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The stomach receives both sympathetic and parasympathetic innervation. The sympathetic fibers reach the stomach via celiac plexus. The parasympathetic fibers reach the stomach through the left and right vagus nerves. The anterior vagal trunk, which is derived mainly from the left vagus nerve, enters the abdominal cavity through the esophageal hiatus in the diaphragm. Its gastric branches are distributed on the anterio-superior surface. The posterior vagal trunk, which is derived mainly from the right vagus nerve, also enters the abdomen through the esophageal hiatus in the diaphragm on the posterior surface of the esophagus. Its gastric branches are distributed on the posterio-inferior surface of the stomach.
Besides the extrinsic innervation described above, the stomach contains an extensive enteric nervous system in the form of submucosal Meissner's plexus and Auerbach's plexus situated between the two layers (circular and longitudinal) of the muscle coat. Various neurons of the enteric nervous system produce norepinephrine, acetylcholine, vasoactive intestinal peptide (VIP), substance P, somatostatin, or nitric oxide.
The sympathetic supply chiefly controls the blood vessels and muscular coat of the stomach. Sympathetic stimulation decreases gastric motility. Parasympathetic stimulation increases gastric motility as well as the secretion of oxyntic (parietal) cells, chief cells and G cells of the gastric mucosa.
Several specialized cells in the gastric mucosa contribute to the control of acid secretion. G cells in the gastric antrum release the hormone gastrin. Gastrin acts on the enterochromaffin-like cells in the gastric corpus to release histamine, which stimulates parietal cells to secrete acid. Gastrin also stimulates parietal cells directly and promotes growth of enterochromaffin-like and parietal cells.
Fig 10.2. Feedback control of gastric acid. S = somatostatin secreting cell; G = G-cell : P Parietal cell; ECL = enterochromaffin-like cell.
Histamine H2 receptor antagonists act by blocking the effect of histamine on parietal cells. Proton pump inhibitors act by inhibiting the enzyme in parietal cells that catalyses acid production for release into the gastric lumen. G cells, enterochromaffin-like cells, and parietal cells are all regulated by release of the inhibitory peptide somatostatin from somatostatin cells, which are distributed throughout the stomach. The effect of H pylori infection on acid secretion depends on which part of the stomach is most inflamed because this determines which of these cells are affected most.
Motor functions of stomach
Storage of ingested food.
Empty stomach has a capacity of 50 ml only. As food is ingested, the gastric capacity gradually increases. At the end of a meal, the stomach may contain 1000-1500 ml of food, water and gastric juice. The storage function of the stomach is chiefly served by the fundus and body regions, which undergo a gradually increasing vagally mediated reflex receptive relaxation. That is why; after vagotomy, the patients often complain of early satiety as well as post-prandial epigastric fullness.
Mixing, grinding and sieving function
Peristaltic waves passing down the body and pyloric part of stomach produce thorough mixing of food with the gastric juice. The food is macerated into a semi-liquid chyme. The narrow pyloric sphincter acts like a sieve and allows particles less than 1 mm in size to leave the stomach in to the first part of duodenum.
Regulation of gastric emptying:
Distention of stomach or increased gastrin secretion increases the strength of gastric peristalsis. On the other hand, presence of highly acid chyme, hyperosmolar chyme or fat-rich chyme in the duodenum decreases the strength of gastric peristalsis. These duodenal inhibitory influences on gastric emptying ensure that amount of chyme containing acid, and food particles is ideal for the proper digestion and absorption in the small intestine.
Small intestine: functional anatomy and physiology
The small intestine measures approximately, 2.5-3 cm in diameter and 6 meters in length during life. The ligament of Treitz demarcates duodenum from jejunum. Below the duodenum, the upper 40 % of the small intestine is called the jejunum and the remaining 60 % as ileum. There is no anatomic demarcation between jejunum and ileum. The villi, a characteristic feature of small intestinal mucosa are largest and most numerous in the duodenum and jejunum, and become fewer and smaller in the ileum. The ileum ends with the ileocecal valve (sphincter), which regulates the movement of chyme into the large intestine and prevents backward movement of material from the large intestine.
