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Shaistha Zaheeruddin
April 9TH, 2012
Case Study:
Pancreatic Cancer
Outline
 Objective
 Patient Profile
 Disease Background
 Epidemiology
 Pathology
 Etiology
 Symptoms
 Diagnosis
 Treatment
 Nutrition intervention
 Prevention
 Present Illness and Medical Treatment
 Nutrition Care Process
 Assessment, Diagnosis, Intervention , Monitor , Evaluation
 Conclusion
 References
Objective
Overview the medical and
nutritional therapy related
to diagnosis and
complications of
metastatic pancreatic
cancer
Patient Profile (S.L.)
 71 year old
 Male
 Caucasian
 College graduate
 Admitted to St John’s March 15th with complaints of
generalized weakness, chill and fever
 Active diagnosis: generalized weakness, neutropenia,
leukopenia, acute renal failure and Pancreatic
Cancer (PC)
 Recently diagnosed with stage 4 metastatic
Pancreatic cancer in October 2011.
Disease Background
 Cancer – 2nd leading cause of mortality in the US
 Unspecific and universal
 Affects people of any age, gender, ethnicity and
socioeconomic and cultural status
 Cancer is a cluster of more than a 100 conditions that lead
to development of uninhibited growth and multiplication of
abnormal cells
Prevalence of Pancreatic cancer
Epidemiology
 Elderly, 45 years or older
 Men and African Americans
 5-year survival rate is 6% in Caucasians, 4% in Africans Americans
 No improvement over the past 30 years, 1.5% increase in cases every year
Cancer of the Pancreas
 Exocrine
 responsible for making pancreatic juice, enzymes
responsible for digestion of fats, protein and
carbohydrates
 transported via a pancreatic duct which leads into a
common duct and empties into the duodenum
during digestion.
 Endocrine
 AKA islets of Langerhans
 responsible for releasing hormones such as insulin
and glucagon for maintenance of blood sugars
 Most of the cancers of the pancreas are of
the exocrine cells and ducts
 95% are pancreatic ductal adenocarcinoma
 5% are of the endocrine, have different
symptom, diagnosis, treatment and more
favorable prognosis
Pathology
Initiation Promotion Progression
Pancreatic
cancer (PC)
develops in a
multistep
process:
• Initiation
• Promotion
• Progression –
angiogenesis &
metastasis
Is a familial cancer
Prevalent in families
Inherited or acquired
DNA mutations
Etiology
 No known causes of pancreatic cancer have yet been established
 Pancreatic cancer more prevalent in developed countries rather than
developing countries
 Risk associated with
 Cigarette smoking
 Obesity
 Diabetes type 2
 Chronic pancreatitis
(inflammation of the pancreas)
 Liver cirrhosis
 Other infections (e.g. H. Pylori)
 Environmental toxins
12 - Bracci PM. Obesity and pancreatic cancer: overview of epidemiologic evidence and biologic mechanisms.Molecular carcinogenesis. Jan 2012;51(1):53-63.
http://www.heattreat.ca/aging.php
 Cigarette Smoking
 well-established environmental risk factor worldwide
 Risk increases two-fold
 However recent decline in tobacco consumption
has not decreased the incidence of pancreatic cancer
 Alcohol - linked to pancreatitis and liver cirrhosis
 Sedentary Lifestyle
 Physical Inactivity increases risk of PC in both men and women
 Women with a high waist-to-hip ratio have 70 percent higher risk
 Positive correlation between high BMI, total caloric intake, sugary
drinks and dietary fat intake
 Red meat, Pork, and Processed Meats such as sausage and bacon
6- Pancreatic Cancer: What Are the Risk Factors for Cancer of the Pancreas? American Cancer Society (ACS). http://www.cancer.org/acs/groups/cid/documents/webcontent/003131-pdf.pdf.
14 - Lowenfels AB, Maisonneuve P. Epidemiology and risk factors for pancreatic cancer. Best practice & research. Clinical gastroenterology. Apr 2006;20(2):197-209.
