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Treatment of Psychological Distress in Parents of Premature Infants PTSD in The NICU 1st Edition Richard J. Shaw
Treatment of Psychological Distress in Parents of Premature Infants PTSD in The NICU 1st Edition Richard J. Shaw
Treatment of Psychological Distress in Parents of Premature Infants PTSD in The NICU 1st Edition Richard J. Shaw
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Treatment of
Psychological Distress in
Parents of Premature Infants
PTSD in the NICU
Treatment of
Psychological Distress in
Parents of Premature Infants
PTSD in the NICU
Edited by
Acknowledgments
Index
Contributors
References
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2013
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66, 1964
Kazak AE, Stuber ML, Barakat LP, et al: Predicting posttraumatic stress symptoms
in mothers and fathers of survivors of childhood cancers. J Am Acad Child
Adolesc Psychiatry 37(8):823–831, 1998
Kübler-Ross E: On Death and Dying. New York, Macmillan, 1969
Miles MS, Carter MC, Riddle I, et al: The pediatric intensive care unit environment
as a source of stress for parents. Matern Child Nurs J 18(3):199–206, 1989
Miles MS, Funk SG, Carlson J. Parental Stressor Scale: neonatal intensive care unit.
Nurs Res 42(3):148–52, 1993
Resick PA, Monson CM, Chard KM: Cognitive Processing Therapy for PTSD: A
Comprehensive Manual. New York, Guilford, 2017
Shaw RJ, DeBlois T, Ikuta L, et al: Acute stress disorder among parents in the
neonatal intensive care nursery. Psychosomatics 47:206–212, 2006
Shaw RJ, St John N, Lilo EA, et al: Prevention of traumatic stress in mothers with
preterm infants: a randomized controlled trial. Pediatrics 132(4):e886–e894,
2013
Shaw RJ, St John N, Lilo E, et al: Prevention of traumatic stress in mothers of
preterms: 6-month outcomes. Pediatrics 134(2):e481–e488, 2014
Acknowledgments
Causes of Prematurity
The causes of prematurity are poorly understood despite decades of research
and clinical trials. Understanding of risk factors is limited, and interventions to
prevent prematurity have had little impact. The birth of a preterm infant has
significant emotional and economic cost for families and implications for health
insurance, education, and other social support systems. The annual economic
burden associated with preterm birth in the United States was estimated in
2005 at $26 billion (Behrman 2007).
Spontaneous preterm birth is responsible for two-thirds of all preterm
births, while the rest are considered medically indicated to avoid or minimize
maternal and or fetal complications such as maternal preeclampsia and
intrauterine growth retardation. Spontaneous preterm birth is usually
associated with preterm labor and spontaneous rupture of membranes. Risk
factors associated with preterm birth include medical, genetic, environmental,
and socioeconomic factors. Those previously identified include prior preterm
birth, multiple gestation, use of assisted reproductive technology, tobacco and
substance abuse, infections, extremes of BMI, low socioeconomic status,
cervical anomalies, short intervals between pregnancies, and early elective
delivery. One study examined the contributions of known risk factors for both
spontaneous and medically indicated preterm birth in five high-income
countries to see how well preterm birth might be predicted based on various
combinations of known risk factors (Ferrero et al. 2016). Previous preterm
birth and preeclampsia most strongly predicted preterm birth for individual
women, while on a population basis, nulliparity and male infant were the risk
factors that had the highest impact, accounting for 25%–50% and 11%–16%
of risk, respectively. Unfortunately, more than 65% of preterm births lack a
biological explanation, underscoring the importance of research that is focused
on identifying the underlying biological causes of preterm birth. The March of
Dimes began a campaign in 2003 to increase awareness of prematurity and
decrease the preterm birth rate. Their scientific advisory board created a
research agenda targeting six overlapping categories: epidemiology, genetics,
disparities, inflammation, biological stress, and clinical trials (Green et al.
2005). Preterm birth is widely recognized as a common but complex disorder
in need of a multipronged research effort that will ideally lead to specific
interventions that reduce the rate of preterm birth.
Morbidities of Prematurity
Birth prior to 37 weeks’ gestation, particularly for ELBW infants with a birth
weight < 1,000 g, is associated with immaturity of multiple organ systems and
myriad short- and long-term consequences in the NICU and after discharge.
