Download vitreous hemorrhage in post victretomized eye

Grand Rounds Case Presentation
Halloween in July: When the patient sees black and the doctor sees orange
Abstract:
A patient presents to the eye clinic complaining of black spots in his vision out of the left
eye. Dilated fundus exam reveals a bright orange haze distorting views of the left retina.
Case History:
A 75 yo black male presented to the clinic with a chief complaint of decreased vision out
of his left eye and reported seeing “black floating spots”. These symptoms began four
days earlier and have become progressively worse with each day. The blurry vision
involves the entire visual field. He reported no eye pain and he denied any trauma to his
left eye. He also reports he has not used any of his eye drops in his left eye since the
decrease in vision.
His medical history was significant for Diabetes Type 2 for over thirty years, associated
diabetic neuropathies, cervical spondylosis without myelopathy, obesity, and also
treatment compliance problems.
Ocular history was notable for open angle glaucoma OU since 2007 and diabetic
retinopathy OU. The patient also reports a history of previous laser surgery in both eyes
by a local ophthalmologist.
His current medications included Novolin 70/30 bid, albuterol prn, simvastatin qhs,
Cosopt bid OU, Alphagan bid OU, and Travatan qhs OU.
He reported no known drug allergies.
Based on a chart review, the patient had years of uncontrolled high blood glucose levels.
A two-year history of his HbA1C levels ranged from 10.6-16.1. His past eye notes from
a local retinal specialist contained reports of his previous ocular surgeries, which
included a pars plana vitrectomy, epiretinal membrane peel, and panretinal
photocoagulation in the left eye in 2002. The right eye also had a pars plana vitrectomy,
vitreous hemorrhage removal, and panretinal photocoagulation in 2003. Of note, the
patient also had surgeries repairing levator dehiscence and lid ptosis OU. An analysis of
his intraocular eye pressures over the last two years is below. Humphrey visual fields
showed inferior and superior arcuate defects in both eyes.
***IOP-TREATMENT SUMMARY***
MM/YY__T:OD/OS__@Time___Active meds that day________________________
03/07
32/26
0935
NONE
04/07
26/16
0917
TRAVATAN QHS OU
05/07
25/17
0858
TRAVATAN QHS OU; COSOPT BID OU
07/07
14/14
TRAVATAN QHS OU AND COSOPT BID OU
10/07
24/18
0946
TRAVATAN QHS OU ONLY
10/08
26/21
1021
TRAVATAN QHS OU ONLY
10/08
01/09
02/09
04/09
04/09
18/18
29/29
12/14
32/22
24/17
1051
1045
1125
0805
0915
TRAVATAN QHS OU; COSOPT BID OU
TRAVATAN QHS OU; COSOPT BID OU
TRAVATAN QHS OU; COSOPT BID OU
TRAVATAN QHS OU, COSOPT BID OU
(POST-DILATION)
Pertinent Findings:
The patient’s best-corrected acuities were 20/25 OD and counting fingers at face OS.
Pupils were equal and reactive to light but very miotic OU. Extraocular muscle
movements were full and smooth OU. Lids, lashes, sclera, and conjunctiva were quiet
and unremarkable in each eye. The right cornea had a trace amount of superficial
punctuate keratitis inferiorly with mild gutatta. The left cornea also had a trace amount of
SPK inferiorly with 1+ pigment on the endothelium. The right anterior chamber was
deep and quiet. The left anterior chamber was deep with 3+ cells, flare, and plasmoid
appearing aqueous. His intraocular pressures measured 18 mmHg OD and 24 mmHg OS
at 11:45 am.
The patient was then dilated using one drop 1% tropicamide and one drop 2.5%
phenylephrine OU. During the dilated fundus examination, the posterior pole and retinal
periphery were viewed biomicroscopically with a pre-corneal lens and with a binocular
indirect ophthalmoscope. In the right eye the cup-to-disk ratio was 0.75 horizontally and
0.8 vertically with superior and inferior thinning of the neuro-retinal rim tissue. The
macula was flat and dry with an occasional dot hemorrhage in the posterior pole. The
right vitreous was clear. There were scattered panretinal photocoagulation scars in the
peripheral retina 360 degrees around.
