This essay will present a case study of a selected patient, who has been diagnosed with pancreatic cancer and whom I have cared for, whilst my placement in the inpatient setting. This placement was undertaken in an acute surgical ward at a multidisciplinary hospital specialized mainly for vascular patients, also tending after patients with colorectal, upper gastrointestinal, endocrine and breast problems. Informed consent was taken from the patient to proceed with this assignment reiterating the adherence to the guidelines set by the Nursing and Midwifery Council code of professional conduct (2002) for confidential information.
As a result confidentiality and anonymity has been maintained throughout this essay by assigning a pseudonym and omitting some information on the biographic data of the patient. For the purpose of this assignment, a detailed holistic health profile and plan of care using the nursing process with the integration of pathophysiology has been explored. Three nursing diagnosis according to priority has been identified followed with patient outcome, nursing intervention and evaluation of the interventions has also been included.
This essay will also include a discharge plan and will finally conclude with a brief reflection on the care that I carried out on this patient. Pancreatic cancer is the 11th most common cancer in New Zealand, with more deaths attributed to the neoplasm each year. It is considered one of the most deadly malignancies, whereby majority of the patients die within 5 – 12 months of the initial diagnosis. The incidence rate is high amongst the Maori compared to Non – Maori population, with strong evidence linking to deprivation gradient, that is, more deprived groups have a higher incidence of the disease (Ministry Of Health, 2008).
The clinical picture Mrs. Brown (pseudonym) is a 72 yr. old married Cook Islander who presented to the emergency department (ED) with abdominal pain at the epigastric region, jaundice, Per Rectal (PR) bleeding, nausea and fatigue. Bloods were taken and she was admitted to the surgical ward with query pancreatic cancer. I was assigned to look after Mrs. Brown on the third day of her admission when the doctors had already discussed her diagnosis of a metastasized pancreatic cancer and the prognosis of the disease. Following is the assessment that was done on Mrs.
Brown. According to her she noticed that, from last three months she was getting lethargic and was not able to keep up with the housework. She stated that she felt some discomfort in the upper abdomen, lost her appetite and had diarrhea. She noticed a gradual decrease in her weight and also noticed that her urine had suddenly become dark. Her physician who discovered that she was slightly jaundiced ordered for blood test to rule out viral hepatitis as it causes jaundice. However, her condition deteriorated and she had to come to the hospital.
Mrs. Brown lives with her two grandchildren and her husband. Her past medical history is significant for diabetes mellitus type 2 which was diagnosed in 1976 and hyperlipidaemia. Her brother had died of stomach cancer at the age of sixty seven. The only form of exercise is the housework that she engages herself with. She is an outgoing woman, and loves to go to church functions as her husband is a church minister. She also revealed her love of island food which is mostly cooked with coconut cream. Her lifestyle indicates her risk for pancreatic cancer which is diabetes and high fat consumption.
Mrs. Brown is clearly not at ease in the hospital as I could see her fidgeting in the bed and could not lie still. Her facial expression shows that she is in pain. The functional health pattern findings of Mrs. Brown include acute abdominal pain in the epigastric region that radiates to the back whereby pain is worse in supine position but is relieved by sitting forward. She has nausea and vomiting and has anorexia and has gone from size 22 to size 16 in past four months. Recently she has witnessed early satiety. She has constipation, increased flatus, and feels bloated after meals. She is fatigued and feels dizziness while standing.
Her physical assessment reveals slight fever with temperature of 37. 8oC, heart rate of 109beats/min, with blood pressure of 109/85mmHg and respiration rate of 22respirations/min. Her oxygen saturation is at 96% on air. Abdominal palpation showed that she has hepatomegaly, and distended gallbladder. Slight abdominal distension and reduced bowel sounds was also present. Her feces contained frank blood on occasion and tarry colored on other occasions and is quite foul smelling. She has decreased muscle tone, grossly jaundiced with yellowing of the eye sclera as well. She has a dry skin and mucous membrane.
She also complained of generalized body itchiness which is evidenced by scratch marks and bruising. In general, Mrs. Brown presented with debilitation, depression and restlessness. Mrs. Brown’s evaluation included a Computed Tomography of the abdomen, which revealed pancreatic head enlargement, intrahepatic and extrahepatic duct dilation up to 2. 4 cm and dilated pancreatic duct as well. Laboratory blood test on Full blood count was done to see the effect of the disease on the blood components and the presence of inflammation. The result showed a low hemoglobin level of 76g/l and slightly elevated white cell count of 12. g/l indicating inflammation.