Small intestine is the site of final digestion and absorption of foodstuffs. Most of the digestive enzymes that act in the small intestine are secreted by the pancreas (Table 10.2). In addition bile salts present in the bile (formed in the liver) are essential for proper digestion and absorption of dietary fats. The pancreatic and bile ducts open in the second part of duodenum. As a small bolus of chyme leave the stomach, its intimate mixing with pancreatic juice and bile helps in proper digestion and absorption. Presence of food in the upper small intestine is essential for the release of gastrointestinal hormones such as secretin and cholecystokinin which increase the secretion of pancreas and bile. When the duodenum is bypassed (e.g. Billroth II operation) malabsorption commonly occurs. The optimum pH for the activity of pancreatic enzymes is 6-7. Such pH is achieved by neutralization of the highly acidic chyme that leaves the stomach by the alkaline pancreatic and bile juices.
Table 10. 2 Principal digestive enzymes in the small intestine.
The intestinal digestion of foodstuffs results in production of monosaccharides, amino acids and fatty acids. These products and various other components of food such as vitamins, minerals and water are absorbed in specific parts of the small intestine (Table 10. 3). This knowledge becomes significant when a part of the small intestine is to be resected as a treatment of some disorder (e.g. Crohn's disease). Extensive resection of small intestine is most likely to result in intestinal malabsorption (short bowel or short gut syndrome). Short bowel syndrome usually develops when less than 2 meters of the small intestine left after surgery.
Table 10.3. Site of absorption of various foodstuffs in the GIT.
Duodenum and jejunum
Water soluble vitamins
Fat soluble vitamins
Colon : Functional anatomy and physiology
Colon or the large intestine is a tube about 6 cm in diameter and 1.5 meters in length. Mucus (pH 8) is the chief secretion of colon. Absorption of water and electrolytes is the chief function of the large intestine. The colon contains a large number of bacteria which synthesize vitamin K, folic acid and a number of other vitamins included in B complex, which are absorbed in blood circulation
Large intestine cannot absorb carbohydrates, amino acids or fatty acids. These products reach the colon in patients with inadequate digestion / absorption of foodstuffs in the small intestine (maldigestive / malabsorption syndrome). The fermentation of undigested carbohydrates by the colonic bacteria produces large amount of gases (flatus). Undigested fats are hydrolyzed by the bacteria in to fatty acids, which cannot be absorbed. Fatty acids act as irritant to the colonic mucosa, producing diarrhea. Undigested proteins are broken down to by the bacterial deaminases. Thus, even in a case with severe maldigestion, the stools contain the degraded products rather than macromolecules of carbohydrates, fats or proteins as such.
Infantile Hypertrophic Pyloric Stenosis
Pyloric stenosis, also known as infantile hypertrophic pyloric stenosis (IHPS), is the most common cause of intestinal obstruction in infancy. Although less common in Asian population, IHPS is by no means a rarity. It is 4 times more common in male children. Although it can occur any time from the day of birth to about 3 to 4 months, most common presentation is between the 3rd and 6th week of age. The presenting symptoms are almost always projectile non-bilious vomiting in a baby hitherto normal with no other accompanying findings of upper respiratory infection etc. The presence of an ovoid olive-shaped mass in the right upper quadrant area close to the epigastrium is a very important sign.
The lesion is characterized by gastric outlet obstruction and multiple anatomic abnormalities of the pyloric antrum. There is marked hypertrophy and hyperplasia of the mainly circular, but also longitudinal, muscle fibers of pylorus . The antropyloric muscle is abnormally innervated (see below). In addition, further the luminal narrowing is caused by crowded and redundant mucosa. The mucosa usually is edematous and thickened. In advanced cases, the stomach becomes markedly dilated in response to near-complete obstruction.
Fig 10.3 The pyloric sphincter in a normal infant and in a case of hypertrophic pyloric stenosis.
Nitric oxide has been demonstrated as a major inhibitory nonadrenergic, noncholinergic neurotransmitter in the GI tract, causing relaxation of smooth muscle of the myenteric plexus upon its release. Impairment of this neuronal nitric oxide synthase (nNOS) synthesis has been implicated in IHPS, in addition to achalasia, diabetic gastroparesis, and Hirschsprung disease.
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 can be of a projectile 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), leading to metabolic alkalosis. Persistent vomiting is accompanied by loss of not only acid but also fluids from the stomach. The resulting hypovolemia leads to a secondary hyperaldosteronism. The high aldosterone levels cause the kidneys to: (a) avidly retain Na+ (to correct the intravascular volume depletion), and (b)excrete increased amounts of K+ and H+ into the urine , resulting in hypokalemia and further aggravation of alkalosis.
