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72 Cards in this Set
- Front
- Back
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Low birth weight
Extremely LBW |
< 1500g
< 1000g |
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SGA
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IUG was slowed/ delivered at or later then term
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Small for dates, premature
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IUG was retarded/ delivered prematurely
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LGA
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IUG was increased
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Maternal factors assoc w/ growth restriction
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low SES
preclampsia HTN/ chronic renal dx diabetes (advanced) malnutrition cigarette smoking heroin addiction/ ETOH use |
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Fetal factors assoc. w/ IUG
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multiple gestation
congenital malformations chormosomal abnl chronic IU infections (chorio, syph, hsv, cmv) |
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Placental factors assoc w/ IUG
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insufficiency
twin transfusion single umbilical artery (assoc w/ tri 18) |
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Physical charac of growth restriction
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large head
dec chest/ab circumference - dec SQ fat - loose dry skin - pale/polycythemic (not getting enough O2) - thin and long - wide eyed/chronic hypoxia (alert but stressed, skinny umb) |
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2 types of SGA babies
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1) Hypotropic
-DYSPROPORTIONATE, wt. below 10%ile, head and length normal, *dec SQ fat, *HCT dec, *hypoglycemia, *hypoproteinemia Cause: malnutrition LATE in gestation 2) Hypoplastic - PROPORTIONATE in size and wt, %tile of head, length, wt similiar, *skin taut; *intrauterine, nonbacterial infection frequent CAUSE: malnutrition begins in EARLY pregnancy |
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Common problems with SGA
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- perinatal asphyxia
- mec. aspiration - hypoglycemia - heat loss - polycythemia - lower APGAR |
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Is meconium asp a problem with preterm babies?
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No.
mec production begins at 16wks |
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Is cerebral edema a problem w/ SGA babies?
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No. Cerebral edema is seen in full term babies who suffer IU asphyxia.
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Causes of premature labor
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- chronic hypertensive disease
- toxemia - placental previa - abruptio placenta - multiple gestation - cervical incompetence - hx of premature delivery |
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Problems w/ premature infants
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- respiratory distress- HMD (surfactant def)
- immature digestive tract (NEC) - ineffective immune system - infection - thermoregulation problems - cold stress - dec tissue perfusion - hypoxia - inc capillary fragility - IVH - retinopathy of prematurity - anemia |
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Problems w/ postmaturity
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- AGA or SGA
- placental dysfunction - stops working - Wasted - inc HCT (>65%) - polycythemia |
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Fetal factors assoc. w/ IUG
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multiple gestation
congenital malformations chormosomal abnl chronic IU infections (chorio, syph, hsv, cmv) |
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Placental factors assoc w/ IUG
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insufficiency
twin transfusion single umbilical artery (assoc w/ tri 18) |
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Physical charac of growth restriction
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large head
dec chest/ab circumference - dec SQ fat - loose dry skin - pale/polycythemic (not getting enough O2) - thin and long - wide eyed/chronic hypoxia (alert but stressed, skinny umb) |
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2 types of SGA babies
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1) Hypotropic
-DYSPROPORTIONATE, wt. below 10%ile, head and length normal, *dec SQ fat, *HCT dec, *hypoglycemia, *hypoproteinemia Cause: malnutrition LATE in gestation 2) Hypoplastic - PROPORTIONATE in size and wt, %tile of head, length, wt similiar, *skin taut; *intrauterine, nonbacterial infection frequent CAUSE: malnutrition begins in EARLY pregnancy |
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Common problems with SGA
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- perinatal asphyxia
- mec. aspiration - hypoglycemia - heat loss - polycythemia - lower APGAR |
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Causes of premature labor
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- chronic hypertensive dx
- toxemia - placenta previa - abruptio placenta - multiple gestation - cervical incompetence - hx of premature delivery |
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Problems w/ premature infants
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- resp. distress - HMD surf. def.
