Cause and Pathophysiology of Acute Abdomen
a. Acute Appendicitis
Inflammation in the appendix has the same features and follows the same course as inflammation elsewhere in the gut. Its importance is a function of its frequency as a serious surgical condition with significant complications.
Obstruction of the appendiceal lumen by fecaliths with interference of the vascular supply are important features in its pathogenesis. The essential element causing inflammation of the wall of the appendix is invasion by bacteria. The usual organisms in the inflamed appendix are colon bacilli and streptococci, organisms commonly found in the intestinal tract. Obstruction of the lumen and vascular occlusion probably contribute by breaking down the resistance of the wall of the appendix to invasion by potential pathogens in the gut.
The earliest lesion is a superficial ulceration of the mucosa. Spread then occurs from the mucosa to the muscle layers and the serosa and the lumen may become filled with pus. Interference with circulation leads to areas of necrosis and perforation of the appendix, with spread of infection to the peritoneal cavity. If the infection becomes walled off around the appendix a localized abscess may result. Otherwise a generalized peritonitis results.
The same sort of inflammatory process may occur in acute diverticulitis which usually involves the descending and sigmoid colon. This is promoted by the lodging of fecal material in a diverticulum with spread of inflammation to surrounding tissue, and is accompanied by left lower quadrant pain.
In acute cholecystis there is inflammation of the wall of the gall bladder due so chemical damage from the action of concentrated bile, promoted by an obstruction of the cystic duct, usually by stones. Bacterial infection with streptococci or colon bacilli may supervene. In acute cholecystis the gall bladder is large and has a thick edematous wall. The mucosa shows areas of ulceration and necrosis and leukocytes are present in the wall. Pus may fill the cavity, with an empyema of the gall bladder. Necrosis and rupture may occur.
b. Acute Small Bowel Obstruction
Complete obstruction to the passage of intestinal content is caused either by mechanical obstruction of the lumen or by paralysis of the intestinal muscles (paralytic ileus) and may cause death in a relatively short period of time unless relieved. Acute mechanical obstruction of the small bowel is caused most commonly either by strangulated hernia or by adhesions and bands, usually post-operative, with the peritoneal cavity.
Age has a significant influence on the cause of small bowel obstruction. In newborns, congenital problems such as atresia of the gut are important causes of obstruction and in small children intussusception is encountered with frequency. The obstruction may be an entirely mechanical occlusion of the lumen, which is the case with an incarcerated hernia, congenital atresia of the lumen of the gut, and kinking and external compression of the gut by peritoneal adhesions, usually post-operative in origin.
There may, however, be an associated interference with the blood and nerve supply for the intestines, in which case the bowel is said to be strangulated. Obstruction such as an incarcerated hernia, if not promptly reduced, causes increasing edema of the gut with impairment of the blood supply. Volvulus with twisting of the mesentery and intussusception (where one segment of the small bowel invaginates into another) also cause interference with nerve and blood supply. Ischemic necrosis or infarction of the bowel wall occurs unless the blood supply is promptly restored. The involved portion of the intestine becomes in turn congested, edematous, necrotic and finally gangrenous. In general, the higher the site of an obstruction within the intestinal tract, the more severe are the associated symptoms of excessive vomiting with dehydration and chemical disturbances occurring because of a great loss of water and electrolytes.
The most common cause of lower intestinal obstruction is carcinoma of the distal portion of the colon. The development of the clinical picture is slower than in small bowel obstruction and patients do not appear as ill in comparable stages. Usually the acute episode of large bowel obstruction is superimposed on progressive change of bowel habits, with decreasing caliber of the stools and increasing constipation.
Functional intestinal obstruction due to neurogenic factors which cause paralysis of the intestinal muscle and failure of peristalsis is fairly common. It is termed adynamic or paralytic ileus and it occurs to some extent in most patients who have undergone abdominal surgery, and may be associated with shock or any severe trauma, such as hip fracture. Ischemia of the intestine also rapidly inhibits motility and paralytic ileus results. Paralytic ileus is commonly a concomitant of generalized peritonitis. Paralytic ileus is treated nonoperatively by suction and decompression of the intestine, and is adversely affected by anesthesia and surgery. It is important to differentiate a functional from a mechanical obstruction, where surgery is imperative.
Paralytic ileus is the end-result in a mechanical obstruction, unless the compromised blood supply is promptly restored. Otherwise there may be inexorable progression, terminating in gangrene.
c. Mesenteric Vascular Occlusion
Interference with the blood supply to a segment of the intestine, as in thrombosis or embolism of the superior mesenteric vessels, results in a paralytic obstruction without any mechanical blockage. The majority of patients with embolism involving the superior mesenteric artery have a cardiac lesion that is capable of thrombus formation and emboli. Recent myocardial infarction and atrial fibrillation are the two cardiac problems that give rise most often to mesenteric emboli. The segment of intestine which is deprived of its blood supply rapidly becomes congested, edematous and finally necrotic.
d. Perforated Duodenal Ulcer
While all the factors responsible for the development and persistence of chronic peptic ulcers are not thoroughly understood, the one factor of established importance is the action of acidpepsin gastric content on the duodenal mucosa with ulcer formation. In some individuals there seems to be too much gastric acid secretion with respect to the degree of protection provided for the mucosa. Peptic ulcers are constant in location, being found in the pyloric portion of the stomach near the lesser curvature and the first portion of the duodenum proximal to the ampulla. These chronic ulcers appear as deep, punched-out, funnel-shaped craters whose base is covered with grayish necrotic material. The base of the ulcer is composed of fibrous scar tissue which may cause deformity of the duodenal bulb, demonstrable by x-ray.
