Cure Eye Floaters Naturally
Macular degeneration is the leading cause of blindness after age 65, and nothing prevents or delays its progression. Smoking 20 or more cigarettes a day increases the risk of macular degeneration two- to threefold. As with other smoking-related disorders, macular degeneration also appears to be dose related, with the incidence increasing with the number of pack-years (Christen et al., 1996 Thornton et al., 2005). Smoking is also a cause of nuclear cataract, with smokers having two to three times the risk of never-smokers.
Macular degeneration, which is a disease of the retina, is one of the most common causes of vision loss in older adults. In this illness, the macula, which is the central part of the retina, becomes damaged leaving the affected individual with only peripheral vision. Although this illness usually found in individuals aged over 55, Edgar Degas (French 1834-1917) had his first symptom at age 36. The condition, which began in his right eye, eventually affected his left eye as well. Even without central vision, Degas was determined to work. Unable to stand the glare of the sun, Degas painted indoors, creating interior scenes, portraits, and images of ballet dancers. When his eyesight deteriorated so that he could no longer see the fine lines his brush made with oil paint, Degas changed to pastels where the thick chalk lines were easier to see. These pastels are his most popular works. As his vision worsened and Degas could no longer see the chalk lines, he turned to sculpture, using his...
Fig. 19.3 The presence of drusen in a patient with neovascular age-related macular degeneration (Machemer, 2005). Copyright, Online Journal of Ophthalmology, used with permission. Fig. 19.3 The presence of drusen in a patient with neovascular age-related macular degeneration (Machemer, 2005). Copyright, Online Journal of Ophthalmology, used with permission.
An increase in previous floaters or the onset of new floaters may occur in a retinal detachment. Traumatic detachment of the retina can be observed after blunt eye injury, especially in older adults. Retinal detachment may also occur spontaneously, especially in patients with high myopia. The patient may complain of reduced overall brightness in the involved eye or may have continuous light flashes, indicating retinal traction. After eye trauma, it is imperative to inspect not only the central portions of the retina, but the peripheral portions as well. This examination should be performed in a darkened room after instillation of a short-acting mydriatic agent. Any questionable findings should be referred to an ophthalmologist immediately.
Possible cause Retinal detachment, a disorder in which the light-sensitive membrane at the back of the eye is torn, may cause such symptoms. action The earlier treatment for this problem is started, the greater the chance of success. If the tear is small, laser surgery may be used to repair the retina. Otherwise, conventional surgery may be necessary. Following retinal detachment in one eye, there is a considerable risk of developing it in the other eye. Both eyes will therefore be checked regularly.
The majority of aptamers with potential therapeutic utility selected to date target extracellular proteins. Extracellular therapeutic targets, such as growth and coagulation factors of the vasculature, have the advantage of ready access to aptamer intervention without need for enabling aptamer access to cells or tissue spaces. Broad therapeutic areas are represented among aptamers directed against extracellular targets, including angiogenesis oncology (Green et al., 1995, 1996 Nobile et al., 1998 Ruckman et al., 1998 Lupold et al., 2002 Chen et al., 2003 White et al., 2003), inflammation (Wiegand et al., 1996 Rhodes et al., 2000, 2001), anticoagulation and thrombosis (Bock et al., 1992 Gal et al., 1998 Rusconi et al., 2004 Rusconi et al., 2000, 2002 Tasset et al., 1997), and autoimmune disease (Tsai and Keene, 1993 Doudna et al., 1995 Lee and Sullenger, 1997 Kim et al., 2003). The aptamer drug Macugen (pegaptanib) (Ruckman et al., 1998 Eyetech Study Group, 2002, 2003), which is...