- immature digestive tract - NEC - ineffective immune system - infection - thermoregulation problems - cold stress - dec tissue perfusion - hypoxemia - inc capillary fragility - IVH - retinopathy of prematurity - anemia |
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Problems with postmaturity (>42wks)
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- AGA or SGA
- placental dysfunction - stops working - Wasted - inc HCT (>65%) polycythemia - absent vernix - dry cracked skin - mec. staining |
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Complications of the infant of a diabetic mother
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- polycythemia
- HYPOglycemia, -calcemia, -magnesemia -HYPERbilirubinemia -myocardial hypertrophy -cardiomyopathy w/o hypertrophy - reversible when hypoglycemia, hypocalcemia, polycythemia are corrected - resp disfunction - RDS or HMD |
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In diabetic mother what causes infant polycythemia?
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stimulated by hyperglycemia
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In diabetic mother what causes infant hypoglycemia?
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result of hyperinsulinemia - loses the high insulin environ.
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In diabetic mother what causes infant hypocalcemia?
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dec parathyroid function - parathyroid is responsible for telling bones body need Ca
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In diabetic mother what causes hypomagnesemia?
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dec maternal serum magnesemia, dec total ionized Ca, dec phosphorus, and parathyroid function
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Clinical symptoms of hypoglycemia
What is normal range? |
jitteriness, lethargy, feeding intolerance, apnea, cyanosis, seizures. dipstick <50mg/100ml
70-100 mg/dl |
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What are the risk factors for transient hypoglycemia?
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- infant of diabetic mother
- stressed premature infant - sepsis - gram neg - asphyxia or HIE - hypothermia - shock - drugs - terbutaline (drug that inc moms glucose so baby leaves environ.) - polycythemia - inc glucose consumption by RBC mass -IUGR -post term |
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What factors could affect a glucose result
- where should you not take a sample? - what is the least accurate? |
don't sample from umbilical line
test strips are least accurate glucose meters range from 10-20% whole blood values are 10-20% lower then plasma values |
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Management of hypoglycemia
- mild or asymptomatic - symptomatic |
M or A - oral feeding
Sympt - IV glucose: D10W 200mg/kg Glucose infusion 6mg/kg/min to maintain >60 Repeat monitoring q 30-60min after infusion Glucose screen q 1-2h until stable then q 4. |
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Management of recurrent hypoglycemia
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-inc glucose infusion to 16-20mg/kg/min
- Glucagon .3mg/kg/dose - lab before and after admin -Endocrinology consult |
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Most common problem in the nursery?
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Surfactant def. RDS
greatest incident in LBW and ELBW |
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Pathophys of surfactant RDS
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Lipoprotein that prevents alveolar collapse. Present at 22 wks, prominent at 34-46wks.
Def dec lung compliance, inc work of breathing, dec alveolar ventilation, atelectasis, alveolar hypoperfusion. |
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S&S of Surfactant def RDS
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-diff initiating respiration
- *exp. grunting (good but ominous) - sternal and intercostal retractions - *nasal flaring - *cyanosis on room air |
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Management of surfactant RDS
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- surfactant therapy 4ml/kg/dose intratracheally divided into 4 doses
- assisted ventilation - fluid management/ nutrition - 80cc/kg/day 1st day, then switch to TPN & lipids - thermoregulation - cold baby has dec surfactant produc. |
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Transient tachypnea of the newborn
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retention of fetal lung fluid, at or near term infants.
Xray: generalized over expansion of lungs S&S tachypnea exp grunt retractions nasal flaring cyanosis on RA duration of clinical course 2-4days |
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Mec. Asp Syndrome
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-consequence of fetal asphyxia, rare in preterm.
asphyxia inc. peristalsis and relaxes anal sphinc. to release mec. aspirated w/ first breath or in utero w/ fetal gasping obstructive pneu chemical pneumonitis - inflammation |
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Risk factors for MAS
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post term
preeclampsia/ eclampsia maternal hypertension maternal diabetes abnormal FHR SGA infants BPP </= 6 maternal heavy smoking, chronic resp dx, CV dx. |
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How to prevent MAS in labor?
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avoid hypoxic stress and vagal stimulation.
