2. Table of Contents
I. Patient Profile....................................................................................................................................5
II. Disease Background........................................................................................................................7
A. Epidemiology............................................................................................................................7
Pancreatic cancer is cancer of the pancreas, which accounts for about only 2 percent of all
newly diagnosed cancers in the United States each year; however it is currently the fourth
leading cause of cancer-related deaths. The American Cancer Society estimates that 43,920
(22,090 men and 21,830 women) new cases of pancreatic cancer will be diagnosed and about
37,390 patients will die in the United States in the year 2012 (3). The medical prognosis and
survival of patients with pancreatic cancer has shown little improvement over the past 30 years
with a 1.5% increase in cases every year (4). The 5-year survival rate for these patients in the
US is about 6% in Caucasians and 4% in Africans Americans. Pancreatic cancer is most
prevalent in elderly individuals of 45 years or older, and is more prevalent in men, and in
African Americans (5)....................................................................................................................7
B. Pathology and pathophysiology.................................................................................................7
C. Etiology......................................................................................................................................9
D. Symptoms................................................................................................................................11
E. Diagnosis .................................................................................................................................12
F. Medical Treatment...................................................................................................................14
G. Nutritional intervention...........................................................................................................16
The nutrition implication in pancreatic cancer is neither curative nor therapeutic. Once cancer
has developed and metastasized, especially pancreatic cancer, it cannot be reversed with diet,
let alone most drugs today. Most patients with exocrine pancreatic cancer require nutrition
intervention for symptoms related to the cancer, such as loss of appetite and or involuntary
weight loss and weakness. Managing and improving the adverse effects of chemotherapy and
radiation may be the biggest nutritional challenge. Nutrition intervention for pancreatic cancer
2
3. is usually significant in palliative care, to help progression of a comfortable and pain-free
quality of life. Typical nutrition interventions for cancer usually involve advising patients to
eat high-energy foods as well as supplements. Many patients need pancreatic enzymes in form
of pills for digestion in pancreatic carcinomas. Other interventions may involve nutrition
support therapies using Enteral or parenteral nutrition when feasible.......................................16
H. Prevention................................................................................................................................17
III. Present Illness and Medical Treatment........................................................................................18
A. Diagnosis and Treatment ........................................................................................................18
B. Medical Progression and Treatments.......................................................................................20
C. Medications..............................................................................................................................23
Most medications used for S.L. during his stay included antibiotics, anti-inflammatory and anti-
fungal drugs to treat the infection and sepsis. Other medications included lasix, antihypertensive
and diuretic for maintaining blood pressure and edema. Neupogen was used for formation of
blood cells, especiallu neutrophils and white blood cells, which were diminished after
chemotheraphy. Neupogen was highly regulated by the pharmacy by monitoring on serum WBC
levels. Proton pump inhibitors were used to treat gastroesophageal reflus disease (GERD) and
Zofran injections, an antiemetic drug, was used to treat nausea. Xenoderm and cubicin were
used to treat his skin ulcers and wounds. Additionally potassium chloride (oral and intravenous
piggy bag) and calcium gluconate were used as supplements to improve and replace electrolyte
levels. For more information on medications please refer to Appendix 1...................................24
IV. Nutrition Care Process.................................................................................................................25
A. Nutrition Assessment ..............................................................................................................25
B. Nutrition Diagnosis..................................................................................................................30
C. Nutrition Intervention..............................................................................................................30
D. Nutrition Monitoring and Evaluation......................................................................................33
V. Conclusion.....................................................................................................................................34
VI. Appendix 1: Drugs and Nutrition Implications............................................................................36
3
4. VII. Appendix 2: Pertinent labs and Nutrition Implications..............................................................38
VIII. Appendix 3: Nutritional Needs Calculations.............................................................................39
IX. Appendix 4: Nutrition Assessment Day 1 (March 15th)............................................................40
X. Appendix 5: Nutrition Assessment Day 5 (March 19th)...............................................................42
XI. Appendix 6: Nutrition Assessment Day 7 (March 21th).............................................................44
XII. Appendix 7: Nutrition Assessment Day 9 (March 23rd)............................................................46
XIII. Appendix 8: Nutrition Assessment Day 14 (March 27rd).........................................................48
XIV. Appendix 9: Nutrition Assessment Day 17 (March 30th) ........................................................50
XV. References..................................................................................................................................52
4
5. I. Patient Profile
S.L. is a 71 year old Caucasian male who was admitted to the St. John Providence Health
Center with metastatic pancreatic cancer. He was an independent man with no known disabilities
prior to admission and used to live with his wife in a two level home. He has stable living situation
and economically stable with insurance by Medicare and BlueCross. He is a college graduate with
no barriers to learning and speaks English. He doesn’t have any known food or drug allergies, and
denied any social history of recreational drugs or substance abuse. Information from the admission
assessment suggests that he has a lifelong abstinence of alcohol and that he has had no alcohol
containing drinks over the past year. However other healthcare notes stated that he had a history of
heavy drinking in the past. He used to smoke tobacco in the past but has quit smoking for more than
a year. He has a good social and family support system per charts, with no advanced directives
documented. He has a family history significant of prostate cancer; his father was diagnosed and
passed away because of it.
S.L. went to meet his physician with complaints of generalized weakness, chills and fever,
where he was found to be hypotensive and was advised by the physician to be admitted directly to
the hospital. He was presented alone to St John’s Macomb Hospital on March 15th
by the ground
emergency medical services on a stretcher. His initial diagnoses include generalized weakness,
neutropenia, leucopenia, metastatic pancreatic cancer status post chemotherapy induced diarrhea
and acute renal failure. S.L. had recently been diagnosed with stage 4 pancreatic cancer in October
2011 which had metastasized to the liver and lungs. He also has a history of diffuse large B-cell
lymphoma which was diagnosed in 2004. He was currently undergoing a treatment cycle for
pancreatic cancer using a combination chemotherapy regimen, before being admitted.
5
6. S.L.’s admitting diagnoses and symptoms were a result of the adverse side effects from the
chemotherapy regimen he was getting for the metastatic cancer. His symptoms were profound
diarrhea, fever, hypokalemia, febrile neutropenia with suspected sepsis, dehydration, hypotension,
pyrosis, mucositis and mouth sores. He had a poor oral intake for over three days prior to admission
due to the mouth sores. His past medical history is significant for non-insulin-dependent diabetes
mellitus (DM), coronary artery disease (CAD) with stenting, urinary retention with self-
catheterization for retention and benign prostatic hypertrophy. His surgical history includes
MediPort insertion, cardiac catheterization, and lymph node, liver and bone marrow aspiration
biopsies.
The initial treatment plan for S.L.at the hospital was to provide transfusional support (red
blood cells and platelets) for neutropenia, and intravenous (IV) fluid hydration with 0.9% normal
Saline solution. He was placed on anti-diarrheal medication for the around-the-clock. And septic
workup and infectious disease evaluation was ordered to diagnose underlying cause of the diarrhea
and to rule out sepsis. The initial diagnostic procedures conducted were X-rays of the abdomen and
chest, and an ultrasound of the retroperitoneal space. He was initially admitted to the oncology unit,
but he developed serious complications and was transferred to the Step-down unit for close
monitoring, and then to the intensive care unit (ICU) briefly, before being transferred back to the
advanced progressive care and telemetry unit. He was discharged on March 30th
and transferred to
an extended care facility (ECF) for future care and rehabilitation.
6
7. II. Disease Background
Cancer, by definition, is a cluster of more than a 100 diseases and conditions that lead to
development of uninhibited growth and multiplication of abnormal cells (1). This uncontrolled
growth and multiplication is often a result of the disruption of homeostasis between the cells ability
to proliferate and its ability to undergo cell death, or apoptosis (2). Most of these abnormal cells can
grow into discrete tumors and eventually form into malignant neoplasm which can leak into the
circulation and invade and proliferate into other tissues and organs. Cancer is the 2nd
leading cause
of mortality in the USA and prevalent all over the world, and it is unspecific and universally affects
people of any age, gender, ethnicity and socioeconomic and cultural status.
A. Epidemiology
Pancreatic cancer is cancer of the pancreas, which accounts for about only 2 percent of all
newly diagnosed cancers in the United States each year; however it is currently the fourth
leading cause of cancer-related deaths. The American Cancer Society estimates that 43,920
(22,090 men and 21,830 women) new cases of pancreatic cancer will be diagnosed and
about 37,390 patients will die in the United States in the year 2012 (3). The medical
prognosis and survival of patients with pancreatic cancer has shown little improvement over
the past 30 years with a 1.5% increase in cases every year (4). The 5-year survival rate for
these patients in the US is about 6% in Caucasians and 4% in Africans Americans.
Pancreatic cancer is most prevalent in elderly individuals of 45 years or older, and is more
prevalent in men, and in African Americans (5).
B. Pathology and pathophysiology
The pancreas is located in the abdomen, behind the stomach, an organ that contains both
endocrine and exocrine glands. The exocrine glands are responsible for making pancreatic juice,
7
8. which contain enzymes responsible for digestion of fats, protein and carbohydrates which are
transported via a pancreatic duct which leads into a common duct and empties into the duodenum
during digestion. The endocrine cells of the pancreas, also known as the islets of Langerhans, are
responsible for releasing hormones such as insulin and glucagon which are critical in maintenance
of blood sugar levels.
Most common type of pancreatic cancers are of the exocrine glands or the ducts; they are
mostly adenocarcinomas and malignant in nature and account to about 95% of all cases, known as
pancreatic ductal adenocarcinomas (6). Other types of exocrine pancreatic cancers are
adenosquamous carcinomas, squamous cell carcinomas, and giant cell carcinomas. The cancers of
the endocrine cells, are less common, are known as pancreatic neuroendocrine tumors or as islet cell
tumors, which also include carcinoid tumors. The exocrine and endocrine tumors are very different,
having different signs, symptoms, and are diagnosed and treated very differently, with endocrine
tumors having a more favorable prognosis (3). The pancreatic ductal adenocarcinomas cause a mass
effect with disruption of both the exocrine or endocrine function (6).
