lens and cataract surgery

                lens and cataract surgery

 Cataract Terminology

Phakic: When you have your natural lens
Psudophakic eye: When a cataract is replaced with an artificial lens
Aphakik eye: When a cataract is removed but isn’t replaced.

Lens Anatomy
We can’t go any further in our discussion without first describing the anatomy of the lens and how it sits in the eye. When conceptualizing the structure of the lens, you may find it useful to think of it like a yummy peanut M&M candy. Thus, there is an outer capsule like a “hard candy shell” that surrounds the lens. Inside you’ll find the chocolate layer (the lens cortex) and the inner nut (the hard lens nucleus). These three layers are clear, of course, but that’s the general layout.
Cataracts can form at different layers within the lens, and the location can give you clues to the causative insult and explain specific visual complaints. The lens layers become even more relevant during surgery – with cataract extraction, we tear a round hole through the anterior capsule, suck out the cortex and nucleus (the chocolate and the peanut), and inject a prosthetic lens into the remaining capsular bag.
Now, we know the structure of the lens and we know the lens sits behind the iris … but what keeps the lens from falling into the back of the eye? The lens is actually suspended behind the iris by zonular fibers. These zonules attach at the equator of the lens like trampoline springs and attach the lens to the surrounding ciliary body. The ciliary body is a ring of muscle sitting behind the iris. Trauma and surgical mishaps can break the zonules and cause the lens to de-center or even fall into the back of the eye.

Accomodation
Now, I just said that the lens is suspended by spoke-like zonules to the ciliary body. But what is this mysterious ciliary body? The ciliary body is a ring of muscle that sits directly underneath the iris. You can’t see it directly by standard exam without using mirrors, but this ciliary body is important for two reasons: it produces the aqueous fluid that nourishes the eye and it controls lens focusing.
The ciliary muscle can be thought of as a camera diaphragm, or if you prefer a more entertaining description, a sphincter muscle. When this sphincter contracts, the central “hole” gets smaller causing the zonular “springs” to relax. With zonular relaxation, the lens relaxes and gets rounder. This rounding makes the lens more powerful and allows you to read close-up.
Unfortunately, as we age our lens becomes harder and does not “relax” into a sphere very well, no matter how hard the ciliary body contracts. This loss of lens accommodation is called presbyopia and explains why we need the extra power of bifocals to read after the age of 40. 

                                            Cataract 

Nuclear sclerotic cataracts:

NSCs are the most common type of cataract and many consider them to be a normal maturation of the lens. Over time, the lens becomes larger and brunescent (yellow or brown) especially in the denser central nucleus. If this process goes on long enough the opacity eventually leads to visual obstruction and problems with glare. The lens can become so big that it pushes the iris forward, placing the patient at increased risk for angle closure glaucoma.
With far-advanced cataracts the middle cortical layer (the chocolate layer) can liquefy and become milky white and the nucleus layer (the central peanut) gets hard and falls to the bottom of the capsular bag. These end-stage “Morgagnian cataracts” are rarely seen in this country and are particularly hard to remove at surgery.
Some patients with nuclear sclerotic cataracts will develop so called “second sight” where it seems like the vision improves. This is because the round cataract lens is more powerful and offsets the coexisting presbyopia allowing older patients to read better. Their vision really hasn’t really improved, it’s just that their cataracts are working like weak bifocals inside their eyes.

Posterior Subcapsular Cataract:

The PSC cataract forms on the back of the lens, on the inner surface of the posterior capsule bag. These cataracts tend to occur in patients on steroids, with diabetes, and those with history of ocular inflammation. The opacity looks like breadcrumbs or sand sprinkled onto the back of the lens. This posterior location creates significant vision difficulty despite appearing innocuous on slit-lamp exam. PSC cataracts are quite common, and often occur in conjunction with some degree of NSC.

Posterior versus Anterior located cataracts:
Posterior cataracts cause more visual complaints than anterior cataracts. This is because of the optics of the eye. Advanced optics are beyond the scope of this book. Keep in mind, though, that the eye has an overall refractive power of approximately 60 diopters (40 from the cornea, and 20 from the lens). If you simplify the eye to a single 60-diopter lens system, the important “nodal point” of this system is near the back of the lens.
The closer you get to this nodal point, a greater number of light rays will be affected. Thus, small PSC cataracts are more significant than larger anterior cataracts. 

Congenital Cataracts:
Lens opacities in children are of concern because they can mask deadly disease (remember the differential for leukocoria from the pediatric chapter?) but also because they are highly amblyogenic.
Cataracts in the newborn can be idiopathic or inherited. If small or anteriorly located, they may be visually insignificant. However, when approaching a leukocoric pupil, you should first rule out potentially deadly disease. This includes cataract masqueraders like retinoblastoma, and deadly causes of cataract like the TORCH infections and galactosemia.
A true cataract needs to be removed quickly, usually within the first two months of life, because they are highly amblyogenic. Cataract surgery is challenging in this age-group as children have impressive inflammatory responses and are not easy to examine pre- and post-operatively. After taking the cataract out, you don’t implant a prosthetic implant in newborns, but wait a few years because their eyes are still growing. The family must deal with powerful aphakic glasses or contact lens placement until the child is old enough for the secondary lens implantation.

Traumatic Cataract:
A cataract can form after blunt or penetrating injuries to the eye. When the outer lens capsule breaks, the inner lens swells with water and turns white. These injuries typically occur in young men and the lenses are very soft and easy to suck out. Removal and implant placement can be complicated, though, as the blunt force often tears the zonular support. If the lens is barely hanging in position, it may be safer to consult a retina specialist to remove the lens from behind (a pars plana approach) to keep the lens from falling back into the eye. 

Posterior Capsular Opacification (PCO):
A posterior capsule opacification isn’t a true cataract, but an “after cataract” that forms after a cataract surgery. I’ll be talking about the cataract surgery technique in a second, but basically, we suck out the cortex and nucleus (the chocolate and the peanut) and inject a new lens into the remaining capsule (the hard candy shell).
Residual lens epithelial cells are left behind after surgery. These orphaned epithelial cells get confused (and lonely) and can migrate along the back surface of the implant and opacify the posterior capsular bag.
This is a common occurrence and fortunately is easily treated in clinic with a laser. The YAG laser is used to blast a hole in the posterior capsule. We don’t break a large hole, as you don’t want the implant to fall into the back of the eye, but one big enough to clear the visual access. This is known as a YAG capsulotomy.

                                            choose your LENS implant power
Our goal in cataract surgery is to put the ideal power intraocular lens into the eye such that the patient won’t need additional glasses for viewing distant objects. This is not always an easy task, as everyone’s eyes are different and minor anterior-posterior shifts in the lens placement will severely affect the end refraction. There are many formulas designed from both lens theory and regression analysis to help you choose the correct power lens. We won’t be going over these formulas, but keep in mind that we need to measure two things to come up with the right prescription for the implant:

a. The corneal curvature: Remember that the cornea-air interface actually performs the majority of the refractive power of the eye. The cornea performs approximately 40-diopters of refraction, while the lens makes up the last 20-diopters. A person with a powerful cornea will need a less powerful lens. We measure the curvature of the cornea with a keratometer. 

b. The length of the eye: The shorter the eye, the more powerful lens you’ll need to focus images onto the retina. We measure this with the A-scan mode of a hand-held ultrasound.

                               Cataract Surgery                                

1. Anesthesia
Dilate the pupil, prep, and anesthetize the eye. Anesthetic can be given with simple topical eyedrops like tetracaine. We can also perform a retrobulbar block by injecting lidocaine/bupivicane into the retrobulbar muscle cone to knock out sensation through V1, and eye movement by knocking out CN3 and CN6. The trochlear nerve (CN4) actually runs outside the muscle cone, so you can see some residual eye torsion movement after the block. If you’ve never seen a retrobulbar block, you’re in for a treat (it can look gruesome the first time).

