Intestinal Obstruction

Anatomy of the Small Intestine

The small intestine is a convoluted tube, extending from the pylorus to the colic valve,
where it ends in the large intestine. It is about 7 meters long, and gradually diminishes in
size from its commencement to its termination. It is contained in the central and lower
part of the abdominal cavity, and is surrounded above and at the sides by the large
intestine; a portion of it extends below the superior aperture of the pelvis and lies in front
of the rectum. It is in relation, in front, with the greater omentum and abdominal parietes,
and is connected to the vertebral column by a fold of peritoneum, the mesentery. The
small intestine is divisible into three portions: the duodenum, the jejunum, and the ileum.
The Duodenum
Received its name from being about equal in length to the breadth of twelve fingers (25
cm.). It is the shortest, the widest, and the most fixed part of the small intestine, and has
no mesentery, being only partially covered by peritoneum. Its course presents a
remarkable curve, somewhat of the shape of an imperfect circle, so that its termination is
not far removed from its starting-point.
Jejunum and Ileum.The remainder of the small intestine from the end of the
duodenum is named jejunum and ileum; the former term being given to the upper twofifths and the latter to the lower three-fifths. There is no morphological line of distinction
between the two, and the division is arbitrary; but at the same time the character of the
intestine gradually undergoes a change from the commencement of the jejunum to the
end of the ileum, so that a portion of the bowel taken from these two situations would
present characteristic and marked differences. These are briefly as follows:
The Jejunum (intestinum jejunum) is wider, its diameter being about 4 cm., and is thicker,
more vascular, and of a deeper color than the ileum, so that a given length weighs more.
The circular folds (valvul conniventes) of its mucous membrane are large and thickly
set, and its villi are larger than in the ileum. The aggregated lymph nodules are almost
absent in the upper part of the jejunum, and in the lower part are less frequently found
than in the ileum, and are smaller and tend to assume a circular form.
The Ileum (intestinum ileum) is narrow, its diameter being 3.75 cm., and its coats thinner
and less vascular than those of the jejunum. It possesses but few circular folds, and they
are small and disappear entirely toward its lower end, but aggregated lymph nodules
(Peyers patches) are larger and more numerous

Both intestines share a general structure with the whole gut, and is composed of several
layers.
The lumen is the cavity where digested material passes through and from where nutrients
are absorbed.
Along the whole length of the gut in the glandular epithelium are goblet cells.
These secrete mucus which lubricates the passage of food along and protects it from
digestive enzymes.
Villi are vaginations of the mucosa and increase the overall surface area of the intestine
while also containing a lacteal, which is connected to the lymph system and aids in the
removal of lipids and tissue fluid from the blood supply.
Micro villi are present on the epithelium of a villus and further increase the surface area
over which absorption can take place.
Together the microvilli create a mucosal surface known as the brush border. Coating the
brush border is an unstirred layer of fluid that is important for absorption of substances
oher than wastes and electrolytes.
The lamina propia (a connective tissue layer of the mucous membrane) lies beneath the
epithelial cells of the villi and contains lymphocytes; plasma cells, which produce
immunoglobulins and macrophages.
The next layer is the muscularis mucosa which is a layer of smooth muscle that aids in
the action of continued peristalsis along the gut.
The submucosa contains nerves, blood vessels and elastic fibre with collagen that
stretches with increased capacity but maintains the shape of the intestine.
Surrounding this is the muscularis externa which comprises longitudinal and smooth
muscle that again helps with continued peristalsis and the movement of digested material
out of and along the gut.
Lastly there is the serosa which is made up of loose connective tissue and coated in
mucus so as to prevent friction damage from the intestine rubbing against other tissue.
Holding all this in place are the mesenteries which suspend the intestine in the abdominal
cavity and stop it being disturbed when a person is physically active.
Intestinal Digestion and Absorption
The process of digestion is initiated in the stomach by actions of hydrochloric acid and
pepsin. The chyme that passes into the duodenum is a liquid with small particles of
undigested food. Digestion continues in the proximal portion of the small intestines by

