Ординатура / Офтальмология / Учебные материалы / Clinical Diagnosis and Management of ocular trauma
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Clinical Diagnosis and Management of Ocular Trauma |
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C H A P T E R
28Traumatic Retinopathies
Scott Pfahler, T Mark Johnson (USA)
Commotio Retinae
The term commotio retinae (latin for retinal contusion) was coined by Berlin in 1873.1
ETIOLOGYAND PATHOLOGY
Commotio is primarily observed following blunt ocular trauma (anterior contra-coup injury). Electrical injuries have also been described with similar findings.
In both animal and human histological reports, the areas of retinal whitening have been shown to be fragmented outer segment photoreceptors. Later changes include swelling of photoreceptor inner segments and breakdown of the outer blood-retinal barrier.2 Other pathologic findings include cystic spaces, disruption of RPE plasma membranes and loss of RPE apical processes.3 Experimental models suggest that the outer blood-retinal barrier is re-established 7 to 14 days postinjury and that outer segments show evidence of regeneration. Clinical methods of evaluation of the foveal cone pigment has suggested impairment at the time of the acute injury with resolution by 3 months follow-up visits.4
CLINICAL FEATURES
Ophthalmoscopic examination reveals an area of retinal whitening which can be found in both peripheral retina aswellastheposteriorpole.Iftheretinalwhiteningoccurs in the posterior pole, the term Berlin’s edema is used.1 In both animal and human histological reports, the areas of retinal whitening have been shown to be fragmented outersegmentphotoreceptors.Otherpathologicfindings include cystic spaces, disruption of RPE plasma membranes and loss of RPE apical processes.3,5
DIAGNOSTIC TESTING
Fluorescein angiography often reveals early hypofluorescence with late leakage, described by Gass as “acute pigment epithelial edema.”6 Recent reports using OCT have described increased reflectivity at the
Fig. 28.1: OCT of patient with commotio retinae with increased reflectivity at the level of the photoreceptors
level of the photoreceptor outer segments in the area of retinal whitening7,8 (Fig. 28.1).
TREATMENT AND PROGNOSIS
The natural history of commotio retinae has shown to resolve in about 2-3 days, usually with return of visual acuity. If injury occurs in the macula, reports of permanent visual loss has been reported.
Traumatic Macular Hole
The first report case of traumatic macular hole secondary to blunt ocular trauma was reported by Knapp in 1869.9
ETIOLOGYAND PATHOLOGY
The mechanism of traumatic macular hole formation has been thought to be the result of ocular deformation of the posterior pole at the time of trauma. This appears to lead to secondary retinal edema with cystoid changes in the outer retina10,11 (Fig. 28.2).
CLINICAL FEATURES
Macular holes in patients suffering blunt trauma often have different features from the more common
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Clinical Diagnosis and Management of Ocular Trauma |
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Direct trauma can result in contusion necrosis of |
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the choroid with a rupture oriented parallel to the ora |
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serrata. Indirect choroidal ruptures result in a posterior |
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rupture that is concentric to the optic nerve. This occurs |
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following a compressive force upon the posterior pole |
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combined with the anchoring effect of the optic nerve. |
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CLINICAL FEATURES |
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Fig. 28.2: OCT of patient with traumatic macular hole |
Typical findings include intrachoroidal, subretinal and |
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intraretinal hemorrhages. Commotio retinae is often |
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idiopathic macular hole. Given that the pathogenesis |
accompanied with the choroidal rupture.20-22 Following |
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is related to ocular deformation at the time of trauma |
choroidal rupture the local area of injury undergoes |
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rather than abnormal progression of posterior vitreous |
bleeding, fibrovascular tissue proliferation and then |
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detachment a PVD is rarely encountered in these |
RPE hyperplasia. Retinal tissue injury is variable and |
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patients. In one series only 15% of cases had an |
can range from no direct injury to full thickness |
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associated PVD at diagnosis.12 |
fibrovascular proliferation with vitreo retinal |
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Traumatic macular holes are more typically elliptical |
proliferation20 (Figs 28.3A and B). |
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with irregular edges. Traumatic holes tend to be larger |
The most common secondary complication of |
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in size ranging from 0.2 to 0.5 DD.12 At diagnosis the |
