eMedicine Specialties > Pediatrics: Surgery > General Surgery

Hypertrophic Pyloric Stenosis, Surgical Treatment

Author: Michael S Irish, MD, Adjunct Clinical Assistant Professor, Department of Surgery, University of Iowa; Consulting Pediatric Surgeon, Department of Pediatric Surgery, Blank Children's Hospital and Children's Hospital Physicians Group
Coauthor(s): Philip M Bovet, DO, MPH, Resident Physician in Family Medicine, University of Wisconsin Health Clinic
Contributor Information and Disclosures

Updated: Sep 18, 2009

Introduction

Pyloric stenosis (PS) is the most common pediatric surgical disorder of infancy that requires surgery for associated emesis. Autopsy findings of pyloric stenosis were first reported by Blair in 1717, but it was not until 1887, when Hirschsprung presented unequivocal clinical and autopsy findings of pyloric stenosis in 2 infants, that this entity became accepted. Adequate fluid resuscitation followed by pyloromyotomy is the standard curative treatment for pyloric stenosis.

History of the Procedure

Before 1912, early successful operative treatments of pyloric stenosis included gastroenterostomy, pyloroplasty, and forcible dilatation via gastrostomy (Loreta operation). In 1912, Rammstedt observed an uneventful recovery in a patient following pyloroplasty, in which sutures that were used in reapproximating the seromuscular layer had been disrupted. Following this observation, Rammstedt left the split muscle layer unsutured in all subsequent repairs. The Rammstedt pyloromyotomy, whether performed through a right-upper-quadrant incision, an umbilical incision, or via laparoscopy, remains the standard operation for pyloric stenosis today.

Problem

Pyloric stenosis involves hypertrophy of the circular muscle of the pylorus, resulting in narrowing and obstruction of the pyloric channel by compression of longitudinal folds of mucosa (see Image 1). Gastric outlet obstruction results in emesis, which is characteristically nonbilious and projectile. Protracted emesis, as well as failure of the stomach to empty into the duodenum, results in progressive dehydration, electrolyte abnormalities, acid-base disorders, weight loss, and, potentially, shock.

Diagram of the anatomic changes associated with p...

Diagram of the anatomic changes associated with pyloric stenosis.

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Diagram of the anatomic changes associated with p...

Diagram of the anatomic changes associated with pyloric stenosis.


Frequency

Pyloric stenosis reports in the United States have shown as few as 1 case per 3,000-4,000 live births to as many as 8.2-12 cases per 1,000 live births. It is most commonly observed in whites of northern European descent, is less frequently observed in blacks, and is rarely found in patients of Asian or East Indian ancestry. Location also contributes to frequency, with areas in which the population is more than two thirds rural showing an increased risk of 1.79 (95% CI, 1.23-2.61; P <.005).

Pyloric stenosis is more common in males than in females (male-to-female ratio is 4:1). The highest incidence is in first-born males. A genetic predisposition is suggested in families with occurrences of pyloric stenosis reported in at least 3 generations. Involvement in twins has been reported, with an 85.7% concordance rate in monozygotic twins and an 8.4% concordance rate in dizygotic twins. In 1969, Carter and Evans suggested a sex-modified polygenic inheritance of pyloric stenosis.1 Data from more than 1200 families demonstrated a 20% risk in sons and a 7% risk in daughters of females having had pyloric stenosis, whereas data showed only a 5% risk in sons and a 2.5% risk in daughters of males with pyloric stenosis.

Another report showed a 29% increased risk associated with younger maternal age (<20 y), whereas a maternal age exceeding 30 years was associated with a significantly decreased risk.2

Etiology

No conclusive evidence for the etiology of pyloric stenosis exists; however, both hereditary and environmental influences are believed to be contributing factors. Multiple factors, including both neural and hormonal, have been implicated but not substantiated in the development of pyloric stenosis. An association with B and O blood groups and maternal stress during the third trimester has also been suggested. Although pyloric stenosis is now believed to be acquired, cases of pyloric stenosis diagnosed prenatally and in neonates have been reported.

