EXAM 1 (presentations) Flashcards
what is the normal hematocrit at birth?
43-65%
**hematocrit normally elevates in the first few hours/day and normally falls back to normal by 1 week d/t to fluid shift
what is Neonatal Polycythemia ?
hemotacrit >65%
Venous vs Capillary blood r/t to hematocrit
Capillary blood sample will have higher hematocrit
Venous sample is more accurate
what is partial exchange transfusion
treatment to remove polycythemia
–> by infusing saline or a blood product (albumin) to decrease the hematocrit
done through the umbilical artery
Fetal hemoglobin
15g/dL
higher than adult because they have higher affinity for oxygen
Neonate hemoglobin increases up to 6g/dL w/in a few hours after birth (fluid shift)
Hemoglobin peaks at 4-6 hours & decreases to cord blood value w/in 1 week
(left shift on oxygen-hemoglobin dissociation curve meaning that oxygen is more tightly bound to the hemoglobin)
neonatal hemoglobin
14-20g/dL
**newborns have both fetal hemoglobin and adult hemoglobin
**adult hemoglobin slowly takes over
so fetal hemoglobin breakdown faster causing physiological anemia at 6-8 weeks of age. average is 12.0g/dL in a 2 month old.
adult hemoglobin
12g/dL
signs and symptoms of polycythemia
hct >65% or hgb >22g/dL ruddy appearance plethora (high blood content) causes: chronic hypoxemia, maternal smoking altitudes, cyanotic heart disease, IUGR, maternal hypertensive disorders, DM mothers, trisomy 13, 18 & 21, Beckwith-Wiedemann syndrome or congenital adrenal-hyperplasia Uncommon if less than 34 weeks gestation
newborn urinary system
*** fetus–>empty/fill bladder every 20-30min
newborns are born with an adult number of nephrons, however immature.
newborn renin-angiotension system
increases !
as result the renal blood flow increases markedly w/in 24 hours of life
newborn kidneys still have limitations both in structure and function (shorter uterer)
when do newborns begin to regulate urine
at 3 months of age
newborns can only concentrate their urine to half of adult levels
glomerular filtration rate in newborns
doesn’t catch up with respect to body surface area until age 1
this mean in healthy full term newborns the kidney are immature
**at risk for overhydration/dehydration
**at risk for drug toxicity
what is normal –> teaching about urine system of newborn
there is urine in the bladder at birth
patient should expect the first void w/in 24 hours at birth (95%) but up til 48 hours !
urine should be pale straw colored
there are sometimes uric acid crystals present in the urine (1st day or two otherwise it is a sign of dehydration)
how much voids is normal
1 per day for the first 48 hours
6-10 voids per day in day #3-5 (breastfed/bottle fed)
water for baby
water supplements is extremely dangerous for infant d/t risk of water intoxication
GI system (fetal)
primarily to remove the amniotic fluid
at 38 week–> establish suck/swallow/breathing coordination
GI system (newborn)
supplying newborn’s energy nutritional and fluid needs.
intestinal motility tends to be disorganized and slower in NBs. this leads to increased transit time and delayed emptying, putting the NB at risk for regurgitation
NB’s colon does not conserve water as efficiently as adult colon and can lead to severe water loss.
intestinal surface of the newborn
immature intestinal surface leads to DECREASED absorptive surface
decrease turnover of intestinal epithelia cells leads to inadequate functional surface area. this affects digestion, absorption and host defense
- **feeding after birth stimulates the intestinal lining promoting rapid cell turnover and stimulating production of microvillanous enzymes such as amylase, trypsin, and pancreatic lipase
- **most NBs are able to digest and absorb proteins and carbohydrates but not as efficiently as adults **
Glucoamylase
is a brush border enzyme evenly distributed along the small intestine which helps the NB digest glucose polymers found in breast milk and formula
what is gut closure
the GI system serves as a continuation of human immune system
In NB the “gut closure” does not occur til 4-6 months of age. this means macromolecules and bacterial can penetrate the mucosal lining increasing risks for infection and allergies.
