vomiting with failure to thrive

8/11/2019 Vomiting with Failure to Thrive

1/20


2/20

THE CASE

ID: 44 day old term infant directly admitted to the floor from OSH ED.

CC: Vomiting

HPI: Mother reports that infant was feeding well until about 2 weeks

of life when he started vomiting. At first, this was intermittent, but now

infant vomits after every feed. NBNB. Emesis looks like formula and

seems to be the entire volume of feed, but non projectile. About 5 wetdiapers per day. Hard stools every other day. Wakes up to feed

easily and continues to want to feed after vomiting. No coughing or

sputtering. No increased fussiness.

At OSH, infant was noted to be cachectic, but alert and well hydrated.

Started on maintenance fluids of D5 1/2NS and transferred to PCH.


3/20

THE CASE

PMedHx: Term infant. No complications of pregnancy or birth.Unclear history of newborn screening.

Immunizations: Hep B likely received.

Family Hx: No metabolic disorders or infants with FTT.

Social Hx: Lives with mother, father, and 3 healthy siblings.Family works as migrant workers and infant was born in

Tennessee. Parents report that they had visited a pediatrician in

Salt Lake City 2-3 weeks prior to presentation and were told that

vomiting is normal.


4/20

THE CASE

VITALS: Temp 36.7, HR 120, RR 30, BP 84/55, O2 sat 99%

WEIGHT: 2.57 kg which is 89% of BW

General: Cachectic, NADHEAD: NC/AT, anterior fontanelle open, soft, depressed

EYES: Red reflex present, open spontaneously

NOSE: No discharge or obstruction.

OROPHARYNX: MMM. pallet intact.

CV: RRR. No murmur. Femoral pulses 2+. Cap refill 2 secondsLUNGS: CTAB. No increased WOB.

ABDOMEN: Soft, NTND, no mass, sunken

EXTREMITIES: No clubbing, cyanosis, or edema. Thin and boney.

NEUROLOGICAL: Normal tone, movements, level of alertness.

SKIN: No rash. Loose.


5/20

DIFFERENTIAL DIAGNOSIS

44 day old term infant with vomiting and FTT.


6/20

DIFFERENTIAL DIAGNOSIS

VOMITING

NEONATEPhysiologic reflux/GERD

Pyloric stenosis

Necrotizing enterocolitis

Malrotation w/ midgut volvulus

Gastroenteritis

Hirschsprung diseaseCongenital atresia

Congenital stenosis

Congenital webs

Metabolic disorders

Adrenal crisis

Dietary protein intoleranceOverfeeding

INFANTPhysiologic reflux/GERD

Gastroenteritis

Intussusception

Malrotation w/ midgut volvulus

Pyloric stenosis

Hirschsprung diseaseUTI

Toxic ingestion

Adrenal crisis

Increased ICP

Pancreatitis

Dietary protein intoleranceOverfeeding

CHILD/ADOLESCENTGastroenteritis

UTI

Strep pharyngitis

Appendicitis

DKA

Toxic ingestionPeptic ulcer

Eosinophilic esophagitis

Cyclic vomiting

Psychogenic

Increased ICP

Adrenal crisisObstruction

Constipation

Pancreatitis

Bezoar

Celiac disease

IBD


7/20


8/20

WORK UP

LABS:

1352.2

7844

310.47

91

Ca 11.1

iCal 1.19Phos 4.7

Mag 2.0

Protein 6.5

Albumin 3.9

Tbili 1.6

AP 228

ALT 37

AST 45

CBG: pH 7.56 / Co2 45 / Bicarb 42

Hypochloremic

metabolic

alkalosis


9/20

WORK UP

LABS:

1352.2

7844

310.47

91

Ca 11.1

iCal 1.19Phos 4.7

Mag 2.0

Protein 6.5

Albumin 3.9

Tbili 1.6

AP 228

ALT 37

AST 45

CBG: pH 7.56 / Co2 45 / Bicarb 42

Hypochloremic

metabolic

alkalosis

ABDOMINAL ULTRASOUND: The pylorus is enlarged. Pyloric channel

length 1.9 cm, with single layer muscular thickness 0.7 cm.


