Neonatal Flashcards

1
Q

Concerns with neonates?

A
  • Immaturity of organ systems
    • ie, myocytes not fully developed
    • CO is HR dependent. fixed SV
    • immature NM system
  • High metabolic rate
    • increased O2 consumption and decreased reserve
  • Large ratio of body surface area to weight
  • Ease of miscalculating a drug dose
    • also easy to miscalculate fluids. pay close attention
    • use buretrol, on pump etc
  • Nominal amounts of air in lines can be catastrophic
    • Foramen ovale functionally closed but not permanently closed
    • if it opens, any air can cross over and embolize to brain, causing stroke
    • very important to eliminate ALL air
  • unpredictable response to drugs ie NMB
  • very prone to vagal response
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2
Q

How do you calculate post-gestational age?

A

weeks gestation at birth + current age in weeks

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3
Q

What are some maternal health and genetic factors that can impact fetal life?

When does organogenesis happen? Organ function development? Muscle and fat?

When is extra-uterine life possible?

A
  • Maternal health & genetic factors:
    • congenital viral infections,
    • exposure to drugs,
    • nutritional deficits,
    • issues with vascular supply to fetus (eclampsia),
    • maternal illness (diabetes, etc.),
    • genetic predisposition
  • Organogenesis: 1st trimester; formation within 8 weeks of conception
    • Injury or stress: abnormal organogenesis
  • Organ function develops in 2nd trimester
    • Injury or stress: abnormal functional development of organs
  • Muscle & fat are gained in 3rd trimester
    • Injury or stress: smaller organs; reduced muscle or fat mass
  • Extra-uterine life is not possible until ~22-24 weeks
    • 22-24 weekers usually have significant neurocognitive impairment
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4
Q

How does the lung develop in the fetus?

A
  • Lung development begins in utero at approximately 4 weeks’ gestation but lungs are functionally immature until nearing term
  • occurs in five stages:
    • embryonic,
    • pseudoglandular,
    • canalicular,
    • saccular, and
    • alveolar
  • growth of the pulmonary parenchyma and surfactant system occurs during the saccular phase occurring from week 24 through week 40 (36 weeks: magic # for surfactant)
    • maturation & expansion of alveoli occur during the alveolar period which begins near term & continues to mature through childhood
      • 24 mil alveoli at birht, 300 mil by age 8
    • surfactant can be adminitered via ETT in premie infant
  • Alveoli must transition from fluid filled state to air-filled (gas exchanging) parenchyma
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5
Q

What are some respiratory variations in the newborn?

A

Respiratory system newborn variations:

  • Diaphragm is flatter;
  • more compliant chest with cartilaginous ribs;
    • poorly compliant lungs; may see paradoxical breathing;
      • paradoxical breathing= inward movement of chest during inspiration
  • predominantly nose breathers until 4 weeks of age;
  • chest circumference very close in size to head circumference at birth
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6
Q

What is persistent fetal circulation?

What are some precipitating conditions?

Treatment?

A

Also called Persistent Pulmonary Hypertension of the Newborn

  • PA pressures abnormally elevated causing the ductus arteriosus & foramen ovale to remain open (or re-open):
    • leads to hypoxia due to R to L shunting
  • Hypoxia & acidosis with concurrent inflammatory mediators are primary causes
  • Precipitating conditions:
    • severe birth asphyxia,
    • meconium aspiration,
    • sepsis,
    • congenital diaphragmatic hernia,
    • mom’s use of NSAIDS,
    • idiopathic
  • Response to treatment is unpredicatable
  • Initial tx: provide optimal oxygenation
    • (PaO2 60-100,
    • correct stressors like hypoglycemia or polycythemia
  • Other tx: surfactant, inhaled nitric oxide, HFOV, ECMO
    • inhaled nitric oxide only FDA approved treatment
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7
Q

What is a newborn? neonet?

General categories for infants?

What is preterm?

Low birth weight? Extremoly low gestational age?

What are preterms more at risk for?

A
  • Newborn”- 1st 24 hours
  • Neonate: Birth to 30 days
  • General categories: small for gestational age (SGA), appropriate for gestational age (AGA), large for gestational age (LGA)
    • Weight, height, & head circumference are tracked for growth- SGA’s & LGA’s are more likely to have problems
  • Preterm <37 weeks
    • <2500 grams: low birth weight
  • Extremely low gestational age (ELGAN): 23-27 weeks gestation; all organs immature; most vulnerable Peds patient
  • All preterms have potential for:
    • Respiratory distress,
    • apnea,
    • hypoglycemia,
    • electrolyte disturbances (▼Mg++, Ca++) i
    • infection,
    • hyperbilirubinemia,
    • polycythemia,
    • thrombocytopenia
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8
Q

What is normal gestation?

Postmature?

A
  • Normal gestation: 37-42 weeks
    • All gestational ages have risk for →
      • congenital anomalies,
      • viral infection,
      • perinatal depression,
      • fetal alcohol syndrome
  • Postmature > 42 weeks
  • Risks:
  1. irth trauma if large for gestational age (LGA)
  2. hypoglycemia (esp. if mom diabetic)
  3. meconium aspiration
  4. hyperbilirubinemia
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9
Q

What should you always evaluate about perinatal history?

A

Always evaluate perinatal history:

  • gestational age & size at birth;
  • maternal infections,
  • eclampsia,
  • diabetes, or drug abuse;
  • prolonged or traumatic labor;
  • NICU/ intubation following delivery
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10
Q

Major key points to fetal circulation?

What is pre-ductal, post-ductal?

Where is the most oxygenated blood delivered?

