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Major Case Study

Exocrine Pancreatic Cancer: Nutrition and Mechanisms


of Cachexia
Antoinette Burke, February 26, 2015
ABSTRACT
This case study will discuss the medical course, nutrition therapy, and interdisciplinary
treatment for patients diagnosed with exocrine pancreatic cancer, and will highlight one
subject under the care of the writer.

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Table of Contents
Section

Pages

I- Medical Course...
Anatomy & Physiology, Statistics, Risk factors, Signs & Symptoms,
Diagnosis, Treatment, Laboratory analysis, Medications

3-25

II- Medical Nutrition Therapy .


Role of the RD, Goals of Nutrition Therapy, Macronutrient & Micronutrient Needs,
Complications, Supplementation, Palliative Care

26-42

III- Presentation of the Patient.

43

IV- Medical and Surgical Course

44-47

V- Critical Commentary & Summary

48-49

Appendix A- Nutrition Assessments.

50-54

Appendix B- Patient-specific Medication List.

55

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I. Introduction
The topic of pancreatic cancer has been chosen in order to fulfill requirements of the major case
study competency for the Philadelphia Sodexo Dietetic Internship program. The complex biological
features and challenging nature of pancreatic tumors, which distinguish it from many other types of
cancer, are of special interest to the writer. The paper will focus on exocrine tumors located in the head
of the pancreas, and will exclude pancreatic neuroendocrine tumors. In particular, the alterations in body
composition and the prevalence of cachexia in this population are of major significance. The writer
hopes to learn greater details of various dietary interventions that might be used as an anti-cachectic
treatment or as a measure of comfort care.
The patient discussed herein was admitted to on September 30, 2014 with severe obstipation
(severe constipation caused by intestinal obstruction). The patient was picked up by the dietary team
due to reported weight loss and poor appetite. The patient had a previously attempted
pancreaticoduodenectomy (Whipple) at The Hospital of the , however the aforementioned surgical
procedure was unable to be completed due to the severity of metastatic lesions to the liver and
peritoneum. The patient underwent 2 rounds of chemotherapy before his white blood cell count became
too low to proceed with aggressive treatment, despite pharmacologic interventions. The patient was
eventually placed on hospice care at . The patient is a financial investor who celebrated his 58th birthday
during his hospitalization. The writer had the pleasure to see this patient five times before his death on
October 24, 2014.

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II. Anatomy and Function of the Pancreas
In order to gain a comprehensive understanding of the pathophysiology of pancreatic cancer, it
is necessary to first identify the anatomical features of the organ. The pancreas first appears at
approximately 5 weeks gestation as two outpouchings of the endodermal lining.1 The pancreas develops
into a large accessory digestive gland located behind the stomach and opposite both the duodenum and
spleen.2 The pancreas is a retroperitoneal organ, which in adult humans weighs about 80 g.1 It is
customary to refer to various portions of the pancreas as the head, body, and tail with the head lying
near the duodenum and distal part of the common bile duct, and the tail extending toward the spleen
(Figure 1).3 The deep, retroperitoneal location of the pancreas makes diagnosis and treatment of
pancreatic neoplasms difficult.
The pancreas lies close to the stomach, intestines, liver, and biliary system. Due to its proximity
to the biliary structures, pathological processes of the head of the pancreas, such as cancer may lead to
biliary system obstruction or injury.1 The head of the pancreas lies in the upper right abdominopelvic
quadrant, with the body and tail continuing to the left upper quadrant (Figure 2). There is no anatomic
landmark for the division of body and tail of pancreas. However, aleft border of the aorta is sometimes
used to mark this division.3 The pancreas is composed of two major types of tissues; the acini, ducted
exocrine tissues that are responsible for secreting digestive juices into the duodenum; and the islets of
Langerhans, ductless endocrine tissues that secrete hormones directly into the blood.2

Figures 1 and 2. Anatomical position of pancreas (pennmedicine.org)

The pancreas is a unique structure, in that it is the only organ in the body that has both endocrine
and exocrine functions. Endocrine functions of the pancreas revolve around the secretion of insulin and
glucagon. These hormones are pivotal in the metabolism of glucose, fatty acids, and amino acids.
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4

Exocrine functions of the pancreas include secretion of digestive enzymes and bicarbonate, the

release of which are controlled by neurohumoral factors, including gastrin and secretin.4 The enzymes
made by the acinar cells of the exocrine pancreas are made in an inactive form, zymogens, to keep the
pancreas from digesting itself. Three major groups of enzymes are critical for efficient digestion and are:
proteases, which initiate protein digestion; pancreatic lipase, which hydrolyzes fatty acids, and amylase,
which hydrolyzes starch to maltose.5 Collectively, the exocrine pancreas plays a major role in digestion
of all macronutrients. In addition to the proteases, lipase and amylase, the pancreas produces a host of
other digestive enzymes, including ribonuclease, deoxyribonuclease, gelatinase and elastase.5 Disruption
in the normal processes of this organ such as cancer, are known to have major effects on the nutritional
status of a patient.

The anatomic location of pancreatic tumors has been suggested as a potential determinant of
survival. Approximately 65% of pancreatic cancers are occurring in the head (HD) of the pancreas,
15% occurring in the body and tail (BT), and the remaining lesions involving the gland diffusely.

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6 According to

the National Cancer Institute, pancreatic cancer is relatively rare when

compared to other cancers, representing only 2.8% of all new cancer cases in the U.S.7 It should be
noted that while the diagnosis of pancreatic cancer composes a smaller percentage of all cancer
diagnoses, it carries a much higher mortality rate. Between 2007 and 2011, the number of new cases of
pancreas cancer was 12.3 per 100,000 men and women per year and the number of deaths was 10.9
per 100,000 men and women per year.7 It is predicted that 46,420 new cases will be diagnosed in
2014 with 39,590 in estimated deaths.7 These figures represent 6830 persons or 17% surviving. The
percentage of persons surviving 5 years drops dramatically. Between 2004 and 2010, the average 5year survival rate was 6.7% (figure 3).7 The stage of the cancer at time of diagnosis and metastases also
determine the predicted survival rate for the patient. Generally, the earlier a cancer is caught, the better
the person has a chance of surviving. For pancreatic cancer, only 8.8% are diagnosed at the local stage
before the cancer has spread.7 Figure 4 shows the percentage of new diagnoss based on
stage/metastases, while figure 5 shows the five-year survival rate based on stage. What one may deduct
from these graphics is that while localized cancer has the highest survival rate 25.8%, it also accounts
for merely 9% of new diagnoses. Conversely, metastatic or distant diagnoses have the lowest survival
rate 2.3% yet account for more than half of new pancreatic cancer diagnoses. This being said, the
nutritional interventions and goals may alter dramatically based on stage of diagnosis.

Figure 3. Number of New Cases and Deaths Per 100,000 People (All Races, Males and Females),
Age-Adjusted

Localized (9%)
Confined to Primary Site
Regional (28%)
Spread to Regional Lymph Nodes
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Distant (53%)
Cancer Has Metastasized
Unknown (11%)
Unstaged

Figure 4. Percentage of New Cancer Diagnoses by Stage

Figure 5. Five- Year Survival Rate Based on Stage of Diagnosis

III. Risk Factors


The exact causes of pancreatic cancer are not well defined, although there are certain risk
factors that have been identified which may increase the likelihood of developing the disease. There are
both modifiable and non-modifiable risk factors to be considered.
Tobacco use and/or abuse have been identified as one of these primary modifiable factors.
Smoking is a significant risk factor and may cause about 20-30% of all pancreatic cancer cases; people
who smoke cigarettes are 2 times more likely to develop pancreatic cancer than people who do not
smoke.

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8

overweight or obes may also increase risk for development of the disease. Obese people have

a 20% increased risk of developing the disease compared to people who are of normal weight, with the
risk being even higher in people who are obese during early adulthood.8 Furthermore, people with
excessive abdominal fat may have an increased risk independent of general obesity.8 Closely related to
overweight and obesity is the effect that diet may have as a modifiable risk factor. Although the
association of diet and the development of pancreatic cancer are still unclear, a diet high in red and
processed meats is thought to increase the risk of developing pancreatic cancer.8 As with other forms of
cancer, a diet high in fruits and vegetables may decrease the risk. Poor dietary habits may lead to a
plethora of medical conditions such as heart disease, and diabetes. Pancreatic cancer is also more likely
to occur in people who have long-standing (over 5 years) diabetes.8 While diabetes may have a genetic
component, much of the disease can be controlled through lifestyle. Therefore since diabetes may
contribute to developing pancreatic cancer, it is even more important to understand the role of nutrition
in the prevention and management of the condition. One final major modifiable factor that increases the
risk of pancreatic cancer and should not be ignored is alcohol abuse. Alcohol abuse and chronic
pancreatitis are closely related, and persons with chronic pancreatitis are at greater risk for development
of cancer. Chronic pancreatitis is common in individuals who consume large amounts of alcohol for
many years.8 It is evident that there are many modifiable risk factors associated with the disease.
However, it is important to note that some risk factors are unable to be altered.
Gender is one such non-modifiable risk factor that is out of patient control. More men than
women develop the condition however; this may be attributed to higher rates of smoking in men.

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8 Age

is also an unchangeable notable factor with most cases of pancreatic cancer being

diagnosed after age 60.8 Race may also be considered when evaluating risk for development of the
disease. African Americans have a higher incidence of pancreatic cancer than Asian, Caucasian, or
Hispanic counterparts; although there is higher prevalence is Ashkenazi Jews.8 As in other conditions, a
family history of pancreatic illness may put a person at a higher risk for developing the same disease.
More specifically, familial presentation of pancreatitis causing recurrent inflammation to the organ should
be identified to evaluate overall risk.8 In totality, those with the highest risk are African American males,
over the age of 60, with a family history of pancreatitis. The associated risk increases if the patient
smokes, uses alcohol, has a poor diet, or has developed diabetes. Since over half of the major risk
factors involve diet and lifestyle, the role of the registered dietitian (RD) in prevention of the disease
begins to present itself. However, in our current medical model of health care, prevention is not always
emphasized, and therefore it becomes necessary to evaluate possible signs and symptoms of the
disease. Monitoring the presentation of classic signs and symptoms may be prudent, especially for
persons with many of the abovementioned risk factors. ancreatic cancer is notoriously difficult, and is
thought to contribute to the low survival rate due to the stage that the tumor(s) have advance to by the
time it is discovered.