As the aging population continues to increase, treatment of retinal diseases has become a major issue and there is clearly an unmet medical need (Velez and Whitcup, 1999). Among the many debilitating retinal diseases that greatly impact on quality of life, age-related macular degeneration is the leading cause of loss of vision in the elderly, with an incidence of200,000+ cases per year in the USA. Treatment options are often limited as therapeutic drug levels at the retina are difficult to attain by eye drops. It has proven to be equally challenging by the systemic route due to the blood-retinal barrier at the RPE. A large systemic drug dose is usually required in order to reach therapeutically effective drug levels at the retina, which invariably are accompanied with unwanted side-effects. Currently approved drugs on the market, including Lucentis and Macugen , require frequent bolus injections on a monthly basis into the vitreous body to manage chronic retinal diseases. These...
The outcomes of research in the fields of tumor angio-genesis and developmental biology have resulted in emerging applications for cardiovascular medicine and other diseases that manifest pathologic angiogenesis such as diabetic retinopathy, macular degeneration, and rheumatoid arthritis. Angiogenesis and vascular remodeling are manifested in several cardiovascular conditions including atherosclerosis, myocardial infarction, myocar-dial hypertrophy, pulmonary hypertension, vasculitis, and vascular malformations. The elucidation of molecular pathways that regulate vasculogenesis, angiogenesis, and the assembly of larger arteries may ultimately lead to therapeutic strategies that manipulate the formation or regression of blood vessels in order to modify some of these diseases. Understanding how angiogenesis is regulated in these angiogenic disease states also provides important insights into their pathogenic or repair mechanisms.
Corneal and scleral lacerations fall within the realm of the ophthalmologist and should be referred immediately after a shield is placed over the eye. Frequently, signs of corneal and scleral lacerations include unequal pupils, decreased IOP, iris prolapse, and hyphema, and a corneal laceration often also involves the lens. It is important to consider posterior injuries to the globe, including retinal detachment, retinal tear, and vitreous hemorrhage (Fig. 41-11). Patients can often be managed as outpatients with oral antibiotics. Intravitreal antibiotics may be given at ruptured-globe repair. Some patients are hospitalized for IV antibiotics, although current intravitreal penetration of many antibiotics is often comparable. Corneoscleral lacerations should be principally repaired at the presenting institution when possible with available ophthalmology services. Hospital transfers delay wound closure or risk wound extension or prolapse of intraocular contents.
Evaluation of the posterior aspect of the eye, including examination of the red reflexes, may indicate an early retinal detachment or retinoblastoma. Optic nerve abnormalities may be associated with midline CNS defects, such as an absent septum pellucidum, agenesis of the corpus callosum, or hypopituitarism. Optic nerve abnormalities such as optic nerve hypoplasia are associated with nystagmus. CT or magnetic resonance imaging (MRI) can identify these abnormalities. Electroretinography (ERG) may be
Glaucoma and other ocular disorders must be ruled out. Examination of the red reflexes by retinoscopy can reveal even minute lens opacities. Direct ophthalmoscopy or reti-noscopy through the child's nondilated pupil is helpful for estimating potential vision in an eye harboring a cataract. Any central opacity or surrounding cortical distortion larger than 3 mm can be visually significant. Generally, the more posterior lens opacity carries more visual significance. The presence of retinal detachment, retinoblastoma, or other ocular pathologies that preclude good visual outcome must be ruled out by indirect ophthalmoscopy or ultrasonography.
The most important causes of central and peripheral visual impairment in older adults include glaucoma, cataract, diabetic retinopathy, and macular degeneration. Most of these conditions can be controlled or, as in the case of cataracts, vision can be restored to a significant level to improve the quality of life. Glaucoma and macular degeneration progression may be slowed with proper treatment. Regular eye examinations for older adults can detect early signs of ocular abnormalities and ensure that proper treatment is initiated. Generally, adults older than 40 years should have a complete examination at least every 3 years. After age 65, the examination should be at 1- to 2-year intervals.
Clinical trials of angiogenesis inhibitors are currently under investigation for the treatment of cancer, macular degeneration, hemangiomas, and arthritis. Angiogenesis itself is a complex biologic process involved principally with the endothelial cell but also with other cell types and biologic processes involved in tissue remodeling. Agents that inhibit this process are diverse because they can be directed at multiple targets and cellular events, such as the endothelial cell itself (proliferation, migration, apo-ptosis, endothelial cell receptors), the availability of en-dothelial cell growth factors, downstream signaling responses of growth factor receptors, the activity of metalloprotease enzymes, and the recruitment of peri-cytes to promote the maturation and stabilization of the newly formed capillary. In the conduct of clinical trials to test the efficacy of angiogenesis regulators for other disease, there may be coincidental treatment-related effects on the cardiovascular...