A
  • (high o2 blood) Placenta → Umbilical vein (high pressure if contraction occurring)→ ductus venosus (DV) *high intrahepatic pressure* → most blood gets shunted away from liver → IVC (most blood)→ RA….
  • PREDUCTAL Circulation (Parallel circulation): IVC→ RA (high rate of flow) → Foramen Ovale (FO)→ LA (high O2 []) → LV → aorta
    • HIGH O2 blood to head, neck, and RUE drained into SVC = then MIXED (high O2-RA→ FO→ LA→ LV)
      • Less oxygenated than blood that went straight to head, neck, arms
  • Postductal Circulation: If stayed in RA → RV → pulmonary artery *high pulm resistance* (only 12% [10-15%] blood goes to lungs) → ductus arteriosus (DA) (~85% blood from RV) → aorta → goes systemic circulation (MIXED BLOOD)
    • Ductus arteriosus- keeps lungs from being overloaded by blood

OVERALL:

  • Pre-ductal: More oxygenated blood going to head, neck, RUE
    • From IVC RA LALVAorta head, neck, RUE SVC
  • Post-ductal: More deoxygenated blood going to system circulation from DA!
    • Liver, kidney, lower extremities
  • High pulmonary vascular resistance and low systemic circulatory resistance
  • Minimal intrauterine pulmonary blood flow: only ~10% of the cardiac output
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11
Q

What CV changes occur at birth to transition from fetal to adult circulation, and why do these changes occur?

A

Changes that allow parallel circulation of the fetus to convert to the series circulation of the adult:

  1. Pulmonary Vascular Resistance DECREASES
    1. 1st breath → expansion of lung → pulm vascular resistance DROPS → increased alveolar O2 → increase in pH
    2. neurohumoral mediators and nitric oxide (NO) relaxes pulmonary vasoconstriction.
  2. FO closes
    1. When placenta separates from uterine wall:
      1. placental BV constrict
      2. SVR & left ventricular afterload increase.
        1. Decrease PVR + increase SVR → increases left atrial pressure above right atrial pressure
          1. Pressure: LA > RA → functionally closes FO “flap valve”
            1. FO not close anatomically for months to years (if ever)
            2. Patent in ~15% adults.
  3. Ductus Arteriosus closes
    1. decrease PVR causes flow through the ductus arteriosus to reverse.
      1. This exposes the ductus to oxygenated systemic arterial blood + rapid decrease prostaglandin E 2 (PGE2) after birth → closes ductus arteriosus
      2. Anatomic closure of the ductus requires several weeks.
    2. D/t Increase PaO2 exposure >60 mm Hg → cause vasoconstriction → functional closure of ductus arteriosus
  4. Ductus Venosus Closes
    1. The ductus venosus closes passively with removal of the placental circulation and readjustment of portal pressure relative to inferior vena cava pressure.
  5. There is a further gradual decline in PVR secondary to structural remodeling of the muscular layer of the pulmonary blood vessels. During fetal life, the central pulmonary vascular bed has a relatively thick muscle layer.
    1. After birth, the muscle coat thins and extends to the periphery of the lung, a process that takes months to years to complete
    2. Expansion of the lungs at birth decreases pulmonary vascular resistance, and the entire right ventricular output is diverted to the lungs

**Overall: Increase SVR + decrease PVR → functional closure of PFO & ductus arteriosus (blood not being oxygenated by lung is NOW going through lungs to be oxygenated) **

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12
Q

What happens to fetal ciruclation of adeuqate ventilation/oxygenation are not established at delivery?

A
  • Fetal circulatory pattern persists
    • increased PVR
    • decreased pulm blood flow
    • Ductus arteriosus & FO remain OPEN
      1. Result: Large R → L intracardiac shunt of desaturated blood to periphery
        • Consequences:
          • Arterial hypoxemia
          • Acidosis
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13
Q

What might cause an infant to have persistent fetal ciruclation in the early weeks of life?

A
  • Period of vulnerability:
    • Hypoxia (acidosis)
    • Hypercapnia (acidosis)
    • Hypothermia
    • Infection
    • Prematurity
  • Preterm infants: ductus arteriosus may remain open for several weeks & can cause hemodynamic instability
    1. tx: prostaglandin inhibitor (indomethacin)
    2. surgical ligation
      • ex: if see sudden hypoxia < 10 days old → suspect flip flow circulation occurring
        • tx: hyperventilate & hyperoxygenate – difficult to correct
  • Phenomenon leads to sudden increases in pulmonary artery pressure and shunting of blood past the lungs through a patent foramen ovale or the ductus arteriosus, which may reopen, particularly during the first 10 days of life
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14
Q

What are the components that make up APGAR scoring? What is the significance of APGAR socring?

A

APGAR scoring:

  • five signs measured/observed in neonates 1 minute & 5 minutes after delivery
    • PREDICTIVE on neonatal distress and need for intervention
    • Components:
      • Most important:
        • heart rate
          • HR < 100 bpm: signifies arterial hypoxemia
        • quality of respiratory effort
      • Least informative:
        • color –
          • healthy neonates have acrocyanosis @ 1 min from cold ambient temps (peripheral vasoconstriction)
          • Persistent cyanosis- acidosis and pulm vasoconstriction most likely causes
  • Scores 3–7: Mild to moderately depressed function
    • may respond to oxygen administration by face mask
    • with or without positive pressure ventilation
  • Score < 3: CONCERN
    • consult NRP algorithm

Score 0-10

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15
Q

What are some essentials to the newborn resuscitation program (NRP)

A

Initial actions for newborn in distress:

  • Clear infant airway
  • Warm/dry them
  • Stimulate
  • Position- sniffing
  • Evaluate: HR, respirations, color
    • Ex: labored breathing and persistent cyanosis- suction
    • HR < 100 bpm- assist w/ PPV
    • HR < 60: intubate, PPV, chest compressions
      • O2 & chest compressions not effective → IV Epi
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16
Q

When taking care of a neonatal patient, what are some questions to ask preoperatively?

A
  • Birth history:
    • Mom received prenatal care? Maternal infections? Gestational diabetes or chronic health disease? Maternal substance abuse?
  • How many weeks gestation? Birth weight? Birth complications? Birth trauma?
  • Admitted to newborn intensive care unit? Length of stay?
  • Any episodes of apnea or tachypnea?
  • Need for oxygen? Need for ventilation? For how long? Discharged to home on a ventilator/on oxygen?
  • Infant discharged home on any medications?
  • Assess for passage of meconium & urination
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17
Q

Essential assessment of the newborn/neonate?

