Neonatology: Vomiting Newborns

Front 1

Name 2 features describing the infant's vomiting that are key in history taking.

Back 1

1. Color: bilious vs. nonbilious

2. Force: projectile vs. non-projectile

Front 2

Name 2 very common non-surgical causes of vomiting.

Back 2

1. Overfeeding

2. Reflux

Front 3

Re overfeeding:

1. What is the typical stomach capacity of a 1 day old infant comparable to?

2. And on the third day?

Back 3

1. A calmamansi lemon (5-7 mL)

2. A siniguelas (hog plum) (22-27 mL)

Front 4

What is the primary question needing an answer when presented with a repeatedly vomiting newborn?

Back 4

Is the vomiting the herald for a serious life-threatening condition that only surgery can fix?

Front 5

Name the most common surgical condition causing vomiting in newborns.

Back 5

Pyloric stenosis

Front 6

Within which timespan is pyloric stenosis diagnosed?

Back 6

Between 2-12 weeks: a very long time ago, it seldom was discovered before 2-3 month of age. (In other words, we're not likely going to see it in the newborn nursery.)

Front 7

What causes pyloric stenosis?

Back 7

The cause is not known: it often runs in families, though exposure of infants to oral erythromycin is one environmental factor talked about.

Front 8

What is the underlying pathophysiology in pyloric stenosis?

Back 8

Pyloric innervation has become abnormal, leading to failure of the pyloric muscle to relax

Front 9

Name 2 "growth factors" whose increased systhesis can cause hypertrophy of pyloric muscle tissue.

Back 9

1. Platelet derived growth factor

2. insulin-derived growth factor

Front 10

What is the incidence of pyloric stenosis in newborns?

Back 10

2-4/1000 live births

Front 11

Name four important historical features about the vomiting seen in pyloric stenosis.

Back 11

1. Term infant

2. Non bilious

3. Projectile vomiting

4. Insidious onset: might be taken for GER at first, then becoming constant with every feed

Front 12

What is the preferred test to order if pyloric stenosis is suspected and name 3 reasons why?

Back 12

Abdominal ultrasound (sensitivity 99.5%, specificity 100%, NO radiation)

Front 13

1. What dimensions of the pylorus are used to determine whether stenosis exists?

2. What else we're looking for?

Back 13

1. More than 16 mm long and 4 mm thick (very young newborns may present with a thickness of 3 mm)

2. Watch for fluid making its way through the pyloric channel (yep, it can be seen)

Front 14

When might an upper GI series be considered (albeit reluctantly) in the diagnosis of pyloric stenosis?

Back 14

Only if the ultrasound fails to give clear findings

Front 15

What two physical findings are associated with pyloric stenosis? When are you likely to find them?

Back 15

1. Visible peristaltic waves best seen in the mid to left upper quadrant of the abdomen

2. Pyloric "olive"

Easiest to find in more dehydrated babies relatively later in the course, hardly ever noticed in the earliest stages

Front 16

Name the typical metabolic imbalance associated with pyloric stenosis.

Back 16

Hypochloremic hypokalemic metabolic alkalosis

Front 17

How does pyloric stenosis cause alkalosis?

(3 steps)

Back 17

1. Non-stop vomiting causes loss of fluids rich in hydrochloric acid.

2. In an attempt to hold on to hydrogen ions, the kidneys start desperately (and futilely) to hoard them at the expense of potassium.

3. If there is nothing done, protons will get excreted into the urine anyway, producing the famed "paradoxical aciduria."

Front 18

Without prompt fluid resuscitation, how does the newborn's body respond to prolonged hypochloremic hypokalemic alkalosis?

Back 18

By compensating for the alkalosis with a respiratory acidosis (i.e., they become apneic, and if they go to surgery in that state, they won't get off the ventilator).

Front 19

What are the two major steps of fluid resuscitation that must be done before sending a newborn with pyloric stenosis to the OR?

Back 19

1. Saline bolus in severe dehydration (20 mg/kg 0.9% saline over 10-30 minutes), followed by

2. D5 half-normal saline with 20 mEq/L KCl at 1.5 times maintenance

Front 20

What happens to sodium during hypochloremic hypokalemic alkalosis associated with unrecognized pyloric stenosis

Back 20

Nothing in particular; sodium might be elevated, low, or within normal ranges

Front 21

At the very least, what 2 electrolyte parameters must be met before allowing the anesthesiologist to get their hot little hands on the baby scheduled for surgery for pyloric stenosis?

Back 21

1. HCO3- < 28 mEq/dL

2. Cl- > 100 mEq/dL

Front 22

1. What is the name of the operation commonly used to correct pyloric stenosis?

2. What does the operation do?

Back 22

1. Pyloromyotomy

2. Extramucosal (mucosa not cut) longitudinal splitting of the pyloric muscle

Front 23

Where is the scar of an old-fashioned open pyloromyotomy found?

