UNIT 13
Alterations in Function of the
Hepatobiliary System and
Exocrine Pancreas
Originally developed by:
Anne Mueller RN, MN
Revised (1993) by:
Dot Hughes RN, Msc, PhD
Updated (2000) by:
Marlene Reimer RN, PhD, CNN (C)
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Unit 13 Table of Contents
Overview ...................................................................................................................... 3
Aim ............................................................................................................................. 3
Objectives .................................................................................................................. 3
Resources ................................................................................................................... 3
Web Links.................................................................................................................. 4
Section 1: Disorders of the Liver .............................................................................. 5
Learning Activity #1 ................................................................................................ 5
Section 2: Disorders of the Liver—Hepatitis ....................................................... 12
Introduction ............................................................................................................ 12
Learning Activity #2 .............................................................................................. 12
Section 3: Disorders of the Exocrine Pancreas..................................................... 14
Introduction ............................................................................................................ 14
Pathophysiology .................................................................................................... 15
Clinical Manifestations .......................................................................................... 17
Learning Activity #3 .............................................................................................. 18
Evaluation and Treatment .................................................................................... 19
Section 4: Disorders of the Gallbladder ............................................................... 22
Introduction ............................................................................................................ 22
Pathophysiology .................................................................................................... 23
Clinical Manifestations .......................................................................................... 25
Evaluation and Treatment .................................................................................... 26
Final Thoughts........................................................................................................... 30
References .................................................................................................................. 31
Glossary ...................................................................................................................... 32
Acronym List .............................................................................................................. 32
Checklist of Requirements...................................................................................... 32
Required Readings ................................................................................................. 32
Learning Activities ................................................................................................. 32
Answers to Learning Activities .............................................................................. 33
Answers to Learning Activity #2 ......................................................................... 33
Structure and Function of the Pancreas .............................................................. 33
Answers to Learning Activity #3 ......................................................................... 34
Answers—Surgical interventions in pancreatitis .............................................. 35
Disorders of the Gallbladder ................................................................................ 36
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
UNIT 13
Alterations in Function of the Hepatobiliary
System and Exocrine Pancreas
The hepatobiliary system may not seem like a very exciting topic, certainly
not as stimulating as cardiology or immunology. You may be approaching
this section with some dread; however, by the end of this unit you may think
differently.
The hepatobiliary system has a profound impact on our very existence.
Without an adequately functioning system we would be unable to process
and utilize nutrients provided through digestion, and would be unable to rid
ourselves of toxic materials. Dysfunction of the hepatobiliary system can lead
to a life of discomfort and restrictions, and may ultimately lead to death.
The hepatobiliary system is comprised of the “accessory organs of digestion.”
You will come to see shortly that these accessory organs are closely linked,
such that disease in one organ can have serious consequences on other
organs. Similarly, disease within one portion of the system can have serious
and sometimes fatal effects on the whole. The knowledge you will acquire in
this section about disorders of the liver, the pancreas and the gallbladder will
strengthen your assessment skills and aid in providing complete, competent
nursing care.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Overview
This unit contains three parts:
1. Disorders of the liver (cirrhosis, hepatitis).
2. Disorders of the exocrine pancreas.
3. Disorders of the gallbladder.
Aim
The general aim of this unit is to assist you in gaining an understanding of
how disorders of the hepatobiliary system and exocrine pancreas affect the
individual. By the end of this section you will appreciate the complexity of
the hepatobiliary system and its impact on total body functioning. You will
accomplish this by integrating knowledge of pathophysiology, clinical
manifestations and treatment regimes.
Objectives
Following the completion of this unit you will be able to:
1. Differentiate between different types of hepatitis.
2. Explain the mechanism behind the clinical manifestations of liver
disease.
3. Describe the clinical manifestations of acute pancreatitis.
4. Describe the pathogenesis of cholelithiasis and cholecystitis.
Resources
Required
Print Companion: Alterations in Function of the Hepatobiliary System and
Exocrine Pancreas
Haicken, B. (1991). Laser laparoscopic cholecystectomy in the
ambulatory setting. Journal of Post Anesthesia Nursing, 6(1), 33-39.
Porth, C. M. (2005). Pathophysiology: Concepts of Altered
Health States (7th ed). Philadelphia: Lippincott. Chapter 40
Peicher, A., & Schiff, E. R. (1988). Acute viral hepatitis. Hospital
Medicine, 24(6), 23-41.
Learning Activities
Activities for this unit include Learning Activities 1, 2, and 3.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Supplemental Materials
Supplemental materials include:
Ambrose, M.S. & Dreher, H.M. (1996). Pancreatitis: Managing a flareup. Nursing 96, 24 (4), 33-40.
Brown, A. (1991). Acute pancreatitis: Pathophysiology, nursing
diagnoses, and collaborative problems. Focus on Critical Care, 18 (2), 121-130.
Covington, H. (1993). Nursing care of patients with alcoholic liver
disease. Critical Care Nurse, 13 (3), 47-59.
Doherty, M.M. & Carver, D. (1993). Transjugular intrahepatic
portosystemic shunt: New relief for esophageal varices. American Journal of
Nursing, 93 (4), 58-63.
.
Web Links
All web links in this unit can be accessed through the Web CT system.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Section 1: Disorders of the Liver
In the unit dealing with disorders of the gastrointestinal system the
pathophysiology of specific units was examined by studying representative
diseases or disorders. The format used led you through an examination of the
disorder’s pathophysiology, clinical manifestations, and treatment. We will
depart from this format while examining liver disorders.
While there are numerous liver disorders, many of them share common
clinical manifestations. These include portal hypertension, ascites, esophageal
varices, hepatic encephalopathy, and jaundice. It is important therefore to
understand the underlying mechanisms of these manifestations so that you
will appreciate their impact on the patient regardless of their underlying
etiology.
Learning Activity #1
Prior to beginning this portion, you are expected to read p. 917-925 in Porth
as this will give you an indepth understanding of the functions, anatomy and
physiology of the liver. When you complete your reading, work through the
following case study and apply your knowledge in answering the case study
questions.
