Presentation on theme: "NICU Overview - FEN, NEC, IVH, and ROP"— Presentation transcript:
1NICU Overview - FEN, NEC, IVH, and ROP Jan Sherman, RN,NNP,PhDAssociate Professor of Clinical PracticeNeonatal Nurse Practitioner CoordinatorDepartment of Child Health University of Missouri - ColumbiaAdjunct Teaching Associate ProfessorCollege of Nursing University of Missouri - St. LouisCollege of Nursing University of Missouri - ColumbiaUpdated
2Objectives Provide an overview of basic neonatal care To assist you in preparing for your NICU rotationThe information is not meant to replace standard neonatal textbooks and only basic information will be discussed in this powerpoint presentation.Additional information can be obtained from the neonatal classic textbooks listed in the references at the end of the presentationInformation specific to the NICU at WCH will be presented to you in the NICU
3Fluids and Electrolyes Fluid and electrolyte management is an important and challenging part of the initial management of any very preterm or critically ill newbornAfter birth, the newborn rapidly must assume responsibility for fluid and electrolyte balancePrimary responsibility lies with caregivers!Challenging for very preterm neonates in whom water loss is large and highly variable
4Body Compositon of Fetus and Newborn Infant Early stages of development, body mostly water3rd month fetal life, TBW = 94% of wt24wks, TBW = 86% of wt40 wks, TBW = 78% of wtECF as gestation progresses59% at 24 wks -> 44% at termIncreasing cell numbers and sizeICF as gestation progesses27% at 24 wks -> 34% at term
5Body Compositon of Fetus and Newborn Infant Neonates are born with an excess of TBW, primarily ECF, which needs to be removedInfants with hydrops have excessive ECF!!After birth, TBW fallsContraction of ECWMobilization of extracellular fluid related to improved renal functionNormal physiologic process
6Water Loss 2 types of water loss IWL Sensible = primarily urinary, account for ~50% of daily fluid requirementsInsensible (IWL) = lost through skin and resp tractIWLLose of water by evaporation30% through resp tract70% through skinInversely proportion to gest age and wtPremature infants surface area compared to wt
8< 750 grams, day 1 – start at 100 ml/kg/day. The graph is only a guideline. Total fluids should be discussed in rounds with the attending. Generally you would start at the low end of the Water Requirements to determine your ml/kg/day of total fluids, i.e.,< 750 grams, day 1 – start at 100 ml/kg/day.Fanaroff, A. A., Martin, R. J., & Walsh, M. C. (2010). Neonatal-Perinatal Medicine: Diseases of the Fetus and Newborn.
9Fluid RequirementsMaintenace Fluids = fluid quantities required to preserve neutral fluid balanceTotal fluid requirements =Maintenance (IWL + urine + stool water) + Growth requirementsStool = 5-10 ml/kg/dayGrowth = weight gain is 70% water, an infant growing gm/day requires mL/kg/day of water
10Calculating Fluid Requirements Take desired ml/kg/day x wtExample: 100 ml/kg/day and 1 kg baby100 x 1 kg = 100 ml ÷ 24 hrs = 4.1 ml/hr total fluidAll of your fluids which the baby is receiving needs to equal 4.1 ml/hrInclude all fluids - drips, TPN, lipids, carrier fluids, etc.Can be a challenge with very small infants!
