IGNACIO, Richelle Angelika E. Dr.

Genevieve Pantig
May 26, 2020 OPHTHALMOLOGY

6TH BLOCK PAPER CASE DISCUSSION

1. What do you see in the slit lamp examination?

Fig. 1 OD Fig 2. OS

In both figures, lids and lashes were normal with quiet conjunctiva and clear corneas. Anterior
chambers were deep and quiet. The irides are normal and well-dilated with no signs of rubeosis iridis.

In figure 1, direct illumination shows a white opacity in the central part of the pupil. Retro illumination
shows a transparent granular appearance of the opacified lens with white deposits in the retina. In figure 2,
direct illumination shows a ring of white opacity at the center; but less opaque compared to OD. Retro
illumination shows an opacity in the posterior aspect with less granular appearance. Neither lens had any
nuclear sclerosis.

2. Describe the fundus findings.

Beading
Beading

Fig. 3 OD Fig.4 OS

Figures 3 and 4 show microaneurysms, which are usually the earliest clinical sign of diabetic
retinopathy. Once these vessels rupture, they produce dot & blot hemorrhages also seen in these figures.
Due to the breakdown of blood-retina barrier and leakage of fluid and proteins from the vessels, macular
edema occurs and hard exudates may be seen. As also seen in both figures is venous beading which occurs
as a sign of progression to proliferative diabetic retinopathy. In figure 4, prominent neovascularization is seen
above the disc, reaching up to the area of macula where hard exudates are deposited. This is indicative of
proliferative diabetic retinopathy.

3. What dilating drops would you use to perform a dilated fundus examination on our patient?
Considering that the patient has uncontrolled hypertension, mydriatics from the class of
sympathomimetics are not recommended due to its other effects (i.e. tachycardia, hyperthermia, palpitations)
Hence, mydriatics from the class of parasympatholytics are preferred. Among the parasympatholytic
mydriatics, Tropicamide is the shortest-acting and most useful. However, given that our patient has
uncontrolled diabetes, his pupils dilate poorly to standard anticholinergic eyedrops, hence, a stronger
mydriatic such as Cyclopentolate or Atropine may be used. However, it should be taken into consideration
if the patient has a companion or if the patient drives before prescribing stronger mydriatics. Another
alternative would be adding Phenylephrine to Tropicamide in order to take advantage of the sensitivity of a
diabetic pupil to sympathomimetics and at the same time the rapid action of Tropicamide, minimizing
accommodative loss.1

4. What precautions would you consider when using dilating drops?

Prior to administering dilating drops, complete history should be done in order to determine which
mydriatic best suits the patient. Due to the increased size of the pupil and the excess amount of light entering
the eye, vision may be blurry and sensitive to light. Hence, patients are not advised to drive or use any
machinery or prolong stay in an area of bright light. Patient is advised to be accompanied by a guardian, to
wear sunglasses that have UV protection, and call the doctor if his eyes stay dilated longer than what was
advised. Moreover, as previously stated, mydriatics that fall under sympathomimetics should be used
carefully as these have effects that may be detrimental to a hypertensive patient like in the case. Acute angle
closure glaucoma and allergic reactions may also arise from the use of mydriatics, hence, patient should be
closely monitored.

5. What is your working impression?

Cataract, both eyes; probably posterior subscapular
Proliferative diabetic retinopathy, both eyes; to consider hypertensive retinopathy

Cataracts are lens opacities that cause visual impairments like blurring, distortion, or blindness. It
occurs frequently in aging, but may also be due to other factors such as poor nutrition, metabolic insults,
excessive exposure to sunlight or other sources of radiation, trauma, and certain medications. Aside from his
ocular findings which points to this diagnosis, risk factors like his age, smoking history, sunlight exposure due
to his occupation, and most especially his uncontrolled diabetes, make this diagnosis likely. Basing from the
slit lamp exam, the lens opacities are coming from the back of the lens, hence, these are most probably
posterior subcapsular cataracts (PSCs).