choroidal rupture is development of choroidal neovas- |
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holes are often associated with other features of trauma |
cularization. Reports of CNV following choroidal rupture |
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including hyphema, commotion retina and vitreous |
have been reported as early as one month post-injury |
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hemorrhage. Secondary retinal detachment may occur. |
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TREATMENT AND PROGNOSIS |
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Spontaneous closure of traumatic macular holes is well |
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described.StudiesofmERGinpatientswithspontaneous |
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closure of traumatic macular holes show improved func- |
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tion with closure though recovery is often incomplete.13 |
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In cases with persistent macular hole vitrectomy is |
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typically recommended. Creation of a posterior |
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vitreous detachment can be challenging in pediatric |
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patients. Autologous plasmin has been used as a |
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surgical adjunct to assist in creation of PVD.14 Removal |
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of the internal limiting membrane may be useful to |
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improving the rate of hole closure though no |
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comparative studies exist in the context of traumatic |
Fig. 28.3A: Post-blunt trauma patient has acute |
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macular holes.15,16 Surgical closure rates have been |
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subretinal hemorrhage |
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reported to range from 87 to 100%.14-17 Visual recovery |
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is variable and is influenced by the underlying ocular |
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injury. Approximately 50% of patients achieve better |
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than 20/50 acuity.18 |
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Choroidal Rupture
Choroidal ruptures can occur after blunt trauma (compression/contusion injuries). The incidence of this type of injury is between 5-10% of all blunt ocular trauma.19
ETIOLOGYAND PATHOGENESIS
Positioned between the elastic scleral and retina, the inelastic Bruch’s membrane/RPE/Choriocapillaris complex is susceptible to rupture and tearing.20-22
Fig. 28.3B: Two weeks later clearance of subretinal blood shows evidence of choroidal rupture
Traumatic Retinopathies |
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to four years later.23-26 A study of 111 patients with choroidal rupture showed that older age and macular choroidal rupture where strongly associated with CNV formation.27 Another study identified proximity to the fovea and length of the rupture as risk factors for developing CNV.28
DIAGNOSTIC TESTING
Indocyanine green angiography and fluorescein angiography may aid in the visualization of ruptures not seen clinically.23,24 Optical coherence tomography may be a useful adjunct in following patients with choroidal ruptures.
TREATMENT AND PROGNOSIS
Current options for treatment of CNV associated with choroidal rupture are thermal laser photocoagulation, photodynamic therapy, photodynamic therapy with adjuvant feeder vessel therapy, anti-VEGF intravitreal injections, submacular surgery. No comparative trials of therapy exist.29-32
The visual prognosis associated with choroidal rupture depends upon the location and the presence of neovascularization. A long-term study (4 years, 32 eyes) of patients with choroidal ruptures secondary in the foveal region, juxtafoveal, and extrafoveal regions had final visual acuities of 20/68, 20/35, and 20/60 respectively over a period of 4.5, 3.5, and 4.4 years.33
Chorioretinitis Sclopetaria
The term chorioretinitis sclopetaria has been used to describe chorioretinal injury from high velocity vehicle, typically a bullet or other high velocity projectile. This phenomenon was first described by Goldzieher in 1901.34
ETIOLOGYAND PATHOGENESIS
Classically these injuries occur following a high velocity missle injury to the orbit. This has been attributed to shock waves within the orbit resulting in ruptures of choroidal and retinal layers with or without hemorrhage. The projectile does not contact the globe structures. The proximity to the globe, the size of the projectile and its velocity may influence the nature of the injury. Following the initial injury, observational and pathologic accounts have described a fibrovascular and pigmentary proliferation with loss of photoreceptors.35
CLINICAL FEATURES
At the time of the acute injury there is extensive retinal edema and hemorrhage. The borders of the injury
Fig. 28.4: Extensive subretinal hemorrhage and retinal edema following blunt trauma with a paintball gun
are often serrated. Due to the extensive fibrosis associated with this injury, retinal detachment is a rare occurrence associated with this condition36 (Fig. 28.4).
