jan sherman, rn,nnp,phd associate professor of clinical practice neonatal nurse practitioner...
TRANSCRIPT
NICU Overview -FEN, NEC, IVH, and ROP
Jan Sherman, RN,NNP,PhDAssociate Professor of Clinical Practice
Neonatal Nurse Practitioner Coordinator Department of Child Health University of Missouri - Columbia
Adjunct Teaching Associate Professor
College of Nursing University of Missouri - St. LouisCollege of Nursing University of Missouri - Columbia
1Updated 07-05-2011
Objectives
Provide an overview of basic neonatal care
To assist you in preparing for your NICU rotation
The 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 presentation
Information specific to the NICU at WCH will be presented to you in the NICU 2
Fluids 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 3
Body Compositon of Fetus and Newborn Infant
Early stages of development, body mostly water3rd month fetal life, TBW = 94% of wt 24wks, TBW = 86% of wt40 wks, TBW = 78% of wt
ECF as gestation progresses59% at 24 wks -> 44% at term
Increasing cell numbers and size
ICF as gestation progesses27% at 24 wks -> 34% at term
4
Body 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 ECW
Mobilization of extracellular fluid related to improved renal function
Normal physiologic process
5
Water Loss
2 types of water lossSensible = primarily urinary, account for ~50%
of daily fluid requirements Insensible (IWL) = lost through skin and resp
tractIWL
Lose of water by evaporation30% through resp tract70% through skin
Inversely proportion to gest age and wtPremature infants surface area compared to
wt 6
7
8Fanaroff, A. A., Martin, R. J., & Walsh, M. C. (2010). Neonatal-Perinatal Medicine: Diseases of the Fetus and Newborn.
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.
Fluid Requirements
Maintenace Fluids = fluid quantities required to preserve neutral fluid balance
Total fluid requirements =Maintenance (IWL + urine + stool water) +
Growth requirements
Stool = 5-10 ml/kg/day
Growth = weight gain is 70% water, an infant growing 30-40 gm/day requires 20-25 mL/kg/day of water
9
Calculating Fluid Requirements
Take desired ml/kg/day x wt
Example: 100 ml/kg/day and 1 kg baby 100 x 1 kg = 100 ml ÷ 24 hrs = 4.1 ml/hr total fluid
All of your fluids which the baby is receiving needs to equal 4.1 ml/hr
Include all fluids - drips, TPN, lipids, carrier fluids, etc.
Can be a challenge with very small infants!
10
To calculate fluid ratesi.e. Need 100 ml total fluids in 24 hours = 4.1
ml/hr total fluids
Currently have the following fluids running Dopamine = .05 ml/hr x 24 hr = 1.2 ml Dobutamine = .05 ml/hr = 1.2 ml UAC fluids (1/2 NS) = 1 ml/hr = 24ml 20% lipids = 0.5ml/hr = 12ml Glucose/insulin drip = 0.5ml/hr = 12ml
11
100 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 TPN
Double 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
12
825 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, 3.6 + 0.6 = 4.2ml/hr) to maintain same TF
Replacement of Deficits and Ongoing Losses
Be careful to calculate all outputChest tubes, repogyl, surgical wounds
Excessive 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 hours NS or LR most commonly used for replacement Can send sample of output for electrolyte analysis
Determine what fluid to use for replacement based on electrolyte content of output
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Fluid Requirements
Be cautious with your fluid administrationIncrease fluids if
Weight loss excessive , i. e. > 10% birth weight
Na+ is rising s/s dehydration: HR, ↓ BP, BUN, metabolic
acidosis
Urine output low (< 2 ml/kg/hr) *** be sure to check BUN/creatinine if renal failure is the cause of ↓ urine output, be
cautious with fluid increases!! Poor perfusion
Cardiac, sepsis15
Fluid Requirements
Decrease fluids if
Excessive wt gain
Na+ is falling – dilutional hyponatremia
Urine output ↓ from renal failure Indocin or Ibuprofen administration may
cause renal dysfunction
Evidence of PDA Fluid overload may worsen a PDA
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Fluid CompositionGlucose
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
concentrations To calculate glucose infusion rate (GIR)
ml/kg/day 24 hr 60 minutes x mg/ml of glucose i.e. 60ml/kg/day of D10W (100mg/ml)60 24 60 x 100 = 4.2 mg/kg/min GIR
If you have multiple sources of glucose, i.e. drips, TPN, calculate each GIR separately and add together for total GIR
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Fluid Composition
Watch for hyperglycemiaGlycosuria
Premature infants may have a low renal threshold for glucose and can spill glucose at chemstrip of 120
Normal threshold is > 180 chemstrip
Osmotic diuresis may occur Rapidly become dehydrated with increased urine
output Calculate the GIR
Baby may be receiving excessive glucose!!Maximum GIR should be discussed with the
attending18
Fluid Composition
Hypoglycemia
Watch IDM and IUGR/SGA infants closely
Both may have high glucose needs > 8mg/kg/min GIR
19
TPN
American Academy of Pediatrics, the clinician’s objective is for the infant (< 1500 grams) to grow as well as in-utero Prevent extrauterine growth restriction!
