Hordeolum (1)

Def: A hordeolum is a common disorder of the eyelid.[1] It is an acute focal infection (usually staphylococcal) involving either the glands of Zeis (external hordeola, or styes) or, less frequently, the meibomian glands (internal hordeola).[2] Pathophysiology There is usually underlying meibomitis with thickening and stasis of gland secretions with resultant inspissation of the Zeis or meibomian gland orifices. Stasis of the secretions leads to secondary infection, usually byStaphylococcus aureus.[3] Histologically, hordeola represent focal collections of polymorphonuclear leukocytes and necrotic debris (ie, an abscess). Hordeola should not be confused with chalazia, which represent focal, chronic, lipogranulomatous inflammation of the Zeis or meibomian glands.[4]Chalazia form when underlying meibomitis results in stasis of gland secretions, and the contents of the glands (sebum) are released into the tarsus and adjacent tissues to incite a noninfectious inflammatory reaction. Histologically, chalazia appear as a granulomatous reaction (ie, histiocytes, multinucleated giant cells) surrounding clear spaces that were once occupied by sebum/lipid before they were dissolved by the solvents used for tissue processing, hence the term lipogranuloma. Essentially, a hordeolum represents an acute focal infectious process, while a chalazion represents a chronic, noninfectious granulomatous reaction. However, chalazia often evolve from internal hordeola.[5] History

edema is present, then it may be difficult to palpate a discrete nodule. These nodules may be unilateral or bilateral, single or multiple. The inflammation associated with hordeola may spread to adjacent tissue and cause a secondary preseptal cellulitis. Patients may also have signs of meibomitis, blepharitis, or ocular rosacea.[6 Differentials

Basal Cell Carcinoma, Eyelid Cellulitis, Preseptal Chalazion Sebaceous Gland Carcinoma Squamous Cell Carcinoma, Eyelid Laboratory Studies

The diagnosis is based on history and clinical examination, and cultures are not indicated in uncomplicated cases. There is no indication to check serum lipid levels, as the association among hordeola, chalazia, and hypercholesterolemia remains unclear Histologic Findings Histopathology of a hordeolum reveals an abscess or a focal collection of polymorphonuclear leukocytes and necrotic tissue. Histologically, chalazia represent a lipogranulomatous inflammatory reaction. Histiocytes, multinucleated giant cells, lymphocytes, plasma cells, and neutrophils surround an optically clear space. This optically clear space represents lipids that were dissolved by solvents during tissue processing. Basal cell carcinoma or sebaceous cell carcinoma of the eyelid can be misdiagnosed clinically as a recurrent hordeolum or chalazion; therefore, histopathologic examination is very important in determining the diagnosis, especially in patients with a persistent or recurrent lesion.[8] Medical Care Hordeola are usually self-limited, spontaneously improving in 1-2 weeks. Medical therapy for hordeola includes eyelid hygiene, warm compresses and massages of the lesions for 10 minutes 4 times per day, and topical antibiotic ointment in the inferior fornix if the lesion is draining or if there is an accompanying blepharoconjunctivitis. Systemic antibiotics may be indicated if the hordeola is complicated by preseptal cellulitis. Oral doxycycline may also be added if there is a history of multiple or recurrent lesions or if there is significant and chronic meibomitis. Internal hordeola may occasionally evolve into chalazia, which may require topical steroids, intralesional steroids, or surgical incision and curettage. Surgical Care Incision and drainage is indicated if the hordeolum is large or if it is refractory to medical therapy. Incision and drainage is done under local anesthesia, and the incision is made through the skin and orbicularis (in the case of external hordeola) or through the tarsal

Hordeola essentially represent focal abscesses; therefore, they will present with features of acute inflammation, such as a painful, warm, swollen, red lump on the eyelid. The eyelid lump may also induce corneal astigmatism and cause blurring of vision. The patient often has a past history of similar eyelid lesions or risk factors for hordeola, such as meibomian gland dysfunction, blepharitis, or rosacea.[6] Clinically differentiating hordeola from acute chalazia may be difficult, because they both present with acute inflammation and tender eyelid lumps. However, chronic chalazia represent a granulomatous reaction and, thus, appear firm and nontender on clinical examination Causes Hordeola are associated with S aureus infection.[3] Patients with chronic blepharitis, meibomian gland dysfunction, and ocular rosacea are at greater risk of developing hordeola than the general population.[6] There are published case reports where multiple recurrent hordeola have been associated with selective immunoglobulin M (IgM) deficiency.[7]The lipid component of chalazia has been found to have large cholesterol content and is dissimilar to the lipid found in meibomian glands. Studies have reported an association between multiple chalazia and elevated serum cholesterol levels. Some studies have even suggested that elevated serum lipid levels may increase the risk of blockage to oil glands of the eyelids and, therefore, predispose to hordeola and chalazia. On examination, a tender erythematous subcutaneous nodule is present near the eyelid margin, which may undergo spontaneous rupture and drainage. If sufficient

conjunctiva and tarsus (in the case of internal hordeola). The specimen should be sent for histopathological evaluation to confirm the diagnosis and to rule out a more sinister pathology (eg, basal cell carcinoma). Medication Summary The goals of pharmacotherapy are to treat the infection, to reduce morbidity, and to prevent complications. Antibiotics Class Summary A course of oral antibiotics is indicated if the hordeolum is complicated by preseptal cellulitis. First-generation cephalosporin often used in skin or skin structure infections (eg, acute hordeolum) caused by staphylococci or streptococci. Administered orally and has a half-life of 50-80 min. Only 10% is protein bound and greater than 90% recovered unchanged in urine. Erythromycin base (E-Mycin) Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNAdependent protein synthesis to arrest. Indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections. Further Outpatient Care Patients should be followed within 2-4 weeks of institution of medical therapy to assess response to therapy and need for surgical incision and curettage Deterrence/Prevention Try to prevent recurrences by minimizing or eliminating risk factors, such as blepharitis and meibomian gland dysfunction, through daily lid hygiene and warm compresses. Complications Large lesions of the upper eyelid have been reported to cause decreased vision secondary to induced astigmatism or hyperopia resulting from central corneal flattening. Prognosis Hordeola are usually self-limited and spontaneously resolve within 1-2 weeks. The resolution is hastened with the use of warm compresses and lid hygiene. Internal hordeola may occasionally evolve into chalazia, which may require topical or intralesional steroids or even incision and curettage.[9] Patient Education For excellent patient education resources, visit eMedicine's Eye and Vision Center. Also, see eMedicine's patient education articles Chalazion (Lump in Eyelid) and Sty.