Upon examining the left eye, there was a very poor view of the fundus due to a dense,
bright orange vitreous haze. The optic nerve was slightly visible and there was evidence
of previous panretinal photocoagulation scars in the periphery as well.
Differential Diagnosis:
The differential diagnosis included:
 Retinal detachment
 Vitritis or Posterior Uveitis
 Vitreous Hemorrhage
There are 3 types of retinal detachments: rhegmatogenous, exudative, and tractional.
1. The symptoms of a rhematogenous retinal detachment (RRD) include the
following: flashes of light, floaters, a curtain or shadow moving over the field of
vision, peripheral or central vision loss or both. The main clinical sign involves
elevation of the retina from the retinal pigment epithelium by fluid in the
subretinal space due to an accompanying full-thickness retinal break. Other
clinical signs include anterior vitreous pigmented cells, vitreous hemorrhage,
posterior vitreous detachment (PVD), and usually lower IOP in the affected eye.
The detached retina is often corrugated and partially opaque in appearance and a
mild retinal afferent pupillary defect (RAPD) may be present.
2. The symptoms of an exudative retinal detachment are minimal to severe visual
loss or a visual field defect that may change with different head positions. The
clinical signs include a serous elevation of the retina with shifting subretinal fluid.
There is no retinal break and the fluid accumulation is due to a breakdown of the
normal inner or outer blood-retinal barrier. The detached retina is smooth and
may become quite bullous. A mild RAPD may also be present.
3. The symptoms of a tractional retinal detachment are vision loss or a visual defect.
A patient with a tractional RD may also be asymptomatic. The main clinical sign
is a detached retina that appears concave with a smooth surface. There can be
cellular and vitreous membranes exerting traction on the retina, and retinal striae
extending from these areas may also be seen. The detachment may become a
convex RRD if a tractional retinal tear develops. The retina can be immobile and
a mild RAPD may also be present.
Posterior uveitis commonly presents with symptoms of blurred vision, floaters, pain,
redness and sometimes photophobia. Clinical signs include cells in the anterior and/or
posterior vitreous, vitreous haze, retinal or choroidal inflammatory lesions, and sheathing
with exudates around the retinal vessels.
A vitreous hemorrhage usually presents with symptoms of sudden, painless loss of vision
or the sudden appearance of black spots, cobwebs, or haze in ones vision. The most
common clinical sign is an absent red fundus reflex. The vitreous hemorrhage may be so
dense that no view of the fundus can be obtained. Red blood cells may be seen in the
anterior vitreous, and a chronic vitreous hemorrhage can present with a yellow ochre
appearance from hemoglobin breakdown. The most common etiology is from diabetic
retinopathy but can also be due to a posterior vitreous detachment, retinal break, retinal
detachment, retinal vein occlusion, exudative macular degeneration, Sickle cell disease,
trauma, intraocular tumor, subarachnoid hemorrhage and Eales disease [10].
Diagnosis and Discussion:
Due to the clinical signs and the patient’s symptoms, a diagnosis of vitreous haze
secondary to vitreous hemorrhage versus retinal detachment was made. The patient was
referred to the ophthalmology clinic and a B-scan ultrasound was obtained.
Multiple ocular complications can accompany the presence of systemic diabetes mellitus
(DM) of long duration. These changes are mainly characterized by exudates,
microaneurysms, hemorrhages, and neovascularization, all of which can lead to a
decrease in visual acuity and eventual blindness. Annually, between 12,000 and 24,000
diabetic patients in the US become legally blind as a result of complications of diabetic
retinopathy. Many risk factors contribute to the rate at which diabetic retinopathy
progresses. These risk factors include age, race, obesity, smoking, proteinuria,
depression, dyslipidemia, duration of DM, cardiovascular diseases, uncontrolled systemic
hypertension, parental history of DM, and poor glycemic control [1]. The best predictor
for diabetic retinopathy is the duration of the disease. The prevalence of retinopathy 10
years after the onset of type 2 diabetes ranges from 23% to 67% according to different
studies [2]. Because the eye examination is so critical in diagnosing many of these
changes, the American Diabetes Association’s Clinical Practice Guidelines for examining
the patient who has diabetic retinopathy include performing comprehensive eye
examinations within 3 to 5 years of the onset of DM in type 1 diabetics, and immediately
after initial diagnosis in type 2 diabetics. Patients should have subsequent annual dilated
fundus examinations and a prompt referral to a retinal specialist with the presence of
macular edema, severe nonproliferative diabetic retinopathy, or proliferative diabetic
retinopathy.