Glucose and protein administration soon after birth of are of primary importance Protein turnover and protein breakdown
increase proportionately with the immaturity of the baby
20
TPN
~1 g/kg/day of amino acids (AA)Helps with protein synthesisKeeps the baby in nitrogen equilibrium
Provides a positive nitrogen balance
Early aggressive use of AA to prevent "metabolic shock.“
Irrepressible glucose production may be the cause of the so-called glucose intolerance
Start with Vanilla TPN at 60ml/kg/day on admission
Remainder of total fluids composed of D5W or D10W < 1000 grams may need D5W in fluids to prevent
hyperglycemia21
Adamkin, D. (2006). Nutrition Management of the Very Low-birthweight Infant I. Total Parenteral Nutrition and Minimal Enteral Nutrition. NeoReviews Vol.7 No.12 2006 e602
Protein
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 periods
22
Adamkin, D. (2006). Nutrition Management of the Very Low-birthweight Infant I. Total Parenteral Nutrition and Minimal Enteral Nutrition. NeoReviews Vol.7 No.12 2006 e602
Lipids
Lipids 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 plasma
23Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
Lipids3 - 7 day delay in supplying lipids leads to
biochemical EFA deficiencyIncreases antioxidant susceptibilityReduces body and brain weights
EFA deficiency can be prevented with introduction of as little as 0.5 to 1 gm/kg/day of lipids
Discuss amount of lipids in rounds with the attendingAlways use 20% lipids, not 10% Limit lipids to 40 – 50% of total calories (Gomella, 2009.
Page 78) May cause ketosis
24Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
Potential Adverse Effects of Parenteral Lipids
Increased risks of sepsis coagulase-negative staphylococci (CONs)
Displacement of bilirubin from albumin Increased unbound bilirubin -> increased risk
of kernicterus
Pulmonary complications Deposition of fat globules Increase in pulmonary vascular resistance Activation of inflammatory mediators
25Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
Practical Tips for LipidsFat is a concentrated energy source, providing 9
kcal/g.
Use of 20% lipid emulsion is preferable to a 10% solutionSmaller volume to administer Decrease the risk of hypertriglyceridemia,
hypercholesterolemia, and hyperphospholipidemia.
Plasma triglycerides are monitoredDiscuss with attending when to checkSerum triglycerides should be <200 mg/dL
If the infant has severe hyperbilirubinemia or severe respiratory diseaseConsider discontinuing lipids or decrease dose
26Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
Practical Tips for Lipids
Maximum lipid dosage is usually 3 gm/kg/day
Calculate ml of lipids Gm/kg/day ÷ 0.2 gm fat x kg = ml to give i.e. 1.5 kg, 2 gm/kg/day lipids 2 gm/kg/day ÷ 0.2 x 1.5 kg = 15 ml lipids in 24 hours = 0.6 ml/hr of lipids
Hourly infusion should not exceed 0.12 g/kg/hour Give over 24 hours
27Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
Enteral Nutrition The timing of initial feedings for the preterm
infant has been debated for nearly a century remains controversial!
