PEDIA CONCEPTS 2:

FROM RESPIRATORY
PROBLEMS TO HEMATOLOGIC

MS. ANN EMBRADURA, RN, MN

MS. VALERIE MAE MAGALE, RN
JANUARY TO FEBRAURY 2010
•
• PROBLEMS
RELATED TO
DISTURBED
RESPIRATORY
FUNCTION
•
APNEA OF PREMATURITY
(AOP)
• Etiology: is a common phenomenon in the
preterm infant. Characteristically,
preterm infants are periodic breathers;
they have periods of rapid respiration
separated by periods of very slow
breathing, and often short periods with
no visible or audible respirations.
• Apnea is classified as central, obstructive,
or mixed.
•
•
•
•
•
•
•
• Central: Central apnea is defined as
the cessation of both airflow and
respiratory effort
• Obstructive apnea
is the cessation
of airflow in the
presence of
continued
respiratory effort.
• Mixed apnea
contains
elements of both
central and
obstructive
apnea (see
Media file 2),
either within the
same apneic
pause or at
different times
during a period
• Apnea of infancy
• Apnea of infancy (AOI) occurs when
apnea persists in a neonate older than
37 weeks after conception. The
physiologic aspects of apnea of
prematurity and AOI coincide, though
further studies are needed to determine
their exact relationship.
• Periodic breathing
• Periodic breathing is defined as periods of
regular respiration for as long as 20
seconds followed by apneic periods of
10 seconds or less that occur at least 3
times in succession
•
 • Pathophysiology: the respiratory
reflexes are less mature, which may
be the contributing factor in the
etiology.
•
• Dx:
• Lab studies
• A CBC count and cultures of
blood, urine, and spinal fluid
are necessary if a serious
bacterial or fungal infection
is suspected in patients with
apnea of prematurity
(AOP).Appropriate viral
cultures or collection of
body fluid for polymerase
chain reaction (PCR)
analyses are performed if a
viral pathogen was
suspected.
• Dx:
• Imaging:
• Chest radiography and/or a
nuclear medicine milk
scanning can be helpful if
the child has persistent but
unexplained lower airway
symptoms (eg, wheezing
and/or repetitive
regurgitation after feeding,
rumination)
Treatment and medication
• Goal of medical therapy
• The principal goals of treating apnea
of prematurity (AOP) are to
address its cause and to provide
appropriate medical management.
For example, bacterial sepsis that
causes apnea is treated with
antibiotics and other supportive
therapies, whereas seizures
require anticonvulsants.
•
• Medication
• Methylxanthine: may help reduce
the incidence of events in a
neonate with central apnea,
though apnea in 15-20% of infants
does not respond to
methylxanthines.
• Aminophylline appears to stimulate skeletal
and diaphragmatic muscle contraction,
increase the sensitivity of the ventilatory
center to CO2, and stimulate the central
respiratory drive.
• Aminophylline, theophylline, and caffeine
act as nonspecific inhibitors of adenosine
A1 and adenosine A2a receptors.106 It is
this last effect that raises concerns about
the safety of methylxanthine therapy in
Nursing care mgt
• Physical examination should include
observation of the infant's breathing
patterns while he or she is asleep and
awake. The prone or supine sleeping
positions and other lying postures may
be important during this clinical
observation.
• Weight patient, document
•
• Signs of theophylline or caffeine toxicity
are tachycardia (rate greater than 180-
190bpm) at rest, irritability, restlessness,
diuresis, dysrhytmias, jittiriness and
gastritis (hemorrhagic).
•
• When the alarm in the machine sounds,
infants are first assessed for color and
for presence of respiration. If they
display the usual color and respirations,
the nurse should investigate possible
causes of a false alarrm, such as faulty
lead placement, detached or
disconnected leads, improper alarm
setting or mechanical failure
RESPIRATORY DISTRESS
SYNDROME
• Respiratory distress syndrome (RDS), also
known as hyaline membrane disease
(HMD), occurs almost exclusively in
premature infants. The incidence and
severity of respiratory distress
syndrome are related inversely to the
gestational age of the newborn infant.
•
• Is a breathing disorder of premature newborns in
which the air sacs (alveoli) in a newborn's
lungs do not remain open because the
production of a substance that coats the alveoli
(surfactant) is absent or insufficient.
• Little or no surfactant, as occurs in prematurity and
in infants whose mother has diabetes, is a risk
factor for respiratory distress syndrome.
