Effects of Living Skin Equivalent
Effects of Living Skin Equivalent
Dialysis-dependent patients with calciphylaxis-induced skin wounds are poor candidates for autologous skin grafting because of the risk of creating new wounds at donor sites. To determine if a bilayered living skin equivalent (LSE) aids in the closure of these wounds, case studies of a 79-year-old woman and a 27-year-old woman with multiple calciphylaxis-induced necrotic skin wounds are presented. Wounds were debrided and covered with pieces of LSE. LSE therapy effectively closed the wounds. Reduction in wound size was noted by five to fourteen days. Reepithelialization occurred within three to four weeks in one patient and four to sixteen weeks in the other. The largest wound, which originally measured 450cm2, healed completely. Thus, full wound closure was achieved with calciphylaxis-induced necrotic skin wounds treated with LSE. These results suggest the benefits of this therapy for this difficult-to-treat condition.
Systemic calciphylaxis is a rare but limb-threatening and potentially lethal complication seen in patients with chronic renal failure. It occurs in approximately 1 of 100 hemodialysis patients per year, although the number of reported cases has grown in recent years, perhaps as a result of the increasing number of hemodialysis-dependent chronic renal failure patients. Calciphylaxis is marked by soft tissue calcium deposition in and around small- to medium-sized blood vessels, leading to acute ischemic skin necrosis that rapidly progresses to necrotic ulceration and/or gangrene accompanied by intractable ischemic pain.
The pathogenesis of calciphylaxis remains poorly understood. Ischemia is believed to be caused by medial calcification and intimal hyperplasia of small arteries. Resultant thrombosis, occlusion, or prominent luminal narrowing of small arteries causes hypoxia. The condition is sometimes accompanied by calcification of periarticular tissues and the viscera, especially the kidneys, lungs, gastrointestinal tract, and cardiovascular system. However, in many instances, calcium deposition is limited to the skin and/or the blood vessels.
What predisposes certain dialysis patients to calciphylaxis is also not well understood. While the condition is frequently associated with hyperparathyroidism and a high serum calcium and phosphorous product, such secondary hyperparathyroidism occurs in 80 percent of patients with chronic renal failure, but calciphylaxis only occurs in about one percent. Other factors must also contribute to its development. For instance, either rapid alkalinization during dialysis or immunosuppressive drugs might lead to the calcium phosphate precipitation seen in calciphylaxis and could explain the onset of skin necrosis seen soon after onset of dialysis or after renal transplantation. Still others have suggested that functional protein C deficiency, similar to that seen in Warfarin necrosis, may lead to calciphylaxis and may be paradoxically triggered by oral anticoagulation therapy.
The prognosis of calciphylaxis is poor. Amputation or autoamputation of gangrenous distal extremities is common, and death frequently occurs from sepsis. A meta-analysis of all published cases of calciphylaxis found proximal lesions on the trunk, buttocks, and thighs to be associated with a mortality rate as high as 63 percent to 86 percent, compared with 23 percent to 32 percent when lesions are more distally located. Quick diagnosis and effective closure of wounds are important to prevent the life-threatening sequelae of the condition.
Wound closure is not a simple matter in calciphylaxis. Continuing ischemia in the surrounding skin makes wound closure difficult. The high risk of infection necessitates aggressive wound care with drainage, debridement, and antibiotics, but debridement often leads to enlargement of the wounds, and, in the authors' experience, autologous skin grafting may lead to the creation of new defects. Because of our awareness of these difficulties and the dire nature of this condition, we sought a ready, nonautologous source of grafting material to close calciphylaxis-induced wounds in two patients with chronic renal failure. We used a bilayered living skin equivalent* (LSE) composed of a dermal layer containing fibroblasts and a stratified epidermal layer. Because this construct has been used effectively to close other nonhealing wounds, we decided to use this therapy in our centers.
In this report, we describe the use of LSE for treatment of two patients with calciphylaxis-induced necrotic skin lesions.