 Metabolic Syndrome
 Elevated serum glucose, glucose intolerance,
high insulin concentrations, presence of insulin
resistance, and high insulin receptor expression
 Leptin and ghrelin, hormones which are commonly elevated
during obesity are also associated
 Obesity and diabetes are part of metabolic syndrome, which
can cause inflammation, a key regulator of carcinogenesis
 Obese individuals tend to have high levels of angiogenetic
factors which help to promote metastasis of tumor cells
Symptoms
 Not specific to PC, symptoms are very mild and non-
specific, and appears when the tumor grows big enough to
cause discomfort and pain
 Jaundice (tumor blocks the bile duct)
 Dark urine (bilirubin)
 Light color stool (bilirubin in plasma)
 Loss of appetite or food intolerance
 Epigastric or back pain
 Constipation
 Weakness
 Nausea, Vomiting
 Anorexia and unexplained weight loss
The symptoms are individually treated, or misdiagnosed.
Pancreatic cancer usually goes undetected
Diagnosis
 More than 50% of cases are metastasized and only 10% are localized by
the time of diagnosis
 Lack of screening methods
 Poor early diagnosis by conventional endoscopy and physical exams
because of location of pancreas
 Current diagnosis for symptomatic patients are
 Elevated serum bilirubin, alkaline phosphate, and brown or dark urine
 those with jaundice, or metastasis to liver
 Unusually bulky stools, greasy or tend to float
 lack of pancreatic enzymes and malabsorption
 Serum tumor marker antigen CA 19-9 and CEA
 Released by exocrine pancreatic cells, not sensitive for small tumors
 Enlarged gallbladder or swelling of metastasized areas (lymph nodes)
 Deep vein thrombosis (DVTs)
 Metastasized PC to liver – enlarged liver; to Lungs – cough and difficulty breathing
Diagnostic tests are Endoscopic ultrasound and Biopsy
Medical Treatment
 Presently, surgical resection is the only curative procedure,
however it is not always indicated when tumors have
metastasized.
 3 types of treatments for exocrine PC:
 Surgical Resection
 Pancreaticoduodenectomy (Whipple procedure)
 Distal pancreatectomy
 Total pancreatectomy
Palliative Surgeries
 Radiation therapy
 External beam radiation therapy
 Chemotherapy
 Gemcitabine, fluorouracil monotherapy or
5-fluorouracil (5-FU), leucovorin
 Combinations, e.g. FOLFOX consists of 5-FU, leucovorin,
and oxaliplatin
better outcome, severe side effects
nausea, vomiting, loss of appetite, hair loss, mouth sores, diarrhea,
fatigue and shortness of breath and low blood count
Nutrition Intervention
 Nutrition cannot cure or reverse PC
 Nutrition can impact quality of life, help relieve symptoms
and manage adverse effects of therapy
 Typical nutrition interventions are:
 Pancreatic enzyme replacements
 Enteral or parenteral nutrition support
 Prevent or correct nutritional deficiencies
 Minimize weight loss
 Encourage high-energy foods and supplements
 Improve nutritional status
 Individualized therapies for patient’s specific symptoms, complains and
preferences including
 taste aversions, dysphagia, decreased saliva, GI intolerances, and early
satiety
Prevention
 There are no established guidelines to prevent PC
 Studies suggest negative correlation with:
 Diets high in fruits and vegetables
 High vitamins A, E and D
 have shown to decrease oxidative stress and oxidation of fatty
acids, ultimately preventing carcinogenesis
 Eating high levels of the healthy fats, omega-3 and omega-6
 Exercise and high levels of physical activity
 Cigarette smoking cessation
Present Illness
Present Illness
 S.L 71 Y.O. male with stage 4 metastatic PC, to liver and
lungs. Was in between chemotherapy cycles of FOLFOX (5-
FU, leucovorin and oxaliplatin)
 Found to have hypotension, hypokalemia, dehydration and
suspicion for sepsis and was admitted March 15th
 Leukopenia, febrile neutropenia, acute renal failure
 Prior to admission S.L. was experiencing
 Significant diarrhea, painless with about 4 to 6 bouts daily
 Mucositis, oral pain, difficulty in chewing, some odynophagia and
dysphagia,
 Cough
 Some epigastric pain and discomfort
Previous History
 Previous Medical Hx:
 Enlarged prostate
 Previous multiple UTIs
 Urinary retention and self-
catheterization
 Type 2 Diabetes
 Coronary artery disease
 Diffuse large B-cell lymphoma,
stage 4 (2004)
 Cirrhosis
 High cholesterol
 High blood pressure
 Kidney stones
 Anemia
 Macular degeneration (right
eye)
 Previous Surgical Hx:
o cardiac catheterization with
stent placement
o Mediport insertion
o lymph node and bone
marrow aspiration biopsy
 Social history:
o Smoker (quit > 1yr)
o Alcohol abuse (abstinence for
1 yr)
o Denied illicit drug use
Diagnostic Tests
 Chest X-Ray:
 showed no acute pulmonary disease or interval change
 Abdomen X-Ray (r/o ileus)
 nonspecific bowel gas patterns, no evidence of obstruction or free air
with possible left renal calculus
 Braden score of 19
 suggesting moderate risk for pressure ulcers
 Speech therapy for swallow evaluation
 mild deficits with suspected pharyngeal dysphagia
 Rec.: Regular texture diet and thin liquids as tolerated
 Ultrasound of retroperitoneal cavity
 bilateral renal cysts and urinary bladder wall thickening.