IV. Signs and Symptoms


There are six major signs and symptoms used to evaluate appearance of the disease, which include
jaundice, abdominal pain, weight loss, digestive problems, gallbladder enlargements, and blood clots.
Jaundice, or yellowing of the eyes and skin often occurs as one of the first signs of pancreatic cancer.

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9 Referring back

to the anatomical position of the organ in relation to the biliary structures can help

explain the presentation of this symptom. Blockage of the common bile duct, either by a tumor
originating in the head of the pancreas or one that has traveled there from the body or tail of the organ
may prevent the bile from entering the intestines and will cause jaundice.9 Cancers that have
metastasized to the liver may also exhibit signs of jaundice. Abdominal and/or back pain is also a
common presentation in persons with pancreatic cancer. Although many other conditions may cause
abdominal or back pain, it is thought to be associated with the size of the tumor(s) pressing on nearby
organs or nerves.9 Weight loss and poor appetite can manifest in many types of cancer. The tumor itself
may require extra energy; the patient may be experiencing too much pain to tolerate oral intake, or the
patient may become nauseated upon eating. In conjunction, these symptoms can lead to unintended
weight loss. Weight loss and poor appetite are further affected by physiologic changes in digestion.
Digestive problems are common in patients with pancreatic exocrine tumors as they may block
necessary secretions into the duodenum (ACS). Greasy stools are often a sign of improper digestion.
As described previously, the pancreas plays a crucial role in the disintegration of fat. Without the
powerful pancreatic juices, fat will pass through the gastrointestinal tract largely undigested, and end up
as greasy feces, which will float. Nausea or vomiting may occur if cancerous lesions spread to the
stomach, thereby leading to an even greater decrease in oral intake.9 Gallbladder enlargement may
occur if the cancer spreads to the bile duct.9 This enlargement usually can be felt upon physical
examination. Finally, if a cancer has spread to the blood vessels, it may cause them damage and
potentially lead to blood clots.9 If blood clots develop, persons may be at risk for deep vein thrombosis
and/or pulmonary embolism.
Many of these symptoms can be attributed to other conditions, making early diagnosis complex
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and challenging. For this reason, pancreatic disease is colloquially referred to as a silent killer,
not unlike hypertension. Figure 6 surmises some of the most common symptoms associated with the
disease. A range of thorough, analytic measures may be performed to exclude or affirm cancer
diagnosis.

Figure 6. Major symptoms of pancreatic cancer10


V. Diagnosis
Analytic measures used to affirm cancer diagnosis include physical examination, imaging tests,
ultrasound, and blood tests. These measures will be used in conjunction with one another to assure
comprehensive assessment. During the physical examination, the abdomen will be checked for
enlargements, masses, or fluids in the gallbladder and liver. Because of the pancreas' deep location,
tumors are rarely palpable until the tumor grows large enough to interfere with the function of nearby
structures such as the stomach, duodenum, liver, or gallbladder.11 The skin and the whites of eyes will
be checked for jaundice related to liver and biliary function.9 The lymph nodes above the collarbone
and in other locations will be assessed carefully for lumps or swelling that might indicate metastases.9
Imaging tests aid in determining the exact location of the suspected cancer, as well as provide
information about regions of metastases. The most common types of imaging studies used in diagnosis of
pancreatic cancer are computed tomography (CT), magnetic resonance imaging (MRI), and magnetic
resonance cholangiopancreatography (MRCP). A CT scan is an imaging method that uses x-ray to
create pictures of cross sections in the body.

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12

CT offers the best visualization of pancreas and other areas cancer may have spread to and

may help to determine if surgery is the best or even a viable option.9 CT may also be used to guide a
needle for biopsy. During a biopsy, sample of tissue is removed, studied microscopically, and analyzed
for cancers.9
Special MRI tests such as a magnetic resonance cholangiopancreatography (MRCP) can be
used in cases of already diagnosed pancreatic cancer. A MRCP can be used to look at the pancreatic
and bile ducts, to see if they are blocked, narrowed, or dilated.9 Endoscopic retrograde
cholangiopancreatography (ERCP) and percutaneous transhepatic cholangiography (PTC) are two
primary subtypes of MRCP used for visualization of the bile duct. During an ERCP, an endoscope is
passed down the throat, through the esophagus, the stomach, and into the first part of the small intestine
where the Ampulla of Vater can be seen.9 The Ampulla of Vater is the location at which the common
bile duct empties into the small intestine. PTC is another way to visualize the bile duct. In this procedure,
a hollow needle is placed through the skin of the abdomen, and into a bile duct within the liver.9
However, this procedure is more invasive and more painful, and therefore is not performed unless
ERCP has already been tried and is unsuccessful for some reason.9 Magnetic resonance angiography
(MRA) may also be used to evaluate involvement of blood vessels. MRA assesses blood vessels that
go to the brain, kidneys, and heart and is used to monitor narrowing, stenosis or aneurysms.13
Ultrasound may also be used to create a picture of the deep organ. However, ultrasound uses
sound waves to create its images. There are two types of ultrasound devices used in the management of
pancreatic cancer, which are transabdominal and endoscopic ultrasound (EUS).

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14 Transabdominal ultrasound

is used to evaluate various echo patterns. The echoes made by

most pancreatic tumors differ from those of normal pancreas tissue.9 During an EUS, a thin, lighted tube
is passed through the patient's mouth and stomach into the small intestine to take a picture of the
pancreas.14 This procedure is very specialized and requires a gastroenterologist. This procedure is
beneficial as it may aid in visualization of small tumors.14 If the CT or ultrasound procedures do not
provide a thorough enough examination, a positron emission tomography (PET) scan may be used. This
exam will in combination with a CT scan to provide a more complete picture of the area being
examined.14 During a PET scan, a radioactive sugar known as fluorodeoxyglucose or FDG is injected
into the blood, and because cancer cells in the body grow quickly, tending to use energy quickly, they
will absorb large amounts of the radioactive sugar.9
Blood tests may also be used to investigate the involvement of other organs in the progression of
the disease. Moreover, they are frequently used to monitor effectiveness of treatment. Tests such as
bilirubin, AST/ALT, alkaline phosphatase, and albumin are markers of liver function. These tests will
help distinguish whether symptoms of jaundice are caused by disease in the liver itself, or by a blockage
of bile flow. Blockage most frequently originates from a gallstone, a tumor, or other disease.

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15

Tumor markers are another group of blood tests that are frequently performed. They monitor

substances that can sometimes be found in the blood when cancer is present.15 Two tumor markers that
may be helpful in diagnosing pancreatic cancer are CA 19-9 and carcinoembryonic antigen (CEA). CA
19-9 is a substance released into the blood by exocrine pancreatic cancer cells, although it often cant
be detected until the cancer is already advanced.15 Carcinoembryonic antigen (CEA) is another tumor
marker that might help detect advanced pancreatic cancer in some people, but it is not used as often as
CA 19-9.15 It is important to note that neither of these blood tests will be used definitively to diagnose
cancer but they may help track the success of treatment.
If signs, symptoms, and examination favor the diagnosis of cancer, a biopsy will likely be taken in
order to solidify suspicions. Biopsy is the only way to be certain if a tumor or mass is cancerous or not.
During a biopsy, a sample of tissue will be obtained and studied microscopically to look for
abnormalities. There are 3 main methods of performing a biopsy: percutaneous, endoscopic, and
surgical.9 Percutaneous biopsy, also known as a fine needle aspiration (FNA) utilizes images from
ultrasound or CT scan to guide a fine needle into place through the skin over the abdomen into the
pancreatic tumor.15 Percutaneous FNA is an established means of diagnosing the cause of pancreatic
masses, has been shown to have a low complication rate (3- 6.7%), and has been proven to have 81%
accuracy in diagnosing pancreatic masses.16 Transabdominal percutaneous biopsy may be difficult if the
patient is obese and/or is suffering from abdominal distention related to liver dysfunction. As previously
discussed, it may be common for many patients to have both of these presentations.
Endoscopic sonography (and related biopsy) was developed in the 1990s to overcome
limitations of transabdominal sonography caused by intervening gas and fat.

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Endoscopic biopsy involves the passage of a thin, flexible, tube with a small video camera on

the end through the throat and into the small intestine near the pancreas to obtain a tissue sample.15
Endoscopic sonographically-guided FNA biopsy of the pancreas has been used for the past 10 years,
with a documented accuracy of 76%.16 Surgical biopsy is another method of obtaining tissue sample but
may be more invasive than percutaneous or endoscopic methods. Surgical biopsy, or laparoscopy is a
procedure whereby a small telescope is inserted inside the abdomen through a small surgical incision
and can detect the spread of a tumor not identified on CT scanning.17 This procedure is also known as
a keyhole surgery.17 Surgical biopsies are now done less often than in the past, however they may be
useful if the surgeon is concerned the cancer has spread beyond the pancreas and wants to look at
and/or biopsy other organs in the abdomen.15 After the tumor(s) have been identified, it is possible to
stage the degree of the disease. Staging may help determine plan of care, estimated survival time, and
the necessity or type of nutrition intervention warranted.
VI. Staging
The extent of a cancer at time of diagnosis is a key factor used to define treatment and to assess the
chance of successful treatment outcome.