Common morbidities of ELBW infants include bronchopulmonary dysplasia
(BPD), late-onset sepsis, NEC, severe intracranial hemorrhage (ICH),
periventricular leukomalacia (PVL), and retinopathy of prematurity (ROP)
(Figure 1–6).
FIGURE 1–6. Neonatal morbidities for infants born at gestational
ages 22–28 weeks.
BPD = bronchopulmonary dysplasia; ICH = intracranial hemorrhage; LOS = late-onset sepsis;
NEC = necrotizing enterocolitis; PVL = periventricular leukomalacia; ROP =retinopathy of
prematurity.
Source. Adapted from Stoll et al. 2015.
RESPIRATORY SYSTEM
Apnea of Prematurity
Apnea is defined as cessation of breathing for ≥ 20 seconds or a shorter period
when accompanied by bradycardia < 100 beats per minute, cyanosis, or pallor.
It is due to immature respiratory control. Apnea may be further classified as
central, with cessation of breathing effort; obstructive, with lack of airflow
usually at the pharyngeal level; or mixed. Apnea is common in preterm infants,
and the incidence increases as gestational age decreases. It occurs in all
premature infants born < 29 weeks’ gestation and decreases to 20% of infants
born at 34 weeks’ gestation (Henderson-Smart 1981). Apneic events were
shown to resolve by 37 weeks’ postmenstrual age in 92% and by 40 weeks’
gestation in 98%. Infants born at lower gestational ages were more likely to
have longer persistence of apneic events (Eichenwald et al. 1997). The
Collaborative Home Infant Monitoring Evaluation study documented that
extreme events resolved by 43 weeks’ postmenstrual age in premature infants
(Ramanathan et al. 2001). No data have suggested that apnea of prematurity
is associated with an increased risk of SIDS, although the risk of SIDS is higher
in premature infants. Apnea of prematurity is treated most commonly with
methylxanthines, and caffeine is used due to its longer half-life and high
therapeutic index. A large trial of caffeine use for apnea or to facilitate
extubation found that caffeine-treated infants had a shorter duration of
mechanical ventilation, lower risk of BPD, and improved neurodevelopmental
outcomes at 18 months of age (Schmidt et al. 2006). Other treatments used
for apnea of prematurity include CPAP or high-flow nasal cannula in
combination with caffeine therapy. Management of apnea in newborns
approaching discharge varies, but the usual requirement is for infants to be
free of spontaneously occurring apnea and bradycardia for 5–7 days prior to
discharge.
Air Leaks
Pulmonary air leaks occur when air escapes from the lung, with rupture of
overdistended alveoli dissecting along the perivascular connective tissue
sheath, resulting in pneumothorax, pneumomediastinum, pulmonary interstitial
emphysema, and pneumopericardium. The incidence is highest in preterm
infants with lung disease requiring positive-pressure ventilation. Mechanical
ventilation is most apt to increase the risk of air leak when it involves high
peak inspiratory pressure, large tidal volume, or long inspiratory time. Air leak
can be asymptomatic, noted on routine chest radiograph, or can present
dramatically with sudden clinical deterioration. Treatment for pneumothorax,
the most common form of air leak, involves needle aspiration of the air, often
followed by chest tube placement. Small pneumothoraces in asymptomatic or
minimally symptomatic newborns who are not on positive-pressure support
may be observed without specific treatment.
Bronchopulmonary Dysplasia
BPD, also known as chronic lung disease, is an important cause of morbidity,
affecting more than 25% of very low birth weight (VLBW) infants and
approximately 40% of ELBW infants. Lung development is interrupted by
preterm birth, and alveolarization and normal lung growth are significantly
impaired even without supplemental oxygen and mechanical ventilation.
Genetic factors, intrauterine and postnatal infection and inflammation, and
oxidant stress are some of the other potential causes of impaired lung
development leading to BPD (Higgins et al. 2018) (Figure 1–7). The definition
of BPD has changed since the 1990s. The definition used most commonly is
oxygen use at 36 weeks’ postmenstrual age. Rates of BPD have been
increasing in recent years, likely due to the survival of smaller and less mature
infants; a large observational study found an increase in BPD from 32% in
1993 to 45% in 2008–2012 (Stoll et al. 2015). Certain factors such as
intrauterine growth restriction increase the risk of BPD.
