| Article Access Statistics|
| Viewed||6445 |
| Printed||90 |
| Emailed||4 |
| PDF Downloaded||0 |
| Comments ||[Add] |
Click on image for details.
|Year : 1987 | Volume
| Issue : 2 | Page : 81-3
Idiopathic necrotising myofascitis of the anterior abdominal wall : a new modality of management.
Pikale HS, Shah DM, Nair HT, Hirve SH, Shenoy SG
|How to cite this article:|
Pikale H S, Shah D M, Nair H T, Hirve S H, Shenoy S G. Idiopathic necrotising myofascitis of the anterior abdominal wall : a new modality of management. J Postgrad Med 1987;33:81
|How to cite this URL:|
Pikale H S, Shah D M, Nair H T, Hirve S H, Shenoy S G. Idiopathic necrotising myofascitis of the anterior abdominal wall : a new modality of management. J Postgrad Med [serial online] 1987 [cited 2020 Sep 29];33:81. Available from: http://www.jpgmonline.com/text.asp?1987/33/2/81/5300
Necrotising myofascitis involving the rectus sheath, rectus muscle and the peritoneum is an uncommon condition where in there is a spreading necrosis of these structures without much involvement of the skin. This is usually associated with anaerobic infection. Diagnosis becomes difficult in such cases as an infra-abdominal pathology cannot be definitely ruled out. We had 3 such cases under our care over a period of 4 months. The present paper describes the findings and management of these three cases.
All the 3 patients were young, apparently healthy males between 25 and 35 years of age. There was no history of trauma, fever or any other major illness preceeding this episode. One patient had undergone anal stretching for a fissure-in-ano, 48 hours prior to admission. None of the patients was diabetic, alcoholic or drug addict. All had involvement of the rectus sheath, rectus muscle and the peritoneum but the skin was spared. The parts affected were black, gangrenous, non-bleeding with foul smelling discharge. All were in septicemia with tachycardia, tachypnoea and low blood pressure.
After aggressive resuscitation with intravenous fluids and blood transfusion, the patients were subjected to exploratory laparotomy. The sub-cutaneous tissue and muscles contained a foul- smelling discharge and a radical excision of half of the rectus muscle, peritoneum and the rectus sheath was carried out after exploring the peritoneal cavity for any intra-peritoneal pathology, one patient in whom anal stretching was done seemed to have a suspicious looking, black-coloured lesion at the recto-sigmoid junction on the left postero-lateral side with loss of serosal cover. Hence, a temporary loop sigmoid colostomy was performed.
The discharge was cultured anaerobically and aerobically. Coagulase positive Staphylococci were isolated in all cases. One showed E. coli and the other two showed Peptostreptococci and B. fragilis not sensitive to gentamicin, ampicillin and other routine antibiotics.
Post-operatively, the patients were put on broad spectrum antibiotics, metronidazole and oxygen by mask. Suitable changes in the anti- biotic therapy were made on receiving the sensitivity reports. All patients were given hyper-immune-immunoglobulin 3000 mg intramuscularly in divided doses. Two patients were given hyperbaric oxygen for a total of 10 sittings. All patients recovered by 1½ months and were discharged. There was no residual abscess or deformity.
Necrotising fascitis was first described by Joseph Jones (Quoted by Miller, 1983) during the American Civil War as hospital gangrene. Meleny described it as hemolytic streptococcal gangrene. Various terms are now a day used for the same.
This fascitis is usually seen in males over 40 years. But in our series, all the three patients were young healthy males, below the age of 35 years. It is known to occur following minor trauma, operations like appendicectomy, muscle biopsy etc., It is however not described following peri-anal surgery. It is also associated with diabetes mellitus or occlusive venous disease. However, none of our patients had diabetes or thrombo-angiitis obliterans. The clinical features described are muscular and fascial necrosis, cellulitis, edema, gangrene and toxaemia. Loss of sensation of the skin over the involved area is reported to be associated with high fever, toxicity, tachypnoea and hypotension. The laboratory investigations may show anemia, leucocytosis and hypocalcemia, consistent with our findings.
Treatment consisted of infusion intravenous fluids and whole blood transfusions. The antibiotics selected initially should be effective against multiple organisms. Subsequent change of antibiotics may be necessary after the availability of the sensitivity reports. Wide excision of the affected tissues with debridement is required.
Hyperbaric oxygen may help these patients by increasing the oxygen content (pO2) at the site of infection which is usually anaerobic. These patients with septicemia normally tend to have low pO2 levels.
Due to progressive impairment of blood flow, there is organ failure particularly of the brain, liver and lungs, presenting as shock and/or respiratory distress syndrome. Hence blood gases and lactate levels form an important part of investigations for prognosis. The patients with hypogammaglobulinemia usually tend to have severe pyogenic infection. Hence, septicemia and severe infections like necrotising myofascitis tend to occur in these patients. The immunoglobulin injection may help these patients by increasing their globulin concentration. This is comparable to the views by David-son et al.
The mortality of necrotising fascitis varies from 3.7 to 4.6%. Higher mortality has been reported amongst patients over 50 years of age and diabetics. However, there was no mortality in our series as compared to that found by Deodhar et al.
Necrotising fascitis is usually caused by staphylococci, streptococci, anaerobes and rarely Gram-negative bacilli. Coagulase positive staphylococci were isolated in all the three cases. Ketona et al attributed the increased incidence of staphylococcal infection to T-cell defect in the presence of high levels of IgE. High levels of IgE due to parasitic infection are common in our country with the resultant T-cell defect causing minor, unnoticed trauma leading to fulminant infection.
In conclusion, for better outcome of patients with necrotising myofascitis, we suggest (a) radical excision, (b) hyperbaric oxygen and (c) injection of immunoglobulins, all these modalities at a time.
We thank the Dean, Seth G. S. Medical College and K.E.M. Hospital, Bombay for allowing us to publish this data.
|1.||Baxter, C. R.: Surgical management of soft tissue infection. Surg. Clin. North Amer., 52: 1483-1499, 1972. |
|2.||Deodhar, S. D., Shirahatti, R.G. P. Sareen, A. A., Bharucha, M. A. and Bhave, Geeta, G.: Necrotising fascitis. A report of 5 cases. J. Postgrad. Med., 31: 170-172, 1985. |
|3.||Ketona, I. M., Tata, G., Scanlon, R. T. and Bellanti, J. A.: Hyper IgE syndrome; A disease with suppressor T-cell deficiency. Ann. Allerg., 45: 295-300, 1980. |
|4.||MacLeod, J.: Immunological factors in disease. In, "Davidson's Principles and Practice of Medicine. 13th Edition, ELBS and Churchill Linvingstone, 1981, p. 42. |
|5.||Mcleny, F. L.: Haemolytic streptococcal gangrene. Arch Surg., 9: 317-364, 1924. |
|6.||Miller, J. D.: The importance of early diagnosis and surgical treatment of necrotising fascitis, Surg. Gynaecol. & Obstet., 157: 197-200, 1983. |
|7.||Rea, W. J. and Wyrick, W. J.: Necrotising fascitis. Ann. Surg., 172: 957-964, 1970. |