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The most widely used staging system among clinicians is the TNM system maintained by the

American Joint Committee on Cancer (AJCC) and the International Union for Cancer Control
(UICC).18 This system codes the extent of the primary tumor (T), regional lymph nodes (N), distant
metastases (M) and provides a stage grouping based on T, N, and M.18 T describes the size of the
primary tumor and whether it has grown outside the pancreas and into nearby organs; N describes the
spread to nearby lymph nodes; and M indicates whether the cancer has metastasized to other organs
of the body, the most common of which are the liver, lungs, and peritoneum.15 Numbers or letters
appear after T, N, and M provide further details about each of these factors.
Once the T, N, and M categories have been determined, a process called stage grouping is
performed. The defined TNM information is combined and evaluated to assign an overall numerical
stage of 0, I, II, III, or IV.

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Details of this delineation are outlined in figure 7. Note that stage IV cancer has any tumor,

any involvement of the lymph nodes, and metastatic involvement. As well as staging, the tumor(s) may
be characterized as resectable, borderline resectable, or unresectable. Tumors are deemed to be
resectable if the cancer is only in the pancreas or has spread just beyond it, and the surgeon believes the
entire tumor can be removed.15 Borderline resectable tumors describe some cancers that might have
just reached nearby blood vessels, but which the doctors feel might still be removed completely with
surgery.15 Unresectable tumors cannot be removed entirely by surgical methods.15 Unresectable tumors
may be classified as locally advanced, or metastatic. Cancer is considered locally advanced if it has not
yet spread to distant organs but it still cannot be removed completely with surgery.15 Often the reason
the cancer cant be removed is because it has grown into or surrounded nearby major blood vessels.15
Metastatic cancers are often perceived as a diagnosis of poor prognosis. This term means the cancer
has spread to distant organs, and cant be removed completely.15 Surgery might still be done but the
goal would be to relieve symptoms, not to cure the cancer.15 The TNM classification of the tumor, as
well as its overall stage can help to determine the type of treatment best suited for a patient.

Figure 7. Numerical classification of pancreatic tumors based on T, N, M 18


VII. Treatment
Treatment of pancreatic cancer may aim to be either curative in nature, or palliative. The most
common curative measures in practice are surgery, ablative techniques, and adjuvant therapies.
Palliative measures include paracentesis, bowel regimens, and pain management. The most widely
known surgical intervention for pancreatic cancer is the traditional pancreaticoduodenectomy (PD), or
Whipple procedure. The Whipple procedure is a complex, high-risk surgical procedure, with the lowest
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operative mortality rates and best long-term outcomes being demonstrated at high-volume
centers.19 In experienced hands, the median operative time for the Whipple procedure is 5.5 hours, with
a median blood loss of 350 mL and mortality of less than 4 percent.19 This procedure involves removal
of the pancreatic head, duodenum, first 15 cm of the jejunum, common bile duct, and gallbladder, and a
partial gastrectomy (Figure 8).19 The majority of exocrine pancreatic cancers (85 percent) are
adenocarcinomas with only 15 to 20 percent of patients being candidates for surgery due to the late
presentation of the disease.19 The prognosis of pancreatic cancer is poor even in those with potentially
resectable disease and as mentioned with diagnostics, preoperative imaging evaluation determines
candidacy for resection. Although only 15 to 20 percent of patients are candidates for surgery, and the
traditional procedure has a low mortality rate when performed by skill surgeons, side effects of resection
are still a topic of contention and will be discussed later in greater detail.
Modifications of the conventional pancreaticoduodenectomy procedure have been developed
in an attempt to improve outcomes or minimize the morbidity associated with the operation. It has been
proposed that preservation of the pylorus during resection may decrease incidences of postoperative
complications. The pylorus is a muscular feature of the distal end of the stomach that connects it to the
duodenum. A pylorus- preserving pancreaticoduodenectomy (PPPD) preserves the gastric antrum,
pylorus, and the proximal 3 to 6 cm of the duodenum, which is anastomosed to the jejunum to restore
gastrointestinal continuity (Figure 9).20
This procedure may decrease the incidence of postoperative dumping typically associated with any
gastric resection. The available data suggest that, for suitable cases, perioperative morbidity and
mortality and long-term survival are not adversely affected using a pylorus-preserving technique.

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Irrefutably, some patients will choose aggressive measures such as surgery but they are not without

complication and do not guarantee long-term survival.


While it is theorized that the PPPD may reduce postoperative side effects, there are definite
complications for both the traditional and modified surgery. Common complications for both procedures
include delayed gastric emptying (DGE) and septic complications with intra-abdominal abscess and
abdominal hemorrhage of particular notability.21 DGE has emerged as the leading procedure-related
patient morbidity.21 It should be known that there are no current criterion or set definition for DGE in
studies evaluating the occurrence of these symptoms. Treatment consists of nasogastric decompression,
attention to nutritional support, reassurance and watchful waiting.21 The pancreatico-enteric anastomosis
is the Achilles heel of PD and its modifications however, if it leads to retroperitoneal sepsis with abscess
formation and/or destruction of the surrounding tissues and blood vessels with the potential for severe
hemorrhage.21

Figure 8. Traditional Whipple

Figure 9. Pylorus- Preserving Pancreaticoduodenectomy

Ablative techniques may be implemented in addition to, or in place of traditional or modified


surgeries. Ablative techniques are methods of destroying or removing cancerous tissue. One common
type of ablation is removal of damaged tissue radiofrequency. This technique uses high frequency
current and heat to destroy cancer cells, and is most commonly used for cancers that are difficult to
remove surgically.
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22

Adjuvant therapy will be used in addition to surgery, and can be understood as accessory care

that is intended to complement a primary treatment. Most often, the adjuvant therapies associated with
cancer are chemotherapy and radiation. These additional therapies comprise treatment of pancreatic
cancer due to its high rate of recurrence. Systemic recurrence is seen in >80 percent of cases, local
recurrence is seen in >20 percent (UpToDate).
Chemotherapy uses chemicals or drugs in the treatment of neoplasms. It has been shown to
improve overall survival by reducing systemic recurrence and it is currently recommended that all
patients undergoing surgical resection also begin some form of chemotherapy.23 For obese cancer
patients with a large body surface area (BSA), chemotherapy drug doses are often reduced because of
concern for excess toxicity.23 Since the prevalence of obesity is widely understood, it is necessary to be
aware that various practitioners may adjust pharmacologic doses in relation to body weight. However,
there is no evidence that fully dosed obese patients experience greater toxicity from chemotherapy for
pancreatic cancer.23 Medications used as chemotherapeutic agents, including mechanism of action and
common gastrointestinal side effects can be found in further detail in section IX; medications.
Chemotherapeutic drugs are generally administered to a patient through an implantable port. Implantable
ports are placed under the skin, into a vein for people requiring frequent IV access. This procedure
requires maintenance but prevents the patient from constant needle sticks.
Radiation therapy uses high-energy beams to destroy cancer cells. In pancreatic cancer, it has
been shown to reduce local recurrence of cancer but there are no high-quality studies demonstrating an
effect on survival that is independent of systemic chemotherapy.23 Both chemotherapy and radiation
treatments carry significant effects on the nutritional status of a patient, and will be discussed in the
medical nutrition therapy portion of this document.
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Palliative measures are treatments that aim to make the patient more comfortable without
attempting to cure the condition. Paracentesis is one form of palliative care that is often utilized to reduce
abdomen distention and make the patient more comfortable. Paracentesis may be necessary in patients
whose cancer has become metastatic, has traveled to the liver, and has resulted in fluid buildup around
the abdomen, otherwise known as ascites. Abdominal paracentesis is a simple bedside or clinic
procedure in which a needle is inserted into the peritoneal cavity and ascitic fluid is removed.24
Therapeutic paracentesis refers to the removal of 5 liters or more of fluid to reduce intra-abdominal
pressure and relieve the associated dyspnea, abdominal pain, and early satiety.25 Paracentesis may aid
in improving appetite and oral intake by decreasing abdominal pressure and pain. Pharmacologic
treatment that may be considered therapeutic involves the use of anti-emetics, opiates, pain relievers,
and cannabinoid derivatives. A bowel regimen may also be implemented to relieve constipation
associated with narcotic use, and lingering distention. Both curative and palliative measures will likely be
necessary to effectively combat pancreatic cancer.

VIII. Laboratory Findings 26


A. Comprehensive Metabolic Panel
-A series of 14 tests used as a broad screening tool to evaluate organ function and check for
conditions
-Includes glucose, calcium, albumin, total protein, Na, K, Cl, CO2, BUN, creat, ALP, AST, ALT,
bilirubin
-Abnormal test results or groups of test results are usually followed up with other specific tests to
confirm or rule out a suspected diagnosis.
B. CA 19-9
-Tumor marker used to differentiate between cancer of the pancreas and other conditions, such as
pancreatitis
-Used to monitor a person's response to pancreatic cancer treatment and/or cancer progression or
to watch for pancreatic cancer recurrence
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-Moderate to high levels are found in pancreatic cancer
-Highest levels of CA 19-9 are seen in cancer of the exocrine pancreas
C. CEA (Carcinoembryonic Antigen)
-Used in combination with other tumor markers in the evaluation of cancer
-Ordered when a person has been diagnosed with colon cancer or other specific types of cancer
-Measured before therapy is initiated and then on a regular basis to evaluate the success of treatment
and to detect recurrence
D. Amylase
-Used to help diagnose and monitor acute pancreatitis; often ordered along with lipase test.
-Used to diagnose and monitor chronic pancreatitis and other disorders that may involve the
pancreas
-Significantly increased in people with pancreatic duct obstruction and pancreatic cancers
E. Fecal Fat
-Positive results indicate that fat is likely not being absorbed normally and that the person may have
impaired digestion or malabsorption; Malabsorption is seen with a wide variety of diseases and
conditions.
-Causes of malabsorption include: Pancreatic insufficiency caused by chronic pancreatitis or
pancreatic cancer
F. Stool trypsin
Ordered
along with other tests, such as a fecal fat, to evaluate pancreatic insufficiency
-Negative result is not diagnostic, but indicative that further testing for pancreatic insufficiency may be
indicated
G. Serum trypsinogen
-Ordered when patient presents with symptoms suggesting pancreatic dysfunction such as persistent
diarrhea, foul-smelling, bulky greasy stools, malnutrition, and vitamin deficiency
-Elevation may indicate abnormal pancreatic enzyme production, pancreatitis, or pancreatic cancer
Elevated
levels may be a false positive and require further testing
H. Lipase
-Ordered when a person has symptoms of acute pancreatitis or another pancreatic disorder
-May be ordered at intervals to monitor pancreatic conditions and to evaluate the effectiveness of
treatment
-High levels may indicate the presence of a condition affecting the pancreas
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IX. Medications 27
A. Abraxane (Paclitaxel Albumin-stabilized Nanoparticle Formulation)
-Antimicrotubule agent exhibiting a unique mechanism of action
-Inhibits of normal dynamic reorganization of the microtubule network required for vital interphase
and mitotic cellular functions
Side
effects: Nausea, vomiting, diarrhea (N/V/D), loss of appetite
-