Cancers develop in a multistep process including initiation, promotion, malignant
conversion, and tumor progression or metastasis. Pancreatic cancer development can be triggered
by several environmental, physiological and genetic factors. Most pancreatic cancers are familial
which means it runs in some families, where most patients inherit mutated genes from their patients
that cause abnormal cell growth and lead to the development of cancer cells, which may be
responsible for about 10% of cases (6). Studies have shown that pancreatic cancer development is
regulated by a multiple subset of genes which are altered by point mutations or amplifications in the
DNA, which either act by activating oncogenes (genes responsible for causing the cancers) or by
inactivating the tumor suppressor genes (7). Some of the genes, that are mutated, are known to be
involved in growth-factor mediated signal transduction pathways which stimulate a cascade of
8
9. uncontrollable events leading to cell growth and proliferation (8). Studies have also shown that
mutations, deletions and hypermethylation (8) of certain genes in the DNA, may inactivate the
naturally occurring tumor suppressor genes, which inhibit the correction pathways of DNA
mutation, and defected cells are not automatically programmed for cell death (apoptosis), instead
the the begin to proliferate and become tumors.
Oxidative stress and prolonged inflammation, related to stress and infections, has also been
associated to development of tumors from preneoplastic to neoplastic cells (9). Many environmental
factors can lead to cell and DNA damage. Some tumors may develop at sites of infection and that
approximately one-fourth of all cancer cases are linked to chronic infection and inflammation (10).
The production of reactive oxygen species (ROS), free radicals and inflammation collectively and
independently play a significant role in all stages of cancer initiation, development, progression and
metastasis, by altering the cells normal physiology and redox state, and inducing cytotoxic effects
and DNA damage and instability (11). These oxidative and reactive species can be generated by
environmental and lifestyles habits such as smoking, poor dietary habits and sedentary lifestyle.
Pancreatic cancer risk has also been associated with obesity (12), sedentary lifestyle, poor dietary
habits, cigarette smoking, diabetes, chronic pancreatitis (inflammation of the pancreas), liver
cirrhosis and other infections (13). With these physiological and genetic changes, pancreatic cancer
develops gradually over the years and progresses slowly, unnoticed, in to a malignant tumor.
C. Etiology
No known causes of pancreatic cancer have yet been established, but evidence and research
indicate several risk factors. The risk of pancreatic cancers increases with age, smoking, type 2
diabetes, chronic pancreatitis and obesity. Pancreatic cancer was found to be more prevalent in
developed countries rather than developing countries which may suggest lifestyle habits and
environmental factors as key players in its progression. The risk of pancreatic cancer increases two-
9
10. fold with tobacco consumption (14). Smoking the most well-established environmental risk factor
for pancreatic cancer worldwide but recent decline in tobacco consumption has not decreased the
incidence of pancreatic cancer.
Lifestyle and Environment
The distribution of pancreatic cancer worldwide is uneven suggesting environmental may
have a profound causal effect on development of the cancer. Epidemiological studies have linked
physical inactivity to increased risk of pancreatic cancer in both men and women (12). One research
showed that women with a high waist-to-hip ratio have 70 percent higher risk of developing the
disease (14). There is a correlation between high Body Mass Index (BMI), total caloric intake,
sugary drinks and dietary fat intake (especially foods high in red meat, pork, and processed meat
such as sausage and bacon) with an increased incidence of pancreatic cancer (6). There is some
speculation that high consumption of coffee may increase risk of pancreatic cancer however this has
not been confirmed (6).
Exposures to toxic environmental pollutants such as certain pesticides, dyes, and chemicals
used in metal refining might be associated with increased risk of developing pancreatic cancer (6).
Other social factors such as heavy alcohol consumption have also been associated with increased
risk because heavy drinking may lead to liver cirrhosis and chronic pancreatitis, which are also risk
factors (13, 14). Cirrhosis, a chronic liver disease, a result of hepatitis or alcohol abuse has been
linked to an increased risk of pancreatic cancer development. Other infections, such as gastric ulcers
caused by Helicobacter pylori bacteria and also increased gastric acid may be associated with
increased risk of pancreatic cancer (6).
Metabolic Syndrome
10
11. Most patients with pancreatic cancer have co-existing diabetes, in many cases the two
diseases are diagnosed concurrently. It is not been well established whether diabetes is the cause or
consequence of this carcinoma. Type 2 diabetes however is associated with obesity and may pose as
an independent risk factor for pancreatic cancer. Elevated serum glucose, glucose intolerance, high
insulin concentrations, presence of insulin resistance, and high insulin receptor expression have all
been correlated with high incidence of pancreatic adenocarcinoma (16, 17). High levels of leptin
and ghrelin, hormones which are commonly elevated during obesity are also associated with the
development of pancreatic cancer (18). Obesity and diabetes are part of metabolic syndrome, which
can cause inflammation, a key regulator of carcinogenesis. High levels of insulin and insulin like
growth factors due to insulin resistance during obesity and diabetes can promote the growth of
tumor cells (18). Obese individuals tend to have high levels of angiogenetic factors which help to
promote metastasis of tumor cells, helping the tumors cells to break into the blood stream and
invade other organs (18).
Chronic pancreatitis
Pancreatitis is the inflammation of the pancreas, when enzymes in the pancreas are activated
within the pancreas rather than in the duodenum. Pancreatitis is usually caused by alcohol, gall
bladder stones or certain medications. There is an increased risk of pancreatic cancer with patients
with chronic pancreatitis (14); however the association is stronger in smokers. Chronic pancreatitis
may also be a result of an inherited gene mutation, these people have about 40 to 70% higher
lifetime risk for developing pancreatic cancer (6).
D. Symptoms
Pancreatic cancer is one of the most lethal cancers because it has very mild symptoms which
can easily be unnoticed. The most common symptoms of pancreatic cancer include jaundice, loss of
11
12. appetite or food intolerance, epigastric or back pain, dark urine, light stool or constipation,
weakness, nausea, vomiting, anorexia and unexplained weight loss (13). These symptoms are non-
specific, because of which pancreatic cancer often goes undetected. These symptoms usually
develop when the tumor is large enough to cause discomfort by pushing on nerves or organs,
leading to abdominal or back pain. In some cases the cancer grows around the bile duct, blocking
the passage of bile which leads to symptoms of jaundice such as yellow eyes and skin (6, 13).
Involuntary weight loss of about 5 pounds per month may be experienced, which may be caused by
diarrhea, anorexia, early satiety, hypermetabolism; or may also be a consequence of steatorrhea
which is caused by pancreatic duct obstruction, leading to malnutrition, and cachexia (13).
By the time the “mild” symptoms begin to surface the cancer would have already grown and
in some cases metastasized to other organs. More than 50% of cases of pancreatic cancers are
metastasized and only 10% of pancreatic cancers are localized by the time of diagnosis (12). Once
the cancer has metastized to other organs other symptoms may appear. Most pancreatic carcinomas
have distant metastases especially to the liver, lung, peritoneum, pleural, bones and adrenal glands
(7). Even small pancreatic cancers of less than 2 cm are also associated with metastasis. Autopsy
studies suggest that pancreatic cancer patients have metastatic sites can range from 10 to 1000
metastases (7).
E. Diagnosis
Since the pancreas is located deep, behind the stomach, this makes the pancreas hard to
reach and tumors hard to be detected by conventional endoscopic approaches. Because of its
location and almost asymptomatic growth, there is a lack of effective screening procedures, and
lumps or tumors cannot be seen or felt in physical exams, making diagnosis difficult at early stages.
Usually by the time pancreatic adenocarcinomas have been detected or symptoms appear, the tumor
have grown or metastasized to distant organs, and are usually surgically unresectable (13).
12
13. Currently there is no specific diagnostic procedure or specific blood tests available for early
detection of pancreatic cancer. For symptomatic patients a complete physical examination, and
serum bilirubin and alkaline phosphate levels may indicate to pancreatic cancer, but is not
diagnostic (6).
Serum bilirubin may be high for some patients who present with jaundice because of an
obstruction of the bile duct or metastasis to liver, about half of patients with pancreatic cancer may
have jaundice (6). These patients may also have brown or dark urine due to high levels of bilirubin
in blood, and also have light color stools, because the bilirubin is no longer being excreted through
stool. However, jaundice may be a marker or underlying cause of other diseases and is not specific
to pancreatic cancer. Some patients may notice their “stools to be unusually pale, bulky, greasy and
may tend to float in the toilet which may be due to malabsorption because of the lack of pancreatic
enzyme secretion to the intestine (6).
A serum tumor marker antigen CA 19-9, released by exocrine pancreatic cancer cells, could
be used to confirm the diagnosis however this antigen is not sensitive or specific for patients at early
stages because the antigen is not at a detectable concentration. (6, 13). This antigen is mostly used
during, in-between and after treatments to measure the effectiveness of the therapy and progress.
Another antigen, known as the carcinoembryonic antigen (CEA), may be useful in detecting
advance stages of the adenocarcinoma (13). Genetic testing and screening may be another tool used
for people, with a known history of pancreatic cancer to determine their risk.
A physical exam or imaging tests of enlarged gallbladder may indicate the tumor is blocking
the bile duct, artificially enlarging the gallbladder. The cancer may metastasize to the lymphnodes,
so physical screening for swellings may be indicative. A physical observation of uneven adipose
tissue under the skin could indicate alteration in pancreatic function. Typical diagnosis of pancreatic
13
14. cancer is after a detection of deep venous thrombosis (DVT), which sometimes also may lead to
pulmonary embolism (6). Patients with pancreatic cancer with metastasis to the liver may have
enlarged liver and jaundice, while those with metastasis to the lungs may experience cough and
difficulty in breathing.
Imaging tests such as Computed tomography (CT or CAT) scan may be a useful tool to
detect tumors of the pancreas and helpful in staging the cancer or for guiding a biopsy. Magnetic
resonance imaging (MRI), ultrasonography (ultrasound or US) or somatostatin receptor scintigraphy
(or OctreoScan) and endoscopic retrograde cholangiopancreatography (ERCP) can also be used for
diagnosing pancreatic carcinomas (6). A combination of CT and Positron emission tomography
(PET) may be an effective diagnostic tool; however endoscopic ultrasound is most accurate method
of detection of pancreatic cancer and can be used for biopsies as well. The only definite way to be
confirm the diagnosis of pancreatic cancer is to do a biopsy, most often used method is a fine needle
aspiration (FNA) biopsy. If surgery is indicated a biopsy may not be needed, however if plans for
chemotherapy or radiation is warranted a biopsy is necessary to confirm the diagnosis (6).
