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Specic lineage commitment is order nitroglycerin 2.5mg with visa, therefore nitroglycerin 2.5mg with visa, dependent on the contextual cues provided by competing signaling molecules discount nitroglycerin 2.5 mg on-line. Moreover, a limited set of interacting secreted signaling factors and a related network of intracellular signaling cascades and transcription factors can clearly drive divergent differentiation from a common cohort of stem cells. The core pluripotency network arguably emerged early in vertebrate evolution to support two main functions, to promote stem cell renewal while simultaneously suppressing differentia- tion, and appears to be largely similar from one stem cell compartment to the next. Differ- entiation, on the other hand, is likely to involve a diversity of maturation genes that adapt differentiating cells to specic tissues and organs. It is likely therefore that there is a layer of cellular regulation that adapts the common pluripotency network to cell-, tissue-, and even organism-specic differentiation. Several pieces of evidence indirectly point to an intervening regulatory layer between stem cell renewal and differentiation. Green boxes indicate core transcription factors necessary for osteoblast and adipocyte lineage specic differentiation. Secondly, the biology of stem cells is intimately associated with evolution and speciation. Similar types of stem cells in different organisms produce diverse body plans and exhibit divergent regen- erative capacities. Stem cells in amphibian [12] and mammalian species [4,5] make use of an over- lapping complement of pluripotency factors, yet amphibian, but not mammalian stem cells have the capacity to regenerate complex tissues like limbs. Finally, not only do stem cells in older organisms exhibit diminished regenerative capacities [22], but stem cells can exhibit altered patterns of lineage commitment with age; i. The question is why is there such diversity in stem cell differentiation potential from tissue type, speciation, and age? One answer to this question might lie in the existence of a new and relatively poorly understood network of regulatory mechanisms collectively termed, epigenetics. At the level of the organism, epigenetics serves to promote adaptation and is increasingly thought to be a major mechanism for speciation, and at the molecular level, a mechanism to control cellular differentiation and homeostasis. Epigenetic regulatory networks are increasingly being found to be critical facilitators of the successful 508 transformation of stem cells into tissues and organs, but may also serve the aberrant trans- formation of stem cells in cancer. A detailed and comprehensive overview of the eld of epigenetics is well beyond the scope of this chapter. Excellent recent reviews have outlined the history and basic mechanisms underlying epigenetics [24], and detailed their relevance to tissue and organism development [25,26] and to cancer mechanisms [27]. A variety of cellular mechanisms that regulate nuclear chromatin structure and control gene transcription and translation are collectively classied as epigenetic mechanisms, if these mechanisms result in relatively irreversible changes in the function of cells and tissues. Similarly, post-translational histone modications can also alter the compactness of nucleosomes to regulate gene expression. The methylation of histones, such as di- or trimethylation of histone H3 on lysine-4 (H3K4me2 and H3K4me3), result in increased activation, whereas di- and trimethylation on H3K9 and histone acetylation are associated with repression [29]. The methylation and demethylation of chromatin is an important component of the stem cell differentiation process. For example, adipose-derived mesenchymal stem cells exhibit de- methylation at Dlx5 and other osteoblast-specic transcription factors during the process of transformation into osteoblasts [30]. The dominant model for transcription at these loci is that it proceeds from the remaining active allele. Frequently, the non-silenced allele exhibits post- translational histone modications like trimethylation of lysine 4 (H3K4me3) that are known to facilitate transcription activation [31]. The human genome is predicted to contain as many as 156 imprinted genes [32], and many of these do not overlap with the cohort of imprinted genes in the mouse [33], suggesting the likelihood of shifts in imprinting with mammalian speciation. The net effect is to decrease the gene dosage in tissues and the emergence of this phenomenon with mammalian evolution is thought to be a mechanism for the control of fetal size. Paternal alleles are thought to promote, while maternal alleles are thought to constrain, fetal growth (reviewed in [34]). The implication of imprinting as an epigenetic phenomenon that regulates stem cells is enormous. Because of their capacity to control