Swallowed amniotic fluid may play in nutrition and in the development of the gastrointestinal tract By 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 infant
28
Adamkin, D. (2006). Nutrition Management of the Very Low-birthweight Infant .I. Total Parenteral Nutrition and Minimal Enteral Nutrition. NeoReviews Vol.7 No.12 2006 e602
Enteral Nutrition TPN does little to support the function of the
gastrointestinal tract Animals studies have shown that intraluminal
nutrition is necessary for normal gastrointestinal structure and functional integrity
Prevents intestinal atrophy
Enteral feedings Have both direct trophic effects and indirect
effects due to the release of intestinal hormones
29
Enteral Nutrition Feeding volumes are to be discussed in
rounds with the attendings
General feeding guidelinesVLBW infant (<1000 gm, < 28 wks)
Gavage feed only PO feeds after 32 – 34 weeks PMA when
suck/swallow coordination has developed Start at 10-20 ml/kg/day, every 3 hours bolus Advance per attending – generally 10 -20 ml/kg/day Breast milk is ideal, if no breast milk use Special
Care 20cal Advance to 24cal after full feedings attained or at
direction of the attending 30Gomella, 2009. Page 92 -95
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 infants Rarely see until after feedings are initiated10 – 30% mortality associated with NEC
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Minimal Enteral Nutrition NEC occurs rarely in infants who are not being fed
Association between feedings and NEC Feedings thought to act as vehicles for the introduction of
bacterial or viral pathogens or toxins into the gut
Efforts aimed at minimizing the risk of NEC
Focused on the time of introduction of feedings Feeding volumes Rate of feeding volume increments
Gut priming, minimal enteric feedings, hypocaloric feedings, or trophic feedings are all different names for gut stimulation
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Enteral Nutrition – Feeding IntoleranceResiduals – examine infant and if exam benign
< 20% of feeding can be refed (Gomella, 2009. Page 92) and full volume feedings given
if > 20% consider subtracting volume of residual from feeding volume i.e. feeding to be given = 20ml – 5ml residual = 15ml of new
feeding and return the 5ml of residual
Persistent 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 abdomen
look for distention, bowel loops, guarding , discolorationObtain KUBHold feedings until KUB seen and condition discussed with
attending 33
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Radiographic Determination of NEC
Radiographs can help predict the severity of NEC
Duke 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 scores
The 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 intervention
36
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. 2009 Nov;193(5):1408-13.
.
Duke Abdominal Assessment Scale (DAAS)
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38
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
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The plain abdominal film shows:1) air in the portal vein2) air in the bowel
walls3) a large
pneumoperitoneum [subdiaphragmatic free air
4) perihepatic free air5) double wall sign
(blue arrows)6) triangle sign (green
arrows)7) falciform ligament
(red arrow)
air in the portal vein – portal venous air
Management of NECNPORespiratory support
May need fluid boluses and pressors to maintain adequate blood pressure
Obtain CBC, CRP, blood gas, and blood culture
Antibiotic coverageUsually Vanc, Gent, and Clindamycin or Flagyl
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Management of NEC
Serial abdominal films to watch for perforationUsually every 6 – 12 hoursSooner if change in exam notedCan transilluminate abdomen to check for
perforationBowel rest and decompression with repogyl
to low intermittent suction
Surgical consult as needed
41
Fluid Composition: Potassium
PotassiumIdeal lab range is 3.5-5.5 mEq/L.
Discuss supplemental K+ in the first days of life with the attending Be cautious with potassium administration! Don’t automatically add potassium to IV fluids
in preterm infants
42Gomella, 2009. Pages 304-307.
Hyperkalemia
Serum K+ > 6mEq/L.
EtiologyHeelstick vs central
Heelstick values may be hemolyzed giving false elevations. Redraw by venous or arterial sample to confirm
Excessive supplemental K+
BruisingRenal failureRenal immaturity
Infants < 800 gram, first 2-3 days of lifePathologic hemolysis of RBC from IVH or other
thrombusNEC – tissue necrosisAdrenal insufficiency
43Gomella, 2009. Pages 304-307.
Hyperkalemia
Metabolic acidosisdecrease in pH by 0.1 unit -> increase in K+ by
0.3-1.3 meq/l
Medications which can cause hyperkalemiaDigoxin -> redistribution of K+
Aldactone – K+ sparing Indomethocin -> renal dysfunction
44Gomella, 2009. Pages 304-307.
Hyperkalemia
Look at EKG pattern on the infant’s monitor
If no EKG changes stop supplemental K+
Consider Lasix if renal function is adequate
Consider Kayexalate (sodium polystyrene sulfonate)Binds K+
Dose = 1 gram/kg/dose rectally q 2-6 hrs 1 gram resin removes ~ 1 meq K+
Works slowly!!
Watch lytes closely with frequent labs
45Gomella, 2009. Pages 304-307.
Hyperkalemia
If EKG changes -> medical emergency
Give Calcium gluconate IV Decreases myocardial excitability
Correct any acidosis with NaHCO3
Glucose – insulin drip
Inhaled albuterol
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Monitoring Fluid and Electrolyte Balance
Normal valuesUrine output = > 2ml/kg/hrUrine SG = 1.008-1.012Weight loss no greater than 10 - 15% of BW
Calculate daily and report to attending in rounds i.e. down 12% of birth weight today
Base deficit < - 6 Watch closely for acidosis in preterm infants BD > - 6 needs attention!
After full feedings or full TPN attained infant should gain 10-30 gm/kg/day20-30 gm/kg/day ideal
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References
Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
Adamkin, D. (2006). Nutrition Management of the Very Low-birthweight Infant I. Total Parenteral Nutrition and Minimal Enteral Nutrition. NeoReviews Vol.7 No.12 2006
e602
Christensen, 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. 2009 Nov;193(5):1408-13.
