module 11 pediatric Flashcards
children more susceptible to airway issues
infant trachea has more mucus producing glands
trachea lumen, bronchi and bronchioles are narrower
- inc. risk obstruction
- higher resistance to air flow
increased work of breathing required for ventilation
- large volume of dead space
- immature alveoli and smaller number of alveoli
- ventilation primarily done by diaphragm and abd.
infants nose breathers
anatomical differences in peds
process of alveolar development continues through age 8
collateral ventilation not well developed -> inc. risk of atelectasis
lung tissue very compliant and prone to over-distention
bronchiectasis
obstructive and suppurative (pus forming) disease
dilation of bronchi
acquired or congenital
peds inc risk d/t: small, soft elastic bronchi
-> easily damaged from inflammation/infection
3 types of bronchiectasis
saccular: cavity like dilations
cylindrical: widening of bronchial walls
fusiform: combo of both
bronchiectasis pathogenesis
inflammation -> destruction of walls in central bronchi and obliteration of peripheral bronchi/bronchioles
most common cause: H. influenza
bronchiectasis s/s
chronic productive cough copious amounts of purulent, foul, yellow/green sputum hemoptysis fever night sweats moist crackles rhonchi bad breath skin pallor
bronchiectasis complications
malnutrition
recurrent pneumonia
RV failure
secondary visceral abscesses
bronchiolitis
widespread inflammation of bronchioles, production of thick mucus -> airway obstruction, atelectasis and hyperinflation
RSV, influenza virus, bacteria, occasionally allergic reactions
bronchiolitis s/s
wheezing r/t bronchospasm crackles dec. breath sounds retractions inc. sputum dyspnea inc. RR low fever
bronchiolitis pathogenesis
causal agent -> proliferation and necrosis of bronchiolar epithelium -> obstruction and inc. mucus production -> airway obstruction, atelectasis, hyperinflation
bronchiolitis 3 mechanisms of obstruction
development of inflammatory exudate, displaces surfactant
chemical mediators -> bronchiolar constriction
inflammation -> fibrosis and narrowing
cystic fibrosis
autosomal recessive disorder of exocrine glands
most common genetic lung disease
classified as either obstructive or suppurative
dysfunction of CFTR gene
CFTR gene
encodes a membrane chloride channel in sweat glands, lungs, pancreas, and intestinal tract
with cystic fibrosis
- alteration in chloride and water transportation across epithelial cells
-> dehydrated mucus, hypersecretion of thick mucus that is hard to clear
pathogenesis of cystic fibrosis
mucus producing glands enlarge
- excessive secretion in GI tract
- plug the glands and duct of pancreas acini and gallbladder -> dilation and fibrosis, dec. pancreatic enzymes for digestion -> inc. fat and protein in stool
- thick, tenacious mucus in bronchopulmonary system -> airway obstruction, atelectasis, hyperinflation, dec. ciliary action -> mucus stasis -> infection
cystic fibrosis s/s
causes infertility in males cough thick sputum recurrent infections/bronchitis RSHF exercise intolerance dyspnea clubbing (late) inc. retractions unequal breath sounds/crackles barrel chest and hyperresonant pancreatic insufficiency cirrhosis of liver DM gallstones nasal polymps fatty stools
cystic fibrosis dx
ABG: hypoxemia, hypercapnia
PFT: dec. VC, flow rate, and TV. Inc. resistance, FRC
sputum cx
CXR: patchy atelectasis, bronchiectasis, obs. emphysema, cystic lung fields, peribronchial thickening
stools for fat
pilocarpine iontophoresis (sweat test)
genetic testing
72 hr stool collection w/ diet hx to determine fat absorption and fecal fat rate
complications of cystic fibrosis
anorexia
dec. growth rate
dec. midarm indices
acute tracheobronchial obstruction
foreign body trauma tumors swelling malpositioned ET tube larynogospasm epiglotitis post-surgical blood clot - requires immediate tx - w/ inhaled foreign bodies R. side affected > than left d/t angle of anatomic extension of R. main bronchus
