Pyloric stenosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Synonyms and keywords: Congenital hypertrophic pyloric stenosis; infantile hypertrophic pyloric stenosis; pyloric stenosis
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
Infantile pyloric stenosis is a condition that causes severe vomiting in the first few months of life.There is narrowing (stenosis) of the opening from the stomach to the intestines, due to spasm and hypertrophy of the muscle surrounding this opening (the pylorus). Pyloric stenosis also occurs in adults where the cause is usually a narrowed pylorus due to scarring from chronic peptic ulceration. This is a completely different condition from the infantile form. There is chloride loss due persistent vomiting that results in hypochloremia which impairs the kidney‘s ability to excrete bicarbonate. Infantile hypertrophic pyloric stenosis must be differentiated from other diseases that cause vomiting, poor feeding and dehydration, such as adrenal insufficiency, gastroenteritis, UTI, inborn errors of metabolism and acute renal failure. The hallmark of infantile pyloric stenosis is progressively worsening vomiting within the first few weeks to months of life. A positive history of bottle feeding and cesarean section delivery is suggestive of infantile pyloric stenosis. Palpation of the abdomen may reveal a mass in the epigastrium. This mass consists of the enlarged pylorus smooth muscle and it is called olive.Ultrasonography is the the modality of choice for the diagnosis of infantile pyloric stenosis. Infantile pyloric stenosis is typically managed with surgery. Ranstedt’s extramuscular pyloromyotomy is the gold standard of treatment. After the surgery, once the stomach can empty into the duodenum, feeding can be started. There is occasionally recurrence in the immediate post-operative period, but the condition generally has no long-term impact on the child‘s future.
Historical Perspective
In 1717, Dr. Patrick Blair reported autopsy findings of pyloric stenosis for first time. In 1911, Conrad Ramstedt witnessed complete recovery of a patient with pyloric stenosis after undergoing pyloroplasty.
Classification
There is no established system for the classification of pyloric stenosis. It may be subclassified as infantile pyloric stenosis and adult-onset hypertrophic pyloric stenosis.
Pathophysiology
The pathogenesis of infantile hypertrophic pyloric stenosis is not completely understood. However, infantile hypertrophic pyloric stenosis may result from abnormal innervation of the pyloric smooth muscle. The chloride loss due persistent vomiting results in hypochloremia which impairs the kidney‘s ability to excrete bicarbonate. This factor significantly prevents correction of the alkalosis. The secondary hyperaldosteronism develops due to the hypovolaemia. The body’s compensatory response to the metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO2. In relatives of probands of infantile hypertrophic pyloric stenosis patients and monozygotic co-twins the recurrence pattern did not depict a single major inheritance. The incidence of infantile pyloric stenosis is approximately 400 per 100,000 individuals worldwide and it is four times more common in males. Most common laboratory findings consistent with the diagnosis of infantile pyloric stenosis and adult type pyloric stenosis include hypokalemia, hypochloremia, and metabolic alkalosis.
Causes
The causes of infantile pyloric stenosis are unknown, but genetic and environmental factors might play a role in pathogenesis of infantile pyloric stenosis. common causes of adult-onset hypertrophic pyloric stenosis (HPS) include persisting duodenal hyperacidity, inheritance of a parietal cell mass (PCM) at the upper end of the normal range which causes persisting duodenal hyperacidity.
Differentiating Pyloric stenosis overview from Other Diseases
Infantile hypertrophic pyloric stenosis must be differentiated from other diseases that cause vomiting, poor feeding and dehydration, such as adrenal insufficiency, gastroenteritis, UTI, inborn errors of metabolism and acute renal failure. Projectile vomiting and and palpation of an olive in abdominal physical examination are very helpful to distinguish infantile pyloric stenosis from other common causes of vomiting in infants.
Epidemiology and Demographics
The incidence of infantile pyloric stenosis is approximately 400 per 100,000 individuals worldwide and it is four times more common in males. It usually affects individuals of the Caucasian race. Asians individuals are less likely to develop Infantile pyloric stenosis. The prevalence of infantile pyloric stenosis in the course of 11 years (1989-1999) was approximately 7.3 per 100,000 individuals in one study. Studies showed the mortality rate of pyloric stenosis is very low and usually results from delays in diagnosis that causes sever dehydration and shock.
