pyloric sphincter

ANATOMY/HISTOLOGY: The pylorus is the distal stomach, and the pyloric sphincter is a thickened ring of the inner circular smooth muscle layer of the muscularis externa. It separates the pyloric antrum/canal from the duodenal bulb (first part of the duodenum). It lies at the transpyloric plane (L1) and is marked on the surface of the stomach by the prepyloric vein of Mayo. Blood supply: right gastric artery (from the proper hepatic artery), right gastroepiploic artery (from the gastroduodenal artery), and the supraduodenal artery. Innervation: parasympathetic via the vagus nerve (anterior and posterior vagal trunks), and sympathetic via celiac plexus (T6-T9 greater splanchnic nerves).

PHYSIOLOGY: The sphincter is normally tonically contracted. It relaxes briefly when peristaltic waves from the antrum push chyme through, releasing small amounts (about 1-3 mL) of well-mixed chyme into the duodenum. This regulates the rate of gastric emptying and limits regurgitation of duodenal contents (bile, pancreatic secretions) back into the stomach. Gastric emptying is slowed by duodenal feedback: fat and acid in the duodenum release CCK and secretin, and the enterogastric reflex also contributes. Both CCK and secretin increase pyloric sphincter tone. Gastrin and vagal stimulation increase antral motility. Nitric oxide and VIP mediate relaxation. Liquids empty faster than solids. Carbohydrates empty faster than proteins, and fats empty slowest.

CLINICAL SIGNIFICANCE: 1) Hypertrophic pyloric stenosis (infantile): hypertrophy of the pyloric smooth muscle, typically in first-born males at 2-6 weeks of age. Presents with projectile NON-bilious vomiting after feeding, a palpable "olive-shaped" mass in the epigastrium or RUQ, and visible peristalsis. Labs show hypochloremic, hypokalemic metabolic alkalosis, with paradoxical aciduria in severe cases. Diagnose with ultrasound (muscle thickness 3 mm or more, channel length 15 mm or more) and treat with fluid and electrolyte correction followed by pyloromyotomy (Ramstedt). Risk factors: macrolide exposure (erythromycin) in early infancy, bottle feeding, and a family history. It is associated with Turner syndrome and trisomy 18. 2) Gastric outlet obstruction (adults): from peptic ulcer disease (especially pyloric channel or duodenal ulcers with scarring), gastric antral cancer, or extrinsic compression (pancreatic cancer). Presents with early satiety, nausea, and vomiting of undigested food. Also causes hypochloremic, hypokalemic metabolic alkalosis. Succussion splash may be heard. 3) Gastroparesis: delayed gastric emptying without mechanical obstruction (diabetes, post-viral, medications). Treat with prokinetics such as metoclopramide (D2 antagonist) or erythromycin (motilin agonist). Pyloric botulinum toxin injection, G-POEM, and pyloroplasty are options for refractory cases. 4) Bile reflux gastritis: incompetent or surgically bypassed or disrupted pylorus (e.g., after pyloroplasty, Billroth II, or gastrectomy) allows bile to reflux into the stomach. 5) Dumping syndrome: after gastric surgery that removes or bypasses the pylorus, rapid emptying of hyperosmolar chyme causes early symptoms (abdominal pain, diarrhea, vasomotor signs) and late symptoms (reactive hypoglycemia from insulin surge). 6) Vagotomy: truncal vagotomy impairs pyloric relaxation, so it is paired with a drainage procedure (pyloroplasty).

HIGH-YIELD PEARLS: Non-bilious vomiting indicates an obstruction proximal to the ampulla of Vater (pyloric stenosis), whereas bilious vomiting suggests a distal obstruction (e.g., malrotation with midgut volvulus). The pylorus is a true anatomic and functional sphincter, unlike the lower esophageal sphincter. Duodenal ulcers on the posterior wall can erode the gastroduodenal artery, and anterior ulcers tend to perforate.