Senile macular degeneration occurs in nearly 10 of the geriatric population, affecting more women than men. It represents the most common cause of legal blindness in the United States. There is painless and progressive loss of central vision. The patient frequently complains of difficulty reading. Because only the macula is involved, peripheral vision is spared, and complete blindness does not result. See Figures 10-121 to 10-123.
Degenerative changes in the iris, vitreous humor, and retina may impair visual acuity, reduce the fields of vision, and lead to the development of floaters (muscae volitantes). Senile macular degeneration (see Figs. 10-121 to 10-123) and retinal hemorrhages are other medically significant causes of decreases in visual acuity.
Focuses on the use of postures (asanas) and breathing exercises (pranayama) traditionally used in India to purify the body and maximize the impact of meditation practice many different schools must be used with caution by those with glaucoma, retinal detachment, or at high risk for muscle strain or fracture.
Preclinical and phase 1A clinical evaluation of an anti-VEGF pegylated aptamer (EYE001) for the treatment of exudative age-related macular degeneration. Retina 22, 143-152. Eyetech Study Group (2003). Anti-vascular endothelial growth factor therapy for sub-foveal choroidal neovascularization secondary to age-related macular degeneration phase II study results. Ophthalmology 110, 979-986.
Figure 10-141 shows a giant retinal tear. A large area of bare choroid is visible through the break. progressive constriction of the peripheral fields and eventually blurred vision. Evaluation of the retina reveals the very characteristic picture of black ''bone spicule'' pigmentary changes, particularly in the midperipheral retina. Macular degeneration occurs in late stages. No treatment is available. Figure 10-142A is the classic picture of retinitis pigmentosa. A close-up photograph of the ''bone spicules'' is seen in Figure 10-142B. A staphyloma is an outward bulging of the sclera and protrusion of intraocular contents at a point where the sclera is too thin to support the ocular structure. When present in the posterior pole, as shown in Figure 10-143, it is associated with degenerative high myopia. Macular holes, retinal tears, and retinal detachment are common. Staphylomas may be congenital or may occur after trauma or chronic inflammation that has weakened the scleral wall. In...
The cardiovascular system is the first organ system to develop and reach a functional state in an embryo (Hamilton et al. 1962). The initial steps in blood vessel development consist of vasculogenesis, the differentiation of endothelial cell precursors, the angioblasts, from the hemangioblasts (Risau and Flamme 1995). The juvenile vascular system evolves from the primary capillary plexus by subsequent pruning and reorganization of endothelial cells in a process called angiogenesis (Risau 1997). More recent evidence suggests that incorporation of bone-marrow-derived endothelial precursor cells contributes to the growing vessels, complementing the sprouting of resident endothelial cells (Asahara et al. 1997 Rafii et al. 2002). The development of a vascular supply is also essential in the adult for wound healing and reproductive functions (Folkman 1995). In addition, angiogenesis is implicated in the pathogenesis of a variety of proliferative disorders age-related macular degeneration,...
Retrolental fibroplasia (RLF) is the result of oxygen-induced retinal vasoconstriction, with obliteration of the most immature retinal vessels and subsequent new vessel formation at the site of damage in the form of a proliferative retinopathy. Leakage of intravascular fluid leads to vitreoretinal adhesions and even retinal detachment. Retrolental fibroplasia occurs in infants exposed to hyperoxia in the paediatric intensive care unit and is related not to the -F C 2 per se, but to an elevated retinal artery Po2. It is not known what the threshold of Pa02 is for the development of retinal damage, but an umbilical arterial P02 of 8-12 kPa (60-90 mmHg) is associated with a very low incidence of RLF and no signs of systemic hypoxia. It should be stressed, however, that there are many factors involved in the development of RLF in addition to arterial hyperoxia.
