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244 Cards in this Set
- Front
- Back
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premature newborn
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<37 weeks gestation
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term newborn
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>37 weeks gestation
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newonate
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1 d - 1 mo
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infant
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1 m - 1 y
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children
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1-11 y
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adolescent
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12-18 y
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effect of altered gastric pH
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acid-labile drugs achieve higher serum concentrations in premature (AG, nafcillin)
weakly acidic drugs achieve lower serum concentrations in preemies (phenytoin, phenobarbital, APAP) |
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infants have ___ gastric emptying
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delayed
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infants have ___ intestinal motility
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decreased
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IM/SQ absorption in infants is
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reduced
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exception to IM/SQ injection in infants
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use if >2 kg: hepC vaccine
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topical absorption is ____ in preemies and children
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exposure to topically applied medications can result in toxic effects
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rectal absorption in young children is ____ due to ___
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enhanced
immature hepatic metabolism |
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rectal administration is ___ in neonates and ____ in older infants and children
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avoided
useful |
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body water in neonates
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increased due to immature processing of sodium and water
increased insensible losses due to increased S:V ratio |
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body fat ___ with age, therefore ____
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increases
fat soluble drugs may have higher serum concentrations when administered to neonates |
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newborns have
____ plasma protein ____ bilirubin causing |
decreased albumin
increased bilirubin increased free fraction of highly protein bound drugs, increased drug activity, drug toxicity |
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kernicterus
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deposition of bilirubin in brain leading to neurologic dysfunction that may be permanent if untreated
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low Vd is ass'd with
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high water solubility
high protein binding |
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high Vd is ass'd with
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high lipid solubility
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CNS penetration is ____ in neonates
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increased
immature BBB |
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metabolism is ___ in neonates
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slower
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Phase I enzymes summary in neonates
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to increase water solubility
oxidation: 50% reduction: 100% hydrolysis: takes 10-12 months demethylation: takes 15 weeks |
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1A2 affects which drugs
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caffeine
theophylline exceeds adult levels |
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2D6 affects which drugs
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codeine
oxycodone normal level by childhood |
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2C9 affects which drugs
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ibuprofen
phenytoin increased as a neonate |
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2E1 affects which drug
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APAP
controversial |
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3A4 affects
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carbamazepine
methadone over-expressed then decreases |
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Phase II summary
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methylation: higher - theophylline
glucuronidation: takes 2-3 years - chloramphenicol sulfation: developed: APAP, theophyllin, morphine |
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kidneys in neonates
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not fully functional
rapid, but variable renal maturation requires frequent dosage adjustment and titration |
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Schwartz Equation for calculating CrCl
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K x Ht (cm) / SCr
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moa of vancomycin
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inhibits bacterial cell wall synthesis
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vanco has ___ dependent killing
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time
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coverage of vanco
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gram +
MRSA Strep |
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gentamicin and tobramicin have ____ dependent killing
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concentration
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gentamicin and tobramycin cover
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gram -
Pseudomonas |
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phenytoin moa
