Managing Lower Extremity Wounds In Obese Patients

Given the challenges of treating wounds in obese patients, these authors discuss key factors ranging from excess adipose tissue and venous insufficiency to oxidative stress and lymphedema, and offer insights from the literature on treatment options including compression wraps and complete decongestive therapy. 

Obesity is a chronic disease that has proven to complicate the management of lower extremity wounds. This worldwide pandemic has not only affected the management of lower extremity diseases but has had profound impacts on the global healthcare system at large.

In 2014, the World Health Organization found that about 2 billion people were overweight, half of whom were obese.¹ An estimated 2.8 million people die each year from obesity and obesity-related medical problems.¹ The United States spends roughly $100 billion annually on treating obesity and its complications.

Today, obesity can be linked to many comorbidities such as diabetes, coronary artery disease, hypertension, osteoarthritis, chronic kidney disease, cancer, metabolic syndrome and others.² According to the Obesity Society, about 90 percent of people living with type 2 diabetes are obese.² These rising numbers, in addition to the many effects diabetic complications have on wound healing, contribute to the difficulty podiatric surgeons face when treating wounds in the obese population.

Lymphedema and venous insufficiency are among the most notable complica-tions that arise in obese patients. In addition, excessive adipose tissue can increase the risk for infection and compromise the vasculature needed for wound healing.^3,4

Accordingly, let us take a closer look at the intricacies of how lymphedema and excess adipose tissue impact wound healing in the bariatric population. Having a strong understanding of these issues will help optimize care when managing lower extremity wounds in patients with obesity.

A Closer Look At Adipose Tissue Anatomy

Authors have previously described adipose tissue as relatively avascular. However, a study by Markman and colleagues took a closer look at the anatomy and physiology of adipose tissue.⁵ The authors found that adipose tissue is separated into lobules, each made up of thousands of fat cells carrying large vessels and neurons. Excess adipose tissue increases the demand on the circulation. Accordingly, obesity leads to vascular insufficiencies because the capillary density does not increase proportionately to the increase in adipose tissue.^5,6 This newly created fibrotic and rigid environment within the adipose tissue further restricts capillary proliferation. Obese patients have a greater number of large vessels. Due to a greater diffusion barrier, larger vessels are not able to deliver oxygen as efficiently as capillaries.^4,5 All things considered, the increased number of larger vessels and decreased density of capillaries contribute to the hypoxic environment of excessive adipose tissue.

Understanding the delicate anatomy of fat lobules and capillary diffusion enables the podiatric surgeon to decrease the rate of graft failure when applying full-thickness skin grafts. Residual adipose tissue attached to the graft inhibits epithelial cell migration and capillary ingrowth into the donor skin, which is essential for the graft’s survival.^5,7 The terminal capillary inflow of fat lobules in combination with fewer capillary links impedes revascularization of the graft, leading to failure. Therefore, one should remove residual adipose tissue from the inferior aspect of the graft before application to the donor site for maximum results.  

What You Should Know About Decreased Vascularity In Obese Patients

There are many studies debating the overall vascularity of adipose tissue. Many studies support the inherent decreased vascularity as we mentioned above. However, a few studies argue that undisturbed adipose tissue is well perfused and that trauma and surgical incisions stimulate ischemic conditions.⁸ Regardless, most studies support the findings of heightened release of certain glucocorticoids with increased adipose tissue as a result of increased type VI collagen. Glucocorticoids inhibit angiogenesis.⁹ In addition, tissue hypoxia leads to overexpression of type I and III collagen, which further stimulates a fibrotic environment within fat lobules.⁴ Overexpression of these factors suppresses the angiogenic process needed to support revascularization and provide an optimal medium for wound healing.

Venous insufficiency is another problem bariatric patients face. Venous insuffi-ciency causes chronic wounds and delays wound healing, thus increasing the risk for infection. Once venous function in the lower extremity is disrupted, fibrosis and clots occur in the capillaries as a result of the protein accumulation in the interstitium surrounding these smaller vessels.^10,11 An inflammatory response tends to occur from the leaked intravascular components as a consequence of the increased hydrostatic pressure. Altogether, these factors create a barrier around capillaries and subsequently decrease the diffusion of oxygen and nutrients needed to supply tissue and support wound healing.^4,10,11 Pro-inflammatory mediators and leukocytes can leak into the interstitium, where they become trapped, leading to further tissue destruction.  

Key Insights On Oxidative Stress

Obesity also predisposes patients to tissue damage and impaired wound healing by oxidative stress. This is partly due to a deficiency in adiponectin, a cytokine that protects against oxidative stress and inflammation. Adiponectin plays a crucial role in the reepithelialization of wounds and stimulation of angiogenesis in response to ischemia. Therefore, a deficiency in adiponectin impairs perfusion and the tissue repair of wounds.