A
  • Accurate weight critical
    • Unclothed/undiapered
  • Essentials:
    • Assessment of overall appearance
    • skin color
    • breathing pattern
    • degree of alertness
  • Color: assess mucous membranes
    • acrocyanosis: cool and cyanotic hands and feet
      1. normal finding in healthy infants
      2. d/t immature peripheral vasomotor tone
    • central cyanosis: needs investigation
      1. not normal
    • jaundice- hyperbilirubinemia
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18
Q

Airway assessment in newborn

A
  • assess mucous membranes;
  • look at tongue size/ mobility- look at frenulum of tongue (impact feeding);
    • a short tight lingual fenulum attached to inferior tip of tongue may impede movement of tongue and breastfeeding
  • evaluate chin (retrognathia?- diff intubate);
  • nasal patency/ discharge;
  • intact hard and soft palate?;
  • presence of natal teeth (< 1 mo old- fall out easily)?
    • teeth that erupt in first month of life, typically central incisors
    • similar to normal teeth but lack developed root system and may fall out
    • no indication for removal unless concern for aspiration or interference with feeding
  • unrestricted neck movement
    • congenital torticollis- means that a baby is born with an odd position of the neck. The odd position is because of a tight, short neck muscle
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19
Q

Heart and lung assessment in newborn/neonate?

A
  • assess for tachypnea, flaring grunting, retractions
    • respirations may be “regularly irregular” with pauses (pauses should not last >20 seconds)
    • Periodic breathing: more common in infants, particularly preterm infants; probably due to inadequate development of the medullary respiratory centers
      • Assess length of pause
  • assess clavicles
    • Clavicular fractures are a common birth injury occurring in 0.2%–3.5% of births. Usually left untreated
  • assess upper & lower extremity pulses
    1. risk of CHD- impact perfusion to extremities
  • Murmurs common in newborns
    1. Systolic murmur- not as concerning
    2. Diastolic murmur – concerning!!
      • PDA: murmur best heard along the left lower sternal border
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20
Q

Neuro and musculoskeletal assessment in newborn/neonate

A
  • Neuro assessment:
    • Posture,
    • muscle tone,
    • movement,
    • seizure activity;
    • head control,
    • quality of cry;
    • response to light and sound;
    • fontanelles (Anterior and posterior)
    • Back: Spinal contour; presence of cysts, sinuses, dimples, tufts of hair
  • ·Musculoskeletal:
    • Normal: Inward flexion resting position of upper and lower extremities
    • Abnormal: rigidity or extension
      *
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21
Q

Relevant labs for newborn?

A

o point-of-care glucose testing

o complete blood count or hematocrit

o blood type

o Coombs

o bilirubin

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22
Q

Blood and fluid requirement for newborn/neonate?

A
  • Amount of insensible water losses are inversely proportional to gestational age
    • Ex: younger pt → more insensible loses we have to account for
      • Reasons:
        1. higher skin permeability
        2. higher ratio of body surface area to weight
        3. higher metabolic demand
          • radiant warmers and phototherapy increase insensible losses** = more volume deficit!
  • Neonatal kidneys are unable to excrete large amounts of excess water or electrolytes
    • newborn daily fluid requirement: 70ml/kg/day
      1. gradually increases throughout 1st wk
    • generally started w/ 10% glucose to prevent hypoglycemia for 1st wks of life (if going to surgery)
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23
Q

Considerations for fluid and blood requirement?

A
  • Hct < 30% → risk of apnea higher (neonates and preterm infants)
    • Optimize Hct to decrease postop apnea
  • Crossmatching not always needed
    • Weak expression of ABO antigens at birth
  • Transfused blood has higher levels of hemoglobin A → (better release of oxygen to tissues)
    • Better release of O2 than FetalHgb provides
  • Transfusion associated graft-versus-host risk:
    • **Use leukoreduced, irradiated blood is preferred (radiation destroys lymphocytes)
  • Ionized hypocalcemia risk (esp w/ FFP administration in neonates- see in any blood products)
    1. decreased ability to mobilize calcium and metabolize citrate → depresses CV function
    2. monitor ionized calcium and prepare to replace
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24
Q

Considerations for venous access in newborn?

A

Peripheral access: can often be obtained once resuscitated

  • Common sites: dorsum of the hand, antecubital fossa, dorsum of foot, and scalp (very common in neonates/ small infants)
    • Venous cutdown may be needed in difficult access (common site is saphenous)
      1. cutdowns are avoided (try ultrasound first)

Central lines: common sites are internal jugular, subclavian, or femoral line

  • PICC lines placed in the axillary vein have low rates of complications
    • IO access is preferred in urgent situations as central venous access can be time consuming

Umbilical vein: may be used in newborn for vascular access

  • A small amount of the cord is cut and then umbilical tape is applied to stop the bleeding
    1. one large, thin-walled umbilical vein and two smaller, thick-walled arteries can be seen and are catheterized with sterile technique
  • Complications: Infection, bleeding, hemorrhage, perforation of vessel, thrombosis with distal embolization, ischemia or infarction of lower extremities, bowel, or kidney, arrhythmia if catheter is in the heart, air embolus
  • Contraindications umbilical vein:
    1. omphalocele
    2. gastroschisis
    3. peritonitis
  • Considerations umbilical vein use:
    1. May be patent up to 2 wks after birth- can be used in an emergency
    2. Potential for accidental placement in portal vein- xray required
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25
Q

Consideraiton with umbilical artery catherization?

A
  • Umbilical artery cannulation is common in neonates
    • Ability to obtain arterial blood and continuously measure arterial BP.
    • Tip of catheter location:
      1. at or just above level of aortic bifurcation
      2. below the level of renal arteries (L2) (would cause hypoperf of renal arteries)
  • When stable → peripheral a-line inserted and umbilical artery catheter should be removed
    • Considerations:
      • All arterial catheters have the potential to cause distal thromboembolic disease
      • Flush gently to prevent cerebral or cardiac emboli
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26
Q

How do you monitor pre/post ductal ABG in neonate?

