Foot gangrene: signs and treatment options

Foot gangrene is tissue necrosis due to critically reduced blood flow, infection, or a combination of both; it most often develops against the background of atherosclerotic lesions of the arteries of the lower extremities and diabetes mellitus. Clinically, a distinction is made between the "dry" ischemic form with tissue mummification, the "wet" form with infection and edema, and the "gas" form due to clostridial infection. Treatment tactics depend on tissue viability, the severity of ischemia, the presence of deep infection, and overall cardiovascular risk. A modern approach relies on teamwork: a vascular surgeon, an infectious disease specialist, an endocrinologist, a podiatrist, and a wound care team. [1]

Code according to ICD-10 and ICD-11

ICD-10 uses several coding methods, depending on the etiology. For atherosclerosis of the arteries of the extremities with gangrene, the category I70.2 is used with the specification "with gangrene" in national extensions, and for the primary description of gangrene without specifying the cause, R02 "Gangrene, not elsewhere classified" is used. For diabetes mellitus with gangrene, national versions often use combined codes from blocks E10-E14 and I70, reflecting the cause and manifestation. It is important to follow local coding rules. [2]

In ICD-11, the base code for gangrene is MC85 "Gangrene," to which the underlying disease code is added via post-coordination, such as atherosclerotic occlusive disease of the arteries of the leg or diabetic foot. For diabetic ulcer and necrosis, ICD-11 uses the root code BD54 "Diabetic foot ulcer" with severity and infection modifiers. This cluster approach more accurately reflects causes and complications. [3]

Table 1. Coding examples

System	Code	When appropriate
ICD-10	I70.2 with the clarification "with gangrene"	Atherosclerosis of the arteries of the extremities with gangrene
ICD-10	R02	Gangrene without apparent cause in the diagnosis
ICD-11	MC85 + post coordination	Gangrene as a manifestation with an indication of the cause
ICD-11	BD54 + modifiers	Diabetic foot ulcer, including with necrosis

Epidemiology

Chronic lower extremity arterial disease affects hundreds of millions of people worldwide, and the risk increases sharply with age and diabetes. Diabetic foot infections account for a significant proportion of lower extremity hospitalizations and amputations; according to the IWGDF, foot infections remain the most common cause of hospitalization in people with diabetes. The lifetime prevalence of foot ulcers in people with diabetes is estimated to be approximately 15-25 percent. Increasing life expectancy and the high prevalence of risk factors support a steady increase in incidence. [4]

Table 2. Epidemiological landmarks

Indicator	Grade
Proportion of people with diabetes who ever develop a foot ulcer	15-25%
The leading cause of hospitalization in people with diabetes	Foot infections
The main predictor of amputation	Chronic limb-threatening ischemia and infected necrosis

Reasons

The main causes of foot gangrene are critical ischemia due to atherosclerosis of the aortoiliofemoral segment and the arteries of the lower leg, as well as infection due to ulcers, especially in diabetes mellitus and neuropathy. The ischemic component leads to "dry" gangrene with tissue mummification, while the infectious component forms "wet" gangrene with edema and foul-smelling discharge. The gas form is associated with clostridial myonecrosis and requires emergency surgery. Often, both factors are present: ischemia reduces healing potential, and infection accelerates tissue destruction. [5]

Risk factors

Modifiable factors include smoking, dyslipidemia, hypertension, hyperglycemia and poor glycemic control, obesity, chronic kidney disease, and a sedentary lifestyle. Non-modifiable factors include age, diabetes duration, the presence of peripheral neuropathy, and a history of ulcers or amputations. The combination of several factors dramatically increases the risk of ulceration, infection, and necrosis. Tobacco cessation and intensive lipid-lowering therapy reduce the risk of progression and amputations. [6]

Table 3. Risk factors for foot gangrene

Category	Examples	Practical significance
Vascular	Smoking, dyslipidemia, hypertension	Accelerate atherosclerosis and ischemia
Metabolic	Hyperglycemia, obesity	Impair immune response and healing
Neuropathic	Diabetic polyneuropathy	Loss of protection and foot injury
Medical history	Previous ulcer, amputation	High risk of relapse

