Peds Advanced Patho Flashcards
prematurity
birth before 37 weeks gestation
low-birth-weight
<2500 g
very-low-birth-weight
<1500 g
extremely-low-birth-weight
<1000 g
five anatomical structures in the airway that are different in pediatric patient versus adult
- tongue
- position of larynx
- epiglottis
- vocal folds
- subglottis
tongue in pediatric patient
- infant’s tongue relatively large in proportion to rest of the oral cavity
- contributes to easy obstruction of infant’s airway
- oral airway helps to relieve the obstruction
other differences in pediatric airway
- narrow nasal passages
- more secretions from salivary glands
- large tonsils and adenoids
position of larynx in pediatric patient
- higher (more cephalad) for neonates to 2 years of age
- larynx seems more anterior
- located C3-C4 infants (C4-5 adults)
- a straight laryngoscope blade more effectively lifts the tongue from the field of view
epiglottis in pediatric patient
- adult = flat and broad with axis parallel to trachea
- infant = more narrow, omega shaped and angled away fro the axis of the trachea
- often obstructs the view of the vocal cords and is more difficult to lift
vocal cords in pediatric patient
- infant’s vocal cords have a lower (caudad) attachment anteriorly versus posteriorly
- adult the axis of the vocal cords is perpendicular to the trachea
- can lead to difficult intubation with the tip of the ETT held up at the anterior portion of the folds
trachea in pediatric patient
- shorter than in adults
- infant 4-5 cm
rule of thumb for tube placement in peds
3x size of the tube
subglottic area in pediatric patient
- traditionally taught = this is the narrowest portion of the child’s airway
- recent studies = pediatric larynx is oblong shaped (like a football) and may be more narrow in the AP dimension but wider in the transverse dimension
prematurity and the airway
- small airways, such as those in prematurity, are predisposed to obstruction and difficulty with ventilation
- resistance to airflow inversely proportional to radius of 4th power (poiseuille’s law)
- ETT internal diameter smaller
- partial occlusion of ETT due to kinking or secretions GREATLY increases WOB for premie
- tight fitting ETT compresses tracheal mucosa and can cause damage/edema
diseases that narrow the airway
- subglottic stenosis
- tracheal stenosis
- tracheobronchomalacia
subglottic stenosis
- 90% of acquired subglottic stenosis are result of ETT and prolonged intubation
- often requires placement of smaller ETT
tracheal stenosis
-often occurs at carina and creates added resistance distal to ETT
tracheobronchomalacia
- intrathoracic airway collapses during exhalation
- PEEP and CPAP are helpful to stent open airway
when does surfactant production begin?
23-34 weeks gestation
-concentration of surfactant often inadequate until 36 weeks post-conception
lung maturation
- prenatal = alveoli are thick, fluid filled sacs that are deficient in surfactant and require GREAT pressures to expand
- structure and function of immature lungs predisposes infant to alveolar collapse and hypoxia
- leads to reduced lung volumes, decreased lung compliance, increased intrapulmonary shunting and V/Q mismatch
intercostal and diaphragmatic musculature in infants
- low numbers of type I muscle fibers (marathon muscles, slow twitch; do not develop adequate until > 6-8 months)
- chest wall more horizontal and pliable, minimal vertical movement so less room for lung expansion
- result = early fatigue and propensity for apnea
respiratory system in children
- changes occur from 8 mo-12 yo
- episodic respirs in utero
- passage through birth canal forces fluid out of lungs
- RR elevated in infant and small child
- O2 consumption 2-3x higher (6-10 mL/kg/min)
- Vt/kg remains constant throughout development
- decreased FRC and increased CC
- immature hypoxic and hypercapnic drives
respiratory control in children
- premies have biphasic ventilatory response to hypoxia
- initial = ventilation increases, but after several minutes, ventilation decreases and bradycardia/apnea may occur
- ventilatory response to hypothermia and CO2 is also decreased
- increased risk of hypoxia, hypercapnia, and apnea in post-op period because of these things combined with anesthesia
BPD
- bronchopulmonary dysplasia
- form of chronic lung disease that occurs in patients who have survived severe neonatal lung disease
- cause = uncertain
- most likely related to increased end-inspiratory lung volumes + frequent collapse and reopening of alveoli
potential causative factors of BPD
- oxygen toxicity
- barotruama of PPV
- inflammation
- ETT intubation on immature lungs
BPD presentation
- need oxygen
- lower airway obstruction
- air trapping
- CO2 retention
- atelectasis
- bronchiolitis
- bronchopneumonia
ventilation strategy for BPD
- small tidal volume (4-6 mL/kg)
- greater RR
- PEEP
- minimize FiO2
RDS of newborn
- breathing disorder affects newborns, common in premies more than 6 weeks early
- develops secondary to lack of surfactant
- result = airway collapse and hypoxia
- treatments may lead to BPD
anesthetic concerns with RDS
- anemia
- history of apnea, residual chronic respiratory disease, impaired gas exchange
- history of prolonged ventilation, residual subglottic stensosis (from ETT)
apnea in premie
- inversely related to postconceptional age
