The Charcot joint was originally described as tabetic arthopathy and published in 1868. This occurs in approximately 0.2% of people with diabetes and usually involves a prior peripheral neuropathy. Other factors involved in the pathogenesis of this osteoarthropathy are autonomic neuropathy & trauma.
A 74-year-old male presented in August 2004 with a subacute history of right foot swelling & discomfort. There was no discreet history of preceding trauma but he had reported regular walking 2 months prior.
He has had type 2 diabetes since 1984 with HBA1c values often <7%. He does not have photographic evidence of retinopathy and clinical examination did not reveal a peripheral neuropathy. He has impaired renal function with a serum creatinine of 200 μmol/litre and protein excretion of 0.73 g over 24 hours. His chronic renal impairment is thought to be secondary to prolonged NSAID therapy, although he has a history of gout (serum urate 0.22) previous renal calculi & prostatism. He is not anaemic but has evidence of secondary hyperparathyroidism.
Other medical history includes hypertension and a Dukes C1 sigmoid adenocarcinoma which was completely resected in 1998 followed by six months of 5-fluoro-uracil chemotherapy (C1 T3 N1).
A Right warm, swollen ankle was visible with good vibration sense at the great toe as well as elicited ankle reflexes and foot pulses. A formal neurological examination by a neurologist confirmed no obvious evidence of a clinical peripheral neuropathy. Subsequent EMG studies revealed reduced sensory action potentials consistent with a mild sensory-motor axonal polyneuropathy. Autonomic function test results were normal as well as other metabolic parameters. Imaging was entirely consistent with a charcot joint. His foot was offloaded with an air cast walker with subsequent quiescence of the charcot joint activity.
This describes a case of Charcot without predominant features of a neuropathy or other microvascular complications.
07 - 09 Nov 2005
Society for Endocrinology