• Affected infants have severe difficulty breathing and
may appear blue due to a lack of oxygen in the
blood.
• The diagnosis is based on symptoms, oxygen levels
in the blood, and chest x-ray results.
• Without treatment, the syndrome may cause brain
damage or death.
•
• Patho:
• Acute respiratory failure with ↑pulmonary
capillary permeability, pulmonary
edema, refractory hypoxemia, and
↓lung compliance. The lungs appear
deep purplish red and are liver-like in
consistency. Microscopically, extensive
atelectasis with engorgement of the
interalveolar capillaries and lymphatics
can be observed.
•
•
• Clinical manifestations:
• Tachypnea, respiratory alkalosis are
early signs followed by
tachycardia.
• The natural course of untreated
RDS is characterized by
progressive worsening of cyanosis
and dyspnea. If the condition is
inadequately treated, blood
pressure may fall; fatigue,
cyanosis, and pallor increase, and
grunting decreases or disappears
as the condition worsens
• DX;
• Labs
• Blood gases are usually obtained in
respiratory distress syndrome
(RDS), as clinically indicated,
from an indwelling peripheral or
central (umbilical) arterial catheter
or by means of arterial puncture
• Pulse oximetry is used as a
noninvasive tool to monitor
oxygen saturation, which should
be maintained at 90-95%.
• Dx:
• Imaging
• Chest radiographs of a
newborn infant with
respiratory distress
syndrome reveal bilateral,
diffuse reticular granular or
ground-glass appearances,
air bronchograms, and poor
lung expansion
Therapeutic MGT:
• Prevention: Administration of
betamethasone to women 48 hr before
the delivery of fetuses between 24 and
34 wk of gestation significantly reduces
the incidence, mortality, and morbidity of
RDS
• Corticosteroid treatment at recognition of a
risk of preterm delivery is indicated. If
the mother does not deliver within 1
week, retreatment may be considered;
most perinatologists administer a single,
12-mg dose of betamethasone, rather
than 2 doses.
• The mortality rate of respiratory distress
syndrome decreased by approximately
50% over the last decade with the
advent of surfactant therapy.
• Oxygenation and CPAP
• Vapotherm: Vapotherm with heated and
humidified high-flow nasal canula (>2
L/min) has been used for respiratory
support of neonates and to facilitate
early extubation
•
• Assisted ventilation
• High-frequency ventilation (HFV)
•
• Nitric oxide (NO)
• Supportive therapy:
• Temperature regulation: Hypothermia
increases oxygen consumption, further
compromising neonates with respiratory
distress syndrome who are born prematurely.
Therefore, prevent hypothermia in neonates
with respiratory distress syndrome during
delivery, resuscitation, and transport. Care for
these patients in a neutral thermal
environment with the use of a double-walled
incubator or radiant warmer.
•
• Circulation and anemia: Assess the baby's
circulatory status by monitoring his or
her heart rate, peripheral perfusion, and
blood pressure
• Antibiotic administration: Start antibiotics in
all infants who present with respiratory
distress at birth after blood cultures, a
CBC count with differential, and C-
reactive protein levels are obtained.
• Support the family
Nursing care management
• Observe carefully especially be mindful of
the constant threat of hypoxemia and
acidosis
• Continuous monitoring and close
observation bcause the oxygen
saturation changes rapidly.
• Record at least hourly the pulse oximetry
readings
• Arterial blood is drawn from the umbilical
arterial catheter; assist aseptically when
necessary
• Suctioning should be done ONLY when
necessary. Should never be carried out
as a routine procedure as it may cause
bronchospasm, bradycardia because of
the vagal stimulation; hypoxia and inc
intracranial pressure
• Improper suctioning technique may cause
infection, airway damage r even
pnuemothorax
• Mouth care, as the infant is taking nothing
by mouth.
MECONIUM ASPIRATION
SYNDROME
• The first intestinal discharge from
newborns is meconium, which is a
viscous, dark-green substance
composed of intestinal epithelial cells,
lanugo, mucus, and intestinal secretions
(eg, bile). Intestinal secretions, mucosal
cells, and solid elements of swallowed
amniotic fluid are the 3 major solid
constituents of meconium..
