Ocular Complications in IV Drug Users
Ocular Complications in IV Drug Users
Two case reports illustrate the visually devastating risks associated with the use of injectable street drugs.
By Amanda S. Legge, O.D.
Review of Optometry, 11/19/2012
Intravenous drug use is directly associated with a variety of localized and systemic complications. In addition, it can yield numerous ophthalmological consequences. The most devastating ocular side effects of intravenous drug use include the formation of choroidal and retinal nodules, infarction and inflammation. Typically, such associated lesions form in the posterior pole near the macula.
Eliciting a thorough patient history is crucial for appropriate testing, culturing and treatment. Prompt diagnosis and management is of utmost importance to decrease both ocular and systemic morbidity.
The following case reports describe complicated infections and potential posterior segment damage secondary to intravenous drug abuse.
CASE 1
History
A 30-year-old white male presented to our office for the first time with a chief complaint of decreased visual acuity (O.S.>O.D.). His vision had decreased suddenly about two weeks earlier but had remained stable O.U. since. He denied the presence of floaters, photopsia, diplopia, pain or discomfort.
The patient’s medical history was remarkable for post-traumatic stress disorder, bipolar affective disorder, chronic cluster headaches and depression. He did not take any medications.
The patient’s ocular history was unremarkable because he reported never undergoing a formal eye exam. His family ocular and medical histories were unremarkable.
Prior to vision loss, the patient experienced low-grade fevers, severe cluster headaches and diffuse joint pain for one month. His primary care physician (PCP) performed an extensive lab work-up, which included complete blood count (CBC), partial thromboplastin time, international normalized ratio, lupus anticoagulant, amylase, lipase, fluorescent treponemal antibody (FTA), rheumatoid factor, antinuclear antibodies, rapid plasma reagin (RPR), urinalysis and HIV screening.
All test results returned within normal limits. The patient also had a negative CT scan of the head and chest without contrast. He had not seen his PCP since receiving these results.
Upon further questioning, the patient admitted to injecting crack cocaine dissolved in vinegar intravenously. He said that he had injected the drug approximately 10 to 15 times per week for the past five years. He stated that he was aware of the risks of his behavior, but had not sought any counseling or rehabilitation.
Diagnostic Data
The patient’s uncorrected visual acuity measured 20/40 O.D. and 10/300 O.S. with direct fixation. No improvement was observed upon pinhole testing. He achieved 20/200 O.S. with eccentric fixation. His pupils were equal, round and reactive to light, without evidence of afferent defect O.U. Extraocular motility testing showed no restrictions in muscle movement. Confrontation visual fields were full to finger counting O.U.
Intraocular pressure measured 11mm Hg O.D. and 12mm Hg O.S. Anterior segment examination was unremarkable. We detected no inflammatory cells or protein flare in the anterior chamber.
Gonioscopy revealed that the most posterior structure in all quadrants was the ciliary body face O.U.
No sign of microhyphema, microhypopyon, peripheral anterior synechiae or neovascularization was noted O.U. Posterior segment evaluation revealed multiple choroidal and retinal infarcts of varying duration (figure 1) as well as the presence of Roth’s spots throughout the posterior pole O.U. (figure 2).
Nerve fiber layer hemorrhages and exudates as well as retinal infiltrates were noted, indicating a septic chorioretinitis. The optic nerves appeared flat, pink and distinct, with no sign of disc edema O.U.
The left macula was affected dramatically by multiple infarcts and intraretinal edema, which correlated with the severe visual decrease in that eye.
The right eye exhibited subtle macular edema and exudates, accounting for the mild decrease in vision.
Following the examination, we ordered additional blood work, including another CBC with
platelet count and differential, troponin I, Westergren sedimentation rate, C-reactive protein (CRP) and a blood culture.
Diagnosis and Follow-Up
We tentatively diagnosed our patient with septic chorioretinitis, pending further testing. We educated the patient about the emergent nature of this condition and informed him that it likely was caused by bacterial endocarditis. We made an immediate referral to a local hospital, and indicated the need for a transesophageal echocardiogram (TEE) to confirm the diagnosis and begin prompt administration of intravenous antibiotics.
He did not report to the hospital as recommended. Upon investigation, a relative informed us that he had died from a gunshot wound to the head. Apparently, he was murdered the night of the referral. We later confirmed this report.
The lab results were received within 48 hours, revealing an elevated troponin I, sedimentation rate and CRP. The CBC remained within normal limits. The blood culture revealed growth of Staphylococcus aureus, which may have been methicillin resistant.
Although the TEE could not be obtained to confirm, we presumed the diagnosis to be bacterial endocarditis secondary to S. aureus infection, very likely due to street drug use.
CASE 2
History
A 42-year-old white female presented with a chief complaint of severe blurred vision in her right eye that had persisted for a week. Her vision decreased rapidly and painlessly over the course of two to four days and had remained stable since that time. She did not complain of pain, irritation, diplopia, photopsia or floaters. Additionally, she exhibited no associated systemic signs or symptoms.
The patient’s medical history was unremarkable, but she admitted that she had not seen a PCP in at least 10 years. Her ocular history was unremarkable; however, she reported wearing glasses since age 12. Her current prescription was at least four to five years old. The patient’s family ocular and medical histories were unremarkable.
Upon additional questioning, the patient admitted to intravenous heroin use since age 15. She reported that, during the past year, she had reduced her drug usage to “just a few times a month.” However, she admitted to using heroin up to six times per day in the past. She acknowledged the risks of her behavior, and had attended multiple counseling sessions during the last five years. Still, she never enrolled in a formal rehabilitation program.