Chalazion
Background A chalazion (Greek for hailstone) is a lipogranuloma of either a meibomian gland or a Zeis gland. When the former is involved, the lid nodule is a characteristically hard and painless lid nodule; if the latter is involved, it is marginal or superficial. Examples of a chalazion are shown in the images below. Pathophysiology Lipid breakdown products, possibly from bacterial enzymes (as free fatty acids) or from retained sebaceous secretions, leak into the surrounding tissue and incite a granulomatous inflammatory response. The resulting mass of granulation tissue and chronic inflammation (with lymphocytes and lipid-laden macrophages) distinguishes a chalazion from an internal or external hordeolum, which is primarily an acute pyogenic inflammation with polymorphonuclear leucocytes and necrosis with pustule formation. However, one condition can result in the other because of their close proximity. Upon clinical examination, the single, nontender, firm nodule (or, in rare cases, multiple nodules) is located deep within the lid or the tarsal plate, whereas a hordeolum is more superficial and is typically centered on an eyelash. Eversion of the lid may reveal the dilated meibomian gland and chronic inspissation of adjoining glands. With judicious pressure on the lid, the thick secretions can be seen extruding like toothpaste, resulting in tear debris. Epidemiology Frequency United States Chalazia are common, but the exact incidence or prevalence is unknown. International No data about the prevalence or incidence are available. Mortality/Morbidity Acute inflammatory exacerbation can result in a rupture anteriorly (through the skin) or posteriorly (through the conjunctiva), forming a granuloma pyogenicum. Race No information about prevalence or incidence with respect to race is available. Sex Male and females seem equally affected, but precise information about prevalence and incidence is not available. Contrary to popular opinion, research has not shown that the use of eyelid cosmetic products either causes or aggravates the condition. Age Chalazia occur in all age groups. Chalazia are more common in adults than in children, as androgenic hormones increase sebum viscosity. Although they are uncommon at extremes of age, pediatric cases may be encountered. Hormonal influences on sebaceous secretion and viscosity may explain clustering at the time of puberty and during pregnancy. However, the large number of patients without evidence of hormonal alteration suggests that other mechanisms also apply.

History Patients with chalazia usually present with a short history of recent lid discomfort, followed by acute inflammation (eg, redness, tenderness, swelling). They frequently have a long history of previous similar occurrences, because chalazia tend to recur in predisposed individuals. Physical Chalazia are more common on the upper lid than on the lower lid because of the increased number and length of meibomian glands present on the upper lid. Chronic inspissation of the meibomian secretions may be apparent as meibomian gland dysfunction. This condition is characterized by pressure on the eyelids that produces copious toothpaste-like secretions instead of the normal small amount of clear, oily secretion. Sebaceous dysfunction and obstruction elsewhere (eg, comedones, oily face) are the only associated features or specific general findings. Rosacea is a frequent associated finding. When present, rosacea demonstrates very specific findings, such as facial erythema; telangiectatic and spider nevi on the malar, nasal, and lid skin; and rhinophyma. Causes Chalazia may arise spontaneously due to blockage of a gland orifice or due to an internal hordeolum. Chalazia are associated with seborrhea, chronic blepharitis, and acne rosacea. Poor lid hygiene is occasionally associated with chalazia, although its causal role needs to be established. Although stress is often apparently associated with chalazia, it has not been proven as a cause, and the mechanism by which stress acts is unknown. Differential Dx Actinomycosis Basal Cell Carcinoma, Eyelid Blepharitis, Adult Cellulitis, Orbital Cellulitis, Preseptal Conjunctivitis, Bacterial Contact Lens Complications Dacryoadenitis Dacryocystitis Demodicosis Dermatitis, Atopic Dermatitis, Contact Dermatochalasis Dermoid, Orbital Distichiasis Floppy Eyelid Syndrome Hemangioma, Capillary Hemangioma, Cavernous Herpes Simplex Herpes Zoster Hordeolum Juvenile Xanthogranuloma Kaposi Sarcoma Lacrimal Gland Tumors Melanoma, Conjunctival Molluscum Contagiosum Nasolacrimal Duct, Congenital Anomalies Nasolacrimal Duct, Obstruction Neurofibromatosis-1 Ocular Manifestations of HIV Papilloma, Eyelid Pigmented Lesions of the Eyelid Psoriasis Ptosis, Adult

Red Eye Evaluation Sarcoidosis Sebaceous Gland Carcinoma Spider Bites Squamous Cell Carcinoma, Conjunctival Squamous Cell Carcinoma, Eyelid Sturge-Weber Syndrome Trichiasis Tuberculosis Tumors, Orbital Xanthelasma Laboratory Studies Clinical findings and responses to therapy in patients with chalazia are usually specific. The material obtained from a chalazion shows a mixture of acute and chronic inflammatory cells, as well as large, lipid-filled, foreign body-type giant cells. Lipid analysis may reveal fatty acids with long carbon chains resulting in an increased melting point. This finding possibly accounts for the blockage of secretions. Bacterial culture findings are usually negative. However, Staphylococcus aureus, Staphylococcus albus, or other cutaneous commensal organisms can be isolated. Propionibacterium acnes may be present in the glandular contents. Imaging Studies Infrared photographic imaging of the meibomian glands can demonstrate abnormally dilated and inspissated secretions, which are visible on the tarsal surface of the everted lid. Other Tests Pressure directly over the tarsal plate of the lid results in the extrusion of lipids, especially of thick viscous material with meibomian gland dysfunction Histologic Findings Histology reveals a chronic granulomatous reaction with numerous lipid-filled, Touton-type giant cells. Typically, the nuclei of these cells are arranged around the periphery of a central foamy cytoplasmic area that contains the ingested lipid material. Other typical mononuclear cells (eg, lymphocytes, macrophages) also may occur around the periphery. In the event of secondary bacterial infection, an acute necrotic reaction with polymorphonuclear cells may ensue. Destruction of the fibrocartilage of the tarsal plate may be evident. Foreign bodies (eg, embedded polymethyl methacrylate [PMMA] contact lenses) in the tarsal plate have been encountered in chronic chalazia. Medical Care Small, inconspicuous, asymptomatic chalazia may be ignored. Conservative treatment with lid massage, moist heat, and topical mild steroid drops usually suffices.[1] Acute therapy with oral tetracycline (eg, doxycycline 100 mg or minocycline 50 mg every day for 10 d) minimizes the infectious component and decreases the inflammation, reputedly by inhibiting polymorph degranulation. Chronic therapy with low-dose tetracycline (eg, doxycycline 100 mg orally every week for 6 mo) frequently prevents recurrence. If tetracycline cannot be used, then metronidazole has been used in a similar fashion. In most cases, surgery should be performed only after a few weeks of medical therapy.