Since 1976, several reports and cohort retrospective studies have appeared in the literature suggesting an association between pyloric stenosis and exposure to macrolide antibiotics (erythromycin). In 2002, Cooper et al suggested that early exposure to erythromycin (at 3-13 days of life) is associated with a nearly 8-fold increased risk of pyloric stenosis (adjusted incident-rate ratio, 7.88; 95% CI, 1.97-31.57). No increased risk of pyloric stenosis was observed in infants exposed to erythromycin after 13 days of life.3

In 1993, Huang et al, by homologous recombination, generated mutant mice (knockout mice) lacking the neuronal nitric oxide synthase (NOS) gene. Nitric oxide (NO) mediates nonadrenergic noncholinergic smooth muscle relaxation throughout the gut. The stomachs of homozygous mutant mice were larger than normal in this group, and the circular muscle layer of the stomach and pylorus was hypertrophied. Wild-type mouse stomachs contained NOS in the myenteric plexus and nerve fibers of the circular muscle layer, whereas mutant homozygous mice lacked NOS in both locations. Applying these observations to the human condition, Huang et al hypothesized that the stomach and pylorus may be particularly dependent on NO and prone to dysfunction in its absence. Although human pyloric stenosis does not appear to be due to a complete absence of neuronal NOS gene product, the absence of NOS in this area may result in pyloric smooth muscle hypertrophy.4

In a more recent study, Huang et al (2006) collected biopsy samples of the pylorus in 13 patients with infantile hypertrophic pyloric stenosis and found decreased expression of neuronal nitric oxide synthase (nNOS) and demonstrated that plasma nitrite levels can be valuable for diagnosing pyloric stenosis.5

Regarding other factors that contribute to smooth-muscle control and hypertrophy, one study of 81 pyloric stenosis pedigrees used SNP-based linkage analysis to identify two pertinent functional genes on loci 11q14-22 and Xq23. These areas are thought to play a part in the canonical transient receptor potential (TRPC) family of ion channels and may contribute to the development of pyloric stenosis in infants.6

Associated anomalies, though rare, have been reported with pyloric stenosis. Approximately 4%-7% of infants with pyloric stenosis have associated anomalies, with hiatal and inguinal hernias being the most common. Other anomalies include congenital heart disease, esophageal atresia, tracheoesophageal fistulas, renal abnormalities, rubella, and chromosomal abnormalities such as Turner syndrome and trisomy 18.

Jackson et al (1993) found that 3.8% of infants (12 of 308) with de Lange syndrome had pyloric stenosis. Infants with a developmental delay called FG syndrome and those with Smith-Lemli-Opitz (SLO) syndrome, a type of cholesterol deficiency, are reported to be at an increased risk for pyloric stenosis.7 Additionally, Liede et al (2000) proposed a convincing argument of a common genetic association between endometriosis, breast cancer, and pyloric stenosis in several families.8

Pathophysiology

Pyloric stenosis involves hypertrophy of the circular muscle of the pylorus, resulting in narrowing and obstruction of the pyloric channel by compression of longitudinal folds of mucosa. Grossly, the pylorus is enlarged, resembling a tumor approximating the size and shape of an olive (ie, 2 cm long, 1 cm diameter). Microscopically, the circular muscle hypertrophies, with increased connective tissue in the septa between the muscle bundles. An increase of chondroitin sulfate within the extracellular matrix may account for the cartilaginous quality of the pyloric tumor.

Gastric fluid loss is associated with the loss of H+ and Cl-. This fluid loss is unlike that in conditions caused by vomiting with an open pylorus, which involves losses of gastric, pancreatic, biliary, and intestinal fluid. Hypochloremic hypokalemic metabolic alkalosis is the characteristic biochemical disturbance observed in pyloric stenosis. Urinary Na+ and HCO3 - losses, which compensate for Cl- losses, perpetuate this alkalosis.

With protracted vomiting, an extracellular volume deficit ensues, and urinary excretion of K+ and H+ increases in an attempt to preserve Na+ and volume. The initially alkalotic urine then becomes acidotic (paradoxic aciduria). This sign of protracted dehydration should alert the clinician to the severity of the volume and total body K+ deficit. The severity of electrolyte abnormalities depends on the duration of vomiting before resuscitation. Greater awareness of the presenting signs of pyloric stenosis by pediatricians and primary care physicians, along with ultrasonographic examination, has resulted in earlier diagnosis and less severe electrolyte and acid-base abnormalities.

Presentation

History

Pyloric stenosis most often occurs in neonates and infants aged 1-10 weeks (mean, 5 wk), with a range of age 5 days to 5 months. Although uncommon in premature infants younger than corrected age for a full-term infant, pyloric stenosis has been detected on prenatal sonograms and could be considered in the differential diagnoses for nonbilious vomiting in the newborn. Pyloric stenosis is observed in premature infants older than corrected age for a full-term baby.

