Ординатура / Офтальмология / Учебные материалы / Color Atlas of Ophthalmology The Quick-Reference Manual for Diagnosis and Treatment
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1 Ocular Trauma 11
flare in th e an terior ch am ber at slit-lam p exam in at ion . A com plete oph th alm ic evalu at ion sh ou ld be perform ed, in cluding ton om et r y an d fu n dus exam in at ion . Treat m en t t ypically con sists of cycloplegic agen t s. In refractor y cases an d if n o cor- n eal epith elial defect is detected, a steroid drop could be given . Pat ien ts sh ou ld be re-evalu ated w ith in a w eek; if irit is is resolved, m edicat ion can be discon t in u ed .
Iris Sphincter Tear
Blun t inju r y often causes tears in th e sph in cter p upillae of th e iris.
Presentation
Th e pat ien t m ay be asym ptom at ic or m ay h ave glare an d ph otoph obia. Th e tears in th e pupillar y m argin can be visu alized on slit lam p exam in at ion (Fig. 1.10)
Differential Diagnosis
Oth er causes of a dilated p upil (e.g., ph arm acological m ydriasis)
Management
A th orough ocu lar exam in at ion is don e to ru le ou t any oth er coexist ing dam age. It m ay be left alon e un t reated . If cau sing sym ptom s, an d if cat aract ext ract ion is also being plan n ed, on e m ay perform a pupilloplast y or use an iridia segm en t s.
Traumatic Cataract
Trau m at ic cataract can develop after various t ypes of in sult: blun t or perforat ing t raum a, elect ric sh ock, in frared, UV, an d ion izing radiat ion . Blun t t rau m a is th e m ost com m on cause, an d cou p an d con t recoup inju ries, along w ith equ atorial expan sion , are th e path ophysiological m ech an ism respon sible for ocu lar dam age. As regards len s inju r y, “coup” is th e cau se for Vossius ring (iris pigm en t rem ain s im prin ted on th e an terior capsule), an d “con t recou p” is respon sible for th e sh ock w aves th at m ay lead to an terior or posterior capsular ru pt u re an d su bsequ en t len s opacificat ion . Th e equatorial st retch ing can disr upt th e zon ules an d capsu le. Th e
Fig . 1.10 Sphincter tear. (Courtesy of Amar Agarwal, Dr.
Agarwal’s Eye Hospital, Chennai, India)
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release of len s protein s du e to capsu le rupt u re can lead to ph acoan aphylact ic uveit is, ch aracterized by th e presen ce of polym orph on uclear leukocyte (eosin oph ils) an d gian t cell in filt rat ion su rroun ding len s m aterials. Th e occlusion of th e t rabecu - lar m esh w ork du e to len s protein s an d m acroph ages can lead to an acu te rise in in t raocular p ressure. Glaucom a can also be secon dar y to relat ive pup illar y block du e to posterior syn ech iae or len s sw elling (ph acom orph ic glaucom a).
Presentation
If no perforating traum a or traum a-related sym ptom atic iritis occurs, the patient could w ait for days, weeks, or m onths before searching for m edical care. The patient usually presents w ith a history of traum a and m ay com plain of decreased vision and m onocular diplopia. At slit lam p exam ination, cataract associated w ith blunt traum a usually appears as stellate or roset te-shaped “visual axis” opacification located in - axis and involving the posterior capsule. Perforating traum a leads to cortical opacification at the site of injur y. This opacification usually rem ains localized, but if the capsular tear is large enough, the entire lens m ay opacify. Hyphem a, signs of iritis, and lens dislocation or sublu xation m ay be present (Fig. 1.11A,B).
A
B
Fig. 1.11 (A) Cataract and iridodialysis secondary to severe penetrating trauma. (B) Post traum atic endophthalmitis.
