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Biomedical subjects

Andrew S Gurwood

Publications and source records attributed to Andrew S Gurwood.

8 recordsLinked to original sources

Acute onset of halos and glare: bilateral corneal epithelial edema with cystic eruptions--atypical presentation of amiodarone keratopathy.

BACKGROUND: Amiodarone (Cordarone; Wyeth, Ayerst, New York) is a potassium channel blocking antiarrythmal medication indicated for recurrent ventricular fibrillation and recurrent hemodynamically unstable ventricular tachycardia. Chemically, it is classified as an iodinated benzofuran derivate antiarrythmal drug not chemically related to any other available antiarrhythmic drug. Documented side effects of amiodarone include neurologic, gastrointestinal, dermatologic, cardiovascular, and ophthalmic. The ophthalmic abnormalities include optic neuropathy, optic neuritis, papilledema, corneal deposits, photosensitivity, lens opacities, and macular degeneration. Corneal microdeposits are seen in virtually all patients who receive amiodarone for more than 6 months. Corneal microdeposits result secondary to the secretion of amiodarone by the lacrimal gland with accumulation on, and absorption by, the corneal epithelium. Approximately 10% of these patients become symptomatic with glare and halos; however, that alone is usually not enough to precipitate intervention. CASE REPORT: A 69-year-old woman presented to our office with a 2-week history of halos and glare in both eyes (OU). Her ocular history was significant for occasional contact lens wear. Her systemic history was significant for atrial fibrillation, for which she was taking amiodarone daily for the last 6 years. Six weeks before the onset of her chief complaint, her daily amiodarone dosage was increased from 100 mg to 300 mg. Ophthalmic examination found decreased visual acuities OU, amiodarone keratopathy (subepithelial verticillata), and diffuse corneal epithelial edema with diffuse sodium fluorescein staining OU. The corneal compromise was treated in 2 ways: the source medication was discontinued, and the ocular signs were medicated with a prophylactic topical antibiotic along with supportive preparations (tears/lubricants) and monitored over 2 weeks until full elimination of the pathologic signs and their symptoms. Even after complete resolution of the acute keratitis, the infiltrative keratopathy persisted along with the initial complaints of halos and glare. The supportive treatments were maintained over the course of 2 months until full recovery. CONCLUSION: By exclusion, it was determined that the subepithelial depositions and cystic formations were secondary to an acute amiodarone dosage increase by a new practitioner. Prompt communication resulted in the physician discontinuing that medicine.

Aged↗

Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is an acute, demyelinating polyneuropathy involving the spinal roots, peripheral nerves, and often the cranial nerves. Although its exact mechanism remains unclear, an autoimmune etiopathology is theorized. It is characterized by rapidly progressing, symmetrical muscular weakness starting in the legs and ascending to the trunk and arms. Additionally, deep tendon reflexes are lost. Approximately half of the patients with GBS have cranial nerve palsies, with unilateral or bilateral facial nerve (CN VII) palsy being the most common. Paralysis of the muscles of the tongue, lips, palate, larynx, and pharynx from lesions involving cranial nerves IX, X, and XI and weakness of the muscles of mastication (CN V) are the next most common cranial nerve abnormalities. Ocular muscle palsy is not common, only occurring in approximately 10% of patients. The Miller Fisher variant of GBS is a distinct syndrome in which the only neurologic deficits are oculomotor palsies, areflexia, and ataxia. We present the rare case of a 45-year-old woman with GBS whose ocular muscles were affected. The oculomotor disturbance and limb weakness occurred within a few days of one another. Basic anatomic considerations are reviewed along with the pathophysiology and clinical features of GBS.

Diagnosis, Differential↗

Leber's hereditary optic neuropathy: a case report.

BACKGROUND: Leber's hereditary optic neuropathy (LHON) is a bilateral optic neuropathy of mitochondrial inheritance that produces significant painless, central vision loss and dyschromatopsia. LHON usually occurs in young males between the ages of 15 and 30 years and manifests an episode of subacute or acute vision loss in one eye, with the opposite eye becoming involved weeks to months later. Approximately 80% to 90% of all LHON patients are male. While the disease usually presents itself around the third decade of life, its onset ranges anywhere from 5 to 80 years. CASE REPORT: We report a case of an uncooperative 12-year-old Hispanic boy who was brought to our group practice following referral from an outside optometrist for amblyopia therapy. Following the workup by the binocular vision clinician, a neuro-ophthalmic consultation was obtained, eventually leading to the diagnosis and confirmation of LHON. CONCLUSION: Leber's hereditary optic neuropathy may manifest signs and symptoms that mimic common ophthalmic entities. Teenage males often are reluctant to report its subtle clinical findings, making its discovery even more challenging. LHON should be kept in mind as a possibility for anyone who manifests unexplained visual loss.

