Jan Sherman, RN,NNP,PhD
Associate 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. Louis
College of Nursing University of Missouri - Columbia
Updated 07-05-2011
1
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 newborn
 After birth, the newborn rapidly must assume
responsibility for fluid and electrolyte balance
 Primary 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
water
 3rd month fetal life, TBW = 94% of wt
 24wks, TBW = 86% of wt
 40 wks, TBW = 78% of wt
 ECF  as gestation progresses
 59% at 24 wks -> 44% at term
 Increasing cell numbers and size
 ICF  as gestation progesses
 27% 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 removed
 Infants with hydrops have excessive ECF!!
 After birth, TBW falls
 Contraction of ECW


Mobilization of extracellular fluid related to improved renal
function
Normal physiologic process
5
Water Loss
 2 types of water loss
 Sensible = primarily urinary, account for ~50% of daily
fluid requirements
 Insensible (IWL) = lost through skin and resp tract
 IWL
 Lose of water by evaporation
 30% through resp tract
 70% through skin
 Inversely proportion to gest age and wt
 Premature infants  surface area compared to wt
6
7
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.
8
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 rates
 i.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 hours
 115 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 output
 Chest tubes, repogyl, surgical wounds
 Excessive output needs to be replaced to avoid
dehydration – watch urine output closely!!
 Generally replace output ml:ml
 May use ½ replacement – discuss with attending
 General 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
14
Fluid Requirements
 Be cautious with your fluid administration
 Increase 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, sepsis
15
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
16
Fluid Composition
 Glucose
 Basic metabolic needs for glucose are 4-8 mg/kg/min
 Do not give > D10W in a peripheral line without discussing
with the attending
 Central 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 hyperglycemia
 Glycosuria

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 attending
18
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 synthesis
 Keeps 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 socalled 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
hyperglycemia
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
21
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
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
22
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 days
 High energy density
 Energy efficiency
 Isotonic with plasma
Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
23
Lipids
 3 - 7 day delay in supplying lipids leads to biochemical EFA
deficiency
 Increases antioxidant susceptibility
 Reduces 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 attending
 Always use 20% lipids, not 10%
 Limit lipids to 40 – 50% of total calories (Gomella, 2009. Page 78)

May cause ketosis
Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
24
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
Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
25
Practical Tips for Lipids
 Fat is a concentrated energy source, providing 9 kcal/g.
 Use of 20% lipid emulsion is preferable to a 10% solution
 Smaller volume to administer
 Decrease the risk of hypertriglyceridemia, hypercholesterolemia,
and hyperphospholipidemia.
 Plasma triglycerides are monitored
 Discuss with attending when to check
 Serum triglycerides should be <200 mg/dL
 If the infant has severe hyperbilirubinemia or severe
respiratory disease
 Consider discontinuing lipids or decrease dose
Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
26
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
Adamkin, D. (2007). Use of Intravenous Lipids in Very Low-birthweight Infants. NeoReviews Vol.8 No.12 2007 e543
27
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
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
28
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 guidelines
 VLBW 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
Gomella, 2009. Page 92 -95
30
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 initiated
 10 – 30% mortality associated with NEC
31
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
32
Enteral Nutrition – Feeding Intolerance
 Residuals – 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 output
 Exam infant’s abdomen
 look for distention, bowel loops, guarding , discoloration
 Obtain KUB
 Hold feedings until KUB seen and condition discussed with
attending
33
34
35
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 NEC
 Patients 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 severity
 For 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
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.
.
36
Duke Abdominal Assessment Scale (DAAS)
37
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
38
air in the portal vein –
portal venous air
The plain abdominal film
shows:
1) air in the portal vein
2) air in the bowel walls
3) a large
pneumoperitoneum
[subdiaphragmatic free
air
4) perihepatic free air
5) double wall sign (blue
arrows)
6) triangle sign (green
arrows)
7) falciform ligament (red
arrow)
39
Management of NEC
 NPO
 Respiratory support
 May need fluid boluses and pressors to maintain adequate
blood pressure
 Obtain CBC, CRP, blood gas, and blood culture
 Antibiotic coverage
 Usually Vanc, Gent, and Clindamycin or Flagyl
40
Management of NEC
 Serial abdominal films to watch for perforation
 Usually every 6 – 12 hours
 Sooner if change in exam noted
 Can transilluminate abdomen to check for perforation
 Bowel rest and decompression with repogyl to low
intermittent suction
 Surgical consult as needed
41
Fluid Composition: Potassium
 Potassium
 Ideal 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
Gomella, 2009. Pages 304-307.
42
Hyperkalemia
 Serum K+ > 6mEq/L.
 Etiology
 Heelstick vs central





Heelstick values may be hemolyzed giving false elevations.
Redraw by venous or arterial sample to confirm
Excessive supplemental K+
Bruising
Renal failure
Renal immaturity

Infants < 800 gram, first 2-3 days of life
 Pathologic hemolysis of RBC from IVH or other thrombus
 NEC – tissue necrosis
 Adrenal insufficiency
Gomella, 2009. Pages 304-307.
43
Hyperkalemia
 Metabolic acidosis
 decrease in pH by 0.1 unit -> increase in K+ by 0.3-1.3
meq/l
 Medications which can cause hyperkalemia
 Digoxin -> redistribution of K+
 Aldactone – K+ sparing
 Indomethocin -> renal dysfunction
Gomella, 2009. Pages 304-307.
44
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
Gomella, 2009. Pages 304-307.
45
Hyperkalemia
 If EKG changes -> medical emergency
 Give Calcium gluconate IV

