Gastrointestinal and Abdominal: Liver Flashcards
Liver: Anatomy and Physiology
The liver is located in the right upper quadrant of the
abdomen and is bounded superiorly and posteriorly by
the diaphragm, laterally by the ribs, and inferiorly by
the gallbladder, stomach, duodenum, colon, kidney,
and right adrenal. It is covered by Glisson capsule and
peritoneum. The right and left lobes of the liver are
defined by the plane formed by the gallbladder fossa
and the inferior vena cava. The falciform ligament
between the liver and diaphragm is a landmark
between the lateral and medial segments of the left
lobe. The coronary ligaments continue laterally from
the falciform and end at the right and left triangular
ligaments. These ligaments define the bare area of
the liver, an area devoid of peritoneum. The liver
parenchyma is divided into eight segments on the basis
of arterial and venous anatomy (see Color Plate 5).
Segment 1 is also known as the caudate lobe. It is not
visible from the ventral surface of the liver, being
tucked behind segment 4. The caudate is juxtaposed to
the inferior vena cava and has venous branches that
drain directly into the cava. These branches are quite
fragile and must be carefully controlled if resection of
the caudate is required. Segments 2, 3, and 4 form the
left lobe of the liver, whereas segments 5, 6, 7, and 8
comprise the right lobe. Segment 4 may be divided
into cranial segment 4a and caudal segment 4b.
Liver: Anatomy and Physiology: Part 2
The hepatic circulation is based on a portal circu-
lation that provides the liver with first access to all
intestinal venous flow. Seventy-five percent of total
hepatic blood flow is derived from the portal vein,
which is formed from the confluence of the splenic
and superior mesenteric veins. The remaining blood
supply comes from the hepatic artery via the celiac
axis. The right hepatic artery arises from the superior
mesenteric artery in 15% of patients. When this
occurs,
the artery will run posterior to the bile duct on the
right side of the hilum, and it is termed a replaced
right hepatic artery. The left hepatic artery arises
from the left gastric in 15% of patients, called a
replaced left hepatic artery. In this instance, the artery
will run in the cranial portion of the gastrohepatic lig-
ament. Other arterial variants include a completely
replaced hepatic artery, which arises from the supe-
rior mesenteric artery, and a middle hepatic artery,
which occurs when the segment 4 branch arises in
the hilum. Blood leaving the liver enters the inferior
vena cava via the right, middle, and left hepatic veins.
Often there is an accessory right hepatic vein that
leaves the liver caudad to the principle right hepatic
vein. This vein must be controlled separately during
right hepatic lobectomy.
Liver: Anatomy and Physiology: Part 3
The hepatic hilum can be palpated by placing a
finger through the foramen of Winslow (epiploic
foramen) into the lesser sac (Fig. 6-1). This is an
important maneuver because it provides control of
the hepatic hilum (hepatoduodenal ligament), within
which runs the hepatic artery, portal vein, and bile
duct. A Pringle maneuver, which involves placing a
clamp on the hilum, disrupts most blood flow to the
liver and can greatly reduce bleeding during liver
resection (Fig. 6-2). This maneuver also makes the
liver ischemic and can cause arterial thrombosis. As
a result, it should be used for a limited amount of
time and only when necessary.
Liver: Anatomy and Physiology: Part 4
The liver is the site of many critical events in energy
metabolism and protein synthesis. Glucose is taken up
and stored as glycogen, and glycogen is broken down, as
necessary, to maintain a relatively constant level of
serum glucose. The liver is able to initiate gluconeogen-
esis during stress, and the liver can oxidize fatty acids to
ketones, which the brain can use as an energy source.
Proteins synthesized in the liver include the coagulation
factors fibrinogen, prothrombin, prekallikrein, high-
molecular-weight kininogen, and factors V, VII, VIII,
IX, X, XI, and XII. Of these, prothrombin and factors
VII, IX, and X are dependent on vitamin K. The anti-
coagulant warfarin (Coumadin) affects these vitamin
K–dependent pathways, resulting in an increased pro-
thrombin time. Albumin and alpha globulin are
pro-
duced solely in the liver.
Liver: Anatomy and Physiology: Part 5
The digestive functions of the liver include bile
synthesis and cholesterol metabolism. Heme is used
to form bilirubin, which is excreted in the bile after
conjugation with glycine or taurine. Bile emulsifies
fats to aid their digestion and plays a role in vitamin
uptake. Bile salts excreted into the intestine are reab-
sorbed into the portal circulation. This cycle of bile
excretion and absorption is termed the enterohepatic
circulation. Total body bile circulates approximately
10 times per day in this loop. More than 95% of
excreted bile is reabsorbed, and the remainder must
be resynthesized. The rate-limiting step of cholesterol
synthesis involving the enzyme 3-hydroxy-3-methyl-
glutaryl–coenzyme A reductase occurs in the liver, as
does cholesterol metabolism to bile salts.
