I review the notes made by the ophthalmic assistant regarding the pupils. I correlate any noted RAPD with visual field findings [30]. It is worth reviewing old photos, including those on a driver’s license, for a history of anisocoria (unilateral use of miotics or dilating agents, old trauma, Horner’s syndrome [31] (Fig. 11.2), Adie’s tonic pupil [32]) or other unusual pupil findings. Pupils that do not readily dilate with drops may have had long-term exposure to miotics, posterior synechiae, or previous surgery or trauma. An attack of acute angle-closure glaucoma with very high IOP may result in a nonmotile iris even after the attack is broken [33].

I note the presence (or absence) and location of iridotomies (previously narrow angles or acute angle closure), heterochromia (Fig. 11.3) (Fuchs’ heterochromic iridocylcitis [34, 35] (Fig. 11.4), siderosis [36], congenital Horner’s syndrome [37], unilateral use of HLs), rubeosis [38] (Fig. 11.5a, b) (neovascularization of the iris: CRVO, proliferative diabetic retinopathy, ischemic syndrome), transillumination defects [39] (pigmentary dispersion syndrome or glaucoma) (Fig. 11.6), pseudoexfoliation (Fig. 11.7a, b) material at the pupil margin [40], moth-eaten appearance of the iris (iridocorneal–endothelial (ICE) syndrome [41] (Fig. 11.8) or related diseases), and nodules [42] (Koeppe nodules, inflammatory cell precipitates at the pupillary margin found in nongranulomatous as well and granulomatous uveitis; Busacca nodules on the iris surface, which are pathognomonic for granulomatous uveitides such as sarcoidosis). Iris bombe (Fig. 11.9), a forward bowing of the iris, occurs when the pupil margin is completely bound down to the lens with posterior synechia. The forward pressure of the fluid in the posterior chamber causes the bowed appearance. Portions of the iris may be touching the corneal endothelium. Peripheral laser iridotomies, often needed in several places around the iris, will relieve this forward pressure and allow the iris to flatten to its normal position. Iris bombe may occur in both phakic and pseudophakic eyes with untreated uveitis [43–45].

The patient is requested to look downward while I simultaneously lift their upper lid. I inspect the superior conjunctiva for the presence of a filtering bleb (Fig. 11.10), and if it is found, I note its location, size, shape, and quality (cystic, flat, overhanging the cornea, scarred, etc.) If glaucoma tube shunt surgery has occurred, I described the conjunctiva’s appearance and the presence of any scleral patch graft. I notice if there are any leaks from either kind of glaucoma surgery (Seidel’s test, using sterile fluorescein strips to “paint” the area of the bleb that appears to leak). I release their upper lid and ask them to look forward. I note any hyperemia, possible secondary to chronic use of glaucoma medications (and also ask about itching, burning, etc.). I look for the presence and location of any subconjunctival hemorrhages (Fig. 11.11) and review the patient’s use of aspirin, Plavix, Coumadin, etc. I ask them to look upward and inspect the lower portion of the bulbar conjunctiva. Upper and lower palpebral conjunctival areas are examined if there is significant lid margin disease or symptomatic complaints by the patient. If glaucoma surgery is being contemplated I search for areas of “virgin” conjunctiva to place new incisions.

The epithelial surface, stroma, and endothelial layers of the cornea are examined using both broad and thin slit beams. I have found it increasingly helpful to take the 15 s of extra “chair time” required to do a tear breakup time (TBUT) [46, 47] test for each eye. Chronic exposure to glaucoma medications, which contain toxic benzalkonium chloride (BAK) [48] as well as the natural aging process, may lead to symptoms of ocular surface disease [49] and patient distress. Place a drop of fluorescein with anesthesia on the eye, have the patient blink, and observe the corneal surface through the slit lamp with the blue light engaged. Normal TBUTs are 10 s or longer in duration. Additionally, damaged epithelium may be detected using sterile lissamine green strips [50]. It stains devitalized corneal and conjunctival epithelium and is much gentler to the eye and patient friendly than rose bengal [51] solution.