F. Medical Treatment
Presently, surgical resection is the only curative procedure for patients with pancreatic
cancer, however it is not always indicated when tumors have metastasized. There are 3 types of
medical treatments for exocrine pancreatic cancer, including surgical resection, radiation therapy,
and chemotherapy. Depending on the stage of the cancer, some of these treatments may be
combined. Surgery is usually performed when the tumor is localized. The most common type of
resection surgery include pancreaticoduodenectomy (Whipple procedure) which involves removal
of the head of the pancreas and sometimes the body of the pancreas as well and some part of the
stomach, small intestine, and lymph nodes near the pancreas, gallbladder and part of the common
bile duct. Most patients may die as a result of complications after surgery. The other types of
14
15. surgeries are distal pancreatectomy that remove only the tail of the pancreas and some part of
spleen; and a total pancreatectomy, that removes the entire pancreas and the spleen. If surgery is not
indicated, in some cases a palliative surgery may be done to relieve symptoms or to prevent certain
complications like a blocked ducts (6).
Many drugs and chemotherapeutic regimens are being studied, both single and multi-agent;
however they have not shown survival or improved prognosis. Gemcitabine, fluorouracil
monotherapy or 5-fluorouracil (5-FU), leucovorin are being used for chemotherapy treatment. Other
drugs are also used in combination with the above, which include cisplatin, irinotecan, paclitaxel,
docetaxel, capecitabine, or oxaliplatin (6). Chemotherapy drugs due to their cytotoxic nature,
usually lead to adverse side effects, depending on the type, concentration and duration of drug
usage. Common short-term side effects include nausea, vomiting, loss of appetite, hair loss, mouth
sores, diarrhea, fatigue and shortness of breath and low blood count. This could also result in
increased incidence of infections and delayed wound healing, due to a shortage of platelets. The
oxaliplatin can cause neuropathy, nerve damage and lead to symptoms of numbness, tingling,
and/or pain in the hands and feet. There is also often pain during swallowing. Another combination
therapy that have currently been used in clinical trials is called FOLFOX, which consists of 5-FU,
leucovorin, and oxaliplatin, and has shown to have a better outcome and prognosis (19), however it
can have much more severe side effects than regular chemotherapies.
Intra-operative radiation therapy is also used on locally advanced disease, but with little
effect on metastasized cancer or survival rate. Radiation therapy use high-energy x-rays to target
and destroy tumor cells (6). The most common radiation therapy used is External beam radiation
therapy, with usually about 5 treatments per week over a period of a few weeks or months. On the
bright side a combination of both radiation therapy and chemotherapy (called chemoradiation or
chemoradiotherapy) has shown significant improvement in survival rate, comparably. Some of the
15
16. common side effects of radiation therapy include mild skin burns and irritation, nausea, vomiting,
diarrhea, fatigue, poor appetite, and weight loss. Radiation can also lower blood counts and can
increase the risk of infections.
There are other non-conventional therapies such as complementary or alternative methods to
medicine which are used for cancers but there are little scientific and evidence – based research for
such therapies. The present surgeries and therapies for pancreatic cancer only improve the length of
survival to a few years but do not have a permanent or complete cure. Prognosis of patients with
pancreatic cancer is positive only if detected at an early stage, before it metastasizes.
G. Nutritional intervention
The nutrition implication in pancreatic cancer is neither curative nor therapeutic. Once
cancer has developed and metastasized, especially pancreatic cancer, it cannot be reversed with
diet, let alone most drugs today. Most patients with exocrine pancreatic cancer require nutrition
intervention for symptoms related to the cancer, such as loss of appetite and or involuntary
weight loss and weakness. Managing and improving the adverse effects of chemotherapy and
radiation may be the biggest nutritional challenge. Nutrition intervention for pancreatic cancer is
usually significant in palliative care, to help progression of a comfortable and pain-free quality
of life. Typical nutrition interventions for cancer usually involve advising patients to eat high-
energy foods as well as supplements. Many patients need pancreatic enzymes in form of pills for
digestion in pancreatic carcinomas. Other interventions may involve nutrition support therapies
using Enteral or parenteral nutrition when feasible.
Nutritional screening and intervention should occur at time of diagnosis and throughout
course of treatment. The goals of nutritional care are to prevent or correct nutritional deficiencies,
minimize weight loss. The biggest challenge is to improve nutritional status with presence of taste
16
17. aversion, dysphagia, decreased saliva, GI intolerances, and early satiety. The timing of food
presentation is very critical, by introducing larger meals earlier in the days and serve small frequent
meals, and make patients aware and reactive to their own new senses and food aversions. High kcal,
high protein diets may be useful to prevent further weight loss. Nutrition therapies and interventions
must be individualized to the patient’s specific symptoms, complains and preferences.
H. Prevention
Like most diseases, pancreatic cancer may also be prevented by diets high in fruits and
vegetables. But not all studies have found such links, and the exact role of diet in relation to
pancreatic cancer is still being studied. There are no established guidelines to prevent pancreatic
cancer but many researchers are studying the correlation of healthy diet in disease prevention.
Foods that are high in vitamins A, E and D have shown to decrease oxidative stress and oxidation of
fatty acids, ultimately preventing carcinogenesis (14). Eating high levels of the healthy fats, omega-
3 and omega-6 have shown some protective effect (20). Exercise and high levels of physical activity
can be protective against pancreatic cancer89 to date there are no significant therapy has passed the
phase III clinical trial (20, 21). Cigarette smoking cessation may also be helpful in preventing
pancreatic cancer.
17
18. III. Present Illness and Medical Treatment
A. Diagnosis and Treatment
S.L. who is a 71 year old male was recently diagnosed with pancreatic cancer in October
2011 which metastasized to the lung and liver and was currently between cycles of chemotherapy at
the time of admission. He was presented to the physician’s office with complains of weakness and
was found to have hypotension, hypokalemia, dehydration and suspicion for sepsis for which he
was admitted to the hospital on March 15th
at 2:22 am. Prior to admission S.L. was experiencing
significant diarrhea, which was painless with about 4 to 6 bouts on a daily basis. He had mucositis
with complain of oral pain and difficulty in chewing, some odynophagia and dysphagia, cough,
some epigastric pain and discomfort. He was on a unique chemotherapy regimen with a
combination of 5-flourouracil (5-FU), leucovorin and oxaliplatin, part of the FOLFOX regimen,
which had been linked to most of the medical diagnosis and conditions for which S.L. was
presented to the hospital.
He was also being followed for enlarged prostate for many years which appeared to have
obstruction based on recent imaging studies. He also has a history of urinary tract infection (UTI) in
the past, and the most recent bladder infection was in November 2011 for which he had been on
antibiotics. His baseline lower urinary tract obstructive symptoms eventually became exacerbated to
full retention, which was not resolved, and he had been on intermittent catheterization at home for
over a month. Based on his history and physical (H&P) and admission assessment, S.L. has a
history of type 2 diabetes, coronary artery disease, enlarged prostate, urinary retention, previous
UTI, metastatic pancreatic cancer with ongoing chemotherapy. He had diffuse large B-cell
lymphoma stage 4 that had been diagnosed in 2004. He also had a cardiac catheterization with stent
placement, Mediport insertion, lymph node and bone marrow aspiration biopsy done in the past.
Based on his admission history he also has a history of macular degeneration to the right eye, high
18
19. cholesterol, high blood pressure, shortness of breath with exertion, heartburn, cirrhosis, anemia and
kidney stones. He had denied any tobacco or illicit drug use, but has a history of heavy drinking in
the past.
On admission S.L. was brought in by a stretcher but was alert and oriented, with a body
temperature of 99.3 °F, pulse of 144 and blood pressure of 113/60. He had decreased breath sounds
bilaterally, with 1+ trace edema on his bilateral ankles upon admission. He appeared to have severe
mouth sores. His initial assessment impressions included febrile neutropenia and profound
diarrhea.. The admitting diagnosis was generalized weakness, neutropenia, leucopenia, pancreatic
cancer and acute renal failure. Febrile neutropenia is a condition with decreased neutrophil count
with infection, and leukopenia is condition with low white blood cell (leukocyte) count. The initial
treatment plan was to provide transfusional support for neutropenia and IV fluids for rehydration
and Lomotil medication for diarrhea, and septic work up and infectious disease consult for possible
infection and sepsis. An indwelling/continuous Foley catheter was also placed (March 14th
) due to
his urinary retention, which had an initial output of 400 cubic centimeters of turbid amber-colored
urine.
Initial diagnostic imaging of abdomen X-ray was performed for suspected ileus and was
found to have nonspecific bowel gas patterns, with no evidence of obstruction or free air with
possible left renal calculus. A chest X-ray showed no acute pulmonary disease or interval change.
The admission assessment of S.L. demonstrated a Braden score of 19 suggesting moderate risk for
pressure ulcers. His abdomen appeared symmetric, rounded and distended, with soft and tender to
palpitation on all quadrants, with bowel sounds present. He continued to have diarrhea upon
admission. He was placed with a one person assist because of generalized weakness with activity.
Because of the oral lesions from chemo, speech therapy did a swallow evaluation and found to have
mild deficits with suspected pharyngeal dysphagia, due to prolonged (although functional)
19
20. mastication, hesitant to delayed swallow response, multiple swallows. The swallow evaluation
recommendations were to continue with regular texture diet and thin liquids as tolerated.
B. Medical Progression and Treatments
Early in morning of March 15th
S.L. had a drop in his blood pressure to 80/48 and heart rate
of 70 and body temperature of 98.1°F, because of this he was transferred to the step-down unit for
close monitoring. He also had a positive blood culture of gram positive cocci and gram negative
bacilli which could have been the cause of the neutropenia and sepsis, possibly as a result of past
UTI and self-catheterizations. His white blood cells (WBC) were significantly low at 0.3 x 103
/cu
mm. The decreased blood count related to the chemotherapy made him highly susceptible to
infections, making his prognosis even weaker. The septic shock and infection was treated by
intravenous (IV) and oral antibiotics. Stool samples were also sent for detection of Clostridium
difficile (C. Diff) as a potential cause of the profound diarrhea.
The treatment for the oral ulcerations and mucositis symptoms was done by using magic
mouthwash topically and a proton-pump inhibitor medication was ordered for the epigastric pain.
Significantly high serum levels of blood urea nitrogen (BUN) of 87 and creatinine of 2.19 and
minimal urinary output were seen upon admission, and was indicative of acute kidney injury or
chronic renal insufficiency diagnosis. This was treated with aggressive hydration from 0.9% normal
saline IV. His serum lactic acid was elevated which was slightly improved with IV hydration. The
IV fluids needed to be very closely monitored to not risk volume overload and respiratory failure.
