Pressure ulcer disease represents a significant medical problem both nationally and internationally. Approximately 1.7 million people in the United States develop these maladies at an annual cost of between $2.2 billion and $3.6 billion.1 With the population aging, assisted living and nursing facilities flourishing and obesity creating catastrophic increases in diabetes and other diseases, it is likely the number of ulcerations will continue to increase. The pressure ulcer is an area of localized damage to the skin and underlying tissue caused by pressure, sheer, friction and/or a combination of these conditions. These lesions were initially characterized as unfortunate sequella of seriously ill patients; however, they often take on a “life of their own,” leaving catastrophe in their wakes.2 Pressure wounds are often predicated on multiple medical diagnoses, age, impaired mobility and decreased mental status. Poor nutritional status, incontinence and impaired circulation are also important indicators. Particularly vulnerable groups include patients with spinal cord injuries, diabetes and patients who have had orthopedic surgery. You should give additional consideration to ICU patients and elderly patients, especially those suffering from dementia, malnutrition, a history of previous ulcerations, low ejection fractions and incontinence.4 The heel is particularly prone to pressure ulcer defects, in part because of its relatively lower resting blood perfusion levels, higher amounts of surface pressure when under stress, and the possibility of compromised local blood flow if the patient has lower extremity arterial disease.5 Depths range from persistent reddened or blue areas of intact skin to very deep destructive wounds with significant tissue loss. Wound bed appearance may vary. Extensive necrotic tissue with significant undermining and tunneling is common. Lesions in the sacrum or coccyx areas may appear as inverted cones with the apex at the skin surface. Underlying bone may be affected and exudates may vary. Well-defined wounds frequently conform to the underlying bone and therefore appear irregularly shaped. You’ll usually see this phenomenon in the large truncal areas. The surrounding skin is usually dry. Maceration secondary to incontinence or excessive perspiration may be an issue in sacral or coccyx areas. Infected ulcers may exhibit periwound erythema and edema. Drainage may be prevalent and copious. The degree of pain varies. Key Tips On Nutritional Testing Healing is predicated on eliminating or reducing pressure, shear and friction, and implementing appropriate skin care.6 Nutritional protocols are important and you should monitor them carefully. Albumin and pre-albumin studies are useful in assessing protein deficiencies. Serum albumin is often used as a basic screening measure for malnutrition. However, because of its relatively long half-life of 18 days, it reflects long-term change and is not a sensitive marker of current nutritional status. Hydration and age affect this test as well. A value of less than 3.5 g/dL is generally indicative of poor nutritional status.7 The pre-albumin has a shorter half-life of two to three days, responds to changes in nutrient balance within seven days and can be performed regularly.8 Indeed, this blood study represents a better indicator of nutritional status. You can monitor dietary interventions and change them accordingly. Studies including serum transferrin and total lymphocyte counts (TLC) may also be of benefit. Order a nutritional consult if you suspect deficiencies. Pinpointing Areas Of Emphasis In Treatment Treatment options include meticulous nursing care (i.e. turning patients every two hours, appropriately lubricating the skin), nutrition and hydration, mobility, pain management and meticulous wound care, including medical and surgical interventions. Educating both the patient and family is critical and should be an ongoing effort.9 With all of this in mind, let’s take a closer look at four challenging case studies involving difficult heel ulcers. Case Study One A 79-year-old Caucasian male presented with a non-healing wound of three months duration at the medial aspect of the left heel. He had surgery on his left knee and subsequently developed this ulcer. Primarily wheelchair-bound, the patient had limited ambulation. He experienced occasional rest pain in his heel and was offloading the area with pillows. His past medical history