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Local anesthesia may be beneficial to facilitate a thorough massage. A wet facecloth, as hot as can be tolerated, can be applied twice daily to promote drainage by melting the lipid secretions. A self-administered technique called the "4 fingers times 10 massage" can be beneficial. This technique is performed as follows: At the conclusion of a bath or shower, the patient warms his or her hands under hot water. Using 1 drop of baby shampoo (which does not sting the eyes), the patient works up a lather, places the index finger over the closed lids at the lid margin, and vigorously massages the lid back and forth 10 times. The patient then repeats the procedure with the middle, ring, and little fingers. Most marginal chalazia are connected to another chalazion located deeper in the substance of the lid. The contents of a purely marginal chalazion may be expressed by rolling 2 cotton-tipped applicators toward the lid margin from both sides of the lid. If the contents cannot be expressed, incise the distal chalazion, and curette the contents. The management of infected chalazia (ie, internal hordeolum) includes heat and topical and/or systemic antibiotics. In select cases, incision and drainage may be beneficial. Evacuate only the pus; overly aggressive curettage can disseminate the infection by breaking down tissue barriers. Topical steroids are necessary to prevent the chronic inflammatory response, as well as the acute noninfectious reaction produced by irritants (eg, free fatty acids liberated by bacterial enzymes) from causing excessive scarring. Once the acute inflammation has subsided, revision and definitive curettage or excision of the granulomatous mass may be required.

Surgical Care Drainage by means of a transconjunctival incision and curettage is optimal. Establish anesthesia by means of a local infiltration, possibly augmented with topical anesthetic cream (eutectic mixture of local anesthetics [EMLAs]) to reduce the pain of the injection in young patients. With recurrent chalazia, it is imperative that a biopsy be performed, with histological evaluation using fat stains (specifically request this on the specimen) to rule out sebaceous cell carcinoma.

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For local nonsurgical care early in the condition, blocked glandular orifices may be opened by means of vigorous massage between 2 cotton wool buds at the slit lamp.

Apply a chalazion clamp to evert the lid and to control bleeding. Vertically incise the lesion with a sharp blade, going no closer than 2-3 mm to the lid margin. Avoid perforating the skin. Curette the contents, including any cyst lining. A few minutes of pressure are usually sufficient to achieve hemostasis. A light pressure bandage should be applied for a few hours to absorb any further oozing. If previous external drainage (or granuloma extension) was performed, an external approach may be recommended. Make the incision horizontally, at least 3 mm from the lid margin in an existing crease. Do not sacrifice normal tissue. After hemostasis, the wound may be closed with appropriate sutures (eg, 7-0 silk). Involvement of both skin and conjunctiva may require offsetting the incisions to avoid fistula formation.

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Cauterization with phenol or trichloroacetic acid after incision and drainage may prevent the recurrence of small chalazia. Large or chronically neglected and excessively fibrotic chalazia may require more extensive surgical excision, including removal of parts of the tarsal plate. Leaving a 3-mm bridge of normal tarsus near the lid margin prevents notching. Multiple chalazia may be excised carefully, without fear of major lid deformity; the fibrous tarsal plate heals without leaving gaps. Even complete tarsal plate removal has been reported not to cause a lid deformity. A local intralesional corticosteroid injection (0.5-2 mL triamcinolone acetonide 5 mg/mL) is administered and can be repeated in 2-7 days.[2] Soluble aqueous preparations are preferred to crystalline suspensions to minimize complications of hypopigmentation, atrophy, or a visible depot of medication. A transconjunctival injection route may also provide a further safeguard. Injection or cautious surgical drainage of a chalazion located near the lacrimal drainage system can prevent serious complications involving tear flow. A study by Simon et al compared triamcinolone acetonide injection with incision and curettage in 94 patients with chalazion.[3] The study determined that intralesional triamcinolone acetonide injection was as effective as incision and curettage and may be considered as an alternative first-line treatment in cases where diagnosis is straightforward and biopsy is not required. Biopsy may be performed by simply excising a section of the remaining edge of the lesion. Do not overlook the specific request to the pathologist to rule out sebaceous cell carcinoma and to especially consider using fat stains (ie, do not have the specimen processed as usual).

Medical therapy for a chalazion is only rarely indicated, except in cases of rosacea, for which a 6-month course of low-dose tetracycline may be of benefit. Doxycycline in dosages of as little as 100 mg every week for 6 months may result in permanent biochemical change, with the sebaceous glands producing shorter-chain fatty acids, which are less likely than longer-chain fatty acids to congeal and block the gland orifices. Although probably innocuous, topical antibiotics do not help this condition, which is not infectious. Systemic tetracycline may be beneficial, but local drops are unlikely to help and are more likely to cause a contact dermatitistype reaction. Topical steroids can be helpful in minimizing inflammation and in reducing edema, thereby facilitating any drainage that may take place. Antibiotics Class Summary Antibiotics are not indicated as treatment of infection. Significant benefit may be derived from low-dose, longterm therapy with tetracycline. Tetracycline (Sumycin) Useful adverse effect is altering bacterial flora in skin and altering lipids to produce shorter-chain fatty acids, lowering melting point of sebaceous secretions, which may prevent blockage of meibomian glands. Doxycycline (Bio-Tab, Doryx, Vibramycin) Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. Alters lipids to produce shorter-chain fatty acids, lowering melting point of sebaceous secretions, which may prevent blockage of the meibomian glands. Minocycline (Dynacin, Minocin)

Consultations Referral to a dermatologist may be beneficial to help treat problems with rosacea or sebaceous dysfunction. Diet Dietary modification has not been evaluated.

