Background: This study aimed to assess the efficacy of the adductor canal block (ACB) in comparison to intra-articular steroid-lidocaine injection (IASLI) to control chronic knee osteoarthritis (KOA) pain. Methods: A randomized, single-blinded trial in an outpatient rehabilitation clinic re-cruiting chronic KOA with pain ≥ 6 months over one year. Following randomization,subjects received either a single ACB or IASLI under ultrasound guidance. Numerical rating scale (NRS) scores for pain, and Knee Injury and Osteoarthritis Outcome Scores (KOOS) were recorded at baseline, 1 hour, 1 month, and 3 months postinjection. Results: Sixty-six knees were recruited; 2 were lost to follow-up. Age was normally distributed (P = 0.463), with more female subjects in both arms (P = 0.564). NRS scores improved significantly for both arms at 1 hour, with better pain scores for the IASLI arm (P = 0.416) at 1st month and ACB arm at 3rd month (P = 0.077) with larger effect size (Cohen’s d = 1.085). Lower limb function improved significantly in the IASLI arm at 1 month; the ACB subjects showed greater functional improvement at 3 months (Cohen’s d = 0.3, P = 0.346). Quality of life (QoL) improvement mirrored the functional scores whereby the IASLI group fared better at the 1st month (P = 0.071) but at the 3rd month the ACB group scored better (Cohen’s d = 0.08, P = 0.710). Conclusions ACB provides longer lasting analgesia which improves function and QoL in chronic KOA patients up to 3 months without any significant side effects.

INTRODUCTIONThis study aimed to determine the risk factors of diabetic Charcot arthropathy of the foot among diabetic patients with and without foot problems.

METHODSThis was a case-control study involving diabetic patients attending the Diabetic Foot Care and Wound Management Clinic at University Malaya Medical Centre, Kuala Lumpur, Malaysia, from June 2010 to June 2011. Data on sociodemographic profiles, foot factors and diabetes characteristics was collected and analysed.

RESULTSA total of 48 diabetic patients with Charcot arthropathy of the foot were identified. Data from these 48 patients was compared with those of 52 diabetic patients without foot problems. Up to 83.3% of patients with diabetic Charcot arthropathy presented with unilateral Charcot foot, most commonly located at the midfoot (45.8%). Patients with a history of foot problems, including foot ulcer, amputation, surgery or a combination of problems, had the highest (26-time) likelihood of developing Charcot arthropathy (odds ratio 26.4; 95% confidence interval 6.4-109.6). Other significant risk factors included age below 60 years, more than ten years' duration of diabetes mellitus and the presence of nephropathy.

CONCLUSIONA history of prior diabetic foot problems is the greatest risk factor for developing diabetic Charcot arthropathy, compared with other risk factors such as diabetes characteristics and sociodemographic profiles. Preventive management of diabetic foot problems in the primary care setting and multidisciplinary care are of paramount importance, especially among chronic diabetic patients.

Arthropathy, Neurogenic ; diagnosis ; epidemiology ; etiology ; Diabetic Foot ; complications ; epidemiology ; Female ; Follow-Up Studies ; Humans ; Incidence ; Malaysia ; epidemiology ; Male ; Middle Aged ; Retrospective Studies ; Risk Assessment ; Risk Factors ; Tertiary Care Centers ; statistics & numerical data

Childhood chronic inflammatory demyelinating polyneuropathy (CIDP) can be misdiagnosed for the more common genetic neuropathies such as Charcot-Marie-Tooth (CMT) disease. We present a case of childhood-onset demyelinating polyneuropathy who was initially diagnosed as CMT before a revised diagnosis of CIDP was made. A 14-year-old boy with bilateral pes cavus presented with progressive history of ataxic gait, generalized areflexia and proprioceptive sensory loss. Nerve conduction studies showed demyelinating features including markedly slow motor conduction velocities and prolonged distal motor latencies resembling CMT1. Despite the absence of a family history of genetic neuropathies, a diagnosis of CMT1 was considered most likely. The patient presented two years later with an acute onset of worsening instability and muscle weakness. A detailed history revealed functional improvement following the last presentation along with two separate episodes of exacerbations suggesting a relapsingremitting form of neuropathy. Cerebrospinal fluid analysis showed cytoalbuminergic dissociation. Nerve ultrasound demonstrated enlarged peripheral nerves, particularly in the proximal and non-entrapment sites. Genetic testing was negative for known mutations in common CMT genes. A course of intravenous immunoglobulin resulted in clinically significant improvement. In conclusion, our patient highlights the diagnostic challenges in childhood-onset demyelinating neuropathies and the importance of not missing a potentially treatable immune-mediated neuropathy.