Risk Factors
The most potent risk factors in the development of infantile pyloric stenosis are male gender, Caucasian race, bottle feeding, caesarean section delivery, first-born infant, preterm birth; and exposure to macrolides, nitrofurantoin, penicillins, and trimethoprim-sulphamethoxazole during pregnancy.
Screening
Screening for pyloric stenosis is not recommended.
Natural History, Complications, and Prognosis
The symptoms of pyloric stenosis usually develop in the first days of life, and start with projectile vomiting. If left untreated, infants with mild infantile pyloric stenosis can develop severe electrolyte imbalances include hypokalemia , hypochloremia, and metabolic alkalosis. In rare cases of untreated pyloric stenosis, patients may develop significant problems on the cognition, receptive language, fine motor, and gross motor skills compared to the normal infants due to long term malnutrition. Complications of infantile pyloric stenosis before surgery include vomiting and failure to gain weight in newborn period. Prognosis is generally excellent and surgery usually provides complete relief of symptoms. Infants usually tolerate small, frequent feedings several hours after surgery
Diagnosis
Ultrasonography is the the modality of choice for the diagnosis of infantile pyloric stenosis. The thickened prepyloric antrum bridging the duodenal bulb and distended stomach and crowded intervening mucosa that protrudes into the distended portion of the antrum (nipple sign) may be seen in Ultrasonography of patients with infantyle pyloric stenosis.
History and Symptoms
The hallmark of infantile pyloric stenosis is progressively worsening vomiting within the first few weeks to months of life. A positive history of bottle feeding and cesarean section delivery is suggestive of infantile pyloric stenosis. The most common symptoms of infantile pyloric stenosis include vomiting, belching, persistent hunger. Less common symptoms of infantile pyloric stenosis include failure to gain weight or weight loss, jaundice, lethargy and decreased urine output. The hallmark of adult type pyloric stenosis is progressively worsening projectile vomiting. A positive history of chronic peptic ulcers and fibrosis near the gastric outlet is suggestive of adult type pyloric stenosis. The most common symptoms of adult type pyloric stenosis include vomiting with occasional relief after vomiting, belching, epigastric pain. Less common symptoms of adult type pyloric stenosis include failure to gain weight or weight loss and symptoms of dehydration like increased thirst, dry mouth and decreased urine output.
Physical Examination
Palpation of the abdomen may reveal a mass in the epigastrium. This mass consists of the enlarged pylorus smooth muscle and it is called olive. Palpation of a hypertrophied pylorus is very useful in diagnosis of hypertrophic pyloric stenosis.Peristaltic waves may be palpated or may be seen in abdominal exam of patients with infantile pyloric stenosis. Hypothermia and tachycardia with regular pulse and tachypnea may be present. In skin examination cyanosis, poor skin turgur, jaundice and pallor may be present.
Laboratory Findings
Most common laboratory findings consistent with the diagnosis of infantile pyloric stenosis and adult type pyloric stenosis include hypokalemia, hypochloremia, and metabolic alkalosis.
Electrocardiogram
There are no ECG findings associated with pyloric stenosis.
Xray
There are no significant abdominal x-ray findings associated with infantile pyloric stenosis.
CT scan
There are no CT scan findings associated with infantile pyloric stenosis.
MRI
There are no MRI findings associated with infantile pyloric stenosis.
Ultrasound
Ultrasonography is the modality of choice for the diagnosis of infantile pyloric stenosis. The thickened pre-pyloric antrum bridging the duodenal bulb and distended stomach could be seen in the ultrasound of patients with infantile pyloric stenosis. Demonstration of the pylorus is achieved by identifying the duodenal cap, distended stomach, and intervening pyloric channel. In patients with pyloric stenosis, the variable hypertrophy of the smooth muscle and crowded intervening mucosa which is thickened to a variable degree, and protrudes into the distended portion of the antrum (nipple sign) may be observed on ultrasonography.
Other Imaging Findings
Upper gastrointestinal series (barium meal) may be helpful in the diagnosis of infantile pyloric stenosis. Findings on an upper gastrointestinal series suggestive of infantile pyloric stenosis include delayed gastric emptying, elongated pylorus with a narrow lumen (string sign), and the pylorus indents the contrast-filled antrum (shoulder sign).
