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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2014  |  Volume : 25  |  Issue : 6  |  Page : 1263-1265
Concurrent emphysematous pyelonephritis and thigh necrotizing fasciitis after intramuscular administration of diclofenac

1 Department of Nephrology, Ziaeian Hospital, Tehran University of Medical Sciences, Tehran, Iran
2 Department of Radiology, Baharloo Hospital, Tehran University of Medical Sciences, Tehran, Iran

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Date of Web Publication10-Nov-2014


Necrotizing fasciitis (NF) is a rapidly progressive, life-threatening soft tissue infec­tion. NF may result from any injury to the skin or from hematogenous spread. However, con­current emphysematous pyelonephritis and necrotizing fasciitis of the left thigh has not been reported. We report a case of emphysematous pyelonephritis and necrotizing fasciitis of the left thigh after intramuscular administration of diclofenac that improved with aggressive management including broad-spectrum antibiotics, nephrectomy and surgical intervention.

How to cite this article:
Amiri FS, Foroughi A. Concurrent emphysematous pyelonephritis and thigh necrotizing fasciitis after intramuscular administration of diclofenac. Saudi J Kidney Dis Transpl 2014;25:1263-5

How to cite this URL:
Amiri FS, Foroughi A. Concurrent emphysematous pyelonephritis and thigh necrotizing fasciitis after intramuscular administration of diclofenac. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2023 Feb 4];25:1263-5. Available from: https://www.sjkdt.org/text.asp?2014/25/6/1263/144264

   Introduction Top

Tissue necrosis is rare, but it is a serious complication of intramuscular administration of medications, including non-steroidal anti-inflammatory drugs (NSAIDs). Pain often occurs at the time of the injection, but tissue necrosis typically becomes apparent a few days later. Necrotizing fasciitis (NF) is charac­terized by rapidly spreading infection with necrosis of fascia and subcutaneous fat. [1]

We report a case of emphysematous pyelo­nephritis and necrotizing fasciitis of left thigh after intramuscular administration of diclofenac that improved with aggressive mana­gement including broad-spectrum antibiotics, nephrectomy and surgical intervention.

   Case Report Top

A 39-year-old female presented to the neph-rology clinic with high-grade fever, chills, nausea, vomiting and right flank pain for the preceding four days. Past medical history was significant for type2 DM since six years ago for which the patient was on oral hypoglycemic agents (glibenclamide and metformin). She received intramuscular injection of diclofenac four days before admission that did not yield any improvement.

On admission, the patient was normotensive but tachycardic (120 beats/min). Physical exa­mination was remarkable only for severe right costovertebral angle tenderness. Laboratory analysis showed an elevated white blood count: 12100/mm 3 , platelet count: 90,000/mm 3 , blood sugar: 344 mg/dL, serum creatinine: 2.1 mg/ dL and ESR: 139 mm/h. Urinalysis re­vealed pyuria (8-10/hpf), proteinuria (1+) and significant bacteriuria.

The patient was aggressively resuscitated with intravenous fluids and she was switched to subcutaneous NPH and regular insulin for glycemic control. We initiated empiric i.v. piperacillin/tazobactam, vancomycin and amphotericin B. A renal sonography showed hydronephrosis of right kidney due to obstruction of right ureter.

Computerized tomography (CT) scan of the abdomen and the pelvis obtained the same day revealed distention of the perirenal fat and right enlarged kidney due to pyelonephritis or ureteropelvic junction stenosis. Two days later, the patient developed decreased brea­thing sounds at the base of the right lung and CXR demonstrated small right pleural effu­sion. A right nephrostomy tube was inserted and dirty amorphous material was removed, but was negative for malignant cells.

The general condition of the patient became better, but fever continued. Urine culture grew Escherichia coli (E. coli), but blood culture was negative. The same day, she developed left buttock pain, pain of motion of left hip joint during internal rotation, elevated muscle and liver enzymes and indirect hyperbilirubinemia.

Left buttock magnetic resonance imaging (MRI) was performed and revealed a signal change lesion in the left gluteal muscle and microabscesses in the lateral side of the left gluteal muscle. Because of continued fever, spiral CT scan of the abdomen/pelvis with contrast showed severe hydronephrosis with multiple gas bubbles in the right kidney and renal pelvis and involvement of renal fascia [Figure 1].
Figure 1: Abdominal CT scan of the patient showing right enlarged kidney. With multiple gas bubbles (arrows).

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For this reason, right nephrectomy was per­formed. Because of the high suspicion of NF, incision and drainage of the left thigh was performed and a great amount of pus was removed. The patient became afebrile and had complete clinical improvement, and wound closure was performed after four months. The pathological examination of the right kidney showed mixed acute and chronic inflammatory cells infiltration in the interstitial tissue with foci of necrosis and abscess formations exten­ding into the renal capsule and the perinephric fat tissue, which were all compatible with acute pyelonephritis.

