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neonatal emergencies Flashcards

1
Q

what is the most common type of tracheo esophageal fistula (TEF)?

A

C (90% of cases. upper esophagus ends in blind pouch and lower esophagus communicates with distal trachea

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2
Q

key diagnostic indicator for TEF?

A

maternal polyhydraminos (because esophageal atresia prevents fetus from swallowing amniotic fluid)

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3
Q

sx of TEF and confirmation

A

unable to pass OG
sx: choking, coughing, cyanosis during PO feeding

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4
Q

VACTERL association

A

Vertebral defects
imperforated Anus
Cardiac anomalies
Tracheoesophageal fustula
Esophageal atresia
Renal Dysplasia
Limb anomalies

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5
Q

approx 20% of neonates with TEF have what? what should you do preop?

A

cardiac defect: (ASD, VSD, TOF, aortic coarctation)
get a preop echo

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6
Q

anesthetic management of TEF patient

A

head up and frequent suctioning for gastric management
awake intubation or mask induction with spontaneous inhalation
gastric decompression before induction
place ETT below fistula but above carina (if placed too high, resp gas is delivered to stomach)
right lung compression during surgery is common. right mainstem intubation will cause rapid desaturation

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7
Q

when do type 2 pneumocytes start producing surfactant and when does production peak?

A

22-26 weeks: start
35-36 weeks: peak

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8
Q

risk factors for respiratory distress syndrome (RDS)

A

LBW (low birth weight)
low gestational age (GA)
barotrauma from positive pressure ventilation
O2 toxicity
endotracheal intubation
maternal DM

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9
Q

dx of RDS:

A

soon after birth. neonate is grunting , tachypnea, intercostal and subcostal retractions, nasal flaring
ABG: hypoxemia, hypercarbia, mixed acidosis

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10
Q

tx of RDS:

A

betamethasone (starts working in 18h, peaks at 48h)

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11
Q

describe L/S ratio and its significance

A

lecithin (surfactant)/sphingomyelin (surfactant precursor) ratio gives advanced warning about state of fetal lung
L/S >2 suggests adequate lung development
L/S < 2 associated with increased risk of RDS

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12
Q

first line tx for neonates after delivery that have not produced enough surfactant

A

CPAP (may progress to mechanical ventilation)

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13
Q

anesthetic implications for patient with lack of surfactant

A

pre ductal SpO2 (RUE) and post ductal SpO2 (LE) should be used. (difference in values suggests pHTN, R to L shunt, return to fetal circulation via PDA

aline- pre ductal artery for ABG’s

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14
Q

what congenital diaphragmatic hernia is MOST likely to occur?

A

D, most commonly occurs through the foramen of bochdalek (usually on the left side)
the orientation- you are in the stomach looking up, NOT the thorax looking down

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15
Q

when is congenital diaphragmatic hernia (CDH) diagnosed?

A

at birth. newborn will have RDS and sunken (scaphoid) abdomen

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16
Q

what happens to the lungs r/t CDH

A

mass effect of abdominal contents impairs lung development, leading to pulmonary hypoplasia.

could include poor pulmonary vascular development, increased pulmonary vascular resistance, impaired airway development, and airway reactivity

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17
Q

respiratory related anesthetic management in a patient with CDH

A

keep PIP <25-30cmH2O
avoid conditions that increase PVR (hypoxia, acidosis, hypothermia)
OLV may be better d/t pulmonary hypoplasia of other lung
abdominal closure may increase PIP. surgeon may create temporary ventral hernia to increase abdominal volume
pulse ox on lower extremity can warn of increased intra abdominal pressure

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18
Q

explain how right to left shunting affects PVR and how to monitor it

A

right to left shunting through the ductus arteriosus leads to hypoxemia and cyanosis where PVR further increases

pulse ox on RUE to monitor pre ductal O2 and BP
pre ductal O2 should be >90%

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19
Q

how long is surgery for CDH delayed and why

A

5-15 days to allow for stabilization of pulmonary, cardiac, and metabolic status

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20
Q

ID each anatomical structure and diaphragmatic abnormality

A
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21
Q

define gastroschisis

A

congenital defect where abdominal wall does not develop fully and no membrane covering (sac) to protect the viscera

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22
Q

what is gastroschisis highly associated with?