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stabilizes neuronal membranes via sodium ion flux
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toxicity of phenytoin is measured
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clinically
affected by levels of albumin and bilrubin |
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digoxin moa
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increases the influx of calcium ions through the inhibition of Na and K ions in the myocardial membrane
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draw digoxin trough if
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concerned about toxicity, ONLY
-renal fxn changes -compliance -interactions |
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total body water percentage
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60% men
50% women |
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intracellular compartment is ___ of TBW
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60%
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extracellular compartment is ___ of TBW
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40%
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interstitial space is ___ of EC
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75%
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intravascular space is ___ of EC
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25% (plasma)
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unique property of albumin
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pulls fluid into the intravascular space
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surface area method of calculating fluid volumes
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(children <10kg): 1-2L/m2/d
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body weight method
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100 (10 kg) + 50 (X-10 kg) + 20
mL/kg |
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maintenance sodium dose
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3-4mEq/kg/d
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maintenance potassium dose
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2-3mEq/kg/d
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alteration of fluids
in fever |
↑ by 5ml/kg/d for each degree over 38C
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alteration of fluids
in hyperventilation |
↑ by 10-60ml/100 kcal BEE (basal energy expenditure)
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alteration of fluids
in sweating |
↑ by 10-25ml/100 kcal BEE
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alteration of fluids
in diarrhea |
↑ on a ml/ml loss basis
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alteration of fluids
in hyperthyroidism |
25-50%
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alteration of fluids
in renal failure |
maintenance fluids are equal to insensible losses(300ml/m3) +urine replacement (ml/ml)
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alteration of fluids
in renal disease |
monitor and analyze output, adjust accordingly
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Extremely low birth weight
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<1kg
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Very low birth weight
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<1.5 kg
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Low birth weight
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<2.5 kg
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Small for gestational age
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<10th percentile
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Appropriate for gestational age
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10-90th percentile
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Large for gestational age
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>90th percentile
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neonatal vitals
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↑HR
↑RR ↑K ↓BP ↓SCr |
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hypertonicity is associated with
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with necrotizing enterocolitis-NEC and intraventricular hemorrhage-IVH
hepatic injury if infused into umbilical or portal vein |
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adjuvants to avoid in infants
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benzyl alcohol
propylene gylcol sorbitol |
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effects of benzyl alcohol
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gasping syndrome, displaces bilirubin
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effects of propylene glycol
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respiratory depression
seizures lactic acidosis arrhythmias hypotension |
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effects of sorbitol
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diarrhea
abdominal pain gas (large doses) |
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routine care of newborns
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erythromycin
vitamin K hepatitis B vaccine |
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pathophysiology of respiratory distress syndrome
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Respiratory failure with decreased ling compliance, hypoxemia, atalectasis, small airway epithelial damage, pulmonary edema
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cause of RDS
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pulmonary surfactant deficiency
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timeline of RDS
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30-32 weeks – synthesis and secretion
34-36 weeks – surfactant sufficient for normal lung function |
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how to delay premature labor to decrease risk of RDS
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use tocolytic
terbutaline indomethacin nifedipine magnesium sulfate • Antenatal corticosteroids – decrease the incidence of RDS |
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how to decrease the incidence of RDS
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adrenal corticosteroids
-betamethasone -dexamethasone |
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treatment of RDS