   Discussion Top

NF is an infection of the superficial fascia. It may result from any insult to the integu­mentary system or from hematogenous spread. NF may develop at the site of a skin biopsy, laceration, insect bite, needle puncture (parti­cularly delineated in users of illicit drugs), herpes zoster, surgical wound, skin abscess or areas affected with a chronic venous leg ulcer. Risk factors for the development of NF in­clude diabetes mellitus, old age, surgery, trau­ma, chronic skin infection and immune system impairment. [2] A single species of bacteria or polymicrobial infection may be responsible for the NF.

Polymicrobial NF typically consists of anae­robic and facultative bacteria that synergistically cause what may initially be mistaken for as a simple wound cellulitis.

There are two main forms of necrotizing fasciitis; necrotizing fasciitis, type I and II. The majority of the cases are due to a polybacterial infection, while the latter is mainly due to group A beta-hemolytic streptococcal infec­tion. There is another subtype due to marine Vibrio species (e.g. V. vulnificus), which is usually associated with exposure to fish or sea water.

X-ray might show subcutaneous gas, but it was reported to be present in a few of the patients. Ultrasonography has also been used to improve the diagnosis of necrotizing fasciitis. A diffuse thickening of the subcuta­neous tissue, with a layer of fluid accumu­lation greater than 4 mm in depth in the deep fascial layer, would suggest a diagnosis of necrotizing fasciitis. CT scan and MRI may aid the diagnosis.

The keystones for survival of the infected patients include early diagnosis and prompt treatment with surgical drainage, debridement, broad-spectrum antibiotics and intensive care. Hyperbaric oxygen therapy has also been recommended based on the possibility of anae­robic infection and the rapid tissue necrosis due to the obstruction of the microvasculature. Intravenous immunoglobulin has also been used in selected cases. [3]

The use of NSAIDs may predispose to the NF. Several reports of serious or fatal com­plications from NSAID injections have been published. [4],[5],[6] NSAIDs increase the risk of developing gas necrotizing fasciitis, impede its timely recognition and management and acce­lerate the course of infection. [7]

The pathogenesis explaining skin necrosis is uncertain, but damage to an end-artery is a plausible hypothesis. Other causes to consider, especially when deep tissue necrosis is also present, are the cytotoxic effect of the drug or additives to the drug in the injection. [8]

In this context, Nicolau syndrome (embolia cutis medicamentosa) is an uncommon comp­lication of intramuscular injection that results in variable degrees of necrosis of skin and underlying tissues. [9],[10]

Finally, we believe that in our patient, the intramuscular injections caused a locally asep­tic necrosis, which was secondarily invaded by E. coli. Since this incident, our policy was developed to avoid the use of intramuscular injections of diclofenac and other NSAIDs in cases of potentially infectious diseases. Fur­thermore, concomitant soft tissue infections should be looked for if a case of necrotizing fasciitis is suspected.

Conflict of interest: None.

   References Top

Kihiczak GG, Schwartz RA, Kapila R. Necrotizing fasciitis: A deadly infection. J Eur Acad Dermatol Venereol 2006;20:365-9.  Back to cited text no. 1
Cox NH. Streptococcal necrotizing fasciitis and the dermatologist. Br J Dermatol 1999; 141:613-14.  Back to cited text no. 2
Siu AY, Kwok SL, Chung CH, Lai KK. A rare cause of necrotizing fasciitis: Psoas abscess. Hong Kong J Emerg Med 2005;12:242-5.  Back to cited text no. 3
McGee AM, Davison PM. Skin necrosis fol­lowing injection of non-steroidal anti-inflam­matory drug. Br J Anaesth 2002;88:139-40.  Back to cited text no. 4
Okan G, Yaylaci S, Ince U, Zorer S. Necrotizing fasciitis following intramuscular diclofenac injection. J Eur Acad Dermatol Venereol 2008;22:1521-2.  Back to cited text no. 5
Pillans PI, O'Connor N. Tissue necrosis and necrotizing fasciitis after intramuscular admi­nistration of diclofenac. Ann Pharmacother 1995;29:264-6.  Back to cited text no. 6
Aronoff DM, Bloch KC. Assessing the Relationship between the Use of Non-steroidal Anti-inflammatory Drugs and Necrotizing Fasciitis Caused by Group A Strepto-coccus. Medicine 2003;82:225-35.  Back to cited text no. 7
Velissaris D, Matzaroglou C, Kalogeropoulou C, Karamouzos V, Filos K, Karanikolas M. Sepsis requiring intensive care following intra­muscular injecttions: Two case reports. Cases J 2009;2:7365.  Back to cited text no. 8
Mutalik S, Belgaumkar V. Nicolau syndrome: A report of 2 cases. J Drugs Dermatol 2006; 5:377-8.  Back to cited text no. 9
Rygnestad T, Kvam AM. Streptococcal myositis and tissue necrosis with intramuscular administration of diclofenac (Voltaren). Acta Anaesthesiol Scand 1995;39:1128-30.  Back to cited text no. 10

Correspondence Address:
Dr. Fateme Shamekhi Amiri
Imam Khomeini Hospital, Tehran
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.144264

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