tissue growth [35],it is likely that imprinted genes play an important role in stem cell maturation [36]. The species variation in gene imprinting suggests that the epigenetic controls over stem cell renewal and maturation are likely to be species-specic. Moreover, gene imprinting may vary as a function of the state of cellular differentiation. These data suggest that the epigenetic programming of stem cells may 509 vary as a function of both species and tissue of origin, and that the replication of tissue- and species-specic epigenetic programs will be critical for the successful therapeutic manipulation of stem cells. Sequencing the human genome has shown unexpectedly that the human genome contains a surprisingly small number of protein-coding genes [40]. Clearly the protein coding gene content of animal chromosomes does not change dramatically with vertebrate and mammalian evolution. These apparently contradictory data suggest that Myc-mediated epigenetic programming is complex, but taken as a whole, prevents cell cycle arrest. Some genes that are moderately methylated during stem cell renewal, become hypomethylated, while others exhibit increased methylation. Collectively, these factors contribute to Myc-mediated epigenetic control over stem cell renewal and maintenance of pluripotency. Myc also directly binds to, and strongly represses, the transcription of Gata6, a transcription factor that promotes endoderm differen- tiation of stem cells. Other members of the pluripotency network are also subject to epigenetic regulatory programs. The human genome contains six pseudogenes for Oct3/4 and ten pseudogenes for Nanog, compared to a relative paucity of psuedogenes for other non-pluripotency-related transcription factors [64]. The Oct4 pseudo- gene family has been recently found to exert complex and mutually interdependent epigenetic regulation of the Oct4 promoter. Imprinted gene loci play an important role in tissue growth in mammals and therefore an analysis of how they control stem cell differentiation is particularly important for the thera- peutic use of stem cells. The Mest/Peg (Paternally-Expressed Gene)-1 locus is a good example of the role of epigenetics in stem cell maturation. Inter- estingly, these regions, particularly at the second CpG island also coincide with a high density of activation acetylation (H3K27Ac) and methylation (H3K4me3 and H3K4Me1) marks on histones, suggesting differential activation of maternal and paternal alleles. We previously discussed evidence, for example, that Wnt signaling directs mesenchymal stem cells towards osteoblast-specic differentiation and inhibits adipocyte differentiation. However, miR335 also acts as a direct negative regulator of Runx2, a factor required for osteogenic differentiation [73]. For example, researchers have reported the loss of X-chromosome inactivation in well-established human embryonic stem cell lines [80] suggesting that stem cells can experience epigenetic drift. This suggests that the environment can reprogram epigenetic controls over stem cell renewal and maturation. Most epigenetic changes do not lead to alterations in the primary sequence of genes and are potentially reversible. However, some epigenetic mutations do lead to genetic mosaicism in somatic stem cells, potentially leading to permanent alterations in differentiation. The retro- transposon genes, which constitute approximately 45% of the sequence of the human genome [82] are a good example of how mutations in the epigenome may produce genetic drift among somatic cells, and perhaps even among stem cells. However, epigenetic mutations may contribute to senescence of adult tissue stem cells, compromising their regenerative capacity [22]. Moreover, epigenetically driven genetic diversi- cation of somatic cells means that these cells may not be equipped to recapitulate native pluripotency states of embryonic stem cells derived from the blastocyst. The authors were able to show vascularization, osteogenesis, and successful functional engraftment of the engineered mandible into a patient. A clearer understanding of the epigenetic landscape of the stem cell during renewal and through successive stages of maturation will be a critical requirement for the development of effective stem cell therapy. A reserve stem cell population in small intestine renders Lgr5-positive cells dispensable. Reprogramming with dened factors: from induced pluripotency to induced transdifferentiation. Sprouty1 Regulates Neural and Endothelial Differentiation of Mouse Embryonic Stem Cells. Induction of chondro-, osteo- and adipogenesis in embryonic stem cells by bone morphogenetic protein-2: effect of cofactors on differentiating lineages. Downregulation of Dlx5 and Dlx6 expression by Hand2 is essential for initiation of tongue morphogenesis. Comparison of human stem cells derived from various mesenchymal tissues: superiority of synovium as a cell source.