• Factors that promote the passage of
meconium in utero include the following:
• Placental insufficiency
• Maternal hypertension
• Preeclampsia
• Oligohydramnios
• Maternal drug abuse, especially of tobacco
and cocaine
• Maternal infection/chorioamnionitis
• Fetal gasping secondary to hypoxia
• Inadequate removal of meconium from the
airway prior to the first breath
• Use of positive pressure ventilation (PPV)
prior to clearing the airway of meconium
•
• Pathophysiology
• n utero meconium passage results
from neural stimulation of a
mature GI tract and usually results
from fetal hypoxic stress. As the
fetus approaches term, the GI
tract matures, and vagal
stimulation from head or cord
compression may cause
peristalsis and relaxation of the
rectal sphincter leading to
meconium passage.
• Clinical manifestations:
• Severe respiratory distress may be
present. Symptoms include the
following:
• Cyanosis
• End-expiratory grunting
• Alar flaring
• Intercostal retractions
• Tachypnea
• Barrel chest in the presence of
air trapping
• Auscultated rales and rhonchi (in
some cases)
• Yellow-green staining of fingernails,
umbilical cord, and skin may be
• DX:
• Labs
• Acid-base status
• Serum electrolytes: Obtain
sodium, potassium, and
calcium concentrations when the
infant with MAS aged 24 hours
because the
syndrome of inappropriate secretion of
antidiuretic hormone (SIADH) and
acute renal failure are frequent
complications of perinatal stress.
• CBC count
• Imaging:
• Chest radiography is essential
•
Treatment and medication
• Prevention of meconium aspiration
syndrome (MAS)Prevention is
paramount.
• Respiratory gases
• Inhaled nitric oxide (NO) has the
direct effect of pulmonary
vasodilatation without the adverse
effect of systemic hypotension. It
is approved for use, if concomitant
hypoxemic respiratory failure
occurs.
• Morphine, used for analgesia and sedation
• Pediatric0.05-0.2 mg/kg/dose IV
over 5 min q2-4h prn
• Fentanyl (Sublimaze)
• Potent opioid used for analgesia, sedation,
and anesthesia. Has a shorter duration
of action than morphine.
• Phenobarbital (Luminal)
• An anticonvulsant that may be used as a
sedative. Suppresses the CNS from the
reticular activating system (ie,
presynaptic, postsynaptic).
• Pentobarbital (Nembutal)
• CNS sedative and hypnotic that acts
primarily on the cerebral cortex and
reticular formation through decreased
neuronal synaptic activity.
•
• Neuromuscular blocking agents
• These agents are used for skeletal
muscle paralysis to maximize
ventilation by improving
oxygenation and ventilation. They
are also used to reduce
barotrauma and minimize oxygen
consumption.
• Pancuronium (Pavulon)
•
•
Nursing care mgt
• Nursing care in oxygen therapy
AIR LEAK SYNDROMES
• Asymptomatic pneumothorax, usually
unilateral, is estimated to occur in 1–2%
of all newborn infants; symptomatic
pneumothorax and pneumomediastinum
are less common
• . Pneumothorax occurs more frequently in
males than in females and in term and
post-term infants than in premature
ones.
• Etiology and pathophysiology
• Extraneous air collection
• May occur in normal
neonates,
• Can result from congenital
renal or pulmonary
malformation, and
• Often complicates
underlying respiratory
disease and its therapy
• PIE
•
• Tension pneumothorax:
• occurs if an accumulation of air
within the pleural space is
sufficient to elevate intrapleural
pressure above atmospheric
pressure.
• Presence of asymetrical chest,
altered cardiac sounds-muffled,
shifted or diminished, palpable
liver, and spleed, and
subcutaneous emphysema
• Clinical manifestations
• early manifestations of
pneumothorax include
tachypnea, restlessness, and
irritability, lethargy, grunting, nasal
flaring, and retractions.
• Symptomatic pneumothorax is
characterized by respiratory
distress, which varies from only an
increased respiratory rate to
severe dyspnea, tachypnea, and
cyanosis. Irritability and
restlessness or apnea may be the
earliest signs.
• Pneumomediastinum occurs in at least
25% of patients with pneumothorax and
is usually asymptomatic.
• Pulmonary interstitial emphysema (PIE)
may precede the development of a
pneumothorax or may occur
independently and result in increasing
respiratory distress as a result of
decreased compliance, hypercapnia,
and hypoxia
DX
• The diagnosis of pneumothorax is
established by x-ray, with the edge of
the collapsed lung standing out in relief
against the pneumothorax;
pneumomediastinum is diagnosed by
hyperlucency around the heart border
and between the sternum and the heart
border. Transillumination of the thorax is
often helpful in the emergency diagnosis
of pneumothorax; the affected side
transmits excessive light. Associated
renal anomalies are identified by
ultrasonography.