was remarkable for myocardial infarction, transient ischemic attack, CVA, hypertension, anemia and diabetes with neuropathy. He exhibited a moderate nutritional risk. A physical examination revealed an afebrile male in no acute distress. He was oriented well to time and space. He had weakly palpable pedal pulses bilaterally. The hand-held Doppler exam revealed a biphasic left dorsalis pedis pulse and a right monophasic dorsalis pedis. The patient had sparse hair distribution and his skin was dry, atrophic and cool to the touch. We noted varicosities and pitting edema at +1 over +4 in both legs and +3 over +4 in both ankles. His deep tendon reflexes were symmetrical and had diminished vibratory and sharp/dull sensation. The Semmes- Weinstein was greater than 5.07. The patient complained of numbness and tingling consistent with diabetic neuropathy. The dermatological exam revealed a wound at the left heel measuring 20mm by 41mm by 1mm. Epithelialization was less than 100 percent with the functional assessment rating of 1. The wound showed necrosis and marked fibrin deposition. There was fluctuance and the periwound tissue was necrotic. There was periwound hyperemia with no active cellulites; however, we had concerns that the patient was not mounting a physiological response. Due to the wound’s chronicity, we suspected underlying osteomyelitis. What Is The Diagnosis? Possible differential diagnoses included: • ulceration of the posterior aspect of the left heel (probably related to pressure); • peripheral vascular disease; • diabetes mellitus with neuropathy; • possible osteomyelitis; or • multiple medical problems. How To Treat Patient One We topically anesthetized the wound with a 4% lidocaine topical solution and debrided it free of skin and subcutaneous tissue. We proceeded to take cultures and sensitivity studies. We emphasized a topical wound dressing, consisting of a mixture of Bactroban ointment and Accuzyme twice daily. In addition, we ordered a L’Nard splint that the patient could use in the wheelchair and in bed. We ordered serum albumin and pre-albumin levels to determine the possibility of underlying protein malnutrition. To guage the possibility of underlying osteomyelitis, we ordered X-rays of the left heel and a Ceretec scan. Finally, we ordered an arterial Doppler and scheduled the patient for weekly visits. The X-rays and Ceretec scans were negative for osteomyelitis. In this case, we procured cultures because it was possible the patient was not mounting a physiological response to infection. However, if a wound does not appear to be clinically infected, we usually will not obtain cultures. The arterial lower extremity Doppler did show diminished perfusion. However, it was the opinion of the vascular consultant that the patient had adequate collateralization. We continued weekly debridements with sharp dissection as well as offloading. We followed the patient’s pre-albumin on a regular basis and found it normal throughout his treatment course. At week 10, we applied an Apligraf skin construct and continued offloading protocols, hydration and appropriate nursing care. At week 16, the patient was completely healed. Treatment Discussion Points It is imperative to do a complete history and physical examination prior to treatment. Meticulous wound management, including sharp wound debridements (if feasible), is imperative. We obtained appropriate consultation with a vascular surgeon to confirm the patient’s relative healing potential. We mixed an antibiotic ointment with an enzymatic agent because, in some cases when debridement occurs, senescent cells separate from the underlying wound bed, potentially increasing the bioburden. Once tissue exfoliation had occurred (after approximately two weeks), we discontinued the enzymatic debriding agent and topical antibiotic mixture in favor of a hydrogel to create a moist wound healing environment. We continued offloading throughout the entire treatment course and utilized the Apligraf skin construct when beefy red granulation was evident. This modality further augmented the healing process by bathing the tissue with growth factors and stimulating granulation tissue. Case Study Two A 72-year-old Caucasian male presented with a wound of approximately three months duration at the posterior aspect of the right heel. The patient described his pain as severe. He had a course of intravenous vancomycin for five weeks through a Groshong