Other Diagnostic Studies
There are no other diagnostic studies associated with pyloric stenosis.
Treatment
Medical Therapy
Decompression of stomach by suction via nasogastric tube and Initial correction of fluid and electrolyte imbalance, oral administration of atropine sulfate, and oral feeding with 10 ml of 10% glucose are important in treatment of pyloric stenosis.
Surgery
Infantile pyloric stenosis is typically managed with surgery. Ranstedt’s extramuscular pyloromyotomy is the gold standard of treatment. After the surgery, once the stomach can empty into the duodenum, feeding can be started. There is occasionally recurrence in the immediate post-operative period, but the condition generally has no long-term impact on the child‘s future.
Primary Prevention
There are no established measures for the primary prevention of pyloric stenosis.
Secondary Prevention
There are no established measures for the secondary prevention of pyloric stenosis.
References
Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
In 1717, Dr. Patrick Blair reported autopsy findings of pyloric stenosis for first time. In 1911, Conrad Ramstedt witnessed complete recovery of a patient with pyloric stenosis after undergoing pyloroplasty.
Historical Perspective
- In 1717, Dr. Patrick Blair first reported autopsy findings of pyloric stenosis.[1]
- In 1887, Harald Hirschsprung, a Danish pediatrician described the clinical picture and pathology of pyloric stenosis.[2]
Landmark Events in the Development of Treatment Strategies
- In 1911, Conrad Ramstedt witnessed complete recovery of a patient with pyloric stenosis after undergoing pyloroplasty.[2]
- Till date, Ramstedt pyloromyotomy is understood to be the standard procedure in patients with pyloric stenosis.[3]
References
- ↑ T. E. C., Jr. (1978). “IS DR. PATRICK BLAIR’S DESCRIPTION OF PYLORIC STENOSIS IN 1717 THE EARLIEST ON RECORD?”. Pediatircs. 62 (1).
- ↑ 2.0 2.1 Nafe, Cleon A. (1947). “CONGENITAL HYPERTROPHIC PYLORIC STENOSIS”. Archives of Surgery. 54 (5): 555. doi:10.1001/archsurg.1947.01230070564006. ISSN 0004-0010.
- ↑ St. Peter, Shawn D.; Holcomb, George W.; Calkins, Casey M.; Murphy, J Patrick; Andrews, Walter S.; Sharp, Ronald J.; Snyder, Charles L.; Ostlie, Daniel J. (2006). “Open Versus Laparoscopic Pyloromyotomy for Pyloric Stenosis”. Transactions of the … Meeting of the American Surgical Association. 124: 29–36. doi:10.1097/01.sla.0000234647.03466.27. ISSN 0066-0833.
Classification
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
There is no established system for the classification of pyloric stenosis. It may be subclassified as infantile pyloric stenosis and adult-onset hypertrophic pyloric stenosis.
Classification
There is no established system for the classification of pyloric stenosis. It may be subclassified as infantile pyloric stenosis and adult-onset hypertrophic pyloric stenosis.[1]
References
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
The pathogenesis of infantile hypertrophic pyloric stenosis is not completely understood[1]. However, infantile hypertrophic pyloric stenosis may result from abnormal innervation of the pyloric smooth muscle.[1] The chloride loss due persistent vomiting results in hypochloremia which impairs the kidney‘s ability to excrete bicarbonate. This factor significantly prevents correction of the alkalosis. The secondary hyperaldosteronism develops due to the hypovolaemia. The body’s compensatory response to the metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO2. In relatives of probands of infantile hypertrophic pyloric stenosis patients and monozygotic co-twins the recurrence pattern did not depict a single major inheritance.
Pathophysiology
The pathogenesis of infantile hypertrophic pyloric stenosis is not completely understood.