11To calculate fluid rates i.e. Need 100 ml total fluids in 24 hours = 4.1 ml/hr total fluidsCurrently have the following fluids runningDopamine = .05 ml/hr x 24 hr = 1.2 mlDobutamine = .05 ml/hr = 1.2 mlUAC fluids (1/2 NS) = 1 ml/hr = 24ml20% lipids = 0.5ml/hr = 12mlGlucose/insulin drip = 0.5ml/hr = 12ml
12100 ml total fluids in 24 hours (Use this number as the initial ml of TPN or primary glucose solution to order – other fluids are subtracted from this initial mo and the amount left will determine the rate of the TPN/glucose solution)- 2.4 ml (Dopamine and Dobutamine)= 97.6 ml- 24 ml (UAC fluids)= 73.6 ml-12 ml (lipids)= 61.6 ml- 12 ml (glucose/insulin drip)= 49.6 ml left to be used for TPN= 49.6 ÷ 24 hours = 2 ml/hr TPNDouble check your calculations by adding up all of your hourly rates to be sure it equals your original calculation, i.e 4.1 ml/hr
13825 grams with total fluids (TF) = 140ml/kg/day .825gm x 140 ml/kg/day = 115ml in 24 hours115 ml- 16 ml (feeds = 2 ml q 3 hours)= 99 ml- 12 ml ( lipids = 12 ml)= 87 ml left to be used for TPN= 87 ÷ 24 hours = 3.6 ml/hr TPN** if make baby NPO will need to increase IV fluids to 4.2 ml/hr (16 ml ÷ 24 hr = 0.6 ml/hr, = 4.2ml/hr) to maintain same TF
14Replacement of Deficits and Ongoing Losses Be careful to calculate all outputChest tubes, repogyl, surgical woundsExcessive output needs to be replaced to avoid dehydration – watch urine output closely!!Generally replace output ml:mlMay use ½ replacement – discuss with attendingGeneral guideline to consider replacement is if output is > 5ml/kg every 4 hoursNS or LR most commonly used for replacementCan send sample of output for electrolyte analysisDetermine what fluid to use for replacement based on electrolyte content of output
15Fluid Requirements Be cautious with your fluid administration Increase fluids ifWeight loss excessive , i. e. > 10% birth weightNa+ is risings/s dehydration: HR, ↓ BP, BUN, metabolic acidosisUrine output low (< 2 ml/kg/hr)*** be sure to check BUN/creatinineif renal failure is the cause of ↓ urine output, be cautious with fluid increases!!Poor perfusionCardiac, sepsis
16Fluid Requirements Decrease fluids if Excessive wt gain Na+ is falling – dilutional hyponatremiaUrine output ↓ from renal failureIndocin or Ibuprofen administration may cause renal dysfunctionEvidence of PDAFluid overload may worsen a PDA
17Fluid Composition Glucose To calculate glucose infusion rate (GIR) Basic metabolic needs for glucose are 4-8 mg/kg/minDo not give > D10W in a peripheral line without discussing with the attendingCentral lines (UVC or PICC) may run higher glucose concentrationsTo calculate glucose infusion rate (GIR)ml/kg/day 24 hr 60 minutes x mg/ml of glucosei.e. 60ml/kg/day of D10W (100mg/ml)60 24 60 x 100 = 4.2 mg/kg/min GIRIf you have multiple sources of glucose, i.e. drips, TPN, calculate each GIR separately and add together for total GIR
18Fluid Composition Watch for hyperglycemia Calculate the GIR Glycosuria Premature infants may have a low renal threshold for glucose and can spill glucose at chemstrip of 120Normal threshold is > 180 chemstripOsmotic diuresis may occurRapidly become dehydrated with increased urine outputCalculate the GIRBaby may be receiving excessive glucose!!Maximum GIR should be discussed with the attending
19Fluid Composition Hypoglycemia Watch IDM and IUGR/SGA infants closely Both may have high glucose needs > 8mg/kg/min GIR
20TPNAmerican Academy of Pediatrics, the clinician’s objective is for the infant (< 1500 grams) to grow as well as in-uteroPrevent extrauterine growth restriction!Glucose and protein administration soon after birth of are of primary importanceProtein turnover and protein breakdown increase proportionately with the immaturity of the baby
