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Gas gangrene of a different origin in trauma patients- report of 2 cases

Mariusz Stasiak*, Jerzy Lasek*, Alfred Samet**, Anna Śledzińska**, Zbigniew Witkowski*, Ewa Augustynowicz***, Wojciech Marks*, Janusz Ślusarczyk***

*Department of Trauma Surgery Medical University of Gdańsk, Poland
**Department of Clinical Microbiology Public Hospital No.1 Medical University of Gdańsk, Poland
***Department of Sera and Vaccine Evaluation, National Institute of Hygiene, Warsaw, Poland

Address for Correspondence

Mariusz Stasiak
Department of Trauma Surgery Medical University of Gdańsk,
Ul. Dębinki 7 Gdańsk 80-211  Poland
Phone : +48583492402
E-mail :

J.Orthopaedics 2007;4(1)e15


Gas gangrene is an extremely severe surgical infection with high mortality (1-6). It is a fulminant necrotizing soft tissue infection caused by anaerobic bacteriae belonging to genus Clostridium which are Gram positive, cylindrical in shape bacilli and produce endospores (1,2,3,7). Pathogenic Clostridia produce toxins developing tissue necrosis (1,7). The main pathogens in gas gangrene are: C. perfringens type A (85- 90%) (1,7,8) and C. septicum, C. novyi, C. histolyticum, C. sordelli, C. fallax, C. carnis (1,3,4). Clostridial infections are usually polymicrobial (1).

Representatives of the genus Clostridium are found mainly as endospores in soil, dust and constitute a common component of the bowel flora in humans and animals (C. perfringens) or female genitourinary tract (mainly C. septicum) (1,2,3). In general Clostridia are widely distributed in nature (1,2).

In this paper we present two patients with severe gas gangrene syndromes of a completely  different origin in order to present that patients following trauma may develop infections originating both from their own bacterial flora and from an  external source (1,2,5). Clostridial infections in these patients were confirmed by positive cultures.

Case reports:

Case 1.

A 65 old male, was admitted to our Department following severe shotgun injury of the chest and left shoulder girdle. He shot himself accidentally during the poaching expedition while using a sewed-off shotgun. At the admission he was under the influence of alcohole (serum ethanole level 2.29 0/00). The patient was in a profound traumatic shock, with poor respiration, unconscious. Resuscitation procedures were initiated and after performing X-rays multifragmental left scapula fracture, multiple left rib fractures, left haemopneumothorax, vast subcutaneous thoracic emphysema were diagnosed. It was decided to operate on the patient. A left latero-posterior thoracotomy was performed,  vast pleural haematoma was evacuated and lacerations of the lung tissue were sutured; pleural suction drainage was installed. After the surgery the patient was admitted to the ICU, intubated with controlled mechanical  ventilation. Wide-spectrum empirical antibioticotics was administered- piperacillin+tazobactam (Tazocin) 3x4,5/day i.v. During three postoperative  days the  patient was stable- chest X-ray examination showed parenchymal densities in the left lung, bronchofiberoaspiration (BFA) was performed, pleural cavity drainage reached 150-200 ml/day. The patient’s temperature was mildly elevated- 37oC. On the fourth day a serosanguineous exsudate from the postoperative wound was observed; surrounding tissues were mildly reddened, oedematous. Subcutaneous crepitations were noted. An urgent surgical intervention was instituted with the vast excision of necrotic tissues (Fig.1). Tissue and fluid specimens were microbiologically examined and cultured. Direct microscopic examination showed large number of Gram positive cylindrical- and spheric- shaped forms. Cultures revealed multibacterial growth- C. perfringens, Staphylococcus aureus and Enterococcus sp.  C. perfringens strain  was identified as type A (alpha, theta and kappa toxins producing). The patient was transferred to the Hyperbaric Medicine Department (head dr Z.Sićko). He stayed there for 8 days, receiving 15 sessions of hyperbaric oxygen therapy (HBO). Antibioticotherapy was modified- the patient was given intravenously penicillin (3x10 mln u./day) and metronidazole (3x0.5/day i.v.). Besides he was given a complete parenteral alimentation. The wound dressings were changed every day with further surgical debridement; dissinfectants (Octenisept, Hibitane) were used locally. Further microbiological procedures showed no anaerobic growth; hospital multi-resistant strains of Enterococcus faecium and Acinetobacter baumannii were cultured. These findings forced further antibioticotherapy modifications due to pathogens susceptibility- vancomycin (2x1.0/day i.v.) and netilmycin (3x0,05/day i.v.) instead of penicillin; with further therapy with metronidazole. After 8 days the patient left the ICU. Another surgical excision of necrotic tissues from the left axillar region was performed. Two consecutive skin transplantations were also performed. Full rehabilitation program was introduced. After 67 days of hospitalisation the patient went home in good condition.