Back 23

RUQ of the abdomen

Front 24

What does the scar of a laparoscopic pyloromyotomy look like?

Back 24

Actually, there are 3 very small ones: one inferior to the umbilicus, and 2 more in the epigastric area.

Front 25

1. If an infant can't have surgery to correct pyloric stenosis, what drug can provide an alternate treatment?

2. How is it given?

3. How long the hospital stay?

4. What is the average number of days that oral atropine is taken?

5. What's the success rate?

Back 25

1. Atropine

2. IV, then P.O.

3. A median of 13 days

4. 44 days

5. 85%

Front 26

What does bile-stained emesis mean for a newborn?

Back 26

This is a cardinal sign of neonatal intestinal obstruction requiring a surgical consult, pronto!

Front 27

Name 2 commoner conditions causing intestinal obstruction in newborns

Back 27

1. Malrotation/volvulus of the intestine

2. Intestinal atresias: duodenal, jejunalieal, and colonic.

Front 28

In normal persons, what happens to the midgut in the 2nd month of embryonic life?

Back 28

It rotates 3 separate counterclockwise rotations of 90 degrees each, making a total of 270 degrees, using the superior mesenteric artery as its pivot.

Front 29

1. What does the Ligament of Treitz do, especially for radiologists?

2. Where should it be located?

Back 29

1. It marks the duodenal-jejunal junction

2. Following the successful rotation of the midgut, it suspends the distal duodenum by attaching itself in the LUQ, left of the spine and above the pylorus.

Front 30

What 2 things happen following malrotation of the midgut (i.e,. if the rotating process if messed with, at any time, at any stage)?

Back 30

1. The bowel is inadequately fixed, held by a narrow-based mesentery.

2. The ileocecal junction can't anchor itself in the right lower quadrant as it should; instead it attaches itself the best it can by forming Ladd's bands with adjacent structures

Front 31

What happens to the intestinal anatomy if there's no rotation of the midgut at all? (2 things)

Back 31

1. The ligament of Treitz is left in the RIGHT hemiabdomen.

2. Cecocolic limb in the LEFT hemiabdomen.

Front 32

1. What is the incidence of malrotation?

2. When is it typically discovered?

Back 32

1. 1/6000 live births (1 per year at BH-D)

2. 75% diagnosed in the first month of life; 90% by the end of the first year (meaning 10% are not discovered until maybe much later)

Front 33

Name 3 possible presentations of malrotation of the intestine.

Back 33

1. Acute bowel obstruction in infancy

2. Intermittent chronic abdominal pain (after the first year)

3. No symptoms at all; discovered as an incidental finding in older kids

Front 34

If malrotation presents as acute bowel obstruction, how will it progress if left alone? (Name 5 steps)

Back 34

1. Bilious, greenish emesis

2. Abdominal pain, distention

3. Inconsolability (think colic)

4. Metabolic acidosis

5. Dehydration and hypovolemic shock

Front 35

Name 3 late signs indicating you've waited too long to deal with the bowel obstruction related to malrotation of the intestine.

Back 35

1. Hematemesis

2. Melena

3. Erythema abdominal wall

Front 36

What should be ordered first in the work-up of suspected malrotation, and what are we looking for?

Back 36

Upper GI (without SBFT) is the "gold standard."

We're looking for:

1. Plain film: findings variable, nonspecific (gastric and/or duodenal distention, gasless abdomen)

2. The position of the Ligament of Treitz: is it in the LUQ where it's supposed to be?

Front 37

What causes the obstruction, when present, in malrotation of the intestine?

Back 37

The formation of Ladd's bands, usually from the ileocecal junction trying to attach itself, which act like post-surgical bowel adhesions, either causing volvulus or trapping the duodenum beneath them.

Front 38

Name three things that must be done to prep an infant with obstruction associated with malrotation of the intestine.

Back 38

1. Prompt fluid resuscitation to treat hypovolemia and electrolyte imbalances.

2. IV prophylactic antibiotics

3. NG decompression

Front 39

Name the primary goal of surgical management of catastrophic malrotation of the intestine.

Back 39

Prevention of loss of portions of the entire midgut that starts at the Ligament of Treitz and extends about 2/3 of the way through the transverse colon.

Front 40

Name the operation used to correct malrotation of the midgut, and the 6 steps it entails.

Back 40

Ladd procedure

1. Evisceration of the abdomen

2. Untwisting of the intention

3. Division of the offending Ladd's bands

4. Broadening of the mesentery to make the bowel be in a "safe" malrotated postion

5. Incidental appendectomy, because the cecum will be left in the LUQ

6. Small bowel stays in right hemiabdomen; the colon remains on the left.

Front 41

Name the major morbidity associated with obstruction associated with malrotation of the intestine.

Back 41

Short bowel syndrome seen in 18%, caused by midgut volvulus.