Pathophysiology of peptic ulcer
It is a physiological marvel that gastric juice can easily digest the swallowed pieces of meat but normally, it has no corrosive action on the gastric mucosa itself. Several factors seem to be involved in the protection of gastric mucosa from autodigestion. These factors, collectively known as gastric mucosal barrier, include:
(a) Mucus secreted by surface epithelial cells and mucus neck glands which forms a water insoluble visco-elastic gel with poor diffusion coefficient for H+ .
Bicarbonate secreted by surface epithelial cells into the boundary zone between the epithelial cells and the mucus layer. The secretion of mucus and bicarbonate is believed to be mediated through prostaglandins.
Tight junctions between the adjacent cells of gastric surface epithelium.
Rapid turnover of surface epithelial cells, and rich blood supply.
Prostaglandins. Endogenous prostaglandins stimulate secretion of gastric mucus as well as gastric and duodenal mucosal bicarbonate. Prostaglandins also participate in the maintenance of gastric mucosal blood flow and integrity of mucosal barrier and promote epithelial cell renewal in response to mucosal injury.
Under normal conditions, a physiologic balance exists between peptic acid secretion and gastro-duodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs, H pylori, alcohol, cigarette smoking, psychogenic stress (excessive acid, and pepsin) or Zollinger Ellison syndrome can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury.
Mechanisms of injury differ distinctly between duodenal and gastric ulcers. Duodenal ulcer is essentially an H. pylori-related disease and is caused mainly by an increase in acid and pepsin load, and gastric metaplasia in the duodenal cap. Gastric ulcer, at least in Western countries, is most commonly associated with NSAID ingestion, although H. pylori infection might also be present. Chronic, superficial and atrophic gastritis predominate in patients with gastric ulcers, when even normal acid levels can be associated with mucosal ulceration. Basically in both conditions, ulcer is associated with an imbalance between protective and aggressive factors, with inflammation being a leading cause of this imbalance.
Fig. 10.4. Helicobactor pylori bacterium.
Role of Helicobacter pylori
Helicobacter pylori is a gram-negative bacillus responsible for one of the most common infections found in humans worldwide. H pylori organisms are spiral-shaped gram-negative bacteria that are highly motile because of multiple unipolar flagella. They are microaerophilic (need less oxygen) and potent producers of the enzyme urease. H pylori inhabits the mucus adjacent to the gastric mucosa. The most common route of H pylori infection is either oral-to-oral: kissing (stomach contents are transmitted from mouth to mouth) or fecal-to-oral (from stool to mouth) contact. Parents and siblings seem to play a primary role in transmission
Helicobacter pylori bacteria colonize the stomach and induces chronic gastritis. It is widely believed that in the absence of treatment, H. pylori infection-once established in its gastric niche-persists for life. In Western countries the prevalence of Helicobacter pylori infections roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80, etc). Prevalence is higher in third world countries. Most individuals infected by H. pylori will never experience clinical symptoms despite having chronic gastritis. Approximately 10-20% of those colonized by H. pylori will ultimately develop gastric and duodenal ulcers. A larger proportion of people will get non-specific discomfort, abdominal pain or gastritis (Fig. 10.5). The severity of the inflammation is likely to underlie H. pylori-related diseases. Duodenal and stomach ulcers result when the consequences of inflammation allow the acid and pepsin in the stomach lumen to overwhelm the mechanisms that protect the stomach and duodenal mucosa from these caustic substances.
The type of ulcer that develops depends on the location of chronic gastritis, which occurs at the site of H. pylori colonization. In those with duodenal ulcer, H. pylori colonizes the antrum. The inflammatory response to the bacteria causes destruction of somatostatin-producing D cells in the pylorus. Consequently, the G cells in the antrum secrete more of the hormone gastrin, which travels through the bloodstream to the corpus. Gastrin stimulates the parietal cells in the corpus to secrete more acid into the stomach lumen. Chronically increased gastrin levels eventually cause the number of parietal cells to also increase, further escalating the amount of acid secreted. The increased acid load damages the duodenum, and ulceration may eventually result.
In contrast, gastric ulcers are often associated with normal or reduced gastric acid production, suggesting that the mechanisms that protect the gastric mucosa are defective. In these patients H. pylori can also colonize the corpus of the stomach, where the acid-secreting parietal cells are located. However, chronic inflammation induced by the bacteria causes further reduction of acid production, and eventually atrophy of the stomach lining. Gastric atrophy may lead to gastric ulcer and increases the risk for stomach cancer.