Regardless of age, projectile vomiting typically occurs and is always nonbilious but may have brown discoloration or a coffee-ground appearance due to associated gastritis, particularly if emesis has persisted for several days. The vomiting occurs within 30-60 minutes after feeding. The infant remains hungry and usually attempts to feed immediately after vomiting. Weight loss and evidence of dehydration (eg, decreased tearing and urinary output, with poor skin turgor) are present if vomiting is allowed to continue for more than a few days.

Physical examination of the infant is conducted in a warm environment with the baby quiet or sleeping. A general sense of hydration is assessed first (see Table below), with particular attention paid to the baby's level of consciousness (arousability if sleeping), eyes, fontanelles, skin turgor, mucous membranes, and tearing. Infants with depressed fontanelles and decreased skin turgor have at least a 5% deficit of total body water. The lungs should be examined carefully, looking for signs of aspiration pneumonia in any infant who presents with a history of vomiting.

Clinical Findings in Dehydrated Infants With Pyloric Stenosis

Open table in new window

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Table
Level of DehydrationMildModerateSevere
Estimated Volume Deficit5% (50 mL/kg)10% (100 mL/kg)15% (150 mL/kg)




Clinical Findings


Skin (touch)NormalDry, paleClammy
Skin turgorNormalTentingNone
Mucus membranesMoistDryParched
EyesNormalDeep-setSunken
TearingPresentReducedNone
FontanelleNormal (flat)SoftSunken
CNSNormalIrritableLethargic/obtunded
Heart rateNormalSlightly increasedIncreased
Pulse qualityNormalWeakFeeble/impalpable
Capillary refillNormal~2 sec>3 sec
Urine outputNormalDecreasedAnuric
Level of DehydrationMildModerateSevere
Estimated Volume Deficit5% (50 mL/kg)10% (100 mL/kg)15% (150 mL/kg)




Clinical Findings


Skin (touch)NormalDry, paleClammy
Skin turgorNormalTentingNone
Mucus membranesMoistDryParched
EyesNormalDeep-setSunken
TearingPresentReducedNone
FontanelleNormal (flat)SoftSunken
CNSNormalIrritableLethargic/obtunded
Heart rateNormalSlightly increasedIncreased
Pulse qualityNormalWeakFeeble/impalpable
Capillary refillNormal~2 sec>3 sec
Urine outputNormalDecreasedAnuric

The infant is best examined from the right, with mild pressure applied by the first 3 fingers of the right hand in a cephalad direction (see Image 2). Ideally, the infant should be examined with the stomach decompressed with a nasogastric or orogastric tube, which prevents the pyloric channel from being obscured by an overlying dilated stomach. Careful examination reveals an oblong, smooth, hard mass that is 1-2 cm in length. This mass is the hypertrophied pylorus, commonly referred to as an olive or pyloric tumor, and is located in the epigastrium just above the umbilicus, either in the midline or just to the right. Although a superficially located pyloric mass may be palpated with relatively gentle pressure, identification of masses lying deeper or masses in crying infants requires firmer deep palpation.

Technique used for examining an infant with pylor...

Technique used for examining an infant with pyloric stenosis. The infant is best examined from the right, with mild pressure applied using the first 3 fingers of the right hand in a cephalad direction. Careful examination reveals an oblong, smooth, hard mass that is 1-2 cm in length. This mass is the hypertrophied pylorus and is commonly referred to as an olive.

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Technique used for examining an infant with pylor...

Technique used for examining an infant with pyloric stenosis. The infant is best examined from the right, with mild pressure applied using the first 3 fingers of the right hand in a cephalad direction. Careful examination reveals an oblong, smooth, hard mass that is 1-2 cm in length. This mass is the hypertrophied pylorus and is commonly referred to as an olive.


Upon identifying a suspected olive (pyloric tumor), the examiner must attempt to outline or palpate discrete borders of the mass to avoid mistaking the liver edge, contracted rectus muscle, or the upper pole of the right kidney for the mass. With persistence and experience, the pyloric tumor should be palpated in 85%-100% of cases. Difficulty in locating the mass is encountered if the mass is obscured by the liver, a distended stomach, or tense rectus muscles in crying infants.

Feeding the patient a small volume of warm sugar water may be useful in the examination, for 2 reasons: (1) a feeding infant cannot cry and, thus, does not tense the abdominal muscles, thereby making the examination of the pylorus easier and (2) observation of the abdomen of the infant with pyloric stenosis after feeding often reveals visible gastric contractions occurring in a wavelike manner from left to right across the abdomen. These waves generally terminate in emesis and are often associated with, but are not pathognomonic for, pyloric stenosis. Further examination of the abdomen is facilitated by nasogastric decompression and by lifting the lower extremities to help relax the abdominal musculature.

