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Diabetic Muscle Infarction of the Peroneus Brevis: a Case Report

Posted on: Saturday, 18 February 2006, 03:03 CST

By Lim, Y W; Thamboo, T P

ABSTRACT

Diabetic muscle infarction of the peroneus brevis is a rare complication of diabetes mellitus. It often presents with an acute leg pain without any obvious signs. Due to poor awareness of this condition, it is often misdiagnosed and results in anxiety of the patient and unnecessary investigations. It is ominous as it usually indicates vascular disease of the end organs. We report a case where the patient presented to several physicians for leg pain without any other clinical signs. The diagnosis was suspected on ultrasound and confirmed with biopsy. The symptoms improved dramatically after excision. Although most literature suggests conservative treatment by non-weight bearing and analgesia, the recovery period can last for more than 6 weeks, with a recurrence rate of 50%. We feel that there is a role for excision biopsy of the lesion for both diagnosis and treatment. In this case, symptoms improved remarkably and the patient was able to ambulate without pain 2 days after the operation without needing any analgesia.

Key words: diabetic angiopathies; infarction; muscle

INTRODUCTION

Diabetic muscle infarction is a rare complication of diabetes. It was first reported in 1965 by Angervall and Stener1; however, only few cases have been published since then. It has been reported as myonecrosis, ischaemic myonecrosis, and tumoriform focal muscular degeneration. Clinical presentation is usually an acute onset of leg pain over the affected muscle and occasionally a palpable mass. The differential diagnosis is extensive and diabetic muscle infarction is often misdiagnosed clinically.

Figure Necrotic skeletal muscle fibres are surrounded and infiltrated by acute and chronic inflammatory cells (H&E, x100).

CASE REPORT

A 59-year-old Chinese man with newly diagnosed type-2 diabetes presented to the orthopaedic surgery out-patient clinic of Alexandra Hospital, Singapore in November 2003. The patient had excruciating pain on the right lateral leg for the previous 3 weeks. The pain was progressively affecting his sleep and worsened with activity. There was no history of trauma or penetrating injury to the site. He reported no erythema, warmth, or swelling of the lower extremity. There were also no systemic symptoms of fever, chills, rigors, or weight loss, as well as no numbness or pain radiating to the legs.

The patient was recently diagnosed as having diabetes mellitus 2 months prior to the leg pain. He was subsequently started on subcutaneous insulin therapy. He had no history of nephropathy or visual complaints and denied any injection to his leg. He was thin and frail, measuring 168 cm in height and 62 kg in weight, with a blood pressure of 130/80 mm Hg. Physical examination of the leg was unremarkable except showing tenderness over the peroneal compartment of the right leg 15 cm below the fibula head and 5 cm from the anterior border of the tibia. The patient had pain on active eversion of the foot and was unable to bear weight. However, superficial skin changes including erythema, swelling, oedema, and Homans sign were absent. The pulses of dorsalis pedis and posterior tibialis were strong, and the vibratory sense and proprioception were normal.

The total white blood cell count was 9.42x10^sup 9^/l, haemoglobin level was 143 g/1, and platelet count was 371x10^sup 9^/ l. The electrolyte and creatinine levels were also normal. Aldolase was 5.8 U/l and creatine kinase was <10 U/l, which was not within the normal range (38-164 U/l). C-reactive protein was 145.31 mg/l, which was another blood investigation not within the normal level (<5 mg/1). Ultrasound of the lateral compartment of the leg revealed a hypoechoic well-marginated lesion measuring 7x0.7 cm within the muscle. No abscess or fluid collection was noted, and radiographs of the tibia and fibula were normal.

An open excision biopsy revealed a segment of pale-looking peroneal brevis muscle at 15 cm below the joint line and 5 cm lateral to the anterior border of the tibia. Histology subsequently revealed necrotic skeletal muscle with acute and chronic inflammatory cells (Fig.). Stains for fungi and acid-fast bacillus were negative.

The next day after surgery, the patient felt significant pain relief and analgesia was withdrawn.

DISCUSSION

Diabetic muscle infarction was first described in 1965 by Angervall and Stener.1 It is a rare complication of diabetes and a sign of underlying vascular disease. Diagnoses in most of the 30 cases reported in the literature were delayed because of failure to recognise the condition. The clinical differential diagnoses are extensive, ranging from muscle strain, rupture, haematoma, myositis, abscess, deep vein thrombosis, thrombophlebitis, fracture, and tumour.

