158 IRIS LACERATIONS 364.74, IRIS HOLES 364.74, AND IRIDODIALYSIS 369.76

Iridodialysis and158Holes,CHAPTERIris Lacerations, Iris •

Injuries Nonmechanical and Mechanical • 14 SECTION

COMMENTS

Iris injury due to blunt ocular trauma may result from one of two possible mechanisms. The first mechanism is that of direct corneal compression with resulting expansion of the globe in the coronal plane. This expansion directly stresses the area of the iris root and ciliary body. The second possible mechanism is that of a compression wave created in the aqueous as a result of blunt trauma. The subsequent posterior and lateral flow of the aqueous could cause sphincter or iris damage due to iris displacement.

Iris lacerations, holes, and iridodialyses by themselves do not commonly cause symptoms or ocular complications. Their primary significance lies in raising suspicions regarding injury to other ocular structures. Only if the iris defect creates significant symptoms should treatment be considered.

REFERENCES

Crouch ER, Williams PB: Trauma: ruptures and bleeding. In: Tasman W, Jaeger EA, eds: Duane’s clinical ophthalmology. Philadelphia, Lippin- cott-Raven, 1997:IV:1–3.

Hanna C, Roy FH: Iris wound healing. Arch Ophthalmol 88:296–304, 1972.

Hersh PS, Zagelbaum BM, et al: Blunt iris injury. In: Albert DM, Jakobiec FA, eds: Principles and practice of ophthalmology. Philadelphia, WB Saunders, 2000:5208–5209.

Steinert RF: Iris trauma. In: Shingleton BJ, Hersh PS, Kenyon KR, eds: Eye trauma. St Louis, CV Mosby, 1991:95–103.

Wachler BB, Drueger RR: Double-armed McCannel suture for repair of traumatic iridodialysis. Am J Ophthalmol 122:109–110, 1996.

Waubke TN, Mellin KB: Treatment of iris injuries. In: Blodi F, Mackensen G, Neubauer H, eds: Surgical ophthalmology. Berlin, Springer, 1992: II:516–518.

159 ORBITAL IMPLANT EXTRUSION

996.59

Mark R. Levine, MD, FACS

Beechwood, Ohio

Amarpreet Singh, MD

Cleveland, Ohio

The loss of an eye because of enucleation or evisceration is emotionally traumatic, and is exacerbated by extrusion of an orbital implant. In general, the implant size used in enucleations is 18 to 22 mm. This (along with the prosthesis) maximally replaces the 6 mL of volume lost, prevents enophthalmos, superior tarsal sulcus deformity, and avoids the need for an oversized prosthesis and the complications associated with it. The implant in evisceration is as large as can be fit into the scleral envelope, which can be augmented with expansion sclerotomies or posterior placement of the implant.

There are three categories of implants used:

●Integrated: hydroxyapatite or porous polyethylene (Medpore);

●Non-integrated: silicone or acrylic spheres (methylmethacrylate);

●Biological: dermis fat grafts.

Problems formerly created by the rough surfaces of hydroxyapatite (HA) and porous polyethylene (PP) implants have been

FIGURE 159.1. Extruding tantalum mesh from anophthalmic socket.

minimized by the recent refinement and smoothing of these surfaces as well as the use of wrapping materials. A secondary implant is always desirable to maintain orbital volume, minimize superior tarsal sulcus deformity, promote motility, and maximize cosmetic acceptability. It is important that the implant be centrally placed to facilitate the proper fit of a prosthesis.

ETIOLOGY

Extrusions may occur early in the postoperative period or many years after the initial implant (Figure 159.1). The causes of early extrusion are edema, hemorrhage, infection, too large an implant, and faulty surgical technique. Late extrusion is caused by erosion of the tissue covering the anterior surface of the implant. This erosion is a result of friction from a rough prosthesis or rough implant, such as hydroxyapatite, covered only by conjunctiva and Tenon’s capsule. The erosion leads to extrusion either because of a secondary infection or because of epithelialization of the socket, with resulting contraction of the orbital tissues.

COURSE/PROGNOSIS

In evisceration, if the conjunctiva and Tenon’s capsule have retracted but the scleral incision is intact, re-epithelialization may occur. If the sclera dehisces, exposing the implant, the likely course will be further wound dehiscence and extrusion. At this point, re-suturing the sclera is rarely effective.

