D) Reparación del efecto
3.2. ARCOS
Once the diagnosis of a ruptured globe is made, further examination should be deferred until the time of surgical repair in the operating room. This is to avoid placing any pressure on the globe and risking extrusion of the intraocular contents. Diagnosis should be made by penlight, or if possible, by slit-lamp examination (with very gentle manipulation). Once the diagnosis is made, then the following measures should be taken:
1. Protect the eye with a shield at all times.
2. Obtain CT scan of the brain and orbits (axial and coronal views, 1-mm sections) to rule out IOFB in most cases.
3. Gentle UBM may be needed to localize posterior rupture site(s) or to rule out intraocular foreign bodies not visible on CT scan (nonmetallic, wood, etc.). However, UBM should not be done in patients with an
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Figure 3.14.1. Ruptured globe showing flat anterior chamber, iris prolapse, and peaked pupil.
obvious anterior rupture for the risk of extrusion of intraocular contents. A trained ophthalmologist should evaluate the patient before UBM or other manipulation is performed on a ruptured globe suspect.
4. Admit patient to the hospital with no food or drink (NPO).
5. Place patient on bed rest with bathroom privileges. Avoid bending over and Valsalva maneuvers.
6. Systemic antibiotics should be administered within 6 hours of injury. For adults, give cefazolin 1 g i.v.
q8h or vancomycin 1 g i.v. q12h. Also give ciprofloxacin 400 mg p.o./i.v. b.i.d. (fourth-generation fluoroquinolones, such as gatifloxacin 400 mg q.d. or moxifloxacin 400 mg q.d. may have better vitreous penetration). For children <12 years, give cefazolin 25 to 50 mg/kg/ day i.v. in three divided doses, and gentamicin 2 mg/kg i.v. q8h.
7. Administer tetanus toxoid p.r.n. (see Appendix 2, Tetanus Prophylaxis).
8. Administer antiemetic (e.g., prochlorperazine (Compazine) 10 mg i.m. q8h) p.r.n. for nausea and vomiting to prevent Valsalva.
9. Consider pain medicine before and after surgery p.r.n.
10. Determine the time of the patient's most recent meal. The timing of surgical repair is often influenced by this information.
11. Arrange for surgical repair to be done as soon as possible.
Note
Antibiotic doses may need to be reduced if renal function is impaired. Gentamicin peak and trough levels are obtained one-half hour before and after the fifth dose, and blood urea nitrogen and creatinine levels are evaluated every other day. See Pharmacopoeia.
Note
In any severely traumatized eye in which there is no chance of restoring vision, enucleation should be considered initially or within 7 to 14 days after the trauma to prevent the rare occurrence of sympathetic ophthalmia.
Infection is more likely to occur in eyes with dirty injuries, retained intraocular foreign bodies, rupture of lens capsule, and in patients with a long delay until primary surgical repair. In patients at high risk of infection, some groups recommend intravitreal antibiotics (see 12.15, Traumatic Endophthalmitis).
3.15 Intraocular Foreign Body Intraocular Foreign Body Symptoms
Eye pain, decreased vision, or may be asymptomatic; often suggestive history (e.g., hammering metal).
Signs
(See Figure 3.15.1.)
Critical. May have a clinically detectable corneal, scleral perforation site, hole in the iris, or an IOFB.
Intraocular foreign bodies are often seen on CT scan, UBM, or both.
Other. See 3.14, Ruptured Globe. Also, microcystic (epithelial) edema of the peripheral cornea (a clue that a foreign body may be hidden in the AC angle in the same sector of the eye). Longstanding iron-containing intraocular foreign bodies may cause siderosis, manifesting as anisocoria, heterochromia, corneal endothelial and epithelial deposits, anterior subcapsular cataracts, lens dislocation, and optic
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atrophy.
Types of Foreign Bodies
1. Frequently produce severe inflammatory reactions and may encapsulate within 24 hours if on the retina.
a. Magnetic: Iron and steel.
b. Nonmagnetic: Copper and vegetable matter (may be severe or mild).
2. Typically produce mild inflammatory reactions.
a. Magnetic: Nickel.
b. Nonmagnetic: Aluminum, mercury, zinc, vegetable matter (may be severe or mild).