The cause of pancreatic cancer is unknown; however, the incidence of pancreatic cancer is high with smokers. It is also associated with high calorie intake and nitrosamines, whose formation is enhanced with high temperatures as in frying. Diabetes is another risk factor but it is not clear whether cancer follows diabetes or diabetes follows cancer (Porth, 2002). In the above case study the patient already had diabetes for thirty – three years. When normal cells are exposed to carcinogens, example, cigarette smoke, there is genetic damage to the DNA repair genes, resulting in DNA damage and eventually mutation of cell genes.
A gene called K-ras is found to be altered in up to 95% of ductal carcinoma of the pancreas (Chernicky & Endy, 2008). These mutations of the gene leads to the activation of proto – oncogenes that promote normal cell growth and anti – oncogenes that inhibit growth. The result is unregulated cell growth and differentiation ending into a malignant neoplasm. The unregulated, cell growth results into proliferation of cells with a mass and because pancreas is an organ that lies just under the curvature of the stomach and deep within the abdomen the doctors usually miss an early diagnosis during the abdominal assessment.
This cancerous process may arise in any part of the pancreas that is the head, body and the tail. Most of it occurs in the head. As cancer has no regard to normal anatomical boundaries, the proximity of the head of the pancreas to other abdominal structures like the common bile duct and the ampulla vater causes obstruction of these structures as neoplasm grows. The result is obstructive jaundice that occurs. Uncoordinated growth and lack of contact inhibition in neoplasm than have the ability to break loose because the cells are less well differentiated.
As a result they can enter the circulatory circulation or lymphatic systems and form secondary malignant tumors at other sites (Porth, 2002). In our case study the liver is also affected. The symptoms that Mrs. Brown presented with are the common manifestations of the pancreatic cancer. Abdominal pain, anorexia, rapid and progressive weight loss, nausea and jaundice are the most common ones. She presented with these symptoms when her cancer had well progressed and had metastasized because the onset of pancreatic cancer is insidious most of the time.
Presence of jaundice usually indicates the progression of the disease to its late stage. Unfortunately there is no screening available for this cancer unlike other cancers (Bryant and Knights, 2007). In Porth (2002), anorexia which is one of the main symptoms of pancreatic cancer occurs because of the exocrine function the pancreas plays in the body. From an anatomical view point, the pancreas passes its exocrine contents which contains enzyme lipase, protease and amylase for digestion of fats, proteins and carbohydrates respectively, through the pancreatic duct into the duodenum.
In the normal physiological condition there is digestion of all three food groups in the duodenum by the pancreatic enzymes. However, in the pathological state, when there is pancreatic duct obstruction as the case study presents, obstruction to the flow of the pancreatic juices will cause poor absorption of food leading to weight loss. Apart from the malabsorption of nutrients that occur there is another phenomenon about weight loss. Cancer cachexia is the term that describes the weight loss and wasting of body fat and lean protein in cancer patients.
Cachectin which is identical to Tumor Necrotic Factor (TNF) is released from the macrophages in response to tumor growth, causes anorexia by suppressing satiety centers causing early satiety. This contributes to fatigue and weakness and other psychosocial factors like depression. TNF is also an endogenous pyrogen that induces fever by its action on hypothalamic regulatory regions which probably explains SB’s fever TNF is also said to activate inflammatory response and coagulation system explaining why Mrs. Brown probably had a high WCC and elevated APTT.
Jaundice is the result of obstruction of the biliary tract and duodenum. This occurs when the hepatic or extrahepatic biliary tracts are occluded, causing decrease in flow of bile. Bile which is produced by the hepatocytes (liver cells) contains bilirubin (heme degradation product) and bile salts, whose function is to emulsify fats. The bile moves from the liver into the duodenum through biliary tract, into the common bile duct which passes through the head of the pancreas before passing through the ampulla of vater.
Because of the obstruction of the common bile duct from the head of the pancreatic tumor the flow of bile together with bile salts is obstructed from entering the duodenum. As a result bilirubin is unable to empty into the duodenum and it backs up the biliary tree into the liver and crosses over into the blood in the systemic capillaries. It then binds to elastic tissue causing the characteristic color change of yellow skin and sclera and often causes debilitating pruritis.
By the time the patient presents with jaundice the cancer has already metastasized and the prognosis is really poor whereby surgical resection of the tumor becomes impossible (Porth, 2002). Tea colored urine is also due to high bilirubin in the blood which causes increased filtration of bilirubin by the kidneys into the urine giving it the dark coloration. Obstruction of bile flow into the duodenum also causes decreased fat emulsification because of low or absent bile salts causing decreased fat digestion and absorption resulting in high fecal fat excretion.