We examine the endothelial surface for Krukenberg spindles [52] – an isosceles triangle-shaped deposition of melanin pigment found in the central posterior cornea (Fig. 11.12) associated with pigmentary dispersion syndrome (see Fig. 11.6) and glaucoma – and correlate this finding with possible radial slit-like iris transillumination defects. Transillumination defects may best be observed by making the slit-lamp beam bright and small and shining it directly through the pupil with the beam oriented directly in front of the eye, not obliquely. Pigmentary dispersion syndrome and pigmentary glaucoma are discussed in greater detail in Chap.​ 16.

Inflammatory keratic precipitates (KP) (Fig. 11.13) seen on the corneal endothelial surface are indicative of uveitis. These are collections of inflammatory cells. When the uveitis is active, they appear white. They may appear as pigmented residua from old, burned-out inflammatory disease. So-called “mutton-fat” KP are larger, have a greasy appearance, and are generally associated with granulomatous diseases (e.g., sarcoidosis). They contain both macrophages and epithelioid cells. KP may be present in all forms of nonspecific anterior uveitis. In Posner–Schlossman syndrome [53, 54] (Fig. 11.14), the KP may at first appear small and white, later taking on the appearance of pigmented rings with white centers. In Fuchs’ heterochromic iridocyclitis [55], the KP may be small and have a stellate appearance (Fig. 11.15). All forms of anterior segment inflammation may at first lead to increased intraocular pressure because of cellular debris and an inflamed trabecular meshwork, while later inflammation of the ciliary body may lead to a decreased production of aqueous humor and a fall in intraocular pressure [56].

Aging changes of the corneal endothelium may appear as guttata, focal thickenings of Descemet’s membrane (Fig. 11.16). These may be indicative of early Fuchs’ endothelial dystrophy [57–59] (Fig. 11.17), a dominantly inherited, usually bilateral disease more common in women than men, usually presenting in patients older than 60 years of age. Patients with early or late Fuchs’ endothelial dystrophy may be more likely to suffer bullous keratopathy (corneal edema) after intraocular surgery (cataract or glaucoma filter). Younger, asymptomatic individuals may exhibit Hassall–Henle bodies [60], wartlike guttata at the peripheral regions of the corneal endothelium.

If present, I comment on the appearance of an arcus senilis (Fig. 11.18), which represents lipid deposition in the peripheral corneal stroma. When opaque, an arcus may make it difficult to aim laser light through the cornea blocking the attempt to create a truly peripheral iridotomy for patients with narrow anterior chamber angles. Arcus may appear in some persons at a young age (often associated with familiar hyperlipidemia), but is more commonly found in the elderly (hence the name).

Finally, I describe the condition (e.g., clear and compact, edematous, folds in Descemet’s membrane, neovascularized, opaque) of any penetrating keratoplasty (PKP, corneal transplant) that may be present. The presence or absence of sutures, and whether or not the knots are buried, is described in the chart notes.

The anterior chamber (AC) is evaluated for its depth (normal, shallow centrally, or peripherally) and whether or not inflammation is present. The presence and degree of cells, flare (protein), hyphema (blood), or hypopyon (layered white cells) are noted. Cells and flare are evaluated by using a thin and narrow slit beam in a darkened room, to observe the Tyndall effect of light scattering off particles (cells) in a suspension. This is similar to the phenomenon of observing dust particles in the light beam of the projector in a darkened movie theater. Patients with uveitis are often light sensitive and are discomforted by light intensities that need be no stronger than that found in indoors with normal incandescent lighting levels. This patient symptom and complaint suggests uveitis and directs your examination to search for cell and flare. Uveitic glaucomas are more fully explored in Chap.​ 19.

Blood in the AC (hyphema) may be diffused or layered. Trauma is the most likely cause. Fragile abnormal blood vessels on the iris (rubeosis) or in the angle may bleed. This neovascularization may be due to proliferative diabetic retinopathy, following central retinal vessel occlusion, branch retinal vein occlusion, or ocular ischemic syndrome. Inquiries must be made about blood dyscrasias (including sickle cell anemia) and the use of anticoagulants. Blood cells can clog the trabecular meshwork and raise intraocular pressure [61]. If the IOP is raised high enough and long enough, blood staining of the cornea may occur [62].

Mechanical chaffing of the iris by an intraocular lens, usually an anterior chamber lens, can liberate blood and cause the so-called UGH syndrome (uveitis, glaucoma, and hyphema) [63, 64].