In enucleation, retraction of the conjunctiva and Tenon’s capsule with implant exposure leads to a natural course of extension of the exposure, with or without infection. If a porous implant is wrapped in fascia and the fascia is exposed, re-epi- thelialization and vascularization may occur. This is more likely if the defect is only 2 to 3 mm and the prosthesis is removed or vaulted. Larger defects of 10 to 15 mm will only occasionally re-epithelialize and vascularize.

Infection is another complication of orbital implant surgery. The fascial wrap may become infected or may resorb, during which time significant mucus production will be noted. An infection is more likely to develop from the combination of a moist socket, low-grade bacteria (usually Staphylococcus

epidermidis), and the presence of a prosthesis. In the case of an infection, extrusion of the implant is usually inevitable.

DIAGNOSIS

The presence of a defect in the conjunctiva and Tenon’s capsule and visualization of the implant require immediate attention. Significant muco-purulent discharge should alert the clinician to the possibility of socket infection and implant exposure, be it large or small.

TREATMENT

Systemic

●Systemic antibiotics when the socket is infected.

Local

●Good lid hygiene, using moist swabs as often as necessary.

●Observation for enlarging defects (keeping in mind that defects up to 3 mm usually resolve with conservative management).

●Removal or vaulting of the prosthesis to remove pressure from the affected area.

●Obtaining of a culture and sensitivity of any low-grade infection and use of appropriate topical antibiotics.

Surgical

Complete extrusion in cases of enucleation (no infection present)

●Immediate replacement with a fascia-enveloped sphere.

●Conjunctiva and Tenon’s capsule are dissected from the rest of the orbital contents, taking care not to injure the recti muscles.

●A cavity may be present within the muscle cone if extrusion occurred within 2 to 3 weeks of placement of the implant. More commonly, the extraocular muscle and Tenon’s capsule will have retracted into a small fibrotic mass.

●Sharp dissection is used to create a cavity in this mass.

●Excision of scar tissue posteriorly, or a posterior dissection, is carried out until Tenon’s capsule and the muscles can stretch over the implant.

●A piece of autogenous fascia (either fascia lata, removed from the leg or temporalis fascia from the temple) is wrapped around an appropriately sized implant (16 to 20 mm), and sutured with 5-0 vicryl. Note that fascia as a wrap adds an additional 1 to 2 mm to the implant size.

●Sutures of 4-0 double-armed vicryl are placed in each of the four quadrants of the fascia-enveloped sphere.

●The implant is placed in the socket and the sutures are brought out from each socket quadrant between the recti muscles, through Tenon’s capsule and the conjunctiva, and fixed externally to position the implant.

●Tenon’s capsule posterior to the recti muscles is sutured over the fascial ball with interrupted 5-0 vicryl, taking bites of the fascia to create a barrier and centrally fix the implant.

●The recti muscles, if found, are gently approximated with 5-0 vicryl.

●Anterior Tenon’s capsule is closed with 6-0 vicryl and the conjunctiva is closed with locking 6-0 chromic catgut suture.

●A small conformer is inserted so as not to place tension on the suture line.

●Two 4-0 silk tarsorrhaphies are performed, and a pressure patch is applied for 3–4 days.

Notes

●The choice of implant can be either PP, HA, silicone or acrylic sphere. The implant should be wrapped for added support and provide an additional barrier to extrusion.

●In the case of a porous implant, it too should be wrapped with fascia; however, multiple window defects are placed in the fascia to enhance vascular ingrowth.

●If the socket is infected, it is filled with antibioticimpregnated gauze and replaced often until the infection is resolved (5 to 10 days); a secondary implant is placed at a later time.

Implant replacement in an evisceration

●The scleral pouch is irrigated with antibiotics.

●The implant of choice is placed in the scleral pouch so there is no tension on the scleral closure.

●If the scleral pouch is a too small, expansion sclerotomies are made with either radial or circumferential cuts. This is particularly important for vascular ingrowth if a HA or PP implant is being placed.

●The sclera is closed with running 5-0 vicryl, and Tenon’s capsule and the conjunctiva are closed with locking 6-0 chromic catgut.

●Tarsorrhaphy is performed, and pressure patches are applied. A conformer is not needed, as the cul-de-sacs are formed and there will be no pressure on the suture line.