Remember that your goal is to work through how the pathophysiology results in
certain clinical manifestations, not to simply reproduce those manifestations in your
answers.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Disorders of the Liver: Case Study
Patient Name:
Age:
Occupation:
Accommodation:
Marital Status:
John Smith
32
house painter
lives alone
single
Presentation to Hospital:
On November 12, 1989, John came to the emergency department complaining of
generalized malaise, anorexia, nausea, and vomiting. These symptoms had become
progressively worse over the past few days. John was obviously jaundiced in
appearance and upon questioning admitted that people had been commenting on his
“yellow” appearance. John’s history revealed that he had a ten-year history of alcohol
abuse involving 26 ounces of liquor and “a few bottles of beer” daily. He was a
nonsmoker, denied the use of street drugs, and his only medication has been 5 or 6
Tylenol per day for headaches. John had no known allergies.
John’s physical exam revealed:
CNS:
somnolent but cooperative, oriented
CVS:
vital signs T. 38 P. 100 R. 20 BP. 100/60
normal heart sounds, elevated jugular vein pressure 5 cm. above
clavicular
bilateral edema to the knees
jaundiced skin and sclera
easy bruising, occasional severe nosebleeds
several spider nevi
CHEST:
good air entry, chest clear
GI:
protuberant abdomen, tender right upper quadrant
liver palpable 14 cm. below the costal margin
swollen varicose veins draining up from the umbilicus
normal colored stools
GU:
dark yellow urine
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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John was admitted to an acute medical unit where his admitting laboratory work
revealed the following (normal values are shown in brackets):
Hgb
113
(135-180 g/L)
Hct
RBC
3.13
(4.5-6.3 X 1012/L)
WBC 16.3 (4-10.0 X 109/L)
Platelets
126
(150-400 X 109/L)
PT
16.8
(9-11.7 sec.)
0.34
(0.40-0.54 L/L)
PTT
63.9
(24.0-36.5 sec.)
AST
78.7
(8-20 U/L)
INR (International Normalized Ratio) 1.7 (0.8-1.1)
ALT
52.3
(5-35 IU/L)
Electrolytes were found to be normal.
Total Bilirubin 25 umol/L (<17.0 umol/L)
Direct Bilirubin 12 umol/L (<8
umol/L)
An ultrasound of the abdomen showed a large but homogeneous and smooth liver, a
mildly enlarged spleen, and normal kidneys. A pelvic ultrasound showed a small
amount of fluid in the pelvis.
Upon admission John was placed on bed rest with bathroom privileges, a low sodium,
low protein diet, and a fluid restriction. His medications included Berroca C 2 ml. OD,
Thiamine 50 mg. IM BID, Vitamin K 10 mg. SC X 2, Aldactone 25 mg. PO BID, Lactulose
30 cc. PO TID, Solu-Cortef 100 mg. IV q12h.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Questions related to Case Study
1.
John has been diagnosed with cirrhosis of the liver. What is cirrhosis of
the liver? How is it diagnosed?
2a. What explanation would you give for the varicose veins on John’s
abdomen?
b. Where else do they appear?
c. Why are these varicose veins significant?
d. How would they be treated?
3.
John’s peritoneal tap was positive for ascitic fluid. What does this mean?
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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How is ascites managed?
5a. Describe the mechanisms underlying jaundice.
b. Briefly describe two other forms of jaundice.
6.
At the present time John is fairly alert and oriented.
a. If you perceived a deterioration in his mental status, what complications
would you expect is/are developing?
b. Discuss management.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
7.
As you are reviewing John’s blood work results you note that his
PT/NR is elevated. You also are aware that John bruises easily and that he
occasionally suffers serious nosebleeds.
a. Explain this complication in relation to his liver disorder.
b. How would this complication be treated?
8.
John’s blood work also reveals elevated levels of ALT and AST.
a. What is the significance of this enzyme elevation?
b. John was taking Tylenol at home. Why may Tylenol cause an increased
level?
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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9a. What occurs in liver disease that causes elevation in direct (conjugated)
Bilirubin?
b. In total Bilirubin?
c. Why is John’s urine dark yellow?
10a. Why was John prescribed Thiamine and Berroca C?
b. Why was he prescribed Solu-Cortef?
11. What is John’s prognosis?
These answers to the case study will be discussed in the case study time
during the term. If you have any questions please contact the course
professors.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Section 2: Disorders of the Liver—Hepatitis
Introduction
The preceding case study reviewed your understanding of alcoholic liver
disease. As health professionals, we must be familiar with another common
liver disorder, hepatitis.
Hepatitis is a disease which is highly transmittable and which may have
serious consequences if untreated. As health care workers we must be able to
recognize its presentation, understand its pathophysiology, and promote
effective treatment options.
Learning Activity #2
Read: You are required to read the section in your text addressing hepatitis,
pp. 927-932.
After you have completed these readings, complete the post-test. The
answers are in Appendix A.
If you discover areas that you require a review or more information, go back
to the text or refer to the articles in the references. In particular the article by
Marx, J.F. (1998). Understanding the varieties of viral hepatitis. Nursing 98,
July, 43-49 may be helpful.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Hepatitis Post-Test
Indicate whether the following statements are true (T) or false (F), and
then check your answers against those in Appendix A.
1. _______
Hepatitis A may lead to chronic hepatitis.
2. _______
The incubation period for Hepatitis B is 60-180 days.*
3. _______
Hepatitis A is endemic in countries with poor
sanitation.
4. _______
Body fluid precautions are essential in preventing the
spread of Hepatitis A in hospitalized patients.
5. _______
The virus responsible for Delta Hepatitis is known.
6. _______
Diagnosis of Hepatitis B is based on the presence of
HBsAg.
7. _______
Diagnosis of Hepatitis A also is based on the presence
of an antigen.
8. _______
.
The Delta virus is dependent on the presence of
Hepatitis B for replication
9. _______
Inflammation of the hepatocytes may lead to
cholestasis and obstructive jaundice.
10. _______
Liver damage in Hepatitis B tends to be more severe
than in Hepatitis A.
11. _______
Delta Hepatitis is a mild form of hepatitis.
12. _______
Hepatitis B may go on to become chronic.
13. _______
Immunization against hepatitis B is not available.
14. _______
Immunization against hepatitis A is available.
Well done, you have worked your way through this section.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Section 3: Disorders of the Exocrine Pancreas
Introduction
Now that you are familiar with the role of the liver in digestion and its
associated pathophysiology in selected illnesses, you will look at another
accessory organ of digestion, the pancreas. If you would like to refresh your
memory of the pancreas’ structure and function, fill in the blanks in the
following statement. If not, move on. Answers are included in Appendix B.
