N935 Premie Patho Flashcards
(57 cards)
1
Q
LBW (in g)
VLBW
ELBW
A
LBW = <2500 g
VLBW = <1500 g
ELBW = <1000 g (<1 kg!)
2
Q
survival of extremely premie babies in low-income countries vs high-income settings
A
low-income >90% die within 1st few days
high-income <10% die in 1st few days
3
Q
4 ways premie deaths in low-income countries could be prevented
A
- warmth
- breastfeeding
- basic care for infxns
- safe O2 use for breathing difficulties
4
Q
WHO is coordinating clinical trials that examine effectiveness of what, for premies
A
antenatal corticosteroids
immediate kangaroo mother care (putting baby to mom’s chest)
5
Q
peds anatomy compared to adults:
tongue
larynx
epiglottis
vocal folds IRT trachea
subglottis
A
tongue is larger
larynx is higher (C3-4, compared to C4-5 in adults)
epiglottis is omega shaped and FLOPPY
vocal folds are attached more caudad anteriorly (compared to just about perpendicular in adults)
subglottis is narrowest part of larynx (until about age 8)
compared to adults, whose narrowest is the glottic opening
6
Q
peds oral and nasopharynx
A
tongue is large so there’s easy obstruction of the aw
oral airways relieve obstruction, NPAs rarely used
nasal passages are narrow
^^^ salivary secretions
large tonsils/adenoids
7
Q
peds larynx
A
- more cephalad, until 2 yrs old
- larynx is more anterior
- glottic opening C3-C4 (adult C4-C5)
- a straight laryngoscope blade more effectively lifts the tongue from the field of view
- Dr. Funk uses a straight blade until ~2 yrs of age, such as the Philips blade which is straight with a curve on the end. After 2 yrs old, she switches back to MAC
8
Q
PIC of phillips blade
A
9
Q
peds epiglottis and VCs
A
- (adult epiglottis: flat, broad, axis parallel to the trachea)
- epiglottis: narrower, omega-shaped, angled away “for the axis of the trachea” (think she meant angled away from the trachea), often obstructs the view of VCs, and is more difficult to lift. Great.
- VCs: more caudad attachment anteriorly, tip of ETT could get caught on the anterior portion of the folds, or hit the anterior trachea –> would have to rotate the tube to get it down
- (as opposed to adults which are attached perpendicularly)
10
Q
how do you figure out the length of peds ETT
A
3 x (size of tube)
11
Q
peds trachea, subglottic area
A
- trachea: shorter than adults
- infants are 4-5 cm long
- adults are 10-12 cm
- subglottic area
- traditionally, the narrowest portion of the peds pt (up to 8 yrs old), funnel shaped
- recent studies show that peds larynx is probably oblong shaped - narrower in AP plane, and wider in the transverse plane
12
Q
prematurity and the airway:
who’s law? resistance to airflow is inversely proportional to the radius
A
- Poisseuille!
- Q = (ΔP) (r^4) (π) / 8 n l
- ETT internal diameter
- 2-2.5-3 mm micropremie
- 5 mm child
- 7 mm adult
- a tight-fitting ETT that compresses the tracheal mucosa may cause edema = reduced luminal diameter
13
Q
name 3 dz’s that cause narrowing of the airway
A
- subglottic stenosis - 90% of the time are d/t previous prolonged intubation. requires that you place a smaller ETT, duh.