- However, infantile hypertrophic pyloric stenosis (IHPS) may result from abnormal innervation of the pyloric smooth muscle.[1]
- Evidence of increased collagen production and abnormal amounts of extracellular matrix proteins has also been observed in patients with hypertrophic pyloric muscle.[1]
- The gastric outlet obstruction due to the hypertrophic pylorus impairs emptying of gastric contents into the duodenum. As a consequence, all ingested food and gastric secretions can only exit via vomiting, which is projectile in nature. The vomited material does not contain bile because the pyloric obstruction prevents entry of duodenal contents (containing bile) into the stomach. This results in loss of gastric acid (hydrochloric acid). The chloride loss results in hypochloremia which impairs the kidney‘s ability to excrete bicarbonate. This factor significantly prevents correction of the alkalosis.[2]
- A secondary hyperaldosteronism develops due to the hypovolaemia. The high aldosterone levels causes the kidneys to:[3]
- Avidly retain Na+ (to correct the intravascular volume depletion).
- Excrete increased amounts of K+ into the urine (resulting in hypokalaemia). The body’s compensatory response to the metabolic alkalosis is hypoventilation resulting in an elevated arterial pCO2.[4]
| Hypertrophic pylorus | |||||||||||||||||||
| Gastric outlet obstruction | |||||||||||||||||||
| Impaired emptying of gastric content into duodenum | |||||||||||||||||||
| All ingested food and gastric content exit through vomiting | |||||||||||||||||||
| Hypochloremia and alkalosis | |||||||||||||||||||
Genetics
In relatives of probands of infantile hypertrophic pyloric stenosis patients and monozygotic co-twins the recurrence pattern did not depict a single major inheritance.[5]
Associated Conditions of Infantile Hypertrophic Pyloric Stenosis
Various conditions associated with infantile pyloric stenosis include:[6]
- Neuromuscular disorders
- Connective tissue disorders
- Metabolic disorders
- Intracellular signalling pathway disturbances
- Intercellular communication disturbances
- Ciliopathies
- DNA-repair abnormalities
- Transcription regulation disorders
- MAPK-pathway abnormalities
- Lymphatic abnormalities
- Environmental factors
Gross Pathology
On gross pathology, characteristic findings of pyloric stenosis include:
- Hypertrophic muscularis mucosa
- Protrusion of gastric mucosa into the smooth muscle layer[7]
Microscopic Pathology
The following observations may be seen in pyloric stenosis:[8]
- Smooth muscle cells are in a proliferative phase and there is very few gap junctions between smooth muscle cells in pyloric stenosis.
- The circular muscle layer is characterized by very few large granular vesicle-containing nerve fibers.
- The number of nerve cell bodies in the myenteric plexus, and the total number of ganglia is lower than normal.
- Interstitial cells of Cajal are almost completely absent.
References
- ↑ 1.0 1.1 1.2 1.3 Ohshiro K, Puri P (1998). “Pathogenesis of infantile hypertrophic pyloric stenosis: recent progress”. Pediatr Surg Int. 13 (4): 243–52. doi:10.1007/s003830050308. PMID 9553181.
- ↑ Ahmad, J.; Thomson, S.; Taylor, M.; Scoffield, J. (2011). “A reminder of the classical biochemical sequelae of adult gastric outlet obstruction”. Case Reports. 2011 (jan29 1): bcr0520102978–bcr0520102978. doi:10.1136/bcr.05.2010.2978. ISSN 1757-790X.
- ↑ Booth RE, Johnson JP, Stockand JD (2002). “Aldosterone”. Adv Physiol Educ. 26 (1–4): 8–20. PMID 11850323.
- ↑ Javaheri S, Shore NS, Rose B, Kazemi H (1982). “Compensatory hypoventilation in metabolic alkalosis”. Chest. 81 (3): 296–301. PMID 6799256.
- ↑ Mitchell LE, Risch N (1993). “The genetics of infantile hypertrophic pyloric stenosis. A reanalysis”. Am J Dis Child. 147 (11): 1203–11. PMID 8237916.
- ↑ Peeters B, Benninga MA, Hennekam RC (2012). “Infantile hypertrophic pyloric stenosis–genetics and syndromes”. Nat Rev Gastroenterol Hepatol. 9 (11): 646–60. doi:10.1038/nrgastro.2012.133. PMID 22777173.
- ↑ Spicer RD (1982). “Infantile hypertrophic pyloric stenosis: a review”. Br J Surg. 69 (3): 128–35. PMID 7039756.
- ↑ Langer JC, Berezin I, Daniel EE (1995). “Hypertrophic pyloric stenosis: ultrastructural abnormalities of enteric nerves and the interstitial cells of Cajal”. J Pediatr Surg. 30 (11): 1535–43. PMID 8583319.
