Etiology
Gas gangrene is a type of anaerobic bacterial infection caused by Clostridium species, leading to myonecrosis or myositis. This condition progresses rapidly and is associated with a poor prognosis. Several species of Clostridium are known, with Clostridium perfringens being the most common pathogen. Infections are typically polymicrobial rather than caused by a single organism. These bacteria are widely found in animal and human feces and in the surrounding environment, particularly in soil. Although contamination of wounds by these bacteria is common, actual infection is relatively rare, as the bacteria require an anaerobic environment to grow and reproduce within the human body. Situations with higher infection risk include open fractures with vascular injury, crush injuries involving deep muscle damage, prolonged tourniquet use, overly tight plaster casts, and severe trauma in regions near the perineum or anus.
Pathophysiology
These bacteria produce various exotoxins and enzymes that are harmful to human tissue. Some enzymes generate large amounts of gas—such as hydrogen sulfide and nitrogen—through processes like deamination and fermentation, causing gas accumulation in tissues. Other enzymes dissolve tissue proteins, leading to necrosis, exudation, and severe edema. The rapid expansion caused by the combination of gas and fluid increases local tissue tension, which may cause the skin to become board-like in firmness. The subfascial pressure rises dramatically, compressing microvasculature and further worsening ischemia, hypoxia, and tissue death—creating a vicious cycle that favors bacterial proliferation. Enzymes such as lecithinase and hyaluronidase also facilitate bacterial spread by enabling penetration through tissue planes.
Once established, the infection may spread longitudinally along muscle fascicles or muscle groups. The affected muscles turn brick-red and resemble cooked meat, losing their elasticity. If the subcutaneous tissues are involved, gas, edema, and necrosis can rapidly spread along fascial planes. Biopsy of living tissue may reveal gas bubbles between muscle fibers and numerous large, Gram-positive bacilli.
Clinical Manifestations
Symptoms usually develop 1 to 4 days after injury, though onset may occur as early as 8 to 10 hours or as late as 5 to 6 days. The clinical course is marked by rapid deterioration. Patients may become restless, agitated, and display signs of fear or euphoria. Pallor of the skin and lips, profuse sweating, tachycardia, and gradually rising fever are common. As the disease progresses, hemolytic anemia, jaundice, hemoglobinuria, and metabolic acidosis may occur.
Patients often describe the affected limb as heavy or increasingly painful, with pain resembling bursting or tearing—often out of proportion to the initial trauma and unrelieved by analgesics. Swelling typically exceeds what would be expected from the injury and rapidly spreads. Serous or serosanguinous discharge may be profuse, soaking through thick dressings; gas bubbles may be seen escaping when dressings are removed. Subcutaneous emphysema may produce crepitus on palpation. Local pressure may blanch the skin, and impaired superficial venous return can create a marbled skin appearance. Due to tissue liquefaction, decomposition, and gas production (including hydrogen sulfide), a foul odor is often present. On exploration, subfascial infections may reveal degenerated and swollen subcutaneous fat, high fascial tension, and muscle that does not bleed on incision.
Diagnosis and Differential Diagnosis
Due to the rapid progression, early diagnosis is crucial. Local clinical signs are key to early recognition. Identification of large, Gram-positive rods on wound exudate smear and evidence of gas in soft tissues on radiographs can confirm the diagnosis. Differential diagnosis should consider the following:
Gas accumulation in tissues is not exclusive to Clostridium infections. Rupture of certain organs (e.g., esophagus or trachea) from surgery, trauma, or pathology can cause subcutaneous emphysema and crepitus, but these are typically not accompanied by systemic toxicity, severe local swelling, or skin changes, and the gas tends to be absorbed over time.
Some facultative anaerobes, such as Escherichia coli and Klebsiella species, can also produce gas—mainly CO2, which is water-soluble and less likely to accumulate in tissues, and the gas lacks a distinctive odor.
Anaerobic streptococci may also generate gas, but systemic toxicity is milder, and progression is slower. If managed promptly with decompressive incisions, thorough drainage, and antibiotic therapy, the prognosis is generally favorable.
Prevention
The key to prevention lies in prompt and thorough debridement, which includes the removal of nonviable and ischemic tissues as well as the elimination of foreign bodies, particularly non-metallic ones. Deep and irregular wounds should be fully opened for drainage to avoid the formation of dead spaces. In cases of increased subfascial tension, early fasciotomy should be performed to relieve pressure. For wounds suspected of developing gas gangrene, irrigation or wet dressings with 3% hydrogen peroxide or 1:1,000 potassium permanganate solution may be used. In soft tissue injuries such as contusions or crush injuries, tissue viability is often difficult to determine in the early stage, and clearer demarcation generally appears within 24 to 36 hours; during this period, close observation is necessary. Penetrating abdominal injuries, especially those involving the colon, rectum, or perineum, should also raise suspicion for potential infection. Early administration of high-dose penicillin and metronidazole is recommended in these cases.
Treatment
Once the diagnosis is established, immediate and aggressive treatment is necessary to minimize tissue necrosis and reduce the risk of amputation. The main therapeutic approaches include:
Emergency Debridement
The extent of deep tissue involvement often exceeds what is visible on the surface; therefore, wide and multiple incisions should be made in the affected area, including regions with edema or subcutaneous emphysema surrounding the wound. Intraoperatively, the area should be fully exposed and examined, with complete removal of discolored, non-contractile, and non-bleeding muscle tissue. Since bacterial spread often surpasses the visually apparent lesions, entire muscle groups—including their origins and insertions—should be excised when necessary. If the infection is confined to a specific fascial compartment, the entire muscle group within that compartment should be removed. In cases of extensive infection throughout a limb, amputation may be necessary to save the patient's life. If the infection extends beyond the planned amputation level, the fascial compartments proximal to the level should be fully opened, followed by postoperative irrigation with oxidizing agents, wet dressings, frequent dressing changes, and further debridement if required.
Antibiotic Therapy
Penicillin is the first-line treatment, as Clostridium perfringens and related species are generally sensitive to it. However, high doses are needed, typically exceeding 10 million units per day. Macrolide antibiotics (e.g., roxithromycin, midecamycin) and nitroimidazoles (e.g., metronidazole, tinidazole) may also provide therapeutic benefits. Aminoglycosides (e.g., kanamycin, gentamicin) have been shown to be ineffective against these pathogens.
Hyperbaric Oxygen Therapy
Increasing oxygen levels in tissues helps create an environment that inhibits anaerobic bacterial growth and reproduction. This method can improve cure rates and reduce disability.
Systemic Supportive Care
This includes blood transfusions, correction of fluid and electrolyte imbalances, nutritional support, and symptomatic treatment as needed.