TREATMENT AND PROGNOSIS
No treatment has been described to date. Visual prognosis is dependent upon the location of the injury, with the worst visual prognosis involving the posterior pole.
Purtscher’s Retinopathy
The term “Purtscher’s retinopathy” was derived from Otmar Purtschers original description of with multiple retinal white spots scattered throughout the posterior pole after trauma in 1912. He suspected that these white spots were caused by lymphatic extravasations associated with increased intracranial pressure associated with head trauma.37
ETIOLOGYAND PATHOGENESIS
Purtscher’s retinopathy arises following severe head trauma or chest compression without direct globe injury. It is generally considered to be a rare phenomenon with the incidence of Purtscher’s retinopathy estimated at 0.24 cases per million population per year in the United Kingdom.
The pathogenesis of Purtscher retinopathy has been widely debated, possible causes include fat emboli, air embolization, venous reflux with endothelial swelling, and severe angiospasm.38-43,45 A common link between many cases has been leukocyte aggregation by activated complement factor 5 (C5a) which can occur in the conditions mentioned previously. Despite the wide range of opinions regarding the etiology the apparent occlusion of capillaries on IVFA suggest an emboli
nature.40, 43,44
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Clinical Diagnosis and Management of Ocular Trauma |
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CLINICAL FEATURES |
have been described for large subhyaloid hemorrhages |
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Typically findings in Purtscher retinopathy are bilateral |
that obscure the macula. Treatment options include |
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but there have been reports of unilateral cases. Visual |
Nd:YAG laser hyaloidotomy, krypton laser membro- |
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acuity typical ranges from 20/200 to CF with possible |
tomy, or vitrectomy with membrane peel.55,56 The |
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visual recovery to pre-event levels. Findings often |
prognosis in this condition is good, with vision often |
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include inner retinal whitening polygonal in shape |
returning following resolution of the hemorrhage. |
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which spare areas near the vasculature. Often upon |
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resolution of the retinal edema/cotton-wool spots, there |
Shaken Baby Syndrome/ |
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is nerve fiber layer dropout, mottling of the RPE in |
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the involved areas and possible optic atrophy.45 |
Child Abuse |
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DIAGNOSTIC TESTING |
ETIOLOGYAND PATHOGENESIS |
IVFA findings can vary from staining and leakage of the vasculature early in the course of the disease to capillary non-perfusion late in the disease. ICGA can reveal choroidal hypofluorescent areas.
TREATMENT AND PROGNOSIS
Some reports suggest high dose corticosteroids as therapy for Purtsher’s retinopathy but there are no randomized trials to evaluate this treatment.45
Valsalva Retinopathy
ETIOLOGYAND PATHOGENESIS
Retinopathy caused by a sudden increase in venous pressure in the retinal capillary network has been reported. With the valveless nature of the venous system in the head and neck, increases in abdominal or intrathoracic pressure can be transmitted to the head and neck resulting in a sudden increase in the capillary venous pressure with subsequent retinal hemorrhage.46 Reports of this phenomenon have been associated with the Valsalva maneuver, heavy lifting, childbirth, motor-vehicle airbags, sexual activity, choking, vigorous dancing, refractive surgery.50-54
CLINICAL FEATURES
Visual loss can occur with hemorrhages in the macular region. Peripheral hemorrhages are often asymptomatic. More extensive hemorrhages can occur with sub-internal limiting membrane hemorrhages and the possibility of breaking through and becoming subhyaloid or vitreous hemorrhages.47 One published case report using OCT showed that the anatomic location was likely sub-ILM.48, 49
TREATMENT AND PROGNOSIS
Most Valsalva hemorrhages are minimally symptomatic and do not require treatment. Many symptomatic hemorrhages will resolve spontaneously. Treatments
The presence of retinal hemorrhages in a child is highly suspicious for abuse and non accidental head trauma. Retinal hemorrhages are a common finding in childhood abuse cases and are the most common ocular finding in children with manifestations of child abuse occurring 11-23% of abused children and 5080% of shaken babies.57 Conversely direct, accidental head trauma in children rarely produces intraocular hemorrhages.58 In a series of 241 infants hospitalized with subdural hematomas 77.5% of children with shaken baby syndrome had intraocular hemorrhage compared with 0% with a history of direct, accidental trauma.58
The likely cause of these hemorrhages are the sudden, severe acceleration/deceleration head and neck movementts. Children are usually age three or younger in age.60 Similar ophthalmic findings have been described in abused children that are older.61 Macular retinoschisis is a characteristic autopsy finding that is not observed with other forms of head trauma.62
CLINICAL FEATURES
Involvement of ophthalmologists in the screening for shaken baby syndrome is of paramount importance. 55 % of non-ophthalmologists involved in shaken baby cases fail to examine the retina.59 External signs of shaking or child abuse may be absent with only retinal hemorrhages and subdural/subarachnoid hemorrhages present. In one case series of 75 cases of shaken baby syndrome 93 % had subdural hematoma, 44 % cerebral edema and 16 % subarachnoid hemorrhage.63 Clinical features include intraretinal, preretinal and sub ILM hemorrhages (Fig. 28.5).