The pancreas is a _________, __________ organ that is situated with its
_________ close to the_________. It has an endocrine function, the secretion of
_________ and _________; and an exocrine function, the secretion of
_________ _________ into the duodenum.
The functional units of the exocrine pancreas are the _________. These
__________ are grape-like clusters made up of single layers of __________ or
__________ cells which surround a__________ into which pancreatic juices
are emptied.
Pancreatic juices are necessary for __________ and contain _________,
_________, and _________.
These digestive enzymes include _________, _________ and _________ which
digest _________, _________ and _________ respectively.
The pancreas is normally protected from autodigestion because these
enzymes are stored in an _________ form until reaching the _________. Once
they enter the duodenum, _________, the precursor to trypsin, is activated by
enzymes in the duodenum. Trypsin then goes on to activate the other
enzymes in the pancreatic juice.
Can you anticipate what might happen if these enzymes were to back up into
the pancreas? We will examine this in a review of pancreatitis. The answers
to questions posed throughout this section can be found in Appendix B.
Definitions
Historically there has been considerable confusion and disagreement as to
the proper definition of the terms acute and chronic pancreatitis. In 1963,
physicians at the Marseille Symposium met to classify pancreatic
inflammatory diseases.
From this conference the following definitions were derived:
Acute pancreatitis: an acute condition typically presenting with abdominal
pain, and usually associated with raised pancreatic enzymes in blood or
urine, due to inflammatory disease of the pancreas.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Chronic pancreatitis: a continuing inflammatory disease of the pancreas,
characterized by irreversible morphological change, and typically causing
pain and/or permanent loss of function.
Prevalence
Pancreatitis is considered a relatively rare disease; however, it is estimated to
be clinically evident in 0.9 to 9.5 percent of alcoholic patients and
pathologically evident in 17 to 45 percent of alcoholics.
Population at Risk
Pancreatitis is equally common among men and women, and most
commonly begins in the fifth decade. As previously stated, alcohol
consumption increases one’s risk of developing pancreatitis. The average
length of alcohol consumption prior to onset of pancreatitis is 11 to 18 years
and the average amount of alcohol consumed is 144 to 150g/day (e.g., 6-10
drinks/day).
Individuals with gallstones also are at higher risk of developing a form of
pancreatitis known simply as gallstone pancreatitis, which is thought to
result from obstruction of the pancreatic duct by a gallstone.
A small percentage of pancreatitis is caused by conditions such as
hyperlipemia, hypercalcemia, trauma, drug ingestion, and genetic
predisposition. There also remains a group of individuals (10% to 20% of
cases) who develop pancreatitis for no known reason.
Pathophysiology
Etiology
Pancreatitis is one of those frustrating diseases in which the pathogenesis and
etiology are not fully understood. Determination of the etiology of
pancreatitis is somewhat dependent on the location of the investigation and
the zeal of the investigator. The location of the investigation may affect
etiology in that affluent suburban populations often differ in their
presentation compared to poor inner city populations: the former having a
higher incidence of gallstone disease and the latter alcohol abuse. Biliary tract
disease and alcohol are associated with 65% to 90% of all cases of acute
pancreatitis (Brown, 1991). It also should be noted that one individual may
exhibit overlapping etiologies. Accepting these facts, let us look at some of
the known etiologies of pancreatitis.
An association between biliary tract stone disease and pancreatitis has been
demonstrated, but the exact mechanism behind it is not clearly understood.
Some theories suggest gallstones become impacted in the distal end of the
biliopancreatic duct thereby allowing bile to reflux into the pancreatic duct.
Other researchers feel an incompetent sphincter of Oddi may allow reflux of
duodenal contents into the pancreas. Finally, other theorists think obstruction
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
of the pancreatic duct by a gallstone leads to ductal hypertension, the rupture
of small ducts, and leakage of pancreatic juice into the parenchyma.
Other sources of obstruction, such as, strictures, tumors, and lesions have
been implicated in the development of pancreatitis.
It should be noted that correction of the obstruction leads to resolution of the
disease in the acute form, whereas chronic obstruction leads to chronic
pancreatitis.
In chronic pancreatitis, inflammation results in irreversible changes in the
endocrine and exocrine tissues. The normal parenchyma becomes fibrotic
and intraductal calcification occurs. These changes usually take place
“silently” and independently of acute episodes. It is thought that acute
pancreatitis rarely leads to chronic pancreatitis (Banks, Frey, & Greenberger,
1989).
Alcohol clearly has been accepted as a cause of both acute and chronic
pancreatitis, although the majority of alcohol related cases show
morphological changes reflecting chronic pancreatitis (Hootman & Ondarza,
1993). The exact effect of alcohol is unknown: theories include a direct or
indirect toxic effect, alcohol induced spasm of the sphincter of Oddi and
associated ductal hypertension, and hyper-secretion of the gland. In addition,
the nutritional status of many alcoholics is compromised and studies indicate
that diets high in protein or high in fat influence the development of
pancreatitis in the presence of alcohol.
Acute and chronic pancreatitis also have been associated with scarlet fever,
mumps, Coxsackie and parasitic infections, familial hyperlipemia, abdominal
surgery, trauma, Crohn’s disease, cystic fibrosis, poor nutrition, certain
drugs, elevated serum calcium level and scorpion stings (Hootman &
Ondarza, 1993). Smoking has been found to have a relationship to the
development of chronic pancreatitis but its role in acute pancreatitis is
unclear (Brown, 1991).
Pathogenesis
As you discovered in the previous section pancreatitis has been associated
with a number of etiologies but as of yet there is no clearly defined cause and
effect. We will examine a few of the many theories which exist.
You will recall that alcohol or its metabolites may play a direct or indirect
role in damaging pancreatic tissue. It has been noted that alcohol results in
the secretion of pancreatic juice which is high in protein, low in bicarbonate
and low in secretory trypsin inhibitors. It is hypothesized that excess protein
results in the formation of protein plugs. These plugs also may result from a
decreased amount of a specific type of protein, pancreatic stone protein,
which actually inhibits the precipitation of calcium in pancreatic juice.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Regardless of the mechanism, obstruction leads to ductal hypertension which
results in pancreatic ischemia. Ductal permeability increases, thereby
allowing toxic substances to diffuse into the pancreas. Pancreatic edema and
interstitial inflammation occur. Enzymes which have leaked into the tissue
become activated and a process of “autodigestion” occurs. Tissue and cell
membranes are destroyed resulting in vascular damage, ischemia, edema,
necrosis, hemorrhage and pain.
