NICU Resident Orientation
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Transcript NICU Resident Orientation
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
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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.
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
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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 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
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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
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Cloherty, J. P., Eichenwaid, E. C., Stark, A. (2007). Manual of Neonatal
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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
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Taeusch, H. W., Ballard, R. A., & Gleason, C. A. (2004). Avery’s
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Jobe, A. H., The New BPD. NeoReviews, Oct 2006; 7: e531 - e545.
88