Ghost cells – pale tan remnants of blood in the vitreous – may be seen in slit beam or may layer inferiorly in the anterior chamber (Fig. 11.19). They may also clog the trabecular meshwork, usually transiently, and can cause a rise in intraocular pressure [65]. Chapter 21 elaborates on these phenomena.

Hypopyon – a layering of inflammatory cells inferiorly in the anterior chamber – may be sterile or infection related (Fig. 11.20). Hypopyon can result from infectious endophthalmitis, from neoplastic diseases such as leukemia or lymphoma and from inflammatory diseases of many etiologies [66–72]. IOP may increase with both inflammation of the TM and clogging caused by the cellular components.

I perform gonioscopy, in a darkened room, at the initial examination of all glaucoma patients or suspects, without regard to how obviously open the angle appears to be on slit-lamp examination. The anterior chamber angle cannot be seen directly through the cornea, because light coming from structures in the angle undergoes total internal reflection. A goniolens replaces the cornea–air interface with a different interface having a refractive index greater than that of the cornea. Direct gonioscopy provides a direct view of the angle and indirect gonioscopy shows a reflected image from a mirror of a portion of the angle across the anterior chamber. Direct gonioscopy using Koeppe lenses is rarely performed outside of the academic environment.

I prefer to use the indirect Posner goniolens (Fig. 11.21a, b) or the similar Zeiss goniolens. These have four mirrors and thin metal handles. The indirect Sussman lens does not have a handle. While a bit more difficult to manipulate than the more traditional three-mirror Goldmann lens, the Posner and Zeiss devices have two advantages: (1) they may be used for indentation gonioscopy [73], especially helpful when evaluating narrow or slightly appositional angles, and (2) they use the patient’s tear film as an interface, requiring no gooey goniogel coupling agent [74]. Further observations of the eye are thus unimpeded by a corneal surface that is not coated with sticky methylcellulose. With the Posner/Zeiss goniolenses, this portion of the glaucoma examination is simpler for the physician and easier for the patient. Regardless of which goniolens is used, the patient’s eye must first be anesthetized with a topical agent such as proparacaine.

Please note that the silvered outer surface of these prisms may be scratched easily. When I first take possession of a new Posner or Zeiss goniolens, I coat the outer surface with two layers of clear nail polish that seals the surface and prevents scratches.

I take note of the following anterior chamber angle structures (Fig. 11.22):
There is an art as well as a science to appropriately examining the anterior chamber angle by gonioscopy (see Chap.​ 10). Dr. Wallace Alward, of the University of Iowa, has created a superb website (http://​www.​gonioscopy.​org/​) dedicated to teaching gonioscopy skills through videography.

Gonioscopy is inexpensive, convenient, and a skill learned fairly easily. Academic medical centers may have access to anterior segment optical coherence tomography (AS-OCT) [81] and/or ultrasound biomicroscopy (UBM) [82, 83]. UBM can visualize anterior segment structures from the cornea to the ciliary body. Higher-frequency ultrasound gives better resolution but poorer penetration. UBM employs immersion techniques similar to B-scan ultrasonography. AS-OCT has higher resolution than UBM but poorer penetration. Newer AS-OCT machines have good sensitivity and specificity for diagnosing appositional angles [84].

These newer imaging modalities have been useful in examining anterior segment tumors [85, 86] as well as elucidating mechanisms behind pupillary block and plateau iris syndrome [87, 88].

Each machine has proponents advocating its use for determining the potential occludability of anterior chamber angles [89]. Devices under development may automate the process of determining the depth of the anterior chamber angle [90].

Our group has not had the luxury of using these various instruments in the community setting. Fortunately, laser peripheral iridotomy has a high benefit-to-risk ratio, so the occasional eye that is lasered because the angle appears occludable on gonioscopy but is not truly occludable seems a reasonable price to pay for those many eyes that will avoid acute angle closure.

Dilating drops are placed in the new patient’s eyes after they have undergone the anterior segment slit-lamp exam (excluding the lens), gonioscopy, and visual field testing. The patient then sits in a waiting area for about 20 min to allow for maximum effect of the drops. Their chart is placed into a bin adjacent to one of the examining lanes being used by the physician.