Diabetic muscle infarction (DMI) is an unknown complication of poorly controlled long standing diabetes. Presentation, though is well characterised with sudden onset of painful swelling, mostly of the thigh without history of trauma or features of infections. The differential diagnosis is extensive and it is frequently misdiagnosed clinically and treated as polymyositis, pyomyositis and rhabdomyolysis. The uniform clinical presentation and characteristic T2 weighted imaging is sufficient to make the timely diagnosis of DMI and excluding other clinical entities, thus avoiding unnecessary investigations and interventations.
An-81- year old diabetic female presented with severe pain and swelling of left thigh in the emergency department in January, 2011. The previous night she woke up suddenly because of the severe pain in her left thigh. The pain was so severe that she couldn’t touch her thigh nor could she move it. She denied having any other symptoms. On examination, she was a febrile with pulse rate of 90 beats/min; respiratory rate of 16 breath/min and blood pressure was 160/100 mmHg. Systemic examination of chest, heart and abdomen was also normal. On local examination left thigh was swollen with difference of 12 cm between left and right, indurated and was excruciatingly tender to touch, maximum on anterolateral aspect without any erythema and cellulitis but was warmer than right thigh. Funds examination showed hypertensive along with background diabetic retinopathy changes. Peripheral pulses were symmetrical. There were no muscle fasciculations, muscle atrophy and tenderness of the spine. There was no evidence of neurovascular compromise. Neurological examination revealed absent ankle reflexes and absent vibration sensation at big toe and ankle bilaterally. Her urea was 86 mg % (10-35 mg%) and creatinine was 1.9 mg% (0.5-1.0 mg%) and rest of her routine blood tests were normal. Her random blood sugar was 320 mg% and blood ketones was negative. Twenty four hour urine revealed 800 mg of protein. D-dimer and antinuclear antigenwere negative. Creatine kinase was raised two time of the normal. Compressive Ultrasonography of left thigh was normal. MRI of pelvis and thighs showed high T2 signal and hypodense signal on T1 images of left thigh characteristic of fluid affecting subcutaneous and quadriceps with maximum involvement of vastes lateralis muscle of left thigh [Figures 1 and 2]. On i.v gadolinium there was uniform enhancement of the muscle with central non-enhanced area of necrotic muscle [Figure 3a and b]. Fine needle aspiration was done which showed of muscle fibres in various stages of degeneration. Moreover, Sudden onset of excruciating pain and swelling without weakness in the thigh and with no signs of local and systemic inflammation, without any evidence of neurovascular compromise with small increase in creatine kinase, negative collagen network in a long standing diabetic woman having underlying micro vascular complications in the form of retinopathy, nephropathy and neuropathy is highly suggestive of diabetic muscle necrosis in our patient. The highly characteristic MRI findings further support the clinical diagnosis. The patient was treated conservatively with bed rest, analgesics and insulin. She starts showing improvement and was discharged after 24 days.
Diabetic muscle necrosis first diagnosed by Angervall and Stener in 1965, is a very uncommon complication of diabetes and predominately occurs in type 1 diabetes (70% of cases) or long standing poorly controlled type 2 diabetic patients. DMI typically presents acutely as a localised exquisitely painful and tender swelling of the involved muscle, associated with restricted movement of the involved limb without redness and systemic signs of infection. DMI most commonly affects thighs, with quadriceps being involved in 84% of cases and calves in about 19% of cases. Among quadriceps, vastes lateralis and vastis medialis are the most frequently involved muscles. Bilateral involvement of thighs is seen in 8 to 30% of cases. Diabetic muscle infarction occurs more frequently in poorly controlled diabetic women, typically having underlying micro vascular complications. Though; exact pathogenesis is unknown but probably is related to a diffuse microangiopathic process resulting into hypoxia-reperfusion injury. Diabetic muscle infarction must be differentiated from other painful swelling in an extremity because of various infective, inflammatory, neurological, neoplastic, traumatic and vascular disorders. However, inflammatory conditions such as polymyositis and pyomyositis present with proximal muscle pain and swelling and raised creatine kinase are the most common clinical entities to be differentiated from diabetic muscle infarction. In polymyositis, proximal muscle weakness rather than intense pain is the dominant presentation and muscle biopsy establish the diagnosis. Absence of systemic and local signs of infections strongly argues against an infectious process such as pyomyositis. The diagnosis of diabetic muscle infarction is clinical and radiological. The clinical possibility should be entertained in a long standing poorly controlled diabetic patient who presents with abrupt onset of exquisitely painful and tender swelling of thighs without erythema and cellulites with mild rise of creatine kinase. In radiology, MRI of the extremity is the modality of choice, characteristically shows an increased signal from affected muscle (intramuscular and perimuscular area) and subcutaneous fat on T2 weighted images and isointense or hypointense areas on T1 weighted images, highly suggestive of fluid from edema and inflammatory changes.
Gadolinium enhancement though not required routinely, characteristically show enhanced margin of the infracted muscle with central nonenhanced area of necrotic tissue. Muscle biopsy may prolong the recovery it is not needed routinely, it indicates only if diagnosis is uncertain, response to treatment is poor and presentation is atypical. The biopsy when done shows an areas of muscle necrosis and edema surrounded the muscle fibres, which are in various stages of degeneration and regeneration with hyalinosis and arterioles thickening. Conservative management in the form of bed rest, leg elevation and good analgesia is the mainstay of treatment as no evidence based recommendation is available. Exercise during acute phase may increase pain and swelling, hence should be avoided. Poor diabetic control prolongs the recovery, strict diabetic control is important. No evidence based recommendation support the use of steroid. There is no role of surgery in diabetic muscle infarction. In fact surgery may worsen the outcome, should be avoided. In acute phase the recovery is good but the recurrence is high (48%), which may affect other muscle in 39% of cases. Long term prognosis is not good in diabetic muscle infarction, with 10% mortality over next two years.
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