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CASE REPORT |
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Year : 2021 | Volume
: 17
| Issue : 4 | Page : 143-145 |
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An extensive anterior abdominal wall Meleney’s gangrene following bull gore injury
Jayabal Pandiaraja
Department of General Surgery, Dr. Mehta Hospital Global Campus, Chennai, Tamil Nadu, India
Date of Submission | 07-Jul-2021 |
Date of Acceptance | 16-Jul-2021 |
Date of Web Publication | 10-Mar-2022 |
Correspondence Address: Dr. Jayabal Pandiaraja Department of General Surgery, Dr. Mehta Hospital Global Campus, 26/1, Kaveri Street, Rajaji Nagar, Villivakkam, Chennai 600049, Tamil Nadu. India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/AMJM.AMJM_31_21
Meleney’s gangrene is a rapidly spreading gangrene of skin, subcutaneous tissue, and fascia. It has the highest mortality approximately 40% and more in immunocompromised and diabetic patients. The initial presentation mimics cellulitis and most of the cases are misdiagnosed. Delayed diagnosis and treatment increase mortality by approximately 100%. Our case is initially diagnosed as bull gore injury and underwent treatment of the same. Later patient developed extensive Meleney’s gangrene of the entire anterior abdominal wall and genitalia. Even with extensive wound debridement with antibiotic coverage fails to save the patient life. Therefore, early diagnosis and prompt surgical debridement in boll gore injury will reduce the chance of developing Meleney’s gangrene. Keywords: Abdominal wall infection, bull gore injury, Meleney’s gangrene, septic shock, synergistic gangrene
How to cite this article: Pandiaraja J. An extensive anterior abdominal wall Meleney’s gangrene following bull gore injury. Amrita J Med 2021;17:143-5 |
Introduction | |  |
Meleney’s gangrene is caused by synergistic infection of Staphylococcus aureus and streptococcus organisms. It is more common in immunocompromised individuals and diabetics following surgery and trauma. It is called synergistic gangrene because of the destructive nature of multiple bacteria. Most of the reported cases of Meleney’s gangrene develop following postoperative wound infections.
Case Presentation | |  |
A 47-year-old male, nondiabetic individual presented in our center in a state of extensive anterior abdominal wall infections with septic shock. He had a history of small bull gore injury on the right groin region before 1 week for which local wound debridement primary suturing done in a primary health center. Now patient presented with extensive abdominal wall infections with foul-smelling discharge for the past 5 days. He had a history of fever with chills and rigors for the past 2 days. He was not a known case of diabetes, hypertension, tuberculosis, ischemic heart disease, and retroviral infection. He was not on any immunosuppression drugs. There was no history of alcohol consumption. There was no history of previous surgery.
On examination, the patient was febrile (temperature 103°F, blood pressure 90/60 mm Hg, pulse rate 110 /min, and respiratory rate 32 /min). Local examination showed there was extensive necrosis of the abdominal wall from the umbilicus to groin. There was a foul-smelling purulent discharge present.
The blood investigations showed the following findings: hemoglobin 7.0gm/dL, total count 39,000, platelet 1.3 lakhs, urea 54 mg/dL, creatinine 2.2 mg/dL, random blood sugar 102 mg/dL, HbA1c 5.5, HIV 1 and 2 negative, HbsAg nonreactive, and HCV nonreactive. Post resuscitation computed tomography (CT) was done to rule out any intra-abdominal organ injury following bull gore injury. CT abdomen showed extensive anterior abdominal wall necrosis with a subcutaneous collection without extension into the peritoneal cavity.
The patient was taken for emergency wound debridement under general anesthesia. Necrotic tissue along with slough was excised starting from the umbilicus to the groin [Figure 1]. Pus was taken for culture and sensitivity. The patient was started on empirical antibiotics of cefoperazone with sulbactam 1.5g q12h and metronidazole 500 mg q8h. Aminoglycosides were avoided due to increased renal parameters. The patient is not showing any signs of improvement following debridement and continues to deteriorate. The patient is not responding to resuscitation with intravenous fluid, inotropes, and other supportive measures. He was declared dead on third postoperative day. | Figure 1: Postoperative image of the patient showing extensive anterior abdominal wall necrosis, from the umbilicus to groin
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Discussion | |  |
Meleney’s gangrene mostly affects the skin and subcutaneous tissue. Sometimes it also affects the deeper tissue like fascia and muscle.[1] It is more common following pelvic surgery, abdominal wall surgery, colorectal surgery, cesarean section, sterilization, and genitourinary surgery.[2] Most of Meleney’s gangrene is associated with diabetes, prolonged steroid intake, patient on immunosuppression, chronic renal failure, obesity, malnutrition, retroviral positive, intravenous drug abuse, and chronic alcoholic.
Meleney’s gangrene is usually misdiagnosed as an abscess or cellulitis.[3] Sometimes it may be confused with gas gangrene. Meleney’s gangrene may be differentiated from gas gangrene by the absence of crepitus and the absence of gas on plain X-Ray.