Occasionally, inflamed tissue walls off pockets of pancreatic juice, blood, and
necrotic debris in what is termed a pseudocyst. As these have a risk of
rupture, surgical resection is often indicated. Pseudocysts are more often
associated with chronic pancreatitis.
When toxic substances are released into the blood stream, blood vessels and
other organs such as the lungs and kidneys may be affected.
Clinical Manifestations
Acute pancreatitis can range in severity from mild to life threatening. This
range of seriousness may result from different etiologies, diagnostic criteria,
or management. Some estimate that 80 percent of individuals will recover
uneventfully, while 20 percent will develop life-threatening complications,
and 10 percent will die. Diagnosis is difficult because the gland cannot be
directly visualized, except during surgery or autopsy. Blood serum and
radiographic studies aid in the diagnosis of acute pancreatitis (Brown, 1991).
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Learning Activity #3
Complete the following questions and compare your answers to those in
Appendix B.
Considering the pathogenesis of acute pancreatitis, what symptoms would
you expect to see? What lab values would you expect and why?
In contrast, what are the signs and symptoms of chronic pancreatitis? How
do lab findings differ in chronic pancreatitis? Include rationale.
In addition to laboratory tests, what diagnostic tests aid in the diagnosing of
pancreatitis? Include rationale.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Evaluation and Treatment
The goals of management of acute pancreatitis are three-fold:
1. To limit the degree of inflammation.
2. To prevent the development of complications.
3. To treat complications which do arise.
Limiting the Degree of Inflammation
Reducing stimulation of the pancreas is one way of reducing inflammation.
Secretin, an intestinal hormone, stimulates the pancreas to release enzymes
and bicarbonate, in response to acidic chyme in the duodenum. Methods of
reducing this stimulation include nasogastric suctioning, antacids via
nasogastrial tube, histamine receptor blockers (Cimetidine, Ranitidine), and
no oral intake.
Although studies suggest that mortality rates are not improved with
antibiotics, some recommend the administration of a broad spectrum
antibiotic such as a Cephalosporin in patients with gallstone pancreatitis and
those with severe disease.
Preventing the Development of Complications
Close monitoring of fluids and electrolytes is essential in preventing
complications. As many of these patients will lose fluid into the peritoneum,
accurate recording of intakes and outputs is necessary. For some patients
central venous catheters are necessary to monitor central venous pressures
(CVP) and to provide parenteral nutrition. Potassium replacement is
common, as is close monitoring of calcium levels.
Another complication is respiratory insufficiency. You will recall that pleural
effusion, especially on the right side is associated with acute pancreatitis.
Some estimate that 40 percent of patients with acute pancreatitis will develop
respiratory insufficiency, and therefore recommend close monitoring of
arterial blood gases (ABG’s) during the first 72 hours of diagnosis. Most
patients will respond to monitoring and oxygen administration, but some
with more severe disease will require mechanical ventilation, fluid
restrictions, and diuretic therapy. Pain and abdominal distention will also
contribute to respiratory complications. Table 15.1 in this unit summarizes
the various complications during the three stages of acute pancreatitis.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Table 15.1 Complications of Acute Pancreatitis
Early
Bleeding, stress ulcers, and erosive gastroduodenitis
Erosion of pancreatic and parapancreatic vessels
Fistulas (biliary-duodenal, colonic, pancreatic, small bowel, gastric)
Infected necrosis
Metabolic disorders (e.g., hyperglycemia, hypercalcemia)
Renal insufficiency
Respiratory insufficiency
Shock
Intermediate
Abscess
Pseudocyst
Late
Chronic pancreatitis
Colonic Stenosis
Diabetes
Treating Complications
Individuals with chronic pancreatitis may require pancreatic enzyme
supplements and oral histamine receptor blockers to help improve digestion
and absorption. A diet low in fat is recommended to reduce steatorrhea and
discomfort. Obviously, cessation of alcohol ingestion is central to treatment in
alcohol related pancreatitis.
The pain associated with acute pancreatitis is usually treated with parental
analgesics such as meperidine (Demerol). You will recall that morphine can
cause spasm of the sphincter of Oddi, resulting in increased pain.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Based on your readings and your present understanding of the etiology of
pancreatitis, list some of the types of surgical interventions you might see in a
patient with this disease.
1. __________________________
2. __________________________
3. __________________________
4. __________________________
5. __________________________
It should be noted at this point that surgical intervention in pancreatitis is
associated with a number of concerns. Firstly, patients requiring surgery are
often very ill thereby increasing their perioperative risk. Patients undergoing
pancreatic surgery are at risk of respiratory complications and intraabdominal sepsis. Those individuals undergoing extensive pancreatic
resection are also at risk of developing diabetes. Resection of the pancreas is
thought to be a difficult procedure due to the soft, spongy nature of
pancreatic tissue.
Trajectory of Disease
The prognosis for acute pancreatitis in individuals who obtain treatment and
eliminate the precipitating factor such as gallstones is very good. The
prognosis for alcohol-induced pancreatitis is not as favourable.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Section 4: Disorders of the Gallbladder
Introduction
In the final section of this unit we will examine the gallbladder. The material
in this section has been pulled together for you from a number of sources, so
you should not have to “track down” additional information. Periodically
throughout this section you will be asked questions to stimulate your
thinking and enhance your learning. The answers to the questions posed can
be found in Appendix C. Let’s begin.
You will recall that the gallbladder is a hollow, pear shaped organ which is
“tucked” in under the liver in the right upper quadrant. Its primary function
is the storage and concentration of bile received from the liver. Food in the
duodenum stimulates the sphincter of Oddi to relax and the gallbladder to
contract, thereby allowing bile to pass into the duodenum where it is used to
emulsify fats. As with any internal organ, dysfunction of the gallbladder may
result from trauma, cancer, and complications secondary to other disease
conditions. However, the most common disorders of the gallbladder are
primary disorders of inflammation and obstruction. The two most common
diagnoses associated with these disorders are cholelithiasis and
cholecystitis.
Cholelithiasis refers to the formation of gallstones primarily in the
gallbladder.
