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Anatomy

Anterior Abdominal Wall


Inguinal Canal, Hernias
Inguinal Hernia: the Laparoscopic Approach
Parts of the Peritoneal Cavity
Parts of the Digestive Tract
Esophagus
Gastresophageal Junction
Stomach
Duodenum
Pancreas
Spleen
Liver and Biliary System
Boundaries of the Epiploic Foramen (of Winslow)
Jejunum and Ileum
Large Bowel
Blood Vessels of Gut Tube
Foregut Vessels
Gut Sensation: Pain
Lymph Drainage of the Gut Tube
Foregut: Stomach, Liver, Spleen, Pancreas, Duodenum
Midgut and Hindgut
Rectum and Anal Canal
Levator Ani
Ischioanal (Ischiorectal) Fossa
Rectum
Anal Canal
Watersheds in the Anal Canal
Anal Sphincters

Anterior Abdominal Wall

Transpyloric plane: vertebral level L1.

Tip of the ninth costal cartilage

About half way between the suprasternal notch and the pubic symphysis, or about halfway
between the xiphoid process and the umbilicus

Level of several internal structures (pylorus, gallbladder, renal hila, origin of superior
mesenteric artery, etc.)

Epigastrium: stomach, aorta is slightly to the left of the midline; pain from foregut structures
(as far the duodenal papilla) is usually referred here.

Umbilical region: aorta palpable above the umbilicus; pain from midgut structures (duodenal
papilla to splenic flexure of colon) referred here.

Hypogastrium or suprapubic region: enlarged pelvic organs (uterus, bladder); pain from
hindgut structures (descending colon onwards) referred here.

Hypochondriac region. On the right, the liver and the gallbladder may be palpable. Murphy's
point: tip of the right ninth costal cartilage, the usual surface marking of the fundus of the
gallbladder. On the left an enlarged spleen may be palpable.

Lumbar region. The lower poles of the kidneys may be palpated here, and the descending
colon may be palpable on the left.

Lower quadrant or inguinal region. McBurney's point (base of appendix surface marking): one
third of the way along a line from the right anterior superior iliac spine to the umbilicus. The
cecum or ascending colon may be palpable on the right. The descending and sigmoid colon
may be palpable on the left.

Dermatomes: xiphoid process T8, umbilicus T10, pubic symphysis T12/L1.

Midline incisions. The linea alba is a nerveless and comparatively bloodless plane.

Paramedian incisions. Nerves enter rectus abdominis muscles from the lateral aspect, so in
paramedian incisions, retract rectus abdominis muscle laterally so as not to tear the nerves.

L1 nerves (ilioinguinal and iliohypogastric) are in the vicinity of an incision over McBurney's
point. Damage to the iliohypogastric might weaken the muscles in the inguinal region,
increasing the possibility of subsequent inguinal hernia.

Inguinal Canal, Hernias


Deep (internal) inguinal ring. A defect in transversalis fascia about 2 cm above the
femoral pulse at the inguinal ligament. It is immediately lateral and superior to the inferior
epigastric artery.
Superficial (external) inguinal ring. A triangular opening in external oblique aponeurosis,
the base of which is medial to the pubic tubercle, and the apex of which points up and

laterally so that most of the superficial ring is more-or-less directly above the pubic
tubercle.
The anterior wall of the canal is formed by external oblique aponeurosis throughout
reinforced laterally (over the deep ring) by internal oblique.
The posterior wall of the canal is formed by transversalis fascia throughout, reinforced
medially (deep to the superficial ring) by the conjoint muscle (united internal oblique and
transversus abdominis) attached to the pubic tubercle.
The roof of the canal is made up of the fibers of internal oblique arching over the contents
of the inguinal canal to form the conjoint muscle.

Inguinal Hernia: the Laparoscopic Approach


The ductus deferens (round ligament in the female) and gonadal vessels approach the deep
inguinal ring from different directions. As they do so, they form the apex of a triangle deep to
which, hidden under peritoneum, are the external iliac vessels. These must not be damaged in
laparoscopic herniorrhaphy.
The gonadal vessels are usually easy to identify at laparoscopy, whereas the ductus deferens
is not. It is usually safe to assume that the ductus, as it approaches the deep ring, forms an
angle with the gonadal vessels such that if you avoid the area medial to the gonadal vessels
within a 60 angle at the deep ring, you are unlikely to damage important structures.

Parts of the Peritoneal Cavity

Supracolic compartment

Superior to the transverse colon. Includes the esophagus,


stomach, most of the duodenum, liver and biliary system

Infracolic compartment

Inferior to the transverse colon. Includes jejunum, ileum, cecum,


ascending and descending and sigmoid colon, rectum.

Paracolic gutters

Lateral to ascending and descending colons.

Paravertebral gutters

Between ascending and descending colons and the vertebral


column.

Hepatorenal (Morison's) pouch Superior end of the right paracolic gutter between liver and
kidney, also known by some as the right subhepatic
(subdiaphragmatic) space.
Subphrenic (subdiaphragmatic) The liver and diaphragm developmentally are different parts of
and subhepatic spaces

the same thing (septum transversum) and they remain attached


to each other at the bare area of the liver. The recesses of the
peritoneal cavity partially separate the two structures. The
anatomy of the liver, mainly a right sided organ, means that these
spaces are on the right side of the body:
Posterior subphrenic posterior to the liver, between it and the
space

posterior diaphragm, continuous with


Morison's pouch.

Anterior subphrenic anteriorly between the liver and the


space
Lesser and greater sacs

diaphragm.

The lesser sac lies behind the stomach and lesser omentum and
anterior to the pancreas. The spleen is at its left extremity and on
the right a small opening called the foramen of Winslow connects
the lesser sac with the rest of the peritoneal cavity. The rest of the
peritoneal cavity with its supracolic and infracolic compartments
is called the greater sac.

Parts of the Digestive Tract

Esophagus
Vertebral level T4 (surface marking: sternal angle of Louis): the esophagus is indented by the
arch of the aorta.
Vertebral level T5: the esophagus is slightly to the left of the trachea and is indented by the left
main bronchus.
Below this, the esophagus is behind the left atrium, separated from it only by the oblique sinus of
the pericardial cavity. This is useful: transesophageal echocardiography.
The esophagus does not hold sutures well because there is little connective tissue in the
submucosa.

Gastresophageal Junction

The esophagus passes through the diaphragm at vertebral level T10 slightly to the left of the midline,
but the muscle fibers of the gastresophageal sphincter arise from the right diaphragmatic crus.
At the junction, the stratified squamous (wear and tear) epithelium that has lined the alimentary tract
so far changes abruptly to a simple columnar (digestive) epithelium.

Stomach
The size and position of the stomach vary depending upon body shape, degree of
distension, and posture.
The pylorus normally lies at about vertebral level L1, the tr

anspyloric

plane.
The greater omentum, adheres to the transverse
mesocolon.
Branches of the vagus run in the lesser curvature. One of them is the
nerve of Latarjet to the pyloric region.

Duodenum
The gastroduodenal artery, which may be eroded by posterior ulcers of the first part.
The duodenal papilla marks entry of bile and pancreatic ducts, and it indicates the end
of embryonic foregut.
The third part passes horizontally to the left at about vertebral level L2/3, crossing the
midline in front of the abdominal aorta. Ulcers here may erode the aorta.
At the duodenojejunal (d-j) flexure or junction, about vertebral level L1, the gut once
again becomes mesenteric as the jejunum. It is anchored by the ligament of Treitz,
which passes down from the diaphragm.

Pancreas
The tail is the only part that is not retroperitoneal and extends into the splenorenal ligament
to reach the hilum of the spleen.
There is usually an accessory pancreatic duct opening into the second part of the
duodenum above the main duct.
Pancreatic pain is often felt in the back as well as generally in the abdomen anteriorly.
The pancreas develops from two foregut outgrowths, which, after some rotation around the
gut tube, fuse. Congenital anomalies include a condition in which pancreatic tissue forms a
ring around the duodenum - annular pancreas. This may cause duodenal obstruction.

Spleen
This is situated posteriorly on the left, related to ribs 9, 10 and 11. It is anterior to the left
costodiaphragmatic recess of the pleural cavity. It does not normally extend any further
anteriorly than the midaxillary line and is therefore not normally palpable.
The spleen is in danger from trauma to the left lower rib cage.

Liver and Biliary System


The liver occupies the right and central upper abdomen, roughly from the fourth intercostal
space (nipple in a lean male) to the costal margin. A very rough approximation is to draw a
triangle joining the two nipples and the tenth right costochondral junction.
Part of the liver is in direct contact with the diaphragm with no intervening peritoneum: this
is the bare area. The margins of the bare area, where the hepatic visceral peritoneum is
reflected on to the under surface of the diaphragm, form the coronary ligament, and the
right and left extremities of this are the right and left triangular ligaments.
The inferior vena cava passes through the bare area of the liver and the diaphragm
(vertebral level T8). In this region the right adrenal gland is posterior to the IVC and
intimately related to the bare area of the liver.