Relevant Anatomy

Pyloric stenosis involves hypertrophy of the circular muscle of the pylorus, resulting in narrowing and obstruction of the pyloric channel by compression of longitudinal folds of mucosa. Gastric distention results (see Image 1). Intraoperatively, the surgeon must pay strict attention to the serosal demarcation between the duodenum and the pylorus. The prepyloric vein, or Mayo vein, is located at this junction. The risk of duodenal perforation is prevented by stopping the distal extent of the myotomy 1-2 mm short of this point.

Diagram of the anatomic changes associated with p...

Diagram of the anatomic changes associated with pyloric stenosis.

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Diagram of the anatomic changes associated with p...

Diagram of the anatomic changes associated with pyloric stenosis.


Contraindications

Adequate preoperative resuscitation is essential. Fluid resuscitation is guided by adequate urine output (1 mL/kg/h) and by normalization of acid-base disturbances and electrolyte and bicarbonate levels.

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References
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References

  1. Carter CO, Evans KA. Inheritance of congenital pyloric stenosis. J Med Genet. Sep 1969;6(3):233-54. [Medline].

  2. Pedersen RN, Garne E, Loane M, Korsholm L, Husby S. Infantile hypertrophic pyloric stenosis: a comparative study of incidence and other epidemiological characteristics in seven European regions. J Matern Fetal Neonatal Med. Sep 2008;21(9):599-604. [Medline].

  3. Cooper WO, Griffin MR, Arbogast P. Very early exposure to erythromycin and infantile hypertrophic pyloric stenosis. Arch Pediatr Adolesc Med. Jul 2002;156(7):647-50. [Medline].

  4. Huang PL, Dawson TM, Bredt DS, et al. Targeted disruption of the neuronal nitric oxide synthase gene. Cell. Dec 31 1993;75(7):1273-86. [Medline].

  5. Huang LT, Tiao MM, Lee SY, Hsieh CS, Lin JW. Low plasma nitrite in infantile hypertrophic pyloric stenosis patients. Dig Dis Sci. May 2006;51(5):869-72. [Medline].

  6. Everett KV, Chioza BA, Georgoula C, Reece A, Capon F, Parker KA, et al. Genome-wide high-density SNP-based linkage analysis of infantile hypertrophic pyloric stenosis identifies loci on chromosomes 11q14-q22 and Xq23. Am J Hum Genet. Mar 2008;82(3):756-62. [Medline].

  7. Jackson L, Kline AD, Barr MA. de Lange syndrome: a clinical review of 310 individuals. Am J Med Genet. Nov 15 1993;47(7):940-6. [Medline].

  8. Liede A, Pal T, Mitchell M. Delineation of a new syndrome: clustering of pyloric stenosis, endometriosis, and breast cancer in two families. J Med Genet. Oct 2000;37(10):794-6. [Medline]. [Full Text].

  9. Teele RL, Smith EH. Ultrasound in the diagnosis of idiopathic hypertrophic pyloric stenosis. N Engl J Med. May 19 1977;296(20):1149-50. [Medline].

  10. Nagita A, Yamaguchi J, Amemoto K. Management and ultrasonographic appearance of infantile hypertrophic pyloric stenosis with intravenous atropine sulfate. J Pediatr Gastroenterol Nutr. Aug 1996;23(2):172-7. [Medline].

  11. Kawahara H, Takama Y, Yoshida H. Medical treatment of infantile hypertrophic pyloric stenosis: should we always slice the "olive"?. J Pediatr Surg. Dec 2005;40(12):1848-51. [Medline].

  12. Tan KC, Bianchi A. Circumumbilical incision for pyloromyotomy. Br J Surg. May 1986;73(5):399. [Medline].

  13. Blumer RM, Hessel NS, van Baren R. Comparison between umbilical and transverse right upper abdominal incision for pyloromyotomy. J Pediatr Surg. Jul 2004;39(7):1091-3. [Medline].

  14. Alberti M, Cheli M, Locatelli G. A new technical variant for extramucosal pyloromyotomy, The Tan-Bianchi operation moves to the right. J Ped Surg. 2004;39:53-6. [Medline].

