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Flexible bronchoscopy is a widely used procedure with multiple therapeutic and diagnostic uses. Although considered fairly low risk, ocular complications including subconjunctival hemorrhage and Valsalva retinopathy
have been reported. We present a case of serous retinal detachment (SRD) that was primarily caused by a hypertensive emergency occurring during bronchoscopy.
A 66-year-old man presented for acute unilateral right vision loss after diagnostic bronchoscopy. His ocular history was notable for left amblyopia and bilateral cataract surgery. He was otherwise known for chronic kidney disease with nephrotic proteinuria caused by focal segmental glomerulosclerosis, hypertension on multiple antihypertensive agents, coronary artery disease, peripheral vascular disease, dyslipidemia, and benign prostatic hyperplasia.
The bronchoscopy was performed under mild sedation for investigation of a chronic cough of unknown etiology. The blood pressure (BP, mm Hg) immediately before the procedure was 169/90, which was higher than the patient's estimated baseline of (138/75). The procedure itself was unremarkable except for an elevated BP (max. 188/87) throughout the procedure. Although a significant gag reflex was observed, there was no associated emesis or excessive coughing. However, 15 minutes after the procedure, the patient noted blurry vision OD that persisted until 2 days later, upon which he was seen at our retina clinic.
At presentation, visual acuity (VA) was 20/150 correcting to 20/60−2 OD and 20/150+1 OS. A year ago, VA was 20/20−1 OD and 20/80 OS. Fundus examination of the right eye revealed a macular SRD, an Elschnig spot, and focal chorioretinal pigmentary changes in the posterior pole (Fig. 1). Optical coherence tomography (OCT) showed subretinal fluid and marked irregularity of the retinal pigmented epithelium contour with a dome-shaped elevation superior to the fovea (Fig. 2). On ultrasonography, the choroid measured 1.6 mm in thickness in this area. Fluorescein angiography (FA) showed choroidal ischemia (Supplementary Fig. 1A, 1B; available online). The examination of the fellow eye, including ancillary testing, was normal except for small macular drusen and mild choroidal thickening at 259 µm on OCT. It was postulated that the patient had a retinal detachment after hypertensive choroidopathy with other contributing factors after bronchoscopy. His blood pressure was still elevated at 171/81.
Follow-up at 1 week revealed significant resolution of the retinal detachment, and the pigmentary changes along the superior arcade were no longer visualized. The dome-shaped elevation of the retinal pigmented epithelium was markedly reduced on OCT. Choroidal ischemia was still present on FA and indocyanine green angiography (Supplementary Fig. 2; available online). His follow-up 1 month thereafter demonstrated complete resolution of the exudative retinal detachment and reperfusion of the choroidal zone of ischemia (Supplementary Fig. 3; available online). At 6 months post-bronchoscopy, SRD was completely resolved. His final VA OD was 20/20.
We present a unilateral SRD after a hypertensive emergency precipitated by diagnostic bronchoscopy. We postulate that uncontrolled hypertension and induced Valsalva manoeuvres during procedure, exacerbated by the patient's underlying comorbidities, including chronic kidney disease, were important factors leading to this previously undescribed complication.
Hypertensive emergency is recognized among reported causes of SRD. Lee et al. described 45 eyes of 24 patients with hypertensive emergency who exhibited SRD. OCT angiography imaging suggested that choroidal circulation hypoperfusion from hypertension was a key mechanism in hypertensive choroidopathy and ischemia, predisposing patients to subsequent SRD.
In our patient, the choroidal ischemia shown on FA and indocyanine green angiography suggests the role of impaired choroidal vascular perfusion and interstitial fluid extension into the subretinal space as an underlying mechanism. The persistent hypertension seen during bronchoscopy and later visits likely maintained the SRD by increasing hydrostatic pressure according to the Starling equation. The Elschnig spot is also suggestive of hypertension as a physiopathological mechanism.
Another possible component contributing to the SRD is the Valsalva manoeuvre, associated with increased intrathoracic pressure. The bronchoscopy procedure notes described a significant gag reflex in this patient, which could be one of several factors responsible for an elevated venous pressure, leading to venous stasis and ischemia causing the SRD.
We also speculate that the dome-shaped elevation of the retinal pigmented epithelium, which later resolved, was caused by a small suprachoroidal hemorrhage, despite absence of a reddish hue on fundoscopy. This self-limited suprachoroidal hemorrhage may have occurred as a result of an increased pressure gradient in the ciliary vessels during Valsalva manoeuvre.
This patient was also at higher risk for SRD given the presence of nephrotic syndrome caused by focal segmental glomerulosclerosis, which decreases vascular oncotic pressure. This can cause an imbalance in the Starling equation, favouring movement of fluid from the choroidal capillaries to the subretinal space. Ang et al. suggested this possible mechanism in their case of bilateral choroidal detachments with associated SRD in a patient with severe hypoalbuminemia and graft-versus-host disease.
Our patient's findings were highly asymmetrical despite being caused by systemic factors that should affect both eyes. Indeed, the left eye showed mild choroidal thickening without any signs of hypertensive retinopathy. Retinopathy was also absent in the affected eye. Lee et al. have shown that 97.8% of patients with hypertensive emergency and SRD in at least 1 eye exhibited hypertensive retinopathy features.
In conclusion, SRD can occur after hypertensive emergencies precipitated by any procedure requiring conscious sedation, such as diagnostic bronchoscopy. Clinicians should be wary of this possibility, and we suggest that hypertension control should be achieved before proceeding, as well as adequate sedation and anaesthesia provided, in order to minimize significant BP rise and Valsalva during the procedure. Clinical evolution of this complication can be favourable without additional treatment.
Footnotes and Disclosure
The authors have no proprietary or commercial interest in any materials discussed in this article.