Judith G. Hall, M.D.

• University of British Columbia
• Dept. of Pediatrics, BH Children? Hospital
• Vancouver, British Columbia, Canada

Timolol maleate gel is used once a day Mode of action?It reduces aqueous secretion erectile dysfunction pump surgery purchase super avana now. Side effects?Bronchospasm erectile dysfunction treatment kolkata buy super avana without prescription, bradycardia icd 9 code erectile dysfunction due diabetes cheap generic super avana uk, low blood pressure and corneal anaesthesia erectile dysfunction treatment in pune order super avana online pills, depression and fatigue erectile dysfunction caused by performance anxiety discount super avana 160 mg amex. It is a cardioselective beta-adrenergic blocking agent which has the advantage of having little effect on cardiopulmonary system erectile dysfunction raleigh nc purchase 160 mg super avana with visa. It is there fore best choice for patients with open angle glaucoma having associated hyper lipideamia or athero-sclerotic cardiovas cular disease. Side effects Local?Conjunctival hyperaemia, allergic blepharoconjunctivitis, nasolacrimal obstruction, adrenochrome deposits in the conjunctiva, angle closure glaucoma and cystoid maculopathy. Mode of action?It acts by reducing aqueous production and also by increasing uveoscleral outflow. Side effects?Allergic conjunctivitis, xerostomia, drowsiness and fatigue may occur. It is not suitable for long-term use because of tachyphylaxis and higher incidence of local side effects. Dorzolamide (2%, 2-3 times a day) It is a recently introduced topical carbonic anhydrase inhibitor. It is water soluble and has excellent corneal penetration Mode of action-It lowers intraocular pressure by decreasing aqueous secretion Side effect?It may cause allergic blepharo conjunctivitis. Brinzolamide (1% three times a day)?It is similar to dorzolamide but there is lower incidence of ocular allergy. Anterior uveitis and cystoid macular oedema may occur in predisposed eyes, hence should be used with caution in uveitic glaucoma. Combine Drugs Therapy Combine preparations are more effective, convenient and improve patients? compliance. Sustained action capsules of acetazolamide 250-500 mg (substitute) are given once or twice daily iii. Side effects of acetazolamide Mode of action?There is decreased formation of bicarbonates which causes less secre tion of aqueous from the ciliary epithelium (diuretic effect is not a factor in the reduction of intraocular pressure). Pilocarpine 3-4 times Ciliary muscle contraction, Miosis and spasm, induced myo 1%, 2%, 4% daily miosis, opens spaces in pia, hyperaemia, risk of retinal trabecular meshwork detachment, cataract, iris cyst 2. Timolol Twice Reduces aqueous Bronchospasm, bradycardia, Maleate daily secretion arrhythmia, low blood 0. Selective beta blockers Reduces aqueous Same as timolol except no Betaxolol Twice secretion corneal anesthesia. Epinephrine Twice Increases aqueous outflow Irritation, conjunctival 1% Dipive daily by their beta agonist action congestion, cystoid macular frine 0. Latanoprost Once Enhances uveoscleral Hyperaemia, iris pigmentation, (Xalatan) daily outflow allergy, risk of cystoid macular 0. Travoprost Once Enhances uveoscleral Conjunctival hyperaemia (Travatan) daily outflow 0. Bimatoprost Once Enhances both trabecular More conjunctival hypercaemia (Lumigan) daily and uveoscleral outflow but fewer headache and less 0. Dorzolamide 2-3 times Decreases aqueous Allergy, superficial punctate 2% (topical) daily production keratitis, blurring dryness ii. Brinzolamide 2-3 times Decreases aqueous Similar to dorzolamide but lower 1% daily production incidence of stinging and local allergy 276 Basic Ophthalmology Side effects?Paraesthesia, malaise complex, gastric irritation, renal stone formation, Stevens Johnson syndrome and blood dyscrasias. Hyperosmotic Agents Mode of action?These agents increased the plasma tonicity or osmolality to draw water out of the eyes. Surgical Treatment Trabeculectomy, a filtering operation is done when the miotics and? Mode of action?Discrete laser beam causes a shrinkage of the collagen on the inner surface of the trabecular ring, thereby, opening the intertrabecular spaces. Extent?180o Viewing power?The slit-lamp is utilised with a gonioscopic lens with 25-fold ocular viewing power. Glaucoma 277 Placement of the argon-laser beam focus Direction?The beam is to be focused at the junction between the pigmented and non-pigmented trabeculum. Laser filtration?It is done with virtually any laser coupled to a fiberoptic delivery system. The advantage over routine filtering operations are fewer complications by use of smaller or no incision. Seton valves?These include filtration devices such as the Molteno (silicon tube) and Krupin (supramid tube) implants. It is a subconjunctival implant connected to a tube that enters the anterior chamber. Aqueous is shunted through the implant and diffuses away in the subconjunctival tissue. Non-penetrating surgery?The anterior chamber is not entered and the internal trabecular meshwork preserved. There is no bleb formation which means the aqueous does not drain into the subconjunctival space. Glaucoma 279 Investigation Perimetry should be done at 4-6 monthly interval to demonstrate progression before starting medical treatment. If nocturnal drop of blood pressure is present, avoid high dose of antihypertensive medication. Relative pupil block?Normally pupillary margin just touches the anterior surface of the lens. Physiological iris bombe?On dilatation of the pupil there is crowding of the iris in the angle of anterior chamber causing obsruction to the flow of aqueous from the posterior to the anterior chamber at the level of the pupil. Irido-trabecular contact?It totally cuts off the drainage channel by forming a false angle. It precipitates an attack of raised intraocular pressure (acute congestive attack). Irido-trabecular contact Stages the clinical course of the disease has been divided into five stages. The condition however does not necessarily progress from one stage to the other in an orderly sequence. Absolute primary angle-closure glaucoma Mechanism of closed angle glaucoma Glaucoma 281 1. The pigmented trabecular meshwork is not visible (Shaffer grade 1 or 0) without indentation or manipulation in at least three quadrants. The patient is asked to lie down in a dark room, in the prone (face downwards) position for 1 hour without sleeping. It is confirmed in one eye during an attack of acute congestive angle closure in the other eye usually. An optical section of the peripheral cornea and anterior chamber is made with the illumination and viewing arms at 60 degrees to each other. It is a corneal topography mapping system which combines scanning slit with placido disc technology. Treatment Prophylactic peripheral laser iridotomy in both eyes will prevent an acute attack. If untreated, the risk of acute pressure rise during the next 5 years is approximately 50%. The normal diurnal variation Intermittent angle closure occurs in an anatomically predisposed eye in which physiological factors such as reading in dim illumination or watching television in a dark room precipitates a pupillary block due to mydriasis. This causes a sharp rise in intraocular pressure for a short period of time followed by a spontaneous resolution of the pupillary block possibly due to: i. Sleep (As the pupil becomes constricted) Emotional stress may also be a precipitating factor. Coloured halos around lights?There is accumulation of fluid in the corneal epithelium and corneal lamellae which alters the refractive conditions of the cornea. As halos are seen as coloured rings around lighted bulb, they are observed only after dark. The colours are distributed as in the spectrum of rainbow with red colour being outside and violet inner most. Course Some eyes may develop an acute attack or may progress into chronic primary angle-closure glaucoma. Diagnosis Diagnosis in the early stages (angle-closure suspect and intermittent or subacute angle-closure) is important since adequate treatment at this stage is easy and certain to prevent the loss of vision. If the patient gives a vague history, the halo can be demonstrated by him on looking through a thin layer of lycopodiun powder enclosed between two glass plates made up as a trial lens. Provocative tests Rise in tension can be tested by the provocative tests even if the tension is normal. Dark room test?The patient lies awake in the prone (with face downward) position in a dark room for 1 hour. The pupil dilates and if the rise in tension is more than 8 mm Hg (Schiotz), it is pathological. Full miosis is achieved after the test by the instillation of pilocarpine eyedrops as precaution. Lenticular halos?These are typically seen in early cataractous changes in the lens. It is typically seen in the case of incipient cataract due to the prismatic effect of the wedge-shaped peripheral cortical opacities where the halos make and brake. Halo in conjunctivitis?This is due to the sticking of conjunctival discharge on the cornea. The stenopaeic test (Fincham test) Treatment Prophylactic peripheral laser iridotomy is performed in both eyes of all the patients because if untreated the risk of acute pressure rise during the next 5 years is very high (50% approximately). Glaucoma 285 Mechanism of the rise in intraocular pressure in angle-closure glaucoma Pathogenesis the crisis is due to acute ischaemia associated with liberation of prostaglandin-like substances. If the attack lasts for several hours or days, irreversible damage may occur to the ocular tissues. Severe unilateral headache, nausea, vomiting and prostration are often associated. There is sudden onset of intense unbearable pain in the eye due to stretching of the sensory nerves. It is mainly due to ischaemia due to optic neuropathy and partially due to corneal oedema stasis and increased permeability of the capillaries. Redness, lacrimation and photophobia are present due to corneal oedema erosion and conjunctival and ciliary congestion. This is due to the imbibation of fluid in the cornea caused by the dysfunction of the endothelial pump? as a result of raised intraocular pressure. Lens?Glaucoma fleckens are small greyish white anterior subcapsuler opacities seen in the lens in the pupillary area. Fundus examination?There may be difficulty in visualizing the fundus due to hazy cornea. Gonioscopy?It reveals abnormally narrow angle of the anterior chamber with or without anterior synechiae. Peripheral anterior synechiae (organized exudates) occur as a result of prolonged and repeated acute congestive attack. The perfusion of optic nerve head is affected due to decreased blood flow in the capillary and in annulus of Zinn which supplies nutrition to the laminar and post-laminar optic nerve head. It usually passes into the stage of chronic primary angle-closure glaucoma as the angle becomes slowly and progressively closed. Treatment Although the treatment of primary angle-closure glaucoma is essentially surgical, the initial treatment is medical in order to control the raised tension. Medical Treatment It is useful in lowering the raised tension particularly in the acute congestive attack preoperatively. The patient should be positioned supine (lying straight) to allow the lens to shift posteriorly. Carbonic anhydrase inhibitors?It reduces the formation of aqueous by inhibiting the action of carbonic anhydrase enzyme. Acetazolamide 500 mg intravenously and 500 mg orally and/or intravenous mannitol is given after making sure that the patient is not suffering from cardiovascular disease. Pressure with moist cotton swab can be applied on the central part of the cornea if the pupil remains blocked. Pilocarpine (2%)?It should be started half to one hour after commencement of systemic treatment, i. Initially pilocarpine is instilled every 30 minute and later hourly till maximum miosis is achieved. This is effective in pulling the iris away from the angle and opening the drainage channels. However, the tension is lowered by medical treatment before surgery to prevent occurrence of expulsive haemorrhage. Technique A drop of topical pilocarpine is instilled frequently 30 minutes before laser therapy. The laser with an anterior offset is then used to make an opening measuring 150-200 microns in size is made in the periphery of iris. By making a hole in the periphery of iris, pupillary block is relieved permanently. Trabeculectomy?It is done when extensive peripheral synechiae are present (more than 50% angle closure). A partial thickness of a part of limbus (trabecular meshwork and canal of Schlemm) is excised under a scleral flap. A conjunctival flap is dissected anteriorly 10 mm away from the limbus in the upper part of cornea (12 O?clock position). The aqueous seeps out from the anterior chamber into the scleral window > It passes in between the two scleral flaps > It flows into the subconjunctival space. Postoperative management Topical broad spectrum antibiotic drops and ointment, cycloplegic and corticosteroids are given for a period of 2-3 weeks. Pathogenesis Type 1(Creeping)?It is caused by gradual and progressive closure of the angle by synechiae over atleast 180 degrees. Type 2 (Subacute)?It is caused by synechial angle closure as a result of subacute (intermittent) attacks secondary to the pupillary block.

This is an important step as it recognizes that total arsenic in foods is not appropriate for evaluating food safety low libido erectile dysfunction treatment discount super avana 160 mg visa. The total arsenic content of 150 paddy rice samples collected from different areas of Bangladesh erectile dysfunction hormones proven super avana 160mg. The variation in arsenic concentrations in rice was only partially consistent with the pattern of arsenic concentrations in drinking water tube wells erectile dysfunction treatment uk discount super avana 160mg with mastercard. Processing of rice (parboiling and milling) reduced arsenic concentrations in rice by an average of 19% erectile dysfunction freedom purchase 160 mg super avana with amex. Human exposure to arsenic through rice would be equivalent to half of that in water containing 50 g/kg for 14% of the paddy rice samples at rice and water intake levels of 400 g and 4 L/cap/day erectile dysfunction inventory of treatment satisfaction questionnaire cheap super avana online mastercard, respectively (Duxbury et al erectile dysfunction at 65 order super avana 160 mg overnight delivery. Although the amount of arsenic in rice varies that may be due to inadequate number of samples, area from which it is collected and method of estimation. There are two varieties of rice: uncooked rice (atap chal; local language) and cooked rice (sidha chal; local language). When the paddy is cooked with high concentration of arsenic contaminated water twice, once at the processing of rice and another just before intake as boiled rice (Misbahuddin, 167. However, boiling of rice for 5 min will reduce the arsenic concentration by 20% and for 25 min the concentration will reduce by 65% (Chakravarty et al. A rice sample (with undetectable amount of arsenic) showed arsenic in the cooked rice (bhat) when it was cooked with arsenic-contaminated water. The quantity of arsenic was higher when water and rice were cooked so that all the water was absorbed by the rice by the time it was well-cooked (Huq et al. Bangladeshi cook rice with more amount of water and when the rice was well-cooked, the liquid starch was decanted. Cooked rice collected from households during the field survey showed concentrations of arsenic from 0. Another study shows that the content of arsenic ingested by a person from cooked rice is 0. Different strains of rice show different degrees of arsenic uptake, and arsenic levels in rice are affected by concentration in irrigation water and soils. For example, three to four decades ago Bangladeshi preferred to eat bowl full rice (Figure 9. Total arsenic content of raw rice may be reduced 35 to 45% in cooked rice after rinse washing of raw rice and cook with high volume (6: 1, water: rice) of water (Raab et al. Although rice in arsenic endemic area has quite high amount of arsenic as well as antioxidants. If someone uses arsenic contaminated water, then there is chance of more intake of arsenic. Among the vegetables, leafy vegetables contain relatively low concentration of arsenic (Table 9. Arum is a common vegetable in rural Bangladesh for easy to cultivate and available throughout the whole season. The higher values of arsenic in arum may be due to the use of contaminated water from hand pump tube well for its cultivation in the home garden. In an arsenic endemic area, it is impossible to eat any vegetable after estimating its arsenic level. In reality, it is difficult to avoid the intake of arum by the poor Bangladeshi leaving in rural arsenic endemic area. There are some vegetables which have compound(s) that can reduce the body arsenic load. The total calorie can be replaced by shifting the diet habit of potato, maize, etc. On a dry weight basis, some vegetables have much higher levels of arsenic than rice. However, a typical Asian diet includes much more rice than vegetables, so intake from rice remains the principal arsenic exposure through food. Meanwhile, in a bid to reduce the amount of arsenic taken up by rice, researchers are attempting to design rice plants that do not absorb as much arsenic. The proportion of inorganic arsenic ingested through food may be significant, even when the arsenic concentration of drinking water is higher than 50 ppb. For example, a recent study conducted in Mexico, where the concentration of arsenic in drinking water was as high as 400 ppb, found that even so 30% of inorganic arsenic intake came from food (DelRazo et al. In conclusion, people of arsenic endemic area must change the food habit in order to reduce intake of arsenic from foodstuffs. For example, Bangladeshi must change their diet manu like combination of rice (small amount), chapati, dal, vegetable, boiled corn, boiled bean, and yogart (Figure 9. In an arsenic endemic area, the arsenic contaminated hand pump tube wells are marked with red color in order to encourage the people not to drink that water. Unlike water intake, it is not possible to estimate the arsenic content of any food before intake. Most of the epidemiological studies show a close relationship between arsenic intake through water and the development of symptoms. Survey of arsenic in total diet food composites and estimation of the dietary intake of arsenic by Canadian adults and children. Arsenic concentrations in rice, vegetables and fish in Bangladesh: A preliminary study. Food chain aspects of arsenic contamination in Bangladesh: Effects on quality and productivity of rice. Journal of Environmental Science Health, Part A: Toxic/Hazardous Substance Environmental Engineer, 38(1), 61-69. Arsenic contamination in food-chain: Transfer of arsenic into food materials through groundwater irrigation. Arsenic contamination of Bangladesh paddy field soils: Implications for rice contribution to arsenic consumption. Speciation of arsenic in rice and vegetables from arsenic exposed areas in Bangladesh. Total and inorganic arsenic concentrations in rice sold in Spain, effect of cooking, and risk assessments. Market basket and duplicate portion estimation of dietary intakes of cadmium, mercury, arsenic, copper, manganese, and zinc by Japanese adults. Increase in rice grain arsenic for regions of Bangladesh irrigating paddies with elevated arsenic in groundwaters. Even then, S scientists and physicians are trying to relieve the symptoms of arsenicosis by reducing body arsenic load as well as complications. Body arsenic load can be reduced by a) stoppage of drinking arsenic contaminated water; b) intake of low arsenic contaminated food; c) avoid inhalation of arsenic contaminated air; and d) take drug that enhances biotransformation and excretion of arsenic. However, it is a difficult task to make an animal model of skin manifestations of arsenicosis. Most of the animal studies show the effect of drug in reducing the body arsenic load as well as the evidence of oxidative stress. Based on these limitations, some of the antioxidant vitamins and minerals are suggested to be effective in the treatment of arsenicosis. The use of antioxidant is due to the development of arsenic-induced oxidative stress. The administration of 1 g of sodium thiosulfate orally or intravenously causes a rapid and pronounced increase in the excretion of arsenic. The oral administration of sodium thiosulfate (20 and 40 g) significantly decreased the arsenic load in milk, urine, and hair of cattle in arsenic endemic area after 1 month of treatment (Ghosh et al. It can also be administered intravenously and has adverse effects like nausea, joint pain, muscle cramp, blurred vision, agitation, and hallucinations. However, their role in the treatment of arsenicosis remains inconclusive due to inadequate studies on patient. Major drawbacks of dimercaprol include (a) its low therapeutic index, (b) its tendency to redistribute arsenic to brain and testes, for example, (c) the need for intramuscular injection which is painful and (d) its unpleasant odor. This effect may be due to increased urinary excretion of arsenic during the period of therapy. However, it recurs when a patient starts to drink arsenic contaminated water again. In some of the arsenic endemic areas, almost all the hand pump tube wells are contaminated with high concentration of arsenic. In addition, the emphasis should be given on the provision of a diet rich in protein and vitamins. Treatment of keratosis: Stoppage of drinking arsenic contaminated water or shifting of highly arsenic contaminated hand pump tube well to low arsenic contaminated hand pumped tube well is necessary. Keratosis present in the palm and sole can be treated by topical application of salicylic acid with or without urea, propylene glycol, and neem. Orally administered compounds are beta-carotene, retinoid, ascorbic acid, alpha-tocopherol, zinc, selenium, spirulina, alpha-lipoic acid, and folic acid. Among the vegetables, ceraels and spices that can be used include: spinach, corn, amaranth leaf, garlic, curcumin and kala jeera oil. The topical use of 10% boric acid ointment containing 6% salicylic acid in arsenical keratosis for treatment purpose has a long history (Hall, 1946). There was confusion about the percentage of salicylic acid that can be used in arsenical keratisis. Therefore, a randomized control trial on 150 cases with severity of disease (mild, moderate and severe), concentration of salicylate (5, 10, 20 and 30%), and duration of treatment (1, 3 and 6 months) was conducted (Islam et al. Almost all cases of mild and moderate forms of keratosis were found to be improved (97. About 90% improvement was observed using 20 or 30% concentration in mild keratosis within 1 month and 100% improvement with 10, 20 or 30% concentrations within 3 months of treatment. In the case of moderate keratosis, more than 90% improvement was found using 5% concentration or more after 6 months of treatment. More than 90% improvement was noted in the severe form of keratosis only by using 30% concentration salicylic acid for 6 months. The urea enhances the penetration of salicylic acid and produces the systemic adverse effects of salicylate. Propylene glycol: Propylene glycol is usually used as a dissolving media for pararcetamol. A randomized study was conducted on 60 patients of arsenical palmer keratosis treated topically with three different concentrations (15, 30 and 45%) of propylene glycol once daily at both palms at bedtime for eight weeks (Dina & Misbahuddin, 2010). Both roughness and thickness of arsenical palmer keratosis can be reduced using propylene glycol and as the concentration of the drug increases, its effectiveness is increased without any significant adverse effect. Therefore, 45% proplylene glycol is recommended for topical use in the treatment of arsenical keratosis. Topical application of dichloromethane extract of neem (Azadirachta indica) once daily (overnight) for 12 weeks showed significant improvement in palmar arsenical keratosis (Ferdous and Misbahuddin, 2014). So, topical application of neem extract may be recommended for the treatment of arsenical keartosis. Vitamin A: the serum concentration of retinol in patients with non-malignant skin lesions is not significantly changed from the control (Chung et al. However, oral administration of vitamin A (150,000 units) daily for three months was effective in arsenical keratosis following medicinal use of arsenic (Hall, 1946). Open clinical trial on arsenicosis shows its effectivenesss when combination of vitamin A, C and E were used. The effectiveness of vitamin A does not mean that the patient of arsenical keratosis has avitaminosis, hypovitaminosis or dysvitamino-sis. The serum concentration of beta-carotene in patients with non-malignant skin lesions in West Bengal (India) is not significantly changed from the control (Chung et al. However, patients of arsenic-induced skin cancer in Taiwan have low level of beta-carotene in blood (Hsueh et al. A total of 29,133 male smokers 50 to 69 years of age from southwestern Finland were randomly assigned to one of four regimens: alpha-tocopherol (50 mg per day) alone, beta carotene (20 mg per day) alone, both alpha-tocopherol and beta-carotene, or placebo. Total mortality was higher among the participants who received beta-carotene than among those who did not (The alpha-tocopherol beta-carotene cancer prevention study group, 1994). Low dose may not produce any effect whereas excessive dose may cause selenium toxicity. One study shows that supplementation with L-selenomethionine for 6 months shows slight improvement in non-malignant skin lesions in patients, although the improvement was not statistically significant (Verret et al. Selenium reduces the oxidative damage and oxidative stress related gene expression in rat liver under chronic poisoning of arsenic (Xu et al. Ascorbic acid: Isolated liver tissues of rat were first loaded with arsenic within the test tube at 37?C and then treated with ascorbic acid (20 g/mL) (Saha, 2006). However, chronic intake of ascorbic acid may cause stone formation in the urinary tract. Alpha-tocopherol: the serum concentration of alpha-tocopherol in patients with non-malignant skin lesions is not significantly changed from the control (Chung et al. There is 3-fold increased secretion of vitamin E from the skin of chest and back of arsenicosis in comparison to control or arsenic exposed individual (Yousuf et al. A study on the vitamin E levels in the buccal cells of patients shows significantly low concentration in comparison to healthy volunteers. Supplementation with alpha-tocopherol for 6 months shows slight improvement in non-malignant skin lesions, although the improvement was not statistically significant (Verret et al. A study conducted in southwestern Finland shows that alpha-tocopherol had no apparent effect on total mortality, although more deaths from hemorrhagic stroke were observed among the men who received this supplement than among those who did not (The alpha-tocopherol beta carotene cancer prevention study group, 1994). Co-administration of ascorbic acid and alpha-tocopherol to arsenic-exposed rats 183. Vitamin E ameliorates arsenic-induced toxicities in the liver and kidney of mice (Verma et al. Alpha-lipoic acid: In vitro experiment with small pieces of isolated liver tissue of rats incubated first in presence of arsenic and then with different concentrations of?

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Striate melanokeratosis Striate melanokeratosis refers to pigment lines located in the epithelium erectile dysfunction 40s quality super avana 160mg, which extend from the limbus toward the central cornea (Fig erectile dysfunction what kind of doctor purchase super avana visa. These lines normally occur in darkly pigmented individuals but also can occur in lighter pigmented individuals after injury or inflammation erectile dysfunction 23 years old super avana 160mg with mastercard. The deposits are probably the result of migration of pigmented limbal stem cells onto the cornea erectile dysfunction and testosterone injections 160 mg super avana amex. Epithelial iron lines Iron deposits in the epithelium have a yellow-brown coloration (Fig impotence at 50 order super avana visa. Pooling of tears in the region of topographic irregularities allows iron from the tear film to be deposited within the epithelium xatral impotence order super avana 160mg with mastercard. Spheroidal degeneration Spheroidal degeneration produces golden-yellow globular deposits within the interpalpebral area (Fig. In primary spheroidal degeneration, the deposits are bilateral and initially located in the nasal and temporal cornea; they can extend onto the conjunctiva. Secondary spheroidal degeneration is associated with ocular injury or inflammation. The deposits in secondary spheroidal degeneration will aggregate near the area of corneal scarring or vascularization. Adrenochrome deposition Adrenochrome deposits are usually found within the conjunctiva, but rarely may occur on the corneal surface (Fig. These brown-black deposits occur in patients treated with epinephrine eye drops for glaucoma. Nonpigmented deposits Subepithelial mucinous corneal dystrophy Subepithelial mucinous corneal dystrophy is an autosomal dominant condition, which results in the deposition of glycosaminoglycans in the subepithelial stroma (Fig. Irregular gray-white opacities also may be seen centrally; these deposits may be raised. These rings develop when a rust ring from an iron foreign body is not entirely removed. Calcific band keratopathy Hypercalcemia and chronic ocular inflammation are the most common conditions associated with calcific band keratopathy (Fig. Clinically, subepithelial chalky white deposits are found in the interpalpebral zone. The deposition initially begins in the peripheral cornea, with a clear margin separating the deposit from the limbus. Fluoroquinolone deposits Topical ciprofloxacin[18] and norfloxacin[19] therapy can result in the deposition of a chalky white precipitate within an epithelial defect (Fig. Although they are predominantly white in appearance, a crystalline pattern also may be observed. Mucin balls Mucin balls are round white deposits that accumulate between the posterior surface of a contact lens and the corneal epithelium (Fig. When the contact lens is removed, the mucin balls may be blinked away, but in some cases they remain adherent to the cornea for several hours. They are more common with rigid soft contact lens material such as high-Dk silicone lenses. These cysts appear gray on direct illumination, but with retroillumination are transparent and are thus better viewed. Gelatinous droplike dystrophy Gelatinous droplike dystrophy is an autosomal recessive disorder that results in the bilateral accumulation of amyloid deposits in the anterior corneal stroma (Fig. This condition, as well as lattice dystrophy, is a form of primary localized corneal amyloidosis. Clinically, subepithelial raised, gelatinous deposits appear within the first or second decade. These deposits are refractile on indirect illumination, limited to the central cornea, and have been likened to the appearance of a mulberry. The deposits are located within the epithelium and subepithelial space of the central cornea (Fig 22. The deposits can assume a dendritic pattern and can be confused with herpetic keratitis; however, they do not stain with fluorescein. Gout (urate) Patients with gout may have fine, yellow, scintillating crystals in the superficial cornea (Fig. The corneal findings include a diffuse, granular, yellow-brown pigmentation located throughout the stroma, although usually more dense in the deep stroma (Fig. Light exposure probably plays a role in the pathogenesis because the deposits are denser in the interpalpebral region. With very high doses, cornea verticillata or conjunctival pigmentation may be seen. Corneal blood staining Corneal blood staining most commonly occurs in the presence of a hyphema and elevated intraocular pressure. With continued presence of the hyphema, a rust-colored opacity of the stroma develops. This opacity can involve the entire cornea and clears over several years, beginning at the limbus and progressing centrally. Bilirubin Elevated levels of bilirubin secondary to advanced liver diseases such as hepatitis, cirrhosis, or biliary obstruction can lead to a yellow staining in the peripheral cornea (Fig. The staining is found throughout the corneal stroma but is more extensive in the deep stroma. It typically occurs in the setting of a metallic intraocular foreign body, although systemic causes of iron overload such as hemochromatosis can also lead to the condition. The cornea can occasionally be affected by siderosis if the foreign body is localized within the anterior chamber. Nonpigmented deposits Granular dystrophy Granular dystrophy is an autosomal dominant condition that affects the central corneal stroma of both eyes (Fig. Focal white bread crumb? deposits that assume irregular shapes are located throughout the stroma, but tend to be concentrated anteriorly. The deposits initially appear within the first decade of life, and the intervening stroma is clear. Over time, the deposits tend to coalesce, and the intervening stroma assumes a ground-glass appearance. Macular dystrophy Macular dystrophy is an autosomal recessive disorder that results in the accumulation of glycosaminoglycans (predominantly keratin sulfate) within stromal keratocytes and the intervening stroma (Fig. Clinically, small, gray-white nodular deposits are seen within a diffuse stromal haze. Fleck dystrophy Fleck dystrophy is an autosomal dominant disorder that results in the bilateral accumulation of glycosaminoglycans and lipid within keratocytes. There are white, comma shaped, stellate, circular, and wreathlike opacities at all levels of the corneal stroma. Histologically, the deposits are formed by distended keratocytes filled with complex lipids and glycosaminoglycans. Lipid deposition Arcus senilis is lipid deposition within the peripheral cornea, possibly secondary to increased permeability of the limbal vasculature. The lipid is initially deposited in the superior and inferior margins of the cornea. Clinically, the deposits appear as a hazy white circumferential band separated from the limbus by a lucid interval (Fig. The outer margin of the deposit is sharply demarcated, and the inner margin is irregular secondary to an arterial diffusion gradient of lipid toward the central cornea and a venous clearing of lipid peripherally. Associated conditions include trauma, interstitial keratitis, and corneal ulceration. Clinically, the lipid may assume either a fan shaped pattern in front of active neovascularization or a disk-shaped pattern within chronic neovascularization. Refractile/crystalline deposits Lattice dystrophy Lattice dystrophy is an autosomal dominant disorder that results in the accumulation of amyloid within the corneal stroma (Fig. The lines are white in direct light and translucent or crystalline in indirect light. Recurrent epithelial erosions are a common finding in this disease and can lead to subepithelial opacification. Clinically, a diffuse gray stromal haze is seen with small crystals scattered throughout the haze. The clinical appearance of the dystrophy varies widely, but it typically presents during the first decade, with progressive opacification over time. The corneal crystals are small and located in the anterior stroma and subepithelial space in the peripheral cornea. The corneal crystals resemble cholesterol or other lipid deposits histologically, and the disorder may represent a systemic defect in lipid metabolism. This progressive condition usually presents in the third decade with symptoms of nyctalopia, poor dark adaptation, peripheral visual field loss, or central visual acuity loss. Systemic diseases with immunoglobulin deposition Corneal crystals have been recognized in systemic diseases that result in excessive immunoglobulin production (Fig. The crystals are seen throughout the stroma, but may be localized in the posterior stroma in some cases. Cystinosis Cystinosis is an autosomal recessive disorder that results in the accumulation of nonprotein cystine in most body tissues. A defect in lysosomal cystine transport allows cystine to accumulate within the lysosomes of the cells. Corneal manifestations are found in all three forms and consist of stromal deposition of iridescent crystals (Fig. These crystals are deposited initially in the anterior peripheral stroma and, with time, the deposition proceeds posteriorly and centrally. Deposits of crystals in the cornea can cause severe photophobia and episodes of recurrent erosions. Because of its peripheral location, gonioscopy may be required to locate the ring in its early stage. Chalcosis Ocular chalcosis refers to the deposition of copper within the eye (Fig. Ocular chrysiasis Ocular chrysiasis occurs in the setting of oral or intramuscular gold therapy for rheumatoid arthritis. The cause is unclear, but it appears to be associated with long-term contact lens wear. Nonpigmented deposits Cornea farinata Cornea farinata is a degenerative disorder characterized by multiple, tan to white, punctate opacities located in the posterior stroma (Fig. The disorder is familial, although the exact pattern of inheritance has not been established. X-linked ichthyosis X-linked ichthyosis is one of a group of hereditary skin disorders that results in hyperkeratosis and scaling of the skin. The disease is inherited in an X-linked recessive pattern, and corneal changes are found in both homozygote males and heterozygote females. They are diffusely spread over the cornea and shaped as dots, commas, or filaments. Ocular argyrosis Ocular argyrosis is the deposition of silver within the eye (Fig. The deposition occurs in the conjunctiva and cornea and is the result of the topical medication Argyrol (a silver nitrate compound rarely used anymore) or industrial exposure to silver. Recent reports of ocular argyrosis have been due to self application of eyelash tint. Almost all cases of corneal deposition are associated with a grayish discoloration of the conjunctiva. Refractile/crystalline deposits Polymorphic amyloid degeneration Polymorphic amyloid degeneration is an age-related change of the cornea that is usually bilateral and does not affect vision. In the deep corneal stroma are polygonal gray-white opacities and lines that are refractile in indirect illumination (Fig. The opacities themselves appear similar to those seen in lattice dystrophy; however, they are usually less extensive, located in the deepest level of the stroma, and are not associated with the sequelae of lattice dystrophy. These deposits are not associated with any systemic disorder of amyloid deposition. Konishi M, Yamada M, Machima Y: Corneal ulcer associated with deposits of norfloxacin. Cohen An estimated 36 million Americans are contact lens wearers, comprising nearly 10% of the United States population. Current variations in types of contact lenses, disinfection methods, and patterns of use all add to the complexity of managing corneal infiltrates in the contact lens wearer. In addition, contact lens users are subject to problems unrelated to contact lens use, such as staphylococcal hypersensitivity marginal keratitis. History A detailed history is the first important step in managing the acutely symptomatic contact lens patient. The history should include the type of contact lens worn, the pattern of lens usage, the cleaning and disinfection regimen, as well as the type and brand of cleaning solution. Breaks in standard contact lens care, such as exposure of the lenses or case to water, should be specifically sought, as this information is rarely volunteered. Any one of these pieces of information alone will certainly not make the diagnosis, but together, along with careful clinical examination, the information will guide initial diagnosis and management. Increasing pain is consistent with active infection, whereas decreasing pain after contact lens removal favors self-limited inflammation. Type of contact lens and pattern of wear It is necessary to determine whether the patient wears disposable (single use), frequent replacement (discards after a few weeks), or conventional lenses, extended or daily-wear soft contact lenses, or rigid gas-permeable lenses. Daily disposable lenses eliminate standard contact lens hazards such as improper hygiene and storage, when used correctly. Hyper-oxygen transmissible silicone hydrogel lenses were designed to reduce corneal hypoxia, hypothesized to be a major risk factor for corneal infection. However, the relative risk of microbial keratitis with silicone hydrogels was not significantly different compared to planned replacement lenses in a studies by Dart et al. Both studies demonstrated that overnight use continues to be the main risk factor for corneal infection.

An incision is made through the deep fascia near the cranial border of the triceps muscle and is continued distally over the extensor muscles erectile dysfunction drugs history buy cheap super avana 160 mg on-line. An incision is started distally in the intermuscular septum between the extensor carpi ra dialis and the common digital extensor muscles erectile dysfunction see urologist buy on line super avana. This incision continues proximally into the periostal origin of the distal half of the extensor carpi radialis muscle erectile dysfunction doctors in connecticut generic 160mg super avana overnight delivery. The extensor carpi radialis muscle is elevated from the bone and underlying joint capsule impotence nhs purchase line super avana, and the capsule is opened with a L-shaped incision discussing erectile dysfunction doctor order super avana mastercard. Small animal orthopedic and neurosurgery page 7 Medial intermuscular approach to the elbow joint Martin Bass erectile dysfunction doctor in mumbai generic 160mg super avana mastercard, Dr. The simple muscular-separating ap proach gives adequate exposure for a fragmented medial coronoid process. The skin incision starts proximal to the elbow joint and extends to proximal third of the ulna. Deep antebrachial fascia is incised on the same line as the skin and retracted to ex pose the flexor muscle group. The division of the flexor carpi radialis and deep digital flexor muscles is done by blunt dis section. The intermuscular incision can alternatively be made between the pronator teres and flexor carpi radialis muscles. Strong retraction between the muscles exposes the joint capsule, which is incised parallel to the muscles. Exposure of the medial coronoid process may require extension of the joint capsule incision parallel to the trochlear notch of the ulna, but the incision should not cross the medial col lateral ligament. Visualization of the medial coronoid process is facilitated by strong pronation and abduction of the antebrachium to open the joint on the medial side. Small animal orthopedic and neurosurgery page 8 Small animal orthopedic and neurosurgery page 9 Medial approach to the elbow joint by epicondylotomy Martin Bass, Dr. The skin incision is centered on the medial humeral epicondyle and follows the humeral shaft proximally and the shaft of the ulna distally. The subcutaneous fat and the deep an tebrachial fascia are incised on the same line. The osteotomy should include all of the origin of both the pronator teres and flexor carpi radialis muscle from the adjacent digital flexor muscles. A suitable glide and tap hole should be drilled now, just distal to the epicondyle. The incisions 1 und 2 are first made by an osteotome to a depth of approximately 5 mm, and then incision 3 is made parallel to the surface of the condyle, taking care not to include articular cartilage. The osteotomized bone with attached muscles and collateral ligaments can be retracted distally after incising the joint capsule. The ulnar ostectomy is also indicated in dogs younger than one year, where overload on the coronoid process is suspected or proven, in order to prevent further damage. The dynamization effect of the procedure is shown to persist also in dogs older than one year. In cases of dogs younger than 6 months of age, a fat graft from the falciforme ligament prevents too rapid bony union. Incision into the fascia antebrachii bertween the tendon of the lateral digital muscle (cra nial) and the lateral ulnar muscle (caudal). The tissue around the osteotomy cuts is prepared, retracted and protected with the help of two periosteal elevators or Hohmann retractors. In young dogs: A fat graft from the ligamentum falciforme is placed be tween the cut ends. Closure of the fascia with interrupted cruciate pattern, subcutaneous tissue and skin are closed with single inter rupted sutures. Hyperextension of the carpus, occuring in midsize and large breed dogs after falls and jumps, is one of the most serious injuries to the carpus. The structures responsible for maintaining the normal 10 to 12 degrees of carpal extension are the palmar ligaments and palmar carpal fibro cartilage. Surprisingly minimal signs of pain and inflammation are associated with hyperextension injuries after a few days. Some animals may be walking on their carpal pads, but others may show only 20 to 30 degrees of extension. In order to select the proper treatment, it is important to know at which joint level the injury has occured. A lateral radiograph is made with the limb stressed to maximal carpal hyperexten sion. In order to check for rupture of the collateral ligaments also valgus and varus stress radiographs are made. If there is also damage to these ligaments, most of the time it will be the medial, a bone tunnel reconstruction has also to be performed or a pancarpal arthrodesis is indicated. Partial arthrodesis involves surgical fusion of only the middle level and carpometacarpal joints. The function of the carpus remains essentially normal because there is little motion normally present in these joint levels. The antebrachiocarpal joint, which is responsible of virtually all flexion of the carpus, remains functional. The pin fixation method has better results than the dorsal plate technique and will be adressed here. The cortical slots must be long enough to allow the pin to bent as it is introduced into the medullary canal. The pins must not penetrate the proximal articular cartilage of the radiocarpal bone. Figure 5: Partial carpal arthrodesis, pin fixation method Small animal orthopedic and neurosurgery page 14 9) Deep fascia is closed to ensure that tendons and vessels are securely held in position. A caudal splint is applied until radiographic signs of fusion are noted, typically 6 to 8 weeks later. Small animal orthopedic and neurosurgery page 15 Craniodorsal Approach to the Hip Joint, Coxofemoral Luxation Katja Voss, Dr. Introduction Surgical approaches to the hip joint include the craniodorsal approach, the caudal approach, the dorsal approach via a trochanteric osteotomy and the ventral approach. The craniodorsal ap proach allows visualization of the craniodorsal aspect of the hip joint and is indicated for femo ral head and neck excision, for cranial acetabular fractures, for femoral head and neck frac tures, for installation of total hip prosthesis and for open reduction and internal fixation of coxofemoral luxations. Coxofemoral luxations are usually the result of external trauma, such as hit by car, which leads to failure of the joint capsule and the round ligament. The femoral head may dislocate in a cra niodorsal direction, the most frequent form, or in a caudodorsal or ventral direction. Closed reduction of the hip joint followed by the use of an external support like the Ehmer sling may be unsuccessful due to persisting remnants of the round ligament, the joint capsule or blood clots in the joint or due to coexisting hip dysplasia. Internal fixation is also advised in animals with concurrent injuries of another leg, which makes the application of an Ehmer sling impossible. Numerous methods have been described for internal fixation after reduction of a coxofemoral luxation. Slocum, consisting of a suture sling between the greater trochanter and the cranial aspect of the acetabulum. This sling, like the Ehmer sling, holds the hind leg in internal rotation, thus preventing reluxation in the postoperative period. The final joint stability is due to joint capsule healing and formation of periarticular fi brosis. Surgical Technique Skin incision from the level of the greater trochanter, along the cranial border of the shaft of the femur, to half of the length of the femur (Fig. The cranial gluteal artery, vein and nerve are avoided where they pass from medial to lat eral over the caudodorsal iliac spine to enter the middle gluteal muscle. Ventral reflection of the middle gluteal muscle (?roll down) permits placement of one screw through the dorsal tuber sacrale into the sacrum. Elevation of the iliacus muscle and digital palpation of the sacrum and of the ilial auricular surface helps for the reduction of the sacroiliac joint. Palpation of the promotorium of the sacrum permits op timal placement of the screw in the body of S1. This approach is pre ferred especially for simultaneous repair of coexisting iliac body fracture. It provides access through muscle separation and subperiosteal elevation rather than transection of muscle. The middle gluteal muscle can be partially or entirely elevated from all but the dorsum of the ilium and reflected dorsally. The deep gluteal muscle is ele vated to allow visualization of the fracture reduction or of placement of implants, if necessary. The superficial glu teal muscle is isolated, incised at its insertion, and re flected dorsally. If necessary, the obturator and gemellus muscles are incised at their insertion at the trochanteric fossa, are tagged and retracted caudodorsally. Inward rotation of the femur allows visualization of the craniodorsal area of the acetabulum. The superficial gluteal muscle is isolated, incised at its insertion on the third trochanter, and reflected dorsally. The osteotomy is started at the level of the third trochanter and is ex tended dorsally to the junction of the greater trochanter and the femoral neck, which is identified with the help of two mosquitos. The middle and deep gluteal muscle are reflected dorsally with the greater trochanter requiring separation of the deep gluteal from the dorsal joint cap sule. After repair of the fracture, the greater trochanter is reattached to the proximal femur with the tension band technique. This approach is recommended for minimal or non dislocated fractures of the acetabulum. The gluteal mus cles are splitted to allow visualisation of the dorsal aspect of the acetabulum. It allows exposure of the caudal aspect of the iliac body, cranial third of the acetabulum, and cranial and dorsal aspects of the femoral head and neck. Retraction of the biceps muscle caudally, the tensor fascia lata cranially and the superficial gluteal muscle caudally exposes the hip joint. It is bordered dorsally by the mid dle and deep gluteal muscle, cranially by the rectus femoris muscles and laterally by the vastus lateralis muscle. Exposure is enhanced by performing a tenotomy of the insertion of the deep glu teal muscle at the greater trochanter. It is recommended for femoral head and neck excisions and repair of femoral head fracturs in dogs and cats. The femoral artery and vein have to be protected the pectineus muscle is transected near its origin on the prepubic tendon. Retraction of the iliopsoas cranially and the adductor and the obturatorius nerve caudally exposes the acetabulum. Introduction the ventral approach to the coxofemoral joint can be used for femoral head and neck excision or for the repair of fractures of the femoral head. Femoral head and neck excision is a com monly performed salvage procedure in cats and small dogs with otherwise untreatable diseases of the hip joint, such as coxarthrosis, Legg Calve Perthes disease or complicated aceatubular and femoral head and neck fractures. After femoral head and neck excision contraction of the pectineus muscle often leads to dorsal displacement of the femur in relation to the pelvis. Per forming the head and neck excision via a ventral approach allows a prophylactic pectineomyec tomy during the same operation. Chronic pain of the hip joint leads to lame ness, associated with contracture of local muscle groups. Local palpation of the medial aspect of the joint may reveal pain on pressure over the contracted pectineus muscle. Pectinotomy and pectinectomy have been used successfully to reduce pain in patients with coxarthrosis. Contracture of the pectineus muscle leads to subluxation of the femoral head and painful stretching of the ventral joint capsule, and reduces the abduction. The tendinous part of the iliopsoas muscle is in direct contact with the ventral joint capsule. During extension of the hip joint it exerts pressure on the inflamed joint capsule of the cox arthrotic dog. The ventral part of the joint capsule is involved in generating pain in dysplastic patients. Sub luxation of the joint distends mostly the ventral joint capsule and nociceptors are concentrated in this area. The obturatorius nerve is mainly responsible for the innervation of the ventral cap sule of the hip joint. The present surgical technique for the treatment of coxarthrosis adds the iliopsoastenotomy and neurectomy of the joint capsule to the classical pectineomyectomy. The outcome is an increased hip joint extension (iliopsoastenotomy) and enhanced pain reduction (neurectomy). Indications for this technique are principally older patients with concomitant orthopedic prob lems. Small animal orthopedic and neurosurgery page 22 After skin incision, the pectineus muscle is subtotally resected while performing optimal hemostasis. During the approach, the obturatorius nerve area is retracted toward cau dally and the femoral vessels to ward cranially. The deep femoral vessels should be preserved dur ing the preparation of the origin Fig. The proximal caudal femoral vessels are retracted in a distal direction during transection of pectineus muscle, in the area of its muscu lotendinous junction (Fig. The iliopsoas muscle is then prepared proximal to its in sertion on the lesser trochanter, which is palpable on the caudal Fig. The tendon has to be re tracted with a curved instrument (Mosquito, small Hohman retrac tor) and transected on its entire width.

References

• Weinstein WM, Ippoliti AF: The diagnosis of Barrett's esophagus: Goblets, goblets, goblets (Editorial). Gastrointest Endosc 44:91, 1996.
• Rapley JH, Crates J, Barber A. Mid-substance peroneal tendon defects augmented with an acellular dermal matrix allograft. Foot Ankle Int. 2010;31(2):136-140.
• Tokuno H, Chowdhury JU, Tomita T: Inhibitory effects of propiverine on rat and guinea-pig urinary bladder muscle, Naunyn Schmiedebergs Arch Pharmacol 348:659, 1993.
• Wiviott SD, Trenk D, Frelinger AL, et al: Prasugrel compared with high loading- and maintenance-dose clopidogrel in patients with planned percutaneous coronary intervention: The Prasugrel in Comparison to Clopidogrel for Inhibition of Platelet Activation and Aggregation-Thrombolysis in Myocardial Infarction 44 trial. Circulation 2007;116:2923-2932.
• Piolatto G, Negri E, La Vecchia C, et al. An update of cancer mortality among chrysotile asbestos miners in Balangero, northern Italy. Br J Ind Med 1990;47(12):810-4.
• Kishimoto Y, Sugio K, Hung JY, et al. Allele-specific loss in chromosome 9p loci in preneoplastic lesions accompanying non-small-cell lung cancers. J Natl Cancer Inst 1995;87:1224-9.
• Pernkopf E. Anatomy, Volume I, Head and neck, 3rd ed. Baltimore: Urban & Schwarzenberg, 1989.
• Nishimura T, Faul J, Berry G, et al: Simvastatin attenuates smooth muscle neointimal proliferation and pulmonary hypertension in rats, Am J Respir Crit Care Med 166(10):1403- 1408, 2002.