2. Enter the eye
The main surgical entry site can be performed several ways. You can enter the eye by cutting through the cornea, or you can spend more time tunneling in from the sclera. A clear-cornea incision is fastest, while the scleral tunnel takes longer but is easier to extend if you run into surgical complications.

3. Capsulorhexis
To get the lens out you need to tear a hole in the anterior capsule (hard candy shell) of the lens. This step is important to get right, because if the rhexis is too small, it will make cortex and nucleus removal harder. Also, the outer capsule you are tearing is finicky and can tear incorrectly, with a rip extending radially outwards to the equator (not good). If you lose your capsule, you can lose pieces of lens into the back of the eye. Poor capsular support also makes implant placement that much harder.

4. Phacoemulsify
We use an instrument called the phaco handpiece to carve up the lens nucleus. This machine oscillates at ultrasonic speeds and allows us to groove ridges into the lens. After grooving, the lens can be broken into pie-pieces and eaten up one-by-one.

5. Cortical removal
After removing the inner nucleus, we can remove the residual cortex (the middle chocolate layer) of the lens. This cortex is soft but wants to stick to the capsular bag. You don’t want to leave too much, as it will cause inflammation and can cause “after cataracts” (posterior capsule opacification). We strip this with suction and vacuum it out.

You need to be careful with your posterior capsule during this cleanup. The surgeon tries to maintain the posterior capsule for a couple of reasons - not only does it create a support structure for the new lens, but it maintains the barrier between the anterior and posterior chambers, keeping the jelly-like vitreous from squeezing into the anterior chamber.

6. Insert the lens
We usually use a foldable lens that can be injected directly into the bag. If we’ve lost capsular support (for example, we managed to break the posterior capsule during phaco or cortex removal), the lens can be placed on top of the entire capsular bag, right behind the iris. If support for this sulcus placement is questionable (i.e. you’ve had a LOT of complications with the case), a lens can be placed in the anterior chamber on top of the iris, or sutured to the back surface of the iris (tricky).

7. Close up
You now close the eye. Many small incision corneal wounds are self-sealing, but some require closure with 10-0 nylon suture that will eventually biodegrade.

8. Postop care:
Immediately after surgery, antibiotics are dropped and a shield is placed over the eye. The patient is then seen the next day and will use antibiotic drops and a steroid drop to decrease inflammation.

Optics

                  Optics

Myopia and Hyperopia

A myopic eye just means a “nearsighted” eye. If we draw a picture of this eye, we see that it looks big (and long) and that light focuses not onto the retina, but in front of the retina within the vitreous jelly! To correct this refractive error we use a minus (concave) lens to diverge the incoming rays of light. This effectively weakens the overall refractive power of the eye and pushes the image back onto the retina where it belongs.

Hyperopic eyes are small, short eyes. The axial length of these eyes is so short that light focuses behind the eye. To get that image onto the retina we have to add power to the overall refractive power of the eye by using a plus (convex) lens. These convex lenses are basically your traditional magnifying glass and can make your patient’s eyes look enormous at high power.

Near-reading and Presbyopia
Once we get a patient corrected for distance vision we need to take care of close-up vision. With distance vision, the incoming light rays are coming in parallel before entering the eye. A near object, however, produces expanding divergent rays of light. When these rays hit the eye they end up focusing behind the eye.

To get this near object in focus the eye needs some more refractive power. Fortunately, we are born with the natural ability to increase the strength of the lens by making it rounder. This morphing process is called “accommodation.”

The lens works because it is suspended like a trampoline by surrounding zonular fibers. These fibers attach 360 degrees around the lens and tether the lens to the surrounding ciliary muscle. When the ciliary sphincter contracts the zonules relax and the lens becomes rounder. This rounding of the lens increases its magnification/refractive power and allows us to see near objects. With age, the lens becomes dense and does not easily round out. This presbyopia presents after age 40 and progresses with age, explaining the need for near-reading glasses in this age-group. 

Astigmatism
The cornea surface provides the majority of the refractive power of the eye. In the examples above we assumed that the cornea surface was perfectly spherical like a basketball. However, many patients have some degree of astigmatism, where the corneal surface is shaped more like a football. Thus, one axis of the cornea is steeper than the other.

Retina

             Retina

                                                      Diabetic Retinopathy

Diabetes is a common disease and many affected patients have vision problems. In fact, diabetics are twenty times more likely to go blind than the general population. Diabetic retinopathy is the term used to describe the retinal damage causing this visual loss. Diabetics have a high prevalence of retinopathy, and one out of every five patients with newly diagnosed diabetes will also show signs of retinopathy on exam.

Mechanism of Vessel Breakdown

 Basically, diabetes is a disease of blood vessels. With large amounts of glucose coursing through the circulatory system, a glycosylation reaction occurs between the sugar and the proteins that make up the vessel walls. Over time, this glycosylation promotes denaturing of collagen protein within the walls, creating capillary thickening and eventually, wall breakdown.

While this process occurs throughout the entire body, the microvasculature of certain organs, such as the kidneys and eyes, are more susceptible to damage. Along these lines, a good predictor of microvasculature damage in the diabetic eye is prior evidence of renal microvasculature disease as measured by proteinurea, elevated BUN, and creatinine.

Because vessel damage accumulates over time, the most accurate predictor of retinopathy is duration of diabetes. After 10 years, more than half of patients will show signs of retinopathy, and after 15 years this number increases to nearly 90%. The relative control of glucose during this time is also important, and studies have shown that patients who maintain lower hemoglobin A1C levels have delayed onset and slower progression of disease. Additional risk factors include smoking, hypertension, and pregnancy.

                                                            Types of Retinopathy

1. Nonproliferative diabetic retinopathy (NPDR)

Most patients (95%) have NPDR. This is the earliest stage of retinopathy and it progresses slowly. Because so many diabetic patients have NPDR, this stage is commonly described as “background retinopathy.” The earliest signs of retinal damage arise from capillary wall breakdown, seen on the fundus exam as vessel microaneurysms. Injured capillaries can leak fluid into the retina and the aneurysms themselves can burst, forming “dot-and-blot hemorrhages.”

Dot-blot hemorrhages look small and round because they occur in the deep, longitudinally-oriented cell layers of the retina. This contrasts with the “flame hemorrhages” of hypertension that occur within the superficial ganglion nerve layer, and thus spread horizontally.

With worsening retinopathy and vessel damage, the retina begins to show early signs of ischemia. Cotton-wool spots, seen with hypertension and stasis, are gray spots with soft edges that indicate ischemia/infarction of the superficial retinal nerve fibers. As vessel damage progresses, you can also see beading of the larger retinal veins and other vascular anomalies.

2. Proliferative Retinopathy

With ongoing injury to the retinal vasculature, there eventually comes a time when the vessels occlude entirely, shutting down all blood supply to areas of the retina. In response, the ischemic retina sends out chemicals that stimulate growth of new vessels. This new vessel growth is called neovascularization, and is the defining characteristic of proliferative retinopathy. Far fewer patients have proliferative retinopathy, which is fortunate as this stage can advance rapidly with half of these patients going blind within five years if left untreated. The mechanism and complications of neovascularization merit study, so let’s take a closer look.

                                                      The Mechanism of Neovascularization
With complete vessel occlusion, parts of the retina become starved for nourishment. The ischemic retina responds by releasing angiogenic molecules like VEGF to promote new vessel growth. These new vessels serve to bypass the clogged arteries in order to resupply the starved retina.

A collateral blood supply seems like a great idea, but unfortunately there is a problem. The newly formed vessels are abnormal in both appearance and function. The new vessels are friable and prone to leaking. They also grow in the wrong place, spreading and growing along the surface of the retina. They can even grow off the retina, sprouting up into the vitreous fluid. The vitreous is mostly water, but it also contains a lattice framework of proteins that the new vessels can adhere to. With vitreous movement or contraction, these new connections pull on the retina and the traction can lead to retinal detachment. Since the vessels are also weak, any vitreous traction can break the vessels and create sudden hemorrhaging with subsequent vision loss as the eye fills with blood. Finally, the new vessels can regress and scar down, creating massive traction on the retina underneath.