Amblyopia↗

Intravenous and indocyanine green angiography.

BACKGROUND: Indocyanine green angiography (ICGA) is an adjunct procedure to intravenous sodium fluorescein angiography (IVFA) for evaluation of disorders of the retina. It has particular application when choroidal pathology is implicated or suspected. Indocyanine green (ICG) dye has been used in the medical field since 1956, when it was approved by the Federal Drug Administration for imaging cardiac and hepatic circulations. Indocyanine green is a well-tolerated, tricarbocyanine dye with a molecular weight of 775 daltons that absorbs light at 790 to 805 nm and has a peak emission at 835 nm. While the substance gives off 4% the fluorescence of sodium fluorescein, its spectral properties allow it to be visualized through ocular pigments, blood, and serous fluids. METHODS: Using search engines and library resources, clinically relevant ICGA studies were reviewed for their purpose, description, outcome, clinical importance, and compared and contrasted to IVFA. RESULTS: Information is presented that represents the current modalities of ICGA. CONCLUSION: ICGA still remains an adjunct therapy to traditional IVFA. However, as the technology improves--allowing easier recording and visualization of ICG angiograms--and as more studies are conducted on the best use of the information obtained from ICGA, this technique may emerge as an important diagnostic tool in the fight to prevent the severe vision loss associated with the various retinal disorders mentioned.

Choroid Diseases↗

The National Eye Institute of The National Institutes of Health: its history and impact on clinical eye care.

BACKGROUND: Research supported by the National Eye Institute (NEI) of the National Institutes of Health (NIH) has contributed to the visual well being of the world. Pertinent citations from the literature were compiled to produce a clinical database reviewing major studies of the NEI and their outcomes. METHODS: Using Internet search engines and library resources, clinical NEI studies were reviewed. Their purpose, description, outcome and clinical importance are summarized. RESULTS: The results of major clinical NEI research are presented and included are the current modalities of treatment for each disease studied. CONCLUSION: Each NEI study yielded results upon which current scientific guidelines for the treatment or prevention of ocular disease are based.

Biomedical Research↗

Giant cell arteritis.

Giant cell arteritis has been considered an enigmatic disease. It is characterised by chronic granulomatous inflammation of the walls of large and medium-sized arteries. The process has a predilection for the extradural cranial arteries, which include the ophthalmic and the posterior ciliary arteries. It is a multi-symptom disease of older individuals and patients often present with challenging issues and diagnostic dilemmas. We review the literature and latest protocols for the diagnosis and management of giant cell arteritis.

Giant Cell Arteritis↗

Herpes zoster ophthalmicus.

BACKGROUND: We examined the literature for the latest information on diagnosis and management of herpes zoster, and compiled a representative database. METHODS: Using search engines and library resources, we reviewed pathology, epidemiology, pathophysiology, differential diagnosis, and management. RESULTS: The varicella zoster virus is a member of the herpes virus family that produces an infection through direct contact with active skin lesions or airborne droplets. The infection resides latent in the trigeminal ganglion until reactivated, often affecting the sensory nerve, skin, eye, and adnexa. CONCLUSION: The varicella zoster virus has the potential to severely disrupt the structures of the eye. Patients less than 50 years of age should be referred for systemic workup to rule out an immunocompromised state. In general, management is often palliative and/or geared toward specific sequelae.

Antiviral Agents↗

Idiopathic intracranial hypertension: pseudotumor cerebri.

BACKGROUND: Idiopathic intracranial hypertension (IIH), as defined by the modified Dandy criteria, is a diagnosis of exclusion. It is important to rule out other sight- and life-threatening causes of optic disk edema. IIH primarily affects obese women of childbearing age. CONCLUSIONS: Permanent visual loss is the primary morbidity associated with IIH. Quantitative perimetry is key in management decision-making to prevent blindness. Treatment consists of weight loss, medication, and surgery.

Diagnosis, Differential↗