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Name the Diagnosis: Why Is My Baby Vomiting?

Paton, Elizabeth A., DNP, RN-BC, PNP-AC, PPCNP-BC, CPEN, FAEN; Brauninger, Anna, BSN, RN, CCRN

Journal of Pediatric Surgical Nursing: July/September 2018 - Volume 7 - Issue 3 - p 75–77
doi: 10.1097/JPS.0000000000000182
Name the Diagnosis

Elizabeth A. Paton, DNP, RN-BC, PNP-AC, PPCNP-BC, CPEN, FAEN Assistant Professor, Department of Acute and Tertiary Care, College of Nursing, University of Tennessee Health Science Center, and Nurse Practitioner, Le Bonheur Children's Hospital, Memphis, TN.

Anna Brauninger, BSN, RN, CCRN Registered Nurse, Cardiovascular Intensive Care Unit, Le Bonheur Children's Hospital, Memphis, TN.

The authors declare no conflict of interest.

Supplemental digital content is available for this article. Direct URL citations are provided in the HTML and PDF versions of this article.

Correspondence: Elizabeth A. Paton, DNP, RN-BC, PNP-AC, PPCNP-BC, CPEN, FAEN, Le Bonheur Children's Hospital, 49 N. Dunlap St., 2nd Floor, Memphis, TN 38105. E-mail: epaton@uthsc.edu

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HISTORY

Finley is a 3-week-old female infant who presents with frequent episodes of “projectile” vomiting after feedings. The nonbilious vomiting started 2 weeks ago and has continued without resolution. Her parents have tried various measures to alleviate the vomiting including small frequent feedings and changing feeding positions. The patient seems to have a good appetite and is still hungry after each episode. She was born full term and was feeding appropriately before discharge.

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ASSESSMENT

The patient has had poor weight gain since birth and is in the 15th percentile of the growth chart. On examination, she is alert and resting quietly in her mother's arms. Her anterior fontanelle is slightly sunken, mucous membranes are tacky, and capillary refill is approximately 2 seconds. Bowel sounds are normoactive with no abdominal tenderness or distention. A small mass is palpated in the right epigastric region. Vital signs are as follows: heart rate = 175, respirations = 52, blood pressure = 72/48, and temperature = 37.1°C.

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What Is Your Diagnosis?

What is the most likely diagnosis based on the list of differentials?

  1. Formula intolerance
  2. Malrotation
  3. Pyloric stenosis
  4. Gastroesophageal Reflux Disease
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The Diagnosis Is:

c. Pyloric stenosis

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CASE PROGRESSION

On the basis of the clinical history and physical examination, a complete metabolic panel and an abdominal ultrasound were ordered.

The complete metabolic panel revealed hypochloremia, hypokalemia, and a metabolic alkalosis (Table 1). The ultrasound exhibited the classic “target” sign with a measurement of pyloric muscle thickness of 3.4 mm and a channel length of 21 mm (Figure 1). Dynamic images also showed failure of the pyloric channel to open and stomach contents to empty (see Video, Supplemental Digital Content 1, http://links.lww.com/JPSN/A11). The ultrasound findings were consistent with a diagnosis of pyloric stenosis. (Bakal, Sarac, Aydin, Tartar, & Kazez, 2016)

Table 1

Table 1

FIGURE 1

FIGURE 1

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RESOLUTION OF THE CASE AND PATIENT OUTCOME

The patient was admitted with a diagnosis of hypertrophic pyloric stenosis (HPS). She was made nothing by mouth and provided intravenous fluid resuscitation including two 20-cc/kg normal saline boluses and 1.5 times of maintenance intravenous fluid. The following day, her electrolytes had normalized with a potassium level of 3.5, a chloride level of 105, and carbon dioxide level of 29.