Dilute thick mec via amnioinfusion of IV fluids Clear mec from airway before gasping or breathing occurs. |
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Treatment of MAS
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Keep intubated if trachea not cleared
ABG - determine need for FiO2 Monitor O2 w/ pulse ox Antibiotics - Amp and Gent Chest xray Supp O2 - may need CPAP or mech vent Check for organ damage d/t perinatal asphyxia |
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Signs of Shock
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*tachycardia
poor perfusion cold extremities w/ normal core temp lethargy weak pulse *apnea & bradycardia tachypnea metabolic acidosis |
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Lab and radiologic studies for shock
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lab: CBC w/ diff, serum glucose, electrolytes, and Ca, Cultures, Kleinhauer-Betke test (fetal/maternal cells - after trauma), ABG
Radiologic tests: chest xray, US if suspect IVH, EKG- arrhythmias, Echo - asses myocardial func in birth asphyxiated infants |
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General Shock Management
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Volume expansion - NS 10mg/kg over 30min IV -> if + response continue
no response - inotropic agent - Dopamine provide resp support |
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Hypovolemic shock management
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NS for emergency
Albumin or plasmate preferred Give volume until get good urine output Blood replacement may be needed - Hct < 40% - PRBC 5-10ml/kg over 30-40min |
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Septic shock management
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Obtain cultures - blood and urine (unless in 1st 24hrs - only blood)
LP for CSF culture (?) Antibiotics - Amp and Gent Volume expansion and inotropic agent PRN |
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Cardiogenic shock management
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1st treat obvious cause
air leak? - remove air from tension pneumothorax arrhythmia? - id and treat metabolic? - correct asphyxia? - hypotension will respond to inotropic agents |
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Sepsis
Early onset vs late onset vs nonsocomial |
Early
- present in first 5-7d - colonized during perinatal pd - Org - viruses, Listeria, Candida, GBS, birth process - Sites of colonization: skin, nasopharynx, oropharynx, conjunctiva, umb. cord Late Onset: - after the first wk - maternal genital tract or human contact - horizontal transmission -antiobodies to mothers own vaginal flora can be transferred to baby, effects which baby will become infected Nonsocomial: -underlying illness - nursery environ, - invasive monitoring - tech procedures - immature immune defense - Org. - staph, pseud, Kebsiella, Serratia, Proteus *prophylaxis antib in nursery |
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Most causitive organisms?
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GBS
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Risk factors for sepsis?
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Prematurity and LBW
PROM >24h Maternal infection (UTI, chorio) Resuscitation at birth Multiple gestation Invasive procedures Infants w/ glactosemia (cant reg glucose) - predisposed to E.coli sepsis Iron therapy - ehances growth org. male infants black infants Low SES - LBW |
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Clinical presentation of sepsis
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temperature instability
lethargy, irritability poor peripheral perfusion, cyanosis, mottling, palor, petechiae, rashes, sclerema (pale, waxy, firm sking), jaundice feeding intolerance tachypnea, resp distress, apnea *tachycardia & hypotension - LATE SIGNS hypo or hyperglycemia metabolic acidosis |
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Lab studies for sepsis?
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Blood cultures
Spinal tap if symptomatic Antigen detection test Gram stain of CSF WBC and diff Plt count < 150,000 C-reactive protein Cytokines - interleukin 6 (mediator of immune response to bacterial infection, inflammatory cytokine, sensitive in drawn w/in 12hrs) |
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Maternal risks of GBS
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PROM >18hrs
Prematurity Fever >38C Chorio GBS bacteruria Age <21 AA 75% assoc w/ maternal risk factors |
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S&S of EARLY ONSET GBS sepsis
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apnea, tachypnea, cyanosis, grunting resp, lethargy, poor tone, feeding intolerance, pallor, tachycardia, chest xray indistinguishable from TTN or RDS, unstable temp
*preterm infants present early |
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S&S of LATE ONSET GBS
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presents as meningitis 50%
generalized septicemia 40% osteomylitis or septic arthritis 10% fever, poor feeding, poor tone, lethargy, irritiability, tachypnea, seizures, shock, neutropenia, coma *full term infants present late (7d-12wks) |
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IP prophylaxis of GBS if