Functionally, the liver is divided into lobes and segments similar to the bronchopulmonary
segments of the lung, each with its own branches of the hepatic artery and portal vein,

and each with its own tributaries of the hepatic vein and the biliary tree.
Portosystemic anastomoses:
At the lower end of the esophagus when left gastric veins normally draining to the
portal system connect with tributaries of the azygos system. These are important
since they can lead to varices in the esophageal submucosa.
In and around the falciform ligament, including a recanalized ligamentum teres
(umbilical vein), and the veins of the anterior abdominal wall: caput Medusae (read
Greek mythology)
Other anastomoses of the posterior abdominal wall, the inferior rectal veins and
bare area of the liver: clinically insignificant.

Boundaries of the Epiploic Foramen (of Winslow)


Anterior: structures in the free edge of the lesser omentum: portal vein,
common hepatic artery, common bile duct
Superior: caudate lobe of liver
Posterior: inferior vena cava
Inferior: duodenum (first part)

Jejunum and Ileum

Approximately the first 2/5 of the mesenteric small bowel is the jejunum.
The jejunum has a richer blood supply, and thicker walls than the ileum.
Meckel's diverticulum. Within about one meter or so of the distal end of the ileum, a
remnant of the vitellointestinal duct may persist: Meckel's diverticulum. It may contain
ectopic gastric mucosa, which secretes acid and causes bleeding when ulcerated.
Peyer's patches. These lymphoid aggregations in the wall of the intestine may enlarge and
form the leading point of an intussusception in infants.
Carcinoid tumor. Neuroendocrine cells scattered throughout the epithelium undergo
neoplastic change resulting in overproduction of pressor amines.

Large Bowel
The surface marking of the cecum and base of the appendix is McBurney's point (see
above). The appendix is of variable length and position: it may extend down to the pelvis
and give rise, when inflamed, to pelvic pain.
Taenia coli converge at the appendix.
The ascending and descending colons are retroperitoneal and so are not usually mobile,
but the transverse mesocolon may be sufficiently extensive for the transverse colon to
loop down for some distance.
The sigmoid colon (mesenteric) becomes the rectum in front of the body of S3, as the gut
tube once again becomes retroperitoneal.

Blood Vessels of Gut Tube


Celiac artery: vertebral level T12: forgut.
Superior mesenteric artery: vertebral level T12/L1: midgut.
Inferior mesenteric artery: vertebral level L1 (approx.): hindgut.
All blood to the liver enters through vessels in the free edge of the lesser omentum.
Bleeding from the liver can be stemmed by compressing it (Pringle's maneuver). If

bleeding continues, look for a tear in the IVC.


Marginal artery of Drummond runs along the mesenteric border of the colon. This
maintains supply to the descending and sigmoid colon even if the inferior mesenteric
artery is ligated. The converse does not hold: the inferior mesenteric artery does not
supply enough blood to the marginal artery to allow the ligation of the superior
mesenteric artery.

Foregut Vessels
Splenic

Passes in the posterior wall of the lesser sac through or


along the top of the pancreas and through the splenorenal
ligament to the spleen. Near the spleen it gives short
gastric arteries to the fundus of the stomach, and the left
gastroepiploic (gastro-omental), which supplies the
greater omentum and the greater curvature of the
stomach.

Common hepatic

Passes to the liver in the lesser omentum. (Rarely the


hepatic artery may be a branch of the superior
mesenteric.) It gives:
Gastroduodenal

passes inferiorly, behind the first part


of the duodenum, and divides into the:
right gastroepiploic (right gastroomental) supplying the greater
curvature

superior pancreaticoduodenal,
which runs between the head of
the pancreas and the duodenum,
supplying them both
Right gastric

lesser curvature

Cystic

to the gallbladder

Right and left

to the liver

hepatic arteries
Left gastric

Lesser curvature and terminal esophagus

Gut Sensation: Pain


Pain from foregut structures is referred to the epigastrium. Gallbladder pain may also be
referred to the tip of the right scapula.
Pain from midgut structures is referred to the umbilical region, and from hindgut structures
is referred to the hypogastric (suprapubic) region.
Appendicitis and pain. The classical picture is central abdominal (periumbilical) pain that
after a time shifts to the RLQ. The explanation usually given is that initially the
inflammation or distention involves only the appendix, and the resulting midgut visceral
sensation is referred to the umbilical region. As the disease progresses the inflamed
appendix enlarges, touching the anterior abdominal wall to which inflammation spreads.
This is then perceived as somatic peritoneal pain.

Lymph Drainage of the Gut Tube

Foregut: Stomach, Liver, Spleen, Pancreas, Duodenum


To celiac nodes, although other structures may be involved.
Lymph drainage of the stomach:
from the greater omentum passes to splenic and pancreatic nodes before reaching
celiac nodes
from the lesser curvature, lymph may pass retrogradely to the liver, leading to hepatic
involvement. This is not uncommon.

from the celiac nodes, lymph passes to the cisterna chyli, the thoracic duct and its
termination at the junction of the left internal jugular and left subclavian veins.

In some cases of upper abdominal malignant disease, particularly stomach cancer,


involvement of a left supraclavicular node may occur, presumably because of their proximity
to the termination of the main thoracic duct. This, when present, is Virchow's node.

Midgut and Hindgut


To nodes in the mesentery, posterior abdominal wall, and around the origin of the mesenteric
arteries.

Rectum and Anal Canal

Levator Ani

The inferior limit of the abdominal cavity is formed by levator ani muscle, also known as
the pelvic floor or pelvic diaphragm. It is a shallow cone of muscle and fascia with its
lowest part just in front of the anal canal: the perineal body.
It separates the pelvic cavity (above) from the perineum (below).
It is where the rectum (above) becomes the anal canal (below). This is a majority view:
opinions differ.

Ischioanal (Ischiorectal) Fossa


The area of the perineum surrounding the anal canal (below levator ani) is the
ischioanal (ischiorectal) fossa (between ischium and anal canal). This contains fat
and glands, which open into the anal canal (see below). Boundaries are anus and
rectum medially, levator superiorly and ischium laterally.

The pudendal nerve (S 2, 3,4) passes on the lateral wall of the ischioanal fossa and
innervates all the structures in the perineum.

Rectum
The rectum begins in front of vertebra S3 where the sigmoid colon loses its mesentery. It
continues downwards and forwards on the superior aspect of the pelvic diaphragm.
Puborectalis part of levator ani muscle holds the feces in the rectal ampulla by 'pulling' the
rectum forwards so that just beneath the ampulla the rectum turns sharply backwards
(approximately 90) and down through the pelvic diaphragm. This angle and the role of
puborectalis are important in the maintenance of fecal continence. Damage to the pelvic
diaphragm or the perineal body may result in incontinence.
Rectal valves. These consist of three mucosal folds, sometimes called the valves of
Houston. These folds project into the lumen, from above down (or below up): from the left,
from the right, and from the left.

Anal Canal
From the puborectalis sling, the anal canal passes down and backwards to the anal
orifice.
The mucosa of the upper part of the anal canal is thrown into, between five and 10
longitudinal mucosal folds, the anal columns.
At their lower end, about halfway along the canal, these folds are joined together by
mucosal ridges, called valves (not to be confused with valves of the rectum) with a small
recess behind, something like a pocket. Mucus glands open into these pockets.
The apparent line formed by the valves is the pectinate or dentate line and it marks the
approximate position of several boundaries or watersheds.
Veins. You might logically suppose that, since the anal canal is a site of anastomoses
between the portal and systemic venous systems, it would be involved in the
manifestation of liver disease in a way similar to esophageal varices. This complication
does occur, but it is not common. Why it is not more common is unclear.

Watersheds in the Anal Canal


Above pectinate (dentate) line Below pectinate (dentate) line
Epithelium

columnar (mucosa)

Stratified squamous (skin)

Arteries

branches of inferior mesenteric,

branches of internal iliac, for example,

for example, superior rectal

inferior rectal

to the portal system (inferior

to the systemic system (internal iliac

mesenteric)

veins)

Veins

Lymph drainage to mesenteric nodes

to internal iliac and inguinal nodes

Nerve supply

Somatic, inferior rectal from pudendal (S

visceral (autonomic): pelvic

splanchnic nerves (S 2, 3, 4 and 2, 3, 4). Pain is sharp and well defined


sympathetic). Pain is dull and
poorly defined

Anal Sphincters
Internal sphincter. Smooth muscle, autonomic innervation. This is the expanded inferior
termination of the circular muscle of the gut tube wall.
External sphincter. Skeletal muscle, voluntary (somatic) innervation (S 2, 3, 4). There are
three parts. From outside (anus) in, these are:
subcutaneous: puckers the anal skin
superficial: level with the inferior edge of the internal sphincter
deep: level with the anal columns
The deep part is functionally related to, and merges with, puborectalis and the perineal
body. This is why damage to the pelvic diaphragm, or to the perineal body, may lead to loss
of sphincter control.

Physiology

Gastrointestinal Tract
Gastrointestinal Motility
Mouth and Esophagus
Stomach
Vomiting
Small Intestine
Large Intestine
Diarrhea
Constipation
Digestion and Secretion
Saliva
Gastric Secretion
Hyposecretion
Hypersecretion
Pancreatic Secretion
Diseases of the Pancreas
Bile
Unconjugated Hyperbilirubinemia
Conjugated Hyperbilirubinemia
Gallstones
Absorption
Generalized Malabsorption
Effects of Generalized Malabsorption
Liver

Gastrointestinal Tract

Gastrointestinal Motility
Transit time can vary from about 20 to 140 hours largely depending on the amount of dietary
fiber. A high fiber diet usually results in a large fecal mass with a short transit time.

