Disease reviewRetinopathy of prematurityIntroductionPreterm infants of low birth weigh Exposed to high ambient oxygen concentrations Retina : temporal retina is susceptible to oxygen damage No blood vessels until the fourth month of gestation Vascular complexes emanating from the hyaloid vessels at optic disc grow towards the periphery Vessels reach the nasal periphery after 8 months of gestation Not reach the temporal periphery until about 1 month after deliveryOxygen's effectPrimary stage : retinal vasoconstriction and vascular occlusion Continuous oxygen exposure ⇒ vasoconstriction (4~6 hours : 80% of caliber) Total stay in oxygen of 10~15 hours ⇒ more anterior and immature peripheral vessel are occludedOxygen's effectSecondary stage : retinal neo-vascularization Residual vascular complexes adjacent to retinal capillaries ablated during hypoxia (posterior to the area of capillary closure) : Removal of oxygen exposure ⇒ Marked endothelial proliferation ⇒ Canalize to form new vessel ⇒rhage Seizure Exchange transfusion Septicemia In utero hypoxia Anemia Patent ductus arteriosus Vitamin E deficiency Xanthine administrationActive retinopathy of prematurityseverity Location Extent Stages Plus disease Screening TreatmentLocationZone 1 Circle the radius of which is twice the distance from the disc to macula. Zone 2 Nasal ora serrata Temporal equator Zone 3 Consists of a residual temporal crescent anterior to zone 2Nasal ora serrataTemporal equatorExtentNumber of clock hours of retina involvedStagingStage 1 : Demarcation lineThin, tortuous grey white line running roughly parallel with the ora serrata separate avascular immature peripheral retina from vascularized posterior retina More prominent in the temporal peripheryStage 2 : ridgeDemarcation line develops into an elevated ridge represents a mesenchymal shunt joining arteriole which vein= Popcorn lesionStage 3 : Ridge with extraretinal fibrovascular proliferationfibrovascular proliferation : posterior, inferior aspect ege 4A : extrafovealLocation : in anterior zone II or in zone III Prognosis : relatively good Frequently detachment will reattach Not affect macular functionStage 4B : retinal detachment including foveaLocation Including fovea, often extended from the disc through zone I to zones II and III Prognosis : poorStage 5 : Total retinal detachmentClassification : divided the funnel into an anterior and a posterior partStage 5 : Total retinal detachmentStage 5 : Total retinal detachmentPlus diseaseSignifies a tendency to progression Gross vascular engorgement of the iris ⇒ failure of the pupil to dilate Development of vitreous haze Dilatation of veins and tortuosity of the arteries in posterior fundus Increasing preretinal and vitreous hemorrhageThreshold diseaseIndication of treatment Five(150˚) contiguous clock hours or eight(240˚) non-contiguous clock hours of Stage 3 disease in Zone1 or Zone 2 and plus diseaseThreshold diseaseScreeningIndication : babies born at or before 31 weeks gestation infants with threshold disease Remainder progress to retinal detachment in spite of treatment Vitreoretinal surgery For tractional retinal detachmentManagementZone III : treatment is rarely Zone II Stage 1 and 2 Large majority of infants undergo spontaneous remission Monitored at regular interval Lesion in posterior zone II : unfavorable prognosis Stage 3 Infants with progressive stage 3+ : cryotherapyManagementZone I Once plus disease : treatment Stage 4 4A : Careful observation at weekly of biweekly Progression of the detachment or 4B Scleral bulking Peripheral ablation with cryotherapy or laser coagulation Paracentesis Despite anatomical reattachment, once detachment involve of macula, visual result is very poor Stage 5 Except for shallow open-open funnel detachment : Scleral bulking Bilateral stage 5 : lensectomy, vitrectomy, membrane peeling surgery Unilateral stage 5 : lens sparing surgeryManagementRegressed retinopathy of prematurity complication Most serious complication :latetinopathy of prematurityManagementHistory of prematurity Careful examination Particular attention should be given to temporal periphery of retinaCicatricial retinopathy of prematurityIntroduction StageIntroduction20% of infants with active develop cicatrical complication More advanced or the more posterior the proliferative disease : worse the cicatrical sequelaeStageStage 1 myopia associated with mild peripheral retinal pigmentary disturbance haze at the vitreous base. Stage 2 Temporal vitreoretinal fibrosis dragging of the macula pseudo-exotropia, due to resultant exaggeration of angle kappaStageStage 3 More severe peripheral fibrosis with contracture Falciform retinal detachment Stage 4 Partial ring of retrolental fibrovascular tissue with partial retinal detachment Stage 5 Complete ring of retrolental fibrovascular tissue with total retinal detachment, a picture formerly known as 'retrolental fibroplasia' forward movement of anterior synechiae ⇒ progressive shallowing of the anterow}
SAH & ICH 차이와 임상경과subarachnoid hemorrhage는 subarachnoid space에 생긴 출혈로, volume 완충역할을 해주는 CSF가 있기도 하고 IICP 시 공간으로 퍼져 버리기 때문에 웅급도가 떨어진다. 초기에는 meningeal irritation sign만 존재하고 국소 신경학적 정후는 없다. 하지만 intracranial hemorrhage는 뇌실질 내에 생긴 출혈로, 더 위험하며 국소 신경학적 정후가 존재하는데 발생빈도가 가장 많은 putamen의 출혈은 corticospinal tract가 지나가는 internal capsule 주위에 위치하므로 운동장애가 나타날 수 있다.SAH는 가장 많은 원인이 aneurysm이 rupture 되어서 발생하는 것으로, supportive care 만으로 서서히 회복된다. 그러나 일반적인 경우, 수술적 치료를 해 주는데, 그 이유는 SAH가 재출혈을 하게 되면 이미 한번 출혈하여 subarachnoid space가 adhesion 되어 있기 때문에 mortality가 매우 높아 수술적 치료로 aneurysm clipping을 해서 재출혈을 막기 위해서이다. 반면에 ICH는 hypertension이 가장 흔한 원인으로, 수술하지 않고 가만히 두면 SAH처럼 나아지지 않고 경과가 나빠지기 때문에 수술적 방법으로 hematoma를 일찍 제거해 주어야 하며, hematoma를 제거해주면 국소 신경학적 증상이 좋아질 수도 있다.SAH1) sudden severe headache: the worst headache in my life2) 그 외 nausea, vomiting, meningismus, altered consciousness3) meningeal irritation sign : neck stiffness, Kernig’s sign(knee extention 시 pain)4) 동맥류 파열 위치에 따른 증상① 전대뇌동맥 동맥류 : 갑작스런 양하지 무력감② 중대뇌동맥 동맥류 : 간질③ 후교통동맥이나 상소뇌동맥 동맥류 : 동안신경 마비(안구 운동 장애와 pupil dilatation 동반, 당뇨병의 경우 동공산대는 없을 수 있음)④ 지주막하출혈이 심한 경우 : 유리체하(subhyaloid) 또는 초자체(vitreous) 출혈을 야기하여 시력감퇴 유발5) 미파열 뇌동맥류에 의해 초래될 수 있는 증상 및 징후 : 주위 뇌신경이나 뇌조직을 압박함으로써 나타남① 해면정맥동내 내경동맥의 동맥류 : 뇌신경마비(CN III, IV, VD, 삼차신경의 경우 안면 동통 유발② 안동맥(ophthalmic artery) 동맥류 : 시신경을 압박함으로써 시력 장애나 시야 장애③ 후교통동맥 동맥류 : 동안신경 마비④ 전교통동맥 동맥류 : 시야 변화(optic chiasm 압박), hypopituitarism(pituitary stalk 압박)ICH1) putaminal hemorrhage(피각출혈): 반신 부전 마비, 감각 소실, 시야 결손, 언어 장애, 병소쪽을 향하여 안구 편위, 진행성 신경학적 결손 증세가 진행, 뇌척수액 압력 상승, 혼수, 약측 Babinski sign 양성, 산동, 대광 반사소실, 유두 부종(papilledema), 제뇌 경직 (decerebrate rigidity)2) thalamic hemorrhage(시상출혈): 뇌실(제3뇌실이나 측뇌실)로 파급-)수두중이 발생 신경학적 결손이 피각출혈보다 서서히 발생, 점진적인 반대측 반신 부전 마비 시상핵을 침범하여 반대측 지각소실3) subcortical hemorrhage(피질하 출혈): 측두, 두정, 후두엽내에 호발 의식의 혼미를 초래하는 경우는 드묾, 시야 결손과 지각 결손이 생길 수 있음. 실어증, 읽기 장애(dyslexia), 기억 장애, 피각이나 시상출혈에 비해서 양호한 경과