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empirically treat other causes (Abx)
give exogenous surfactants -beractant, calfactant, poractant -prophylactic use only for extremely premature |
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side effects of exogenous surfactants
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bradycardia, oxygen desaturation, mucous plugging, blood pressure and EEG changes, pulmonary hemorrhage, risk of apnea
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describe bronchopulmonary dysplasia
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o Most common chronic pulmonary disease in infants
o Occurs in newborns on supplemental oxygen and positive-pressure ventilation for other lung diseases (RDS) |
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2 major risk factors for bronchopulmonary dysplasia
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low birth weight
gestational age |
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other risk factors for bronchopulmonary dysplasia
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oxygen toxicity, fluid excess, mechanical ventilation, male, caucaisian, persistent PDA
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causes of bronchopulmonary dysplasia
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immature lung, surfactant deficiency, oxygen toxicity, inflammation, barotraumas, volutrama, infection, nutrient deficiency
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complications of bronchopulmonary dysplasia
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pulmonary HTN, systemic HTN, cor pulmonale, left ventricular hypertrophy, problems with neurodevelopment, nutrition, growth, RSV
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prevention of bronchopulmonary dysplasia
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prevent prematurity, prevent RDS, adequate nutrition, fluid restriction
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Management of BPD
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• Oxygen, mechanical ventilation, fluid restriction, nutrition(hypercaloric)
• Medical management: diuretics, bronchodilators, corticosteroids • Goals: reduce Sx and improve lung function |
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3 classes of Tx of BPD
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diuretics
--furosemide, chlorthiazide, HCTZ, spironolactone bronchodilators -caffeine, theophylline, albuterol, metaprenerol, ipratroprium inhaled corticosteroids -beclomethasone, fluiconide, fluticasone, budesonide |
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describe necrotizing enterocolitis
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most common life-threatening non-respiratory disease, acute interstitial necrosis(AIN)
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Sx of necrotizing enterocolitis
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abdominal distention, bloody stools, apnea, metabolic acidosis, gas in the intestinal mucosa or portal venous systems, free air in the abdomen, usually limited to the ileum and colon, can progress to advanced stages in 24-48h
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causes of necrotizing enterocolitis
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interstitial bacteria and inflammatory mediators
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prenatal causes of necrotizing enterocolitis
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eclampsia, prolonged rupture of membranes, cocaine
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postnatal causes of necrotizing enterocolitis
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PREMATURITY, respiratory distress, ductus arteriosis, hyperosmolar substances, rapidly advancing feeds
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medications that can cause necrotizing enterocolitis
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corticosteroids, indomethacin, H2RAs
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prevention of necrotizing enterocolitis
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• Interstitial priming/trophic feeds, avoid aggressive advancement of feeds, breastfeeding, careful with hyperosmolar medications and formulas, maternal steroids, infection control
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tx of necrotizing enterocolitis
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• Stop feeds – start TPN and bowel rest for 7-14 days
• Decompress abdomen (suction) • Start ABX for 72 hours to rule out or 7-14 days if treating |
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broad spectrum Abx for necrotizing enterocolitis
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ampicillin + gentamicin
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Abx for late onset necrotizing enterocolitis
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vancomycin + gentamicin
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Other Abx for necrotizing enterocolitis
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cefotaxime + ampicillin or vancomycin
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Tx of peritonitis
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give metronidazole or clindamycin for anaerobic coverage
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complications of necrotizing enterocolitis
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interstitial strictures, short-bowel syndrome (malabsorption and malnutrition)
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definition of apnea of prematurity
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stop breathing for >15sec, (less if bradycardia), hypoxemia, cyanosis
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3 types of apnea of prematurity
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central(no respiratory effort)
obstructive mixed |
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incidence of apnea of prematurity is most in
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premies <1kg
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causes of apnea of prematurity
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prematurity, drugs, other illnesses
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Tx of apnea of prematurity
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tactile stimulation, methyxanthines (caffeine, theophylline, methylxanthine), oxygen, oscillation, nasal continuous positive airway pressure, positive-pressure ventilation (usually resolves at 37wks of age)