Mouth and Esophagus


In the mouth, food is broken down by chewing and is mixed with saliva and mucus to aid
lubrication. When the food has been chewed it is forced backwards with the tongue until
pressure on the pharyngeal wall initiates the swallowing reflex. As the bolus is carried by
peristalsis down the esophagus, nervous signals cause relaxation of the lower esophageal
sphincter allowing food to enter the stomach.

Stomach
Regular peristaltic waves, generated within the stomach muscle at a rate of about 3/min
spread from the body of the stomach to the antrum where the strongest contractions occur.
As the contractions reach the pylorus, the pyloric sphincter closes preventing excessive
emptying into the duodenum, so forcing some of the chyme into the duodenum while the bulk
of it is mixed back into the body of the stomach. The strength of contraction increases during
a meal and accelerated gastric emptying occurs as a result of factors such as mechanical
distension, increased parasympathetic activity and the action of gastrin. Gastric emptying is
slowed by the acid or fat in the duodenum thus expediting pH neutralization and intestinal
lipid absorption.

Vomiting
The vomiting center in the medulla is stimulated by a number of factors including tactile
stimulation of the back of the throat, motion sickness, irritation or distension of the stomach
and duodenum, elevated intracranial pressure such as that caused by cerebral hemorrhage,
intense pain arising from a variety of organs and various chemical agents including emetics
and toxic substances. Vomiting is usually associated with nausea and is often preceded by
sweating, pallor and an elevated heart rate. Vomiting results in the loss of NaCl, water and H+
so that dehydration and alkalosis may result.

Small Intestine
Three types of contractile activity:
segmentation, where the muscle contracts simultaneously at regular intervals along
the intestinal wall. This divides the lumen of the gut into a series of discontinuous
segments and moves along the gut contents.
peristalsis, the main propulsive force. The waves of peristalsis only travel a few
centimeters before dying out to ensure that the movement of intestinal contents is
slow to allow adequate time for digestion and absorption.
strongly propulsive migratory motor complexes develop several hours after a meal,
when absorption is largely completed, to help intestinal residue into the large
intestine

Large Intestine
Segmentation in the colon is slow (2-4 contractions/h) though there is a sustained contraction
of the circular muscle immediately after a meal. Mass movements force the colonic contents
into the rectum thereby distending it. Rectal distension gives rise to an awareness of the urge
to defecate. The learned ability to respond to this urge by voluntarily contracting the external
anal sphincter results in the control of defecation (fecal continence).

Diarrhea
Diarrhea is an increased volume of stool causing dehydration, loss of K + and HC03- so
hypokalemia and acidosis may result. It may be caused by:
increased bowel motility in response to inflammation

malabsorption of nutrients from the intestinal lumen leading to fluid retention


excess secretion by the intestinal muscosa for example in response to bacterial toxins

Constipation
Infrequent or difficult defecation, which is reasonably common in the elderly, is often the result of
inadequate dietary fiber.

Digestion and Secretion

Saliva

Saliva is alkaline (as a result of HC03-) which helps buffer the acid in food and thus prevents
dental caries The main constituents are:
mucus which acts as a lubricant
amylase which has a minor role in polysaccharide digestion
lysozyme which protects against bacterial infections by hydrolysing the
peptidoglycan found in some bacterial cell walls

Gastric Secretion
Goblet cells produce mucus
Parietal (or oxyntic) cells secrete hydrochloric acid and intrinsic factor

Chief (zymogenic) cells secrete pepsinogen.


Parietal and chief cells are found in the deeper regions of the gastric pits.
Gastric mucosa also contains cells which secrete histamine and G cells
producing gastrin which control acid secretion from adjacent parietal cells.
Stimulation of gastric secretions occurs by two main pathways:
through the vagus nerve which in turn responds to stimuli from the
cerebral cortex normally resulting from the sight, taste and smell of food
by gastrin released from G Cells in the gastric antrum in response to
distension and the presence of protein in the stomach. Gastrin stimulates
acid secretion, the action being mediated by histamine. Acid in the
pylorus inhibits gastrin secretion by negative feedback inhibition. Alcohol
and calcium may also enhance gastrin secretion and the effect of calcium
may explain the relatively high incidence of peptic ulceration in patients
with chronic hypercalcemia.

Hyposecretion
Reduced secretion is found in patients with pernicious anemia (autoimmune destruction of
parietal cells). Intrinsic factor deficiency results in impaired vitamin B12 absorption.
Hyposecretion may also be caused by chronic gastritis and carcinoma of the stomach.

Hypersecretion

Excessive gastric secretion may result in gastric and duodenal ulceration.


In the Zollinger-Ellison syndrome acid hypersecretion is due to high levels of gastrin
caused by gastrinomas. Approximately 90% are found in the pancreas.
More than 80% of peptic ulcers are caused by Helicobacter pylori. Individuals (up to 30%
of the population) with this bacterium also have an increased risk of developing stomach
cancer. The Helicobacter pylori reside in the stomach's thick mucus layer where they
contribute to ulcer formation by secreting toxins that cause a persistent inflammatory
response which weakens the gastric mucosal barrier. The bactericidal effects of gastric
HCl are minimized as the bacteria settles in the antrum, which has no acid-producing
parietal cells. The bacteria also produce the enzyme urease, which breaks down urea into
NH3 and CO2. The NH3 can neutralize stomach acid thereby facilitating Helicobacter pylori
survival.

Tests to detect the bacteria measure ammonia or radiolabeled carbon dioxide in the
breath of the patient after ingestion of urea.
Other factors contributing to ulcer formation include alcohol abuse, nonsteroidal antiinflammatory drugs for example aspirin and ibuprofen.
Where Helicobacter pylori is implicated, therapy should include antibiotics. Palliative
treatment with antacids and surgery (vagotomy or removal of the gastric antrum) have
been largely replaced with H2 blockers (cimetidine) and proton pump inhibitors
(omeprazole).

Pancreatic Secretion
The two major components of pancreatic secretions are bicarbonate (HC0 3-), which
neutralizes gastric acid entering the duodenum, and a number of powerful digestive
enzymes that are required for the digestion of all the major macromolecules.
Protein. Proteolytic enzymes are synthesized and stored as inactive precursors or
zymogens (for example trypsinogen, chymotrypsinogen) which prevents autodigestion of
the pancreas. The zymogens are converted to active enzymes (for example trypsin and
chymotrypsin) by enzymatic degradation in the small intestine. Trypsin and chymotrypsin
and other pancreatic peptidases hydrolyze dietary proteins into small peptides and amino
acids.
Carbohydrate. Pancreatic amylase hydrolyzes dietary polysaccharides such as starch and
glycogen into disaccharides and limit dextrins.

Fat. Lipase and cholesterol esterase convert triglycerides and cholesteryl esters into
monoglycerides, cholesterol and fatty acids. Fat is emulsified prior to digestion by bile
salts.
Pancreatic secretion is stimulated by the presence of food and acid in the duodenum
which triggers the release of two intestinal peptide hormones cholecystokinin pancreozymin (CCK-PZ) and secretin. CCK-PZ, which is secreted by the upper small
intestine in response to proteins and fatty acids, stimulates pancreatic enzyme secretion
and increases small intestine motility. Secretin is formed in the duodenal and upper jejunal
epithelium. Its release, in response to H+, enhances HC03- secretion.

Diseases of the Pancreas


Cystic Fibrosis. The most common lethal inherited metabolic disease in
Caucasians with a frequency of 1/2,500 live births. It is a recessive condition in
which defective chloride transport results in viscous pancreatic and bronchial
secretions which cause obstructive diseases. Pulmonary dysfunction is the
most common cause of death and pancreatic insufficiency occurs in

approximately 85% of cases.


Acute Pancreatitis. An often lethal disease characterized by the premature
activation of proteolytic and lipolytic enzymes within the gland. The effect is to
destroy the pancreas and its blood vessels. The presence of pancreatic
enzymes in the peritoneal cavity cause severe abdominal pain and shock.
Pancreatitis is most commonly the result of obstruction of the pancreatic duct or
of regurgitation of bile along this duct. The most important predisposing factors
are alcoholism, gallstones and biliary tract disease. Serum amylase levels
greater than 10 times the upper limit of normal are virtually diagnostic of acute
pancreatitis.
Chronic Pancreatitis. Most commonly the result of alcohol abuse although it
may also follow severe attacks of acute pancreatitis. Inflammation with
subsequent fibrosis often results in exocrine insufficiency and generalized
malabsorption.
Carcinoma of the pancreas. Patients usually present with abdominal pain,
weight loss or jaundice.

