Case of the Month

Edited by Robert N. Johnson, MD

Case #119, May, 2019

Presented by Joseph Alsberge, MD

A 60-year-old man with loss of vision in his left eye

Figure 1: Color fundus photo of the right macula. Note scattered small and large drusen through out the macula.

Figure 2: Color fundus photo of the left macula. Note the large area of preretinal hemorrhage obscuring much of the macula.

Case History

A 60-year-old man presented for evaluation of decreased vision in the left eye.

On examination, visual acuity was 20/40 in the right eye and 3’/200 in the left eye. The anterior segment examination was unremarkable. Dilated examination of the right eye showed scattered large drusen throughout the macula and posterior pole. In the left eye he had a large subhyaloid hemorrhage in the macula, mild vitreous hemorrhage, and scattered drusen in the posterior pole (Figures 1 and 2). Fluorescein angiography showed a large area of blockage in the macula of the left eye due to the preretinal hemorrhage (Figure 3).

Figure 3: Mid-phase fluorescein angiogram of the left eye. Note the large area of blockage due to the subhyaloid hemorrhage.

What is your Diagnosis?

Differential Diagnosis

Ruptured retinal arterial macroaneurysm, choroidal neovascularization due to age-related macular degeneration, retinal neovascularization (multiple potential etiologies, e.g. branch retinal vein occlusion), valsalva retinopathy, Terson’s syndrome, leukemic retinopathy.


Additional History and Diagnosis

The patient reported no past medical history and he was not taking any systemic medicines. He had no recent history of head trauma. On further questioning he revealed that the vision loss in the left eye developed shortly after a recent episode of severe vomiting. Given this information and the exam and imaging findings, the most likely diagnosis was felt to be valsalva retinopathy. The decision was made to monitor the hemorrhage with the expectation that it would resolve on its own over the course of several weeks.

The patient returned two weeks later with the complaint of worsening floaters. On exam, the subhyaloid hemorrhage appeared more yellow in color but remained quiet dense, and there was increased breakthrough of the hemorrhage into the vitreous cavity (Figure 4). At this point, the patient desired to more rapidly restore his vision. The options of ongoing observation versus intervention were discussed, and the patient elected to proceed with vitrectomy for removal of the blood.

At the time of vitrectomy, there was blood present in the sub-internal limiting membrane (ILM) potential space. The ILM was removed and noted to be thickened and blood-stained. Upon full inspection of the macula, there was no evidence of retinal arterial macroaneurysm or neovascularization, confirming the diagnosis of valsalva retinopathy (Figure 5).

Figure 4: Fundus photo of the left macula 2 weeks after initial presentation. Note that there has been some breakthrough hemorrhage into the vitreous and the yellowing of the subhyaloid hemorrhage due to dehemoglobinzation.

Figure 5: Fundus photo of the left eye 5 weeks following vitrectomy. Note the presence of large and soft drusen similar to the right eye (Figure 1) as well as the absence of other pathology.


Valsalva retinopathy, described by Duane in 1972,1 is classically characterized by sub-ILM and subhyaloid hemorrhage that develops following an exertion-related sudden increase in intraabdominal or intrathoracic pressure against a closed glottis (i.e., “the Valsalva maneuver”).2

The proposed pathophysiology of Valsalva retinopathy is that the sudden increase in venous system pressure from the Valsalva maneuver leads to a secondary increase in intravenous pressure within the eye, and subsequent rupture of superficial retinal capillaries.3 The hemorrhage then accumulates in the sub-ILM potential space and can then break through into the subhyaloid space and vitreous cavity. This type of retinal hemorrhage may develop following a wide variety of activities that induce the Valsalva maneuver including heavy lifiting, coughing, and vomiting.2 Valsalva retinopathy has been reported to occur in both normal eyes and eyes with pre-existing vascular abnormalities.2

Valsava retinopathy may be observed with the expectation of resolution of the hemorrhage and recovery of normal vision after several weeks to months. Even after resolution of the hemorrhage, the ILM detachment may persist for several weeks before spontaneously reattaching.2 Other therapeutic options for more prompt visual recovery include vitrectomy or Nd:YAG laser membranotomy.3 In Nd:YAG laser membranotomy, a hole is created in the ILM/hyaloid face overlying the preretinal hemorrhage, allowing the blood to drain into the vitreous cavity. The efficacy of laser membrabnotomy, however, may be limited if the blood has already clotted.4

Take Home Points

  • Valsalva retinopathy is characterized by sub-ILM and subhyaloid hemorrhage that develops following a sudden, exertion-related increase in systemic venous pressure.
  • With conservative management (observation alone), Valsalva retinopathy can be expected to resolve over several weeks to months, depending on the initial size of the hemorrhage. The prognosis for visual recovery is excellent.
  • Alternative treatment strategies for more prompt resolution include vitrectomy or Nd:YAG laser membrabnotomy.

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  1. Duane TD. Valsava hemorrhagic retinopathy. Trans Am Ophthalmol Soc 1972;70:298-313.
  2. Agarwal A. Traumatic Retinopathy. In: Agarwal, A. Gass’ Atlas of Macular Diseases. Fifth ed. Elsevier:714.-753
  3. Chen Y, Mingwei Z, Zhou P. Traumatic Chorioretinopathies. In: Ryan SJ, Schachat AP, Sadda SR, eds. Retina. Fifth ed. Elsevier:1564-1570.
  4. Kuruvilla O, Munie M, Shah M, et al. Nd:YAG membranotomy for preretinal hemorrhage secondary to valsalva retinopathy. Saudi Journal of Ophthalmology 2014;28:145-151.