21TPN ~1 g/kg/day of amino acids (AA) Helps with protein synthesisKeeps the baby in nitrogen equilibriumProvides a positive nitrogen balanceEarly aggressive use of AA to prevent "metabolic shock.“Irrepressible glucose production may be the cause of the so-called glucose intoleranceStart with Vanilla TPN at 60ml/kg/day on admissionRemainder of total fluids composed of D5W or D10W< 1000 grams may need D5W in fluids to prevent hyperglycemiaAdamkin, D. (2006). Nutrition Management of the Very Low-birthweight InfantI. Total Parenteral Nutrition and Minimal Enteral Nutrition. NeoReviews Vol.7 No e602
22Protein Maximum AA intake is usually 3 gm/kg/day Intakes of 3.5 g/kg/day for infants weighing less than 1,200 g may be appropriate when enteral feedings are extremely delayed or withheld for prolonged periodsAdamkin, D. (2006). Nutrition Management of the Very Low-birthweight InfantI. Total Parenteral Nutrition and Minimal Enteral Nutrition. NeoReviews Vol.7 No e602
23LipidsLipids are essential components of parenteral nutrition for preterm infants to provide essential fatty acids (EFAs)Parenteral lipids are an attractive source of nutrition in the first postnatal daysHigh energy densityEnergy efficiencyIsotonic with plasmaAdamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No e543
24Lipids3 - 7 day delay in supplying lipids leads to biochemical EFA deficiencyIncreases antioxidant susceptibilityReduces body and brain weightsEFA deficiency can be prevented with introduction of as little as 0.5 to 1 gm/kg/day of lipidsDiscuss amount of lipids in rounds with the attendingAlways use 20% lipids, not 10%Limit lipids to 40 – 50% of total calories (Gomella, Page 78)May cause ketosisAdamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No e543
25Potential Adverse Effects of Parenteral Lipids Increased risks of sepsiscoagulase-negative staphylococci (CONs)Displacement of bilirubin from albuminIncreased unbound bilirubin -> increased risk of kernicterusPulmonary complicationsDeposition of fat globulesIncrease in pulmonary vascular resistanceActivation of inflammatory mediatorsAdamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No e543
26Practical Tips for Lipids Fat is a concentrated energy source, providing 9 kcal/g.Use of 20% lipid emulsion is preferable to a 10% solutionSmaller volume to administerDecrease the risk of hypertriglyceridemia, hypercholesterolemia, and hyperphospholipidemia.Plasma triglycerides are monitoredDiscuss with attending when to checkSerum triglycerides should be <200 mg/dLIf the infant has severe hyperbilirubinemia or severe respiratory diseaseConsider discontinuing lipids or decrease doseAdamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No e543
27Practical Tips for Lipids Maximum lipid dosage is usually 3 gm/kg/dayCalculate ml of lipidsGm/kg/day ÷ 0.2 gm fat x kg = ml to givei.e. 1.5 kg, 2 gm/kg/day lipids2 gm/kg/day ÷ 0.2 x 1.5 kg = 15 ml lipids in 24 hours= 0.6 ml/hr of lipidsHourly infusion should not exceed 0.12 g/kg/hourGive over 24 hoursAdamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No e543
28Enteral NutritionThe timing of initial feedings for the preterm infant has been debated for nearly a centuryremains controversial!Swallowed amniotic fluid may play in nutrition and in the development of the gastrointestinal tractBy the end of the third trimester, amniotic fluid provides the fetus with the same enteral volume intake and ~ 25% of the enteral protein intake of a term, breastfed infantAdamkin, D. (2006). Nutrition Management of the Very Low-birthweight Infant .I. Total Parenteral Nutrition and Minimal Enteral Nutrition.NeoReviews Vol.7 No e602