Neovascularization isn’t just limited to the retina, but can also occur on the iris itself. NVI (neovascularization of the iris) is an ominous sign, as the new vessels can cover the trabecular meshwork and create a sudden neovascular glaucoma.

Macular Edema
Despite the neovascularization phenomenon and its potential for detachments and hemorrhage, the most common cause of blindness in diabetic patients is from macular edema. This occurs when diffuse capillary and microaneurysm leakage at the macula causes the macular retina to swell with fluid.

Macular edema occurs in about 10% of patients with diabetic retinopathy and is more common with severe retinopathy. On exam the macula looks cloudy and mildly elevated, and you can see past evidence of edema in the form of yellow-colored “hard exudates”. These exudates are fatty lipids that are left behind after past macular swelling subsides, similar to a dirt ring in a bathtub.

                                                                         Treatment 

Laser Treatment
In cases of macular edema, an argon laser can be used to seal off leaking vessels and microaneurysm in the retina by burning them. If the leakage or microaneurysm is small and well-defined, it can be selectively sealed off. With larger areas of leaking capillaries, such as diffuse macular edema, the laser can lay down a “grid photocoagulation” pattern over the entire area.

With advanced retinopathy and neovascularization, a different approach is taken. Instead of individually targeting vessels, PRP (pan-retinal photocoagulation) is performed. With PRP, the ophthalmologist burns thousands of spots around the peripheral retina. This destroys the ischemic retina, decreasing the angiogenic stimulus, and commonly leads to regression and even the complete disappearance of the new vessels. This treatment may seem drastic, but it has proven to be effective. Naturally, there are side effects, with peripheral vision loss and decreased night vision (from the rod photoreceptor loss), but this is acceptable if the central vision is saved. I’ve never seen anyone actually complain of decreased vision, but it’s possible and should be stressed during consent.

Vitrectomy

A vitrectomy may also need to be performed and is often done in conjunction with other surgeries. This surgery involves removing the vitreous humor from the eye and replacing it with saline. This allows removal of hemorrhaged blood, inflammatory cells, and other debris that may obscure the visual axis. While removing the vitreous, the surgeon also removes any fine strands of vitreous attached to the retina in order to relieve traction that might have, or will, cause a detachment.

Glaucoma

                                             Glaucoma

Open vs. Closed-Angle Glaucoma
There are two categories of glaucoma and they have very different mechanisms. Open-angle glaucoma is the most common type in our country. It occurs from decreased aqueous drainage caused by an unidentified dysfunction or microscopic clogging of the trabecular meshwork. This leads to chronically elevated eye pressure, and over many years, gradual vision loss.
This differs from closed-angle glaucoma, also called “acute glaucoma,” which occurs when the angle between the cornea and iris closes abruptly. With this closure, aqueous fluid can’t access the drainage pathway entirely, causing ocular pressure to increase rapidly. This is an ophthalmological emergency and patients can lose all vision in their eye within hours.
Let’s examine each of these types of glaucoma in more detail. 

Open-Angle Glaucoma
The majority of glaucoma patients (about 80% ) have chronic open angle glaucoma. Most patients are over the age of 40. This condition is more common in African Americans, and has a strong familial inheritance. The major risk factors are family history, age, race, high eye pressure, and large vertical nerve cupping. More recently, thin-corneas have been found to be a major risk factor, though this mechanism is not well understood.
The underlying mechanism for open-angle glaucoma involves degeneration of the trabecular meshwork filter, usually by unknown causes, that leads to aqueous backup and chronically elevated eye pressure. With prolonged high pressure, the ganglion nerves in the retina (the same nerves that form the optic nerve) atrophy. The exact mechanism for this nerve damage is poorly understood and proposed mechanisms include stretching, vascular compromise, and glutamate transmitter pathways. As the ganglion nerves are progressively destroyed, vision is gradually lost.
Open-angle glaucoma has the reputation of being the “sneaky thief of sight” because the visual loss occurs so slowly that many patients don’t realize they have the disease until it is far advanced.
Because the disease is otherwise asymptomatic, detecting open-angle glaucoma requires early pressure screening. Free screening clinics also use different types of automated visual-field testing to detect subtle peripheral vision loss. 

Presentation
Open-angle glaucoma patients usually present with three exam findings: elevated eye pressures, optic disk changes, and repeatable visual field loss patterns.

1. Pressure: The most accurate way to measure eye pressure is with the Goldman applanation tonometer. This is a device mounted on the slit-lamp that measures the force required to flatten a fixed area of the cornea. Normal pressures range from 10 to 20 mm Hg, while glaucoma patients can measure over 21 mm Hg. Keep in mind that eye pressure can fluctuate throughout the day (typically highest in the morning) so the pressure should be checked with each visit and the time of measurement should be noted. Also, some glaucomatous eyes have a “normal” pressure. In other words, a “good pressure” doesn’t rule out glaucoma, nor does a high pressure necessarily indicate glaucoma. 


2. Fundus Exam: The optic disk looks striking in advanced glaucoma. In normal patients, the optic disk has a physiological indentation or “cup” that is less than one-third the disk diameter. With glaucoma, the ganglion nerve layer slowly dies away, and, as fewer ganglion nerves course through the optic disk, the amount of cupping increases. A cup to disk ratio greater than 0.5 or an asymmetry between the eyes suggests ganglion atrophy caused by glaucoma.

3. Visual Loss: The vision loss from chronic glaucoma occurs in characteristic patterns that can be followed by automated perimetry (machines that map out the peripheral vision). The central vision is typically spared – in fact, late stage patients may have 20/20 central vision, but be otherwise legally blind because of peripheral blindness.

Treatment:
Since IOP is the only risk factor we can treat, the primary treatment of glaucoma focuses on decreasing eye pressure to less than 20 mm Hg or even lower depending upon the severity of disease. Treatment may be either medical or surgical. 

Medical Treatment
Topical beta-blockers are the traditional therapy for these patients and have been around for decades. Beta-blockers work by decreasing aqueous humor production at the ciliary body. Unfortunately, systemic side effects can occur from nasal absorption, making it especially important to ask your patients about history of asthma, COPD, and cardiac problems.
These days, many physicians are using newer drugs like topical CAIs, alpha-agonists, and prostaglandin analogues for first-line therapy, as they have fewer systemic side effects.
Prostaglandin analogues like latanoprost (Xalatan™) are the newest of these glaucoma drugs, and they are very popular as a first-line agent. They work by increasing aqueous humor outflow. They do have some side effects, though. They can make eyelashes grow longer (many patients actually like this), and in a few patients may darken the iris color, turning green and blue eyes brown. 

Surgical Treatment for Chronic Glaucoma
If eyedrops aren’t working, there are several surgical techniques available to relieve eye pressure. One common surgery is the trabeculectomy, where an alternate drainage pathway is surgically created. A small hole is cut through the superior limbus, creating a drainage tract from the anterior chamber to a space under the conjunctiva. This can be very effective in decreasing pressure, but if the patient is a rapid healer the shunt can scar down and close, so anti-metabolites like mitomycin-C are often applied to the site. If this surgery doesn’t work, a plastic tube-shunt can be inserted into the anterior chamber that drains to a plate fixed under the conjunctiva further back.

Several laser procedures can also help. Argon laser trabeculoplasty (ALT) can be used to burn portions of the trabecular meshwork itself. The resulting scarring opens up the meshwork and increases outflow. A laser can also be used to burn the ciliary body to decrease aqueous production at its source. 

                                                                            Acute Glaucoma

Acute glaucoma is a medical emergency. The most common mechanism is pupillary block. This occurs when the lens plasters up against the back of the iris, blocking aqueous flow through the pupil. This resistance produces a pressure gradient (this is a good buzz word to memorize) across the iris that forces the iris and lens to move anteriorly. When the iris moves forward, the irido-corneal angle closes, blocking the trabecular meshwork. Without an exit pathway, aqueous fluid builds up, eye pressure increases rapidly, and the retina is damaged from stretching and decreased blood supply.
The outflow angle can close for many reasons, and people with naturally shallow anterior chambers such as hyperopes (far-sighted people with small eyes) and Asians are predisposed to developing angle closure. One inciting condition that is typical in acute glaucoma is pupil dilation — many patients describe onset of their symptoms occurring while in the dark or during stressful situations. When the iris dilates, the iris muscle gets thicker and the irido-corneal angle becomes smaller, making it more likely to spontaneously close. Along those lines, medications that dilate the eye, such as over-the-counter antihistamines and cold medications, also predispose angle closure. 

