Pancreatitis

58 Pancreatitis




Overview/pathophysiology


The pancreas serves both endocrine (hormonal) and exocrine (nonhormonal) functions. (Pancreatic endocrine function is discussed in “Diabetes Mellitus,” p. 348.) The exocrine portion comprises 98% of its tissue mass. Exocrine secretions, which are produced by the acini cells, empty through a series of lobular ducts into the main pancreatic duct, where they are released into the duodenum. Exocrine function is the secretion of potent enzymes, proteases, lipases, and amylases that act to reduce proteins, fats, and carbohydrates respectively into simpler chemical substances. Pancreatic proteases (trypsin, chymotrypsin, carboxypeptidases A and B, elastase, and phospholipase A) aid in protein digestion. Pancreatic lipase acts on fats to produce glycerides, fatty acids, and glycerol; pancreatic amylase acts on starch to produce disaccharides. The pancreas also secretes sodium bicarbonate to neutralize the strongly acidic gastric contents as it enters the duodenum. The resultant mixture of acids and bases provides an optimal pH of 8.3 for activation of pancreatic enzymes.


Pancreatitis, which can be acute or chronic, is an inflammation of the pancreas with varying degrees of edema, hemorrhage, and necrosis. The damage can lead to fibrosis, stricture, and calcifications. Acute pancreatitis occurs when pancreatic ductal flow becomes obstructed and digestive enzymes escape from the pancreatic duct into surrounding tissue. Self-destruction of the pancreas produces edema, hemorrhage, and necrosis of pancreatic and surrounding tissue. Biochemical abnormalities and disruption of cardiopulmonary, renal, metabolic, and gastrointestinal (GI) function are likely. Pancreatitis has been associated with gallstones, alcoholism, surgical manipulation, abdominal trauma, abdominal vascular disease, heavy metal poisoning, infectious agents (viral, bacterial, mycoplasmal, parasitic), medications, and some allergic reactions. Pancreatitis also is associated with familial hyperlipidemia and can be induced by endoscopic retrograde cholangiopancreatography (ERCP). The majority of acute pancreatitis cases are mild, require a short hospitalization, and leave no long-term adverse effects. Severe acute pancreatitis involving multiple organ failure occurs in approximately 25% of cases but accounts for 98% of deaths associated with acute pancreatitis. Complications of acute pancreatitis include pancreatic abscess, hemorrhage, pancreatic pseudocyst, fistula formation, and transient hypoglycemia. Acute, life-threatening complications include renal failure, hemorrhagic pancreatitis, septicemia, adult respiratory distress syndrome (ARDS), shock, and disseminated intravascular coagulation (DIC).


Chronic pancreatitis is characterized by varying degrees of pancreatic insufficiency, which results in decreased production of enzymes and bicarbonate and malabsorption of fats and proteins. The digestion of fat is affected most severely. As a result, a high-fat content in the bowel stimulates water and electrolyte secretion, which produces diarrhea. The action of bacteria on fecal fat produces flatus, fatty stools (steatorrhea), and abdominal cramps. Often diabetes mellitus (DM) occurs as a result of chronic pancreatitis because of damage to the insulin-producing beta cells and resultant deficient insulin production. Chronic pancreatitis is also associated with complications of DM, chronic pain, maldigestion, pseudocysts, and bleeding.



Health care setting


Primary care with hospitalization for acute pancreatitis and complications of chronic pancreatitis



Assessment




Acute pancreatitis:


Symptoms vary according to severity of the attack. Sudden onset of constant, severe epigastric pain often occurs after a large meal or alcohol intake. Pain frequently radiates to the back or left shoulder and is somewhat relieved by a sitting position with the spine flexed. It is caused by biliary tree obstruction, enzymes irritating pancreatic and surrounding tissue, and the resulting edema. Nausea and vomiting, sometimes with persistent retching, usually occur and are caused by bowel hypermotility or ileus. Pain may be increased after vomiting because of increased pressure on the ducts, leading to further obstructions of secretions and tissue damage. Fever is usually present as well as hypotension and tachycardia. Jaundice suggests biliary tree obstruction. Extreme malaise, restlessness, respiratory distress, and diminished urinary output may be present. Hypovolemic shock may be present with hemorrhagic events, or distributive shock may occur secondary to systemic inflammatory response syndrome.



Physical assessment:


Diminished or absent bowel sounds, suggesting presence of ileus; mild to moderate ascites; generalized abdominal tenderness; tachypnea, crackles (rales) at lung bases related to atelectasis, and interstitial fluid accumulation; diminished ventilatory excursion related to splinting and guarding with pain; low-grade fever (37.7°-38.8° C [100°-102° F]) or pronounced fever with abscess or sepsis; and agitation, confusion, and altered mental status may occur because of electrolyte/metabolic abnormalities or acute alcohol withdrawal. Gray-blue discoloration of the flank (Grey Turner’s sign) or blue-red discoloration around the umbilicus (Cullen’s sign) sometimes is present with pancreatic hemorrhage.