Newborn intestine
intestine are sterile at birth but rapidly colonize
intestinal bacteria are an important source of vit. K, but it take up to 6 weeks for NB to build an adequate supply
*in breastfed infants maternal secretory IgA working at local level restricts immune activation and bacterial attachment
why passage of meconium is important
because it is essential step in initiation of intestinal function. if meconium stays in the gut over a prolonged period there is an increased risk of hyperbilirubenemia !
GI colonization process
change in symbiotic relationship with beneficial organisms which promote immune homeostasis
**disrupt of immune homeostasis has been found to increase the incidence of asthma and other immune diseases later in life.
Oligosaccharides
found in breast milk, act as prebiotics which preferentially promote the proliferation of bifidobacteria and lactobacillus.
implications for practice regarding GI system of newborn
–> breastfeeding promotion and support during antenatal intrapartum and postpartum
–> Skin to skin with mom right after birth with breastfeeding w/in 1 hour of birth
if mom unable to breastfeed expressed milk can be used to feed the baby
Documentation of passage of meconium
monitor NB for excessive wt. loss
teaching to parents about GI system
start breastfeeding as soon as baby is born can help protect baby against common diseases
Colostrum is easily swallowed and digested by baby it also helps with intestines to begin maturing faster
colostrum help baby pass meconium
most baby pass meconium by 24-48 hours after birth
better to breastfeed exclusively
do not introduce regular food til baby is at least 6 months old
fetus circulatory system
- -> neonate child & adult require more oxygen than fetus
- ->fetus is able to compensate by increase its oxygen perfusion rate (higher than of an adult) to maximize oxygen delivery to vital organs
- ->fetal lungs are in a collapsed state and the pulmonary arteries are thickened, creating a state of high pulmonary vascular resistance (increase PVR)
- -> increase PVR minimizes blood flow to lungs and encourages the return of blood to the placenta for oxygenation
umbilical vein
bring OXYGENATED BLOOD from placenta into the fetus
ductus venosus
BYPASSED the liver and connects to the inferior vena cava (IVC)
the oxygenated blood mixes with deoxygenated blood in the (IVC) and is transported into the right atrium (RA ) of the heart.
foramen ovale
connect the RIGHT ATRIUM to the LEFT ATRIUM and moves majority of the blood from the right to left
from left atrium blood moves to left ventricle and is ejected into the ascending aorta to deliver well oxygenated blood to the head neck and upper limbs via the left carotid, coronary and subclavican arteries
ductus arteriosus
connect PULMONARY ARTERY to the DESCENDING AORTA and BYPASSes approximately 90% of blood past the lungs to return it to the placenta
umbilical arteries
SPIRAL around umbilical vein and return the blood from internal iliac arteries to the placenta for reoxygenation.
neonatal circulation
-first breath
-placenta is removed
- foramen ovale: close w/in few hours
-ductus arteriosis : 10-96 hours close , total closure 1-2 mos
-ductus venosus: few days to one week.
umbilical vein close w/in few days turn into ligament .
umbilical arteries : clot quickly turn to ligament
physiologic changes
lung start working to oxygentate the bldy
closure of ductus arteriosus forament ovale, and ductus venosus
umbilical arteries constricts after birth
umbilical vein remains patent for some time
vascular pressure changes after birth
systemic vascular resistance (SVR) INCREASE
pulmonary vascular resistance (PVR) DECREASE
blood flow in the LEFT side of the heart INCREASE
Cardiac exam reveals systolic murmur and high pitch heart tones
in healthy newborn, functional murmurs, clicks, hums, and high pitch sounds of greater intensity can be normal findings as the newborn functionally transitions to extrauterine life.
MURMUR self resolve ! Murmurs are heard in approximately 1/3 of healthy infant though the firs 24 hours of life and 2/3 thought he first 48 hours of life.