There are no approved pharmacologic treatments for nonneovascular AMD. The Age-Related Eye Disease Study showed that a supplement containing ascorbic acid 500 mg, vitamin E 400 IU, -carotene 15 mg, zinc oxide 80 mg, and cupric oxide 2 mg reduced the rate of clinical progression of all types of AMD by 28 in patients with at least intermediate macular degeneration.28 No benefit was seen in patients with earlier stages of AMD however, the duration of the study may have been insufficient to 28
The adverse effects of pilocarpine are caused by the induction of miosis. The contraction of the ciliary muscle causes the lens to displace forward, which can lead to accommodation spasm and myopia, and can lead to brow ache. Pupillary constriction can also affect night vision. Pilocarpine should be avoided in patients with severe myopia as it increases the risk of developing retinal detachment. Systemic effects may occur at higher concentrations and include nausea, vomiting and diarrhea, and brady-cardia.
A fold of detached retina is seen drooping well in front of the posterior pole giving the appearance of a three-dimensional fundus. (Photo contributor Department of Ophthalmology, Naval Medical Center, Portsmouth, VA.) Retinal detachment Retinal Detachment. Undulating, out-of-focus, elevated retina is seen with few vessels in focus. (Photo contributor Richard E. Wyszynski, MD.)
ADCA with retinal degeneration is an autosomal dominant disorder that is distinct from other types of ADCA in that it has the constant additional feature of retinal degeneration. ADCA with retinal degeneration has also been named ADCA-II. y The gene locus of ADCA-II, SCA7, has been mapped to chromosome 3p. y , y All available data suggest that ADCA-II is a genetically homogeneous disorder. Recently, a protein containing a polyglutamine expansion was detected in the brains of patients with SCA7, suggesting that SCA7 is caused by a CAG repeat expansion. y The clinical observation of marked anticipation in ADCA-II families also points toward an unstable mutation. Neuropathological examinations of ADCA-II patients have consistently revealed the presence of OPCA. All patients have primarily macular degeneration, which then spreads to involve the retina. There is often secondary atrophy of the optic nerve.
Angiogenesis plays a critical role in numerous physiological and pathological states. Vascular endothelial growth factor (VEGF) is the best characterized factor involved in benign and neoplastic angiogenesis and represents a promising target in anticancer and other anti-angiogenic therapies (Rosen, 2001, 2002). Elevated VEGF levels are associated with ocular neovascularizations including diabetic retinopathy (Adamis et al., 1994), retinopathy of prematurity (Pierce et al., 1995), and macular degeneration (Kvanta et al., 1996). Several selections have been performed against a 165-amino acid form of VEGF (VEGF165) (Jellinek et al., 1994 Green et al., 1995) with the latest of this series being a 2'-fluoropyrimidine RNA selection (Ruckman et al., 1998). Ruckman and co-workers performed 12 rounds of selection and isolated three aptamers with Kd-values ranging from 5 to 50pmol L (Ruckman et al., 1998). All but two of the 2'-OH purine positions were modified with 2'-O-methyl substitutions to...
There were no serious adverse events considered to be attributable to Macugen itself in either of these two concurrent Phase III studies (Gragoudas et al., 2004). Non-serious adverse events were generally transient, mild to moderate in severity, and tended to be attributable to the injection process rather than the study drug. These included eye pain, vitreous floaters, punctate keratitis, cataracts, vitreous opacities, anterior chamber inflammation, visual disturbances, eye discharge, and corneal edema. Of the adverse events attributable to the injection procedure (Gragoudas et al., 2004), the most serious was endophthalmitis, an intraocular infection often associated with significant loss of vision. Overall, 12 patients (all in the Macugen injection groups) developed endophthalmitis, but only one patient experienced severe vision loss as a result. Interestingly, this patients enrollment was, in retrospect, a protocol violation because of an active periocular soft tissue infection at...