29Enteral NutritionTPN does little to support the function of the gastrointestinal tractAnimals studies have shown that intraluminal nutrition is necessary for normal gastrointestinal structure and functional integrityPrevents intestinal atrophyEnteral feedingsHave both direct trophic effects and indirect effects due to the release of intestinal hormones
30Enteral NutritionFeeding volumes are to be discussed in rounds with the attendingsGeneral feeding guidelinesVLBW infant (<1000 gm, < 28 wks)Gavage feed onlyPO feeds after 32 – 34 weeks PMA when suck/swallow coordination has developedStart at ml/kg/day, every 3 hours bolusAdvance per attending – generally ml/kg/dayBreast milk is ideal, if no breast milk use Special Care 20calAdvance to 24cal after full feedings attained or at direction of the attendingGomella, Page
31So why aren’t we more aggressive with feeding… So why aren’t we more aggressive with feeding…. Necrotizing Enterocolitis (NEC)NEC is defined as an ischemic and inflammatory necrosis of the bowel primarily affecting premature infants (Gomella, 2009)10% of cases are seen in term infantsRarely see until after feedings are initiated10 – 30% mortality associated with NEC
32Minimal Enteral Nutrition NEC occurs rarely in infants who are not being fedAssociation between feedings and NECFeedings thought to act as vehicles for the introduction of bacterial or viral pathogens or toxins into the gutEfforts aimed at minimizing the risk of NECFocused on the time of introduction of feedingsFeeding volumesRate of feeding volume incrementsGut priming, minimal enteric feedings, hypocaloric feedings, or trophic feedings are all different names for gut stimulation
33Enteral Nutrition – Feeding Intolerance Residuals – examine infant and if exam benign< 20% of feeding can be refed (Gomella, Page 92) and full volume feedings givenif > 20% consider subtracting volume of residual from feeding volumei.e. feeding to be given = 20ml – 5ml residual = 15ml of new feeding and return the 5ml of residualPersistent large volume residuals, bilious or bloody aspirates, emesis, bloody stools, abdominal distention, increased apnea and bradycardia, hypotension, acidosis, change in LOC, decreased urine outputExam infant’s abdomenlook for distention, bowel loops, guarding , discolorationObtain KUBHold feedings until KUB seen and condition discussed with attending
36Radiographic Determination of NEC Radiographs can help predict the severity of NECDuke abdominal assessment scale (DAAS)Tool for predicting the severity of disease in neonates and infants with suspected NECPatients with higher DAAS scores were more likely to undergo surgical intervention than patients with lower scoresThe DAAS provides a standardized 10-point radiographic scale that increases with disease severityFor every 1-point increase in the DAAS score, patients were statistically significantly more likely to have severe disease as measured by need for surgical interventionCoursey, C.A., Hollingsworth, C. L. Wriston, C. Beam, C. Rice, H., & Bisset, G. (2009). Radiographic predictors of disease severity in neonates and infants with necrotizing enterocolitis. AJR Am J Roentgenol Nov;193(5):.
38Pneumatosis intestinalis gives a bubbly appearance to bowel Pneumatosis intestinalis gives a bubbly appearance to bowel . May see persistent dilated static loop of bowel, portal venous air or pneumoperitoneum if the bowel has perforated.Bubbles are filled with hydrogen gas
