Ординатура / Офтальмология / Английские материалы / Clinical Medicine in Optometric Practice_Muchnick_2007

EMERGENCY INTERVENTION

AND THE LAW

Good Samaritan laws exist to protect the rescuer in the event that the patient is hurt or dies during emergency intervention. These laws extend, at least partially, to the optometric private practice. As long as the optometrist intervenes in a medical emergency in an appropriate manner, and is deemed to have followed a protocol that any reasonable optometrist would follow in the event of a medical emergency in the optometric office, then the optometrist would most likely not be found to be negligent, even if injury to the patient results from the intervention.

If, however, the optometrist is found to have caused injury or death because of the inappropriate application of emergency procedures, or the failure to have adequate knowledge to appropriately intervene in a medical emergency, the optometrist may be found culpable on the basis of negligence, and good Samaritan laws may not apply in this case to trained professionals.

What, then, does a reasonable optometrist need to know to meet the standard of care in emergency situations as it applies to optometry? First, it would be expected that all optometrists be certified in CPR, and take recertification to prevent expiration. It may also be expected that at least some office personnel be trained in CPR.

Second, an office manual with emergency protocols may demonstrate to a jury that you are aware of the potential medical emergencies that can occur in your office and that you and your staff prepared in advance for a crisis.

Third, a reasonable optometrist should have a blood pressure cuff and stethoscope. In addition, orange juice and sugar for diabetic emergencies may be essential in the office.

You should contact your state board of optometry to ask if your state therapeutic bill requires emergency medication or devices in your office. If your bill allows for indictable, then you should keep an insect sting kit in your office.

The optometrist would not likely be expected to have sublingual nitroglycerin tablets, oxygen canisters, injectable antihistamines, or a defibrillator in the office. Therefore, failure to possess these items would not constitute negligence in a medical emergency.

BIBLIOGRAPHY

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Emergency Response Training: Student primer, 1994, Oxygen Therapy Institute, p. 19, 22.

Ferri FF: Practical guide to the care of the medical patient, ed 3, St Louis, 1995, Mosby, p. 556.

Grambart S, Decker TL: Common office emergencies, Clin Podiatr Med Surg 19:1163-1185, 2002.

Heiberger MH, Madonna RJ, Nehmad L: Emergency care in the optometric setting, New York, 2004, McGraw-Hill.

Idris AH, Gabrielli A: Advances in airway management, Emerg Med Clin North Am 20:4843-57, 2002.

Kapoor WN: Evaluation and management of the patient with syncope, JAMA 268:18, 1992.

Laskowski-Jones L: Responding to an out-of-hospital emergency, Nursing 32:936-42, 2002.

Limmer D, et al: Emergency care, Upper Saddle River, N.J., 2001, Prentice-Hall.

Manolis, AS et al: Syncope: current diagnostic evaluation and management, Ann Intern Med 112:850, 1990.

National Safety Council: CPR manual (for SOS Technologies), Sudbury, 1996, Jones and Bartlett, p. 12.

National Safety Council: Private Communication, 1997. O’Callahan W, Renzi, FP: Neurologic emergencies. In Stine RJ,

Chudnorsky CR, eds: A practical approach to emergency medicine, ed 2, Boston, 1994, Little Brown and Co., p. 830.

O’Callahan W, Renzi, FP: Neurologic emergencies. In Stine RJ, Chudnorsky CR: A practical approach to emergency medicine, ed 2, Boston, 1994, Little Brown and Co., p. 831.

Orland MJ: Endocrine emergencies. In Stine RJ, Chudnorsky CR, eds: A practical approach to emergency medicine, ed 2,

Boston, 1994, Little Brown and Co., pp. 199-213.

Riela AR: Management of seizures, Crit Care Clin 5:4, 1989. Scheuer ML, Pedley JA:The evaluation and treatment of seizures,

N Engl J Med 323:21, 1990.

Sendrowski DP, Maher JF: Emergency medicine. In Muchnick BG: Clinical medicine in optometric practice, St Louis, 1994, Mosby, pp. 350-356.