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Differential Diagnosis
Sen ile cat aract , ectopia len t is, angle recession glaucom a, an d hyph em a
Management
Mech an ism of injur y an d past ocular h istor y sh ould be invest igated first . Th en a rupt ured globe an d in t raocular foreign body sh ou ld be ru led ou t an d a com plete oph th alm ic exam in at ion sh ou ld be perform ed . Type an d exten t of len s opacificat ion an d th e presen ce of ocu lar in flam m at ion , hyph em a, ph acodon esis, iridodon esis, angle recession , len s sw elling, len s dislocat ion , or sublu xat ion sh ould be docum en ted . Zon u lar disru pt ion m ay be detected gon ioscopically th rough a dilated pu pil. Posterior segm en t t rau m a-related p ath ology sh ould be invest igated by fu n du scopy. If opacificat ion obst ruct s th e view of th e posterior segm en t , u l- t rason ography m ay be h elpfu l. Medical t reat m en t sh ou ld be directed to focal an d off-a xis opacit ies, in flam m at ion , an d in t raocular pressu re rise. Miot ics can h elp to obt ain a clear visual axis, in flam m at ion can be con t rolled w ith cor t icosteroids, in creased in t raocu lar pressu re can be t reated w ith st an dard ocu lar hypoten sive m edicat ion s. How ever, su rgical rem oval of th e len s u sually resolves th ese com plicat ion s. Decreased visual acu it y, len s-in duced in flam m at ion or glau com a, capsular rupt ure w ith len s sw elling, an d poor visualizat ion of posterior segm en t path ology are in dicat ion s for su rger y. St an dard ph acoem u lsificat ion is preferred if th e len s capsule is in tact an d th ere is su fficien t zon u lar su ppor t; in t racapsu lar ext ract ion is in dicated for zon ular in st abilit y or an terior dislocat ion . In cases of posterior dislocat ion or posterior capsular rupt u re, pars plan a len sectom y an d vit rectom y m ay be preferred . As regards len s im plan tat ion , capsu lar fixat ion is in dicated if zon u lar su ppor t an d th e len s capsu le are in tact; capsu lar ten sion rings m ay h elp in cases of lim ited zon ular dialysis. If th e posterior capsule is com prom ised but sufficien t zon ular su ppor t rem ain s, su lcus fixat ion sh ould be ch osen . A sut u re fixat ion ap - proach w ou ld be th e best if both zon u lar an d capsu lar su ppor t are in adequ ate. If n o posterior supp or t is m ain t ain ed, an terior ch am ber posit ion ing sh ou ld be con sidered . Com plicat ion s associated w ith t raum at ic cat aract in clude glau com a (pup illar y block glau com a, p h acolyt ic glaucom a, ph acom orph ic glau com a, angle recession glaucom a), ph acoan aphylact ic uveit is, hyph em a, ret in al det ach m en t , ch oroidal ru pt u re, t raum at ic opt ic n eu ropathy, an d globe rupt u re.
Lens Dislocation/Subluxation
Su blu xat ion is par t ial disrupt ion of th e zon u lar fibers; th e len s is decen tered bu t rem ain s par t ially in th e pu pillar y apert u re. Dislocat ion is com plete disru pt ion of th e zon ular fibers; th e len s is displaced ou t of th e pu pillar y apert u re. Trau m a (m ost com m on cau se), Marfan syn drom e, h om ocyst in u ria, Weill–March esan i syn - drom e, acqu ired syph ilis, congen it al ectop ia len t is, an iridia, Eh lers–Dan los syn - drom e, Crou zon disease, hyperlysin em ia, sulfite oxidase deficien cy, h igh m yopia, ch ron ic in flam m at ion s, an d hyperm at ure cat aract are som e of th e cau ses of len s su blu xat ion .
Presentation
Decreased vision an d dou ble vision th at persist w h en covering on e eye (m on ocu lar diplopia) are th e m ain sym ptom s. Crit ical sign s are decen tered or displaced len s, iridodon esis (qu ivering of th e iris), an d p h acodon esis (qu ivering of th e len s). Oth er sign s in clu de m arked ast igm at ism , cataract , angle closure glaucom a as a resu lt of pupillar y block, acqu ired h igh m yopia, vit reou s in th e an terior ch am ber, an d asym m et r y of th e an terior ch am ber depth (Fig. 1.12)
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Fig. 1.12 Lens subluxation and zonular disruption.