What would yous see if ductus arteriosus shunting or foramen ovale shunting are present?

A
  • Differences in A-Lines:
    • Preductal ABG- RIGHT radial arterial catheter
    • Postductal ABG: umbilical artery
      • Ex: for pt w/ PDA and pulm HTN
        • Pulmonary hypertension: Preductal and postductal oxygenation should be measured to assess right-to-left shunting
  • ABG Gas:
    • Ductus ateriosus shunting suggested if:
      • Preductal PaO2 15-20 mm Hg > postductal PaO2
    • Foramen Ovale shunting:
      • Decreased predicted value of preductal PaO2
      • will not produce a gradient compared w/ post ductal PaO2
  • Preductal arterial oxygen saturation (SaO2 ) reflects cerebral oxygenation
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27
Q

Pharmacokinetic difference in newborn/neonate?

A
  • Larger volume of distribution: increased dose for water soluble meds
    • Ex: AntiX and Succs
  • Decreased protein binding: increased free fraction of primarily protein bound drugs
    • Ex: More drug available to exert effects
  • Decreased body fat percentage: higher levels of drugs that are primarily redistributed to muscle and fat
    • Less redistribution that takes place
  • Immature renal and hepatic function
28
Q

Pharm reminders and “pearls?

Versed and opioid use?

Propfool?

Morphine?

remi?

NDNMB? Vec? Cis?

NMB Reversal?

Lidocaine

A
  • Versed and opioids combined in neonates can lead to severe hypotension- titrate carefully
  • Propofol: variability in elimination in neonates and preterm infants
    • may see longer elimination times
  • Morphine clearance directly correlated with gestational age
    • r/t immaturity of kidneys
    • → reduce frequency of admission
  • Remifentanyl has similar PK to older children making it a reliable choice for an intraoperative opioid
    • Independent of liver/kidneys
  • Sch dose increased
    • DOSE: 3 mg/kg
    • Pretreatment: w/ atropine
  • NDNMB:
    • have significant variability and unpredictability in this population- titrate carefully
    • Will always need reversal in neonates**
  • Vecuronium: considered a “long acting” NDNMB in infants <1 yo due to liver immaturity
  • Cisatracurium produces reliable recovery due to Hoffman elimination
    • TEMP & PH MUST BE NORMAL
    • laudanosine → can decrease seizure threshold
  • Lidocaine has a longer half life and volume of distribution in the neonate
29
Q

What are some urgent problems at time of birth?

A
  • meconium aspiration
  • choanal stenosis and atresia
  • diaphragmatic hernia
  • hypovolemia
  • hypoglycemia
  • tracheoesophageal fistula (TEF)
  • laryngeal anomalies

all of these require immediate attention!

30
Q

What is retinopathy of prematurity?

A
  • Can lead to blindness if left uncorrected
    • incidence inversely proportional to gestational age (increase w/ more prematurity)
  • Exact cause is unknown
    • Ass. w/ prematurity, low birth weight, supplemental oxygen therapy, postnatal hypotension, use of surfactant or inotrope, and need for mechanical ventilation
    • Pathogenesis of Supplemental O2 therapy:
  • initiated by oxygen-induced retinal vasoconstriction and endothelial cell death → followed by unchecked neovascularization from angiogenic factors (VEGF) that do not respond to normal regulation because of immaturity
  • Tx: cryotherapy, laser photocoagulation, scleral buckling surgery, and/or vitrectomy
  • Considerations:
    • Hyperoxia should be avoided if at all possible
    • suggested SpO2 target range of 91% to 95%
31
Q

What is a subgaleal hemorrhage?

A
  • Occurs in 1.5 to 30 per 10,000 births
  • Patho:
    • Venous bleeding between aponeurosis and periosteum (large hematoma over cranial surface not restricted by suture line )
    • Can increase considerably in size over 1st hrs to days of life
  • S/s:
    • large boggy, shifting collection of fluid over the cranial surface
      • unrestricted by the suture lines
    • may extend to neck and behind ears (lifting the ears forward)
  • Consequences:
    • Hypovolemia (d/t bleeding into large Subaponeurotic space) bleeding
    • Hyperbilirubinemia after RBC breakdown occurs
    • May remain asymptomatic & be observed for 24-48 hours
32
Q

What is meconium?

Pathophys and consequences of meconium aspiration?

A
  • Meconium: the breakdown product of swallowed amniotic fluid, gastrointestinal cells, and secretions
    • Usually present after 34 weeks’ gestation

Patho:

  • Fetal distress (ex: intrauterine arterial hypoxemia) @ > 34 weeks→ can cause increased gut motility & defecation
  • Fetal distress also causes gasping → inhale amniotic fluid → debris into the lungs
    • Birth w/in 24 hours of aspiration: meconium in major airways and is distributed throughout lungs with onset of spontaneous breathing
      1. Delivery delayed >24 hours? meconium is broken down and excreted from the lungs

Consequences:

  • Obstruction of small airways → ventilation/perfusion mismatching
  • RR >100 breaths per minute
  • Decreased Lung compliance (levels seen in infants w/ resp distress syndrome)
  • Pneumothorax risk
  • Severe cases:
    • pulmonary hypertension + R-to-L shunting through PFO and DA (persistent fetal circulation) →
      • **hypoxemia
33
Q

What was historic txmt of meconium aspiraiton?

Current treatment/recommendations?

A
  • Historic tx: ETT immediately after delivery with suctioning of meconium from newborn’s airways
  • Roughly 10% of newborns have meconium staining- routinely intubating all leads to complications of advanced airway in many who do not need it.
  • Currently tx: more conservative
    • NRP guidelines updated (2010): do NOT recommend routine oropharyngeal/nasopharyngeal suctioning with either clear or meconium-stained amniotic fluid
  • Endotracheal suctioning IS indicated for nonvigorous meconium-stained newborns
    • Recommendation: meconium present →
      • Tx:
        • 1st: orally suction
          • vigorous & crying- no further action.
        • If still depressed:
          • intubate & suction
            • If vigorous → pull the tube and reintubate (don’t want merconium in tube)
            • If not → keep tube → move to PPV.