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The role of Lrp5/beta-catenin activation in cardiovascular calcification and osteoblast bone formation: Connection with the bone axis Bone and cartilage are major tissues in the vertebrate skeletal system 6.5 mg nitroglycerin fast delivery, which is primarily composed of three cell types: osteoblasts order nitroglycerin 2.5 mg amex, chrondrocytes generic nitroglycerin 6.5mg mastercard, and osteoclasts. In the developing embryo, osteoblast and chrondrocytes, both differentiate from common mesenchymal pro genitors in situ, where as osteoclasts are of hematopoietic origin and brought in later by in vading blood vessels. Osteoblast differentiation and maturation lead to bone formation controlled by two distinct mechanisms: intramembranous and endochondral ossification, both starting from mesenchymal condensations. The transcription factor Cbfa1 [51] has all the attributes of a master gene differ entiation factor for the osteoblast lineage and bone matrix gene expression. During embryonic development, Cbfa1 expression precedes osteoblast differentiation and is restrict ed to mesenchymal cells destined to become osteoblast. In addition to its critical role in os teoblast commitment and differentiation, Cbfa1 appears to control osteoblast activity, i. We have shown previously that cholesterol upregulates Cbfa1 gene expression in the aortic valve and atorvastatin decreases the gene expression [6] in an animal model. We have also demonstrated that Sox9 and Cbfa1 are expressed in human degenerative valves removed at the time of surgical valve replace ment [16]. The regulatory mechanism of osteoblast differentiation from osteoblast progeni tor cells into terminally differentiated cells is via a well orchestrated and well studied pathway which involves initial cellular proliferation events and then synthesis of bone ma trix proteins, which requires the actions of specific paracrine/hormonal factors and the acti vation of the canonical Wntpathway [52]. This data supports a potential regulatory mechanism that these matrix proteins play a critical role in the development of biomineralization. To date, many of these markers have been shown to be critical in the extracellular mineralization and bone formation that develops in 268 Oxidative Stress and Chronic Degenerative Diseases - A Role for Antioxidants normal osteoblast differentiation (Fig. Rajamannan have extensive experience in osteoblast cell biology and will contribute to the translational studies in the aortic valve involving the differentiation and mineralization [53, 54]. These groups have shown in in vitro and in vivo studies that lipids decrease bone formation and increase vascular calcification. This studied correlated the-/- important understanding of chronic kidney disease with decreased bone formation rates and increase in vascular calcification. This study demonstrates that accelerated vascular cal cification found in patients with end stage renal disease may be related to multifactorial mechanisms including traditional atherosclerotic risk factors and elevated serum phosphate levels. Giachelli has also studied extensively the hypothesis of a sodium phosphate abnor mality in the vascular smooth muscle cell [61]. Her group has also shown that osteopontin expression by vascular smooth muscle cells may have an inhibitory effect in the develop ment of calcification [62] which further defines the complexity of the matrix synthesis phase of bone formation. Demers laboratory has also studied extensively the correlation of lipids with vascular calcification and osteoporosis via inhibition of Cbfa1 in osteoblast cells [60, 63]. This paradoxical finding between the calcifying vascular aorta and osteoporosis is an important link in the hypercholesterolemia hypothesis. The development of cardiovascular calcification is a multifactorial process which includes a number of mechanisms. Studies in the different laboratories provide important evidence towards the development of therapies depending on the patient population i. Our lab (43) and Towlers laboratory (44) have shown that the Lrp5/Wnt/beta-catenin path way plays an important role in the development of vascular and valvular calcification. To determine a potential signaling pathway for the development of aortic valve disease there are numerous pathways which may be implicated in this disease process [50, 74, 75]. Recent evidence suggests that the Wnt pathway regulates the expression of bone mineral markers in cells responsive to the Wnt pathway. This background outlines the potential for lipids in the regulation of aortic valve mineralization via the canonical Wnt pathway. It is the test of choice to quantify the severity of valve stenosis and pressure differential across the aortic valve. There are a increasing number of studies which have demonstrated the utility of calculating the volume of