H pylori infection and its association with gastric malignancy have been well described in several epidemiologic studies. However, the course of progression from inflammation to cancer remains unclear. One model describes the stepwise progression of H pylori infection to hypochlorhydria, chronic gastritis, atrophic gastritis, intestinal metaplasia, and gastric cancer. Increased production of the cytokine interleukin -1Î² has been linked to an increased risk of hypochlorhydria and gastric cancer in infected subjects.
Fig.10.5 . Consequences of H pylori infection.
Complications of peptic ulcers
Hemorrhage: Mild to severe hemorrhage is the most common complication of peptic ulcer disease. It may occur even when the ulcer pain is not severe. Symptoms include hematemesis (fresh blood or "coffee ground" material); passage of bloody stools or black tarry stools (melena); and weakness, syncope, thirst, and sweating caused by blood loss. However, small amounts of blood in the stool may not be noticeable but, if persistent, can still lead to anemia
A peptic ulcer may penetrate the wall of the stomach. If adhesions prevent leakage into the peritoneal cavity, free penetration is avoided and confined perforation occurs. Ulcers on the front surface of the duodenum, or less commonly the stomach, can go through the wall, creating an opening to the free space in the abdominal cavity. Perforation often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to the back.
An ulcer may penetrate the muscular wall of the stomach or duodenum and continue into an adjacent organ, such as the liver or pancreas.
Gastric outlet obstruction: Gastric outlet obstruction is the third most frequent complication of peptic ulcer disease after bleeding and perforation. It can occur during the acute phase of the disease or in chronic disease. Gastric outlet obstruction has traditionally been considered synonymous with pyloric stenosis as a result of peptic ulcer disease in adults.
Obstruction may be caused by scarring, spasm, or inflammation from an ulcer. Symptoms include recurrent, large-volume vomiting, occurring more frequently at the end of the day and often as late as 6 h after the last meal. Loss of appetite with persistent bloating or fullness after eating also suggests gastric outlet obstruction. Prolonged vomiting may cause weight loss, dehydration, and alkalosis.
People with ulcers caused by Helicobacter pylori have 3 to 6 times the chance of developing stomach cancer later in life. There is no increased risk of developing cancer from ulcers that have other causes.
POST GASTRECTOMY SYNDROMES
Modern treatment of peptic ulcer has led to a decline in the frequency of gastrectomies and therefore, the incidence of postgastrectomy syndromes has declined to a great extent. A 10-fold reduction has occurred in elective operations for peptic ulcer disease in the last 20-30 years. The advent of histamine-2 receptor antagonists and proton pump inhibitors has accelerated the decline. Helicobacter pylori treatment and eradication in patients with peptic ulcer disease have further decreased the need for surgery. Newer gastric operations, such as proximal gastric vagotomy (which produces minimal disturbance of gastric emptying mechanisms), are associated with a much lower incidence of postgastrectomy syndromes.
Although the need for elective surgery for peptic ulcer disease has declined, the need for emergency surgery has remained the same over the last 20 years. Emergency surgery tends to be more mutilating to the stomach. This increases the incidence of more severe symptoms
The stomach serves as the receptive and storage site of ingested food. The primary functions of the stomach are to act as a reservoir, to initiate the digestive process, and to release its contents downstream into the duodenum in a controlled fashion. The capacity of the stomach in adults is approximately 1.5-2 liters, and its location in the abdomen allows for considerable distensibility. Gastric motility is regulated by the enteric nervous system, which is influenced by extrinsic innervation and by circulating hormones. Alterations in gastric anatomy after surgery or interference in its extrinsic innervation (vagotomy) may have profound effects on gastric emptying. These effects, for convenience, have been termed postgastrectomy syndromes.
Postgastrectomy syndromes include small capacity, dumping, bile gastritis, post-gastrectomy malnutrition, and afferent loop syndrome.
Partial gastric resection
A partial gastrectomy may be used in the treatment of ulcers that are resistant to standard therapy, ulcers that continue to recur despite aggressive treatment or ulcers that cause severe complications. Partial gastrectomy is also used as treatment for gastric malignancies restricted to the antrum. Such an operation involves removal of the gastrin-secreting antrum (up to 75% of the distal stomach). Reconstruction is performed with anastomosis of the remaining gastric segment to the duodenum, called Billroth I (BI), or to the side of the jejunum (approximately 15 centimeters distal to the ligament of treitz), called Billroth II (BII) operation. The duodenal stump is preserved in the Billroth II to allow continued flow of bile salts and pancreatic enzymes. However, because of dysynchrony of food and bile/enzyme entry, patients with a BII may still have inadequate mixing.