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use methylxanthines in apnea of prematurity when
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>3 episodes of apnea lasting >20-30 seconds, accompanied by bradycardia/cyanosis, not controlled by non-pharm therapy
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toxicities of methylxanthines
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tachycardia, agitation, irritability, hyperglycemia, feeding intolerance, GERD, emesis
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preferred methylxanthine
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caffeine
↓ADE, less monitoring, less frequent dosing |
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dosing of caffeine
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LD 10 mg/kg/dose
MD 5 mg/kg/dose |
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monitoring of caffeine
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watch for 7-10 days
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describe neonatal abstinence syndrome
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Withdrawal Sx caused by maternal use of illicit drugs or pain medications/opiates etc
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Sx of neonatal abstinence syndrome
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Dehydration, vomiting, poor feeding, excessive weight loss, seizures, severe hyperactivity, irritability
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nonpharm Tx of neonatal abstinence syndrome
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↓sensory stimulation, frequent small feedings
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pharm Tx of neonatal abstinence syndrome
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Tincture of opium, methadone, morphine, phenobarbital (for non-narcotic or polydrug use), diazepam, lorazepam
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define SIRS
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Systemic inflammatory response syndrome
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criteria for SIRS
|
2/4, 1 has to be temp or WBC
temp <36 or >38.5C WBC (↑,↓ for age or >10%N) bradycardia tachycardia tachypnea |
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sepsis
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SIRS (at least 2) + infection
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severe sepsis
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sepsis + one of the following (CV dysfunction, acute respiratory distress syndrome-ARDS, two or more organ dysfunctions)
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septic shock
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sepsis with refractory hypoperfusion
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neonatal sepsis
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Sepsis occurring within the first month of life
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early onset of neonatal sepsis
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<7 days old
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RF for early onset neonatal sepsis
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preterm delivery, prolonged rupture of membranes, maternal group B strep, chorioamnionitis, maternal fever >38C within 24hours of delivery, intrauterine monitoring devices or the use of obstetrical foreceps
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source of pathogen in early onset neonatal sepsis
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maternal genital tract
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pathogens in early onset neonatal sepsis
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group B strep
E. coli Listeria monocytogenes |
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Tx of early onset neonatal sepsis or home discharge late onset neonatal sepsis
|
ampicillin
--B strep, L mono, S pneumo AG --E coli, Klebsiella, H flu, synergy cefotaxime --E.coli, klebsiella, H. flu |
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timing of late onset neonatal sepsis
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>7 days old
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risk factors of late onset neonatal sepsis
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low birth weight, IV catheters or indwelling devices, parenteral nutrition, unknown maternal risk factors, community acquired infections
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source of pathogen in late onset neonatal sepsis
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nosocomial or maternal genital tract
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pathogens in late onset neonatal sepsis
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coagulase negative staph
S. aureus Pseudomonas anaerobes candida or early onset |
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Tx of hospitalized late onset neonatal sepsis
|
Vanco – MRSA, CoN staph, B strep
AG – E.coli, klebsiella, H. flu, synergy |
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screening of neonatal sepsis
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At 35-37 weeks gestation with risk factors whose mother received <4 hours of antibiotic treatment prior to delivery or who are symptomatic
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duration of therapy in neonatal sepsis
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• Asymptomatic after 48hrs of Tx→ DC
• Symptomatic Sepsis→ 7-10 days |
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define pediatric sepsis
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Defined as sepsis beyond the neonatal period
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Tx pediatric sepsis when...
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clinical suspicion of infection and evidence of SIRS
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risk factors of pediatric sepsis
|
indwelling catheters
asplenic or sickle cell pts immunosuppressed pts |
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Bugs in pediatric sepsis in healthy children
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N. meningitis, H flu, S. pneumo, S. aureus, Salmonella
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Tx of pediatric sepsis in healthy children
|
vanco + cefotaxime