systolic murmurs are more audible approximately 15% of healthy newborns for 5-6 hours after birth as DUCTUS ARTERIOSUS begins to close
implications for practice
recognize normal vs abnormal :
not uncommon to see baby with blueish extremities d/t acyanosis –>oxygen more to brain
Mindful resuscitation
it is estimated that approx. 1 out of 10 healthy newborns will require assistance with their first breath
life-saving interventions should benefit mother-infant interaction and unnecessary procedures (eg. routine suctioning immediate separation from mothers) should be discontinued
early and prolonged skin to skin has been shown to promote cardiopulmonary stability as well as decrease the distress level of the infant
innate immunity
barriers
inflammation
adaptive immunity
cellular
antibody mediated (humoral)
–> active acquire
—>passive acquire
physical mechanical and chemical BARRIERS of innate immunity
epithelial cells of the skin & mucous membranes
coughing and sneezing
mechanical cleaning and sloughing of cells
ciliary action
biochemical secretions such as mucous, perspiration, saliva, tears, and earwax
presence of protective proteins call antimicrobial peptides
normal bacterial flora
INFLAMMATORY response
–> heat redness edema & pain
vasodilation following an injury increases blood flow and capillary permeability goal is to dilute toxin producing bacteria
the vascular changes allow for delivery of leukocytes, plasma proteins and other biochemical mediators to the site of injury
Acute phase of Inflammatory response
there are 3 plasma protein system which play roles in inflammatory response
(1) complement system
(2) clotting system
(3) kinin system
* ***they work in conjunction w/ one another with anitmicrobial peptides and the cellular level to prevent bacterial invasion
* **cells involve in the inflammatory process include mast cells, neutrophils, monocytes, macrocytes, eosinophils, NK cells, platelets and nonleukocytic cells.
Mast cells (role in inflammatory response)
central role to all types of physical injuries and allergies reactions
neutrophil (role in inflammatory response)
aka POLYMORPHONUCLEUS NEUTROPHILS (PNM) are arrive w/in 6-12 hours and ingest bacteria damaged cells and debris
monocytes (role in inflammatory response)
produced in bone marrow migrate to the site & then transform into macrophages. Macrophages assist with cleaning the area and healing promotion
macrophages stimulate the activation of the adaptive immune system
eosinophil (role in inflammatory response)
minimize the extent of the inflammatory response which reduces healthy tissue damage. they also fight against parasitic invasion
NK cells
specializes in the elimination of viruses, abnormal cells and cancer cells
platelets
promote bleeding cessation and aid in inflammatory control
Antigen Binding & Destruction
can occur with only 3 types of lymphocyte receptors complexes :
(1) antibodies
(2) B-lymphocytes (B-cell receptor )
(3) T-lymphocytes (T-cell receptor)
Antibody
or immunoglobulin –> is a serum glycoprotein produced by plasma cells in response to presences of an antigen. There are 5 types : IgG IgM, IgA, IgD, and IgE
- *purpose: with lymphocytes to identify and eliminate the offending antigen
- *Primary exposure to antigen creates an ability to form memory cells, which speed response time to subsequently exposure
Adaptive Immunity (acquired)
produced by the host after either being exposed to the antigen or having received immunization
passive immunity (acquired)
does not require action from the host’s immune system
antibodies are transferred directly to the host
ex: transfer antibodies from a pregnant women to her fetus or through immunotherapy.
Newborn’s Immune system
Immature in many ways
limited adaptive immunity
Innate immunity is the main defense for neonate.
Innate Immunity for NB
1st line of defense to an infectin
Vernix as a shield on the newborn’s body
breastfeeding is powerful stimulant of innate immunity
higher risk of systemic infection than adults
Adaptive Immunity
Acquired as a response to specific pathogens
CD8 and CD4 cell (memory cells) present in low levels in neonate and increase slowly throughout childhood
4-6 weeks after birth experience minimal protection by T-cells
B-cell response also deficient and have delayed onset & short duration
passive immunity
NB are born with passive immunity d/t passage of IgG through the placenta from mother
Protects the infant for approximately 6 months
Dependent on this type of immunity since IgG is not produced by the infant until 6 months of age
IgA is present in breast milk and colostrum
passively acquired antibodies provide protection against pathogens that the mother was immune
preventive measure for healthy immune system
–> recommend vaccines in pregnancy such as Tdap vaccine
vaginal birth
practice standard precautions at all times
vit. K injection at birth
encourage breastfeeding provide lactation education and support
educate the mother regarding good hygeine and habits ways to prevent infection
monitor. newborn for s/sx infection d/t immature immune system following delivery
understand normal newborn labs and when to recognize any deviation suggestive of infection
signs of infection in a newborn
can be subtle
look for changes in activity, tone, color, or feeding
lack of fever DOES NOT mean there is no infection
vaginal birth and breastfeeding establish microbial colonization and effect that persists throughout infancy
if at all possible breastfeed your infant
protect infant from infection by limiting exposure to crowds sick individuals or toddlers in the first month of life.