Hemorrhage may result from erosion of large vessels in the base of the ulcer. Perforation may result when the ulcer continues to penetrate deeply and erodes through the wall of the duodenum into a remarkable series of dramatic changes. Spillage of acidpeptic gastric juice, bile, and pancreatic juice causes a marked chemical inflammation of the peritoneum comparable to a burn. Bacterial invasion may soon follow. Within a short time massive amounts of extracellular fluid may be extravasated into the area of peritoneal injury and this loss of fluid may bring about hypovolemic shock.
Acute pancreatitis may closely simulate a perforated duodenal ulcer. The effects are caused by the escape of lytic pancreatic enzymes into the gland itself. These act on the parenchyma of the gland, blood vessels and fatty tissue causing edema, necrosis, hemorrhage, and suppuration of varying degree. It appears to be due to increased pancreatic secretion with partial or complete obstruction of outflow and raised intraductal pressure. It may occur suddenly with severe abdominal pain, peripheral vascular collapse or shock, and may be fatal.
e. Peritonitis
The peritoneal cavity, lined by serous peritoneal membranes which cover the viscera and the parietal walls, is a closed sac except for the openings of the fallopian tubes in the female. General inflammation of the peritoneal cavity is usually caused by bacterial invasion, which may result by spread: 1) from a ruptured viscus such as a perforated peptic ulcer or gangrenous appendix; 2) through an ischemic and necrotic but unruptured bowel wall, as in strangulated hernia, mesenteric occlusion, or volvulus; or 3) as a result of extension of infection from abdominal organs such as occurs with a liver abscess or a pelvic inflammatory disease.
The majority of cases of peritonitis involve organisms found in the normal flora of the gastrointestinal tract. Perforation of a hollow viscus is most frequently the source of entry of these organisms. The peritoneal infection may become walled off and limited to a localized area as in an appendiceal abscess, or there may be generalized peritonitis, which may be a serious complication of any of the diseases described above in a-d.
a. Acute Appendicitis
Inflammation in the appendix has the same features and follows the same course as inflammation elsewhere in the gut. Its importance is a function of its frequency as a serious surgical condition with significant complications.
Obstruction of the appendiceal lumen by fecaliths with interference of the vascular supply are important features in its pathogenesis. The essential element causing inflammation of the wall of the appendix is invasion by bacteria. The usual organisms in the inflamed appendix are colon bacilli and streptococci, organisms commonly found in the intestinal tract. Obstruction of the lumen and vascular occlusion probably contribute by breaking down the resistance of the wall of the appendix to invasion by potential pathogens in the gut.
The earliest lesion is a superficial ulceration of the mucosa. Spread then occurs from the mucosa to the muscle layers and the serosa and the lumen may become filled with pus. Interference with circulation leads to areas of necrosis and perforation of the appendix, with spread of infection to the peritoneal cavity. If the infection becomes walled off around the appendix a localized abscess may result. Otherwise a generalized peritonitis results.
The same sort of inflammatory process may occur in acute diverticulitis which usually involves the descending and sigmoid colon. This is promoted by the lodging of fecal material in a diverticulum with spread of inflammation to surrounding tissue, and is accompanied by left lower quadrant pain.
In acute cholecystis there is inflammation of the wall of the gall bladder due so chemical damage from the action of concentrated bile, promoted by an obstruction of the cystic duct, usually by stones. Bacterial infection with streptococci or colon bacilli may supervene. In acute cholecystis the gall bladder is large and has a thick edematous wall. The mucosa shows areas of ulceration and necrosis and leukocytes are present in the wall. Pus may fill the cavity, with an empyema of the gall bladder. Necrosis and rupture may occur.
b. Acute Small Bowel Obstruction
Complete obstruction to the passage of intestinal content is caused either by mechanical obstruction of the lumen or by paralysis of the intestinal muscles (paralytic ileus) and may cause death in a relatively short period of time unless relieved. Acute mechanical obstruction of the small bowel is caused most commonly either by strangulated hernia or by adhesions and bands, usually post-operative, with the peritoneal cavity.
Age has a significant influence on the cause of small bowel obstruction. In newborns, congenital problems such as atresia of the gut are important causes of obstruction and in small children intussusception is encountered with frequency. The obstruction may be an entirely mechanical occlusion of the lumen, which is the case with an incarcerated hernia, congenital atresia of the lumen of the gut, and kinking and external compression of the gut by peritoneal adhesions, usually post-operative in origin.