3. Inert foreign bodies: Carbon, gold, coal, glass, lead, plaster, platinum, porcelain, rubber, silver, and stone. Brass is also relatively nontoxic. However, even inert foreign bodies can be toxic to the eye because of a coating or chemical additive. Most BBs and gunshot pellets are made of 80% to 90% lead and 10% to 20% iron.
Work-Up
1. History: Composition of foreign body and time of last meal.
2. Perform ocular examination, including visual acuity assessment and careful evaluation of whether the globe is intact. If there is an obvious perforation site, the remainder of the examination may be deferred until surgery. If there does not appear to be a risk of extrusion of the intraocular contents, the globe is inspected gently to localize the site of perforation and to detect the foreign body.
a. Slit-lamp examination; search the AC and iris for a foreign body and look for an iris TID. Examine the lens for disruption, cataract, or embedded foreign body. Check the IOP.
b. Consider gonioscopy of the AC angle if no wound leak can be detected and the globe appears intact.
c. Dilated retinal examination using indirect ophthalmoscopy.
3. Obtain a CT scan of the orbits and brain (coronal and axial views with 1-mm sections through the orbit).
MRI is contraindicated in the presence of a metallic foreign body. It may be difficult to visualize wood, glass, or plastic on a CT scan, especially acutely.
4. Gentle UBM of the globe and orbit. Intraocular air can mimic a foreign body. UBM should be deferred in Figure 3.15.1. Intraocular foreign body.
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patients with an anterior rupture given risk for extrusion of intraocular contents.
5. Culture the wound site, if it appears infected.
6. Determine whether the foreign body is magnetic (e.g., examine material from which the foreign body came).
Treatment
1. Hospitalization with no food or drink (NPO) until repair.
2. Place a protective shield over the involved eye.
3. Tetanus prophylaxis as needed (see Appendix 2, Tetanus Prophylaxis).
4. Antibiotics (e.g., vancomycin 1 g i.v. q12h; and ceftazidime 1 g i.v. q12h or ciprofloxacin 400 mg i.v.
q12 hr or moxifloxacin 400 mg i.v. q.d. or gatifloxacin 400 mg i.v. q.d.).
5. Cycloplegic (e.g., atropine 1% t.i.d.) for posterior segment foreign bodies.
6. Urgent surgical removal of any acute IOFB is advisable to reduce the risk of infection. For some metallic foreign bodies, a magnet may be useful during surgical extraction. Copper or contaminated foreign bodies require especially urgent removal. A chronic IOFB may require removal if associated with severe recurrent inflammation, if in the visual axis, or if causing siderosis.
7. If endophthalmitis is present, treat as per 12.15, Traumatic Endophthalmitis.
Note
Fluorquinolones are contraindicated in children and pregnant women.
Follow-Up
Observe the patient closely in the hospital for signs of inflammation or infection. If the surgeon is uncertain as to whether the foreign body was entirely removed, postoperative imaging should be
considered. Periodic follow-up for years is required; watch for a delayed inflammatory reaction. When an IOFB is left in place, an electroretinogram (ERG) should be obtained as soon as it can be done safely.
Serial ERGs should be followed to look for toxic retinal metallosis, which will often reverse if the foreign body is removed.
3.16 Commotio Retinae Commotio Retinae Symptoms
Decreased vision or asymptomatic; history of recent ocular trauma.
Signs
(See Figure 3.16.1.)
Confluent area of retinal whitening. When occurring in the macula is called Berlin edema. The retinal blood vessels are undisturbed in the area of retinal whitening. However, other signs of ocular trauma may be noted including retinal hemorrhages.
Note
Visual acuity does not always correlate with the degree of retinal whitening.
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Etiology
Contrecoup injury. Blunt trauma to the globe causes shock waves which travel posteriorly and lead to disruption of the photoreceptors. The whitening is the result of intracellular edema and fragmentation of the photoreceptor outer segments and intracellular edema of the retinal pigment epithelium (RPE). There is little to no intercellular edema.
Differential Diagnosis
z Retinal detachment: Retina elevated associated with retinal break or dialysis. See 11.3, Retinal Detachment.
z Branch retinal artery occlusion: Rarely follows trauma. Whitening of the retina along the distribution of an artery. See 11.7, Branch Retinal Artery Occlusion.
z White without pressure: Common benign peripheral retinal finding. May be associated with a prominent vitreous base.