Temporal arteritis is a systemic autoimmune disorder. Pathologically, there is a granulomatous inflammation of large and medium-sized arteries. It generally occurs in patients older than 55 years, with no gender predilection. Involvement may occur in any organ system. Ocular involvement is generally associated with inflammation of the posterior ciliary arteries. General symptoms include amaurosis fugax, headaches, scalp tenderness, jaw claudication, occasional ear pain or arthralgias, pain and tenderness on one or both temples, malaise, and intermittent fevers. Ocular symptoms include loss of vision, diplopia, pain, red eye, and ocular-ischemic syndrome. The workup of patients suspected to have giant cell arteritis includes a careful history of nonvisual symptoms, examination, and laboratory studies to include erythrocyte sedimentation rate (ESR), C-reactive protein, and complete blood count with differential. Using the Westergren method, the value for a normal ESR is 30 mm hr for a...
Patients may complain of the gradual and usually painless onset of the following visual sensations floaters, scintillating scotomas (quivering blind spots), decreased peripheral visual field, and metamorphopsia (wavy distortion of vision). Cytomegalovirus (CMV) infiltrates appear as focal, small (but may be larger, confluent) white lesions in the retina that look like cotton wool spots. CMV is a necrotizing virus that is spread hematogenously, so that damage is concentrated in the retina adjacent to the major vessels and the optic disk. Often hemorrhage is involved with significant retinal necrosis (dirty white with a granular appearance), giving the pizza pie or cheese and ketchup appearance. Optic nerve involvement and retinal detachments can be present.
The temporal profile of the visual loss suggests possible diagnoses, and its monocularity or binocularity helps in localization. As a general rule, acute or subacute visual deficits result from ischemic or inflammatory conditions or may be caused by a vitreous hemorrhage or retinal detachment. Chronic or progressive visual loss, in turn, may result from a compressive, infiltrative, or degenerative process. Cataracts, refractive error, open-angle glaucoma, and retinal disorders such as age-related macular degeneration or diabetic retinopathy also need to be considered when visual symptoms are insidious.
Most ophthalmic operations are not urgent and patients should be optimized medically before surgery. Patients requiring ophthalmic surgery are often elderly and suffer from coincidental medical conditions, including diabetes, cardiorespiratory disease, and renal impairment.12 Conditions such as trauma, retinal detachment, or malignant glaucoma necessitate emergency surgery, and all present challenges for the anesthesiologist. Before planning the anesthetic care for surgery, the anesthesiologist must have a good understanding of ocular anatomy and physiology.121 In addition, the anesthesiologist must understand the ophthalmologist's preferred conditions for the procedure. Ophthalmic surgeries can broadly be subdivided into intra-and extraocular procedures. Intraocular surgery usually requires globe and conjunctival anesthesia, globe and orbital hypotonia, and extraocular muscle and orbicularis muscle akinesia. With advances in surgical techniques for cataract surgery, nonakinetic...
The orbits are involved in Le Fort II and III fractures and diplopia and restriction of eye movements may be evident. There may be marked proptosis of the eyes due to intraorbital bleeding and oedema. The eyes must be examined carefully to exclude any serious globe damage the incidence of which varies in different case series but around 20 is a likely figure, with around 10 permanent visual loss. In craniofacial injuries there may be visual field changes. Retinal detachments and other intraocular injuries must be excluded to avoid their deterioration during mobilisation of the midface or intraorbital surgical intervention. Usually, if 7-10 days are allowed to elapse it becomes safe to operate on the orbit. Careful examination of the lids and surface of the eye will identify lacerations and other injuries an early ophthalmic assessment is advisable.
Blindness can occur with severe pressure on the optic nerve or from its avulsion in major trauma. Fundal examination is essential, to detect this and injuries such as retinal detachments, choroidal tears and lens dislocations. Persistent diplopia can result from damage to muscles or persistent trapping and failure to reposition prolapsed orbital contents. Enophthalmos persists following loss of orbital contents or an increase in orbital size following poor surgery.