* -glottic opening looks fine, but distal to it the opening is teeeeeeny* - tracheal stenosis - offen at carina, makes ^ resistance distal to the ETT
- tracheobronchomalacia - intrathoracic airway collapses during exhalation. PEEP/CPAP are helpful to stent open the airway
14
Q
Tell me about prenatal alveoli,
lung maturation, surfactant
A
prenatal alveoli are thick-walled, fluid-filled sacs that don’t have surfactant – require greater pressure to initially expand
- surfactant prod occurs between 23-24 wks gestation. Concentration of surfactant is usually inadequate until ~36 wks post-conception
- The structure/fn of immature lungs predisposes the infant to alveolar collapse and hypoxia
- –> lead to decreased lung volumes/lung compliance, increased intrapulmonary shunting, and V/Q mismatch
15
Q
intercostal and diaphragmatic musculature
A
- low numbers of Type I muscle fibers - 10-25%
- marathon, slow-twitch muscles
- used for prolonged activity
- bebes don’t dev adequate Type I fibers until >6-8 months
- adults have 55% of these
- chest wall is more horizontal and more pliable
- minimal vertical expansion
- diaphragmatic ventilation - movement is more horizontal
- this results in early fatigue and propensity for apnea
16
Q
respiratory system, in general
(changes occur when, RR in infant/smol child, Vt, FRC/closing capacity compared to adults, hypoxic/hypercapnic drives)
A
- changes in resp system from infancy - 8 yrs old
- episodic respirs in utero
- passage thru birth vanal - takes fluid from the lungs, 90 mLs (~30 mL/kg) taken out via “vaginal squeeze”
- C-sxn babies may have more residual fluid in lungs
- VO2 is 2-3x higher (6-10 mL/kg/min)
- Vt is the same throughout development, always (~6 mL/kg)
- decreased FRC, increased CC
- immature hypoxic AND hypercapnic drives
17
Q
respiratory control
A
- biphasic ventil response to hypoxia - at first ventilation increases in response to hypoxia, but after a few minutes they become bradycardic and apneic
- ventil response to hypercarbia and CO2 is decreased also
- immature resp control + anesthesia effects + immature intercostal/diaphragmatic muscles = ^ r/f hypoxia, hypercapnia, and apnea in the postop period
18
Q
(BPD) bronchopulmonary dysplasia
A
- form of chronic lung dz, in pts hwo have survived severe neonatal dz
- cause is uncertain, but maybe d/t ^ end-inspiratory lung volumes, and frequent collapse and reopening of alveoli … (or O2 toxicity, barotrauma of PPV, inflammation, ETT intubation on immature lungs)
- may require supplemental O2, may develop lower aw obstruction/air trapping, CO2 retention, atelectasis, bronchiolitis, bronchopneumonemia
19
Q
ventilation strategy for (BPD) bronchopulmonary dysplasia
A
small Vts (4-6 mL/kg)
higher RR
PEEP
minimize inspired FiO2
ICU therapy: ^calories to meet the higher energy expenditure d/t ^WOB, respiratory support, diuretics, bronchodilators, alternative modes of ventilation (ECMO, high-freq ventilation)
20
Q
RDS - respiratory distress syndrome, what is it
A
- breathing d/o that affects newborns, common in premies born >6 wks early
- this develops 2/2 to lack of surfactant - airway collapses with hypoxia
- tx of RDS may lead to BPD (but like… you have to treat it so that sucks)
21
Q
RDS - respiratory distress syndrome, anestethic concerns
A
- anemia
- hx of apnea, residual chronic resp disease, impaired gas exchange
- hx of prolonged ventilation, residual subglottic stenosis
22
Q
what is the postconceptual age (PCA)
A
conceptual age + postnatal age
23
Q
how does apnea related to PCA
+ additional risk factors
A
- apnea is inversely related to PCA (conceptual + postnatal age)
- apneic ep’s (>15 secs) include failure to breath (central apnea) and failure to maintain a patent airway (obstructive apnea)
- may be accompanied by bradycardia and desaturation
- additional risk factors: LBW, anemia, hypothermia, sepsis, neuro abnormalities, type of surgery
24
Q
apnea/periodic breathing:
neonates <2500 g
<1000 g
A
- <2500 g = 25% risk for apnea/periodic breathing
- <1000 g = 85% risk for apnea/periodic breathing
- reduction of 50% occurs after 44 weeks PCA
25
when does apnea occur perioperatively in premies?
* apnea occurs most commonly after anesthesia and surgery in preterm infants
* continues 48 hours postop
* can still occur with regional anesthesia!
*Why? The general stress of surgery, and how their little immature brains process it*
26
mgmt of periop apnea
* admit \<60 wk postconception age, with continuous apnea/bradycardia monitoring for 24-48 hrs
* defer elective surgeries until \>44-50 wks PCA
* IV caffeine (5-10 mg/kg)
* nasal CPAP or tracheal intubation with ventilation
27
fetal heart differences
* more CT
* less organized contractile elements (not much of an SVR to pump against)
* ^ dependence on extracellular Ca++
28
why is the premie at a greater risk of CV collapse from anesthesia/surgery?
other that they're so weetle
* fetal heart differences (^CT, less contractiles, more dep on ECF Ca++)
* less compliant tissue that's **less sensitive to catecholamines** (EPI \> ephedrine)
* small circ volumes (mL/kg)
* autoregulation not well developed
* no ^ in HR irt hypovolemia --\> decreased BF and O2 delivery with not that much blood loss
29
circulating blood volumes
micropremie 110
premie 100
FT neonate 90
infant 80
child 70
30
neonatal myocardium + what it can handle
\*IMMATURE\* \*DECREASED MYOFIBRILS\*
* decreased inotropy, decreased relaxation (lusitropy)
* afterload increases poorly tolerated
* preload decreases poorly tolerated
* reliant on serum Ca++
* decreased response to volume loads
* RV = LV
* PSNS innervation is well developed. Hello, they keep getting bradycardic.