Management
Fam ily, person al, m edical, an d t rau m a h istor y is ver y im port an t . System ic exam i- n at ion sh ould evalu ate st at u re, ext rem it ies, h an ds, an d fingers as n ecessar y. Rapid plasm a reagin test an d fluorescen t t rep on em al an t ibody absorpt ion test , sodiu m n it ropru sside test , ech ocardiography, an d urin e ch rom atography to rule out h o- m ocyst in uria are n eeded .
Lens dislocated into the vit reous: Surgically rem ove th e len s.
Lens capsule intact, pat ient asym ptom at ic no signs of inflam m at ion: Obser ve.
Lens capsule broken eye inflam ed: Len sectom y is don e eith er th rough th e pars plan a or by using a lim bal approach
Sublu xat ion
Asym ptom at ic: Obser ve.
High uncorrectable ast igm at ism or m onocular diplopia: Su rgical rem oval of th e len s.
Sym ptom at ic cataract: Opt ion s in clu de surgical rem oval of th e len s.
Pupillary block: Treat m en t is iden t ical to th at for aph akic pup illar y block.
Marfan syndrom e is present: Refer th e pat ien t to a cardiologist for an an n u al ech ocardiogram an d m an agem en t of any cardiac-related abn orm alit ies. Prophylact ic system ic an t ibiot ics are required if th e p at ien t un dergoes su rger y (or a den tal procedu re) to preven t en docardit is.
Hom ocyst inuria is present:
Adm in ister pyridoxin e, 50 to 1000 m g by m outh fou r t im es a day.
Redu ce diet ar y m eth ion in e.
Avoid su rger y if possible becau se of th e risk of th rom boem bolic com plicat ion s. If surgical in ter ven t ion is n ecessar y, an t icoagu lan t th erapy is in - dicated .
Microhyphema/Hyphema
Trau m at ic hyph em a is defin ed by post inju r y accu m ulat ion of blood w ith in th e an - terior ch am ber. Microhyph em a con sist s of su spen ded er yth rocytes in th e an terior ch am ber, gen erally visible at slit lam p . Equatorial expan sion after blu n t t raum a in duces st ress to angle st ru ct u res, w h ich can lead to ru pt u re of iris an d ciliar y body
1 Ocular Trauma 15
vessels w ith su bsequen t h em orrh age. Lacerat ing injur y can be associated w ith direct dam age of blood vessels an d hypotony. Som e con dit ion s such as ru beosis iridis, juven ile xan th ogran u lom a, h em oph ilia, leu kem ia, an d th e use of dr ugs th at alter platelet or th rom bin fu n ct ion m ay facilit ate th e on set of hyph em a. A sign ifican t n um ber of sigh t-th reaten ing com plicat ion s m ay develop, w h ich requires careful follow -u p for hyph em a pat ien ts.
Presentation
Pat ien ts usu ally presen t w ith a h istor y of blun t t rau m a. Pain an d blu rred vision are com m on sym ptom s. Hyph em as are graded on th e am ou n t of blood w ith in th e an terior ch am ber: grade I is less th an on e th ird filling of th e an terior ch am ber, grade II hyph em as h ave m ore th an on e th ird but less th an on e h alf of th e an terior ch am ber filled w ith blood, grade III is m ore th an on e h alf bu t less th an total filling, grade IV is a total hyph em a, also kn ow n as eigh t-ball hyph em a (Fig. 1.13).
