Editor, V alsalva manoeuvre, the forced exhalation against a closed glottis, leads to increased intrathoracic pressure and central venous pressure. Preretinal haemorrhage caused by the subsequent venous hypertension is termed valsalva retinopathy (Duane 1972). Valsalva manoeuvre has also been reported as a cause of Purtscher’s retinopathy (Kocak et al. 2003) and retinal vein occlusion (Sbeity & Mansour 2004). A 38-year-old man presented with unilateral, sudden onset, decreased vision in his left eye that occurred while straining to defaecate. Snellen visual acuity was 6 ⁄6 in the right eye and 6 ⁄ 12 in the left. There were several subconjunctival haemorrhages in the left eye (Fig. 1). Fundus examination of the left eye showed dilated and tortuous retinal veins but no retinal oedema or haemorrhages (Fig. 2). Intraocular pressure was 12 and 16 mmHg right and left, respectively. There was a petechial rash involving his face and neck (Fig. 3). Blood pressure was normal. Investigations for cardiovascular risk factors and thrombophilias did not reveal any abnormality. Ten days later his vision had improved to 6 ⁄ 6 in his left eye; however, retinal venous dilation remained. Retinal venous dilation is a common finding in retinal vein occlusion and we believe the same common process of venous hypertension has produced the findings reported here. Unlike vein occlusion, the venous hypertension reported here was transient and transmitted from raised intrathoracic pressure. Capillary rupture, the underlying process in valsalva retinopathy (Duane 1972), was not observed in the globe but was observed in the conjunctiva and the skin. This provides further evidence of venous hypertension within regional venous and capillary networks. It was unclear why the patient’s visual acuity was affected but we hypothesize that there was transient sub-clinical retinal oedema. A similar process of raised venous pressure leading to retinal oedema has been proposed for Purtscher’s retinopathy (Marr & Marr 1962; Sbeity & Mansour 2004). The pathophysiology of Purtscher’s retinopathy is controversial, with vasculitic and embolic events also proposed. We believe that this case highlights a unique way in which the retinal vasculature has responded to transient venous hypertension. In addition, it highlights how valsalva retinopathy and Purtscher’s retinopathy may share a common pathological process in venous hypertension.