• Treatment:
• Without a continued air leak,
asymptomatic and mildly
symptomatic small
pneumothoraces require only
close observation.
• Frequent small feedings may
prevent gastric dilatation and
minimize crying, which can further
compromise ventilation and
worsen the pneumothorax.
Nursing care mgt
• Most effective function is EARLY
DETECTION
• And close vigilance for possible
susceptible infants.
• For infants at risk, needle aspiration
equipment (30ml syringe, three-way
stopcock, and a 23-,to 25-gauge
needles) should be at the bedside for
emergency use.
• Assess breath sounds freq, monitor the
efficacy of gas exchange, and regulating
oxygen therapy.
Bronchopulmonary Dysplasia
• Is sometimes referred to as chronic lung
dysplasia or syndrome, it is a
pathologiic process that may develop in
primarily ELBW, and VLBW infants with
RDS.
• This may also develop in infants with MAS,
persistent pulmonary hypertension,
pneumonia, and cyanotic heart disease.
• Pathophysiology
• The pathogenesis of
bronchopulmonary dysplasia
remains complex and poorly
understood
• The pulmonary changes are
characterized by interstitial edema
and epithelial swelling followed by
thickening and fibrotic proliferation
of the alveolar walls and
squamous mettaplasia of the
bronchiolar epithelium
• Clinical:
• Physical examination may reveal
tachypnea, tachycardia, increased work
of breathing (with retractions, nasal
flaring, and grunting), and significant
weight loss during the first 10 days of
life.
• Infants with severe bronchopulmonary
dysplasia are often extremely immature
and had a very low birth weight. Their
requirements for oxygen and ventilatory
support often increase in the first 2
weeks of life.
•
• Diagnosis
• ABG assessment in patients with
bronchopulmonary dysplasia (BPD)
may reveal acidosis, hypercarbia,
and hypoxia (with increased oxygen
requirements).
• Continuously monitor oxygenation by
using pulse oximeter because of
frequent desaturations.
• Chest radiography is helpful in
determining the severity of
bronchopulmonary dysplasia and in
differentiating bronchopulmonary
dysplasia from atelectasis,
pneumonia, and air leak syndrome
• Treatment
• Nutrition supplementation
• Fluid restriction
• Diuretics
• Inhaled bronchodilators
• O2 supplementation as
needed
• Respiratory syncytial virus
(RSV) monoclonal antibody
•
Nursing Care Mgt
• Provide adequate hydration...care not to
overhydrate as it might affect his heart
status.
• Infants with BPD may become difficult or
maladaptive feeders if they are aware of
hunger yet compromise by not easting
fast enough
• One may decrease oxygenation
requirements during feedings,
decreasing environmental stimuli,
fortifying feedings, and provide more
contact with primary caregiver.
 • Problems
related to
infectious
processes
•
SEPSIS/SEPTICEMIA
• Refers to a generalized bacterial infection in the
bloodstream. Infections are a frequent and
important cause of neonatal and infant morbidity
and mortality.
• Neonatal sepsis occurs in 0.5 to 8.0/1000 births.
The highest rates occur in low-birth-weight
(LBW) infants, those with depressed respiratory
function at birth, and those with maternal
perinatal risk factors.
• A neonate may be predisposed to sepsis by
obstetric complications, eg, premature rupture
of membranes (PROM) occurring ≥ 18 h before
birth or maternal bleeding (placenta previa,
abruptio placentae), toxemia, precipitous
delivery, or maternal infection (particularly of the
urinary tract or endometrium, most commonly
manifested as maternal fever shortly before or
during parturition).
• Etiology
• Early-onset sepsis (ie, within 7 days
of birth) usually results from
organisms acquired intrapartum.
In > 50% of cases, early-onset
sepsis appears within 6 h of birth,
and most cases occur within 72 h.
Late-onset sepsis (after 7 days) is
often acquired from the
environment
•
 Patho
• The physical and chemical barriers to
infection in the human body are present in
the newborn but are functionally deficient.
Skin and mucus membranes are broken
down easily in the premature infant.
Neonates who are ill and/or premature are
additionally at risk because of the invasive
procedures that breach their physical
barriers to infection.
• Defense mechanisms of neonates are further
hampered by a low level of complement,
diminished opsonization ability, monocyte
dysfunction and a reduced number and
inefficient functionsof leucocytes.