( Fig. 10.6). Nowadays, BI operations are rare and are used primarily for very small tumors in the antrum.
BI and BII operations may or may not involve vagotomy. Furthermore, the type of vagotomy may differ. A truncal vagotomy severs the vagus on the distal esophagus. It significantly reduces acid secretion and creates gastric stasis and poor gastric emptying and is therefore combined with a drainage procedure (pyloroplasty or gastrojejunostomy). A selective vagotomy divides and severs the vagus nerve branches that supply the parietal cells while preserving those that innervate the antrum and pylorus. Thus, a drainage procedure is unnecessary, and the innervation to other organs is preserved. Unfortunately, a selective vagotomy is more technically difficult and is associated with a higher rate of ulcer recurrence.
Total gastrectomy ( TG)
Total gastrectomies are performed for gastric malignancies that affect the middle or upper part of the stomach. Total gastrectomy, by nature, involves a functional vagotomy, removing cholinergic drive and eliminating acid production.
Fig.10.6 Principles of Billroth operations
Changes after gastrectomy
Decreased Intrinsic Factor
Decreased pancreatic enzymes
Decreased mixing of food with acid, pepsin, and bile.
Decreased absorption of proteins, calcium, vitamin D & B, Fe, fat
Rapid absorption of glucose.
Increased intestinal motility
Creation of a "blind loop" i.e. afferent loop.
1. Dumping Syndrome
Postprandially, the function of the stomach is to store food and to allow the initial chemical digestion by acid and proteases before transferring food to the gastric antrum. In the antrum, powerful peristaltic contractions pulverize the solids, reducing the particle size to 1-2 mm. Once solids have been reduced to the desired size, they are able to pass through the pylorus. An intact pylorus prevents the passage of larger particles into the duodenum. Gastric emptying is controlled by fundic tone, antropyloric mechanisms, and duodenal feedback. Gastric surgery alters these mechanisms in several ways.
Gastric resection can reduce the fundic reservoir, thereby reducing the stomach's capacity to accommodate a large meal. Similarly, vagotomy limits receptive relaxation of the stomach. An operation in which the pylorus is removed, bypassed, or destroyed increases the rate of gastric emptying. Duodenal feedback inhibition of gastric emptying is lost after a bypass procedure, such as gastrojejunostomy. Accelerated gastric emptying of stomach is a characteristic feature and a critical step in the pathogenesis of dumping syndrome. Gastric mucosal function is altered by surgery, and acid and enzymatic secretions are decreased. Also, hormonal secretions that sustain the gastric phase of digestion are affected adversely. All these factors interplay in the pathophysiology of dumping syndrome.
The concept of pathophysiology of dumping syndrome discussed above is supported by the fact that a change of dietary habits usually bring partial or even complete relief in most of the patients. People who have gastric dumping syndrome are advised to eat several small meals (e.g. six small meals rather than the usual three large meals) a day. The food should be low in carbohydrates, avoiding simple sugars. The patient is advised to drink liquids between meals, not with them. Fiber-rich food also helps since it delays gastric emptying and reduce insulin peaks.
Incidence and severity of symptoms in dumping syndrome are related directly to the extent of gastric surgery. An estimated 25-50% of all patients who have undergone gastric surgery have some symptoms of dumping. However, only 1-5% patients are reported to have severe disabling symptoms.
Dumping syndrome manifestations
Early dumping: When symptoms of dumping syndrome occur during a meal or 30-60 min postprandial: they may include:
Abdominal pain, cramps
Heart palpitations, rapid heart rate
Late dumping: When signs and symptoms develop later, usually one to three hours after eating: they may include:
Feelings of anxiety, nervousness
Symptoms of early dumping syndrome (30-60 min postprandial) are believed to result from accelerated gastric emptying of hyperosmolar chyme into the small bowel. This leads to fluid shifts from the intravascular compartment into the bowel lumen, resulting in rapid small bowel distention and an increase in the frequency of bowel contractions. Experimentally, rapid instillation of liquid meals into the small bowel has been shown to induce dumping symptoms in healthy individuals. Bowel distention may be responsible for GI symptoms, such as crampy abdominal pain, bloating, and diarrhea. Intravascular volume contraction due to osmotic fluid shifts is perhaps responsible for vasomotor symptoms, such as tachycardia and lightheadedness.