Detoxification occurs in the liver through two path-
ways. Phase I reactions involve cytochrome P450 and
include oxidation, reduction, and hydrolysis. Phase II
reactions consist of conjugation. These reactions are
critical to destruction or renal clearance of toxins. The
dosing of all oral drugs is determined only after con-
sidering the first-pass effect of the drug through the
liver. The initial hydroxylation of vitamin D occurs
in the liver. Immunologic functions are mediated by
Kupffer cells, the resident liver macrophages.
Benign Liver Tumors: Pathology
Benign liver tumors include hepatocellular adenoma
(see Color Plate 6), focal nodular hyperplasia,
hemangioma, and lipoma. Hemangiomas are catego-
rized into capillary and cavernous types, the former
being of no clinical consequence and the latter capa-
ble of attaining large size and rupturing.
Benign Liver Tumors: Epidemiology
Only 5% of liver tumors are benign, with hemangioma
being the most common. Approximately 7% of people
have a cavernous hemangioma at autopsy. The inci-
dence of adenoma is one per million in women with-
out a history of oral contraceptive use. These medicines
increase the risk by a factor of 40. This lesion most
commonly occurs in women between 30 and 50 years
of age. Adenoma and focal nodular hyperplasia are five
times more common in female patients.
Benign Liver Tumors: History
Patients with adenomas and hemangiomas can be
asymptomatic or present with dull pain; rupture can
produce sudden onset of severe abdominal pain.
These lesions can also become large enough to cause
jaundice or symptoms of gastric outlet obstruction,
including nausea and vomiting. Focal nodular hyper-
plasia is rarely symptomatic.
Benign Liver Tumors: Physical Examination
Large lesions can be palpated. Jaundice may occur in
patients if the tumor causes bile duct obstruction.
Benign Liver Tumors: Diagnostic Evaluation
These lesions are most often found incidentally at
laparotomy or on imaging studies requested for other
reasons. Laboratory evaluation is often unremarkable,
although hemorrhage in an adenoma can lead to
hepatocellular necrosis and a subsequent increase in
transaminase levels. Hemangioma can cause a con-
sumptive coagulopathy. Ultrasound differentiates cystic
from solid lesions. Triple-phase computed tomography
(CT) is the best study for distinguishing between vari-
ous types of benign and malignant lesions, but in certain
cases, this determination is not possible. Adenomas are
typically low-density lesions; focal nodular hyperplasias
may appear with a filling defect or central scar, whereas
hemangiomas have early peripheral enhancement after
contrast administration. Hemangiomas should not be
biopsied because of the risk of bleeding.
Benign Liver Tumors: Treatment
Patients with adenoma who are using oral contracep-
tives should stop. If the lesion does not regress, resec-
tion should be considered in otherwise healthy indi-
viduals because of the risk of malignant degeneration
or hemorrhage. Relative contraindications to resec-
tion include a tumor that is technically difficult to
resect or tumors of large size in which a large portion
of the liver would need to be removed. Symptomatic
hemangiomas should be resected, if possible. Because
focal nodular hyperplasia is not malignant and rarely
causes symptoms, it should not be resected unless it
is found incidentally at laparotomy and is small and
peripheral enough to be wedged out easily.
Liver Cancer: Pathology
Liver cancers are hepatomas, also known as hepato-
cellular carcinoma, or metastases from other primar-
ies (see Color Plate 7).
Liver Cancer: Epidemiology
Ninety-five percent of liver tumors are malignant.
Hepatoma is one of the most common malignancies
in the world, but rates in the United States are rela-
tively low (approximately two per 100,000). It is
more common in male than in female patients.
Liver Cancer: Etiology
Cirrhosis is a predisposing factor to hepatoma; as such,
hepatitis B, the leading cause of cirrhosis, and alco-
holism are associated with hepatoma development.
Fungal-derived aflatoxins have been implicated as
causes of hepatoma, as have hemochromatosis, smok-
ing, vinyl chloride, and oral contraceptives.
Liver Cancer: History
Patients with hepatoma may complain of weight loss,
right upper quadrant or shoulder pain, and weakness.
