Gas gangrene or clostridium myonecrosis is an acute, rapidly progressive, gas-forming necrotizing infection of muscle and subcutaneous tissue. Myonecrosis is a condition of necrotic damage that is specific to the muscles.
Gangrene refers to a type of tissue death caused by the inadequate blood supply. It is a complication of necrosis, characterized by decay of body tissue.
The typical incubation period for gas gangrene is usually less than 24 hours.
Tissue turns black and or dark green and also malodorous
What are the types of gangrene?
There are two main types of gangrene
- Dry gangrene
- Wet gangrene.
In dry gangrene, there is an obstruction or slowing of blood flow into the part of the body that is affected. Mostly seen in type 1 and type 2 diabetes patients due to damage to blood vessels.
This type of gangrene is characterized by cold, painless and dry and shriveled up affected parts.
Wet gangrene, on the other hand, occurs when infection and bacteria invade deeper tissues.
Massive tissue swelling is due to the release of the toxins from the invading bacteria. This causes blockage of the blood supply and worsening of the infection as the white blood cells cannot reach the area affected via blood vessels.
This type of gangrene can spread much quicker than dry gangrene.
Other types of gangrene are:
- Necrotizing fasciitis,
- Meleney’s synergistic gangrene,
- Fournier’s gangrene,
- Noma or cancrum oris,
- Internal gangrene.
You can learn about Fournier’s gangrene in detail in our article here.
Gas gangrene that we are covering in this article is a kind of wet gangrene
What are the causes of gangrene?
Clostridial organisms are common causes.
Facultative anaerobic spore-forming gram-positive bacilli. They produce a number of toxins and the most prevalent and lethal one is known as alpha-toxin.
Of these clostridia, perfringens is the most common cause found in about 90% of the wounds.
Other clostridium bacteria are clostridium nivyi, clostridium septicum, clostridium histolycum, clostridium bifermentans, and clostridium fallax.
There are two main mechanisms that these microbes enter the body. Either due to infection, or ischemia and common in lower extremities.
It can be seen in post-trauma, post-operative situations, and in deep penetrating dirty wounds. It causes a progressive invasion and destruction of healthy tissues
Pathophysiology of gas gangrene
Gas gangrene is commonly caused by toxin-producing clostridial microbes that are found in the soil of normal flora. C perfringens produces a kind of toxin known as an alpha-toxin that is known to be lethal and also known as lecithinase or phospholipase C.
In C. septicum, the alpha-toxin forms pores and induces necrosis by causing the rapid loss of intracellular potassium and depletion of adenosine triphosphate (ATP). This increases vascular permeability and leading to necrosis or death of the tissues. Then the bacteria when they get entry they invade and proliferate in the dead or necrotic tissue producing more and more toxins. These toxins then damage the neighboring tissues very rapidly while producing gas.
The C perfringens also produce a toxin known as kappa-toxin which is a collagenase responsible for the destruction of blood vessels and connective tissue.
The fermentation of glucose is an apparent mechanism of gas production in gas gangrene.
It is often difficult to identify the extent of the infection because the clostridium perfringens can work deeper in the fascial layers below the skin. The discharge is different from other anaerobic infections in that it is non-purulent but is thinner than the normal puss and described as sweetly putrid. This is due to the fact that lecithinase and other toxins cause lysis of the neutrophils.
These produced exotoxins can cause severe hemolysis leading to a drop in levels the levels of hemoglobin to very low levels and, when occurring with hypotension, may cause acute tubular necrosis and renal failure
The alpha-toxin is the virulence factor in the pathogenesis of gas gangrene.
Traumatic and post-operative infection or non-traumatic means associated with conditions such as diabetes mellitus, alcoholism, peripheral vascular disease, intravenous drug abuse, malignancies.
What are the toxins produced by clostridium perfringens?
Clostridium perfringens produces at least 20 known exotoxins but the most important exotoxins are as follows:
The alpha-toxin also is known as lecithinase is lethal, necrotizing, hemolytic and cardiotoxic
Iota toxin and Beta toxin – necrotizing and lethal
Epsilon toxin is Lethal, and permease
Delta toxin is lethal, and hemolysin
Phi toxin is a hemolysin and cytolysin
Kappa toxin is lethal, collagenase, gelatinase and necrotizing
Lambda toxin is a protease
Mu toxin is a hyaluronidase
Nu toxin is also lethal, deoxyribonuclease, hemolytic and necrotizing
signs and symptoms
Diagnosis starts from a good clinical examination
The patient will present with the following features.
A sudden pain of the extremities or the affected body part
Tachycardia (rapid heart rate) that is nonproportional to the fever
Bronzing of the skin on the affected areas whereby they turn purple or red
Crepitus caused by gas escaping from the necrotic tissue.