NOTES

●In the case where the volume of the scleral pouch is inadequate even after expansion sclerotomies, a posterior placement of the implant can be performed. The posterior sclera is cut from 3 to 9 o’clock and the implant placed within the muscle cone behind the posterior sclera. The posterior sclera is closed with running 5-0 vicryl and the anterior sclera is sutured to the posterior sclera with running 5-0 vicryl. The conjunctiva and Tenon’s is closed with 6-0 chromic catgut. This permits a large enough sphere without placing tension on the sclera.

Large defects with implant exposure of 10 to 15 mm

●Immediate patch grafting with fascia.

●The conjunctiva and Tenon’s capsule are dissected off the implant for several additional millimeters.

●The defect is irrigated with antibiotic solution copiously.

●Burr down the implant to reduce the size and remove areas of superficial infection.

●A piece of autogenous fascia (either fascia lata, removed from the leg or temporalis fascia from the temple) is placed over the implant, extending into all four quadrants of the socket.

●5-0 vicryl sutures are placed into the fascia through Tenon’s capsule, exiting through the conjunctiva in all four quadrants and tied.

●The conjunctiva and Tenon’s capsule are closed over the fascia, taking bites of the fascia every third suture.

●If there are inadequate conjunctiva and Tenon’s capsule, a bipedicle conjunctival flap is brought down from the upper fornix to cover the defect, and the upper fornix is allowed to heal by secondary intention.

159ExtrusionCHAPTERImplant Orbital •

Injuries Nonmechanical and Mechanical • 14 SECTION

FIGURE 160.1. Shaken baby syndrome.

shaken baby syndrome, they are highly suggestive of a shaking or impact injury and several studies have shown that they are usually absent in pediatric accidental head trauma. Retinal hemorrhages often occur in all layers of the retina with no identifiable predominant location. Additional ocular findings include other forms of posterior segment injury such as vitreous hemorrhage, retinal detachment, retinoschisis, choroidal rupture, retinal folds, and optic nerve injury (Figure 160.1).

Laboratory findings

Diagnostic testing depends on the stability of the patient and may be limited for critically ill infants requiring life support. Neuroimaging should be performed in all cases of shaken baby syndrome to quantify the degree of head trauma. Computed tomography (CT) of the head should be the initial image of choice, preferably with intravenous contrast and bone and softtissue windows. CT is ideal for detection of subdural/subarachnoid hemorrhages and mass effect. Magnetic resonance imaging (MRI) of the head should be used as an adjunct to CT if patient stability is present and can be performed several days after initial testing. MRI can greater define intraparenchymal brain lesions and has a greater rate of detection for subdural hematomas. A skeletal survey should be performed once patient stability is achieved to evaluate for fractures of the hands, feet, long bones, skull, spine, and ribs. A repeat skeletal survey 2 weeks after the initial evaluation can demonstrate healing fractures that may have been missed on initial films.

Differential diagnosis

Retinal hemorrhages are an important clinical finding in diagnosis of shaken baby syndrome, but they are not pathognomonic for the syndrome. The most likely causes of retinal hemorrhages in an infant or young child include birth trauma, hematological disorders, Terson syndrome, severe accidental head trauma, infection, cardiopulmonary resuscitation, and child abuse. An estimated 15%–30% of infants have retinal hemorrhages from birth trauma, but they are often associated with a traumatic birth and resolve by 4 weeks of age. Hematologic testing can rule out coagulopathies such as hemophilia, von Willebrand disease, and vitamin K deficiency, and laboratory testing can help with confirmation of an infection. Several reports have shown that retinal hemorrhages are rare findings in accidental head trauma.

COMMENT

The wide variety of injuries that may occur in the syndrome require a multidisciplinary team approach in management and should include a pediatrician, neurologist, radiologist, ophthalmologist and/or a pediatric neurosurgeon. A child abuse specialist, social worker, law enforcement officer and child protection services must also work closely with the medical team. Appropriate documentation of injuries is imperative for future legal investigations with careful and detailed documentation of history, presentation, and examination as a high proportion of these cases develop into legal investigations.