Postprandial release of gut hormones, such as enteroglucagon, peptide YY, pancreatic polypeptide, vasoactive intestinal polypeptide, glucagon-like peptide-1 (GLP-1), and neurotensin, is higher in patients with dumping syndrome compared to asymptomatic patients after gastric surgery. Some or all of these peptides are likely to participate in the pathogenesis of dumping syndrome. One of the effects of these hormones is the retardation of proximal GI motility and the inhibition of secretion. This function is called the ileal brake. Some authors have suggested that the accelerated release of these hormones is an attempt to activate the ileal brake, thereby delaying proximal transit time in response to rapid delivery of food to the distal small bowel.
Late dumping occurs 1-3 hours after a meal. The pathogenesis is thought to be related to the early development of hyperinsulinemic (reactive) hypoglycemia. Rapid delivery of a meal to the small intestine results in an initial high concentration of carbohydrates in the proximal small bowel and rapid absorption of glucose. This is countered by a hyperinsulinemic response. The high insulin levels are responsible for the subsequent hypoglycemia. Experimentally it is has been shown that intra-jejunal glucose induces a higher insulin release than intravenous infusion of glucose, even when serum glucose levels are the same in both experiments. Two hormones are thought to play a pivotal role. These are gastric inhibitory peptide (GIP) also known as glucose-dependent insulinotropic peptide and glucagon like peptide -1(GLP-1). In human studies, an increase in GLP-1 response has been noted after an oral glucose challenge. An increased GLP-1 response has been noted in patients after total gastrectomy, esophageal resection, and partial gastrectomy. Furthermore, a positive correlation has been found between the rise in plasma GLP-1 and insulin release. Exaggerated GLP-1 response likely plays an important role in the hyperinsulinemia and hypoglycemia in patients with late dumping. The reason why some patients remain asymptomatic after gastric surgery, while others develop severe symptoms, remains elusive.
2. Bile gastritis
Bile reflux gastritis can be a disabling post- partial-gastrectomy condition characterized by abdominal pain, bilious vomiting, and weight loss. The syndrome appears to be caused by free enterogastric reflux of bile and other proximal small bowel constituents. The effects of bile salts on gastric mucosa appear to be similar to the effects of nonsteroidal anti-inflammatory drugs. Both will break down the gastric mucosal barrier thereby increasing the risk of inflammation, ulcer development and associated symptoms of pain and bleeding. The same effects have been shown in animal models using bile as the irritant. With mucosal barrier disruption there is a back diffusion of hydrogen ions and the subsequent destruction of the mucosal cell.
There is a wide range of presentation in patients with bile gastritis. Most commonly it is asymptomatic and is a coincidental finding on endoscopy. The other extreme is the development of severe nausea, bilious vomiting, abdominal pain, and anorexia and weight loss. It is most commonly seen in patients with a Bilroth II operation. This procedure allows bile to pass the anastomosis with increased chance of reflux into the stomach.
3. Post-gastrectomy malnutrition
Gross malabsorption syndrome
Anemia - either iron deficiency or megaloblastic
Vitamin B deficiency
Metabolic bone disease
Post-gastrectomy malnutrition results from nutritional intolerance and deficiencies. Combination of fat maldigestion and lactose intolerance is most likely responsible for acute post-operative weight loss, the most frequent complication of gastrectomized patients. Nutrient deficiencies develop months to years after gastric resections and can result in deleterious clinical consequences. Anemia and bone disease are the most common manifestations of the nutritional deficiency seen in these patients.
Protein malnutrition may result from several frequently associated pathogenic factors. Insufficient protein intake is reported in most of the cases. The consequences of such an inadequate diet are aggravated in patients who are alcoholic or of a poor socio-economic status. Another important cause of protein malnutrition is malabsorption of ingested proteins due to a deficient pancreatic secretion.
The gastric stump empties itself early and the gastric content moves rapidly through the upper digestive tract, reaching the jejunum and ileum sooner than the pancreatic enzymes. Other factors may contribute to a post-gastrectomy malnutrition. Bacterial invasion of the small intestine resulting from achlorhydria and stasis in the afferent loop accounts sometimes for steatorrhea. Primary malabsorption due to an atrophy of the intestinal villi is sometimes responsible for malnutrition in a gastrectomized patient.