B. Adrucil (Fluorouracil)
-Antimetabolite of the pyrimidine analog type, considered to be cell cyclespecific for the S phase
of cell division.
-Activity results from its conversion to an active metabolite in the tissues, and includes inhibition of
DNA and RNA synthesis
-Side effects: N/V/D, esophago pharyngitis, loss of appetite, stomatitis
- Afinitor (Everolimus)
-Binds to and inhibits the mammalian Target Of Rapamycin (mTOR)
Prevents
protein synthesis and cell proliferation
-Side effects: nausea, decreased appetite, abdominal pain, constipation
C. Erlotinib Hydrochloride (Tarceva)
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-Reversibly inhibits tyrosine kinase activity of the epidermal growth factor receptor (EGFR)
-Inhibition of autophosphorylation of tyrosine residues associated with EGFR and dampened tumor
cell signalling, survival, and proliferation
-Side effects: N/V/D, abdominal pain, loss of appetite, indigestion, flatulence, inflammatory disease
D. Sunitinib Malate
-Multi-targeting receptor tyrosine kinase inhibitor
-Decreases tumor cell proliferation and angiogenesis
-Abdominal pain, constipation, diarrhea, indigestion, inflammatory disease of mucous membrane,
loss of appetite, nausea, pain of oral cavity structure, altered taste, vomiting

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Medical Nutrition Therapy
I. Role of the RD
Proper management for patients dealing with complex diseases such as cancer may require health
care from many specialties. A registered dietitian (RD) is a professional with expertise in nutrition
recommendations appropriate for people suffering from a variety of illnesses. Regarding oncologic
treatment, the RD may offer suggestions for prevention of cancer and may help the patient minimize
symptoms of gastrointestinal (GI) distress. Although food might not seem like a critical component of
care in light of such a devastating diagnosis, proper nutrition will help the patient maintain strength and
energy to fight the disease. The RD may also help the patient distinguish fact from fiction-based or
pseudo-scientific recommendations regarding nutrients, supplements, vitamins, etc. The RD may work in
an outpatient setting for those with standard therapeutic regimens, or may become visible in the inpatient
setting in cases of extreme weight loss, poor oral intake, intractable nausea, vomiting, or diarrhea. The
RD is also responsible for accounting of psychosocial factors such as mental status, family support,
income, and religious beliefs. Most often, the RD is seen in conjunction with patients experiencing the
following: loss of appetite, significant weight change, sore mouth or throat, dry mouth, difficulty
swallowing, dental and gum problems, changes in sense of taste or smell, nausea/vomiting, diarrhea,
constipation, or when requiring alternate forms of nutrition such as enteral/parenteral nutrition.28
II. Goals of Nutrition Therapy
In addition to considerations specifically made to address GI symptoms, nutrition therapy addresses
other relevant goals in this population. These objectives include: the prevention or reduction in

nutrient deficiencies, preservation of lean body mass, improved tolerance to treatment,


maintenance or improvement in strength and/or functional ability, enhancement of immune
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function by decreasing risk of infection, maximization of quality of life, increase in


independence, improved ability to perform activities of daily living (ADL), and relief of
symptoms rather than reversal of malnutrition or weight gain.29 In order to meet these
goals, loose recommendations have been made to guide nutrition professionals to a
competent and caring practice.
III. Macronutrients, Micronutrients, and Digestive Enzymes
Although there are no validated parameters for determining nutrition needs of patients with cancer,
there have been studies to evaluate energy expenditure in various types of cancer.29 The following table
summarizes the current caloric and protein estimations published by the Academy of Nutrition and
Dietetics (AND).29
Condition

Caloric
Requirements
kcal/kg

Condition

Protein
Requirements
g/kg

25-30

Normal maintenance

0.8-1.0

30-35

Non-stressed cancer patients

1.0-1.2

35

Patients undergoing treatment

1.2-1.5

Non-ambulatory sedentary adults


Slightly hypermetabolic, wt gain
Hypermetabolic, malabsorption

In addition to calories and protein, the micronutrient content of the diet may also be analyzed.
Micronutrients include the vitamin and mineral status of the patient. It should be noted that according to
the AND, specific measurement of vitamins and minerals is not considered routine assessment, and
there are no standardized indications for this type of treatment.

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29

The use of dietary supplements such as vitamins minerals, hormones, and herbs is a topic of

considerable controversy, especially in the cancer treatment phase.30 Generally speaking, patients and
the public at large should always try to obtain nutrients from food first, and the pill form of these
elements should never be considered an adequate substitute for a nutrient-dense diet.
The use of vitamin and mineral supplements at doses higher than recommended levels can raise
safety concerns, as is the case with mega-doses of vitamins C and E.30 Furthermore, vitamin
supplements that contain high levels of folic acid, or eating fortified food products that contain high levels
of folic acid may be counterproductive when taken during the administration of certain chemotherapy
agents.30 It is evident that there are still many unanswered questions and research needed on the
risk/benefit ratio of supplementation. However, it is currently recommended that patients undergoing
chemotherapy or radiotherapy should not exceed the upper intake limits of the dietary reference intakes
(DRIs) for vitamin supplements.30
While many patients and their family members may be willing to try methods of complimentary care,
it should be emphasized that medicines, including over the counter products should be taken under the
direct discretion of the physician. A reasonable health recommendation for a patient with pancreatic
cancer is to use a balanced multiple vitamin and mineral supplement (once or twice a day) to correct
possible deficiencies.

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30

Recommendations made to adhere to upper limits have been made in view of the restricted

dietary pattern of tumor patients. An exception to the abovementioned recommendations is the use of
vitamin D. Depending on the basal 25-OH-D3 plasma level, the vitamin D supply should amount to
1800-4000 IU/ day (45-100 g/day of cholecalciferol) in order to reach the desirable plasma
concentration of >75 nmoll/l in most oncological patients.31,32 As vitamins, minerals, and herbal
remedies are easily accessible, and the popularity of health food and specialized supplementation
stores rises, it is necessary that the entire medical team communicating cohesive information to the
patient at this vulnerable time. Patients should be directed towards other remedies that may alleviate or
prevent nutrient deficiencies.
Specifically in the case of pancreatic cancer, pancreatic enzymes can be supplemented to counteract
the malabsorption of food. These enzymes include amylase, lipase, and trypsin. Most often
malabsorption syndrome is characterized by a patients inability to digest fat or protein.29 Common
symptoms of malabsorption include bloating, indigestion, diarrhea, constipation, steatorrhea, and muscle
weakness. Steatorrhea is defined as fat malabsorption, and is characterized by stools that look oily,
frothy, are foul smelling or may float in water. Enzymes are taken orally and will in turn help the patient
receive the maximal nutrition from ingested food.
Electrolytes may also become unbalanced due to tumor-related processes and chemotherapyrelated side effects. Of note, a patient may become hyponatremic due to an increase in abdominal fluid.
Further disruptions in electrolytes are related to prolonged or intractable vomiting and diarrhea.
Frequent emesis or stool weight greater than 200 grams per day may disrupt sodium, potassium,
magnesium, chloride, and bicarbonate. Patients with severe disruptions in electrolytes may require IV
hydration and replacement or correction of losses. Additionally, chemotherapy may carry an inherent ri
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sk of nephrotoxicity, which may alter renal function and potentially exacerbate electrolyte
imbalances. Aside from a general multivitamin/mineral recommendation, the physicians and nursing staff
are responsible for corrections. RDs may have a greater impact on preserving a patients lean body
mass, strength, immunity, weight loss, and quality of life.

IV. Cancer Cachexia Syndrome


The loss of lean body mass (LBM) is largely accepted as a side effect of cancer and subsequent
treatment. This loss may be accounted for due to the tumor itself, cancer cachexia syndrome (CCS),
early satiety, inflammation, GI symptoms, and alterations in absorption.
It has been hypothesized that the tumor(s) will release certain cytokines, or cell-signaling messengers
that affect various metabolic pathways and may contribute to anorexia and a hypercatabolic state. These
pathways can be divided into central pathways, which are hypothalamus-mediated, and peripheral
pathways, which involve direct lipolysis and proteolysis.33 The response from the hypothalamus may
become inappropriate due to the increased cytokine expression from tumor growth.33 This disruption in
the hypothalamic response and relation to food intake may be understood at the most basic level by
acknowledging there are a number of neuropeptides located in the brain that control hunger and satiety,
thus leading to anorexia. Peripherally, the cytokines have also been shown to induce lipolysis, muscle
catabolism, and the hepatic acute phase protein response (APPR) through various pathways.33 Both the
central and peripheral pathways lead to the development of muscle and tissue mass loss. This loss of
muscle mass is further aggravated by the advancement of cachexia.