Another diagnosis seen in the patient is diabetic retinopathy (DR) as seen in the fundus examination.
Given the presence of neovascularization, the proliferative type is highly likely in this case, which is the
advanced stage of retinopathy. However, hypertensive retinopathy also exhibit the same manifestations,
especially the fundus exam shows AV crossing defects, which are more characteristic of hypertensive
retinopathy. Given that the patient shows history of both uncontrolled diabetes and hypertension, the latter
cannot totally be ruled out.

6. What systemic disease is most likely responsible for the fundus findings of our patient?
In the patient’s case, his uncontrolled diabetes is responsible for both PSC and PDR. It is the long-
standing hyperglycemia that initiates tissue damage to the retina leading to detrimental changes that affect
cellular metabolism, retinal circulation and capillary competency. However, it should not be ignored that
chronic hypertension may also damage the retina as well. Increase in blood pressure is transferred directly
to the retinal vessels which initially constricts. But further increases in blood pressure overcomes this
compensatory tone and damage to the muscle and endothelium ensues. 3

7. What is the mechanism of visual impairment in this condition for our patient?
There are several mechanisms by which cataracts form in a diabetic patient. One of which is through
the polyol pathway wherein the enzyme aldose reductase catalyzes the reduction of glucose to sorbitol. The
intracellular accumulation of sorbitol leads to osmotic changes resulting in hydropic lens fibers that
degenerate and form “sugar cataracts”. Furthermore, the sorbitol buildup causes osmotic stress in the lens,
which induces lens epithelial cells leading to cataract development. Aside from these, increased glucose
levels in the aqueous humor induces glycation of lens proteins, which results in generation of superoxide
radicals and formation of advanced glycation end-products. In addition to the increased free radicals, diabetic
lenses also have an impaired antioxidant capacity, which increases their susceptibility to oxidative stress. 4
Aside from his diabetes, aging can contribute largely in cataract formation, given that the patient is elderly.
As the patient ages, the lenses become less flexible, less transparent, and thicker. This, in addition to
metabolic insults, causes tissues within the lens to break down and clump together forming white opacities
that cloud small areas within the lens. As it develops, it becomes denser until it involves a bigger area and
blocks the light that passes through the lens, preventing a sharp image to reach the retina, resulting to blurred
vision.5

Like in cataracts, diabetic retinopathy, by several mechanisms (polyol pathway, AGE products), is a
result of uncontrolled blood sugar level which leads to several changes in the retina, mainly, abnormal vessel
permeability and occlusion with ischemia and subsequent neovascularization. Structural changes that take
place such as loss of retinal pericytes, thickening of capillary basement membrane, and outpouchings of
capillary walls (microaneurysms) lead to closure of retinal capillaries causing retinal ischemia and disruption
of blood retinal barrier. Once blood vessels have been damaged, fluid leaks into the macula causing it to
swell (macular edema), resulting in blurred vision. Subsequently, neovascularization occurs to compensate
for the impaired blood circulation in the retina by promotion of growth factors in response to hypoxia. The
newly formed, fragile, abnormal blood vessels can leak blood posterior to the eye and block the vision.

8. What ophthalmic treatment options are available for our patient’s case?
Prior to treatment, further diagnostic tests should be done to confirm the impression. In the patient’s
case, it is useful to undergo fluorescein angiography as it is used to determine ischemia and retinal vascular
abnormalities. In this case, microaneurysms, neovascularizations, and intraretinal microvascular
abnormalities (IRMAs) may be seen as hyperfluorescences while ischemia may appear as
hypofluorescences. Optical coherence tomography may also be used because it allows visualization of each
retinal layer making retinal thickness measurements possible. Through this, macular edema may be
determined to be clinically significant or not, and subsequently, may be used to measure effectiveness of
therapy depending on the macular swelling.