Pathogenesis

Ischemic gangrene develops when blood flow is critically low, with perfusion falling below thresholds that support healing. Clinically significant benchmark thresholds include systolic pressure at the toe of less than 30 mmHg and transcutaneous oxygen tension below 25-30 mmHg, at which point the chance of healing without revascularization is extremely low. Infection aggravates ischemia through edema, microthrombosis, and a systemic response, accelerating necrosis and the risk of sepsis. In the gas form, clostridia produce toxins that cause rapid myonecrosis and systemic intoxication. [7]

Table 4. Threshold perfusion values for predicting healing

Indicator	Unfavorable threshold	Comment
Systolic pressure on the finger	<30 mmHg	Low probability of healing without revascularization
Transcutaneous oxygen tension	<25-30 mmHg	Indicates severe tissue ischemia
Ankle-brachial pressure index	≤0.90 pathology; ≥1.40 non-compressible arteries	In case of medial calcinosis, evaluate digital pressures

Symptoms

In "dry" gangrene, the area becomes cold and dry, with a clear boundary between living and dead tissue. Pain can range from moderate to severe, especially at night. "Wet" gangrene is characterized by swelling, an unpleasant odor, cloudy discharge, perifocal redness, and a systemic reaction. The gas form is accompanied by severe pain disproportionate to the physical examination, crepitus under the skin, and rapid deterioration. Precursors are often present: a non-healing ulcer, increasing pain at rest, coldness, and discoloration of the fingers. [8]

Classification, forms and stages

In practice, a distinction is made between "dry," "wet," and "gas" gangrene, which helps assess the urgency of debridement. The Society for Vascular Surgery's WIfI system is useful for stratifying limb threat: the wound, ischemia, and infection are assessed, after which the stage of amputation threat and the feasibility of revascularization are calculated. For planning revascularization in chronic limb-threatening ischemia, global guidelines are used, taking into account patient risk, limb threat, and the anatomy of the lesion. Standardized assessment allows for predicting healing and choosing the correct sequence of debridement and restoration of blood flow. [9]

Table 5. Key landmarks of the WIfI classification

Component	Range	What does it reflect?
Wound	0-3	From no ulcer to deep necrosis with exposed bone
Ischemia	0-3	From normal perfusion to critically low pressures
Infection	0-3	From absence to systemic infection and fasciitis

Complications and consequences

Without treatment, "wet" and gas gangrene quickly lead to sepsis, multiple organ failure, and high mortality. Even with the localized "dry" form, continued loss of perfusion threatens progression of necrosis and the need for further amputation. Long-term, patients have an increased risk of myocardial infarction and stroke as manifestations of systemic atherosclerosis. Timely targeted revascularization and debridement of the lesion reduce the risk of amputation and improve survival. [10]

When to see a doctor

Immediate assistance is required if signs of a systemic infection, increasing pain, rapidly expanding necrotic area, crepitus, or foul-smelling discharge appear. Urgent care is required if a non-healing ulcer, pain at rest, coldness or discoloration of the toes, or a sudden weakening or absent pulse in the arteries of the foot occurs. Any changes in people with diabetes should be considered potentially dangerous and require evaluation within the next few hours. Early referral to a vascular surgeon and an infection specialist is critical. [11]

Diagnostics

Step 1. Clinical assessment. Tissue viability, signs of deep infection, pain at rest, temperature, and hemodynamic stability are determined. Both feet are examined simultaneously, and the area of necrosis, its boundaries, odor, discharge, and the presence of crepitus are described. Probing to the bone of the ulcer is performed to rule out osteomyelitis. Laboratory markers of inflammation are obtained. [12]

Step 2. Microbiology. Culture material is taken from deep tissue after surgical debridement of the wound or from bone if osteomyelitis is suspected. Superficial smears are of little value. The first line of treatment is classical culture microbiology with susceptibility testing; molecular methods are reserved for special situations. [13]

Step 3. Perfusion assessment. Measure the ankle-brachial pressure index, finger pressures, and, if necessary, transcutaneous oxygen tension. Finger systolic pressure values less than 30 mmHg and transcutaneous oxygen tension less than 25-30 mmHg indicate extremely low healing potential without restoring blood flow. In medial calcification, finger tests are used as a guide. [14]

Step 4. Visualization. To plan revascularization, tomoangiography or magnetic resonance angiography is performed, and invasive angiography is performed if necessary. Magnetic resonance imaging is informative for osteomyelitis; alternatives include positron emission tomography and leukocyte scintigraphy. In cases of severe infection and ischemia, a consultation with a vascular surgeon is scheduled without delay. [15]