  15. Mullassery D, Shariff R, Craigie RJ, Losty PD, Kenny SE, Baillie CT. Umbilical pyloromyotomy: comparison of vertical linea alba and transverse muscle cutting incisions. J Pediatr Surg. Mar 2007;42(3):525-7. [Medline].

  16. Alain JL, Grousseau D, Terrier G. Extramucosal pylorotomy by laparoscopy. J Pediatr Surg. Oct 1991;26(10):1191-2. [Medline].

  17. Michalsky MP, Pratt D, Caniano DA. Streamlining the care of patients with hypertrophic pyloric stenosis: application of a clinical pathway. J Pediatr Surg. Jul 2002;37(7):1072-5; discussion 1072-5. [Medline].

  18. Puapong D, Kahng D, Ko A. Ad libitum feeding: safely improving the cost-effectiveness of pyloromyotomy. J Pediatr Surg. Dec 2002;37(12):1667-8. [Medline].

  19. Yoshizawa J, Eto T, Higashimoto Y. Ultrasonographic features of normalization of the pylorus after pyloromyotomy for hypertrophic pyloric stenosis. J Pediatr Surg. Apr 2001;36(4):582-6. [Medline].

  20. Pranikoff T, Campbell BT, Travis J. Differences in outcome with subspecialty care: pyloromyotomy in North Carolina. J Pediatr Surg. Mar 2002;37(3):352-6. [Medline].

  21. Safford SD, Pietrobon R, Safford KM. A study of 11,003 patients with hypertrophic pyloric stenosis and the association between surgeon and hospital volume and outcomes. J Pediatr Surg. Jun 2005;40(6):967-72; discussion 972-3. [Medline].

  22. Hendrickson RJ, Yu S, Bruny JL, Partrick DA, Petty JK, Bensard DD. Early experience with laparoscopic pyloromyotomy in a teaching institution. JSLS. Oct-Dec 2005;9(4):386-8. [Medline].

  23. Yagmurlu A, Barnhart DC, Vernon A. Comparison of the incidence of complications in open and laparoscopic pyloromyotomy: a concurrent single institution series. J Pediatr Surg. Mar 2004;39(3):292-6; discussion 292-6. [Medline].

  24. Campbell BT, McLean K, Barnhart DC. A comparison of laparoscopic and open pyloromyotomy at a teaching hospital. J Pediatr Surg. Jul 2002;37(7):1068-71; discussion 1068-71. [Medline].

  25. [Guideline] International Pediatric Endosurgery Group. Guidelines for surgical treatment of infantile hypertrophic pyloric stenosis. Los Angeles, Calif: International Pediatric Endosurgery Group;. 2002;[Full Text].

  26. Haricharan RN, Aprahamian CJ, Morgan TL, Harmon CM, Georgeson KE, Barnhart DC. Smaller scars--what is the big deal: a survey of the perceived value of laparoscopic pyloromyotomy. J Pediatr Surg. Jan 2008;43(1):92-6; discussion 96. [Medline].

  27. Cosper GH, Menon R, Hamann MS, Nakayama DK. Residency training in pyloromyotomy: a survey of 331 pediatric surgeons. J Pediatr Surg. Jan 2008;43(1):102-8. [Medline].

  28. Zhang YX, Nie YQ, Xiao X, Yu NF, Li QN, Deng L. [Treatment of congenital hypertrophic pyloric stenosis with endoscopic pyloromyotomy]. Zhonghua Er Ke Za Zhi. Apr 2008;46(4):247-51. [Medline].

  29. Abel RM. The ontogeny of the peptide innervation of the human pylorus, with special reference to understanding the aetiology and pathogenesis of infantile hypertrophic pyloric stenosis. J Pediatr Surg. Apr 1996;31(4):490-7. [Medline].

  30. Alain JL, Grousseau D, Longis B, et al. Extramucosal pyloromyotomy by laparoscopy. J Laparoendosc Surg. Mar 1996;6 Suppl 1:S41-4. [Medline].

  31. Ankermann T, Engler S, Partsch CJ. Repyloromyotomy for recurrent infantile hypertrophic pyloric stenosis after successful first pyloromyotomy. J Pediatr Surg. Nov 2002;37(11):E40. [Medline].

  32. Ashcraft KW, Holcomb GW III, Murphy JP. Lesions of the stomach, laparoscopy. In: Pediatric Surgery. 4th ed. Philadelphia, Pa: WB Saunders Co; 2005:407-10, 680-1.

  33. Atwell JD, Levick P. Congenital hypertrophic pyloric stenosis and associated anomalies in the genitourinary tract. J Pediatr Surg. Dec 1981;16(6):1029-35. [Medline].

