Muscular infarction, though rare, is a notable complication of diabetes mellitus in patients undergoing hemodialysis. Its pathophysiology remains elusive. Herein, we present two cases, one involving a young woman and the other a young man, both manifesting muscular pain with subsequent diagnosis of muscular infarction. This review emphasizes the rarity of this diagnosis and underscores the importance of considering it in clinical practice.

• Diabetes mellitus ; Muscular infarction ; Hemodialysis

Driss N, Sallemi N, Younsi F, Agerbi S (2024) Muscle Infarction: An Uncommon Complication in Diabetic Hemodialysis Patients. J Clin Nephrol Res 11(1): 1119.

Diabetic muscular infarction is an infrequent complication observed in individuals with long-standing, poorly controlled diabetes, particularly in the context of degenerative complications. Since its initial description over 45 years ago by Angervall and Stener [1,2], fewer than 200 cases have been documented in the medical literature. Formerly labeled as septic myonecrosis, ischemic myonecrosis, or tumor-forming focal muscle degeneration,[3] its clinical presentation ty-pically involves acute, focal muscle pain. Diagnosis primarily relies on magnetic resonance imaging (MRI), obviating the necessity for muscle biopsy. We report two cases encountered in our department.

Case 1

A 35-year-old female, diagnosed with type 1 diabetes 17 years prior, presented with poor glycemic control and diabetic complications, including retinopathy and stage V nephropathy necessitating hemodialysis for two years. She developed sudden severe swelling of the left thigh with associated edema and functional impairment of the left lower limb. Labo-ratory investigations revealed hyperglycemia, anemia, elevated C-reactive protein, and creatine phosphokinase indica-tive of moderate rhabdomyolysis.

Venous Doppler ultrasonography ruled out deep-vein thrombosis. Soft tissue ultrasonography revealed significant sub-cutaneous edema and a heterogeneous, predominantly hypoechoic appearance of the left quadriceps, with no evi-dence of hematoma [Figure 1].

Figure 1: Ultrasound depicting hypoechoic lesions within the quadriceps, suggestive of inflammatory infiltrate.

Magnetic resonance imaging (MRI) depicted edematous infiltration of the subcutaneous fat of the left thigh, along with hypotrophy and diffuse hypersignal of the quadriceps muscle, without any focal lesion. Additionally, there was a moderately large knee joint effusion [Figure 2].

Figure 2: MRI revealing T2 hypersignal lesions within the quadriceps.

The patient was initiated on a treatment regimen consisting of analgesics, non-steroidal anti-inflammatory drugs, and vasodilators, which led to partial regression of the clinical symptoms after 15 days of treatment.

Case 2

10. This is a 45-year-old man with type 2 diabetes of 15 years’ duration, poorly controlled, complicated by retinopathy, nephropathy at the hemodialysis stage for 6 years, and peripheral neuropathy. During his routine hemodialysis session, he developed acute pain in the upper third of his left calf, along with functional impairment. On clinical examination, the patient was afebrile and hemodynamically and respiratorily stable. He exhibited asymmetry of both lower limbs without associated inflammatory signs, experienced pain upon both active and passive mobilization of the limb, and had a firm calf upon palpation. Laboratory assessment revealed an inflammatory syndrome: C-reactive protein level was 58 mg/l. Blood count and muscle enzyme levels were within normal range. Glycated hemoglobin was measured at 9.8%. Doppler ultrasound of the left lower limb ruled out deep-vein thrombosis and indicated extensive edematous infiltration of the subcutaneous soft tissues [Figure 3].

Figure 3: MRI demonstrating T2 hypersignal with thickening of the lateral gastrocnemius muscle and edema, along with enhancement defect extending over 3 cm with interposition of a few fibres of marked enhancement.

Muscle MRI revealed a T2 hypersignal with thickening of the lateral gastrocnemius muscle and edema after gadolinium injection. The patient’s condition improved following limb rest and treatment with analgesics and vasodilators. Subsequently, he was readmitted to the endocrinology department for diabetes management.

Pathogenesis

The pathophysiology of myocardial infarction in diabetic patients remains uncertain [4]. Several hypotheses have been proposed, including diabetic microangiopathy and atherosclerotic lesions that are responsible for thromboembolic events and a cascade of intense inflammatory reactions leading to edema, hyperemia, and release of free radicals, resulting in ischemia-reperfusion injury, intense muscular ischemia, and tissue necrosis [5,6]. Additionally, emerging research suggests a potential role for chemokines in mediating inflammatory processes and tissue damage in diabetic myocardial infarction [7]. Other hypotheses include alterations in the coagulationfibrinolysis system with hypercoagulability and increased factor VII concentration, presence of antiphospholipid antibodies, vascular lesions observed in both type 1 and type 2 diabetes, as well as decreased levels of prostacyclin, antithrombin, and tissue plasminogen activator [8-10]. Despite these hypotheses, the precise pathophysiology of myocardial infarction in diabetic patients remains the subject of ongoing research.

Clinical and Laboratory Presentation

Muscle infarction is most commonly observed in patients with long-standing, poorly controlled diabetes. It typically manifests as muscle swelling and acute limb pain, often in the absence of fever. In diabetics, muscle infarction predo-minantly affects the anterior thigh in 55% of cases, the posterior thigh and calf in 15%, and the upper limb in only 5% of cases [1]. Recurrence of symptoms in different muscle groups is observed in 55% of cases [1,3].

Biologically, an inflammatory syndrome may be detected in 50% of cases [11]. Rhabdomyolysis is rare, and according to an American review published in 2015, CPK values were normal in 70% of cases [1].

While muscle biopsy remains the gold standard for diagnosis, it is generally not recommended due to its invasive na-ture, which carries a high risk of exacerbating necrosis and delaying healing. Its use is reserved for cases of diagnostic uncertainty or therapeutic inefficacy. When performed, muscle biopsy typically reveals areas of muscle necrosis, in-flammatory cell infiltrates, microvascular abnormalities, and fibrotic lesions [3].

Muscle MRI serves as an alternative diagnostic method with excellent specificity and sensitivity, effectively ruling out differential diagnoses such as deep vein thrombosis, myositis, muscle tumors, and infiltrative diseases. Characteristical-ly, it demonstrates a T2-weighted hypersignal and a T1-weighted isosignal or hyposignal attributable to the elevated water content of perimuscular edema [12].

Additionally, soft tissue ultrasonography can aid in diagnosis by revealing hypoechoic intramuscular lesions traversed by characteristic echogenic lines, while the absence of anechoic lesions helps exclude abscesses and muscle tumors [1].

Management and Prognosis

Multiple studies advocate for analgesic therapy coupled with strict limb rest and optimal glycemic control [10,13,14]. Some studies have proposed the utilization of low-dose aspirin for patients with microangiopathic lesions and non-steroidal anti-inflammatory drugs (NSAIDs) to mitigate edema and inflammation [15]. However, physiotherapy and surgery are generally not recommended [1]. Similar to other diabetic complications, maintaining diabetes control is pivotal in both treatment and prevention of recurrence. Muscle infarction in diabetic patients typically carries a poor prognosis, emphasizing the significance of addressing microvascular complications in therapeutic strategies.

Muscular infarction is a rare complication in diabetic patients, necessitating vigilance in diagnosis, particularly in hemodialysis recipients. Awareness of this entity is crucial to prevent misdiagnosis and optimize patient outcomes.

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