Meleney’s gangrene is caused by polymicrobial agents namely microaerophilic nonhemolytic streptococcus, beta-hemolytic Staphylococcus, anaerobes, and coliforms organisms. In most reported cases, 45%–58% of Meleney’s gangrene is due to hemolytic Staphylococci and 20%–28% of Meleney’s gangrene is due to nonhemolytic Streptococcus. The remaining 14%–35% of cases are due to polymicrobial organisms. Other reported polymicrobial organism includes pseudomonas, coliform organisms, diphtheroid, proteus, and Bacteroides.
Polymicrobial organisms are usually inoculated in the subcutaneous tissue following surgery or trauma. After initial inoculation of bacteria, an infection spread rapidly through the subcutaneous fascial plane. After inoculation, bacteria release proteolytic enzymes, hemolytic enzymes, and bacterial toxins. It causes nonspecific inflammatory changes, arteriolitis, and thrombosis of small blood vessels. During this period there will not be many skin manifestations in Meleney’s gangrene. After thrombosis of small blood vessels, there will be patch gangrene of skin followed by secondary gangrene of entire abdominal wall skin. In an immunocompromised individual, the organisms spread via subcutaneous tissue and produce small vessel thrombosis followed by tissue necrosis.[4] Most reported cases of Meleney’s gangrene occur following postoperative wound infection in the diabetic patient.[5] Our patient is a nondiabetic developed Meleney’s gangrene following bull gore injury. Most reported cases present in a septic shock with foul-smelling discharge.[4] It is a surgical emergency. Extensive aggressive surgical debridement is the cornerstone of the treatment for Meleney’s gangrene.[6] The antibiotics selected depend on the culture and sensitivity report.
A study conducted by Shah et al.[7] showed that increased white blood cell count, hyponatremia, hypoalbuminemia, anemia, and increased renal parameters were considered poor prognostic factors in a patient with necrotizing soft tissue infections. Most of the cases required multiple wound debridement followed by reconstruction using grafting or flap cover.
Romanoff et al.[8] reported a case of necrotizing fasciitis following perforated acute appendicitis, which was managed by laparotomy with abdominal wall debridement. Meleney’s gangrene has variable presentation and sometimes it was misdiagnosed as other intra-abdominal conditions. Wong et al.[9] reported a case of Meleney’s gangrene presenting with features of pyelonephritis and later diagnosed as Meleney’s gangrene on further investigations. It leads to delayed diagnosis and increases morbidity and mortality related to the disease process.
It is not always mandatory to have immunocompromised status or diabetes for the development of Meleney’s gangrene. A case reported by Chhetry et al.[10] revealed Meleney’s gangrene can occur in an immune-competent individual with the monomicrobial organism. Makhdoomi et al.[11] reported fast recovery and less morbidity in an immunocompetent patient with Meleney’s gangrene.
Conclusion | |  |
Prompt surgical debridement with adequate antibiotics is the cornerstone treatment for Meleney’s gangrene. Delayed presentation of Meleney’s gangrene increases both morbidity and mortality. Apart from diabetes and immunocompromised state, bull gore injury must be considered one of the risk factors for Meleney’s gangrene.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
References | |  |
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3. | Losa-Iglesias ME, Becerro-de-Bengoa-Vallejo R. A rare case of meleney’s ulcer after partial chemical matricectomy. Rev Esp Quimioter 2013;26:128-31. |
4. | Vayvada H, Demirdover C, Menderes A, Karaca C. Necrotising fasciitis in the central part of the body: diagnosis, management and review of the literature. Int Wound J.2013 Aug;10(4):466-72. doi: 10.1111/j.1742-481X.2012.01006.x. |
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7. | Shah AK, Kumar NB, Gambhir RP, Chaudhry R. Integrated clinical care pathway for managing necrotising soft tissue infections. Indian J Surg 2009;71:254-7. |
8. | Romanoff A, Freed J, Heimann T. A case report of necrotizing fasciitis of the abdominal wall: A rare, life-threatening complication of a common disease process. Int J Surg Case Rep 2016;28:355-6. |
9. | Wong CH, Song C, Ong YS, Tan BK, Tan KC, Foo CL. Abdominal wall necrotizing fasciitis: It is still “Meleney’s minefield”. Plast Reconstr Surg 2006;117:147e-50e. |
10. | Chhetry M, Banerjee B, Subedi S, Koirala A. Necrotizing fasciitis of anterior abdominal wall following cesarean section in a low-risk patient. J Surg Case Rep 2016;2016:rjw122. |
11. | Makhdoomi MA, Haraga A, Joseph M, Habeeb YA. Necrotising Fasciitis of lower anterior abdominal wall post lower segment ceaserian section. Int Surg J 2018;5:3760-3. |
[Figure 1]
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