CARDIOVASCULAR SYSTEM
Hypotension
Extremely preterm infants who are critically ill often experience hypotension
after birth. There are no widely accepted definitions for normal blood pressure,
and this has led to significant practice variation. Treatments for hypotension
include volume boluses, blood transfusion, and vasoactive drugs and are used
with the belief that blood pressure is a proxy for tissue perfusion and that by
increasing blood pressure, tissue perfusion will improve and adverse outcomes
will lessen. Laughon et al. (2007) studied blood pressures in 1,507 newborns
between 23 weeks’ and 27 weeks, 6 days’ gestation and the use of treatments
for hypotension. He found that 80% of newborns received treatment for
hypotension, and the lowest blood pressures were seen in the lowest
gestational age babies and increased with chronological age. Lower birth
weight, male sex, and higher severity of illness were associated with
treatment, although institutions varied significantly in their use of therapies for
hypotension. Batton et al. (2013) prospectively studied blood pressure and
treatment of hypotension and found that 55% received treatment for
hypotension. Surprisingly, treatment was also administered to 28%–41% of
infants without hypotension. Treated infants were significantly more likely than
untreated infants to experience adverse outcomes, including severe
retinopathy, severe IVH, or death. In a follow-up study, infants given an
antihypotensive therapy had a significantly higher rate of death or NDI when
compared with the untreated group, and this difference could not be explained
by other markers such as severity of illness (Batton et al. 2016).
INFECTIONS
Prematurity places infants, particularly ELBW infants, at risk for infection due
to immaturity of the immune system as well as for prolonged hospitalization
and invasive procedures, such as endotracheal intubation and use of
intravenous central lines. The term neonatal sepsis is generally used to
describe a systemic infection of bacterial, viral, or fungal origin, with
associated clinical manifestations. This definition includes the isolation of a
pathogen from a usually sterile body fluid (e.g., blood, cerebrospinal fluid,
trachea, or urine); however, the clinical features can be present without
identification of an organism, because small volume collections of body fluids
often fail to identify the organism responsible. This is called culture-negative
sepsis or suspected sepsis.
Neonatal sepsis can be classified as either early or late-onset sepsis
depending on the age of onset. Early onset sepsis is an invasive bacterial
infection occurring in the first 3 days after birth. It is strongly associated with
perinatal risk factors and likely represents vertical mother-to-infant
transmission. It almost always is accompanied by clinical symptoms in the first
24 hours after birth. The most common pathogens are Escherichia coli in the
preterm infant and group B Streptococcus in the term infant (Stoll et al. 2011).
The frequency of early onset sepsis has changed dramatically with the use of
intrapartum prophylaxis for early onset group B streptococcal sepsis (Figure 1–
8). The rate of occurrence is 0.98 infections per 1,000 births, with the highest
rates found in preterm infants—10.96 per 1,000 live births.
Gastroesophageal Reflux
Gastroesophageal reflux is the transient relaxation of the lower esophageal
sphincter, often accompanied by poor coordination of esophageal motility,
allowing reflux of gastric contents into the esophagus. The premature infant
may also have delayed gastric emptying. Reflux is common and physiological
in all newborns in the first few months of life and causes few symptoms. It is
seen more frequently in premature infants and may be associated with feeding
problems, such as frequent emesis, feeding aversion, poor weight gain,
grimacing, aspiration, and exacerbation of chronic lung disease. Numerous
studies have failed to demonstrate a temporal association of gastroesophageal
reflux and apnea in preterm infants or a worsening of apnea when reflux is
present (Peter et al. 2002). Nonpharmacological treatment consists of
elevating the head of the bed and positioning the infant left side down so that
the lower esophageal sphincter is in a higher position. The most common
pharmacological intervention is a histamine H2 blocker or proton pump
inhibitor to decrease gastric acidity.
Necrotizing Enterocolitis
NEC is one of the most common gastrointestinal emergencies in newborn
infants. Diagnosis is typically made radiographically by identifying air in the
bowel wall, pneumatosis intestinalis, free air in the abdomen,
pneumoperitoneum, or portal venous air. A classification system was suggested
by Bell that differentiated suspected (Stage I), proven (Stage II), and
advanced (Stage III) NEC (Table 1–2) (Bell et al. 1978). Most affected infants
are premature, with an increasing incidence as gestational age decreases. The
exact etiology is unknown; however, important risk factors include prematurity,
intestinal ischemia, enteral feeding, and bacterial colonization. An
observational study of preterm infants performed by the NICHD NRN found an
overall incidence of 9% (Stoll et al. 2015). The incidence seems to be
declining, likely related to quality improvement efforts aimed at reducing risk,
including use of antenatal steroids, human milk feedings, and avoiding
prolonged antibiotic use. Classic NEC in preterm infants occurs from 10 to 25
days of age, with a peak at 32 weeks’ gestation. Clinical presentation can vary
from slowly increasing feeding intolerance or bloody stools without other signs
of illness to fulminant disease with a shock-like picture.