Adverse effect alters lipids to produce shorter-chain fatty acids, lowering melting point of sebaceous secretions, which may prevent blockage of the meibomian glands. Metronidazole (Flagyl) Taken PO, may tetracyclines. Corticosteroids Class Summary Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the immune response of the body to diverse stimuli. Triamcinolone acetonide (Kenalog, Aristocort) Advantages of Kenalog over other depot corticosteroids (eg, Celestone) are less discomfort and reduced cost. For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Used to minimize scarring and inflammation. Further Outpatient Care Routine follow-up at approximately 1 month should reveal resolution of the chalazion, with no swelling, redness, or persistent lump. Any persistence of a nodule suggests the diagnosis included not simply a chalazion but also sebaceous cell carcinoma or other lid lesion. benefit patients unable to take

Similar advice given to manage severe acne may be appropriate in certain individuals. This advice is as follows: avoid or decrease the ingestion of coffee, chocolate, and highly refined foods, as well as fried foods and those containing saturated fats. On average, most of the public is not consuming sufficient amounts of vegetables and fruits, fresh or cooked, to meet the minimum recommendations of the American Dietary Association. Dietary supplements with omega-3 and omega-6 fatty acids, available in flax seeds or in flax seed oil, may be beneficial. A practical and simple intervention is to use a coffee grinder to grind flax seeds into meal. One tablespoon per day of fresh meal is an excellent dietary supplement and quite palatable Activity Regular habits of sufficient sleep, moderate sun exposure, exercise, and fresh air may be of benefit to cutaneous health and hygiene of the skin and glands of the eyelids. Stress is often associated with episodes of recurrent chalazia, although a causal role has not been established. Medication Summary

For further evaluation and management, appropriate specimens of tissue should be obtained for histologic evaluation. Because sebaceous cell carcinoma is best evaluated by using lipid stains, alert the pathologist to perform tissue processing without dehydration (ie, frozen section). The specimen should still be prepared in formalin to avoid autolysis; formalin does not remove the lipid, but rather, the alcohol baths used in paraffin sectioning remove the lipid. Transfer Urgent transfer to an experienced orbital and/or ophthalmic plastic surgeon is mandatory after biopsy results are documented or if the clinical findings suggest sebaceous cell carcinoma.

Hordeolum (2)
Bintitan disebabkan sering mengintip? Sama sekali SALAH tuh. Bintitan bukan terjadi sebab sering mengintip orang, namun bintitan itu sendiri sebenarnya adalah tergolong infeksi mata. Gejala yang timbul pada bintitan adalah kelopak mata terasa bengkak dan nyeri (kemeng), kadang keluar kotoran mata, dan pada perabaan sering terasa nyeri. Pada bintitan (hordeolum), terjadi infeksi bacterial pada kelenjar Meibom maupun kelenjar Zeiss dan Moll. Penyebab tersering dari bintitan ini sendiri adalah Staphylococcus aureus and Staphylococcus epidermidis. Bintitan ini sendiri harus diobati dengan benar, sebab apabila berlangsung lama, maka infeksi tersebut berubah menjadi infeksi granulomatus yang disebut Chalazia. Apabila infeksi bintitan ini tidak diobati dengan baik, juga dapat menyebabkan penyebaran infeksi ke kelenjar disekitar kelopak mata yang dapat menimbulkan suatu preseptal selulitis. Bintitan ini sebenarnya terdiri dari dua fase, yaitu fase infiltratif dimana gejalanya masih meradang dan nyeri, serta fase supuratif yaitu fase dimana kondisi peradangan sudah reda namun bintitan sudah memasuki tahap untuk memerlukan incisi dan kuretase. Pada bintitan yang masih dalam tahap awal, maka pengobatan dapat dilakukan secara medika mentosa (konservatif), yaitu berupa kompres dingin untuk mengurangi inflamasi dan obat-obatan seperti tetes mata, salep mata, maupun obat oral yang mengandung antibiotika. klik gambar untuk melihat lebih jelas

STYE
An external stye (pronounced /sta/), also could be spelled as styor hordeolum (/hrdilm/) is an infection of the sebaceousglands of Zeis at the base of the eyelashes, or an infection of theapocrine sweat glands of Moll.[1] External styes form on the outside of the lids and can be seen as small red bumps. Internal styes are infections of the meibomian sebaceous glands lining the inside of the eyelids. They also cause a red bump underneath the lid with only generalized redness and swelling visible on the outside. Styes are similar to chalazia, but tend to be of smaller size and are more painful and usually produce no lasting damage. Styes are characterized by an acute onset and usually short in duration (710 days without treatment) compared to chalazia that are chronic and usually do not resolve without intervention.

Cause Styes are commonly caused by a Staphylococcus aureus bacterial infection, or by the blocking of an oil gland at the base of the eyelash. Although they are particularly common in infants, styes are experienced by people of all ages. Styes can be triggered by poor nutrition, sleep deprivation, lack of hygiene or rubbing of the eyes. Sharing of washcloths or face towels should be curtailed to avoid spreading the infection between individuals.[2][3] Styes can last from one to two weeks without treatment, or as little as four days if treated properly.[4] Medical professionals will sometimes lance a particularly persistent or irritating stye with a needle to accelerate its draining.[5] A stye's expansion can also be fought with erythromycin ophthalmic ointment.[6] Medical professionals may also treat styes with other antibiotics, such as chloramphenicol or amoxicillin.[7] Chloramphenicol is used successfully in many parts of the world, but contains a black box warning in the United States due to concerns about aplastic anemia, which on rare occasions can be fatal. Erythromycin ointment enjoys widespread use, and may add to comfort and aid in preventing secondary infections. However, it is poorly absorbed when used topically, and usually requires oral dosing to reach the infection with therapeutic levels inside of a stye. Azasite, a topical eye drop form of azithromycin, does appear to penetrate eyelid tissues fairly well, and may be a topical treatment for styes used in the future. If a stye bursts, care must be taken to cleanse the wound to prevent reinfection. Signs and symptoms The first sign of a stye is a small, yellowish spot at the center of the bump that develops as pus expands in the area.[8] Other stye symptoms may include: A lump on the top or bottom eyelid Localized swelling of the eyelid Localized pain Redness Tenderness to touch Crusting of the eyelid margins Burning in the eye Droopiness of the eyelid Scratchy sensation on the eyeball Blurred vision Mucous discharge in the eye Irritation of the eye[9] Light sensitivity Tearing

Apabila bintitan sudah memasuki tahap supuratif, maka pengobatan oral maupun topical sudah tidak dapat dilakukan. Satu-satunya jalan adalah membuatkan 'jalan' atau melakukan insisi dan kuretase pada hordeolum tersebut. Untuk pencegahan bintitan, hindari menggosok kelopak mata dengan tangan, terutama apabila tangan kita kotor karena dapat menyebabkan infeksi pada kelenjar di kelopak mata tersebut.

