Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Adenocarcinoma: Linitis Plastica The rate of gastric adenocarcinoma has decreased drastically in the United States, but makes up 90-95% of all gastric cancer cases. Globally, a decrease has also occurred and is attributed to environmental and socioeconomic changes. Despite the drop, over 798,000 new cases of gastric cancer are diagnosed worldwide each year. Prognosis for patients is based on tumor extent, nodule involvement, extension of the tumor beyond the gastric walls, and sometimes the grade of the tumor (1). The depth of invasion, or extension into muscularis propria is used to distinguish between early and advanced stages. Overall, the 5 and 10 year survival rates for advanced carcinoma are 46% and 35%, respectively. Survival rate is higher when the tumor infiltrates only the distal two-thirds of the stomach. Tumor size is directly correlated with survival rate in advanced carcinoma. Despite radical treatment procedures, predictors of poor prognosis are >70 years old, tumor stage, and need for total gastrectomy (2). Linitis Plastica (3) Pa tholog y a nd Na tura l History of Ga stric Ca nc er 287 Gastric Linitis Plastica (GLP), also known as Brinton’s Disease or leather bottle stomach, involves diffuse infiltration of the stomach lining. This causes thickening and stiffening of gastric walls from the Figure 23–8 Linitis plastica form of gastric cancer. Note the classical leather bottle–like appearance. The wall is diffusely thickened. Figure 23–10 Diffuse carcinoma. The individual tumor cells are widely spaced andin supported by a dense desmoplastic fundus to the pylorus and occurs 3-19% of allstroma. gastric cancer cases. Linitis Plastica Common tumor typ es Tubular adenocarcinomas contain prominent dilated or slit-like and branching neoplastic tubules varying in diameter; acinar structures may be present (Fig. 23–11). Individual tumor cells may be columnar or cuboidal, or they become flattened by intraluminal mucin. The cells superficially resemble those found in colonic adenocarcinomas. Clear cells also may be present. The degree of cytological atypia varies from low to high grade.25,26 Poorly differentiated variants are sometimes called solid carcinomas. Tumors with a prominent lymphoid stroma sometimes are called medullary carcinomas or gastric carcinomas with lymphoid stroma (Fig. 23–12).27 The degree of desmoplasia varies and may be conspicuous in these neoplasms. Papillary adenocarcinomas are well-differentiated exophytic carcinomas with elongated finger-like processes lined by cylindrical or cuboidal cells supported by fibrovascular connective tissue cores. Goblet cells may be present. The cells tend to maintain their polarity. Some tumors show tubular differentiation. Rarely, a micropapillary architecture is present. The degree of cellular atypia and the mitotic index vary, and severe nuclear from surrounding structures. often The tumor may inhas a 1:1.3 female dominancedemarcated and occurs more inbeyoung individuals. These atypia may be present. Usually the invading tumor edge is sharply filtrated by acute and chronic inflammatory cells. Mucinous adenocarcinomas are tumors composed of more than 50% extracellular mucinous pools. The two major growth patterns are (1) glands lined by a columnar mucus-secreting epithelium together with interstitial mucin (well-differentiated type) and (2) chains or irregular cell clusters floating freely in mucinous lakes (Fig. 23–13). The latter pattern results from glandular rupture. Mucin also may be present in the interglandular stroma. Scattered signet ring cells, when present, do not dominate the histological picture. Signet ring cell carcinomas are adenocarcinomas in which more than 50% of the tumor consists of isolated or small groups of malignant cells containing intracytoplasmic mucin (Fig. 23–14). Superficially, cells lie scattered in the lamina propria, often widening the distances between the pits and glands. The tumor cells can also be quite subtle and can be easily missed when they are few in number. The tumor cells have five morphologies: (1) nuclei that push against cell membranes, creating a classical signet ring cell appearance because of an expanded, globoid, optically clear cytoplasm; these contain acid mucin and stain with Alcian blue at pH 2.5; (2) bland-appearing cells with central nuclei that are easily mistaken for histiocytes because they show little or no mitotic activity; (3) small, deeply eosinophilic patients show a significantly lower survival rate. A study based on surgical intervention of 102 individuals resulted in a median survival time of 5.7 months. Diagnosis of GLP regularly occurs late and the tumor is often non-resectable. It is staged using a esophagogastroduodenoscopy (EGD) with biopsy barium swallow and thoracoabdominal CT (3). The disease is believed to be correlated with heredity, poor diet, lack of exercise, or H. pylori infection. Preserved, processed or smoked foods and poor quality water contain nitrites, which form the potentially carcinogenic compound N-nitroso. Nitrite, found in these foods, is a precursor to N-nitroso