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Description : Overview the medical and nutritional therapy related to diagnosis and complications of metastatic pancreatic cancer

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Published on : Apr 04, 2023 | Views : 2005 | Downloads : 1

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Shaistha Zaheeruddin April 9th, 2012 Case Study: Pancreatic Cancer
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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
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Objective Overview the medical and nutritional therapy related to diagnosis and complications of metastatic pancreatic cancer
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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.
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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
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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
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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
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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
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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
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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.
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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
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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
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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
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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
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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
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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
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Present Illness
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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
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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: cardiac catheterization with stent placement Mediport insertion lymph node and bone marrow aspiration biopsy Social history: Smoker (quit > 1yr) Alcohol abuse (abstinence for 1 yr) Denied illicit drug use
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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
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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
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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
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Nutrition Care Process
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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)
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Biochemical Data
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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
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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.
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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
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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
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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
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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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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.