Hypertrophic Pyloric Stenosis and Lesions of the Stomach Flashcards
A 5-week-old boy has a 5-day history of nonbilious vomiting and weight loss of 0.4 kg (from 4.0 to 3.6 kg). His anterior fontanelle is flattened, and his mucous membranes are dry. Laboratory data are as follows (in mEq/L): sodium 132, potassium 3.2, chloride 91, and bicarbonate 28. Which of the following statements about this infant is true?
A. Characterization of the emesis as nonbilious is crucial to aid in the diagnosis.
B. Palpation of the abdomen will not help with the diagnosis.
C. Ultrasound imaging of the abdomen will not add to the diagnosis.
D. This condition is more likely to affect females.
E. Laboratory results are likely to demonstrate a metabolic acidosis.
ANSWER: A
COMMENTS: The differential diagnoses in this child include intestinal stenosis, pyloric stenosis, intussusception, and malrotation.
Age is important in sorting out the differential diagnoses in children.
Duodenal atresia is seen in newborns since it is congenital.
This child has hypertrophic pyloric stenosis, which typically produces symptoms in infants between 3 and 12 weeks of age and is more common in males.
Intussusception most commonly occurs in children between 3 and 18 months of age.
Infants with pyloric stenosis usually present with nonbilious vomiting that progressively becomes projectile since the blockage is proximal to the ampulla of Vater.
Duodenal atresia most commonly occurs distal to the ampulla of Vater, and therefore the vomitus is bilious in about 80% of cases.
Duodenal stenosis distal to the ampulla may present in a similar manner.
Malrotation also presents with bilious emesis.
The extent of dehydration and electrolyte imbalance depends on the duration of the symptoms.
Early in the course, fluid and electrolyte levels may be normal. If the condition is diagnosed late, infants are more likely to have severe metabolic derangements and dehydration.
Palpation during physical examination may reveal the pathognomonic olive-sized mass of the thickened pylorus in the upper mid to right abdomen.
Sometimes gastric waves are seen through the epigastrium.
If the pyloric mass cannot be palpated by an experienced examiner, ultrasound is the first choice for diagnostic imaging.
Correction of fluid and electrolyte abnormalities takes precedence over surgery, which can be undertaken once electrolyte imbalances are corrected.
For the infant with pyloric stenosis, which of the following is the
most common electrolyte abnormality?
A. Hypokalemia
B. Hyperkalemia
C. Hypocalcemia
D. Hyperchloremia
E. Hypercalcemia
ANSWER: A
COMMENTS: Infants with a gastric outlet obstruction due to hypertrophic pyloric stenosis typically present with hypokalemia, hypochloremic metabolic alkalosis, and paradoxical aciduria.
The electrolyte abnormalities reflect the extensive loss of gastric contents from emesis in hypertrophic pyloric stenosis.
Paradoxical aciduria and hypokalemia result from the urinary loss of acid (H+) and potassium at the expense of sodium and water retention to preserve the fluid volume.
Hypochloremia is secondary to the loss of bicarbonate from emesis with resulting contraction alkalosis.
Disturbances in calcium are not common in this setting. Correction of fluid and electrolyte imbalances is essential before proceeding to surgery.
This patient with hypertrophic pyloric stenosis presented with laboratory values of sodium 132 mEq/L, potassium 3.2 mEq/L, chloride 91 mEq/L, and bicarbonate 28 mEq/L. Which of the following intravenous fluids administered prior to surgery can decrease the risk of respiratory distress?
A. Dextrose 5% and water with 20 mEq of potassium chloride (KCl)
B. Lactated Ringer’s
C. 1 unit of packed red blood cells
D. Dextrose 5% with one-half normal saline and 20 mEq of KCL
E. Dextrose 5% with one-half normal saline
ANSWER: D
COMMENTS: Hypertrophic pyloric stenosis presents with a hypochloremic, hypokalemic, and metabolic alkalosis. A serum bicarbonate < 25 mEq/L is a slight deficit, 26 to 35 mEq/L is a moderate deficit, and >35 mEq/L is severe.
