms in 60% of chronic wounds, defined as open for at least 30 days, versus 6% of acute wounds. Unlike most infections, a mature biofilm develops within 10 hours and remains indefinitely while the wound remains open.⁴¹ Once matured beyond the 48 hours, the biofilm becomes increasingly resistant to antibiotics.³⁶ It is important that the physician recognizes the 6 most common features that identify the presence of a bacterial biofilm in human chronic wounds⁴²: a pale wound bed, friable granulation tissue, a yellow discharge, necrotic tissue, a clear slime, and a putrid smell. In DFUs, a biofilm diagnosis is generally derived from clinical signs (ie, wound bed color change, friable granulation tissue, abnormal odor, increased serous exudates, and pain at wound site) and symptoms of inflammation. 

Due to the duration of development and slow healing times, virtually all chronic diabetic wounds contain bacteria. The level of infection may range from contamination, colonization, or critical colonization to infection.⁴³ The impact of bacteria in a wound depends on 3 factors: bacterial load, bacterial strain virulence, and the capability of the host to mount resistance. In patients with diabetes, the effect of bacterial loads can be observed even at a lower count or with the normal skin flora due to the patient’s weak immune system and impaired leukocyte function. In patients with DFUs, the associated infections are most commonly polymicrobial and contain both aerobic and anaerobic bacteria.⁴⁴ The most common bacteria observed in chronic wound infections are Staphylococcus aureus (93.5% of ulcers), E faecalis (71.7%), Pseudomonas aeruginosa (52.2%), coagulase-negative staphylococci (45.7%), Acinetobacter baumannii (13%), and Klebsiela pneumonia (6.5%).^40,45 

Studies^46,47 also have reported the presence of antibiotic-resistant bacterial species in biofilms, in particular methicillin-resistant S aureus (MRSA), vancomycin-resistant Enterococcus, and multidrug-resistant A baumannii. It is important to perform a preoperative wound swab in order to identify subclinical bacterial wound bed colonization as well as specific strains of bacteria, such as P aeruginosa or S aureus, which can have detrimental effects on graft take.^48,49 However, physicians frequently question whether a near-sterile wound bed is required for successful skin grafting, because not all wounds can be cleared from bacteria despite prolonged antibiotic administration and sustained wound bed preparation.¹¹ In an analysis by Aerden et al,²⁵ wound swabs that were taken immediately before grafting showed that about half of the wound beds (53%) had been contaminated, while the other half (47%) were found to be sterile. In 5 cases, MRSA was detected, and either P aeruginosa or S aureus was detected in 23% of the wounds. Contaminated wounds did not display a lower mean graft take percentage than near-sterile wounds (87% vs. 90%, respectively). Wounds containing either P aeruginosa or S aureus were found to have an inferior outcome (mean take percentage, 78.9% vs. 91.3%, respectively), whereas diabetes also appeared to be a deteriorating factor in graft take success (mean take percentage, 83.0% vs. 90.7%).²⁵ 

Surgeons often employ debridement techniques in order to reduce the bacterial burden within the wound. It also controls ongoing inflammation and encourages the formation of granulation tissue.⁴³ The goal of debridement is to create a chronic wound molecular and cellular environment that resembles that of acute wounds in order to allow rapid healing. For this to occur, it is often found that nonhealing wounds may require repeated debridement before an adequate wound site has been prepared.¹¹

Another useful technique available to the surgeon involves the use of NPWT to stimulate granulation tissue and help remove fibrotic tissue formation.^5,18,50 Negative pressure wound therapy has been shown to provide many aspects of graft success by promoting the growth of granulation tissue, lowering bacterial counts, and removing accumulated fluid, such as hematoma/seroma^10,50-56; it also can be a useful tool in biofilm reduction. Morykwas et al⁵⁷ and Timmers et al⁵⁸ suggest NPWT promotes and shortens wound healing time through the evacuation of unwanted fluid, promotion of angiogenesis, granulation tissue formation, and biofilm reduction. Gabriel et al⁵⁹ demonstrated fewer days of treatment, more rapid wound closure, and fewer hospital days with the use of NPWT. This therapy finds a role both before and after skin grafting. It decreases bacterial load, assists with wound bed preparation, helps fixate the graft, and reduces fluid accumulation. Graft take and complication rates have significantly been improved since the introduction of NPWT.¹¹ 

