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PEDS > Apex- neonatal emergencies > Flashcards

Apex- neonatal emergencies Flashcards

1
Q

where should ETT go?

A

C

AKA “Type C”

Upper esophagus ends in a blind pouch
Lower esophagus communicates with distal trachea
ETT should be below fistula but above the carina

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2
Q

What is the most common congenital defect of the esophagus?

A

Esophageal atresia

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3
Q

If mom has what, you should be worried about TEF?

A

Polyhydraminos - key diagnostic factor for TEF

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4
Q

How is TEF confirmed?

A

by the inability to pass a gastric tube itno the stomach

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5
Q

What % of neonatese with esophgeal atresia will have a signfificant cardaic defect?

What do they need preop?

A

20%!

think EA - potential cardiac issue (VSD/ASD/TOF/Aortic coarctation)
*ECHO

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6
Q

Anesthetic considerations for neonates with esophgeal atresia and TEF

  1. Position
  2. Induction technique
  3. Placement of tube
  4. Use of something otherwise uncommon
A
  1. head up, frequent gastric suctioning to minimizie aspiration
  2. maintain SV (PPV can cause gastric distention)
  3. Place ETT below fistula but above carina
  4. Precordial can be placed on left chest /left axillary to immediately detect a right mainstem intubation
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7
Q

T/F: most neonates with esophageal atresia also have a TEF

what is EA?

what other symptoms might be observed?

A

True

esophagus doesnt form properly

choking, coughing, and cyanosis during oral feeding

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8
Q

What is VACTERL associatied with and what does it stand for

A

It’s associated with TEF (50-70% of these patients have one of these other anomolies and should be throughoughly worked up)

Vertebral defects
Anus imperforated
Cardiac anomolies
TEF
Esophageal atresia
Renal dysplasia
Limb anomalies

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9
Q
A
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10
Q

What lecithin/sphinogomyelin ratio suggest fetal lung maturity?

A. 0.5
B. 1.0
C. 1.5
D. 2.0

A

D. 2.0

*An LS ratio < 2 suggets immature fetal lungs and may place the fetus at risk for RDS

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11
Q

Type (1 or 2) Pneumocytes begin producing sufactant at how many weeks?

Peak production @ how many weeks?

A

Type 2 pneumocytes

22-26 weeks
35-36 weeks

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12
Q

How to hasten fetal lung maturity before and after delivery (1/3)

A

Before - maternal corticosteroids
After- CPAP/vent/exogenous surfactant

*Beamethasone - onset 18hrs, peak 48

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13
Q

What can preductal and postductal o2 sat monitoring assess for (3)?

is a pre or post ductal artery preferred for arterial sampling

Where are they placed?

A

pulm htn
right to left shunt
and return of fetal circulation via the PDA

preductal

Preductal- RUE
Postductal- Lower extremity

*differences between the values suggest the above.

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14
Q

PPV in the pt with poor lung commpliace increases the risk of what?

A

PTX

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15
Q

Equation for law of la place

A

P = 2T/R

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16
Q

according to the law of la place, the tendcy of an alveolus t ocollapse is:

(directly proportional/inversely proportional) to (alveolar radius/surface tension)

A

directly proportional to surface tension (more tension, more likely to collapse)

inversely proportional to alveolar radius (smaller radius = more likely to collapse)

P = 2T/R

maybe whatever the denominator of the euqation is is what is inversely proportional
…..hmm took me long enough

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17
Q

T/F- each alveolus contains the same amount of surfactant

A

True- its the concentration that differs

-larger ones have a smaller concentration
-smaller ones have a higher concentration

as the radius changes, so does the concentration of the surfactant- keeps alveolor pressures constant, preventing smaller alvoli from collapsing iand emptyig into larger ones

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18
Q

What does surfactant do?

short and sweet

A

Equalizes surface tensions and prevents alvolar collapse

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19
Q

CDH - congenital diaphramatic hernia

CDH most commonly occurs through what?

A

D.

the foramen of Bochdalek (usually on the left)

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20
Q

So if CDHs allow the abdominal contents to enter the thoracic cavity, what can this lead to? consequences (2 main concepts)

A

can lead to pulmonary hypoplasia

  1. poor pulmonary vascular development > increased PVR > pulm HTN
  2. impaired airway development > airway reactivity
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21
Q

3 big considerations for anesthetic mangement of congenital diaphrgamatic hernia

how long should surgery be delayed and why?

