An Orthopaedist's Review of Diabetic Foot Wounds and Osteomyelitis

Matthew R. DeSanto, BS; Luke V. Weber, BS; Emmanuel Nageeb, BS; Kyle Petersen, MD; Jeffrey Junko, MD


Curr Orthop Pract. 2020;31(5):423-428. 

In This Article


The pathoanatomy of diabetic foot ulcers is a complex multifactorial process. Diabetes itself stems from either inadequate endogenous insulin release, insulin receptor desensitivity, or hypoactivity. This ultimately confers an increased risk for elevated blood sugar, otherwise known as hyperglycemia. Hyperglycemia is believed to induce nerve cell damage as a result of neuronal cells' inability to excrete internal glucose and production of reactive oxygen species.[12] Diabetic foot ulcers commonly stem from both sensory and motor neuropathy, as well as an autonomic neuropathy. The neuropathy typically begins distally in the toes as the microvasculature is most susceptible to ischemia and damage; progression occurs proximally in a sock-like distribution.[13] Overall, these neuropathies lead to loss of protective foot sensation, high foot pressures, improper shifting of weight, foot deformities, gait disturbances, and the diminishment of microbial defense.[14–17]

Autonomic neuropathy, assumed to be the first neuropathy affecting diabetics, leads to pathophysiologic alterations in the sweat glands. There is a significant reduction in sweating, altering thermoregulation and possibly microbial defense.[18] Fissuring and problematic bacterial infections are linked to these pathologic conformities, and this complicates diabetic foot ulcer treatment. In addition to this, demyelination of vascular nerve axonal segments leads to arteriovenous shunting, poor nutrient profusion, and decreased wound healing potential.[13,19] On top of this, higher rates of atherosclerosis and microvascular disease are often seen in this patient population from a variety of other comorbidities. Deteriorated vasculature decreases the healing potential of the wound beds and can directly lead to ulceration.[20,21]

Sensory neuropathy, present in 50% to 60% of diabetics, can often lead to diabetic foot ulcers because of unrecognized microtrauma and loss of protective sensation.[13,22,23] Pathology of these changes follows the patterns of autonomic neuropathy consisting of hyperglycemia induced microvascular and axonal damage. A 10 gram or 5.07 gauge Semmes Weinstein monofilament can be utilized to determine sensory deficits and predict the capacity of protective sensation from noxious stimuli.[24,25] This loss of protective sensation and increased plantar pressure has been shown to be closely correlated with diabetic foot ulcers in multiple observational studies.[26–28] The most typical anatomical sites for Semmes Weinstein monofilament testing are the plantar aspect of great toe, third metatarsal, and fifth metatarsal.

Motor neuropathy is considered to be a later complication of diabetes. Motor endplate damage results in the declination of intrinsic musculature and resulting deformity. These changes are often observed congruently with the gait instability frequently displayed in diabetics.[23] Overcompensation of intrinsic muscles leads to clawing of the toes and depression of the metatarsal heads, two common places for diabetic foot ulcers to occur.[13,29] The damage caused by these differing neuropathies provides the basis for diabetic foot ulceration.