Discomfort during blinking[10] Sensation of a foreign body in the eye Treatment

throughout the body) is extremely rare, and only a few instances of such spread have been recorded.[13] Prognosis Although styes are harmless in most cases and complications are very rare, styes often recur. They do not cause intraocular damage, meaning they do not affect the eye. Styes normally heal on their own by rupturing within few days to a week, causing the relief of symptoms. Few people require surgery as part of stye treatment. With adequate treatment, styes tend to heal quickly and without arising any type of complications. The prognosis is better if one does not attempt to squeeze or puncture the stye, as infection may spread to adjacent tissues. A stye usually will heal within a few days to a week, but if it does not improve or it worsens within two weeks, a doctor's opinion should be sought. Also, patients are recommended to call a doctor if they encounter problems with vision, the eyelid bumps becomes very painful, the stye bleeds or reoccurs or the eyelid or eye becomes red.[14] Prevention Stye prevention is closely related to proper hygiene. Proper hand washing can not only reduce the risks of developing styes, but also all other types of infections. Upon awakening, application of a warm washcloth to the eyelids for one to two minutes may be beneficial in decreasing the occurrence of styes by liquefying the contents of the oil glands of the eyelid and thereby preventing blockage. Some studies suggest oral flaxseed supplementation to prevent the occurrence of styes.[15] To prevent developing styes, it is recommended to never share cosmetics or cosmetic eye tools with other people. People should also keep their eye tools clean and generally practice proper eye hygiene. It is recommended to remove makeup every night before going to sleep and discard old or contaminated eye makeup.

Stye on lower part of a person's eye The primary mode of treatment for a stye is application of warm compresses. Incision and drainage is performed if resolution does not begin in the next 48 hours after warm compresses are started. As a part of self-care at home, patients may cleanse the affected eyelid with tap water or with a mild, nonirritating soap or shampoo (such as baby shampoo) to help clean crusted discharge. Cleansing must be done gently and while the eyes are closed to prevent eye injuries.[11] Patients are highly advised to not lance the stye, as serious infection can occur as a result. The infection could spread to the surrounding tissues and areas. Eye stye sufferers should avoid eye makeup (e.g., eyeliner), lotions and wearing contact lenses, since these can aggravate and spread the infection (sometimes to the cornea). Medical treatment can also be provided by a doctor and it is aimed on relieving the symptoms. Pain relievers such asacetaminophen may be prescribed and in some cases, antibiotics may be needed. Antibiotics are normally given to patients with multiple styes or with styes that do not seem to heal, and to patients who also suffer from blepharitis orrosacea. Commonly, the ophthalmologist prescribes oral or intravenous antibiotics, such as doxycycline, only when the infection has spread. Topical antibiotic ointments or antibiotic/steroid combination ointments can also be administered in stye treatment. Surgery is the last resort in stye treatment. Styes that do not respond to any type of therapies are usually surgically removed. Stye surgery is performed by an ophthalmologist, and generally under local anesthesia. The procedure consists of making a small incision on the inner or outer surface of the eyelid, depending if the stye is pointing externally or not. After the incision is made, the pus is drained out of the gland, and very small and unnoticeablesutures are used to close the lesion. It is common for the removed stye to be sent for histopathological examination to rule out the possibility of skin cancer. Complications Stye complications occur in very rare cases. However, the most frequent complication of styes is progression to achalazion that causes cosmetic deformity, corneal irritation, and often requires surgical removal.[12] Complications may also arise from the improper surgical lancing, and mainly consist of disruption of lash growth, lid deformity or lidfistula. Styes that are too large may interfere with one's vision. Eyelid cellulitis is another potential complication of eye styes, which is a generalized infection of the eyelid. Progression of a stye to a systemic infection (spreading

Ulkus Kornea, Referat.