A
  1. Risk of PTX in the good lung > keep PIPS < 25-30cm H20
  2. Avoid increases in PVR (hypoxia, acidosis, hypercarbia, hypothermia)
  3. Monitor pre-ductal o2 sat (RUE)

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

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22
Q

Label hernias

normal structures

A

green = parasternal hernia (morgagni)
orange = paraesophogeal hernia
purple - posterolateral nernia (Bochdalek)

blue- IVC
pink- esophagus
Red- Aorta

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23
Q

Okay so say you have a baby with a CDH and you know you want to keep PIPS < (what) to minimize barotrauma nad the risk of PTX in the good lung.

Your ETCO2 starts rising and you know you also want to avoid acidosis (anything that can increase PVR). So what do you do?

A

Allow permissive hypercarbia

-although it increases PVR, it’s the lesser of the two evils

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24
Q

If they are closing the abdomen after repair of the CDH and your PIPS start going wild, what can the surgeon do?

A

create a temporary ventral hernia to increase the abdominal volume

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25
Q

During a CDH repair, what is something that can warn you of increased abdominal pressure?

A

a pulseox on the lower extremity

26
Q

If one-lung ventilation is needed for a CDH repair, how can this be accomplished?

A

advance the ETT into the mainstem bronchus of the good lung

*There are no DLT or bronchial blockers available for neonates

27
Q

What condition is MOST cloely associated with gastroschisis?

A. Prematurity
B. Congenital heart disease
C. Beckwith-Weidemann syndrome
D. Trisomy 21

A

A. Prematurity

28
Q

what are these

what causes them?

A

Omphalocele

Gastroschisis

Omphalocele- failure of gut to migrate from the yolk sac into the abdomen
Gastroschisis- occlusion of hte omphalomesenteric artery during gestation > viscer and intestines herniate on the right of the umbilicis > exposed viscera to air > inflmmation and edema

29
Q
A
30
Q

How would it be determined if a omphalocele or gastrochisis surgery closure needs to be staged or not?

A

if PIPs > 25-30cm H20, then staging may be required

31
Q

How does increased abdominal pressure lead to decreased systemic perfusion?

A

increase IAP → decreased venous return → decreased CO → decreased systemic perfusion

32
Q

What is a late finding in the patient with untreated pyloric stenosis?

A. Hyponatremia
B. Hyperkalemia
C. Metabolic Acidosis
D. Alkaline urine

A

C. Metabolic acidosis

vomitting causes infant to lose H+ and lytes so common findings =
-metabolic ALKALOSIS
-hyponatermia
-hypokalemia
-alkaline urine

→ if dehydration persists and dehydration isnt corrected, impared tissue perfusion increases lactic acid production (metabolic acidosis =)

33
Q

Olive shaped mass felt below the xiphoid process

A

pyloric stenosis

*hypertrophy of the pyloric muscle creates a mechanical obstruction at the gastric outlet

34
Q

What anomoly are you concerned for if the infant starts with non-bilious projectile vomitting

(5 things this will lead to)

A

pyloric stenosis

  1. hyponatermia
  2. hypokalemia
  3. hypochloremia
  4. metabolic alkalosis
  5. compensatory respiratory acidosis
35
Q

T/F- pyloric stenosis is a surgical emergency

A

False -medical

patient must be optimized prior to pyloromyotomy
-fluids/lytes/acid-base

36
Q

plan for induction of a infant with pyloric stenosis?

A

Empty stomach with gastric tube prior to induction
awake intubation vs RSI (considered full stomach)

awake extubation

37
Q

When will pyloric stenosis typically present?

more common in males or females

A

in the first 2-12 weeks of life (1-3months)

non-binary obvi …..(males)

i should make up a timeline of things…. im gonna start that now

38
Q

What other congential issues are typically associated with pyloric stenosis?

A

none

39
Q
A
40
Q

Which way would the oxyhemoglobin diassociation curve be shifted in pyloric stenosis and why

A

left- decreased H+ions from vomitting

-reduces oxygen release at the tissue level

41
Q

why does the infant with pyloric stenosis end up with alkaline urine?