Been offered, depending on the location of the cause of blindness. A retinal prosthesis can make use of the selective survival of inner layer retinal cells for people with macular degeneration or retinitis pigmentosa by directly stimulating them, bypassing damaged photorecep-tors. With complete retinal or optic nerve damage, the stimulation must include the occipital visual cortex. One approach captures images with a camera and a stimulating device activates an implanted microarray. The density of the array and just what properties it signals determines the size of the visualized pixels.49 As the number increases, especially beyond a matrix of pixels that is approximately eight by eight, visual acuity improves enough to make out coarse features.
Limiting the disability of diabetes mellitus has been greatly advanced with laser control of retinal disease. The onset of retinopathy is the appearance of microaneurysms indicative of diabetic angiopathy. Microaneurysms represent the beginning of a progression from background to proliferative reti-nopathy with neovascularization. Advanced retinopathy is caused by continuing capillary failure with leakage, hemorrhage, and closure, producing zones of retinal ischemia. The resulting compensatory capillary proliferation in the isch-emic parts of the retina is prone to leak and rupture, causing gross hemorrhage. A reabsorbing hemorrhage in the vitreous can exert a pull on the retina resulting in retinal detachment with onset of blindness. Capillary hemorrhage can be detected by inspection or imaging modalities. Treatment by laser application decreases angiogenesis and further hemor-rhagic risks. Vitreous hemorrhage can be removed, restoring vision and eliminating the risk of retinal...
It may not be a coincidence that the only FDA-approved antisense drug (Vitra-veneTM) and the first approved aptamer drug (MacugenTM) are both administered to the eye by intravitreal injection. The eye is a relatively small and independent compartment. As a consequence systemic toxicity and cost-of-goods issues are favorable when compared with most other dosing strategies. Macugen (pegaptanib) is a 5'-40kDa-polyethylene glycol-terminated, 3'-inverted dT-terminated 27-mer in which all of the pyrimidines are 2'-fluoro and all of the purines are 2'-O-methyl except for two 2'-hydroxy adenosines. Macugen successfully completed Phase III clinical trials and Phase II clinical trials are reported in the literature (Eyetech Study Group, 2003). Macugen binds to VEGF, which is implicated in the overproliferation of vasculature that accompanies age-related macular degeneration. The Phase II data report that patients received multiple intravitreal injections, that these were well-tolerated and...
As the world population ages and more people face debilitating visual diseases and their quality of life is severely threatened, the development of a drug delivery system that is effective, convenient, and of low risk will surely benefit many. The ever-advancing polymer delivery systems, especially those in periocular drug delivery, for the treatment of age-related macular degeneration, retinitis pigmentosa, and the many other retinal diseases, hold great promise as new therapeutic agents are discovered.
Del Priore LV, Kaplan HJ, Hornbeck R, Jones Z, Swinn M (1996) Retinal pigment epithelial debridement as a model for the pathogenesis and treatment of macular degeneration. Am J Ophthalmol 122 629-643 4. Campochiaro PA, Soloway P, Ryan SJ, Miller JW (1999) The pathogenesis of choroidal neovascularization in patients with age-related macular degeneration. Mol Vis 5 34
The scientific staff at NeXstar were faced with an interesting problem. As a group we were largely academic (in beliefs, in approaches, in politics, all of it) and we were trying to make drugs using a new technology. We were facing a pharmaceutical industry that had not yet learned that injected drugs (like therapeutic antibodies or other biologicals) were a legitimate idea and, on top of that, aptamers had a short academic history. The scientists at NeXstar were asked to choose a protein target for therapeutic intervention, identify a neutralizing aptamer with high affinity and specificity, and convince Pat Mahaffy and me that the commercial opportunity for that aptamer was significant. We were lucky to have on the scientific staff Nebojsa Janjic, a scientist more than up to those tasks. Early on, Nebojsa had decided that angiogenesis was often pathological and should be a target for therapeutic intervention, and as such he and his team began successful aptamer development programs...