Hepatic metastases are often indistinguishable from
primary hepatocellular carcinoma.
Liver Cancer: Diagnostic Evaluation
Laboratory examination may reveal abnormal liver
function tests.
-Fetoprotein is a specific marker for
hepatoma but can also be elevated in embryonic
tumors. Radiographic studies are used to differentiate
benign and malignant lesions. Ultrasonography can
distinguish cystic from solid lesions, whereas CT or
magnetic resonance imaging can reveal multiple lesions
and clarify anatomic relationships (Fig. 6-3). They can
also demonstrate nodularity of the liver, hypersplenism,
and portal hypertension, indicative of underlying
liver
disease. Hepatic arteriography can diagnose a heman-
gioma. Because most cancers occur in the setting of
liver disease and cirrhosis, it is important to perform
viral studies for hepatitis.
Liver Cancer: Treatment
Before consideration of resection, the underlying
health of the liver should be assessed using the Child-
Turcotte-Pugh scoring system (Table 6-1). Patients
with Child class C disease will generally not tolerate
a resection; patients with Child class B disease may
tolerate a limited resection.
If the patient is a surgical candidate, treatment
involves resection of the tumor. Survival without treat-
ment averages 3 months; resection can extend survival
to 3 years, with a 5-year survival rate of 11% to 46%.
The decision to resect the tumor depends on comorbid
disease and the location and size of the tumor. When
possible, wedge resection should be performed, because
formal hepatic lobectomy does not provide any addi-
tional survival benefit. Patients with small tumors who
are not candidates for resection because of tumor loca-
tion or concomitant cirrhosis should be considered for
liver transplantation. Liver transplantation is becoming
an increasingly attractive option for these patients, pro-
viding good long-term survival. Patients who meet the
Milan criteria (tumor less than 5 cm or no more than three
tumors, the largest of which is less than 3 cm) will receive extra
points on the liver transplant list.
Metastatic disease occurs in decreasing frequency
from lung, colon, pancreas, breast, and stomach. When
colon cancer metastasizes to the liver, resection of up
to three lesions has been shown to improve survival
and should be attempted as long as the operative risk
is not prohibitive. In general, liver metastases from
other tumors should not be resected.
Liver Abscess: Epidemiology
Pyogenic abscesses are responsible for fewer than one
in 500 adult hospital admissions. Amebic abscesses
occur in 3% to 25% of patients with gastrointestinal
amebiasis (Fig. 6-4). Risk factors include HIV, alcohol
abuse, and foreign travel.
Echinococcus
is most com-
monly seen in Eastern Europe, Greece, South Africa,
South America, and Australia; although rare in the
United States, it is the most common cause of liver
abscesses worldwide (Fig. 6-5).
Portal Hypertension: Complications
Bleeding varices are a life-threatening complication of
portal hypertension. When portal pressures increase,
flow through the hemorrhoidal, umbilical, or coro-
nary veins becomes the low-resistance route for blood
flow. The coronary vein empties into the plexus of
veins draining the stomach and esophagus (Fig. 6-6).
Engorgement of these veins places the patient at risk
of bleeding into the esophagus or stomach.
Portal Hypertension: Treatment
Patients with portal hypertension are placed on beta-
blockers to decrease the risk of bleeding. Endoscopic
surveillance and banding are useful in preventing bleed-
ing episodes.
For patients with upper gastrointestinal bleeds, large-
bore intravenous lines and volume resuscitation should
be started immediately. A nasogastric tube should be
placed to confirm the diagnosis. If the patient cannot
be lavaged clear, suggesting active bleeding, emer-
gency endoscopy is both diagnostic and therapeutic.
Endoscopy is >90% effective in controlling acute bleed-
ing from esophageal varices. Should this fail, balloon
tamponade with a Sengstaken-Blakemore tube and
vasopressin infusion should be considered. Use of the
Sengstaken-Blakemore tube involves passing the gastric
balloon into the stomach, exerting gentle traction on
the tube, and then inflating the esophageal balloon to
tamponade bleeding. Although effective in stopping
life-threatening hemorrhage, the tube can produce gas-
tric and esophageal ischemia and must be used with
extreme caution. Transjugular intrahepatic portosys-
temic shunting has a high rate of success in controlling
acute bleeding and is usually preferred to an emergent
surgical shunt, although this is also an option (Fig. 6-7).
Approximately 40% of patients with varices will
develop a bleeding complication. Seventy percent of
patients with a first episode will rebleed. For this rea-
son, a definitive procedure should be considered after
the initial episode is controlled.