Cholecystitis refers to inflammation of the gallbladder and occurs when
gallstones obstruct the flow of bile through the cystic duct.
Occasionally, inflammation may result from an infectious agent but for the
purposes of our discussion cholecystitis will refer to inflammation associated
with cholelithiasis. Throughout this section references will be made to both
cholelithiasis and cholecystitis, so please keep in mind that they are two
distinct conditions, which may or may not occur together.
Prevalence
Diseases of the gallbladder are very common in developed countries with an
estimated prevalence of 10 to 20 percent. In the United States 20 million
Americans (15 million women and 5 million men) are thought to have
cholelithiasis at any given time. Approximately one million cases of
cholelithiasis are diagnosed annually and 600,000 cholecystectomies are
performed. The economic impact of this disease is reflected in the fact that it
accounts for 2.5 percent of the health expenditure of the United States, or $2
billion dollars annually!
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Population at Risk
Through your clinical practice, you may have gained an understanding of the
role that risk factors play in guiding preliminary assessments. Keep the
following information in mind when examining patients who are
complaining of abdominal pain.
Historically, individuals who were “fair, fat, female, and forty” were
considered typical sufferers of gallbladder disease. If you are close to meeting
this description don’t panic, while some of these characteristics remain, the
risk factors have broadened. Predisposing risk factors are now thought to
include obesity, a sedentary lifestyle, high cholesterol diet, female gender,
multiple parity in women, American Indian ancestry, middle age, and a
positive family history. Medical conditions associated with gallbladder
disease include pancreatic or ileal disease, diabetes mellitus, and jejunoileal
bypass for morbid obesity.).
Pathophysiology
Etiology
As stated earlier, cholelithiasis refers to the formation of gallstones.
Gallstones are categorized as either cholesterol or pigment stones.
Cholesterol gallstones are composed of 74 to 96 percent cholesterol and 5
percent bilirubin whereas pigment stones are 3 to 26 percent cholesterol and
40 to 60 percent bilirubin plus other organic and inorganic materials. Ninetyfive percent of gallstones in North America and Europe are cholesterol
stones. On the surface this may seem like superfluous information but it has a
significant impact on the choice of treatment as noncholesterol stones cannot
be dissolved with noninvasive techniques.
The formation of pigment stones may be associated with altered
concentrations of conjugated and unconjugated bilirubin and calcium,
gallbladder stasis, and gallbladder mucin hypersecretion.
Pathogenesis
The exact pathogenesis of gallstones is unknown; however, cholesterol stones
appear to develop when bile becomes supersaturated with cholesterol.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
A number of theories exist as to why the liver may secrete bile which is high
in cholesterol. Think back over your readings and list some of the theories.
(Answers to questions posed in this section on Disorders of the Gallbladder
can be found in Appendix C.)
1. __________________________
2. __________________________
3. __________________________
4. __________________________
Gallstones form when the cholesterol in the bile changes from liquid form to
a solid crystal or microstone. As more crystals precipitate macrostones
develop. The crystallization of cholesterol may be affected by bile stasis,
excessive gallbladder mucin secretion, the presence of nucleating agents, or
the absence of antinucleating agents. It is interesting to note that these
gallstones can range in size from sand-like particles, sometimes referred to as
sludge, to large, golf ball-sized stones which almost fill the gallbladder.
Ninety percent of individuals with cholelithiasis have associated
cholecystitis. The development of cholecystitis is thought to result from the
impaction of a gallstone in the cystic duct. With extended obstruction, the
gallbladder becomes distended, edematous and ischemic. Prolonged
ischemia leads to necrosis and eventually gangrene and perforation of the
gallbladder may result.
In addition to obstructing the outflow of bile from the gallbladder, gallstones
also can become lodged in the common bile duct and obstruct the drainage of
bile into the duodenum.
Take a moment to visualize the biliary system and then describe what you
think might happen if an obstruction of the common bile duct was
prolonged. Draw a diagram if it would be helpful to your learning.
In addition to travelling into the common bile duct, in rare circumstances,
gallstones may erode through the gallbladder wall into the small intestine
and cause a gallstone ileus.
Approximately ten percent of cases of cholecystitis occur in the absence of
gallstones and are known as acalculous cholecystitis. This form is thought to
be caused by ischemia resulting from vasculitis, and has been associated with
diabetes mellitus, systemic lupus erythematosus, rheumatoid arthritis, and
previous trauma.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Clinical Manifestations
As you probably have noted from your readings, there are differing opinions
as to what constitutes symptomatic cholelithiasis. To begin with there are
individuals who are truly asymptomatic, having what are termed “silent”
gallstones. Thus discovery of cholelithiasis is through diagnostic tests or
surgery for other problems. The development of symptoms may take many
years, with the average time lapse between developing gallstones and
symptoms being 25 months.
Historically, it was believed that intolerance to fatty foods, heartburn,
belching, bloating and flatulence were indicators of gallstones. However, it is
now felt that these symptoms are just as common in individuals without
cholelithiasis and as such should not be the basis for surgical treatment.
While these manifestations may be present in individuals with gallstones, the
cardinal symptoms of cholelithiasis are abdominal pain and jaundice. The
pain of cholelithiasis is caused by gallstones blocking the cystic duct, thereby
obstructing the outflow of bile during contraction of the gallbladder.
A “gallbladder” attack typically occurs following the ingestion of food, often
high in fat, and results in pain which escalates over 30-60 minutes and then
plateaus for several hours. The pain is intense, usually in the right upper
quadrant and sometimes radiating to the back or right shoulder. Although
often referred to as biliary colic, the pain is more often steady than “colicky”
during an attack. Following an attack the individual may have some short
term residual soreness and then be symptom free for weeks or months.
Individuals often present with complaints of anorexia, nausea and vomiting.
You know that the suffix “itis” describes an inflammatory process.
Considering this, what clinical manifestations would you expect to see in a
patient with acute cholecystitis?
Diagnostic Tests
A number of diagnostic investigations are available to determine the
presence of gallstones in the gallbladder. As nurses, we are often not familiar
with the techniques used in diagnostic imaging. The following is a brief
summary of the four main techniques that may be used to diagnose
gallbladder disease.
At present, the test of choice is abdominal ultrasonography (ultrasound) as it
is rapid, noninvasive, radiation free, and easy to perform even in pediatrics
and obstetrics. The test involves “bouncing” sound waves off the gallbladder.