Silverstein MD, et al: Patients with syncope admitted to medical intensive care units, JAMA 248:1184, 1982.

Starr Larry:The control of anxiety in lifesaving method (Calm),

In: Emergency response training student primer, 1994, Oxygen Therapy Institute, p. 2.

Stine RJ, Harding MH: Environmental emergencies, In Stine RJ, Chudnorsky CR, eds: A practical approach to emergency medicine, ed 2, Boston, 1994, Little Brown and Co., pp. 390-391.

Inflammation of the anterior uveal tissues may be caused by the presence of systemic disease. Anterior uveitis is often the first symptom of a serious underlying disorder. Therefore, the management strategy often involves topical therapy in addition to laboratory testing and multidisciplinary involvement to identify

an associated systemic etiology.

In at least 1 of 6 cases of anterior uveitis, an associated systemic disease can be ultimately identified. In approximately 3 of 4 cases of anterior uveitis, however, an etiology of any type is never found. Consequently, the disease can be frustrating to both doctor and patient.

In general, anterior uveitis is fairly straightforward to diagnose. The presence of white blood cells in the anterior chamber of the eye is pathognomonic of the disease. The treatment is typically effective and simple, and in most cases anterior uveitis resolves with no significant sequelae.

Although typified by an uneventful resolution, anterior uveitis may cause severe and permanent ocular complications. For example, the presence of keratic precipitates on the corneal endothelium may reduce the effectiveness of the corneal endothelial pump and disrupt normal corneal physiology, thus leading to stromal clouding. In addition, anterior and posterior synechiae can lead to uveitis-related glaucoma, and chronic anterior uveitis increases the risk of cataract formation.

Anterior uveitis becomes particularly challenging in recurrent, bilateral, chronic, or recalcitrant cases, in addition to those that involve the posterior segment. These characteristics, in addition to cases unresponsive to treatment, often indicate the presence of an underlying disorder. The management of such complicated cases becomes compounded by the need for laboratory investigation and medical specialty involvement.

300 THE EYE IN SYSTEMIC DISEASE

The diagnosis and treatment of anterior uveitis without considering the possibility of an underlying systemic disease is considered inadequate medical interdiction. Minimally, an extensive uveitis history on every patient who presents with anterior uveitis can help screen for a potential systemic disorder. Any indication of an associated disease, whether by history, uveitic characteristics, or concurrent systemic signs or symptoms, warrants a laboratory evaluation.

CLASSIFICATION OF ANTERIOR UVEITIS

Anterior uveitis is a broad definition used to denote inflammation of the tissue components of the anterior uveal tract. Inflammation confined to the anterior chamber indicates involvement of the iris and is consequently known as iritis. If only the ciliary body is inflamed, then the disorder is termed cyclitis. Iridocyclitis is defined as inflammation to both the iris and ciliary body. The more posterior the inflammation, the greater the likelihood that it is caused by a systemic disease and the more difficult it will be to treat.

Acute uveitis is typically intraocular inflammation that lasts no longer than 6 weeks, while chronic cases persist longer. In general, the more posterior the inflammation, the longer it will last. Chronic uveitis increases the likelihood of an associated systemic disease, and short-lived acute cases are more likely to be caused by local or environmental factors.

Anterior uveitis may be unilateral or bilateral in presentation. Bilateral uveitis has a greater association with systemic disease than the unilateral presentation.

A uveitis that is seen more than once is known as recurrent uveitis. Recurrent uveitis has a greater risk of associated systemic disease. A patient with a first-time occurrence of anterior uveitis is considered at low risk for systemic disease, unless other factors are present such as concurrent systemic symptoms, bilaterality, posterior segment involvement, intraocular complications, and resistance to treatment.

If the etiology of the uveitis is never discovered, then the inflammation is termed idiopathic. Idiopathic inflammation is the most common form of anterior uveitis, because in most cases the cause of the disease is never discovered.