glycogen
stored form of glucose
glucagon
pancreatic hormone that stimulates the conversion of glycogen to glucose
gluconeogenesis
the production of glucose from non-carbohydrates such as lactate, amino acids and glycerol
glycogenesis
the metabolic process by which glucose is stored as glycogen
glycogenolysis
breakdown of glycogen to glucose for engergy
ketogenesis
the process by which ketone bodies are created by fatty acid breakdown
lipogenesis
process by which simple sugars are stored as fats
fetal glucose regulation
the fetus depends on maternal transfer of glucose fatty acid ketones glycerol and amino acids for energy
as gestation progreses: energy is produced by anabolic metabolism of glucose to lactic acid in order to conserve glucose in preparation for birth
glycogen is stored in the liver and in cardiac and skeletal muscle of a much higher rate than adults
liponeogenesis increases in the third trimester
–>fatty acids and ketones serve as secondary fuel source after birth.
newborn glucose regulation
while the fetus primarily use glucose for energy, the neonate uses more FATTY ACID oxidation and ketones
Gluconeogenesis begins after clamping of the umbilical cord when the maternal glucose supply ceases
neonatal glucose levels fall rapidly in the postnatal period usually dropping to the lowest point at 1 hour of life and returning to higher values by 2-3 hours of life.
this drop is thought to activate glucose production in the newborn through the rapid process of glycogenolysis
—> glucose concentration vary considerably between individual newborns during the first few hours of birth
metabolic changes postnatal period
metabolic changes cont. occur throughout the postnatal period.
–>hepatic glycogen stores last about 10 hours, then gluconeogenesis and ketogenesis kick-in as fuel sources
by the THIRD DAY of life, neonatal blood glucose regulation is no longer glucose dominant but regulated by INSULIN
at this point the infant’s serum glucose levels approximate those of a normal adult.
optimal plasma glucose range
70-100mg/dL
hypoglycemia in the healthy full term neonate
common occurence seen in 5% to 15% of normal newborns
–> the risk of persistent or recurrent neonatal hypoglycemia include brain injury and neuronal necrosis that may result in permanent neurological damage.
signs of neonatal hypoglycemia
apnea irregular respiration cyanosis hypothermia seizure tremors jitteriness hypotonia poor feeding, lethargy, irritability high pitched cry OR asymptomatic !
Asymptomatic hypoglycemia can also be caused by
mask clinical sign as brain compensates by increasing cerebral blood pressure, epinephrine secretion, and utilization of ketones, lactate, and cerebral glycogen stores.
management of hypoglycemia
promote normoglycemia and intervene promptly for plasma glucose levels <40-45mg/dL
there are no evidence-based guidelines for tx neonates w/ low plasma glucose levels.
first management
–check neonate glucose level ?
risk factors
symptoms
–>recheck w/in 30 after feed (1st glucose check is VENOUS sample draw and REFER
Pathophysiological of neonatal hypoglycemia
inadequate glucose supply
altered endocrine regulation: hypopituitarism, hypothyroidism, adrenal insufficiency, or immature hepatic enzymes required for glucose production
elevated hematocrit level leading to increased red blood cell utilization of glucose
increased glucose utilization r/t hypothermia or asphyxia
DM mom resulting in initial neonatal hyperglycemia
Pseudoglandular period
6-16w
Canalicular period
16-26w
LUMINA of the bronchi and TERMINAL bronchioles become larger (airway lengthens and growns in diameter)
Lung tissue now highly vascular (increased pulmonary/capillary beds)
by 24 week TERMINAL BRONCHIOLES branch into 3 or more respiratory bronchioles which branch into 3-6 primordial alveolar ducts
At the end of this stage, well vascularized THIN WALLed TERMINAL SACS develop at the end of the respiratory bronchioles making RESPIRATION POSSIBLE
terminal sac stage
26-birth
Blood-air barrier established allowing adequate gas exchange for survival
proliferation of pulmonary vascular beds
Continuation of terminal sac development
—> squamous epithelia cells of endodermal origin make up the terminal sac lining
(1) type I pneumocytes: where GAS exchange occurs
(2) type 2 pneumocytes: produces, store and secrete pulmonary SURFACTANT (complex mixture of phospholipids and proteins)
alveolar period
32-8 years old
transition from the terminal sac stage to the alveolar stage is marked by the ALVEOLUS
terminal sacs remain at the end of respiratory bronchioles and are divided by connective tissue. They represent future alveoli ducts
Throughout this period, alveoli increase in size, number, and shape. They enlarge become deeper to maximize surface area for gas exchange.
