Intern Report Case Discussion 2.5

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Presented by Matt Steimle, MD

Chief complaint: “I can’t see”

28 year old female comes to the ER for loss of vision for 2 days, patient states that this happened suddenly after she was vomiting. Patient is 6.5 months pregnant and has hyperemesis gravidarum that has persisted through her entire pregnancy. She denies any eye pain and the vision has not improved. She says she is unable to see anything from the left eye. Previous to this she has not had any trouble with her vision, other than wearing reading glasses. She decided to come to the ER because her vision still has not improved. She has history of hypertension but no longer requires medication. Denies any headache, fever, chills, chest pain, palpitations, shortness of breath, abdominal pain diarrhea, constipation, dysuria, vaginal bleeding or discharge, no recent travel, no sick contacts.

ROS: negative except as noted per HPI.
PMH: Hx of Hypertension no longer on medication
Surg hx: none
Gyn: G1P0, good prenatal care
Meds: Prenatal vitamins
Allergies: Vicodin causes “throat to close”
FH: Hypertension and diabetes run in the family
SH: No tobacco/alcohol/drugs

PE: vitals: T 98.7, HR 76, BP 110/56, RR 18, pulse ox 100% RA, weight 231, 5’5’’
General: 28 year old, African American female, sitting converses without difficulty
Skin: No rashes or scars
Head: normocephalic, atraumatic
Eyes: EOMI, PERRLA constricting from 6 to 3 mm bilaterally with light, no afferent pupillary defects, Pt has 20/20 VA in right eye, left eye able to finger count correctly at 5 ft. In her left eye her vision is more clear in her peripheral fields than centrally, intraocular pressure R eye 12, L eye 13, peripheral fields are intact by confrontation, on fundoscopy there were no distinct optic discs visualized, no pallor, no icterus
Nose: symmetric, no discharge
Mouth, throat: No erythema or exudates
Neck: No tracheal deviation or masses
Heart: RRR, S1, S2 heard no murmurs rubs or gallops
Respiratory: CTA BIL
Abd: gravid uterus above the umbilicus consistent with 26 week gestation, soft NT ND,
CNS: Alert and oriented x 3, cranial nerves: II, III, IV, and VI see eye exam above, good eyelid opening bilaterally; V, corneal reflex intact bilaterally facial sensation intact bilaterally in V1,V2, V3, good jaw opening, and bite strength; VII, eyebrow raise, eyelid close, smile, frown, pucker, and taste all intact and equal bilaterally; VIII equal auditory acuity to finger rub bilaterally; IX good swallow reflex, positive gag reflex; XI good lateral head rotation, neck flexion, shoulder shrug bilaterally; XII midline tongue protrusion and equal strength on lateral deviation bilaterally. Equal strength in the upper and lower extremities bilaterally, speech and gait are normal.
Extremities: no peripheral edema, all peripheral pulses are felt, good range of motion, no weakness

Questions

1.  After you dilate the pupil this is your fundoscopic exam. Your diagnosis is?

_______________________________________________

A. acute glaucoma

B. vitreous hemorrhage

C. central retinal vascular occlusion

D. valsava retinopathy

E. central retinal vein occlusion

2. The patient should be advised which of the following?
A. use aspirin

B. sleep in a sitting position

C. decrease fiber intake

D. resume normal physical activity

E . all of the above

3.Which of the following are risk factors for the above diagnosis?
A.diabetes

B.hypertension

C.anemia

D. idiopathic thrombocytopenic purpura

E. all of the above

Answers:

1. D

2. B

3. E

Discussion:

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
Migraine

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
Migraine
Vertebral basilar insufficiency
Cerebrovascular disease
Toxins (methanol, salicylates, quinine, ergot)
Optic or retrobulbar neuritis
Hysteria
Malingering

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

Retinal vein occlusion

______________________

Central retinal artery occlusion

___________________

Vitreous hemorrhage

_____________________

References:
1.Retinopathy, Valsalva, eMedicine http:emedicine.medscape.com/article/1228106
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
5.http://www.virginiaretina.org/pix/vitreous_hemorrhage.jpg, Virginia Retina Foundation

_______________________

This case discussion presented by Dr Matt Stemile

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