If a cause is isolated, however, then the uveitis may be noninfectious or infectious. Causes of noninfectious anterior uveitis include systemic disease-associated uveitis and trauma. Infectious uveitis may be the result of bacterial, viral, fungal, or parasitic infection.

Uveitis may be associated with a granulomatous condition. In granulomatous uveitis a deposition of large, fatty-appearing congregations of white blood cells known as “mutton-fat” keratic precipitates is present, primarily on the corneal endothelium. These precipitates may also occur on the iris, lens, vitreous,

and retina. The presence of granulomatous uveitis increases the likelihood of an associated granulomatous systemic disease. Nongranulomatous uveitis fails to reveal any evidence of a granulomatous nature and the keratic precipitates will be small and discrete. Nongranulomatous uveitis has a reduced risk of associated systemic disease.

The term “posterior uveitis” indicates inflammation of the posterior uveal tract. More specifically, choroiditis is used to describe an inflammation of the choroid. Posterior uveitis is rarely confined to just the choroidal tissue, however, because of the intimacy of the retina. If the pars plana becomes inflamed it is termed “pars planitis,” or intermediate uveitis. Inflammation of the overlying retina, or retinitis, is typical in many cases of choroiditis. Active cases of retinitis often produce inflammation of the overlying vitreous, or vitritis.

In extreme cases of uveitis, all the internal tissues of the eye may become involved. This is known as endophthalmitis. Panophthalmitis describes the inflammation of both internal and external tissues of the eye.

On the basis of these definitions, the relative risk of a systemic disease associated with a uveitis can be predicted to some degree. The least risk for a systemic disease occurs in a patient with a first occurrence of unilateral, noninfectious, acute nongranulomatous iritis. The greatest risk for a systemic disease occurs in a patient with recurrent, bilateral chronic granulomatous anterior uveitis with posterior involvement.

PATHOPHYSIOLOGY OF ANTERIOR UVEITIS

Inflammation of the iris is not visualized well because the tissue swells along the anteroposterior axis of the eye. As such, a thickened iris could only be detected in cross-section by use of ultrasound biomicroscopy. Visual assessment of the inflamed iris in the slit lamp reveals no indication of its edematous condition except for possible narrowing of the anterior chamber angle. Likewise, swelling of the ciliary body is practically undetectable, and may only cause some accommodative changes in the uveitis patient. The swelling of these tissues is detected by their release of white blood cells into the aqueous. Cells detected in the anterior chamber indicate an iritis, and cells visualized in the potential space between the iris and the vitreous are produced by an inflamed ciliary body.

Inflammation of the iris promotes migration of white blood cells and protein into the anterior chamber by causing a breakdown of the blood-aqueous barrier. These extravasated cells help mediate the inflammatory response, and are a crucial element in the immune response of the eye. In the absence of anterior uveitis, the anterior chamber should be free of cells.

The cells that migrate into the aqueous from the iris or ciliary body are primarily lymphocytes, though there may be a significant number of neutrophils present in the aqueous. Other white blood cell types can also be identified in almost all cases of uveitis.

The diverse cell types found in the aqueous of uveitis patients indicates that elements of all four hypersensitivity reactions are present in almost all cases of anterior uveitis. Type I hypersensitivity reactions, mediated by antibodies such as immunoglobulin E (IgE), binds mast cells to basophils, causing their breakdown and release of histamine. An example of a Type I reaction is hay fever, but the role of mast cells and basophils in anterior uveitis is still unclear.

Type II reactions are mediated by cytotoxic antibodies and cause hemolytic disorders (such as blood transfusion reactions), and are of little impact in the typical case of anterior uveitis.

Type III reactions are known as immune complexmediated inflammatory response. In these cases, antibodies bind to antigens, causing deposition of these complexes with activation of the complement cascade and ultimate attraction of tissue-destroying cells. This type of reaction is a limited contributor to the inflammation produced in anterior uveitis.