calci um and the rate of progression of the disease process in the aortic valve [76-80]. Confir mation of hemodynamic valve stenosis by echo will provide the degree of valve stenosis using ultrasound techniques. Development of future medical therapies for calcific aortic stenosis The natural history studies of valvular aortic stenosis as defined by clinical and histopatho logic parameters have provided landmark developments towards the understanding of this disease. There are a number of experimental models which demon strate the potential for treating the vasculature with statins to inhibit matrix formation [24, 25], cellular proliferation [6] and vascular aneurysm formation [82]. Although valve replace ment is the current treatment of choice for severe critical aortic stenosis, future insights into the mechanisms of calcification and its progression may indicate a role for lipid lowering therapy in modifying the rate of progression of stenosis. There are a growing number of retrospective studies demonstrating that statins may have benefits in slowing the progression of aortic stenosis [83-85]. A recent clinical trial by Cowell et al, demonstrated that high dose atorvastatin did not slow the progression of aortic steno sis in patients [86]. However, the timing of the initiation of the statin therapy was at a later stage of aortic valve disease. The studies planned in this application should lead to an important understanding of the molecular and cellular mechanisms of aortic valve disease. With the decline of acute rheu matic fever, calcific aortic stenosis has become the most common indication for surgical valve replacement. Despite the high prevalence of aortic stenosis, few studies have investi gated the mechanisms responsible for aortic valve disease. Previously, we and others have demonstrat ed that aortic valve calcification is associated with an osteoblast bone-like phenotype [14, 15]. This bone phenotype is regulated by the canonical Wnt pathway in experimental cardio vascular calcification [5, 17]. We have alsoshown that the canonical Wnt/Lrp5 pathway is upregulated in diseased human valves from patients with valvular heart disease [16]. These studies implicate that inhibition of the canonical Wnt pathway provides a therapeutic ap proach for the treatment of degenerative valvular heart diseases. A recent study [88], discov ered that a loss of function mutation in Notch1 was associated with accelerated aortic valve calcification and a number of congenital heart abnormalities. This Notch1 splicing may be the regulatory switch important for the activation of the Wnt pathway and downstream calcification in these diseased valves [5, 17, 90]. The elucidation of these risk factors have provided the experimental basis for hypercholesterolemia as a method to induce aortic valve disease [4-8. Echocardiography hemodynamics was also performed to determine the timing of stenosis in bicuspid vs. Histology of the aortic valves from human bicuspid calcified valves compared to normal aortic valves re moved at the time of surgical valve replacement; Panel A. Bicuspid Aortic Valve Removed from patient at the time of surgical valve replacement. Cholesterol diets increased the members of the canonical Wnt pathway and Atorvastatin diminished these markers significantly (p<0. The importance of cell- cell communication within a stem cell niche is necessary for the development of valvular heart disease. The two corollaries necessary for an adult stem cell niche is to first define the physical architecture of the stem-cell niche and second is to define the gradient of prolifera tion to differentiation within the stem-cell niche. These cells interact with the subendothelial cells that are resident below the endothelial layer of cells. In the aortic valve the com munication for the stem cell niche would be between the aortic valve endothelial cell and the adjacent myofibroblast cell located below the aortic lining endothelial cell. Conditioned media was produced from untreated aortic valve endothelial cells for the microenvironment that activates signaling in the myofibroblast cell. A mitogenic protein (Wnt3a) was isolated from the conditioned media and then tested directly on the responding mesenchymal cell, the cardiac valve myofibroblast [93, 96,95]. This transfer of isolated protein to the adjacent cell was necessary to determine if the cell would proliferate directly in the presence of this protein. This system is appealing because the responding mesenchymal cell is isolated from the anatomic region adjacent and immediately below that of the endothelial cells producing the growth factor activity along the fibrosa surface. Very little is known regarding the char acterization of the endothelial cell conditioned media. These experiments test the corollary that the physical architecture described above is necessary for disease development in the aortic valve.