39air in the portal vein –portal venous airThe plain abdominal film shows:air in the portal veinair in the bowel wallsa large pneumoperitoneum [subdiaphragmatic free airperihepatic free airdouble wall sign (blue arrows)triangle sign (green arrows)falciform ligament (red arrow)
40Management of NEC NPO Respiratory support May need fluid boluses and pressors to maintain adequate blood pressureObtain CBC, CRP, blood gas, and blood cultureAntibiotic coverageUsually Vanc, Gent, and Clindamycin or Flagyl
41Management of NEC Serial abdominal films to watch for perforation Usually every 6 – 12 hoursSooner if change in exam notedCan transilluminate abdomen to check for perforationBowel rest and decompression with repogyl to low intermittent suctionSurgical consult as needed
42Fluid Composition: Potassium Ideal lab range is mEq/L.Discuss supplemental K+ in the first days of life with the attendingBe cautious with potassium administration!Don’t automatically add potassium to IV fluids in preterm infantsGomella, Pages
43Hyperkalemia Serum K+ > 6mEq/L. Etiology Heelstick vs central Heelstick values may be hemolyzed giving false elevations. Redraw by venous or arterial sample to confirmExcessive supplemental K+BruisingRenal failureRenal immaturityInfants < 800 gram, first 2-3 days of lifePathologic hemolysis of RBC from IVH or other thrombusNEC – tissue necrosisAdrenal insufficiencyGomella, Pages
44Hyperkalemia Metabolic acidosis decrease in pH by 0.1 unit -> increase in K+ by meq/lMedications which can cause hyperkalemiaDigoxin -> redistribution of K+Aldactone – K+ sparingIndomethocin -> renal dysfunctionGomella, Pages
45Hyperkalemia Watch lytes closely with frequent labs Consider Lasix Look at EKG pattern on the infant’s monitorIf no EKG changes stop supplemental K+Consider Lasixif renal function is adequateConsider Kayexalate (sodium polystyrene sulfonate)Binds K+Dose = 1 gram/kg/dose rectally q 2-6 hrs1 gram resin removes ~ 1 meq K+Works slowly!!Watch lytes closely with frequent labsGomella, Pages
46Hyperkalemia If EKG changes -> medical emergency Give Calcium gluconate IVDecreases myocardial excitabilityCorrect any acidosis with NaHCO3Glucose – insulin dripInhaled albuterol
48Monitoring Fluid and Electrolyte Balance Normal valuesUrine output = > 2ml/kg/hrUrine SG =Weight loss no greater than % of BWCalculate daily and report to attending in roundsi.e. down 12% of birth weight todayBase deficit < - 6Watch closely for acidosis in preterm infantsBD > - 6 needs attention!After full feedings or full TPN attained infant should gain gm/kg/day20-30 gm/kg/day ideal
49ReferencesAdamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No e543Adamkin, D. (2006). Nutrition Management of the Very Low-birthweight InfantI. Total Parenteral Nutrition and Minimal Enteral Nutrition. NeoReviews Vol.7 No e602Christensen, R. D. (2000). Hematologic Problems of the Neonate.Cloherty, J. P., Eichenwaid, E. C., Stark, A. (2008). Manual of Neonatal Care, 5th ed. Lippincott.Coursey, C.A., Hollingsworth, C. L. Wriston, C. Beam, C. Rice, H., & Bisset, G. (2009). Radiographic predictors of disease severity in neonates and infants with necrotizing enterocolitis. AJR Am J Roentgenol Nov;193(5):Fanaroff, A. A., & Martin, R. J. (2002). Neonatal-Perinatal Medicine: Diseases of the Fetus and Newborn.Gomella, T. L. (2009). Neonatology management, procedures, on-call problems, diseases and drugs.Polin, R. A., Fox. W. W., Abman, S. H. (2004). Fetal and Neonatal Physiology.Taeusch, H. W., Ballard, R. A., & Gleason, C. A. (2005). Avery’s Diseases of the Newborn. 8th ed.