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Bugs in pediatric sepsis in immunocompromised children
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CoNS, enterrococcus, viridian strep, enterrobacter, anaerobes, candida, viral
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Tx of pediatric sepsis in immunocompromised children
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vanco + antipseudomonal agent
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adjunctive/supportive care of pediatric sepsis
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Fluids/electrolytes (10-20ml/kg isotonic saline or LR), vasopressors, blood products, respiratory support, nutrition, glycemic control, steroids
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if GBS use
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PCN
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if enterococcus, use
|
amp or vanco ± gent
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if Listeria, use
|
amp ± gent
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if S. aureus, use
|
nafcillin or vanco
|
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If S. epidermidis, use
|
vanco
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If E.coli/kelbsiella/citrobacter , use
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amp ± AG/cefotaxime
|
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If enterobacter/serratia, use
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beta lactam + AG
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If P. aeruginosa, use
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antipseudomonal beta lactam
|
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if anaerobe, use
|
metronidazole or clindamycin
|
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if candida, use
|
fluconazole or ampho B
|
|
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If HSV, use
|
acyclovir
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Tx of early onset neonatal meningitis
|
ampicillin + AG or cefotaxime
|
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Tx of late onset neonatal meningitis
|
vancomycin + AG or cefotaxime
|
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Tx if risk factors present or suspicion of HSV
|
add acyclovir
|
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meningococcemia specific Sx of pediatric meningitis
|
petechiae and purpura (death will result if untreated for 24hrs)
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H flu specific Sx of pediatric meningitis
|
joint involvement
|
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most common pathogens of pediatric meningitis
|
o H. flu – 7 days
o S.pneumo – 10-14 days o N. mengingitidis – 7 days |
|
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• Bugs and treatment resistance
|
o H. flu – ampicillin resistant
o S. pneumo – penicillin and beta-lactam resistant o N. meningitides – penicillin resistant (use 3rd gen ceph) |
|
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dexamethasone use in meningitis
|
• Only recommended for HiB meningitis (hardly used)
|
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long term complications of meningitis
|
seizures, hearing loss, learning/behavioral problems
|
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Px of long term complications of early onset meningitis
|
intrapartum chemoprophylaxis(PCN to mom), prevention of preterm delivery
|
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Px of long term complications of late onset meningitis
|
judicious use of ABX
|
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vaccinations and meningitis
|
HiB, pneumococcal, meningococcal
|
|
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cause of kawasaki's disease
|
unknown, believed to be infectious, disease of exclusion, mainly affects children <5yo,
|
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epidemiology of kawasaki's disease
|
higher in Asian population, higher in boys, higher seasonally (Jan and June/July)
|
|
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etiology of kawasaki's
|
linked to being infectious d/t seasonality, linked with coronavirus
|
|
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pathogenesis of kawasaki's
|
idiopathic, but cytokines are increased
|
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presentation of kawasaki's
|
o Begins with fever (not responsive to APAP or IBU) that could persist for weeks
o Skin rash (trunk and groin), red eyes, red mucous membranes in the mouth(cracked lips, strawberry tongue), bilateral conjunctivitis, lymphadenopathy in the neck area(>1.5cm), erythema or desquamation of the palms or soles |
|
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lab findings of kawasaki's
|
o CRP and ESR(acute phase reactants), CBC, UA, serum alanine aminotransferase, serum albumin
|
|
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cardiac complications of kawasaki's
|
• Coronary artery aneurysm
|
|
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RF for Coronary artery aneurysm
|
age <1yo or >6yo, male, fever >14d, serum sodium >135, Hct <35%, white cell counts >12K
|
|
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cause of coronary artery aneurysm
|
unknown, related to inflammation
|
|
|
nonvascular complications of Kawasaki's
|
• Urinary abnormalities and renal disease
• GI abnormalities • Macrophage activation syndrome |
|
|
Tx of Kawasaki's
|
IVIG
glucocorticoids Add'l specific Tx |
|
|
Dose of IVIG*****
|
• 2gm/kg x1 dose over 12 hours
o Start slow and increase q15-30min as tolerated |
|
|
infusion reactions of IVIG
|
fever, chills, hypotension, HA
|
|
|
how to premedicate for IVIG
|
APAP, diphenhydramine, and/or steroids (methylpred, dex)
|
|
|
post IVIG medication
|
ASA
• 80-100mg/kg/day (divided every 8 hours) • Reduce to 3-5mg/kg/day after acute phase • If coronary artery changes, consider the addition of clopidogrel, warfarin, or heparin |
|
|
prognosis of Kawasaki's if no cardiac involvement
|
return to normal w/o signs and Sx related to the heart
|
|
|
prognosis of Kawasaki's if early Dx
|
5% cardiovascular complications, half will resolve in 1-2 years
MI risk is highest in 1st year after onset |
|
|
Worst prognosis of Kawasaki's is with
|
giant aneurysm, progress to steroids
|
|
|
Which vaccines are given subQ
|
MMR, MMRV, varicella, MPSV4
|
|
|
Which vaccine is given as an oral suspension?
|
RV
|
|
|
What is used multiple times throughout the winter and has a max of 3 doses/yr for healthy patients?
|
RSV
|
|
|
Which vaccines require 1 dose?