This deficit guides resuscitation as well as operative timing.
It is important to correct alkalosis so that the serum bicarbonate level is <30mEq/L prior to operative intervention.
If uncorrected, this can lead to respiratory insufficiency and prolonged intubation as the baby’s system attempts to correct the acid–base balance by hypoventilation.
In addition to alkalosis, these patients also have hypokalemia.
Therefore adding potassium to the intravenous fluid is essential, making the optimal resuscitative fluid D5 with one-half normal saline and 20 mEq of KCL.
If electrolyte abnormalities are severely deranged at presentation, very close intensive care unit monitoring and gradual resuscitation should be performed to prevent rapid shifts in electrolytes that could lead to seizures and other serious complications.
Ref.: 4
A five-week-old baby has been projectile vomiting for two weeks, is losing weight, is dehydrated with visible gastric peristalsis and has a palpable mass in epigastrium. The most likely diagnosis is:
A. Gastroesophageal reflux.
B. Pyloric stenosis.
C. Duodenal stenosis.
D. Duodenal atresia.
E. Gastric volvulus.
B. Pyloric stenosis.
All features in question are suggestive of pyloric stenosis.
Syed/MCQ
Regarding the ultrasound finding to label hypertrophied pyloric stenosis, the most correct statement is:
A. Pyloric muscle thickness is 4 mm or more, and pyloric channel length is 16 mm or more.
B. Pyloric muscle thickness is 2 mm or more, and pyloric channel length is 14 mm or more.
C. Pyloric muscle thickness is 2 mm or more, and pyloric channel length is 16 mm or more.
D. Pyloric muscle thickness is 16 mm or more, and pyloric channel length is 10 mm or more.
E. Pyloric muscle thickness is 8 mm or more, and pyloric channel length is 12 mm or more.
A. The pyloric muscle thickness 4 mm or more and pyloric channel length 16 mm or more.
Syed/MCQ
The preferred site of incision for pyloromyotomy is:
A. Anterosuperior surface.
B. Posterior surface.
C. Posterosuperior surface.
D. Posteroinferior surface.
E. Inferior surface.
A. Anterosuperior surface. This is relatively bloodless area.
Syed/MCQ
The metabolic derangement in pyloric stenosis is:
A. Hyperchloremic, hyperkalemic metabolic alkalosis.
B. Metabolic acidosis.
C. Hypochloremic, hypokalemic metabolic acidosis.
D. Hypochloremic, hypokalemic metabolic alkalosis.
E. Hypochloremic, hyperkalemic metabolic alkalosis.
D. Hypochloremic, hypokalemic metabolic alkalosis.
Hypochloraemia because of loss of chloride in vomitus.
Hypokalaemia because of K+ loss in vomitus and activation of rennin-AG-ALD system will produce loss of K+ in urine.
With K+ loss in urine, it gets reabsorbed in distal tubule with loss of H+ worsening, leading to metabolic alkalosis and production of acidic urine.
Initially, alkaline urine and, later, paradoxical aciduria is noted, in order to prevent hypokalaemia.
Metabolic alkalosis also because of loss of H+ in vomitus, decreased secretion of pancreatic CHO3-, increased CHO3- presented to distal tubule and eliminated, producing an alkaline urine.
Additionally, hyponatraemia occurs because of loss of Na+ in vomitus, decreased absorption of Na+, and loss of Na+ in urine until kidney adjusts to increased CHO3- load.
Syed/MCQ
Pyloric atresia. Which of the following statements is true?
A. A common presentation is bilious vomiting in the first few days of life.
B. Radiological features are similar to duodenal atresia.
C. It is associated with epidermolysis bullosa.
D. Pyloromyotomy is the treatment of choice.
E. It is more common in males.
C
Pyloric atresia is rare and accounts for 1% of all intestinal atresias. Its incidence is about one per 100 000 live births. There is an equal male-to-female ratio. There are three recognised forms of pyloric atresia, types A, B and C. In type A (57%) there is a pyloric membrane or web occluding the lumen; in type B (34%) the pyloric channel is a solid cord, and in type C (9%) there is a complete gap between the stomach and duodenum.