- apneic episodes include central and obstructive apnea
- may also be accompanied by bradycardia and desaturations
risk factors for apnea in premie
- LBW
- anemia
- hypothermia
- sepsis
- neurological abnormalities
- type of surgical procedure
postconceptional age
-the sum of the conceptional age and the post natal age
neonates < 2500g
25% risk for apnea/periodic breathing
neonates < 1000g
85% risk for apnea/periodic breathing
44 weeks postconceptional age
50% reduction of risk for apnea/periodic breathing
apnea risk and anesthesia
- apnea occurs commonly after anesthesia and surgery in preterm infants
- can continue to occur up to 48 hours post op
- apnea can still occur with regional
mangement of apnea + anesthesia in bebes
- DO NOT SEND HOME; plan for in=house admit for all premature infants <60 weeks PCA with continuous apnea + bradycardia monitoring
- deferment of elective surgery until 44-55 weeks PCA
- IV caffeine (5-10 mg/kg)
- nasal CPAP or tracheal intubation with ventilation
premie + CV system
-greater risk of CV collapse during anesthesia and surgery
differences in premie/fetal heart
- more connective tissue
- less organized contractile elements
- increased dependence on extracellular calcium
- less compliant tissue and less sensitive to catecholes
- small circulating blood volumes (relatively small surgical blood loss can result in hypovolemia and hypoperfusion_
- autoregulation not well developed
- HR may not increase with hypovolemia
micropremie blood volume
110 mL/kg
premie blood volume
100 mL/kg
full term neonate blood volume
90 mL/kg
infant blood volume
80 mL/kg
child blood volume
70 mL/kg
neonatal myocardium
- immature and decreased number of myofibrils (reduced contractility and relaxation)
- afterload increases poorly tolerated
- preload reductions poorly tolerated
- reliant on serum level of iCal
- decreased response to volume loads
- R and L ventricles are equal
- PSNS innervation well developed
failure of ductus arteriosus to close
- further increases risk of CV collapse during major surgery
- 20-30% of infants born before 34 weeks
- PDA promotes Pulm HTN and CHF
- changes in systemic or pulmonary vascular resistance result in change of blood flow direction through the PDA
right to left shunting
- occurs with an increase in PVR
- result = hypoxia, hypercarbia, acidosis
left to right shunting
- occurs with increase in SVR
- hypotension and pulmonary volume overload
three shunts in fetal circulation
- ductus venosus
- foramen ovale
- ductus arteriosus
ductus venosus
oxygenated blood from umbilical vein to bypass the liver and go straight to the heart
foramen ovale
small hole located in the septum between the two atria of the heart
ductus arteriosus
connection between the aorta and the pulmonary artery
two umbilical arteries
originate from the fetal internal iliac arteries and deliver fetal blood to the placenta where it is oxygenated
one umbilical vein
carries oxygenated blood from the placenta to the fetus
umbilical vein blood
majority bypasses the liver via ductus venosus and empties into the IVC where it mixes with less oxygenated blood from the lower half of the body
IVC blood
enters RA and directed by the eustachian valve across the foramen ovale into the LA
LV
pumps this blood from the LA to the upper body through the great vessels of the aortic arch
SVC blood
deoxygenated; enters the RA and primarily crosses the tricuspid valve into the RV
-only a small amount of SVC blood enters the LA via the PFO
HIGH PVR
forces RV output to enter the systemic circulation via ductus arteriosis (which originates from the PA and inserts into the aorta at the point just distal to the origin of the left subclavian artery)
fetal circulation characteristics
- high PVR secondary to fluid filled lungs
- low SVR secondary to large SA of the low resistance utero-placental bed
- the most oxygenated blood from the umbilical vein perfuses the brain and heart by shunting across the liver via the ductus venosus and shunting across the R heart via the foramen ovale
PaO2 of umbilical vein
30-35 mmHg
-oxygen transport exists in relatively hypoxic environment
fetal hemoglobin maintenance of CaO2 in fetal circulation
- HgB F is left shifted and more saturated than adult HgB
- hemoglobin levels in utero are elevated which also raises CaO2
- effect of left shifted hemoglobin F and polycythemia produce and oxygen carrying capacity in the fetus that nearly equals the adult
p50 of Hgb F
19 mmHg
when does transition from fetal to adult circulation occur?
clamping of umbilical cord and inflation of lungs
- cord clamping = removes low resistance placenta and raises SVR
- lung inflation = increases PaO2 and DRAMATICALLY lowers PVR
foramen ovale closure
- LA pressure rises above RA pressure, closing the flap of tissue covering the PFO
- functional closure occurs quickly
- anatomic closure usually requires weeks
- PFO that is probe patent persists in 20-25% of adults
ductus arteriosus closure
- patent in utero due to hypoxia, mild acidosis, and placental prostaglandins
- removal of these factors after delivery causes functional closure
- reverse flow pressure and increase in local PaO2 (>50-60 mmHg) causes muscular wall of ductus to constrict
- permanent anatomic closure usually complete in 5-7 days BUT may persist until 3 weeks
PDA when? WHY?