Posterior subscapular cataract

Given that there are two conditions to be treated, initial ophthalmologic assessment must be done to
evaluate what proportion or aspect of visual impairment is accounted for by the cataract. The only treatment
for cataract is its extraction and subsequent replacement of the opacified lens, which is preferably done by
phaecoemulsification with IOL implant. Phaecoemulsification is done using ultrasound waves to break the
cataract into particles small enough that it can be aspirated. Once this is accomplished, replacement of the
cataract is done by placing an intraocular lens, which can either be put in the anterior or posterior chamber. 6
Prior to surgery, application of povidone-iodine should be done to lower risk of postoperative
endophthalmitis in intraocular surgery. Post-surgery, pain may be felt within the first 24 hours and patient
may be prescribed with acetaminophen. Patient will be seen one week and one month after surgery to monitor
complications and proper healing. Some complications that should be watched out for are endophthalmitis,
corneal edema, IOL lens malposition, retinal detachment, and the risk for macular degeneration.

Proliferative diabetic retinopathy

In the case of the patient where there is already macular edema with visual acuity impairment, a
combination of anti-VEGF agents for the macular edema and panretinal photocoagulation for the PDR should
be given as both have shown to be effective in preventing progression of PDR and its subsequent vision loss.
In treating this patient, it is important to administer first the anti-VEGF therapy because PRP may possibly
aggravate the macular edema. Anti-VEGF intravitreal injections work by stopping the abnormal blood vessels
leaking, growing, and bleeding under the retina. It arrests neovascularization and reduce chances for vision
loss. Possible adverse effects are transient increases in IOP and injection-related infectious endophthalmitis;
hence these should be watched out for. Panretinal photocoagulation, on the other hand, works by coagulating
the retinal pigment epithelium and the adjacent photoreceptors, thereby reducing oxygen consumption of
photoreceptors and return the balance of oxygen demand and supply. 7 Some of its adverse effects are pain
during treatment, transient increases in intraocular pressure, corneal abrasions, mydriasis due to damage of
nerves in the uveal tract, and macular edema among others. When the condition progresses with non-clearing
vitreous hemorrhage, vitrectomy should be considered.

9. What other parameters (non-ophthalmic) would you want monitored and managed in this patient
to reduce his ongoing risk of complications?
Considering that both the patient’s conditions stem from diabetes, controlling it and maintaining an
HbA1c level in the 6-7% range are the goals for this patient. Good glycemic control is the primary preventive
measure in managing DR. Good blood pressure control and lipid-lowering therapy should also be observed
as these slow down the progression of DR and cataract formation. 8 Since the patient discontinued his
medications, he should consult his physician in order to update the management plan for his comorbidities.
Compliance with follow-ups and medications should be emphasized. Lifestyle changes such as regular
exercise and a nutritious diet are also advised. Systemic checkup should also be warranted as diabetic
patients are predisposed to acquiring renal and cardiac diseases.

References:
1. Huber, M. J., Smith, S. A., & Smith, S. E. (1985). Mydriatic drugs for diabetic patients. British Journal of
Ophthalmology, 69(6), 425-427. https://doi.org/10.1136/bjo.69.6.425
2. Hypertensive retinopathy - StatPearls - NCBI bookshelf. (2020, January 8). National Center for Biotechnology
Information. https://www.ncbi.nlm.nih.gov/books/NBK525980/
3. Hypertensive retinopathy. (2019, January 4). https://eyewiki.aao.org/Hypertensive_retinopathy
4. Diabetic cataract—Pathogenesis, epidemiology and treatment. (2010, June 17). Publishing Open Access research
journals & papers | Hindawi. https://www.hindawi.com/journals/joph/2010/608751/
5. Cataracts - Symptoms and causes. (2018, June 23). Mayo Clinic. https://www.mayoclinic.org/diseases-
conditions/cataracts/symptoms-causes/syc-20353790
6. Cataract. (2018, June 16). https://eyewiki.aao.org/Cataract#Ophthalmic_Examination
7. Stefánsson, E. (2009). The mechanism of retinal Photocoagulation – How does the laser work? European
Ophthalmic Review, 02(01), 76. https://doi.org/10.17925/eor.2009.02.01.76
8. Fraser, Claire. et.al. 2019. “Diabetic Retinopathy: Prevention and Treatment.”
UpToDate. Available at:
www.uptodate.com/contents/diabetic-retinopathy-prevention-and-treatment .
https://emedicine.medscape.com/article/1225122-overview