A 66-year-old retired man (Han Chinese) was referred to the endocrinology unit of the First Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, due to poor plasma glucose control and severely painful lower limbs on April 21, 2020. He reported sleepiness, fatigue, swelling of the face, and occasional lower limb convulsions for the past 2 months. He complained of pain, redness, and swelling in the lower limbs for 3 days and gradually worsening symptoms, which severely affected his daily activities and sleep quality. The patient had a history of type 2 diabetes for 22 years. Due to the poor effect of metformin, he had been injecting mixed recombinant human insulin (30/70) 44 U/day for the past 5 years. His fasting blood glucose fluctuated around 9.0 mmol/L. The patient reported no history of trauma, excessive exercise, fever, drinking alcohol, and medication (other than insulin) in the past 6 months. The patient reported no family genetic history. Physical examination on admission showed stable vitals, with a heart rate of 72 bpm and blood pressure of 130/70 mmHg, but dry and pale skin and slow speech. The whole body was swollen, especially the lower limbs, and the anterior shin of both legs were red and swollen. Local skin tension was high, and tenderness was obvious. The blood investigations revealed serum creatine kinase (CK) at 9774 U/L (reference: 50–310 U/L), CK isoenzyme (CK-MB) at 115.2 U/L (reference: 0–24 U/L), cardiac troponinI (cTnI) at 0 U/L, myoglobin (Mb) at > 3811 μg/L (reference: 0–70 μg/L), albumin (Alb) at 48.8 g/L (reference: 40–55 g/L), alanine aminotransferase (ALT) at 46 U/L (reference: 9–50 U/L), aspartate aminotransferase (AST) at 139 U/L (reference: 15–40 U/L), lactate dehydrogenase (LDH) at 579 U/L (reference: 120–250 U/L), and α-hydroxybutyrate dehydrogenase (HBDH) at 419 U/L (reference:72–182 U/L), suggesting RM. Blood glucose was 13.7 mmol/L (reference: 3.9–7.7 mmol/L), HbA1c was 10.6% (reference: 3.9–6.2%), hemoglobin was 159 g/L (reference: 130–175 g/L), white cell counts was 11.98 × 109/L (reference: 3.5–9.5 × 109/L), and platelet count was in the normal range (125–350 × 109/L). Free triiodothyronine (FT3) was 0.06 pg/ml (reference: 2.3–4.2 pmol/L), free thyroxine (FT4) was 2.78 pmol/L (reference: 7.5–17.4 pmol/L), and TSH was 145.6 mIU/L (reference: 0.35–5.5 mIU/L). Subsequent tests were suggestive of Hashimoto’s thyroiditis, with raised thyroid peroxidase antibodies at 661.8 IU/ml (reference: 0–34 IU/ml) and positive antithyroglobulin antibody at 366.20 KIU/L (reference:0–115 KIU/L). Blood electrolytes, renal function, coagulation function, brain natriuretic peptide, chest radiograph, and abdominal ultrasound were normal. There were no erythrocytes on microscopic examination, although his urine was bloody in appearance. Ultrasound of both lower extremities suggested uneven thickening of the arteries and media of the lower extremities with plaques and no abnormalities in the veins of both lower extremities. Swelling of the lower limbs caused by vascular occlusion and thrombosis was excluded. There was no ST-T segment change on the ECG. Considering RM, fluid replacement, maintenance of water and electrolyte balance, diuresis, alkalized urine, penicillin, insulin, thyroid hormone replacement, and loxoprofen for pain relief were given immediately. The lower extremity swelling continued to progress, with high tension and thin skin. Tension blisters appeared on the right ankle on April 22, and muscle enzymes increased progressively, urine was dark brown, urine output was 3500 ml/day. On April 23, creatinine did not elevate [116 μmol/L (reference: 57–111)], but CK rose at 48,118 U/L (reference: 50–310 U/L). Mb was > 3811 μg/L, ALT was 196 U/L, AST was 1027 U/L, LDH was 1422 U/L, and HBDH was 798 U/L. An orthopedist was consulted and suggested lower limb OCS. Surgery could not be considered due to the high risk of open decompression and complications such as poorly healing incision because of poor blood glucose control and hypothyroidism. Hemofiltration was started on the evening of April 23. The lower limb pain and redness gradually reduced, and the levels of CK, CK-MB, Mb, ALT, AST, LDH, and HBDH gradually decreased. CK fell to 8301 U/L (reference: 50–310 U/L) and Mb to 1183 μg/L on April 28. Blood Alb and hemoglobin gradually decreased, and APTT and PT were prolonged. On April 29, there were large ecchymoses on the right waist and right thigh, and the anterior tibial swelling of the two lower legs was aggravated again. Ultrasound showed intermuscular hematoma of both lower legs and subcutaneous hematoma of the right thigh. The feet were drooping and could not stretch back. The worsening of the disease was considered related to abnormal blood coagulation caused by RM. Considering the necrosis of the soft tissue of the anterior tibia, ceftriaxone (2 g/qd) was given from April 29 to May 7. On April 30, the levels of CK again increased to 14,292 U/L. Blood filtration, fluid replacement, gradually increasing the dose of thyroid hormone (75 μg/d) and insulin (insulin pump therapy, basic dose 30 U, high dose 10 U before meals), infusion of albumin (20 g/day, continued for 1 week), and other treatments (glutathione 1.8 g/day and esomeprazole 40 mg/12 h) were continued. The condition of the patient gradually stabilized. On May 6, hemofiltration was stopped due to the improvement of the redness and swelling of the lower limbs, and APTT was normal. Since the levels of CK (4650 U/L) and Mb (232.0 μg/L) were still higher than the normal range, treatment was continued. Afterward, the lower limbs were slightly red but without pain and swelling. Muscle enzymes continued to decline, with CK from 4650 U/L to 1547 U/L and Mb to normal. FT3/FT4 gradually rose. Fasting blood glucose fluctuated around 7.0 mmol/L, and postprandial blood glucose fluctuated around 10.0 mmol/L. The foot drop did not recover. The patient was discharged on May 19. The lower limbs were slightly red but without pain and discomfort. CK was 1547 U/L, and Mb was normal. CK was checked every 10 days and FT3/FT4 every month after that. Rehabilitation was recommended. On May 30, the patient was able to stand, but walking was slightly unstable. CK was 818 U/L, and Mb was normal. On July 12, the patient’s feet were still drooping; there was no redness or swelling in the lower limbs and occasional swelling of the ankles. The levels of TSH, FT3, FT4, and CK were normal. The patient is undergoing rehabilitation. The patient’s treatment process is shown in Fig.. The changes in related laboratory indicators are shown in Supplementary Tables,, and.