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.
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CNS
One 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 subtentorial
Generally related to birth trauma, hypoxic-ischemic events, coagulopathies (thrombophilias or thrombocytopenia)
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Gomella, 2009. pg 549 - 557
CNS
Preterm infants tend to have: Intraventricular (IVH)
Generally originates from vascular rupture in the germinal matrix
Incidence of IVH decreases with increasing gestational age Rare in newborns > 32 weeks’ gestational age or >
1,500 gm birthweight
Periventricular leukomalacia (PVL) PVL of the white matter may occur in isolation or
follow an IVH May occur in preterm and term infants
51
52Coronal View
53
54Sagittal View
The occipital horn of the lateral ventricle is filled with choroid plexus. The choroid tucks up in the caudothalamic groove in the floor of the lateral ventricle and may be echogenic.
Germinal matrix -located in the caudo-thalamic groove
CNSGeneral presentation
SeizuresRapid drop in hematocritSudden deterioration in condition
DiagnosisPreterm
HUS to look for IVH – can be done at the bedside
Term HUS CT scan – rapid test, will show hemorrhagic damage MRI –
Generally done with more stable infant – time consuming Specific for hemorrhage and hypodensities
55Gomella, 2009. pg 549 - 557
CNSThe most widely used classification system
for IVH is that originally described by Papile and associates
Grades from 1 to 4 with increasing severity
56
Rhine, W. D. & Blankenberg, F. G. , (2001). Cranial Ultrasonography. NeoReviews Vol.2 No.1 January 2001
CNS
ICH usually begins within the first 24 to 72 hours of lifeMay have occurred antenatal
Ask the attending when to obtain the HUS – generally the HUS will be done at 7 days of age in our NICU
HUS may be obtained sooner on very sick infants or infants who have:Unexplained hematocrit dropAcidosisChange in neurologic status 57
58
Grade 1 IVH –
Referred to as a germinal matrix or subependymal hemorrhage
Seen on HUS as an abnormally increased number of echoes in the caudothalamic groove (ie, notch) in the expected location of the germinal matrix.
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Bilateral small germinal matrix hemorrhages http://www.google.com/imgres?imgurl=http://neuropathology.neoucom.edu/chapter3/images3/3-ivh.jpg&imgrefurl=http://neuropathology.neoucom.edu/chapter3/chapter3dGmh.html&usg=__O5BiBTF-DXt_6r1m7R0DbzMgNLo=&h=446&w=500&sz=170&hl=en&start=5&itbs=1&tbnid=3kwwgVKjog8fYM:&tbnh=116&tbnw=130&prev=/images%3Fq%3DGrade%2B1%2BIVH%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1
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Grade 2 describes extension of a germinal matrix/subependymal hemorrhage into the ventricles without any ventricular enlargement
A. 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.
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Grade II IVH
http://www.google.com/imgres?imgurl=http://neuropathology.neoucom.edu/chapter3/images3/3-ivh.jpg&imgrefurl=http://neuropathology.neoucom.edu/chapter3/chapter3dGmh.html&usg=__O5BiBTF-DXt_6r1m7R0DbzMgNLo=&h=446&w=500&sz=170&hl=en&start=5&itbs=1&tbnid=3kwwgVKjog8fYM:&tbnh=116&tbnw=130&prev=/images%3Fq%3DGrade%2B1%2BIVH%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1
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Grade 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.
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Grade 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).
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Grade IV IVH
http://www.google.com/imgres?imgurl=http://neuropathology.neoucom.edu/chapter3/images3/3-ivh.jpg&imgrefurl=http://neuropathology.neoucom.edu/chapter3/chapter3dGmh.html&usg=__O5BiBTF-DXt_6r1m7R0DbzMgNLo=&h=446&w=500&sz=170&hl=en&start=5&itbs=1&tbnid=3kwwgVKjog8fYM:&tbnh=116&tbnw=130&prev=/images%3Fq%3DGrade%2B1%2BIVH%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1
Treatment of IVH
SupportiveVentilationVolume expansion and pressors as
neededPRBC and platelets as needed
Check CBC frequentlyCorrect anemia and thrombocytopenia
as directed by attendingCorrect acidosis
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PVL 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 CUS
However, PVL can arise without ICH and vice versa.
Affects white matter tracts of the brain and can cause severe neurological problems with movement.