31
failure of the PDA to close
(incidence in premies, what does it cause)
* ^s risk of CV collapse during surgery
* 20-30% of infants born before 34 wks
* PDA promotes pHTN and CHF
* changes in SVR/PVR alter direction of flow thru the PDA
* R --\> L shunting (d/t ^ PVR) --\> hypoxia, hypercarbia, acidosis
* L --\> R shunting --\> hypotension, pulmonary volume overload
32
describe normal fetal circulation
* placenta - umbilical vein - (most) ductus venosus (bypasses liver)
* IVC - RA - (Eustachian valve across foramen ovale) - LA - aortic arch
* SVC - RA - RV (small amt to LA thru PFO) - PA - ductus arteriosus
33
describe fetal circulation in general (no #s)
* high PVR 2/2 fluid in lungs
* low SVR d/t large surface area/low resistance of utero-placental bed
* most oxygenated blood from umbilical vein to brain and heart (ductus venosus - foramen ovale)
34
fetal circulation:
PaO2, oxyhgb
* umbilical vein PaO2 30-35 mmHg
* Hgb F (fetal) is left shifted, more saturated than adult Hgb
* P50 is 19 mmHg, as opposed to adults 26.8 mmHg
* ^ Hgb in utero --\> raises CaO2
* left shifted Hgb F + polycythemia = O2 carrying capacity similar to adults
35
SVR/PVR changes at birth
* cord clamp = ^ SVR
* reversese flow thru PDA
* lungs fill with air = lowers PVR, ^s PaO2
* lower PVR - increased BF to LA
* closes PFO
* ^ PaO2 causes decreases prostaglandin --\> closure of PDA
36
describe foramen ovale closure
| (PFO incidence)
lower PVR - more BF thru pulmonary system - more BF to LA - LAP \> RAP - functional closure of PFO
anatomic closure requires weeks (murmur in newborns is normal!)
PFO in 20-25%
37
describe ductus arteriosus closure
| (PDA)
was kept open in utero bc of **hypoxia**, **mild acidosis**, placental **prostaglandins**
* removal causes fn'l closure of PDA
* \*reverse flow pressure and \*increased PaO2 (\>50-60 mmHg) causes muscular wall to constrict
* permanent anatomic closure between 5-7 days (but as long as 3 wks)
* PDA often persists in premies **with lung dz** (blood follows path of least resistance)
* before anatomic closure, if any stressors such as hypothermia, hypercarbia, acidosis, hypoxia, sepsis, ^PVR, can cause the newborn to revert back to fetal circulation
38
PDA in premies + sequelae
* delayed closure is common in premies, esp \<34 wks
* changes in PVR, SVR alter the direction of blood
* ^ PVR --\> R-to-L shunting (bad)
* p. edema from ^ blood flow promotes pHTN
* worsened with hypoxia, ^CO2, acidosis, hypothermia
* PDA causes CHF, low DBP
## Footnote
*basically a leak in the aortic pressure from blood going back to pulmonary circ, so DBP is low --\> distal perfusion is low*
39
describe pre- and post-ductal saturation
* aortic arch from our L → R is brachiocephalic (leads to R subclavian and R common carotid), L common carotid, L subclavian
* preductal = pulse ox on RH or ear
* postductal = pulse ox on LE
* lower sat here tells you that pHTN has changed!
* is the baby too light? Do you need to add N2O?
40
prematurity and the CNS
* myelination of nerve fibers is incomplete
* cerebral cortex less developed
* BBB is immature, rendering the dev brain more vulnerable to drugs/toxins
* neural pathways allowing for pain perception in 1st, 2nd and 3rd trimesters
41
CBF and IVH in premies
+ predisposing factors
* developing cerebral vessles are more fragile than adult
* cerebral autoregulation sucks in sick neonates → CBF is pressure-dependent
* rupture leads to ICH and IVH (intraventricular hemorrhage)
* predisposing factors
* (all the same as what keeps the PDA open)
* hypoxia, hypercarbia, acidosis
* fluctuations in pressure
* low Hct
* overtransfusion
* rapid infusion of hypertonic fluids (NaBicarb or Dextrose) - these need to be diluted, as they're damaging to vessels
42
IVH in premies:
what is it?
risk factors, causes, sx's
sequelae
* spontaneous bldg into/around the lateral ventricles of the brain
* at risk: small birth weight, preterm (1/3 of micropremies)
* causes: RDS, hypoxia, acute BP changes, trauma, acidosis, distress
* sx: hypotonia, apnea, sz's, loss of sucking reflex, bulging anterior fontanelle (which tells you there's an ^ ICP)
* graded I-IV (hemorrhage limited to subependymal matrix → grade I-III but extension into brain tissue)
43
what is ROP
what does the optic nerve (ON) do?