Table 6. Diagnostic markers and their interpretation

Test	Threshold of unfavorable prognosis	Practical conclusion
Pressure on the toe	<30 mmHg	Low chance of healing without revascularization
Transcutaneous oxygen tension	<25-30 mmHg	Restoration of blood flow is required
Probing to the bone	Positively	High probability of osteomyelitis
Magnetic resonance imaging	Bone edema, sequestration	Confirmation of osteomyelitis

Differential diagnosis

It is important to distinguish gangrene from necrotizing fasciitis, severe cellulitis, diabetic neuroosteoarthropathy syndrome, and deep trophic ulcers without necrosis. Necrotizing fasciitis is characterized by pain disproportionate to the physical examination, rapid progression, systemic instability, and requires immediate extensive surgical debridement and intensive care. Gas gangrene is characterized by the presence of gas in the tissues and severe intoxication. When in doubt, the decision is made in favor of early surgical exploration. [16]

Table 7. What simulates gangrene of the foot

State	Distinguishing features	Tactics
Necrotizing fasciitis	Rapid spread, severe disproportionate pain, systemic toxicity	Urgent radical sanitation and antibiotics
Severe cellulite	Diffuse redness and swelling without necrosis	Systemic antibiotics and monitoring
Neuroosteoarthropathy	Foot deformity, warm skin, minimal pain	Unloading and exchange control
Deep ulcer without necrosis	The bottom is granulated, without black scabs.	Wound therapy and infection prevention

Treatment

The basic principle is "saving lives first, then limbs." If signs of sepsis, necrotic tissue, or gas formation are present, immediate surgical exploration and debridement of the lesion are required, along with the simultaneous initiation of broad empirical antibiotic therapy and intensive support. Removal of necrotic tissue reduces the microbial load, toxemia, and creates conditions for further healing. The decision on the extent of debridement is made intraoperatively, taking into account tissue viability. [17]

Antibiotic therapy is selected based on the likely pathogens and the severity of the infection. For mild soft tissue infections in temperate climates, initial coverage of aerobic gram-positive cocci is advisable, while for moderate to severe infections, a broad regimen covering gram-negative bacteria and anaerobes is required until culture results are available. Empirical coverage of Pseudomonas aeruginosa is not recommended in temperate climates without risk factors. Duration of treatment is typically up to 2 weeks for soft tissue infections, up to 3 weeks after minor amputations with positive bone margins, and approximately 6 weeks for osteomyelitis without bone resection. [18]

Early and complete surgical debridement is key to infection control. For moderate to severe infections, early surgery within 24-48 hours is recommended, followed by repeated wound revision as indicated. For osteomyelitis, resection of the infected bone is preferred, along with systemic antibiotics; in some patients with forefoot lesions, a conservative approach is possible with strict selection. The choice of approach is determined by a multidisciplinary team. [19]

Restoring blood flow is the second cornerstone of successful treatment, especially in cases of ischemia and necrosis. The decision to revascularize is based on limb risk stratification, perfusion parameters, and the anatomy of the lesion. The goal is to establish a direct arterial line to the wound bed, taking into account the priority artery in the foot. Endovascular methods and open bypass surgeries are used; the choice depends on the anatomy and overall risk. [20]

Endovascular interventions include balloon angioplasty, stenting, and the use of modern coated devices. Their advantages include less invasiveness and faster recovery, especially in patients with high surgical risk. For extensive lesions and calcification of the leg, experience and careful selection of instrumentation are preferred, sometimes in combination with directional atherectomy. Patency is monitored clinically and using noninvasive tests. [21]

Open reconstructions remain valuable in cases of complex anatomy and where long-lasting results are expected. Bypass grafting to the distal arteries of the foot remains an option for "refractory" ischemia in the presence of a suitable vein. The choice of amputation level when blood flow cannot be restored is determined by perfusion parameters and tissue viability. The goal is to create a functional stump and maintain weight-bearing capacity. Rehabilitation begins early with the introduction of orthotics. [22]