The Type IV hypersensitivity reaction is mediated solely by T cells and is termed a cell-mediated immune response. The response seen in anterior uveitis is predominantly a T-cell-mediated mechanism.

The aqueous of the inflamed eye may demonstrate not only white blood cells, but also the presence of red blood cells, indicating hyphema, and pigment cells. The presence of even a trace amount of leukocytes in the anterior chamber is the strongest indicator of anterior uveitis. Erythrocytes in the anterior chamber indicate possible trauma or a severe acute iritis. The most common causes of pigment cells in the anterior chamber are the pharmacological introduction of topical phenylephrine (for pupil dilation), trauma, pigment dispersion syndrome, pigmentary glaucoma, and anterior uveitis.

Protein in the anterior chamber appears as flare, or a fog, visualized in the slit-beam of the biomicroscope. In the absence of anterior uveitis, only a slight amount of flare at most should be detected under the brightest illumination. Flare is a significant indicator of a breakdown in the blood-aqueous barrier. This sign is typical in cases of acute, severe iritis, but may be present chronically after ocular surgery or several bouts of anterior uveitis. Flare, in the absence of cells, does not require treatment, because it is not an indicator of active uveitis. The most common cause of flare is traumatic uveitis, because the concussive shock wave causes immediate and dramatic dilation of iris and ciliary body blood vessel. Traumatic effects on the intraocular tissues allow protein ample opportunity to

escape the blood-aqueous barrier and leak into the anterior chamber.

Resolution of the anterior uveitis, either with or without treatment, occurs as the cellular components of the inflammation are reabsorbed into the trabecular meshwork. During time, an eventual clearing of the cells and protein occurs. The longer these immune components exist in the anterior chamber, the greater the chance of complications arising from their presence. Therefore, it is imperative to institute treatment as quickly as possible to expedite the clearing of these immune products from the aqueous.

SYMPTOMS OF ANTERIOR UVEITIS

The issue of photophobia is significant in the diagnosis of anterior uveitis. The most common complaint of patients with acute iritis is an aversion to bright light. Although some patients would describe photophobia as painful, more often it is an irritation that arises when exposed to brilliant illumination. The patient who arises in the morning with an iritis that developed during the night usually complains of photophobia when opening the shades of his or her bedroom and looking at sunlight, but photophobia is much less frequent in cases of chronic uveitis. Because chronic anterior uveitis is more often associated with systemic disease, the complaint of photophobia will decrease, but not eliminate, the possibility of an associated systemic disorder.

Vision is rarely affected by anterior uveitis. In most cases, only a mild subjective complaint of some visual blur will be present. Several factors can cause the subjective complaint of blurred vision. In anterior uveitis, lid, tear film, corneal, anterior chamber, iris, lenticular, and posterior tissue involvement may be present.

Ptosis can occur in anterior uveitis when the patient forcibly holds shut the upper lid of the involved eye until seeking help. This mechanical ptosis is transient, and not directly related to the uveitis, but still can cause blurry vision when the patient attempts to use the eye.

Profuse tearing is not uncommon in cases of acute uveitis, and increases with photophobia. Chronic and low-grade uveitis has much less associated tearing. A large tear lake is often responsible for the complaint of visual blur.

If a significant amount of immune product is deposited on the corneal endothelium, a degradation of the corneal endothelial pump may be present. A reduction in the effectiveness of this pump can lead to corneal swelling and cloudiness that patients describe as a visual blur or halos around lights. The patient may describe the vision as “foggy,” or like “looking through a cloud.”

An elevation in intraocular pressure can also cause a reduction in the effectiveness of the corneal endothelial

302 THE EYE IN SYSTEMIC DISEASE

pump. Uveitis-associated glaucoma can lead to visual blur because of corneal swelling. The glaucoma may be the result of a closed angle from a swollen iris, or a pupillary block secondary to posterior synechiae. In the case of pupillary block, a subsequent iris bombe forces the iris forward and closes the angle. In most cases of anterior uveitis, a reduction of intraocular pressure is present that is mostly the result of an increase in the uveoscleral outflow mechanism and a slight reduction in aqueous production. In this manner, an elevation in intraocular pressure that would be expected because the trabecular meshwork is clogged with cellular debris is offset by an increase in uveoscleral outflow and reduced aqueous production.