Front 42

What's the mortality rate for symptomatic infants diagnosed with intestinal malrotation?

Back 42

3-9%: seen in patients suffering with volvulus, bowel necrosis, prematurity and other abnormalities.

Front 43

Name the three major locations of intestinal atresias.

Back 43

1. Duodenum

2. Jejunoileal

3. Colonic

Front 44

Which is the most common type of intestinal atresia?

Back 44

1. Duodenal

Front 45

Name 2 possible presentations of duodenal atresia. What presentation is usually not seen?

Back 45

1. Bilious vomiting

2. "Feeding intolerance"

But abdominal distention is seldom seen!

Front 46

The presence of which 3 anomalies should always be searched for in newborns with duodenal atresia?

Back 46

1. Cardiac anomalies, seen in one-half

2. Renal (19%)

3. Down's syndrome in 20-25%

Front 47

What is an abdominal x-ray likely to show us in an infant with duodenal atresia?

Back 47

"Double bubble"

Front 48

Name the 5 steps of surgical management in duodenal atresia.

Back 48

1. Fluid resuscitation

2. Gastric decompression

3. Total parenteral nutrition

4. Search for cardiac and renal anomalies

5. Duodenoduodenostomy: the anastomosis of the proximal and distal sections of normal bowel.

Front 49

Name 2 additional anomalies that might be discovered during surgery for duodenal atresia.

Back 49

1. Annular pancreas (46%)

2. Malrotation (39%)

Front 50

What is most likely to kill an infant with duodenal atresia in the initial stages?

Back 50

The cardiac anomalies when present

Front 51

What is the best explanation for the presence of jejunoileal atresia in a newborn?

Back 51

A late intrauterine mesenteric vascular accident

Front 52

Which 3 findings appear in a typical presentation of jejunoileal atresia?

Back 52

1. Bilious emesis

2. Abdominal distention (in contrast to duodenal atresia)

3. Failure to pass meconium

Front 53

Name 3 other findings associated with jejunoileal atresia.

Back 53

1. Prematurity (44%)

2. Gastroschisis (16%)

3. Omphalocele (1.5%)

Front 54

1. If intestinal obstruction is suspected in the lower GI tract (the problem being in the jejunum and more distally), which xray should be ordered first?

2. What 2 things should we expect to see?

3. What would we order next?

Back 54

1. Abdominal X-ray

2. We'd see:

a. Dilated intestinal loops

b. Air fluid levels

3. Contrast enema, searching for microcolon

Front 55

Name the 4 anatomic types of jejunoileal atresia, with subtypes if needed.

Back 55

1. Type I: mucosal web blocking passage

2. Type II: fibrous cord

3. Type III:

a. Mesenteric gap defect, no connection between the segments

b. "Apple-peel" deformity

4. Type IV: Multiple atresias, resembling a string of sausages

Front 56

Name the 3 anatomic types of duodenal atresia .

Back 56

1. Type I: mucosal web, can resemble a windsock

2. Type II: the atretic ends of the duodenum are connected by a fibrous cord

3. Type III: Complete separation of the atretic ends

And... there also exists "duodenal stenosis"

Front 57

How does colonic atresia present?

Name 3 findings.

Back 57

Hard to distinguish from jejunoileal atresia:

1. Bilious emesis also

2. Abdominal distention also

3. Also--failure to pass meconium

Front 58

How is colonic atresia managed in the OR?

Describe the operation used.

Back 58

Segmental resection of affected bowel with primary anastomosis

Front 59

Name the main genetic cause of functional intestinal obstruction.

Back 59

Hirschsprung's disease

Front 60

What is the underlying problem affecting the intestine in Hirschsprung's disease?

Back 60

Absence of enteric ganglia along a variable length of intestine

Front 61

What is the incidence of Hirschprung's disease?

Back 61

1/5000 live births (about once a year at BH-D)

Front 62

Name three parts of the GI tract affected by Hirschsprung's disease.

Back 62

1. Large bowel (in varying lengths, in 5% the entire colon is involved and the clinical picture starts resembling a lower GI atresia.

2. Stomach

3. Esophagus

Front 63

In which 2 ways can Hirschsprung's disease present in the nursery?

Back 63

1. Failure to pass meconium in the first 48 hours of life

2. Abdominal distention relieved by rectal stimulation and/or washouts

Front 64

Name three classifications of Hirschsprung's disease based on their extent.

Back 64

1. Short segment (80%)

2. Long segment

a. Total colonic aganglionosis

b. Total colonic involvement and small bowel aganglionosis as well

3. Ultra short segment involvement

Front 65

What two steps usually are taken to diagnose Hirschprung's disease?

Back 65

1. Barium enema: identifies the "transition zone"

2. Rectal biopsy to determine absence of ganglion cells

Front 66

When confronted with Hirschprung's disease, what blood test should be ordered early on and why?

Back 66

Chromosome studies: anomalies found in about 12%