Case 2.

A 60 year-old male was admitted to our Department for an elective operation in order  to remove osteosynthesis implants. The patient underwent osteosynthesis a year before because of pertrochanteric right femur fracture. Complete bone union of the fractured bone was achieved. The patient was homeless, suffered from gastric and duodenal ulcerative disease. Surgical removal of an angled plate from the femur was performed. On the third postoperative day the wound region became painful, with pale, oedematous marigins, and serosanguineous exsudate. The wound was opened in the upper part and a  drain was installed. The fluid from the wound was taken for microbiological examination. Empirical antibioticotherapy was initiated- ampicillin+sulbactam (Unasyn) 2x1,5/day i.v. No disorders of consciousness were present.  On the fifth postoperative day positive bacterial cultures revealed- C. perfringens, C. bifermentans. The wound was widely reopened (Fig. 2); necrotic tissues, with cooked-like muscles were extensively excised. Microbiological examinations were repeated revealing the same bacteriae- C. perfringens, C. bifermentans. C. perfringens strain  was identified as type A (alpha, theta and kappa toxins positive). The patient was transferred to the Hyperbaric Medicine Department. He was treated with HBO for 3 days; 5 sessions of HBO. The patient was given intravenously penicillin (3x8 mln u./day) and metronidazole (3x0.5/day i.v.). The wound dressings were changed every day; necrotic tissues were removed; dissinfectants (Octenisept, Hibitane, Betadine) were used locally. A significant local improvement was observed; on the 18-th day after the operation the wound was resutured. Rehabilitation was initiated. On the 40-th postoperative day the patient was excribed home in good condition.

Both patients’ C. perfringens isolates were cultured on the Columbia Sheep Blood Agar anaerobically. They were further identified by a classical method and VITEK ANI cards (bioMerieux). Patients’ cultured strains from the genus Clostridium were  isolated and kept in lyophilised at the Department of Sera and Vaccines Evaluation at the National Institute of Hygiene in Warsaw, Poland. C. perfringens strains were identified by Gram staining, urease and lecithinase assays, and other biochemical tests (9). The biotype of C. perfringens strains was determined by seroneutralization of lethality using intravenous injection in mice at the time of strain identification during (9). Multiplex PCR to detect C. perfringens were performed with primers designed for plc, cpb1, etx, and iap genes fragments. Primers sequence and PCR conditions were previously described (9). Classical biotyping of analysed C. perfringens collection, performed by the seroneutralisation of lethality by intravenous injection in mice revealed that both C. perfringens strains were of biotype A ( alpha, theta and kappa toxins positive). Similar data of toxin type determination were obtained by multiplex PCR for both C. perfringens strains, as amplification was successful for 402 bp product for cpa1/cpa2 primers designed for plc gene, and there were no products for cpb3/cpb4, cpe1/cpe2, and cpi1/cpi2 primers designed for detection of cpb1, etx, and  iap genes, respectively.

Fig. 1: The debrided area of the wound revealing devitalized muscles and tissue.
Fig. 2: Open wound with characteristic pale disintegrating muscles and exsudate.

Discussion :

During the World War I in the Northern Europe the incidence of gas gangrene was 12% with the mortality of 25% (1). The introduction of early wound excision resulted in a significant decrease of gas gangrene down to 1% by the end of WW I (1) . During the WWII the incidence of this infection among British soldiers ranged from 0.3 to 0.8 %; the incidence among American troops varied from 0 to 4.5 % (1) with 5% rate in severe wounds (2). Nowadays, the morbidity is assumed to be less than 0.08 %, with no mortality(1).

In the 1970s, according to the British and American authors the incidence of gas gangrene in civilian practice varied from 0.1 to 1 per million population per year and is connected mainly with trauma (1).  According to Abella BS, Kuchnic P, Hiraoka T et al. about 1000 cases of gas gangrene are recorded each year in the USA (2). There are no precise epidemiologic data concerning this issue in Poland .

It is estimated that about 50% of clostridial infections are posttraumatic, 35% develop in vast surgical wounds, 15% are spontaneous, atraumatic or metastatic (2).

In the above described cases the most severe type of clostridial infection- i.e. myonecrosis with extensive muscle involvement and severe toxemia was observed. In such cases clinical symptoms of gas gangrene may appear as early as 6-8 hours from the onset (1,7). The linear progress of the inflammation may be as fast as several cm per hour (1,2,7). The incidence of septic shock and multiorgan failure (MOF) in such cases is estimated at 50%, and mortality rate rises up to 40% (7).