 Stool culture to r/o C. diff
 Septic work up, and infectious disease consult
Medical Treatment
 Antibiotics – Vancomycin, Flagyl, Cefazolin, Cefepime, Rocephin, Maxipime
 Sepsis, infection
 IV fluids – 0.9% Normal Saline
 Dehydration from diarrhea
 Transfusional support (packed RBCs, Platelets) - Neupogen
 Neutropenia, and leukopenia
 Medications – Protonix, Lomotil, Zofran, Flomax
 Diarrhea, epigastric pain, nausea, enlarge prostate
 Mineral Supplements
 Calcium gluconate, K-Dur, KCl
 Foley Catheter placement
 Urinary retention
 Placed on one person assist
 Weakness
 Magic Mouthwash, oral care
 Mouth sores
 Day 1 (March 15th)
 Dropped blood pressure and was transferred to step-down
 Found to have positive cultures/sepsis, low WBC count
 Day 2 (March 16th)
 Transferred to ICU
 Continued profound diarrhea, flexiseal placed
 Day 4 (March 18th)
 Diminished lung sounds, severe watery diarrhea
 Severe mouth pain, refused meals and PO medication, PICC line
placement
 Stage I pressure ulcer
 Day 5 (March 19th)
 Signs of jaundice, nausea, no oral intake
 SLP unable to evaluate due to severe pain
 TPN feedings initiated
Nutrition Care Process
Nutrition Assessment
 Anthropometric
 Ht: 6 feet
 Wt: 174 lb (79 kg)
 UBW: 237 lbs (107 kg; had BMI 32)
 BMI: 24
 IBW: 178 lbs (81 kg)
 % IBW: 98%
 % UBW: 74%
 Wt change: 26% involuntary weight loss
 Estimated Nutrition Needs:
 Calories: 1975 – 2370 kcal (25-30 kcal/kg)
 Protein: 79 – 95g (1.0 – 1.2 g/kg for high BUN and Cr labs)
 Fluids: 1975 – 2370 ml (25-30 ml/kg)
 Biochemical Data
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%
 Nutrition-Focused Physical Findings
 Throat & mouth pain, fatigue, weakness - poor oral intake
 Nausea
 Severe Diarrhea
 + Flexiseal: 1L dark liquid stool
 Skin: Stage 1 bilateral buttocks
 Edema: 1+ generalized
 No sign/symptoms of hyper/hypoglycemia
 Lethargic, decreased alertness, and ADLs
 Client History
 No known food allergies and intolerances
 Prior Diabetic instructions, unable to determine compliance (no Hgb
A1C labs)
 Alcohol and smoking history
Nutrition Diagnosis
 Problem:
 Suboptimal protein-energy intake
 Etiology (related to)
 poor appetite
 medical condition
 nausea
 Pain
 Taste changes
 Sign/Symptom (as evidenced by)
 consumption of less than 50% of meals
 involuntary weight loss of 26%
 delayed wound healing with stage 1 pressure ulcers.
Nutrition Intervention
 The initial treatment plan was to provide adequate oral intake by:
1) Liberalize diet to 2000 kcal Diabetic, to improve oral intake and provide
more meal choices
2) Glucerna shakes to provide 220 calories and 9.9g protein each, three times
daily
3) Encourage oral intake and 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
 When it was clear that his oral intake would not increase, and he was degraded
by Swallow evaluation to Dysphagia II diet
 Initiate TPN at rate of 75 ml/h with 20% Dextrose (1100ml), 15% Amino
Acids (700ml) with 20% Lipids (500ml) 3 times weekly (M-W-F)
 Provides 1597 kcals, 105 g protein.