Differential Diagnosis
Uveit ic glau com a an d cau ses of spon tan eou s hyph em a such as juven ile xan th o- gran ulom a, iris cavern ous h em angiom a, hyper ten sion , an d bleeding disorders
Management
Mech an ism an d t im e of inju r y sh ou ld be invest igated carefully. A h istor y of sickle cell t rait or disease sh ou ld be sough t ou t . In spect ion for gross ocu lar injur y an d evaluat ion of th e adn exa sh ou ld be perform ed . A ru pt u red globe sh ould be ruled ou t . A com plete ocu lar exam in at ion is im perat ive an d m ust in clu de in t raocu lar pressure m easu rem en t an d dilated fun du scopic evalu at ion . Gon ioscopy sh ould be deferred un t il hyph em a resolves to detect poten t ial rebleeding sites an d angle recession . A draw ing of th e hyph em a docum en t ing sh ape an d size sh ou ld be recorded at ever y oph th alm ic evalu at ion . Depen ding on th e pat ien t’s h istor y, h em oglobin opath ies an d bleeding disorders sh ou ld be invest igated . B-scan u lt rason ography m ay be u sefu l in pat ien t s w ith large hyph em as, w h en oph th alm oscopy is n ot feasible. Non com plian t pat ien t s or th ose w ith in creased risk of rebleeding, u n con t rolled
Fig . 1.13 Post traum atic hyphema. Grade II hyphemas have more than one third but less than one half of the anterior chamber filled with blood.
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glaucom a, posit ive sickle cell t rait , or an em ia sh ou ld be con sidered for inpat ien t h ospitalizat ion . Th e elevat ion of th e pat ien t’s h ead to 30 to 45 degrees w h ile lying su pin e m ay facilit ate th e set tling an d layering of th e hyp h em a in th e in ferior an terior ch am ber, allow ing an easier classificat ion of th e hyph em a, an earlier evalu at ion of th e posterior pole, an d a m ore rap id im provem en t in visual acu it y. A t ran sparen t plast ic sh ield sh ould be u sed to protect th e involved eye from fur th er inju r y. It s t ran sparen cy allow s recogn izing rebleeding or su dden visu al loss.
Medical t reatm ent in cludes topical cycloplegics (1 drop of 1% at ropin e three tim es a day for up to 5 days) to in crease the pat ient’s com fort (con sider th e risk of precipitating acute glaucom a in pat ien ts w ith a n arrow ch am ber angle) and topical steroids (0.1%dexam eth ason e) to decrease inflam m at ion, reduce anterior ch am ber reaction , an d prevent the incidence of secon dar y hem orrh age (caution sh ould be exerted if steroids are used for a prolonged period because th ey can in crease the risk of cataract an d glaucom a). Topical and system ic an tifibrin olytics, such as am i- nocaproic acid, could be used to prevent rebleeding an d retarding clot lysis. Th e m ore com m on side effects of am in ocaproic acid in clude vom iting, diarrhea, and post ural hypoten sion . Its system ic use sh ould be avoided in patien ts w ith hepatic or ren al disease. Persistent in creased in traocular pressure should be treated in i- tially w ith topical
-blockers. If th is treatm en t is unsuccessful, topical
-agon ist or carbonic an hydrase in hibitor m ay be added in patients w ith out sickle cell t rait or disease. Aspirin an d other NSAIDS should be discont in ued . Un con trolled elevated int raocular pressure (at least 45 m m Hg for 5 days) could be surgically t reated w ith paracentesis and an terior ch am ber w ashout . Other indicat ions to surger y are early corneal staining or rebleeding hyph em as. Sm aller hyphem as are usually self-lim iting an d clear w ith in 5 days. Large hyphem as are associated w ith com plication s an d th e w orst progn osis. Such com plicat ions are secon dar y h em orrhage, corneal blood stain ing, glaucom a, an terior an d posterior syn ech iae, cataract, an d opt ic atrophy.
Ruptured Globe
A rupt ured globe is a devastating injur y w ith significant long-term con sequen ces for the pat ien t . It represen ts a discont in uit y of the eye’s outer m em branes caused by blunt or pen et rating t raum a. Rupt ures resulting from blunt traum a usually occur at th e sites w here the sclera is w eakest, such as at th e in sertion of th e extraocular m uscles, around the opt ic ner ve, an d at the lim bus. Sh arp objects w ith sufficient m om en t um m ay directly perforate th e globe. Globe rupt ure is m ore com m on in young m ales ow ing to their occupation al and recreation al preferen ces. High m yopia and previous eye surger y can m ake t issues m ore vulnerable to rupture. A rupt ured globe is an ophth alm ic em ergen cy and requires surgical repair as soon as possible. Th e visual outcom e depends largely on early recogn ition and prom pt in ter vent ion .