50CNSOne of the primary concerns for infants in the NICU is the development of intracranial hemorrhage which can cause later neurologic issuesTerm infants tend to have:Subdural, subarachnoid, or subtentorialGenerally related to birth trauma, hypoxic-ischemic events, coagulopathies (thrombophilias or thrombocytopenia)Gomella, pg
51CNS Preterm infants tend to have: Intraventricular (IVH) Generally originates from vascular rupture in the germinal matrixIncidence of IVH decreases with increasing gestational ageRare in newborns > 32 weeks’ gestational age or > 1,500 gm birthweightPeriventricular leukomalacia (PVL)PVL of the white matter may occur in isolation or follow an IVHMay occur in preterm and term infants
54Sagittal View Germinal matrix -located in the caudo-thalamic groove The occipital horn of the lateral ventricle is filled with choroid plexus. The choroid tucks up in the caudothalamic groove in the floor of thelateral ventricle and may be echogenic.Sagittal View
55CNS General presentation Diagnosis Seizures Rapid drop in hematocrit Sudden deterioration in conditionDiagnosisPretermHUS to look for IVH – can be done at the bedsideTermHUSCT scan – rapid test, will show hemorrhagic damageMRI –Generally done with more stable infant – time consumingSpecific for hemorrhage and hypodensitiesGomella, pg
56CNSThe most widely used classification system for IVH is that originally described by Papile and associatesGrades from 1 to 4 with increasing severityRhine, W. D. & Blankenberg, F. G. , (2001). Cranial Ultrasonography.NeoReviews Vol.2 No.1 January 2001
57CNS ICH usually begins within the first 24 to 72 hours of life May have occurred antenatalAsk the attending when to obtain the HUS – generally the HUS will be done at 7 days of age in our NICUHUS may be obtained sooner on very sick infants or infants who have:Unexplained hematocrit dropAcidosisChange in neurologic status
58Grade 1 IVH –Referred to as a germinal matrix or subependymal hemorrhageSeen on HUS as an abnormally increased number of echoes in the caudothalamic groove (ie, notch) in the expected location of the germinal matrix.
60Grade 2 describes extension of a germinal matrix/subependymal hemorrhage into the ventricles without any ventricular enlargementA. The sagittal view demonstrates the echogenic bulbous collection of blood that bears no resemblance to the normal germinal matrix that tapers as it courses anteriorally in the caudothalamic groove and also never is seen anterior to the foramen of Monro.B. Coronal view, showing a bulbous echogenic collection of blood in the left caudothalamic groove.C. A sagittal view through the anterior fontanelle that is angled slightly more posteriorly shows an echogenic clot filling the occipital horn posterior to the calcar avis. The choroid plexus never is seen in the occipital horn.
62Grade 3 has blood extending into the ventricles and causing ventriculomegaly at the time of the initial observation of IVH.Grade 3 germinal matrix hemorrhage 3 and 10 days after birth.A. On day 3 of life, the coronal view demonstrates massive bilateral IVH and germinalmatrix hemorrhage with ventricular dilation.B. The sagittal view confirms the presence of massive IVH and germinal matrix hemorrhage.On day 10 of life, progressive posthemorrhagic hydrocephalus is evident on the coronal (C) and sagittal (D) views.
63Grade 4 describes a germinal matrix hemorrhage that dissects and extends into the adjacent brain parenchyma, irrespective of the presence or absence of IVH.It is also referred to as an intraparenchymal hemorrhage(IPH) when found elsewhere in the parenchyma.Bleeding extending into the periventricular white matter in association with an ipsilateral IPH has been classified as periventricular hemorrhagic venous infarction(PHVI).
65Treatment of IVH Supportive Ventilation Volume expansion and pressors as neededPRBC and platelets as neededCheck CBC frequentlyCorrect anemia and thrombocytopenia as directed by attendingCorrect acidosis
66PVL in weeks 1 and 4 of life.A. Coronal view of the frontal lobe region demonstrates abnormally increased periventricular echogenicity bilaterally at week 1.B. Follow-up coronal view at week 4 demonstrates cystic degeneration, involution of the periventricularwhite matter and mild ventricular dilation.PVL describes a characteristic pattern ofcystic degeneration over the next 2 to 3 weeks, resulting in a “swiss cheese” pattern of white matter loss that canbe detected readily with CUSHowever, PVL can arise without ICH and vice versa.Affects white matter tracts of the brain and can cause severe neurological problems with movement.