Extensive corneal endothelial deposits may themselves reduce vision by obscuring the visual axis.

Several factors, if present in the anterior chamber of the inflamed eye, may cause visual blurring. Cells and flare, if profuse and centrally located, can cause complaints of hazy vision. Hypopyon, a thick cellular and dramatic response, can cover the visual axis and obscure vision. In some extreme cases of recalcitrant uveitis that resists treatment, the hypopyon may be cultured using fine-needle paracentesis to identify a possible pathogen (Figure 21-1).

Hyphema, a deposition of blood in the anterior chamber, may also be so thick and profuse that it too covers the visual axis, thus obscuring the vision of the patient (Figure 21-2).

Posterior synechiae, the abnormal attachment of the iris to the anterior lens capsule, can obscure the visual axis and cause blurred vision. This condition is rare, however, because most posterior synechiae form along the pupillary border and away from the visual axis.

Anterior uveitis can contribute to the formation of cataracts. Chronic or recurrent uveitis can be so disruptive to normal intraocular physiology that the clarity of the lens cannot be preserved. In addition, topical steroids used to treat anterior uveitis can cause the formation of posterior subcapsular cataract.

FIGURE 21-1 ■ Fine-needle aspiration (paracentesis) of a hypopyon for culturing and pathologic evaluation.

FIGURE 21-2 ■ Resolving hyphema in a case of juvenile xanthogranuloma. Note dark area of blood in the anterior chamber transversing the view of the inferior pupil and iris.

More posterior causes of visual blur include vitritis, retinitis, choroiditis, vasculitis, macular edema, and disc edema. Any case of anterior uveitis warrants a dilated posterior evaluation to monitor for any of these conditions. A uveitis that involves posterior structures will be more difficult to treat, has a greater risk of complications, and has a greater frequency of systemic disease association. In addition to visual blur, the most common symptom of a posterior involvement of the uveitis is the presence of floaters. These floaters are usually cellular debris and immune products that form in the vitreous and are seen by the patient, often against a blue sky or a white wall.

Finally, the patient with anterior uveitis may complain of a red eye. Acute uveitis has greatest risk of red eye, and chronic anterior uveitis may be seen with a white and uninvolved conjunctiva. Therefore, the patient with uveitis who is seen with a white eye is at greater risk of an associated systemic disease than the patient with red-eyed uveitis.

In summary, systemic disease should be suspected in cases of chronic anterior uveitis when the patient with a nearly white conjunctiva who has minimal photophobia complains of significant blurring of vision and floaters. Acute anterior uveitis with severe photophobia and redness, but hardly any visual blur or floaters, is less likely to be associated with a systemic disease.

HISTORY

The uveitic patient will often wait no longer than 2 days after the onset of symptoms to seek help. On the first day, the involved eye typically becomes red and photophobic. On the second day, the condition worsens to the point that the patient cannot work because

of extreme light sensitivity and ocular irritation or pain. Any patient who calls with complaints of a red, photophobic eye, should be seen immediately to confirm the presence of anterior uveitis.

The examination of the patient with a red, photophobic eye should be directed toward the detection and confirmation of an anterior uveitis. To this end, the history should narrow quickly to specifics about the ocular inflammation. After anterior uveitis is confirmed, a uveitis history is taken with regard to systemic disease.

The general history should include all patient demographics, because these can have an impact later on the search for a systemic disease. It is important to note whether this episode of inflammation has occurred in the past, whether it was ever evaluated or treated, and whether any systemic diseases were suspected. The names and addresses of previous treating practitioners should be noted so that previous episodes can be confirmed, thus helping establish the diagnosis of recurrent uveitis.