Ocular defects in Sturge-Weber syndrome include glaucoma, hemangiomas of the choroid, conjunctiva, or episclera, retinal detachment, vascular tortuosity, strabismus, and buph-thalmos. Of these lesions, glaucoma is the most common oph-thalmologic finding, affecting between 30 and 50 of patients with Sturge-Weber syndrome. This finding is often unilateral and ipsilateral to the facial nevus. In addition, it is often congenital or develops before age 2. Trabeculotomy may be required for the treatment of this condition. Rarely, choroidal hemangiomas may cause retinal or choroidal detachment with visual loss, necessitating surgical intervention, external-beam irradiation, or photocoagulation.
The presenting complaint of CMV retinitis is usually unilateral floaters or decreased visual acuity. Ophthalmological examination demonstrates large white-colored areas with perivascular exudates and hemorrhages. Initially these abnormalities are found at the periphery of the fundus, but if left untreated, lesions progress to involve the macula and the optic disk. '130'
Cataract, choroidal rupture, vitreous hemorrhage, angle recession glaucoma, and retinal detachment are often associated with traumatic hyphema and compromise the final visual acuity prognosis. It is important to recognize that the prognosis for visual recovery from traumatic hyphema is directly related to three factors (1) amount of associated damage to other ocular structures (e.g., choroidal rupture or macular scarring), (2) presence or absence of secondary hemorrhage, and (3) presence or absence of complications
Acute painless visual loss is caused by either a vascular accident or a retinal detachment. Painless loss of vision over a longer period occurs with compression of the optic nerve or tract or radiation. Glaucoma is often the cause of chronic, insidious, painless loss of vision. Acute narrow-angle glaucoma, however, may be responsible for transient loss of vision in association with intense ocular pain. Episodes of migraine may produce transient episodes
An optic pit is a congenital anomaly of the optic disc. It is a small depression, located temporally in 75 of cases, in the optic nerve and is usually gray or yellow. In 85 of cases, it is unilateral. Figure 10-79A shows an optic pit. Retinal tears and detachment can occur in 50 of patients with an optic pit, as shown in Figure 10-79B that patient has an optic pit and a retinal tear involving the macula of the left eye. Can be normal with aging Age-related macular degeneration
Some retinal lesions are recognized because of visual impairment and retinal detachment. y Obliteration of these lesions has been accomplished with cryocoagulation or photocoagulation. Cerebellar hemangioblastomas are removed surgically in about 90 percent of patients, who have a risk of recurrence of about 15 percent. Small renal tumors should be judiciously removed because the presence of multiple tumors is a possibility. In patients with cystic renal disease, nephrectomy should be considered, followed by dialysis.
The vast majority of ophthalmic operations, whether involving the anterior segment of the eye (e.g., cataract extraction and corneal transplantation), the posterior segment of the eye (e.g., retinal detachment, vitrectomy, scleral buckling), or the ocular adnexa (e.g., strabismus, ptosis surgery), as well as evisceration of the eye, can all be done under regional anesthesia. Very lengthy procedures, however, may constitute a relative contraindication to regional anesthesia because the patient may become tired or restless.
Mannitol is an osmotic diuretic which reduces the volume of the vitreous humour. Infusions in doses of up to 1.5 g kg-1 are given before surgery over a period of 30-45 min. There is an initial increase in circulating blood volume followed by a diuresis and decrease in blood volume. When combined with the induction of general anaesthesia, haemodynamic instability may occur. Particular caution must be exercised in patients with cardiovascular disease. A urinary catheter should be inserted preoperatively if patients are to receive mannitol in this way.
Towards the end of a retinal detachment procedure, the surgeon often injects a bubble of sulphur hexafluoride (SFg) or per-fluoropropane (C Ffj ) into the eye to tamponade the retina. Some minutes before this is done, the anaesthetist must discontinue administration of nitrous oxide but continue to maintain anaesthesia with air, oxygen and additional volatile agent. The use of a continuous intravenous propofol technique is a suitable alternative. If the nitrous oxide is not eliminated beforehand, it equilibrates with the tamponading gas during the operation, but at the end of the anaesthetic the nitrous oxide diffuses out and reduces the pressure in the gas bubble. The inhaled anaesthetic gas mixture at the time of injection of SFg or C3F8 should approximate as nearly as possible to normal room air. As soon as there is sufficient recovery from anaesthesia, the patient is turned to the prone position so that the bubble exerts upward pressure on the area of the retinal detachment.