Formation of blebs or bullae
Thin serosanguinous exudate and sweet odor
Rapid local extension
In about 3 days the patient is extremely sick, looking toxic and moribund.
Obtunded sensorium and features of systemic toxicity
The infection progresses rapidly to toxemia and shock therefore these patients may present with features of systemic toxicity.
Take a good history and physical assessment of the patient taking into consideration the clinical evidence of crepitus in soft tissue.
Soft tissue x-rays of the involved area are taken to detect gas dissecting along the fascia planes
The absence of gas does not exclude a significant disease.
Stat gram stain of wound exudate for gram-positive bacillus with a paucity of leucocytes
Diagnostic tests and interpretation
Laboratory tests performed are
Complete blood count with differentials will show hemolytic anemia, electrolyte levels, blood urea nitrogen and creatinine levels.
The CBC count may show hemoconcentration and extreme leukocytosis is systemically toxic patients.
These patients will have elevated lactate dehydrogenase (LDH) level
Evaluate the patient for hemolysis
Stat gram stain for wound exudates
Anaerobic cultures of wounds or tissue biopsy
Imaging studies performed include
A radiograph of the affected body part which may show features of soft tissue gas
A CT scan may be done if the affected area is the abdomen or flank.
All patients with gas gangrene must undergo surgical debridement
The differential diagnosis for gas gangrene include;
- Necrotizing fasciitis
- Nonclostridial myositis and myonecrosis
- Othe causes of gas in tissues as from dissection from respiratory or gastrointestinal tracts
Treatment of gas gangrene
Prehospital treatment includes the establishment of intravenous access and infusion with isotonic fluids.
The initial stabilization therapy entails the management of the airway and resuscitation of the patient if necessary.
This can be done by rapid sequence intubation or supplemental oxygen
Cardiac and oxygen saturation monitors should be placed to monitor the oxygenation of the patient
Intravenous access is recommended in these patients. central venous pressure monitoring and sepsis control protocol is appropriate
Aggressive volume expansion using crystalloids, plasma, packed red blood cells and albumin if there is a septic shock.
Parenteral antibiotic therapy in gas gangrene
The initial empiric therapy should cover clostridium species and group A streptococcus as well as mixed aerobes and anaerobes.
Primary definitive therapy includes the use of penicillin G and clindamycin.
Alternative therapy is the use of ceftriaxone or erythromycin
If mixed infections are present then penicillin plus clindamycin or vancomycin and gram-negative coverage with gentamycin are appropriate
in patients with penicillin allergy, a combination of metronidazole and clindamycin is used.
A combination of penicillin and metronidazole may be antagonistic and is not recommended
In the management of sepsis follow te local sepsis protocols.
Gas gangrene is not subtle and should prompt immediate return to the operating room for wound reopening and washout
Surgical consultation for daily debridement, amputation of the affected extremity or fasciotomy for compartment syndrome is required.
Copious irrigation with sterile normal saline solutions and/or 3% liquid hydrogen peroxide should be performed.
Wound cleaning and leave them open with negative-pressure wound dressing therapy or just a sterile dressing.
Hyperbaric oxygen therapy can be used as adjunctive therapy: Early transfer to hyperbaric oxygen facility may be life-saving. From studies, this has suggested benefits. The oxygen saturates the infected tissues preventing the growth of obligate anaerobic clostridia
Tetanus prophylaxis using a tetanus toxoid
Observe for major complications such as acute respiratory distress syndrome, renal failure, myocardial irritability, and disseminated intravascular coagulation.
The medications used are
- Ceftriaxone 2 grams intravenously twice a day in adults and in pediatrics is 100mg/kg/24 hours with a maximum of 4 grams
- Clindamycin 900 mg intravenously three times a day in adults. For pediatrics is 40mg/kg/day every 6 hours.
- Erythromycin 1 gram intravenously every 6 hours in adults and 50mg/kg/day every 6 hours in pediatric patients.
- Gentamycin 2mg/kg intravenously every 8 hours in adults and pediatrics
- Metronidazole 500 mg intravenously every 8 hours in adults
- Penicillin G 24 million IU in 24 hours intravenously every 4-6 hours. In pediatrics, the dosage is 250,000 IU/kg per day.
- Tetanus immune globulin 500IU intramuscularly and
- Tetanus toxoid 0.5mg intramuscularly
Primary definitive therapy for clostridial species is the combination of penicillin G and clindamycin
All patients with gas gangrene and evidence of myonecrosis must be admitted for surgical debridement and intravenous antibiotics.
The use of hyperbaric oxygen therapy is an important adjunctive therapy for these patients.
No patient with acute gangrene should be discharged.
Pearls and pitfalls.
Bacteremia occurs in about 15% and can progress quickly to intravascular hemolysis.
HBO and adjunctive therapy to surgical debridement and early antibiotics if a patient id hemodynamically stable.