Recommendation: meconium present- 1st orally suction, if vigorous and crying- no further action. If still depressed then intubate and suction- if then vigorous, pull the tube and reintubate. If not- keep tube and move to PPV.

34
Q

What is respiratory distress syndrome in neonate/newbown?

A
  • Primary Cause: Lack of surfactant
    • decreased number of branching airways and alveoli
    • atelectasis
    • impaired gas exchange
    • hypoxemia
    • poor lung compliance & propensity for alveolar collapse
  • Incidence inversely proportional to gestational age & birth weight (< 36 wks → more likely to have RDS b/c less surfactant in alveoli)
  • S/S:
    • Tachypnea
    • Tachycardia
    • Cyanosis
    • Grunting
    • Retractions
    • flaring
      *
35
Q

What is the treatment and long-term effects of respiratory distress syndrome?

A
  • Tx: surfactant (delivered via ETT)
    • Anesthesia: Limit hypoxemia while avoiding hyperoxia
      • follow ABG’s
  • Consequences:
    • Long term: bronchopulmonary dysplasia
  • Surfactant initially appears at 23 to 24 weeks and increases in concentration during the last 10 weeks.
  • Surfactant is released into the alveoli at about 36 weeks’ gestation, thus making normal extrauterine life possible.
36
Q

What is bronchopulmonary dysplasi?

Symptoms? Treatment

A
  • Chronic lung disease of infancy
    • Occurrence: d/t trauma of mech ventilation on immature lung (major cause)
      • ·born premature
      • extensive mechanical ventilation
      • high FiO2 during mech vent
      • The lungs are hyperinflated
  • S/s: intercostal retractions
    • nasal flaring
    • wheezing
    • hypercapnia
    • hypoxia
  • Tx: supportive care
    • Adequate caloric intake
    • Respiratory support (mechanical ventilation, CPAP) PRN
    • diuretics
    • bronchodilators PRN
37
Q

What is laryngomalacia and bronchomalacia?

What are vascular rings?

A
  • Congenital or acquired
  • Excessive flaccidity of laryngeal structures
    • → prone to airway collapse
  • Laryngomalacia:
    • often congenital (>85%)
    • Laryngeal anomalies at birth: stridor present
  • Bronchomalacia
    • likely sequelae of prolonged NICU admission – intubated
  • ·Vascular rings:
    • anomalies of the aorta that may compress the trachea → produces both inspiratory and expiratory obstruction.
    • May be difficult to advance ETT beyond obstruction produced by vascular rings** (ventilate but cant intubate probs)
38
Q

What is choanal atresia?

s/s?

A
  • Abnormal embryogenesis (formation) of neuroectodermal cell linen → obstructing nasal passage
    • functional atresia may also occur resulting from obstruction (blood, mucus, or meconium)
      • ~90%: bony
      • 10% : membranous

Considerations:

  • Nasal obstruction should be suspected when good breathing efforts but in whom air entry is absent
    • Recall- infants are obligate nasal breathers
  1. 40% of term infants can convert to oral breathing if nasal airway is obstructed (60% cant)
  2. 5 mo- Almost all infants can easily convert to oral breathing

*

39
Q

s/s and treatment of choanal atresia?

A

s/s:

  • cyanosis (develops if these infants are forced to breathe with their mouths closed)
  • Respiratory distress at birth
    • worsen w/ feeding
  • Improve w/ crying (bc breathing out mouth)
  • Airway obstruction
  • stridor
    • paradoxical cyanosis (normally, newborns turn pink when crying as they begin to breathe through their open mouth).
  • 1/2 of children with choanal atresia have other congenital issues – also look for ear defomiries. can be s/s of other congenital syndromes
    • CHARGE association:
      • Coloboma- eye deformity
      • heart disease
      • atresia [choanal]
      • retarded growth
      • genital abnormalities
      • ear deformity
  • Unilateral atresia: rarely a surgical emergency,
    • often intervention can be delayed.
  • Dx: Unilateral or bilateral choanal stenosis
    • based on inability to pass a small catheter through each nare
  • Tx:
    • Congenital choanal atresia requires surgical treatment during the neonatal period
      • Use of an oral airway may be necessary until surgical correction can be accomplished
    • Functional choanal atresia is treated by nasal suctioning
40
Q

When can infants easily convert to oral breathing?

A
  • 8% preterm neonate (31-32 weeks PCA) and 40% term infants can convert to oral breathing if nasal airway obstructed
  • almost all infants can convert to oral breathing by 5 months
    • most convert to oral breathing if obstruction lasts longer than 15 seconds
41
Q

What is a congenital diaphragmatic hernia?

Location? Consequences? s/s

A
  • 1 in 3000-5000 births
  • Herniation of abdominal viscera through a defect in diaphragm
    • Locations of Herniations:
      1. Foramen of Bochdalek (on the left side): most common site
      2. Anterior foramen of Morgagni herniation: occurs in only 2%.
  • Consequences: Lungs are underdeveloped d/t compression in utero
    • Alveolar & Vascular hypoplasia
  • S/S:
    • Severe respiratory distress at birth
    • Cyanosis
    • scaphoid abdomen (collapsed abdomen)
    • Chest x-ray: abdominal contents in thorax
    • Associated anomalies (40%-50% pts)
      1. CNS- meningomyelocele
      2. CHD- most common
42
Q

Initial treatment for congenital diaphragmatic hernia in deliveyr room?

A
  • Initial treatment in delivery room:
    • avoid aggressive mask ventilation
    • urgent intubation
    • decompress stomach
    • maintenance of PaCO2 <40
    • optimal oxygenation
  • Problems: must avoid iatrogenic volutrauma (over ventilating)!!!
    • High risk pneumothorax on the side opposite the hernia if attempts are made to expand the ipsilateral lung
    • Hypoxemia secondary to pulmonary hypoplasia & pulmonary hypertension
    • Hypotension d/t overdistention of stomach & mechanical kinking of great vessels
43
Q

Treatment and management of congenital diaphragmatic hernia

A
  • Tx:
    • Supportive care rather than immediate surgery after birth: ECMO, HFOV, & nitric oxide (manage PHTN)
  • Management:
    • awake intubation without positive pressure ventilation
    • adequate IV access
    • a-line
    • opioids
    • muscle relaxation
    • maintain optimal oxygenation (PaO2 >100)
    • ventilation
    • avoid nitrous oxide (d/t bowel distention)
      • anticipate ICU postop
44
Q

What is apnea of prematurity? treatmnt?