67Hypoxic-ischemic Encephalopathy (HIE) Birth DepressionHIE in both preterm and term neonates may cause a wide range of CNS injuries that may not be visible by HUSIn the term newborn, severe HIE can lead initially to generalized cerebral edemaIncluding small, slit-like ventriclesPoor gray-white signal differentiation on HUS
68Treatment of HIE Head and Body Cooling Supportive Ventilation Volume expansion and pressors as neededCorrection of acidosisHead and Body CoolingRecent advance has been development of hypothermia in which the body and brain are cooled down to about 92°F (33.5°C)Hypothermia is appropriate for full-term babiesGenerally must begin treatment within 6 hours of birth
69Retinopathy of Prematurity Retinopathy of prematurity (ROP) is a disorder of retinal vascular development in preterm infants.It remains a major cause of childhood blindness worldwideRetinal vascular development is incomplete in preterm infants.Postnatal interference with normal development may lead to ROP
70Pathogenesis of ROP Still unknown Current concept of the pathogenesis of ROP suggests that preterm birth interrupts the normal processes of retinal blood vessel developmentPostnatal developing retina is exposed to a less stable and relatively hyperoxic oxygen environment
71Pathogenesis of ROPNormal physiologic hypoxia “drive” of angiogenesis is reduced.Local and systemic concentrations of growth factors, notably insulin-like growth factor 1 (IGF-1) are lowProcess of retinal vascularization is delayedPeripheral retina remains avascular
72Pathogenesis of ROPPreterm infants have low circulating concentrations of IGF-1, which increase with postnatal growthWhen tissue concentrations of IGF-1 reach a critical threshold level, vascular endothelial growth factor (VEGF) signaled angiogenesis is permittedRapid-onset, excessive VEGF effects are seen in the retinal blood vessels
73Pathogenesis of ROPExtra-retinal new vessels grow into the vitreous (stage 3 ROP)Posterior retinal blood vessels become dilated and tortuous (plus disease)If the condition is untreated, a progressive gliosis of the retina and vitreous occursLeads to retinal detachment and blindness (stage 4 and stage 5 ROP)
74Screening Examination of the Retina Most infants born at less than 28 weeks’ gestation develop some degree of ROPIn most, the disease is mild and regresses spontaneouslyA small proportion of infants, even up to 32 weeks’ gestation (and if SGA at even greater gestations), develop potentially severe retinopathyScreening of infants at risk can monitor the progress of retinopathyTimely intervention has a good chance of preventing progression and preserving vision
75Screening Examination of the Retina AAP Guidelines on Timing of First Eye Exam Based on Gestational Age at BirthGestational Age at Birth, wk Age at Initial Examination, wk Postmenstrual Chronologic age22a23a31b32bShown is a schedule for detecting pre-threshold ROP with 99% confidence, usually well before any required treatment.Infants with a birth weight of less than 1500 g or gestational age of 30 weeks or less (as defined by the attending neonatologist) and selected infants with a birth weight between 1500 and 2000 g or gestational age of more than 30 weeks with an unstable clinical course, including those requiring cardiorespiratory support and who are believed by their attending pediatrician or neonatologist to be at high risk, should have retinal screening examinations performed after pupillary dilation using binocular indirect ophthalmoscopy to detect ROP."a = This guideline should be considered tentative rather than evidence-based for infants with a gestational age of 22 to 23 weeks because of the small number of survivors in these gestational age categories.b = If necessaryPOLICY STATEMENT ERRATA: Section on Ophthalmology, American Academy of Pediatrics; American Academy of Ophthalmology (2006). American Association for Pediatrics Ophthalmology and Strabismus. Screening Examination of Premature Infants for Retinopathy of Prematurity. PEDIATRICS 2006;117:572–576.
