Valsalva Retinopathy

All content on Eyewiki is protected by copyright law and the Terms of Service. This content may not be reproduced, copied, or put into any artificial intelligence program, including large language and generative AI models, without permission from the Academy.

Article initiated by:

Lorena Lam, MD

All contributors:

Christine Evans, Vinay A. Shah M.D., Lorena Lam, MD, Patricio J Rodríguez-Valdés, MD, Koushik Tripathy, MD (AIIMS), Neelakshi Bhagat, MD, FACS, Jennifer I Lim MD, Peter A.Karth, MD, Jacqueline Erdahl

Assigned editor:

Neelakshi Bhagat, MD, FACS

Review:

Assigned status Up to Date

 by Neelakshi Bhagat, MD, FACS on May 8, 2026.

add
Contributing Editors:	add

Valsalva Retinopathy

ICD-9

362.10

Disease Entity

Valsalva retinopathy

• ICD-9-CM 362.10 Background retinopathy, unspecified

Disease

Valsalva retinopathy is a preretinal hemorrhage caused by a sudden increase in intrathoracic or intraabdominal pressure with an acute rise in pressure in retinal capillaries leading to their rupture into the vitreous, subhyaloid or sub-internal limiting membrane spaces. It was first described by Duane in 1972 as hemorrhagic retinopathy of Valsalva. It can occur in otherwise healthy eyes and spontaneous resolution is common.

Epidemiology

There are insufficient epidemiological data to determine whether race, age, or sex predisposes individuals to Valsalva retinopathy. Current knowledge is largely derived from case reports and case series. The condition has been reported in otherwise healthy individuals across a wide range of ages.

Pathophysiology

During the Valsalva maneuver, a sudden rise in intrathoracic or intraabdominal pressure against a closed glottis, reduces venous return to the heart and stroke volume, consequently increasing venous system pressure. The rise in venous pressure is transmitted to the ocular circulation through absent or incompetent valves of the head and neck venous system, increasing retinal venous pressure and leading to rupture of small superficial capillaries of the macula. This results in unilateral or bilateral retinal hemorrhages and subsequent extravasation of blood into the retina, usually under the internal limiting membrane (ILM), but may also bleed to the vitreous cavity (due to a breakthrough bleed via a rupture in the ILM) or subhyaloid space.

Risk Factors

Precipitating Events

Valsalva retinopathy may occur after events that cause an increase in intrathoracic or intraabdominal pressure. Reported precipitating factors include:

• coughing
• vomiting
• heavy lifting
• straining during defecation
• strenuous exertion
• sexual intercourse
• labor and vaginal delivery
• blowing musical instruments
• compression injuries

Precipitating Conditions

Valsalva retinopathy usually occurs in otherwise healthy eyes but certain risk factors may increase occurrence, such as retinal vascular abnormalities either acquired (diabetic or hypertensive retinopathy) or congenital (retinal telangiectasias and congenital retinal artery tortuosity). Systemic hematologic conditions such as anemia has been reported as a possible contributing factor in individual cases, potentially increasing vascular susceptibility through hypoxia induced vasodilation; however, evidence is limited to case reports.

Diagnosis

Clinical Presentation

Patients may present with a history of a Valsalva event preceding sudden, painless loss of vision or scotoma centrally. Blurred vision is another common complaint. It is usually unilateral, although may rarely be bilateral. Visual acuity is variable depending on the location, size and degree of the preretinal hemorrhage.

Slit lamp examination of the anterior segment is usually normal, although subconjunctival hemorrhages could be present. Fundus examination reveals a preretinal hemorrhage typically located in the premacular area, below the internal limiting membrane, but may show break through to the sub hyaloid or intravitreal space. Hemorrhages vary in size. Blood located under the internal limiting membrane usually appears a well-circumscribed, round or dumbbell-shaped red elevation, causing a hemorrhagic detachment of the internal limiting membrane. Dissection of the blood beneath the retina may occur if bleeding occurs in the foveal region, although subretinal hemorrhage is rarely seen. Choroidal hemorrhage, although rare, has been described. The blood is initially bright red, but dehemoglobinizes to yellowish white after several days to weeks. A fluid level may be seen. Serous detachment may persist up to weeks until complete resolution. A double ring sign has been described which is characterized by the separate margins of sub hyaloid hemorrhage (outer ring) and sub-ILM hemorrhage (inner ring).

Diagnostic Procedures

Diagnosis is primarily based on history and funduscopic exam findings, although ancillary diagnostic imaging may be used to determine the extent and location of the hemorrhage or exclude alternative diagnoses. Optical coherence tomography may be used to determine the location of the hemorrhage (subhyaloid, sub-ILM, etc). Retinal fluorescein angiography can be used to rule out retinal neovascularization or other active leakage, if suspected. Serial imaging with fundus photography may be carried out to monitor the progression of recovery. When clinically indicated, laboratory testing may be considered to evaluate for alternative causes such as diabetes, sickle cell disease, or other blood dyscrasias. When the fundus is obscured by vitrial hemorrhage, a B-scan may be used to exclude retinal detachment or other structural abnormalities.

Differential Diagnosis

• Posterior vitreous detachment
• Diabetic retinopathy
• Hypertensive retinopathy
• Sickle cell retinopathy
• Purtscher retinopathy
• Terson’s syndrome
• Ruptured macroaneurysm
• Intraocular parasite
• Severe anemia

Complications

Most cases resolve without complication. A full thickness macular hole has rarely been described in association with Valsalva retinopathy, possibly due to traction at the vitreofoveal interface. Rarely, prolonged premacular hemorrhage may be associated with persistent visual impairment due to pigmentary macular changes, epiretinal membrane formation, or retinal injury from prolonged exposure to blood products and their catabolites.

Management

General treatment

Conservative management is observation of spontaneous resolution, which occurs within weeks to months. Anticoagulant or antiplatelet therapy should be reviewed with the prescribing clinician. Advise patients to avoid strenuous physical activity. Stool softeners may be utilized in cases of constipation. No medical therapy has proven benefit.

Surgery

Neodymium:YAG (Nd:YAG) laser, krypton laser, and argon laser membranotomy are suitable treatment options for large hemorrhages causing significant visual impairment. Laser membranotomy disrupts the ILM or posterior hyaloid leading to drainage of the blood into the inferior vitreous cavity, producing a faster resolution. The procedure is most suitable when the hemorrhage remains liquid and there is sufficient separation between the target membrane and the underlying retina; delayed treatment may be less effective after the blood has coagulated. Complications associated with laser membranotomy include macular hole, retinal detachment, and epiretinal membrane formation. In rare cases of dense premacular hemorrhage with insufficient spontaneous reabsorption, particularly when Nd:YAG laser drainage is not feasible or has been unsuccessful, pars plana vitrectomy with release of the ILM and evacuation of the sub-ILM hemorrhage may be considered.

Prognosis

The prognosis for Valsalva retinopathy is favorable, with most patients recovering near or at their baseline visual acuity after weeks to months. Persistent visual impairment is uncommon but may occur in cases involving submacular hemorrhage or associated structural complications such as a macular hole.