Clostridium genus multiply and produce toxins responsible for the clinical symptoms of the disease only when the oxidation-reduction potential of the tissues is below + 74 mV (normal values are from +126 to +246 mV) (1). Such conditions occur as a consequence of local or systemic tissue anoxia.(i.e caused by posttraumatic, cardiogenic or hypovolemic shock) (1,2). Gunshot wounds cause extensive tissue damage by temporary and permanent cavities and disturb local tissue perfusion (1). Crush injuries of limbs are connected with significant blood loss and poor perfusion (1). Inadequacies in management of limb injuries i.e application of tourniquets and too tight plasters, missed diagnosis of vessels injuries cause similar conditions (1). Any damage involving the skin is of great importance as potential invasion gates of the infection (1,2,4,5). Metal implants might carry the pathogens (1,6). There are more sources of contamination: missiles and their fragments, pieces of clothing and tissues (1,6). Soil that contaminates the wound usually contains large numbers of aerobic bacteria like  Escherichia coli and Proteus sp (1). They contribute to the initiation of anaerobic bacterial growth by decreasing the oxidation-reduction potential. This enables the spores of Clostridium to change into vegetative forms, multiply and produce toxins responsible for clostridial infection symptoms (1,5,7). This course of events is typical for posttraumatic gas gangrene. Gas gangrene may also develop after elective surgery, i.e amputation for obliterative arterial disease, surgical stabilisation of lower limb fractures, gastrointestinal surgery especially including bowel and  biliary tract, artificial abortions (1,2,5). Microorganisms resposible for the infection in these cases come from the endogenous flora of the buttock and tight skin and mucosa (1-6). The application of bloodless field techniques, insufficient haemostasis, excessive use of diathermy, aggressive operative procedures enable these bacteria to infiltrate the damaged tissues (1,5).

Clinical symptoms of gas gangrene may coexist with those  induced by the trauma like: contusions, abrasions, fractures and tight plasters. A suprisingly strong pain results from the tension of the affected tissue (1,2,4). Other specific symptoms are: crepitus (when the infection begins in deep layers of the wound it is not always present), typical unpleasant, foul smell, oedema, erythema, blisters filled with serous or saiguinoserous fluid (1,2,5). The margins of the wound are necrotic and its inner parts reveal pale, disintegrated muscles (1). The arterial pulse may be impalpable and the rigidity of muscles may be observed.

General symptoms depend on the level of toxemia, including symptoms of toxic shock and multiorgan failure (1,2,3,6). Frequent pulse, inadequate to the mild rise of body temperature is one of the early ones (1,2). Disorders of the patients’ consciousness are manifestation of process affecting the central nervous system- encephalopathy(5). When they appear at the onset of the disease, the prognosis is usually poor. Encephalopathy is a result of damage of cerebral blood vessels by clostridial toxins (7,8). Further progress of the disease may result in significant downfall of arterial blood pressure, eventually resulting in shock  (2,3,5,6). Body temperature rises moderately, and the lack of fever may suggest poor prognosis. Haemolytic anaemia, throbocythopenia and jaundice, acute renal failure may be observed (1,2,5,6). Gas gangrene may lead to clostridial sepsis and haematogenic spread of the infection resulting in secondary focus of infection (1,3).

“Key toxins” are: alpha toxin and theta toxin (1,7,8). Alpha toxin possesses activities of  lecithinase (PLC) and haemolysine (1,7,8). High concentrations  of alpha toxin are required to cause clinical symptoms of gas gangrene (2,7,8). Alpha toxin causes  damage, lysis of cell membranes which has a lethal effect to various tissues i.e. haemolysis, lysis and aggregation of platellets, lesion of leucocytes and endothelial cells, creation of conglomerates of fibrin, leucocytes, platelets  which obliterate blood vessels, lesion of myocardium cells resulting in arrythmias, bradycardia, hypotension, cardiogenic shock (7,8). Alpha toxin has got also dermonecrotic properties (7). Alpha toxin inhibits  functions of neutrophils, which are unable to penetrate the infected tissues (leucostasis) (2,7,8). It is assumed that alpha toxins pathogenicity is bound with the arachidonic acid cascade (7,8). Theta toxin is called a lethal haemolysin or perfringolysin O. It is responsible for the necrosis of tissues. It also increases permeability of blood vessels and is cardiotoxic (7,8). The synergic interactions of both toxins is of great importance, as they decrease tissues perfusion by damaging  capillaries (7,8).

While performing bacteriological diagnosis of gas gangrene it is essential to obtain biological materials from the “borderline” of the infected area (fragments of tissues, discharge) (1,4,6). Smears taken from the wound are not recommended. The biological samples undergoes direct examination by Gram staining(1,2,4,5,6). Members of genus Clostridium present themselves in microscopic examination as cylindrically shaped, gram-positive forms(1,2,4).  A positive culture is the final confirmation of the diagnosis (1,4,5). Histopatologic examinations of the possibly infected tissue might be helpful in establishing quick  diagnosis (1,2).