2 |
Meningitis (MPSV4, MCV4)
|
|
|
Which vaccines require 2 doses?
4 |
Hep A, varicella, MMR, MMRV
|
|
|
Which vaccines require 3 doses?
4 |
HPV, rotavirus, Hep B, IPV
|
|
|
Which vaccines require 4 doses?
2 |
PCV
HiB |
|
|
Which vaccines require 5 doses?
1 |
DTaP
|
|
|
3 common household substances that cause poisoning
|
cleaning solution
pesticides pharmaceutical toxins |
|
|
pH of most cleaning solutions ingested
|
alkaline
|
|
|
Sx of cleaning solution toxicity
|
excessive salivation, bloody vomit, coughing, erythema, ulceration
|
|
|
Initial Tx of cleaning solution toxicity
|
airway management (emesis NOT recommended)
|
|
|
common pesticides that cause toxicity
|
Organophosphates (irreversible cholinesterase inhibitors)
|
|
|
most common neurologic Sx of pesticide toxicity
|
seizures, coma, agitation, areflexia, pin-point pupils
|
|
|
most common GI Sx of pesticide toxicity
|
SLUDGE
salivation, lacrimation, urindation, defectaion, GI motility, emesis |
|
|
most common cardiopulmonary Sx of pesticide toxicity
|
bronchospasm, tachycardia, respiratory failure
|
|
|
Initial nonpharm Tx of pesticide toxicity
|
• Organophosphate levels should be obtained
• Gastric lavage (remove stomach contents) • Seizure management |
|
|
Initial pharm Tx of pesticide toxicity
|
activated charcoal
anticholinergics -atropine |
|
|
S/Sx of APAP toxicity
|
non-specific, N/V, myocardial damage, hepatic damage, renal damage, neurologic Sx like coma, metabolic acidosis, hematological abnormalities, pancreatitis
|
|
|
Physiology of APAP toxicity
|
glucoronidation and sulfation, pathways become saturated and metabolism by P450 takes over
• P450 pathway makes NAPQI → binds to cells in the liver →apoptosis, resulting in hepatic degeneration |
|
|
monitoring of APAP toxicity
|
• Labs can be pulled 24-36 hours after ingestion, acute overdose may cause severe hepatotoxicity which may not be detected for up to 4 days after ingestion
-• Upon admission get labs drawn for AST, ALT, total bilirubin, INR • 4 hour post-ingestion plasma level to determine if NAC is indicated • Do not delay NAC administration if levels are not back, start the loading dose • Do not DC if levels drop below Tx level after 1st dose |
|
|
Who to Tx for APAP toxicity?
|
Single ingestion >6-8gm for an adult or 200-250mg/kg for a child
|
|
|
Tx for APAP toxicity
|
• Activated charcoal – give ASAP, especially in the 1st few hours
• NAC |
|
|
MOA of NAC
|
augments the glutathione reserves and together with glutathione directly bind to toxic metabolites, protects the liver from NAPQI toxicity
|
|
|
dosing of NAC
|
o 1st dose: 150mg/kg in 200ml of D5W over 60 minutes
o 2nd dose: 50mg/kg in 500ml of D5W over 4 hours o 3rd dose: 100mg/kg in 1000ml of D5W over 16 hours |
|
|
central effects of clonidine toxicity
|
impaired consciousness, hypotonia, hyporeflexia, miosis, bradycardia, hypotension, respiratory depression, apnea, hypothermia
|
|
|
peripheral effects of clonidine toxicity
|
hypertension, tachycardia at first, then hypotension and bradycardia
|
|
|
onset of clonidine toxicity
|
30min-4 hours post-ingestion
|
|
|
monitoring of clonidine toxicity
|
no specific lab work, monitor for CNS depression, vitals, ECG, pulse ox if symptomatic
|
|
|
Tx of clonidine toxicity
|
• Activated charcoal
• Fluids – for the hypotension • Nitroprusside – severe initial hypertension • Naloxone – for respiratory depression, hypotension, and coma |
|
|
S/Sx of antidepressant toxicity
|
can be mild Sx, serotonin syndrome, seizures, CNS depression
• 30x daily dose - Minor Sx • 50-75x daily dose – vomiting, CNS depression, tremor • >150x the daily dose or in the presence of alcohol – fatalities |
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Presentation of serotonin syndrome
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autonomic instability, mental status changes, increased neuromuscular tone
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Tx of serotonin syndrome
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supportive care and close monitoring
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Sx of iron toxicity
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vomiting, diarrhea, lethargy, stupor, shock, acidosis, bloody vomit, bloody diarrhea, coma
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clinical course of iron toxicity
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• Phase 1 (0.5-2hr)
• Vomiting, hematemesis, abdominal pain, diarrhea, hematochezia, lethargy, shock, acidosis, coagulopathy • Phase 2 • Apparent recovery and false sense of security • Phase 3 (2-12 hours after phase 1) • Shock, acidosis, cyanosis, fever • Phase 4 (2-4 days later) • Hepatotoxicity, lung injury • Phase 5 • GI scarring and strictures |