 Also recommend adding the TPN bag with 80 mEq KAcetate & 100 mEq NaCl
 When oral intake improve, decrease TPN to half, and provide diet education when
medically stable
Teaching Plan
 Evaluation of Education
 S.L. provided feedback and verbalized understanding.
 Barriers to learning
 Acuity of illness and emotional state
 Teaching needs
 Needs further teaching and reinforcement, showed interest & receptiveness to education
Key Pt/Topics Objective Method Activity Aids
1) High Calorie
and Protein
Eat small, more
frequent meals
Explanation One-on-One
discussion
Printed
Materials
Eat energy dense
foods
Examples and
Handout
One-on-One
discussion
Printed
Materials
2)Neutropenic Use low microbial
foods
Examples and
Handout
One-on-One
discussion
Printed
Materials
Properly wash Explanation One-on-One
discussion
Printed
Materials
3) Managing
diarrhea, taste
aversions,
mouth sores
Give survival tips
to improve oral
food/bev intake
Explanation
and examples
One-on-One
discussion
Printed
Materials
Monitoring and Evaluate
 Monitor
 Diet order
 Monitor and documentation of oral intake
 Tolerance to oral diet
 Intake and acceptance of supplements
 Parenteral nutrition order, intake and tolerance
 Flexiseal outputs
 Blood glucose levels and adjusting insulin as needed
 GI profile
 Nutrition quality of life
 Nutrition-focused physical findings
 Protein profile: serum albumin and prealbumin levels
 Renal panel profile
 Evaluated initial interventions and made new recs to
 Consider change appetite stimulant to Marinol due to compromised renal functions triggered by
megace
 Protein levels improved, prealbumin levels of increased from 5 to 12 mg/dl.
 Oral intake began to improve slightly, and he started consuming the glucerna shakes
regularly, and TPN was discontinued
Conclusion
 S.L. was discharged to ECF for further rehabilitation and PT and OT
 Most of S.L’s symptoms where a result of the adverse side effects of
aggressive chemotherapy
 S.L. was immunocompromised and became a host to many pathogens
 Nutrition and Parenteral nutrition helped improved his nutrition
status, improved is protein levels
 Pancreatic cancer has poor prognosis and many complications but
nutrition intervention was needed too improve his quality of life and
manage compromised symptoms
References
1. What is Cancer? American Cancer Society. Available at: http://www.cancer.org/Cancer/CancerBasics/what-is-cancer. Accessed April 2nd, 2012
2. Grabenbauer GG, Suckorada O, Niedobitek G, et al. Imbalance between proliferation and apoptosis may be responsible for treatment failure after postoperative radiotherapy in
squamous cell carcinoma of the oropharynx. Oral oncology. Jul 2003;39(5):459-469.
3. Siegel R, Naishadham D, Jemal A. Cancer statistics, 2012. CA: a cancer journal for clinicians. Jan-Feb 2012;62(1):10-29.
4. American Cancer Society. Cancer Facts & Figures 2012. Atlanta, Ga: American Cancer Society; 2012.
5. Hayat MJ, Howlader N, Reichman ME, Edwards BK. Cancer statistics, trends, and multiple primary cancer analyses from the Surveillance, Epidemiology, and End Results
(SEER) Program. The oncologist. Jan 2007;12(1):20-37.
6. Pancreatic Cancer: What Are the Risk Factors for Cancer of the Pancreas? American Cancer Society (ACS). Available at:
http://www.cancer.org/acs/groups/cid/documents/webcontent/003131-pdf.pdf. Accessed April 02, 2012
7. Yachida S, Iacobuzio-Donahue CA. The pathology and genetics of metastatic pancreatic cancer. Archives of pathology & laboratory medicine. Mar 2009;133(3):413-422.
8. Sarkar FH, Banerjee S, Li Y. Pancreatic cancer: pathogenesis, prevention and treatment. Toxicology and applied pharmacology. Nov 1 2007;224(3):326-336.
9. Borrello MG, Degl'Innocenti D, Pierotti MA. Inflammation and cancer: the oncogene-driven connection. Cancer letters. Aug 28 2008;267(2):262-270.