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This method classifies wounds according to the likelihood or rate of wound infection buy 6.5mg nitroglycerin with amex. Clean-contaminated: Minor break in technique purchase nitroglycerin 6.5mg with visa, oropharynx entered discount nitroglycerin 2.5 mg otc, gastrointestinal or respiratory tracts entered without significant spillage, genitourinary or biliary tracts entered in absence of infected urine or bile. If other serious conditions exist, which endanger the patients life, the wound should be covered with sterile gauze and priorities attended to. However, the goal in all cases is to establish a good environment to assist wound healing and prevent infection. Proper wound care includes the following measures: Adequate hemostasis locally to stop bleeding. It provides a reliable drainage and opportunity for repeated inspection and debridement as necessary. There is no specific management needed except local compress and analgesics if pain is severe. Management: - It usually gets absorbed spontaneously and should be left - Local compress to alleviate pain - Aseptic evacuation or aspiration only if very large (expanding) or over a cosmetic area or leading to compression of vital structures. Management: - Cleanse using scrubbing brushes - Use antiseptic or lean tap water and soap - Analgesic Punctures These may be compound wounds which involve deeper structures. Management: - Careful inspection - Adequate cleansing - Closure, if feasible, under appropriate anesthesia - Proper wound debridement if needed - Appropriate antibiotic prophylaxis - Tetanus Prophylaxis - Analgesics as needed Crush and avulsion wounds These are compound complicated wounds. They are usually associated with systemic involvement and have more extensive damage than may appear. Management: - Correct associated life threatening conditions - Proper wound debridement - Early skin cover if possible or late graft, wound left open if contaminated - Appropriate antibiotics - Tetanus Prophylaxis - Analgesics as needed Missile injuries These are type of wounds which are compound and complicated. They usually present with severe life threatening conditions and should be carefully managed. Human bites These are relatively rare but more heavily contaminated than those of most animalss due to polymicrobial nature including anaerobic organisms as a normal oral flora. To avoid this complication the animal must be kept for observation for at least 10 days. Management should include: First aid measures: - Local wound irrigation - Apply pressure bandage proximally to avoid or reduce venom spread with caution on the blood supply - Immobilize the limb to minimize venom absorption - Transport patient immediately to nearby hospital Hospital Measures: - Identify the species - Conduct necessary laboratory investigations like hemoglobin, renal function... Local: Local complications may manifest as one or more of the following conditions- - Hematoma - Seroma 55 - Infection - Dehiscence - Granuloma formation - Scar formation - Contracture leading to loss of joint function etc Systemic: - Death may occur if un controlled sepsis or hemorrhage - Systemic manifestations of hemorrhagic shock due to massive bleeding - Bacteremia and sepsis from a source of locally infected wound 56 Review Questions 1. A) Duration of injury B) The circumstance of wounding C) The mechanism of injury D) Local appearance of the wound E) All of the above 2. A) Bullet wound of one hour duration B) Human bite of 30 minutes duration C) Glass laceration of five hours duration D) Crush injury of the leg following car accident E) None of the above 3. A proper wound care includes all measures except A) Removing all devitalized tissue B) Removing foreign bodies impregnated to the wound C) Wound inspection following primary management D) Inadequate hemostasis of a bleeding artery E) Decision to close a wound primarily 4. A) Forearm laceration from a knife B) Dog bite to the calf of one hour duration C) Blast wound to the thigh of two hours duration D) Stick wound to the scalp of four hours E) B and C are correct 5. In a contaminated wound left open to heal without closure, healing is effected by A) First intention B) Second intention C) Third intention D) Purely by epithelialization E) All of the above 7. A) Presence of foreign body B) Systemic illness C) Sex of the patient D) Poor patient nutritional state E) Presence of infection 58 Key to the Review Questions 1. It can be defined broadly as an infection related to or complicating a surgical therapy and requiring surgical management. Many infections occupy a non-vascularized space of tissue, thus are likely to respond to non-surgical treatments. These types of infection therefore definitely require surgery as a primary or definitive therapeutic approach. On the other hand, any infection that is related to surgical therapy but that may not definitely require surgery is also categorized as a surgical infection. Examples: - Urinary tract infections after catheterization for surgical purpose - Pulmonary complications following intubation