Bile
Hepatocytes secrete bile into the bile canaliculi, which open into the bile ducts. Between
meals, bile is stored and concentrated in the gallbladder. Following a meal the gallbladder
is stimulated to contract by cholecystokinin, which also stimulates pancreatic secretion.
Bile consists of an aqueous alkaline fluid with NaHCO 3, similar to pancreatic secretions,
and organic constituents such as bile salts, cholesterol, lecithin and bilirubin.
Bile salts are derivatives of cholesterol. They have a steroid nucleus and are usually
conjugated with an amino acid. Bile salts are important in both the digestion and
absorption of lipids. They emulsify fat.
The main pigment is bilirubin, which is formed from the heme component of hemoglobin.
At the end of their lifespan of approximately 120 days, red blood cells are broken down by
the reticuloendothelial system mainly in the spleen. Following lysis the released
hemoglobin is split into globin which enters the general protein pool and heme, which
after the removal of iron, is converted to bilirubin.
Bilirubin is transported to the liver bound to albumin. This is unconjugated bilirubin and, in
the liver, it is transported to the smooth endoplasmic reticulum where it is conjugated with
two molecules of glucuronic acid to form water-soluble bilirubin diglucuronide, or
conjugated bilirubin. Conjugated bilirubin is excreted via the bile canaliculi and ducts.

Intestinal bacteria convert bilirubin diglucuronide to urobilinogen. Some is excreted in the


feces (stercobilinogen). The remainder is reabsorbed from the intestine and is re-excreted
in bile (enterohepatic circulation). A small amount is excreted in urine.

Unconjugated Hyperbilirubinemia
Prehepatic jaundice: increased production of bilirubin as a result of hemolysis
(for example in hereditary spherocytosis) or of the breakdown of large amounts
of blood after hemorrhage , specifically into the retroperitoneum.
Neonatal jaundice. This is common particularly in premature babies and is
usually the result of inadequate conjugating capacity. The jaundice is usually
transitory though high levels of bilirubin could result in kernicterus (deposition of
bilirubin in the brain).
Gilbert's disease is harmless and may be the result of defects in several factors
involved in the hepatic uptake and conjugation of bilirubin.
Crigler-Najjar Syndrome (serious) is the result of a congenital deficiency of
UDP-glucuronyl transferase.

Conjugated Hyperbilirubinemia
Conjugated bilirubin is water soluble and can be excreted in urine. Bilirubinuria is
always pathological. In most cases of jaundice in adults, both conjugated and
unconjugated bilirubin fractions are increased which is indicative of the
hepatocellular damage.

Gallstones
Although most gallstones contain all biliary constituents, one of them usually
predominates.
Pigment stones: associated with chronic hemolytic states such as hereditary
spherocytosis or biliary infection.
Cholesterol stones.
Mixed stones contain a mixture of bile constituents usually with a cholesterol nucleus.
In patients with cholestasis there is a characteristic elevation in plasma levels of
conjugated bilirubin and alkaline phosphatase (produced by cells lining bile
canaliculi).

Absorption

Absorption largely takes place in the small intestine and involves the transfer of the
products of digestion and small dietary molecules including water, vitamins and minerals
from the lumen of the gut into the blood.
Lipids. Micelles, which contain bile salts, monoglycerides, cholesterol, fatty acids,
phospholipids and fat soluble vitamins passively traverse microvillous spaces into intestinal
cells where lipids are packaged with proteins into chylomicrons. Chylomicrons pass
through the cell wall into the lymphatics and enter the systemic circulation.

Carbohydrates. Glucose and galactose are absorbed into the duodenum by a common
active process requiring energy. Na+ is cotransported with the glucose (or galactose) and it
thus moves from a region of high concentration (in the intestinal lumen) to a low
intracellular concentration. The Na+ / K+ ATPase uses the energy released from ATP
breakdown to pump Na+ out again and thus maintain a low Na+ concentration inside the
cell. The glucose and galactose diffuse into the plasma in the mucosal capillaries. Fructose
is absorbed by a different mechanism called facilitated diffusion, which doesn't require
energy.

Protein. Amino acids are absorbed by active transport again using Na + cotransport.

Vitamin B12 is absorbed only when it has formed a complex with intrinsic factor a
glycoprotein secreted by the parietal cells in the stomach. This complex is resistant to
proteolytic digestion and binds to specific receptors in the distal ileum from where it is
absorbed. Vitamin B12 deficiency may thus be the result of either gastric or ileal disease.
Some intestinal bacteria need Vitamin B12 for growth and may also prevent its absorption
by competing for it with intestinal cells. Deficiency of Vitamin B12 causes megaloblastic
anemia and subacute combined degeneration of the spinal cord.
Water Soluble Vitamins (Other than B12). Absorbed mainly in the upper small intestine.
Clinical deficiencies with the exception of folate are uncommon.
Sodium and Potassium. Probably absorbed by an active process throughout the small
intestine. Many other active transport mechanisms depend on the energy provided by the
sodium pump.
Chloride. Absorbed in the small intestine down the electrochemical gradient created by the
absorption of Na+ and other anions.
Water. Passively absorbed along the osmotic gradient created by the absorption of Na +,
sugars, amino acids and so on. Final water absorption occurs in the colon.
Calcium. Actively absorbed in the upper small intestine. Its absorption is inhibited by the
formation of insoluble salts with phosphate or fatty acids. Calcium absorption also requires
1,25 dihydroxycholecalciferol (active Vitamin D).
Iron. Absorption in the duodenum and upper jejunum is stimulated by anemia.

Generalized Malabsorption
The generalized malabsorption of fat, carbohydrate, protein and other nutrients
may be the result of either intestinal disease (reduced absorption) or pancreatic
disease (impaired digestion). Intestinal diseases include those which result in a
reduction in surface area for example celiac disease (gluten enteropathy) or
tropical sprue (probable bacterial etiology). In these cases flattening of the
mucosal villi may be demonstrated by intestinal biopsy.
Chronic inflammatory diseases like Crohn's disease may also cause
malabsorption. Pancreatic diseases such as chronic pancreatitis and cystic
fibrosis may cause a generalized malabsorption as a result of the incomplete
digestion of dietary foodstuffs.

Effects of Generalized Malabsorption

Steatorrhea. The most common finding in generalized malabsorption is


impaired fat absorption with an increased fat output in the stools (>18mmol (56g) fat/day). Fat malabsorption may also be the result of biliary obstruction
because of the requirement of bile salts for the emulsification of fat prior to
digestion. Fat soluble vitamin deficiencies occur as these are absorbed
together with other lipids in the micelles and this may result in impaired calcium
absorption (vitamin D), hemorrhagic diathesis with a prolonged prothrombin
time (vitamin K) and night blindness (vitamin A). Vitamin E deficiency is rarely
clinically evident.
Protein Malabsorption. Prolonged disease causes generalized tissue wasting,
a lowering of plasma proteins and osteoporosis (a reduction in the mass of
bone matrix with a secondary loss of calcium).

Liver
The liver contains two principal cell types:
Hepatocytes or parenchymal cells (about 40%)

Kupffer cells which form part of the reticuloendothelial network (about


30%)
Liver cell damage causes the release of intracellular constituents (including
enzymes) into the blood stream. Alanine (ALT, GPT) and aspartate (AST, GOT)
transaminase levels rise in plasma as a result of damage to cyloplasmic and/or
mitochondrial membranes. Gamma-glutamyl transferase is the most sensitive
indicator of alcohol abuse.
Synthetic Function. Hepatocytes synthesize many compounds including
plasma proteins, clotting factors, lipoproteins and bile acids. The liver has a
large functional reserve and there may be extensive liver damage before
deficiencies in synthetic function can be detected. Severe disease results in low
levels of plasma proteins (leading to bleeding states).
Cholestasis. Plasma conjugated bilirubin and alkaline phosphatase are
increased.

Pathology

Esophagus
Congenital Anomalies
Motor Dysfunction
Barrett's Esophagus
Esophageal Tumors
Stomach
Congenital Anomalies
Gastritis, Ulceration
Benign Tumors
Malignant Tumors
Small Intestine and Colon
Congenital Anomalies
Ischemic Bowel Disease
Malabsorption Syndromes
Ulcerative Colitis
Crohn's Disease (Regional Ileitis)
Diverticular Disease
Carcinoid Tumor

Tumors of Large Intestine


Genetic Factors
Staging and Prognosis
Appendix
Liver Disease
Hepatitis, Alcohol, Cirrhosis
Liver Tumors
Gallstones
Pancreatic Disease

Esophagus

Congenital Anomalies
Atresia and fistulas are usually discovered soon after birth and may be
incompatible with life. They are often associated with congenital heart diseases
and other malformations. In 80% of cases, a fistula connects with trachea or main
stem bronchus. Stenosis may be congenital or may be secondary to esophageal
injury following gastresophageal reflux, radiation or caustic injury. Mucosal rings
are protrusions of mucosa and when present in the upper esophagus are called
webs.

Motor Dysfunction
Achalasia is due to a failure in relaxation of the lower esophageal sphincter
resulting in proximal esophageal dilation, dysphagia and regurgitation.
Complications include candidal esophagitis, diverticula, aspiration pneumonia and
a risk of carcinoma.
Hiatus hernia: sliding (90%) and paraesophageal (<10%). Hiatus hernia may cause
retrosternal chest pain due to regurgitation and can lead to ulceration and
strangulation.

Barrett's Esophagus
This is columnar metaplasia of the distal esophageal epithelium in response to
prolonged injury such as long-standing reflux. It is not itself neoplastic but it carries
a risk of ulceration and stricture and is associated with an increased risk of
adenocarcinoma (up to 30 times).