10. Sorci G, Faivre B. Inflammation and oxidative stress in vertebrate host-parasite systems. Philosophical transactions of the Royal Society of London. Series B, Biological
sciences. Jan 12 2009;364(1513):71-83.
11. Khandrika L, Kumar B, Koul S, Maroni P, Koul HK. Oxidative stress in prostate cancer. Cancer letters. Sep 18 2009;282(2):125-136.
12. Bracci PM. Obesity and pancreatic cancer: overview of epidemiologic evidence and biologic mechanisms. Molecular carcinogenesis. Jan 2012;51(1):53-63.
13. Freelove R, Walling AD. Pancreatic cancer: diagnosis and management. American family physician. Feb 1 2006;73(3):485-492.
14. Lowenfels AB, Maisonneuve P. Epidemiology and risk factors for pancreatic cancer. Best practice & research. Clinical gastroenterology. Apr 2006;20(2):197-209.
15. Chari ST, Leibson CL, Rabe KG, Ransom J, de Andrade M, Petersen GM. Probability of pancreatic cancer following diabetes: a population-based study. Gastroenterology. Aug
2005;129(2):504-511.
16. Stolzenberg-Solomon RZ, Graubard BI, Chari S, et al. Insulin, glucose, insulin resistance, and pancreatic cancer in male smokers. JAMA : the journal of the American Medical
Association. Dec 14 2005;294(22):2872-2878.
17. Li D. Diabetes and pancreatic cancer. Molecular carcinogenesis. Jan 2012;51(1):64-74.
18. Gumbs AA, Bessler M, Milone L, Schrope B, Chabot J. Contribution of obesity to pancreatic carcinogenesis. Surgery for obesity and related diseases : official journal of the
American Society for Bariatric Surgery. Mar-Apr 2008;4(2):186-193.
19. Rathkopf D, Dickson MA, Feldman DR, et al. Phase I study of flavopiridol with oxaliplatin and fluorouracil/leucovorin in advanced solid tumors. Clinical cancer research : an
official journal of the American Association for Cancer Research. Dec 1 2009;15(23):7405-7411.
20. Silverman DT, Swanson CA, Gridley G, et al. Dietary and nutritional factors and pancreatic cancer: a case-control study based on direct interviews. Journal of the National
Cancer Institute. Nov 18 1998;90(22):1710-1719.
21. Schernhammer ES, Hu FB, Giovannucci E, et al. Sugar-sweetened soft drink consumption and risk of pancreatic cancer in two prospective cohorts. Cancer epidemiology,
biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. Sep
2005;14(9):2098-2105.

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Case Study_Pancreatic Cancer patient with TPN

  • 1. Shaistha Zaheeruddin April 9TH, 2012 Case Study: Pancreatic Cancer
  • 2. Outline  Objective  Patient Profile  Disease Background  Epidemiology  Pathology  Etiology  Symptoms  Diagnosis  Treatment  Nutrition intervention  Prevention  Present Illness and Medical Treatment  Nutrition Care Process  Assessment, Diagnosis, Intervention , Monitor , Evaluation  Conclusion  References
  • 3. Objective Overview the medical and nutritional therapy related to diagnosis and complications of metastatic pancreatic cancer
  • 4. Patient Profile (S.L.)  71 year old  Male  Caucasian  College graduate  Admitted to St John’s March 15th with complaints of generalized weakness, chill and fever  Active diagnosis: generalized weakness, neutropenia, leukopenia, acute renal failure and Pancreatic Cancer (PC)  Recently diagnosed with stage 4 metastatic Pancreatic cancer in October 2011.