It is important to establish how the inflammation was first detected by the patient, what its course has been, and whether the patient is self-medicating. Any symptomology, such as pain, tearing, or photophobia, should be established. It is significant to note any concurrent body wide symptoms, because these may help in the detection of systemic disease. Such symptoms include hot or cold spells, malaise, rashes, cough, headache, or neck ache. It is appropriate to wait until the uveitis is established before asking these medical questions as part of a comprehensive uveitic history.

DIAGNOSIS

Visual Acuity

Most patients will be evaluated with the Snellen chart, which is adequate for patients with good visual acuity (VA). In patients with subnormal vision, low vision charts are a good option. For bedside patients, the “C- PAC” pocket low vision chart created by Dr. Connie Chronister is a portable and reliable method of establishing visual acuities in low-vision patients with uveitis. In acute, anterior uveitis, the VA is typically unaffected or reduced by only a line or two. The greater the reduction in visual acuity, the greater the risk of posterior involvement.

External Examination

The skin of the lids should be evaluated closely in patients with uveitis. Any growths or tumors of the lids should be measured and a referral to dermatology be considered for eventual biopsy. Granulomas of the skin or lid may occur in association with anterior uve-

itis and indicate an underlying granulomatous condition (Figure 21-3). The presence of any lid lesions in association with an anterior uveitis increases the likelihood of a systemic disease.

Extraocular Muscles

It is unusual to find extraocular muscle involvement in cases of anterior uveitis. If a finding of tropia or internuclear ophthalmoplegia in association with a uveitis is present, a common causal etiology may exist within the central nervous system. Multiple sclerosis, sarcoidosis or non–Hodgkin’s lymphoma should be suspected in any patient who has anterior uveitis with diplopia, tropia, or extraocular muscle palsy.

Pupils

Anterior uveitis typically produces a miotic pupil on the involved side. Therefore, anisocoria is usually present in cases of acute unilateral anterior uveitis. The miosis is not the result of a neurologic lesion but is an effect of chemical inflammatory mediators on the receptor sites of the pupillary sphincter.

Unlike acute uveitis, recurrent uveitis may yield iris atrophy, mydriasis, and reduce the speed of pupillary constriction. Fuch’s heterochromic iridocyclitis, for example, causes iris atrophy and pupil dilation when compared with the uninvolved side (Figures 21-4 and 21-5). Often the speed of pupil constriction on the involved side is reduced and almost extinguished.

In general, pupillary miosis is more common in acute iritis than in chronic anterior uveitis. Therefore, miosis is not an indication of an associated systemic disease.

Posterior synechiae may reduce pupillary functioning, cause a permanent distortion of the pupil, and eventually become cosmetically unappealing.

FIGURE 21-3 ■ Sarcoidosis with lid granulomas. Biopsy of these lid lesions can confirm the presence of sarcoid.

Intraocular Pressure

Intraocular pressure (IOP) is best measured using applanation tonometry with anesthetic but without fluorescein, because fluorescein can enter the anterior chamber and obscure the amount of cell and flare that is present. In addition, fluorescein may obscure posterior segment evaluation for as long as 24 hours and prevent the use of fluorescein angiography if it is necessary.

The IOP typically elevates in the first hours of an anterior uveitis, because aqueous cells get swept into the angle and physically clog the trabecular meshwork. This effect is short-lived and rarely observed in the office, because most patients are not seen within hours of the onset of anterior uveitis. Rather, the patient with uveitis is usually seen a day or 2 after its onset, by which time the IOP has decreased below

normal. This drop in IOP is the result of the inflammatory effect on the uveoscleral outflow mechanism. In addition, uveitis has a slight effect on reducing aqueous production from the ciliary body. Therefore, most uveitis patients exhibit a reduced IOP on the side of the uveitis. This accounts for the time honored, and not particularly accurate phrase, “A sick eye is a soft eye.”

