Case Studies In Unusual Wounds

Given the preponderance of wounds one sees in practice, podiatrists inevitably see wounds of an unusual shape or wounds that demonstrate a unique pattern of soft tissue trauma. Accordingly, this author discusses underlying factors with these abnormal presentations and offers a few challenging case studies involving unusual wounds.

The management of lower extremity ulcerations is a complex task. It is necessary that physicians involved in wound care and limb preservation address both the systemic and local factors that interact to generate significant comorbidity and mortality in this complex patient population.

   Numerous authors have previously described the efficacy of an interdisciplinary team approach to specifically address the common factors that combine to lead to ulceration, wound infection and subsequent lower extremity amputation.1,2 Research has demonstrated that such interdisciplinary models are highly effective in reducing the incidence of non-traumatic amputations around the world.3

   In the management of lower extremity ulcerations, clinicians involved in lower extremity wound care can appreciate a harmony of themes — wounds that present in similar ways and respond in a consistent fashion — and one can appreciate that these wound presentations are a consequence of complex interactions of various risk factors. These risk factors include neuropathy, vasculopathy, musculoskeletal deformity and trauma associated with repetitive stress across a wound site.4-6 To ensure progression through wound healing to wound closure, clinicians must address each of these factors.

   Despite the commonality of wound presentation, one must remember that each patient is unique and consequently each wound can be similarly unique. Often, unusual wounds require a fresh approach and a new paradigm to effectively progress toward wound healing.

What You Should Know About The Chronic Wound Environment

Prior to any discussion regarding unusual wounds, it is valuable to discuss the central concepts associated with wound healing and those factors that contribute to wound chronicity. Sheehan and colleagues found that a wound that does not reduce in area (simple length x width) by at least 50 percent in four weeks has a greater than 90 percent likelihood of not healing at 12 weeks.7 Therefore, should a wound appear to be progressing too slowly, it is appropriate to alter the treatment algorithm as necessary in an effort to restart healing.5,8

   In those instances in which delayed healing occurs, this delay is commonly secondary to multifactorial etiology and pathological variations in the wound environment. In addition to being populated largely by senescent cells, chronic wounds commonly demonstrate increased levels of inflammatory cells as well as imbalances in the endogenous proteases found in the wound bed. These enzymatic imbalances lead to persistent degradation of the provisional wound matrix components that are necessary for wound healing.

   Among these proteases, matrix metalloproteases (MMPs) play an important role in damaging the extracellular matrix and the extracellular growth factors present in a chronic wound.9,10 These MMPs are synthesized by multiple cell types, including neutrophils, fibroblasts and macrophages, at the direction of chemical mediators such as inflammatory cytokines. In the acute wound environment, MMPs function to debride away denatured elements of the extracellular matrix, thus exposing areas of the intact functional matrix that are needed for wound healing.

   This process is highly regulated and controlled via tissue inhibitors of metalloproteases (TIMPs). In chronic wounds, in addition to an excess number of MMPs, there is a failure in the regulation of protease activity between the MMPs and TIMPs, which can result in further degradation of the extracellular matrix.11,12 This is followed by the destruction of growth factors, inhibition of angiogenesis and breakdown of granulation tissue.

   Currently, common wound healing modalities seek to address these imbalances and new advanced wound healing modalities, such as bioengineered alternative tissues, provide dermoinductive and dermoconductive wound healing properties to help convert a stagnant wound into an acute, healing wound.13,14

   In this context, dermoconductive products serve as a scaffold matrix, which allows for an organized infiltration of cells from the surrounding wound tissue. Dermoinductive products are impregnated with living cells that synthesize growth factors, subsequently inducing the formation of neodermis and stimulating the development of healthy granulation tissue.

What Makes A Wound Unusual?

Central to any discussion regarding the usualness or unusualness of wounds, it is helpful to establish definitions to distinguish between normal wounds and those that might be considered abnormal. One could argue that the most “usual” would be an absence of ulceration altogether. Despite our familiarity with lower extremity wounds — seeing them daily in the clinic — we as clinicians must never forget that the development of lower extremity ulceration is a pivotal event in a patient’s life, one that requires a redoubling of efforts to effectively address any underlying pathology that may be present. It is not normal to have a wound.