Figure 10. Hypothalamic Role in Mediating Appetite. Note interactions with gherlin and leptin.
These two hormones respectively are responsible for communicating hunger and satiety cues.
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Cachexia is a complex metabolic state that leads to depletion of energy and muscle stores in cancer
patients.29 Similar to tumor-mediated loss, cachexia leads to skeletal wasting as well as loss of adipose.
Cancer-associated cachexia occurs in up to 80 percent of patients with pancreatic cancer.33
Dissimilarly, these losses are not entirely associated with poor appetite or decreased caloric intake.
More accurately, inappropriately accelerated resting energy expenditure may contribute to the energy
deficits.33 This rise in energy expenditure is thought to be due to inflammatory markers such as tumor
necrosis factor (TNF-) interleukin-6 (IL-6).
TNF- was first identified as a cachexia-inducing factor in chronic diseases, and mouse models
have shown that TNF- may induce muscle protein degradation through formation of reactive oxygen
species (ROS).34 IL-6 secretion is induced by TNF-; it acts synergistically with TNF- in many of its
actions including stimulation of other cytokines.35 Circulating levels of IL-6 correlate with weight loss
and reduced survival in pancreatic cancer patients.34 IL-6 is known to activate the hepatic acute phase
protein response (APPR) and trigger tissue catabolism.35 The activation of hepatic APPR subsequently
results in hypercatabolism through reprioritization of body protein metabolism from skeletal muscle to
production of acute phase proteins.35 Production of these acute phase proteins by the liver can lead to
mobilization of peripheral amino acid stores primarily from skeletal muscle contributing to the loss of
lean tissue and catabolism. Overproduction of IL-6 and elevated APPR have been associated with
decreased survival in patients with pancreatic cancer cachexia.34 In totality, production of IL-6 and
TNF- conclude in loss of skeletal muscle and lean body mass.
The RD may be influential in helping the cancer patient understand the physiological changes within
the body during treatment. The RD must also keep in mind that among patients with cancer, cancerassociated cachexia syndrome is an independent risk factor for mortality.
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33

Straightforwardly, this means that presenting with cachexia increases the risk of dying in a disease

already characterized by a low survival rate. Therefore, it is of utmost importance for the RD to build
strong relationships with the oncologist, and nursing team to assure cognizance of this concept. Along
with nutrition intervention, pharmacology will likely become involved in the maintenance of CCS.
Although many agents have been evaluated for the treatment of cancer-associated cachexia syndrome,
only corticosteroids and progesterone analogs have proven benefit in palliation of the anorexia
associated with this syndrome; however the primary benefits associated with these drugs are increased
appetite and weight gain, not improved survival or quality of life.33 Weight loss is further complicated by
sensory changes in taste and smell. Moreover, as a patient receives each subsequent chemotherapeutic
treatment, a decrease in white blood cell count may occur. This decrease represents a linear correlation
to immune function, and is termed neutropenia. Patients in the hospital setting will often be placed on
neutropenic precautions. These types of patients must be treated with extra care regarding
transmission of infection, which includes certain dietary restrictions. Of note, these patients are generally
advised to refrain from consumption of fresh or raw fruits and vegetables. These items are thought to
increase infection rate and may limit the diet further. The RD should take responsibility in monitoring
certain parameters and contributing factors, which may indicate CCS.

Figure 11. Chemotherapy-induced weight loss

Weight loss is one major indicator that should be assessed frequently by the RD. Body weight
should be evaluated initially and routinely in all oncology patients, and assessment of body weight should
be based on change from usual body weight.

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29

Usual body weight (UBW) is a preferred method of analysis rather than ideal body weight

(IBW), especially in the elderly or obese. Weight loss of greater than 10% is correlated with lower
survival rates than those who are well nourished.29 The general parameters used to assess risk are: 5%
over 1 month, and 10% over 6 months. As implied previously, the weight loss may be due to a
combination of reduction in muscle mass and adipose tissue, referred to as proteolysis, and lipolysis
respectively.
Proteolysis is also thought to be tumor-mediated. Proteolysis-inducing factor (PIF) is a tumor
byproduct that has been indicated in the development of muscle catabolism and inhibition of protein
synthesis.29 PIF has been implicated for increased turnover of body protein stores and muscle
degradation.29 Furthermore, loss of body weight is not commensurate to protein loss. A loss of 30%
body weight has been correlated to a loss of 75% of skeletal muscle mass.29 For example, consider a 5
foot 11 inch man who weighs 260 pounds prior to illness, and loses 30% of his usual body weight; this
percent weight loss would equate to 78 pounds, with 58.5 pounds being attributed to loss of lean body
mass. This patient now at 182 pounds would be at a more appropriate weight for his height and have a
body mass index (BMI) within the normal range, yet this is still undesirable in the oncologic population.
Lipolysis is similar to proteolysis in that there are abnormalities in lipid mobilization. Although the precise
etiology this irregularity is not as well understood as with PIF, it is still thought to be related to the
release of cytokines, which decrease lipogenesis, and lipid mobilizing factor (LMF), and thus increase
lipolysis.29 LMF seems to act directly on adipocytes, causing release of free fatty acids and glycerol.36
In addition to definitive changes at the cellular and neurohormonal level, weight changes may also be
associated with early satiety, fatigue, and depression.
V. Further dietary complications
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Early satiety in the cancer patient may be caused by a variety of factors, including, delayed gastric
emptying, abdominal bloating, lack of gastroparesis, or obstruction. Pancreatic cancer patients
presenting at an advanced stage or with metastases may exhibit this symptom more frequently than
newly diagnosed or well controlled patients. This irregular feeling of fullness, combined with the wasting
factors as mentioned above leads to patients at great nutritional risk. Fatigue may also be an instrument
in loss of weight. Patients simply may be too tired to eat. Fatigue may be from exhaustive
chemotherapeutic treatments, stress, and other ongoing medical procedures. Fatigue is further
exacerbated by muscle and fat loss, and is therefore a cyclical symptom requiring attention.
Moreover, depression in the chronically ill population should not be ignored. Depression is often
classified as situational or chronic (non-situational). Cancer patients, especially ones that represent that
group with the lowest survival may experience both kinds of depression. The first or situational
depression may be caused by the realization of the loss in health. However, if the patient is unable to
move out of the depressive situation, he or she may become chronically depressed. Depression should
be taken seriously and may be managed medically, artistically, by development of coping skills, or by
involvement in support groups. In addition to the disease process itself, the related treatment also poses
undeniable challenges for the patient; of note are the prominent side effects.
The side effects of cancer treatment typically refer to the intensity and frequency of nausea and
vomiting. Nutrition interventions become difficult for the oncology patient due to intractable emesis, or
fear of future episodes. Although nausea and vomiting can result from surgery, opiates, or radiotherapy,
chemotherapy-induced nausea and vomiting (CINV) is potentially the most severe and most distressing.

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37

Adjustments to a patients medications or time of treatment may be made in attempts to diminish

side effects. Three distinct types of CINV have been defined, with important implications for both
prevention and management:
1.

Acute emesis, which most commonly begins within one to two hours of chemotherapy and
usually peaks in the first four to six hours37

2.

Delayed emesis, occurring more than 24 hours after chemotherapy37

3.

Anticipatory emesis, occurring prior to treatment as a conditioned response in patients37


who have developed significant nausea and vomiting during previous cycles of chemotherapy

CINV is thought to be caused by a complex set of mechanisms, including direct stimulation of the
chemoreceptor trigger zone, damage to the GI mucosa, and neurohormonal etiology.38
Figure 12. Etiologies of Nausea and Vomiting. Note the central portion labeled:
Chemoreceptor trigger zone.

Recurrent emesis carries serious implications such as dehydration, malabsorption of nutrients and
medication, vitamin deficiency, poor outcomes postoperatively, and disturbances in acid-base balance.
A singular or a combination of these responses may be a life-threatening condition. Nausea and vomiting
may also be caused by variations in bowel habits.
People with pancreatic cancer may often suffer from constipation. The inability to move stool may
be caused by a decreased digestive ability, or a reaction to antineoplastic treatment such as
chemotherapy or pharmaceuticals targeted for pain management. Commonly, opioid medications are
prescribed for pain. This class of medications is known to cause constipation in most people by slowing
GI motility and allowing stools to harden. In some cases, the stools may become so hard that they cause
an intestinal obstruction. Other general causes of constipation include decreased fluid intake, decreased
physical activity and decreased intake of fiber-containing foods. It is best to begin any patient on an
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opioid regimen with a concurrent bowel regimen to prevent these occurrences. Bowel regimens may
include the use of enemas or laxative. However, inclusion of a bowel regimen may result in diarrhea.
Development of diarrhea may indicate laxative disbursement that is either too strong or too aggressive.
Failure to correct diarrhea may result in similar negative consequences as outlined with intractable
vomiting.
VI. Supplementation
As recognized in depth in the preceding paragraphs, the ability to eat, digest and absorb food in the
pancreatic cancer patient is highly altered. An effort should be taken to rectify malabsorption. There are
three major principles underlying the management of patients with malabsorption and maldigestion, and
appropriate care of such patients in the majority of cases necessitates that each of these three are
addressed: (1) identification and treatment of the underlying disease, (2) treatment of the diarrhea that
often accompanies these disorders, and (3) identification and correction of nutritional deficits.39
Supplementation may be necessary for patients who are unable to consume adequate amounts of
calories through traditional diet alone. Supplements may refer to oral products, enteral nutrition,
parenteral nutrition, or a combination of all three.
Oral nutrition supplements (ONS) are taken by the mouth as the name suggests. These products are
available over the counter, online, and through health care facilities. These specialty goods have evolved
over time to include drinks, powders, bars, gels, jellos, puddings, ice creams, and freezer pops. Often,
these supplements are the first option utilized for auxiliary nutrition. Products of these categories are
usually less expensive and present a smaller possibility of complications. The intention of oral
supplementation is to provide extra calories and protein to patients unable to tolerate large volumes of
food. Furthermore formulas supplemented with eicosapentaenoic acid (EPA) and docosahexaenoic acid
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(DHA) may interfere with signaling pathways of pro-inflammatory cytokines and proteolysisinducing factor, which contributes to tumor-induced weight loss; a daily recommended serving size of 2
g has been shown to limit tumor-induced weight loss.29 Oral nutrition supplements are the preferred and
primary method of preventing or correcting inadequate energy intake. However, other options will be
considered if the patient is still unable to meet his or her needs. These secondary and tertiary methods
include enteral nutrition (EN) or total parenteral nutrition (TPN).
EN is a process of feeding the patient either directly into the stomach, or into the small intestine. This
method of feeding is the secondary choice for optimizing nutrition in patients who are unable to take
sufficient calories and protein orally, and is preferred to TPN. The American Society of Parenteral and
Enteral Nutrition (ASPEN) has detailed criteria for the appropriateness of implemental EN, or tube
feeding as they are called colloquially. If a patient is deemed to be malnourished, has lost a significant
amount of weight, cannot tolerate oral intake >10 days, and is suspected to be nil per os (NPO) for >7
days, enteral nutrition EN may be considered.40 EN may also be indicated perioperatively, or if any of
the gastrointestinal tract has become compromised, and the patient is experiencing obstructions or
suboptimal /absent digestive capacity.29 This type of feeding is intended to prevent the weight loss and
lean body wasting that acts as independent risk factor for increased mortality, as previously discussed.
However, although an impaired nutritional status is associated with reduced quality of life, lower activity
level, increased treatment-related adverse reactions, reduced tumor response to treatment and reduced
survival a causeeffect relationship has not yet been established between nutritional status and the
clinical course of the disease or overall prognosis.41
The goals of nutrition therapy for cancer patients include prevention and/or reversal of malnutrition,
improvement in the quality of life, and to reduce adverse effects of anti-tumor therapies.
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41