Work-Up
Complete ophthalmic evaluation, including dilated fundus examination. Scleral depression is performed except when a hyphema, microhyphema, or iritis is present.
Treatment
No treatment is required because this condition usually clears without therapy.
Follow-Up
Dilated fundus examination is repeated in 1 to 2 weeks. Patients are instructed to return sooner if retinal detachment symptoms are experienced (see 11.3, Retinal Detachment).
3.17 Traumatic Choroidal Rupture Traumatic Choroidal Rupture Symptoms
Decreased vision or asymptomatic; history of ocular trauma.
Signs
Figure 3.16.1. Commotio retinae.
(See Figure 3.17.1.)
Critical. A yellow or white crescent-shaped subretinal streak, usually concentric to the optic disc. It may be single or multiple. Often the rupture cannot be seen until several days or weeks after trauma because it may be obscured by overlying blood.
Other. Rarely, the rupture may be radially oriented. Choroidal neovascularization (CNV) may develop later. Traumatic optic neuropathy may be present.
Differential Diagnosis
z Lacquer cracks of high myopia: Often bilateral. A tilted disc, a scleral crescent adjacent to the disc, and a posterior staphyloma may also be seen. A CNV also may develop in this condition. See 11.22, High Myopia.
z Angioid streaks: Bilateral subretinal streaks that radiate from the optic disc, sometimes associated with a CNV. See 11.23, Angioid Streaks.
Work-Up
1. Complete ocular examination, including dilated fundus evaluation to rule out retinal breaks and to detect CNV which is best seen using slit-lamp biomicroscopy with either a fundus contact or 60- or 90-diopter lens.
2. Consider fluorescein angiography to confirm the location of a CNV.
Treatment
Laser photocoagulation should be considered when a CNV is extrafoveal (>200 µm from the center of the fovea). Treatment should be applied within 72 hours of obtaining the fluorescein angiogram. Surgical removal of the CNV, intravitreal anti-VEGF drugs, or photodynamic therapy may be options for subfoveal lesions, although experience with these options is limited. See 11.17, Neovascular or Exudative (Wet) Age-Related Macular Degeneration, for more information on treatment of subfoveal CNVs.
Follow-Up
After ocular trauma, patients with hemorrhage obscuring the underlying choroid are reevaluated every 1 to 2 weeks until the choroid can be well visualized. If a choroidal rupture is present, patients are instructed in the use of an Amsler grid and told to return if a change in the appearance of the grid is noted (see Amsler Grid). Although CNVs are rare overall, ruptures that are longer or closer to the fovea
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Figure 3.17.1. Choroidal rupture.
are at greater risk for development of CNV. Fundus examinations may be performed every 6 to 12 months depending on severity and risk of progression to CNV. Patients treated for a CNV must be followed closely after treatment to watch for a persistent or new CNV (see 11.17, Neovascular or Exudative (Wet) Age-Related Macular Degeneration, for further follow-up guidelines).
3.18 Chorioretinitis Sclopetaria Chorioretinitis Sclopetaria Symptoms
Visual loss, severity depends on region of involvement, history of high-velocity missile injury to orbit (e.g., a BB, bullet, or shrapnel).
Signs
(See Figure 3.18.1.)
Critical. Areas of choroidal and retinal rupture and necrosis leaving bare sclera on fundus examination;
subretinal, intraretinal, preretinal, and vitreous hemorrhage often involving the macula. Eventually blood is resorbed and the resultant defects are replaced by fibrous tissue.
Other. Intraorbital foreign body, “claw-like” break in the Bruch membrane and choriocapillaris. Can have associated avulsion of vitreous base which can cause peripheral retinal dialysis.
Etiology
Caused by a high-velocity missile passing through the orbit without directly contacting the
globe. Shock waves produced by the missile's passage through the orbit lead to the chorioretinal injury.
Differential Diagnosis
z Ruptured globe: Severe subconjunctival hemorrhage and chemosis, often with deep or shallow AC, low intraocular pressure, and peaked, irregular pupil. See 3.14, Ruptured Globe and Penetrating Ocular Injury.
z Choroidal rupture: White or yellow crescent-shaped subretinal streak usually concentric to the optic nerve. No retinal break is present. Initially retinal hemorrhage in the posterior pole may obscure a choroidal rupture which then becomes apparent only over the following several weeks as the blood clears. See 3.17, Traumatic Choroidal Rupture.