  34. Banieghbal B. Rapid correction of metabolic alkalosis in hypertrophic pyloric stenosis with intravenous cimetidine: preliminary results. Pediatr Surg Int. Mar 2009;25(3):269-71. [Medline].

  35. Barksdale EM. Pyloric stenosis. In: Ziegler MM, ed. Operative Pediatric Surgery. Stamford, Conn: Appleton and Lange; 2003:583-8.

  36. Battaglia A, Chines C, Carey JC. The FG syndrome: report of a large Italian series. Am J Med Genet A. Oct 1 2006;140(19):2075-9. [Medline].

  37. Behrman RE, Kliegman RM, Jenson HB. Nelson Textbook of Pediatrics. 16th ed. 2000:1130-1.

  38. Boneti C, McVay MR, Kokoska ER, Jackson RJ, Smith SD. Ultrasound as a diagnostic tool used by surgeons in pyloric stenosis. J Pediatr Surg. Jan 2008;43(1):87-91; discussion 91. [Medline].

  39. Bufo AJ, Merry C, Shah R, et al. Laparoscopic pyloromyotomy: a safer technique. Pediatr Surg Int. Apr 1998;13(4):240-2. [Medline].

  40. Castanon J, Portilla E, Rodriguez E, et al. A new technique for laparoscopic repair of hypertrophic pyloric stenosis. J Pediatr Surg. Sep 1995;30(9):1294-6. [Medline].

  41. Caty MG, Azizkhan RG. Acute surgical conditions of the abdomen. Pediatr Ann. Apr 1994;23(4):192-4, 199-201. [Medline].

  42. Chaves-Carballo E, Harris LE, Lynn HB. Jaundice associated with pyloric stenosis and neonatal small-bowel obstructions. Clin Pediatr (Phila). Apr 1968;7(4):198-202. [Medline].

  43. Chuang JH, Chen MJ. Membranous atresia of esophagus associated with pyloric stenosis. J Pediatr Surg. Nov 1987;22(11):988-90. [Medline].

  44. Cook-Sather SD, Tulloch HV, Cnaan A. A comparison of awake versus paralyzed tracheal intubation for infants with pyloric stenosis. Anesth Analg. May 1998;86(5):945-51. [Medline].

  45. Croitoru D, Neilson I, Guttman FM. Pyloric stenosis associated with malrotation. J Pediatr Surg. Nov 1991;26(11):1276-8. [Medline].

  46. Desai K, Mazziotti M. Pediatric surgery, pyloromyotomy. In: Jones DB, Wu JS, Soper NJ, eds. Laparoscopic Surgery: Principles and Procedures. 2nd ed. New York, NY: Marcel Dekker, Inc; 2004:522.

  47. Dodge JA. Infantile hypertrophic pyloric stenosis in Belfast, 1957-1969. Arch Dis Child. Mar 1975;50(3):171-8. [Medline].

  48. Foulkes D. Clinical observations in dehydration. In: Gunn VL, Nechyba C, eds. Harriett Lane Handbook: A Manual for Pediatric House Officers. 2002. 16th ed. St Louis, Mo: CV Mosby Co; 235.

  49. Franken EA Jr, Saldino RM. Hypertrophic pyloric stenosis complicating esophageal atresia with tracheoesophageal fistula. Am J Surg. May 1969;117(5):647-9. [Medline].

  50. Fujimoto T, Lane GJ, Segawa O, et al. Laparoscopic extramucosal pyloromyotomy versus open pyloromyotomy for infantile hypertrophic pyloric stenosis: which is better?. J Pediatr Surg. Feb 1999;34(2):370-2. [Medline].

  51. Hamada Y, Tsui M, Kogata M, et al. Surgical technique of laparoscopic pyloromyotomy for infantile hypertrophic pyloric stenosis. Surg Today. 1995;25(8):754-6. [Medline].

  52. Haricharan RN, Aprahamian CJ, Celik A, Harmon CM, Georgeson KE, Barnhart DC. Laparoscopic pyloromyotomy: effect of resident training on complications. J Pediatr Surg. Jan 2008;43(1):97-101. [Medline].

  53. Hollands CM, Tantoco J. Telerobotically-assisted pediatric surgery. In: Ballantyne GH, Marescaus J, Giulianotti PC, Marescaux J, eds. Primer of Robotic & Telerobotic Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2004:181-6.

