What exactly is the role of the OD in managing retinal conditions? I’d bet if you ask 10 people, you’d get 10 different answers. Some answers will center on timely referral to retina with referral back to the OD upon completion of the treatment, where as other options at the other end of the spectrum are more hands on for the part of the OD.  

While OD’s are for the most part not performing retinal surgery, and the majority are not performing fluorescein angiography, many retinal diseases can be managed primarily by the OD, with ophthalmological involvement for surgery or injections only. It’s similar to situations that arise in clinic, where, for example, a patient presents with a calcific retinal emboli; they can be referred out for all management, or they can be directed by the OD to the appropriate care. In the latter case, it’s certainly feasible that the OD orders the neuroimaging and vascular imaging that is part and parcel of the work up of these patients, making the referral directly to the ED for the acute care, and then directly scheduling the referral for a carotid endarterectomy or stenting (if one is needed).

The management of retinal vein occlusions is generally the same, whether the vein occlusion is a central, hemispheric or branch vein occlusion. We play an incredibly valuable role in helping to determine what caused the VO to begin with, and also following up the patient after the onset of the VO.

Presented here is a rather dramatic case of a central retinal vein occlusion, and how this patient has been managed over many years, with the OD making the call on the frequency and need for anti-vegf injections, as well as the initial work up.

At the time of initial presentation in 2016, this Caucasian male was 56 years old and taking only Prilosec and the occasional allergy medication. He reported an intolerance to aspirin secondary to peptic ulcers, but had no allergies to medications. He presented urgently with complaints of decreased and worsening vision in the left eye of 5 days duration. Visual acuities at that time were 20/20 OD and 20/60 OS. He reported the vision in the left eye as ‘blotchy’.

His anterior segments bilaterally were completely normal. There was an equivocal APD on the left side. IOPs were 15mmHg OD and 16mmHg OS. His crystalline lenses were clear.

Through dilated pupils, the fundus image seen in Figure 1 below was the initial presentation of the left eye; that of the right was completely normal except for grade 2 arteriolarsclerotic retinopathy. Blood pressure was 132/86 RAS at the initial visit.

Figure 1: Initial presentation of the left eye.

As seen in Figure 1, there is a classic presentation of evolving CRVO, with venular dilation and tortuosity, NFL hemorrhages and deep blot and dot hemorrhages. Also present are numerous cotton wool spots indicative of retinal ischemia. An initial diagnosis of ischemic CRVO was made. Also, as seen in Figure two, there is some early macular edema that needs to be addressed by the retinologist, but ultimately, there is a more pressing issue that needs to be identified.

Figure 2: Initial macular OCT showing mild retinal edema that can also be seen fundoscopically on physical examination.

While the diagnosis is pretty clear just from the presenting fundus image, the question remains as to the cause of the VO in this particular eye. While there are many possible causes of VO, the majority are related to the same causative factors in the development of retinal arterial atherosclerosis, namely diabetes, hypertension, hypercholesterolemia, smoking and obesity. Of course there are coagulability issues that may be at play as well.

The initial work up of these patients should include lab studies related to the aforementioned conditions. This patient did have a PCP whom he saw yearly, so I ordered several studies from the PCP’s office, namely a CBC with differential, ESR, CRP, Sed Rate, anti-phospholipid antibodies, Factor 5 Leiden, and a complete lipid panel. I also asked him to see his PCP for possible BP fluctuations.

While I was waiting on the results of the lab studies, the patient did see the PCP who determined that the blood pressure was not an issue as his is historically low; perhaps it was borderline in my office related to the nature of his visit, namely decreased vision.

Importantly here, though is the presence of an ischemic retina, and the importance of facilitating adequate reperfusion of the retina.

The basic physiology of RVOs is decreased drainage from the eye through the venular system. Certain clotting conditions can play a role in this condition without structural vascular changes as the etiology, and they were being evaluated with aforementioned the blood work. But the other eye really held the key to this case: the arteriolarsclerosis. So how does arteriolar sclerosis of the arteries, cause a drainage problem of the veins? The answer is simple; hard walled arteries, especially those with structural signs of atherosclerosis, can partially compress a thin walled vein, creating a perfect storm for a clot to form. What’s the easiest way to cause a clot? Slow blood down and make it turbulent. Retinal veins already have slow rates of blood flow through them, which is under low pressure; all they need is an overlying artery to partially compress them, slow blood even further, and make what blood that is passing through the constriction turbulent. Perfect storm for a clot to form in the vein, restricting venous drainage even further!!