Unlike in critical illness, or sepsis, there are no data from controlled studies to suggest a cancer-

specific enteral formula, such as formula enriched with glutamine or other immune modulating substances
on the nutritional status of cancer patients, aside from perioperative nutrition.41 However, a patient may
benefit from a high calorie, high protein, limited volume formula if he/she is experiencing early satiety or
abdominal distention. While it may seem ideal to treat the patient in this fashion, there are circumstances
in which provision of EN is not warranted, and furthermore may be a detriment to the patient. EN is
contraindicated if the patient has severe short bowel syndrome (<100 cm remaining), persistent
postoperative ileus, high output fistulas, severe gastrointestinal bleeding, severe gastrointestinal
malabsorption (i.e. radiation enteritis), hypotension (with a mean arterial pressure less than 60
millimeters of mercury), bowel obstruction, or simply if EN is not appropriate or desired.29 While the
RD may desire to make interventions related to the most favorable outcomes, the patients needs and
desires must always be considered first. If neither ONS nor EN are successful, and aggressive measures
are still being taken for the patient, the use of TPN may be indicated.

Figures 13 and 14. Development of Cancer-Related Malnutrition

TPN should only be used when EN is not possible due to the lack of access to the gastrointestinal
tract or to unavoidable dysfunction including severe malabsorption, high output fstula, dysmotility, or
abdominal pain.42 TPN is associated with an increased rate of infection, and a decline in the integrity of
the GI tract. As with the commencement of EN, there are strict standards for the use of TPN in the
clinical setting. In 2002, the American Society for Parenteral and Enteral Nutrition published the
following guidelines for the use of nutrition support in cancer patients:
1.

Specialized nutrition support should not be used routinely in patients undergoing major
cancer operations.40

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2.

3.

Perioperative specialized nutrition support may be beneficial in moderately or severely


malnourished patients if administered for 7 to 14 days preoperatively, but the potential benefits
of nutrition support must be weighed against the potential risks of the specialized nutrition
support itself and of delaying the operation.40
Specialized nutrition support should not be used routinely as an adjunct to chemotherapy.40

4.

Specialized nutrition support should not be used routinely in patients undergoing head and
neck, abdominal, or pelvic irradiation.40

5.

Specialized nutrition support is appropriate in patients receiving active anticancer treatment


who are malnourished and who are anticipated to be unable to ingest and/or absorb adequate
nutrients for a prolonged period of time.40

6.

The palliative use of specialized nutrition support in terminally ill cancer patients is rarely
indicated.40

Complications of both EN and TPN may include refeeding syndrome, whereby nutrients are rapidly
taken into the cells, leaving the bloodstream devoid. The most common nutrients to be altered are
glucose, potassium, magnesium, and phosphorus. Dramatic changes in these electrolytes may lead to
cardiac, respiratory, and neurological complications.29 The decision to begin nutrition support of any
kind should be agreed upon by the entire medical team and will require daily supervision. If it is deemed
that the patient is with poor prognosis, the healthcare team should reprioritize the patients comfort and
quality of life as the superior goals of treatment.
VII. Palliative Care
Comfort care, comfort measures only, or palliative care are all terms used clinically that refer to the
transition of care from a curative objective to one with a focus on relief of symptoms. Palliative care is a
specialization includes medical expertise in symptom management, psychosocial care, communication,
complex decision making, end-of-life care, and is a fundamental component of cancer care.

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43

Caring for people in this regard may help the patient come to terms with end-of -life process and

provide them with the opportunity to enjoy his or her remaining months. The management of pancreatic
cancer today is an interdisciplinary team effort. Palliative therapy has been shown to improve quality of
life, decrease symptom intensity, and elevate mood, as well as minimize unnecessary resource
consumption by patients whose survival is limited.44 Although some countries have already integrated
palliative care into routine oncology practice, the United States has a national cancer control plan that
envisions the inclusion of palliative care as a routine part of comprehensive cancer care for all patients
by 2020.45,46
Unfortunately in many cases, the involvement of the RD will usually will not present until the patient
is at an advanced stage and he or she is already considering comfort care. Prior to this decision, the
patients family may have many questions related to the nutritional status of their loved one. It is
acceptable to provide them with techniques for management of symptoms and to explain that aggressive
measures such as EN or TPN as mentioned antecedently may not be appropriate. Furthermore, the
presence of a RD at the bedside who has the time to sit with the patient and discuss his or her concerns
may help to comfort the family. It may also reveal information that may have been missed otherwise by
the medical staff. Although interventions may be limited, it is still worth visiting these palliative care
patients.

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Presentation of the Patient
Diagnosis: Obstipation/intestinal obstruction secondary to pancreatic cancer with metastases to the liver
and peritoneum (retroperitoneal and mesenteric nodes); adenocarcinoma at head of pancreas
Other issues: abdominal distention, aspiration pneumonia, atrial fibrillation, constipation, normocytic
anemia
Allergies: Metaxalone (muscle relaxant)
Duration of Illness: diagnosed late August 2014; attempted Whipple at HUP. Patient traveled to Johns
Hopkins for a second opinion where he was put on a bowel regimen and told to build up his strength
and nutrition. Patient had planned on returning to Johns Hopkins for chemotherapy when he presented
at Doylestown Hospital with obstipation.
Past Medical History: hypertension, atrial fibrillation, diabetes mellitus (II), gastroesophageal reflux
disease, arrhythmia, high cholesterol; failed Whipple with post-op GI bleed, mitral valve repair x 2,
biliary stent
Age: 57/58
Sex: M
Race: Caucasian
Family History: Noncontributory
Social History: Patient lives with his wife in a one-story home. Patient was independent with activities of
daily living and ambulation prior to admission. Patient does not smoke and has no history of alcohol
abuse. Pat works as a financial advisor and has one son at Lehigh University.

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The Medical/Surgical/Nutritional Hospital Course
Refer to Appendix A for ADIME assessments
September
30
Patient admitted; abdomen distended/tender, hypoactive/distant BS; intractable nausea; vomiting;
abdominal discomfort rated 4/10 post pain meds
MOM (milk and molasses) enema given
CAT scan and rectal exam given
Initial nutrition care note; picked up pt for reported wt loss >33 lbs; Unintended weight loss
October
1
Paracentesis (5 L)
Placed on full liquid diet
Oncology consulted
2
Management of symptoms
Intermittent nausea; Zofran provided; eating less than 50% of meals
Pt NPO for port placement
2nd nutrition care note: inadequate oral intake

3
CTX port placed
Cycle 1, day 1 palliative gemcitabine and abraxane
Pt with some fullness; no nausea; no vomiting; poor PO

intake; fatigue

4
Rest

5
Obstruction series; showed distended loops of large bowel, no
Pt c/o pain (7/10); abdomen continues to be painful, distended
Medicated with 4 mgs PO Dilaudid
Pt refusing NG tube due to pain

obstruction

6
Pt remains NPO
Medicated with Compazine IV
Medicated with5/10 with IV Morphine and

PO Dilaudid for c/o abdominal pain and generalized


discomfort (5/10)
Repeat paracentesis (1.7 L)
Third nutrition care note: Inadequate oral intake
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7
Pt feeling reasonably well
Pt eating small amounts of eggs and

other semi-solids; no vomiting; passing gas but no BM x 3 days

8
Pt with difficulty tolerating diet
Pt with significant pain and nausea requiring IV meds
Unable to discharge patient at this point in time; discussed with oncology.
Planned continued supportive care with anticipated chemotherapy
Pt requiring IV narcotics and around the clock antiemetics
Pts cousin would like a dietitian to be involved with patient's care to increase his PO
Family requested palliative care consult
Plain xray; shows resolution of bowel dilation seen on xray 10/5/2014.
4th nutrition care note: Inadequate oral intake

intake

9
Pt celebrates 58th birthday
Repeat paracentesis (6.7 L)
Pt states he wishes to proceed

with additional chemo; states he would like his pain and nausea to be
under better control; states he wishes he could eat more
Pt asks if it was possible to be "pain-free and comfortable" if/when he wished no more treatment
Pt educated briefly about hospice care
10
Second CTX; Gemzar and Abraxane
Pt states he is more nauseous today while receiving chemo
Pt with increased Fentanyl/Dilaudid dose; no vomiting
5th nutrition care note: Inadequate oral intake

11
Pt with poor performance status and increasing pain
Sister at bedside asking about TPN
Pt reports he is feeling nauseous, very tired and weak; trying to

eat small amounts of food

12
Repeat obstruction series; unremarkable; no
Pt eating virtually nothing
Nausea medicines made round-the-clock

clear reason for continued nausea

13
Family continues to wish to aggressively treat the pt's underlying disease hoping he will improve
Family gently informed that pts options remain of limited usefulness
Lengthy, 45 minute family conference with patient, wife, and sister, palliative care team, and oncology
Pt able to eat and drink small to moderate amounts of food and liquid (water and Ensure liquid)
Pts family requests to take him home; provided resources for obtaining homecare services,

accommodations, etc.
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6th

nutrition care note; consult for tips for providing kcal/pro at home; pt family unavailable;
inadequate oral intake

14
Marinol administered for appetite stimulant
Family asking again about TPN; discouraged by P.A. unless performance status drastically improves
Frank discussion with pt today about his overall prognosis and that he should think about how he would

like to spend his time.