The final metabolic pathway that causes diabetic retinopathy is unknown. There are
several theories including aldose reductase mediated damage, vasoproliferative factors,
and abnormalities of platelet and blood viscosity function. The earliest histologic effects
of diabetes mellitus are the loss of retinal vascular pericytes (supporting cells of retinal
endothelial cells), thickening of the vascular endothelium basement membrane, and
alterations of blood flow. With increasing loss of pericytes, the retinal vessel wall
develops microaneurysms and become fragile [3]. The earliest stage of diabetic
retinopathy is nonproliferative (NPDR). In some patients, there is progression to
proliferative retinopathy (PDR). Microaneurysms are the first ophthalmoscopically
detectable change in diabetic retinopathy, seen as small red dots in the middle retinal
layers. Macular edema, or retinal thickening, is an important manifestation of NPDR and
represents the leading cause of legal blindness in diabetics. The intercellular fluid comes
from leaking microaneurysms or from diffuse capillary incompetence. The edema causes
scattering of light by the multiple interfaces it creates in the retina by separated retinal
cells. The pockets of fluid in the outer plexiform layer, if large enough, can be seen as
cystoid macular edema. Usually cystoid macular edema is seen in eyes that have other
signs of severe NPDR such as numerous hemorrhages or exudates. In advanced NPDR,
signs of increasing inner retinal hypoxia appear, including multiple retinal hemorrhages,
cotton-wool spots, venous beading and loops, intraretinal microvascular abnormalities
(IRMA), and large areas of capillary nonperfusion depicted on fluorescein angiography.
The ETDRS found that IRMA, multiple retinal hemorrhages, venous beading and loops,
widespread capillary nonperfusion, and widespread leakage on fluorescein angiography
were all significant risk factors for the development of proliferative retinopathy.
Interestingly, cotton-wool spots were not [2].
Proliferative diabetic retinopathy (PDR) is a very advanced stage of the disease. These
new vessels usually arise from the retinal veins and often begin as a collection of fine
vessels. Once the stimulus for growth of new vessels is present, subsequent new vessel
growth is along the path of least resistance and seems to grow more easily on a performed
connective tissue framework. Thus, the true internal limiting membrane on the disc and a
shallowly detached posterior face are frequent sites of new vessels. As PDR progresses,
the fibrous component becomes more prominent and is found in association with vessels
that extend into the vitreous cavity. Neovascular vessels do not “grow” forward into the
vitreous cavity but are pulled into it by the contracting vitreous to which they adhere. It
has been long assumed that sudden vitreous contractions tear the fragile new vessels,
causing vitreous hemorrhage. However, the majority of diabetic vitreous hemorrhages
occur during sleep, possibly because of an increase in blood pressure secondary to early
morning hypoglycemia or to rapid eye movement during sleep [2]. The extravasation of
blood fills the space limited anteriorly by the posterior lens capsule, posteriorly by the
internal limiting membrane, and laterally by the ciliary body and lens zonular fibers. In a
vitrectomized eye, blood can remain in a liquefied state and often requires the use of high
gain settings in dynamic B-scan ultrasound to visualize and diagnose the hemorrhage [4].
A pars plana vitrectomy is known to be effective in preserving and restoring visual
function in patients with proliferative diabetic retinopathy [5]. The Diabetic Retinopathy
Vitrectomy Study (DRVS) provided sufficient data to support early vitrectomy in eyes
known or suspected to have very severe proliferative diabetic retinopathy as a means of
increasing the chance of restoring or maintaining good vision [7]. The unique
presentation of the appearance of our patient’s vitreous hemorrhage in this case was due
to his history of a pars plana vitrectomy procedure in the left eye. The dispersed nature of
the hemorrhage was likely secondary to the infusion solution (balanced saline solution)
that replaced the vitreous during surgery. When blood from the hemorrhage mixed with
the saline solution, it created an opaque solution that presented as a bright orange haze
during biomicroscopy. Because of the opaque appearance it was necessary to refer this
patient to the ophthalmology clinic in order to obtain a B-scan ultrasound. This should
always be done in order to rule out a retinal detachment.
