This patient was about to have juxtafoveal laser photocoagulation for a chronic detachment. A retrobulbar anesthetic was used and the needle penetrated the posterior segment. The yellowish material represents the anesthetic agent
(left) . There is also hemorrhage from the penetration. One day later, the anesthetic resolved and the retina flattened out (right).
This patient experienced a penetrating injury from a retrobulbar needle. There is exudate at the fovea
(arrows), which was the terminal point of the penetration.
A myopic patient who experienced a needle perforation through the macular region. The track of the needle is clearly visible clinically and angiographically.
Courtesy of David Boyer, MD
This cataract surgery patient received retrobulbar anesthesia and sustained a double perforating injury. Subsequent vitrectomy surgery for vitreous hemorrhage revealed two perforating sites. There was an entrance site inferotemporally near the equator
(arrow) , and a second needle exit site superior to the optic disc (arrow) . Fortunately, there was no evidence of retinal detachment. Following vitrectomy surgery, the patient recovered vision to 20/30.
This patient was given a nasopharyngeal injection of a corticosteroid suspension. There was obstruction of retinal arterioles
(left), along with whitening of the retina and a plaque of the suspension in a retinal vessel (arrow) . The drug can be seen in the choroidal circulation as well (multiple yellowish particles in the image on the right).
This patient was injected in the nasopharyngeal area for chronic sinusitis. A corticosteroid suspension obstructed arteriolar and choriocapillaris vessels. Note the whitening of the retina on the color photograph and the multifocal areas of absent perfusion on the fluorescein angiogram.
Courtesy of Dr. Kurt Gitter
This patient developed epistaxis and received a nasal packing that contained corticosteroids. The patient lost vision and was noted to have corticosteroid particulate matter in the retinal arterioles, along with a central retinal artery occlusion. There was minimal visual recovery.
Courtesy of Scott R. Sneed, MD
Intravitreal Triamcinolone Injection
This patient was injected with triamcinolone. This formulation precipitated within the vitreous as irregular lesions
(arrowheads) . The vitreous is otherwise cloudy from endophthalmitis.
Intravitreal Vancomycin Injection
This patient had been administered a triamcinolone suspension for chronic edema and a branch vein occlusion. Note the suspension of the particulate matter in the vitreous. There appears to be a vasotrophic orientation of the drug as it adheres to larger retinal vessels
This patient was suspected of having endophthalmitis, and vancomycin was injected into the vitreous. This suspension formulation left multiple variably sized particulates in the vitreous. This finding is in distinct contrast to the reported cases of immune-mediated vascular abnormalities reported with the utilization of intracameral vancomycin (see “Intracameral Vancomycin” below).
Courtesy of Dr. Jeffrey Shakin
Mechanical Retinal Vascular Obstruction (from Injections)
Mechanical retinal vascular obstruction may occur in the course of ocular surgery from an injection into the optic nerve sheath during anesthesia. Complications range from a retrobulbar hemorrhage with elevation of the intraocular pressure and/or a sudden rise in the intraocular pressure during the course of a closed vitrectomy operation, with resultant central artery occlusion.
Optic Nerve Sheath Injection
This patient had a combined artery and venous obstruction from an intrasheath injection of the nerve, as captured on a CT scan
(arrow) . As the pressure in the optic nerve sheath rises, it cuts the venular outflow and eventually the arteriolar inflow will be cut off, resulting in combined whitening of the retina and intraretinal and pre-retinal hemorrhages. In the photo on the right, there is axoplasmic debris within the retina, indicative of retinal ischemia.
Left and middle images courtesy of Dr. Gary Brown
This patient had an inadvertent optic nerve sheath injection that resulted in peripapillary retinal ischemia and pre-retinal hemorrhage or a Terson-like syndrome
(left) . Eventually the hemorrhage localized in the subhyaloidal area (middle) . Three months later, there was complete resolution of the serosanguineous exudative changes, but there was atrophy of the optic nerve (right) .