Presentation
These patients will present with an extremely red and painful eye, often complaining of nausea and vomiting. On exam, you’ll find their pupil sluggish and mid-dilated. Pressures in the affected eye can be very high, often 60 mm Hg or higher. The eye will feel rock hard, and you can actually palpate the difference between the eyes with your fingers. One classic sign that patients often describe is seeing halos around lights. This occurs because the cornea swells as water is pushed under high pressure through the endothelium into the corneal stroma. This corneal swelling also makes it hard for you to see into the eye, further complicating diagnosis and treatment.

Acute Glaucoma Exam Techniques:
Ophthalmologic examination for acute glaucoma involves measuring the eye pressure, accessing the anterior chamber angle, and a fundus exam.
One trick to determine whether an angle is shallow is to shine a simple penlight across the eyes. If the iris is pushed forward, it will cast a shadow. Additionally, an ophthalmologist can visualize the angle directly through gonioscopy. Here’s how it works: 

Gonioscopy:
Normally, the inside angle cannot be seen with a microscope because the cornea-air interface creates “total internal reflection.” However, we can use a goniolens, which is a special glass lens with mirrors on its sides, to look directly at the angle. When the glass lens is placed directly onto the cornea, the cornea-air interface reflection is broken and light from the angle can escape and be seen through the mirrors.

Acute Glaucoma Treatment
In cases of acute glaucoma, you want to decrease the pressure in the eye as quickly as possible. A “kitchen sink” approach is often used, throwing many treatments on at once. You can decrease aqueous production using a topical beta-blocker like Timolol and a carbonic anhydrase inhibitor like Diamox. Also, osmotic agents such as oral glycerin or IV mannitol (even ethanol, in a bind) can be given systemically to draw fluid out of the eye and back into the bloodstream. Finally, a miotic such as pilocarpine may be helpful in certain cases to constrict the pupil and thus open up the outflow angle. You can also use topical glycerin to transiently dehydrate/clear the cornea to aid with examination.
Ultimately, these patients need surgical treatment to avoid recurrence of their angle closure. A high intensity laser can burn a hole through the iris and create a communication between the posterior and anterior chambers, relieving the pressure gradient  across the iris, and allowing it to move back into a normal position. This opens up the trabecular meshwork and allows aqueous fluid to flow freely out of the eye. This procedure is typically performed on both eyes because these patients are predisposed to having attacks in the other eye as well.

Other types of glaucoma

1. Neovascular Glaucoma:
This can occur in diabetic patients or those with a retinal vein occlusion.  

2. Pigment Dispersion Syndrome (PDS):
Occurs when the pigmented back-surface of the iris rubs against the radial zonules supporting the lens.

3. Pseudoexfoliation Syndrome (PXF)
In this systemic condition, basement membrane-like material is deposited throughout the body. This material adheres to the anterior lens capsule, creating a rough surface. As the overlying iris dilates and contracts with daily activity, pigment is rubbed off and clogs the trabecular drain. These patients also suffer from zonular instability, making cataract operations difficult.   

Eye Trauma

                      Eye Trauma

Corneal Abrasions:
The surface of the cornea is covered by a thin layer of epithelium. The cornea contains more nerve innervation (per surface area) than any other place in the body so these abrasions “hurt like the dickens,” with patients complaining of excruciating pain and intense photophobia. Abrasions are easy to see, even without a microscope, as the raw surface will uptake fleurosceine and glow bright green under a blue light.

Fortunately, abrasions recover quickly and will often completely heal within 24 hours. Until complete epithelial healing you treat with aggressive lubrication and follow these eyes closely to insure the raw wound doesn’t become infected. Many physicians will treat an abrasion with empiric erythromycin ointment as well, reserving more aggressive antibiotics like ciprofloxacin for contact lens wearers and “dirty wounds” caused by tree branches, etc..
If an abrasion does become infected, you’ll see a white infiltrate at the wound. Any abrasion with an infectious infiltrate is officially called a “corneal ulcer.” Depending upon the size and location of an ulcer, you may need to culture the wound and tailor your antibiotic coverage accordingly.

Corneal Lacerations:
Most corneal scratches only involve the surface epithelial layer. If the injury goes deeper into the stroma, then you have a laceration. With any laceration you want to insure that the cornea hasn’t perforated. You can check corneal integrity with the “Seidel test.” You wipe a strip of fluorescein paper over the wound and see if dye flows down the corneal surface, indicating leaking aqueous fluid.
If a patient is “Seidel positive” than you have an open-globe injury - time to call in your seniors for possible surgical repair! 

Orbital Wall Fractures:
The bony orbital walls are thin and tend to break with blunt impact to the eye. This is especially true of the orbital floor and medial wall. These orbital fractures are common and you will see them weekly (usually at two in the morning). 
Most of the time these orbital bones heal fine with no long-term problems, with patients merely having a great deal of orbital and periorbital swelling that resolves over a few weeks. However, sometimes the broken bone creates a “hinge” or “trapdoor” that entraps fat or extraocular muscles. If there is significant entrapment or enophthalmos, we need to repair the break. During surgery we can release the muscle and bolster the floor to keep orbital contents from herniating back through the defect. This surgery is usually performed by an oculoplastics specialist.

Lid Lacerations:
When evaluating lid lacerations, you need to determine if the laceration involves the lid margin and how close the cut is to the canalicular (tear drainage) system. Most of these lid lacerations are straight-forward to repair, though special effort is made to align the lid margins to avoid lid notching and misdirected eyelashes.
If the laceration is medial (near the nose) you need to worry about the canalicular tear system - repair of this drain is much more involved and involves threading silicone tubes down into the nose to keep the canaliculus patent. 

Metal :
Small pieces of metal can fly into the eye – an unfortunate event occurring primarily in welders or construction workers. Particles of metal stick onto the cornea causing small abrasions and discomfort. Metal rusts quickly and will form a rust ring within a day. You can remove metal objects and rust rings at the slit-lamp using a needle. You can also use a small dremel-like drill to drill off the rust-ring. If the rust is deep, or aggressive pursuit seems to be making the situation worse, you can leave the residual rust in place as most of it will eventually migrate to the surface by itself.
Anytime you have metal-striking-metal injuries, you must entertain the possibility of an intraocular foreign body. Small metal fragments can enter the eye at high speed and leave little or no signs of injury. Metal is very toxic to the retina and can kill the retinal cells if not detected. If you have any suspicion for penetrating injury, you should always order a thin-slice CT scan of the head to look for metal pieces not obvious on exam. You want to avoid MRI in this setting to avoid creating a moving projectile inside the eye.

                                                                         Chemical Injuries:
 The first thing you do with any chemical injury is:

Irrigate, Irrigate, Irrigate, Irrigate

The final visual outcome for a chemical burn is going to depend upon how quickly the chemical is washed out of the eye. If a patient calls you with a chemical conjunctivitis, tell them to immediately wash their eyes out! If the ER calls you with a chemical conjunctivitis, tell them to start irrigating immediately - several liters in each eye. Then grab your equipment and pH paper and head on down there!
Acids are less dangerous than bases as acids tend to precipitate denatured proteins and this limits tissue damage. Bases, on the other hand, just keep on going like the proverbial Energizer Bunny so you need to continually irrigate and check the pH until it normalizes.
On exam you want to carefully check the state of the cornea – hopefully, it is still clear. A red, inflammed conjunctiva is actually a good finding: if the conjunctiva is white, that means its blanched out from extreme damage. Be sure to flip the lids and irrigate/sweep the fornices to remove any material that may be retaining chemicals.
Chemical injuries can lead to significant scarring that may require corneal transplant if bad enough, so you want to be very aggressive with that irrigation!! The emergency room has access to a simple device called a Morgan lens to help irrigate via a suspended saline bag. Little kids hate this thing and have to be restrained when using it. 