- in premies with lung disease
- during period before anatomic closure certain physiologic stressors can cause newborn to revert to fetal circulation
what physiologic stressors cause reversion to fetal circulation?
- hypothermia
- hypercarbia
- acidosis
- hypoxia
- sepsis
- raised PVR
PDA negative effects
- increase in PVR–> increased R to L shunt (BAD)
- pulmonary edema
- pulmonary hypertension
- CHF
- low diastolic pressure (leak, blood just going to lungs so p in aorta drops –> decreased DBP)
preductal
pulse ox R hand
postductal
pulse ox in lower limb
shunting occurs
increased pre, decreased post
prematurity and CNS
- myelination of nerve fibers incomplete
- cerebral cortex less developed
- BBB immature, rendering developing brain more susceptible to toxins
- neural pathways allowing for pain perception develop in first, second and third trimesters
Cerebral blood flow
- developing brain more fragile
- cerebral autoregulation impaired so blood flow pressure dependent
- preterm infants have VERY fragile cerebral vessels - rupture leads to IVH
predisposing factors to IVH
- hypoxia
- hypercarbia
- hypernatremia
- fluctuations in pressure
- low HCT
- over transfusion
- rapid admin of hypertonic fluids
IVH
- spontaneous bleed into and around lateral ventricles of brain
- at risk = small birth weight and preterm
- causes = RDS, hypoxia, acute BP alterations, trauma, acidosis, distress
- graded I-IV
- can progress –> hydrocephalus, parenchymal infarction, periventricular matter injury
S/S IVH
- hypotonia
- apnea
- seizures
- loss of suck reflex
- bulging anterior fontanelle
retinopathy of prematurity (ROP)
- arrest of normal retinal vascular development in exchange for neovascularization and fibrous tissue formation in retina
- can lead to retinal detachment and fibrosis
- infant retina continues to mature until 42-44 weeks
- fluctuating oxygen levels may be more damaging than high oxygen tensions
ROP risk factors
- low birth weight
- prematurity
- oxygen exposure
- apnea
- blood transfusions
- sepsis
- CO2
anesthesia sat goal
90-94%
metabolism and temperature in premie
-peds patients have larger SA per kg than adults, thin skin, lower fat content and higher SA = increased risk for heat loss
four routes of heat loss
- radiation (39%)
- convection (34%)
- evaporation (24%)
- conduction (4%)
heat production mechanism
- non-shivering thermogenesis during first 3 months of life -metabolism of brown fat - shivering severely limited in premies, thermogenesis inhibited by volatiles
- crying
- movement
most effective means of keeping bebe warm?
HEAT the room
volatiles effect on temperature
- depress hypothalamus = reduction in already reduced ability to warm themselves
- cutaneous vasodilation
hypothermia of peds patient can result in
- delayed awakening from GA
- cardiac instability
- respiratory depression
- increased PVR
- altered drug response
what can be done to combat these effects of anesthesia on temperature
- transport child in incubator or on heating pad
- warm OR (78-80 degrees) and warm fluids
- limit skin exposure
- cover child’s head
- use forced air devices and warmers ALWAYS
- heat lamps
prematurity and renal system
- significantly reduced ability to compensate for large swings in volume
- glomeruli continue to form post-natally until approximately 40 days
- renal clearance of drugs reduced
- reduced proximal tubular reabsorption of sodium and water
glucose homeostasis in neonate
- neonate have very low glycogen and body fat stores
- predisposed to hypoglycemia during stress
- however, decreased insulin production with infusion of dextrose predisposes to hyperglycemia
- impaired glucose excretion by kidneys can work to offset these problems
- should be maintained on IV dextrose when NPO and close monitoring of BG is vital
normoglycemia
45-90 mg/dL
prematurity and hepatic system
- CYP450 reaches ~50% adult values at birth
- phase II reactions are impaired until ~1 year of age
- limited glycogen stores
- limited ability to handle large protein loads
- reduced albumin synthesis (greater amount of unbound drugs)
calcium homeostasis
- calcium actively transported across placenta in utero
- after birth, infant relies on extracellular calcium and calcium reserves BUT parathyroid not fully functional, vitamin D store inadequate, and albumin + Protein reserves lower
- anticipate hypocalcemia esp in preterm, illness, and following blood transfusions
- symptomatic hypocalcemia requires tx
- central line preferred for calcium infusion