This patient underwent cataract surgery, and no problem was noted until the visit on postoperative day one. The patient sustained a central retinal artery occlusion along with a small amount of intraocular hemorrhage, as is seen in the accompanying color photograph. Visual acuity was bare light perception. MRI of the orbit did not show any definite abnormality (though was obtained two days following the cataract surgery). Vision recovered only to hand motions over the next two months, in spite of eventual reperfusion of the retinal arteries.
This patient developed a combined retinal artery and vein occlusion presumably from an intrasheath injection prior to cataract surgery. There are elements of Terson syndrome or pre-retinal hemorrhage contiguous with the nerve and extending into the vitreous. A slow rise in intraocular pressure induced the venous obstruction and bleeding, which resulted in arteriolar ischemia.
Retrobulbar hemorrhage may result in venous insufficiency, central vein occlusion
(top), or even a central retinal artery occlusion with a variable degree of venous insufficiency (bottom).
These two patients experienced combined venous and arteriolar occlusion from a retrobulbar hemorrhage. As the intraocular pressure rose there was development of venous occlusion and retinal hemorrhages. Continued elevation of the pressure produced arteriolar obstruction and ischemic whitening of the retina. Each patient ended up with optic atrophy from the antecedent ischemia.
This patient developed an ophthalmic artery occlusion following a retrobulbar injection with localized hemorrhage. Note the complete absence of filling of the choroidal as well as the retinal circulation. There was no visual recovery, and the patient gradually developed optic nerve atrophy, severe vascular attenuation, and diffuse retinal pigment mottling
(right image) .
Courtesy of David Boyer, MD
Choroidal Ischemia (Outer Retinal Infarction)
Some intraocular procedures may cause choroidal ischemia, which simulates retinal vascular occlusive disease. While rare, it is particularly known to occur in the course of a closed vitreoretinal procedure.
This patient has an accumulation of white subretinal axoplasmic debris from choroidal insufficiency or infarction. The peripapillary insufficiency resulted in a pale nerve
(middle image) . The fluorescein angiogram shows reperfusion, typical of a compressive event.
This patient experienced severe inner choroidal vascular insufficiency or outer retinal infarction during phacoemulsification. Notice the relative sparing of the optic nerve and the complete sparing of the perifoveal area, producing a “cherry-red-like” spot.
This patient experienced choroidal insufficiency at the time of vitrectomy surgery. The cherry-red spot is due to subretinal whitening, not retinal vascular ischemia. There is no optic nerve head edema.
In another patient with choroidal insufficiency, the fluorescein angiogram shows that there is adequate retinal vascular perfusion in this eye.
This patient experienced severe choroidal ischemia following a closed vitrectomy. There is outer retinal whitening with hemorrhages, but sparing of the retinal vasculature, optic nerve, and fovea. A “cherry-red-like” spot is seen at the fovea. After reperfusion of the choroid, there are atrophic and pigment epithelial changes, producing a “bull’s-eye” pattern. The acuity was not affected, but there was constriction of the peripheral field.
This is a patient who also experienced choroidal insufficiency during a vitrectomy procedure. After resolution of the acute manifestations, there was widespread pigment epithelial atrophy and hyperplasia. The retinal circulation was adequately perfused throughout the course of the complication, and there was sparing of the nerve and disc.
Courtesy of Dr. Sohan Singh Hayreh
Antibiotic Toxicity During Intraocular Surgery
Aminoglycoside toxicity is an uncommon though well-known clinical entity in intraocular surgery. When administered intravitreally, the toxic effect will depend up on the concentration and dose of the drug. Injection into the anterior chamber may also cause prominent uveitis with associated iris complications. Intraocular usage of gentamicin has become quite limited over the past 15 to 20 years. More recently, intracameral vancomycin has been shown to produce an apparent immune-mediated retinal vasculitis, with profound visual impairment. While this has only occurred in a very small number of patients, the precise etiology of this reaction is not entirely clear.
When the vitreous is intact, the effect is generally concentrated in a localized area of the posterior pole. The drug can diffusely spread throughout the posterior segment after a vitrectomy procedure. Following resolution of the acute toxic effect of the retina and the associated obliteration of the circulation, there is seldom any reperfusion.