An elevated IOP in cases of anterior uveitis may be caused by glaucomatocyclitic crisis (or PossnerSchlossman syndrome), or uveitic glaucoma. Intraocular tumors may contribute to an elevated IOP in association with cells in the anterior chamber. A diligent search for an intraocular tumor should be initiated whenever there is unilateral elevation of the IOP in association with cells in the anterior chamber.

Slit-Lamp Biomicroscopy

Conjunctiva

The classic conjunctival injection pattern of the acute anterior uveitis is a red circumcorneal flush. This limbal injection is often noted to be almost 360 degrees around the cornea. It represents a reflection on the conjunctival surface of deeper iris or ciliary body inflammation.

This limbal injection is to be differentiated from the injection patterns of conjunctivitis (Figure 21-6). In bacterial conjunctivitis, a deep red injection pattern is typically present that is greatest in the fornices and lessens towards the limbus. In viral conjunctivitis a superficial pink injection is usually present that is uniform over the entire bulbar conjunctiva, and in allergic conjunctivitis a classic swelling of the conjunctiva occurs so that the cornea appears to be sunk into it in a classic “watchglass” appearance.

The circumlimbal flush is typical in acute iritis but nearly or completely absent in chronic anterior uveitis. Therefore, the absence of circumcorneal injection in a case of anterior uveitis increases the likelihood of a systemic disease as a cause of the ocular inflammation.

Cornea

Convection currents are established in the anterior chamber by the aqueous rising up near the warm iris and then falling near the relatively cooler cornea. White blood cells circulate along these aqueous currents, being driven into the superior anterior chamber and then falling along the corneal endothelium toward the inferior angle. When the white blood cells hit the

A

C

corneal endothelium they may get caught in irregularities such as guttata. The deposited cells send out chemical messengers to attract other white blood cells to the site. Accumulations of these white blood cells are known as keratic precipitates (KPs) (Figure 21-7). They typically form in the inferior cornea and frequently take on the shape of an inverted triangle (Arlt’s triangle).

Neutrophils, macrophages, and lymphocytes are typically found within the KP. Large deposits are known as “mutton-fat” KPs and are typical of granulomatous disease (Figure 21-8). Small KPs are usually nongranulomatous and less likely to be associated with systemic disease.

FIGURE 21-7 ■ Keratic precipitates on the corneal endothelium. These small KPs are usually the result of nongranulomatous disease.

B

D

306 THE EYE IN SYSTEMIC DISEASE

FIGURE 21-8 ■ “Mutton-fat” keratic precipitates. These larger KPs are likely the result of granulomatous disease processes.

After resolution of the uveitis, KPs may take from weeks to years to clear from the cornea. The risk of an associated systemic disease increases as the size and number of KPs increases. Granulomatous KPs indicate the presence of a granulomatous systemic disease.

Anterior Chamber

Neutrophils and lymphocytes spill over from the inflamed iris or ciliary body into the aqueous and can be observed on slit-lamp exam. The presence of these cells is pathognomonic of anterior uveitis (Figure 21-9). The anatomical classification of anterior uveitis can be determined by the position of the cells. White blood cells confined to the anterior chamber indicate the presence of an iritis, and if the anterior chamber is clear but cells are present just behind the lens and in front of the vitreous, then a cyclitis is present. Iridocyclitis causes cells to migrate to both positions. The further posterior the position of the cells, the greater the likelihood of systemic disease, the greater the risk of complications, and the more difficult it will be to treat the uveitis.

A profuse cellular response (Figure 21-10) may congeal with fibrin to produce a hypopyon that collects in the inferior angle of the eye (Figure 21-11). The presence of a hypopyon also increases the risk of an associated systemic disease, particularly Behçet’s disease.

Flare, a proteinaceous exudate from the inflamed iris or ciliary body, is typical of acute and traumatic iritis, and is thus not indicative of an associated systemic disease (Figure 21-12). Permanent flare, in the absence of a cellular response, typically occurs because of multiple ocular surgeries or recurrent, chronic anterior uveitis. Flare does not require treatment unless some associated sign of active ocular inflammation is present.