TINJAUAN PUSTAKA III.1 Definisi Ulkus Kornea adalah keadaan patologik kornea yang ditandai oleh adanya infiltrat supuratif disertai defek kornea bergaung, diskontinuitas jaringan kornea dapat terjadi dari epitel sampai stroma. Ulkus kornea merupakan hilangnya sebagian permukaan kornea akibat kematian jaringan kornea. Ulkus kornea yang luas memerlukan penanganan yang tepat dan cepat uuntuk mencegah perluasan ulkus dan timbulnya komplikasi seperti desmetokel, perforasi, endoftalmitis. III.2 Etiologi Penyakit kornea adalah penyakit mata yang serius karena menyebabkan gangguan tajam penglihatan, bahkan dapat menyebabkan kebutaan. Ulkus kornea merupakan hilangnya sebagian permukaan kornea akibat kematian jaringan kornea. Ulkus biasanya terbentuk akibat; infeksi oleh bakteri (misalnya stafilokokus, pseudomonas, atau pneumokokus), jamur virus (misalnya herpes) atau protozoa akantamuba, selain itu ulkus kornea disebabkan reaksi toksik, degenerasi, alergi dan penyakit kolagen vaskuler. Kekurangan vitamin A atau protein, mata kering (karena kelopak mata tidak menutup secara sempurna dan melembabkan kornea). Faktor resiko terbentuknya antara lain adalah cedera mata, ada benda asing di mata, dan iritasi akibat lensa kontak. III.3 Patofisiologi Bila pertahanan normal pada mata seperti epitel kornea mengalami gangguan, resikoterjadinya infeksi sangat tinggi. Penyebab yang mungkin seperti trauma langsung pada kornea, penyakit alis mata yang kronis, abnormalitas tear film yang mengganggu keseimbangan permukaan bola mata dan trauma hipoksia akibat pemakaian lensa kontak. Koloni bakteri patologi pada lapisan kornea bersifat antigen dan akan melepaskan enzim dan toksin. Hal ini akan mengaktifkan reaksi antigen antibodi yang mengawali proses inflamasi. Sel sel PMN pada kornea akan membentuk infiltrat. PMN berfungsi memfagosit bakteri. Lapisan kolagen stroma dihancurkan oleh bakteri dan enzim leukosit dan proses degradasi berlanjut meliputi nekrosis dan penipisan. Karena penipisan lapisan ini, dapat terjadi perforasi menyebabkan endoftalmitis. Bila kornea telah sembuh, dapat timbul jaringan sikatrik yang menyebabkan penurunan tajam penglihatan. Bakteri gram positif lebih banyak menjadi penyebab infeksi bakterialis di dunia bagianselatan. Psaeudomonas aeruginosa paling banyak ditemukan pada ulkus kornea dan keratitis karena lensa kontak. Terbentuknya ulkus pada kornea mungkin banyak ditentukan oleh adanya kolagenase yang dibentuk oleh sel epitel baru dan sel radang.Dikenal ada 2 bentuk tukak pada kornea, yaitu sentral dan marginal/perifer. Tukak kornea sentral disebabkan oleh infeksi bakteri, jamur, dan virus.Sedangkan perifer umumnya disebabkan oleh reaksi toksik, alergi, autoimun, dan infeksi.Infeksi pada kornea perifer biasanya disebabkan oleh kuman Stafilokok aureus, H. influenza, dan M. lacunata. III.4 Jenis III.4.1 Ulkus Kornea Sentral

Ulkus kornea sentral dapat disebabkan oleh pseudomonas, streptococcus, pneumonia, virus, jamur, dan alergi. Pengobatan ulkus kornea secara umum adalah dengan pemberian antibiotika yang sesuai dan sikloplegik.Pembentukan parut akibat ulserasi kornea adalah penyebab utama kebutaan dan gangguan penglihatan di selu ruh dunia. Kebanyakan gangguan penglihatan ini dapat dicegah, namun hanya bila diagnosis penyebabnya ditetapkan secara dini dan diobati secara memadai. Ulserasi supuratif sentral dahulu hanya disebabkan oleh S pneumonia. Tetapi akhir-akhir ini sebagai akibat luasnya penggunaan obat-obat sistemik dan lokal (sekurangkurangnya di negara-negara maju), bakteri, fungi, dan virus opurtunistik cenderung lebih banyak menjadi penyebab ulkus kornea daripada S pneumonia. Ulkus kornea sentral dengan hipopion Ulkus sentral biasanya merupakan ulkus infeksi akibat kerusakan pada epitel. Lesi terletek di sentral, jauh dari limbus vaskuler. Hipopion biasanya (tidak selalu) menyertai ulkus. Hipopion adalah pengumpulan sel-sel radang yang tampak sebagai lapis pucat di bagian bawah kamera anterior dan khas untuk ulkus sentral kornea bakteri dan fungi. Meskipun hipopion itu steril pada ulkus kornea bakteri, kecuali terjadi robekan pada membran descemet, pada ulkus fungi lesi ini mungkin mengandung unsur fungi. Ulkus Kornea Bakterialis Ulkus kornea yang khas biasanya terjadi pada orang dewasa yang bekerja di bidang konstruksi, industri, atau pertanian yang memungkinkan terjadinya cedera mata. Terjadinya ulkus biasanya karena benda asing yang masuk ke mata, atau karena erosi epitel kornea. Dengan adanya defek epitel, dapat terjadi ulkus kornea yang disebabkan oleh mikroorganisme patogen yang terdapat pada konjungtiva atau di dalam kantong lakrimal. Banyak jenis ulkus kornea bakteri mirip satu sama lain dan hanya bervariasi dalam beratnya penyakit. Ini terutama berlaku untuk ulkus yang disebabkan bakteri oportunitik (misalnya Streptococcus alfa-hemolyticus, Staphylococcus aureus, Staphylococcus epidermidis, Nocardia, dan M fortuitum-chelonei), yang menimbulkan ulkus indolen yang cenderung menyebar perlahan dan superficial. Ulkus sentral yang disebabkan Streptococcus beta hemolyticus tidak memiliki ciri khas. Stroma kornea disekitarnya sering menunjukkan infiltrat dan sembab, dan biasanya terdapat hipopion yang berukuran sedang. Kerokan memperlihatkan kokus gram (+) dalam bentuk rantai. Obat obat yang disarankan untuk pengobatan adalah Cefazolin, Penisillin G, Vancomysin dan Ceftazidime. Ulkus kornea sentral yang disebabkan Staphylococcus aureus, Staphylococcus epidermidis, dan Streptococcus alfa-hemolyticus kini lebih sering dijumpai daripada sebelumnya, banyak diantaranya pada kornea yang telah terbiasa terkena kortikosteroid topikal. Ulkusnya sering indolen namun dapat disertai hipopion dan sedikit infiltrat pada korneasekitar. Ulkus ini sering superficial, dan dasar ulkus teraba padat saat dilakukan kerokan. Kerokan mengandung kokus gram (+) satu-satu, berpasangan, atau dalam bentuk rantai. Keratopati kristalina infeksiosa telah ditemukan pada pasien yang menggunakan kortikosteroid topikal jangka panjang, penyebab umumnya adalah Streptococcus alfa-hemolyticus. Ulkus Kornea Fungi