PATHOGENESIS OF ASCENDING
BACTERIAL INFECTION

• In most cases, the fetus or neonate

is not exposed to potentially
pathogenic bacteria until the
membranes rupture and the infant
passes through the birth canal
and/or enters the extrauterine
environment.
• Chorioamnionitis results from
microbial invasion of amniotic
fluid, often as a result of
prolonged rupture of the
chorioamniotic membrane
• Clinical
• A few neonatal infections are easily
recognized: pyoderma, conjuctivitis,
ompahlitis.
• Cardiac signs: In overwhelming sepsis, an
initial early phase characterized by
pulmonary hypertension, decreased
cardiac output, and hypoxemia may occur
• Metabolic signs: Hypoglycemia,
hyperglycemia, metabolic acidosis, and
jaundice all are metabolic signs that
commonly accompany neonatal sepsis
syndrome
• Neurologic signs: Meningitis is the common
manifestation of infection of the CNS
• Hematologic signs: The platelet count in
the healthy newborn is rarely less than
100,000/µL in the first 10 days of life.
• GI signs: The intestinal tract can be
colonized by organisms in utero or at
delivery by swallowing infected amniotic
fluid
• Dx
• Labs
• Blood, cerebrospinal fluid (CSF),
and urine culturesAerobic and
anaerobic cultures are
appropriate for most of the
bacterial etiologies associated
with neonatal sepsis.
• A Gram stain provides early
identification of the gram-
negative or gram-positive status
of the organism for preliminary
identification.
• Urine cultures are most
• Imaging studies
• Chest radiography may reveal segmental or
lobar infiltrate but more commonly
reveals a diffuse, fine, reticulogranular
pattern, much like what is observed in
respiratory distress syndrome (RDS).
Pleural effusions may also be observed.
• MRI
•
• Treatment and medication:
• Antibiotics
• Vancomycin has been favored for
this coverage; however, concern
exists that overuse of this drug
may lead to vancomycin-resistant
organisms, Oxacillin therapy is
preferred by some clinicians
because of this.
• Additional therapies include
granulocyte transfusion,
intravenous immune globulin
(IVIG) replacement, exchange
transfusion, and the use of
recombinant cytokines.
• Granulocyte transfusion has been shown
to be suitable for infants with significant
depletion of the storage neutrophil pool
• IVIG infusion
• Recombinant human cytokine
administration to stimulate granulocyte
progenitor cells has been studied as an
adjunct to antibiotic therapy
•
• Diet
• The neonate may need to be given nothing
by mouth (NPO)
• Feeding may be restarted via a nasogastric
tube for the infant with serious
compromise.
• Activity
• The infant with temperature instability
needs thermoregulatory support with a
radiant warmer or incubator.
• Once the infant is stable from a
cardiopulmonary standpoint, parental
contact is important.
•
• Medications:
• Antibiotics
• Ampicillin
• Gentamicin
• Cefotaxime (Claforan)
• Vancomycin (Vancocin)
• Metronidazole (Flagyl)
• Oxacillin (Bactocill)
• Piperacillin
• Erythromycin (Erythrocin)
•
• Meds
• Antivirals
• Acyclovir (Zovirax)
• Zidovudine (Retrovir, ZDV, AZT)
• Antifungals
• Fluconazole (Diflucan)
• Amphotericin B (Fungizone)
• Amphotericin B, liposomal
(AmBisome)
•
• Prognosis
• With early diagnosis and treatment, term
infants are not likely to experience long-
term health problems associated with
neonatal sepsis; however, if early signs
and/or risk factors are missed, the
mortality rate increases. Residual
neurologic damage occurs in 15-30% of
neonates with septic meningitis.
•
 Nursing care mgt
• Prompt recognition of the warning signs
• Knowledge of the side effects of the specific
antibiotics and proper regulation and
administration of the drug are vital.
• In addition, antibiotics predispose the infant to
growth of resistant organisms and
superinfection from fungal or mycotic agents,
(C. Albicans)
• Provide an optimum thermoregulated
environment. Anticipate dehydration and
hypoxia
• Proper handwashing and disposal of excretions.
•
 NECROTIZING ENTEROCOLITIS
• is the most common life-threatening emergency of
the gastrointestinal tract in the newborn period
• The disease is characterized by various degrees
of mucosal or transmural necrosis of the
intestine.
• The incidence of NEC is 1–5% of infants in
neonatal intensive care units.
• Symptoms and signs include feeding intolerance,
lethargy, temperature instability, ileus, bloating,
bilious emesis, hematochezia, reducing
substances in the stool, apnea, and sometimes
signs of sepsis.