Esophageal Tumors
Benign tumors are rare.
Squamous cell carcinoma formerly accounted for over 80% of primary esophageal
carcinomas. It is usually seen in adults over 50 and is more common in men. The
middle esophagus is involved in 50% cases, upper esophagus in 20% and lower
esophagus in 30% cases. The carcinomas are usually moderately to well
differentiated and spread by lymphatics and directly to neighboring structures. Five
year survival for superficial cancer is 75%, for advanced resectable carcinoma
25% but only 5% for non resectable disease.

Adenocarcinoma represents 25% of esophageal cancers and its relative incidence


is on the increase. Most are in the distal third of the esophagus. The overall 5 year
survival is 15%.

Stomach

Congenital Anomalies
Diaphragmatic hernias are due to a defect or weakness in the diaphragm resulting
in herniation of part or all of stomach and occasionally small bowel and liver, into
the chest leading to respiratory impairment. Pyloric stenosis consists of
hypertrophy of pyloric circular muscle. It occurs in 1:3000 to 1:9000 live births,
more commonly affecting males, but after the neonatal period (3-6 weeks of age).

Gastritis, Ulceration
Acute gastritis may be caused by bacterial or viral infections, NSAIDs, alcohol and
acid production with back diffusion, decreased bicarbonate, reduced mucosal
blood flow and mucosal damage. Chronic gastritis may result from chronic infection
(Helicobacter pylori), immunological damage (autoimmune gastritis), toxins
(alcohol), postantrectomy bile reflux, radiation, inflammatory bowel disease and
graft versus host disease. It may progress to ulceration and carcinoma.
Chronic peptic ulceration is more common in the duodenum than in the stomach.
Other sites include Meckel's diverticulum, the lower esophagus and
gastroenterostomy stoma. Favored locations are the anterior or the posterior wall
of the first part of duodenum, and the lesser curvature of the stomach.
Complications include perforation, hemorrhage, stenosis and malignancy. Severe
recurrent gastric ulceration may be due to the Zollinger-Ellison syndrome (gastrinproducing tumors).

Benign Tumors

Gastric polyps may be inflammatory, neoplastic or hamartomatous. Benign gastric


adenomas are likely to become malignant. Leiomyomas may also cause polyps in
the stomach. Hamartomatous polyps arise in Peutz-Jegher syndrome.

Malignant Tumors
Gastric carcinomas are 90-95% of stomach malignancies. They are associated
with chronic gastritis, pernicious anemia, previous partial gastrectomy and blood
group A. Microscopically they are divided into early (confined to mucosa and
submucosa) and late (invasion deep to the submucosa). Presentation is usually
with dyspepsia, anorexia and hematemesis, but patients may present with
metastases. Spread is by local invasion, lymphatics, and blood vessels and the
transcelomic route. Prognosis depends on the depth of invasion with a 90% 5 year
survival in early cancers (confined to the mucosa and submucosa) and only 10% 5
year survival in advanced cancers.
Metastases to the stomach are rare. Lymphomas are usually non-Hodgkin's B Cell
lymphomas and often arise from MALT. The most common gastric sarcoma is a
gastrointestinal stromal tumor (GIST) or leiomyosarcoma.

Small Intestine and Colon

Congenital Anomalies
Meckel's diverticulum arises from persistence of part of the vitellointestinal duct. It
is found within 30 inches of the ileocecal valve. Heterotopic gastric or pancreatic
mucosa may cause symptoms of peptic ulceration and it may present as anemia.
The diverticulum may also become perforated, incarcerated or intussuscepted and
when inflamed may mimic appendicitis.
Hirschsprung's disease is due to arrested migration of neural crest cells into the
gut (proximal to distal) leading to an aganglionic colonic segment causing
functional obstruction. The incidence varies from 1 in 5000 to 8000 live births.
Diagnosis is confirmed by an absence of ganglion cells in the affected segment of
the bowel.

Ischemic Bowel Disease


This may be due to arterial or venous ischemia or occlusion. Predisposing
conditions include arterial atheroma and or thrombosis, arterial emboli, (thrombus
or cholesterol), venous thrombosis and nonocclusive ischemia resulting from
shock. Other causes include arteritis and mechanical causes such as volvulus.
Pathological patterns include transmural infarction, mucosal infarction or chronic
ischemia, which results in fibrous stenosis. Transmural infarction may cause death
in 50 - 75% of patients.

Malabsorption Syndromes
Impaired digestion may be due to chronic pancreatitis or previous pancreatic
resection. Impaired absorption by the mucosa may be due to celiac disease, blind
loop syndrome, Crohn's disease, intestinal resection, tropical sprue, previous
radiation etc.

Ulcerative Colitis
This inflammatory disease of unknown etiology most commonly affects the sigmoid colon
and the rectum. It has a chronic relapsing nature with periods of remission.
Macroscopic appearance:
mucosal congestion and linear, continuous ulcers along the long axis of the
intestine
pseudopolyps, due to granulation tissue are common
Back wash ileitis: may cause ulceration in a small segment of terminal ileum.
Whether back wash ileitis really occurs in ulcerative colitis is disputed. Most
such cases are probably Crohn's disease.
Ulcerative colitis does not show skip lesions and will not cause inflammation of the full
thickness of the bowel wall unless toxic megacolon supervenes. Complications include
hemorrhage, malnutrition, perforation, toxic megacolon and malignancy in long standing
cases. Other manifestations include sacroiliitis, sclerosing cholangitis and erythema
nodosum.

Crohn's Disease (Regional Ileitis)


This is a chronic remitting and relapsing inflammatory process of unknown etiology.
It can affect the gastrointestinal tract from the mouth to the anus but most
commonly affects the ileum. Unlike UC by gross inspection, skip lesions are seen
(normal mucosa between affected areas). The so-called gross skip areas have
been shown to have changes in the neural plexuses and small blood vessels by
electron microscopy.
Macroscopic appearance:
single or multiple patchy penetrating ulcers
thickening of the bowel wall and fistula formation
Microscopic appearance:
ulceration and inflammation with skip areas
gland distortion, fissure and fibrosis, and granuloma formation
transmural inflammation
Local complications include stenosis and obstruction, perforation, fistulas to
adjacent organs. Anal tags are characteristic. Malabsorption may cause anemia
due to Fe, B12, or folic acid deficiency, or weight loss and hypoproteinemia. Other
manifestations include sacroiliitis, iritis and erythema nodosum.

Diverticular Disease
This is common and occurs particularly on the left. Complications include
diverticular abscess, fistula formation, strictures and hemorrhage.

Carcinoid Tumor
This is a malignant neuroendocrine tumor. It arises in amine secreting cells (neural
crest) and so can be found anywhere in the body, but is most often found in
appendix, ileum, stomach and colon. It secretes pressor amines, particularly
serotonin.

Tumors of Large Intestine


Nonneoplastic polyps
lymphoid
inflammatory
metaplastic
hamartomatous
Neoplastic polyps
tubular adenoma
tubulovillous adenoma
villous adenoma, also called papillary adenoma: polyps composed of
dysplastic epithelium which may develop into carcinomas. Polypectomy
may be adequate if the excision margin is > 2 mm and if the dysplasia is
not high grade.
Carcinoma of colon
adenocarcinoma
predisposing factors include certain neoplastic adenomatous polyps, and
ulcerative colitis
reduced fiber in a high fat diet
sites: rectum and rectosigmoid

Genetic Factors
Genetic evaluation has revealed a progression of genetic events in the
development of adenomas into carcinomas. Relevant genes include P53, Ras,
mismatch repair genes, APC and DCC genes. Two genetic syndromes are
associated with carcinoma of the colon, familial adenomatous polyposis coli and
the Lynch Syndrome (hereditary nonpolyposis coli).

Staging and Prognosis


Dukes' staging of colonic carcinoma:
A: confined to bowel wall, not involving the serosa 80% 5 year survival
B: invades bowel wall and involves serosa 50% 5 year survival
C: involves lymph nodes 25% 5 year survival
TNM staging is also used.

Appendix
Acute appendicitis. Acute inflammatory cells are present within the wall. It may
suppurate and lead to general peritonitis, abscess formation and adhesions.
Carcinoid tumor, sometimes an incidental finding in acute appendicitis, may be the
cause of the inflammation. A mucocele is a dilation of the appendix lumen by
mucinous secretions caused by mucosal hyperplasia, a mucinous cystadenoma or
a mucinous cystadenocarcinoma.

Liver Disease

Hepatitis, Alcohol, Cirrhosis

Hepatitis B virus is spread by blood. It has a relatively long incubation period. Liver
damage produces a variety of clinical syndromes: acute fulminating hepatitis, chronic
persistent hepatitis, chronic active hepatitis, cirrhosis, hepatocellular carcinoma. The
immunological response of the patient to the hepatitis B virus determines the severity and
chronicity of liver disease. Delta antigen is a defective RNA virus which only becomes
pathogenic in the presence of hepatitis B virus. It aggravates the consequences of
hepatitis B virus infection. Hepatitis C virus causes chronic liver disease and is spread by
blood. It is more indolent than hepatitis B infection, but has a risk of development of
cirrhosis and hepatocellular carcinoma.
Alcohol causes acute hepatocyte necrosis or chronic liver disease culminating in
cirrhosis. Always do LFTs and a coagulation screen before operating on these patients.
Chronic hepatitis results from a variety of agents: hepatitis B virus, hepatitis C virus, delta
antigen, alcohol, autoimmune processes, drugs, hemochromatosis and Wilson's disease.
Cirrhosis represents the end stage of chronic hepatitis and is characterized by nodules of
regenerating hepatocytes surrounded by bands of fibrosis, resulting in characteristic
fibrotic bands.