Pyloric atresia is seen in association with other congenital defects in 30%–50% of cases (malrotation, cardiac defects, vaginal agenesis and tracheo-oesophageal anomalies). Eighteen per cent of cases of pyloric atresia are associated with epidermolysis bullosa, which is a cutaneous genetic disease of variable severity. There is usually a maternal history of polyhydramnios, and affected infants present in the first few days of life with non-bilious vomiting and complete gastric outlet obstruction. unlike duodenal atresia, which has a classic double-bubble appearance on plain radiograph, pyloric atresia is diagnosed with a single gastric bubble with no distal gas beyond pylorus. If distal gas is seen, the diagnosis may be confirmed with a contrast study to rule out an incomplete pyloric membrane.
In type A, excision of a complete or partial diaphragm with Heineke-mikulicz’s or Finney’s pyloroplasty is the most straightforward corrective procedure. In types B and C, with atretic ends separated by a cord or discontinuous segment, a repair is usually with a Billroth type I (gastroduodenostomy) anastomosis.
Which of the following is true regarding hypertrophic pyloric stenosis?
A The male-to-female ratio is identical.
B Premature infants are diagnosed later than term/post-term infants.
C It is more common in first-born female infants.
D The risk is greater with older maternal age.
E Offspring risk is higher if father had hypertrophic pyloric stenosis.
B
Hypertrophic pyloric stenosis occurs at a rate of 1–4 per 1000 live births with a male-to-female ratio of 4 : 1. Risk factors include family history, younger maternal age, first-born infant (more common in males), maternal feeding pattern (breast feeding protective), erythromycin exposure and transpyloric feeding of premature infants.
Premature infants are diagnosed with hypertrophic pyloric stenosis later than post-term infants. The risk of hypertrophic pyloric stenosis in offspring of mothers who had pyloric stenosis as a baby is greater than if the father has pyloric stenosis.
Which of the following is true regarding the metabolic derangement seen in hypertrophic pyloric stenosis?
A hypochloraemia B hyperkalaemia C hypernatraemia D metabolic acidosis E respiratory alkalosis
A
The cardinal features of pyloric stenosis are non-bilious projectile vomiting, visible peristaltic waves in the left upper quadrant, and metabolic derangement of hypokalaemic, hypochloraemic metabolic alkalosis in a full-term neonate between 2 and 8 weeks of age. There are large losses of hydrogen and chloride ions due to vomiting of gastric secretions.
The chloride loss results in hypochloraemia, which impairs the kidney’s ability to excrete bicarbonate. This is the significant factor that prevents correction of the alkalosis. Secondary hyperaldosteronism develops because of the hypovolaemia. The high aldosterone levels cause the kidneys to:
● avidly retain Na + (to correct the intravascular volume depletion)
● excrete increased amounts of K + into the urine (resulting in hypokalaemia).
As potassium depletion worsens, sodium is reabsorbed across the renal tubules in exchange for hydrogen ions. Hence, despite having a metabolic alkalosis, the child will develop a ‘paradoxical aciduria’. The compensatory response to metabolic alkalosis is hypoventilation resulting in elevated arterial PCo2 (respiratory acidosis).
The only means of breaking this cycle is to rehydrate the child, and surgery should be deferred until the metabolic derangement has been reversed.
Which of the following is true regarding management of hypertrophic pyloric stenosis?
A Diagnostic feature on ultrasonography is length of pylorus >14 mm.
B Diagnostic feature on ultrasonography is the pylorus muscle thickness >3 mm.
C Urgent pyloromyotomy is the treatment of choice.
D Postoperative emesis is a common occurrence.
E Postoperative contrast study is useful in the evaluation of completeness of myotomy.
D
A definitive diagnosis can be made on clinical examination in 75% of cases, by palpating a pyloric mass. However, if the diagnosis is unclear after a thorough physical examination, radiological evaluation is warranted. ultrasonography is the gold standard investigation for confirming the diagnosis of pyloric stenosis.