The immune system requires oxygen to combat against infection. A defective oxidase system in the adipose tissue of obese patients may predispose them to developing infections from surgical sites and ulcers. A study by Anaya and coworkers showed that a deficiency in the oxidase system of leukocytes interrupted the efficacy of phagocytosis due to a block in the oxygen consumption required for bacterial death.¹² The authors’ research demonstrated that without oxygen, leukocytes could ingest bacteria but not kill them. Researchers have found bacteria cultured from infected wounds of obese patients to be similar to longstanding wounds of patients with chronic granulomatous disease, in whom the main issue is a defective oxidase system.^4,12

Collagen synthesis is an integral aspect of wound healing because it contributes to the integrity and tensile strength of the wound. The absence of oxygen inhibits fibroblasts from synthesizing collagen.¹⁰ The combination of impaired oxygen perfusion and insufficient vascular supply hinders damaged tissue from producing collagen to necessitate healing in the setting of trauma or ulcer development.^10,13 Wound healing is impaired in obese patients because the mechanical strength is inadequate due to the disorganized collagen fibers lacking the efficiency for appropriate wound recovery.         
                                                                                                         
When Obese Patients Develop Lymphedema

Lymphedema is an incurable, chronic, progressive disease common in obese patients. Several studies have postulated that specific gene sequences are responsible for abnormal lymphatic system development, which can cause site-specific fat deposition.¹⁴

Physicians often confuse lymphedema with lower extremity edema caused by medical issues such as cardiac failure, kidney failure, deep vein thrombosis, malignancy and venous insufficiency. It is caused by the accumulation of protein-rich fluid in the lymphatic system. It presents similar to venous insufficiency in the fact that hydrostatic pressure builds up and pulls protein-rich fluid into the interstitium, where an inflammatory process may begin due to the leaked pro-inflammatory cytokines from the vascular network. Without early treatment, the limbs may enlarge due to fibrosis and hypertrophy of adipose tissue from the inflammation with profound tissue damage and subsequent skin breakdown. This can become a debilitating process from the lack of mobility and pain from ulcerations.

There are several modalities at the physician’s disposal for identifying lymphedema when the cause of lower extremity swelling is unclear. A study by Monnin-Delhom and coworkers found computed tomography (CT) to be 93 percent sensitive and 100 percent specific for diagnosing lymphedema.¹⁵ Research by Kerchner and colleagues found a honeycombed subcutaneous edema pattern on magnetic resonance imaging (MRI) to be specific for lymphedema.¹⁶ However, lymphoscintigraphy has been considered the gold standard in identifying the cause of lower extremity swelling. From a clinical standpoint, the swelling in lymphedema often occurs in the digits in comparison to other types of edema that usually spare the digits.

Most obese patients who walk into the podiatric office will have secondary lymphedema, which is caused by disruption or obstruction of the lymphatic pathways. The problem most obese patients with lymphedema face is lack of recognition of lower extremity swelling, late diagnosis and absence of treatment by the caregiver, whether it be the primary care doctor or podiatrist.¹⁷ A study by Maclellan and colleagues found that two-thirds of all lymphedema cases go undiagnosed or have a late recognition.¹⁷ This creates a slew of problems for podiatric physicians when addressing wounds or follow-up appointments for patients with diabetes. A study by Ridner and coworkers found that patients with lower extremity lymphedema are predisposed to a greater chance of infection and more frequent hospitalization.¹⁸

What Challenges Do Pressure Ulcers Pose In Obese Patients?

The bariatric population is extremely susceptible to pressure ulcers. The excessive weight gain predisposes soft tissue breakdown over areas of bony prominences that have been exposed to external pressures long enough to cause cellular necrosis.

Tissue pressures that exceed 32 mmHg for an extended period of time will cause pressure necrosis.¹⁹ The onset of ulceration presents a new challenge for the obese patient to self-manage, often leading to non-adherence.

A Guide To Treating Wounds In Obese People

When managing wounds in the obese patient, podiatric caregivers must remember that they are not only treating the wound but complications correlating to obesity as well.

Treatment of ulcerations secondary to venous insufficiency should be geared toward preventing infection of the ulcer.

Active infections can pose a serious threat in the obese population. While clinicians should start antibiotics in the setting of active infection, adequate delivery to tissues can be difficult due to the relative avascular environment present in excessive adipose tissue along with impaired diffusion across larger vessels as we mentioned earlier.⁴ If the ulcer is not infected, treatment should consist of providing an environment where the wound can heal. Accordingly, treatment can consist of the application of hydrocolloids, enzymatic debridement agents and non-adherent dressings.

In addition, one should apply compression wraps if there is no history of cardiac failure. A Profore compression wrap (Smith and Nephew) is a good choice in treating patients with an ulcer while also combating the lower extremity swelling. However, like most dressings, Profore wraps are only as durable as the environment patients put them in. The everlasting battle with many patients is non-adherence. Profore wraps can stay on up to a week and the expectation of keeping this compression wrap clean and intact can be unrealistic. The infected ulcer may require a trip to the operating room for debridement. Patients with venous ulcerations tend to be neurologically intact and office debridements can be too painful for the patient to tolerate. Surgical debridement may offer a better alternative in addition to compression therapy.

