Hypertrophic pyloric stenosis (HPS) is one of the most common surgical conditions in infancy, affecting 3 in 1,000 newborns. It is most common in white firstborn males. It presents between the 2nd and 12th week of life with postprandial non-bilious emesis. The etiology is unclear. Diagnosis can be made solely on clinical grounds, with the presence of a palpable “olive” having a high specificity. Ultrasound examination has at least 99 % sensitivity and specificity for this diagnosis. A pyloric channel measuring 15–20 mm, with a wall thickness of 3–5 mm and lack of relaxation are considered positive findings.

Treatment is the Ramstedt pyloromyotomy, a procedure in which the serosa and muscular layers are transected longitudinally, leaving the mucosa intact. In cases in which the mucosa is penetrated, it should be repaired. Current recommendations include closure of the original myotomy site, with creation of a new myotomy at a different site [1, 2].

The stomach is a rather mobile organ, held in place at either end by the phrenoesophageal ligament proximally and the duodenum distally. This degree of motility allows it to rotate along its axis, creating a gastric volvulus. Gastric volvulus can be organoaxial (i.e., along the longitudinal axis or cascade volvulus along its horizontal axis). The most important predisposing factors are gastric distention and the shape of the stomach itself. Long, vertically oriented stomachs are prone to organoaxial volvulus, whereas broad horizontally oriented stomachs are predisposed to a cascade volvulus. Gastric volvulus has not been associated to gastric banding [3] (Fig. 12.1).

Due to its mobility, the stomach is often used to replace the esophagus in the chest. In order to mobilize the stomach, the short gastric vessels, the left gastric artery, the right gastric artery, and the left gastroepiploic artery are divided. In such cases, the right gastroepiploic artery may feed the entire stomach [4].

The stomach is attached to other abdominal organs through the derivatives of the ventral and dorsal mesogastria. The ventral mesogastrium forms the lesser omentum, which may harbor accessory or replaced left hepatic arteries arising from the left gastric artery. The dorsal mesentery forms the gastrosplenic ligament (which encases the short gastric vessels), the splenic capsule, and the splenophrenic ligament [5].

Gastric acid secretion is the sole function of the parietal cells. This is a finely regulated process, under the influence of neural, hormonal, and intraluminal stimuli. Parietal cells are located exclusively in the fundus and body of the stomach, which is the basis of limiting highly selective vagotomy to the branches of the nerve of Latarjet going to this portion of the stomach.

Located in the antrum, G cells, through gastrin production, are the most important positive regulators of acid secretion. They are stimulated by vagal efferents as well as by the presence of food in the gastric lumen. Gastrin reaches the oxyntic region of the stomach (fundus and body), where it stimulates the production of acid by parietal cells directly and indirectly, by inducing histamine release from enterochromaffin-like cells. The acidification of the gastric lumen stimulates somatostatin-producing D cells in the antrum, which inhibit G cells in a paracrine manner.

Interestingly D cells are also found in the oxyntic region of the stomach; however, in this location, they lack luminal receptors and do not respond to gastric acidification. Instead, they respond to the hormones released by duodenal acidification, namely, CCK, secretin, and gastric inhibitory peptide, and further downregulate gastric production.

M cells produce mucus. While they are located throughout the stomach, they are most abundant in the antrum. Chief cells share their location with parietal cells. They produce intrinsic factor, pepsin, and other digestive enzymes [6, 7] (Fig. 12.2).

Celiac artery compression syndrome, also known as median arcuate ligament syndrome, celiac band syndrome, or Dunbar’s syndrome, mostly affects young and middle-aged women. The compression of the celiac trunk leads to intermittent gastric ischemia, causing symptoms of epigastric pain, mostly in the postprandial period, and is classically accompanied by an epigastric bruit and weight loss.

However, it has been suggested that while necessary, celiac compression may not be sufficient to produce this syndrome. As noted above, up to 25 % of the population has some degree of celiac trunk impingement, with symptomatic disease being much less common. It has been hypothesized that a disturbance in the rich collateral circulation of the stomach must also be present for symptoms to occur.

During deep inspiration, descent of the diaphragm and slight cephalad displacement of the aorta increase the degree of compression on the celiac trunk. This is best seen on lateral views through conventional angiography or CT scanning. Another key finding is the poststenotic dilatation of the celiac trunk and the formation of prominent collateral vessels.

