Gas gangrene has often erroneously been associated (almost exclusively) with trauma.A surprisingly large number of gas gangrene cases in which trauma was not a factor have alsobeen reported.Aetiological factors can be divided into post-traumatic, post-operative (non-traumatic)and spontaneous (neither injury nor surgery). A review of 284 reported cases of gas gangrenerevealed the following distribution of aetiological factors:- traumatic 49%- surgical 35%- spontaneous 16%.Posttraumatic aetiological factors can include compound fractures, gastro-intestinaltrauma, burns, criminal abortions and even bee stings, injections and venepunctures.Clostridial sepsis of the abdominal wall can occur post-operatively (no trauma) andit can follow, in descending order of importance, surgical procedures involving the appendix,biliary tract, small intestine or upper gastrointestinal tract. Endogenous sources of Clostridiasuch as the skin or gastrointestinal tract are implicated in elective surgical cases. Lastly, itmust be noted that spontaneous clostridial sepsis (no injury or surgery) can occur. Theunderlying conditions implicated in the development of this spontaneous sepsis includecolonic malignancies, diabetes mellitus, burns, peri-rectal abscesses, ileus, acute cholecystitisand arteriosclerotic peripheral vascular disease.PathophysiologyIf tissue (mainly muscle tissue) is contaminated with Clostridia and anaerobicconditions exist, or are created for any reason whatsoever, the organisms then have anenvironment in which they can multiply and liberate the exotoxins which initiate thefulminant phase of the process: an intense oedema develops around the area of necrosis withlittle or no inflammatory response. This swelling in itself comprises the blood supply,reducing the availability of leucocytes and lowering the oxygen tension of the tissues, leadingto rapid spread of the necrotizing process, with a fulminating toxaemia as a result of theexotoxins.Clostridium perfringens is known to produce 12 toxins that are active in the tissues,as well as an enterotoxin. In infections by this organism, five major and a number of minorexotoxins responsible for local and systemic changes have been identified. The alpha-toxin,a C-lecithinase (a phospholipase), is the major lethal toxin that splits lecithin. It causeshaemolysis, platelet destruction, capillary damage and necrosis. It is also oxygen stable, i.e.it remains active when exposed to hyperbaric oxygen at 2 or 3 atmospheres absolute (ATA).The haemolysis leads to anaemia, haemoglobinuria, jaundice, oliguria and renal failure.The remainder of the exotoxins are responsible for destroying, liquifying, and dissecting intoadjacent unaffected tissue, thus promoting rapid fulminating spread of the process. Otherenzymes involved include fibrinolysins, hyaluronidase, collagenase, haemolysin and cytolysin.The oedema and development of gas in the fascial compartments cause expansion with raisedintracompartmental pressure. At first the muscles are haemorrhagic and friable. Later the34
muscle tissues change to a dark colour and lose their contractility with secretion of a brickred,foul-smelling fluid and the development of gas-containing bullae.Systemic effects such as cardiotoxicity, brain dysfunction and renal failure may be theresult of proteolytic and saccharolytic enzymes which are responsible for the production ofhydrogen sulphide. The various species of Clostridia liberate their own specific endotoxins,i.e. the alpha-toxin of Clostridium novyi predominantly increases vascular permeability.Clinical PresentationThe incubation period in the trauma and post-surgical groups ranges from eight hoursto 20 days, with an average of four days after the initiating event.It must be noted that patients with gas gangrene remain remarkably alert with extremesensitivity to their surroundings, despite profound shock, impairment of renal function andadvancing palpable crepitus. They realise their impending doom and a sense of terror becomesevident in their facial expression. Just before death they mercifully lapse into a toxic deliriumand coma.Successful management depends on early diagnosis of this condition - thus a highindex of suspicion should be maintained to ensure recognition of the early signs of theinfection, which include subtle changes such as:- pain in a wound or a surgical incision which increases progressively in intensity andis disproportionately severe- a tachycardia disproportionate to the fever- shiny oedematous skin around a wound, and- apathy.Suspicion should also be high in any situation where the patient is compromised byshock, vascular impairment, oedema, tight-tension skin sutures, abdominal distension or atight plaster cast. Progressive changes can take place towards the classic presentation of thedisease.smell"These include:- oedema- a discoloured wound with brown to brick-red watery discharge with a "foul-sweet- haemorrhagic bullae and rapid extention of the surrounding erythema.Palpable crepitations are only found later. Subsequently, shock and renal failure ensue.35