A
  • Inversely proportional to gestational age
  • Immaturity of the respiratory control centers of the brainstem → decreased sensitivity to elevations in CO2
  • Both central apnea & obstructive apnea
    • Dx:
      • apneic periods >15-20 seconds
      • apnea with HR < 80-100
      • apnea with desaturation
  • Tx:
    • Methylxanthines- primary tx
    • Others:
      • aminophylline
      • caffeine
45
Q

Pathology behind neontal hypoglycemia?

A
  • The most common problem in newborns & young infants
  • Patho:
    • Early in gestation, the fetal liver begins to store glycogen while a continuous supply of glucose is delivered by transplacental transfer from the mother.
    • In the third trimester, glycogen stores begin to develop in fetal skeletal and cardiac muscle, as well as in the kidneys, intestines, and brain. (but still immature)
      • Birth → neonatal glucose concentrations decrease rapidly to 30 mg/dL w/in 1st 1-2 hrs
        • → stimulates glycogenolysis & gluconeogenesis
        • → glucose flux usually stabilizes at values > 45 mg/dL by 12 hours post birth
46
Q

S/S or neonatal hypoglycemia

Highest risk for neonatal hypoglycemia?

A
  • S/s:
    • Hypotension
    • Tremors
    • Seizures
      • can be masked by anesthesia
      • Other sx: respiratory distress, apnea, cyanosis, high-pitched cry, irritability, limpness, lethargy, eye-rolling, poor feeding, temperature instability, and sweating
  • Highest risk: Infants with intrauterine growth restriction; diabetic mothers; severe intrauterine fetal distress
    • Premature infants:
      • prone to hypoglycemia owing to immature glucoregulatory mechanisms,
      • reduced levels of glycogen storage,
      • increased energy demands,
      • limited adipose stores (reduced free fatty acids and ketones available as alternative sources of energy)
    • Also at risk: Full-term infants who have been excessively fasted, small-for-gestational-age (SGA) infants, and infants of diabetic mothers
47
Q

What is hypoglycemia defined as in the full term and preterm infants?

Prevention of hypoglycemia?

A
  • Full term neonates:
    1. < 40 mg/dL glucose [] during 1st 24 hours after birth
    2. < 60 mg/dL at 36 hours
  • Premature infants:
    1. < 45 mg/dL at 1st 24 hrs
    2. < 50 mg/dL > 24 hrs after birth
  • Prevention:
    • 1st 48 hours MIVF:
      • contains 10% glucose in 0.2% saline with 20 mmol/L K
    • > 48 hours:
      • 5% glucose supplementation is usually okay
      • preterm infants will have increased requirement
48
Q

Treatment for hypoglycemia?

A
  • Acute dose: bolus 0.25 - 0.5 g/kg (1–2 mL/kg of D25 W or 2.5–5 mL/kg of D10 W)
    1. → then increase glucose in MIVF (to prevent stimulation of insulin production)
      • A single bolus of glucose without subsequent infusion can stimulate insulin production with consequent return to the hypoglycemic state
  • All other fluids (e.g., to replace third-space losses, blood loss, and fluid deficits) should be glucose-free to avoid hyperglycemia
  • Check blood sugar frequently
  • TPN- do not stop suddenly without bridging with a glucose containing fluid
49
Q

What are the 3 main forms of calicum in the body?

what causes hypocalcemia in neonates?

s/s

A
  • 3 forms of Ca in body:
      1. Protein bound
      1. Chelated to bicarb, phos, and citrate
      1. Free or Ionized- physiologically active component
        * Not always clear relationship b/t total serum Ca and iCa (correlation is poor with hypoalbuminemia or acid-base disturbances, as seen in premature and critically ill neonates)
  • Hypocalcemia:
    • iCa: < 1 mmol (in both premature and neonate pop)
    • Hypocalcemia is defined as a total serum calcium concentration less than 8 mg/dL (2 mmol/L) in full-term infants and less than 7 mg/dL (1.75 mmol/L) in premature infants. An iCa 2+ less than 4 mg/dL (1 mmol/L) defines hypocalcemia in both populations.
  • At birth → abrupt loss of maternal calcium
    • by 3rd day of life, serum calcium concentrations in the full-term neonate to return to normal
      • Infants who are born prematurely do not benefit from the transfer of maternal calcium
  • Hypocalcemia present in nearly 40% of critically ill neonates
    • Causes: PTH insufficiency, inadequate calcium supplementation, and altered calcium metabolism caused by transfusion with citrated blood products, bicarbonate administration, or diuretics (e.g., furosemide)
  • Hypocalcemia s/s:
    • asymptomatic or…
    • nonspecific symptoms such as neuromuscular irritability (myoclonic jerks, exaggerated startle, or seizures), tachycardia, prolonged QT interval, and decreased cardiac contractility
50
Q

Treatment of symptomatic hypocalcemia in neonate?

A
  • Tx:
    • Slow IV infusion over 5-10 min w/ → (2 txs)
      • 1. 90 mg/kg calcium gluconate
        • May be given IV but is vesicant!! (tissue necrosis and subcutaneous calcification deposits with extravasation)
      • 2. 30 mg/kg calcium chloride
        • Infused through central line**
      • Monitor for bradycardia!!! (seen with rapid increases in the serum concentration of calcium)
  • Consider need for Magnesium supplementation as well
51
Q

What do newbornws with CHD present with?