–>thin ALVEOLOCAPILLARY MEMBRANE allows for GAS EXCHANGE
–>most mature alveoli form after birth. Approximately 5% of mature alveoli are present at term. Alveolar development is usually complete by age 3, but new alveoli may be added until age 8.
24-26w
newborn only survive with intensive care
beginning of surfactant production
prior to this time, there are not enough pulmonary capillary beds in place to help distribution of gas exchange (think of capillary bed as the trucks that carry the oxygen)
surfactant
production begins at 20w reaching adequate levels late in fetal development
forms a monomolecular film over the interior walls of the alveolar sacs
lowers surface tension at the air-alveolar interface facilitating expansion of the terminal sacs
infant born before 34 weeks benefits from corticosteroids to stimulate production of pneumocytes I & 2
adequate surfactant at birth decreases the respiratory pressure needed to inflate the alveoli thus decreasing the workload of breathing.
corticosteroids
the use of antenatal corticosteroids and postnatal surfactant replacement is often necessary to increase likelihood of survival for the premature infant
antenatal corticosteroid: increase development of pneumocyte I and pneumocyte 22 cells
corticosteroid use was limited to the gestational period of 24 to 34 weeks as there are lack evidence for use earlier in gestation, however new research has recently emerged effecting guidelines.
transition of life outside uterus (lungs)
activation of epithelial sodium channels resulting in shift of fluid out of the fetal lungs ** begin days before labor **
increasing production of surfactant
transformation of lungs into gas exchanging organs
shifts from fetal circulation to neonatal circulation
first breaths
help enable the conversion from fetal to adult circulation
decrease pulmonary arterial pressure
establish pulmonary function of the newborn
establish neonatal lung volume
—> functional residual capacity (FRC)
empties the lungs of fluid
over time will expand ALL alveoli
mechanical stimuli : first stage of labor
mechanical stimuli: 2nd stage of labor
THORACIC SQUEEZE
creates negative intrathoracic pressure
clears approx. 1/3 of the fluid
mechanical stimuli: Mechanical GASP reflex
caused by the elastic recoil of the thorax following vaginal delivery
mechanical stimuli: Clamping of the umbilical cord
initiates freestanding neonatal circulatory system
cord clamping
increase systemic vascular resistance : coincides with the first breaths
increase in O2 causes vasculature to relax: decrease in pulmonary vascular resistance (PVR)
Closure of Ductus arteriosis
shift in pressure causes increased blood flow into the pulmonary system.