DIAGNOSTIC TESTING
All cases of suspected abuse need to be evaluated by a multi-disciplinary team. Neuroimaging is important due to the frequent association with intracranial hemorrhage.
Recent studies involving optical coherence tomography have shown evidence of vitreomacular traction
Traumatic Retinopathies |
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ment is possible. Animal models of high velocity projectiles suggest that direct corneal trauma tended to produce tenting of the nasal retinal while peripheral trauma produced direct retina effects.69 High speed cinematography describes four phases of globe deformation from high velocity trauma: (1) compression of the globe with decreased axial length and equatorial expansion; (2) decompression with an increase in axial length and a decrease in equatorial diameter; (3) overshoot with a rebound in axial lengthening and equatorial shortening and (4) oscillation of small movement of the eye.70 Retinal breaks appear to develop via two mechanisms: (1) vitreous base contraction with traction on the anterior retina or (2) contusion necrosis
Fig. 28.5: Extensive preretinal hemorrhages in of the retina secondary to direct trauma. shaken baby syndrome
CLINICAL FEATURES
associated with preretinal blood. In addition evidence of perimacular folds and hemorrhagic macular retinoschisis were documented.64
TREATMENT AND PROGNOSIS
Management of this condition necessitates prompt notification of children services authorities in the community and treatment of underlying retinal hemorrhagic and neurologic sequelae. In one series of 241 infants 82% of intraocular hemorrhages resolved within 4 weeks.58 In cases of premacular hemorrhage that obscure the visual axis vitrectomy should be considered to reduce the risk of ambyopia.
Retinal Tears, Retinal Dialysis
and Detachments
ETIOLOGYAND PATHOGENESIS
In many case series, blunt force trauma causes the majority of traumatic retinal detachments (70-86%) The most common age and sex demographic is young males, who overall account for the majority of trauma cases.65-67 A large case series consisting of 160 patients with retinal detachment showed that signs of detachment manifested within two years of injury in most cases, however, a wide range exists. 12% of detachments are noted within 24 hours. Some presentations may be delayed by many years.68
The pathological mechanism thought to cause retinal tears and detachments is the rapid anteriorposterior compression of the globe/vitreous structure which causes a degree of vitreous base traction and subsequent retinal tears. If the vitreous has not liquefied the break may remain stable but if liquid vitreous accumulates near the break, a future retinal detach-
Traumatic retinal detachments differ from routine rhegmatogenous detachments by the nature of the pathologic retinal break. Traumatic detachments are more likely to arise from dialyses (55% of traumatic detachments versus 5% of rhegmatogenous detachments) or giant retinal tears (16 % of traumatic detachments versus 2 % of rhegmatogenous detachments).71 Lattice degeneration is much less commonly observed in traumatic retinal detachment series.
