Diabetic myonecrosis can occur in both types 1 and 2 DM, with mixed reports about which type is more prevalent.1,3 The first reported DMN cases were 2 patients with DM who presented with painful, circumscribed, elongated swelling in the thigh that was initially thought to be tumors.4 Biopsy revealed hemorrhagic necrosis surrounded by homogenous muscle fibers with regressive changes separated by wide edematous spaces.4 A 2015 systematic review reported 126 cases published in English; 68 cases (54%) were females, and the mean age at DMN presentation in all patients was 44.6 years (range, 20–67 years).1 Although short-term prognosis is good, long-term prognosis is poor because of underlying microvascular disease with a 2-year mortality of 10% and recurrence in approximately half of patients.2,5 Of note, recurrence is typically at a different site.
The exact etiology of DMN is unknown.1 However, it is thought to be associated with vasculopathy such as diabetic microangiopathy and atherosclerosis.1 Arteriosclerosis obliterans is another possible contributor suggested by Chester and Banker.6 Umpierrez et al7 suggested vasculitis phenomenon associated with fibrinoid necrosis in these patients. Other theories include alteration in the coagulation fibrinolysis system.8 Gargiulo et al9 and Palmer and Greco10 suggested antiphospholipid antibodies as causative factors. Galtier-Dereure et al11 pointed to a high association of antiphospholipid antibodies in types 1 and 2 DM patients.
Diabetic myonecrosis usually presents as subacute to acute pain and swelling of the affected area, with or without accompanying induration and erythema. It is an atraumatic, noninfectious process, often with no systemic signs and symptoms of infection. However, an inflammatory reaction to muscle infarction may be present, and a few cases are described as having mild fever.1,3,7 It also generally presents as unilateral muscle pain, although bilateral involvement can occur.3 The anterior thigh is the most commonly affected location (55%), followed by the calf and posterior thigh (15.3%), anterior upper extremities (5%), and posterior forearm (<5%). Within the thigh, the most commonly affected muscle groups are the quadriceps (65%), hip adductors (13%), hamstrings (8%), and hip flexors (2%).1
Radiographically, MRI, CT, and ultrasound are useful tools for diagnosis of DMN, and MRI is the test of choice.1 Most often, MRI findings include loss of intermuscular septae, especially on T1-weighted images. T1-weighted images are characterized by tissues with high fat content appearing bright and fluid appearing dark. In DMN, T2 images show diffuse enlargement of involved muscle, subcutaneous edema, and hyperintense muscle. On T2-weighted MRI images, fluid-filled compartments appear bright, and tissues with high fat content appear dark.2,12
Ultrasound and CT can assist in differentiating between diagnoses that may present in a similar fashion. Ultrasound can be used to diagnose intramuscular hematoma, venous thrombosis, and intramuscular abscess.13 A CT scan can identify localized abscess, tumor, and bone destruction and may demonstrate muscle swelling.14 Ultrasound in DMN usually has nonspecific findings of hypoechoic regions (regions less reflective of sound waves that appear darker than neighboring structures). Internal linear structures (lines) coursing through these regions represent muscle fibers, and there is an absence of fluid motion with pressure from the transducer.15 In contrast, abscesses on ultrasound are typically seen as anechoic (regions that do not reflect sound waves at all and appear black on ultrasound) or hypoechoic, with posterior acoustic enhancement (regions that appear lighter than surrounding structures and are usually present behind a structure that does not transmit sound waves), and possibly have intrinsic motion of fluid with pressure from the transducer.15
Patients with DMN typically have a history of uncontrolled DM and present with pain but do not usually have signs or symptoms of sepsis. However, in DMN, imaging will not reveal a well-circumscribed fluid collection as with an abscess.
Laboratory values, such as white blood cell count, creatinine phosphokinase, and inflammatory markers (eg, erythrocyte sedimentation rate, C-reactive protein), are considered nonspecific as they can range from normal to elevated in DMN patients.1 One review included a discussion of laboratory values obtained for DMN patients and noted that inflammatory markers were elevated in most cases but found no consistency in diagnostic usefulness.1
Muscle biopsy is reserved for atypical patients with an unclear diagnosis after radiologic imaging. The main pathologic findings of biopsies are muscle necrosis and edema.1 Biopsies are usually avoided because of the risk of infection and poor wound healing.1 When a biopsy is performed, MRI guidance should be used for its ability to localize the lesion.12
Management options for DMN include a conservative approach with bed rest, antiplatelet therapy, and nonsteroidal anti-inflammatory drugs (NSAIDs),16 which counteract the endothelial damage, platelet-associated imbalance, and inflammatory reactions that create the prothrombotic state of DMN.1 However, tight glycemic control is the mainstay of the treatment.17 In contrast with the aggressive management of cellulitis and necrotizing soft tissue infections, early recognition of DMN avoids antibiotic use in the absence of superimposed infections, surgery, and biopsy.1,16 Surgery and biopsy prolong recovery time, whereas NSAIDs decrease recurrence.1 The recurrence risk associated with surgery is 50%, and the mean time to resolution with biopsy is 60.8 days compared with 29.5 days without biopsy.1
Diabetic myonecrosis is an uncommon complication of poorly controlled, long-standing DM that can present in a similar fashion to many other diagnoses such as cellulitis, abscess, DVT, hematoma, pyomyositis, fasciitis, and malignancy. Therefore, a high index of suspicion is required by providers for prompt and accurate diagnosis. Magnetic resonance imaging is the diagnostic test of choice, and treatment includes bed rest, antiplatelet therapy, NSAIDs, and, most importantly, tight glycemic control. As illustrated in the case presentation, early diagnosis can help prevent unnecessary surgical intervention. Diagnostic acuity can also eliminate unwarranted use of antibiotics. Future studies, possibly using animal-based models, are needed to further delineate the exact cause of DMN in order to improve awareness and prevention.
- Diabetic myonecrosis is an uncommon complication of poorly controlled DM. The etiology is unknown but is thought to be associated with vasculopathy.
- A high index of suspicion is required because DMN presents in a similar fashion to cellulitis, abscess, DVT, and hematoma.
- Magnetic resonance imaging is the diagnostic test of choice.
- Treatment includes bed rest, antiplatelet therapy, NSAIDs, and glycemic control.
- Antibiotics and surgical intervention are not indicated as treatment options. Operative management has been shown to double the time to healing.
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Keywords:Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
aseptic myonecrosis; cellulitis; diabetic myonecrosis; diabetic muscle infarction; diabetic complications; muscle necrosis; necrotizing soft tissue infections