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Dose of elemental iron per tab
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FSG 359
• Fumarate divide by 3, sulfate divide by 5, gluconate divide by 9 |
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o Treatment for Fe ingestion (based on quantity of elemental iron ingestion)
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• <30mg/kg – ER if Symptomatic
• 30-50mg/kg – syrup of ipecac • >50 or unknown – syrup of ipecac, if no success gastric lavage |
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o Treatment for Fe ingestion based on serum toxicity
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• 400-450 ug/dl and symptomatic – deferoxamine (iron chelator) 10-15 mg/kg/hr IV in D5W (NTE 6gm/d)
• 500-550 ug/dl deferoxamine • 600-800 ug/dl deferoxamine and whole bowel irrigation • If asymptomatic after 6 hours – no Tx is necessary |
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MOA of salicylate toxicity
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• Uncouples oxidative phosphorylation, producing metabolic alkalosis
• Acts as a CNS and respiratory stimulant producing respiratory alkalosis |
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severities of salicylate toxicity
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• Determine quantity ingested
• Mild tox: <150mg/kg, moderate: 150-300, life-threatening >300, severe >500 |
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monitoring of salicylate toxicity
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• Obtain serum level within 3-4 hours, monitor blood gases, electrolytes, and blood sugar
• Repeat every 4 hours until stable • If the pt is asymptomatic and the 3-4 hour level is less than 30mg/dl there is no need for repeat testing unless the pt took enteric coated preparations |
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Tx of salycilate toxicity
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• Alkalinize the urine with sodium bicarbonate (2-3mEq/kg over 4-6 hours)
• 80mEq/L of D5W • Infusion rate: 5-10 mk/kg/hr for 1-2 hours • Continue hydration: after 2-3 hours of bicarb dose |
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activated charcoal summary
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o Binds drug and prevents absorption, best if <1hr from ingestion
o CI: overdoses involving caustics, solvents, or altered mental status o Dose: adults 25-100gm, children <12yo 25-50gm, infants <1yo 1g/kg |
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2 types of congenital heart defects
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o Structural – defects in the walls, valves, arteries or veins
o Functional - affects blood flow |
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causes of congenital heart defects
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• Genetics – chromosome abnormalities
• Environmental – maternal infections(rubella), drug exposure during pregnancy(isotretinoin, lithium, etc.), maternal disease states (diabetes), alcohol consumption |
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3 main shunting systems in fetal circulation
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ductus arteriosis, foramen ovale, ductus venosus
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course of fetal circulation
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• Oxygenated blood comes from the placenta
• 50% bypasses the liver and goes to the inferior vena cava(via ductus venosus) and onto the right atrium • Right atrium to left atrium via foramen ovale→ then to the left V. and out to heart, brain, and body • Right atrium to the right ventricle |
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when the Right atrium to the right ventricle
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o Blood mixes with the deoxygenated blood from the superior vena cava (high pulmonary vascular resistance-PVR)
o Right ventricle to the aorta (via ductus arteriosis) and out to body, umbilical arteries, and returning to placenta |
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describe transitional circulation
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• Transfer of oxygen exchange from placenta to lungs, arterial and venous circulations become separate
• First breath lungs become functional, ↓ pulmonary resistance and ↑ pulmonary blood flow • Clamping of the umbilical cord: ↑ systemic vascular resistance, ↑ pulmonary venous return, leading to ↑ left arterial pressure (closure of foramen ovale @3mo) and ventricular afterload • Removal of placenta – closure of the ductus venosus • Closure of the ductus arteriosis – begins at 10-15 hours and completes by 2-3 weeks |
