Pernicious Ankle Wound in a Woman Whose Opposite Leg Has Been Amputated

HISTORY An 85-year-old woman is seen in the nursing home where she lives because of a nonhealing ulcer near the right medial malleolar area. She has angiographically proven severe coronary artery disease and aortoiliofemoral arterial blockages and has undergone coronary angioplasty. There is great concern that the ulceration resulting from ongoing critical arterial stenoses may lead to a second and even more devastating leg amputation: the same sequence eventuated in left above-knee amputation last year. Patient did better than expected both psychically and in rehabilitation after the left leg was amputated, but she has run out of emotional and physical reserves. Active bilateral amputees among the aged are few. Present ulcer has not improved in the several months since right leg angioplasty. PHYSICAL EXAMINATION  Pleasant, somewhat stoic woman. Normotensive despite history of hypertension. In her remaining leg, faintly palpable dorsalis pedis pulse; skin of foot is cool but not ice cold or mottled. No gangrene. Mitral regurgitation murmur. No S3. Neurologically intact. Cognitively near perfect, rarely struggles to find a particular word. Expresses deep concern about the limb and shows appropriate mixture of anxiety and depression. WHAT’S YOUR DIAGNOSIS?     ANSWER: NONHEALING ARTERIAL ULCER The image shows a large, moderately deep, and sharp-edged ulcer that lies superoposterior to the right medial malleolus. Its base is clean, although less red than one would wish (Figure 1). A paler stripe crosses the midportion craniocaudad (horizontally in this view) and suggests tendon. However, when this hypothesis is tested by having the patient dorsiflex and plantarflex the foot, no movement occurs at the stripe, proving that it is not tendon. An array of indentations near the right proximal edge of the image represents the bulbs from a nearinfrared device (Anodyne) that was being tried (Figure 2), based both on promising results reported in the literature and on desperation, because all other measures—including endosurgical revascularization—had manifestly failed. Dried applications of skin protectant that had not yet been wiped off have produced brown glops, especially anterior and distal to the wound and near the array of indentations. The heel and the sole appear adequately perfused, at least insofar as color and lack of gangrene or ulcers permit us to judge.1-3 CAUSES OTHER THAN ARTERIAL INSUFFICIENCY Leg ulcers have myriad causes, and many “What’s Your Diagnosis?” columns—and an immense literature—have been devoted to them. Many sound points have been made about the bedside assessment and differentiation of common causes such as arterial versus venous ulcers.1,2,4,5  Older classification schemes that pronounced some ulcers diabetic and others hypertensive have tended to be replaced by descriptions, since the final common pathway of unresolving tissue injury is not specific to a single cause, even in cases of the usually dialysis-related calciphylaxis.6 Uncommon causes range from vasculitis via microvascular occlusion7 to thrombotic diatheses that can produce the same downstream ischemia even though the vessel wall is normal,8  to the devastating effects of certain specific infections.9-11  Abnormal matter in the skin can press upward from beneath and cause a pressure injury with ulceration.12 PRESSURE ULCERS Many ulcers of vascular origin are mislabeled with the catchall term “bedsores” (pressure sores, pressure ulcers). This error can have adverse consequences because it will direct attention and interventions toward pressure relief. Such relief is an essential element in the healing of pressure sores, but is insufficient if there are multiple contributing causes or if the lesion results primarily from arterial or venous insufficiency.13,14  The Achilles tendon is subject to pressure injury in the bedbound patient who habitually lies on his or her back, but nursing measures and special devices such as Multipodus boots usually prevent this. In the present instance, the wound lies too far forward to blame that area; spares the heel, which is typically affected; and is distinct from the malleolus. Nursing care had been expert and attentive. The patient was well aware of the need to shift position and regularly did so using a bed trapeze. So although pressure sores are always kept in mind, they were not a factor in this case. SPECTRE OF CANCER AND ROLE OF THE SURGEON Dermatologists always remind us that even without rolled edges or a ragged look, a sore that does not heal could be a primary skin cancer. In the present context, we stopped just short of requesting a biopsy. Surprisingly, evidence shows that tissue sampling does not impair the healing of venous ulcers, which tend to heal back to the point of biopsy but not beyond. However, because of the patient’s severe arterial disease, the biopsy option was deferred. The patient and the primary care clinicians looking after her were helped at every step by the vascular surgeon, whose review and advice were as valuable as his reassurance and apt conservatism. He shared our opinion that biopsy was not yet indicated. EVOLUTION OF THE LESION During the next 10 months (Figures 3 to 9), wonderful healing took place, albeit at a pace that taxed the patience of all. One can only speculate on the relative contributions to this good outcome: exceptionally devoted and expert nursing care, a primary nurse who cared for the wound with marvelous skill and consistency, close overall medical management, the patient’s own strong will and excellent compliance, sound nutrition, and the skilled use of the near-infrared device by both rehabilitation and nursing staff. Certainly credit was due to all, and the outcome exceeded expectations. The patient retains the limb and her mobility, and is pleased that there is no further attenuation of her quality of life and no immediate threat to the limb. I plan to re-photograph the area in another 6 months to provide a brief further follow-up in these pages. Schneiderman H. Multifactorial improvement in a chronic leg ulcer attributable to severe peripheral arterial insufficiency in an octogenarian with above-knee amputation. CONSULTANT. 2005;45:1131-1138. REFERENCES: 1. Schneiderman H, Pitegoff G. Dry gangrene of the toes after vascular surgery. Consultant. 1997;37:141-145. 2. London N, Donnelly R. ABC of arterial and venous disease: ulcerated lower limb. BMJ. 2000;320:1589-1591. 3. Christensen JH, Freundlich M, Jacobsen BA, Falstie-Jensen N. Clinical relevance of pedal pulse palpation in patients suspected of peripheral arterial insufficiency. J Intern Med. 1989;226:95-99. 4. Schneiderman H. Dermatitis venosa, venous ulcers, and other foot-and-ankle ulcers. Consultant. 1996;36:109-110. 5. Schneiderman H. Diabetic ulcer with exposed bone: an ominous physical finding. Consultant. 1996;36:795-800. 6. Schneiderman H, Yun HC. Calcific uremic arteriolopathy (calciphylaxis). Consultant. 2000;40:539-541. 7. Schneiderman H. Vasculitic lupus ulcers on the breast, and disastrous lupus vasculitis of the feet and hands. Consultant. 1997;37:991-998. 8. Uwaifo GI, Schneiderman H. Sickle cell leg ulcers: cutaneous manifestation of vascular occlusion in hemoglobinopathy. Consultant. 1999;39:783-788. 9. Schneiderman H. Digital and pedal gangrene due to peripartum toxic shock syndrome. Consultant. 1998;38:1271-1272. 10. Schneiderman H. Fournier’s gangrene of the scrotum (necrotizing perineal infection). Consultant. 1994;34:1431-1432. 11. Iloeje U, Schneiderman H. Chiclero ulcer of cutaneous leishmaniasis. Consultant. 1997;37:2920- 2924. 12. Noyes-Duguay L, Beliveau MM, Schneiderman H. Gouty tophi and tophus ulcers. Consultant. 1995;35:221-224. 13. Schneiderman H. Multiple stage III and stage IV pressure ulcers (decubitus ulcers, bedsores) in an elderly debilitated man. Consultant. 1990;30(12): 47-52. 14. Schneiderman H. Pressure ulcer (bedsore), Shea stage I. Consultant. 1995;35:523-524.