Description

A woman in her 30s presented with reduced left visual acuity (VA) and a left inferior altitudinal visual field defect days after a massive postpartum haemorrhage (PPH) following elective caesarean section, requiring 10 units of blood transfusion. The field defect faded from black to a ‘yellow-green haze’ over 24 hours. Medical history was significant for postural hypotension. There was no ophthalmic history and pregnancy was uneventful without steroid treatment (ie, no haemolysis, elevated liver enzymes and low platelets, that is, HELLP syndrome nor pre-eclampsia).

Ophthalmic examination 3 days post partum revealed best corrected VA of 6/6 and 6/9 in right and left eyes, respectively. There was no relative afferent pupil defect. Anterior segments and intraocular pressures were normal (10 mm Hg). There was no optic disc swelling/atrophy and optical coherence tomography (OCT) showed normal retinal nerve fibre layer thickness bilaterally. There were no retinal arteriolar or venous occlusions, and no signs of hypertensive retinopathy (figure 1A,B). Macular OCT showed left subfoveal oedema without pigment epithelial detachment (figure 1C). OCT angiography showed no capillary dropout or neovascularisation (figure 1D). Subretinal oedema spontaneously resolved by 1 month review (figure 2A), with return to 6/6 VA. Autofluorescence imaging demonstrated speckled multifocal hyperautofluorescence in the superior hemiretina, indicative of a resolved choroidal effusion (figure 2B). She had mild anaemia (haemoglobin 125 g/L) and elevated B12 (625 ng/L). Mean corpuscular haemoglobin, mean corpuscular volume, iron, ferritin and liver function were normal.

• Download figure
• Open in new tab
• Download powerpoint

Figure 1

(A) Colour photograph (FF450plus, Carl Zeiss MediTec, Dublin, California, USA) of the left fundus showing a diminution of the foveal reflex and central macular oedema without other acute or chronic abnormalities. (B) Fundus autofluorescence image (FAF, FF450plus camera) demonstrating a multifocal speckled hyperautofluorescent focus superior to the optic nerve head. (C) Optical coherence tomography (Cirrus 5000, Carl Zeiss Meditec, Dublin, California, USA) images of the left eye showing subretinal oedema underlying the fovea and extending temporally. (D) OCT angiography (Cirrus 5000) showing no choriocapillaris dropout in the superior fundus.

• Download figure
• Open in new tab
• Download powerpoint

Figure 2

(A) OCT showing spontaneous resolution of subretinal oedema with maintained photoreceptor architecture 1 month later. (B) FAF image of the left eye showing focal speckled hyperautofluorescence at the superior arcades and peripapillary region.

PPH is defined as blood loss from the genital tract ≥500 mL following vaginal delivery, >1000 mL post-Caesarean section, reducing haematocrit ≥10%.1 2 PPH is the primary cause of maternal death globally (140 000 annually).3 Maternal mortality risk from PPH is 1000× higher in developing nations than developed nations (1:1000 vs 1:1 000 000 deliveries, respectively).4 Overall, 99% of maternal deaths secondary to PPH occur in developing countries.5 These disproportionate death rates observed in developing countries are consequences of factors including limited medical resources and delayed access to adequate emergency healthcare.4 6

The resulting hypovolaemia secondary to PPH with shunting of perfusion to critical structures (ie, brain) may cause ischaemic damage to visceral organs and ocular tissue in surviving patients.7 8 There are very few published reports of PPH-associated visual loss (PPHAVL) in the literature; one case of non-arteritic anterior ischaemic optic neuropathy and one case of bilateral posterior ischaemic optic neuropathy.9 10 It is likely that areas in the developing world with greater rates of PPH have higher PPHAVL incidence. To our knowledge, there are no previous reports of PPH-associated choroidopathies in the literature.

We present an unusual case of transient PPHAVL, whereby transient hypovolaemia from PPH led to choroidal hypoperfusion resulting in choroidal effusion. Possible pathophysiological mechanisms include (1) choroidal ischaemia and (2) reduced choriocapillaris oncotic pressure (ie, loss of plasma proteins). The prognosis for visual recovery after PPHAVL is largely unknown; however, prolonged PPH (ie, delayed haemostasis/resuscitation) and underlying vascular risk factors (eg, diabetes mellitus, hypertension and smoking) likely confer a poorer prognosis. In this case, the patient had a complete return to baseline vision likely due to rapid vascular resuscitation and lack of other comorbidities.