Most patients with diabetic muscle infarction are young with a mean age of 37 years. They usually have had diabetes mellitus for 5 to 30 years and are on insulin therapy. The female:male ratio is 1.7:1.2 Usual sites of occurrence are: quadriceps (62%), hip adductors (13%), hamstrings (8%), and hip flexor (2%) muscles. Rarely the calf and anterior tibial muscles are involved. We are not aware of any report involving the peroneal brevis muscle. The pathogenesis of diabetic muscle infarction is still unclear but a diffuse microangiopathic process possibly associated with hypoxia- reperfusion injury has been implicated as a cause.3-5

Magnetic resonance imaging is the preferred diagnostic instrument. It reveals swollen and oedematous muscles under increased signal intensity of T2-weighted images.6,7 Ultrasound findings of this patient also revealed typical diabetic muscle infarction, namely a well-marginated, hypo-echoic, and intramuscular lesion with features of internal linear echogenic structures coursing through the lesion, an absence of internal motion or swirling of fluid transducer pressure, and a lack of a predominantly anechoic area. These findings may help to differentiate diabetic muscle infarction from a necrotic mass or abscess.

Histology shows irregular areas of haemorrhages, necrosis of myocytes with regeneration, and atrophy of surrounding fibres. Small vessel walls are thickened and hyalinised with luminal narrowing or complete occlusion.8,9

Diabetic muscle infarction is a rare and easily misdiagnosed disease that occurs in patients on insulin therapy. Any patient presenting with leg pain should have diabetic muscle infarction as one of the differential diagnoses. The muscle infarction can sometimes be complicated by a secondary infection. Although some physicians advocate magnetic resonance imaging for diagnosis and choose analgesia and short-term immobilisation as treatment, the infrequent presentation of this entity makes such recommendations for all patients less convincing. Most of the literature suggests treating the condition with non-weight bearing and analgesia; however, the recovery period can last for more than 6 weeks with a recurrence rate of 50%.'" Our patient suffered excruciating pain despite receiving diclofenac acid, naprosyn, and codeine phosphate for weeks. After surgery, he felt immense pain relief and was able to bear weight fully without using any analgesia. Given the presence of a necrotic muscle, there is always a risk of it forming a nidus for secondary infection. We feel that there is a role for excision biopsy of the lesion for both diagnosis and treatment. As in this case, the patient symptoms improved remarkably after surgery. He was able to ambulate without analgesia 2 days after the operation.

More ominous, however, is the underlying vascular disease that diabetic muscle infarction is associated with. Most patients have been reported to succumb to a cardiovascular event within several years of diagnosis. Therefore, patients should undergo evaluation for all end-organ manifestations of diabetes.

REFERENCES

1. Angervall L, Slener B. Tumoriform focal muscle degeneration in 2 diabetic patients. Diabelologia 1965;1:39-42.

2. Chason DP, Fleckenstein JL, Burns DK, Rojas C. Diabetic muscle infarction: radiological evaluation. Skeletal Radiol 1996; 25:127- 32.

3. Grigoriadis E, Fam AG, Starok M, Ang LC. Skeletal muscle infarction in diabetes mellitus. J Rheumatol 2000;27:1063-8.

4. Silberstein L, Britton KE, Marsh FP, Raftery Mj, D'Cruz D. An unexpected cause of muscle pain in diabetes. Ann Rheum Dis 2001;60:310-2.

5. Toh V, Winocour P. Bilateral lower limb pain and swelling in a young girl with type 1 diabetes mellitus. Hosp Med 2001;62: 783-5.

6. Aboulafia AJ, Monson DK, Kennon RE. Clincal and radiological aspects of idiopathic diabetic muscle infarction. Rational approach to diagnosis and treatment. J Bone Joint Surg Br 1999;81:323-6.

7. Spengos K, Wohrle JC, Binder J, Schwartz A, Hennerici M. Bilateral diabetic infarction of the anterior tibia muscle. Diabetes Care 2000;23:699-701.

8. Umpierrez GE, Stiles RG, Kleinbart J, Krendel DA, Watts NB. Diabetic muscle infarction. Am J Med 1996;101:245-50.

9. Bingham C, Hilton DA, Nicholls AJ. Diabetic muscle infarction: an unusual cause of leg swelling in diabetic on continuous ambulatory peritoneal dialysis. Nephrol Dial Transplant 1998;13:2377- 9.

10. Mac Isaac RJ, Jerums G, Scurrah L. Diabetic muscle infarction. Med J Aust 2002;177:323-4.

YW Lim

Department of Orthopaedic Surgery, Changi General Hospital, Singapore

TP Thamboo

Department of Pathology, National University of Singapore, Singapore

Address correspondence andreprint requests to: Dr YW Lim, Associate Consultant, Department of Orthopaedic Surgery, Changi General Hospital, 2 Simei Street 3, 529889, Singapore. E-mail: yeow_wai_lim@cgh.com.sg

Copyright Western Pacific Orthopaedic Association Dec 2005

Source: Journal of Orthopaedic Surgery

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