  54. Honein MA, Paulozzi LJ, Himelright IM. Infantile hypertrophic pyloric stenosis after pertussis prophylaxis with erythromycin: a case review and cohort study. Lancet. Dec 18-25 1999;354(9196):2101-5. [Medline].

  55. Keller H, Waldmann D, Greiner P. Comparison of preoperative sonography with intraoperative findings in congenital hypertrophic pyloric stenosis. J Pediatr Surg. Oct 1987;22(10):950-2. [Medline].

  56. Kelley RI. Smith-Lemli-Opitz syndrome. Baltimore, Md: Clinical Mass Spectrometry Laboratory. Kennedy Krieger Institute;1996. [Full Text].

  57. Klein A, Cremin BJ. Racial significance in pyloric stenosis. S Afr Med J. Oct 3 1970;44(39):1131. [Medline].

  58. Kol A, Steinman A, Levi O. Congenital pyloric stenosis in a foal. Isreal J Vet Med. 2005;60(2):59-62. [Full Text].

  59. Ladd AP, Nemeth SA, Kirincich AN. Supraumbilical pyloromyotomy: a unique indication for antimicrobial prophylaxis. J Pediatr Surg. Jun 2005;40(6):974-7; discussion 977. [Medline].

  60. Leaphart CL, Borland K, Kane TD, Hackam DJ. Hypertrophic pyloric stenosis in newborns younger than 21 days: remodeling the path of surgical intervention. J Pediatr Surg. Jun 2008;43(6):998-1001. [Medline].

  61. Mack HCA. A history of hypertrophic pyloric stenosis. Bull Hist Med. 1942;12:465-595.

  62. McVay MR, Copeland DR, McMahon LE, Cosper GH, McCallie TG, Kokoska ER, et al. Surgeon-performed ultrasound for diagnosis of pyloric stenosis is accurate, reproducible, and clinically valuable. J Pediatr Surg. Jan 2009;44(1):169-71; discussion 171-2. [Medline].

  63. Meeker CS, Denicola RR. Hypertrophic pyloric stenosis in a newborn infant. J Pediatr. Jul 1948;33(1):94-7. [Medline].

  64. Moore KL, Dalley AF. Abdomen. In: Clinically Oriented Anatomy. 4th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 1999:231.

  65. Mullassery D, Mallappa S, Shariff R, Craigie RJ, Losty PD, Kenny SE, et al. Negative exploration for pyloric stenosis--is it preventable?. BMC Pediatr. Sep 24 2008;8:37. [Medline].

  66. O'Neill JA Jr, Grosfeld JL, Fonkalsrud EW. Hypertrophic pyloric stenosis. In: O'Neill JA Jr, Grosfeld JL, Fonkalsrud EW, Coran AG, Caldamone AA, eds. Principles of Pediatric Surgery. 2nd ed. St Louis, Mo: Mosby; 2003:467-70.

  67. Pickard RH. Hypertropic Pyloric Stenosis. Disease Topic 3463. MedPix Medical Imaging Database, Bethesda, MD;Departments of Radiology and Biomedical Informatics; Uniformed Services University: 2004. Available at http://rad.usuhs.mil/medpix/radpix.html?mode=single&comebackto=mode%3Dgeo_browse&recnum=3463.

  68. Ravitch M. The story of pyloric stenosis. Surgery. Dec 1960;48:1117-43. [Medline].

  69. Rowe MI, O'Neill JA, Grosfeld JL, et al. Hypertrophic pyloric stenosis. In: Rowe MI, ed. Essentials of Pediatric Surgery. St. Louis, Mo: Mosby Yearbook; 1995:481-5.

  70. SanFilippo A. Infantile hypertrophic pyloric stenosis related to ingestion of erythromycine estolate: A report of five cases. J Pediatr Surg. Apr 1976;11(2):177-80. [Medline].

  71. Schärli A, Sieber WK, Kiesewetter WB. Hypertrophic pyloric stenosis at the Children's Hospital of Pittsburgh from 1912 to 1967. A critical review of current problems and complications. J Pediatr Surg. Feb 1969;4(1):108-14. [Medline].

  72. Shuman FI, Darling DB, Fisher JH. The radiographic diagnosis of congenital hypertrophic pyloric stenosis. J Pediatr. Jul 1967;71(1):70-4. [Medline].

  73. Sitsen E, Bax NM, van der Zee DC. Is laparoscopic pyloromyotomy superior to open surgery?. Surg Endosc. Jun 1998;12(6):813-5. [Medline].

