Lesions of The Stomach

Published on 26/02/2015 by admin

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Last modified 26/02/2015

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Lesions 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 and obesity, are covered elsewhere.

Hypertrophic Pyloric Stenosis

Hypertrophic pyloric stenosis (HPS) is one of the most common surgical conditions of the newborn.1–9 It occurs at a rate of 1 to 4 per 1,000 live births in Caucasian infants, but is seen less often in non-Caucasian children.14 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.4,9,10 Premature infants are diagnosed with HPS later than term or post-term infants.4

Etiology

The cause of HPS is unknown, but genetic and environmental factors appear to play a large role in the pathophysiology. Circumstantial evidence for a genetic predisposition includes race discrepancies, the increased frequency in males, and the birth order (first-born infants with a positive family history). Environmental factors associated with HPS include the method of feeding (breast vs formula), seasonal variability, exposure to erythromycin, and transpyloric feeding in premature infants.5–7 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.8,9 Thus, the etiology of HPS is likely multifactorial with environmental influences.

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 gastroesophageal reflux disease. 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 may be palpable in 72–89% of patients.11,12 To palpate the hypertrophied pylorus, the baby must be relaxed. Techniques for relaxing the infant include bending the 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 and down, trying to trap the ‘olive.’ Palpating the hypertrophied pylorus requires patience and an optimal examination setting. If palpated, no further studies are needed. If the pylorus cannot be palpated, ultrasound (US) should be performed.

Ultrasound 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 greater than or equal to 4 mm and a pyloric channel length greater than or equal to 16 mm (Fig. 29-1).12 A thickness of more than 3 mm is considered positive if the neonate is younger than 30 days of age.13 The study is dependent on the expertise of the ultrasound technician and radiologist.

There are reports of non-radiologists performing ultrasound for HPS, which would obviously reduce the need for the ultrasound technician.14,15 If the ultrasound findings are equivocal, then an upper gastrointestinal series can be helpful in confirming the diagnosis (Fig. 29-2).

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 ultrasound facilitates an earlier diagnosis and treatment. However, the complete differential diagnosis for nonbilious vomiting should be considered. This includes medical causes such as gastroesophageal reflux, 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.

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 therapy and are often not effective.16–20

Once the diagnosis of HPS is made, feedings should be withheld. Gastric decompression is usually not necessary but occasionally may be required for extreme cases. If a barium study was performed, it is important to remove all of the contrast material from the stomach to prevent aspiration and pulmonary complications.

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 less than 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 resuscitation. Initially, a 10–20 mL/kg bolus of normal saline should be given if the electrolytes are abnormal. Then, D5/1/2NS with 20–30 mEq/L of potassium chloride is started at a rate of 1.25 to 2 times the calculated maintenance rate. Electrolytes should be checked every six hours until they normalize and the alkalosis has resolved. Subsequent fluid boluses are given if the electrolytes remain abnormal. It is important to appreciate that HPS is not a surgical emergency and resuscitation is the initial priority. Inadequate resuscitation can lead to postoperative apnea due to a decreased respiratory drive secondary to metabolic alkalosis.

The pyloromyotomy can be performed by the standard open technique or by the minimally invasive approach. The anesthesiologist should pass and leave a suction catheter in the stomach for decompression and for instilling air after the pyloromyotomy to check for a mucosal leak.

The Open Approach

Several incisions have been described for the open approach. The typical right upper quadrant transverse incision seems to be used most commonly (Fig. 29-3). 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 initially 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 pyloromyotomy. 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 evaluated 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.

The Laparoscopic Operation

Neonatal laparoscopy has grown in popularity with the refinement 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).21 Since then, this procedure has been accepted by most pediatric surgeons. Critics of this approach argue that laparoscopic pyloromyotomy exposes the patient to undue risks compared with the open technique. However, recent randomized prospective trials have not shown any difference in complication rates.22,23 Operative times can vary depending on the experience of the surgeon. The minimally invasive approach for pyloromyotomy is similar to laparoscopic appendectomy in terms of acceptance and has become the standard technique for pyloromyotomy in many centers.

The technique involves entering the abdomen through an umbilical incision. A Veress needle is inserted at the base of the umbilicus between the umbilical arteries. It is paramount 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 mm or 5 mm port is introduced for the telescope and camera. Two stab incisions are made. One 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 instilled at all incisions. An atraumatic bowel grasper is inserted through the patient’s right incision, and a pylorotome or spatula cautery tip is introduced through the patient’s left incision (Fig. 29-4). 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 the knife or cautery in a similar manner as the open technique (Fig. 29-5). Initially, a retractable arthrotomy knife was used; however, it is no longer available in the USA. Thus, most USA pediatric surgeons now use an unguarded arthrotomy knife or the cautery. Once the seromuscular layer is incised, a laparoscopic pyloric spreader or a box-type grasper is inserted to perform the myotomy. Completeness of the myotomy and mucosal integrity are checked in a similar manner as the open technique. Omentum can be placed over the myotomy to help with hemostasis. 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 (see Fig. 29-4B).