1 Loy Maslen, MSN, RN, NNP-BC, CPHM Perinatal Clinical Nurse Specialist UW/Valley Medical Center April 2015 PREMATURITY: CLINICAL ISSUES PART TWO 1 The Long Journey Home Birthweight: 2 ½ lbs 1920 2 Born in1974, BW: 600 gm 3 LEARNING OBJECTIVES • Discuss neurologic factors affecting preterm infants and strategies for minimization • List causes and interventions for ROP • Review Infant Blood Protocol for and reasons for anemia of prematurity • Apply knowledge of apnea of prematurity and hyperbilirubinemia to appropriate interventions • Analyzes the fluid and electrolyte needs of infants • Discuss nutritional needs and feeding complications of the preterm infant 4 NEUROLOGICAL The third trimester is a time of rapid brain growth and development which continues on through the first year. 5 36 weeks 32 weeks 28 weeks 6
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PREMATURITY: CLINICAL ISSUES PART TWO · 2015-08-26 · 2 NEUROLOGICAL •Cortical neurons are generated in the periventricular germinal matrix. •Almost all neurons have actually
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1
Loy Maslen, MSN, RN, NNP-BC, CPHM
Perinatal Clinical Nurse Specialist
UW/Valley Medical Center
April 2015
PREMATURITY: CLINICAL ISSUES
PART TWO
1
The Long Journey HomeBirthweight: 2 ½ lbs
1920
2
Born in1974,
BW: 600 gm
3
LEARNING OBJECTIVES
• Discuss neurologic factors affecting preterm infants and strategies for minimization
• List causes and interventions for ROP
• Review Infant Blood Protocol for and reasons for anemia of prematurity
• Apply knowledge of apnea of prematurity and hyperbilirubinemia to appropriate interventions
• Analyzes the fluid and electrolyte needs of infants
• Discuss nutritional needs and feeding complications of the preterm infant
4
NEUROLOGICAL
The third trimester is a time of rapid brain growth and development which continues on through the first year.
5
36 weeks
32 weeks28 weeks
6
2
NEUROLOGICAL
• Cortical neurons are generated in the
periventricular germinal matrix.
• Almost all neurons have actually been
generated by 25 weeks.
7 8
NEUROLOGICAL
• Neurons then migrate out towards the
surface of the cortex, branch out, and
form synapses.
• By 32-34 weeks, focus of development
shifts to the cortex
• Germinal matrix tissues themselves
undergo involution.
9
NEUROLOGICAL: HEMORRHAGE
At 24-28 weeks, the supportive
structures around the germinal
matrix are still very fragile, making
the baby vulnerable to hemorrhage
into the ventricles.
10
11
NEUROLOGICAL
The autonomic control of cerebral blood
flow is poorly developed in the preemie,
allowing fluctuations in cerebral blood
flow which can lead to bleeding and/or
ischemia.
12
3
13
INTRAVENTRICULAR HEMORRHAGE (IVH)
• Risk Factors:
• <34 weeks
• <1500 grams
• “unstable”
• Incidence:
• Has decreased over the past 20 years to about 10-20% of VLBW babies in most NICUs. (Down from over 50%)
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INTRAVENTRICULAR HEMORRHAGE (IVH)
• Clinical Presentation:
• Ranges from catastrophic (least common) to silent (most common)
• Risk period: first 3-4 days of life
• Diagnosis:
• Cranial Ultrasound at 1 week of age detects 95% of all IVH or at time of dramatic condition change
15 16
INTRAVENTRICULAR HEMORRHAGE (IVH)
• Management
• Serial ultrasounds
• CSF taps or drainage for progressive
hydrocephalus
• Ventricular-peritoneal shunt
17 18
4
INTRAVENTRICULAR HEMORRHAGE
(IVH)
• Prognosis
• Neurodevelopmental outcome of
preemies with grade I or II hemorrhage
similar to comparable babies with no
hemorrhage.
• Some increased risk in visual motor
integration skills.
19
INTRAVENTRICULAR HEMORRHAGE
(IVH)
• 30-40% of those with moderate (Grade III ) bleeds have major neurologic sequelae (higher with periventricular infarct or PVL)
• “Major” neurologic sequelae
• Blindness
• Deafness
• Cerebral Palsy
• Severe mental retardation
20
PERIVENTRICULAR LEUKOMALACIA (PVL)
• Necrosis of white matter in a characteristic
distribution dorsal and lateral to the lateral
ventricles. It is the primary ischemic lesion of
the premature infant.
• Currently the major form of brain injury in
preterm infants.
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PERIVENTRICULAR LEUKOMALACIA
• Risk Factors
• Prematurity – 23-32 weeks
• Postnatal illness – hypoxia, ischemia,
inflammation
• Maternal cocaine and methamphetamine
use
• Maternal smoking
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PERIVENTRICULAR LEUKOMALACIA (PVL)
Pathophysiology
• Pressure passive cerebral circulation
• Rapidly growing cerebral white matter has high metabolic needs
• Periventricular vascular anatomic factors
• Low blood flow leading to necrosis, hemorrhage, and cysts
• Initial insult plus damage to process of myelinization
23 24
5
PERIVENTRICULAR LEUKOMALACIA (PVL)
• Clinical Presentation
• Generally silent, picked up on ultrasound. Delay
before evident on ultrasound.
• Prognosis
• Major long term sequela is spastic diplegia,
especially affecting legs.
• High risk for developmental problems.