Hyphema:
A hyphema describes blood floating in the anterior chamber, a common finding after blunt eye trauma. If the bleed is large, the blood will settle out in a layer at the bottom of the anterior chamber. If the entire AC is filled with blood, you’ll see an “8-ball hyphema.” Most of the time, however, the bleeding is microscopic and can only be seen as “red cells” floating in the aqueous fluid.

Open Globe Injuries:
The eye can be perforated many ways , firecracker explosions, gunshot wounds, car wrecks, and domestic accidents . Visual outcome is usually terrible and a blind, painful eye may need later enucleation.
If you suspect an open globe injury you need to evaluate the eye in the operating room. One thing to remember - if you suspect an open globe injury, cover the eye with a shield and don’t push on it. You could extrude the eye contents  if you push on the eye. 

Eye infections

                 Eye infections

The eye is well protected from infection by the conjunctiva and the corneal epithelium. In addition, the tear film contains antimicrobials while the tear flow itself tends to wash away pathogens. The eye also harbors a host of non-pathogenic bacteria that competitively prohibit new bacteria growth. However, these eye-defenses can be breached by trauma, improper tearing, or contact lens wear and lead to an infection. An eye infection not only threatens vision, but the orbit can act as an entry portal to the rest of the body and infections can progress to systemic involvement, meningitis, and even death.

RED Eye: three types of Conjunctivitis
The conjunctiva is the semi-transparent skin covering the white part of the eye. This layer protects the eye from foreign bodies, infections, and irritants. However, the conjunctiva itself is susceptible to irritation and infection from virus and bacteria. Conjunctivitis, or “pink eye,” is the term used to describe inflammation of the conjunctiva and commonly occurs from three different sources: viral, bacterial, or allergic.

1. Viral conjunctivitis is the most common type, making up half of all cases of conjunctivitis in the adult. It is usually caused by an adenovirus, often following an upper respiratory infection or cold. Viral conjunctivitis is quite contagious and other family members may also complain of having “red eye.” Infected patients typically present with eye redness and watery tearing, but little mucous discharge. Often, only one eye is infected, but the infection may hop to the other side before the end. Two specific signs on exam are enlarged follicular bumps on the inside of the eyelids (these look like tiny blisters) and swelling of the preauricular node located in front of the ear. Most of these infections clear up on their own within a few days. Like the common cold, treatment is geared toward relieving symptoms. Viral conjunctivitis is so contagious that I also recommend good hygiene and no towel/makeup sharing in the home. A lot of people at our hospital present with pink-eye, and this diagnosis is often an instant three-day vacation from work as we don’t want to spread the infection to patients. 

2. Bacterial conjunctivitis presents with a mucupurulent (pus) discharge. This creamy discharge may cause your patient to complain of sticky eyelashes, with patients finding their eyes matted shut upon waking in the morning. Bacterial conjunctivitis often develops a papillary conjunctival reaction (red bumps on the inside of the lids) and, unlike viral infections, typically does NOT have preauricular node enlargement.


The most common culprits are staph and strep, although with children you should also consider Hemophilus influenza bacteria. In addition, sexually active adults may harbor chlamydial and gonococcal infections (especially with severe or sudden discharge). We treat most conjunctivitis with erythromycin
ointment. 

3. Allergic Conjunctivitis: Finally, patients with allergic conjunctivitis present with red, watery eyes. The hallmark symptoms of allergy are itching and swelling. On exam you may see swelling around the eyes that we call “allergic shiners.” Patients often have a history of seasonal allergies and will usually present with other allergic symptoms such as a stuffy nose and cough. Treatment for allergic conjunctivitis involves avoidance of the offending allergens. These patients may need antihistamines, mast-cell stabilizers, and possibly steroids.

                                                   Pathognomonic symptoms include:
1. Viral: watering, follicles, swollen lymph nodes
2. Bacterial: creamy discharge, unilateral
3. Allergy: bilateral itching and swelling

Blepharitis:
Blepharitis means inflammation (itis) of the eyelids (bleph), specifically the eyelid margin. This condition is a common diagnosis in an eye clinic, with patients complaining of stinging, tearing, and a “gritty” sensation in their eyes.
The primary treatment for blepharitis involves good lid hygiene. Most cases can be relieved in a few weeks by having your patient wash their eyelashes daily with baby shampoo and a washcloth. Warm compresses will also help as they open up the orifices of the meibomian glands , also may require topical some times oral antibiotics.

Chalazion:
Chalazions are granulomatous inflammations of the meibomion gland. These glands produce the lipid component of the tear film and are deeply located within the supporting tarsal plate of the lid. Chalazions occur when meibomian gland pores become clogged (such as in blepharitis) — lipid backs up into the gland, and a noninfectious inflammatory granuloma reaction occurs.
On exam, the patient will have a firm and mobile nodular bump on their eyelid. When you evert the lid, you’ll often see the chalazion bump more clearly. They are non-tender and are not painful.
Early treatment involves warm compresses, massage, and lid scrubs in an attempt to reopen the meibomian pore and allow the material to flow out. If this doesn’t work, we flip the lid and incise/drain the chalazion from the inner eyelid surface. Some people are more prone to developing chalazions and they tend to reoccur.

Chlamydial Conjunctivitis:
Chlamydia causes two different kinds of conjunctivitis: inclusion conjunctivitis and trachoma. 

Gonococcal Infection:
While gonococcal infection is much rarer than chlamydial infection, it is very serious as gonorrhea can progress rapidly. These patients will present with redness of the conjunctiva and profuse mucopurulent discharge. This is a serious infection, as the organism can penetrate through a healthy cornea and perforate within 24-48 hours, leading to endophthalmitis and loss of the eye. The eye can also act as an entry portal for meningitis and septicemia.

Corneal Abrasions and Ulcers:
Corneal abrasions are very common and the most common consult that we get from the ER. Superficial epithelial defects can occur after trauma, infection, or from exposure. The cornea contains more nerve endings per area than anywhere else in the body, so scratches here are painful, and patients will often have photophobia (pain with bright lights) with the sensation that “something is in the eye.” Fortunately, with aggressive lubrication, the superficial epithelial layer heals quickly, literally within a day or two, and the patient feels better. We’ll often treat the eye with empiric erythromycin until the epithelium reforms.
If an epithelial defect has an associated bacterial infiltrate, this is called a corneal ulcer. Ulcers are treated aggressively with antibiotics and should be followed on a daily basis until the epithelial defect has closed. For straightforward, small ulcers, we typically use a fluoroquinolone like ciprofloxacin. If the ulcer is large, centrally located, or not healing, then we culture and tailor antibiotics accordingly.

Contact lens:
Contact lens wearers are more likely to have a dangerous infection with pseudomonas. In these patients, we cover with ciprofloxacin. If the ulcer looks bad, we’ll admit for hourly fortified antibiotics (ex. vancomycin and amikacin). Also, we treat any “dirty” ulcer (i.e., caused by tree branch, fingernail, soil) with more aggressive antibiotics.
With sterile epithelial defects you can patch the eye to promote lubrication and speed healing. However, you don’t want to patch an eye with a potential infection and you should follow patched eyes on a daily basis to make sure a perforating ulcer isn’t brewing under that patch.