Dialysis-dependent patients with calciphylaxis-induced skin wounds are poor candidates for autologous skin grafting because of the risk of creating new wounds at donor sites. To determine if a bilayered living skin equivalent (LSE) aids in the closure of these wounds, case studies of a 79-year-old woman and a 27-year-old woman with multiple calciphylaxis-induced necrotic skin wounds are presented. Wounds were debrided and covered with pieces of LSE. LSE therapy effectively closed the wounds. Reduction in wound size was noted by five to fourteen days. Reepithelialization occurred within three to four weeks in one patient and four to sixteen weeks in the other. The largest wound, which originally measured 450cm2, healed completely. Thus, full wound closure was achieved with calciphylaxis-induced necrotic skin wounds treated with LSE. These results suggest the benefits of this therapy for this difficult-to-treat condition.
Systemic calciphylaxis is a rare but limb-threatening and potentially lethal complication seen in patients with chronic renal failure. It occurs in approximately 1 of 100 hemodialysis patients per year, although the number of reported cases has grown in recent years, perhaps as a result of the increasing number of hemodialysis-dependent chronic renal failure patients. Calciphylaxis is marked by soft tissue calcium deposition in and around small- to medium-sized blood vessels, leading to acute ischemic skin necrosis that rapidly progresses to necrotic ulceration and/or gangrene accompanied by intractable ischemic pain.
The pathogenesis of calciphylaxis remains poorly understood. Ischemia is believed to be caused by medial calcification and intimal hyperplasia of small arteries. Resultant thrombosis, occlusion, or prominent luminal narrowing of small arteries causes hypoxia. The condition is sometimes accompanied by calcification of periarticular tissues and the viscera, especially the kidneys, lungs, gastrointestinal tract, and cardiovascular system. However, in many instances, calcium deposition is limited to the skin and/or the blood vessels.
What predisposes certain dialysis patients to calciphylaxis is also not well understood. While the condition is frequently associated with hyperparathyroidism and a high serum calcium and phosphorous product, such secondary hyperparathyroidism occurs in 80 percent of patients with chronic renal failure, but calciphylaxis only occurs in about one percent. Other factors must also contribute to its development. For instance, either rapid alkalinization during dialysis or immunosuppressive drugs might lead to the calcium phosphate precipitation seen in calciphylaxis and could explain the onset of skin necrosis seen soon after onset of dialysis or after renal transplantation. Still others have suggested that functional protein C deficiency, similar to that seen in Warfarin necrosis, may lead to calciphylaxis and may be paradoxically triggered by oral anticoagulation therapy.
The prognosis of calciphylaxis is poor. Amputation or autoamputation of gangrenous distal extremities is common, and death frequently occurs from sepsis. A meta-analysis of all published cases of calciphylaxis found proximal lesions on the trunk, buttocks, and thighs to be associated with a mortality rate as high as 63 percent to 86 percent, compared with 23 percent to 32 percent when lesions are more distally located. Quick diagnosis and effective closure of wounds are important to prevent the life-threatening sequelae of the condition.
Wound closure is not a simple matter in calciphylaxis. Continuing ischemia in the surrounding skin makes wound closure difficult. The high risk of infection necessitates aggressive wound care with drainage, debridement, and antibiotics, but debridement often leads to enlargement of the wounds, and, in the authors' experience, autologous skin grafting may lead to the creation of new defects. Because of our awareness of these difficulties and the dire nature of this condition, we sought a ready, nonautologous source of grafting material to close calciphylaxis-induced wounds in two patients with chronic renal failure. We used a bilayered living skin equivalent* (LSE) composed of a dermal layer containing fibroblasts and a stratified epidermal layer. Because this construct has been used effectively to close other nonhealing wounds, we decided to use this therapy in our centers.
In this report, we describe the use of LSE for treatment of two patients with calciphylaxis-induced necrotic skin lesions.
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