Hypoxic-ischemic Encephalopathy (HIE)
Birth Depression
HIE in both preterm and term neonates may cause a wide range of CNS injuries that may not be visible by HUS
In the term newborn, severe HIE can lead initially to generalized cerebral edemaIncluding small, slit-like ventriclesPoor gray-white signal differentiation on HUS
67
Treatment of HIE
SupportiveVentilationVolume expansion and pressors as neededCorrection of acidosis
Head 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 68
Retinopathy of Prematurity
Retinopathy of prematurity (ROP) is a disorder of retinal vascular development in preterm infants.It remains a major cause of childhood
blindness worldwide
Retinal vascular development is incomplete in preterm infants. Postnatal interference with normal
development may lead to ROP
69
Pathogenesis of ROP
Still unknownCurrent concept of the pathogenesis of ROP
suggests that preterm birth interrupts the normal processes of retinal blood vessel development
Postnatal developing retina is exposed to a less stable and relatively hyperoxic oxygen environment
70
Pathogenesis of ROP
Normal physiologic hypoxia “drive” of angiogenesis is reduced.
Local and systemic concentrations of growth factors, notably insulin-like growth factor 1 (IGF-1) are low Process of retinal vascularization is delayed
Peripheral retina remains avascular
71
Pathogenesis of ROP
Preterm 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 permitted
Rapid-onset, excessive VEGF effects are seen in the retinal blood vessels
72
Pathogenesis of ROP
Extra-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)
73
Screening 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 retinopathy
Screening of infants at risk can monitor the progress of retinopathy
Timely intervention has a good chance of preventing progression and preserving vision
74
Screening Examination of the Retina AAP Guidelines on Timing of First Eye Exam Based on Gestational Age at Birth
Gestational Age at Birth, wk Age at Initial Examination, wk Postmenstrual Chronologic age22a 31 923a 31 824 31 725 31 626 31 527 31 428 32 429 33 430 34 431b 35 432b 36 4
Shown 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 necessary
POLICY 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.
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Classification of Clinical ROP
LocationThe retina is divided into three zones – I, II, and III
Zone 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 disc
Zone II extends from zone I forward to the anterior edge of the retina (ora serrata) on the nasal side of the eye Centered on the optic disc. Ora serrata is closer to the optic disc on the nasal side than
on the temporal side of the eye
Zone III is the retina anterior to zone II Only present on the temporal side
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ROP Zones
Classification of Clinical ROPIn the absence of
retinopathy, the retina of the very preterm infant merges imperceptibly from vascularized centrally to avascular peripherally
ROP affects the entire retina 78
Normal immature retina, not fully vascularized
Classification 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 retina
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Stage 2 ROP, indicated by the development of a ridge between the vascular and avascular retina
Classification of Clinical ROP
Stage 3 ROPNeovascularizati
on can be seen within the ridge, and extraretinal vascularization extends out of the retina
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Stage 3 ROP, showing neovascularization within the ridge and extraretinal vascularization out of the retina. Courtesy of Professor Michael O’Keefe, Dublin, Ireland.
Classification of Clinical ROP
Stage 4 ROPPartial retinal detachment occurs, May be extrafoveal or foveal
Stage 5 ROPEventually total retinal detachment may occur
With resulting complete blindness
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Classification of Clinical ROP
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Plus disease:
Indicated by tortuosity of the posterior retinal vessels
Treatment of ROP
The finding of threshold ROP, as defined in the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity, may no longer be the preferred time of intervention
Treatment 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
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Treatment of ROPBIO-delivered diode laser ablation of the
peripheral avascular retina has become the usual method of treating ROPcryotherapy is used rarely
Aim is to produce almost confluent burns of all areas of the avascular retina anterior to the ROP ridge, extending to the ora serrata
Careful primary treatment, ensuring complete cover of the retina and avoiding untreated “skip” areas, reduces the risk for retreatment 84
Treatment of ROPNew approach to ROP treatment is under
investigationIntravitreal 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 vitreous
A volume of 0.025 mL is used A single injection appears to be sufficient in most
cases.
Normal retina is not subjected to laser ablationPermanent scarring Some reduction of the peripheral visual field
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References
Fleck, B. W. & McIntosh, N. (2009). Retinopathy of Prematurity: Recent Developments. NeoReviews 2009;10;e20-e30. DOI: 10.1542/neo.10-1-e20
AAP 2006 Position Statement: Screening Examination of Premature Infants for Retinopathy of Prematurity. PEDIATRICS Vol. 117 No. 2 February 2006, pp. 572-576 (doi:10.1542/peds.2005-2749)
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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.
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Jobe, A. H., The New BPD. NeoReviews, Oct 2006; 7: e531 - e545.
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