Other impressions and diagnosis included pancytopenia (reduction of red blood cells, white blood
cells and platelets) related again to the chemotherapy, and was treated with blood transfusions of
packed red blood cells and platelets. His first physical showed some erythema on bilateral buttock
which was treated with antifungal medications and topical ointments.
20
21. On day 2, March 16th
, S.L. had continued significant diarrhea over night of yellow or green
loose stools, and dark yellow urinary output probably related to increased serum bilirubin. Flexiseal,
a fecal containment device was placed. An ultrasound of the retroperitoneal cavity was done to
study the kidneys and showed bilateral renal cysts and urinary bladder wall thickening. His wounds
progressed to stage 1 pressure ulcer on bilateral buttock by day 3. On day 4, March 18th
, S.L. had
become pale and had diminished lung sounds and continued to have severe watery diarrhea. He had
an intensity of 9 out of 10 pain in his mouth, complaining of a sense of burning, and he refused to
eat or take any medications. A total parenteral nutrition (TPN) feeding became indicated due to
poor appetite and intake due to complains of mouth and throat pains, so a peripheral inserted central
catheter (PICC) line was placed on his right forearm to initiate TPN feedings.
By day 5, March 19th
, S.L.’s Braden score was 10 due to very limited mobility from debility
and muscle atrophy secondary to intubation, and poor nutrition due to nausea, mouth sores and
continued loose dark stools and dark urine. His bowel sounds were hyperactive and his skin
appeared pale, dry and yellowish, showing signs of jaundice. The speech therapist tried to evaluate
his ability to swallow oral diet and appropriate consistency but was not able to do so because S.L
refused any intake by mouth, thus TPN feeding recommendations were made and started. On day 6,
March 20th
, S.L. was found to have arrhythmia, with atrial fibrillation with rapid ventricular
response. He was given digoxin and metoprolol to maintain heart rhythms and blood pressure. He
continued to have severe diarrhea (black and green, watery) and pain in mouth with decreased
mobility and little to no improvements in his medical condition. He also developed generalized 2+
mild, non-pitting and pitting edema. He was also experiencing nausea, decreased urine output, and
delayed wound healing with little to no improvements.
On March 21st
, day 6 of hospitalization, a chest X-ray was repeated and found small right
pleural effusion and right basilar subsegmental atelectasis. His intake was still nothing by mouth
21
22. (NPO) and he was still getting TPN feedings. His diarrhea did not improve, however stools were
found to be negative for C. Diff infection. His abdomen was distended and appeared to have some
ascetic fluid. The urine analysis was positive for protein and large blood, his WBC improved from
before but still lower at 1.5 x 103
. The BUN and creatinine continued to be high, with normal limits
of phosphorus and potassium. He was getting potassium replacement. His blood glucose was
monitored and insulin was regulated using insulin sliding scale. His dehydration was resolving with
some signs of hypervolemia. Acute kidney injury with possibility of underlying stage 1 chronic
kidney disease wad suspected.
On March 22nd
, day 7, S.L. had more wounds present in addition to stage 1 pressure ulcer at
buttock, and also developed erythema and excoriation due to incontinence, in medial buttock and on
the scrotum. He also developed 2+ pitting edema in the pretibial, ankle and pedal. A swallow re-
evaluation was done to attempt to begin oral intake, which showed that S.L. could tolerate oral diet
with no signs or symptoms of aspiration, and was recommend diet texture of regular with thin
liquids. By day 8 of hospitalization, March 23rd
, his edema was slightly reduced to generalized 1+
mild, pitting bilaterally. However his condition remained afebrile, with persistent diarrhea and he
also developed metabolic acidosis. He continued to have extensive sacral and perianal wounds
which extended from lower back into lower gluteal area and groins. Skin became inflamed, red,
excoriated and had draining serous fluid, with multiple open tissue wounds scattered throughout the
area. The area around the flexiseal rectal catheter had increased draining which caused the area to
become very tender to palpation and susceptible to damage.
Due to no improvement over a week, the health care team was discussing possible hospice
care if his blood pressure and kidney functions continue to deteriorate. However, his condition
improved over the next 24 hours with elevated levels of WBC count, and this showed a positive
sign and more care was drawn to improving his quality of life and activities of daily living (ADL).
22
23. On March 26th
, S.L. was started on lasix medication for edema. He was experiencing difficulty in
breathing and a chest X-ray was performed with evidence of increasing abnormal density at the
right base of the lung. His BUN and creatinine levels remained high and only slight improvement
with diarrhea and wounds were seen. On March 27th
physical and occupational therapy were
attempted, to increase mobility and ADL to improve quality of life to progress to baseline, however
he seemed to have difficulty in basic activities of daily living, coordination and functional mobility
and had increased risk of falls. He needs maximum assistance and became dependent in most basic
ADLs. His cognitive level seemed to have declined with increased confusion and he was not
oriented to time and place. He was continuously weak, tired, fatigued and very lethargic; and unable
to tolerate 3 hours of rehab therapy.
His diarrhea continued but was slightly resolved. By March 28th
his white blood cells
increased above normal range. However a swallow re-evaluation showed S.L. to have some
dysphagia, and his diet was downgraded to Dysphagia III (mechanical soft) diet and thin liquids,
with softer and smaller bites of food to manipulate help increase oral intake. Although he still had
some intermittent bouts of diarrhea although the flexiseal catheter was removed on March 29th
. By
March 30th
much of the wounds improved with some perirectal and sacral redness and excoriation,
and an unstageable right gluteal wound. The social worker along with S.L.’s wife discussed
discharge plans with potential transfer to extended care facility for increased rehab, because the
wife also could not continue to take care of her husband at home with decreased ADLs, and needed
S.L. to return to baseline prior to returning to home. He was transfer on March 30th
at 5pm to an
ECF via ambulance for further rehabilitation.
C. Medications
23
24. Most medications used for S.L. during his stay included antibiotics, anti-inflammatory and
anti-fungal drugs to treat the infection and sepsis. Other medications included lasix,
antihypertensive and diuretic for maintaining blood pressure and edema. Neupogen was
used for formation of blood cells, especiallu neutrophils and white blood cells, which were
diminished after chemotheraphy. Neupogen was highly regulated by the pharmacy by
monitoring on serum WBC levels. Proton pump inhibitors were used to treat
gastroesophageal reflus disease (GERD) and Zofran injections, an antiemetic drug, was used
to treat nausea. Xenoderm and cubicin were used to treat his skin ulcers and wounds.
Additionally potassium chloride (oral and intravenous piggy bag) and calcium gluconate
were used as supplements to improve and replace electrolyte levels. For more information
on medications please refer to Appendix 1.
24
25. IV. Nutrition Care Process
A. Nutrition Assessment
Anthropometric Measurements
S.L. is 6’0” (72 inches or 182.8 cm) tall and weighed 174 pounds (79 kg) when he was
admitted to the hospital. His present body mass index (BMI) was 24, suggesting a normal weight.
His ideal body weight for his height of 72 inches; is about 81 kg (178 pounds) and percent ideal
body weight at admission was 98%. During admission assessment by a registered nurse, it was
found that S.L. had a 63 pound weight loss over the past few months. His usual body weight was
237 pounds, and he is currently 74% his usual body weight, indicating a severe weight loss of 26%.
This weight loss was involuntary and unexplained, which is most probably related to
hypermetabolism from the metastatic disease and pre-existing medical conditions and
chemotherapy.
Food/Nutrition-Related History
Due to S.L.’s acute medical condition, it was not possible to obtain a detailed history of his
typical daily food intake and dietary habits, however based on his medical records he used to follow
a diabetic diet at home. He has been diagnosed with diabetes for an unspecified period of time, and
was documented to have previous diet instructions for managing diabetes. According to the medical
records, he is aware of the basics of carbohydrate counting and meal planning. S.L. also has a
history of heavy alcohol consumption in the past, with complete abstinence in the past year. He
denied use of tobacco or other recreational drugs. He has no known food allergies or intolerances.
Without a detailed diet history and the cognitive stated of S.L. it was not possible to determine
whether he followed the diabetic diet plan or his compliance with a regimen. There are no available
25
26. labs values of glycohemoglobin to determine past blood glucose levels to make any assumptions of
past diabetic diet compliance.
While admitted, S.L. had a very poor intake, which was related to decrease appetite from
him medical conditions, and the mouth sores which were developed as a result of his aggressive
chemotherapy. His appetite and oral intake was documented to about zero percent for the first few
days of admission. The diet prescription at admission was 1800 calorie diabetic and neutropenic
diet. The diabetic diet limits caloric intake to no more than 1800 per day with restrictions on high
carbohydrate foods such as pizza and other sugary soft beverages. The neutropenic diet is a diet for
patients with who are neutropenic, with low neutrophil count, to avoid contamination of pathogens
and infection from food sources. Most of these foods are well cooked and properly handled to avoid
pathogens.
S.L. used to refuse meals or intake of anything by mouth including medication, because he
had severe mucositis pain in the mouth and throat that resulted from the chemotherapy regimen. At
most visits, S.L. would be too disoriented, confused or lethargic to be able to provide details and
communicate. It was not possible to determine reasons for or even verify the involuntary weight
loss and reasons for decreased appetite. However he did complain of sherbet being too painful to
consume. We had provided him some standard diabetic supplement of strawberry flavored Glucerna
shakes to be delivered with meal trays (three times a day) to increase caloric and protein intake.
Based on the information on e-care and charts, his estimated energy and protein needs were
determined. Since he is currently of normal body weight, with BMI of 24, his current body weight
of 79 kg was used to determine his estimated needs. Based on the estimated energy needs of kcal
per 25 to 30 kilogram body weight per day, his estimated energy needs were between 1975 to 2370
calories (kcal); and using 1.2 grams per kilogram body weight per kilogram, his estimated protein
needs were 95g.
