Case Details

Emergency Medicine Orthopedic Surgery

Indian Doctors Network posted a case

16 days ago

Case report: A delayed extensor pollicis longus tendon repair,following a rupture secondary to multifactorial causes

Courtesy: Nirav Y Gandhi*; Raimand Morad; Hemant Kumar

Case Report
We present a case of a left-handed, 65-year-old, Caucasian gentleman who presented in August 2015 to the plastics outpatients trauma clinic as a routine referral. During the initial assessment it was clinically deemed that he had ruptured a tendon in his left thumb.
His extensive past medical history included: polycystic kidney disease, chronic renal failure of over 15 years requiring haemodialysis via an arterio-venousfistula, ulcerative colitis, primary sclerosing cholangitis, ischaemic heart disease, inflammatory arthropathy and prostatic adenocarcinoma. The only medication of note was long-term (5 years) ciprofloxacin on an intermittent basis for recurrent urinary tract infections. The patient had no known allergies. He was also noted to have a history of untreated Achilles tendon rupture. Subsequent ultrasound imaging confirmed a distal Extensor Pollicis Longus (EPL) rupture in his left hand, the red arrows indicating the location of the rupture.) Following this, he was advised to
wear a volar thumb splint for a period of 4-6 weeks and to return to clinic to assess any improvements or the need for further treatment.
A follow-up clinic appointment at 2 months revealed that the patient had no functional improvement and was still unable to extend his thumb. Understandably, this was causing him increasing frustration, as he had difficulty with daily activities. He denied any other sensorimotor symptoms. During this appointment the patient was advised of the possible options for his left EPL tendon repair and the risks of delayed treatment. He then underwent a primary suture repair in October 2015. Surgical intervention was delayed until this point, owing to the initial underlying inflammation.

The patient underwent a repair of his EPL tendon with a transfer of the Extensor Indicis Propius (EIP) tendon. The distal end of the EPL tendon was revealed by a sigmoid incision at its distal attachment.
The operation was complicated by various factors, primarily the presence of an Arterio-Venous (AV) fistula in proximity to the operative field. This prevented the use of a tourniquet and the limited the extent of dissection in view of tracing the proximal end of the EPL tendon. The EIP tendon was found via an incision near its distal end and divided at a level proximal to the metacarpophalangeal joint and tunneled to lie in line with the distal end of the EPL. The free ends were sutured in place and the tendon function was tested intra-operatively.

In this specific case, there are multiple relevant predisposing factors. The patient is diagnosed with ESRF requiring dialysis, with subsequent development of secondary hyperparathyroidism (current PTH levels are within normal range: 31pg/ml due to treatment with a calcimimetic). In addition, the patient had only stopped his long-term steroid therapy and ciprofloxacin before his initial presentation. It is important to realise that although literature may suggest individual causes for tendon rupture, the cumulative effect of these factors increases this risk even further as evidenced by the patient’s history of multiple tendon

Gao et al. demonstrated that tendinopathy was more common in haemodialysis patients although rupture was a rare end-point. Case series, reports and literature reviews suggest that end stage renal failure and haemodialysis are major predisposing factors for tendinopathy and tendon rupture. Other factors also significantly contribute; the duration of dialysis (15 years in the presented case), secondary hyperparathyroidism, accumulation of beta-2-microglobulin, corticosteroids, quinolone antibiotics, malnutrition and chronic acidosis have all been identified.
It is postulated that secondary hyperparathyroidism is important in the process of tendon rupture. The elevated levels of parathyroid hormone seen in ESRF patients leads to sub-tendinous bone resorption at the insertion sites. This leads to a weakened insertion site with eventual tendon rupture.

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