The diagnostic criteria are a combination of a muscle thickness greater than or equal to 4 mm and a length of greater than or equal to 16 mm.
In neonates younger than 30 days, a thickness of more than 3 mm is considered positive.
Pyloric stenosis is not a surgical emergency, and the mainstay of therapy is initial resuscitation and correction of metabolic and electrolyte abnormality.
Once the metabolic derangement is corrected the operative procedure of choice is a Ramstedt pyloromyotomy. This can be performed via an open approach or laparoscopically.
Complications after pyloromyotomy are minimal and include mucosal perforation (1%–2%), wound infection (1%–2%) and incisional hernia (1%). Postoperative emesis is common and can occur in up to 80% of cases.
However, prolonged emesis is less common (2%–26%) and is usually secondary to gastro-oesophageal reflux (24%–31%), but can be secondary to incomplete myotomy (0%–6%).
Frequent vomiting persisting beyond 3–4 days may suggest an incomplete myotomy or an unsuspected perforation.
A postoperative contrast study may demonstrate a leak but is not helpful in evaluating the completeness of the myotomy.
It can take several weeks for the radiographic appearance of the pylorus to improve.
Persistent and frequent vomiting 1 week beyond the pyloromyotomy may require re-exploration.
Regarding the ultrasound finding to label hypertrophied pyloric stenosis, the most correct statement is:
A. Pyloric muscle thickness is 4mm or more, and pyloric channel length is 16mm or more.
B. Pyloric muscle thickness is 2mm or more, and pyloric channel length is 14mm or more.
C. Pyloric muscle thickness is 2mm or more, and pyloric channel length is 16mm or more.
D. Pyloric muscle thickness is 16mm or more, and pyloric channel length is 10mm or more.
E. Pyloric muscle thickness is 8mm or more, and pyloric channel length is 12mm or more.
A. Pyloric muscle thickness is 4mm or more, and pyloric channel length is 16mm or more.
The preferred site of incision for pyloromyotomy is:
A. Anterosuperior surface
B. Posterior surface
C. Posterosuperior surface
D. Posteroinferior surface
E. Inferior surface
A. Anterosuperior surface
What is the embryology of the stomach?
The stomach forms from the foregut and is recognizable by the fifth week of gestation.
It then elongates, descends, and dilates to form its familiar structure by the seventh week of gestation.
The vascular supply to the stomach is very robust, and ischemia of the stomach is rare.
The stomach is supplied by the right and left gastric arteries along the lesser curvature, the right and left gastroepiploic arteries along the greater curvature, and the short gastric vessels from the spleen.
There is also contribution from the posterior gastric artery, which is a branch of the splenic artery, as well as the phrenic arteries.
In this chapter we discuss common and unusual conditions of the stomach that are treated surgically. Some topics relevant to the stomach, such as gastroesophageal reflux disease (GERD) and obesity, are covered elsewhere.
H&A
What is the etiology of hypertrophic pyloric stenosis?
Hypertrophic pyloric stenosis (HPS) is one of the most common surgical conditions of the newborn.
It occurs at a rate of 1–4 per 1000 live births in white infants but is seen less often in nonwhite children.
Males are affected more often with a 4:1 male-to-female ratio.
Risk factors for HPS include family history, gender, younger maternal age, being a first-born infant, and maternal feeding patterns.
Premature infants are diagnosed with HPS later than term or post-term infants.
ETIOLOGY
The cause of HPS is unknown, but genetic and environmental factors appear to play a significant role in the pathophysiology.
A genetic predisposition has been inferred from race discrepancies, the increased frequency in males, and the association with birth order (first-born infants with a positive family history).
Variants near several loci including MBNL1, NKX2-5, and APOA1 have been associated with HPS.
Environmental factors associated with HPS include the method of feeding (breast vs formula), seasonal variability, exposure to erythromycin, environmental pesticides, and transpyloric feeding in premature infants.
Additionally, there has been interest in several gastrointestinal peptides or growth factors that may facilitate pyloric hypertrophy.
Some of these include excessive substance P, decreased neurotrophins, deficient nitric oxide synthase, and gastrin hypersecretion.