26
27. Biochemical Data
During the initial nutrition assessment, on the day of admission, his albumin level was 3.0,
suggesting mild protein store depletion, elevated levels of BUN and creatinine which could be a
consequence of altered lab values due to dehydration, but the levels of BUN and creatinine
remained elevated even after sufficient IV hydration which suggests the possibility of renal
dysfunction which was correlated with the diagnosis of increased renal insufficiency and acute
kidney injury. His electrolytes were within normal limits however, the calcium labs were 8.3,
slightly lower than normal range. However, since calcium is bound to albumin, a decrease in serum
albumin can cause a false decline in serum calcium levels, thus corrected calcium levels were
calculated to be [(4.0 - 3.0) x 0.8 + 8.3 (calcium level) =] 9.1 which is within the normal range. The
total serum bilirubin was also elevated at admission, which correlated well with pancreatic cancer
diagnosis, due to possible bile duct obstruction from the metastasized tumor, which causes bilirubin
to build up in blood rather than be excreted. S.L. also had significantly lower levels of WBC, RBC,
neutrophils and platelets. His blood glucose was elevated, at 239 mg/dl corresponding to diabetes.
The next time we followed up with S.L., on March 19th
(day 5) his albumin was found to be
2.2, suggesting severe protein store depletion. This sudden drop in albumin could be a consequence
of severe hypermetabolism and prolonged suboptimal oral intake. The calcium level in serum was
low in correlation to serum albumin, and corrected calcium levels again were within normal limits.
The BUN and creatinine levels were still elevated, but levels of sodium, magnesium and chloride
were elevated above the normal range, and the level of bicarbonate had dropped. The elevation of
serum sodium could be due to dehydration or from the sodium from the IV fluids, elevation of
magnesium may be a result of possible renal failure, dehydration or the antacid medication. The
disruption of chloride and bicarbonate levels could be a result of dehydration, renal insufficiency or
27
28. metabolic acidosis. The complete blood count of WBC, RBC and platelets remained below normal
limits.
S.L.’s albumin and prealbumin levels continued to drop, with prealbumin of 5 (on March
20th
) and albumin of 1.2 (on March 21st
) indicating severe protein store depletion; possibly due to
his medical condition and inadequate oral intake. Appendix 2 shows the pertinent lab values of S.L.
during his admission and their possible implications.
Nutrition-Related Physical Findings
S.L. appeared to have some muscle wasting, and seemed confused and lethargic at time of
most visits. He had pressure ulcers on his buttock and scrotum which healed slowly, indicating
potential malnutrition. He had pale skin, sometimes even yellowish suggesting possible symptoms
of jaundice. His skin was often reported to be dry probably related to dehydration. He did not
appear underweight, maybe because he was well nourished before the exacerbation of his condition.
He was mumbling during conversations, which was due to pain and sores in mouth. He had edema
of +1 to 3+ pitting edema on his bilateral lower extremities including pedal, ankle and pretibial, or
in arms; and some days the edema was generalized. Other signs of gastrointestinal distress were
nausea, abdominal pain, diarrhea (significant), and other signs related to hyperglycemia such as
frequent urination, and dry mouth were being observed and monitored.
Client History
S.L. had good dentition with natural teeth, and no known swallowing or chewing problems
before chemotherapy. Prior to admission he had difficulty in eating due to the mouth sores, making
him unable to eat for three days before admission. S.L. has a history of type 2 diabetes with
previous diet instructions. He also has a history of heart disease such as coronary artery disease,
high cholesterol, high blood pressure, shortness of breath with exertion and catheterization with
28
29. stent placement; which could suggest that he did not have a heart healthy lifestyle, but this cannot
be determined due to lack of information. He also has a history of heavy alcohol consumption and
cirrhosis. Other medical conditions such as previous UTI, metastatic pancreatic cancer and previous
diffuse large B-cell lymphoma, macular degeneration to the right eye, heartburn, anemia and kidney
stones may impact his nutrition status and prognosis. Prior to admission S.L. was independent with
ADLs.
S.L. was diagnosed with diffuse B-cell lymphoma in 2003 and then with metastatic
pancreatic cancer in October 2011. His father had passed away with prostate cancer, which may
suggest a familial or inherited cause and development of the cancer. It may be possible that
pancreatic cancer was the primary cancer and could not be diagnosed until it had metastasized. He
was undergoing aggressive chemotherapy and was in between his cycles when his neurtophil and
white blood cell count dropped and caused him to develop sepsis with polymicrobial infections.
His involuntary weight loss of 63 pounds or 26% was probably a consequence
hypermetabolism due to metastatic cancer, the aggressive chemotherapy combination, which is
known for its severe adverse effects, or could also have been a result of sepsis, fatigue, weakness
and an inability to prepare or consume a proper balance diet. It was not possible to obtain
information about his compliance to recommendations and medications especially insulin, however
while he was admitted he had refused medications and meals, but it was related to acuity of his
illness and may not be a good indication of his normal routine. By the time S.L. was medically
stable he was not oriented to time and place and was not a good historian, and did not understand
his medical condition or therapy and became dependent with most ADLs.
During his admission he had many diagnoses and medical complications from dehydration,
infection, renal failure, renal cysts, plural embolisms, persistent diarrhea, as well as nausea,
neutropenia, leukopenia and pancytopenia; edema and pressure ulcers, which in addition to
29
30. underlying diagnosis of metastatic cancer, made him a candidate of very poor prognosis. The
nutritional implications of his diagnoses and lethargic state and inability to independently feed
himself or tolerate a diet necessitated aggressive nutrition therapy as well. He was also evaluated by
the speech therapist and had to be downgraded to mechanical soft diet, to be able to tolerate diet
well, which had also not been successful.
B. Nutrition Diagnosis
The most significant problem facing S.L. nutritionally was that he was not able to tolerate
oral intake and was not getting sufficient nutrients to meet his minimal needs. He was eating
minimal and refusing to eat, he even complained of the sherbet being too painful to consume, and
was not drinking the Glucerna Shakes which were ordered with each meals three times daily,
indicating poor nutritional status. Thus TPN had to be initiated to meet his minimal needs. Enteral
nutrition was not indicated because of the significant diarrhea and altered GI function and profile,
including abdominal distention. For the next few days while he was on TPN with oral diet, his
serum albumin continued to drop from 3.0 to 2.2 then to 1.3, and his prealbumin was 5 indicating
severely depleted visceral protein stores. In addition his weight loss of 26% and a 78% usual body
weight put S.L at severe nutritional risk.
The nutrition diagnosis for S.L was suboptimal protein-energy intake related to poor
appetite, medical condition, nausea, pain and taste changes, as evidenced by consumption of less
than 50% of meals, involuntary weight loss of 26%, and delayed wound healing with stage 1
pressure ulcers.
C. Nutrition Intervention
Based on nutrition diagnosis of suboptimal protein-energy intake and poor nutrition status
and severe nutrition risk, there was a need for aggressive nutritional intervention. The initial
30
31. treatment plan was to provide adequate oral intake by: 1) Liberalizing the diet to regular, to improve
oral intake and provide more meal choices; 2) continue with glucerna shakes to provide 220 calories
and 9.9g protein each, three times daily. 3) Recommend appetite stimulant, 4) consider palliative
care consult, 5) increase assistance with meal choices, 6) discussed nutritional management with
health care team to consider adding multivitamin and mineral supplements and 7) possibly
recommending a calorie count to determine if S.L. would be able to meet the minimal nutrition
needs.
After it was clear that oral diet was not feasible with the decline in S.L.’s ADLs and
medical status, a modification was made to the initial intervention. The modification was initiation
of parenteral nutrition, at rate of 75 ml/h with 20% Dextrose (1100ml), 15% Amino Acids (700ml)
with 20% Lipids (500ml) three times weekly (Monday-Wednesday-Friday), to provide 1597 kcals,
105 g protein. We also recommended adding the TPN bad with 80 mEq KAcetate & 100 mEq NaCl
as discussed with nephrologist to maintain electrolyte balance. This recommendation was made
with the help of the registered dietitian. We recommended discontinuing insulin added to TPN bag
because S.L. was initiated on insulin drip. We also notified the care team to continue ordering
electrolytes, phosphorus, magnesium, calcium daily; and triglycerides and prealbumin weekly to
make appropriate TPN adjustments. We also recommended the care team to document all infusions,
TPN rate, oral intake, flexiseal output and urine output.
Once the TPN feedings were initiated, the electrolytes and glucose were carefully
monitored and when the WBC counts had increased and S.L. became more medically stable we
recommended referral to speech therapy to do a swallow re-evaluation. Then, based on the new
recommendations made by the speech therapist of regular with thin liquids consistency, we
recommended changing the diet prescription to 2000 kcal diabetic diet with neutropenic restrictions
to provide more caloric options and maintain stable glucose levels. We also recommended
31
32. continuing current supplements, and encouraged oral intake of the meals & supplements. We also
recommended beginning to wean off of TPN feedings, if oral diet was improved, by reducing
infusion rate from 75 to 35 ml/h and complete the current hanging bag; then discontinue the TPN.
The final intervention was to provide a diet education when S.L. becomes hemodynamically
stable and more oriented and alert. The education was provided on March 30th
before S.L. was
discharged. The main topics to discuss were diabetic, neutropenic and high kcal/protein diet; and
some instructions on ways to managing taste changes, mouth sores and diarrhea. For diabetes
education, the objective was to give S.L. key survival tips for managing diabetes by discussing one-
on-one about not skipping meals and not spreading meals out more than 3 to 4 hours apart, and
encouraging frequent meals. Printed handouts and materials were also provided.
The key instructional points for high caloric dense and neutropenic diet were given by
providing few examples of food that have high protein and calories while making him aware that
foods should be well washed or cooked before eating to avoid infections. He was encouraged to eat
small, frequent meals, keep snacks handy; use nutritional supplements such as Ensure, Boost, and
adding butter, margarine, whipped cream, half and half, cream cheese, sour cream, salad dressings,
mayonnaise, honey, jam, sugar, granola, dried fruits, cottage or ricotta cheese, whole milk,
powdered milk, ice cream, yogurt, eggs, nuts, seeds, wheat germ, and peanut butter when possible.
Some printed documents with recommended and non-recommended foods where provided as well
and asked for verbalization of understanding.
And lastly simple tips were given on managing nausea, diarrhea and mouth sores while
maintaining good oral intake. All this information was briefly discussed and printed materials were
given and asked for feedback. Information for managing taste changes, diarrhea and xerostomia
given was to eliminate unpleasant odors and food, drinking fluids with meals and frequently
throughout the day to moisten oral mucosa. Encouraging taking sips of water before swallowing,
32
33. cleansing mouth every 2-4 hours, and drinking 2-3 liters of fluid daily and keeping lips moistened,
and avoiding citrus and dry foods , using sauces and gravies with food to provide extra moisture and
if needed use saliva substitute. He was again encouraged to eat small, frequent meals, fatty foods to
prevent diarrhea, and foods that cause gas. He was encouraged to eat foods high in soluble fiber
(bran, granola, nuts, seeds, vegetables) and avoiding alcohol and caffeine.