for surgery - Tracheotomy site infection All wounds that follow operative procedure or incision are also grouped as surgical infections. According to temporal relation to surgery, surgical infections are grouped into three types. Ante/pre operative infections: These infections happen before a surgical procedure. Example: - Accidents - Appendicitis - Boils - Carbuncle - Pyomyositis Operative infections: These are types of surgical infections that happen during a surgical procedure. It can occur either due to contamination of the site or poor tissue handling technique. These include: - An infectious agent - A susceptible host - Favorable external factors or local condition with closed, less or non-per fused space. An infection becomes overt only when the equilibrium between the bacterial and host factors becomes disturbed. The common organisms in decreasing order are:- 1- Aerobic bacteria - Staphylococcus aureus - Streptococci - Klebsiella - E. Host Susceptibility: Reduced immune host defense predisposes to surgical infections. Local and external factors: Closed spaces, usually with poor vascularization, are areas susceptible to infection. Favorable situations under such condition contributing to infection include:- - Poor perfusion of blood and oxygen - Presence of dead tissue 63 - Presence of foreign bodies - Closure under tension etc. External factors like a break in the sterility technique also contribute to the development of surgical infection. Post-Operative Wound Infection This is contamination of a surgical wound during or after a surgical procedure. Source of infection: The source of contamination in more than 80% cases is the patient (endogenous). In about 20% of cases, the source is from the environment, operating staff or unsterile surgical equipment (exogenous). It contains necrotic tissue and suppuration from damage by the bacteria, and white blood cells. It is surrounded by area of inflamed tissue due to the bodys response to limit the infection. Clinical features: Patients with an abscess anywhere in the body may present with the following findings. It usually involves the extremities and identifiable portal of entry is detectable. Etiology: The most common etiologic organisms are - Beta hemolytic streptococci - Staphylococci - Clostridium perfringens Clinical Features: There is usually an identifiable portal of entry which can be a surgical wound, puncture site, skin ulcer or dermatitis. Clinical Pictures: - Series of small intra epithelial abscesses, multiple - Bullous lesions - Skin erosion and - Crust formation. Poor hygiene, immune suppressive diseases and irritation are known contributing factors. Clinical feature: - There is an intense local irritation of acute onset - Painful firm, reddish, round swelling initially, which later becomes fluctuant - Suppuration and central necrosis occurs later - The condition subsides and is self-limited to recur in multiple lesions (chronicity) Treatment: It may subside spontaneously without suppuration (Blind boil) Incision /Excision if complicated Antibiotics Carbuncle Carbuncle is an infective gangrene of subcutaneous tissue which commonly occurs in patients with diabetes and other immune suppressive conditions. Clinical Feature: Formed by multiple furuncles Pain Erythema Induration Progressive suppuration of thick pus Tissue loss with shallow and deep ulcer surrounded by smaller areas of necrosis 67 Treatment: Adequate systemic antibiotics in early stages Aggressive debridement Local wound care Detect and treat predisposing factors like diabetes mellitus Pyomyositis Pyomyositis is an acute bacterial infection of skeletal muscles with accumulation of pus in the intra-muscular area. It usually occurs in the lower limbs and trunk spontaneously or following penetrating wounds, vascular insufficiency, trauma or injection. Poor nutrition, immune deficiency, hot climate and intense muscle activity are highly associated factors. Clinical Features: It usually has sub-acute onset and can present with Localized muscle pain and swelling, late tenderness Induration, erythema and heat Muscle necrosis due to pressure Fever and other systemic manifestations later after some days Treatment: Immediate intravenous antibiotics before surgery Surgical drainage of all abscess Excision of all necrotic muscles Supportive care Madura Foot This is a chronic granulomatous disease commonly affecting the foot with extensive granulation tissue formation and bone destruction. The disease is common in the tropics and occurs through a prick in barefoot walkers in 90% of cases. Etiology: The causative microorganisms for this infection are various fungi or actinomycetes found in road dust. Treatment: Sulphonamides and Dapson (prolonged course) Broad spectrum antibiotics for secondary infection Amputation if severe and disfiguring infection Necrotizing fasciitis This is an acute invasive infection of the subcutaneous tissue and fascia characterized by vascular thrombosis, which leads to tissue necrosis. It is idiopathic in origin but minor wounds, ulcers and surgical wounds are believed to be initiating factors.