  • 5. Disease Background  Cancer – 2nd leading cause of mortality in the US  Unspecific and universal  Affects people of any age, gender, ethnicity and socioeconomic and cultural status  Cancer is a cluster of more than a 100 conditions that lead to development of uninhibited growth and multiplication of abnormal cells Prevalence of Pancreatic cancer
  • 6. Epidemiology  Elderly, 45 years or older  Men and African Americans  5-year survival rate is 6% in Caucasians, 4% in Africans Americans  No improvement over the past 30 years, 1.5% increase in cases every year
  • 7. Cancer of the Pancreas  Exocrine  responsible for making pancreatic juice, enzymes responsible for digestion of fats, protein and carbohydrates  transported via a pancreatic duct which leads into a common duct and empties into the duodenum during digestion.  Endocrine  AKA islets of Langerhans  responsible for releasing hormones such as insulin and glucagon for maintenance of blood sugars  Most of the cancers of the pancreas are of the exocrine cells and ducts  95% are pancreatic ductal adenocarcinoma  5% are of the endocrine, have different symptom, diagnosis, treatment and more favorable prognosis
  • 8. Pathology Initiation Promotion Progression Pancreatic cancer (PC) develops in a multistep process: • Initiation • Promotion • Progression – angiogenesis & metastasis Is a familial cancer Prevalent in families Inherited or acquired DNA mutations
  • 9. Etiology  No known causes of pancreatic cancer have yet been established  Pancreatic cancer more prevalent in developed countries rather than developing countries  Risk associated with  Cigarette smoking  Obesity  Diabetes type 2  Chronic pancreatitis (inflammation of the pancreas)  Liver cirrhosis  Other infections (e.g. H. Pylori)  Environmental toxins 12 - Bracci PM. Obesity and pancreatic cancer: overview of epidemiologic evidence and biologic mechanisms.Molecular carcinogenesis. Jan 2012;51(1):53-63. http://www.heattreat.ca/aging.php
  • 10.  Cigarette Smoking  well-established environmental risk factor worldwide  Risk increases two-fold  However recent decline in tobacco consumption has not decreased the incidence of pancreatic cancer  Alcohol - linked to pancreatitis and liver cirrhosis  Sedentary Lifestyle  Physical Inactivity increases risk of PC in both men and women  Women with a high waist-to-hip ratio have 70 percent higher risk  Positive correlation between high BMI, total caloric intake, sugary drinks and dietary fat intake  Red meat, Pork, and Processed Meats such as sausage and bacon 6- Pancreatic Cancer: What Are the Risk Factors for Cancer of the Pancreas? American Cancer Society (ACS). http://www.cancer.org/acs/groups/cid/documents/webcontent/003131-pdf.pdf. 14 - Lowenfels AB, Maisonneuve P. Epidemiology and risk factors for pancreatic cancer. Best practice & research. Clinical gastroenterology. Apr 2006;20(2):197-209.
  • 11.  Metabolic Syndrome  Elevated serum glucose, glucose intolerance, high insulin concentrations, presence of insulin resistance, and high insulin receptor expression  Leptin and ghrelin, hormones which are commonly elevated during obesity are also associated  Obesity and diabetes are part of metabolic syndrome, which can cause inflammation, a key regulator of carcinogenesis  Obese individuals tend to have high levels of angiogenetic factors which help to promote metastasis of tumor cells
  • 12. Symptoms  Not specific to PC, symptoms are very mild and non- specific, and appears when the tumor grows big enough to cause discomfort and pain  Jaundice (tumor blocks the bile duct)  Dark urine (bilirubin)  Light color stool (bilirubin in plasma)  Loss of appetite or food intolerance  Epigastric or back pain  Constipation  Weakness  Nausea, Vomiting  Anorexia and unexplained weight loss The symptoms are individually treated, or misdiagnosed. Pancreatic cancer usually goes undetected
  • 13. Diagnosis  More than 50% of cases are metastasized and only 10% are localized by the time of diagnosis  Lack of screening methods  Poor early diagnosis by conventional endoscopy and physical exams because of location of pancreas  Current diagnosis for symptomatic patients are  Elevated serum bilirubin, alkaline phosphate, and brown or dark urine  those with jaundice, or metastasis to liver  Unusually bulky stools, greasy or tend to float  lack of pancreatic enzymes and malabsorption  Serum tumor marker antigen CA 19-9 and CEA  Released by exocrine pancreatic cells, not sensitive for small tumors  Enlarged gallbladder or swelling of metastasized areas (lymph nodes)  Deep vein thrombosis (DVTs)  Metastasized PC to liver – enlarged liver; to Lungs – cough and difficulty breathing Diagnostic tests are Endoscopic ultrasound and Biopsy