Thus, the etiology of HPS is likely multifactorial with environmental influences.
H&A
How is hypertrophic pyloric stenosis diagnosed?
DIAGNOSIS
The classic presentation of HPS is nonbilious, projectile vomiting in a full-term neonate who is between 2 and 8 weeks old.
Initially, the emesis is infrequent and may appear to be symptomatic of GERD.
However, over a short period of time, the emesis occurs with every feeding and becomes forceful (i.e., projectile).
The contents of the emesis are usually the recent feedings, but signs of gastritis are not uncommon (“coffee-ground” emesis).
On physical examination, the neonate usually appears well if the diagnosis is made early.
However, depending on the duration of symptoms and degree of dehydration, the neonate may be gaunt and somnolent.
Visible peristaltic waves may be present in the mid to left upper abdomen.
The pylorus is palpable in 70–90% of patients.
To palpate the pyloric mass (i.e., “olive”), the neonate must be relaxed.
Techniques for relaxing the patient include bending the newborn’s knees and flexing the hips, and using a pacifier with sugar water.
These techniques should be attempted after the stomach has been decompressed with a 10 French to 12 French orogastric tube.
After palpating the liver edge, the examiner’s fingertips should slide underneath the liver in the midline.
Slowly, the fingers are pulled back down, trying to trap the “olive.”
Palpating the pylorus requires patience and an optimal examination setting. If palpated, no further studies are needed. If the hypertrophied pylorus cannot be palpated, ultrasound (US) is the next step.
US has become the standard technique for diagnosing HPS and has supplanted the physical examination at most institutions.
The diagnostic criteria for pyloric stenosis is a muscle thickness of ≥4 mm and a pyloric length of ≥16 mm.
A thickness of >3 mm is considered positive if the neonate is younger than 30 days of age.
The study is dependent on the expertise of the US technician and radiologist.
There are reports of nonradiologists performing US for diagnosing HPS, which would obviously reduce the need for the US technician.
If the US findings are equivocal, then an upper gastrointestinal series can be helpful in confirming the diagnosis.
In the past, the diagnosis was often delayed and profound dehydration with metabolic derangements was common.
Today, however, primary care physicians are more aware of the problem and the availability of US facilitates an earlier diagnosis and treatment of HPS.
However, the complete differential diagnosis for nonbilious vomiting should be considered.
This includes medical causes such as GERD, gastroenteritis, increased intracranial pressure, and metabolic disorders.
Anatomic causes include an antral web, foregut duplication cyst, gastric tumors, or a tumor causing extrinsic gastric compression.
H&A
How is hypertrophic pyloric stenosis managed?
TREATMENT
The mainstay of therapy is typically resuscitation followed by
pyloromyotomy.
There are reports of medical treatment with atropine and pyloric dilation, but these treatments require long periods of time and are often not effective.
Once the diagnosis of HPS is made, feedings should be withheld. Gastric decompression is usually not necessary but occasionally may be required in extreme cases.
If a barium study was performed, it is important to remove all of the contrast material from the stomach to prevent aspiration.
The hallmark metabolic derangement of hypochloremic, hypokalemic metabolic alkalosis is usually seen to some degree in most patients.
Profound dehydration is rarely seen today, and correction is usually achieved in <24 hours after presentation.
A basic metabolic panel should be ordered, and the resuscitation should be directed toward correcting the abnormalities.
Most surgeons use the serum carbon dioxide (<30 mmol/L),
chloride (>100 mmol/L), and
potassium (4.5–6.5 mmol/L) levels
as markers of adequate resuscitation.
Initially, a 10- to 20-mL/kg bolus of normal saline should be given if the electrolyte values are abnormal.
Then D5/½NS with 20–30 mEq/L of potassium chloride is started at a rate of 1.25–2 times the calculated maintenance rate.
Electrolytes should be checked every 6 hours until they normalize and the alkalosis has resolved.
Subsequent fluid boluses are given if the electrolytes remain abnormal.
Then the patient can safely undergo anesthesia and operation.