10/20

WORK UP

LABS:

1352.2

7844

310.47

91

Ca 11.1

iCal 1.19Phos 4.7

Mag 2.0

Protein 6.5

Albumin 3.9

Tbili 1.6

AP 228

ALT 37

AST 45

CBG: pH 7.56 / Co2 45 / Bicarb 42

Hypochloremic

metabolic

alkalosis

ABDOMINAL ULTRASOUND: The pylorus is enlarged. Pyloric channel

length 1.9 cm, with single layer muscular thickness 0.7 cm.

DIAGNOSIS: Pyloric stenosis


11/20

WORK UP


12/20

WORK UP


13/20

TREATMENT

HYDRATION AND RESOLUTION OF ALKALOSIS: 20 ml/kg NS then D5NS+20

meq/L KCl at 1.5 maintenance rate. IV replacement potassium. NPO.

PYLOROMYOTOMY: incision through the longitudinal and circular muscles of the

pylorus until mucosa bulges through incision.

OP NOTE: The duodenum adjacent to the pylorus was grasped providing

stabilization of the pylorus. The pylorus was then incised in a longitudinal fashionwith an arthrotomy knife. The muscular fibers were then spread. A complete

pyloromyotomy was performed as demonstrated by independent movements of

the 2 halves of the pylorus. Careful inspection showed no evidence of

perforation.


14/20


15/20

TREATMENT

NUTRITION: Feeds started at 15 ml q 3 hours and held at this rate for 24hours. Increased by 6 ml per feed every 6 hours to goal of 50 ml q 3

hrs.

MONITORING FOR REFEEDING: RFP and Mg levels q 6 hours during thefirst 24 hours. Consider EKG monitoring. Watch for hypophosphatemia,hypokalemia, hypomagnesemia, signs of Wernicke encephalopathy 2/2thiamine deficiency.

PREVENTION OF REFEEDING: Slow introduction of feeds.Recommendations vary: 10 kcal/kg/day or 25% of daily calorie goal onday one. Pretreatment with thiamine.


16/20

PYLORIC STENOSIS

EPIDEMIOLOGY:

2-3/1000 live births

Males>females

Symptoms begin around 3-5 weeks of life, rare after 12 weeks

ETIOLOGY:

Unclear

Likely a combination of genetic and environmental factors

Macrolide antibiotics?

Formula feeding?


17/20

PYLORIC STENOSIS

CLINICAL PRESENTATION:

Vomiting in a 3-6 week old infant

Age at presentation has changed (mean 5.4 weeks in 1975 and 3.4 weeks in

1995)

Emesis is immediately post prandial and may be projectile

Infant typically desires to feed soon after vomiting, happy spitters

Emaciated, dehydrated, with palpable olive sized mass in the RUQ at lateral

aspect of rectus abdominus with possible peristaltic waves


18/20

PYLORIC STENOSIS

LABORTATORY FINDINGS:

Hypochloremic metabolic alkalosis

Hypokalemia

Elevation of BUN and creatinine

CBC normal

Elevation of unconjugated bilirubin possible, icteropyloric syndrome

ULTRASOUND FINDINGS:

Increased pyloric muscle length, diameter and thickness

95% sensitive and specific if done by experienced examiner


19/20

PYLORIC STENOSIS

TREATMENT:

Rehydration

Pyloromyotomy

Reimplementation of nutrition

PROGNOSIS:

A review of cases from the Royal Hospital for Sick Children in Glasgow, Scotlandshowed a decrease in mortality of IHPS from 59 percent in 1925 to 0 percent in

1975, as a result of surgical intervention Mucosal perforations occur in about 1 percent of patients and are readily

recognized intraoperatively

Wound complications occur in about 3 percent of patients treated with alaparoscopic approach and 7 percent of those undergoing open pyloromyotomy.

The pyloromyotomy is incomplete in 2 to 6 percent of patients treated with a

laparoscopic approach and is rare in those undergoing the open procedure.


20/20

RESOURCES

Parashtte KR. Vomiting. Peds in Review 2013; 34307-319.

Olive, A, et al. Infantile hypertrophic pyloric stenosis. Up to date. Accessed8/2014.

vomiting with failure to thrive

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