   Lower extremity wounds generally present as a consequence of more or less common underlying factors. However, perhaps a better description of such wounds is to consider these lower extremity ulcerations as “usual” wounds presenting or responding to therapy in an unusual way, either through a lack of response or an exuberant response to therapy. Alternatively, perhaps these unusual wounds are unusual simply because of the patients themselves and their individual responses to this potentially life threatening manifestation of some greater morbidity.15

   The underlying etiology of “usual” wounds is well understood and numerous authors have described this.16,17 Particularly in the context of lower extremity diabetic ulcerations, there exists a triad of disease that predisposes patients to wound development. Vascular status, infection and pressure are known as the “VIPs” of diabetic wound healing.18 It is necessary that one address those predisposing factors that contribute to wound development, progression and chronicity. Without appropriate diagnosis and management of these VIPs, wounds will not heal, regardless of the modalities clinicians utilize.

   It is helpful to consider that patients who demonstrate “unusual” lower extremity wounds may indeed be suffering from unrecognized underlying factors. While these factors persist, they can contribute to wound propagation and chronicity. Additionally, some wounds, particularly those related to lower extremity trauma, may be categorized as unusual simply due to the pattern of complex soft tissue trauma, which is related to the specific mechanism of injury.

An Emerging Correlation Between Wound Geometry And Wound Chronicity

It is becoming increasingly understood that there is a correlation between wound geometry and wound chronicity. Perhaps one could use wound shape to help categorize unusual wounds. One study noted a proportional relationship between the change in the square root of wound area and movement of the wound margins.19

   Gowland and co-workers further quantified this relationship as the ratio of the change in wound area to the average size of the perimeter between measurements.20 From these findings, Gowland and colleagues hypothesized that one could standardize a linear healing rate between wounds of different perimeters, sizes and shapes to demonstrate wound healing outcomes. This linear healing rate demonstrated a proportional change in wound area and wound perimeter when researchers compared them in the same dimension.20 Consequently, those wounds that demonstrate irregular wound geometry may demonstrate abnormal healing and clinicians can classify these wounds as “unusual.”

   Accordingly, let us take a closer look at a few cases that highlight patients who presented with what could be described as “unusual” wounds. In each case, I discuss the course of care as well as the challenges posed by the unusual nature of the wound presentation.

Case Study One: When A Crush Injury Causes Multiple Fractures And A Large Fracture Blister

This patient is a pleasant 48-year-old female, who sustained a crush injury to her left foot. She presented with multiple fractures of the left lower extremity and a large fracture blister on the dorsal aspect of the foot just proximal to the metatarsophalangeal joints (MPJs). She presented four days after her injury and was unable to bear weight in the affected extremity due to increased pain and swelling.

   The patient’s past medical history consists of hypertension and hyperlipidemia. Her past surgical history is non-contributory. The patient notes social alcohol consumption and denies tobacco and drug usage.

   A computed tomography (CT) scan of the extremity demonstrated non-displaced fractures at the cuboid, the base of the third metatarsal, and the medial and middle cuneiforms.

   The patient initially received conservative treatment both for the fractures and the fracture blister. I applied a moist, non-adherent dressing to the patient’s large dorsal blister and the patient wore a Jones compression dressing with a posterior splint.

   During follow-up care, the patient developed eschar in the area of the previous dorsal fracture blister. The blister itself had resolved but the underlying tissue demonstrated evidence of compromise from the previous crush injury. The patient demonstrated appropriate vascular status with palpable pulses at the dorsalis pedis and posterior tibial arteries as well as appropriate capillary filling time in the digits. Her pain level remained moderate but this was well controlled with oral opioids.

   There was fibrous slough around the eschar margins. We initiated enzymatic debridement therapy while waiting for the tissue to demarcate further. She was non-weightbearing at this time. Following two weeks of enzymatic debridement, the patient went to the operating room for surgical debridement and possible dermal replacement grafting.

   In the operating room, I removed the dorsal left foot eschar in total, identifying and removing a significant amount of nonviable tissue. Soft tissue specimens sent for pathological evaluation demonstrated thrombosed capillaries and inflammatory infiltrate. Following the removal of all apparent nonviable tissue, the wound was quite deep and the dorsal surfaces of the third and fourth metatarsals were exposed. The extensor digitorum longus tendons to the third and fourth toes were intact and the wound bed was bleeding freely.

