Gas gangrene (clostridial myonecrosis)

Gas gangrene (clostridial myonecrosis)

Gas gangrene is a dreaded consequence of late-presenting missile wounds and crushing injuries. It is a rapidly progressive, potentially fatal condition characterised by widespread necro sis of the muscles and soft-tissue destruction. The common causative organism is Clostridium perfringens , a spore-forming, Gram-positive saprophyte that flourishes in anaerobic condi tions. Other organisms implicated in gas gangrene include Clostridium bifermentans , Clostridium septicum and Clostridium sporogenes . Non-clostridial gas-producing organisms such as coliforms have also been isolated in 60–85% of cases of gas gangrene. C. perfringens produces many exotoxins but their exact role is unclear. Alpha-toxin, the most important, is a lecithinase that destroys red and white blood cells, platelets, fibroblasts and muscle cells. The phi-toxin produces myocardial suppres sion while the kappa-toxin is responsible for the destruction of connective tissue and blood vessels. Devitalised tissue or premature wound closure pro vides the anaerobic conditions necessary for spore germination. The usual incubation period is <24 hours but ranges from 1 hour to 6 weeks. A vicious cycle of tissue destruction is initiated by rapidly multiplying bacteria and locally and systemically act ing exotoxins. This causes spreading necrosis of muscle and thrombosis of blood vessels. The typical feature of this con dition is the production of gas that spreads along the muscle planes. Systemically , the exotoxins cause severe haemolysis and, combined with the local e ff ects, this leads to the rapid progression of the disease, hypotension, shock, acute kidney injury and acute r espiratory distress syndrome. Pain that rapidly increases in severity is the earliest symptom. The limb swells up and the wound exudes a serosanguineous discharge. The skin is involved secondary to muscle necrosis, turning brown and progressing to a blue–black colour with haemorrhagic bullae ( Figure 33.17 ). The characteristic sickly sweet odour and soft-tissue crepitus appear with established infection but their absence does not exclude the diagnosis. These local signs are accompanied by pyrexia, tachycardia, tachypnoea and altered mental status. The diagnosis is made on the basis of history and clinical features. A peripheral blood smear may suggest haemolysis eals large Gram-positive and a Gram stain of the exudate rev bacilli without neutrophils. The biochemical profile may show metabolic acidosis and renal failure. Radiography can visualise gas in the soft tissues and is particularly useful in patients with - chest and abdominal involvement. Patients should be admitted to the ICU and treated aggressively with careful monitoring. High-dose penicillin G - , and clindamycin, along with third-generation cephalosporins should be given intravenously . Surgical treatment is the same as for necrotising fasciitis (see Necrotising fasciitis ). In estab - lished gas gangrene with systemic toxicity , amputation of the involved extremity is life-saving and should not be delayed. No attempt is made at closure; amputation stumps are left open and the wound is lightly packed with saline-soaked gauze and then dressed. T he role of HBO is not as clear as in necrotising fasciitis. - However, considering the frequent catastrophic outcomes, it le. is recommended in severe cases if the facilities are availab Summary box 33.9 Gas gangrene /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF

Figure 33.17 Typical picture of spreading gas gangrene caused by a crush injury. Caused by C. perfringens Spores are present in the soil Thrives in anaerobic conditions and produces many exotoxins Treat with radical and regular surgical excision Give oxygen and penicillin Early amputation may be life-saving

Gas gangrene (clostridial myonecrosis)

Gas gangrene is a dreaded consequence of late-presenting missile wounds and crushing injuries. It is a rapidly progressive, potentially fatal condition characterised by widespread necro sis of the muscles and soft-tissue destruction. The common causative organism is Clostridium perfringens , a spore-forming, Gram-positive saprophyte that flourishes in anaerobic condi tions. Other organisms implicated in gas gangrene include Clostridium bifermentans , Clostridium septicum and Clostridium sporogenes . Non-clostridial gas-producing organisms such as coliforms have also been isolated in 60–85% of cases of gas gangrene. C. perfringens produces many exotoxins but their exact role is unclear. Alpha-toxin, the most important, is a lecithinase that destroys red and white blood cells, platelets, fibroblasts and muscle cells. The phi-toxin produces myocardial suppres sion while the kappa-toxin is responsible for the destruction of connective tissue and blood vessels. Devitalised tissue or premature wound closure pro vides the anaerobic conditions necessary for spore germination. The usual incubation period is <24 hours but ranges from 1 hour to 6 weeks. A vicious cycle of tissue destruction is initiated by rapidly multiplying bacteria and locally and systemically act ing exotoxins. This causes spreading necrosis of muscle and thrombosis of blood vessels. The typical feature of this con dition is the production of gas that spreads along the muscle planes. Systemically , the exotoxins cause severe haemolysis and, combined with the local e ff ects, this leads to the rapid progression of the disease, hypotension, shock, acute kidney injury and acute r espiratory distress syndrome. Pain that rapidly increases in severity is the earliest symptom. The limb swells up and the wound exudes a serosanguineous discharge. The skin is involved secondary to muscle necrosis, turning brown and progressing to a blue–black colour with haemorrhagic bullae ( Figure 33.17 ). The characteristic sickly sweet odour and soft-tissue crepitus appear with established infection but their absence does not exclude the diagnosis. These local signs are accompanied by pyrexia, tachycardia, tachypnoea and altered mental status. The diagnosis is made on the basis of history and clinical features. A peripheral blood smear may suggest haemolysis eals large Gram-positive and a Gram stain of the exudate rev bacilli without neutrophils. The biochemical profile may show metabolic acidosis and renal failure. Radiography can visualise gas in the soft tissues and is particularly useful in patients with - chest and abdominal involvement. Patients should be admitted to the ICU and treated aggressively with careful monitoring. High-dose penicillin G - , and clindamycin, along with third-generation cephalosporins should be given intravenously . Surgical treatment is the same as for necrotising fasciitis (see Necrotising fasciitis ). In estab - lished gas gangrene with systemic toxicity , amputation of the involved extremity is life-saving and should not be delayed. No attempt is made at closure; amputation stumps are left open and the wound is lightly packed with saline-soaked gauze and then dressed. T he role of HBO is not as clear as in necrotising fasciitis. - However, considering the frequent catastrophic outcomes, it le. is recommended in severe cases if the facilities are availab Summary box 33.9 Gas gangrene /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF

Figure 33.17 Typical picture of spreading gas gangrene caused by a crush injury. Caused by C. perfringens Spores are present in the soil Thrives in anaerobic conditions and produces many exotoxins Treat with radical and regular surgical excision Give oxygen and penicillin Early amputation may be life-saving

Gas gangrene (clostridial myonecrosis)

Gas gangrene is a dreaded consequence of late-presenting missile wounds and crushing injuries. It is a rapidly progressive, potentially fatal condition characterised by widespread necro sis of the muscles and soft-tissue destruction. The common causative organism is Clostridium perfringens , a spore-forming, Gram-positive saprophyte that flourishes in anaerobic condi tions. Other organisms implicated in gas gangrene include Clostridium bifermentans , Clostridium septicum and Clostridium sporogenes . Non-clostridial gas-producing organisms such as coliforms have also been isolated in 60–85% of cases of gas gangrene. C. perfringens produces many exotoxins but their exact role is unclear. Alpha-toxin, the most important, is a lecithinase that destroys red and white blood cells, platelets, fibroblasts and muscle cells. The phi-toxin produces myocardial suppres sion while the kappa-toxin is responsible for the destruction of connective tissue and blood vessels. Devitalised tissue or premature wound closure pro vides the anaerobic conditions necessary for spore germination. The usual incubation period is <24 hours but ranges from 1 hour to 6 weeks. A vicious cycle of tissue destruction is initiated by rapidly multiplying bacteria and locally and systemically act ing exotoxins. This causes spreading necrosis of muscle and thrombosis of blood vessels. The typical feature of this con dition is the production of gas that spreads along the muscle planes. Systemically , the exotoxins cause severe haemolysis and, combined with the local e ff ects, this leads to the rapid progression of the disease, hypotension, shock, acute kidney injury and acute r espiratory distress syndrome. Pain that rapidly increases in severity is the earliest symptom. The limb swells up and the wound exudes a serosanguineous discharge. The skin is involved secondary to muscle necrosis, turning brown and progressing to a blue–black colour with haemorrhagic bullae ( Figure 33.17 ). The characteristic sickly sweet odour and soft-tissue crepitus appear with established infection but their absence does not exclude the diagnosis. These local signs are accompanied by pyrexia, tachycardia, tachypnoea and altered mental status. The diagnosis is made on the basis of history and clinical features. A peripheral blood smear may suggest haemolysis eals large Gram-positive and a Gram stain of the exudate rev bacilli without neutrophils. The biochemical profile may show metabolic acidosis and renal failure. Radiography can visualise gas in the soft tissues and is particularly useful in patients with - chest and abdominal involvement. Patients should be admitted to the ICU and treated aggressively with careful monitoring. High-dose penicillin G - , and clindamycin, along with third-generation cephalosporins should be given intravenously . Surgical treatment is the same as for necrotising fasciitis (see Necrotising fasciitis ). In estab - lished gas gangrene with systemic toxicity , amputation of the involved extremity is life-saving and should not be delayed. No attempt is made at closure; amputation stumps are left open and the wound is lightly packed with saline-soaked gauze and then dressed. T he role of HBO is not as clear as in necrotising fasciitis. - However, considering the frequent catastrophic outcomes, it le. is recommended in severe cases if the facilities are availab Summary box 33.9 Gas gangrene /uni25CF - /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF

Figure 33.17 Typical picture of spreading gas gangrene caused by a crush injury. Caused by C. perfringens Spores are present in the soil Thrives in anaerobic conditions and produces many exotoxins Treat with radical and regular surgical excision Give oxygen and penicillin Early amputation may be life-saving