compounds. Nitrite reacts with amines, amides and other protein to form N-nitroso compounds (4,5). Nitrate does not react the same way, but can be reduced to nitrite by bacterial spoilage and the bacteria in the mouth and upper GI tract (6). Studies found that patients with a higher caloric, saturated fat, and oleic acid intake also had a higher incidence of gastric adenocarcinoma. It has been hypothesized that fruits and vegetables have a protective effect against gastric carcinoma. The most significant effects seen have come from non-citrus and raw fruit. Fruits and vegetables with nitrite scavenging properties of varying mechanisms may be protective against stomach cancer. Vitamin C and E, Selenium, and B-carotene/carotenoids are all potent antioxidants that scavenge free-radicals. Vitamins C and E also inhibit intragastric formation of N-nitroso compounds (5,7). Presentation and Complications: Patients initially present with early satiety, postprandial abdominal pain, and weight loss. These, along with other factors such as anorexia, intestinal obstruction, taste changes, chemotherapy and radiation side effects, and depression can contribute to malnutrition (8, 9). Patients with gastric cancer usually require a partial or total gastrectomy with esophagojejunal anastomosis. Malnutrition prior to surgery can lead to altered cellular immunity, increasing the risk of infection and delaying wound healing. Patients with significant weight loss, or reduced caloric intake for 2-24 weeks pre or post surgery are at risk for macro- and micronutrient deficiencies. Post operatively, signs of significant weight loss, gastric stasis, dumping syndrome, fat maldigestion, and iron, calcium, and B12 deficiency all need to be monitored (4,10). Dumping syndrome is one of many complications of extensive stomach resection. Other complications can include fat malabsorption, gastric stasis, lactose intolerance, anemia’s, and metabolic bone disease (11). Dumping syndrome occurs in 25-50% of patients and begins when large amounts of food or liquid, especially those high in simple carbohydrates, rapidly enter the small intestine (10). The body’s response to dilute the high osmotic bolus results in gastrointestinal and vasomotor symptoms such as abdominal cramps, diarrhea, nausea, vomiting, flushing, faintness, diaphoresis, and tachycardia. (11). Dumping syndrome can be classified as either early or late dumping. Early dumping happens within 10-30 minutes after meal consumption. Patients will often experience a feeling of fullness and nausea attributed to small bowel distention plus a fluid shift into the small intestine. Gastrointestinal and vasomotor symptoms are experienced: hypotension, flushing, rapid heartbeat, faintness, vomiting, diarrhea, and headache. Late dumping syndrome occurs 1-3 hours after a meal and is related to hypoglycemia. The rapid delivery, hydrolysis, and absorption of CHO cause insulin to rise with a subsequent decline in blood glucose. Patients experience vasomotor symptoms and may perspire, feel anxious, weak, shaky, or hungry, and have difficulty concentrating. Patients who experience dumping syndrome often loose weight due to fear and anxiety associated with the symptoms (10, 11). Malabsorption and steatorrhea occur secondary to rapid transit, loss of gastric, lipase, or pancreatic/biliary insufficiency. Anemia, osteoporosis, and vitamin and mineral deficiencies occur as the result of this malabsorption or due to limited intake. Loss of gastric acid secretions and intrinsic factor may cause iron complications. Gastric acid cleaves B12 from protein while intrinsic factor forms the necessary complex with B12 for absorption in the ileum. Sometimes, the duodenum and jejunum begin producing intrinsic factor, but if it is not produced in sufficient quantities, pernicious anemia will result. Bacterial overgrowth in the small intestine also causes a reduction in B12 absorption due to the bacteria completing for its use. Many patients need prophylactic B12 injections (10, 11). Other common deficiencies include calcium, folate (use RBC folate to diagnose) and fat soluble vitamins. Patient Information: SM is a 35 year old female of El Salvadorian decent who works at Costco. She is a single mother to one child and estimated to be of moderate socioeconomic status based on reported residence. She initially presented with complaints of early satiety and mild emesis since February 2011. SM has no past medical history and is taking no medications upon initial visit to physician. She does not smoke or drink, but does have a history of poor eating habits. She has a family history of colon and prostate cancer, leukemia, liver disease, and heart disease. SM underwent an EUS where it was determined she has stage IIB gastric cancer. She had three cycles of chemotherapy involving the antineoplastic drugs epirubicin, oxaliplatnum, and zolotin (EOX). SM tolerated the Chemotherapy well with good oral intake, no weight loss, and no GI complaints. After three rounds of chemotherapy, a CT of the abdomen and pelvis was done, showing no significant change in the poorly differentiated tumor’s size, but also no metastatic