Gallstones are “visualized” as echogenic shadows within the gallbladder. In
addition to visualizing gallstones, ultrasound can reflect the patency of the
hepatic and common bile duct and detect thickening of the gallbladder wall
which is suggestive of inflammation. The accuracy rate of ultrasound of the
gallbladder is 90 to 99 percent; however, difficulties may occur in visualizing
stones in the common bile duct and in very obese individuals.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
When ultrasound is inconclusive, oral cholecystography allows visualization
of the gallbladder via a contrast medium. Once the test of choice,
cholecystography involves the inges tion of an oral contrast medium
followed by abdominal x-rays. The disadvantages of this test are 1) patient
preparation requires the ingestion of the contrast medium the evening before
the test and 2) in many cases it must be repeated due to poor initial
visualization resulting from failure to ingest the tablets, hepatic dysfunction,
vomiting or malabsorption.
A third diagnostic test available is endoscopic retrograde
cholangiopancreatography (ERCP). This is an invasive test which involves
passing a catheter through the mouth and down into the duodenum, at
which point it is fed into the common bile duct to enable visualization of the
biliary tree.
Finally computed tomography (CT) is used occasionally and is estimated to
have a 45 to 90 percent accuracy rate in detecting gallstones in the common
bile duct. It also is thought to be more sensitive than other diagnostic tests in
detecting partially calcified stones and therefore may be of more use in the
future in therapies aimed at dissolving gallstones.
Evaluation and Treatment
The treatment of asymptomatic cholelithiasis is somewhat controversial and
greatly depends upon the individual case. Some estimate that asymptomatic
individuals have a 70-90 percent chance of remaining so for 10-25 years and
when these individuals become symptomatic they do not usually develop
serious complications.
However, some factors should be considered when deciding whether or not
to postpone surgery: geographical access to medical facilities, the presence of
gallstones over 3 cm. in diameter, and the likelihood of developing
cholecystitis and complications. The decision to postpone surgery is
influenced by the fact that exploration of the common bile duct is necessary
twice as often among individuals who delay surgery for a year after the onset
of symptoms. Obviously, exploration of the common bile duct significantly
increases complications and mortality rates.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Non-Surgical Management
Cholelithiasis often progresses to acute cholecystitis. The management of
acute cholecystitis is aimed at reducing or eliminating inflammation and
promoting comfort until more definitive intervention is necessary.
What are some of the measures you could employ to assist in meeting these
two goals?
Gallstones which go on to produce acute cholecystitis are usually resolved
with surgery; however, for those individuals who do not require such
immediate relief alternate treatments are available. These treatments include
dissolving the gallstone(s) through the ingestion of oral bile salts or the direct
application of solvents, removing the stones through endoscopy, and
crumbling them with shock wave lithotripsy.
Oral bile salts slowly dissolve gallstones over a period of months to years but
are only effective with cholesterol stones. One agent, chenodiol, has been
shown to elevate LDL cholesterol levels and to cause gastritis in some
patients, and therefore is not recommended for use in individuals with
atherosclerosis or gastric ulcers. This drug also can cause diarrhea requiring
antidiarrheal agents or discontinuation of therapy. The second agent,
ursodiol, does not appear to elevate cholesterol or cause significant diarrhea.
Neither drug is recommended for use in individuals with liver disease.
Gallstones within the gallbladder or common bile duct may be dissolved via
direct application of a solvent. Stones in the gallbladder are accessed via a
transhepatic catheter and are bathed in methyl tertiary butyl ether. The ether
is flushed in and out of the gallbladder until evidence of gallstone dissolution
is noted in fluoroscopy. The process usually is completed within hours.
Another topical solvent, monooctanoin, is used when stones are in the
common bile duct. A nasal-biliary tube or a T-tube is used to access the
stone, which subsequently is washed with monooctanoin on a continuous
basis for 3 to 21 days. Evidence of stone dissolution is obtained through
cholecystograms.
A third method of stone removal is through endoscopy. An endoscope is fed
through the mouth and down to the sphincter where the common bile duct
enters the duodenum. The sphincter is slightly incised to allow a catheter,
which is equipped with a basket or balloon tip, into the common bile duct.
Once the catheter has passed the stones, the balloon is inflated or the basket
opened to allow the stones to be pulled or scooped out of the duct.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
The final nonsurgical technique is shock wave lithotripsy. The individual is
either immersed in water or a water filled bag is placed over the abdomen in
the area of the stones. Series of shock waves are directed at the stones with
the assistance of ultrasound until they break up. The individual may require
analgesia or occasionally anaesthesia. If the gallstones are in the common bile
duct, transhepatic or nasal-biliary catheters may be used to visualize the
stones with contrast media. Some individuals are placed on oral bile salts to
dissolve any remaining fragments following lithotripsy, endoscopy, or
solvent therapy.
Surgical Management
The decision of when to perform surgery on patients with acute cholecystitis
depends upon the patient’s condition. Ideally, individuals with acute
cholecystitis improve with supportive therapy and surgery can be performed
when they stabilize or at a later date on an elective basis. However, acute
cholecystitis that persists with therapy is associated with perforation of the
gallbladder, gangrene, and sepsis, and therefore, emergency surgery is
sometimes necessary. Fortunately, advances in diagnostic techniques allow
earlier detection and treatment of cholecystitis in individuals with no prior
history. With the advent of laser and laparoscopic technologies the patient
need not suffer frequent acute attacks and concomitant complications. The
procedure is simple, fast and relatively free of complications (Haicken, 1991).
Traditional Open Abdominal Surgery
The surgical procedure, a cholecystectomy, involves an upper midline or
right subcostal incision (6 to 8 inch). Following the removal of the gallbladder
many surgeons perform an intra-operative cholangiogram to ensure that the
common bile duct is free of stones. If the common bile duct is manipulated
through examination or removal of stones, a T-tube is placed in the duct to
ensure patency. The T-tube is positioned so that the short end of the “T” lies
in the common bile duct and the long end is brought out through the skin
and attached to a drainage bag. Occasionally, surgeons also will place a drain
in the gallbladder bed to promote evacuation of blood or bile. This is usually
removed in 72 hours. Time lost from work for convalescence is generally 4 to
6 weeks (Haicken, 1991).
