Surgical Management of the Diabetic Foot
Surgical Management of the Diabetic Foot
Wounds of the foot are the most common reason for diabetes-related hospital admissions. In many of these cases, surgical intervention is the best option. This article will review the risk factors for foot wounds in people with diabetes, discuss preventative and surgical strategies, and present surgical management techniques to treat ulceration and chronic infection in these wounds.
Diabetes is a common condition in the United States, affecting more than 10 million adults. Wounds of the foot are the most common reason for hospitalization in patients with diabetes; it is estimated that 15% to 20% of patients with diabetes will develop an ulcer on their foot at some point, and for many of these cases, the most appropriate treatment results in some form of surgery.
The foot is highly specialized to cope with a large degree of repetitive stress. Fatty tissue on the plantar surface and a thickened dermis and epidermis cushion and absorb repeated forces of compression, torsion, and shear during locomotion and standing. However, the pathophysiology of diabetes can significantly alter the wound healing process, leading to an increased risk for foot ulceration. McNeely et al found that a transcutaneous oxygen tension (TcPO2) of less than 30 mmHg, absence of the Achilles' tendon reflex, and foot insensitivity are 3 factors that are strong predictors of ulceration.
A simple test for sensation involves pressing a nylon monofilament against the skin to the point of buckling. Patients who cannot feel the monofilament are at particular risk for ulceration. In patients without sensation, the likelihood for ulceration is 9.9 times higher and the likelihood of amputation is 17 times higher than in patients who can feel the monofilament.
The pathogenesis of ulceration is complex and involves the interaction of angiopathy, neuropathy, and immunopathy. Briefly, vascular impairment has been found to correlate with the development of diabetic foot ulcers, probably through ischemic skin changes leading to ulceration. There is debate about the precise role of angiopathy in the microvasculature, but it is likely that thickening of the capillary basement membrane impairs the flow of nutrients and possibly white blood cell migration, yet there is no evidence of impairment of oxygen diffusion.
Neuropathy is the most significant risk factor for diabetic foot ulcers and is present in over 80% of patients with diabetes and foot lesions. All aspects of nerve function including the motor fibers to the intrinsic muscles of the foot are affected. With the loss of function, the toes become drawn up into a claw-foot position, creating points of increased pressure or friction beneath the metatarsophalangeal joints, over the dorsum of the toes or at the tip of the toes. Autonomic dysfunction also results in the shunting of blood through direct arteriole-venule passages, reducing the extent of tissue perfusion. The decreased awareness of sensation and nerve-induced deformity predispose the diabetic foot to ulceration by causing imbalances in the tendons that shift the load-bearing areas to unprotected parts of the plantar surface. In the absence of a neuro-inflammatory response, infection may occur without the patient being alerted by the usual clinical signs of inflammation.
Although there does not appear to be any significant impairment of humoral immunity in diabetes, at the cellular level, impaired leukocyte function and intracellular killing have been noted and these can be partly or completely reversed with improved diabetic control. Cell-mediated immune responses are also impaired by elevated glucose levels.
Wounds of the foot are the most common reason for diabetes-related hospital admissions. In many of these cases, surgical intervention is the best option. This article will review the risk factors for foot wounds in people with diabetes, discuss preventative and surgical strategies, and present surgical management techniques to treat ulceration and chronic infection in these wounds.
Diabetes is a common condition in the United States, affecting more than 10 million adults. Wounds of the foot are the most common reason for hospitalization in patients with diabetes; it is estimated that 15% to 20% of patients with diabetes will develop an ulcer on their foot at some point, and for many of these cases, the most appropriate treatment results in some form of surgery.
The foot is highly specialized to cope with a large degree of repetitive stress. Fatty tissue on the plantar surface and a thickened dermis and epidermis cushion and absorb repeated forces of compression, torsion, and shear during locomotion and standing. However, the pathophysiology of diabetes can significantly alter the wound healing process, leading to an increased risk for foot ulceration. McNeely et al found that a transcutaneous oxygen tension (TcPO2) of less than 30 mmHg, absence of the Achilles' tendon reflex, and foot insensitivity are 3 factors that are strong predictors of ulceration.
A simple test for sensation involves pressing a nylon monofilament against the skin to the point of buckling. Patients who cannot feel the monofilament are at particular risk for ulceration. In patients without sensation, the likelihood for ulceration is 9.9 times higher and the likelihood of amputation is 17 times higher than in patients who can feel the monofilament.
The pathogenesis of ulceration is complex and involves the interaction of angiopathy, neuropathy, and immunopathy. Briefly, vascular impairment has been found to correlate with the development of diabetic foot ulcers, probably through ischemic skin changes leading to ulceration. There is debate about the precise role of angiopathy in the microvasculature, but it is likely that thickening of the capillary basement membrane impairs the flow of nutrients and possibly white blood cell migration, yet there is no evidence of impairment of oxygen diffusion.
Neuropathy is the most significant risk factor for diabetic foot ulcers and is present in over 80% of patients with diabetes and foot lesions. All aspects of nerve function including the motor fibers to the intrinsic muscles of the foot are affected. With the loss of function, the toes become drawn up into a claw-foot position, creating points of increased pressure or friction beneath the metatarsophalangeal joints, over the dorsum of the toes or at the tip of the toes. Autonomic dysfunction also results in the shunting of blood through direct arteriole-venule passages, reducing the extent of tissue perfusion. The decreased awareness of sensation and nerve-induced deformity predispose the diabetic foot to ulceration by causing imbalances in the tendons that shift the load-bearing areas to unprotected parts of the plantar surface. In the absence of a neuro-inflammatory response, infection may occur without the patient being alerted by the usual clinical signs of inflammation.
Although there does not appear to be any significant impairment of humoral immunity in diabetes, at the cellular level, impaired leukocyte function and intracellular killing have been noted and these can be partly or completely reversed with improved diabetic control. Cell-mediated immune responses are also impaired by elevated glucose levels.
