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The presence of blood or blood debris in the anterior chamber can increase
intraocular pressure (IOP). Vitreous hemorrhage can also lead to secondary
glaucoma, producing a "ghost cell glaucoma" (GCG).1,2
Ghost cells (GCs) are degenerated spherical erythrocytes that partially lose
their hemoglobin content by aging for a long period in the vitreous. Changes
begin after a few days and are usually completed within 3 weeks. Hemoglobin
abandons the red blood cell and forms clumps that adhere to vitreous bands.
Hemoglobin that remains in the red blood cell becomes denatured and binds
to the internal surface of the cell membrane, forming granules (Heinz bodies).3 Once formed, GCs may remain intact for months,
moving freely within the vitreous. Neither fresh erythrocytes nor GCs are
able to pass through an intact anterior hyaloid membrane; thus, a hyaloid
injury must be present for these cells to be found in the anterior segment.2,3 Since GCs are rigid, they have
difficulty passing through the trabecular meshwork. They tend to accumulate
in its middle and external portions, whereas fresh erythrocytes pass 3 times
more easily to the external portion and from there to the Schlemm canal.1,3
Increased IOP usually occurs about 2 to 4 weeks after the injury, but
it may also take from 1 week to many months to develop.2,3
It is a complication that often requires surgical intervention with profuse
and repeated lavage of the anterior chamber or vitrectomy to remove the hemorrhagic
We describe a patient who developed vitreous hemorrhage and GCG after
a snake bite. There was no evidence of anatomic alteration of the anterior
Report of a Case
A 44-year-old male farmer was seen in the emergency department of our
institution (Hospital San Juan de Dios, National University of Colombia, Bogotá)
72 hours after sustaining a snake bite (Bothrops athrox) in his right foot. The patient was admitted to the hospital and treated
for respiratory distress syndrome and hemorrhagic syndrome with renal and
cerebral involvement. Two days later, after recovery from respiratory distress
and renal failure, he complained of bilateral visual loss.
On examination, his visual acuity was hand motions in the right eye
and light perception in the left eye. The left eye showed inferior and temporal
subconjunctival hemorrhage (Figure 1),
stromal and epithelial corneal edema, ++++ cells and flare in the anterior
chamber, and dense anterior vitreous hemorrhage (Figure 2). The IOP was 17 mm Hg OD and 40 mm Hg OS. Dilated indirect
ophthalmoscopy showed a dense vitreous hemorrhage in both eyes. Results of
B-scan ultrasonography confirmed bilateral vitreous hemorrhage with incomplete
posterior vitreous detachment.
Left inferior subconjunctival
hemorrhage as part of hemorrhagic syndrome.
Left slitlamp photograph showing
corneal edema and elevated number of ghost cells in anterior chamber.
With an initial diagnosis of GCG in the left eye, a paracentesis and
aqueous sampling were performed in the left eye. Cytologic examination of
the aqueous humor disclosed the presence of GCs. Meanwhile, the IOP in the
right eye rose to 28 mm Hg, and treatment was begun with 0.4% apraclonidine
hydrochloride twice daily, 0.4% timolol maleate twice daily, and a prostaglandin
derivative 3 times daily in both eyes. A diagnostic paracentesis in the right
eye confirmed the presence of GCs.
Results of B-scan ultrasonography performed 2 weeks later showed little
or no resolution of the vitreous hemorrhage. Both eyes were treated with standard
3-port posterior vitrectomy. Cytologic examination of the vitreous showed
the presence of GCs (Figure 3).
Bilateral indirect ophthalmoscopy showed optic nerve pallor with a cup-disc
ratio of 0.2 and attenuated retinal vascular tree and fovea reflex loss. The
IOP normalized in the right eye and visual acuity improved to 20/70. The IOP
normalized in the left eye, but the visual acuity was counting fingers at
40 cm because of a rhegmatogenous retinal detachment with macular involvement.
Spherical erythrocytes with vacuoles
and partial loss of hemoglobin (ghost cells) in vitreous (Papanicolaou, original
Bilateral GCG secondary to snake poisoning has not yet been described
in the literature, based on our MEDLINE search of the medical literature since
the initial description of GCG in 1976 to the present.
Ghost cell glaucoma has been associated with diabetic vitreous hemorrhage
in a phakic eye without previous trauma or surgery as well as in other rare
cases.5,6 Snake venoms,
especially those from crotalids, as in the case of Bothrops, contain proteolytic enzymes capable of breaking tissue proteins,
thereby acting as hemorrhagic factors. Thrombinogenic and thrombinoid enzymes
with fibrinolytic action have also been detected. Viper's venom alters vascular
resistance and, often, vascular integrity. It produces changes in blood cells
and coagulation mechanisms as well as alterations in central nervous system,
cardiovascular, and pulmonary dynamics.7
Hyaluronidase is also present in all American viperous poisons studied to
date.8 Hyaluronidase, collagenase, and other
proteolytic enzymes present in the Bothrops venom
may decrease the vitreous viscosity and alter the anterior hyaloid permeability.
This physiologic disruption may allow migration of the GCs in the aqueous,
causing the secondary glaucoma affecting both eyes.
Ghost cells were identified by cytologic examination of vitreous and
aqueous humor, centrifuged and stained with Papanicolaou stain9
(Figure 1). Sometimes, the vitreous
has "hemolytic cells" that are actually macrophages with hemosiderin and erythrocyte
Ophthalmologists should be aware that snake bite can cause visual loss.
Early diagnosis and prompt treatment to reduce the number of blood cells and
GCs may increase the potential for recovery.
Corresponding author: Ledy Rojas, MD, Departamento de Oftalmología,
Hospital San Juan de Dios, Carrera 10 Calle 1, Bogotá, Colombia (e-mail: email@example.com).
Rojas L, Ortiz G, Gutiérrez M, Corredor S. Ghost Cell Glaucoma Related to Snake Poisoning. Arch Ophthalmol. 2001;119(8):1212–1213. doi:
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