Pt very frustrated because his family keeps pushing him to eat today eat but reports worsening of nausea
No progression during this hospitalization; oral intake remains minimal due to persistent nausea; on

maximum nausea medication; cousin inquiring about TPN; informed her and the patient that in the
scheme of things if it would be of meaningful benefit; nevertheless remain quite interested
Pt not cleared for discharge today; still has issues with pain management and nutrition/nausea
Family receives hospital bed for home
7th nutrition care note: second attempt to educate family on providing high kcal/pro foods at
home; Inadequate oral intake
15
Dramatic drop in WBC despite daily Neupogen injections
Pt with 300 mL bile colored emesis
Repeat paracentesis (6.3 L)
Pt informed he is unable to undergo further CTX due to further decrease in WBC
Miserable prognosis discussed with pt; Suggested his son come home from college ASAP

to be with him;

life expectancy measurable in weeks; family undecided about hospice


16
Pt continuing to

request chemotherapy, if able; explained he would not qualify for until his white count is
dramatically improved; pt understands but continues to hold out hope
Son home from college for the day
17
Pt with continued nausea; development of hiccups; increasing pain
Wife signs hospice consent
IVF d/c
Pt placed on inpatient hospice at DH
DNR status confirmed
Morphine drip initiated 1mg/hr
8th nutrition care note: Inadequate oral intake

18
Pt with intermittently restlessness
Morphine increased to 3mg/hr
Pt states that he is "hurting and uncomfortable"
Morphine increased to 4 mg/hr
Pt having increased pain with movement.
Morphine increased to 5 mg/hr

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Pt reports an intolerable amount of pain

19
Patient reports pain is OK.

Still has intermittent nausea.

20
Patient continues with pain particularly with repositioning,

anxiety and nausea; reluctant to accept

increased pain medication choosing to be more alert.


Morphine drip maintained at 9 mg/hr.
21
Pt with many visitors this evening but became restless and
Ativan given
Patient c/o increased pain, unable to rate pain level
Increased Morphine drip to 10mg/hr

anxious

22
Continues with intermittent agitation; receiving Lorazepam for management
Support offered to spouse
Morphine at 11 mg/hr
Patient restless attempting to get up out of bed. Patient also lethargic and very weak

on bilateral lower

extremities.
23
Pt restless grabbing at foley,

pulling gown off, generally restless. Pt does open eyes at times but pt us
clearly groggy, medicated. Pt with some hiccups
Morphine drip increased to 14mgs/hour
Medicated with Compazine.
Pt continues with occ. harsh non productive cough. Attempts were made to suction the back of pts throat
which were unsuccessful in getting secretion from back of throat. Pt was suction naso-pharyngeal.
Suctioned for a moderate amount of thick yellow secretions. Mouth care given.
24
Pt was resting comfortably for most of shift but became very restless with care.
Received Ativan and Zofran at midnight.
Morphine drip increased to 16 mg/hr.
Mouth care given freq and suctioned for small amt yellow thick mucus.
Patient essentially unresponsive today, scattered rhonchi and oral secretions present.
Patient's son to visit today, family feels this might be the closure the patient needs.
Son arrived at 13:25.
Pt found unresponsive; pronounced dead at 14:25 pm

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Critical Commentary

This patient presented with a very advanced disease to an intern with approximately 1 month of
clinical experience in a conservative hospital setting. The patient frequently commented on his appetite,
stating that he wished he could eat more. The family was also very invested in the patients nutrition,
frequently asking about venous feeding. Although the patient experienced intractable nausea, and
vomiting, TPN was still not appropriate considered his functioning GI tract, low immune function with
chemotherapy, untreatable condition, and poor prognosis of the patient. Nutrition support was
recommended multiple times, however the patient refused a NG tube placement due to pain. The
patient was NPO upon admission for his suspected bowel obstruction but was placed on a regular diet
after its resolution. The patient was supplemented orally with Ensure BID, and Ensure Clear once the
traditional supplement became intolerable. For a brief period of time, it seemed as if the family would
take the patient home, and again they consulted nutrition for education on providing adequate calories
and protein. The patient would go consecutive days, often 4-5, without eating anything prior to
placement on hospice.
The patient verbalized frustration with his family wanting him to eat but being unable to. Until
September 15th when the patient experienced a dramatic drop in white blood cell count, he was still a
candidate for chemotherapy. In retrospect, more aggressive dietary measures could have been taken to
match the level of medical treatment he was given. Although the medical team noted poor prognosis
prior to the patient becoming neutropenic, the family and patient had not yet withdrawn care. Despite
constant attempts by both the family and patient to increase nutrition, the patient was only offered simple
interventions such as oral nutrition supplements, Marinol and anti-emetics to correct anorexia.
Furthermore, this patient had been seen at Johns Hopkins and related specific instructions to build up
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nutrition in order to initiate treatment there. The decision to continue with aggressive measures
was noted multiple times by the medical staff, along with anorexia, skeletal wasting, odynophagia,
dysphagia, nausea, hyperemesis, and desire to build up nutritional status. It is likely that further
interventions were deemed futile by the medical staff, or they were unwilling to risk failure.
Retrospectively, a nasojejunal tube would have been a viable option considering the patients requests
to keep fighting his disease. Improvements in feeding could have been implemented rather than
aggressive consultations with palliative care. In this particular case, a traditional jejunostomy tube would
have been contraindicated due to significant ascites and peritoneal metastases. Considering that
placement of NG tube was not wanted by the patient, and his life expectancy was weeks, palliative
measures were appropriate.
Summary
The summation of nutrition care for this patient was palliative measures. Since the passing of this
patient, the writer has encountered many more oncologic patients and was much more assertive in their
care. Future encounters with this population led to more in depth assessments (including physical
examinations), frank discussions with the family and patients about the necessity and importance of
nutrition during treatment, greater interdisciplinary communication with nursing, quicker
recommendations of supplements and/or artificial feeding, a greater understanding of physiologic
functions of the pancreas, and an overall improvement in comfort level dealing with diagnoses of
terminally patients. No further contact has been made with the family.