Corneal abrasions are associated with inadequate eye protection, especially during transfer or use of the prone position. The use of adhesive tape to close the eyelids is also a risk factor. Lubricated dressings such as sterile paraffin gauze may be a preferable method of securing the eyelids. Mechanical pressure to the globes should be avoided at all times, because of the risk of retinal ischaemia and permanent blindness. Retinal detachment has been reported with extreme Trendelenburg positioning and as a result of pressure exerted on the eye in patients placed in the prone position.
It is extremely important to ascertain the acuteness of the loss of vision and the presence or absence of pain. Sudden, painless loss of vision may result from a retinal vascular occlusion or a retinal detachment. Sudden, painful loss of vision occurs in attacks of acute narrow-angle glaucoma. Gradual, painless loss of vision commonly occurs in chronic simple glaucoma.
In all cases, generally the first observed clinical abnormality is hepatosplenomegaly. In addition to the systemic organopathy, patients develop progressive neurological deterioration with motor and mental decline. Macular degeneration occurs, and a cherry-red spot appears in about 25 percent of patients with type A disease, 8 usually in the first year of life. Seizures may develop, and as the disease progresses, children become inexorably obtunded and difficult to feed. Recurrent infection is often a major problem, and death occurs before 2 years of age. In some cases, peripheral nervous system involvement is detected with slow nerve conduction velocities. In type C disease, the childhood or adult form, deterioration occurs more slowly, and the patients usually seem normal until 2 years of age or even young adulthood. They often develop dystonia with selectively swollen cells in the basal ganglia. In such patients, foamy histiocytes can be found in bone marrow and spleen, and hepatic...
Patients with posterior uveitis usually present with a reduction in vision and vitreous floaters. They may have clinical signs of retinal vasculitis, retinal ischemia, optic nerve edema, and exudative retinal detachment. On careful inspection, cells may be visible floating in the vitreous. Common causes of posterior uveitis are toxoplasmosis, sarcoidosis, cytomegalovirus, Epstein-Barr virus, Beh et's disease, and Bartonella infection. Toxoplasmosis accounts for up to 30 of cases and may destroy the macula or other important visual structures. Characteristically, there is an exudation in the retina caused by an inflammatory process. Toxocara canis may also present as uveitis.
The diagnosis of retinoblastoma is made by the patient presenting with a white pupil (leukocoria) in 61 of cases, strabismus in 22 of cases, and sometimes with a retinal detachment, red painful eye, or spontaneous hyphema (Fig. 41-25). Generally, patients with small retinoblastomas have problems with vision or strabismus. More advanced lesions present with leukocoria and occasionally secondary glaucoma. The advanced lesions may metastasize to the orbit and produce proptosis through the orbital spread. In addition, patients with retinoblastoma may have systemic metastases to the CNS, skull bones, lymph nodes, and other organs.
Painless monocular visual loss may also occur following a vitreous hemorrhage. Affected patients often report seeing large floaters in the affected eye, and blood within the vitreous impedes a complete fundus examination. These hemorrhages can result from neovascularization (e.g., diabetic) or acutely elevated intracranial pressure associated with a subarachnoid hemorrhage (Terson's syndrome). Common causes of subacute monocular visual loss evolving over hours that involve the retina include retinal vein occlusions and retinal detachments. A patient with a central or branch retinal vein occlusion generally reports a painless loss of vision. Funduscopic examination reveals retinal hemorrhages cotton wool spots edema and tortuous, dilated retinal veins. Peripheral visual loss may be reported, and decreased visual acuity suggests macular involvement or optic nerve ischemia. Retinal detachments are usually preceded by floaters and flashes of light (photopsias). If the macula becomes...
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