The progress of gas gangrene is rapid. Prognosis therefore relies on the time of diagnosis. Two elements are necessary to establish proper diagnosis: the typical clinical course and the presence of cylindrical, gram-positive forms in direct microscopic examination (4,5).(2,4). It involved radical excision of all the affected tissues and amputation procedures (2,4,5). The results of amputations were often unsatisfactory as they were not radical enough and patients required higher limb reamputations. Other historical methods of treatment included dressing the wound using H2O2, chloramine and other oxygen “carriers” combined with wide incisions of the affected soft tissues. Deep intramuscular injections of pure oxygen were also performed. These methods were generally ineffective; they could not stop  progress of the disease. Antitoxin also did not prove to be a satisfactory treatment of gas gangrene. HBO was introduced in the mid 70’s (1,10). Nowadays it is generally accepted as the treatment of choice in anaerobic infections, especially in cases of gas gangrene (2,4,5,10). It decreases mortality and shortens the time of treatment; it inhibits the production of toxins and significantly improves the oxygenation of the damaged  tissues and the cytotoxic abilities of phagocytes (10).

Successful treatment of gas gangene is always a combined one (4,5,10). HBO therapy should be completed by surgical procedures, empirical antimicrobial therapy and application of antiseptics. Antiseptics effective against Clostridium spp, including spores are: 0,1% Octenisept, 10%  Betadine, 5% Hibitane (4). Based on our clinical experience we prefer to use Octenisept because of its high antibacterial efficacy, good tolerance and safety.

Clostridia associated with wound infections are susceptible to several antimicrobial agents: penicilin (2,5) combined with lincosamides i.e clindamycin or metronidazole(5,6).

However surgery still plays an essential part in the proper management of gas gangrene. Nowadays the operations are not as radical as they used to be in the past. They include incisions widening  the wounds, relieving tension of the soft tissues (2,5). The necrotic tissues are removed but the excision should not be too radical because they undergo a demarcation during hyperbaric oxygen therapy (5,10). Lately amputations in posttraumatic cases are rarely performed (5).

A detailed knowledge of the clinical course, pathophysiology, diagnostic and up to date methods of treatment of gas gangrene are essential for surgeons and emergency medicine specialists. In cases of this infection rapid and adequate management usually results in saving patient’s life and allows to avoid serious body disability. All cases with surgical soft tissue infections should be monitored microbiologically (5).

It is worth considering that patients planned for elective surgical procedures should have a rectal tamponage with dissinfectants (Octenisept, Betadine, Hibitane) in prevention of endogenous infections of the opperative field.

Proper management of gas gangrene should be based on close cooperation between a surgical staff and a microbiological laboratory experienced in problems of clostridial infections.

Reference :

  1. Sussmann M, Boriello SP, Taylor DJ. Gas gangrene and other clostridial infections. In: Collier L, Balows A, Sussman M, eds. Topley and Wilsons’ Microbiology and Microbial infections, Ninth edition. London, Arnold; 1998:669-684.
  2. Abella BS, Kuchnic P, Hiraoka T et al. Atraumatic clostridial myonecrosis: case report and literature review. J Emerg Med. 2003;4:401-405.
  3. Chew SSB, Lubowski DZ. Clostridium septicum and malignancy. ANZJ Surg. 2001;71:647-649.
  4. Lorea P, Baeten Y, Chahindi N, Franck D, Moermans JP. A severe complication of muscle transfer: clostridial myonecrosis. Ann Chir Plast Esthet. 2004;49:32-35.
  5. Voros D. Anaerobic infections of the soft tissues and bones. Anaerobe. 1997;3:117-119.
  6. Dunham CM, Coates S. Clostridial septic shock following an isolated, hepatic gunshot wound. Injury. 1996;4:291-293.
  7. Stevens DL, Bryant AE. The role of clostridial toxins in the pathogenesis of gas gangrene. CID. 2002; 35 (Suppl. 1):593-600.
  8. Awad MM, Ellemor DM, Boyd RL, et al. Synergistic Effects of Alpha-Toxin and Perfringolysin O in Clostridium perfringens-Mediated Gas Gangrene. Infect  Immun. 2001; 12:7904–7910.
  9. Augustynowicz E, Gzyl A, Ślusarczyk J. Molecular epidemiology survey of toxinogenic Clostridium perfringens  strain types by multiplex PCR. Scand J Infect Dis. 2000;32 :637-641.
  10. Strauss MB, Bryant B. Hyperbaric oxygen. Orthopedics. 2002;3:303-310.


This is a peer reviewed paper 

Please cite as : Mariusz Stasiak:Gas gangrene of a different origin in trauma patients- report of 2 cases

J.Orthopaedics 2007;4(1)e15





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