All the information was taught to the patient, family were not available at the time of visit,
but S.L. provided feedback and verbalized understanding. His barriers to learning were his acuity of
illness and emotional state, and the method of teaching was one on one explanation, and printed
materials. Although while he verbalized understanding, he still needs further teaching and
reinforcement, however he began reading the printed handouts while I was leaving and showed
interest and receptiveness to the education.
D. Nutrition Monitoring and Evaluation
After the intervention was written, we recommended monitoring of the diet order; parenteral
nutrition order, intake and tolerance; monitor and documentation of oral intake, tolerance to oral
diet, flexiseal outputs; monitoring blood glucose levels and adjusting insulin as needed; monitoring
gastrointestinal profile, and the nutrition quality of life and nutrition-focused physical findings;
monitoring protein intake and serum albumin and prealbumin levels; and renal panel profile, and the
intake and acceptance of supplements.
Once S.L. began oral diet in conjunction with TPN feedings, he was given Megace as an
appetite stimulant, and when we re-evaluated the initial interventions and made new
recommendations to consider changing appetite stimulant to Marinol due to compromised renal
functions triggered by megace. And after meeting and talking with S.L. before he was discharged
from the hospital we added an intervention of providing fortified chocolate ice cream two times
33
34. daily, because it was requested upon visit with S.L. As a result of our interventions S.L.’s protein
levels were improved, with prealbumin levels of increased from 5 to 12 mg/dl. His oral intake
began to improve slightly, and he started consuming the glucerna shakes regularly, stating he like
them and is able to tolerate them with no taste aversions to it. He said that his oran condition is
improving however he continued to state that he could not tolerate foods because of altered taste.
As S.L. was being discharged His TPN was discontinued and he was provided with the education
materials and information as a guide for future dietary considerations as mentioned above under
intervention section.
V. Conclusion
Overall, pancreatic cancer like many diseases can be very devastating for the individuals
experiencing it, but nutrition can impact all stages of disease from prevention to decreasing
incidence to progression and eventually treatment and improvement of symptoms. Pancreatic
cancer, although rare is currently fatal with very poor prognosis and almost always leads to
mortality within 5-years of diagnosis. S.L. was one of the unfortunate persons to undergo this
metastatic cancer and had to suffer the many consequences of the disease and its treatment. It is
rarely expected that treatment of diseases can lead to severe complications. However, S.L.
underwent chemotherapy using a combination regimen of 5-FU, leucovorin and oxaliplatin which
caused him to become immunocompromised and became a host to many pathogens, which lead to
the development of sepsis in addition to the other adverse side effects of the regimen, such as mouth
sore and weight loss. Because of compromised and poor nutrition status, S.L. had to begin nutrition
support administration because he was unable to tolerate oral diet. However the aggressive
treatment and constant monitoring helped S.L. to become more medically stable and was able to be
discharged to an ECF for further rehabilitation treatment. Although prognosis of metastatic
34
35. pancreatic cancer is poor with a small survival rate in 5-years, proper nutrition intervention may be
helpful during both the therapeutic and supportive care of these patients.
This study posed many difficulties, because of the complication of the pateints’ conditions
and comorbidities. It was difficult to have a single focus, and the metastatic disease though was the
underlying cause of the medical condition, the chemotherapy and its side effects were the most
prevalence cause of the complications in this patient. It was an eye opener, for me as a researcher to
see that not only the disease (which is always the focus of much scientific research) but the
treatment of the disease can have significant impact on a persons survival and quality of life. It was
difficult to follow the patient and see him deteriorate, but it was a very rewarding experience when
the patient was allowed to be discharged, and showed improved ADLs. When we first saw him, he
could not communicate but while he was leaving he was given diet instructions and handouts,
which he was reading and receptive to follow.
35
36. VI. Appendix 1: Drugs and Nutrition Implications
Drugs used for treatment of S.L., their uses, adverse effects and nutrition implications.
Name Drug Class Action Adverse effects Nutrition
Implications
Calcium
gluconate
Mineral
supplement
Calcium
supplement, used
as anti-diarrhea
Diarrhea, lowers phosphorous Anorexia
Cefazolin Cephalexine Antibiotic Diarrhea, decrease renal
function, lowers AST, ALT,
WBC
Cefepime
Maxipime
and Rocephin
Cephalosporin Antibiotic Eoscinophelia, increases
Creatinine, AST, ALT, and
bilirubin
Anorexia, use with
low Na+ diet and
may need K+
supplements
Cubicin Cyclic-
lypopeptide/
daptomycin
Antibiotic for skin
infections
Nausea, constipation, diarrhea,
headache. Decrease glucose,
K+ Mg++ and electrolyte
disturbance. UTI and renal
failure
Decrease appetite,
anemia, nausea
Digoxin Cardiotonic Antiarrhythmetic,
CHF treatment
Nausea, vomiting, and
diarrhea. Low Mg++ and
platelets, renal function
Anorexia. Diet
with lower Na+
and with adequate
Mg++ and Ca++
Fentanyl
patch
Analgesic Arcotic and opioid Dry mouth, dyspepsia, N/V,
abdominal pain, constipation,
diarrhea, depression, dyspnea,
urinary retention
Anorexia
Flagyl Antibiotic Metallic taste, N/V, epigastric
distress, diarrhea. Low WBC,
platelets, TG and glucose
Anorexia. Avoid
Alcohol
Flomax Alpha-
adrenergic
blockers
Treatment of
enlarged prostate,
Antihypertensive
Lower BP, drowsiness,
palpitations
Increase wt
Fluconazole Antifungal,
anticandidiasis
Taste changes, dry mouth,
dyspepsia, Headache. Elevated
ALT, AST, bil, Alk phos
Hydrocortiso
ne
Corticosteroid Antiinflammatory,
immunosuppresant
Ca++ wasting, edema, high
BP, delayed healing,
osteoporosis, necrosis, muscle
wasting. High Na+, and
glucose, Low K+ and Ca++
Increased appetite,
and wt, except
anorexia.
K-Dur
(Potassium
chloride)
Potassium
supplement
N/V, GI irritation, abdominal
pain, diarrhea, flatulence
Diet no salt
substitutes.
Furosemide Diuretic, lasix Diuretic,
antihypertensive –
to treat edema
associated with
CHF, renal or
hepatic disease
Low BP, possible hypotension.
Low K+, Mg+, Na+, Cl-, Ca
and high glucose.
Anorexia, high
thirst. High K+,
high Mg and low
Na+ diet
36
37. Megace Appetite stimulant,
antineoplastic
Edema, depression, insomnia,
High Na+, glucose, LDL, Alk
Phos, bil, AST, ALT. Low
HDL
High appetite, wt
Neupogen Filgrastim,
Colony
stimulating
factor
High production
and activity of
neutrophils. High
WBC and
neutrophils
Bone pain, splenomegaly, nose
bleeds. High uric acid, Alk
phos. Low platelets.
Hematouria
Protonix Proton pump
inhibitor
Anti-GERD, Anti-
secretory, anti-ulcer
High GI pH, diarrhea, High
gastrin
May lower
absorbance of iron
and vitamin B12.
Avoid Alcohol
Vancomycin Antibiotic, to treat
staph species
Allergic reaction, rash, Lower
WBC and platelets. High
BUN, Cr
Bitter taste, nausea
Zofran Ondansetron Anti-emetic, anti-
nausea (post
operative or
chemotherapy)
Dry mouth, abdominal pain,
constipation and diarrhea,
fatigue. Urinary retention
37
38. VII. Appendix 2: Pertinent labs and Nutrition Implications
Pertinent biochemical lab values on day 1, 6 and 10 of S.L.’s hospitalization, corresponding normal
ranges and their nutrition implications
Pertinent labs Normal
ranges
(Day 1)
March
15th
(Day 6)
March
21st
(Day 10)
March
25th
Nutrition implications
Glucose
(mg/dl)
70 - 200 163 332 ↑ 187 Elevated with diabetes, hyperglycemia
BUN (mg/dl) 8 – 23 94 ↑ 81 ↑ 93 ↑ Elevated with renal failure, shock,
dehydration, infection, diabetes
Creatinine
(mg/dl)
0.4 – 1.2 2.29 ↑ 2.47 ↑ 2.61 ↑ Elevated with acute and chronic renal
disease, muscle damage, starvation,
diabetic acidosis
Sodium
(mEq/L)
136 - 144 142 143 147 ↑ Elevated with dehydration
Potassium
(mEq/L)
3.5 – 5.0 3.8 3.8 3.8 Elevated with renal failure.Decreases
with IV fluids, diarrhea, vomiting,
chronic stress or fever, renal disease
Chloride
(mmol/L)
98 - 107 109 119 ↑ 115 ↑ Elevated with dehydration, renal
insufficiency, diarrhea
Bicarbonate
(mmol/L)
22 – 29 21 ↓ 16 ↓ 24 Decreases with metabolic acidosis, renal
failure, diarrhea, starvation
Calcium
(mg/dl)
8.4– 10.2 7.6 ↓ 6.8 ↓ 6.1 ↓ Decreases with hypoalbuminemia,
diarrhea, hyperphosphatemia, starvation
Phosphorous
(mg/dl)
2.3 – 5.0 - 2.9 - Decreases with low vitamin D,
alcoholism, diabetes, hyperinsulinism,
hyperthyroidism
Magnesium
(mEq/L)
1.3 – 2.1 *2.3 ↑ 1.9 - Elevated with renal failure, diabetic
acidosis, dehydration, use of anacid
Albumin
(g/dl)
3.5 – 5.0 - 1.6 1.5 Decreases with edema, hepatic disease,
diarrhea, ESRD, cancer, overhydration,
low protein diet
WBC
(x103
/ul)
3.2– 10.6 0.5 ↓ 1.5 ↓ 33.3 ↑ Decreased with infection, chemotherapy
and radiation
Neutrophils 44 - 76% 3% ↓ 27% ↓ 50%
38
40. IX. Appendix 4: Nutrition Assessment Day 1 (March 15th
)
Nutrition Current Medical Course
71 y.o. male admitted on 03/15/12 for Neutropenia, Pancreatic cancer s/p chemotherapy
RD consult system generated due to 63# weight loss in three months
Current diet: 1800 ADA/ Neutropenic diet + strawberry Ensure TID
Patient transferred from 5C to Stepdown due to low blood pressure.
