Ch. 33 Infant with Nonbilious Emesis Flashcards
Most likely diagnosis for non-bilious vomiting in infant?
Infantile hypertrophic pyloric stenosis (HPS)
** shows up around 3 weeks
** usually seen in firstborn boys
Why is it important to distinguish b/w bilious and nonbilious vomiting in an infant?
Presence or absence of bile in the emesis = useful diagnostic info
If obstruction is proximal to the pylorus, emesis will always be nonbilious… bile-stained emesis implies that obstruction is distal to ampulla of Vater
Children w/ bilious emesis presumed to have surgical problem unless proven otherwise
Classic history for HPS
Projectile, nonbilious vomiting (1-2 weeks) in healthy infant, but emesis will become progressively more forceful and voluminous
baby is hungry and eager to eat again after he vomits… by the time they are seen, they are dehydrated, with visible gastric peristaltic waves and palpable “olive-size” mass in RUQ
Classic Physical Exam Findings
- Dehydrated infant (sunken fontanelle)
- Palpable mass (“olive”) in RUQ –> thickened and elongated pyloric muscle
- Reverse peristaltic waves
Pathophysiology of this condition?
Hypertrophy + hyperplasia of circular muscle layer of the pylorus
Muscle thickening causes pyloric channel to become increasingly narrowed and elongated –> gastric outlet obstruction
Smooth muscle of stomach hypertrophies/dilates in response to vigorous peristalsis against obstructed pylorus –> stomach dilates and peristaltic contractions become stronger –> classic projectile vomiting of a large volume of gastric content occurs
Workup:
What is the first imaging study to obtain?
Additional study?
If no palpable “olive,” gold-standard = U/S (measures pyloric channel length, muscle thickness, diameter)
UGI contrast study - string sign at level of pylorus
What electrolyte abnormalities would you expect?
Hypochloremic, hypokalemic metabolic alkalosis
Chloride ions lost in gastric secretions / alkalosis initially caused by loss of gastric HCl / hypokalemia = result of combination of potassium ions being lost with vomiting and dehydration / dehydration and subsequent hypovolemia inc. aldosterone secretion –> leads to activation fo Na+/K+ pump in renal tubules
In an attempt to increase water reabsoprtion, Na+ is conserved at the expense of K+… as K+ levels in blood decrease, the kidney preferentially uses Na+/H+ pump to maintain Na+ and water reabsorption and prevent profound hypokalemia… this change leads to H+ secretion and worsening metabolic alkalosis
Urinalysis often reveals paradoxical aciduria
Mgmt:
What is the most important immediate management issue?
Secure IV access and begin fluid resuscitation
DEHYDRATION = most common issue due to prolonged, high-volume emesis
(isotonic fluid - normal saline - bolus of 20 ml/kg followed by resuscitation with 5% dextrose 0.45% NaCl at 1.5x typical maintenance rate)
What is the treatment?
Surgery –> Ramstedt pyloromyotomy
(abdomen entered either laparoscopically or through small transverse RUQ incision)
Pylorus ID’ed an incision made through overlying serosa and the thickened pyloric muscularis –> pylorus muscle is then spread apart until intact submucosa and mucosa are seen
What is the timing of surgery?
Surgery is delayed until effective fluid resuscitation and electrolyte replacement have been performed