• Etiology : In infants who develop NEC, 3 intestinal
factors are usually present: a preceding ischemic
insult, bacterial colonization, and intraluminal
substrate (ie, enteral feedings).
•
• Dx
• CBC count
• Platelet count
• Blood culture
• Serum sodium: Hyponatremia is a
worrisome sign that is consistent with
capillary leak and "third spacing" of fluid
within the bowel and peritoneal space.
• Arterial blood gasses
•
Treatment and medication
• Stoppage of feedings: if NEC is suspected
• Double lumen, NGT for decompression
• Fluid resuscitation
• Broad-spectrum antibiotics
• TPN
• Possibly surgery
•
• medication
• Gentamicin
• Vancomycin (Vancocin, Vancoled)
• Metronidazole (Flagyl)
• Vasopressors
• Dopamine (Intropin)
• Dobutamine (Dobutrex)
• Epinephrine (Adrenaline)
• Naloxone (Narcan)
• Volume expanders
• Albumin (5% and 25%)
• Sodium chloride 0.9% (Normal saline, NS,
Isotonic saline)
• Fresh frozen plasma
•
•

•
• Glucocorticosteroids
• Hydrocortisone sodium succinate (Solu-
Cortef)
• Opioid analgesics
• Morphine sulfate (Duramorph, Astramorph)
• Fentanyl (Sublimaze)
• Antifungal
• Probiotics
• Lactobacillus acidophilus/Bifidobacterium
infantis (Infloran)
•
Nursing care mgt
• Prompt recognition
• Observe for early development of
NEC by checking the abdomen
frequently for distention
(measuring abdominal girth,
measuring residual gastric
contents before feedings, and
listening for the presence of bowel
sounds), and performing all
routine assessments for high risk
neonates
• Conscientious attention to nutrition a
d hydration
• STRICT HANDWASHING
•CARDIO-
VASCULAR
•AND

HEMATOLOGIC
COMPLICATIONS
PATENT DUCTUS
ARTERIOSUS
• During fetal life, most of the pulmonary
arterial blood is shunted through the
ductus arteriosus into the aorta
•
AO = aorta;
LA = left
atrium; LV =
left ventricle;
PA =
pulmonary
artery.

In patent ductus arteriosus, pulmonary

blood flow, LA and LV volumes, and
ascending AO volume are increased.
• Clinical manifestation:
• When the defect is large, CHF with
dyspnea and poor weight gain or
failure to thrive are the main
presentations.
• Tachypnea
• Tachycardia
• Diaphoresis
• Cyanosis
• Bounding peripheral pulses and wide pulse
pressure
• Hyperactive precordium: Systolic thrill
• Clubbing
•
• Dx
• Laboratory Studies
• Pulse oximetry/arterial blood
gas analysis
• Imaging Studies
• Chest radiography
• Echocardiography/Doppler
imaging - Procedure of
choice to confirm a
diagnosis of PDA
• Contrast echocardiography
• Cardiac catheterization
• Computed tomography
• Magnetic resonance imaging
(MRI)
Treatment and medication
• General measures
• Pulmonary support
• Oxygen to correct hypoxemia
• Sodium and fluid restriction
• Correction of anemia
• Medical management consists of
amelioration of CHF symptoms.
• No exercise restriction is required in the
absence of pulmonary hypertension.
• Prophylaxis against infective endocarditis
is recommended.
•
• Medication
• Indomethacin is currently the drug of
choice for closure of the ductus in
premature infants.
• When surgical ligation is not
indicated, prostaglandin inhibitors
(eg, NSAIDs) are used to close
the ductus arteriosus.
• A few com;lications
• Left heart failureP
• ulmonary hypertension
• Right heart hypertrophy and failure
• Eisenmenger physiology (Pulmonary
hypertension usually develops in patients
with a large PDA who do not undergo
surgical treatment)
• Bacterial endocarditis
• Myocardial ischemia
• Necrotizing enterocolitis
Nursing care mgt
• Responsibilities:
• Assisting in early detection
• Careful assessing of cardiovascular
status
• Monitoring for complications after
implementation of therapy
• Assess renal function (BUN,
Creatinine levels)
• Post op: monitor for pneumothorax,
bleeding, s/s of infections,
supportive respi care, pan mgt
Persistent Pulmonary
Hypertension of the Newborn
• Persistent pulmonary hypertension of the
newborn is the persistence of or
reversion to pulmonary arteriolar
constriction, causing a severe reduction
in pulmonary blood flow and right-to-left
shunts through both the foramen ovale
and the ductus arteriosus.