In the literature there are case reports of a procedure in which a YAG laser capsulotomy
outside of the optic of the IOL was used to treat remaining vitreous cavity hemorrhage.
The purpose of the procedure was to provide a safe noninvasive method to clear the
hemorrhage without returning to the operating room. The procedure is to use the laser to
create an opening in the peripheral lens capsule and zonule to allow fluid and red blood
cells to pass easily from the vitreous cavity into the anterior chamber. The results
appeared to show that this was a safe and effective management procedure in treating
postvitrectomy hemorrhage in diabetic patients who had previously undergone cataract
surgery with posterior chamber lens implant. The vitreous hemorrhage cleared
completely in all five cases [11]. Several papers have been published evaluating the
safety and efficacy of anti-VEGF pre-treatments for a pars plana vitrectomy in order to
reduce the incidence of postoperative vitreous hemorrhage. The conclusion of these
studies determined that pre-treatment was not associated with any observed
complications, but also did not influence the rates of postoperative vitreous hemorrhage
or final visual acuity [12].
Treatment and Management:
The B-scan ultrasound showed a flattened attached retina 360 degrees and no intraocular
masses in the left eye. The patient was instructed to sleep with his head raised above a 45
degree incline for the next 3-4 weeks. Many times hemorrhages will resolve through
hemolysis and phagocytosis. The patient was told to continue his glaucoma medications
at this time. At his return visit 4 weeks later, the vitreous hemorrhage still showed no
signs of clearing. He was scheduled to return in 2 weeks for surgical retinal rounds to
evaluate and possibly schedule a second vitrectomy for removal. (As of this case report,
the patient had not yet had that follow-up appointment.)
Conclusion:
This patient was diagnosed with a vitreous hemorrhage that was found to be dispersed in
the infusion solution from a previous pars plana vitrectomy. Eye care professionals
should be aware that this condition can present with a unique color and consistency in a
post-vitrectomized eye. A B-scan ultrasound should be performed to rule out a retinal
detachment. Treatment options first include monitoring and sleeping with the head
elevated. After a timely follow-up, if the hemorrhage has not adequately resolved,
surgical intervention should be considered.
References:
1. Tumosa N. Eye Disease and the Older Diabetic. Clinics In Geriatric Medicine
2008; 24: 515-527
2. Yanoff & Duker: Ophthalmology, 3rd ed. 2008. Mosby, An Imprint of Elsevier.
Online edition
3. Kronenberg: Williams Textbook of Endocrinology, 11th ed. 2008. Saunders, An
Imprint of Elsevier. Online edition.
4. Sharma S, Ventura AC, Waheed N. Vitreoretinal Disorders. Ultrasound
Clinician. 2008; 3: 217-228
5. Okamoto F, Okamoto Y, Fukuda S, Hiraoka T, Oshika T. Vision-Related Quality
of Life and Visual Functon Following Vitrectomy for Proliferative Diabetic
Retinopathy. American Journal of Ophthalmology 2008; June: 1031-1036
6. Singh RP, Lewis H. Innovations in Eye Surgery. Clinics In Geriatric Medicine
2006; 22: 659-675
7. http://www.nei.nih.gov/neitrials/viewstudyweb.aspx?id=56
8. Novak M, Rice TA, Michels RG, Auer C. Vitreous hemorrhage after vitrectomy
for diabetic retinopathy. Ophthalmology 1984; 91: 1485-1489
9. Benjamin Borish’s Clinical Refaction. 1988. Pg 177
10. The Wills Eye Manual. 5th edition. 2008. Lippincott Williams and Wilkins
11. Landers MB, Perraki AD. Management of Post-Vitrectomy Persistent Vitreous
Hemorrhage in Pseudophakic Eyes. American Journal of Ophthalmology 2003;
December: 989-994
12. Lo WR, Stephen KJ. Visual Outcomes and Incidence of Recurrent Vitreous
Hemorrhage After Vitrectomy in Diabetic Eyes Pretreated with Bevacizumab
(Avastin). The Journal of Retinal and Vitreous Diseases 2009; Volume 29
Number 7: 926-932