Causes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
The causes of infantile pyloric stenosis are unknown, but genetic and environmental factors might play a role in the pathogenesis of infantile pyloric stenosis. Common causes of adult-onset hypertrophic pyloric stenosis (HPS) include persisting duodenal hyperacidity, inheritance of a parietal cell mass (PCM) at the upper end of the normal range which causes persisting duodenal hyperacidity.
Causes
Causes of pyloric stenosis include:
- Causes of adult-onset hypertrophic pyloric stenosis
- Persisting duodenal hyperacidity.[1]
- Inheritance of a parietal cell mass (PCM) at the upper end of the normal range which causes persisting duodenal hyperacidity.
- Causes of infantile pyloric stenosis
- The causes of infantile pyloric stenosis are unknown, but genetic and environmental factors might play a role in the pathogenesis of infantile pyloric stenosis.[2]
References
- ↑ Rogers IM (2006). “The true cause of pyloric stenosis is hyperacidity”. Acta Paediatr. 95 (2): 132–6. doi:10.1080/08035250500431385. PMID 16449017.
- ↑ Eyal O, Asia A, Yorgenson U, Nagar H, Schpirer Z (1999). “[Atypical infantile hypertrophic pyloric stenosis]”. Harefuah. 136 (2): 113–4, 175. PMID 10914175.
Differentiating Pyloric stenosis from other Diseases
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
Infantile hypertrophic pyloric stenosis must be differentiated from other diseases that cause vomiting, poor feeding and dehydration, such as adrenal insufficiency, gastroenteritis, UTI, inborn errors of metabolism and acute renal failure. projectile vomiting and and palpation of an olive in abdominal physical examination are very helpful to distinguish infantile pyloric stenosis from other common causes of vomiting in infants.
Differentiating Infantile Pyloric stenosis from Other Diseases
Pyloric stenosis must be differentiated from other diseases, such as:[1][2][3][4]
- Adrenal insufficiency
- Gastroenteritis
- Inborn errors of metabolism
- Urinary tract infections and pyelonephritis
- Acute renal failure
Preferred Table
| Diseases | History and Symptoms | Physical Examination | Laboratory Findings | |||||
|---|---|---|---|---|---|---|---|---|
| Vomiting | Persistent hunger | Failure to gain weight | Dehydration | Palpation of an olive in abdomen | Hypokalemia | Acidosis or Alkalosis | Hypochloremia or hyperchloremia | |
| Infantile pyloric stenosis | ++ | ++ | ++ | ++ | +/- | + | Alkalosis | Hypochloremia |
| Adrenal insufficiency | +/- | +/- | + | + | – | Hyperkalemia or normal | Acidosis | Hypochloremia |
| Gastroenteritis | ++ | – | +/- | ++ | – | + | Acidosis | Hypochloremia |
| UTI | +/- | – | – | +/- | – | + | Acidosis or alkalosis | Hypochloremia or hyperchloremia |
| Acute renal failure | +/- | – | – | + | – | Hyperkalemia | Acidosis | Hyperchloremia |
References
- ↑ Puttanna, A.; Cunningham, A. R.; Dainty, P. (2013). “Addison’s disease and its associations”. Case Reports. 2013 (jul26 1): bcr2013010473–bcr2013010473. doi:10.1136/bcr-2013-010473. ISSN 1757-790X.
- ↑ Elliott, E. J. (2007). “Acute gastroenteritis in children”. BMJ. 334 (7583): 35–40. doi:10.1136/bmj.39036.406169.80. ISSN 0959-8138.
- ↑ Gil-Ruiz, Maite Augusta; Alcaraz, Andrés José; Marañón, Rafael José; Navarro, Nelia; Huidobro, Belén; Luque, Augusto (2011). “Electrolyte disturbances in acute pyelonephritis”. Pediatric Nephrology. 27 (3): 429–433. doi:10.1007/s00467-011-2020-9. ISSN 0931-041X.
- ↑ Chambers JK (1987). “Fluid and electrolyte problems in renal and urologic disorders”. Nurs Clin North Am. 22 (4): 815–26. PMID 3317287.