NEUROLOGICAL SYSTEM
Intraventricular Hemorrhage
IVH is the most common type of intracranial pathology seen in the premature
infant. Preterm infants are at risk for impaired autoregulation, which results in
increases in cerebral blood flow leading to rupture of the fragile blood vessels
in the germinal matrix. The germinal matrix, a periventricular structure
between the caudate nucleus and the thalamus, progressively decreases in
size as gestational age advances, with nearly complete involution by 36 weeks
of gestation. In the premature newborn, the germinal matrix contains a fine
vascular network without supportive stroma. The risk of IVH increases with
decreasing maturity; it is more common in EPT infants born earlier than 28
weeks’ gestation and is rare after 32 weeks. Most hemorrhages occur in the
first 48 hours and almost all in the first week of life. IVH is often
asymptomatic, but occasionally it will be accompanied by lethargy, seizures,
drop in hematocrit, hypotension, or metabolic acidosis. The Papile grading
system (Papile et al. 1978) has been used to classify IVH (Table 1–3). The
incidence of IVH declined significantly following the widespread use of
antenatal steroids and postnatal surfactant in the 1990s. The percentage of
babies with severe IVH, defined as grade 3 or 4, also declined significantly
between 1993 and 2012 in infants born at 26–28 weeks’ gestation but not in
infants born at 22–25 weeks’ gestation (Stoll et al. 2015).
Grade Description
Periventricular Leukomalacia
PVL is described as multifocal areas of necrosis that form cysts in the deep
periventricular white matter, occurring in a specific distribution dorsolateral to
the external angles of the adjacent lateral ventricles. Perinatal inflammation
and cerebral ischemia are two factors known to contribute to PVL. In a recent
study, cystic PVL occurred in 6% of premature infants ≤ 26 weeks’ gestation
and was found to be transient in 18%, persistent in 20%, and appearing late
in 62%; all were associated with NDI and cerebral palsy (CP) (Sarkar et al.
2018).
Seizures
The incidence of seizures in the term neonatal population had been estimated
at 1–5 per 1,000 live births, with higher rates of 9–11 per 1,000 live births
among premature newborns. These studies did not account for the low
diagnostic accuracy of clinical observation alone. It is now recognized that
neonatal seizures are frequently either subtle or often subclinical, and thus the
rate of seizures is likely much higher. Both continuous electroencephalography
and amplitude-integrated encephalography are being used with more
frequency in the NICU, resulting in improved detection of seizure activity.
Premature infants with neonatal seizures have been found to have an
increased risk of adverse neurodevelopmental outcome, independent of
multiple other confounding factors (Davis et al. 2010). The adverse outcome
may be related to both the underlying cause of the seizures and the impact of
seizure activity on the developing brain.
Retinopathy of Prematurity
ROP is the abnormal growth of blood vessels in the retina of premature
infants. It leads to a wide range of outcomes, from normal vision to blindness.
A review of interventions and short-term outcomes over a 20-year period by
the NRN reported ROP stage 3 or higher in about 15% of infants born ≤ 28
weeks’ gestation, with incidence of ROP and high-grade ROP increasing
significantly as gestational age decreased (Stoll et al. 2015). ROP is more
common in infants with a longer duration of mechanical ventilation, prolonged
oxygen administration, and other indicators of illness severity. Careful
monitoring of oxygen saturation reduces but does not eliminate ROP.
Restriction of supplemental oxygen has been used to reduce ROP, and clinical
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toute sorte que la Prusse rencontra jusqu’à la dernière heure [34] .
C’est une curieuse page d’histoire et qui mérite d’être connue chez
nous.
[34] Die Kæmpfe um Reichsverfassung und
Kaiserthum 1870-71, von Dr Wilhelm Busch, Tübingen,
1906.
I
LES ANNÉES D’APPRENTISSAGE.