Dengue is a mosquito-borne viral disease
transmitted by Aedes aegypti. It is caused by one of four dengue virus
serotypes (DENV-1 to DENV-4) from the Flavivirus family.
Ophthalmic complications range from
subconjunctival hemorrhage and anterior uveitis to severe optic neuritis,
retinal vasculitis, maculopathy, and panophthalmitis. Other diverse ocular
effects include central retinal artery occlusion, bilateral vitreous hemorrhage,
and uncommonly acute angle-closure glaucoma (AACG).
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From: Pierre Filho Pde T |
Dengue can directly inflame ocular
anatomical tissues. The ocular structures have a particularly poor tolerance
for inflammatory insult and disruption of vessel regulation due to their rich
choroid and ciliary body vasculature. These structures are involved in vascular
leakage, which causes forward displacement of the lens-iris diaphragm and
narrowing of the anterior chamber angle, potentially leading to AACG.
Edema in the ciliary body exacerbates the
mechanical crowding of the angle structures, increasing outflow resistance
through the trabecular meshwork.
AACG can also be precipitated by certain
drugs used to treat dengue complications, or by medications that patients may
have been taking before hospitalization. For example, sulfonamide-based
antibiotics and anti-epileptics, such as topiramate, have been associated with
drug-induced AACG due to ciliochoroidal effusion and angle closure. Severe
dengue may cause systemic capillary leak syndrome, which acts synergistically
with these pharmacologic triggers to worsen anterior segment crowding and
precipitate glaucoma. In addition, systemic hypovolemia and electrolyte
imbalances may exacerbate vascular instability in ocular tissues, leading to
fluid extravasation and segmental edema.
Dengue may have an associated
autoimmune-mediated inflammation in the anterior segment. Such immune responses
would further augment ciliary body edema, interfere with aqueous production and
outflow, and have detrimental effects on IOP regulation. In addition, genetic
predispositions associated with human leukocyte antigen (HLA) alleles could
participate in the autoimmune eye inflammation induced by the dengue virus and
need to be further studied.
Hypothesized Sequence of Events:
Dengue virus infection generates a systemic
inflammatory response mediated by cytokines. This, in turn, leads to vascular
permeability and extravasation of fluid from the ciliary body, resulting in
ocular edema. The resulting anterior segment anatomical changes lead to
narrowing or closure of the anterior chamber angle, ultimately leading to AACG.
Additionally, the dengue pathophysiology, medications, individual anatomical
predispositions, and possibly autoimmune pathways provide a multifactorial
basis for AACG development in dengue-affected individuals.
REFERENCE:
Al-Essa A (April 11, 2025) Acute
Angle-Closure Glaucoma as an Ocular Complication of Dengue Fever: A
Comprehensive Review. Cureus 17(4): e82119. doi:10.7759/cureus.82119.
Pierre Filho Pde T, Carvalho Filho JP, Pierre ET. Bilateral acute angle closure glaucoma in a patient with dengue fever: case report. Arq Bras Oftalmol. 2008 Mar-Apr;71(2):265-8. doi: 10.1590/s0004-27492008000200025. PMID: 18516431.
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