Keratoconus is classically defined as a non-inflammatory corneal ectasia, with progressive corneal stromal thinning and abnormal conical curvature of the cornea, usually centrally or inferiorly, resulting in irregular astigmatism and visual distortion (Downie and Lindsay 2015; Rabinowitz 1998; Romero-Jimenez et al. 2010). Four of the five classical signs of inflammation (redness, swelling, pain and heat) are not present, although there is loss of function, and proinflammatory mediators have been found to be elevated in the tear film of eyes with keratoconus (Lema and Duran 2005; Lema et al. 2009), whilst tear film anti-inflammatory substances are reduced (Acera et al. 2011; Balasubramanian et al. 2012). Thus, it has recently been proposed that keratoconus is redefined as a ‘quasi-inflammatory’ disease (McMonnies 2015). The disease is usually bilateral, but asymmetric, and spectacles often cannot provide adequate correction of the irregular astigmatism, especially as the disease becomes more advanced, resulting in reduced visual acuity (Downie and Lindsay 2015; Lim and Vogt 2002; Nadaran et al. 2015; Rabinowitz 1998; Romero-Jimenez et al. 2010). Keratoconus is usually diagnosed in the second decade of life, although it can present at any time (Romero-Jimenez et al. 2010). After the third to fourth decade, progression tends to halt and the condition stabilises (Rabinowitz 1998). Thus the disease develops over some of the most active years of a person’s life; education, work and family life are ongoing concerns at the time of diagnosis and progression of the condition. Optimal visual correction is therefore vital to maintain good quality of life. Equally, detecting and, where possible, preventing progression or complications are very important.