A
  • Newborns with significant congenital heart disease commonly have either cyanosis or CHF
    • Present as CHF: See in →
      1. VSD
      2. PDA
      3. Critical aortic stenosis
      4. Coarctation of the aorta
    • Present as cyanotic: See in →
      1. Tetralogy of Fallot
      2. Transposition of the great arteries
      3. Hypoplastic left heart syndrome
52
Q

S/S of CHF in newborn?

Treatment CHD?

When might ductus arteriosus be maintained open?

A
  • Newborn s/s of CHF:
    • poor feeding, irritability, sweating, tachycardia, tachypnea, decreased peripheral pulses, poor cutaneous perfusion, and hepatomegaly (swollen liver)
    • pulmonary edema may present as tachypnea without retractions
  • Initial tx of CHD → aimed at relieving CHF:
    • improving systemic perfusion
    • improving/maintaining pulmonary BF
  • Ductus arteriosus must be maintained open in:
    • hypoplastic left heart syndrome
    • aortic stenosis or atresia
    • interrupted aortic arch
    • symptomatic neonatal coarctation of the aorta
    • tx: prostaglandin E 1(PGE) sustains life until surgical palliation is performed

Overall: Assess for murmurs, and habits (poor feeding) that alert you to CHD

Understand present w/ cyanosis or CHF

53
Q

What is a meningomyelocele?

Anesthesia considerations?

Treatment?

A
  • Hernial protrusion of a part of the meninges and spinal cord through a defect in the vertebral column
    • To protect the defect, it is placed on a “doughnut” and towels are placed under the head
  • Anesthesia:
    • Plan for positioning for intubation to protect defect
    • Anticipate larger insensible losses – membranous sac
    • High possibility of hydrocephalus
    • Possibility of cranial nerve (vocal cord) palsy leading to respiratory distress/ stridor
    • Potential for brainstem herniation
    • Higher incidence of latex allergy:
      1. always use latex precautions
  • Meningomyelocele usually have an Arnold-Chiari malformation and may have stridor from vocal cord paralysis
    • caudal displacement of the medulla
    • treatment:
      1. relief of the hydrocephalus
      2. possible cervical decompression of the herniation
      3. tracheotomy and long-term mechanical ventilation may be required (if VC paralysis)
54
Q

What is esophageal atresia or TEF? when to suspect it

s/s?

dx test?

what other anomalies might be present?

anesthesia consideraitons?

A
  • The inability to swallow amniotic fluid in utero results in polyhydramnios
  • Five plus different configurations
    • esophageal communication with trachea causes aspiration pneumonitis
  • Suspect in polyhydramnios
  • Esophageal atresia: the esophagus ends in a blind pouch
  • s/s: Copious amounts of oropharyngeal secretions are usually present
  • Diagnostic test: inability to pass a suction catheter into the stomach
  • Suspect other anomalies:
    • VATER association ( V , vertebral; A , anal; TE , tracheoesophageal; R , renal) or
    • VACTERL association (VATER and C , cardiac; and L , limb).
  • Echocardiogram advised before anesthesia

Prematurity and polyhydramnios are associated with TEF. The inability to swallow amniotic fluid in utero results in polyhydramnios

55
Q

What are the types of tracheoesophageal fistulas?

A
  • Classification by Gross
  • Type C is the most common (~ 85% of TEFs)

A—Esophageal atresia without fistula

B—Esophageal atresia with communication of the upper esophageal segment to the trachea

C—Esophageal atresia with communication of the lower esophageal segment to the trachea

D—Esophageal atresia with both upper and lower esophageal segments communicating with the trachea

E—No esophageal atresia but TEF

F—Esophageal stenosis without fistula

56
Q

Anesthesia managment of esophageal atresia?

A
  • Anticipate presence of aspiration pneumonia
    • may have to receive treatment before stable for surgery
    • g-tube may be placed for nutrition
  • Airway management:
    • withhold feedings
    • place soft suction in esophagus to drain saliva
    • position prone in a head-up position
      • Plan:
        1. awake intubation with sedation (fentanyl/ versed/ topicalization)
        2. Intentional right mainstem then back out to Bil BS → hope is that ETT is past fistula
    • ETT placement is CRITICAL- it is possible to ventilate one lung, both lungs, and/or the fistula depending on tube placement with 1-2 mm movement
      • Ventilation:
        1. spontaneous assisted ventilation → best to avoid stomach over distention until the fistula is ligated or g-tube placed
    • SpO2 placement should be pre-ductal and post-ductal
    • Consider left precordial stethoscope (under left axilla)
      • continuously monitor for endobronchial intubation
    • May require postoperative ventilation but may trial extubation depending in surgeon preference
    • Postoperative pain may be managed with a caudal catheter

Miller suggestion: 0.5 to 1 μg/kg of fentanyl and 25 to 50 μg/kg of midazolam and topicalizes the tongue, larynx, and vocal cords with no more than 5 mg/kg of lidocaine (1.0%)

Stomach can rupture if large volumes of air are being instilled with positive pressure ventilation

57
Q

What is an omphalocele? Gastrochisis?

complications?

A
  • Major defects in the closure of the abdominal wall that result in exposure of viscera
    • omphalocele: covered by peritoneum
      • typically ass. w/ anomalies (very sick)
      • W/in umbilical cord
    • gastroschisis: not covered by peritoneum
      • not ass. w/ anomalies
      • periumbilical
  • Complications:
    • severe dehydration and massive fluid loss from the exposed visceral surfaces
    • heat loss
    • complex surgical closure
  • High association with prematurity and other congenital defects
    • cardiac abnormalities common (omphalocele ∼20%)
58
Q

Management of omphalocele/gastroschisis?

A
  • ECHO before anesthesia
  • Anticipate need for postop ventilation
  • May be a staged repair
    1. Early repair: reduces the potential for infection and compromise of bowel function; minimizes fluid & heat loss
  • Must optimize fluid and electrolyte balance before surgery
  • Obtain good IV access
    1. anticipate need for TPN postop- central line placement
  • Expect invasive monitoring if associated cardiac defect is present
  • Expect liberal use of muscle relaxants for closure of the defect
  • Anticipate hypotension secondary to tension on a major organ (liver) or caval compression (tight space fitting everything)
  • Increased abdominal pressure after a tight closure
    1. Impairs ventilation
    2. Risk of abdominal compartment syndrome → may alter hepatic/ renal function & metabolism
  • Omphalocele has association with Beckwith-Wiedemann syndrome
    • → profound hypoglycemia, hyperviscosity syndrome, congenital heart disease, and associated visceromegaly
59
Q

What is hirschprung disease?

