It is also called Clostridia MYOSITIS or MYONECROSIS.
It is a dangerous acute wound infection caused by anaerobic gas-forming organisms.
Etiopathology
The infection is characterized by inflammation gas formation and necrosis of muscles with severe toxemia. Extensive laceration and penetration of muscles of the buttock, thigh, or calf with F.B inside e.g. bomb splinters, dirty clothing, etc., produce a good breeding ground for gas gangrene organisms.
Gas gangrene organisms act in symbiosis with pyogenic organisms. The latter utilizes the oxygen and makes the wound partly anaerobic, where the gas gangrene organisms can flourish. The lowered oxygen tension is further helped by a large hematoma, thigh bandage, tourniquet, or plaster casing.
Gas gangrene organisms (gram-positive, anaerobic, spore-bearing) are in two groups:
A. Saccharolytic group -
Cl. Welchii,
Cl. Oedematiens,
Cl. septicum,
Cl. Aerogenes capsulatus.
B. Proteolytic group -
Cl. Sporogenes,
Cl. Fallux,
Cl Bifermentans
The damaged muscles containing a large amount of glycogen are good media for the growth of a saccharolytic group of organisms. They produce tissue destruction and extension of solid edema. Their exotoxin is highly depressive which is responsible for generalized toxemia with myocardial depression and peripheral circulatory failure. They also liberate hemolysin which gets free iron from myo-hemoglobin
The acid inhibits the growth of the saccharolytic group when the action of the proteolytic group comes into play. The proteolytic group split the protein and liberates H2S to form iron sulfide which responsible for the black discoloration of the muscles. At an early stage, the striated muscles are brick red, edematous, and non -contractile. The discharge from the wound is thin blood-stained with no pus. The fluid is highly toxic and full of gas gangrene organisms. Later the muscles turn greenish or blackish. The infection may be complicated with septicemia and other organs may contain gas. The liver is riddled with gas and is known as the foaming liver.
Sign and Symptoms or Clinical features
The incubation period is between hours to few days.
Pain: Complaint of severe pain at the site of injury for increased tension in muscles.
Toxemia: There is a sudden deterioration of the patient's condition. The pulse is rapid, tachycardia is disproportionate to temperature, B.P falls, Subnormal temperature. The patient looks pale, alert, and apprehensive. There may be jaundice.
Gas crepitus: The limb is tense, swollen and palpation reverts gas crepitus.
Wound: On examination of the wound, the stitches are seen to the under tension, and through the pouting edges, thin brownish fluid exudate, which possesses a sickly foul odor.
Investigation
Blood picture: There is no leukocytosis.
X-Ray: Will demonstrate the presence of gas in intramuscular planes. Gas and foul fluid form in the cellular spaces contractibility of the muscles soon lost and their color changes from dull red to green and then black.
Treatment
A. Prevention: Early thorough excision of dead and devitalized tissues is the best prophylaxis measure. The partial suture is sufficient and secondary suture can excision of the wound, it is better to keep it open.
Inj. A.G.S to be given after intradermal test.
Inj. Penicillin in repeated doses.
B. An Established case
General:
Isolation
Infusion of fluid and blood transfusion to combat toxemia and circulatory collapse.
In hypotension (persisting) vaso-pressure drugs may be necessary.
Inj. A.G.S to be repeated hourly
High doses of penicillin and streptomycin or Broad-spectrum antibiotic hourly I.V.
Nursing in a Hyperbaric Oxygen chamber.
Local:
Under general aesthesis adequate excision of all affected groups of muscles through the long incision.
In massive cases with fracture amputation or disarticulation is life shaving.
When condition under control secondary suture and skin grafting.
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