  74. Stang H. Pyloric stenosis associated with erythromycin ingested through breastmilk. Minn Med. Nov 1986;69(11):669-70, 682. [Medline].

  75. Tan HL, Blythe A, Kirby CP, Gent R. Gastric Foveolar Cell Hyperplasia and its Role in Postoperative Vomiting in Patients with Infantile Hypertrophic Pyloric Stenosis. Eur J Pediatr Surg. Feb 25 2009;[Medline].

  76. Tashjian DB, Konefal SH. Hypertrophic pyloric stenosis in utero. Pediatr Surg Int. Sep 2002;18(5-6):539-40. [Medline].

  77. To T, Wajja A, Wales PW. Population demographic indicators associated with incidence of pyloric stenosis. Arch Pediatr Adolesc Med. Jun 2005;159(6):520-5. [Medline].

  78. Van der Horst R, Frankel J, Grace J. Congenital hypertrophic pyloric stenosis in phenotypic female twins with X-XX mosaicism. Arch Dis Child. Aug 1971;46(248):554-6. [Medline].

  79. Warner BW. Townsend CM, Beauchamp RD, Evers BK, Mattox K, eds. Sabiston Textbook of Surgery. 17th ed. Philadelphia, Pa: Saunders; 2004:2107-8.

  80. Yokomori K, Oue T, Odajima T, Baba N, Hashimoto D. Pyloromyotomy through a sliding umbilical window. J Pediatr Surg. Dec 2006;41(12):2066-8. [Medline].

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Further Reading

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Keywords

hypertrophic pyloric stenosis, HPS, PS, pyloric tumor, pyloric olive, congenital hypertrophic pyloric stenosis, infantile hypertrophic pyloric stenosis, IHPS, gastric outlet obstruction, pyloromyotomy, open pyloromyotomy, laparoscopic pyloromyotomy, metabolic alkalosis, acid-base disorders, acid base disorders, Mayo vein, prepyloric vein, metabolic abnormalities

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Contributor Information and Disclosures

Author

Michael S Irish, MD, Adjunct Clinical Assistant Professor, Department of Surgery, University of Iowa; Consulting Pediatric Surgeon, Department of Pediatric Surgery, Blank Children's Hospital and Children's Hospital Physicians Group
Michael S Irish, MD is a member of the following medical societies: International Pediatric Endosurgery Group and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Philip M Bovet, DO, MPH, Resident Physician in Family Medicine, University of Wisconsin Health Clinic
Philip M Bovet, DO, MPH is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, American Osteopathic Association, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Aviva L Katz, MD, Assistant Professor of Surgery, University of Pittsburgh School of Medicine; Consulting Staff, Division of General and Thoracic Surgery, Children's Hospital of Pittsburgh
Aviva L Katz, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, Association of Women Surgeons, Physicians for Social Responsibility, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Gail E Besner, MD, John E Wilson Endowed Professor of Neonatal Research, Nationwide Children's Hospital; Professor of Surgery and Pediatrics, Department of Surgery, Ohio State University College of Medicine; Director, Pediatric Surgical Research, Department of Surgery, Nationwide Children's Hospital
Gail E Besner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Burn Association, American College of Surgeons, American Gastroenterological Association, American Medical Association, American Medical Women's Association, American Pediatric Surgical Association, Association for Academic Surgery, Federation of American Societies for Experimental Biology, Society of Critical Care Medicine, Society of Surgical Oncology, and Society of University Surgeons
Disclosure: Nothing to disclose.

CME Editor

H Biemann Othersen Jr, MD, Professor of Surgery and Pediatrics, Emeritus Head, Division of Pediatric Surgery, Medical University of South Carolina
H Biemann Othersen Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, American Cancer Society, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, American Society for Parenteral and Enteral Nutrition, American Surgical Association, American Thoracic Society, British Association of Paediatric Surgeons, Society for Surgery of the Alimentary Tract, Society of Critical Care Medicine, South Carolina Medical Association, Southeastern Surgical Congress, Southern Medical Association, Southern Society for Pediatric Research, and Southern Thoracic Surgical Association
Disclosure: Nothing to disclose.

Chief Editor

Marleta Reynolds, MD, Professor of Surgery, Feinberg School of Medicine, Northwestern University; Interim Head, Department of Surgery and Surgeon in Chief, Head, Division of Pediatric Surgery, Children's Memorial Hospital of Chicago
Marleta Reynolds, MD is a member of the following medical societies: American Pediatric Surgical Association
Disclosure: Nothing to disclose.

 
 
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