Postnatal breathing : sensory stimuli
sensory stimuli cause excitation of respiratory center of the brain stimulating the infant to take a breath
- ->changes in temp (cold)
- ->light
- ->noise
- ->pain
- ->tactile stimulation
chemical stimuli
fetus has increased plasma levels of :
–>CATECHOLAMINES (primarily epinephrine)
–>GLUCOCORTICOIDS
–>SURFACTANT( in the lungs)
the increased level of stress hormones lead to improved lung compliance
clearing of lungs by decreasing secretion of lung fluids
increasing fluid absorption into the lymphatic system
cesarean birth
baby is NOT receive the hormonal and mechanical benefits provided during labor and birth processes
–> increased risk for Transient Tachypnea of Newborn (TTN) and respiratory distress syndrome (RDS)
maintenance of breathing
secondary to central brain stem activity
specialized cells in the carotid body
chemoreceptors of the carotid body initiate increases in ventilatory effort
—> response to ACIDOSIS and HYPERCAPNIA
–> decreased ventilatory effort r/t hypocapnia
what is the normal blood volume of neonate
70-80ml/kg
volume shared between placenta & fetus
400
100 (placenta)
300 (baby)
–> the timing of cord clamping impacts blood volume and initial Hgb levels, delayed clamping increases blood volume
benefits of delayed cord clamping
- increase oxygen -bolus
- increase blood volume ~80ml –> promote pulmonary perfusion, volume expander :alveoli attached to capillary so when blood come it will pullled alveoli open
- fewer blood transfusions
- decreased iron deficiency
- improves neonatal transition
disadvantages
polycythemia
increased risk for hyperbilirubinemia
midwife practice (cord clamping)
early education about delayed cord clamping with parent : include benefit vs risk
baby to abdomen immediate following birth w cord attached for 1-3 minutes while drying and stimulating infant
do not milk the cord
if resuscitation measures are necessary for baby at least 30 sec to 60 sec delay in the cord clamping has shown to be beneficial to infant
thermal neutral environment
environment at which newborns maintain low metabolic expenditures while retaining normal body temp
- *prevent cold stress leading to
(1) hypothermia
(2) hypoglycemia
(3) respiratory distress
normal newborn temperatures
core temp : 97.7-99.5 (36.5-37.5) axillary temp: 97.7-99.0 (36.5-37.5) abdominal temp: 96.8-97.7 (36-36.5) rectal temp: no longer recommended tympanic temp: least reliable
lack of thermoregulation
cold stress and hypothermia
- -> acidosis
- ->hypoxemia
- ->hypoglycemia
- ->infection
***shivering in a newborn is a late sign of compromise !!!
how a neonate maintains his/her own temp
NST (nonshivering thermoregulation)
BAT (brown adipose tissue)
posturing
peripheral vasoconstriction or acrocynosis
Brown Adipose Tissue
stores begin at around 25 weeks gestation and cont. through early weeks after birth
majority found around kidneys and adrenal glands
majority function of BAT is heat production
Quickly metabolizes to produce heat and extends it to peripheral circulation
metabolism of BAT dependent on oxygen, glucose and ATP
–> hypoxia acidosis and hypoglycemia inhibit BAT metabolism !!!
posturing
flexed position decreases heat loss by minimize surface area
prone position for LBW infants can lower metabolic output while maintaining warm temp
voluntary movement such as crying restlessness and hyperactivity are heat generators
peripheral vasoconstriction
vasomotor control through thermal receptors shunt blood away from the extremities to core
—> result is acrocyanosis
challenges of thermoneutrality
- large body surface area
- Insipidus water loss
- trigeminal receptors
challenges of a thermoneutral environment
conduction
radiation
evaporation
convection
conduction
heat transfer from infant to object in contact with the body
–> MATTRESS
–> CLOTHING
if there is a large discrepancy in temps then heat loss will increase at faster rate
radiation
transfers heat away from baby onto surrounding objects not in contact with infant
–> SIDE OF BASSINET WINDOW WALLS
the amount of radiation loss is affected by how cool the surrounding objects are
–> independent of air temp air movement
evaporation
moisture on skin and in respiratory tract dissipate into surrounding environment
–> most prominent source of heat loss immediately follow birth
convection
heat is carried away from the body onto moving air particles –>open window fans air conditioner units
window draft heat moves into air around boundary of infant then disperses farther into room atmosphere
actions for neutral thermal environment
warm room temp
dry wet baby
contact with warm surface –>skin to skin , warm blankets
avoid contact with cold objects or spaces
delay baths
early breastfeeding - preferably 1st hour
head covered and wrapped or skin to skin for 48 hours.
physiologic jaundice
- increased bilirubin availability
–> increased RBC
–>decreased RBC lifespan -80-100d term infant
(120 d -adult, preterm 60-80d, extreme lowbirth 35-50d)
–>increased early bilirubin
-Decreased clearance
–> of bilirubin
–>from plasma
–>decreased hepatic metabolism
incidence of physiologic jaundice
visible jaundice occur in 60% or more in normal newborns
onset : 36 hours
peak: 5-12mg/dL & 7-14mg/dL (breastfed or Asian)
—>total serum bilirubin is 5.5mg/dL in caucasians and african american but 10mg/dL in Asian by 3rd day of life
goal: tx bilirubin conc. that might be potentially harmful
risk factors
asian delayed passage of meconium meconium ileus intestinal obstruction severe hyperbilirubinemia preterm infants
lack of breast milk jaundice
breastfed infant have higher total serum bilirubin in 1st day
9% in breastfed infants and 2% in formula fed infant
onset: 2-4 days
peak >12mg/dL
incidence in full term neonates:
**the infant has decreased intake with increased enterohepatic circulation **
***may be an important indication of inadequate breast milk supply/nursing
–> infant that is not feeding well may be lethargic and less likely to have effective feeding make it a difficult cycle.