A

so they will have metabolic alkalosis due to loss of /h+ ions through vomitting
kidneys will try and compensate by increasing bicarb excretion > this alkalizes the urine

42
Q

severe dehydration of a kid with pyloric stenosis should be corrected with what?

maintenance fluids of kid with pyloric stenosis

A

20ml/kg of 0.9%NaCl (BEFORE SURGERY)

1.5x calculated maintenance rate with D51/2NS

43
Q

Why is postop apnea common following pyloromyotomy

A

pyloromyotomy- done to correct pyloric stenosis
pyloric stenosis = metabolic alkalosis (loss of H+ ions)
postop apnea is thought to occur secondary from the CSF remaining alkalotic even after serum acid-basis status is normalized
-decreased co2 = decreased drive to breathe

44
Q

What is necrotizing enterocolitis

2 most imporant risk factors

A

necrosis of the bowel

  1. prematurity (<32 weeks)
  2. low birth weight (<1500g)
45
Q

What is NEC likely the result from?

A

Early feeding → impaired absoprtion by the gut → stasis, bacterial overgrowh, infection → bowel perforation

46
Q

Are babies with NEC managed medically or surgically?

what acid-base imbalance

A

medically - however bowel perforation necessitates bowel resection and usually a colostomy

metabolic acidosis
*substantial fluid replacement usually required

47
Q

NEC affects what 2 regions of the bowel

A

terminal ileum and proximal colon

48
Q

2 most important risk factors for retinopathy of prematurity

A

prematury and hyperoxia

49
Q

when is retinal maturation complete and how should o2 administration be required until then?

where should pox be monitored??

A

44weeks after conception

-minimize supplemental o2 and maintain sat of 89-94%

preductal pox (RUE)

50
Q

Normal PaO2 in urtero vs after delivery

A

in urtero = 20-30mmHg
after delivery = 55-85mmHg

51
Q

What is retinopathy of prematurity?

A

abdomral vascular development in the retina creating vascular injury; scars form and then retract leading to retinal detatchment and blindness

52
Q

Why would you place a pulseox on a kids RUE with ROP?

A

bc preductal spo2 better correlates with the oxygen saturation in the retinal vessels

53
Q

Based on experimental animal data, which anesthetic agent is LEAST likely to cause apoptosis?

A. Ketamine
B. Nitrous oxide
C. Dexmedetomidine
D. Midazolam

A

C. Dex

*drugs that antagonize the NMDA receptor (ketamine, nitrous), stimulate GABA (propofol, halogenated agents, etomidate, barbituates, benzos) may cause apoptosis

54
Q

Where does bilirubin come from?

A

the breakdown of RBCs

55
Q

If a parent says they saw that anesthetic agents can kill nerurons and potentially cause neurocognitive delays later in life, how should you respond?

A

There are early studies that MIGHT suggest that, but there is not enough evidence that support witholding anesthetics during surgery.

There are also many studies that link recurrent stress and pain contrbute to poor neurological development- so theres a risk with either side

we will make every effort to use the least amount possible to achive comfort and even supplment with one particuular drug that has been shown to have a realitively safe profile in order to use less of the others

I will care for your child as if I were anesthetizing my own

56
Q

T/F- opioids are associated with apoptosis

A

false - dex and opioids and xenon have an “unknown” effect

57
Q

What metabolizes bilirubin

why is this an issue with babies?

A

glucuronyl transfersase (phase 2 reaction)

they cant metabolize it at birth, leaving them vulnerable 1st few days

58
Q

what is kernicterus

what can cause it

risk factors (3), treatment (2)

A

fetal encephalopathy

anything that increases serum bilirubin

risk factors: prematurity, low plasma concentration, acidosis
tx of hyperbilirubinemia: phototherapy and exchange transfusion (rarely needed)

59
Q

A child whith what congenital condition would receive the GREATEST benefit from awake intubation

A. ROP
B. TEF
C. Gastroschisis
D. NEC

A

B. TEF

PPV can cause gastric distension, reducing thoracic compliance, and increasing PIPS needed to ventilate adequately

60
Q

Prematurity is a risk factor for which condition (select 2)

A. Kernicterus
B. TEF
C. CDH
D. NEC

A

A. Kernicterus
D. NEC

TEF and CDH occur during fetal development so prematurity does not cause these conditions (they were already there)

PEDS (6 decks)

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