Shaken baby syndrome is a leading cause of morbidity and mortality in infants and young children. All infants suspected of child abuse and shaken baby syndrome must have a careful evaluation with a complete physical exam including a dilated fundus examination. A multidisciplinary healthcare team is imperative in diagnosis and management of victims suffering from shaken baby syndrome. With an increasing incidence and high probability of underdiagnosed or unreported cases, a thorough physical and ophthalmologic examination can be critical in diagnosis of shaken baby syndrome. A greater understanding of this syndrome is important for the education of not only health care providers, but also the public, as prevention is the only method for alleviation of this abusive syndrome.

REFERENCES

Caffey J: The whiplash shaken infant syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pediatrics 54:396–403, 1974.

Kivlin JD, Simons KB, Lazoritz S, Ruttum MS: Shaken baby syndrome. Ophthalmology 107:1246–1254, 2000.

Levin AV: Ophthalmology of shaken baby syndrome. Neurosurg Clin N Am 13:201–211, 2002.

Pierre-Kahn V, Roche O, Dureau P, et al: Ophthalmologic findings in suspected child abuse victims with subdural hematomas. Ophthalmology 110:1718–1723, 2003.

Tsao K, Kazlas M, Weiter JJ: Ocular injuries in shaken baby. Int Ophthalmol Clin 42:145–155, 2002.

161 THERMAL BURNS 940.9

F. Hampton Roy, MD, FACS

Little Rock, Arkansas

The thermally burned patient may present a challenging management problem for the ophthalmologist. Although many seriously burned individuals with total-body burns may initially escape direct damage to the globe of the eye, complications resulting from the overall injury can have a devastating effect on the ocular system.

ETIOLOGY

Many severely burned patients may escape direct injury to the cornea and conjunctiva because of Bell’s phenomenon and the protection of the eyelids. On the other hand, many do suffer direct corneal and conjunctival injuries that are thermal in nature, caused by the flame itself or by hot gases. Some corneal

161 CHAPTERBurns Thermal •

Injuries Nonmechanical and Mechanical • 14 SECTION

given to the eyes. A tarsorrhaphy protects the corneas during this phase of the therapy in a severely burned patient.

COMMENTS

For severe conjunctival burns caused by exploding liquids or molten metal, severe necrosis of the conjunctiva and cornea may occur. These injuries behave like severe acid or alkali burns. Local mucosal grafts may be applied in such cases, and the use of symblepharon rings may also help to prevent symblepharon. Because these injuries are similar to severe chemical burns, the articles on acid and alkali burns provide further information on the management of these cases.

In large, total-body burns, the acute phase of the injuries requires frequent operations for debridement as well as skin grafting. Until these patients are totally covered with skin, they are susceptible to infections both systemically and locally. These patients need frequent follow-up care after the application of large tarsorrhaphies. Once tarsorrhaphies are healed, examinations may be less frequent, provided that the blood cultures remain negative and signs of orbital cellulitis do not occur.

When the entire burned area is covered, the reconstructive phase of therapy can begin. When reconstruction of the eyelids with skin grafting is successful, tarsorrhaphies may be released.

Significant corneal complications such as corneal ulcers caused by Pseudomonas species may be prevented by tarsorrhaphies; this technique is preferable to treating such an infection, especially in combination with lid retraction and exposure keratitis. For this reason, the need for adequate and early tarsorrhaphies to protect the corneas in the severely burned patient cannot be overemphasized.

REFERENCES

Bloom SM, Gittinger JW, Jr, Kazarian EL: Management of corneal contact thermal burns. Am J Ophthalmol 102:536, 1986.

Children’s Hospital Boston: Fire safety and burns. Online. Available at: Injury Statistics and Incidence Rates Children’s Hospital Boston Web site. Accessed April 22, 2005.

Deutsch TA, Feller DB: Paton and Goldberg’s management of ocular injuries. 2nd edn. Philadelphia, WB Saunders, 1985:99–103.

Guy RJ, Baldwin J, Kwedar S, Law EJ: Three-years’ experience in a regional burn center with burns of the eyes and eyelids. Ophthalmic Surg 13:383–386, 1982.

Kulwin DR, Kersten RC: Management of eyelid burns. In: Focal points: clinical modules for ophthalmologists. San Francisco, American Academy of Ophthalmology, 1990:8:module 2:1–10.

Wibbenmeyer LA, Amelon MJ, Torner JC, et al: Population-based assessment of burn injury in southern Iowa: identification of children and young-adult at-risk groups and behaviors. J Burn Care Rehabil 24(4): 2003.