Diagnostic Data
Upon evaluation, the patient’s corrected visual acuity measured 20/100 O.D. and 20/20 O.S. No improvement was documented upon pinhole testing. Her pupils were equal, round and reactive to light, with no evidence of afferent defect. Extraocular motility testing showed no restrictions in muscle movement. Confrontation visual fields were full to finger counting O.U.
On color vision testing, the patient correctly identified 14/14 Ishihara plates O.U. No red desaturation was detected.
Her intraocular pressure measured 18mm Hg O.D. and 19mm Hg O.S. The anterior segment examination was unremarkable, with no evidence of inflammatory cells or protein flare in the anterior chamber. Gonioscopy revealed that the most posterior structure in all quadrants was the ciliary body face O.U. We documented no sign of microhyphema, microhypopyon, peripheral anterior synechiae or neovascularization O.U.
The posterior segment evaluation revealed a round, yellow-white pre-retinal lesion (figure 3) with surrounding telangiectasia (figure 4) and 2+ posterior vitreous cells in her right eye. Furthermore, we noted trace to 1+ cells in the anterior vitreous.
The right optic nerve had blurred margins. This presentation likely was caused by traction and vitreal inflammation rather than true disc edema, because no afferent defect was noted on pupil testing and color vision was normal.
The fundus examination of the left eye was unremarkable.
Diagnosis and Follow-Up
Immediately, we referred her to the hospital for blood work and intravenous antimicrobial therapy. The patient received an MRI of the brain and orbits, both with and without contrast. Additionally, she underwent FTA, RPR, HIV screening, Lyme titer, angiotensin-converting enzyme, Toxocara screening, purified protein derivative, chest X-ray, CBC testing and a blood culture.
Further, a vitreal culture was taken the following day. A mold infection of unknown species was identified in the vitreal cultures. All other blood testing was negative. The patient was started on intravenous amphotericin B, because of its broad-spectrum coverage. The mold did not reproduce in the mycology lab, which was necessary for species identification.
Because amphotericin B has poor vitreal penetration when prescribed orally, the patient also was started on 5µg/0.1mL intravitreal injection of the drug. She received two in-patient intravitreal injections during the five-week hospitalization period. Following discharge, the patient was transitioned from intravenous to oral amphotericin B by her infectious disease specialist. Recently, she reported a moderate improvement in vision with mild distortion. Approximately five and a half weeks after the initial diagnosis, her visual acuity measured 20/50 O.D. and 20/20 O.S.
Vitreous cells were not observed at follow-up. The pre-retinal nodule had formed into a fibrotic scar, causing retinal traction and striae (figure 5). Blood cultures were performed again both two and four weeks after hospital admittance; all cultures returned negative. Eight weeks after initial culture, we identified the mold as a Malbranchea species.
During the next year, we will closely monitor the patient for advancing retinal traction and a potential detachment O.D. We educated her extensively on the risks associated with intravenous drug abuse, and she promised to begin an official rehabilitation program as soon as possible.
DISCUSSION (abridged)
Recreational injection of street drugs directly is associated with a variety of local and systemic complications. It is also linked to the transmission of infectious diseases through needle sharing and sexual activity. The most serious ocular complications have been reported from the use of crack or crack-cocaine, methylenedioxymethamphetamine or diamorphine (heroin) injections.
Ophthalmological complications include corneal ulcers, reduced corneal sensitivity, microtalc retinopathy, retinal or choroidal infarcts, central retinal artery or vein occlusion, endophthalmitis, nystagmus, and cerebrovascular accidents that cause neuro-ophthalmic manifestations.
Retinal or choroidal infarct, inflammation or infiltrates cause some of the most devastating visual sequelae, because they typically are located in the posterior pole. These signs are indicative of general septic chorioretinopathy. The underlying cause is bacterial or fungal (or, less commonly, parasitic). Inflammatory causes of chorioretinopathy must also be ruled out.
Eliciting a history of illicit intravenous drug abuse is imperative when septic chorioretinopathy is suspected. This helps to facilitate prompt testing for the most commonly associated pathogens and also could help guide the most appropriate treatment regimen.
Bacterial pathogens, specifically those of the Staphylococcus genus, are the most common cause of infection in intravenous drug users. Without question, eye care clinicians should be most concerned about the potential for methicillin-resistant Staphylococcus aureus. Other common pathogens associated with this behavior include streptococci, gram-negative bacilli, enterococci, Fusarium, Aspergillus and Candida.
The development of Roth’s spots is one of the most serious presentations in intravenous drug users who are suspected of bacterial chorioretinitis or endocarditis. Roth’s spots are white-centered hemorrhages that classically are indicative of bacteremia and bacterial endocarditis; however, they also are seen in diseases such as leukemia, pernicious anemia, sickle cell disease and connective tissue disorder.
In bacterial endocarditis, Roth’s spots are formed as a result of thrombocytopenia and a low-grade, disseminated, intravascular coagulopathy. The clinically viewed, white-centered hemorrhages are most likely caused by anoxia, which causes a sudden increase in venous pressure. This causes capillary rupture and extrusion of whole blood. Platelet release causes the coagulation cascade to initiate, eventually causing a platelet-fibrin thrombus surrounded by heme.
Because of this specific pathology, Roth’s spots are now part of the standard used to determine a diagnosis of bacterial endocarditis.
[Full article with pics and references here:
http://www.revoptom.com/content/c/37817/]