Liver Tumors
Benign tumors are usually asymptomatic but may occasionally cause
hemoperitoneum due to spontaneous rupture.
Secondary tumors (metastases) are the most common malignant liver tumors,
and the most usual primary sites are, in order, gastroinestinal tract, lung and
breast.
Hepatocellular carcinoma. Etiological agents include aflatoxins, hepatitis B
virus and hepatitis C virus. It may be single or multiple, and metastasizes late.
In 30% of cases, serum alpha fetoprotein is elevated. It may be difficult to
distinguish from metastatic adenocarcinoma on liver biopsy. Primary
hepatocellular carcinoma does not secrete mucin so the presence of mucin
indicates a metastasis or a primary cholangiocarcinoma.
Cholangiocarcinoma arises from bile duct epithelium. It may be difficult to
differentiate histologically from metastatic adenocarcinoma as both may show
the presence of mucin. There is no specific tumor marker.

Angiosarcoma is a malignant tumor arising from sinusoidal endothelium.


Etiological agents include vinyl chloride and Thorotrast. It is aggressively
malignant.
Hepatoblastoma is rare and usually occurs in children under 5. The prognosis
is poor.

Gallstones

Risk factors are: female, diabetes mellitus and obesity. Three types of gallstones are found:
pure cholesterol stones, pure bile pigment stones, or a mixture. Cholesterol gallstones occur
when there is an imbalance between the ratio of cholesterol and bile salts in the bile. Pigment
stones arise from infection or pigment overload. Complications include cholecystitis
(inflammation of the gallbladder), obstruction of the biliary tract resulting in jaundice,
empyema of the gallbladder, mucocele, cholangitis, pancreatitis and carcinoma of the
gallbladder.

Pancreatic Disease

Acute pancreatitis may be life threatening. The commonest causes include gallstones and
excess alcohol, and it may arise in shock (not common) (the pancreas is supplied by end
arteries). It is associated with elevated serum amylase. Chronic pancreatitis is also related to
excess alcohol intake and gallstones and is difficult to distinguish from carcinoma of the
pancreas.

Carcinoma of the pancreas is an adenocarcinoma arising from duct epithelium. The etiology
is unknown. Presentation is generally late with obstructive jaundice if the tumor is in the head
of the pancreas. Some cases develop thrombophlebitis migrans (Trousseau's sign). The
diagnosis is often only made at laparotomy and the prognosis is extremely poor.

Investigations

Radiological Imaging
Abdominal Trauma
Abdominal Pain
Chronic Abdominal Pain
Abdominal Masses
Intestinal Obstruction
Peritonitis/Abscesses
GI Hemorrhage
Abdominal Hernias

Abdominal Fistulas

Radiological Imaging

Abdominal Trauma
In cases of abdominal trauma, close correlation with the history and examination is
required to best select the most appropriate radiological investigation. Imaging modalities
available include:

Plain film
Contrast studies
Ultrasound
CT
Penetrating Injury
Plain film of the abdomen and erect chest x-ray may show evidence of free air.

Contrast studies: A nonionic low osmolar contrast agent may be used to demonstrate
a leak from the esophagus, stomach, duodenum, rectum or bladder.
Ultrasound may be used to look for free fluid or a solid organ laceration. Overall
sensitivity is low and ultrasound is not the first line investigation of choice. It is highly
dependent on experience of ultrasonographer.
CT is used in all cases of major trauma. It is fast, accurate and more sensitive than
US in detecting free fluid and visceral lacerations.
Blunt Trauma
Plain film is rarely of use in the acute setting. It may demonstrate free air, particularly
in cases of a ruptured duodenum following an auto accident. In addition, the bones
may be evaluated, for example, the vertebrae following a fall from a height and the
pelvis following an auto accident or fall.
CT has largely replaced diagnostic peritoneal lavage (DPL) in cases of major trauma.
CT is of great value particularly if the abdomen cannot be examined in an
unconscious patient. Free air can be detected with greater accuracy than on plain
film. Visceral laceration can be clearly seen if intravenous contrast is administered
during a dynamic study.

Abdominal Pain
Acute Abdominal Pain
A good history and examination are essential to guide the radiological investigation, given the
diversity of causes. A modality based table is probably the best approach to adopt to cover
such a widespread list.
Plain Film of the Abdomen (PFA):
Renal colic: 90% of renal stones are radiopaque.
Only 10% of gallstones are radiopaque. The presence of gallstones does not
automatically imply that the cause of the pain is related to gallstones.
The presence of a fecolith in the setting of right lower quadrant pain is highly suggestive
of appendicitis.
Free air, implying perforation, may be seen. Dilated loops of bowel indicative of
obstruction may also be seen.

IVU:
This is useful in renal or ureteric colic and was previously considered the gold standard
investigation. Noncontrast CT has now taken over this role.

Contrast:
Contrast studies of the GI tract are used to demonstrate the site and possible cause of
obstruction. They are also useful in the diagnosis of volvulus and inflammatory bowel
disease.

US:
This is the investigation of choice for the biliary tree. It can also detect renal calculi but is of
limited use in the detection of ureteric calculi. In this case, an obstructing calculus will cause
hydronephrosis which can best be seen on US. US has a limited role in diagnosing
appendicitis and diverticular abscess.

CT:
This is the single most useful study in the investigation of acute abdominal pain. It is by far

the best modality for diagnosing inflammatory causes of abdominal pain. It is also useful in
diagnosing the site and cause of obstruction. Free air, tumors, hernia and inflammatory
bowel disease can all be seen well on CT.

An algorithm for a disease-based approach to imaging is given below.


Inflammation

CT for all causes


Barium studies for IBD

Perforation

Plain Film of Abdomen (PFA) and

erect CXR
Contrast studies
CT
Obstruction

PFA
Contrast studies
CT

Colic

PFA
IVU for ureteric now replaced by
CT
US for biliary

Infarction

CT
Angiography
MR Angiography

Chronic Abdominal Pain


The role of imaging in chronic abdominal pain is more limited. The radiological
investigation needs to be tailored to the suspected pathology.
Chronic pancreatitis: Specks of calcification may be seen on the PFA in the
region of the pancreas. US may also demonstrate calcification. CT shows a
shrunken gland with punctate calcification.

Mesenteric ischemia: This is an uncommon cause of postprandial pain in the


aging population. Diagnosis is made on either conventional or MR angio.

Chronic ulceration: This is best seen on a barium meal. Out pouchings of


barium must be seen in two planes to be diagnostic. A scarred and contracted
duodenal cap is seen in long-standing cases. Ulcers seen beyond the first part
of the duodenum are suggestive of Zollinger-Ellison syndrome.

Other unsuspected causes of chronic abdominal pain may be picked up by CT.


Such causes include lymphoma, and retroperitoneal sarcoma. Radiology has a
role in surveillance of known diseases of the abdomen such as inflammatory bowel
disease or malabsorption syndromes although this role is limited.

Abdominal Masses
The history and examination are again important in this area. The appropriate radiological
examination will depend on whether the mass is clinically apparent or if surveillance of
known disease is required. In addition, as imaging improves, smaller lesions are being
detected, which are increasingly difficult to characterize. Plain film has little role in the
detection and follow up of abdominal masses. Secondary signs such as obliteration of
normal fat lines may be seen. An organ-based approach is the best way to cover the imaging

of abdominal masses.
Liver
US is excellent in differentiating solid from cystic lesions.

CT has a greater sensitivity for detecting liver lesions especially following intravenous
contrast. Lesions as small as a few mm can be detected. CT cannot however,
differentiate between solid and cystic lesions. Triphasic spiral CT scanning or CT
arterioportography are the best ways to assess liver metastases prior to surgery.

MRI, using many sequences, can further characterize many but not all lesions. Those
which remain uncharacterized must be either biopsied or followed radiologically,
whichever is deemed most clinically appropriate.
Renal
IVU may demonstrate a space occupying lesion but cannot completely characterize the
lesion.
US is the modality of choice to differentiate solid from cystic lesions. It can also
differentiate a simple cyst from a complex cyst.

CT with precontrast, postcontrast and delayed images is the single most useful
examination in characterizing renal masses. Both benign lesions such as an
angiomyolipoma, and malignant lesions can be characterized by CT.

MR is seldom required in the evaluation of renal masses.


Spleen
US and CT are the most useful modalities in the assessment of splenic masses. Simple
splenic cysts can be diagnosed confidently on US. Solid splenic lesions are more likely to be
malignant, either metastases or lymphoma. Assessment by CT may demonstrate either a
primary site or other features of lymphoma.

Pancreas
US may not be able to visualize a pancreatic mass well due to patient obesity and the
depth of the gland.
CT is the modality of choice for investigating pancreatic masses. Good detail is obtained
and the difference between tumor and pancreatitis is usually apparent. CT scanning of
pancreatic masses should use a "pancreatic protocol" with very thin (1mm) sections.