25 26
ventricle
27
DIFFUSE CELLULAR PVL
• MRI can detect diffuse PVL on cellular level
• May play a role in intellectual deficit
28
STRATEGIES BEFORE BIRTH
• Prevent/delay premature birthparental education
• Tocolytics
• Antenatal steroids
• Magnesium Sulfate for neuroprotection
29
NEUROPROTECTIVE STRATEGIES:
• Delayed umbilical cord clamping
• Stable BP and oxygenation
• Maintain good glucose levels
• Avoid rapid infusion of bicarb or any medication
• Avoid low pCO2 levels
• Keep head in neutral (midline) position for first few days of life
• Gentle handling, developmental support30
6
RETINOPATHY OF PREMATURITY
(ROP)
31
RETINOPATHY OF PREMATURITY (ROP)
• ROP describes an abnormality of growth and development
of the retina of the premature infant.
• Untreated, it may progress to retinal detachment and
blindness.
• In the US, approximately 500 to 700 infants lose their
vision due to ROP each year.
• Additionally, 4500 infants will develop complications of
ROP including myopia, strabismus, and late-onset
retinal detachment/blindness.
32
NORMAL RETINAL DEVELOPMENT
• The retina begins to develop at the 16th week of gestation.
• Blood vessels grow out of the optic disc and slowly advance outward.
• The retina is not completely vascularized until 36 to 40 weeks gestation.
• Preterm infant has immature formation of antioxidant enzymes and free radical scavengers.
33
PATHOPHYSIOLOGY OF ROP
• Initial hyperoxic injury
• Elevated oxygen levels (oxygen saturations >95%) cause severe
vasoconstriction and destruction of immature retinal vessels
• The vasoconstriction severely inhibits blood flow to the retina (retinal
ischemia)
• By about 30-34 weeks gestation the ischemic retina attempts to
restore its blood flow by releasing growth factors to stimulate
new blood vessel growth (neovascularization)
• This “catch-up” growth is abnormal and poorly controlled, and may
result in retinal detachment and blindness.
34
PATHOPHYSIOLOGY OF ROP
Hyperoxia (high O2 saturations)
Vessel constriction/destruction
Neovascularization(abnormal vessel growth)
35
ROP: PREVENTION
• Avoid hyperoxia (O2 sat >95%),
especially in the first few weeks of
life
• Avoid large fluctuations in oxygen
saturations
36
7
RETINOPATHY OF PREMATURITY
(ROP): SCREENING GUIDELINES
• 30 weeks or less at birth
• <1500 grams at birth
• Consider screening if premature, 1500-1800 grams at birth, and unstable
• Start 4 to 6 weeks after birth at 31 to 33 weeks corrected gestational age.
(AAP Guideline April 2006-rev. Sept 2006)
37 38
Stage 1: Demarcation Line Stage 2: Ridge
Stage 3: Ridge with Extraretinal
Vascular Proliferation
Plus Disease: Dilated
& Tortuous Vessels 39
STAGES OF ROP: STAGE 4
Stage 4:
Subtotal retinal detachment beginning at the ridge.
The retina is pulled anteriorly into the vitreous by the fibrovascular ridge.
REFERENCES• AMERICAN ACADEMY OF PEDIATRICS Section on Ophthalmology, AMERICAN ACADEMY OF
OPHTHALMOLOGY, AMERICAN ASSOCIATION FOR PEDIATRIC OPHTHALMOLOGY AND STRABISMUS
and AMERICAN ASSOCIATION OF CERTIFIED ORTHOPTISTS (2013). Policy Statement: Screening Examination of Premature Infants for Retinopathy of Prematurity. Pediatrics 2013; Vol 131; p. 189
• AMERICAN ACADEMY OF PEDIATRICS COMMITTEE ON INFECTIOUS DISEASES AND BRONCHIOLITIS
GUIDELINES COMMITTEE (2014). Policy Statement: Updated Guidance for Palivizumab Prophylaxis
Among Infants and Young Children at Increased Risk of Hospitalization for Respiratory Syncytial Virus
Infection. Pediatrics August 2014, Vol. 134, pp. 415-420
• Bull, MJ, Engle, WE, and The Committee on Injury, Violence, and Poison Prevention and the Committee on Fetus and Newborn (2009). Safe Transportation of Preterm and Low Birth Weight Infants at Hospital
Discharge. Pediatrics May 2009; 123:5 1424-1429.
• Gardner, S., et.al. (2011) Merenstein & Gardner’s Handbook of Neonatal Intensive Care (Seventh Edition)
Mosby Elsevier.
• Infant-Directed Oral Feeding for Premature and Critically Ill Hospitalized Infants: Guideline for Practice
(2013). National Association of Neonatal Nurses.
• Maisels, MJ, Watchko, JF, Bhutani, VK, and Stevenson, DK (2012) An approach to the management of
hyperbilirubinemia in the preterm infant less than 35 weeks gestation. Journal of Perinatology Vol 32, 660-664
130
REFERENCES CONT
• Perinatology. 36(4):737-62.
• Malusky, S. & Donze, A. (2011). Neutral head positioning in premature infants for intraventricular hemorrhage prevention: An evidence-
based review. Neonatal Network. 30(6), 381-390.
• Nist, M., Backes, C., Moorehead, P., & Wispe, J. (2012). Blood pressure support in the very low birth weight infant during the first week
of life. Advances in Neonatal Care. 12(3): 158- 163.
• American College of Obstetricians and Gynecologists. (2012). Timing of umbilical cord clamping after birth. Obstetrics & Gynecology.