Case 09 - Retina and vascular pathology

Unresponsive Patient with Bilateral Fundus Changes

25-year-old man - Brought to ER unresponsive - Stable vitals - Bilateral florid NVD

Illustrated eye for pathology case review

Case 09Proliferative Diabetic Retinopathy

Clinical Presentation

A 25-year-old man is brought into the emergency center. He is unresponsive to verbal stimuli, but his vital signs are stable. The photograph illustrates fundus appearance, similar in both eyes.

Learner Questions

Describe the ophthalmoscopic findings.
How would the ocular findings affect your diagnosis and management of this unconscious patient?
Explain how visual loss occurs in PDR.
What modes of treatment are employed for this ocular condition?

Answer Framework

Findings

Neovascularization of the disc (NVD) - frond-like new vessels at/near optic disc. NVE (neovascularization elsewhere). Pre-retinal/subhyaloid hemorrhage. Fibrovascular proliferation. Dot-blot hemorrhages. Dilated tortuous veins. = High-risk PDR (DRS criteria: NVD + vitreous hemorrhage, or NVD >=1/4-1/3 disc area).

Visual loss mechanisms

1. Vitreous hemorrhage - fragile NV rupture -> sudden painless VL (floaters, blackout). 2. Tractional RD - fibrovascular contraction pulls retina from RPE -> macula detachment -> central VL. 3. DME - VEGF-driven macular edema (most common cause overall). 4. Neovascular glaucoma - rubeosis iridis -> angle closure -> high IOP -> optic neuropathy.

Unconscious patient

Bilateral florid PDR in a 25-year-old = long-standing T1DM -> likely hypoglycemic coma or DKA. STAT fingerstick glucose -> D50 if hypoglycemic; IV fluids + insulin if DKA. BMP, ABG, HbA1c, urine ketones, ECG (hyperkalemia in DKA). Thiamine before glucose if alcohol suspected.

Treatment

PRP (panretinal photocoagulation): gold standard; ablates ischemic retina -> down VEGF -> NV regression (DRS trial). Anti-VEGF (bevacizumab/ranibizumab/aflibercept): PROTOCOL S = non-inferior to PRP with less DME/field loss (requires compliance). Vitrectomy: for non- clearing VH >1-3 months or TRD threatening macula.

Teaching Pearl

PDR in a 25-year-old = long-standing T1DM. 'Triple threat': vitreous hemorrhage, tractional RD, neovascular glaucoma. PROTOCOL S (DRCR.net): anti-VEGF ≈ PRP for PDR over 2 years but requires monthly injections and patient compliance. HbA1c reduction of 1% = ~35% down in microvascular complications (UKPDS).

Original answer transcript

Findings Visual loss mechanisms
Neovascularization of the disc (NVD) - frond-like new vessels at/near optic disc. NVE 1. Vitreous hemorrhage - fragile NV rupture -> sudden painless VL (floaters, blackout). 2.
(neovascularization elsewhere). Pre-retinal/subhyaloid hemorrhage. Fibrovascular Tractional RD - fibrovascular contraction pulls retina from RPE -> macula detachment ->
proliferation. Dot-blot hemorrhages. Dilated tortuous veins. = High-risk PDR (DRS criteria: central VL. 3. DME - VEGF-driven macular edema (most common cause overall). 4.
NVD + vitreous hemorrhage, or NVD >=1/4-1/3 disc area). Neovascular glaucoma - rubeosis iridis -> angle closure -> high IOP -> optic neuropathy.
Unconscious patient Treatment
Bilateral florid PDR in a 25-year-old = long-standing T1DM -> likely hypoglycemic coma or PRP (panretinal photocoagulation): gold standard; ablates ischemic retina -> down VEGF -> NV
DKA. STAT fingerstick glucose -> D50 if hypoglycemic; IV fluids + insulin if DKA. BMP, ABG, regression (DRS trial). Anti-VEGF (bevacizumab/ranibizumab/aflibercept): PROTOCOL S =
HbA1c, urine ketones, ECG (hyperkalemia in DKA). Thiamine before glucose if alcohol non-inferior to PRP with less DME/field loss (requires compliance). Vitrectomy: for non-
suspected. clearing VH >1-3 months or TRD threatening macula.
TEACHING PEARL
PDR in a 25-year-old = long-standing T1DM. 'Triple threat': vitreous hemorrhage, tractional RD, neovascular glaucoma. PROTOCOL S (DRCR.net): anti-VEGF ≈ PRP for PDR
over 2 years but requires monthly injections and patient compliance. HbA1c reduction of 1% = ~35% down in microvascular complications (UKPDS).