TREATMENT AND PROGNOSIS
The preferred treatment of retinal breaks and detachments secondary to trauma vary but include laser retinopexy, cryopexy, pneumatic retinopexy, scleral buckle, pars plana vitrectomy, or combinations of these treatments. The prognosis depends up the extent and duration of the retinal break or detachment.68 Treatment options for traumatic retinal dialysis can include laser demarcation for small inferior temporal dialysis, while scleral buckling has been shown to be successful in 9698% of eyes with trauma associated retinal dialysis .72-75
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Har JCD, Natisikos VE, Raistrick ER, et al. Indirect |
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Jacob HS, Craddock PR, Hammerschmidt DE, et al. |
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Fuller B, Gitter KA. Traumatic choroidal rupture with later |
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serous detachment of macula: report of successful argon |
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laser treatment. Arch Ophthalmol 1973;89:354-55. |
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Ophthalmic findings. J Pediatr Ophthalmol Strabismus |
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2004;41:80-88. |
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in a case of traumatic asphyxia. Am J Ophthalmol 1973; |
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children with abusive head injury: Does shaken-child |
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47. Duane TD. Valsalva hemorrhagic retinopathy. Trans Am |
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syndrome exist? Pediatrics 2006;117:1039-44. |
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62. Gnaanaraj L, Gilliland MG, Yahya RR, et al. Ocular |
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48. Tatlipinar S, Shah SM, Nguyen QD. Optical coherence |
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manifestations of crush head injury in children. Eye |
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63. Morad Y, Kim YM, Armstrong DC, et al. Correlation |
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retinopathy.Can J Ophthalmol 2007;42;129-30. |
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between retinal abnormalities and intracranial |
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49. Shukla D, Naresh KB, Kim R. Optical coherence |
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abnormalities in the shaken baby syndrome. Am J |
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64. Sturm V, Landau K, Menke MN. Optical Coherence |
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50. Friberg TR, Braunstein RA, Bressler NM. Sudden visual |
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Tomography Findings in Shaken Baby Syndrome. Am |
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51. Ladjimi A, Zaouali S, Messaoud R, et al. Valsalva |
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ocular complications of boxing. Ophthalmology 1987; |
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52. Ho LY, Abdelghani WM. Valsalva retinopathy associated |
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nontraumatic retinal detachment. Ophthalmology 1982; |
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with the choking game. Semin Ophthalmol 2007;22; |
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53. Bar-Sela SM, Moisseiev J. Valsalva retinopathy associated |
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detachment. Mod Probl Ophthalmol 1972;10:479-89. |
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with vigorous dancing in a discotheque. Ophthalmic Surg |
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68. Cox MS, Schepens CL, Freeman HM. Retinal detachment |
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due to ocular contusion. Arch Ophthalmol 1966; |
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Valsalva-like retinopathy following hyperopic laser in situ |
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keratomileusis. Ophthalmic Surg Lasers Imaging. |
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globe under high speed impact: Its relation to contusion |
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injury. Invest Ophthalmol Vis Sci 1969;8;2901-301. |
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Ophthalmol 2007. |
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accuracy in diagnosing retinal hemorrhages in the shaken |
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C H A P T E R
29Management of Endophthalmitis
Pei-Chang Wu, Hsi-Kung Kuo (Taiwan)
Introduction
Endophthalmitis is defined by marked inflammation of intraocular fluids and tissues. When caused by microorganisms, endophthalmitis often results in severe visual loss. The broad categories of endophthalmitis include postoperative (acute-onset, chronic or delayed onset, bleb-associated), post-traumatic, endogenous and miscellaneous, such as intravitreous triamcinolone associated endophthalmitis, microbial keratitis and suture removal (Table 29.1). These categories are important in predicting the causative organism and guiding therapeutic decisions before microbiological confirmation.
TABLE 29.1: Classification of endophthalmitis and most frequent organisms
1.Postoperative
a.Acute-onset: coagulase (-) staphylococci (Staph. Epidermidis), Staphylococcus aureus, Enterococcus species, Streptococcus species, gramnegative bacteria (Pseudomonas)
b.Chronic: P. acnes, coagulase (-) staphylococci, fungi
c.Bleb-associated: Streptococcus species, Hemophilus influenza, Staphylococcus species
2.Post-traumatic: Bacillus species, Staphylococci
3.Endogenous: Candida species, gram-negative bacteria (Klebsiella pneumoniae), S. aureus
4.Miscellaneous
a.Corneal ulcer perforation: Pseudomonas, Staphylococcus species
b.Intravitreous triamcinolone associated
c.Suture removal associated.