S/S? Tx?

A
  • The absence of parasympathetic ganglion cells in the large intestine- a nonperistaltic segment in gut of variable length, a tonically contracted anorectal sphincter, and delayed passage of meconium
    • Functional obstruction occurs at the level of the affected segment
    • ~ 60% of patients will have an associated anomaly.
  • S/S:
    • consistent with bowel obstruction
      • bilious vomiting
      • abdominal distention
  • Left untreated it can lead to toxic megacolon
  • Tx:
    • volume replacement
    • vasopressor support
  • Surgical repair
    • varies: anorectal myomectomy, mucosal resections, diverting colostomies, and transanal pull-throughs
60
Q

Lower GI obstruction in neonate?

s/s?

mgmt?

anesthesia?

A
  • Lower GI obstruction usually develops 1-7 days after birth
    • Ex: Imperforate anus, duodenal atresia, jejunoileal atresia, intussusception, malrotation, volvulus, choledocal cyst, meconium ileus
  • S/s: Vomiting secondary to obstruction → fluid shifts
    • Increased intra-abdominal pressure can lead to respiratory compromise
  • Management:
    • Optimize pre-op:
      1. Na+ 130mEq/L
      2. UOP 1-2 ml/kg/hr
  • Anesthesia:
    • fluid and electrolyte resuscitation
    • full stomach precautions (awake intubation or RSI)
    • N2O avoided
    • adequate muscle relaxation req
    • consider remifentanil infusion if planning to extubate → indep of renal/liver for metabolism
  • Look for other congenital anomalies:
    • association w/ trisomy 21, cystic fibrosis, imperforate anus, or renal abnormalities
61
Q

What is pyloric stensosi? considerations? mgmt?

A
  • Not a surgical emergency, correct metabolic derangement before surgery
    • normally revealed in the first 3 to 6 weeks of life
    • have severe projectile vomiting
  • Considerations: ALL electrolytes/fluids SHOULD BE CORRECTED
    • full stomach
    • metabolic alkalosis with hypochloremia and hypokalemia
    • sodium deficits
    • severe dehydration
  • Management:
    • NGT BEFORE induction: suction stomach in the supine and the right and left lateral positions
    • Awake intubation or RSI w/ cricoid pressure after →
      • atropine (0.02 mg/kg)
      • propofol (3 mg/kg)
      • succinylcholine (2 mg/kg) administration
62
Q

What is NEC?

A

Necrotizing enterocolitis

  • Typically affects premature infants but may be seen in term newborns
    • Patho: immature intestine has decreased absorptive ability leading to stasis
      1. the stasis promotes bacterial proliferation and sepsis;
    • ischemia and infection can lead to intestinal necrosis and perforation
  • Medical management:
    • NPO
    • Antibiotics
    • OG tube
    • F&E
    • hemodynamic support
  • Unresponsive to medical management: Ex lap
    • Extremely ill patient
      1. RSI with cardiac stable agent (ketamine)
      2. caution with Sch if hyperkalemic from dead bowel
    • 25-50% mortality
  • Maintenance:
    1. avoid nitrous oxide
    2. very judicious with inhalational agent if unstable (use opioids as primary anesthetic) low VA
    3. Anticipate need for blood products; expect massive fluid losses
    4. Anticipate postoperative continuation of intubation and ventilation
63
Q

Use of NMB iin neonatal pt?

A
  • Neonatal (term and preterm) response to muscle relaxants varies greatly from patient to patient
    • Best practice: titrate to response
    • Dose:
      1. reduce 30%-50% trach intubation dose w/ potent inhaled agent
    • atracurium/ cisatracurium: advantage is Hoffman elimination since renal/ hepatic are immature
    • vecuronium: very prolonged duration in newborns (approaching pancuronium)
      1. good b/c no histamine
64
Q

Postop apnea in neonate?

A
  • Former preterm infants < 60 wks PGA→ greatest risk
    • (especially < 46 weeks PCA)
  • Anemia (hgb <10 gm/dL) adds to this risk
  • Incidence is inversely related to gestational age and postconceptual age at the time of surgery
  • Regional anesthesia may reduce incidence but is not improved when combined with sedation
  • Occurs with all inhaled anesthetics including desflurane and sevoflurane
    • Overall: ADMIT IF < 60 WKs
  • ALL former preterm infants younger than 60 weeks’ PCA should be evaluated for admission to monitored beds (see individual institutional policy but err on the side of caution)
  • Pauses in respiration with a combination of desaturation and bradycardia are most significant
  • Delay in postop apnea can occur (up to 12 hours after receiving anesthesia)
  • Tx: High-dose caffeine (10 mg/kg)- short half life
  • Even in full-term infants:
    • postoperative admission and apnea monitoring should be considered if younger than 1 month

majority of infants in whom postanesthesia apnea develops are younger than 46 weeks’ PCA; however, apnea occurs up to 60 weeks’ PCA

65
Q

Caudal anesthesisa in neonates?

A
  • Landmarks:
    • Coccyx
    • the two sacral cornua
    • posterior superior iliac spines
  • The sacral cornua are identified.
  • A styletted needle is introduced into the caudal space through the sacral hiatus.
  • A “pop” is felt as the sacrococcygeal ligament is accessed. After aspiration, 0.8 to 1 mL/kg of local anesthetic solution is injected.
  • Most common: 0.125% bupivacaine, 0.25% bupivacaine, or 0.2% ropivacaine. Epinephrine, 1:200,000, is added for recognition intravascular injection
  • This provides analgesia for hernia repair, circumcisions, and lower abdominal surgeries
  • Analgesia lasts 6-8 hours