It is important to appreciate that HPS is not a surgical emergency and resuscitation is of the utmost priority.
Inadequate resuscitation can lead to postoperative apnea due to decreased respiratory drive secondary to metabolic alkalosis.
After general anesthesia has been induced, an abdominal examination should be performed to physically check for an “olive” if one was not detectable preoperatively.
The pyloromyotomy may be performed by the open technique or by the minimally invasive approach.
The laparoscopic technique has become the standard approach in the last 5–10 years.
The anesthesiologist can pass and leave a suction catheter in the stomach for decompression and for instilling air after the pyloromyotomy to check for a leak.
H&A
How is an open pyloromyotomy performed?
The Open Approach
Historically, several different incisions have been described for the open approach.
The typical right upper quadrant transverse incision seems to be used most commonly.
An alternate, more cosmetically pleasing incision involves an omega-shaped incision around the superior portion of the umbilicus followed by incising the linea alba cephalad.
With either incision, the pylorus is exteriorized through the incision.
A longitudinal serosal incision is made in the pylorus approximately 2 mm proximal to the junction of the duodenum and is carried onto the anterior gastric wall for approximately 5 mm.
Blunt dissection is used to divide the firm pyloric fibers.
This can be performed using the handle of a scalpel.
Once a good edge of fibers has been developed, a pyloric spreader or hemostat can be used to spread the fibers until the pyloric submucosal layer is seen.
The pyloromyotomy is then completed by ensuring that all fibers are divided throughout the entire length of the incision.
This is confirmed by visualizing the circular muscle of the stomach proximally as well as a slight protrusion of the submucosa.
The most common point of mucosal entry is at the distal part of the incision at the duodenal-pyloric junction.
Therefore, care must be exercised when dividing the fibers in this region.
The pyloromyotomy can be checked for completeness by rocking the superior and inferior edges of the myotomy back and forth to ensure independent movement.
The mucosal integrity can be checked by instilling air through the previously placed suction catheter.
If there are no leaks, the air should be suctioned.
Minor bleeding is common and should be ignored because it will cease after the venous congestion is reduced when the pylorus is returned to the abdominal cavity.
The abdominal incision is then closed in layers.
H&A
How is a laparoscopic pyloromyotomy performed?
The Laparoscopic Operation Neonatal laparoscopy has grown in popularity with the refinements in technique and smaller instruments.
The first reported laparoscopic pyloromyotomy in the English language was in 1991 (the authors had reported the first case in the French literature in 1990).
Since then, this procedure has been accepted by most pediatric surgeons.
Critics of the procedure argue that laparoscopic pyloromyotomy exposes the patient to undue risks compared with the open technique.
However, randomized prospective trials and subsequent meta-analyses have not shown any difference in complication rates.
More recent analysis of the NSQIP database shows that open pyloromyotomy is associated with in increased length of stay compared to laparoscopic pyloromyotomy.
The minimally invasive approach is similar to laparoscopic appendectomy in terms of acceptance and has become the standard technique for pyloromyotomy in most centers.
The technique involves entering the abdomen through an umbilical incision.
A Veress needle is placed at the base of the umbilicus between the umbilical arteries.
It is important to ensure proper placement of the Veress needle before insufflation.
This can be done by several simple methods, including the “blind man’s cane” sweep and the water drop test.
Alternatively, an open approach can be used to introduce the umbilical cannula.
The abdomen is then insufflated to a pressure of 10 mmHg and a 3- or 5-mm port is introduced for the telescope and camera.
Two stab incisions are made. One stab incision is in the right paramedian side of the abdomen at the level of the umbilicus, and the other is in the left paramedian side of the abdomen just superior to the umbilicus.
Local anesthesia is used at all incisions. An atraumatic bowel grasper is placed through the left incision, and a knife or long cautery tip is introduced through the right incision.
The duodenum is grasped firmly just distal to the pylorus, and the pylorus is maneuvered into view.
Occasionally, a transabdominal stay suture wrapping around the falciform ligament is helpful to elevate the liver away from the pylorus.
