Flashcards in pyloric stenosis Deck (29):
non-bilious projectile vomiting in a lethargic 13 day old infant (born at 35 weeks) with a 3 cm mass below the right costal margin. what is the likely diagnosis?
what metabolic derangement is most likely?
hypochloremic, hypokalemic, hyponatremic metabolic alkalosis with compensatory respiratory acidosis
what tests confirm the diagnosis?
abdominal u/s, UGI with barium
would you proceed to surgery?
no, not immediately. the lethargy indicates this is a medical emergency and should be stabilized before proceeding to the OR.
when would you proceed with surgery?
the patient will need to be hydrated and have adequate urine output, as well as correction of the metabolic derangements. specifically, i would like:
what metabolic derangements do you expect to see?
persistent vomiting of stomach contents results in loss of Na, K, Cl, and H ions. i would expect the patient to be hypochloremic, hyponatremic, hypokalemic, and have metabolic alkalosis. the loss of H ions will also trigger the kidneys to waste alkalotic bicard so i think HCO3 will be lower.
why is rehydration important to correct the metabolic alkalosis?
dehydration and the sodium loss from vomiting interfere with the kidney's compensatory mechanism for metabolic alkalosis.
initially, the kidneys secrete bicarb to compensate for the metabolic alkalosis, however as dehydration and hyponatremia worsen, the conservation of sodium takes precedence and bicarb is also resorbed, further excretion of sodium, and increased bicarb formation. this worsens the metabolic alkalosis.
what fluids are ideal for medical optimization?
normal saline to replace volume and electrolyte deficits. after urine output is established, i would supplement with potassium. i may add glucose as necessary if hypoglycemia were present.
LR should probably be avoided since lactate is converted to bicarb.
what is the composition of NS and LR?
154 mEq/L Na, 154 mEq/L Cl, 0 mEq/L K, 0 lactate, 308 osm (slightly hypertonic)
130 mEq/L Na, 109 mEq/L Cl, 4 mEq/L K, 28 mEq/L lactate, 275 osm (slightly hypotonic)
how would you evaluate the neonates volume status?
assess physical signs such as: sunken fontanelles, skin turgor, capillary refill, heart rate, BP, mental status, frequency of vomiting and wet diapers
what rate would you start fluids out to resuscitate this neonate?
bolus of 10-20 mg/kg and then titrate to urine output and electrolyte normalization.
pt will likely also need maintenance fluids.
D5 1/4 NS at: (4kg)(4ml/kg/hr) = 16 ml/hr
that hct is 51. is this normal?
it may be high normal. term neonates are born with hct of about 55%, which then gradually declines to 30% at 3 months of age. it may be due to dehydration.
how would you induce this patient after she has been optimized?
a large concern is risk of aspiration. as such, i would place and apply suction to an ng or ogt in the lateral, supine, and prone positions to remove as much of the gastric contents as possible. i would then preoxygenate fully and perform RSI with cricoid pressure to further reduce the risk of aspiration. since there is a risk of significant bradycardia with succinylcholine in the pediatric population, i would pretreat with atropine.
what are the doses of medications you will give?
atropine 0.01 mg/kg
propofol 2-4 mg/kg
succinylcholine 2-3 mg/kg
fentanyl 1 mcg/kg
the surgeon asks for ancef. how much will you give?
what will you use to intubate?
miller 0, 3.0 9cm deep
what are some of the risks of giving succinylcholine to a neonate?
bradycardia and sinus arrest, hyperkalemia and cardiac arrest, rhabdomyolysis, masseter muscle spasm, malignant hyperthermia
why is the dose of succinylcholine higher in children than adults?
children have a relatively larger volume of distribution
is inhalation induction faster or slower in children when compared to adults?
faster in a neonate, secondary to a higher minute ventilation to FRC ratio and increased BF to vessel-rich organs. additionally, the blood/gas coefficient is lower in neonates compared to adults.
what is the blood gas coefficient?
it describes how soluble an anesthetic agent is in blood. it compares the the ratio of the concentration that is in blood to the concentration that is in gas that is in contact with blood as the same partial pressure.
the higher the coefficient, the more soluble it is, the slower the induction
you place the ETT and are unable to ventilate. what do you do?
i would increase to 100% FiO2, check the circuit, ensure the ETT was not kinked and verify proper placement with auscultation and direct laryngoscopy. if it was directly visualized through the VC my differential diagnosis would move to bronchospasm. i would apply positive airway pressure, deepen the anesthetic by increasing the inhaled agent and giving more propofol, and administering a beta2-agonist (to dilate bronchial smooth muscle).
i would be assess the oropharynx also for gastric contents as this could have caused the bronchospasm.
bronchospasm breaks, bilateral BS have improved, but airway pressures remain high. what will you do?
again confirm proper placement (rule out mainstem intubation), apply gentle PPV, administer beta2-agonist, and ensure sufficiently deep anesthesia.
my ddx would be residual bronchospasm, atelectasis, aspiration.
i would make the surgeon aware that aspiration was a possibility, however, bronchoscopy/lavage/antibiotics are probably not indicated, even if gastric contents were confirmed in the oropharynx.
are you concerned about hypothermia?
it is very important to avoid hypothermia, given its association with delayed awakening, respiratory depression, cardiac irritability, and increased PVR
neonates are particularly susceptible to hypothermia bc of low fat content, thin skin, and higher surface area to weight ratio.
how is temperature regulation in the neonate different than in the adult?
heat production occurs primarily through non shivering thermogenesis, which involves brown fat metabolism. it is very inefficient and may be further limited by volatile anesthetics adn in premature/sick neonates
would you extubate this patient in the OR? how?
assuming there is adequate spontaneous ventilation (6-10 mL/kg), normocapnia, and has undergone full reversal of any NDNMB, i would extubate her in the OR. however, given the continuing risk of aspiration, i would require that she be fully awake and in the lateral position. i do recognize that she had a significant bronchospasm intraoperatively and to mitigate the risk of this recurring, i would administer a beta2-agonist and narcotics just prior to lightening of anesthesia, and lidocaine just prior to extubation.
what concerns do you have for her postoperative course?
i am concerned about continued risk of aspiration and subsequent pulmonary dysfunction.
additionally, i am concerned about the increased risks associated with prematurity and general anesthesia such as: hypothermia, hypoglycemia, ROP and postop apnea
is she at increased risk of postop apnea?
yes because she is less than 50 weeks postconceptual age. additionally, metabolic alkalosis increases the risk also because the CSF will be alkalotic and cause central respiratory depression..
what are the risk factors of postop apnea?
low gestational age at birth, history of chronic lung disease, history of apnea/bradycardia, sepsis, anemia, multiple congenital anomalies, neurologic abnormalities. additionally, anything that exacerbates respiratory depression, such as narcotics.
caffeine (10 mg/kg) or aminophylline can be given to reduce risk.