The internationally recognized standard of care for lymphedema is complete decongestive therapy, which simply breaks down into the following essential components: skin care, manual lymphatic drainage, compression and exercise. Complete decongestive therapy is divided into two phases based on the intensity required for the severity of the disease.

Phase 1 is typically indicated for inpatient therapy by a lymphedema therapist with the goal being maximal volume reduction and normalization of tissue. According to Foldi and Foldi, phase 1 is indicated for patients who require at least two therapy sessions a day or if previous outpatient therapy has failed.²⁰ However, in the United States, lymphedema treatment primarily happens in an outpatient setting, where services do not have the necessary means of providing the appropriate therapeutic intensity for patients with severe disease and mobility restrictions.

Phase 2 of complete decongestive therapy involves the patient assuming the responsibility of care for maintaining the results achieved in phase 1. Phase 2 ultimately becomes a lifelong process that the patient will have to undergo. Patients may require an adjustment in blood pressure medications by their primary care physician.

Boris and coworkers did a study on 18 patients with unilateral lower extremity lymphedema, four patients with bilateral lower extremity lymphedema and 16 patients with upper extremity lymphedema.²¹ Treatment consisted of complete decongestive therapy for four hours a day. The patients with upper extremity lymphedema had an average reduction in their lymphedema of 73 percent and those with unilateral lower extremity lymphedema averaged an 88 percent reduction.

Another study by Lieo and coworkers examined 30 women, 18 with unilateral upper extremity lymphedema and 12 with unilateral lower extremity lymphedema.²² Patients had complete decongestive physical therapy consecutively for four to 21 days with the average length of intervention being 13.13 ± 4.68 days. The average reduction in lymphedema volume following intervention was 67.8 percent ± 33.2 percent for the upper extremity and 68.1 percent ± 35.9 percent for the lower extremity.

Despite the effectiveness of complete decongestive therapy, much of the literature is confined to the upper extremity with lymphedema secondary to breast cancer. There are several limitations to complete decongestive therapy. It can be labor intensive and therapy sessions can last up to four to six hours. Depending on the severity of the disease, patients could require an average of four sessions a week. Furthermore, insurance coverage tends to be a limiting factor for many obese patients that require more extensive therapy.

Once wounds become stable, compression therapy appears to be the mainstay of treatment for lower extremity swelling whether it is a pneumatic compressive device or a multilayered wrap the patient wears once he or she is able to ambulate in public or at home. A FarrowWrap (Jobst USA) offers a good alternative form of compression in those patients who have difficulty putting on a compression stocking or have upper extremity weakness. A FarrowWrap is an easy to slip on compression garment with multiple adjustable bands that patients tighten individually from distal to proximal on the lower extremity. This offers different levels of compression based on the degree of swelling and the patient’s activity level.

Damstra and colleagues performed a prospective, randomized controlled study on the autonomous use of custom adjustable compression wraps to treat moderate to severe lower extremity lymphedema in an inpatient setting.²³ The authors found significantly greater volume reduction after 24 hours in comparison to multilayer compression bandaging.

In Conclusion

Podiatric surgeons face many different obstacles when treating wounds in the bariatric population. First and foremost, it is important for the podiatric caregiver to distinguish between the causes of peripheral edema to exclude different underlying etiologies and direct appropriate management, especially when treating wounds.

Bariatric patients have difficulty managing their own wounds and this often creates more problems for the podiatric surgeons from an adherence standpoint. Patients with severe obesity are unable to change their dressings and apply the proper wound care products, which increases the risk for infection. People with lower extremity edema and lymphedema reportedly have lower household income and inadequate insurance coverage.²⁴ This further leads to missed follow-up appointments and non-adherence issues in the self-management of wound care and lower extremity swelling.

There are numerous wound care products at a podiatrist’s disposal. However, one must consider the cost in their application from an insurance perspective. With that said, expensive wound products can prove ineffective in the setting of excessive adipose tissue. Ulcerations can be the result of excessive weight gain leading to greater plantar pressures in the foot, inflammatory processes from excessive hydrostatic pressure buildup and impaired angiogenesis from excessive adipose tissue. In the context of wound healing, it only makes sense to target therapy toward the etiology of the wound in addition to maintaining a healthy environment for the wound to heal and avoid infection.

Current and older literature reports that treating only the wound without ad-dressing the obesity-linked complications of lymphedema or venous insufficiency is futile. Working with the primary caregiver to combat both is crucial for a successful outcome of wound healing in the bariatric population.

Dr. Garwood is an Assistant Professor in the Department of Plastic Surgery at MedStar Georgetown University Hospital in Washington, DC.

Dr. Mizuo is a first-year resident in the Department of Plastic Surgery at MedStar Georgetown Washington Hospital Center in Washington, DC.

References

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