the action of the pancreatic enzymes and bile salts. There carbohydrates are broken down
to monosaccharides and disaccharides; proteins are degraded further to amino acids and
peptides; and fats are emulsified and reduced to fatty acids and monoglycerides. These
nutrients along with water, vitamins, and electrolytes are absorbed across the intestinal
mucosa by active transport, and diffusion. Products of carbohydrate and protein
breakdown move into villus capillaries and then to the liver through the portal vein.
Digested fats move into the lacteals or lymphatic channel and eventually reach the liver
through the systemic circulation. Intestinal motility exposes nutrients to a large mucosal
surface area by mixing chyme and moving it through the lumen. Different segment of the
gastro intestinal tract absorb different nutrients.
Intestinal Obstruction
Intestinal obstruction is a broad term, which entails cessation of the normal progression
of the intestinal contents. Intestinal obstruction can be segregated into complete and
incomplete blockage, and be due to mechanical or functional etiologies.
Mechanical obstruction is a term usually applied when there is an actual physical barrier
blocking the intestinal lumen, such as bands of adhesion, strangulated hernias, and
pressure from pelvic tumors. In contrast, adynamic ileus is used to describe disorders of
propulsive motility of the bowel.
Intestinal Obstruction can be caused by any condition the prevents the normal flow of
chyme through the intestinal lumen
Causes

Description

Hernia

Diverticulosis

Protrusion of the intestine through a weakness in the abdominal muscles or

through the inguinal ring.
Telescoping of one part of the intestine into another; this usually causes
strangulation of the blood supply; more common in infants 10-15 months of
age than in adults.
Twisting of the intestine on its mesenteric pedicle, with occlusion of the
blood supply; often associated with fibrous adhesions; occurs often in
middle-aged men.
Inflamed saccular herniations of the mucosa and submucosa

Tumor

Tumor growth in the intestinal lumen

Paralytic ileus

Loss of Peristaltic motor activity in the intestine.

Intussuception
Torsion
(volvulus)

Pathophysiology of Intestinal Obstruction

Intestinal
Obstruction

Sequestration of gas and fluid

proximal to the obstruction

Distention

Pressure on the
Diaphragm

Decrease
Respiratory Volume
Atelectasis

Colicky Abdominal Pain

Nausea and Vomiting

Decrease Food Intake,
Nutrient Absorption and
Carbohydrate reserves.
Ketosis
Alkalosis (early)

Pneumonia

Loss of water and

electrolytes
Acidosis (late)
Dehydration

Hypovolemia

Shock

Distention

Prolonged increase of
intraluminal wall tension

Decreased venous return

Intestinal bowel edema

Increased Capillary
Permeability

Bacterial Translocation

Release of Toxins

Fever
Peritonitis

Pathophysiology
Postoperative paralytic ileus results from inhibitory reflexes, inflammatory
mediators, and the influence of exogenous and endogenous opioids. If the obstruction is
at the pylorus or high in the small intestine, metabolic alkalosis develops initially as a
result of excessive loss of hydrogen ions that normally would be absorbed from the
gastric juice. With prolonged obstruction or obstruction lower in the intestine, metabolic
acidosis is more likely to occur because bicarbonate from pancreatic secretions and bile
cannot be reabsorbed. Hypokalemia can be extreme, promoting acidosis and atony of the
intestinal wall. Metabolic acidosis also may be accentuated by ketosis, the result of
declining carbohydrates stores caused by starvation. If pressure from the distention is
severe enough, it occludes the arterial circulation and causes strangulation leading to
perforation. Lack of circulation permits the buildup of significant amounts of lactic acid,
which worsen the metabolic acidosis. Bacteria also proliferate and may cross the mucosal
barrier and cause peritonitis and sepsis.
Clinical Manifestations
Colicky pains followed by vomiting are the cardinal symptoms. Typically the pain
occurs intermittently and intensifies for seconds or minutes as a peristaltic wave of
muscular contraction meets the obstruction. Sweating, nausea, and hypotension occur as
an autonomic response. The passing of the wave is followed by pain free interval. With
severe distention, the pain may diminish in intensity. If strangulation occurs, the pain
looses its colicky character becoming more constant and severe as ischemia progresses to
necrosis and peritonitis.
Vomiting and distention vary, depending on the level of the obstruction.
Obstruction at the pylorus causes early, profuse vomiting of clear gastric fluid.
Obstruction in the proximal small intestine causes mild distention and vomiting of bilestained fluid. Obstruction lower in the intestine cause more pronounced distention, and
vomiting may or may not occur or may occur later and contain fecal material. Partial
obstruction can cause diarrhea or constipation, but complete obstruction causes
constipation only. Early in the course of complete obstruction, the frequency of bowel
sounds increases and they may be tinkly and accompanied by peristaltic rushes and
crampy, abdominal pain as the bowel contracts to overcome the obstruction. Signs of
dehydration, hypovolemia, and metabolic acidosis may be observed as early as 24 hours
after the occurrence of complete obstruction. Distention may be severe enough to push
against the diaphragm and decrease lung volume. This can lead to Atelectasis and
pneumonia, particularly in debilitated individuals.