catheter. A recent triple phase bone scan (TPBS) was negative for osteomyelitis. A vascular surgeon was evaluating and following up on the patient on a regular basis. The patient’s past medical history was significant for a longstanding, 30-year history of insulin-dependent diabetes mellitus (IDDM), hypertension, hypothyroidism and prostate disease. A nutritional profile (including pre-albumin) of the patient was within normal limits. The vascular examination revealed non-palpable dorsalis pedis and posterior tibial and popliteal pulses bilaterally. The patient also had delayed capillary refill. He had no hair distribution below the knee. His skin texture was dry, his varicosities were present and he had pitting edema at +3 over +4. The patient had a negative Homan’s sign. We noted no intermittent claudication. In regard to the patient’s neurological exam, he had symmetrical deep tendon reflexes. While his vibratory and sharp/dull sensation was intact, his Semmes Weinstein was greater than 5.07. The wound itself was 54 mm x 25 mm x 1 mm, had no undermining and was primarily filled with fibrin. There was very scant pink granulation tissue and slight periwound hyperemia. We observed no malodor and noted only serous drainage. We probed the wound to bone. Osteomyelitis of the heel was still of concern despite a negative TPBS. What Is The Diagnosis? Possible differential diagnoses included: • recalcitrant non-healing wound of the posterior aspect of the right heel with history of infection; • possible osteomyelitis; • peripheral vascular disease with ischemia; or • diabetes mellitus with neuropathy. How To Treat Patient Two Iinitially, we used the 4% lidocaine topical and then debrided skin and subcutaneous tissue with sharp dissection. We procured a culture and sensitivity and instituted Santyl ointment enzymatic debridements once a day. We ordered a repeat TPBS as well as a Ceretec scan. The “probe to bone” test is usually 85 percent accurate for diagnosing osteomyelitis. We also ordered an arterial Doppler. The patient had an L’Nard splint but had difficulty ambulating with it, so we placed him in a Reverse IPOS heel relief shoe. The patient wore a foam cradle boot in bed and in his wheelchair. Antibiotic therapy was managed by infectious diseases physicians, who provided us with reports and the patient’s vascular surgeon did the same. The TPBS was negative, yet the Ceretec scan was positive. To ensure appropriate protein nutrition, we obtained nutritional counseling and ordered pre-albumin studies once a week. We treated the patient for almost 56 weeks. He had initially refused vascular surgical intervention but his pain escalated and we discussed amputation as an alternative. The patient ultimately consented to a distal bypass surgery. Subsequently, we performed debridements of soft tissue and bone. The patient eventually underwent a partial calcanectomy with temporary coverage utilizing cadaveric skin allograft. We used vacuum-assisted closure (VAC) therapy for almost 12 weeks and ultimately applied Apligraf coverage. The patient continued offloading and we monitored his nutrition meticulously. The patient ultimately achieved complete wound closure. Treatment Discussion Points This patient required protracted treatment and the collaboration of several specialists and auxiliary personnel. He first needed a distal vascular bypass surgery to profuse the limb. Be aware that TPBS may be inaccurate in diabetic patients with vascular disease because it is blood flow dependent. The Ceretec scan is less blood flow dependent and more specific for detecting osteomyelitis. You may use both tests in tandem. Dual peak imaging may give us better anatomical perspective. In addition, we used VAC therapy for 12 weeks. This form of therapy involves negative pressure, which stimulates granulation tissue, contraction and wound closure. The patient also had several operating room debridements, culminating in a calcanectomy with temporary coverage with a cadaveric allograft. This allograft prevents the bone from desiccating and decreases pain. Ultimately, the patient did develop granulation tissue to cover all bone and tendon and we applied Apligraf. With meticulous offloading, nutritional support and follow-up, the patient’s wound subsequently healed. However, without these measures, he would have probably required a major amputation. Case Study Three An 80-year-old, Caucasian female presented with a pressure