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Figure 3.18.1. Chorioretinitis sclopetaria.
z Optic nerve avulsion: Decreased vision with RAPD on examination and depression or excavation of the optic disc if partial or retraction of entire nerve if complete. Often associated with vitreous
hemorrhage. No treatment is available and visual prognosis depends on extent of injury. See 3.11, Traumatic Optic Neuropathy.
Work-Up
1. History: Known injury with a projectile?
2. Complete ocular evaluation including dilated retinal examination. Look for areas of retinal and choroidal rupture with underlying bare sclera. Carefully examine the conjunctiva and anterior sclera ruling out ruptured globe. Rule out IOFB. Carefully examine the retinal periphery for retinal tears or dialysis especially if the vitreous base has avulsed.
3. Protect the eye with a shield.
4. Obtain CT of the orbits (axial and coronal) to check for intrascleral, intraocular, or intraorbital foreign body. UBM may be helpful to rule out intraocular or intraorbital foreign body.
Treatment
There is no effective treatment, and typically patients are observed. Complications, including retinal dialysis and retinal detachment, are treated appropriately. Surgery can also be considered for nonclearing VH.
Follow-Up
Sequential examinationss are required every 2 to 4 weeks looking for signs of retinal detachment as blood clears. Patients should be followed until an atrophic scar replaces areas of hemorrhage.
3.19 Purtscher Retinopathy Purtscher Retinopathy Symptoms
Decreased vision, often sudden, can be severe. There may be a history of compression injury to the chest, head, or lower extremities, but not a direct ocular injury.
Signs
(See Figure 3.19.1.)
Critical. Multiple cotton wool spots and/or superficial hemorrhages in a configuration
around the optic nerve; can also have larger areas of superficial retinal whitening. Changes are typically bilateral but may be asymmetric or unilateral.
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Other. Serous macular detachment; dilated tortuous vessels; hard exudates; optic disc edema, though the disc usually appears normal; RAPD; optic atrophy when chronic.
Differential Diagnosis
z Pseudo-Purtscher retinopathy: Several entities with the same or similar presentation that are not associated with trauma (Purtscher retinopathy by definition occurs with trauma). Causes include acute pancreatitis, collagen vascular diseases (systemic lupus erythematosis, scleroderma, dermatomyositis, Sjögren syndrome), thrombotic thrombocytopenic purpura (TTP), chronic renal failure, amniotic fluid embolism, retrobulbar anesthesia, orbital steroid injection, and long bone fractures.
z Central retinal vein occlusion: Unilateral, multiple hemorrhages and cotton wools spots diffusely throughout the retina. See Section 11.8, Central Retinal Vein Occlusion.
z Central retinal artery occlusion: Unilateral retinal whitening with a cherry-red spot, see Section 11.6, Central Retinal Artery Occlusion.
Etiology
Not well understood. It is felt that the findings are due to occlusion of small arterioles in the peripapillary retina by different particles depending on the associated systemic condition: complement activation, fibrin clots, platelet–leukocyte aggregates, or fat emboli.
Work-Up
1. History: Determine if there is a history of compression injury to the head or chest. If not, then inquire as to symptoms associated with causes of pseudo-Purtscher (see above e.g., renal failure, alcoholism).
2. Complete ocular examination including dilated retinal evaluation. Rule out direct globe injury.
3. If the characteristic findings occur in association with severe head or chest trauma, then the diagnosis is established and no further work-up is required. However, if not, then the patient needs a systemic work-up to investigate other causes (e.g., amylase, lipase).
4. CT of the head, chest, or long bones as indicated.
5. Fluorescein angiography shows patchy capillary nonperfusion in regions of retinal whitening.
Treatment
No ocular treatment available. Must treat the underlying condition if possible to prevent further damage.
Figure 3.19.1. Purtscher retinopathy.
Follow-Up
Repeat dilated fundus examination in 2 to 4 weeks. Retinal lesions resolve over a few weeks to months.
Visual acuity may remain reduced or may return to baseline in 50% of cases.
3.20 Shaken Baby Syndrome/Inflicted Childhood Neurotrauma Shaken Baby Syndrome/Inflicted Childhood Neurotrauma Definition
Syndrome of intracranial hemorrhage, skeletal fractures and/or multilayered retinal hemorrhages thought due to the acceleration-deceleration forces of violent shaking. May be associated with other injuries (e.g., long bone or rib fractures). External signs of trauma are frequently absent.