Adrenal
Adrenal masses have been discussed elsewhere.
GIT (Gastrointestinal Tract)
GIT masses may be evaluated by a combination of barium studies and CT. Benign GI
masses such as a leiomyoma may grow to a very large size before detection.

Bladder
Bladder masses are best evaluated by US. CT is useful to determine the extent of disease
and to look for any local or distant metastases.
Prostate
Prostate masses are best seen on transrectal US. Most tumors occur in the peripheral lobe

of the gland and can be biopsied under US guidance. Again, CT is useful to assess any local
or distant spread. MRI plays an increasingly important role in evaluating prostatic carcinoma.

Ovary/Uterus
Gynecological masses are best evaluated by transvaginal US. This gives the clearest
indication of the origin of the mass which is not always possible on CT. Tubo-ovarian
abscesses may be drained by the transvaginal route. MRI is being used more commonly to
evaluate uterine fibroids especially in follow up cases of fibroid embolization.
Soft tissue; Retroperitoneal; Intraperitoneal
This miscellaneous group is best evaluated by either CT or MRI, the modality of choice being
very much dependent on the clinical situation.

Intestinal Obstruction
The three most important things to remember when dealing with suspected
obstruction are the level, the cause and the site(intraluminal, within the wall or
extraluminal). The three main levels are stomach, small bowel and large bowel.
Stomach
PFA: This may show a dilated gastric air bubble. There may be a paucity of
bowel gas elsewhere.

Contrast study: A dilated contrast filled stomach with little or no emptying is


seen.

Small Bowel

PFA: Dilated loops of small bowel with normal large bowel caliber. The
differentiation between small and large bowel may be made by:
location of the loops(central in SBO)

caliber of the dilated loops


presence of plicae circulares

Contrast: contrast studies will show dilated loops of small bowel proximally with
a transition zone to normal caliber bowel at the point of obstruction. There may
also be an indication as to the cause of the obstruction with the characteristic
appearances of tumor, infarction or intramural hematoma.

CT: Appearances are similar to the contrast studies. Dilated loops of bowel with
a transition zone are seen. The cause may also be demonstrated.
Large Bowel
PFA: The plain film will show dilated loops of large bowel. If the ileocecal valve
is competent then the small bowel will not be dilated. More commonly, however,
the valve is incompetent and the small bowel is also dilated. This appearance
must be differentiated from paralytic ileus. Thumbprinting, which represents
mucosal edema and indicates colitis, may sometimes be seen.

Contrast passed per rectum may delineate a point of obstruction. This is


particularly useful in cases of sigmoid volvulus.

CT may demonstrate the site and cause of colonic obstruction.

Peritonitis/Abscesses
Plain film may very occasionally demonstrate a mottled gas pattern in an unusual
location indicating an abscess. This may be associated with a localized ileus. CT is the
investigation of choice for detecting an intra-abdominal abscess. Abnormal soft tissue
density with extraluminal air are the key signs.There may also be evidence of the
underlying cause. US is occasionally used in ICU patients. A negative US however, does
not exclude an abscess and a CT will be required.

GI Hemorrhage

There are many causes of GI hemorrhage. If the cause is not apparent on EGD or
colonoscopy then barium studies are rarely useful. There are two radiological
approaches: angiography and nuclear medicine scanning.
Angiography is invasive and carries all the associated risks of an interventional
procedure. One advantage is that should an actively bleeding lesion be found, then
a therapeutic option may be taken simultaneously to embolize the bleeding vessel.

Nuclear medicine scanning involves labeling RBC's with a radioisotope and


injecting this back into the patient. This is more sensitive than angiography and has
the added advantage that the patient does not necessarily need to be actively
bleeding at the time of the examination. However, it is relatively poor at localizing
the exact point of bleeding.

Abdominal Hernias
Imaging is of less importance than an accurate history and examination in the
diagnosis of hernias. However, it can be useful in uncertain cases.
CXR: A hiatus hernia may frequently be seen as an air-fluid level behind the
heart.

PFA: An inguinal hernia may be seen on a plain film if bowel loops are seen
below the pubic ramus.

Barium: Barium studies may be useful to confirm hiatal hernias and inguinal
hernias.

CT: May demonstrate hiatal, inguinal, incisional, obturator and spigelian


hernias.

Abdominal Fistulas
Imaging may demonstrate fistulas extremely well but the sensitivity is poor. As a
result, examinations are often performed looking for fistulas but are rarely
conclusive.
Common causes include:
Crohn's disease
Radiation therapy
Tumor
Diverticulitis

Fistulas may occur anywhere but are most common in the pelvis, following surgery
and radiotherapy for gynecological malignancy.
Common types include:
Vesicovaginal
Colovesical

Enterocolic
Enteroenteric
Enterocutaneous

Plain film may show air in an abnormal location, for example in the bladder.
Contrast studies are rarely positive. A vesicovaginal fistula may be seen on a
micturating cysto urethrogram. Fistulas may be seen on CT either with or without
oral contrast. However, they are often undetected.

Surgical Techniques

Femoral Hernia Repair


Open Inguinal Hernia Repair
Laparoscopic Inguinal Hernia Repair Preperitoneal
Closure of an Ileostomy or Colostomy
Laparotomy for Abdominal Trauma
Laparotomy for a Bleeding Peptic Ulcer
Laparotomy for Intestinal Obstruction

Femoral Hernia Repair


Anesthesia: General. Local or spinal may be used.
Position: Supine
Incisions:
Low approach is suitable for reducible 'elective' hernias; oblique skin crease over
the femoral canal just distal to the inguinal ligament.
McEvedy approach allows access above and below the inguinal ligament in
'complicated' hernias; vertical oblique above the medial end of the inguinal ligament.
The anterior rectus sheath is incised upwards and the rectus muscle is retracted
medially. This allows preperitoneal access to the femoral ring and neck of the

hernia. The peritoneum can also be opened should gangrenous bowel need
resection.

Inguinal approach is as for an inguinal hernia repair with access to the femoral ring
preperitoneally and through the back wall of the inguinal canal.
Procedure:
USING THE LOW APPROACH
The wound is deepened through the layers of connective tissue and fat around the
hernia sac
The inguinal ligament is exposed and the neck of the hernia at the femoral ring is
cleared

The femoral sac is opened and the contents are inspected and reduced if viable
If it is difficult to reduce the contents through the neck of the sac, the femoral ring
may be widened by passing a finger up through the ring outside the sac
If nonviable omentum is encountered this is excised. Should nonviable bowel be
seen, it is safest to perform a short lower abdominal incision to effect control and
bowel resection.
The empty hernial sac is transfixed, excised and the neck reduced, so displaying
the margins of the femoral ring
The femoral ring is closed using two or three interrupted nonabsorbable sutures on
a j-needle placed from the pectineal ligament to the inguinal ligament. Care must be
taken not to catch or occlude the femoral vein lying lateral to the canal.

FOR APPROACHES ABOVE THE INGUINAL LIGAMENT


The femoral canal is closed similarly by approximating the inguinal ligament to the
pectineal ligament from above

Closure and Drainage: In layers with the option of a closed suction drain.
Main Postoperative Complications: Hematoma formation and recurrence, which is
unusual.

Open Inguinal Hernia Repair


Anesthesia: General, spinal or local
Position: Supine
Incision: It is made 2 cm above and parallel to the medial half of the inguinal
ligament.
Procedure:
The wound is deepened to the external oblique aponeurosis and the
inguinal ligament is exposed.
The inguinal canal is entered 1 cm above the ligament by dividing the
aponeurosis along its length. The ilioinguinal nerve is carefully identified
and protected

The spermatic cord is mobilized off the inguinal ligament and the
posterior wall. If it is now evident that a direct hernia is present, it is
reduced and may be held in position with an absorbable suture. It is not
opened.

Otherwise, the spermatic fascia and cremaster is incised longitudinally to


enter the cord.

Here an indirect sac will be identified by separating the cord structures.


The sac is then dissected from the cord to the level of the internal ring. (If
the sac runs into the scrotum, it may be divided and any distal sac left in
place.
The indirect sac is opened and any contents reduced back into the
abdomen.
The neck of the sac is transfixed and the sac excised.
Many repairs of the posterior wall of the inguinal canal have been
described. The repair with arguably the best results is the Lichtenstein
repair:
A piece of synthetic (e.g. polypropylene) mesh is trimmed to size and
sutured without tension from the pubic tubercle along the inguinal
ligament below, to the internal oblique aponeurosis above, using
nonabsorbable sutures. The lateral limit of the mesh encircles the cord at
the internal ring.

Closure and Drainage: In layers. Drains are rarely necessary.


Main Postoperative Complications: Wound hematoma and infection. Later on
are ilioinguinal neuropathy due to damage, and hernia recurrence.

Related Operations:
The preperitoneal laparoscopic approach is particularly suitable for 1) bilateral
hernia repairs, because both sides can be repaired through the same ports, and 2)
when recurrence occurs after open hernia repairs.