Inadvertent injection of aminoglycosides into the vitreous may gravitate to the posterior pole, producing a necrotizing, obliterative vasculopathy, seen here in these two patients. Often there is a “cookie cutter” distribution of the toxicity producing an ovoid or circular whitening of the retina. There may also be retinal and pre-retinal hemorrhage from necrosis and infarction of retinal vessels. The toxicity specifically does not follow the geographic distribution of the retinal vasculature, though better corresponds to the gravitational effect of the intravitreal injection as the patient is supine during the surgical procedure.
This patient also has a “cookie cutter” necrotizing, ischemic retinopathy centrally. The concentration of the drug may have something to do with the posterior pre-retinal cortical pocket. One of the vessels along the course of the superior temporal vasculature has segmental staining from inflammation, but no obstruction
This patient has a necrotizing obliterative vasculopathy centrally, which appears as non-perfusion on the fluorescein angiogram. There are also scattered hemorrhages along the arcades, which produce hypofluorescence.
This patient experienced severe aminoglycoside toxicity with diffuse whitening of the retina from infarction
(left). Only a few central retinal vessels are perfusing, and they are leaking extensively from inflammation.
This patient had severe aminoglycoside toxicity (gentamicin) with diffuse whitening of the retina, scattered hemorrhages, and disc edema. There is some sparing of the superior paramacular region
(arrows), which received a lower dose of the drug. The fluorescein shows marked hypofluorescence from blockage of the choroid and ischemic necrosis of the retinal vasculature.
This patient had aminoglycoside toxicity (gentamicin) during a vitrectomy operation. The toxic drug spread toward the peripheral retina due to the removal of the vitreous. There is infarction of the retina and inflammation of the retinal vasculature. There is also pruning of one of the vessels
(arrow), presumably from white blood cell aggregation. The fluorescein angiogram (right) was carried out after the acute toxic effect resolved. Note that there is limited reperfusion unlike a typical arteriolar infarction.
This patient also had aminoglycoside (apramycin) toxicity during cataract surgery. The dark area on the fluorescein angiogram corresponds to necrotizing vascular obliteration and the segmental staining of the arteriolar and venular retinal vessels corresponds to inflammation in the walls of those vessels due to the toxicity.
This fluorescein angiogram shows the segmental dilation and staining from aminoglycoside toxicity. It is surrounded by a capillary closure, which appears as hypofluorescence. This vessel was not completely obliterated by the drug, but its wall was compromised to produce a permeability defect or leakage.
Courtesy of Dr. Antonio Ciardella
In these three patients with severe aminoglycoside toxicity, the lower half of the retina is more involved. Whitening of the retina and hemorrhage can be seen. There is a detachment
(arrows) from the necrotizing obliterative retinopathy in the upper image. The fluorescein angiogram shows the absence of perfusion in the necrotic retina and staining vessels.
Fundus photograph of both eyes demonstrating a severe bilateral hemorrhagic occlusive retinal vasculitis following cataract surgery with utilization of prophylactic intracameral vancomycin. The cataract surgeries were spaced one week apart. Unfortunately, this immune-mediated event may take a week or so to manifest its features. The fluorescein angiogram exhibits extensive non-perfusion. Visual recovery was very limited.
Courtesy of Stephen Russell, MD
Decompression retinopathy results from a sudden drop in intraocular pressure. It is usually a complication of glaucoma surgery such as trabeculectomy, which is performed under either local or general anesthesia. Hemorrhages, both deep and superficial, may be seen in the posterior segment or diffusely throughout the fundus. There is no venous tortuosity or increased transit time, distinguishing this hemorrhagic event from venous occlusive disease.
These patients experienced hemorrhage in the posterior segment of the eye and into the vitreous from decompression. The hemorrhages on the venous side of the circulation are presumably caused by a sudden drop in pressure and a compensating surge of blood perfusion into the venous bed. The hemorrhages do not coincide with the geographic distribution of veins.
Only gold members can continue reading.
Premium Wordpress Themes by UFO Themes
WordPress theme by UFO themes