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If necessary buy 2.5mg nitroglycerin visa, you can also use a medical assistant to test the visual acuity and examine the book or newspaper discount nitroglycerin 6.5mg with amex. A locally available torch is adequate: it can be easily you should be able to darken it 6.5mg nitroglycerin overnight delivery. This instrument is not subsequent visit; and record your results, so that you will much seen nowadays, but is still very useful. Stand him 6m from the slit lamp useful, although you can diagnose uveitis without one. If necessary, you can use any helpful to get him to point with fingers in the direction of fine scissors. Use special fine If you shine a torch into each of the 4 quadrants of the instruments listed above. For operations on the globe an operating visual field, can he tell you where it is coming from? For repeated use, attach the card to the insides of each lens of a Look for pus or mucopus in the inferior fornix. If there is This is present in all cases of bacterial conjunctivitis, and an uncorrected refractive error, the vision will be significantly improved to 6/9 or 6/12. Is it shining and clear, reflecting the light of a torch, or its surface irregular? Is there clouding superiorly (trachoma, of the position of the eyes, or any protrusion (best judged 28. Ask the patient to look down and keep looking down, but not to actively close the eyes. Put the tips of both your If you suspect the surface is injured or ulcerated, index fingers on one of the globes, so as to feel the sclera instil 1 drop of 2% fluorescein, or dip the end of a through the upper lid above the upper border of the tarsal fluorescein impregnated filter paper inside the lower lid plate. Mop out the excess fluorescein with Gently press with alternate finger tips towards the centre tissue paper. Then ask the patient to look up, pupils with a mydriatic such as cyclopentolate 1%, grasp the bottom lid, and slip the lower blade of the or do your examination in a dark room. Adjust the arm of the speculum until This is however ineffective where the vitreous or cornea is the eye is exposed, and then tighten the locking nut. Use your right hand and your right eye for the that the lashes are in their normal position. Hold the sight hole of the ophthalmoscope close to junction, this occurs in iritis and corneal ulcer. If it is your eye, resting it against your nose and orbit, and move maximal at the periphery but often extending all over, it is it with you as if it was attached to your head. Ask him to open both eyes, and look straight up at a gently raise the upper lid clear of the pupil. Start with the ophthalmoscope 20cm from the eye, With the 55g weight in place, put the tonometer plunger gently on the and shine the light into the pupil; it should glow centre of the cornea with the eye open, and read the scale. Ask the patient to look straight ahead, and move as close as you can to the eye without touching the eyelashes or cornea. Find and look at the optic disc: it is 15 to the nasal side of the optical axis of the eye. This allows good examination of the anterior & posterior segments at much less cost than a slit lamp: It is also portable (28-5). After Chaudhury A, Chugh A, Role of Indirect Ophthalmoscopy in Rural Settings, Rural Surgery 2009;5(3):19-20. It is not hindered, as is the standard ophthalmoscope by a hazy media or scleral or central opacification. With the addition of a +20dioptre condensing lens, by varying the illumination and viewing angle, you can readily look at both the anterior and posterior segments. Examine layer by layer: lid margin conjunctiva cornea anterior chamber lens vitreous. The scale is merely an example; use the scale which is supplied with Note its size and shape after instilling fluorescein and your instrument. If you happen to find one, clean the instrument with a pipe cleaner and Lens: diffuse opacity, discolouration? Using the standard 55g weight and the metal footpad, make sure the Vitreous: Particles from a recent posterior uveitis, instrument is calibrated to zero. The former