Decreases myocardial excitability
 Correct any acidosis with NaHCO3
 Glucose – insulin drip
 Inhaled albuterol
46
47
Monitoring Fluid and Electrolyte Balance
 Normal values
 Urine output = > 2ml/kg/hr
 Urine SG = 1.008-1.012
 Weight 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/day
 20-30 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.
49
CNS
 One of the primary concerns for infants in the NICU is
the development of intracranial hemorrhage which
can cause later neurologic issues
 Term infants tend to have:
 Subdural, subarachnoid, or subtentorial

Generally related to birth trauma, hypoxic-ischemic events,
coagulopathies (thrombophilias or thrombocytopenia)


Gomella, 2009. pg 549 - 557
50
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
Coronal View
52
53
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 the
lateral ventricle and may be echogenic.
Sagittal View
54
CNS
 General presentation
 Seizures
 Rapid drop in hematocrit
 Sudden deterioration in condition
 Diagnosis
 Preterm

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
Gomella, 2009. pg 549 - 557
55
CNS
 The most widely used classification system for IVH is
that originally described by Papile and associates
 Grades from 1 to 4 with increasing severity
Rhine, W. D. & Blankenberg, F. G. , (2001). Cranial Ultrasonography.
NeoReviews Vol.2 No.1 January 2001
56
CNS
 ICH usually begins within the first 24 to 72 hours of
life
 May 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 drop
 Acidosis
 Change in neurologic status
57
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.
58
Bilateral small germinal matrix hemorrhages
http://www.google.com/imgres?imgurl=http://neuropathology.neoucom.edu/chapter3/images3/3ivh.jpg&imgrefurl=http://neuropathology.neoucom.edu/chapter3/chapter3dGmh.html&usg=__O5BiBTFDXt_6r1m7R0DbzMgNLo=&h=446&w=500&sz=170&hl=en&start=5&itbs=1&tbnid=3kwwgVKjog8fYM:&tbnh=116&tbnw=130&prev=/images%3Fq%3DGrade%2B1%2
59
BIVH%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1
 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.
60
Grade II IVH
http://www.google.com/imgres?imgurl=http://neuropathology.neoucom.edu/chapter3/images3/3ivh.jpg&imgrefurl=http://neuropathology.neoucom.edu/chapter3/chapter3dGmh.html&usg=__O5BiBTFDXt_6r1m7R0DbzMgNLo=&h=446&w=500&sz=170&hl=en&start=5&itbs=1&tbnid=3kwwgVKjog8fYM:&tbnh=116&tbnw=130&prev=/images%3Fq%3DGrade%2B1%2
61
BIVH%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1
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 germinal
matrix 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.
62
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).
63
Grade IV IVH
http://www.google.com/imgres?imgurl=http://neuropathology.neoucom.edu/chapter3/images3/3ivh.jpg&imgrefurl=http://neuropathology.neoucom.edu/chapter3/chapter3dGmh.html&usg=__O5BiBTFDXt_6r1m7R0DbzMgNLo=&h=446&w=500&sz=170&hl=en&start=5&itbs=1&tbnid=3kwwgVKjog8fYM:&tbnh=116&tbnw=130&prev=/images%3Fq%3DGrade%2B1%2
64
BIVH%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1
Treatment of IVH
 Supportive
 Ventilation
 Volume expansion and pressors as needed
 PRBC and platelets as needed


Check CBC frequently
Correct anemia and thrombocytopenia as
directed by attending
 Correct acidosis
65
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 periventricular
white matter and mild ventricular dilation.
PVL describes a characteristic pattern of
cystic degeneration over the next 2 to 3
weeks, resulting in a “swiss cheese” pattern
of white matter loss that can
be 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.
66
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 edema
 Including small, slit-like ventricles
 Poor gray-white signal differentiation on HUS
67
Treatment of HIE
 Supportive
 Ventilation
 Volume expansion and pressors as needed
 Correction of acidosis
 Head and Body Cooling
 Recent 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 babies

Generally 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 unknown
 Current 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 growth
 When 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 occurs
 Leads 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 ROP
 In most, the disease is mild and regresses spontaneously
 A 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
22a
23a
24
25
26
27
28
29
30
31b
32b

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.
Age at Initial Examination, wk
31
31
31
31
31
31
32
33
34
35
36
Postmenstrual Chronologic age
9
8
7
6
5
4
4
4
4
4
4
75
Classification of Clinical ROP
 Location
 The 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
76
ROP Zones
77
Classification of Clinical ROP
 In the absence of
retinopathy, the
retina of the very
preterm infant
merges imperceptibly
from vascularized
centrally to avascular
peripherally
 ROP affects the entire
retina
Normal immature retina, not fully
vascularized
78
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
Stage 2 ROP, indicated by the
development of a ridge between the
vascular and avascular retina
79
Classification of Clinical ROP
 Stage 3 ROP
 Neovascularization
can be seen within
the ridge, and
extraretinal
vascularization
extends out of the
retina
Stage 3 ROP, showing neovascularization
within the ridge and extraretinal
vascularization out of the retina.
Courtesy of Professor Michael O’Keefe,
Dublin, Ireland.
80
Classification of Clinical ROP
 Stage 4 ROP
 Partial retinal detachment occurs,
 May be extrafoveal or foveal
 Stage 5 ROP
 Eventually total retinal detachment may occur

With resulting complete blindness
81
Classification of Clinical ROP
Plus disease:
Indicated by tortuosity of the
posterior retinal vessels
82
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
83
Treatment of ROP
 BIO-delivered diode laser ablation of the peripheral
avascular retina has become the usual method of
treating ROP
 cryotherapy 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 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 retinopathy
 Injections 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 ablation
 Permanent scarring
 Some reduction of the peripheral visual field
85
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)
86
References
 Christensen, 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.
87
 Jobe, A. H., The New BPD. NeoReviews, Oct 2006; 7: e531 - e545.
88