Presentation
Th e pat ien t usu ally p resen t s w ith a h istor y of ocu lar t rau m a. Sym ptom s in clude pain , w h ich can be n ot ext rem ely severe in th e case of sh arp injur y, an d decreased vision . Diplopia m ay be presen t du e to ext raocu lar m u scle en t rapm en t or dysfun c- t ion an d t raum a-associated cran ial n er ve palsy. At physical exam in at ion th e globe rupt ure m ay be obviou s or occu lt . A fu ll-th ickn ess corn eal or scleral lacerat ion is a sign of globe perforat ion . Prolapse of th e iris or ext rusion of ocular con ten t s m ay be presen t . Severe conju n ct ival h em orrh age, usually involving 360 degrees of bu lbar conju n ct iva, t ypically in dicates globe ru pt ure. Oth er accom panying sign s in clu de irregu lar pupil, hyph em a, len s injur y, com m ot io ret in ae, vit reou s h em orrh age, ch oroidal rupt ure, ret in al tears an d detach m en ts, an d t raum at ic opt ic n eu ropathy. A ru pt u red globe m ay presen t w ith both en oph th alm os an d exoph th alm os, depen ding on th e presen ce of an associated ret robu lbar h em orrh age (Fig. 1.14).
1 Ocular Trauma 17
Fig. 1.14 Perforating ocular trauma.
Management
Th e m ech an ism an d th e circu m st an ces of injur y an d th e n at ure of th e t raum at izing object sh ou ld be invest igated . Visu al acuit y sh ould be docu m en ted an d ext raocu lar m u scle fu n ct ion sh ou ld be evaluated . Pup ils sh ould be exam in ed for size, sh ape, an d ligh t reflex. Th e diagn osis of a rupt u red globe sh ould be m ade by slit lam p or pen ligh t . Th e orbit an d adn exa sh ou ld be exam in ed for inju ries, foreign bodies, bon e deform it y, an d eyeball displacem en t . In t raocu lar pressu re m easu re- m en t is con t rain dicated to avoid pressure to th e globe. Th e eye sh ou ld be p rotected w ith a sh ield . System ic prophylact ic an t ibiot ics an d an algesics, if advisable, sh ou ld be adm in istered . Th e pat ien t sh ou ld receive tet an u s im m un izat ion if in dicated an d be kept n oth ing per os. Th e im aging st u dy of ch oice is com pu ted tom ography; if it is n ot available a p lain x-ray film sh ou ld be obt ain ed . Magn et ic reson an ce im aging m ay be usefu l to iden t ify soft t issue an d globe inju ries, bu t it is con t rain dicated if a m et allic foreign body is suspected . Careful B-scan ult rason ography m ay be u sefu l to iden t ify th e site of ru pt u re an d in t raocular foreign bodies. Surgical repair sh ou ld be prom pt . If th ere is n o expect at ion to restore vision , en ucleat ion sh ou ld be con - sidered . En dop h th alm it is an d sym path et ic oph th alm ia are possible sigh t-t reat ing com plicat ion s th at sh ould be born e in m in d .
Posterior Segment Trauma
Posttraumatic Vitreous Hemorrhage
Vit reous h em orrh age resu lt s from bleeding in to on e of th e several poten t ial spaces form ed aroun d an d w ith in th e vit reou s body. Th is con dit ion can follow injuries to th e ret in a an d uveal t ract an d th eir associated vascu lar st ru ct u res. Neovascu lariza- t ion occu rring in diseases like proliferat ive diabet ic ret in opathy m ay predispose to bleeding, even if th e t raum a is m ild . Oth er disorders th at p rom ote th e release of angiogen ic vasoact ive factors an d subsequ en t form at ion of n eovascu lar an d fragile vessels th at can easily bleed are isch em ic ret in op athy secon dar y to ret in al vein oc-
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clusion , ret in opathy of prem at u rit y, an d proliferat ive sickle cell ret in opathy. Trau - m at ic vit reou s h em orrh age in ch ildren m ay be a sign of ch ild abu se (sh aken baby syn drom e).