The following day (2.5 days after initial presentation), the blood work was sent my way, and other than slightly elevated total cholesterol and elevated LDL levels, the panel was normal including coagulability indices. The patient’s PCP began statin treatment to mitigate the risk associated with elevated lipids. But we still needed to do what we can to facilitate better venous drainage. Since the patient could not take aspirin and after discussing with the PCP the use of clopidogrel, which he suggested we not use (for the same reason as aspirin was contraindicated), I suggested a medication that has been around for many years, with an incredibly low side effect profile: persantine.  The PCP had not used that medication previously (yes, he was young), and he had no objections to trying it.  I felt as though this would be our best option to facilitate venous drainage, so I prescribed for him 25mg Persantine QD. Also, in the interim, he was scheduled to see the retinologist for reduction of the macular edema with an anti vegf agent.

I next saw the patient a few days later, now about 7 days after ictus, and there was marked improvement is the fundus picture related to the CRVO, as shown in Figure 3.

Figure 3: 7 days post ictus and after only 4 doses of dipyridamole. Note the improvement in the clinical picture as compared to Figure 1.

Shortly thereafter, the patient saw the retinologist and they received the first of 3 scheduled monthly injections of an anti vegf agent.  The administration of the anti vegf had a significant effect in reducing the macular edema, to the point where we were able to begin treat and delay administration after only 3 months. At this point in the case, we are only 3 months out from the initial presentation.

Over the next few years, with a great working relationship with this particular retinologist, I saw the patient frequently and made the referral back to the retinologist at extended time intervals depending on what the OCT demonstrated insofar as the macular edema was concerned. This is standard treat and delay methodology: treat (with an anti vegf agent), and gradually delay further treatments once a set pattern can be seen of no rebound of macular edema  These intervals moved slowly from 4 to 5 to 6 to 8 to 10 weeks, over several years. You and I can determine with the help of our OCTs whether or not the edema is returning; there is no need to bog down a busy retinal surgeon with work that we can do. Let’s enlist their help when they do something we do not do, like anti vegf injections!

Over the next several years, the patients macula typically looked like what we see in Figure 4, namely no macular edema, and an ERM and mild diffuse atrophy atrophy.  Acuity remained at the 20/30 mark for many years in this interim period.

Figure 4: Stable macular OCT without edema present for several years.

Now…..Spin the clock ahead…to current time, December 2023. The patient’s fundus image has remained stable since about 1 year after the ictus, as seen in Figure 5 below. Note the periventricular sheathing and mild venular dilation. That is not a hemorrhage at the temporal aspect of the disc, as this image is a multimodal laser image, not true fundus photograph. Gradually, the intervals between injections have increased to 17 weeks, all of which have been able to keep the patient stable, and he continues to take the daily dose of 25 mg dipyridamole without GI complication.

Figure 5: Fundus image December 2023

Though the fundus image looks stable, and the retinal evaluation was stable, the OCT at the December visit did show some early edema formation as seen in Figure 6. How much of a time interval since the last injection was this OCT?  Interestingly 19 weeks, just as scheduled.

Figure 6: Most recent OCT at 19 week treatment interval.

You would think that after 6 years, and treatment and delay extending to 17 weeks without an issue, extending to 19 weeks would probably be OK, and you’d be correct. But this is exactly why we check periodically.  The underlying problem, sluggish venous flow, still exists.  In fact, the sluggish drainage is just enough to cause backlog in the central retina if the antivegf is extended by two additional weeks. In other words, these are chronic conditions that require continuous observation. We can mitigate the visually significant effects from the VO, but it will always be an 800lb gorilla in this gentleman’s closet.

Also, it will always be our job to follow these patients closely. Of course, now he is developing cataracts that are increasing night glare, but his acuity in this eye is still relatively good at 20/40.

The initial work up of this patient, the interim monitoring, the prescribing of the dipyridamole, and involving the retinologist only when needed, allows for better care, and less redundant care. It happens this same way in many retina clinics that employ ODs. If it can happen there, it can happen in your office as well.

Take charge.  Retinal care is in our wheelhouse.