Edematous or interstitial acute pancreatitis is characterized by interstitial edema, engorgement of capillaries, and dilation of lymphatic vessels. Necrotizing pancreatitis is characterized by pancreatic cell death and may initiate an inflammatory response that extends beyond the pancreas. Surrounding blood vessels may rupture, or the exudate of peritoneal fluid may sequester and become infected, leading to tissue necrosis, peritonitis, shock, and death. Distinction between the two morphologic types is essential for predicting the severity of the course of disease, as well as the outcome. Factors responsible for the transformation of edematous pancreatitis to the necrotizing form are largely unknown (Friedman, 2005; Greenberger & Toskes, 2005).

The pathophysiology of severe pancreatitis can be traced to the extravasation of pancreatic enzymes. These toxic proteolytic enzymes cause widespread chemical inflammation of tissue. As a result, considerable loss and sequestration of protein-rich fluid from the vascular space occurs, leading to hypovolemia, hypotension, and systemic hypoperfusion. Systemic inflammatory response syndrome (SIRS) can occur with the release of systemic inflammatory mediators as a result of pancreatic injury (Greenberger & Toskes, 2005).

Multisystem complications of acute pancreatitis involve almost every organ system and significantly affect the morbidity and mortality associated with this disease. These complications can occur early in the course of the disease or as late as 2 weeks after resolution of the acute phase. The causes of these complications range from enzyme impairment of pancreatic function to pancreatic tissue necrosis (Table 1-1).

BP, Blood pressure; BUN, blood urea nitrogen; Cr, creatinine; Hb, hemoglobin; Hct, hematocrit; LUQ, left upper quadrant; PT, prothrombin time; PTT, partial thromboplastin time.
*Common complications.
Complications Physiologic Mechanism Symptoms
Hypotension* Increased vascular permeability from cytokine release BP <80/60, dizziness
Central Nervous System
Encephalopathy Liver malfunction Confusion, altered mental status, agitation
Bleeding Gastritis, peptic ulcer, Mallory-Weiss tear, pseudocyst rupture or esophageal varices, concomitant liver disease or splenic/portal vein thrombosis Positive hemoccult, hematemesis, abdominal pain, low Hb/Hct, postural hypotension


Coagulation abnormalities

Vascular stasis

Cytokine release from pancreatic cell death
Lower leg pain, erythema, tenderness, swelling, bruising, petechiae, increased PT and PTT, bleeding from orifices


Metabolic acidosis




Pancreatic malfunction

Cytokine release/cell death

Low parathyroid hormone secretion Loss of GI secretions through vomiting
Anxiety, alteration in mental status, diaphoresis, fatigue, leg cramps, nausea and vomiting, polydipsia, polyuria, tetany (↓Ca)

Collection of fluid, tissue, debris, and pancreatic enzymes, caused by blockage, may become infected and develop into abscess Fever (if abscess), palpable tender LUQ abdomen, abdominal pain
Hypoxemia Atelectasis Pleural effusion Acute respiratory syndrome*

Cytokine release from pancreatic cell death, which results in vasodilation, increased vascular permeability, and edema

Hypervolemic from fluid replacement (low BP)
Dyspnea, tachypnea, low PO2 levels
Renal Problems
Prerenal failure Acute tubular necrosis Intravascular volume depletion secondary to leakage of fluids in the pancreatic bed Azotemia, increased BUN/Cr
Pancreatic abscess Infected pseudocyst Peritonitis Infection occurs with pancreatic necrosis Fever, leukocytosis, shock, organ failure, LUQ abdominal pain, elevated C-reactive protein

Differential diagnosis can be difficult, so it is necessary for the clinician to look at the total picture of physical symptoms, laboratory data, and radiologic tests. The goals of treatment are to rest the pancreas, relieve pain, and maintain intravascular fluid volume. Management of secondary complications varies according to the organ system involved. The nurse’s role is to provide supportive care and to assess for signs and symptoms of complications (see Table 1-1).


