Another condition that affects the integrity of the retina and predisposes the patient to retinal and vitreous cavity bleeding is diabetic retinopathy. Patients with significant or active proliferative diabetic retinopathy (PDR) (Fig. 10.2) with the aberrant and uncontrolled blood vessel growth along the posterior eye, are at high risk of bleeding with trauma as seen in Fig. 10.3a-c. Though there is no way of knowing whether a patient has PDR until you thoroughly examine the back of the eye, since the visual acuity may be very good; if there are vision complaints consistent with a retinal detachment in a diabetic patient, the physician’s suspicion should be high.

Finally, lattice degeneration (Fig. 10.4) is another common condition that places people at higher risk of retinal detachment. Lattice degeneration is a common condition, takes many forms and is a disease where thinning in the peripheral retina appears to form a lattice like structure. These thin areas predispose to the development of holes, tears, and detachments after an increase in tension forces in the back of the eye [8]. However, as lattice degeneration is asymptomatic, patients presenting for trauma may not have been diagnosed with the disease. Instead, gathering a good history and performing a good eye exam will help determine the status of the retina. Many retinal detachments are due to lattice degeneration, but not all persons with lattice degeneration develop retinal detachment. In the setting of trauma, it is the trauma itself that leads to retinal detachments in areas of preexisting weakness (concept of locus minoris lesestencia).

So-called, “White without pressure” change (Fig. 10.5a, b) from zonal vitreous base traction on the retina predisposes to retinal tears with blunt eye trauma. This is a common phenomenon, more so in myopic eyes [9]. This condition is so-named because it appears whitened in contrast to the appearance of adjacent areas of retina. The predominant theory is that traction from the peripheral vitreous base area contributes to the appearance of the retina. These patients can be referred for outpatient monitoring with a retinal specialist. White without pressure predisposes to retinal tears in general and is more prevalent in moderate myopia and with trauma.

When examining the back of the eye, it is important to look at the vitreous space. Based on the history of the trauma, the presence of intraocular debris is an emergency and can require surgical intervention. In addition, the type of debris or foreign body will determine the severity of secondary damage inside the eye. This will be expounded upon in later sections.

The next step in evaluating posterior segment trauma should be looking for the presence of bleeding in the back of the eye. There are four major areas where bleeding can arise, each with their own distinct appearance and implications. Though trauma does not adhere to the patterns often described in text, recognizing bleeding patterns can help with triaging patients. Small, round dot-shaped hemorrhages are usually deep within the retina, and when seen in isolation, are not commonly associated with trauma (Fig. 10.6). Flame-shaped hemorrhages are created from the damage of vessels in the superficial retinal fiber layer and are more concerning. Large hemorrhages called boat-shaped preretinal hemorrhages (Fig. 10.3a) are areas of bleeding that have not (yet) broken into the vitreous cavity. Finally, vitreous hemorrhages can be especially worrisome as the murky blood can reduce the ability to examine the state of the posterior eye as seen in Fig. 10.7a, b. A vitreous hemorrhage should be considered due to a retinal tear until proven otherwise (i.e., it cannot be simply blamed on a systemic condition, such as diabetes mellitus and related retinopathy). By becoming comfortable with identifying these patterns of bleeding, the physician can get a better idea of the forces and concepts involved in the trauma and plan further examination and therapy.

On examination, the presence of new visual field loss is very worrisome concerning retinal detachment. This can sometimes be ascertained, but of course not proven with finger counting in all four visual field quadrants with the eyes tested independently. Using an Amsler grid (straight line grid) (Fig. 10.8a), if the patient states they experience distortion or curving of the lines, this could indicate problems in the macular area as depicted in Fig. 10.8b. It is important to understand the process that leads to retinal detachment.

In the posterior portion of the eye, the vitreous body is attached firmly to the retina and in the presence of traumatic tension forces, the vitreous pulls on the retina, potentially causing a hole or a tear and result in acute retinal detachments as seen in Figs. 10.9 and 10.10. This is called a rhegmatogenous retinal detachment (RRD). An area of focal vitreous traction causes tears. Pieces of retina can avulse and come off, leaving small round holes called operculated holes. There can also be small tears in the far periphery of the retina usually in older individuals who have previously undergone cataract surgery. However, more worrisome are flap tears or horseshoe tears, which usually lead to RRD. This is because the vitreous gel remains attached to the flap, exerts anterior-posterior traction, and lets vitreous fluid pass underneath to detach the neurosensory retina. A large flap tear with subretinal fluid and low-bullous retinal detachment is seen in Fig. 10.11. These tears are usually located in the mid-periphery of the retina at the posterior aspect of the vitreous base and will certainly be missed with direct ophthalmoscopy or at the slit lamp. Ultrasound can also help identify tears in the periphery, but only by a very experienced ultrasound operator.