Systemic secondary prevention is mandatory for all patients. High-intensity statins with low-density lipoprotein targets, blood pressure and glycemic control, and complete smoking cessation are recommended. In symptomatic patients and after revascularization, combination antithrombotic therapy with low-dose rivaroxaban in combination with aspirin is considered with an acceptable bleeding risk, which reduces the risk of serious cardiovascular and limb events. [23]

Local wound therapy includes adequate off-loading, regular dressing changes, moisture and biofilm control, and timely correction of wound edges. Negative pressure is appropriate after debridement and with sufficient perfusion; it is not recommended as monotherapy for active infection. Oxygen therapy and topical antibacterial agents are not considered routine treatments for foot infections. [24]

Nutritional support and management of comorbidities improve the chances of healing. Deficiencies of protein, vitamins, and trace elements are associated with protracted disease progression and infectious complications. Patients with chronic kidney disease and heart failure require individualized adjustments to therapy and infusion volumes. Patient education on foot care reduces the risk of recurrence. [25]

Adjuvant methods are used selectively. Hyperbaric oxygenation and local oxygenation are not recommended as treatments for foot infection itself; decisions on their use are made only as part of a comprehensive program after restoration of blood flow and debridement, with specific justification. Experimental methods are considered within the framework of clinical protocols. In the absence of conditions for limb preservation, the emphasis shifts to palliative goals and quality of life. [26]

Table 8. Antibiotic therapy for foot infection in people with diabetes: guidelines

Situation	Starting tactics	Expected duration
Mild soft tissue infection	Covering of aerobic gram-positive cocci	About 1-2 weeks
Moderate to severe infection	Broad regimen covering gram-negatives and anaerobes, then de-escalation	About 2 weeks for soft tissues
After a "minor" amputation with a positive bone margin	Targeted therapy based on sensitivity	Up to 3 weeks
Osteomyelitis without bone resection	Targeted therapy based on sensitivity	About 6 weeks

Table 9. The role of revascularization in gangrene

Target	Endovascular methods	Open shunts
Restore direct flow to the wound pool	Less invasive, faster recovery	High durability with complex anatomy
Symptom control and healing	Effective with appropriate anatomy	Preferred for extended occlusions
Restrictions	Risk of restenosis, need for retherapy	Higher early surgical risk

Prevention

Prevention includes daily foot examinations, proper footwear and insoles, regular nail and skin care, and prompt treatment of calluses and corns. Patients with diabetes should undergo risk stratification at least annually, and more frequently if at high risk, along with training in self-management skills. Smoking cessation and control of blood glucose, lipids, and blood pressure reduce the risk of ulceration and severe outcomes. The presence of any ulcer requires early referral to a specialized multidisciplinary team. [27]

Forecast

The prognosis is determined by the speed of treatment initiation, the depth and extent of necrosis, tissue perfusion, and the effectiveness of debridement. Rapid restoration of blood flow, combined with adequate debridement and appropriate antibacterial therapy, greatly increases the chance of limb salvage. Delays in diagnosis and treatment increase the risk of major amputation and death. The long-term prognosis improves with secondary prevention and observation. [28]

FAQ

Is this really gangrene, not just a "black scab" on the ulcer?
Gangrene is indicated by signs of necrotic tissue with a clear or, conversely, spreading border, changes in temperature and color, an unpleasant odor, and systemic signs of infection. The final decision is made by a doctor after examination and, if necessary, wound revision. Urgent treatment is warranted if there is any doubt. [29]

Is it possible to treat with antibiotics alone, without surgery?
In the presence of necrosis and especially in deep infections, surgical debridement is necessary, as antibiotics poorly penetrate dead tissue; it is combined with antibacterial therapy and restoration of blood flow. Exceptions are limited and require strict selection. [30]

When is revascularization necessary?
If perfusion parameters are low or there are signs of ischemic pain at rest, ulcers are not healing, and necrosis is increasing, restoration of blood flow is indicated as soon as possible. The goal is to ensure direct flow into the wound bed, thereby allowing healing to occur. [31]

Is hyperbaric oxygen therapy worthwhile?
It is not recommended as a treatment for foot infection itself; it does not replace debridement and restoration of blood flow. It is considered only as part of an individual program for clear indications. [32]

What perfusion thresholds are considered critical?
Systolic pressure at the fingertip below 30 mmHg and transcutaneous oxygen tension below 25-30 mmHg typically indicate an extremely low probability of healing without reconstruction. The decision is made based on the overall picture. [33]