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
The incidence of infantile pyloric stenosis is approximately 400 per 100,000 individuals worldwide and it is four times more common in males. It usually affects individuals of the Caucasian race. Asians individuals are less likely to develop infantile pyloric stenosis. The prevalence of infantile pyloric stenosis in the course of 11 years (1989-1999) was approximately 7.3 per 100,000 individuals in one study. It is observed that the mortality rate of pyloric stenosis is very low and usually results from delays in diagnosis that causes severe dehydration and shock.
Epidemiology and Demographics
Incidence
Prevalence
- The prevalence of infantile pyloric stenosis in the course of 11 years (1989-1999) was approximately 7.3 per 100,000 individuals in one study.[2]
Mortality rate
- It is observed that the mortality rate of pyloric stenosis is very low and usually results from delays in diagnosis that causes severe dehydration and shock.[3]
Gender
- Males are more commonly affected by infantile pyloric stenosis than females.[4]
- The male to female ratio is approximately 4 to 1.
Race
- Infantile pyloric stenosis usually affects individuals of the Caucasian race.[1]
- Asians individuals are less likely to develop Infantile pyloric stenosis.
- Incidence of infantile pyloric stenosis according to race include:
- White – 240 per 100,000 individuals
- Hispanic – 180 per 100,000 individuals
- Black – 70 per 100,000 individuals
- Asian – 60 per 100,000 individuals
Age
- Infantile pyloric stenosis commonly affects infants.[1]
References
- ↑ 1.0 1.1 1.2 Schechter R, Torfs CP, Bateson TF (1997). “The epidemiology of infantile hypertrophic pyloric stenosis”. Paediatr Perinat Epidemiol. 11 (4): 407–27. PMID 9373863.
- ↑ Mukhin VN, Moskalenko VZ, Grona VN, Sopov GA, Linchevskiĭ GL (2001). “[Population prevalence of congenital hypertrophic pyloric stenosis in the Donetsk region of Ukraine]”. Tsitol Genet. 35 (5): 60–4. PMID 11944318.
- ↑ Hernanz-Schulman M (2003). “Infantile hypertrophic pyloric stenosis”. Radiology. 227 (2): 319–31. doi:10.1148/radiol.2272011329. PMID 12637675.
- ↑ Chalya, Phillipo L.; Manyama, Mange; Kayange, Neema M.; Mabula, Joseph B.; Massenga, Alicia (2015). “Infantile hypertrophic pyloric stenosis at a tertiary care hospital in Tanzania: a surgical experience with 102 patients over a 5-year period”. BMC Research Notes. 8 (1). doi:10.1186/s13104-015-1660-4. ISSN 1756-0500.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
The most potent risk factors in the development of infantile pyloric stenosis are male gender, Caucasian race, bottle feeding, caesarean section delivery, first-born infant, preterm birth; and exposure to macrolides, nitrofurantoin, penicillins, and trimethoprim-sulphamethoxazole during pregnancy.
Risk Factors
Risk Factors of infantile pyloric stenosis
The most potent risk factor in the development of infantile pyloric stenosis is male gender. Other risk factors include bottle feeding, caucasian race, cesarean section delivery, first born infant, preterm birth and exposure to macrolides, nitrofurantoin, penicillins and trimethoprim-sulphamethoxazole during pregnancy.[1]
Common Risk Factors
Common risk factors for infantile pyloric stenosis include:[2][3][4][5]
- Male gender
- Caucasian race
- Bottle feeding
- Cesarean section delivery
Less Common Risk Factors
Less common risk factors in the development of infantile pyloric stenosis include:[1][5]
- First-born infant
- Preterm birth
- Exposure to drugs during pregnancy
References
- ↑ 1.0 1.1 Nordeng S, Nordeng H, Høye S (2016). “[Use of antibiotics during pregnancy]”. Tidsskr Nor Laegeforen. 136 (4): 317–21. doi:10.4045/tidsskr.15.0451. PMID 26905846.
- ↑ Yang G, Brisseau G, Yanchar NL (2008). “Infantile hypertrophic pyloric stenosis: An association in twins?”. Paediatr Child Health. 13 (5): 383–5. PMC 2532891. PMID 19412365.
- ↑ Schechter R, Torfs CP, Bateson TF (1997). “The epidemiology of infantile hypertrophic pyloric stenosis”. Paediatr Perinat Epidemiol. 11 (4): 407–27. PMID 9373863.