A longitudinal pyloromyotomy is then made with either the knife or the electrocautery in a manner similar to the open technique.
Initially, a retractable arthrotomy knife was used. However, this is no longer on the market in the United States. Most surgeons now use an unguarded arthrotomy knife or the spatula tip electrocautery blade, which appear equivalent in operative time and complications.
A laparoscopic pyloric spreader or a box-type grasper can be used to complete the myotomy.
Completeness of the myotomy and mucosal integrity is checked in a similar manner as the open technique.
Omentum can be placed over the myotomy to help with hemostasis, if necessary.
The stomach can be inflated with air through an orogastric tube to evaluate for perforation.
However, in one study in which there were two perforations, inflating the stomach did not detect the leak. The leaks were detected by careful inspection of the pyloromyotomy.
The pneumoperitoneum is evacuated after the instruments are removed.
The umbilicus is closed with absorbable suture, and the stab incisions are closed with skin adhesive.
H&A
How is postoperative care done post pyloromyotomy?
Postoperative care is similar for both surgical techniques, assuming the submucosa is intact.
Complicated feeding regimens have been advocated in the past. However, recent studies support the use of ad libitum feeds in the early postoperative period. This results in a faster time to full feeds and quicker discharge.
If postoperative emesis is encountered, it is suggested to “feed through it.”
At our institution, we limit the feedings to a maximum of 3 ounces every 3 hours.
There are data to suggest that the degree and duration of metabolic derangement affects postoperative feeding.
Patients who required more complicated resuscitation tend to take longer to reach full feeds and discharge.
Pain is usually controlled with acetaminophen.
Intravenous fluids are discontinued when the patient tolerates a 2-oz feeding twice.
The infant can be discharged when tolerating full feeds, which is usually on the first postoperative day.
H&A
What are complications and outcomes for pyloromyotomy?
The major complications of pyloromyotomy include mucosal perforation, wound infection, incisional hernia, prolonged postoperative emesis, incomplete myotomy, and duodenal injury.
There have been prospective and retrospective studies that do not show any difference in complication rates between the laparoscopic and open techniques.
In pooled analyses, perforation occurs in approximately 1%.
If the disruption occurs at the duodenopyloric junction, a simple interrupted absorbable suture can be placed to close the defect and a patch of omentum can be used to bolster the repair. This can be accomplished laparoscopically depending on the experience of the surgeon.
Otherwise, the operation should be converted to open.
If the perforation is large or in the middle of the myotomy, then the myotomy should be closed with absorbable suture.
A new myotomy can then be made 90–180° from the original incision.
Repairing this injury is difficult to perform laparoscopically, so conversion is usually necessary.
Feedings should be held for 24 hours and then restarted.
A water-soluble contrast study can be performed if desired.
Duodenal injuries also can occur with either the laparoscopic or open approach.
In a 25-year retrospective review of 901 open pyloromyotomies performed between 1969 and 1994, there were 39 duodenal perforations that were recognized intraoperatively and repaired. There were no unrecognized duodenal perforations that developed after the operation.
Incisional hernias and wound dehiscence occurs in approximately 1% of cases. Most hernia defects require repair at some point.
Laparoscopically, port site hernias usually involve omentum protruding through the incision. This can sometimes be managed at the bedside by cleansing the area with povidone-iodine (Betadine), ligating and trimming the extracorporeal omentum, elevating the abdominal wall to get the omentum back into the peritoneal cavity, and using a fine absorbable suture to close the skin.
Laparoscopic pyloromyotomy also appears to have less wound complications.
When the open approach through a right upper quadrant incision is used, the incision usually heals nicely and looks cosmetically pleasing in the early postoperative period. However, later in infancy and into adulthood, these incisions enlarge and often contract, leading to a less cosmetically pleasing appearance.
Postoperative emesis is common, occurring in most patients at some point.
Prolonged emesis is less common and ranges in incidence from 2–26%. Most commonly, this is due to gastroesophageal reflux (25%) but can be secondary to incomplete myotomy (0–6%).
It has been suggested that the laparoscopic approach may be a risk factor for inadequate myotomy, but this is likely related to the surgeon’s experience with this technique.