   I sutured a dermoconductive Integra wound bilayer matrix collagen graft (Integra LifeSciences) into the soft tissue defect and applied a negative pressure wound therapy (NPWT) dressing to promote graft uptake. I changed the NPWT dressing every three days until graft uptake and once there was appropriate dermal tissue regrowth. I then removed the silicone outer layer. The patient then progressed to wound coverage with split thickness skin grafting.

   Why was this wound unusual? The traumatic nature of the wound and the underlying osseous pathology made this wound unusual. Commonly, clinicians observe varying degrees of potential tissue compromise following burn injuries and in cases of frostbite. Crush injuries, much like the one this patient sustained, can also lead to complex soft tissue defects as compromised tissue becomes nonviable and necrotic. In such instances, one must allow the compromised tissue to demarcate between viable and nonviable tissue prior to aggressive, definitive debridement.

Case Study Two: When A Smoker’s Irregularly Shaped, Infected Wound Fails To Heal

This patient is a 55-year-old female who was referred to our office for a second opinion regarding a chronic, non-healing, irregularly shaped ulceration along the anterior aspect of her lower right leg. The ulcer has been present for approximately six months. She says her wound occurred when she scraped her shin along a metal object while at work.

   The patient developed an infection of the wound site and was admitted to a local hospital. She was subsequently evaluated by infectious disease physicians and ultimately discharged to a skilled nursing facility to complete a six-week course of IV vancomycin and piperacillin/tazobactam (Zosyn, Pfizer). At the time of the consultation, the patient was still living at the nursing facility as a consequence of this lower extremity ulceration and she had been treated with numerous courses of parenteral antibiotics. Local wound care has failed to effectively provide for wound closure. She obtained a podiatry consult as a second and final opinion prior to right lower extremity amputation.

   Her past medical history reveals diabetes, hypertension, osteomyelitis, peripheral neuropathy and depression. The past surgical history is non-contributory. The patient smokes half a pack a day. She denies alcohol and drug use.

   Radiographs of the affected extremity demonstrated a “possible permeative lytic process noted in the diaphysis of the tibia, which might represent osteomyelitis.” Subsequent magnetic resonance imaging (MRI) of the right lower extremity demonstrated “No evidence of osteomyelitis or drainable abscess. However, there was evidence to suggest cellulitis and myofascitis.”

   Considering the non-specific and potentially contradictory finding of the imaging studies, I decided to bring the patient to the operating room for a bone biopsy, wound debridement and deep wound culture. I sent a bone sample to histopathology and to the microbiology lab to determine what, if any, bacterial species were present.

   According to the pathology report, the osseous specimens demonstrated distorted fibrovascular tissue with neutrophilic infiltrate that was suggestive, though not diagnostic, of osteomyelitis. Soft tissue biopsy of the wound margins failed to demonstrate malignancy. Tissue cultures demonstrated multi-drug resistant Pseudomonas aeruginosa, which was resistant to the antibiotics that physicians had previously utilized to treat this patient.

   An infectious disease consult addressed the persistent infection and the patient started on IV antibiotics appropriate to the sensitivities obtained from the deep culture. At this time, with serial debridement, appropriate antibiotic therapy and the initiation of smoking cessation therapy, the patient’s wound started to demonstrate interval improvement.

   However, throughout the duration of her care, she demonstrated several instances of wound regression and the development of cellulitis, which coincidently correlated with the patient’s non-adherence and beginning to smoke again. During each instance of cellulitis, deep wound cultures demonstrated the presence of an increasingly aggressive multi-drug resistant pseudomonal infection. The infection was adapting and actively developing resistance to the most recent antibiotics being utilized to treat the infection.

   Ultimately, with the use of numerous advanced modalities, including bioengineered alternative tissues, hyperbaric oxygen therapy (HBOT), thorough aggressive antibiosis via infectious disease consult and smoking cessation therapy, the patient was able to obtain wound closure.

   Why was this wound unusual? There were several factors that made this case unusual. Certainly, one of the complicating factors was the wound shape as researchers have demonstrated that irregularity of wound area is correlated with poor healing outcomes.19

   Additionally, the presence and persistence of a multi-drug resistant bacterial infection made it difficult to maintain an appropriate wound environment for wound healing. A lack of patient adherence further complicated this case as the patient’s unwillingness to engage in smoking cessation further compromised her tissues despite the use of advanced wound healing modalities.