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describe ventricular septal defect
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• Opening between the ventricles, left to right shunt (d/t lower pressure on the right), ↑ oxygenated blood entering the lungs, ↑PVR, eventual development of pulmonary hypertension (4 types based on location)
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if untreated, ventricular septal defect...
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can lead to ventricular hypertrophy, atrial enlargement and heart failure, irreversible pulmonary hypertension
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Presentation of ventricular septal defect depends on
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location and size
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Tx of ventricular septal defects with moderate-large defects with CHF
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high caloric intake, digoxin, and diuretics until stable enough for surgery
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describe arterial septal defect
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• Opening between the atrium, left to right shunt(pressure), ↑ oxygenated blood entering the lungs, ↑PVR, eventual development of pulmonary hypertension (3 types based on location)
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if arterial septal defect is left untreated
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can lead to ventricular hypertrophy, atrial enlargement and heart failure, irreversible pulmonary hypertension
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describe Patent ductus arteriosis
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• Opening between the pulmonary artery and the aorta (bifurcation)
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effects of Patent ductus arteriosis
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• Shunts blood away from the lungs and out to the body, shunting occurs from the right side of the heart to the left side of the heart (d/t ↑PVR and low SVR)
• Remains open due to low oxygen tension and elevated prostaglandins • Normally closes in the first few hours of birth (from ↑O2 tension and ↓PGs) |
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Patent ductus arteriosis is common in
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premies (spontaneously close) but uncommon in term infants (rarely spontaneously close)
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causes of Patent ductus arteriosis
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complicated pregnancies(hypoxemia or rubella), premie, births at high altitude (d/t ↓O2 tension)
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risk factors for Patent ductus arteriosis
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bacterial endocarditis, aneurysms, calcification of the ductus, development of pulmonary HTN/right to left shunting/and CHF
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Tx for PDA
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o IBU 10mg/kg once, followed by 2 doses of 5mg/kg at 24 and 48 hours
• Dilute with dextrose or saline, give within 30 minutes, infuse over 15min, do not mix with TPNs |
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ADRs of IBU for PDA
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↓ urine output, ↓SCr, ↑ risk of necrotizing enterocolitis, ↓ cerebral blood flow, ↓ platelet aggregation(thrombocytopenia)
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why is IBU preferred over indomethacin?
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More renal problems, equally efficacous but not inferior in terms of cerebral blood flow (flow reduction is actually less)
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2 procedures for treating PDA
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• Transcatheter coil closure (reserved for multiple small defects or if no medical intervention is available) not an option for premies
• Surgical ligation (closure via sutures)only failure of medical intervention or large defects |
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CI to medical management of PDA
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• Thrombocytopenia – platelet transfusion prior to meds
• Active bleeding - ↑ risk of other bleeds • Coagulation defects – measure platelets and bleeding risk • Necrotizing enterocolitis – increases risk • Renal insufficiency – worsening issues • Infections • Shunt is needed d/t additional defect |