  • 14. Medical Treatment  Presently, surgical resection is the only curative procedure, however it is not always indicated when tumors have metastasized.  3 types of treatments for exocrine PC:  Surgical Resection  Pancreaticoduodenectomy (Whipple procedure)  Distal pancreatectomy  Total pancreatectomy Palliative Surgeries  Radiation therapy  External beam radiation therapy  Chemotherapy  Gemcitabine, fluorouracil monotherapy or 5-fluorouracil (5-FU), leucovorin  Combinations, e.g. FOLFOX consists of 5-FU, leucovorin, and oxaliplatin better outcome, severe side effects nausea, vomiting, loss of appetite, hair loss, mouth sores, diarrhea, fatigue and shortness of breath and low blood count
  • 15. Nutrition Intervention  Nutrition cannot cure or reverse PC  Nutrition can impact quality of life, help relieve symptoms and manage adverse effects of therapy  Typical nutrition interventions are:  Pancreatic enzyme replacements  Enteral or parenteral nutrition support  Prevent or correct nutritional deficiencies  Minimize weight loss  Encourage high-energy foods and supplements  Improve nutritional status  Individualized therapies for patient’s specific symptoms, complains and preferences including  taste aversions, dysphagia, decreased saliva, GI intolerances, and early satiety
  • 16. Prevention  There are no established guidelines to prevent PC  Studies suggest negative correlation with:  Diets high in fruits and vegetables  High vitamins A, E and D  have shown to decrease oxidative stress and oxidation of fatty acids, ultimately preventing carcinogenesis  Eating high levels of the healthy fats, omega-3 and omega-6  Exercise and high levels of physical activity  Cigarette smoking cessation
  • 18. Present Illness  S.L 71 Y.O. male with stage 4 metastatic PC, to liver and lungs. Was in between chemotherapy cycles of FOLFOX (5- FU, leucovorin and oxaliplatin)  Found to have hypotension, hypokalemia, dehydration and suspicion for sepsis and was admitted March 15th  Leukopenia, febrile neutropenia, acute renal failure  Prior to admission S.L. was experiencing  Significant diarrhea, painless with about 4 to 6 bouts daily  Mucositis, oral pain, difficulty in chewing, some odynophagia and dysphagia,  Cough  Some epigastric pain and discomfort
  • 19. Previous History  Previous Medical Hx:  Enlarged prostate  Previous multiple UTIs  Urinary retention and self- catheterization  Type 2 Diabetes  Coronary artery disease  Diffuse large B-cell lymphoma, stage 4 (2004)  Cirrhosis  High cholesterol  High blood pressure  Kidney stones  Anemia  Macular degeneration (right eye)  Previous Surgical Hx: o cardiac catheterization with stent placement o Mediport insertion o lymph node and bone marrow aspiration biopsy  Social history: o Smoker (quit > 1yr) o Alcohol abuse (abstinence for 1 yr) o Denied illicit drug use
  • 20. Diagnostic Tests  Chest X-Ray:  showed no acute pulmonary disease or interval change  Abdomen X-Ray (r/o ileus)  nonspecific bowel gas patterns, no evidence of obstruction or free air with possible left renal calculus  Braden score of 19  suggesting moderate risk for pressure ulcers  Speech therapy for swallow evaluation  mild deficits with suspected pharyngeal dysphagia  Rec.: Regular texture diet and thin liquids as tolerated  Ultrasound of retroperitoneal cavity  bilateral renal cysts and urinary bladder wall thickening.  Stool culture to r/o C. diff  Septic work up, and infectious disease consult
  • 21. Medical Treatment  Antibiotics – Vancomycin, Flagyl, Cefazolin, Cefepime, Rocephin, Maxipime  Sepsis, infection  IV fluids – 0.9% Normal Saline  Dehydration from diarrhea  Transfusional support (packed RBCs, Platelets) - Neupogen  Neutropenia, and leukopenia  Medications – Protonix, Lomotil, Zofran, Flomax  Diarrhea, epigastric pain, nausea, enlarge prostate  Mineral Supplements  Calcium gluconate, K-Dur, KCl  Foley Catheter placement  Urinary retention  Placed on one person assist  Weakness  Magic Mouthwash, oral care  Mouth sores
