Acute angle closure glaucoma?

At one extreme in the contest of words are those whose use of language could be characterized as ‘loose’, who aver: ‘when I use a word, it means exactly what I choose it to mean’. This provokes in the pedant a clench-fisted, spittle-flecked rage. At the other end of the semantic spectrum is the soothing succour of life-coach-of-the-moment Jordan Peterson, who, in his best-selling book ‘12 Rules for Life: An Antidote to Chaos’, titles the tenth chapter ‘Be precise in your speech’. Acute angle closure glaucoma (AACG) is regarded as a historical term. The most accepted terminology now is acute primary angle closure (APAC). The more emotive option of acute angleclosure crisis seems not to have gained traction in the sober milieu of the scientific literature, probably because of its slightly histrionic overtones. Casson et al. – in their treatise on glaucoma definitions – were explicit in denying APAC a seat at the glaucoma family table: as they say, actual glaucoma involves characteristic optic nerve and visual field changes, which APAC generally does not have (unless the eye has been suffering undiagnosed primary angle closure glaucoma [PACG], such that the attack is acute-on-chronic). Nevertheless, AACG remains – in general hospital emergency departments around the world – a useful trigger-term to exhume a pattern recognition for the non-specialist. Fea et al. are commendably precise in the distinctions they try to make between APAC and PACG in this issue of the Journal. They have sought to determine the presence of glaucomatous optic neuropathy in eyes 5 years following an episode of APAC, compared to fellow eyes without such an acute attack. They show that the eyes affected by the acute attack are more likely to have a greater cup-to-disc ratio and a greater mean deviation on field testing, than the ‘unaffected’ fellow eyes, many of which nevertheless also develop angle closure glaucoma. They confess to the retrospectivity of their paper and the limitations that might entail, which for this discussion may be critical. We do not know the respective angle features in the affected and unaffected eyes prior to APAC – such as narrowing, angle grade or PAS formation – so we cannot speculate as to in what extra way the eye that suffered the APAC was predisposed, nor whether it was thus disposed to worse or more rapidly progressive angle closure glaucoma. In addition, the presence of PACG at 5 years was the determinant of recruitment for the study – 5 cases of APAC which did not go on to PACG were excluded – but while a history of previous glaucoma was an exclusion for the study, the authors were not ultimately able to exclude the possibility that GON was present in some or even many cases prior to the APAC, or in fellow eyes. Their comparison is between the APAC and unaffected eyes 5 years after the attack, not between baseline (APAC) and 5 years for each eye over time. Thus, we cannot assume that each eye was free of PACG prior to the APAC, nor that all the disparity in disc and field features are subsequent to the APAC. Could they be consequent upon the APAC? Following the conventional line, the authors seem to assume that the variations in disc cupping must have been due to a glaucomatous angle-closure process. Although not able to correlate the level of acute IOP or duration of attack with severity of disc or field features in their paper, APAC with markedly elevated IOP may constitute an ischaemic insult to the optic nerve head. Indeed, non-arteritic anterior ischaemic optic neuropathy (NAAION) has been reported in a small number of cases after APAC, but these are usually cases in a clinically designated ‘disk-at-risk’. Could lesser or focal ischaemic insults occur in other disc types? This is a controversial area of speculation. Shen et al. demonstrated a statistically significant increase in optic disc cupping following isolated APAC. In contrast, Chew et al. reported that whilst the RNFL showed thinning after such an attack, there were no changes in disc morphology. This latter view was subsequently contested in a peer-reviewed commentary by Spaeth, but supported by Sng et al. who showed RNFL loss, no change in disc contour on HRT-III, but also reported disc pallor in more than one third of the cases.