. Weight loss usually follows gastric resection with reported loss ranging from 10%-30% of preoperative weight. This loss has been attributed to inadequate dietary intake, malabsorption, rapid intestinal transit time or bacterial overgrowth. More likely, it is a combination of all these factors. Nevertheless, weight gain after surgery is possible. Frequent nutrition follow-up in the early postoperative period is the key to preventing a decline in nutritional status. Indeed, several reports confirm that in the absence of nutrition follow-up, patients become progressively malnourished. Too often, gastrectomized patients are discharged without adequate instruction on what and how much to eat. It is therefore essential for clinicians to provide nutrition intervention and follow-up until patients demonstrate the ability to maintain or gain weight, as the case necessitates.
Studies looking at fat malabsorption after PG and TG have demonstrated excessive fecal fat excretion. The etiology of fat malabsorption appears to be multifactorial. First, the gastric stump empties itself early and the gastric content moves rapidly through the upper digestive tract, reaching the jejunum and ileum sooner than the pancreatic enzymes. Second, decreased transit time prevents sufficient mixing of food with digestive enzymes and bile salts, especially in TG or BII patients. Third, decreased enzyme production reduces the ratio of enzymes to food. One study measuring exocrine pancreatic function in TG patients found that all patients had severe exocrine pancreatic insufficiency three months after surgery. Finally, due to loss of the antrum, and hence its sieving function, larger than normal food particles empty into the jejunum, making enzyme attack more difficult. Qualitative or quantitative fecal fat estimation is useful in the diagnosis of fat maldigestion
Lactase, the enzyme required for lactose absorption, is found primarily on villi in the jejunum. Most gastrectomized patients have an intact jejunum, therefore lactose intolerance, in these patients, is deemed "functional." Patients complaining of abdominal cramping or pain, bloating, diarrhea, flatulence and distention after consumption of lactose may do well to decrease or avoid it. Tolerance to lactose is typically dose-dependent and may improve over time. Many patients may be able to tolerate smaller amounts of lactose containing foods throughout the day. Lactase enzymes are available for patients who wish to continue consuming dairy products.
Although diet therapy may be beneficial in treating nutritional intolerances, it is important to minimize diet restrictions. Superfluous restrictions may cause frustration to the patient and can further aggravate weight loss.
Nutritional anemias resulting from iron deficiency, vitamin B12, or folate are common in gastrectomized patients. Consequences of anemia can be severe. Therefore baseline hemoglobin estimation and periodic monitoring is important. Anemia often presents as a late complication of gastric resection, placing patients with a distant history of the surgery at an even greater risk.
Iron deficiency is the most common anemia following gastric resection.
The reported incidence varies from 5% to 62% of patients with BII.
Alterations in digestion and absorption of dietary iron are thought to be responsible for iron deficiency in TG and PG patients. Duodenum, the primary site for iron absorption, is bypassed (except with BI) and reduced gastric acidity impairs the conversion of ferric iron to the more absorbable ferrous form. Reduced iron intake may also play a role.
Megaloblastic and pernicious anemia
Megaloblastic anemia may be the result of either vitamin B12 or folate deficiency. B12 deficiency may result in PG and TG patients for numerous reasons. Normally, intrinsic factor is complexed to B12 and facilitates its absorption by the terminal ileum. Reduction in intrinsic factor and reduced gastric acidity in gastrectomized patients impairs cleavage of protein bound B12. Bacterial overgrowth and reduced intake of B12 rich foods may also contribute to a deficiency state. Folate deficiency may develop after gastric surgery but is not well reported. Causes of folate deficiency are likely multifactorial including malabsorption (the first site of folate absorption is the duodenum).
Metabolic Bone Disease
Metabolic bone disease, such as osteoporosis, and osteomalacia, is commonly reported in gastrectomy patients leading to a greater risk of bone fractures. A low bone mineral density (BMD) has been reported in 27% to 44% of gastrectomized patients. The etiology of bone disease in gastrectomized patients is uncertain but appears to be a combination of decreased intake of calcium, vitamin D and lactose-containing foods, coupled with altered absorption and metabolism of vitamin D. Vitamin D deficiency may result from decreased intake rather than malabsorption. A significant increase in 25-OHD levels have been recorded when TG and PG patients were supplemented with 400 IU of vitamin D per day.