Case Study Three: How To Address A Diabetic Plantar Wound Of Eight Years’ Duration In A Non-Adherent Patient

The 54-year-old male patient presents upon referral from his primary care physician for evaluation of a plantar wound to the right foot. The patient relates that he has had the wound for approximately eight years and that the wound originated from a rattlesnake bite that he sustained while living in Texas. The patient relates that he has had multiple surgeries to attempt to close the wound and has previously utilized numerous wound healing modalities, including NPWT, that have failed to fully resolve the wound.

   The patient has diabetes and had four previous surgeries on his right foot. He relates social alcohol consumption and denies tobacco and drug use.

   Initial plain film radiographs demonstrated evidence of previous fibular sesamoid resection and evidence of a soft tissue ulcer without evidence of subcutaneous emphysema. We obtained a MRI to evaluate for the possibility of osteomyelitis but this was negative for interosseous changes in the first metatarsal or base of the proximal phalanx. A small fluid collection existed adjacent to the area of the soft tissue defect, which was suspicious for abscess.

   Considering the MRI findings and the appearance and long duration of the wound, I recommended that the patient undergo a surgical debridement with a bone biopsy to evaluate for chronic osteomyelitis. The patient refused this procedure and related that, due to work constraints, he was incapable of taking any time off for risk of losing his job.

   Unable to obtain consent to perform the biopsy, we attempted to offload the ulceration and provide local wound care. Again, however, the patient’s work constraints limited our ability to treat the patient effectively. Working in a local factory, the patient was required to wear steel-toed shoes despite a physician’s note that required him to wear appropriate offloading devices such as a total contact cast or an offloading Royce Medical walker.

   We routinely discussed the risk of ulcer progression, infection and limb loss with the patient. He acknowledged the risk that he was undertaking by not allowing more appropriate and aggressive intervention to address the underlying pathology, which was contributing to wound propagation.

   Considering the limitations imposed by the patient’s abject refusal to comply with physician recommendations and instructions, we initiated a course of palliative wound care. The goal of this care was to attempt to maintain a status quo in his wound to limit wound progression and the potential for infection as much as possible considering the offloading constraints.

   Why was this wound unusual? Apart from the socioeconomic and patient adherence challenges that this case posed, it was unusual that the patient’s wound had been present for eight years without progression toward a fulminate osteomyelitis. Certainly, recent literature data would suggest that chronic wounds such as the one described in this case commonly progress toward infection and limb loss, especially if given nearly a decade to do so.2 To maintain a level of chronicity without a progression toward increased morbidity is certainly unusual.

   Further complicating the issue was the fact that, considering the long duration of this wound, the patient had grown accustomed to considering his wound a minor inconvenience, which ultimately allowed him to justify a cavalier attitude toward the potential for interval worsening and wound progression toward limb loss. Patient attitude is a factor that each of us, as clinicians, must address throughout the treatment process. It is very difficult to provide adequate patient care successfully to a patient who is persistently and willfully non-adherent.

In Conclusion

To promote wound healing effectively in chronic lower extremity ulcerations, one must address all underlying pathology, both regular and perhaps occasionally irregular. In my experience, wounds that present with unusual characteristics do so as a consequence of a failure to fully elicit the underlying etiologies that are contributing to wound development.

   In some cases, this etiology may be physical, as in the case of multi-drug resistant bacterial infection, which is recalcitrant to more conventional therapies. Alternately, the etiology may be psychosocial, in which patient adherence or perhaps the absence of adherence may lead toward wound propagation. This would be considered unusual in comparison to more conventional wound development and progression.

   Clinicians involved in the management of lower extremity ulcerations must elucidate the complex interaction of all underlying factors that will combine to lead toward wound development or wound healing. Ultimately no two wounds are the same and none will respond in exactly the same way. Perhaps it is more appropriate for clinicians to consider any wound as “unusual.” Certainly, the most “usual” scenario in the human condition would be the absence of lower extremity wounds altogether. Patients are unique and their wounds are equally unique.

   Perhaps starting from that refreshed viewpoint, clinicians can critically evaluate each patient who presents with a wound through a new filter — one that looks beyond the standard cause and effect paradigms of conventional wound care — to seek out the deeper, patient-specific underlying connections that lead invariably toward wound development and propagation.

   Dr. Fitzgerald is in private practice at Hess Orthopaedics and Sports Medicine in Harrisonburg, Va.

