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

17

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

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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

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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

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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

48

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

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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

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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

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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

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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

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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)

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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

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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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ReferencesChristensen, 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.

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Jobe, A. H., The New BPD. NeoReviews, Oct 2006; 7: e531 - e545.

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