Take a moment to reflect on the general goals of postoperative nursing care
and then apply these to the cholecystectomy patient. When you are finished
check your list against the one in Appendix C.
Laser Laparoscopic Cholecystectomy (LLC)
Laser and laparoscopic technologies have revolutionized the management of
gallbladder disease. The gallbladder can be removed through four (1/2 inch)
incisions. LLC is performed on an outpatient basis and results in less
postoperative pain and more rapid ambulation and recuperation. Almost half
of patients can have this surgery done without requiring even one night’s
hospitalization. Most people return to work in three days and can resume full
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 15 The Hepatobiliary System and Exocrine Pancreas
29
physical activity in one week. Strong home support is required (Haicken,
1991).
Surveillance/Trajectory of Disease
As you will recall some individuals with asymptomatic cholelithiasis remain
so for their lifetime, whereas others become symptomatic with time
necessitating definitive treatment. In most situations the illness is resolved
following treatment; however, there are cases of continued pain after
cholecystectomy. These people may develop biliary pain after months or
years of no pain. It is recommended that these individuals be investigated for
biliary tract disease, and may require surgery for stones in the common bile
duct.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Final Thoughts
This unit has examined the pathophysiology, clinical manifestations, and
therapeutic regimes of selected disorders of the hepatobiliary system and
exocrine pancreas. In completing this unit you have gained an understanding
of the impact of hepatobiliary disease on patients and their families. The
knowledge you now possess should assist you in assessing and planning care
for the acutely and chronically ill patient with hepatobiliary disease.
Throughout this unit you have been required do to a considerable amount of
work. By working through these exercises many of your questions should
have been answered. If you have discovered areas where you would like
additional information, please utilize the bibliography following to help
guide your search.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 15 The Hepatobiliary System and Exocrine Pancreas
31
References
Ambrose, M.S. & Dreher, H.M. (1996). Pancreatitis Managing a flareup. Nursing 96, 24(4), 33-40.
Brown, A. (1991). Acute pancreatitis: Pathophysiology, nursing
diagnoses, and collaborative problems. Focus on Critical Care, 18(2), 121-130.
Burnett, D. A., & Rikkers, L. F. (1990). Nonoperative emergency
treatment of variceal bleeding. Surgical Clinics of North America, 70(2), 251-266.
Covington, H. (1993). Nursing care of patients with alcoholic liver
disease. Critical Care Nurse 13(3), 47-59.
Doherty, M.M. & Carver, D. (1993). Transjugular intrahepatic
portosystemic shunt: New relief for esophageal varices. American Journal of
Nursing, 93(4), 58-63.
Gust, I. D. (1990). Design of hepatitis A vaccines. British Medical
Bulletin, 46(2), 319-328.
Haicken, B. (1991). Laser laparoscopic cholecystectomy in the
ambulatory setting. Journal of Post Anesthesia Nursing, 6(1), 33-39.
Hootman, S. R., & Ondarza, J. (1993). Overview of pancreatic duct
physiology and pathophysiology. Digestion, 54(6), 323-330.
Mahl, T. C., & Groszmann, R. J. (1990). Pathophysiology of portal
hypertension and variceal bleeding. Surgical Clinics of North America, 70(2),
291-306.
Marx, J.E. (1998, July). Understanding the varieties of viral hepatitis.
Nursing, 98, 43-49.
Porth, C. M. (2005). Pathophysiology-Concepts of Altered Health
States (7th ed). Philadelphia: Lippincott.
Thompson, C. (1992). Managing acute pancreatitis. RN, 55(3), 52-57.
Willis, D. A., Harbit, M. D., & Julius, L. M. (1990). Gallstones
Alternatives to surgery. RN, 53(4), 44-51.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Glossary
acute pancreatits: An acute condition typically presenting with abdominal
pain, and usually associated with raised pancreatic enzymes in blood or
urine, due to inflammatory disease of the pancreas.
cholecystitis: Inflammation of the gallbladder.
cholelithiasis: Formation of gallstones.
chronic pancreatis: A continuing inflammatory disease of the pancreas,
characterized by irreversible morphological change, and typically causing
pain and/or permanent loss of function.
Acronym List
ABG Arterial blood gas
CT
Computed tomography
CVP
Central venous pressure
ERCP Endoscopic retrograde cholangiopancreatography
Checklist of Requirements
Required Readings
Print Companion: Alterations in Function of the Hepatobiliary System and
Exocrine Pancreas

Haicken, B. (1991). Laser laproscopic cholecystectomy in the
ambulatory setting. Journal of Post Anesthesia Nursing, 6(1), 33-34.


Learning Activities

Learning Activity 1—Case Study: Cirrhosis of the liver

Learning Activity 2—Hepatitis Post-Test

Learning Activity 3—Pancreatitis
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary
Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Answers to Learning Activities
Answers to Learning Activity #2
Following are the answers to the hepatitis post-test.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
F
T
T
T/F (The infective period is greatest 10 to 14 days prior to symptoms
and one week following the onset of symptoms, therefore, patients
may be past the contagious period before they are admitted.
However, universal precautions should be practised with ALL
patients regardless of diagnosis.)
TT
F (Diagnosis is based on the presence of anti-HAV.)
T
T
T
F (Delta Hepatitis is a severe form of hepatitis with a higher mortality
rate than other forms.)
T
F
T
Structure and Function of the Pancreas
The pancreas is a soft, spongy organ that is situated with its head close to the
duodenum. It has an endocrine function, the secretion of insulin and
glucagon, and an exocrine function, the secretion of pancreatic juices into the
duodenum.
The functional units of the exocrine pancreas are the acini. These acini are
grape-like clusters made up of single layers of acinar or epithelial cells which
surround a lumen into which pancreatic juices are emptied.
Pancreatic juices are necessary for digestion and contain water, bicarbonate,
and enzymes.
These digestive enzymes include amylase, trypsin, and lipase which digest
starch, protein, and triglycerides respectively. The pancreas is normally
protected from autodigestion because these enzymes are stored in an inactive
form until they reach the duodenum. Once they enter the duodenum,
trypsinogen, the precursor to trypsin, is activated by enzymes in the
duodenum. Trypsin then goes on to activate the other enzymes in the
pancreatic juice.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Answers to Learning Activity #3
Clinical Manifestations of Acute Pancreatitis
Individuals with acute pancreatitis frequently present with midepigastric or
left upper quadrant pain which radiates to the back, and which is associated
with vomiting. Bowel sounds are usually absent due to reflex paralytic ileus.