Giant tears are those which involve three clock hours or more (Fig. 10.12). They are particularly tricky to manage surgically, requiring pars plana vitrectomy, use of perfluorocarbon liquid, and usually primary lensectomy for successful repair.

Retinal dialyses (Fig. 10.13a, b) are radial anterior slit tears, which are usually seen to occur inferiorly. They are seen in younger individuals and are concentric to the ora serrata. They are usually managed with scleral buckling if significant detachment is associated, but sometimes are just treated with observation, laser (as seen in this case) and/ or cryotherapy if pathology is more anterior.

The management of retinal trauma can also vary dramatically depending on the state of the eye. Small retinal tears or detachments in the peripheral retina may not require a trip to the operating room. They may be treated in the eye clinic with laser or cryotherapy at the site of tears or minimal detachment to seal the area and prevent further damage. This will be discussed later.

In younger patients with traumatic detachments, scleral buckling is another commonly used technique (Fig. 10.14). By inserting a silicone band around and suturing the element(s) to the sclera, underneath Tenon’s capsule and the conjunctiva, the structural outer layers of the eye are imbricated/pushed toward the retina, returning the contact of the neuro-retinal tissue with the pigment epithelium; thus restoring the gross structural integrity and allowing proper vascular perfusion. External drainage of subretinal fluid is sometimes simultaneously performed using various means. Either cryotherapy or laser treatments at the time of scleral buckling surgery are also necessary to seal the areas of detachment, preventing recurrence. Laser treatment cannot be performed in areas of detached retina, so it is sometimes used in the acute postoperative period when the retina has reattached. Although its sealing-effect is more immediate, cryotherpy is more pro-inflammatory to the eye than is laser treatment.

More severe retinal tears or detachments may require the injection of long acting gases such as sulfur hexafluoride (SF6) or perfluoropropane (C3F8) to tamponade the retina and push the neuronal film back onto the RPE. These gases work to potentiate the efficacy of laser and cryotherapy treatments by holding the retina in place while they heal together. Gas bubbles sometimes require strict postoperative positioning to ensure proper placement and tamponade, ranging from lying forward on their face, to their side, or remaining upright for several days depending on the location of the pathology. They cannot fly in an airplane or travel to elevated altitudes for any reason with the bubble in place. At higher altitudes (lower atmospheric pressures) and the resulting pressure elevation in the eye will cause severe pain and occlusion of the central retinal artery. Patients who may be unable to properly position are poor candidates for cryotherapy/gas treatments (and pneumatic retinopexy).

Silicone oil is an alternative treatment for severe traumatic detachment or extensive inferior-retinal detachment in patients who may not tolerate gas therapy. The silicone oil acts similarly as a tamponade to push the retina in place, with a shorter time needed for rigid positioning. In contrast, gas is a better tamponade than silicone oil, due to the surface tension intrinsic to a gas. However, with oil, patients may only require one day of lying in a particular position to help with reabsorption of subretinal fluid and may move about normally thereafter. Finally, silicone oil will probably require extraction at a later time, and a secondary procedure will present with its own inherent risks, whereas gas will always reabsorb spontaneously.

Trauma frequently causes inflammation, and thus it can trigger severe fibrous proliferation and scarring in the vitreous and further secondary damage. Coincident vitreous hemorrhage, anterior segment damage, lens damage, and retinal trauma almost always sets in motion a chain of inflammatory event that will usually leads to loss of the eye. For this reason, retinal surgeons often perform pars plana vitrectomy (PPV), which removes some or most of the vitreous body from the eye. This is done in order to cut out and remove sources of tension that pull the retina. Then the surgeon can reposition the retina back onto the underlying structures. Primary PPV is now preferred to scleral buckling in most cases. Luckily, people do not require vitreous humor to see. After the vitreous humor is removed from the posterior segment of the eye, aqueous humor will proceed to fill the space. Many of the procedures mentioned earlier require postoperative time in certain positional states that may not be tolerable for an older patient.

It is important to inform the patient that any damage to the retina results in a guarded prognosis. Patients may be left with permanent visual deficits. If these deficits are in the far periphery of the eye, patients may not notice a change in their vision and will be able to cope easily. However, if the damage is near or involves the macula, the deficit in central vision can be highly disabling, and may require significant coping skills and rehabilitation to manage their impairment.

The macula has the highest density of vision sensing neurons (cones) in the eye and is situated in the central area of the retina. These neurons aggregate and form the crux of a person’s central and color vision. Therefore, damage to the macula can be debilitating to a patient. As a very thin film of neurons in the back of the eye, the macula is susceptible to damage in numerous ways. Significant lasting and demonstrable anatomical and visual defects usually occur with significant trauma to the eye. The macula is highly susceptible to neuronal injury and to bleeding secondary to blunt trauma.

