Diabetes has been associated with greater risk of complications and prolonged postoperative recovery following ankle trauma. Our cohort study reviewed the operative management and outcomes of ankle fractures in diabetic adults relative to non-diabetic adults from Jan 2016–2019. Non-diabetic controls were frequency age-matched 2:1.

34 of 572 ankle fracture presentations were in diabetic patients, 32% managed non-operatively compared to 29% of the matched non-diabetic cohort. The distribution in Lauge-Hansen fracture pattern was comparable between cohorts.

Mean length of follow-up was significantly longer for diabetics (26 weeks) compared to non-diabetics (16 weeks). Post-operative wound complications (superficial wound infection, breakdown, dehiscence) occurred in 48% of the operated diabetic ankles, compared to 5% in non-diabetics (RR 8.1, 95% CI 2.5–26.4). Reoperation (RR 4.3, 95% CI 2.5–26.4, p=0.03) and non-wound complication rates (Charcot joint, mal/non-union, metalware infection) were likewise significantly higher (RR 3.9, 95% CI 1.4–10.8, p=0.008) in diabetics. Amongst diabetics alone, those with an HbA1c >69 mmol/mol (n=14, 41%) demonstrated a significantly higher rate still of non-wound complications (RR 4.3, 95% CI 1.1–18., p=0.03) with a trend towards higher wound complication rates (RR 3, 95% CI 0.52–17, p=0.13).

Poorly controlled diabetes is associated with substantially greater complication rates following ankle fracture than those with well controlled or normal blood sugar; high HbA1c > 69mmol/mol is a significant predictor of complicated follow-up. Locally we recommend management strategies that are influenced by the fracture pattern stability and the presence or absence of complicated or poorly managed diabetes.

Platelet-rich plasma is a new inductive therapy which is being increasingly used for the treatment of the complications of bone healing, such as infection and nonunion. The activator for platelet-rich plasma is a mixture of thrombin and calcium chloride which produces a platelet-rich gel.

We analysed the antibacterial effect of platelet-rich gel in vitro by using the platelet-rich plasma samples of 20 volunteers. In vitro laboratory susceptibility to platelet-rich gel was determined by the Kirby-Bauer disc-diffusion method. Baseline antimicrobial activity was assessed by measuring the zones of inhibition on agar plates coated with selected bacterial strains.

Zones of inhibition produced by platelet-rich gel ranged between 6 mm and 24 mm (mean 9.83 mm) in diameter. Platelet-rich gel inhibited the growth of Staphylococcus aureus and was also active against Escherichia coli. There was no activity against Klebsiella pneumoniae, Enterococcus faecalis, and Pseudomonas aeruginosa. Moreover, platelet-rich gel seemed to induce the in vitro growth of Ps. aeruginosa, suggesting that it may cause an exacerbation of infections with this organism. We believe that a combination of the inductive and antimicrobial properties of platelet-rich gel can improve the treatment of infected delayed healing and nonunion.