- ↑ Krogh C, Biggar RJ, Fischer TK, Lindholm M, Wohlfahrt J, Melbye M (2012). “Bottle-feeding and the Risk of Pyloric Stenosis”. Pediatrics. 130 (4): e943–9. doi:10.1542/peds.2011-2785. PMC 3457615. PMID 22945411.
- ↑ 5.0 5.1 Zhu J, Zhu T, Lin Z, Qu Y, Mu D (2017). “Perinatal risk factors for infantile hypertrophic pyloric stenosis: A meta-analysis”. J Pediatr Surg. 52 (9): 1389–1397. doi:10.1016/j.jpedsurg.2017.02.017. PMID 28318599.
Screening
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
There is insufficient evidence to recommend routine screening for pyloric stenosis.
Screening
There is insufficient evidence to recommend routine screening for pyloric stenosis.
References
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
The symptoms of pyloric stenosis usually develop in the first days of life, and start with projectile vomiting. If left untreated, infants with mild infantile pyloric stenosis can develop severe electrolyte imbalances include hypokalemia , hypochloremia, and metabolic alkalosis.In rare cases of untreated pyloric stenosis, patients may develop significant problems on the cognition, receptive language, fine motor, and gross motor skills compared to the normal infants due to long term malnutrition. Complications of infantile pyloric stenosis before surgery include vomiting and failure to gain weight in newborn period. Prognosis is generally excellent and surgery usually provides complete relief of symptoms. Infants usually tolerate small, frequent feedings several hours after surgery
Natural History, Complications, and Prognosis
Natural History
- The symptoms of pyloric stenosis usually develop in the first days of life, and start with projectile vomiting.
- If left untreated, infants with mild infantile pyloric stenosis can develop severe electrolyte imbalances include hypokalemia , hypochloremia, and metabolic alkalosis.[1]
- In rare cases of untreated pyloric stenosis, patients may develop significant problems on the cognition, receptive language, fine motor, and gross motor skills compared to the normal infants due to long term malnutrition.[2]
Complications
- Complications of infantile pyloric stenosis before surgery include:[1]
Prognosis
- Prognosis is generally excellent and surgery usually provides complete relief of symptoms. Infants usually tolerate small, frequent feedings several hours after surgery.[6]
- Up to 80% of patients continue to regurgitate even after surgical correction.[6]
References
- ↑ 1.0 1.1 Tutay GJ, Capraro G, Spirko B, Garb J, Smithline H (2013). “Electrolyte profile of pediatric patients with hypertrophic pyloric stenosis”. Pediatr Emerg Care. 29 (4): 465–8. doi:10.1097/PEC.0b013e31828a3006. PMID 23528507.
- ↑ Walker K, Halliday R, Holland AJ, Karskens C, Badawi N (2010). “Early developmental outcome of infants with infantile hypertrophic pyloric stenosis”. J Pediatr Surg. 45 (12): 2369–72. doi:10.1016/j.jpedsurg.2010.08.035. PMID 21129547.
- ↑ Spitz L (1979). “Vomiting after pyloromyotomy for infantile hypertrophic pyloric stenosis”. Arch Dis Child. 54 (11): 886–9. PMC 1545582. PMID 526031.
- ↑ Srivastava NT, Parent JJ, Schamberger MS (2017). “Consideration of pyloric stenosis as a cause of feeding dysfunction in children with cyanotic heart disease”. Ann Pediatr Cardiol. 10 (3): 298–300. doi:10.4103/apc.APC_51_17. PMC 5594945. PMID 28928620.
- ↑ Romano C, Oliva S, Martellossi S, Miele E, Arrigo S, Graziani MG; et al. (2017). “Pediatric gastrointestinal bleeding: Perspectives from the Italian Society of Pediatric Gastroenterology”. World J Gastroenterol. 23 (8): 1328–1337. doi:10.3748/wjg.v23.i8.1328. PMC 5330817. PMID 28293079.
- ↑ 6.0 6.1 Gibbs MK, Van Herrden JA, Lynn HB (1975). “Congenital hypertrophic pyloric stenosis. Surgical experience”. Mayo Clin Proc. 50 (6): 312–6. PMID 1127996.
Diagnosis
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Treatment
Treatment
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