ROP is a vasoproliferative retinal d/o, which causes fibrosis and retinal detachment
(*normal retinal vasc devt is exchanged for neovascularization and fibrous tissue formation in the retina)*
the infant retina matures until 42-44 wks (so if normal gestational age is 40 wks, then about a month after birth), and ROP is the leading cause of blindness in the world
44
what are causes of ROP?
2 methods of dx
* inversely related to gestational age (\<37wks) and birth wt (\<1 kg)
* O2 exposure, PaO2 60-80 mmHg
* apnea
* blood tx
* sepsis, infxn
* hypercarbia
* BPD, or surfactant therapy
*fluctuating O2 levels may be more damaging than high O2 "tensions"*
dx with eye exams
* zones (immed around ON and out)
* stages
* DOL 30, and if \<28 wks q2wks
45
anesthesia mgmt to prevent ROP
tx now that you caused it
* SpO2 90-94%
* preop: optimize HD and oxygenation
* intraop: limit hyper- or hypoxemia, avoid swings in oxygen, limit O2 duration
* postop: eye exams. lots of NICUs do eye exams q2wks
* tx:
* intravitreal injxn of steroids or anti-VEGF delays dz progression
* scleral cyrotherapy (Cryo-ROP)
* **laser photocoagulation** \*\*\* laser ablation to peripheral avascular retina
* surgical intervention - lens-sparing vitrectomy
* stage 4 or 5
46
metabolism and temperature
r/f for heat loss
how do they produce heat when cold?
* r/f for heat loss
* larger surface area per kg than adults
* thin skin
* lower fat content
* heat production
* NON-SHIVERING thermogenesis (1st 3 mos)
* metabolism of brown fat, but high metabolic demand to do this
* thermogenesis is inhibited by volatile anesthetics
* (crying, movement) - *can't do this bc we knocked them out*
47
routes of heat loss
radiation (39%) \> convection (34%) \> evaporation (24%) \> conduction (4%)
48
look at this pic of brown fat distribution
49
how do volatiles affect temp
* depresses the hypothalamus - decreases an *already reduced* ability to warm themselves
* cutaneous vasodilation
50
hypothermia in peds sequelae
* delayed awakening from volatiles
* cardiac instability
* resp depression
* increased PVR
* altered drug response
51
what can be done to combat hypothermia (aka prevention)
* transport kid in an incubator or on a heating pad
* warm the OR (78-80 degrees) and fluids
* limit skin exposure
* cover the kid's head
* forced air devices and warmers
* heat lamps
52
prematurity and the renal system
*"decreased renal system"*
* ~ inability to compensate for volume swings
* glomeruli are forming still, until ~40 days old
* decreased renal clearance
* neonates can't handle free H2O or loads
* ^ half-life if excreted by glomerular filtration (eg. abx)
* decreased prox tubular reabsorption of Na+ and H2O
* closely monitor Na+/H2O requirement
53
glucose homeostasis
* low glycogen and body fat stores
* predisposed to hypoglycemia during stress
* surgery is stressful
* but also decreased insulin production
* so too much dextrose = hyperglycemia
* *they can't handle it!*
* impaired glucose excretion by kidneys balances that out
* maintain on IV dextrose (on pump) when NPO
* close BG control
* **normoglycemia is 45-90 mg/dL**
54
prematurity and the hepatic system
* at term, fn'l maturity of liver is somewhat incomplete
* CYP450 (Phase I) ~50% at birth
* Conjugation (Phase II) **impaired until 1 yo**
* limited glycogen
* limited ability to handle large protein loads
* reduced albumin synthesis
* more unbound drugs
55
Ca++ homeostasis
* in utero, Ca++ from placenta, DUR.
* newborn relies on ECF Ca++ and Ca++ reserves, but:
* Parathyroid fn not fully established (*PTH released irt hypocalcemia, nml PTH levels in adults are 8-51 picograms/mL*)
* Vit D stores may be inadequate
* albumin and protein reserves are lower
* anticipate hypoCa++, especially in premies, severe neonatal illness, and following blood transfusions
56
tx for symptomatic hypocalcemia
slow infusion of CaCl2 or CaGluc
central line is preferred - Calcium-containing solutions can cause skin damage and sloughing
57