• Persistent pulmonary hypertension of the
newborn is a disorder of pulmonary
vasculature that affects term or
postterm infants.
• Etiology
• The most common causes involve:
Perinatal asphyxia or hypoxia
• Premature ductus arteriosus or
foramen ovale closure,
• Polycythemia
• Congenital diaphragmatic hernia
• Neonatal sepsis
• Because a patent foramen ovale and
patent ductus arteriosus are normally
present early in life, elevated pulmonary
vascular resistance in the newborn
produces extrapulmonary shunting of
blood, leading to severe and potentially
unresponsive hypoxemia. With
inadequate pulmonary perfusion,
neonates are at risk for developing
refractory hypoxemia, respiratory
distress, and acidosis.
• Clinical
• Upon initial examination, the primary
finding is cyanosis, which is
usually associated with tachypnea
and respiratory distress. Cardiac
examination may reveal a loud,
single S2 sound or a harsh
systolic murmur secondary to
tricuspid regurgitation.
• The patient may have evidence of
poor cardiac function and
perfusion.
• Cynosis
•
• Diagnosis
• Labs
• ABG: (Cyanosis unresponsive
to O2 therapy)
• CBC count
• Serum electrolytes (serum
calcium)
• Imaging
• Echocardiogram
• X-ray to identify underlying
disorders
•
 • Imaging
• Echocardiogram
• X-ray to identify underlying
disorders
•
Treatment and medication
• The care of newborns with persistent
pulmonary hypertension of the newborn
(PPHN) requires meticulous attention to
detail.
• Use a minimal stimulation protocol to
minimize the need to handle the patient
and to perform invasive procedures,
such as suctioning.
• Mechanical ventilation
• Treatment with inhaled nitric oxide (iNO)
• Medication
• Opioid analgesics (Fentanyl
(Sublimaze))
• Neuromuscular-blocking agents
(Pancuronium (Pavulon), Vecuronium
(Norcuron))
• Vasopressors (Dopamine (Intropin),
Dobutamine (Dobutrex), Milrinone
(Primacor).
• surfactants:
•
•
•
Nursing care mgt
• Normal fluid, electrolyte, glucose, and Ca
levels must be maintained. Infants
should be kept in a neutral thermal
environment and treated with antibiotics
for possible sepsis until culture results
are known. Inotropes and pressors may
be required as part of circulatory
support.
• Continuous monitoring for oxygenation,
temperature, CVP, V/S, BP. And acid
base-balance
ANEMIA
• Anemia is a disorder in which there are too
few red blood cells in the blood.
• Anemia can occur when red blood cells
are broken down too rapidly, too much
blood is lost, or the bone marrow does
not produce enough red blood cells.
• If a large amount of blood is lost very
rapidly, the newborn may be in shock,
appear pale, have a rapid heart rate,
and have low blood pressure along with
rapid, shallow breathing.
•
• Normally, the bone marrow does not
produce new red blood cells between
birth and 3 or 4 weeks of age, causing a
slow drop in the red blood cell count
(called physiologic anemia)
• Blood loss is another cause of anemia.
• Symptoms and Diagnosis
• Moderate anemia may result in
sluggishness (lethargy), poor
feeding, or no symptoms.
• Diagnosis is based on symptoms
and is confirmed with blood tests.
• Treatment
• Newborns who have rapidly lost
large amounts of blood, often
during labor and delivery, are
treated with intravenous fluids
followed by a blood transfusion
• Recombinant human erythropoietin
(r-HuEPO) has been used to
prevent or treat chronic anemia
associated with prematurity,
bronchopulmonary dysplasia, and
the hyporegenerative anemia of
erythroblastosis fetalis.
Nursing care mgt
• Careful monitoring
• Sign of anemia in the preterm infant are
poor feeding, decreased oxygen
saturation, systolic murmur, dyspnea,
tachycardia, tachypnea, diminished
activity, and pallor
POLYCYTHEMIA
• Polycythemia is an abnormally high
concentration of red blood cells.
• Plethora, a ruddy, deep red-purple
appearance associated with a high Hct,
is often due to polycythemia, defined as
a central Hct of 65% or higher
• This disorder may result from postmaturity,
diabetes in the mother, or a low oxygen
level in the fetal blood.