breastmilk jaundice
fullterm breastfed infants with persistent hyperbilirubinemia lasting 3-4 weeks after birth
onset: 4-7 days
peak: >10mg/dL
incidence in full term : 2-4%
thought it was possibly an inherent substance (beta-glucuronidase) which increased uptake of unconjugated bilirubin in the milk but not proven theory
possibly a higher level of epidermal growth factors found in jaundiced babies and other mother’s milk
breast milk jaundice is not known to cause bilirubin encephalopathy (if baby is healthy and thriving)
implication for practice
8-10 feedings a day for breastfeeding from mom (avoid pacifier, water, or sugar water
encourage mom to pump after feeding to facilitate milk production
introduce phototherapy
provide trained individuals to mom in first few hours to promote a good latch & effective breastfeeding and skin to skin contact –colostrum is a natural laxative
parental education regarding neonatal jaundice
predischarge bilirubin management : 6h and 12-24h jaundice evaluation
post discharge follow up
re-evaluation at 96 hours after birth
re-evaluation of nutrition, hydration, stooling pattern
–>wt the baby for sig. wt. loss >10%
2-3 stools per day
6 wet diapers per day
breastfeeding 8-10 times per day : swallowing audible
high risk babies follow up sooner at 7 days and 2 weeks for resolution
direct coombs test
used to detect hemolytic disease of the newborn (r/t ABO or Rh incompatibility)
- ->ABO incompatibility : mother has type O blood, the baby has either A or B, 20% of these babies will develop severe jaundice
- ->Rh incapability : mother is Rh negative baby is Rh positive. Rhogam is administered for prevention
- **Production of IgG can coat the surface of RBCs resulting hemolysis. When the Direct Coombs Test is performed the RBCs are washed with saline and mixed with anti-human globulin reagent (Coombs reagent). if the anti-human globulin reagent cause agglutination of RBCs then the test is positive. A negative finding wound indicate no agglutination.
***present of positive Coomb does not necessary result in hyperbilirubinemia but the risk is def. greater for phototherapy & other tx of hyperbilirubinemia
Indirect Coombs Test
used to detect antibodies in the maternal serum that may react and cause harm in the fetus or problems in the newborn
–> ex: Rh titer
The pt. serum cells are mixed with blood sample and washed with saline to remove any unbound antibody. Antihuman globulin is added and if the pt.’s serum contains antibodies, the antihuman globulin will cause the RBCs to agglutinate and test is positive. A negative finding would indicate no agglutination
abnormal values : bilirubin
if the total serum bilirubin is >5mg/dL at 24 hours or >12mg/dL by 48 hours a cause should be examined because it is unlikely to be physiologic
midwife management
do not interrupt breastfeeding unless levels are above 25mg/dL
once levels reach 17mg/dL, cont breastfeeding and start phototherapy, or once levels are in the high risk zone
high risk zone: consider phototherapy, repeat TSB in 6-12 hrs
high intermediate risk zone: repeat in 24 hours TSB
low intermediate risk zone: follow up in 48hr TSB
low risk zone: reassure. follow up in 48 hours
phototherapy
absorption of the light excites the bilirubin molecule and releases the excess energy which the NB can excrete through urine and stool consider phototherapy if : TSB >8mg/dL in 24 hours TSB>13mg/dL at 48 hours TSB>16mg/dL at 72 hours
S/E: retinal damage , neurodevelopmental issues fluid loss, increased temp, lethargy, isolation
skin rashes or burn , altered gastrointestinal function
exchange transfusion
helps to correct the anemia associated with hemolytic disease –very rare
pharmocological agents –>management of hyperbilirubinemia
IV immunoglobulin for Rh or ABO incompatibility
phenobarbital
B-glucuronidas inhibitors