The patient subsequently proceeded to the operating room where she underwent a laparoscopic pyloromyotomy (Figure 2). The procedure was performed without any complications. Once the child awakened from anesthesia, she resumed regular formula feedings ad libitum. She had one small episode of emesis the first night after surgery. She subsequently tolerated three 2-ounce formula feeds without any additional emesis. On Postoperative Day 1, no surgical complications were noted and she was subsequently discharged home. At her postoperative follow-up visit 1 month later, she continued to tolerate feeds and had gained an average of 30 grams per day.

FIGURE 2

FIGURE 2

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INFORMATION ABOUT THE DIAGNOSIS

Infantile HPS typically presents in the first few weeks of life with a history of nonbilious postprandial emesis that increases in intensity. The condition involves hypertrophy of the pyloric sphincter, which then leads to a degree of gastric outlet obstruction (El-Gohary, Abdelhafeez, Paton, Gosain, & Murphy, 2017). The incidence of HPS has been reported to be 2–4 per 1,000 live births (To, Wajja, Wales, & Langer, 2005). It is one of the more commonly treated surgical conditions in pediatrics.

Patients with HPS typically present with a history of postprandial projectile emesis, poor weight gain, and electrolyte abnormalities. The classic laboratory abnormality is a hypokalemic, hyperchloremic, metabolic alkalosis.

The diagnosis is based on a careful history and physical examination and may be confirmed by an abdominal ultrasound. Physical examination may reveal palpation of the hypertrophied muscle in the epigastrium (often referred to as palpating an “olive”). Observation of the abdomen might also show a “peristaltic wave” as the stomach contracts and peristalses in an attempt to empty. An ultrasound is considered consistent with HPS if the pyloric muscle has a thickness of greater than 3 mm, a channel length of greater than 14 mm, and a dynamic demonstration of failure of the channel to open allowing stomach contents to empty.

Initial management of HPS is fluid resuscitation to correct the electrolyte abnormalities. Once the electrolyte derangements are corrected, surgical intervention may ensue. The surgical intervention involves performing a pyloromyotomy. This may be performed via an upper abdominal transverse incision or laparoscopically.

Postoperatively, feeds may be resumed. Multiple studies have been performed evaluating various feeding regimens, and the feeding advancement is institution and surgeon specific (Adibe et al., 2014 ; Graham, Laituri, Markel, & Ladd, 2013). A recent meta-analysis revealed that ad libitum feeds that are initiated once the infant awakens from anesthesia may decrease hospital length of stay and time to full enteral feeds (Sullivan et al., 2015).

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References

Adibe O. O., Iqbal C. W., Sharp S. W., Juang D., Snyder C. L., Holcomb G. W., … Peter S. D. (2014). Protocol versus ad libitum feeds after laparoscopic pyloromyotomy: A prospective randomized trial. Journal of Pediatric Surgery,49(1), 129–132.
Bakal U., Sarac M., Aydin M., Tartar T., & Kazez A. (2016). Recent changes in the features of hypertrophic pyloric stenosis. Pediatrics International,58(5), 369–371. doi:10.1111/ped.12860
El-Gohary Y., Abdelhafeez A., Paton E., Gosain A., & Murphy A. J. (2017). Pyloric stenosis: An enigma more than a century after the first successful treatment. Pediatric Surgery International,34, 21–27.
Graham K. A., Laituri C. A., Markel T. A., & Ladd A. P. (2013). A review of postoperative feeding regimens in infantile hypertrophic pyloric stenosis. Journal of Pediatric Surgery,48(10), 2175–2179.
Sullivan K. J., Chan E., Vincent J., Iqbal M., Wayne C., & Nasr A. (2015). Feeding post-pyloromyotomy: A meta-analysis. Pediatrics,137(1), e20152550. doi:10.1542/peds.2015-2550
To T., Wajja A., Wales P. W., & Langer J. C. (2005). Population demographic indicators associated with incidence of pyloric stenosis. Archives of Pediatric Adolescent Medicine,159, 520–525.

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