Sir,

Choroidal detachment (in the absence of haemorrhage) is caused by the transudation of serum into the suprachoroidal space. This is most commonly due to an increase in orbital transmural pressure, because of trauma, serum exudation, or inflammation.1 To the best of our knowledge, choroidal detachment is unreported in association with pulmonary embolism (PE). We report this previously serious occular complication of acute massive PE.

Case report

An 86-year-old man presented following a collapse outside his general practioner (GP) surgery. On arrival of the paramedics, he was cyanosed, with an unrecordable blood pressure. He was normotensive on arrival at hospital, where an initial electrocardiogram (ECG) showed acute right bundle branch block (RBBB). An arterial blood gas on high-flow oxygen showed hypoxia. The alveolar–arterial oxygen gradient was very high at 85.3.

A D-dimer was raised, as was the troponin. A diagnosis of acute massive PE was made and he was anticoagulated with low molecular weight heparin and warfarin. He was not thrombolysed. A computed tomographic pulmonary angiogram (CTPA) scan, 12 h later, confirmed large bilateral pulmonary emboli.

He complained of blurred vision 24 h later. On examination, visual acuity was 6/60 in the right eye (RE) and light perception in the left intraoccular pressures (IOP) was normal. Pupils were reactive, but sluggish on the left. Anterior segment examination showed folds in the descements membrane. The anterior choroid was quiet. Dilated fundus examination revealed bilateral choroidal detachments with kissing choroids seen on B scan, with appearances consistent with suprachoroidal haemorrhage (Figure 1).

Figure 1
figure 1

B scan of the RE (top panel, a) and LE (lower panel, b), 4 days post PE, showing choroidal detachments with kissing choroids.

Full size image

The patient was managed conservatively. After 10 days later, right visual acuity had improved to 6/18, with counting fingers in the left eye (LE). By 1 month, there was near resolution of the right choroidal detachment, with an RE visual acuity of 6/6 at 2 months. At 6 weeks following the initial insult, he developed a secondary LE vitreous haemorrhage, which failed to improve with conservative management. Anticoagulation was optimal throughout. He underwent a vitrectomy under local anaesthesia, leaving his LE visual acuity at 6/60 with resolved choroidal detachment, a flat retina, and no macular oedema.

Comment

Serous choroidal detachment involves the exudation of serum into the suprachoroidal space. There are several mechanisms for this, including low intraoccular pressure (IOP), which can be a result of ciliary body hypoperfusion.1 We consider the most likely mechanism for this patient's choroidal detachment to be a low arterial perfusion pressure. Acute massive PE leads to an acute rise in pulmonary artery pressure. This leads to reduced pulmonary blood flow and impaired left heart filling, leading to a low systemic blood pressure.2 The low cardiac output state leads to reduced carotid perfusion, and therefore reduced flow in the ophthalmic artery, and other end arteries.1 The raised troponin on admission suggests secondary myocardial damage,3 again owing to a low perfusion pressure. His secondary LE vitreous haemorrhage is likely to be owing to a combination of warfarin anticoagulation in the presence of abnormal choroids.4, 5

Complications of acute massive PE are rare in those who survive the initial insult. Small bowel hypoperfusion (presenting as fluid-filled dilated bowel loops—‘shock bowel’)6 and cerebral hypoperfusion (presenting as fits) are reported owing to the systemic hypotension of acute PE.7 This is, to our knowledge, the first report of bilateral choroidal detachments in association with PE. We could not find any specific reason why this patient should suffer from this complication. Practitioners should be alert to signs of end organ damage following PE, and investigate promptly visual disturbance following a thromboembolic event.