In half of the cases, a low grade fever is present. These symptoms follow
meals in gallstone pancreatitis and alcohol binging in alcoholic pancreatitis.
In hemorrhagic pancreatitis a bluish discoloration may be present over the
flank or periumbilical area and the patient may exhibit signs of shock. There
is no consistent set of laboratory findings in acute pancreatitis as the etiology
of the disease will affect lab values. For example, hemorrhagic pancreatitis
may result in a lowered hematocrit whereas other forms will not, gallstone
pancreatitis may cause slightly elevated serum bilirubin not seen in other
forms. Most patients will have elevated serum amylase levels within six
hours of pain onset, lasting about two days. Serum lipase also elevates for
several days. Urinary amylase also may be elevated. Hyperglycemia and
hypocalcemia may be present also. However, it is important to note that
other gastrointestinal disorders may account for abnormal lab values and
must be ruled out.
Clinical Manifestations of Chronic Pancreatitis
Pain is again a prominent feature in chronic pancreatitis. Initially the pain,
which is deep upper abdominal radiating to the back, comes and goes and
lasts for days or weeks. As the disease progresses the “pain free” periods
diminish and the individual develops chronic pain. The pain is relieved
somewhat by sitting upright while pressing a pillow against the abdomen. It
is exacerbated by lying supine.
Weight loss is a common occurrence as food tolerance decreases with pain
and a decrease in pancreatic enzymes may result in malabsorption. It is
estimated that a 90 percent loss in excretory function is necessary before
malabsorption occurs. Similarly, endocrine function may be affected when
large portions of the exocrine pancreas are diseased, resulting in abnormal
glucose tolerance and possibly diabetes mellitus.
Serum amylase and urinary amylase may or may not be elevated. Many
patients with alcoholic pancreatitis demonstrate abnormal liver function, and
stool samples may reflect elevated levels of undigested fat (steatorrhea).
Diagnostic Tests for Pancreatitis
In addition to the laboratory tests mentioned above, diagnostic tests for
pancreatitis include: abdominal x-rays, endoscopic retrograde
cholangiopancreatography (ERCP), abdominal ultrasound, and secretory
tests in which pancreatic secretions are measured and analyzed following a
standard meal or stimulation with secretin or cholecystokinin. As noted
earlier many of these tests reflect other abnormalities in the gastrointestinal
tract and therefore cannot be thought to be conclusive in isolation.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Answers—Surgical interventions in pancreatitis
1. laparotomy for diagnostic purposes
2. biliary surgery for the removal of gallstones and revision of biliary or
pancreatic ducts
3. resection of associated pseudocysts
4. formation of a feeding jejunostomy
5. pancreatic resection for pain control and decompression: procedures
include distal pancreatectomy or a pancreaticoduodenectomy (Whipple’s
procedure)
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
Disorders of the Gallbladder
Theories of increased cholesterol formation:
1. Hepatocystic synthesis of cholesterol is affected by an enzymatic
defect,
2. Secretion of bile salts, which enhance cholesterol solubility, is
decreased,
3. A lowered bile acid pool as a result of lowered ileal reabsorption of
bile salts, and
4. A combination of mechanisms.
Obstruction of the Common Bile Duct
Obstruction of the common bile duct, by a gallstone, can result in
complications similar to those occurring when liver disease prevents bile
flow through the liver.
Blockage of the common bile duct may prevent drainage of bile from the
liver, thereby resulting in the development of jaundice.
As bile is necessary for the emulsification of fat, the absence of bile in the
intestine prevents fat absorption. Not only does this lead to problems with
nutrition but also with the absorption of fat soluble substances, specifically
vitamin K. As a result the patient may experience problems with clotting.
The presence of excessive amounts of undigested fat in feces results in very
foul smelling fatty stools, steatorrhea. A lack of bile in the intestine also alters
the colour of stool as bile provides the pigment which turns feces brown.
Thus, the presence of clay colored or fatty stool is an important diagnostic
observation.
Clinical Manifestations of Acute Cholecystitis
Individuals with acute cholecystitis present with the symptoms of pain,
nausea, and vomiting, in addition to leukocytosis, fever, and occasionally
chills. Physical examination shows right upper quadrant tenderness and right
sided pleuritic pain on deep inspiration. Jaundice may be present in
individuals who have a gallstone blocking the common bile duct. Laboratory
findings in acute cholecystitis are elevated white cell counts and occasionally
elevated serum amylase, alkaline phosphatase, and bilirubin even in the
absence of stones in the common bile duct or pancreatitis.
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Unit 15 The Hepatobiliary System and Exocrine Pancreas
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Management of Acute Cholecystitis
During the acute attack the gallbladder is rested by withholding oral intake
and occasionally through the removal of gastric secretions via a nasogastric
tube. As many of these individuals are nauseous and vomiting, close
monitoring of fluid and electrolyte status is necessary. Opinions vary on the
role of antibiotics in acute cholecystitis. Some physicians recommend
antibiotics only in the presence of infection, whereas others recommend
antibiotics such as intravenous Ampicillin or Penicillin and Gentamicin in all
but mild, resolving cases (Taylor & Harrington, 1988). Pain, the cardinal
symptom of cholecystitis, is managed through intramuscular analgesics.
Meperidine (Demerol) is recommended as Morphine and its derivatives
cause spasm of the sphincter of Oddi, thereby increasing pain.
The goals of nursing care of the individual with acute cholecystitis are to
promote comfort, prevent fluid and electrolyte imbalances, enhance self-care,
detect early signs of complications, ensure the individual’s understanding of
the disease, tests, and treatments, and if indicated prepare the patient for
surgery.
Goals of nursing care for traditional open surgery patients:
1. To promote comfort
2. To prevent fluid and electrolyte imbalances
3. To prevent respiratory and circulatory complications associated with
surgery
4. To promote effective wound healing
5. To enhance patient understanding of postoperative treatments and
discharge responsibilities (diet, activity, medications)
LLC is becoming an increasingly desirable surgical treatment. Only advanced
age, serious medical conditions and other problems will lead the patient
toward conservative medical treatment (Haicken, 1991). Contraindications
for this type of surgery are basically the same as for open surgery. Obesity
generally is not a limitation.
Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary