At my wound center, I recently had several patients whom I was treating for leg ulcers. At first glance, the ulcers seemed like classic venous wounds. After reviewing the patient histories, the one thing that they all had in common was a history of deep vein thrombosis (DVT). If one refers to venous stasis syndrome occurring after a DVT, an appropriate term is “postthrombotic syndrome.” Prior to this research, I was familiar with postthrombotic syndrome but was unsure of the best way to treat these patients. Postthrombotic syndrome or postphlebitic syndrome is a medical condition that can develop in patients who experience a DVT in the leg. When the body tries to heal from these clots, the valves in the veins are often damaged. The obstruction of the veins and the destruction of valves lead to impaired blood flow. It is a result of venous hypertension, which occurs as a consequence of recanalization of major venous thrombi. This leads to patent but scarred and incompetent valves or, less frequently, persistent outflow obstruction produced by large proximal vein thrombi. Recanalization and valve destruction result in a malfunction of the muscular pump mechanism, which leads to increased pressure in the deep veins of the calf. This high pressure results in progressive incompetence of the valves of the perforating veins of the calf. When this occurs, blood flow directs from the deep vein into the superficial system during muscle contraction, leading to edema and impaired viability of subcutaneous tissues and, in its most severe form, ulceration of venous origin. Symptoms include chronic leg pain, swelling, redness and sometimes ulcers. Post-thrombotic syndrome affects an estimated 330,000 people in the United States with 23 to 60 percent occurring two years following DVT of the leg.1,2 Approximately 60 percent of patients will recover from a leg DVT without any residual symptoms. Forty percent will have some degree of postthrombotic syndrome, 4 percent will have severe symptoms and 10 percent develop venous ulcerations. Symptoms usually occur within the first six months but can occur up two years after the clot. What are the risk factors of postthrombotic syndrome?3 History of proximal deep vein thrombosis (above the knee) Having more than one blood clot in the same leg more than once Still having blood clot symptoms one month after being diagnosed with the blood clot Obesity Difficulty with international normalized ratio levels during the first three months after starting anticoagulants Symptoms include:3 Chronic aching Swelling Fatigue Heaviness Edema Hyperpigmentation Subcutaneous fibrosis in the affected limb Venous claudication Venous leg ulcers Preventing And Treating Postthrombotic Syndrome Prevention is the key to preventing complications after a DVT. If a person has leg swelling after an acute DVT, he or...

The extracellular matrix is the largest component of normal skin, providing skin with its properties of compressibility, elasticity and tensile strength.1 It is comprised of connective tissues and fibers that provide support but are not part of a cell The extracellular matrix’s cellular scaffolding signals the direct cells to divide, differentiate and build themselves into a specific form.1 In healthy skin, the extracellular matrix helps support cells and comprises key components of the basement membrane, which anchors and helps replenish epidermal cells. Extracellular matrices have a variety of functions including: • cell communication within tissue and tissue formation • structural and biochemical support to the surrounding cells • cell adhesion, cell-to-cell communication and differentiation • support, segregating tissues from one another, and regulating intercellular communication • sequestering of a range of cellular growth factors and acts as a local store • regulation of a cell’s dynamic behavior • being an essential component of processes like cell growth, wound healing and fibrosis • holding cells together to form a tissue The components of extracellular matrices include proteins, such as collagens, laminins, fibronectin and elastins. Collagen is the most abundant fibrous protein within the interstitial extracellular matrix and constitutes up to 30 percent of the total protein mass.2 Extracellular matrices also include glycoproteins, glycosaminoglycans and proteoglycans. The extracellular matrix is integral to each phase of wound healing, interacting with cells and growth factors in a dynamic process that eventually results in wound closure. When the extracellular matrix is dysfunctional, wound healing slows or stalls. Chronic wounds contain increased levels of inflammatory cells, giving rise to elevated levels of proteases that appear to degrade the extracellular matrix components, growth factors and receptors that are essential for healing.1 Understanding of the importance of re-establishing a functional extracellular matrix in chronic wounds has led to technical advances and the development of products that reduce excessive protease levels or contribute functional extracellular matrix proteins, thereby facilitating the healing process. Such products include Oasis Wound Matrix (Smith and Nephew), an intact matrix that is derived naturally from porcine small intestinal submucosa. When one applies extracellular matrix to a wound, it does not trigger an immune response. Instead, when it begins to break down into surrounding tissue, it causes the cells in that tissue to start repairing the damage. Cells divide and rebuild, creating new, normal tissue, not scar tissue. References 1. Schultz GS, Ladwig G, Wysocki A. Extracellular matrix: review of its roles in acute and chronic wounds. World Wide Wounds. Available at   http://www.worldwidewounds.com/2005/august/Schultz/Extrace-Matric-Acute-Chronic-Wounds.html . Published August 2005. Accessed Jan. 6, 2015. 2. Boundless. An overview of the extracellular matrix found in animal cells. Boundless Anatomy and Physiology. Available at https://www.boundless.com/physiology/textbooks/boundless-anatomy-and-physiology-textbook/cellular-structure-and-function-3/external-cellular-components-47/an-overview-of-the-extracellular-matrix-found-in-animal-cells-350-11461/ . Published July 3, 2014....

While attending a conference a several weeks ago, I ran into a colleague whose passion and expertise, like mine, is wound care. Our conversation centered upon the topic of nutrition and how often as doctors, we omit the patient’s dietary habits in our treatment strategies. We are so focused on healing the wound that we may overlook the basics that would assist the healing process. Typically as physicians, when we treat an ulcer, we are focused on the wound bed itself. In these situations, the patient often has several comorbidities typically including uncontrolled diabetes, which may translate into a poor diet and eating habits. While patients should be monitoring their blood glucose level daily, we need to monitor their nutritional status. I currently am a physician panelist at a Healogics wound care center in the Washington, DC area. In addition to the standard lab tests, while not mandatory, I have started a new process of ordering baseline nutritional markers to establish a baseline with my patients. Standard lab tests  ● Basic blood work ● Complete blood cell (CBC) with differential ● CHEM-7 panel ● HbA1c Additional nutritional markers ● Albumin (normal 3.4-5.4 g/dL) ● Prealbumin (normal 15-36 mg/dL) ● Any additional labs depending on the patient’s medical history A serum albumin test measures the amount of albumin in the clear liquid portion of the blood. This test can help determine if a patient has liver disease or kidney disease, or if the body is not absorbing enough protein. The body uses prealbumin as a building block to make other proteins. You might order this test if the patient appears to be malnourished or if you want to follow the patient’s nutritional progress. One should monitor the results of these tests periodically and discuss them with patients to educate them on how their nutritional diet impacts their health and the wound healing process. When there are abnormal nutritional results, the patient should get a referral to an endocrinologist or nutritionist for further evaluation. In addition to focusing on the wound, we need to remember to evaluate what is feeding the wound for total patient care. Looking at the whole picture and leveraging a more expanded team approach to include nutrition, in my opinion, is the missing link in wound treatment. Suggested Reading 1. Available at http://www.nlm.nih.gov/medlineplus/ency/article/003480.htm . Published Feb. 13, 2013. Accessed April 22, 2014. 2. Available at http://blog.beckydorner.com/2013/12/use-of-serum-albumin-and-prealbumin-… . Accessed April 22, 2014. 3. Available at http://www.webmd.com/a-to-z-guides/total-serum-protein . Published Nov. 4, 2011. Accessed April 22, 2014. Original Posted on Podiatry...

Recently my organization, the American Association for Women Podiatrists, hosted a scientific conference in San Diego. One of the speakers was Marie Williams, DPM, who discussed the advances in regenerative medicine in wound care. Listening to her presentation left me with more questions. Here is what I found. The Centers for Disease Control and Prevention (CDC) has projected that by 2050, as many as one out of three U.S. adults could have diabetes.1 As many as 25 percent of patients with diabetes will develop an ulceration in their lifetime.1 The goal is to heal these wounds in the fastest manner possible in order to prevent infection, ulceration and amputation. If an ulcer does not respond appropriately to standard care at four weeks, then it requires re-evaluation of the current treatment plan and one should consider an advanced modality.2 Amniotic membrane allograft is a more recent advanced modality in wound care. Since the early 20th century, human amniotic membrane allografts have been in widespread use in a variety of applications including burn care, dentistry, ophthalmic, ear, nose and throat, and spine surgery. Human amniotic membrane products have become a widely accepted form of treatment in ophthalmic surgery, including corneal ulceration, covering of defects in large conjunctival lesions and acute chemical burns of the eye. Recently, physicians have effectively applied amniotic membrane products to help facilitate healing in chronic cutaneous wounds, including diabetic, venous, arterial and decubitus ulcers.3-7 The amniotic membrane derives from the inner layer of the placenta and is composed of conjoined amnion and chorion membranes. The amnion is in contact with the amniotic fluid/fetus and the chorion is in contact with the maternal side of the placenta. Both layers are non-immunogenic. Human amniotic membrane forms the lining of the fetal environment during gestation, separating the developing fetus from the mother in utero. The material used for surgical wound allografts is isolated from the membranous sac surrounding the infant to the point where it adjoins the placenta at the chorionic plate. The amniotic membrane is composed principally of structural collagen, extracellular matrix, biologically active cells and a large number of important regenerative molecules. Collagen types IV, V and VII make up the extracellular matrix, and are substrates that are important for the integrity of the membrane and ingrowth of cells. The membrane also includes proteins such as fibronectin, proteoglycans, glycosaminoglycans and laminins, epidermal growth factor (EGF), transforming growth factor (TGF), fibroblast growth factor and platelet-derived growth factors. Amniotic membrane has both matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Current Insights On The Benefits Of Amniotic Membrane There are a variety of benefits with the use of amniotic membrane products for wound healing.4,6 • The extracellular matrix scaffold...

Recently, I performed an incision and drainage on a patient with gas gangrene. I consulted an infectious disease specialist who said the patient had developed infective endocarditis. Prior to this, I knew very little about the condition. Here is what I have learned from the physician and my research. The patient was a 56-year-old male with diabetes who presented to the hospital with gas gangrene of his right foot. I took him to the OR for an aggressive incision and drainage. His cultures revealed methicillin resistant Staphylococcus aureus (MRSA) in both his foot wound and blood cultures. Bacteremia was a direct result of the foot infection. According to infectious disease specialist Andrew Catanzaro, MD, “If you have a patient who has repeat blood cultures that are positive for bacteremia and it is slow to clear from the blood stream for greater than 48 hours, then you should be suspicious of infective endocarditis.”1 The patient also had a prior history of receiving a peripherally inserted central catheter (PICC) line due to a previous foot infection. He was immunocompromised, which also increased the level of suspicion. Additionally, the patient had increased white blood cells, positive blood cultures and an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Therefore, the next step was to order an echocardiogram to help with confirming infective endocarditis. The patient had initial incision and drainage. Eventually, he had a transmetatarsal amputation after serial debridements. I monitored weekly ESR, CRP and vancomycin levels for this patient. He received six to eight weeks of IV antibiotics and will complete a repeat echocardiogram after his course of IV antibiotics. There was close follow-up with his primary care physician, podiatrist and infectious disease doctor. A Quick Primer On Infective Endocarditis Infective endocarditis is a type of endocarditis of the inner tissue of the heart caused by infectious agents. The incidence is two to 10 episodes per 100,000 people.2 It accounts for one in 1,000 hospital admissions. With this condition, the valves of the heart do not receive any dedicated blood supply. As a result, defensive immune mechanisms cannot directly reach the valves via the bloodstream. If an organism attaches to a valve surface and forms a vegetation, this blunts the host immune response. Many microorganisms can cause infective endocarditis. The damaged part of a heart valve creates a local blood clot. The platelet and fibrin deposits that form as part of the blood clotting process allow bacteria to take hold and develop vegetations. The body has no direct methods of combating valvular vegetations because the valves do not have a dedicated blood supply. This combination of damaged valves, bacterial growth and lack of a strong immune response results in infective endocarditis. Infective endocarditis...

At our wound care center, we recently had a patient who presented with maggots in her wound. At first glance I thought it was worrisome but then I remembered that maggot therapy is still common for wounds that need debridement. I wanted to revisit maggot therapy to see if I should be considering this treatment as an additional option to heal my patients. A maggot is the larva of a fly. Maggot debridement pertains in particular to the larvae of Dipteran flies, specifically Lucilia sericata. Maggots can efficiently consume dead tissue. They consume rotting flesh, leaving healthy tissue intact. In the 1940s, with the rise of penicillin, clinical maggots became less useful but their use returned in the 1990s when the rise of antibiotic-resistant bacteria necessitated alternative treatments. In 2004, the U.S. Food and Drug Administration approved maggot therapy as a prescription treatment indicated “for debriding non-healing necrotic skin and soft tissue wounds, including pressure ulcers, venous stasis ulcerations, neuropathic foot ulcers, and non-healing traumatic post-surgical wounds.”1 Besides debridement as a benefit of maggot therapy, Gwendolyn Cazander, MD, PhD, of Leiden University Medical Center in the Netherlands states there are other benefits.2 The larvae and their secretions have antibacterial effects, reduce inflammation, promote neo-angiogenesis and improve wound healing. Maggots also remove non-viable tissue effectively, which helps combat infection by reducing bioburden and may facilitate the remodeling process. According to Dr. Cazander, maggot therapy occurs in her inpatient and outpatient settings twice weekly.3 John Steinberg, DPM, the Director of Podiatric Surgical Residency at MedStar Washington Hospital Center and MedStar Georgetown University Hospital said, “we do occasionally use maggot therapy for patients who are not candidates for surgical debridement. We probably use them twice per month on inpatients.” After reviewing maggot therapy, my perspective has changed. Maggot debridement will become a treatment I consider in specific patients, especially those who are not responding to conventional treatment. References 1. Gabrielsen P. How maggots heal wounds. Science. Available athttp://news.sciencemag.org/2012/12/how-maggots-heal-wounds . Published Dec. 6, 2012. Accessed Aug. 19, 2014. 2. Cazander G, Pritchard DI, Nigam Y, et al. Multiple actions of Lucilia sericata larvae in hard-to-heal wounds: larval secretions contain molecules that accelerate wound healing, reduce chronic inflammation and inhibit bacterial infection. Bioessays. 2013; 35(12):1083-92. 3. Cazander G, Gottrup F, Jukema GN. Maggot therapy for wound healing: clinical relevance, mechanisms of action and future prospects. J Wound Technology. 2009; 5. Original Posted on Podiatry...