Iris

Large accumulations of inflammatory cells on the surface of the iris are known as iris nodules. Koeppe nodules form on the pupillary border and Busacca nodules form on the ciliary portion of the iris. The presence of nodules increases the likelihood of an associated granulomatous systemic disease.

FIGURE 21-10 ■ Plastic iritis. This severe, acute, nongranulomatous uveitis has flare caused by high fibrin content in the aqueous with Grade 4 cells.

FIGURE 21-9 ■ Cells in the anterior chamber. Grade 2 cells represent a moderate uveitic reaction.

FIGURE 21-11 ■ Hypopyon. Note the subtle area of hypopyon at the most inferior aspect of the anterior chamber. (Courtesy Jane Stein.)

FIGURE 21-12 ■ Flare in the anterior chamber. The bright light reflex on the left is the cornea and on the right is the iris. The normally invisible aqueous is visible as a hazy band extending through the anterior chamber.

Anterior synechiae, an abnormal connection between the anterior peripheral iris to the peripheral corneal endothelium, may occur because of iris swelling in anterior uveitis. The iris swells because of the inflammation in the anteroposterior axis, thus narrowing the angle of the eye. In extreme and rare cases, the angle may close and cause an acute closedangle glaucoma attack secondary to the iritis. The synechiae represents a semipermanent adhesion between the iris and cornea, mostly caused by the presence of fibrin acting as biological glue. Breaking of the anterior synechiae may be accomplished with laser therapy or a surgical approach. Any case of anterior uveitis with elevated IOPs mandates a gonioscopic evaluation of the angles to confirm the presence of anterior synechiae.

Posterior synechiae forms much more often than anterior synechiae in cases of anterior uveitis. Here, an adhesion occurs between the iris and the anterior lens surface, most commonly along the pupillary border of the iris (Figure 21-13). The presence of Koeppe nodules increases the chance of posterior synechiae formation, because fibrin binds the nodule to the anterior lens capsule. Posterior synechiae most commonly occurs in granulomatous reactions of the anterior chamber. The adhesion can usually be broken within the first 72 hours of formation by using strong dilating and cycloplegia agents. After 3 days the pharmacological splitting of a posterior synechiae becomes problematic. Although the synechiae does not represent a significant problem to the functioning of the eye, it may cause a distorted pupil, reduce pupillary functioning, and be cosmetically unappealing. Extensive posterior synechiae may bind down the entire pupil leading to pupillary block with iris bombe. As the iris is pushed anterior by accumulating aqueous behind it, the angle

FIGURE 21-13 ■ Posterior synechiae. These adhesions between the iris and anterior lens surface can cause pupil distortion and block aqueous flow into the anterior chamber.

may close down leading to an acute angle-closure glaucoma attack secondary to pupillary block. An emergency laser peripheral iridectomy may be necessary to allow appropriate aqueous drainage from the posterior chamber and restore normal angle anatomy. The presence of posterior synechiae increases the chance of further adhesions should the uveitis reoccur. Therefore, it is imperative to attempt to break any posterior synechiae that is discovered.

Synechiae are considered a complication of anterior uveitis, and because they are often associated with granulomatous disease and iris nodules, their presence increases the likelihood of an associated systemic disease.

Anterior Chamber Angle

In addition to anterior synechiae, iris neovascularization may be associated with anterior uveitis. Also, an intraocular tumor of the angle or a ciliary body mass may cause a uniocular uveitis. Because of these entities, a gonioscopic evaluation of the angle is imperative in all cases of anterior uveitis.

Lens

Anterior uveitis increases the risk of cataract development caused by a change in normal intraocular physiology. In addition, the use of corticosteroids is associated with the development of subcapsular cataract (Figure 21-14). Lens opacities associated with uveitis are not seen as a marker for systemic disease, but this condition can hinder evaluation of the fundus. In some cases of systemic disease-related uveitis, a retinal evaluation is mandatory to help diagnosis. In some extreme cases, cataract removal is essential to determine whether the patient should be on immunosuppressive therapy.