A

prematurity

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23
Q

most common congenital abdominal wall defects

A

omphalocele and gastroschisis

24
Q

what is omphalocele caused by

A

failure of gut migration from the yolk sac to the abdomen

25
Q

what is gastroschisis caused by

A

occlusion of omphalomesenteric artery during gestation. viscera and intestines herniate on the right of umbilicus. viscera are exposed to air following delivery that results in inflammation and edema of the bowel

25
Q

what is gastroschisis caused by

A

occlusion of omphalomesenteric artery during gestation. viscera and intestines herniate on the right of umbilicus. viscera are exposed to air following delivery that results in inflammation and edema of the bowel

26
Q

compare and contrast omphalocele and gastrotrichosis

A
27
Q

anesthetic management of a patient with abdominal wall defects

A

monitor peak airway pressures. if >25-30, may need to close in stages
closure may increase intra abdominal pressure
increased abdominal pressure decreases venous return, cardiac output, and systemic perfusion
measure SpO2 on LE to monitor for impaired venous return
NO extends the bowel, dont use
anticipate fluid/electrolyte shifts to be significant

28
Q

presentation of an infant with pyloric stenosis (hypertrophy of pyloric muscle)

A

vomiting and losing H+ electrolytes
metabolic alkalosis (hypochloremia)
hyponatremia
hypokalemia
alkaline urine (kidneys excreting bicarbonate to try to compensate for metabolic alkalosis)

29
Q

with pyloric stenosis what can you palpate

A

an olive shaped mass just below the xiphoid process

30
Q

when does pyloric stenosis present

A

within the first 2-12 weeks of life

31
Q

is pyloric stenosis usually associated with other congenital defects?

A

no

32
Q

anesthetic management of a patient with pyloric stenosis

A

its a medical NOT surgical emergency
optimize patient with fluids, lyte correction, good kidney labs
pyloromyotomy can be open or laparoscopic
anticipate full stomach- RSI
plase NGT or OGT post induction. use it to assess for air leak- which would suggest mucosal perforation
postop apnea is common, maybe due to alkalosis

33
Q

volume resuscitation for pyloric stenosis patient (and maintenance)

A

severe dehydration should be corrected with 20mL/kg of NS before* surgery
maintenance should be D5 .45% NaCl at 1.5x the calculated maintenance rate (because aldosterone will kick in and Na retention will start to occur)

34
Q

late stage urine findings for pyloric stenosis

A

acidic due to hydrogen excretion (early stages- alkalotic)

35
Q

two most important risk factors for NEC

A

prematurity (<32w) and LBW <1500g

36
Q

where do you maintain SpO2 to decrease retinopathy of prematurity

A

89-94%
do this until retinal maturation is complete (up to 44w after conception)

37
Q

dx of NEC

A

fixated internal loops, pneumostasis intestinalis (gas cysts), portal vein air, ascites, free air in abdomen

38
Q

NEC affects what region of the bowel?

A

terminal ileum and proximal colon

39
Q

is NEC a medical or surgical emergency?

A

medical but if perf occurs then surgical

40
Q

what action (if taken too early) can cause NEC in a premature baby?

A

early feeding. impaired absorption by the gut leads to stasis, bacterial overgrowth, and infection

41
Q

how does retinopathy of prematurity cause blindness?

A

immature retinal blood vessels are at increased risk for vasoconstriction and hemorrhage. dysfunctional healing creates scars. as the scars retract, they pull on the retina, causing retinal detachment and blindness.

42
Q

two phases of ROP

A

phase 1: inhibited growth of retinal vessels
phase 2: overgrowth of abnormal vessels with fibrous bands that extend to the vitreous gel which can precipitate retinal detachment

43
Q

normal PaO2 in utero

A

20-30mmHg

44
Q

normal PaO2 after delivery

A

55-85mmHg

45
Q

risk factors for ROP

A

two biggest: prematurity and hyperoxia
others: mechanical ventilation, blood transfusion, IVH, sepsis, vitamin E deficiency

46
Q

how to monitor SpO2 in ROP risk patient

A

pre ductal SpO2 preferred because it better correlates with SpO2 in retinal vessels

47
Q

surgical options for late state ROP that doesn’t resolve on its own includes

A

cryotherapy
laser therapy
scleral buckle
vitrectomy

48
Q

drugs that produce apoptosis hit which receptors

A

antagonize NMDA or agonize GABA

49
Q

pathophysiology of kernicterus

A

any condition that increases bilirubin (byproduct of RBC breakdown) can cause kernicterus (fetal encephalopathy).

glucoronyl transferase (phase 2 reaction) metabolizes bilirubin. this pathway is not mature at term which leaves newborn vulnerable for first few days of life.

50
Q

risk factors for kernicterus

A

prematurity
low plasma protein convention
acidosis

51
Q

tx for hyperbilirubinemia

A

phototherapy and exchange transfusion (rare)

52
Q

most likely reason for stridor in the neonate

A

laryngomalacia

53
Q

most common neonatal medical and surgical emergenccy

A

NECC

54
Q

conditions that help with compliance of intracranial space in newborn

A

open fontanelles
cranial sutures

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