Acute Postoperative
Endophthalmitis
Acute postoperative endophthalmitis is defined as the occurrence of intraocular infection within 6 weeks after surgery by the Endophthalmitis Vitrectomy Study (EVS).
PROPHYLAXIS
In recent evidence-based literature, Cillua et al found preoperative irrigation with povidone-iodine (PI) to be a most strongly recommended technique based on the current clinical evidence (Table 29.2).1 PI is a potent antiseptic with a wide spectrum of activity against both gram-positive and gram-negative bacteria, fungi and viruses. Antimicrobial activity contributes to the 1% free iodine released that occurs after contact with the skin for 30 seconds to 1 minute, and this effect will last for 1 hour.2, 3 Iodine penetrates the cell wall and reacts with amino acids and nucleotides, which ultimately disrupt the cell’s protein synthesis. Despite the wide use of PI solutions as disinfectants in hospitals, these solution have been reported to be susceptible to contamination with Pseudomonas cepacia, which could be passed on to the patient.4
Preoperative preparation with 5% PI solution dropped into the conjunctival sac followed by a skin preparation of 10% PI solution has been recommended.5 Our retrospective, case-controlled study found that patients who received 10% PI skin disinfection combined with 5% PI conjunctival disinfection had significantly less risk of developing post-cataract surgery endophthalmitis. However, a modified preparation
TABLE 29.2: Prophylactic methods to prevent bacterial endophthalmitis after cataract surgery1
Prophylacitic intervention |
Clinical |
recommended |
|
|
|
Postoperative subconjunctival antibiotics |
C |
Preoperative lash trimming |
C |
Preoperative saline irrigation |
C |
Preoperative povidone-iodine antisepsis |
B |
Preoperative topical antibiotic therapy |
C |
Irrigating solutions containing antibiotics |
C |
Intraoperative heparin |
C |
Grade ‘A’ is considered very important or crucial to clinical outcome, grade ‘B’ as moderately important, and grade ‘C’ is of questionable use
Management of Endophthalmitis |
|
|
175 |
|
method of 5% PI on both the skin and conjunctiva |
ceftazidime carries a lower risk of retinal toxicity and |
|
||
has been used in many institutes and for simple ocular |
a broader therapeutic index. However, intravitreous |
|
||
surgery, such as intravitreous injection.6,7 Caution should |
ceftazidime was not evaluated in the EVS and it has |
|
||
be taken to avoid touching the lid margin and lashes |
been shown that in-vitro ceftazidime precipitates in |
|
||
when the needle is inserted into the eye. |
vitreous humor at body temperature, irrespective of |
|
||
|
the presence of vancomycin.12 In clinical studies, |
|
||
INTRAOCULARANTIBIOTICS |
ceftazidime has been demonstrated to precipitate in |
|
||
Intravitreal antibiotic therapy could reach far greater |
inflamed eyes resulting in possible subtherapeutic |
|
||
concentration. Reconstitution with normal saline as |
|
|||
intraocular antibiotic concentration than any other |
|
|||
opposed to balanced salt solution produced less |
|
|||
method of administration. It is the main stay of |
|
|||
precipitation. Intravitreous ceftazidime is typically |
|
|||
treatment for infective endophthalmitis. In instances |
|
|||
injected at a concentration of 2.25 mg/0.1 mL.13 Like |
|
|||
of instant and prompt treatment required in order to |
|
|||
vancomycin, half-life is decreased |
in aphakic, |
|
||
save the vision, inaccuracies of gram-staining results |
|
|||
vitrectomized and inflamed eyes. |
|
|
|
|
and unavailable culture results, broad-spectrum |
|
|
|
|
|
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|
|
intravitreal antibiotics covering almost all the gram- |
Aminoglycosides |
|
|
|
positive and gram-negative bacteria are necessary. A |
|
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|
|
Aminoglycosides have a bactericidal effect through |