76Classification of Clinical ROP LocationThe retina is divided into three zones – I, II, and IIIZone I - which is most posterior, consists of a circle with a radius of twice the distance from the optic disc to the center of the macula, centered on the optic discZone II extends from zone I forward to the anterior edge of the retina (ora serrata) on the nasal side of the eyeCentered on the optic disc.Ora serrata is closer to the optic disc on the nasal side than on the temporal side of the eyeZone III is the retina anterior to zone IIOnly present on the temporal side
78Classification of Clinical ROP In the absence of retinopathy, the retina of the very preterm infant merges imperceptibly from vascularized centrally to avascular peripherallyROP affects the entire retinaNormal immature retina, not fully vascularized
79Classification of Clinical ROP Stage 1 ROP:A flat line of demarcation occurs between the vascular and avascular retina.Stage 2 ROP:The line of demarcation acquires volume to become a ridge.Tufts of new vessels may appear on the posterior edge of the ridge, but these vessels still are within the retinaStage 2 ROP, indicated by the development of a ridge between the vascular and avascular retina
80Classification of Clinical ROP Stage 3 ROPNeovascularization can be seen within the ridge, and extraretinal vascularization extends out of the retinaStage 3 ROP, showing neovascularization within the ridge and extraretinal vascularization out of the retina. Courtesy of Professor Michael O’Keefe, Dublin, Ireland.
81Classification of Clinical ROP Stage 4 ROPPartial retinal detachment occurs,May be extrafoveal or fovealStage 5 ROPEventually total retinal detachment may occurWith resulting complete blindness
82Classification of Clinical ROP Plus disease:Indicated by tortuosity of theposterior retinal vessels
83Treatment of ROPThe finding of threshold ROP, as defined in the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity, may no longer be the preferred time of interventionTreatment may also be initiated for the following retinal findings:● zone I ROP: any stage with plus disease● zone I ROP: stage 3—no plus disease● zone II: stage 2 or 3 with plus disease
84Treatment of ROPBIO-delivered diode laser ablation of the peripheral avascular retina has become the usual method of treating ROPcryotherapy is used rarelyAim is to produce almost confluent burns of all areas of the avascular retina anterior to the ROP ridge, extending to the ora serrataCareful primary treatment, ensuring complete cover of the retina and avoiding untreated “skip” areas, reduces the risk for retreatment
85Treatment of ROP New approach to ROP treatment is under investigation Intravitreal injection of anti-VEGF antibodies is used widely in ophthalmology for the treatment of neovascular forms of age-related macular degeneration and diabetic retinopathyInjections are administered under sterile conditions through the sclera adjacent to the cornea into the vitreousA volume of mL is usedA single injection appears to be sufficient in most cases.Normal retina is not subjected to laser ablationPermanent scarringSome reduction of the peripheral visual field
86ReferencesFleck, B. W. & McIntosh, N. (2009). Retinopathy of Prematurity: Recent Developments. NeoReviews 2009;10;e20-e30. DOI: /neo.10-1-e20AAP 2006 Position Statement: Screening Examination of Premature Infants for Retinopathy of Prematurity. PEDIATRICS Vol. 117 No. 2 February 2006, pp (doi: /peds )
87ReferencesChristensen, R. D. (2000). Hematologic Problems of the Neonate.Cloherty, J. P., Eichenwaid, E. C., Stark, A. (2007). Manual of Neonatal Care, 6th ed. Lippincott.Fanaroff, A. A., Martin, R. J., & Walsh, M. C. (2010). Neonatal-Perinatal Medicine: Diseases of the Fetus and Newborn.Gomella, T., et al. (2009). Neonatology: Management, Procedures, On-Call Problems, Diseases, and Drugs. 6th ed.MacDonald, MC, Mullett, MD, & Seshia, MK (2005). Avery’s Neonatology: Pathophysiology & Management of the Newborn. 6th ed.Polin, R. A., Fox. W. W., Abman, S. H. (2004). Fetal and Neonatal Physiology.Taeusch, H. W., Ballard, R. A., & Gleason, C. A. (2004). Avery’s Diseases of the Newborn. 8th ed.
88Jobe, A. H., The New BPD. NeoReviews, Oct 2006; 7: e531 - e545.