161 CHAPTERBurns Thermal •

162 HYPERTENSION 365.04

Jeffrey R. Parnell, MD

Chicago, Illinois

Lee M. Jampol, MD

Chicago, Illinois

Systemic hypertension can be associated with vascular constriction, leakage, and arteriosclerosis, which can affect the function of many target organs throughout the body. The eye is the only target organ in which arteries and veins can be directly viewed in vivo with ease and by noninvasive techniques. Changes in the vasculature observed in the retina in hypertensive patients may reflect the status of the vascular system throughout the body.

The eye has a complex vascular system in which blood supplies to the optic nerve, choroid, and retina are derived from distinct sources, each having special anatomic and physiologic properties. Each vascular system has a unique response to systemic hypertension, and it is useful to separate into categories the different manifestations in the eye. Hypertensive eye disease can take the form of hypertensive retinopathy, hypertensive choroidopathy, hypertensive optic neuropathy, or all three.

ETIOLOGY/INCIDENCE

Systemic hypertension accounts for more visits to physicians than any other disease. As many as 58 million adults in the United States are estimated to have the disease. It is estimated up to 25% of adults and 60% of patients over 60 may be hypertensive. Blacks and males are more often affected.

Over 90% of cases of hypertension are due to essential hypertension for which there is no known cause. Heredity and environmental factors such as a high sodium diet and sedentary life style may play a role.

The remaining 10% of cases can be divided into the secondary causes of systolic and diastolic hypertension or isolated systolic hypertension.

One percent of patients may develop malignant hypertension, a particularly severe and often sudden onset of elevated blood pressure.

●Secondary causes of systolic and diastolic hypertension:

●Renal vascular or parenchymal disease;

●Endocrine disease;

●Coarctation of the aorta;

●Eclampsia or pre-eclampsia;

●Neurologic disorders;

●Increased intravascular volume;

●Isolated causes of systolic hypertension:

●Increased cardiac output due to aortic valve insufficiency, arteriovenous fistula, patent ductus;

●Arteriosus, thyrotoxicosis, beri-beri, hyperkinetic circulation;

●Aortic rigidity.

COURSE/PROGNOSIS

In hypertensive retinopathy, acute elevations of blood pressure lead to retinal arterial vasoconstriction, an auto regulatory response. Persistent hypertension causes irreversible arteriolar narrowing. Chronically elevated pressure also causes sclerotic changes in the media of the arterial wall. Light-reflex changes observed on examination reflect the degree of sclerosis, which, in severe cases, may take on the appearance of burnished copper wire. Arteriolar occlusion may look like silver wire. At arteriovenous crossing sites, where the artery and vein share a common adventitial sheath, compression of the venule causes visible ‘nicking’ (Gunn’s sign) of variable severity. Salus’ sign refers to the abnormal deflection of the venule as it crosses the arteriole at an increasingly obtuse angle or even a right angle. Chronic hypertension may also cause occasional retinal microaneurysms. Arterial macroaneurysms are also seen in association with chronic hypertensive retinopathy. Sclerotic hypertensive vascular changes may contribute to branch or central vein occlusion and branch or central retinal artery occlusions.

Acute, malignant, or accelerated hypertension leads to leakage of the retinal arterioles, with decompensation of the inner blood-retina barrier. This may be manifested as extravasation of blood and lipoprotein into the retina in the form of superficial hemorrhages, cotton wool spots (infarcts), hard exudates (lipid), and capillary occlusions. Malignant hypertension also can cause hypertensive choroidopathy and hypertensive optic nerve changes. In hypertensive choroidopathy, fibrinoid changes in the choriocapillaris result in focal nonperfusion that leads to ischemia of the outer retina and the retinal pigment epithelium. Acute Elschnig’s spots are white or yellow patches of ischemic retinal pigment epithelium overlying occluded choriocapillaris. Acute exudation through the injured retinal pigment epithelium layer can lead to neurosensory detachments. These spots ‘heal’ and become hyperpigmented over time. Linear hyperpigmentation overlying choroidal arteries is called Seigrist’s streaks and represents hyperplastic retinal pigment epithelium. Elschnig’s spots, after healing, are also hyperpigmented.

Conditions or Diseases Unclassified • 15 SECTION