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Appendix A- Nutrition Assessments
No. 1 - September 30, 2014, initial assessment
A- Reviewed due to consult received. Per clinical data pt had indicated a history of wt loss of greater
than 33 lbs. Spoke with pt who stated his weight was running around 270-275lbs. Last weighed this in
march beginning April. CBW reflects a wt loss of 57-62 lbs or 21-22% wt change. Pt states some of
the wt loss was done by design while some was lost due to illness. Unable to provide specifics though
believe most of wt loss was from illness. Discussed case with RN who stated pt received MOM enema
last pm in ER and had positive bm. Per ER documentation and H&P pt was informed he was
constipated as pt informed RN full of stool". As discussed with RN unsure if constipation resolved as
pt still appears very distended. Concur with NPO this time. Would progress diet as tolerated. Needs:
2420 calories, 116 gm protein. Pt needs were based on evidenced based guidelines for ca of 25
calories/kg bw and 1.2 gm protein/ kg bw.
D- Inadequate oral intake related to decreased ability to consume sufficient energy as evidenced by
NPO status
I- To request diet progression as tolerated
-Encourage meal intake when diet initiated to assure pt consuming meals at 50% or greater
-Request to provide ensure plus when diet initiated
*Left note for MD
Recommend to progress diet as medically feasible and as pt can tolerate
Recommend ensure plus bid
Goals- To meet estimated calories and protein needs while hospitalized
Monitor/Evaluation:
-Monitor gi function, ability to progress diet, tolerance to diet, meal intake when diet initiated, weights
per level of care
Level of care: 2- 10/3 FU
No. 2 - October 3, 2014, follow up
A- Follow up as per level of care. Pt admitted with Obstipation, abdomen pain, distention, n/v PMH:
HTN,pancreatic ca-liver mets,DM,arrhythmia, high cholesterol. pt presently receiving a regular diet
with ensure BID as per previous RD request as appropriate to maximize po intake which has been 025%. RD visited with pt and wife, pt noticeably tired falling asleep while talking. Discussed with wife
need to try and get supplements in for pt due to sleeping and being too nauseous to eat. Suggested
trying small portions of ensure be provided to pt through out day to avoid overloading pt with too much
food at one time. pt did say he was able to get some scrambled egg and applesauce down today.
needs were based on evidenced based guidelines for ca of 25 calories/kg bw and 1.2 gm protein/ kg
bw. Labs and meds reviewed. Skin intact.
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D- Inadequate oral intake related to decreased ability to consume sufficient energy as evidenced by
NPO status 10-3 diet advanced new diagnosis
Inadequate oral intake related to decreased appetite as evidenced by poor po intake
I- Nutrition Intervention:
-Provide diet as ordered with ensure BID
-Recommend providing pt with small amounts of ensure at a time to sip on through day. Discussed with
RN
Eval/Monitor: follow as per level of care regarding po intake, wt, labs and skin
level 2 10/6 FU
No. 3 - October 6, 2014, follow up
A- Follow up as per level of care. Pt admitted with obstipation, abdomen pain, distention, n/v PMH:
HTN,pancreatic ca-liver mets,DM,arrhythmia, high cholesterol. Diet downgraded to npo, pt with
vomiting, partial bowel obstruction per progress notes. Pt refusing NGT per nursing notes. Estimated
needs: 2,420 kcal 25 calories/kg bw due to ca and 116 gms protein 1.2 gm protein/ kg bw/ca. Labs
and meds reviewed. Skin intact. CBW 217 lbs BMI 29.4 10/6, noted 4 lb weight gain since admission,
suspect fluid as pt s/p paracentesis today, 1700 ml fluid removed; will monitor. Recommend as
tolerated progression of diet. If diet unable to be advanced consider start EN as pt with >50lb weight
loss in past 7 months, intakes of >75% of only 2 meals in last 7 days and pancreatic ca. RD available
for recommendations as needed.
D- Inadequate oral intake related to decreased appetite as evidenced by poor po intake; 10/6 pt now
npo due to partial bowel obstruction
I- Recommend nutrition support per RD recommendations if diet unable to be advanced.
M/E- follow as per level of care regarding po intake, wt, labs and skin
Level 2 10/9 follow up
No. 4 - October 8, 2014, follow up
A- Level of care follow up note: pt admitted with Obstipation, abdomen pain, distention, n/v PMHx:
HTN, pancreatic ca with liver mets,DM,arrhythmia, high cholesterol. Skin: intact. Labs/meds reviewed
10/8. Current diet: regular (upgraded from NPO 10/6). PO intake ranging from refusal to 80% with an
average of 33% over the past 3 meals. Concur with current diet per pt tolerance and estimated needs of
2,420 kcal (25 calories/kg bw due to ca) and 116 gms protein (1.2 gm protein/ kg bw/ca). CBW 10/8:
221 lb (30.0 BMI) with 4 lb wt gain since previous assessment; suspect fluid wt gain due to positive I/O
of 2590 mL. Pt reports normal appetite but expresses severe pain upon eating, stating "I'd love to eat a
hamburger but I'd barf all over." Pt tolerating small amounts of Ensure. Recommend Ensure clear
instead as the pt might have better tolerance.
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D- Inadequate oral intake related to decreased appetite as evidenced by poor po intake
I- Adjust supplement per RD recommendations
M/E: -RD to monitor PO, wt, skin, and labs as per level of care
Level 2: 10/10 FU
No. 5 - October 10, 2014, follow up
A- Level of care follow up note: pt admitted with Obstipation, abdomen pain, distention, n/v PMHx:
HTN, pancreatic ca with liver mets,DM,arrhythmia, high cholesterol. Skin: surgical only. Labs/meds
reviewed 10/10. Current diet: regular (upgraded from NPO 10/6). PO intake ranging from refusal to
100%, with an average of 52% over the past 6 meals. However, should note average meal pt is eating
is approximately 335 kcal. Concur with current diet but would consider addition of supplement per pt
tolerance and estimated needs of 2,420 kcal (25 calories/kg bw due to ca) and 116 gms protein (1.2
gm protein/ kg bw/ca). CBW 10/10: 218 lb (29.6 BMI) with an 8 lb wt loss since last assessment.
Note previous wt gain and paracentesis x 2. Overall, Pt +5 lbs since admission. Pt reports nausea and
painful abdomen. Pt expressed interest in Ensure Clear (Apple). Recommend supplementation daily.
D- Inadequate oral intake related to decreased appetite as evidenced by poor po intake
I - Addition of supplement per RD recommendations
M/E- RD to monitor PO, wt, skin, and labs as per level of care
Level 2- 10/13 follow up
No. 6 - October 13, 2014, follow up
A- Level of care follow up note: pt admitted with Obstipation, abdomen pain, distention, n/v PMHx:
HTN, pancreatic ca with liver mets,DM,arrhythmia, high cholesterol. Skin: surgical only. Labs/meds
reviewed 10/13. Current diet: regular with Ensure BID. PO intake ranging from refusal to 100%, with
an average of 23% over the past 6 meals and 7 days. Pt only consuming 1/2 bottle of Ensure per day.
Pt declines any further supplementation (Ensure clear, pudding, etc). Concur with current diet due to
estimated needs of 2,420 kcal (25 calories/kg bw due to ca) and 116 gms protein (1.2 gm protein/ kg
bw/ca). CBW 10/10: 220 lb (29.6 BMI) with fluctuations throughout admission; suspect fluid related to
ascites, and paracentesis x 3. Per palliative care note 10/13, pt has been able to eat and drink small to
moderate amounts of food and liquid (water and Ensure liquid); pt reports pain and nausea well
controlled today only. Consult was sent later regarding oncology nutrition, however patient was unable
to receive teaching and family was not present. Education material was left in the paper chart for pt wife
regarding high calorie/high protein food, oncology nutrition tips, and oncology teaching tips. Note to
wife was left along with RD office telephone number. Will attempt education again on 10/14 if pt still
admitted.
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D- Inadequate oral intake related to decreased appetite as evidenced by poor po intake
I- RD available upon pt/pt wife request; follow up with requested education
M/E- RD to monitor PO intake, wt, skin, and labs as per level of care
Level 2- 10/14 FU for education
No. 7 - October 14, 2014, consult for nutrition education
A- Level of care follow up note: Chart reviewed due to consult by pts family. Pt admitted with
obstipation, abdomen pain, distention, n/v PMHx: HTN, pancreatic ca with liver mets,DM,arrhythmia,
high cholesterol. Skin: surgical only. Labs/meds reviewed 10/14. Current diet: regular with Ensure BID.
PO intake ranging from refusal to 100%, with an average of 25% over the past 6 meals. Pt only
consuming 1/2 bottle of Ensure per day. Pt declines any further supplementation (Ensure clear, pudding,
etc). Concur with current diet due to estimated needs of 2,420 kcal (25 calories/kg bw due to ca) and
116 gms protein (1.2 gm protein/ kg bw/ca). CBW 10/14: 222 lb (30.2 BMI) with fluctuations
throughout admission; suspect fluid related to ascites, and paracentesis x 3. Pt and family provided with
education regarding high calorie/high protein food choices as well as shopping/cooking tips for
oncology. Pts family was encouraged to provide small, calorically dense meals throughout the day,
drink between meals instead of with them, and providing calories was now the priority rather than his
previous diabetic restrictions. Pt family asking about possibility of TPN after discharged to home and
was educated on the standards of feeding for patients with functioning GI. Pt may benefit from enteral
nutrition due to continuous poor appetite. RD available for recommendations as appropriate.
D- Inadequate oral intake related to decreased appetite as evidenced by poor po intake
I- Consider nutrition support as appropriate
M/E- RD to monitor PO intake, wt, skin, and labs as per level of care
Level 2- 10/17 FU

No. 8 - October 17, 2014, follow up


A- Level of care follow up note: Dx:pancreatic ca with liver mets, obstipation, s/p chemo 10/3 and
10/10; s/p paracentesis 10/15. PMHx: HTN, DM,arrhythmia, high cholesterol. Skin: stage II: sacrum.
Labs/meds reviewed 10/17. Current diet: regular with Ensure BID. PO intake 0% over the past 4 days.
CBW 10/17: 209 lb (30.2 BMI) with fluctuations throughout admission; suspect fluid related to ascites,
and paracentesis x 4. Most recent paracentesis removed 6300 cc. Estimated needs: 2,375 kcal (25
calories/kg bw due to ca) and 142.5 gms protein (1.5 gm protein/ kg bw/ca and wound). Pt may benefit
from parenteral nutrition due to severe nausea/abdominal pain,
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0% PO intake for the past 4 days, continued poor appetite, and pt desire for treatment.
D- Inadequate oral intake related to poor prognosis metastatic pancreatic ca, severe pain, and nausea
as evidenced by 0% intake over the past 4 days
I- Nutrition support as appropriate; RD available for recommendations
M/E- RD to monitor PO intake/need for nutrition support, wt, skin, and labs as per level of care
Level 2- 10/20 FU
Pt placed on hospice 10/17
No. 9 - October 24, 2014, length of stay
A- Chart reviewed due to length of stay. Pt admitted to hospice on 10/17 after receiving inpatient care
beginning 9/30. Pt will not receive routine dietary follow up care, however RD is available per pt
request or consult. Per current clinical data, full assessment not required.
D- no nutrition diagnosis
I- none
M/E- dietary sign off
Level 4 care
Death pronunciation, 10/24/14 15:14

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Appendix B- Patient Specific Medication Bibliography 27,47
* N- nausea
* V- vomiting
*C- constipation
*D- diarrhea
Medication
Generic brand
Name brand
Acetaminophen
Tylenol
Bisacodyl
Dulcolax
Dexamethasone
Decadron
Dextrose
D5w
Docusate Na
Colace
Dronabinol
Marinol
Fentanyl
Transderm
Filgrastim
Neupogen
Heparin
Lorazepam
Ativan
Morphine
Ondansetron
Zofran
Prochlorperazine
Compazine

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Use

Contraindications

pain/fever relief

hepatic disease

constipation

appendicitis
gastroenteritis
disease of cornea
systemic fungal infect.
caution with DM

CINV prophylaxis
IV Zofran Dilution
Caloric agent
constipation

Side Effects/ NDI


N*/V*/C*
take w/o regard to food
colonic atony; take
with 1.5L-2L fluid
N/V, dyspepsia; take with
food to minimize
no GI side effects

intestinal obstruction
abnormal taste, N/D;
acute N/V
1.5L-2L fluid daily
CINV prophylaxis
hypersensitivity to cannabinoid abdominal pain, dry mouth,
N/V; avoid etoh
breakthrough pain relief paralytic ileus, respiratory
N/V/D/C, abdominal pain,
depression
loss of appetite, indigestion,
dry mouth
febrile neutropenia
hypersensitivity to E.Coli
no GI side effects
derived protein
antithrombotic/port
uncontrolled bleeding
N/V/C, GIB; caution with
flush
DM, ESRD, K+
anxiety/agitation
respiratory insufficiency, sleep N/V/C/D; caution with
apnea, glaucoma
grapefruit, limit caffeine
chronic pain
alcoholism, respiratory
N/V/C/D, anorexia; avoid
ETOH
depression
CINV prophylaxis
hypersensitivity
C/D, dry mouth
severe nausea/vomiting use of CNS depressants
children < 2

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N/V/C, dry mouth; take


with food to decrease
distress; avoid ETOH