are for longer-lasting effect, the latter for immediate and, usually, short-lasting effect. Some drugs are toxic to the eye through systemic use: these include chloroquine and ethambutol. Others are locally toxic, such as penicillin, or dangerous if used for the wrong condition, such as steroids if used when there is a herpetic corneal ulcer present. Certain drugs are specifically used to help examination: cyclopentolate 1%, or phenylephrine 10%, will dilate the pupil for some hours only, so use these when you want a temporary effect for example when using an ophthalmoscope. Remember that an anaesthetized eye is in great ganger if an unnoticed foreign body gets into it, or that an abrasion injury is not felt; so shield it (28-8B) after appropriate examination. Particles in the aqueous and vitreous reflect light, like dust particles illuminated by a sunbeam in a darkened room. To use eye drops, pull the lower eyelid down so that you C, you may be able to see keratic particles directly with bright light. Use this for accurate Close the eye for 2mins to allow the drug to enter the visualization of the anterior part of the eye and its eye. Screw the caps on loosely, and sterilize them in a hot water bath or autoclave at 100C for 30mins, without letting water splash over the necks of the bottles. Refrigerate them; their If the infection is getting worse, repeat the injection the shelf-life is 2months at 2-8C. A severely infected eye is likely to improve, 4months, so this is a useful method. Prepare the face from the hairline to the chin and from ear to ear, using iodine 10% in a non-alcoholic lotion which will not harm the eyes, if it spills on them accidentally. Place another drape across the forehead over the eyebrows, and clip this to the first one. If the patient is intubated, place a third drape over the nose and the mount, which connects the patients endotracheal tube. Sit your assistant on your left for a right eye, and on your right for a left eye. This means you need to have trained your assistant to hand you the right instruments properly. E, subconjunctival injection is an effective way of simply to hold the lids away from the eye while you getting a high concentration of an antibiotic inside the eye. G, stay sutures in place: 2 for the upper and which may press on the eye, and perhaps scratch the 1 for the lower lid. Pull down the lower sutures, just above the lash line and down to the tarsal lid, with your finger on the cheek. In the lower lid insert one suture just below the lash needle on a 2ml syringe (28-8E). Rest the needle flat on the conjunctival surface of the globe, with the bevel facing away from it. Push the needle under the conjunctiva, parallel to the surface of the globe, rotating it gently as you do so. The problem in a busy clinic is that conjunctivitis is so If the conjunctiva or sclera bleed, apply a pad and very much more common that these other causes are easily gentle pressure. So your first task in managing red eyes is to make syringe and an irrigating needle. Touch the bleeding point with this, through the stream of Conjunctivitis can be infectious, allergic, or chemical. This will cool its tip enough to prevent burning, Bacterial conjunctivitis is common (especially from but will leave it hot enough to seal the bleeding vessel. The great danger of an eyepad is that it may rub against an anaesthetized eye, and cause an A corneal ulcer may be due to: abrasion. Shielding it (28-8B) allows it to open and close, without Bacterial infection can follow even a minor injury which anything extraneous touching the cornea, and perhaps damages the epithelium, or it can be spontaneous. A shield is the safest way to protect an Bacteria enter the eye through the anterior chamber. Cut a radius in this, fold it into a cone, Endophthalmitis may be the result of: and maintain the cone with a piece of strapping. Hold the cone in place with two pieces of adhesive (2) a perforating injury of the cornea or sclera, especially strapping, or plastic tape from the forehead to the cheek.

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