Daptomycin-induced rhabdomyolysis complicated with acute gouty arthritis

Introduction

Rhabdomyolysis is a potentially fatal condition caused by the breakdown of skeletal muscle and the subsequent release of intracellular muscle components into the circulation and extracellular space. An elevated creatine kinase (CK) level is the most accurate laboratory test for diagnosing this condition. Clinical manifestations can range from no symptoms with raised CK levels, to myalgia, weakness, and myoglobinuria, to acute renal failure with significantly elevated CK levels and electrolyte disorders. It may result from direct muscular injuries, muscle overuse, infections, hereditary conditions, and the use of specific drugs. Daptomycin is a lipopeptide antibiotic and has been linked to an increased risk of rhabdomyolysis, particularly at high doses. The cornerstone of the treatment is volume expansion and correction of any electrolyte abnormalities.

Case presentation

A 74-year-old man with a past medical history of type 2 diabetes mellitus, hypertension, hypothyroidism, hyperlipidemia, and stage 3 chronic kidney disease presented with a three-day history of severe myalgias, generalized weakness, and oliguria. He was recently admitted one week prior with right elbow pain and swelling. Arthrocentesis was done at that time, and the synovial fluid showed a white blood cell (WBC) count of 70,270/mm ³ with cloudy color. Calcium pyrophosphate crystals were present without monosodium urate crystals. He was treated for a septic right elbow with incision and drainage, a washout procedure, and intravenous antibiotics. He was discharged on a 6-week course of intravenous daptomycin 8mg/kg and oral levofloxacin 750 mg daily. He denied any other medical or surgical history of joint diseases and denied having fevers, hematuria, dysuria, or recent trauma. His drug history included lisinopril 20 mg, hydrochlorothiazide 12.5 mg, and atorvastatin 20 mg daily; he has been compliant for years with no recent dose changes.

On physical examination, there were no signs of redness, swelling, or erythema of any joint, including the right elbow incision from the washout procedure during the last admission. The bedside urinal contained dark yellow urine. Laboratory tests showed blood urea nitrogen of 63 mg/dL, creatinine of 2.7 mg/dL increased from a baseline of 1.2 mg/dL, myoglobin of 7,780 ng/mL, and CK of 10,719 international units/L. The CK increased to 26,250 international units/L the next day. He was admitted to the hospital for acute kidney injury and rhabdomyolysis, and intravenous fluids were started. On hospital day four, he developed severe left knee pain that worsened with movement. There was a significant effusion with warmth presented on examination. On hospital day five, additional pain in the left thenar prominence was reported.

A four-view x-ray of the left knee showed chondrocalcinosis in the medial and lateral compartments of the knee joint consistent with calcium pyrophosphate deposition or pseudogout ( Fig. 1 ). Three-view x-ray of the left hand showed periarticular bony erosions consistent with gout ( Fig. 2 ). Left knee arthrocentesis was done, and fluid analysis revealed monosodium urate and calcium pyrophosphate crystals without bacterial growth. His uric acid was elevated at 10.7 mg/dL; it was previously normal one week prior. A rheumatoid factor, anti-nuclear antibodies, and cyclic citrulline peptide levels were negative.