Surgical repair has traditionally involved release of the median arcuate ligament with restoration of normal blood flow. However, considering the multiple etiologies of celiac artery compression, other procedures such as removal of enlarged lymph nodes or celiac ganglia may be needed. On occasions, the celiac trunk may be chronically scarred, making the creation of an aorto-celiac bypass necessary. More recently, laparoscopic release combined with celiac artery endovascular stenting has been proposed as an alternative. The fact that these interventions are sometimes ineffective highlights both the importance of ruling out other causes of abdominal pain and the complex pathophysiology of this entity [8–10].

The left vagus nerve becomes anterior below the diaphragm and supplies all of the structures that develop in the ventral mesogastrium, i.e., the liver, biliary tree, and head of the pancreas. In a similar fashion, the right vagus, which becomes posterior, supplies the structures that arise in the dorsal mesogastrium (tail of the pancreas and spleen). In addition, the posterior vagus extends along the dorsal mesentery to the entire midgut. This explains why it is larger than the anterior vagus, and may even be comprised by two trunks.

The nerves of Latarjet arise from either vagus and run along the lesser curvature in the gastrohepatic ligament. They supply branches to the fundus and body of the stomach, ending in the pylorus. The nerves of Latarjet supply all the acid-secreting cells and control gastric emptying.

Highly selective vagotomy is also called parietal cell vagotomy. In principle, it divides all branches of the anterior and posterior nerves of Latarjet supplying the fundus and body of the stomach. In this surgery, it is important that the branches to all parietal cells be divided; hence, surgery must start 5 cm above the esophagogastric junction and finish just past the crow’s-foot, in order to totally vagotomize the body and fundus of the stomach (Figs. 12.3 and 12.4).

One of the most often mentioned causes of incomplete vagotomy and ulcer recurrence is the failure to section the “criminal nerve of Grassi.” This nerve is a branch of the posterior vagus, often arising above the diaphragm. When undivided, it may perpetuate gastric acid secretion. Vagal afferents supplying the oxyntic region of the stomach from the greater curvature have also been described [11].

Sympathetic innervation of the stomach arises from the T5 to T10. These fibers end in the celiac ganglia, where they synapse with ganglion cells that reach the stomach following the branches of the celiac artery. Afferent fibers follow the opposite route [12].

It must be remembered that incomplete vagotomy is not the only cause of ulcer recurrence after the surgical treatment of peptic ulcer disease. The possibilities of NSAID abuse, H. pylori infection, retained gastric antrum, gastrinoma, and hypercalcemia must also be considered [13].

The stomach is perhaps the segment of the GI tract with the richest blood supply. The lesser curve receives blood from the left and right gastric arteries, while the greater curve is supplied by the right and left gastroepiploic arteries, with contribution of the short gastric arteries derived from the splenic artery. These four arteries form an anastomotic network such that only one is needed to preserve gastric viability. While these arteries ultimately arise from the celiac trunk, the stomach may also receive blood from the superior mesenteric artery, via the inferior pancreaticoduodenal, which anastomoses to its superior counterpart, ultimately perfusing the right gastroepiploic artery. For example, the right gastroepiploic artery is the only arterial blood supply for the gastric pouch in esophagogastric reconstructions.

The multiple collaterals of the gastric blood supply determine that single ligation of a branch involved in a bleeding ulcer will not achieve hemostasis. In most instances, a three-point ligation is needed.

Dieulafoy ulcers are somewhat of a misnomer, in the sense that a classic peptic ulceration is not present. Rather, these lesions constitute the erosion of an abnormal submucosal arterial plexus. While these lesions where classically described as occurring on the high lesser curvature of the stomach, the term has been expanded to describe similar lesions in the GI tract as a whole [14].

The lymphatic drainage of the stomach forms a very complex network, which confers unpredictability to tumor spread from any given area. In acknowledgment of this fact, the lymphatic drainage of the stomach is not viewed as linear, traveling vascular branches; rather, it is conceived in concentric fashion, with nodal groups describing polygons of increasing diameter [15, 16]. The extent of lymphadenectomy for oncologic surgery coincides with this description [17, 18] (Fig. 12.5a–d).