According to Porth (2002) if there is obstruction to the ampulla of vater there will be more fecal fat excretion because now the excretion of pancreatic enzyme especially lipase for fat digestion is also affected. Hence if there is no lipase there will be no fat digestion. The term to describe this condition is steatorrhoea whereby you have loose, pale, fatty, floating offensive bowel motions, the condition that Mrs. Brown presented with. Mrs. Brown presented with most of the complications arising from pancreatic cancer like obstruction of the duodenum and biliary ducts.
She also presented to the ED, with PR bleeding which is one of the complications due to pancreatic cancer. PR bleeding is due to gastrointestinal hemorrhage when the growing tumor compresses and erodes the portal venous system causing frank bleeding. Fever, another complication is a life threatening condition which can occur when there is neutropenia (low neutrophil count) resulting from cancer which makes the person more prone to infection. Mrs. Brown also has the tendency to develop malignant ascitis which can result from liver metastasis.
From ascitis she can develop respiratory problems, heart failure due to pulmonary edema caused by the diffusion of the peritoneal fluid intravascularly. Splenomegaly can be caused by the encasement of the splenic vein by the tumor. Glucose intolerance can be facilitated even though she already has the history of it. As the tumor grows it can cause gastric outlet obstruction leading to nausea and vomiting. Another complication of pancreatic cancer is migratory thrombophlebitis which is the presence of several blood clots along the veins.
Pain can get intolerable when there is invasion to the autonomic nerves of the pancreas by the tumor. Spinal cord compression from expanding tumor can cause irreversible paraplegia (Chernicky & Endy, 2008). According to the case study presented there are several problems that need addressing for Mrs. Brown. However, three nursing diagnosis according to priority will be discussed. According to Lee and Bishop (2004), “priority diagnosis is those nursing diagnosis… if not managed now, will deter progress to achieve outcomes or negatively affect the client’s functional status”p. 15.
Hence, first nursing diagnosis is fluid volume deficit, relating to nausea, vomiting and PR bleeding as manifested by dry skin and mucous membrane and increased heart rate. Anticipatory short term goal for Mrs. Brown will be that she will verbalize relief from nausea and vomiting, will demonstrate normal heart beat of ? 100 beats/min, absence of blood in stool and exhibit an elastic skin turgor and moist mucous membrane within the end of my shift of seven and a half hours. Nursing implementations included keeping Mrs. Brown Nil By Mouth (NBM) as keeping the stomach empty will reduce the urge to vomit so that more fluids are not lost.
Assured patient has a patent, intravenous access site available for administration of medications. Administration of Intravenous Fluids (IVF) was commenced to maintain fluid and electrolyte balance. Vital signs were monitored every two hourly because of Physiological Unstable Person (PUP) of 2. This was done to monitor cardiovascular changes. According to Brown and Edwards (2008), “When there is mild to moderate fluid volume deficit, compensatory mechanism include sympathetic nervous stimulation of the heart and peripheral vasoconstriction,”p. 354. As a result there is increased heart rate.
If the homeostatic mechanism is not able to compensate then hypotension can occur and the person can have weak pulses eventually leading to hypovolemic shock (Brown and Edwards, 2008). Accurate intake and output of fluids in the 24hr fluid balance chart to detect an imbalance between intake and output was also monitored and documented so that appropriate interventions can be made. For output recordings recorded the urine output and vomitus. Monitored respiratory changes every two hours because respiration rate increases due to decreased tissue perfusion and resultant hypoxia (Brown & Edwards, 2008).
Weight measurement was done in the morning as it was done previously to ensure correct measurement (body weight changes reflect changes in body fluid volume). Administered antiemetic maxalon that relieves nausea and vomiting by blocking dopamine receptors in the chemoreceptor trigger zone (Bryant & Knights, 2007). Monitored Blood glucose regularly so that uncontrolled diabetes can be detected and prevent further fluid loss through diuresis. Abdomen region was assessed for skin turgor and mucous membrane for signs of dehydration.
If there is delay to the return of the pinched skin to its shape the person has a diminished skin turgor (Brown & Edwards, 2008). Urine sample was examined for color and amount as concentrated urine denotes fluid deficit. Urine sample was then sent to the lab for evaluation for increased specific gravity which is the test for dehydration (Brown & Edwards, 2008). Assessed the signs and symptoms of PR bleeding by examining the feces. Presence of frank blood was text paged to the Health surgeon for medical intervention so that appropriate action can be taken to avoid further deterioration on fluid balance resulting in hypovolemia.