In the past, the mortality from pyloric stenosis was considerable and approached 50%. Today, however, mortality is nearly zero with improvement in neonatal resuscitation and anesthesia as well as surgical techniques.
Morbidity is also significantly lower than in the past, with an overall complication rate between 1% and 2%.
In addition, with more pyloromyotomies being performed laparoscopically, the cosmetic advantage of the minimally invasive techniques cannot be overemphasized.
H&A
How is pyloric atresia diagnosed and managed?
Pyloric atresia is a rare disease (1 in 100,000 live births) and presents as symptoms of gastric outlet obstruction.
The disease is difficult to characterize because it is so rare.
However, several generalizations can be made from looking at larger series.
Pyloric atresia may be associated with epidermolysis bullosa and other gastrointestinal anomalies, such as duplications.
Pyloric atresia is diagnosed with a “single bubble” on the abdominal radiograph.
The diagnosis may be confirmed with a contrast study.
Pyloric atresia may occur as a web, a cord, or a gap between the antrum of the stomach and the first portion of the duodenum.
Repair is performed after resuscitation.
These infants may have similar electrolyte abnormalities to infants with HPS.
Repair is usually with a Billroth type I (gastroduodenostomy) anastomosis.
Morbidity and mortality are usually related to the associated anomalies.
H&A
What are the causes of gastric perforation in pediatric patients?
The causes of gastric perforation are spontaneous perforation of the newborn, iatrogenic perforation from instrumentation, peptic ulcer disease, and trauma.
Gastric perforation usually presents as abdominal distention and signs of sepsis or shock related to the perforation.
The diagnosis is suspected when a large amount of extraluminal gas is seen on an abdominal radiograph.
Neonatal gastric perforations most commonly occur in premature infants. About half of neonatal perforations are spontaneous, and the other half are iatrogenic from instrumentation.
Prematurity is associated with an increased mortality.
The perforations are usually managed with laparotomy or laparoscopy.
The perforation can usually be closed primarily with or without an omental patch.
Gastric perforation due to peptic ulcer disease in infants and children is very rare.
Typically, perforation occurs at the site of a prepyloric ulcer.
Again, this may be repaired primarily via laparotomy or laparoscopy with or without an omental patch.
H&A
How is peptic ulcer disease diagnosed and managed in the child?
Peptic ulcer disease and its complications are rarely seen in children.
However, there have been reports of neonatal and pediatric bleeding ulcers, perforated ulcers, and gastric outlet obstruction in children due to peptic ulcer disease.
Peptic ulcer disease appears to be associated with Helicobacter pylori in the majority of pediatric cases.
Treatment is primarily directed at acid reduction and eradication of H. pylori.
Triple therapy with a proton pump inhibitor, amoxicillin, and clarithromycin is typically used initially.
For strains that are resistant to clarithromycin, metronidazole is substituted.
Operative treatment is usually reserved for complications of peptic ulcer disease, such as perforation or gastric outlet obstruction.
If ulcer perforation is suspected, it is reasonable to start with exploratory laparoscopy because there are reports of successful laparoscopic treatment in children.
A gastric resection operation has usually not been needed since the development of effective proton pump inhibitors.
H&A
—
Other causes of gastroduodenal perforations are peptic ulcer disease, gastric volvulus, and iatrogenic causes. Peptic ulcer disease has become quite uncommon but is still seen in children.
Primary ulcers are associated with Helicobacter pylori.
Secondary ulcers can occur as complications of a large number of causes including shock, burns, head injury, malignancy, immunosuppressive disorders, autoimmune disorders, chronic NSAID use, and acid hypersecretion syndromes.
Most perforated ulcers are found in the prepyloric region.
NSAID-associated ulcers occur on the lesser curvature. In the age of effective Helicobacter pylori agents and proton-pump inhibitors, vagotomy or resective procedures for peptic ulcer disease are no longer required. Graham patch closure of the ulcer suffices with postoperative treatment of Helicobacter pylori infection or the underlying etiology.
Sherif