Chronic pancreatitis:


Constant, dull epigastric pain; steatorrhea resulting from malabsorption of fats and protein; weight loss; and onset of symptoms of DM (polydipsia, polyuria, polyphagia).



History of:


Biliary tract disease; chronic excessive alcohol consumption; physical trauma to the abdomen (especially in young people); peptic ulcer disease; viral infection; ERCP; cystic fibrosis; neoplasms; shock; and use of certain medications, such as estrogen-containing oral contraceptives, glucocorticoids, sulfonamides, chlorothiazides, and azathioprine.



Diagnostic tests




Serum amylase:


When significantly elevated (more than 500 units/dL), rules out acute abdomen conditions, such as cholecystitis, appendicitis, bowel infarction/obstruction, and perforated peptic ulcer and confirms presence of pancreatitis. These levels return to normal 48-72 hr after onset of acute symptoms, even though clinical indicators may continue. Sensitivity is limited in patients with alcoholic pancreatitis and hypertriglyceridemia.



Serum lipase:


Has higher specificity and sensitivity than serum amylase. It rises more slowly than serum amylase and persists longer. Both lipase and amylase levels reflect the degree of necrotic pancreatic tissue.



Blood glucose:


Hyperglycemia occurs because of interference with beta cell function. It is transient with acute pancreatitis but common with chronic pancreatitis, during which DM is likely to develop.



Ultrasound, magnetic resonance imaging (MRI), computed tomography (CT) scan:


May reveal an enlarged and edematous pancreatic head or abscess, pseudocyst, or calcification.



MR cholangiopancreatography (MRCP):


Used to visualize pancreatic and common bile ducts and may be used if an ERCP is not feasible.



ERCP:


A combined endoscopic-radiographic tool that is used to study the degree of pancreatic disease via assessment of biliary-pancreatic ductal systems. It allows direct visualization of the ampulla of Vater, diagnoses biliary stones and duct stenosis, and distinguishes cancer of the pancreas from pancreatic calculi. ERCP is not performed until the acute episode has subsided.



Potassium:


Hyperkalemia will occur in the presence of tissue damage, metabolic acidosis, and renal failure in severe cases.



Serum calcium and magnesium:


May be lower than normal. On electrocardiogram, hypocalcemia is evidenced by prolonged QT segment with a normal T wave.



Complete blood count:


Elevated white blood cell (WBC) count caused by inflammatory process. Polymorphonuclear bodies may increase if bacterial peritonitis is present secondary to duodenal rupture. Hematocrit (Hct) may be elevated or decreased.



Blood urea nitrogen (BUN) and serum creatinine:


To evaluate renal function.



Urinalysis:


May show presence of glycosuria, which can signal the onset of DM. Elevated urine amylase levels are useful diagnostically when serum levels have dropped off. An elevated specific gravity reflects the presence of dehydration.



Abdominal x-ray examination:


May show dilation of the small or large bowel and presence of pancreatic calcification in chronic pancreatitis.





Nursing diagnosis:


Acute pain

related to inflammatory process of the pancreas


Desired Outcomes: Within 6 hr of intervention, patient’s subjective perception of discomfort decreases, and it is controlled within 24 hr, as documented by pain scale. Nonverbal indicators, such as grimacing and splinting of abdominal muscles, are absent or diminished.






















ASSESSMENT/INTERVENTIONS RATIONALES
Assess for and document degree and character of patient’s discomfort. Devise a pain scale with patient, rating discomfort on a scale of 0 (no pain) to 10 (worst pain). Pain characteristics may signal varying problems (see Assessment section). Baseline and subsequent use of pain scale helps determine effectiveness of pain relief.
Assess patient’s previous responses to pain and previously effective pain relief measures. Consider possible cultural and spiritual influences. Patient’s previous history of pain and how well it was managed influence perceptions and trust in present pain relief measures. Some cultures allow less outward show of pain, whereas others do not prohibit expressions of pain.
Ensure that patient maintains limited activity or bedrest. Rest helps minimize pancreatic secretions and pain.
Maintain nothing by mouth (NPO) status, and monitor nasogastric (NG) tube function. NPO status and NG suction are initiated early in the course of illness to decrease stimulus for pancreatic secretions and reduce stress in the GI tract. After acute pain and ileus have resolved, the patient is given clear liquids and diet is advanced as tolerated.
Administer analgesics, steroids, histamine H2-receptor blockers, antiemetics, and other medications as prescribed. Be alert to patient’s response to medications, using pain scale.
Analgesics reduce discomfort associated with pancreatitis. Steroids may be given to reduce inflammation in certain types of pancreatitis when infection is not a problem.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Pancreatitis

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