acute trachobronchial obstruction s/s
complete:
- no air movement on auscultation, may have chest movement
- inability to talk
- inc. HR
- cyanosis
- LOC
partial:
- stridor
- retractions
- wheezing
- nasal flaring
- inc. RR
- dyspnea
- inc. HR
- cyanosis (late)
epiglottitis
cellulitis of epiglottis and adjacent soft tissues
- rapid and potentially fatal inflammation/ swelling and airway obstruction
- pain w/ swallowing out of proportion for physical findings
- inability to swallow saliva -> drooling
causative: - HIB
- pneumococci
- strep
- staph
epilottitis s/s
acute respiratory distress drooling dysphagia rapid onset fever dysphonia inspiratory stridor retractions oropharynx edematous and cherry red
croup
acute viral and inflammatory disease of the larynx, trachea, and bronchi causative: - influenza - parainfluenza 1,2, 3 - adenovirus - mycoplasma pneumonia seen more in fall and winter 6mo-3yrs infectious agent -> edema formation in subglottic area
croup s/s
hx uri barky cough stridor low grade/absent fever retractions cyanosis
IRDS: infant respiratory distress syndrome
restrictive lung disease, also known as hyaline membrane disease
charachterized by
- hemorrhagic pulmonary edema
- patchy atelectasis
- hyaline (glassy) membranes
- hallmark: hypoxemia refractory to inc. O2 supplementation
high risk factors for IRDS
earlier than 25 wk gestation - 60% in 30 wk gestation w/out antenatal steroids - 30% in those who received steroids advanced gestational age poorly controlled DM in mom delevery afer antepartum hemorrhage c-section w/out antecedent labor perinatal asphyxia multiple births previous infant with IRDS Rh factor incompatibility
normal labor process
dec. secretion of fetal lung liquid and inc. in absorption of liquid
release of surfactant
inc. catecholamine release
pathogenesis of IRDS
lack of surfactant -> inc. alveolar surface tension and dec. lung compliance
- must generate high intrathoracic pressure to maintain patent alveoli
- infants have soft compliant chest: hard to get pressure where needed
- > inc. WOB amd dec/ ventilation -> atelectasis, inc. pulmonary vascular resistance, hypoxemia, acidosis
IRDS and type 2 alveolar cells
type 2 alveolar cells produce surfactant: inc. in quantity after 32 weeks gestation
- also maintains pulmonary fluid balance
- alteration -> leakage of proteinaceous fluid into alveoli (fibrin, debris) -> hyaline membrane formation
secondary cause of IRDS
- immaturity of capillary blood supply -> V/Q mismatch -> hypoxemia and metabolic acidosis
- progressive damage to basement membrane and respiratory epithelial cells
- > edema and loss of cells -> patchy areas of atelectasis
IRDS s/s
shallow resps retractions dec. breath sounds nasal flaring hypoTN peripheral edema low temp oliguria inc. RR (60-120) dec. HR late: - frothy sputum - central cyanosis - expiratory grunting - paradoxal respirations
inspired O2 with IRDS
maintain between 85-94%
changes in resp. system in children
overproduction of mucus in trachea
smaller diameter of trachea
narrow diameter of bronchi and bronchiolies
- inc. risk airway obstruction
flexible rib cage with less elastic recoil
-> external muscles elevate ribs, ventilation done by diaphragm, inc. WOB, inc. RR
glottis higher in throat
high bifurcation of trachea
larynx higher in neck
- inc. risk aspiration -> infection -> inc. WOB -> inc. RR
changes in resp system in geriatrics
dec. elastin and inc. collagen
-> dec. lung elastic recoil/stiffer chest wall
-> dec. expiratory rate, dec. VC
enlargement of alveoli
-> inc. dead space and dec. surface area
-> inc. risidual volume and V/Q mismatch
-> dec. PaO2 and inc. WOB
hypertrphy of bronchial mucus glands
-> V/Q mismatch
dec. respiratory muscle strength and dec. number and motility of cilia
-> dec. effectiveness of cough
-> dec. PaO2 -> inc. WOB