ulceration of three weeks duration to the left heel. She had been confined to a nursing facility subsequent to a fall. The wound began as a blister but then became necrotic and exceedingly more painful. Her past medical history was significant for hypertension and venous insufficiency. The patient had no allergies. The physical examination revealed a somewhat confused patient in no acute distress. (She went to her first visit with her son.) She was afebrile, had stable vital signs and her blood pressure was 155/81. The vascular exam revealed non-palpable pedal pulses in the affected extremity. The patient was complaining of rest pain and had intermittent claudication. The patient’s skin was dry and atrophic, she had torturous varicosities and brawny edema with lipodermatosclerosis and hemosiderosis. She had a negative Homan’s sign. In regard to her neurological exam, the patient had symmetical deep tendon reflexes. Her vibratory sensations were intact and the Semmes-Weinstein was 5.07. As far as the wound itself, there was periwound erythema and it was palpably tender. There was some streaking up the lateral ankle area. An orthopedic evaluation did not reveal any exposed bone but we had concerns about the possibility of underlying osteomyelitis. What Is The Diagnosis? Possible differential diagnoses included: • pressure ulcer with necrosis at the posterior aspect of the left heel; • ischemic peripheral vascular disease; • cellulitis; • possible osteomyelitis; and/or • venous insufficiency. How To Treat Patient Three We immediately hospitalized the patient and sought vascular and infectious disease consults. An MRI of the affected heel did reveal osteomyelitis. We placed the patient empirically on Zosyn 3.375 q6h. We emphasized offloading protocols with a foam waffle boot and low air mattress. Nursing care included turning the patient q2h and keeping the skin well lubricated. In this case, because the wound was totally necrotic, we began painting with one-quarter strength Betadine paint. In addition, we monitored hydration and nutrition carefully. On several occasions, we performed pre-albumin studies, which were within normal limits. The patient ultimately underwent a distal bypass surgery and this essentially eradicated her rest pain and perfused the affected limb. After the vascular surgery, the patient experienced an increase in cellulitic symptoms. However, this is not an uncommon scenario after you’ve re-established appropriate blood flow. The wound became fluctuant and required operating room debridement. We totally excised the wound, removed any soft infected bone and applied a cadaveric allograft. The patient’s postoperative course was excellent and she was subsequently discharged. Postoperatively, we emphasized daily application of a hydrogel wound dressing and used a L’Nard splint for offloading. The patient ultimately developed beefy red and firm granulation tissue. Subsequently, we applied a split-thickness skin graft. The patient was discharged from active wound care with appropriate orthopedic footwear, including a Sach heel. Treatment Discussion Points Initially, we did not debride this patient’s wound because it was necrotic and dry. Although Betadine is clearly cytotoxic and should not be used full strength on open wounds, literature does support acceptable use to decrease the bioburden in a necrotic dry wound scenario. Be aware that when the wound lacks fluctuance and possesses a stable eschar, it is probably not appropriate to perform extensive debridements. When the wound became fluctuant and we had removed the eschar via debridement, we used a hydrogel to produce a moist healing environment. The patient needed hospitalization and vascular and infectious diseases consults. The patient subsequently had a distal bypass surgery. We took the patient to the operating room for multiple debridements, culminating in a partial calcanectomy. We also used cadaveric skin allograft to decrease pain, prevent desiccation and create a lattice to potentate granulation tissue. Ultimately, we applied a split-thickness skin graft to accomplish healing. Case Study Four An 80-year-old, Hispanic female presented with an ulceration of three months duration at the posterior aspect of the left heel. The patient’s medical history was remarkable for long-standing IDDM, hypertension, peripheral vascular disease and renal failure. A nutritional screen revealed a low nutritional risk. The physical examination