disease. SM was scheduled for a laparotomy, gastrectomy, and Roux-En-Y reconstruction on May 25, 2012. She was admitted to Georgetown Hospital on the day of surgery, and then transferred to inpatient recovery. The procedure resulted in total gastrectomy and R1 resection with the creation of an esophagojejunal anastomosis, plus an additional diagnosis of Linitis Plastica and metastasis to 2 lymph nodes. Post operation day (POD) #6 the patient complained of shaking, chills, palpations, and lightheadedness. Blood glucose was 77. It was determined that patient was experiencing symptoms of late dumping syndrome and diet education was reinforced with patient. Slightly over 3 hours later SM complained of tremoring on her left side which lasted for approximately 2-5 minutes. She complained of left sided tingling and numbness. It was determined she has an acute hemorrhage in her right parietal lobe from transverse venous sinus thrombosis. She underwent both a CT and MRI of the brain. She was transferred to Neurologic Intensive Care Unit (NSICU) where she remains stable but has left sided sensory loss, photophobia, and headaches with pain so great they result in nausea and vomiting. She had been on heparin since POD #0, Coumadin was started POD #8 but D/C’d shortly after. She has also been receiving daily CT scans since POD #8 to monitor spread of bleed and midline shift. Nutrition: SM was NPO the day of her surgery, 5/25/12. She was given D5½NS with KCL at 100mL/hr. The following day she was allowed gum and hard candy. She continued on the D5½NS. On POD #4 she under went an oral glucose intolerance test and radiographic evaluation with the use of gastrographin. She was advanced to sips of liquid, not including concentrated sweets and carbonated beverages. POD #5 SM’s diet was advanced to clear liquid, again no concentrated sweets or carbonated beverages. The following morning, the diet was progressed to full liquid and then to a post gastrectomy diet by dinner. Post gastrectomy diet education was given on 5/31/12 to the patient and her sister. The educational session lasted about 30 minutes and was voice recorded by the family to refer to once outside of the hospital. Main take home points for a post gastrectomy diet include: Eat small, frequent meals, chew foods thoroughly and eat slowly, limit fluid consumption with meals, limit high sugar foods and beverages, eat protein at each meal, and increase fiber intake. Patient and sister were engaged in conversation and verbalized understanding. Discharged was anticipated the following day. After the diet education, the dietitian planned to follow up PRN. Pt was moved to the NSICU 6/1/12, she was trigged for RD referral on 6/6/12 for poor oral intake. After speaking with the patient on 6/6/12, it was determined that she had a poor appetite the past few days, but was feeling hungry most of the day. She had only received a piece of bread for the previous nights dinner, and bread with bacon and grapes for breakfast that morning. SM states that had she been given more than a piece of bread she would have eaten more, the post gastrectomy diet was clarified with catering services. SM remembered a lot of information from her previous diet education, but mentions a fear of eating due to previous complication of dumping syndrome. Patient was briefly re-educated on the post gastrectomy diet and how dumping syndrome occurs. All her questions were clarified, and she appeared more confident in the ability to manage her diet. Nutrition Assessment While completing diet education, SM admitted to previous poor eating habits but since her diagnosis has changed her lifestyle. SM mentioned eating excessive amounts of fried food, a lot of jerky, and consumed large quantities of soda. It is unknown how much jerky SM ate but the curing process could result in an abnormal amount of N-Nitroso compounds. Prior to diagnosis SM was a healthy weight around 50kg. Her weight dropped drastically after her diagnosis, but she regained it during her chemotherapy and radiation treatment. She is currently back to her usual body weight of 52kg. She is 152cm tall, has a BMI of 22, and is at 111% of her 45kg IBW. Shortly after surgery SM’s potassium (3.4mEq/L) and phosphorus (2.0mg/dL) were low, but repleated. Bun and creatinine were consistently low with BUN ranging from 3-6mg/dL and creatinine ranging from 0.26-0.44mg/dL. This could be the result of inadequate protein intake. Sodium ranged from 133-136mEq/L. Over the course of her stay, SM was taking the following medications which have nutritional implications: D5½NS, potassium chloride, magnesium sulfate, sodium chloride, ferrous sulfate, docusate-senna, warfarin, and vitamin C. SM was determined to need 30-35 kcal/kg and 1.5-1.7g protein/kg. She was advanced to a post gastrectomy diet as tolerated, provided with Glucerna three times a day (TID) and given a daily multivitamin. Her oral intake intake is monitored, and though low there is no need for nutrition support at this time. The following goals were set: Eat >75% of meals and supplements and prevent weight loss. She has been gradually increasing the amount of food