  • 22.  Day 1 (March 15th)  Dropped blood pressure and was transferred to step-down  Found to have positive cultures/sepsis, low WBC count  Day 2 (March 16th)  Transferred to ICU  Continued profound diarrhea, flexiseal placed  Day 4 (March 18th)  Diminished lung sounds, severe watery diarrhea  Severe mouth pain, refused meals and PO medication, PICC line placement  Stage I pressure ulcer  Day 5 (March 19th)  Signs of jaundice, nausea, no oral intake  SLP unable to evaluate due to severe pain  TPN feedings initiated
  • 24. Nutrition Assessment  Anthropometric  Ht: 6 feet  Wt: 174 lb (79 kg)  UBW: 237 lbs (107 kg; had BMI 32)  BMI: 24  IBW: 178 lbs (81 kg)  % IBW: 98%  % UBW: 74%  Wt change: 26% involuntary weight loss  Estimated Nutrition Needs:  Calories: 1975 – 2370 kcal (25-30 kcal/kg)  Protein: 79 – 95g (1.0 – 1.2 g/kg for high BUN and Cr labs)  Fluids: 1975 – 2370 ml (25-30 ml/kg)
  • 25.  Biochemical Data 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%
  • 26.  Nutrition-Focused Physical Findings  Throat & mouth pain, fatigue, weakness - poor oral intake  Nausea  Severe Diarrhea  + Flexiseal: 1L dark liquid stool  Skin: Stage 1 bilateral buttocks  Edema: 1+ generalized  No sign/symptoms of hyper/hypoglycemia  Lethargic, decreased alertness, and ADLs  Client History  No known food allergies and intolerances  Prior Diabetic instructions, unable to determine compliance (no Hgb A1C labs)  Alcohol and smoking history
  • 27. Nutrition Diagnosis  Problem:  Suboptimal protein-energy intake  Etiology (related to)  poor appetite  medical condition  nausea  Pain  Taste changes  Sign/Symptom (as evidenced by)  consumption of less than 50% of meals  involuntary weight loss of 26%  delayed wound healing with stage 1 pressure ulcers.
  • 28. Nutrition Intervention  The initial treatment plan was to provide adequate oral intake by: 1) Liberalize diet to 2000 kcal Diabetic, to improve oral intake and provide more meal choices 2) Glucerna shakes to provide 220 calories and 9.9g protein each, three times daily 3) Encourage oral intake and 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  When it was clear that his oral intake would not increase, and he was degraded by Swallow evaluation to Dysphagia II diet  Initiate TPN at rate of 75 ml/h with 20% Dextrose (1100ml), 15% Amino Acids (700ml) with 20% Lipids (500ml) 3 times weekly (M-W-F)  Provides 1597 kcals, 105 g protein.  Also recommend adding the TPN bag with 80 mEq KAcetate & 100 mEq NaCl  When oral intake improve, decrease TPN to half, and provide diet education when medically stable
  • 29. Teaching Plan  Evaluation of Education  S.L. provided feedback and verbalized understanding.  Barriers to learning  Acuity of illness and emotional state  Teaching needs  Needs further teaching and reinforcement, showed interest & receptiveness to education Key Pt/Topics Objective Method Activity Aids 1) High Calorie and Protein Eat small, more frequent meals Explanation One-on-One discussion Printed Materials Eat energy dense foods Examples and Handout One-on-One discussion Printed Materials 2)Neutropenic Use low microbial foods Examples and Handout One-on-One discussion Printed Materials Properly wash Explanation One-on-One discussion Printed Materials 3) Managing diarrhea, taste aversions, mouth sores Give survival tips to improve oral food/bev intake Explanation and examples One-on-One discussion Printed Materials
  • 30. Monitoring and Evaluate  Monitor  Diet order  Monitor and documentation of oral intake  Tolerance to oral diet  Intake and acceptance of supplements  Parenteral nutrition order, intake and tolerance  Flexiseal outputs  Blood glucose levels and adjusting insulin as needed  GI profile  Nutrition quality of life  Nutrition-focused physical findings  Protein profile: serum albumin and prealbumin levels  Renal panel profile  Evaluated initial interventions and made new recs to  Consider change appetite stimulant to Marinol due to compromised renal functions triggered by megace  Protein levels improved, prealbumin levels of increased from 5 to 12 mg/dl.  Oral intake began to improve slightly, and he started consuming the glucerna shakes regularly, and TPN was discontinued
  • 31. Conclusion  S.L. was discharged to ECF for further rehabilitation and PT and OT  Most of S.L’s symptoms where a result of the adverse side effects of aggressive chemotherapy  S.L. was immunocompromised and became a host to many pathogens  Nutrition and Parenteral nutrition helped improved his nutrition status, improved is protein levels  Pancreatic cancer has poor prognosis and many complications but nutrition intervention was needed too improve his quality of life and manage compromised symptoms
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