|
|||
few selected drugs are currently recommended, |
|
|||
including vancomycin, ceftazidime and amikacin. In |
ionic interaction with the cell surface, energy |
|
||
the EVS, the antimicrobial sensitivity profile of amikacin |
dependent uptake phases and binding to ribosomes. |
|
||
Amikacin has a strong bactericidal effect against aerobic |
|
|||
and ceftazidime was similar at 89% against gram- |
|
|||
and facultative gram-negative bacilli. It has a synergistic |
|
|||
negative organism, and all gram-positive cocci were |
|
|||
effect with vancomycin and other cell wall active |
|
|||
sensitive to vancomycin.8 |
|
|||
|
antimicrobials (penicillins and cephalosporins). |
|
||
Vancomycin |
Aminoglycosides such as amikacin and gentamicin |
|
||
have been used for intravitreous injection. Gentamicin |
|
|||
Vancomycin is the drug of choice for gram-positive |
|
|||
has been reported to cause macular toxicity.14 |
|
|||
bacteria in acute postoperative endophthalmitis. It is |
Aminoglycoside-induced macular infarction is thought |
|
||
a bactericidal drug whose primary mode of action is |
to result from an increased concentration by the |
|
||
inhibiting synthesis and assembly of the bacterial cell |
gravity-induced accumulation of drugs on the macula |
|
||
wall. It has a strong antimicrobial effect against gram- |
in a supine patient. Although animal experiments15 |
|
||
positive bacteria, especially Staphylococcus aureus, |
have shown that amikacin is safer than gentamicin, |
|
||
Staphylcoccus epidermidis and enterococcus, including |
a potential for macular toxicity might still exist. Amikacin |
|
||
methicillin-resistant Staphylococcus aureus. In |
has been shown to cause macular infarction with loss |
|
||
intraocular use, concentrations of up to 2 mg/0.1 mL |
of macular capillaries and pre-retinal hemorrhage.16-18 |
|
||
have been demonstrated to be non-toxic to the retina.9 |
The standard intravitreous dose of amikacin is 0.4 |
|
||
The EVS recommended a dose of 1.0 mg/0.1 mL.10 |
mg/0.1 mL. This is the dose used in the EVS. |
|
||
The half-life of the drug is reduced in inflamed eyes |
Pharmacokinetic studies in animals were similar to |
|
||
and prolonged in normal vitreous.11 Even in inflamed |
vancomycin pharmacokinetics in the vitreous cavity. |
|
||
eyes, therapeutic levels are still detected up to 72-84 |
However, levels measured 24 hours after injection were |
|
||
hours after injection. Vancomycin is also cleared more |
equal to or less than the minimal inhibitory concen- |
|
||
rapidly in aphakic, vitrectomized eyes.9, 11 |
tration (MIC) for most organisms sensitive to |
|
||
|
amikacin.19 Lower concentrations in the vitreous may |
|
||
Ceftazidime |
necessitate the need for repeat injections of amikacin |
|
||
if there is no response. No toxicity has been contributed |
|
|||
Ceftazidime is a third-generation cephalosporin that |
|
|||
to a single injection but repeated injections should be |
|
|||
has a bactericidal effect by disrupting cell wall synthesis. |
undertaken with caution due to the possible risk of |
|
||
Third-generation cephalosporins have strong |
macular infarction.18, 19 Nasal side recumbency for |
|
||
antibacterial effects against gram-negative bacilli. They |
about 30 minutes might be suggested after intravitreous |
|
||
also have an added effect against Streptococcus |
injection of amikacin. |
|
|
|
pneumonia, pyogenes and other streptococci. |
Repeated vitreous tapping and injection of |
|
||
Cephalosporins have little effect against Staphylococcus |
antibiotics, together with pars plana vitrectomy, should |
|
||
aureus but a strong effect against Pseudomonas |
be consider if there is no clinical improvement or if |
|
||
aeruginosa. In contrast to the aminoglycosides, |
the condition deteriorates within 48 to 72 hours.20 |
|
||
|
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|