Pre- and Post-septal Cellulitis:
Patients may present with a swollen eyelid that appears to be infected (swelling, erythema, warmth, systemic fever). When approaching a patient with a taut, infected eyelid the important distinction you must determine is whether the infection is located pre- or post-septally.
The “septum” is a layer of connective tissue that runs from the tarsal plate of the eyelid to the surrounding orbital rim. Infections superficial to this septum can look bad, but generally resolve without problems. However, if an infection tracks back behind the septum, you’re in trouble and will need to admit the patient for IV antibiotics and possible surgical abscess drainage. Orbital cellulits occurs most commonly from sinus disease, especially in children, with bacteria eroding through the thin ethmoid bone into the orbit. They can also arise from tooth abscess and even from fungal infections in patients that are immuno-compromised with glycemic problems.
Symptoms of post-septal orbital involvement are pretty obvious: soft-tissue swelling will cause proptosis and chemosis (swelling of the conjunctiva). Intraocular muscle inflammation causes decreased motility and painful eye movement. If the optic nerve is affected they’ll have decreased vision and possibly an APD.
Whenever you see a big swollen eyelid you should always check for these signs of post-septal involvement and if suspected, order a CT scan. Ophthalmology and ENT has to make this distinction frequently, often in the pediatric emergency room. 

Herpes Simplex Virus:
Herpes infection around the eye is quite common - when herpes attacks the cornea, we call this “herpetic keratitis.” Herpetic keratitis is caused by HSV Type-1. This is a common virus, and the vast majority of people contract it during childhood with almost 100% of people over 65 years with latent infection. 

Anatomy of the Eye

              Anatomy of the Eye

Eyelids
The eyelids protect and help lubricate the eyes. The eyelid skin itself is very thin, containing no subcutaneous fat, and is supported by a tarsal plate. This tarsal plate is a fibrous layer that gives the lids shape, strength, and a place for muscles to attach.

Underneath and within the tarsal plate lie meibomian glands. These glands secrete oil into the tear film that keeps the tears from evaporating too quickly. Meibomian glands may become inflamed and swell into a granulomatous chalazion that needs to be excised. Don’t confuse a chalazion with a stye. A stye is a pimple-like infection of a sebaceous gland or eyelash follicle, similar to a pimple, and is superficial to the tarsal plate. Styes are painful, while chalazions are not.

Eyelid Movement 
Two muscles are responsible for eyelid movement. The orbicularis oculi closes the eyelids and is innervated by cranial nerve 7. Patients with a facial nerve paralyses, such as after Bell’s Palsy, can’t close their eye and the eye may need to be patched (or sutured closed) to protect the cornea. The levator palpebrae opens the eye and is innervated by CN3. Oculomotor nerve palsy is the major cause of ptosis (drooping of the eye). In fact, a common surgical treatment for ptosis involves shortening the levator tendon to open up the eye.

Conjunctiva

The conjunctiva is a mucus membrane that covers the front of the eyeball. When you examine the “white part” of a patient’s eyes, you’re actually looking through the semi-transparent conjunctiva to the white sclera of the eyeball underneath. The conjunctiva starts at the edge of the cornea (this location is called the limbus). It then flows back behind the eye, loops forward, and forms the inside surface of the eyelids. The continuity of this conjunctiva is important, as it keeps objects like eyelashes and your contact lens from sliding back behind your eyeball. The conjunctiva is also lax enough to allow your eyes to freely move. When people get conjunctivitis, or “pink eye,” this is the tissue layer affected.

There is a thickened fold of conjunctiva called the semilunar fold that is located at the medial canthus - it is a homolog of the nictitating membrane seen on sharks.

Tear Production and Drainage
The majority of tears are produced by accessory tear glands located within the eyelid and conjunctiva. The lacrimal gland itself is really only responsible for reflexive tearing. Tears flow down the front of the eye and drain out small pores, called lacrimal punctum, which arise on the medial lids. These puncta are small, but can be seen with the naked eye.
After entering the puncta, tears flow down the lacrimal tubing and eventually drain into the nose at the inferior turbinate. This explains why you get a runny nose when you cry. In 2-5% of newborns, the drainage valve within the nose isn’t patent at birth, leading to excessive tearing. Fortunately, this often resolves on it’s own, but sometimes we need to force open the pathway with a metal probe.

Lid Lacerations
Most lacerations through the eyelid can be easily reaproximated and repaired. However, if a laceration occurs in the nasal quadrant of the lid you have to worry about compromising the canalicular tear-drainage pathway. Canalicular lacerations require cannulation with a silicone tube to maintain patency until the tissue has healed.

Warning: Drug absorption through the nasal mucosa can be profound as this is a direct route to the circulatory system and entirely skips liver metabolism. Eyedrops meant for local effect, such as beta-blockers, can have impressive systemic side effects when absorbed through the nose. Patients can decrease nasal drainage by squeezing the medial canthus after putting in eyedrops. They should also close their eyes for a few minutes afterwards because blinking acts as a tear pumping mechanism.

The Eyeball:
The eyeball is an amazing structure. It is only one inch in diameter, roughly the size of a ping-pong ball, and is a direct extension of the brain. The optic nerve is the only nerve in the body that we can actually see (using our ophthalmoscope) in vivo.

The outer wall of the eye is called the sclera. The sclera is white, fibrous, composed of collagen, and is actually continuous with the clear cornea anteriorly. In fact, you can think of the cornea as an extension of the sclera as they look similar under the microscope. The cornea is clear, however, because it is relatively dehydrated. At the back of the eye, the sclera forms the optic sheath encircling the optic nerve.

The eyeball is divided into three chambers, not two as you might expect. The anterior chamber lies between the cornea and the iris, the posterior chamber between the iris and the lens, and the vitreous chamber extends from the lens back to the retina.

The eye is also filled with two different fluids. Vitreous humor fills the back vitreous chamber. It is a gel-suspension with a consistency similar to Jell-O. With age and certain degenerative conditions, areas of the vitreous can liquefy. When this occurs, the vitreous can fall in upon itself – usually a harmless event called a PVD (posterior vitreous detachment). However, this normally benign vitreous detachment can sometimes tug on the retina and create small retinal tears.

Aqueous humor fills the anterior and posterior chambers. This is a watery solution with a high nutrient component that supports the avascular cornea and lens. Aqueous is continuously produced in the posterior chamber, flowing forward through the pupil into the anterior chamber, where it drains back into the venous circulation via the Canal of Schlemm.

The Cornea:
The cornea is the clear front surface of the eye. The cornea-air interface actually provides the majority of the eye’s refractive power. The cornea is avascular and gets its nutrition from tears on the outside, aqueous fluid on the inside, and from blood vessels located at the periphery.

On cross section, the cornea contains five distinct layers. The outside surface layer is composed of epithelial cells that are easily abraded. Though epithelial injuries are painful, this layer heals quickly and typically does not scar. Under this lies Bowman’s layer and then the stroma. The corneal stroma makes up 90% of the corneal thickness, and if the stroma is damaged this can lead to scar formation. The next layer is Descemet’s membrane, which is really the basal lamina of the endothelium, the final inner layer.

The inner endothelium is only one cell layer thick and works as a pump to keep the cornea dehydrated. If the endothelium becomes damaged (during surgery or by degenerative diseases) aqueous fluid can flow unhindered into the stroma and cloud up the cornea with edema. Endothelial cell count is very important as these cells don’t regenerate when destroyed – the surviving endothelial cells just get bigger and spread out. If the cell count gets too low, the endothelial pump can’t keep up and the cornea swells with water, possibly necessitating a corneal transplant to regain vision.

Decemet’s membrane is “deep,” while Bowman’s layer is high up in the “belfry.” A belfry is a room, usually high up in a tower, where bells are hung.

The Anterior Chamber Angle:
The angle formed by the inner cornea and the root of the iris is particularly important in ophthalmology. Here you find the trabecular meshwork with its underlying Schlemms Canal. This is where aqueous is drained, and blockage of this pathway/angle will become important as we discuss glaucoma.

The Uvea:
The iris, ciliary body, and the choroid plexus are all continuous with each other and are collectively called the uvea. This is an important term, as many people can present with painful “uveitis” - spontaneously or in associated with rheumatologic diseases.

The iris is the colored part of the eye and its primary function is to control the amount of light hitting the retina. Sympathetic stimulation of the pupil leads to pupil dilation and parasympathetic stimulation leads to constriction. In other words, if you see a bear in the woods, your sympathetics kick in, and your eyes dilate so you can see as much as possible as you run away. I’ll be using this mnemonic/metaphore many times throughout this book to help you remember this concept.

