neonatal emergencies Flashcards
what is the most common type of tracheo esophageal fistula (TEF)?
C (90% of cases. upper esophagus ends in blind pouch and lower esophagus communicates with distal trachea
key diagnostic indicator for TEF?
maternal polyhydraminos (because esophageal atresia prevents fetus from swallowing amniotic fluid)
sx of TEF and confirmation
unable to pass OG
sx: choking, coughing, cyanosis during PO feeding
VACTERL association
Vertebral defects
imperforated Anus
Cardiac anomalies
Tracheoesophageal fustula
Esophageal atresia
Renal Dysplasia
Limb anomalies
approx 20% of neonates with TEF have what? what should you do preop?
cardiac defect: (ASD, VSD, TOF, aortic coarctation)
get a preop echo
anesthetic management of TEF patient
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
when do type 2 pneumocytes start producing surfactant and when does production peak?
22-26 weeks: start
35-36 weeks: peak
risk factors for respiratory distress syndrome (RDS)
LBW (low birth weight)
low gestational age (GA)
barotrauma from positive pressure ventilation
O2 toxicity
endotracheal intubation
maternal DM
dx of RDS:
soon after birth. neonate is grunting , tachypnea, intercostal and subcostal retractions, nasal flaring
ABG: hypoxemia, hypercarbia, mixed acidosis
tx of RDS:
betamethasone (starts working in 18h, peaks at 48h)
describe L/S ratio and its significance
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
first line tx for neonates after delivery that have not produced enough surfactant
CPAP (may progress to mechanical ventilation)
anesthetic implications for patient with lack of surfactant
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
what congenital diaphragmatic hernia is MOST likely to occur?
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
when is congenital diaphragmatic hernia (CDH) diagnosed?
at birth. newborn will have RDS and sunken (scaphoid) abdomen
what happens to the lungs r/t CDH
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
respiratory related anesthetic management in a patient with CDH
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
explain how right to left shunting affects PVR and how to monitor it
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%
how long is surgery for CDH delayed and why
5-15 days to allow for stabilization of pulmonary, cardiac, and metabolic status
ID each anatomical structure and diaphragmatic abnormality
define gastroschisis
congenital defect where abdominal wall does not develop fully and no membrane covering (sac) to protect the viscera
what is gastroschisis highly associated with?
prematurity
most common congenital abdominal wall defects
omphalocele and gastroschisis
what is omphalocele caused by
failure of gut migration from the yolk sac to the abdomen
what is gastroschisis caused by
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
what is gastroschisis caused by
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
compare and contrast omphalocele and gastrotrichosis
anesthetic management of a patient with abdominal wall defects
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
presentation of an infant with pyloric stenosis (hypertrophy of pyloric muscle)
vomiting and losing H+ electrolytes
metabolic alkalosis (hypochloremia)
hyponatremia
hypokalemia
alkaline urine (kidneys excreting bicarbonate to try to compensate for metabolic alkalosis)
with pyloric stenosis what can you palpate
an olive shaped mass just below the xiphoid process
when does pyloric stenosis present
within the first 2-12 weeks of life
is pyloric stenosis usually associated with other congenital defects?
no
anesthetic management of a patient with pyloric stenosis
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
volume resuscitation for pyloric stenosis patient (and maintenance)
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)
late stage urine findings for pyloric stenosis
acidic due to hydrogen excretion (early stages- alkalotic)
two most important risk factors for NEC
prematurity (<32w) and LBW <1500g
where do you maintain SpO2 to decrease retinopathy of prematurity
89-94%
do this until retinal maturation is complete (up to 44w after conception)
dx of NEC
fixated internal loops, pneumostasis intestinalis (gas cysts), portal vein air, ascites, free air in abdomen
NEC affects what region of the bowel?
terminal ileum and proximal colon
is NEC a medical or surgical emergency?
medical but if perf occurs then surgical
what action (if taken too early) can cause NEC in a premature baby?
early feeding. impaired absorption by the gut leads to stasis, bacterial overgrowth, and infection
how does retinopathy of prematurity cause blindness?
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.
two phases of ROP
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
normal PaO2 in utero
20-30mmHg
normal PaO2 after delivery
55-85mmHg
risk factors for ROP
two biggest: prematurity and hyperoxia
others: mechanical ventilation, blood transfusion, IVH, sepsis, vitamin E deficiency
how to monitor SpO2 in ROP risk patient
pre ductal SpO2 preferred because it better correlates with SpO2 in retinal vessels
surgical options for late state ROP that doesn’t resolve on its own includes
cryotherapy
laser therapy
scleral buckle
vitrectomy
drugs that produce apoptosis hit which receptors
antagonize NMDA or agonize GABA
pathophysiology of kernicterus
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.
risk factors for kernicterus
prematurity
low plasma protein convention
acidosis
tx for hyperbilirubinemia
phototherapy and exchange transfusion (rare)
most likely reason for stridor in the neonate
laryngomalacia
most common neonatal medical and surgical emergenccy
NECC
conditions that help with compliance of intracranial space in newborn
open fontanelles
cranial sutures