revealed an afebrile patient who had vital signs that were within normal limits. The vascular examination revealed palpable pedal pulses bilaterally and a delayed capillary refill. The patient had sparse hair distribution as well as dry and atrophic skin. She had torturous varicosities, brawny edema and a negative Homan’s sign. I did have concerns about the possibility of underlying osteomyelitis. The dermatological exam revealed a fluctuant necrotic ulcer at the posterior aspect of the left heel with ascending cellulitis. Her neurological evaluation revealed no deep tendon reflexes. She also had dimimished vibratory and sharp/dull sensations, and the Semmes-Weinstein was greater than 5.07. What Is The Diagnosis? Possible differential diagnoses included: • decubitis/pressure ulcer on the posterior aspect of left heel with diabetic neuropathy; • cellulitis; and/or • possible osteomyelitis. How To Treat Patient Four The MRI was positive for osteomyelitis of the left heel. We performed several debridements and excised necrotic infected tissue and bone. We applied cadaveric allograft and utilized VAC therapy for approximately 20 weeks. The patient had several other hospital admissions for hypertensive crisis and diabetic coma. Subsequently, we performed Apligraf therapy and continued VAC therapy. The wound ultimately healed. However, the patient subsequently had a myocardial infarction and succumbed. Treatment Discussion Points We performed surgery on several occasions to excise infected tissue and bone. We also found that VAC therapy and cadaveric allograft were very useful. Again, we utilized Apligraf to augment granulation tissue and foster an appropriate healing environment. In this case, we continued VAC therapy after applying Apligraf and found it very useful in accelerated healing. Initially, we used a setting of 125 mm of mercury. However, after Apligraf placement, we employed a setting of 75 mm of mercury. In Conclusion Pressure ulcer disease represents a major health problem both in this country and internationally. The previous case studies outline several etiologies for this illness and various treatment protocols. Keep in mind that the treatments outlined here represent only a portion of the modalities you can utilize for these wounds. It is essential to have an appreciation for the potential seriousness of these seemingly innocuous wounds, particularly in light of comorbid diseases and peripheral vascular disease. Dr. Snyder is the Director of the Wound Healing Center at University Hospital in Tamarac, FL. He is a Diplomate of the American Board of Podiatric Surgery and the American Academy of Wound Management. Ms. Perrigo is a Registered Nurse with an expertise in wound healing and management.
References 1. Beckrich K, Aronoritch SA. Hospital Acquired Pressure Ulcers: A comparison of Costs in Medical Versus Surgical Patients. Advancements in Wound Care. 1998: 11 (Supplement): 3. 2. Weir D. Pressure Ulcers: Assessment Classification in Management. Krasner DL, Rodeheaber GT, Sibbald R. (Editors) Chronic Wound Care: A Clinical Source Book of Healthcare Professionals, Third Edition. Wayne, PA: HMP Communications 2001: 619-627. 3. Bergstrom N, Bennett MA. Carlson CE, et. al. Clinical Practice Guideline Number 15: treatment of Pressure Ulcers. Rockville, Maryland, U.S. Department of Health and Human Services. Agency for Healthcare Policy and Research; 1994. AHCPR Publication 95-0653. 4. Calianno C. Assessing and preventing pressure ulcers. Advances in Skin and Wound Care. September/October 2000; 13(5): 244-246. 5. Mayrovitz HN, Sims N. Effects of Different Cyclic Pressurization and Relief Patterns on Heels, Skin, Blood Profusion. Advances in Skin and Wound Care. July-August 2002: 15 (4): 158-164. 6. Wound Characteristics by Type (Clip and Save) Advances in Skin and Wound Care: The Journal for Prevention and Healing. Jan-Feb 2000; 13 (1): Page 40. 7. Lewis B. Nutrition and wound healing: From: Wound Healing Alternatives in Management, Kloth L, McCulloch JM, eds. 3rd Edition, F.A. Davis Company, Philadelphia, PA. 2002: 35-67. 8. Lipkin EW, et. al. Assessment of nutritional status: the clinician’s perspective. Clinic Lab Med1993; 13: 329. 9. Weir D. Pressure Ulcers: Assessment Classification in Management. Krasner DL, Rodeheaber GT, Sibbald RG (Editors). Chronic Wound Care: A Clinical Source Book of Healthcare Professional, Third Edition. Wayne, PA: HMP Communications 2001: 619-627