The inner iris flows back and becomes the ciliary body. The ciliary body has two functions: it secretes aqueous fluid and it controls the shape of the lens. The ciliary body contains sphincter muscles that change the lens shape by relaxing the zonular fibers that tether to the lens capsule.

The choroid is a bed of blood vessels that lie right under the retina. The choroid supplies nutrition to the outer one-third of the retina which includes the rod and cone photoreceptors. Retinal detachments can separate the retina from the nutritious choroid, which is disastrous for the photoreceptors as they quickly die without this nourishment.

Lens:
The lens sits behind the iris. The lens is unique in that it doesn’t have any innervation or vascularization. It gets its nourishment entirely from nutrients floating in the aqueous fluid. The lens also has the highest protein concentration of any tissue in the body (65% water, 35% protein).

The lens has three layers in a configuration similar to a peanut M&M. The outer layer is called the capsule. The capsule is thin with a consistency of saran wrap and holds the rest of the lens in place. The middle layer is called the cortex, while the central layer is the hard nucleus. Cataracts are described by where they occur such as nuclear cataracts, cortical cataracts, and subcapsular cataracts. With cataract surgery the outer capsule is left behind and the artificial lens is placed inside this suporting bag.

The capsule is held in place by suspensory ligaments called zonules that insert around the periphery and connect to the muscular ciliary body. Contraction of the ciliary muscle causes the zonule ligaments to relax (think about that for a minute), allowing the lens to become rounder and increase its refracting power for close-up reading.

In children the lens is soft but with age the lens hardens and becomes less pliable. After age 40 the lens starts having difficulty “rounding out” and people have problems focusing on near objects. This process is called presbyopia. Almost everyone over 50 needs reading glasses because of this hardening of the lens.

The Retina:
The retina is the sensory portion of the eye and contains layers of photoreceptors, nerves, and supporting cells. Histologically, many cell layers can be seen, but they are not worth memorizing at this point. The important ones include the photoreceptor layer, which is located further out (towards the periphery), and the ganglion nerve layer which lies most inward (toward the vitreous). For light to reach the photoreceptor it has to pass through many layers. After light reaches the photoreceptors the visual signal propagates back up to the ganglion nerves. These ganglion nerves, in turn, course along the surface of the retina toward the optic disk and form the optic nerve running to the brain.

The macula is the pigmented area of the retina that is responsible for central vision. Within the central macula lies the fovea, which is a small pit that is involved with extreme central vision. The fovea is very thin and derives its nutrition entirely from the underlying choroid, making it susceptible to injury during retinal detachments.

The optic disk is the entry and exit point of the eye. The central retinal artery and vein pass through here, along with the the ganglion nerves that form the optic nerve. A physiologic divot or “cup” can be found here that will become important when we talk about glaucoma.

The Orbital Walls:
Seven different bones form the orbital walls: don’t be intimidated by this complexity, however, as these bones are not that confusing when you break them down. For example, the roof of the orbit is a continuation of the frontal bone, the zygomatic bone forms the strong lateral wall, while the maxillary bone creates the orbital floor. This makes sense, and you could probably guess these bones from the surrounding anatomy.

The medial wall is a little more complex, however, but is mainly formed by the lacrimal bone (the lacrimal sac drains tears through this bone into the nose) and the ethmoid bone. The thinnest area in the orbit is a part of the ethmoid bone called the lamina papyracea. Sinus infections can erode through this “paper-thin wall” into the orbital cavity and create a dangerous orbital cellulites.

Despite the fragility of the medial wall, it is well buttressed by surrounding bones, such that it’s the orbital floor that breaks most often during blunt trauma. The maxillary bone fractures downward and the orbital contents can herniate down into the underlying maxillary sinus. This is called a “blowout fracture” and can present with enopthalmia (a sunken-in eyeball) and problems with eye-movements from entrapment of the inferior rectus muscle. We’ll discuss blow-out fractures in more detail in the trauma chapter.

The back of the orbit is formed by the greater wing of the sphenoid bone, with the “lesser wing” surrounding the optic canal. There’s also a little palatine bone back there in the middle, but don’t worry about that one!

The Apex: Entrance into the Orbit
The orbital apex is the entry point for all the nerves and vessels supplying the orbit. The superior orbital fissure lies between the wings of the sphenoid bones, through which many vessels and nerves pass into the orbit.

The “Annulus of Zinn,” a muscular band that serves as the insertion point for most of the ocular muscles, rests on top of the superior orbital fissure. The four rectus muscles attach to the annulus and the optic nerve passes right through the middle.

Eye Muscles:
Four rectus muscles control each eye. These muscles insert at the sclera, behind the limbus, and each pull the eye in the direction of their attachment.

The superior, medial, and inferior rectus muscles are all controlled by the oculomotor nerve (III). The lateral rectus, however, is controlled by the abducens (VI) nerve, which makes sense as the lateral rectus “abducts” the eye.

The remaining two eye muscles are the superior and inferior oblique muscles. The superior oblique also originates in the posterior orbit, but courses nasally until it reaches the trochlea (or “pulley”) before inserting onto the eye. The inferior oblique originates from the orbital floor and inserts behind the globe near the macula. Because of these posterior insertions, the oblique muscles are primarily responsible for intorsion and extorsion (rotation of the eye sideways), though they also contribute some vertical gaze action.

Eye history and physical Exam

        Eye history and physical Exam...

History of Present Illness:


As with all other specialties, a detailed ocular history is crucial to diagnosis. You should explore every complaint with the “basic questions” — when did it start, what’s it like, is there anything that makes it better or worse, are you taking any medications for relieve, etc..

Specific HPI review of systems should also include:

• Floaters and flashing lights: These are the classic symptoms of a retinal detachment and retinal tears so ask EVERY patient about these symptoms. Most patients complain of some floaters - see if they’re actually new or have worsened recently.
• Transient vision loss: Think of migraine vessel spasm in the young and micro-emboli in the elderly. Curtains of darkness might indicate an ischemic event or a retinal detachment, so explore these symptoms in detail.
• Blurry vision: Is the vision always blurry? Does it worsen when reading or watching TV (people blink less when watching TV and develop dry eyes). Is this a glare problem at night that might indicate cataracts? Does the diabetic patient have poor control and hyperglycemic swelling of the lens?
• Red, painful eyes: A common complaint. Be sure to ask about the nature of the pain (is this a scratchy pain, aching pain, or only pain with bright light). Is there discharge that might indicate an infection?
• Chronic itching and tearing: Think about allergies or blepharitis. Is it in both eyes?
• Headaches and scalp tenderness: Think of temporal (giant cell) arteritis and ask about other collaborating symptoms like jaw claudication, polymyalgias, weight loss, and night sweats.

PMH (past medical history):
Past medical history should include the usual health questions, but with the main emphasis on conditions directly contributing to ocular pathology such as diabetes, hypertension, and coronary artery disease. Also, ask about thyroid problems and asthma (you might need to prescribe a beta-blocker and you don’t want to set off bronchospasm).

POH (past ocular history):
Ocular history should inquire about past clinic visits and surgeries. Specifically inquire about cataract surgeries, eye trauma, and glaucoma. You can often piece together your patient’s ocular history by examining their eyedrops.

Family History:Focus on history of glaucoma and blindness. Patients will often confuse glaucoma with cataracts, so be sure to clarify the difference. 

Allergies: List basic allergies and their reaction. We sometimes give Diamox to control eye pressure so make sure your glaucoma patient isn’t allergic to sulfa drugs  

Medications:  Find out what eyedrops your patient is taking, and why. Are they using a regular eyedrop? How about vasoconstricting Visine? Did they bring their drops with them? If your patient can’t remember their medications, it often helps to ask about the bottlecap-color of their drops (ex. all dilating drops have red caps). Also, it’s nice to know if your patient is taking an oral beta-blocker already, in case you want to start a beta-blocking eyedrop.