Symptoms
Change in mental status, new onset seizures, poor feeding, irritability, inability to track or follow with eyes. Child is usually <1 year old and rarely >3 years of age. Symptoms and signs often inconsistent with history.
Signs
Critical. Multilayered (pre-, intra-, and subretinal) retinal hemorrhages are present in ~80%. Unilateral or markedly asymmetric hemorrhages in up to 20% of cases. Hemorrhages can be few in number, exclusively intraretinal, and confined to the posterior pole. In approximately two-thirds of cases, the hemorrhages are too numerous to count and extend to the ora serrata. Macular retinoschisis (hemorrhagic macular cysts) may be seen. Most common brain lesions are subarachnoid and/or subdural hemorrhage.
Other. Subretinal and vitreous hemorrhage less common. Retinal detachment, papilledema, late optic atrophy, optic nerve avulsion, optic nerve sheath hemorrhage, avulsion fractures, periosteal reactions in long bones as well as many signs of acute and old trauma can be seen.
Differential Diagnosis
z Severe accidental injury: Usually accompanied by other external injuries consistent with the history.
Retinal hemorrhages are rarely present and if present, not extensive.
z Birth trauma: Retinal hemorrhages can be extensive but typically resolve within 4 to 6 weeks. Clinical history must be consistent. Likely, most common cause of mild retinal hemorrhage in neonates.
z Coagulopathies, leukemia, and other blood dyscrasias. Rare, but should be ruled out. May be source of extensive retinal hemorrhages.
z Terson syndrome: Intraocular hemorrhage due to intracranial hemorrhage and elevated intracranial pressure. Subhyaloid hemorrhage is classic, but can be in any level (i.e., sub-, intra-, or preretinal, or vitreous hemorrhage). Most often after subarachnoid hemorrhage due to ruptured cerebral aneurysms.
Rarely, if ever, occurs in children.
z Severe hypertension: Peripapillary retinal hemorrhages most common. See 11.10, Hypertensive Retinopathy.
z Norrie disease, Coats disease, persistent hyperplastic primary vitreous, hypotonous retinopathy, CMV retinitis, toxoplasmosis, and retinopathy of prematurity. These are easily distinguished from shaken baby syndrome by the distinctive clinical appearance as well as the clinical setting.
Work-Up
1. Obtain thorough history from caregiver(s), separately if possible. Be alert for history incompatible with P.47
injuries or changing versions of history.
2. Check vitals. Pediatrician to conduct systemic examination.
3. Complete ophthalmic examination, including pupils and dilated fundus examination.
4. Laboratory: Complete blood count, platelet count, PT/INR and PTT. Consider additional
evaluation including fibrinogen, D-dimer, factor levels, von Willebrand factor, as well as other tests based on initial screening results.
5. Obtain appropriate imaging: CT or MRI, as well as a bone scan.
6. If not already done, admit patient to the hospital if shaken baby syndrome is suspected. Requires coordinated care by neurosurgery, pediatrics, psychiatry, and social services.
Note
Careful documentation is an integral part of the evaluation as the medical record may be used as a legal document. Ocular photography is perhaps the gold standard for documenting retinal hemorrhages, though the ability to perform photography cannot be expected.
Treatment
Predominantly supportive. Focus usually initially on systemic complications. Ocular manifestations are usually observed. In cases of dense vitreous hemorrhage vitrectomy may be considered due to the risk of amblyopia and high myopia.
Note
All physicians are legally mandated to report suspected child abuse. There is legal precedence for prosecution of nonreporters.
Follow-Up
Prognosis is variable and unpredictable. Approximately a 30% mortality rate. Survivors can suffer from significant cognitive disabilities and severe visual loss occurs in 20% of children, usually from optic atrophy or brain injury.
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Chapter 4 Cornea
4.1 Superficial Punctate Keratopathy Superficial Punctate Keratopathy Symptoms
Pain, photophobia, red eye, foreign body sensation, mildly decreased vision.
Signs
(See Figure 4.1.1.)
Critical. Pinpoint corneal epithelial defects (stain with fluorescein); may be confluent if severe. Pain is relieved by the instillation of anesthetic drops.
Note
Note