This also was observed by Blume et al⁶⁰ who compared a conventional therapy (CT) dressing (cotton bolster/sterile compressive/stainless steel gauze dressing used for at least 5 days) to NPWT using reticulated open cell foam (ROCF). One hundred forty-two patients underwent STSG placement, of which 79 wounds were DFUs. Grafting area was similar between NPWT/ROCF (45.4 cm²) and CT (47.4 cm²). Mean graft take at the first follow-up was 95% for NPWT/ROCF compared with 86% for CT, with maximum graft take of 96% for NPWT/ROCF compared with 83% for CT. There were significantly fewer repeated STSGs required in the NPWT/ROCF group (3.5%) compared with the CT group (16%). They concluded there were fewer complications (eg, seroma/hematoma/infection) and less graft failure in the NPWT/ROCF group compared with the CT group.⁶⁰ 

A similar conclusion was made by Zhang et al,⁵¹ who found in their prospective case-control study of 81 patients that their study group exhibited a significant lower infection rate and pain score during the removal of the inner layer at the first dressing change after skin grafting compared with those of the control group (P < .05). The time interval between skin grafting and first postoperative change was longer in the study group than that in the control group (P < .01); the study group showed a significantly shorter 95% wound healing time (P < .05).⁵⁷ The survival rate of microskin autografts in the study group was higher than in the control group (P < .05). Their results support the findings that NPWT is beneficial for wound closure after skin autografts and that it prolongs the interval between skin transplantation and first postoperative dressing change, reduces pain during removal of inner layer dressing, increases skin graft survival rate, and shortens wound healing time.⁵¹

Based on the wide range of information and studies that support the use of NPWT, surgeons must take these findings into account when faced with an open wound, regardless of infection status. Negative pressure wound therapy has been found to be a safe, well-tolerated, and effective method in the treatment of DFUs and should therefore be applied before (ie, wound bed preparation) and after (ie, minimizes graft failure) graft application.⁶¹

Open foot wounds are a common complication and comorbidity often seen in patients with diabetes. They are a source of bacterial infection and may lead to systemic infection, amputation, or even death.  Therefore, it is important that the physician recognize this concern and proceed in closing the defect as soon as possible in order to minimize any complications, reduce hospital time spent, and decrease the recovery period. Prior to any procedure, proper patient preparation is imperative. This includes alleviating any local infection that is often present in wound sites since this is a key factor in successful graft application. Once the defect has been prepared, skin grafting provides the best method of wound closure in this population. Skin grafts (STSG and FTSG) combined with NPWT reduced the comorbidities seen in the patient reported herein, while offering a quicker, more cost-effective, and safer technique of wound closure compared with traditional nonoperative methods.

For diabetic wounds, the combination of skin grafts with NPWT before and after graft application reduces the comorbidities and complications often seen in patients with diabetes. Using this method offers a quicker, more cost-saving, and safer technique of wound closure compared with traditional nonoperative methods. 

Authors: Sanda Smuđ-Orehovec, MD¹; Marko Mance, MD¹; Damir Halužan, MD²; Vilena Vrbanović-Mijatović, PhD³; and Davor Mijatović, Prof. PhD¹

Affiliations: ¹University Hospital Rebro, Department of Plastic, Reconstructive and Aesthetic Surgery, Zagreb, Croatia; ²University Hospital Rebro, Department of Vascular Surgery; and ³University Hospital Rebro, Department of Anesthesiology and ICU

Correspondence: Marko Mance, MD, University Hospital Rebro, Department of Plastic, Reconstructive and Aesthetic Surgery, Kišpatićeva 12, Zagreb, Croatia; markomance@gmail.com 

Disclosure: The authors disclose no financial or other conflicts of interest.