References

1. Armstrong DG, Boulton AJ, Andros G, et al., Defining success in clinical trials of diabetic foot wounds: the Los Angeles DFCon consensus. Int Wound J. 2009; 6(3):211-3.
2. Fitzgerald RH, Mills JL, Joseph W, Armstrong DG. The diabetic rapid response acute foot team: 7 essential skills for targeted limb salvage. Eplasty. 2009; 9:e15.
3. Hierner R, Degreef H, Varnckx JJ, et al. Skin grafting and wound healing-the “dermato-plastic team approach.” Clin Dermatol. 2005; 23(4):343-52.
4. McInnes A, Jeffcoate W, Vileikyte J, et al. Foot care education in patients with diabetes at low risk of complications: a consensus statement. Diabet Med. 2001; 28(2):162-7.
5. Snyder RJ, Kirsner RS, Warriner RA, et al. Consensus recommendations on advancing the standard of care for treating neuropathic foot ulcers in patients with diabetes. Ostomy Wound Manage. 2010; 56(4 Suppl):S1-24.
6. Van Acker K, Weyler J, De Leeuw I. The Diabetic Foot Project of Flanders, the northern part of Belgium: implementation of the St Vincent consensus. Sensibilisation and registration in diabetes centres. Acta Clin Belg. 2001; 56(1):21-31.
7. Sheehan P, Jones P, Caselli A, et al. Percent change in wound area of diabetic foot ulcers over a 4-week period is a robust predictor of complete healing in a 12-week prospective trial. Diabetes Care. 2003; 26(6):1879-82.
8. Apelqvist J, Bakker K, van Houtom WH, et al., International consensus and practical guidelines on the management and the prevention of the diabetic foot. International Working Group on the Diabetic Foot. Diabetes Metab Res Rev. 2000; 16(Suppl 1):S84-92.
9. Loo WT, Sasano H, Chow LW. Pro-inflammatory cytokine, matrix metalloproteinases and TIMP-1 are involved in wound healing after mastectomy in invasive breast cancer patients. Biomed Pharmacother. 2007; 61(9):548-52.
10. Manuel JA, Gawronska-Kozak B. Matrix metalloproteinase 9 (MMP-9) is upregulated during scarless wound healing in athymic nude mice. Matrix Biol. 2006; 25(8):505-14.
11. Ladwig GP, Robson MC, Liu R, et al. Ratios of activated matrix metalloproteinase-9 to tissue inhibitor of matrix metalloproteinase-1 in wound fluids are inversely correlated with healing of pressure ulcers. Wound Repair Regen. 2002; 10(1):26-37.
12. Muller M, Trocme C, Morel F, et al. Matrix metalloproteinases and diabetic foot ulcers: the ratio of MMP-1 to TIMP-1 is a predictor of wound healing. Diabet Med. 2008; 25(4):419-26.
13. Kim PJ, Heilala M, Steinberg JS, Weinraub GM, et al. Bioengineered alternative tissues and hyperbaric oxygen in lower extremity wound healing. Clin Podiatr Med Surg. 2007; 24(3):529-46, x.
14. Attinger CE, Janis JE, Steinberg J, et al. Clinical approach to wounds: debridement and wound bed preparation including the use of dressings and wound-healing adjuvants. Plast Reconstr Surg. 2006; 117(7 Suppl):72S-109S.
15. Gouin JP, Kiecolt-Glaser JK. The impact of psychological stress on wound healing: methods and mechanisms. Immunol Allergy Clin North Am. 2011; 31(1):81-93.
16. Jeffcoate WJ, Price P, Harding KG. Wound healing and treatments for people with diabetic foot ulcers. Diabetes Metab Res Rev. 2004; 20(Suppl 1):S78-89.
17. Williams RL, Armstrong DG. Wound healing. New modalities for a new millennium. Clin Podiatr Med Surg. 1998; 15(1):117-28.
18. Armstrong DG. Healing and preventing the diabetic foot wound: where technology, economics and common sense converge. Indian J Med Sci. 2007; 61(6):324-5.
19. Cardinal M, Eisenbud DE, and Armstrong DG. Wound shape geometry measurements correlate to eventual wound healing. Wound Repair Regen. 2009; 17(2):173-8.
20. Gowland E. Studies on the emigration of polymorphonuclear leucocytes from skin lesions in man. J Pathol Bacteriol. 1964; 87:347-52.

   For further reading, see “Current Concepts In Wound Debridement” in the July 2009 issue of Podiatry Today or “Assessing Vascular Complications In Lower Extremity Wounds” in the July 2008 issue.