There may, however, be an associated interference with the blood and nerve supply for the intestines, in which case the bowel is said to be strangulated. Obstruction such as an incarcerated hernia, if not promptly reduced, causes increasing edema of the gut with impairment of the blood supply. Volvulus with twisting of the mesentery and intussusception (where one segment of the small bowel invaginates into another) also cause interference with nerve and blood supply. Ischemic necrosis or infarction of the bowel wall occurs unless the blood supply is promptly restored. The involved portion of the intestine becomes in turn congested, edematous, necrotic and finally gangrenous. In general, the higher the site of an obstruction within the intestinal tract, the more severe are the associated symptoms of excessive vomiting with dehydration and chemical disturbances occurring because of a great loss of water and electrolytes.
The most common cause of lower intestinal obstruction is carcinoma of the distal portion of the colon. The development of the clinical picture is slower than in small bowel obstruction and patients do not appear as ill in comparable stages. Usually the acute episode of large bowel obstruction is superimposed on progressive change of bowel habits, with decreasing caliber of the stools and increasing constipation.
Functional intestinal obstruction due to neurogenic factors which cause paralysis of the intestinal muscle and failure of peristalsis is fairly common. It is termed adynamic or paralytic ileus and it occurs to some extent in most patients who have undergone abdominal surgery, and may be associated with shock or any severe trauma, such as hip fracture. Ischemia of the intestine also rapidly inhibits motility and paralytic ileus results. Paralytic ileus is commonly a concomitant of generalized peritonitis. Paralytic ileus is treated nonoperatively by suction and decompression of the intestine, and is adversely affected by anesthesia and surgery. It is important to differentiate a functional from a mechanical obstruction, where surgery is imperative.
Paralytic ileus is the end-result in a mechanical obstruction, unless the compromised blood supply is promptly restored. Otherwise there may be inexorable progression, terminating in gangrene.
c. Mesenteric Vascular Occlusion
Interference with the blood supply to a segment of the intestine, as in thrombosis or embolism of the superior mesenteric vessels, results in a paralytic obstruction without any mechanical blockage. The majority of patients with embolism involving the superior mesenteric artery have a cardiac lesion that is capable of thrombus formation and emboli. Recent myocardial infarction and atrial fibrillation are the two cardiac problems that give rise most often to mesenteric emboli. The segment of intestine which is deprived of its blood supply rapidly becomes congested, edematous and finally necrotic.
d. Perforated Duodenal Ulcer
While all the factors responsible for the development and persistence of chronic peptic ulcers are not thoroughly understood, the one factor of established importance is the action of acidpepsin gastric content on the duodenal mucosa with ulcer formation. In some individuals there seems to be too much gastric acid secretion with respect to the degree of protection provided for the mucosa. Peptic ulcers are constant in location, being found in the pyloric portion of the stomach near the lesser curvature and the first portion of the duodenum proximal to the ampulla. These chronic ulcers appear as deep, punched-out, funnel-shaped craters whose base is covered with grayish necrotic material. The base of the ulcer is composed of fibrous scar tissue which may cause deformity of the duodenal bulb, demonstrable by x-ray.
Hemorrhage may result from erosion of large vessels in the base of the ulcer. Perforation may result when the ulcer continues to penetrate deeply and erodes through the wall of the duodenum into a remarkable series of dramatic changes. Spillage of acidpeptic gastric juice, bile, and pancreatic juice causes a marked chemical inflammation of the peritoneum comparable to a burn. Bacterial invasion may soon follow. Within a short time massive amounts of extracellular fluid may be extravasated into the area of peritoneal injury and this loss of fluid may bring about hypovolemic shock.
Acute pancreatitis may closely simulate a perforated duodenal ulcer. The effects are caused by the escape of lytic pancreatic enzymes into the gland itself. These act on the parenchyma of the gland, blood vessels and fatty tissue causing edema, necrosis, hemorrhage, and suppuration of varying degree. It appears to be due to increased pancreatic secretion with partial or complete obstruction of outflow and raised intraductal pressure. It may occur suddenly with severe abdominal pain, peripheral vascular collapse or shock, and may be fatal.
e. Peritonitis
The peritoneal cavity, lined by serous peritoneal membranes which cover the viscera and the parietal walls, is a closed sac except for the openings of the fallopian tubes in the female. General inflammation of the peritoneal cavity is usually caused by bacterial invasion, which may result by spread: 1) from a ruptured viscus such as a perforated peptic ulcer or gangrenous appendix; 2) through an ischemic and necrotic but unruptured bowel wall, as in strangulated hernia, mesenteric occlusion, or volvulus; or 3) as a result of extension of infection from abdominal organs such as occurs with a liver abscess or a pelvic inflammatory disease.
The majority of cases of peritonitis involve organisms found in the normal flora of the gastrointestinal tract. Perforation of a hollow viscus is most frequently the source of entry of these organisms. The peritoneal infection may become walled off and limited to a localized area as in an appendiceal abscess, or there may be generalized peritonitis, which may be a serious complication of any of the diseases described above in a-d.
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