Presentation
Pat ien ts w ith t raum at ic vit reou s h em orrh age usually presen t w ith a com plain t of decreased visu al acu it y, floaters, cloudy vision , percept ion of sh adow s, visual h aze, an d ph otoph obia. Pat ien ts m ay n ot rem em ber th e t raum at ic in su lt . Direct oph th al- m oscopy reveals a dim in ish ed red reflex th at can be black in severe cases. In direct oph th alm oscopic exam in at ion discloses th e presen ce of blood in th e an terohyaloid or ret rohyaloid spaces or w ith in th e vit reou s gel. Usu ally a subhyaloid h em orrh age suggest s a source of bleeding an terior to th e ret in a, w h ereas a h em orrh age posterior to th e in tern al lim it ing m em bran e im plies a source of bleeding w ith in th e ret in a. Long-stan ding h em orrh ages can evolve in w h ite m asses (Fig. 1.15).
Differential Diagnosis
Differen t ial diagn osis of t raum at ic vit reous h em orrh age in clu des oth er vit reous h em orrh ages n ot related to t rau m a. Spon t an eou s vit reou s h em orrh age m ay occu r in con dit ion s like proliferat ive ret in opath ies, ch oroidal or ciliar y body m elan om a, ret in oblastom a, uveit is, sarcoidosis, ocu lar m an ifestat ion of syph ilis, or h istoplas- m osis.
Management
A detailed h istor y is ver y im port an t . Un derlying path ologies an d m ech an ism of t raum a sh ou ld be docu m en ted . A com plete eye exam in at ion sh ould be perform ed, in clu ding slit lam p exam in at ion , in t raocu lar p ressure m easu rem en t , an d dilated fun du s evalu at ion . Globe perforat ion an d in t raocu lar foreign body sh ou ld be ruled out . B-scan ult rason ography can be u sed w h en th e fu n dus is difficu lt to visu alize, disclosing th e presen ce of ret in al det ach m en t , ret in al tears, in t raocu lar foreign body, or in t raocular t um or. In it ial th erapy con sist s of bed rest w ith 30to 45-degree h ead elevat ion (allow s th e blood to set tle in feriorly) an d avoidan ce of an t icoagu lat ive drugs an d in ten se Valsalva m an euvers. Con clu sive th erapy is fired at th e u n derlying cau se: ret in al breaks can be closed w ith laser ph otocoagulat ion , an d surger y can resolve ret in al det ach m en t s. Vit rectom y is also in dicated in longstan ding vit reou s h em orrh age (
2 to 3 m on th s) an d w h en vit reous h em orrh age is associated w ith ru beosis an d gh ost-cell glaucom a. Com plicat ion s of vit reou s h em -
Fig. 1.15 Post traum atic vitreous hemorrhage.
1 Ocular Trauma 19
orrh age usu ally develop w h en large am oun ts of blood rem ain for long periods in th e vit reou s cavit y an d in clude en h an ced proliferat ive ret in opathy, h em osiderosis bulbi an d con sequen t iron toxicit y, gh ost-cell glaucom a, am blyop ia (resu lt ing from visu al deprivat ion ), an d m yopic sh ift in in fan t s.
Commotio Retinae
Com m ot io ret in ae is a clin ical en t it y first described in 1873 by Berlin an d is ch aracterized by a t ran sien t w h iten ing at th e deep sen sor y ret in a. Th is con dit ion is com m on ; it h as been sh ow n to be resp on sible for 9.4%of all p ost t raum at ic fu n dus ch anges. Th e m ech an ism of inju r y is th e con t recoup force follow ing blun t ocu lar t raum a th at causes degen erat ion of th e ph otoreceptors’ ou ter segm en t s an d subsequ en t ph agocytosis by ret in al p igm en t epith eliu m cells. Th e presen ce of edem a in th e ou ter plexiform layers, n uclear layers, an d su bret in al space h as been dem on - st rated . Angiograph ic eviden ce h as sup por ted th e belief th at ret in al an d ch oroidal vessels do n ot play a sign ifican t role in th e path ogen esis of th is con dit ion .