Ulkus kornea fungi, yang pernah banyak dijumpai pada pekerja pertanian, kini makin banyak diantara penduduk perkotaan, dengan dipakainya obat kortikosteroid dalam pengobatan mata. Sebelum era kortikosteroid, ulkus kornea fungi hanya timbul bila stroma kornea kemasukan sangat banyak mikroorganisme. Mata yang belum terpengaruhi kortikosteroid masih dapat mengatasi masukkan mikroorganisme sedikit sedikit. Ulkus kornea akibat jamur (fungi) Ulkus fungi itu indolen, dengan infiltrate kelabu, sering dengan hipopion, peradangan nyata pada bola mata, ulserasi superficial, dan lesi -lesi satelit (umumnya infiltrat, di tempat-tempat yang jauh dari daerah utama laserasi). Lesi utama merupakan plak endotel dengan tepian tidak teratur dibawah lesi kornea utama, disertai dengan reaksi kamera anterior yang hebat dan abses kornea. Kebanyakan ulkus fungi disebabkan organisme oportunistik seperti Candida, Fusarium, Aspergillus, Penicillium, Cephalosporium, dan lainlain. Tidak ada ciri khas yang membedakan macam-macam ulkus fungi ini. Kerokan dari ulkus kornea fungi, kecuali yang disebabkan Candida umumnya mengandung unsur-unsur hifa; kerokan dari ulkus Candida umumnya mengandung pseudohifa atau bentuk ragi, yang menampakkan kuncup -kuncup khas. Ulkus Kornea Virus A. Keratitis Herpes Simpleks Keratitis herpes simpleks ada dua bentuk yaitu primer dan rekurens. Keratitis ini adalah penyebab ulkus kornea paling umum dan penyebab kebutaan kornea paling umum di Amerika. Bentuk epitelialnya adalah padanan dari herpes labialis yang memiliki ciri-ciri imunologik dan patologik sama juga perjalanan penyakitnya. Perbedaan satu-satunya adalah bahwa perjalanan klinik keratitis dapat berlangsung lama karena stroma kurang vaskuler sehingga menghambat migrasi limfosit dan makrofag ke tempat lesi. Penyakit stroma dan endotel tadinya diduga hanyalah respons imunologik terhadap partikel virus atau perubahan seluler akibat virus, namun sekarang makin banyak bukti yang menunjukkan bahwa infeksi virus aktif dapat timbul di dalam

BAB I PENDAHULUAN I. 1 Latar Belakang Bilik mata depan adalah ruang yang terdapat antara kornea dan iris. Sedangkan bilik matabelakang adalah ruang yang lebih kecil yang terdapat diantara iris dan lensa. Keduaruangan ini diisi oleh cairan aqueous. Berbagai perubahan yang terjadi pada mata dapatmenyebabkan perubahan dari cairan aqueous dan bilik mata depan. Karena itu gambaranklinis pada bilik mata depan dapat membantu dalam menegakan diagnosa penyakit, jugadalam memantau respons pasien terhadap terapi. Reaksi inflamasi iris dan badan siliar akan memberikan gambaranAnterior chamber cell and flare di bilik mata depan. Diartikan sebagai kumpulan sel dan peningkatan protein (flare) di aqueous humor. Kumpulan sel biasanya terdiri dari sel darah putih, disebut jugahipopion. Kadang bisa juga terdiri dari sel darah merah, disebut sebagai hifema.Kumpulan sel ini akan mengendap di bagian inferior, membentuk lapisan yang dapatterlihat di bilik mata depan.1 Sel darah di bilik mata depan merupakan hasil pelepasan sel darah akibat dilatasipembuluh darah di iris dan badan siliar. Adanya sel di bilik mata depan memberikangambaran penyakit yang onsetnya akut. Sedangkan flare adalah akumulasi dari protein dibilik mata depan. Dapat menetap, bahkan setelah sel darah tidak ditemukan lagi.Mungkin disebabkan karena adanya kebocoran persisten dari blood-aqueous barrier. 1 Karena itu, presentasi flare sendiri tidak bisa dijadikan pegangan sebagai gejala inflamasi yang masih aktif.2 I. 2 Tujuan Penulisan Tujuan dari penulisan referat ini adalah untuk mengenal lebih dalam tentang hipopiondari segi definisi, gambaran klinis, faktor-faktor yang dapat menyebabkan terjadinyahipopion maupun terapinya. Sehingga dapatdilakukan penanganan yang tepat danmencegah terjadinya komplikasi lebih lanjut.

maka toksin dari peradangan kornea dapat sampai ke iris dan badan siliar, dengan melaluimembran Descemet, endotel kornea ke cairan bilik mata depan. Dengan demikian iris danbadan siliar mengalami peradangan dan timbulah kekeruhan di cairan bilik mata depandisusul dengan terbentuknya hipopion. Uveitis Anterior. Peradangan dari iris dan badan siliar. menyebabkan penurunan permeabilitas dari blood-aqueous barrier sehingga terjadi peningkatan protein, fibrin dan sel radang dalam cairan aqueous. Rifabutin. Merupakan terapi profilaksis untuk Mycobacterium avium complex pada penderita dengan HIV. Uveitis merupakan efek samping yang dapat terjadi pada pemakaian Rifabutin. Trauma. Corpus alienum, toxic lens syndrome, post operasi. II. 4Presentasi Klinis Gejala subyektif yang biasanya menyertai hipopion adalah rasa sakit, iritasi, gatal danfotofobia pada mata yang terinfeksi. Beberapa mengalami penurunan visus atau lapangpandang, tergantung dari beratnya penyakit utama yang diderita. 5 Gejala obyektif biasanya ditemukan aqueous cell and flare, eksudat fibrinous, sinekia posterior dan keratitis presipitat.2,3 II. 5 Diagnosa Diagnosa hipopion ditegakan berdasarkan anamnesa dan pemeriksaan menggunakan slitlamp. Pada anamnesa, ditanyakan adanya riwayat infeksi, pemakaian lensa kontak,trauma, pemakaian obat serta riwayat operasi. Pada pemeriksaan dengan slit lamp, ditemukan lapisan berwarna putih pada bagianinferior dari bilik mata depan. Jarang sekali hipopion ini ditemukan pada bagian lain daribilik mata depan. Hipopion biasanya dinilai berdasarkan tingginya, diukur dari dasar bilik mata depandengan satuan milimeter. Atau bisa juga dengan hitungan kasar, misalnya. ringan,moderat, setengah bilik mata depan dan seluruh mata depan. Cara terbaik untuk menilai hipopion adalah dengan terlebih dahulu meminta pasienduduk beberapa saat supaya hipopion dapat mengendap sempurna. Selanjutnya pasiendiminta melihat ke bawah dan sinar diarahkan dari bagian atas-depan iris.1,4 II. 6 Diagnosa Banding Hipopion harus dibedakan dari7: Pseudohipopion yang ditemukan pada retinoblastoma, injeksi steroid okular dan ghost cell glaucoma. Pseudohipopion termasuk dalam kelompok sindrommasquerade. Untuk membedakan harus dilakukan pemeriksaan dengan pupil yangtelah dilebarkan dengan midriatik. Sindrom Masquerade disebabkan oleh iridoskisis, atrofi iris esensial, limfoma maligna, leukemi, sarkoma sel retikulum, retinoblastoma, pseudoeksfoliatif dan tumor metastasis. Pseudohipopion dan infiltrasi tumor di iris Gambar diambil dari http://www.sarawakeyecare.com/Atlasofophthalmology Ghost Cell Glaucoma merupakan glaukoma sekunder sudut terbukadimanatrabecular meshwork mengalami obstruksi oleh sel darah merah yangterdegenerasi, disebut ghost cells. Biasanya didahului oleh trauma. Metastasis ke bilik mata depan, misalnya dari leukemia dan Ca mammae. II. 7 Komplikasi Klinis Struktur dari hipopion yang mengandung fibrin, merupakan reaksi tubuh terhadainflamasi. Tetapi fibrin-