Foveal and macular photoreceptor and RPE damage is irreparable and even minor trauma, from a finger, a pencil, automobile airbag, paintball, soccer or tennis ball can lead to severe injury and be permanently blinding and disabling.

After injury, weakening or breaks in Bruch’s membrane of the choroid layer can trigger bleeding under the macula [10]. This is known as traumatic sub-macular hemorrhage and patients will notice a severe, sudden loss of their vision. Unfortunately, this condition has a poor prognosis as the blood pooling behind the macula is toxic to the tissues due to iron in the hemoglobin. Bleeding underneath the macula can also lead to neovascularization of choroid vessels, worsening the visual acuity. The trauma to the retina and the damage to the macular area can also lead to fibrosis [11].

The fundus exam reveals a red elevation under the macular area, varying in color based on chronicity. Optical Coherence Tomography (OCT) examination can also be performed to visualize the blood pooling underneath the macular region. Retinal specialists may then decide if patients require immediate surgical intervention. Patients with sub-macular hemorrhage can be treated with a combination of vitrectomy, gas tamponade, and injections of tissue plasminogen activator (t-PA) directly into the vitreous cavity [12]. The usage of recombinant t-PA (rt-PA) has been shown to have good outcomes in clearing the sub-macular bleed and has become more accepted as a viable form of treatment. An example of this treatment effect is seen in Fig. 10.15a, b.

This subretinal hemorrhage is very important to note as the changes from the accumulation of blood beneath the retina is toxic and will kill the cone photoreceptors. However, as it is not in the central visual area, patients may not notice changes in their central vision if there is a small area of subretinal bleeding. This damage is time sensitive as well. As the clot organizes, it takes on an ochre-yellow color seen in Fig. 10.16 [13]. The treatment of acute subretinal hemorrhage is the same as sub-macular hemorrhages, but it is important to follow these patients long term.

Cracks in the tissue of Bruch’s membrane that led to the bleed can cause slow degeneration of the vision, if they expand. These cracks can be spotted on examination as linear streaks in the subretinal space or as small spots of hyperpigmentation (known as Fuch’s spots in the case of myopia) (Fig. 10.17a, b) [14]. If these signs are spotted on exam, patients tend to have a poorer prognosis. They often exhibit a degree of associated subretinal fibrosis and scarring (Fig. 10.18a, b). They commonly spawn subretinal neovascular membranes later that also can cause significant bleeding under the retina (Fig. 10.19a, b, c). Choroidal ruptures tend to be circumlinear, can be multiple and are usually concentric in relation to the optic disc (Fig. 10.20a, b).

Holes in the macula can be created secondary to trauma from acute vitreous traction, with a hole forming in the neuronal layer responsible for central vision, one can expect the patient to complain of distortion in their central vision. Less severe holes may simply cause metamorphopsia, or distorted vision, with complaints of warped images [15]. The diagnosis of macular holes can be confirmed with a fundus exam. An older large traumatic hole in the macula is seen in Fig. 10.21. Smaller holes are harder to detect (Fig. 10.22). For physicians with access to optical coherence tomography (OCT), a near histopathologic-microscopic finding confirms the presence of the hole and the diagnosis (Fig. 10.23a, b). Fortunately, small macular holes like this, especially if the overlying vitreous (posterior hyaloid) is separated, can heal with close outpatient observation indicated. Eventually, the macula will seal and the patient’s vision will often return to some extent. However, if there is no spontaneous resolution over a period of time, Retinal surgeons can proceed to surgery and perform a pars plana vitrectomy and internal-limiting membrane peeling with gas tamponade to seal the hole.

Another common type of retinal damage is caused by shockwave damage from blunt trauma to the eye, also called commotio retinae or Berlin’e edema (Fig. 10.24). Commotio (which is anatomic commotion) to the macula generally only occurs in younger individuals where a posterior hyaloid–vitreous separation-detachment (PVD) does not yet exist. Shockwaves from traumatic impact are transmitted to the macula from the attachment of the vitreous triggering shearing of neuronal layers from the nerve fiber layer (Berlin’s edema) all the way down to the photoreceptor layer of the retina [16]. Milder shockwaves may cause poor visual acuity and may only partly resolve. Commotio retina can permanently damage the macula, affecting the ellipsoid (inner-outer segment) junction of the photoreceptors and also the underlying pigmented epithelium (Fig. 10.25a, b). More severe late macular (outer retinal) damage is shown in Fig. 10.26. In this latter instance, with no good treatment options, visual outcomes are quite poor. Ophthalmologists use OCT to look at the state of the layers of the retina and guide followup. Fortunately however, many patients with commotio will recover with time. Monitoring changes to the macular ellipsoid junctional zone and signs of atrophy/RPE hyperpigmentation can help physicians determine the prognosis.