consumed while in the NSICU. Unless there is a significant change in her ability to eat, she will continue on a post gastrectomy diet for life. It will be up to her to determine what foods her body can tolerate, and what foods warrant unwanted side effects. Foods that cause adverse effects should be slowly reintroduced into the diet one at a time. Ideally, she will return to consuming a balanced diet of a large variety within six weeks. Based on research her prognosis is poor, but with her young age, and large support system, it is hopefully that her cancer will remain localized and/or has been completely removed, and will not metastasize. SM was discharged on 6/19/12. Study: Limited Efficacy of Early Enteral Nutrition in Patients after Total Gastrectomy (12). Introduction: Nutritional status has a large impact on surgery outcome. Patients who undergo GI surgery often suffer from malnutrition leading to increased postoperative morbidity and prolonged hospital stay. Artificial intake has been suggested when oral intake will be absent 5-7 days after surgery. Enteral Nutrition (EN) is the preferred method as it has decreased risk of infection than Total Parenteral Nutrition (TPN). The biological and clinical benefits of early EN to patients undergoing gastric surgery due to gastric cancer are currently unknown. This study compares early EN via NJ tube to patients receiving TPN after total gastrectomy. Materials/Methods: Retrospective study of patients with total gastrectomy and Roux-en-Y esophagojejunostom. Total enrolled -116; EN – 62; TPN – 54. Feeding was started within 24 hours with a goal of 20-25kcal/day and was supplemented until at least 1000kcal/day was tolerated. Oral intake was administered on day 6-7 as patient desired. Gradually reduced supplemental nutrition with increased oral intake. TPN contained 50-60% glucose and 40-50% fat. Patient was discharged under the following criteria (1) no fever for 2+ days or signs of inflammation; (2) able to eat more than ½ a solid diet; and (3) able to treat own wounds without any assistance. Results: 116 total patients between 38 and 82 years old. Baseline characteristics (age, gender, BMI, nutritional status, comorbidity, tumor site, operating time, etc) were similar. Post op length of stay, time of flatus passage, and time before starting semi-solid diet were the same in both group. Patients in TPN group started a liquid diet sooner. EN group developed diarrhea and abdominal distention more often, but not of statistical significance. Symptoms from EN could be alleviated by lowering the infusion rate. No significant difference between post op mortality in the two groups. Discussion: About 60% of gastric cancer cases have some form of malnutrition. TPN increased the overall risk of complications by 10% and showed higher rates of hyperglycemia complications. There is no significant difference in major and minor complications postoperatively in EN or TPN groups. Since EN showed no beneficial effects on decreasing risk of complications, the study says EN is not warranted over TPN in patients after total gastrectomy due to possible respiratory infections (no difference in lung infection or pneumonia was reported between the two groups). I would not agree with this outcome – if no difference is reported, EN helps in maintaining normal gut function, reduces risk of infection, and is much less expensive compared to TPN. Works Cited 1. Abbruzzese, JL. Gastrointestinal Oncology. Oxford University Press. 2004; 257264. 2. Nakamura K, Ueyama T, Yao T, Xuan ZX, Ambe K, Adachi Y, Yakeishi Y, Matsukuma A, Enjoji M. Pathology and Prognosis of Gastric Carcinoma. Cancer. 1992; 70(5):1030-1037. 3. Pedrazzini C, Marrelli D, Pacelli F, DiCosmo M, Mura G, Bettarini F, Rosa F, deManzoli G, Roviello F. Gastric Linitis Plastica: Which Role for Surgical Resection?. Gastric Cancer. 2012; 15:56-60. 4. Swann PF. Carcinogenic Risk from Nitrite, Nitrate and N-Nitrosamines in Food. Proceedings of the Royal Society of Medicine. 1977; 70(2):113-115. 5. Kono S, Hirohata T. Nutrition and Stomach Cancer. Cancer Causes Control. 1996; 7(1):41-55. 6. Sandor J, Kiss I, Farkas O, Ember I. Gastric Cancer Mortality and Nitrate Content of Drinking Water: Ecological Study on Small Area Inequalities. Europeal Journal of Epidemiology. 2001; 17(5):443-447. 7. Harrison LE, Zhang ZF, Karpeh MS, Sun M, Kurts RC.The Role of Dietary Factors in the Intestinal and Diffuse Histologic Subtypes of Gastric Adenocarcinoma: A Case-Controlled Study in the U.S. Cancer. 1997; 80(6):1021-8. 8. Scolapio JS, Buchman AL. Clinician’s Guide to Gastrointestinal Oncology. SLACK Inc. 2005; 307-216. 9. Radigan A. Post-Gastrectomy: Managining the Nutrition Fall-Out. Practical Gastroenterology. 2004; 18:63-75. 10. Rogers, C. Postgastrectomy Nutrition. Nutrition in Clinical Practice. 2011; 26(2):126-136. 11. Mahan LK, Escott-Stump S. Krause’s Food & Nutrition Therapy. 12th ed. St. Louis, MI: Saunders Elsevier: 2008: 977, 667-668. 12. Li J, Ji Z, Yuan C, Zhang Y, Chen W, Ju X, Tang W. Limited Efficacy of Early Enteral Nutrition in Patients after Total Gastrectomy. Journal of Investigative Surgery. 2011;24:103-108.