Beberapa keadaan yang dapat memberikan gambaran hipopion, diantaranya5,6: Ulkus Kornea. Apabila terjadi peradangan hebat tapi belum terjadi perforasi dari ulkus,

fibrin ini dapat menyebabkan terjadinya perlengketan antara irisdan lensa (sinekia posterior) Bila seluruh pinggir iris melekat pada lensa disebut seklusiopupil, sehingga cairan dari cop tidak dapat melalui pupil untuk masuk ke coa, iristerdorong ke depan, disebut iris bombe dan menyebabkan sudut coa sempit sehinggatimbul glaukoma sekunder. Kepaniteraan Klinik Ilmu Penyakit Mata Fakultas Kedokteran Universitas Tarumanagara Rumah Sakit Umum Daerah Kota Semarang Periode 07 Juni 2010 10 Juni 2010 7 Peradangan di badan silier dapat juga menyebabkan kekeruhan dalam badan kaca olehsel-sel radang, yang tampak sebagai kekeruhan seperti debu. Peradangan inimenyebabkan metabolisme lensa terganggu dan dapat menimbulkan kekeruhan lensa,hingga terjadi katarak. Pada kasus yang sudah lanjut, kekeruhan badan kaca pun mengalami jaringan organisasidan tampak sebagai membrana yang terdiri dari jaringan ikat dengan neovaskularisasiyang berasal dari sistem retina, disebut retinitis proliferans. Bila membrana ini mengkerut, dapat menarik retina sehingga robek dan cairan badankaca melalui robekan itu masuk ke dalam celah retina potensial dan mengakibatkan ablasi retina.5,6 II. 8 Penatalaksanaan Penatalaksanaan hipopion tergantung dari ringan atau beratnya penyakit. Sel darah putihbiasanya akan di reabsorpsi. Tetapi bila hipopion memberikan gambaran yang berat,maka bisa dilakukan drainase.1,3 Terapi yang lebih spesifik biasanya tergantung dari penyakit utama yang menyebabkan hipopion. Apabila terjadi inflamasi, dapat diberikan kortikosteroid. Anti inflamasi yang biasanya digunakan adalah kortikosteroid, dengan dosis sebagai berikut: Dewasa : Topikal dengan dexamethasone 0,1 % atau prednisolone 1 %. Bila radang sangat hebat dapat diberikan subkonjungtiva atau periokuler : dexamethasone phosphate 4 mg (1 ml) prednisolone succinate 25 mg (1 ml)

Hipopion adalah pus steril yang terdapat pada bilik mata depan yang terlihat sebagai lapisan putih yang mengendap di bagian bawah bilik mata depan. Bangunan yang berhubungan dengan hipopion adalah iris dan badan siliar. Radang irisdan badan siliar menyebabkan penurunan permeabilitas dari bloodaqueous barriersehingga terjadi peningkatan protein, fibrin dan sel radang dalam cairan aqueous,sehingga memberikan gambaran hipopion. Hipopion merupakan reaksi inflamasi di bilik mata depan. Karena itu semua penyakit yang berhubungan dengan uveitis anterior dapat menyebabkan terjadinya hipopion. Diagnosa hipopion ditegakan berdasarkan anamnesa dan pemeriksaan menggunakan slit lamp. Hipopion harus dibedakan dengan pseudohipopion yang merupakan tanda keganasan. Apabila berkelanjutan, hipopion dapat menyebabkan komplikasi berupa glaukomasekunder, katarak, retinitis proliferans dan pada kasus yang berat dapat menyebabkan ablasi retina Penatalaksanaan hipopion biasanya tergantung dari banyaknya lapisan pus di bilik matadepan. Bila proses inflamsi akut sudah diatasi, biasanya hipopion akan direabsorpsi. Bilapresentasi pus sangat banyak, bisa dilakukan drainase. Prognosa dari hipopion tergantung dari penyakit yang menjadi keluhan utama.

triamcinolone acetonide 4 mg (1 ml) methylprednisolone acetate 20 mg Cycloplegic dapat diberikan dengan tujuan untuk mengurangi nyeri dengan memobilisasiiris, mencegah terjadinya perlengketan iris dengan lensa anterior ( sinekia posterior ),yang akan mengarahkan terjadinya iris bombe dan peningkatan tekanan intraocular,menstabilkan bloodaqueous barrier dan mencegah terjadinya protein leakage (flare) yanglebih jauh. Agent cycloplegics yang biasa dipergunakan adalah atropine 0,5%, 1%, 2%,homatropine 2%, 5%, Scopolamine 0,25%, dan cyclopentolate 0,5%, 1%, dan 2%.8 II. 9 Prognosa Hipopion adalah gejala klinis yang muncul sebagai respon inflamasi. Sel darah putihakan diabsorpsi sepenuhnya. Tetapi prognosis tergantung dari penyakit dan komplikasiyang dapat terjadi.1 Kepaniteraan Klinik Ilmu Penyakit Mata Fakultas Kedokteran Universitas Tarumanagara Rumah Sakit Umum Daerah Kota Semarang Periode 07 Juni 2010 10 Juni 2010 9 BAB III KESIMPULAN