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-previous infant w/ GBS disease
-GBS bacteruria this pregnancy - +GBS screen this preg - unknown GBS status & 1) deliv <37wks, 2) AROM >18hrs, or 3) IP temp > 100.4 |
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Clinical picture of PDA
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L to R shunt through PDA
tachypnea tachycardia dec urine output widened pulse pressure - sys and dias diff > 30mmHg inc pericardial activity bounding pulses murmur - continuous long term effects - poor wt gain, recurrent resp infection, & contin ventilator support 60% seen LBW common in infants w/ RDS seen in 12-15% of total newborn population - 40% require tx |
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Diagnosis of PDA
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clinical findings
Echo Xray - lg heart and pulmonary venous congestion w/ clinical signs of PDA suspect in all infants w/ RDS |
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Management
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1) closure of dutus - a) Indomethicin - 1st 7d of age - 80% closure b) ligation
2) monitor for clinical signs |
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Indomethicin
dosage: MofA SE |
dose: .1-.3 mg/kg/dose 3 doses q 12-24hrs
MofA: inhib prostaglandin production SE: renal dysfunction *if creatinine function is > 1.2-1.8mg/dl or UO < 1cc/kg/hr - do not give! dec renal blood flow dec cerebral blood flow impairs platelet function |
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IVH
- clinical picture w/ grades |
50% grades I and II seen in LBW infants; 80% in infants <26wks
incidence dec w/ inc GA; rarely seen after 35-36wks GA - grade I: no clinical signs - grade II & III: stupor, abnl eye movements, unexplained drop in Hct by 10% or >, failure of Hct inc after transfusion grade IV: coma, resp distress, seizures, fixation of pupils, falling Hct, bulging fontanelle, hypotension SIADA |
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Hyperbilirubinemia:
what is a red flag? time that persistent jaundice continues in term and preterm? values indicative of jaundice? |
Jaundice w/in 1st 24h (RED FLAG - pathologic!)
OR persistent visible jaundice after 1 (term) or 2 (preterm) weeks, OR bilirubin values > 12-13mg/dl total/ direct >5mg/dl/day or rise in bilirubin > 5mg/dl/day |
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2 forms of bilirubin and what are they r/t.
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1) Indirect - unconjugated
rare beyond neonatal period greatest concern in newborn fat soluble - deposits in fatty tissue such as skin and brain 2) Direct - conjugated r/t to altered liver function water soluble excreted in stool and urine |
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How is bilirubin formed?
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From the catabolism of hemoglobin
heme - bkdn into iron and bilirubin globin - protein reused in the body |
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Conjugation of bilirubin
Bili changes from ____ into ___ soluble. Binds w/ ____. Travels to ___ for conjugation. Conjugating enzyme ___. Process req ____ & ____. Eliminated by ____ & ___ |
change from fat soluble to water soluble. serum albumin binds w/ albumin and travels to liver for conjugation. conjugating enzyme - glucuronly transferase. Process req O2 and H2O. Conjugated eliminated by urine and stool. Major component of bile and feces.
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Causes of physiologic jaundice
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1) Shorter lifespan of RBC
2) Lower albumin concentrations so dec binding capacity 3) dec conjugating enzyme in liver - low for 1st 24hr; adult levels reached by 6 to 14wks 4) Enterohepatic shunting - dec intestinal activity, absent intestinal flora pattern: levels will rise gradually and begin to dec, reaching normal by abt 10days of life. |
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Causes of pathologic jaundice?
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1) Events that alter liver function - hypoxia, hypoglycemia, dec liver perfusion
2) Hepatic obstruction 3) Hemolytic dx |
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Diagnosis of jaundice
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1) physical exam
2) total (>12-13) and direct bili (>5mg/dl/day) 3) Hg, HCT, reticulocyte count, maternal/infant bl type, Coombs, & RH test 4) RBC smear |
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Management of jaundice
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Phototherapy - bilirubin molecule absorbs light energy
When do you start? blili levels 17-22mg/dl in healthy term infant bili levels 5-8mg/dl perterm infants < 1500gm; 8-12 in 1500-1999gm *prophylactically for VLBW |
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Consequences of phototherapy?
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inc body temp
inc in water loss inc GI motility lethargic or irritable tanning, rashes, burns, bronze baby syn, retinal damage |
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Bilirubin Toxicity
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> 20mg/dl
Kernicterus - lethargy, weak suck, high-pitched cry, hypertonia, opisthotonos, seizures Survivors: CP, hearing loss, MR |