Unable to verify weight loss at this time, patient not stable/ inappropriate for interview at this time per
nursing
Albumin: 3.0 (L), Noted elevated BUN: 94, Cr: 2.29, Glucose random: 210
On neupogen, maxipime, SSI, protonix, zofran
IV fluids: 0.9 Nacl at 75 ml/hour
XR of abdomen: Nonspecific bowel gas pattern
BM: x1 in 24 hour
Nutrition Pertinent Past Medical History
Anemia, Caps/Crowns, Cataract, Chicken Pox, Chronic Constipation/Diarrhea: Self, diarrhea with chemo,
Cirrhosis, Diabetes Mellitus, Enlarged Prostate, Heart Disease, High Blood Pressure, High Cholesterol,
Kidney Stones, Measles, Oncologic pancreatic cancer October 2011, Reflux Disease/Heartburn, SOB with
exertion, Urinary Retention.
Nutrition Assessment
Appetite : Poor
Oral Intake Nutrition : Variable
Supplemental Intake : 2-3/day
Measured Weight in Kilograms : 79.100kg(Converted to: 174lb(s) 6oz)
Measured Height in Inches : 72.00in
Height (cm) : 182.88cm
Weight (kg) : 79.100kg
Body Mass Index : 24m2
Usual Weight : 237.00lb(s)(Converted to: 237lb(s) 0oz, 3,792.00oz)
Percent Usual Weight : 74%
Ideal Body Weight : 81.00kg(Converted to: 178lb(s) 9oz, 178.57lb(s), 2,857.19oz)
Percent Ideal Weight : 98%
Estimated Energy Needs Kcal/day : 1975 - 2370
Estimated Energy Needs Kcal/kg/day : 25 - 30
Estimated Energy: Weight Used : 79 kg/actual body weight
40
41. Estimated Protein Needs gm/day : 79 - 95
Estimated Protein Needs gm/kg/day : 1.0 - 1.2
(Comment: due to high BUN/Cr labs
Estimated Protein Needs: Weight Used : 79 kg
Estimated Fluid Needs mL/day : 1975 - 2370
Estimated Fluid Needs mL/kg/day : 25 - 30
Estimated Fluid Needs: Weight Used : 79 kg
Nutritional Additional Information
On 1800 ADA diet/Strawberry glucerna shakes TID. Current appetite poor/oral intake minimal/refusing to
eat per e-care documentation. Unable to interview patient. Albumin: 3.0, suboptimal intake of nutrients
suggest Malnutrition of mild degree. Refer to intervention.
Nutrition Diagnosis
Diagnosis or Problem : Suboptimal protein-energy intake
Etiology (R/t) : Poor/decreased appetite, Medical condition
Signs/Symptoms (AEB) : Consumption of meals between 26% and 50%, Involuntary weight loss
Status : Current
Goals and Interventions
Nutrition Goals : Adequate oral intake
Nutrition Interventions : Assist w/meal choices, Discuss nutritional management, Recommend calorie
count, Recommend daily weights, Recommend lab checks, Recommend liberalize diet, Recommend provide
mineral supplement, Recommend provide vitamin supplement, Recommend referral
1. Recommend liberalize diet to Regular diet to improve oral intake. Continue with glucerna shakes.
2. Appetite stimulant
3. MVI daily/check prealbumin labs
4. Monitor and cover blood sugars
5. Palliative care consult
Nutrition Monitoring
Diet order, Food/beverage intake, Glucose/endocrine profile, Nutrition-focused physical findings, Protein
intake, Protein profile
Days Until Dietitian Follow-Up : 4
Nutrition related comorbidities : Mild malnutrition (80-90% IBW)
41
42. X. Appendix 5: Nutrition Assessment Day 5 (March 19th
)
Nutrition Current Medical Course
3/19/12 Follow-up/New TPN:
Pt seen resting in bed with family at bedside. Reports throat & mouth pain--using magic mouthwash. +
Nausea. + Flexiseal: 1L dark liquid stool this shift. Pt concerned that ice cream increasing blood glucose.
Encouraged pt to eat, as tolerated.
TPN: 60 mL/h 30% Dextrose, 8.5% Amino Acids with 250 mL 20% Lipids daily = 1479 kcals, 61 g protein
Labs: WBC 0.4; Albumin 2.2; BUN 51; Cr 1.34; Na+ 150; K+ 3.7; Cl- 123; CO2 18; Magnesium 2.2; Phos
1.7; Ca++ 7.4. Blood glucose 3/19/12: 242-425
Meds: magic mouthwash, rocephin, neupogen, fluconazole, solucortef, insulin sliding scale, zofran, protonix,
compazine
Nutrition Assessment
Appetite : Poor
Oral Intake Nutrition : Less than 50%
Supplemental Intake : Pt refuses
Measured Weight in Kilograms : 85.700kg(Converted to: 188lb(s) 15oz)
Measured Height in Inches : 72.00in
Body Mass Index : 26m2
Nutritional Additional Information
3/19/12: Current diet 1800 ADA. Oral intake minimal due to mouth/throat pain. Pt c/o sherbet being too
painful to consume. Not currently drinking Glucerna Shake (ordered TID). TPN providing 1479 kcals, 61 g
protein. Estimated needs unmet. Albumin indicates severe protein store depletion. Prolonged suboptimal
intake & albumin of 2.2 suggests severe protein-calorie malnutrition.
Nutrition Diagnosis
Diagnosis or Problem : Suboptimal protein-energy intake
Etiology (R/t) : Poor/decreased appetite, Current enteral/parenteral support, Medical condition, Nausea,
Pain, Taste changes
Signs/Symptoms (AEB) : Consumption of meals percent less than or equal to 25%, Involuntary weight loss,
Nutrition support not meeting estimated needs
Status : Current
Goals and Interventions
Nutrition Goals : Meet nutrition needs
Nutrition Interventions : Encourage oral feedings, Recommend lab checks, Recommend referral
1. Recommend palliative care consult
2. Modify TPN: 1100 mL 20% Dextrose, 700 mL 15% Amino Acids with 500 mL 20% Lipids = 1597
42
43. kcals, 105 g protein
3. Continue to offer oral foods/supplements, as tolerated
4. Please order prealbumin, triglycerides weekly & electrolytes, magnesium, phosphorus, calcium daily for
TPN adjustments
5. Document oral intake, IV infusions, stool & urine output
Nutrition Monitoring
Electrolyte Profile, Enteral/parenteral nutrition intake, Food/beverage intake, Gastrointestinal profile,
Glucose/endocrine profile, Lipid profile, Nutrition quality of life, Nutrition-focused physical findings,
Protein profile
Nutrition Evaluation : Goal modified
Days Until Dietitian Follow-Up : 2
Nutrition related comorbidities : Severe protein calorie malnutrition
43
44. XI. Appendix 6: Nutrition Assessment Day 7 (March 21th
)
Nutrition Current Medical Course
3/21/12 Follow-up:
Pt seen resting in bed. TPN continues. Oral intake minimal. Nephrology consulted due to increasing BUN,
Cr, electrolyte imbalances. Discussed electrolytes with Nephrologist.
Labs: WBC 1.5; BUN 81; Cr 2.47; Na+ 143; K+ 3.8; Cl- 119; CO2 16; Ca++ 6.8; Phos 2.9; Magnesium 1.9;
Prealbumin 5
Meds: diflucan, magic mouthwash, rocephin, neupogen, solucortef, lantus, zofran, protonix, sandostatin,
insulin drip, levophed
TPN 80 mL/h 30% Dextrose, 8.5% Amino Acids with 250 mL 20% Lipids daily = 1806 kcals, 82 g protein
Skin: Stage 1 bilateral buttocks
Blood glucose: 316 - >400
+ flexiseal; C diff negative
Nutrition Assessment
Appetite : Poor
Oral Intake Nutrition : Less than 50%
Supplemental Intake : Pt refuses
Measured Weight in Kilograms : 84.000kg(Converted to: 185lb(s) 3oz)
Body Mass Index : 25m2
Nutritional Additional Information
3/21/12: Diet unchanged; pt taking sips of liquids. TPN providing1806 kcals, 82 g protein. Prealbumin
indicates severe protein store depletion.
Nutrition Diagnosis
Diagnosis or Problem : Suboptimal protein-energy intake
Etiology (R/t) : Poor/decreased appetite, Current enteral/parenteral support, Medical condition, Nausea,
Pain, Taste changes
Signs/Symptoms (AEB) : Consumption of meals percent less than or equal to 25%, Involuntary weight loss,
Nutrition support not meeting estimated needs
Status : Current
Goals and Interventions
Nutrition Goals : Meet nutrition needs
Nutrition Interventions : Encourage oral feedings, Recommend lab checks
1. Recommend change TPN to 1100 mL 20% Dextrose, 700 mL 15% Amino Acids with 500 mL 20%
Lipids 3 times weekly. 80 mEq KAcetate & 100 mEq NaCl discussed with nephrologist. No insulin in TPN
44
45. bag as pt now on insulin drip.
2. Please continue ordering electrolytes, phosphorus, magnesium, calcium daily & triglycerides, prealbumin
weekly for TPN adjustments.
3. Document all infusions, TPN rate, oral intake, flexiseal & urine output.
Nutrition Monitoring
Electrolyte Profile, Enteral/parenteral nutrition intake, Food/beverage intake, Gastrointestinal profile,
Glucose/endocrine profile, Lipid profile, Nutrition quality of life, Nutrition-focused physical findings,
Protein profile
Nutrition Evaluation : Goal not met
Days Until Dietitian Follow-Up : 2
Nutrition related comorbidities : Severe protein calorie malnutrition
Nutrition Assessment Day 8 (March 22nd)
Nutrition Current Medical Course
3/22/12 Follow-up/TPN:
Spoke with Dr Muyskyj, Dr Nayak & PA regarding TPN. Recommend continue with TPN micro &
macronutrients; however, will re-add 20 units insulin to TPN bag, as well as MVI & trace minerals. Na+
Bicarb infusion ordered. Will monitor renal function/labs.