Presentation
Pat ien ts m ay be asym ptom at ic if com m ot io ret in ae is lim ited to th e periph eral ret in a, or th ey m ay com plain of decreased vision if th e w h iten ing occurs in th e foveal region . Visu al acuit y m ay be variably affected an d does n ot alw ays relate to th e degree of opacificat ion . Oph th alm oscopic exam in at ion reveals a cloudy opacificat ion of th e ret in a, u su ally w ith poorly defin ed m argin s. It can be located anyw h ere w ith in th e posterior segm en t . In som e cases th e en t ire posterior pole can be involved, an d it m ay appear as a pseudoch err y red spot . Ret in al vessels are clearly visible an d ap pear un dist u rbed . Oth er associated t raum at ic path ology m ay be presen t , such as su bret in al, in t raret in al, an d preret in al h em orrh ages; m acu lar h oles; m acu lar detach m en ts, an d ch oroidal ru pt ures (Fig. 1.16).
Differential Diagnosis
Differen tial diagnosis of com m otio ret in ae in cludes retinal detach m ent , cen tral arter y occlusion, bran ch ret in al arter y occlusion , and ret in al w h ite w ith out pressure.
Fig . 1.16 Peripheral comm otio retinae with undefined posterior borders.
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Management
Th e m ech an ism of t raum a sh ou ld be docu m en ted . A com plete op h th alm ic exam i- n at ion sh ould be perform ed, in clu ding dilated fu n dus evaluat ion an d scleral depression if th ere is n o eviden ce of hyph em a, m icrohyph em a, or irit is. Th e ret in al w h iten ing u su ally fades w ith in som e w eeks, an d n o t reat m en t is available, on ly obser vat ion . Abou t 60% of pat ien ts fu lly recover vision , an d 40% su stain perm a- n en t visu al loss. Com plicat ion s of com m ot io ret in ae in clu de cystoid areas th at m ay degen erate in to m acular h oles, ph otoreceptor loss, ret in al p igm en t epith elium (RPE) m igrat ion , degen erat ion , at rop hy, or hyperplasia.
Choroidal Rupture
Traum atic choroidal rupt ure is a com m on occurrence after a blunt ocular traum a (5 to 10%). It is a defect in th e Bru ch m em bran e, th e ch oroid, an d th e ret in al pig- m en t epith eliu m . W h en su dden an teroposterior com pression an d equ atorial expan sion subsequ en t to ocu lar blu n t t raum a t ake p lace, th e sclera h as en ough ten sile st rength an d th e ret in a h as en ough elast icit y to be relat ively protected . Becau se th e Bru ch m em bran e does n ot h ave th ese proper t ies, it is pron e to break. Th e dam age at th e ch oriocapillaris vessels m ay lead to su bret in al, sub-ret in al p ig- m en t epith eliu m , or in t rach oroidal h em orrh age. In th e acute ph ase th e overlying h em orrh age an d th e ret in al edem a m ay obscure th e ch oroidal ru pt ure itself. Typically, during th e h ealing p h ase, ch oroidal n eovascu larizat ion occu rs an d in m ost cases resolves spon t an eou sly. Con dit ion s associated w ith an in creased fragilit y of th e Bru ch m em bran e, su ch as angioid st reaks, are risk factors for t rau m at ic ch o- roidal ru pt u re.
Presentation
Pat ien ts u su ally p resen t w ith a h istor y of ocu lar blu n t t raum a, decreased vision , an d a variet y of visu al field defects (paracen t ral, cen t ral, sector scotom as). At oph - th alm oscopic exam in at ion th e ch oroidal lesion appears as a yellow -w h ite, crescen t-sh aped, su bret in al st reak, con cen t ric to th e opt ic disc. Th e border of th e rup - t u re m ay be hyperpigm en ted or hypopigm en ted . Often th e overlying h em orrh age m ay obscu re th e ch oroidal ru pt u re (Fig. 1.17A,B).
A B Fig . 1.17 (A) Traumatic choroidal rupture. (B) Traumatic choroidal rupture.
