Monday, June 6, 2011

Intern Report Case Discussion 4.1

Case Presentation by Dr. Sarah Hyatt

Case Presentation

Answers: 1. D, 2. B, 3. E
This patient has a Valsava retinopathy. Immediately following a Valsava maneuver, a sudden rise in intraocular pressure causes retinal capillaries to spontaneously rupture. The prognosis for Valsava retinopathy is generally good.

Unilateral manifestations are most commonly seen, but bilateral findings have been reported. Sudden decreased vision occurs in the affected eyes, ranging from complaints of floating spots to complete loss of central vision. Vision often improves over weeks to months, depending on the severity of the retinal findings.

Risk factors for Valsava retinopathy are a history of vascular disease, diabetes, hypertension, sickle cell disease, anemia, idiopathic thrombocytopenic purpura.
Ocular findings are usually described as preretinal hemorrhages. Valsava retinopathy has a predilection for the macula. The ruptured vessels in the perifoveal capillaries usually cause a sudden and painless loss of central vision.

Causes: coughing, weight lifting, vomiting, bungee jumping, aerobic exercise, sexual activity, end-stage labor, colonoscopy procedures, constipation, and blowing musical instruments.

Medical care: patients should be advised to avoid anticoagulants and strenuous activities to prevent a rebleed. Patients should be instructed to sleep in a sitting position to promote blood settling, which may improve visual acuity, stool softeners may need to be considered for those with constipation. A diet rich in fiber is advisable. Physical activity should be limited until the retina has sufficiently healed. The patient should always try to limit activities that cause sudden increases in intrathoracic pressure against a closed glottis. Consultation to ophthalmology is recommended and needed for follow up.
Vision usually returns to normal over a short time period from weeks to months.

Key points:
When testing visual acuity use a Snellen chart at a distance of 20 feet or a Rosenbaum chart at a distance of 14 inches.  If the patient is unable to do this test visual acuity by testing  ability to count fingers (CF), if unable to do this test ability to perceive hand motion (HM), if unable to do this test  ability to perceive light (LP). The result may be recorded as “patient able to count fingers at 5 feet”

Acute angle-closure glaucoma: Pt has a narrow anterior chamber angle; folds of the peripheral iris can block the angle, which prevents aqueous humor outflow. The rapid elevation of intraocular pressure causes optic atrophy if not treated promptly. Patient often complains of nausea, vomiting, and pain. Emergent ophthalmologic consultation is indicated. Acute glaucoma is treated with IV mannitol or glycerol to decrease intraocular pressure by osmotic dieresis, topical miotics (i.e., 2% pilocarpine or 0.5% timolol) to decrease pupil size and increase aqueous outflow, and acetazolamide IV to decrease aqueous production

Vitreous hemorrhage: Suspect if sudden painless monocular loss of vision, more common in diabetics with an obscured red reflex and retinal details. Patients often report seeing flashing lights.  Patients also complain of seeing dark floating spots or floaters, which reflect benign vitreous separations
Central retinal artery and vein occlusion: both occur in middle-aged atherosclerotic patients or elderly hypertensive patients and present as sudden painless loss of vision. Occlusion of the retinal artery or its branches results in a dilated nonreactive pupil with an APD on the affected side. The retina is pale with a cherry-red spot on the macula. Occasionally amaurosis fugax precedes central retinal artery occlusion.
The fundoscopic examination of a central retinal vein occlusion is described as a “blood and thunder fundus” because of the presence of multiple large hemorrhages. Prognosis for both CRAO and CRVO is poor.

Common causes of nontraumatic loss of vision
Transient monocular
Amaurosis fugax
Temporal arteritis

Persistent monocular
Central retinal artery occlusion
Central retinal vein occlusion
Retinal detachment or hemorrhage
Vitreous or macular hemorrhage
Optic or retrobulbar neuritis
Internal carotid occlusion

Acute binocular
Vertebral basilar insufficiency
Cerebrovascular disease
Toxins (methanol, salicylates, quinine, ergot)
Optic or retrobulbar neuritis

Sudden painless loss of vision
Central retinal artery occlusion
Central retinal vein occlusion
Vitreous hemorrhage
Retinal detachment
Ischemic optic neuropathy
Nonarteritic ischemic optic neuropathy
Valsava retinopathy
Functional visual loss, hysterical conversion or malingering

1.Retinopathy, Valsalva, eMedicine
2.Emergency Medicine Secrets, fourth edition, 2006, pages 117-121, Markovchick

3.Rosen’s Emergency Medicine, seventh edition, 2010, pages 870-873, Marx
4.Uptodate, Approach to the adult with acute persistent vision loss, 2010, Leaveque

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