45
46. XII. Appendix 7: Nutrition Assessment Day 9 (March 23rd
)
Nutrition Current Medical Course
3/23/12 Follow up: Oral diet and TPN
Per chart review: mucositis improving, neutropenic fever resolved
Diet: 1800 kcal Diabetic, Neutropenic, and Glucerna shakes TID
Oral intake improved, pt stated he consumed "a waffle, pancake and ice cream and is working on his soup"
Accepting Glucerna shakes. Improving mouth/throat condition per pt.
TPN: D20% (1100ml), 15% Amino acid (700ml) with 20% lipids (500ml) M-W-F, provides 1597 kcal and
105 g protein
Meds: fluconazole, lantus, hydrocortisone, insulin, zofran, nystatin oral, protonix, bicarbonate, octreotide
IV: 0.9% NS at 40ml/h
Labs: (3/23) WBC 7.3, BUN 96 (H), Cr 2.7 (H), Na+ 145, K+ 4.1, Mg++ 1.6, Albumin 1.3, Ca++ 6.2,
Corrected Ca++ 8.36
+Flexiseal: dark loose stools; 900 mL since midnight.
Skin: Stage 1 - buttock, erythema scrotum and buttock
1+ generalized edema
Nutrition Assessment
Appetite : Fair
Oral Intake Nutrition : 50-74%
Supplemental Intake : 1-2/day
Measured Weight in Kilograms : 90.600kg(Converted to: 199lb(s) 12oz)
Body Mass Index : 27m2
Nutritional Additional Information
3/23/12: Oral intake improving, accepting glucerna. TPN provides 1597 kcal and 105 g protein, meeting 81%
kcal needs and 100% protein needs. Albumin 1.3 indicates severe protein store depletion.
Nutrition Diagnosis
Diagnosis or Problem : Suboptimal protein-energy intake
Etiology (R/t) : Poor/decreased appetite, Current enteral/parenteral support, Medical condition, Nausea,
Pain, Taste changes
Signs/Symptoms (AEB) : Consumption of meals between 26% and 50%, Involuntary weight loss, Nutrition
support not meeting estimated needs
Status : Improving
Goals and Interventions
Nutrition Goals : Meet nutrition needs
46
47. Nutrition Interventions : Encourage oral feedings, Recommend advance diet, Recommend discontinue
parenteral nutrition, Recommend lab checks, Recommend provide mineral supplement, Recommend provide
vitamin supplement
1. Change to 2000 ADA diet & continue current supplements
2. Encourage oral intake of meals & supplements
3. Begin wean of TPN by reducing infusion rate to 35 mL/h & finish current hanging bag. Then discontinue
TPN.
4. Please order prealbumin. Monitor electrolytes, phosphorus, magnesium, calcium; replace as needed.
5. Monitor blood glucose; adjust insulin as needed.
6. Document oral intake, diet tolerance, flexiseal output/BMs
7. Consider adding multivitamin supplement
Nutrition Monitoring
Diet order, Electrolyte Profile, Enteral/parenteral nutrition intake, Food/beverage intake, Gastrointestinal
profile, Glucose/endocrine profile, Nutrition quality of life, Nutrition-focused physical findings, Protein
profile, Renal Profile
Nutrition Evaluation : Goal not met
Days Until Dietitian Follow-Up : 4
Nutrition related comorbidities : Severe protein calorie malnutrition
47
48. XIII. Appendix 8: Nutrition Assessment Day 14 (March 27rd
)
Nutrition Current Medical Course
TPN/PPN: D20% (1100 ml), Amino acids 15% (700 ml) + 20% lipids (500 ml) M-W-F = 1597 kcal + 105
gm protein
3/27/12 Follow up:
Current Diet: 1800 cal Diabetic and Glucerna shakes TID
Appetite poor, with no oral intake this AM, tray ordered. Consuming glucerna shakes per PCT. Pt stated
mouth/throat feels better.
TPN: D20% (1100ml), 15% Amino acid (700ml) with 20% lipids (500ml) M-W-F, provides 1597 kcal and
105 g protein
+ Bowel Sounds
+ Flexiseal: brown loose stool (amount not documented)
Skin: sacral and perineal incontinence associated dermatitis - inflamed, red, excoriated and draining serous
fluid, multiple open tissues/wounds scattered throughout the area.
Edema: 3+ (Bil. Arm), 2+ (Bil. pretibial and Bil. ankle), 1+ (Bil.Pedal)
Meds: Calcium gluconate, cefazolin, lantus, insulin sliding scale, magic mouthwash, zofran injection,
protonix, octreotide
IV: D5 in water at 40ml/h = 163kcal
Labs: (3/27) WBC 30.2, POC glucose 183, BUN 92 (H), Cr 2.69 (H), Na++ 144, K+ 3.6, Mg++ 1.4, Ca++
6.3, Corrected Ca++ 8.3 (received Ca++ gluconate); (3/25) Albumin 1.5 (was 1.3), Prealbumin 12
3/26 Chest XR -vague patchy densities at the right base unchanged.
Pt seems lethargic and confused at the time of visit
Nutrition Assessment
Appetite : Poor
Oral Intake Nutrition : Variable
Supplemental Intake : 1-2/day
Measured Weight in Kilograms : 101.200kg(Converted to: 223lb(s) 2oz)
Body Mass Index : 30m2
Nutritional Additional Information
3/27/12: Appetite remains poor. Appears confused. Consuming glucerna shakes per PCT. TPN providing
1597 kcal and 105 g protein, meeting 67 - 81% estimated kcal needs and 88 - 111% estimated protein needs.
Albumin of 1.5 indicates severe protein store depletion, Prealbumin - 12 (trending up) indicates moderate
protein store depletion. Prealbumin - 12, >7 days poor oral intake and delayed wound healing suggests
unspecified protein - calorie malnutrition.
Nutrition Diagnosis
Diagnosis or Problem : Suboptimal protein-energy intake
48
49. Etiology (R/t) : Poor/decreased appetite, Medical condition, Nausea, Pain, Taste changes
Signs/Symptoms (AEB) : Other: pt. and staff reports poor oral intake
Status : Improving
Comment: Prealbumin – 12
Goals and Interventions
Nutrition Goals : Meet nutrition needs
Nutrition Interventions : Encourage oral feedings, Recommend advance diet, Recommend lab checks
Recommend:
1. Continue with current TPN order while pt. with poor oral intake
2. Change to 2200 cal ADA diet & continue current supplements (Glucerna shakes)
3. Continue to encourage increase in food intake.
4. When oral intake improves, consider decrease TPN rate to half (35ml/h) and start weaning.
5. Re-check prealbumin labs weekly to monitor for trend/improvement.
6. Monitor electrolytes and adjust micronutrients in TPN as needed.
7. Monitor blood glucose, adjust meds as needed.
8. Document oral intake, supplement intake and flexiseal output/BMs
9. Consider Vitamin C supplements to help promote wound healing.
Nutrition Monitoring
Diet order, Electrolyte Profile, Enteral/parenteral nutrition intake, Food/beverage intake, Gastrointestinal
profile, Glucose/endocrine profile, Nutrition quality of life, Nutrition-focused physical findings, Nutrition-
related ADLs and IADLs, Protein profile, Renal Profile, Weight change, Other: Supplement intake, Skin
condition, TPN order
Nutrition Evaluation : Goal not met
Pt. continues with poor oral intake per nursing report and current nutrition support does not meet estimated
energy needs. Pt with variable oral intake and nutrition support not meeting estimated nutrition needs
Days Until Dietitian Follow-Up : 3
Nutrition related comorbidities : Unspecified protein calorie malnutrition
49
50. XIV. Appendix 9: Nutrition Assessment Day 17 (March 30th
)
Nutrition Current Medical Course
3/30/12 Follow up:
Current Diet: 2000 kcal Diabetic/ neutropenic, and Glucerna shakes TID
Pt consuming glucerna shakes
PO intake: average 43% per meal in 48 hr
TPN: Discontinued at time of visit.
GI: Abdomen distended. + Bowel sounds. Last BM (x 3) 3/30/12 - with continued diarrhea, however pt
stated it is much better than before. Per chart review- diarrhea resolving. Flexiseal "came out" this AM and
not replaced per PCT.
Skin: unchanged
Edema: 2+ (Generalized) and 2+ (Bil Pedal)
Meds: Now on Megace
Labs: (3/30) POC glucose 238, 249 (H), BUN 82 (H), Na+ 144, K+ 3.9
Plan to D/C to ECF this afternoon
Met with pt at bedside, looks better today, spoke with pt about diabetic and neutropenic diet once discharged,
encouraged oral intake as tolerated. Pt c/o of taste changes; encouraged caloric dense foods and ways to
improve taste of food.
Nutrition Assessment
TPN/PPN : N/A
Appetite : Fair
Oral Intake Nutrition : Variable
Supplemental Intake : 1-2/day
Measured Weight in Kilograms : 103.800kg(Converted to: 228lb(s) 13oz)
Body Mass Index : 31m2
Nutritional Additional Information
3/30/12: Appetite remains poor, started on Megace for appetite stimulance. TPN discontinued. Consuming
glucerna shakes. Plan for D/C to ECF today. Not meeting estimated nutrition needs. Comorbidity remains
unchanged.
Nutrition Diagnosis
Diagnosis or Problem : Suboptimal protein-energy intake
Etiology (R/t) : Poor/decreased appetite, Medical condition, Nausea, Pain, Taste changes
Signs/Symptoms (AEB) : Other: variable food intake
Status : Improving
Comment: Pt. reports improving appetite.
50
51. Goals and Interventions
Nutrition Goals : Meet nutrition needs
Nutrition Interventions : Encourage frequent meals, Encourage oral feedings, Provide diet education
Recommend:
1) Continue current 2000 Cal Diabetic diet and glucerna shakes TID
2) Continue to encourage oral intake
3) Provided diet instruction - 3/30/12
4) Consider change appetite stimulant to Marinol due to compromised renal functions.
5) Will send fortified chocolate ice cream BID - per pt preference, if pt. not discharged
Nutrition Monitoring
Electrolyte Profile, Food/beverage intake, Gastrointestinal profile, Glucose/endocrine profile, Nutrition
quality of life, Nutrition-focused physical findings, Protein profile, Renal Profile, Other: supplement
intake/acceptance
Nutrition Evaluation : Goal not met
Pt. with variable food intake
Days Until Dietitian Follow-Up : 7
Nutrition related comorbidities : Unspecified protein calorie malnutrition
51
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