Laparoscopic Inguinal Hernia Repair Preperitoneal


This is not suitable if there have been previous lower abdominal incisions.
Anesthesia: General
Position: Supine, with arms by patient's sides
Incision and Approach:
A 2 cm transverse incision is made lateral to the lower part of the umbilicus on the
side of the hernia. The anterior rectus sheath is opened transversely and the rectus
muscle is retracted laterally. The operator's finger is passed into and sweeps open
the space behind the rectus muscle.

This space and the retropubic space may be further opened by inflating a balloon
a number of commercial balloons are available for this purpose.

A 10 mm blunt port, with an air-tight seal, is now inserted into the wound and the
space is inflated with carbon dioxide at 15 mmHg. The laparoscope with camera is
then inserted through this port.

Under direct vision two further ports, a 10 mm and a 5mm, are inserted in the
midline into the new preperitoneal space for instumentation.
Procedure:
The peritoneum is separated from the abdominal wall behind the inguinal area,
laterally to the anterior superior iliac spine and medially across the midline.
The inferior epigastric vessels are identified and left attached to the back of the
abdominal wall. A direct sac lies medial to these vessels and is easily withdrawn into
the abdomen.
To find an indirect sac, the cord is first identified lateral to these vessels. When the
outer layer of the cord is separated, the sac will be seen and withdrawn into the
abdomen separating it from the vas and testicular vessels.

A 15 cm x 10 cm polypropylene mesh is then placed over the inguinal area running from
lateral to and covering the deep inguinal ring, and extending across the midline. Metal
tacks can be placed medially to hold it in place.

When the position of the mesh is satisfactory the gas is allowed to vent and the
peritoneum is seen to obliterate the preperitoneal space and secure the mesh
position.

Closure: The ports are withdrawn and the skin is closed.

Main Postoperative Complication: Recurrence

Closure of an Ileostomy or Colostomy


The procedure will depend on whether the closure is for an 'end' or 'loop' ileostomy or
colostomy. An 'end' ileostomy may be taken down or closed, for example, to form an ileal
pouch for a pouch-anal anastomosis. After a Hartmanns procedure, an 'end' colostomy may
be taken down to reanastomose to the rectal stump. We describe here the closure of a 'loop'
stoma, the procedure being similar for either an ileostomy or colostomy.
Postoperative Complications:
Prophylactic antibiotics
Bowel preparation for colostomy (further details are available in The Gastrointestinal
Tract Back to Basics). Fasting for 8-10 hours for an ileostomy.
Anesthesia: General
Incision: After placing four stay sutures at each quadrant to elevate the stoma, an incision is
made in the skin, using a scalpel or cutting diathermy, around and close to the
mucocutaneous junction of the stoma.
Procedure:
Scissors or diathermy dissection is continued through subcutaneous tissues in close
proximity to the bowel wall.

It is important not to injure the intestine or interfere with its vasculature during this
dissection.
The muscular and aponeurotic layers of the abdominal wall are sharply dissected
from around the intestine to allow entry into the peritoneal cavity and to achieve an
intraperitoneal closure.
The dissection continues until the intestine is freely mobile without tethering.
There are a number of techniques to effect intestinal continuity including formal
resection of the stoma ends and reanastomosis, by sutures or stapling.
Most commonly, as shown here, the skin is trimmed from the stoma and, in the case
of an ileostomy, the spout can be reduced with ease. The bowel opening can then
be closed transversely, to avoid narrowing, with synthetic absorbable sutures.

Once continuity is established, the intestine is returned to the peritoneal cavity.

Closure and Drainage: The muscular and aponeurotic layers of the abdominal wall are
closed with interrupted absorbable sutures. The skin and subcutaneous tissue may be left to
heal by secondary intention by leaving a dressing of betadine soaked gauze in situ, or closed
without tension over a small corrugated drain.
Main Postoperative Complications: Subacute intestinal obstruction and wound infection.

Laparotomy for Abdominal Trauma


Preoperative Preparation:

Diagnostic peritoneal lavage or CT scan with contrast


Antibiotics, urinary catheterization and an insulation blanket to counter
hypothermia
Transfusion with blood or fluids as required
Anesthesia: General with endotracheal intubation
Position: Supine
Technique: Middle midline with an option of extending in either direction
Procedure:
Suction of intraperitioneal blood and fluids using two suckers if necessary.
Blood clots are scooped out using large packs.
Identify any bleeding sources and control the hemorrhage using variety of
maneuvers including pressure, packing, arterial forceps or oversewing.
Life-threatening exsanguination may require opening the chest and
crossclamping of the aorta.
A retroperitoneal hematoma associated with pelvic fractures should be
left alone as exploration may lead to uncontrollable hemorrhage.
HOLLOW ORGANS
Identify and repair damaged hollow viscera and resect nonviable
intestine.
Examine both surfaces of the stomach and mobilize the duodenum if you
suspect a duodenal or pancreatic injury.
Defunctioning stomas should be used if there is gross contamination,
impaired healing and especially if the large bowel is injured.
Bladder and ureteric tears can be repaired followed by drainage using
urethral or suprapubic catheters or double-J stents..
Catheterization is avoided if a urethral tear is suspected and this may
complete the tear. This requires specific assessment and treatment.
SOLID ORGANS
For liver injury, substantial hemorrhage may require Pringle's maneuver
placing a soft clamp over the free edge of lesser omentum. Continued
bleeding after clamping suggests hepatic vein or IVC tears. Packing with
gauze swabs is the cornerstone of treatment in this situation and
resection should not be attempted except in certain circumstances. Packs
can be removed at relaparotomy after 24-48 hours.
For splenic injury, splenectomy is the safest option although preservation
can be achieved in some cases.
For renal injury, a pre or perioperative Intravenous urogram is helpful.
Blunt injuries can usually be treated conservatively but severe damage
requires either partial or complete nephrectomy. Remember to check that

the other side is functioning before resection.


Closure and Drainage: As required. In severe contamination, wound may be left
open.

Laparotomy for a Bleeding Peptic Ulcer


Preoperative Preparation:
Appropriate resuscitation with intravenous fluids and blood transfusion.
Central venous line to monitor the volume replacement.
Replenish clotting factors and platelets if a large volume of blood needs to be
given.
Endoscopy to identify bleeding source and to try to control the bleeding with an
injection of an adrenalin solution.
Pass a nasogastric tube and urinary catheter.
Anesthesia: General with an endotracheal tube
Incision: Upper midline
Procedure:
Full laparotomy inspection including opening of the lesser sac to examine the
posterior surface of stomach.
The duodenum is checked for scarring and surface petechiae indicating active
ulcer disease.
If the source of the bleeding is uncertain at endoscopy, two stay sutures are
placed on the stomach proximal to the pylorus.

An anterior gastrotomy incision is made and the opening is held apart with
Babcock forceps.
Blood and clots are sucked and scooped out and an assessment is made as to
whether the bleeding is coming from the stomach or duodenum.
STOMACH ULCER
Extend the incision toward the body of the stomach.
Identify and under run the bleeding ulcer with nonabsorbable sutures until the
hemorrhage is fully controlled.
Close the gastrotomy with a continuous absorbable suture. Alternative options
include local resection plus vagotomy and drainage or, in a fit patient, a partial
gastrectomy, but these are rarely indicated.
If malignancy is suspected, it can be confirmed by frozen section biopsy, and a
gastectomy may be performed provided the patient is fit.
DUODENAL ULCER
Continue the gastrotomy incision across the pylorus extending to the first part of
the duodenum.
The ulcer crater is displayed, which normally is located on the posterior wall,
and under run with nonabsorbable sutures until the hemorrhage is controlled,
being mindful of the posterior proximity of the common bile duct.

An antral specimen should be taken for assessment of the Helicobacter pylori


status.
The pyloric incision is then closed transversely with interrupted absorbable
sutures.
Further definitve ulcer surgery in the form of vagotomy or antrectomy is not now
necessary with current ulcer medication
Closure and Drainage: Routine. Drains are not usually required.
Postoperative Management
Maintain a full course of antiulcer medication and eradicate helicobactor pylori
infection.
Remove ulcer promoting factors.
Main Postoperative Complications: Rebleeding and ulcer recurrence.

Laparotomy for Intestinal Obstruction


Further details are available in Surgical Technique and Technology.
Preoperative Preparation: Nasogastric intubation, fluid replacement, catheterization and
antibiotic and DVT prophylaxis
Anesthesia: General
Position: Supine
Incision: Long midline. The peritoneum is picked up and incised taking with care not to injure
underlying adherent or distended bowel.
Procedure:
The bowel is gently followed until the junction between obstructed and collapsed bowel is
reached.

In the small intestine the usual causes are adhesions and hernias. Adhesions
should be divided by sharp dissection (not diathermy) and the bowel viability
assessed.

Before bowel that is trapped in a hernia sac is released, place a noncrushing clamp
proximal to the obstruction to prevent inadvertent spillage.
Large bowel obstruction is usually due to carcinoma. In the right colon and transverse
colon it is appropriate to perform a right hemicolectomy and primary anastomosis. In the
left colon and rectum it may be treated safely with a Hartmann's operation - resection
followed by an end colostomy and rectal stump closure.

An alternative is on-table colonic irrigation followed by an anastomosis

Before closure, the proximal distended bowel should be emptied by gentle milking,
in a retrograde fashion, back into the stomach which is aspirated with a wide-bore
nasogastric tube.
Closure and Drainage: In layers; drains if indicated

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