Vision, Pupil, and Pressure

Vision, pupil, and pressure are the “vital signs” of ophthalmology. After a brief history, I check these measurements before dilating the eyes. This is because dilating drops will effect vision, pupil size, and potentially elevate our pressure measurements so you need to check these signs first. If you ever consult ophthalmology, we will always ask you …

What’s the vision, pupil, and pressure?

It’s kind of a mantra. I don’t know how many times I’ve been told to “get the vision, pupil, and pressure, then dilate them.”

Visual Acuity:

You measure visual acuity with a standard Snellen letter chart (the chart with the BIG E on it). If your patient can’t read the E on the top line, see if they can count fingers at different distances. Failing this, try hand motion and light. Poor distance vision usually occurs from refractive error (your patient needs better glasses).

You want to check a patient’s “best corrected vision” so have them wear their glasses. You’re going to be amazed at the number of people complaining of “blurry vision” who leave their glasses in their car. You’ll also be impressed by the number of consults you’ll get where the consulting doctor hasn’t bothered to check the patient’s vision. Remember: “I can’t see!” is a relative complaint – for some this means 20/25 vision and for others this means complete darkness.

 Pinhole

A quick and easy way to determine whether refraction is the culprit, short of actually testing different lenses, is with the pinhole test. Punch a small hole in a paper card, and have your patient reread the eye-chart while looking through this pinhole. This can actually improve vision by several diopters. It works because the paper blocks most of the misaligned rays that cause visual blur, and allows the central rays to focus on the retina. If your patient shows no improvement with pinholing, start thinking about other visual impediments like cataracts or other media opacities. Most occluders (the black plastic eye cover used during vision testing) have a fold-down pinhole device for this purpose.

Near Vision

Near vision can be assessed with a near-card or by having your patient read small print in a newspaper. Don’t try using the near-card to estimate distance acuity as distance vision is quite different than close-up acuity. That 20/20 marking printed on the near-card only checks “accommodated” near-vision. Remember that older patients can’t accommodate well and need a plus-power lens (reading glasses) to help them read the card. Carry a +2.50 lens with you when seeing older inpatients as most of these patients leave their reading glasses at home. We’ll cover accommodation and presbyopia in greater detail later in the optics chapter.

Pupils:

The pupils should be equally round and symmetric with each other. You can test reactivity to light with a penlight, but a brighter light like the one on the indirect ophthalmoscope will work much better. When testing the eyes, you will see a direct constriction response in the illuminated eye, and a consensual response in the other eye. These should be equal and synchronous with each other. Also, check the pupils with near-vision, as they should constrict with accommodation.

The Swinging Light Test

If one eye is injured, or not sensing light, then your patient may have an APD or “afferent pupillary defect.” Often these defects are only partial, making them difficult to detect on casual examination. To detect small APDs, you need to perform the “Swinging Light Test.” Here’s how it works:

When you shine a light back and forth between two normal eyes, you’ll find that the pupils constrict, then dilate a fraction as the light beam passes over the nose, and then constrict again. As you go back and forth you’ll see constriction, constriction, constriction, and constriction.

Things look different if one eye is partially blind. As before, when you shine the light in the good eye there is constriction. But, when you cross to the other bad eye, both eyes seem to dilate a little. The bad eye still senses light and constricts, but not as well. So you see constriction, dilation, constriction, and dilation. This phenomenon is also called a Marcus Gunn pupil.

Pressure:

We measure pressure by determining how much force it takes to flatten a predetermined area of the corneal surface. There are several ways to do this and in the ophthalmology clinic we use the “Goldman Applanation Tonometer” that is attached to the slit-lamp microscope.

In the ER, or with patients who are difficult to examine, we can check pressure using a handheld electronic Tono-pen. This little device can be tricky and in the wrong hands becomes a random-numbers generator. I’ll talk more about pressure and its importance within the glaucoma chapter.

Confrontational Fields:

All patients should have their visual fields (peripheral vision) checked. A patient may have great central vision, with perfect eye-chart scores, but suffer from “tunnel vision” resulting from neurological diseases or glaucoma. Your patient may not even be aware of this peripheral visual loss if it has progressed slowly over time.

Confrontational fields are easy to perform but keeping your patient from “cheating” may be tougher. Have your patient cover one eye, and tell them to look straight at your nose. While fixating on your nose, have them count your fingers as you flash them in different quadrants. Be sure to cover your own eye and hold your hands equidistant between you and the patient. This gives you a better idea of what your patient ought to be able to visualize. If you can see your fingers, your patient should be able to see them as well.

EOM (extraocular movements):

Check extraocular movements by having your patient follow your fingers into all quadrants. If the patient has decreased mobility in an eye from nerve paralysis or muscle entrapment, you may notice this from casual inspection or by more sophisticated cover/uncover tests. More often, though, you won’t see anything but your patient will, complaining of double vision.

The Slit-Lamp Exam:

It takes several months to get good at using the slit-lamp microscope. A lot of pathology can be found under the microscope and it’s easy to miss crucial findings. This makes it important to keep yourself organized and describe your findings in the same order with every patient, starting from the outside skin and working your way to the back of the eye. Here’s how we do it:

External Exam (EXT):

With the external exam, make sure the eyes look symmetric and that the patient doesn’t exhibit ptosis (drooping of the eye) or proptosis (extruding eyes or “bug-eyes”). If the patient has a conjunctivitis, check for a swelling of the pre-auricular nodes (in front of the ear) and sub-mandibular/mental nodes.

Lids and lacrimation (L/L):

Always look at the lid margin and lashes for signs of blepharitis. Evert the lids to look for follicles or papillary bumps on the inside of the lids that might indicate infection or irritation.

Conjunctiva and Sclera (C/S):

Check to make sure the sclera is white and non-icteric, and the conjunctival blood vessels aren’t injected (red and inflamed). If they are injected, see if the blood vessels blanch when you dilate the patient with phenylephrine.

Cornea (K):

Look at the corneal surface for erosions and abrasions that might indicate trauma. Does the stroma look clear? Look at the back endothelial surface for folds or gutatta bumps. Fluorescein dye will make surface abrasions easier to spot. 

Anterior Chamber (AC):

Look for cell and flare, which could indicate inflammation or intraocular bleeding. Individual cells are hard to see - you need to turn the lights down and shoot a “ray of light” into the eye. If you compare this light to a projector beam at a movie theater, then “cells” will look like dust flecks while “protein flare” is diffuse and looks like smoke floating in the aqueous. Also, comment if the anterior chamber is deep and well-formed, or shallow and thus a setup for angle-occlusion glaucoma.

Iris (I):

Make sure the iris is flat and the pupil round. If the patient has diabetes or an old retinal vascular occlusion you should comment whether you see any signs of neovascularization of the iris.

Lens (L):

Is the lens clear, or hazy with cataract? Are they phakic (they have their own lens), pseudophakic (prosthetic lens), or aphakic (no lens at all)?

Vitreous (V):

You can look behind the lens into the dark vitreous cavity. If you suspect a retinal hemorrhage or detachment, you may see cells floating here.

Fundus Exam:

The fundus is the only place in the body where you can directly visualize blood vessels and nerves. In our notes we typically comment on four retinal findings:

1. Macula 
2. Vessels 
3. Periphery 
4. Disk

      view the retina:                      

The Direct ophthalmoscope

For non-ophthalmologists the most common way to examine the fundus is with the direct ophthalmoscope. This hand-held device is not easy

to use, especially in an undilated eye. The key to success with this instrument is to get yourself as CLOSE to the patient as possible.

Get really close! Dilating the eye also helps.

 slit-lamp

The best way to look at the posterior fundus in magnified detail is with a lens at the slit-lamp. This is how we look at the optic nerve and macula in the clinic, but it takes practice. We use smaller, more powerful lenses such as a 90-diopter lens.

The Indirect Ophthalmoscope

This is how we look at the peripheral retina in the ophtho clinic. The eye needs to be dilated to get a good image, but the field of view is excellent. We use a larger, 20-diopter lens, for this.