•
• The incidence of neonatal polycythemia is
increased at high altitudes; in postmature
vs term infants; in small for gestational
age vs large for gestational
• during the 1st day of life (peak, 2–3 hr); in
the recipient infant of a twin-twin
transfusion;
• after delayed clamping of the umbilical cord;
in infants of diabetic mothers;
• in trisomy 13, 18, or 21;
• in adrenogenital syndrome; in neonatal
Graves disease, etc....
• which stimulates erythropoietin
production and increases RBC
production.
• Clinical manifestations
• include irritability, lethargy,
tachypnea, respiratory distress,
cyanosis, feeding disturbances,
hyperbilirubinemia, hypoglycemia,
and thrombocytopenia.
• Severe complications include
seizures, stroke, pulmonary
hypertension, necrotizing
enterocolitis, renal vein
thrombosis, and renal failure.
•
• Treatment
• of symptomatic polycythemic
newborns is partial exchange
transfusion (with normal saline)
• Most asymptomatic infants develop
normally.
• Appropriate therapy for correcting
metabolic disturbances....hypoxia,
hypoglycemia, hyperbilirubinemia
Nursing care mgt
• Watch out for these signs: plethora,
peripheral cyanosis, respiratory distress,
lethargy, jitteriness/ seizure activity,
hypoglycemia, hyperbilirubinemia.
RETINOPATHY OF
PREMATURITY
• Retinopathy of prematurity is a disorder in
which the small blood vessels in the
back of the eye (retina) grow
abnormally.
• It can be mild with no visual defects, or it
may become aggressive with new blood
vessel formation (neovascularization)
and progress to retinal detachment and
blindness.
• As smaller and younger babies are
surviving, the incidence of ROP has
increased.
•
• Patho
• ROP is characterized by severe
vascular restriction in the immature
retinal vasculature, followed by
hypoxia in those areas.
• Stimulation of vascular proliferation of
retinal capillaries in to the hypoxic
areas, where veins become
numerous and dilate.
• As new vessels proliferate toward the
lens, the aqueous humor ad vitreous
humor become turbid.
• Retina becomes edematous, and
haemorrhages separate the retina
from its attachment
 Dx
• Stages of ROP
• Stage 0: This is the mildest form of ROP. It is immature retinal
vasculature. No clear demarcation of vascularized and
nonvascularized retina is present
• Stage 1: A fine, thin demarcation line between the vascular and
avascular region is present. This line has no height and no thickness.
• Stage 2: A broad, thick ridge clearly separates the vascular from the
avascular retina.
• Stage 3: The extraretinal fibrovascular proliferation (neovascularization)
may be present on the ridge, on the posterior surface of the ridge or
anteriorly toward the vitreous cavity.
• Stage 4: This stage is a subtotal retinal detachment beginning at the
ridge. The retina is pulled anteriorly into the vitreous by the
fibrovascular ridge.
• Stage 5: This stage is a total retinal detachment in the shape of a
funnel.
• Plus disease is defined as arteriolar tortuosity and venous
engorgement of the posterior pole, iris vascular
engorgement, pupillary rigidity, and vitreous haze, which
are part of the subclassification given to the above stages
• Other terms mentioned with ROP include
the following
• Popcorn: Regressed
neovascularization seen anterior
to the internal limiting membrane.
This is a cicatricial change and
usually regresses completely over
several weeks.
• Hot dog: A "red hot" active ridge,
probably the site of increasing
vascular channels
• Imaging Studies
• a telemedicine study showed that
single-image and multiple-image
telemedicine examinations perform
comparably in the determination of a
recommended follow-up interval and
in the detection of plus disease
• The instruments used are a
Sauer speculum (to keep the
eyes gently open), a Flynn
scleral depressor (to rotate and
depress small eyes), and a 28-
diopter lens (for proper
identification of zones).
Treatment and medication
• Surgical Care
• Cryotherapy was the original mode
of treatment
• Laser surgery (eg, xenon, argon,
diode) has been shown to be as
effective as cryotherapy for ROP
• Scleral buckling surgery and/or
vitrectomy is usually performed for
stages 4 and 5
Nursing care mgt
• Focus on decreasing the constant bright
environment light and stimuli
• Decrease or avoid events known to cause
fluctuations ion systemic blood pressure
and oxygenation
• Intraop: stabilize and monitor v/s, adm of
meds
• Post op: signs of pain and pain mgt
• PARENTS need a considerable amount of
support and assistance in meeting his or
her special development needs.
 •

• Any questions ??????

• Thank you for you attention.
• THE END!
•