The annual incidence of acute pancreatitis in the general population is 5 to 10 people per 100,000; thus, the disorder is relatively common (Turner, 2003) and its occurrence has been increasing. Between 1960 and 1980, the incidence of acute pancreatitis has increased 10-fold (Munoz & Katerndahl, 2006). Up to 25% of patients who develop acute pancreatitis have severe or life-threatening complications (Hale, Moseley, & Warner, 2000); within this percentage, between 2% and 10% of events can be fatal (Munoz & Katerndahl, 2006; Despins, 2005). Necrotizing pancreatitis contributes to the occurrence of acute pancreatitis in 3% to 5% of all patients in whom the condition has been diagnosed; a mortality rate of 50% has been reported (Greenberger & Toskes, 2005). The two major causative factors known to be responsible for acute pancreatitis are intake of alcohol and cholelithiasis. Pancreatitis in the oncology patient is likely to be caused by these same factors, but it also can result from direct tumor infiltration into the gland, metastasis to regional lymph nodes producing ductal obstruction, the complication of tumor lysis syndrome, a presenting manifestation of immunoblastic lymphoma, or complications resulting from medical or surgical therapy (Greenberger & Toskes, 2005; Yahanda & Chang, 2005; Yeo et al., 2005; Sinicrope & Levin, 2000). Other causes of pancreatitis include toxins, biliary obstruction, drugs (Box 1-1), hyperparathyroidism, hyperlipidemia, infection, trauma, ischemia, transplant, vasculitis, and autoimmune disorders (Friedman, 2005; Greenberger & Toskes, 2005).

BOX 1-1


Data from Friedman, L. S. (2005). Liver, biliary tract and pancreas. In L. Tierney, S. J. McPhee, & M. A. Papaealis, et al. (Eds.), Current medical diagnosis and treatment (pp. 671-674). (44th ed.). New York: Lange Medical Books/McGraw-Hill; Greenberger, N., & Toskes, P. (2005). Acute and chronic pancreatitis. In D. Kasper, E. Braunwald, & A. Fauci, et al. (Eds.), Harrisons principles of internal medicine (pp 1895-1902). (16th ed.). New York: McGraw Hill Medical Publishing Division; Sekimoto, M., Takada, T., & Kawarada, Y., et al. (2006). JPH guidelines for the management of acute pancreatitis: Epidemiology, etiology, natural history, and outcome predictors in acute pancreatitis. Journal of Hepatobiliary and Pancreatic Surgery 13:10-24.
Acetaminophen Furosemide Phenolphthalein
Amphetamines Histamine Procainamide
Azathioprine* Hydrochlorothiazide Propoxyphene
Calcium Indomethacin Rifampin
Chlorthalidone Lipids Salicylates
Cholestyramine Manganese Stibogluconate sodium
Cimetidine Mefenamic acid Sulfa antibiotics*
Clonidine Methyldopa Sulindac
Corticosteroids* Nitrofurantoin Tetracycline*
Diazoxide Opiates Thiazides*
Enalapril Pentamidine* Valproic acid*
Ethacrynic acid Phenformin Vitamin D
*Common causes.


Alcohol consumption and abuse: The amount of daily consumed alcohol that is estimated to cause pancreatitis is 50 to 150 g (50 g is equivalent to four 12-oz servings of beer with 3% to 5% alcohol content). The average onset of alcohol-related pancreatitis occurs after 4 to 7 years of drinking (Munoz & Katerndahl, 2000).

Chemotherapy and biotherapy: L-asparaginase produces the highest incidence, reportedly with rates as high as 16% (Yahando & Chang, 2005), but numerous chemotherapy and biotherapy agents may be causative (Box 1-2).

BOX 1-2


Data from Greenberger, N., & Toskes, P. (2005). Acute and chronic pancreatitis. In D. Kasper, E. Braunwald, & A. Fauci, et al. (Eds.), Harrisons principles of internal medicine (pp. 1895-1902). (16th ed.). New York: McGraw Hill Medical Publishing Division; Polovich, M., White, J., & Kelleher, L. (2005). Chemotherapy and biotherapy guidelines and recommendations for practice. (2nd ed.). Pittsburgh: ONS Press; Sinicrope, F. A., & Levin, B. (2000). Complications of cancer and its treatment: Gastrointestinal complications. In R. Bast, D. Kufe, & R. Polock, et al. (Eds.), Cancer medicine (pp. 1035-1040). (5th ed.). Hamilton, Ontario, Canada: B.C. Decker, Inc.; Yahanda, A. M., & Chang, A. E. (2005). Acute abdomen, bowel obstruction and fistula. In M. Abeloff, J. Armitage, & J. Neiderhuber, et al. (Eds.), Clinical oncology (pp. 1030-1031) St. Louis: Elsevier; Yeo, C., Yeo, T., & Hrubcin, R., et al. (2005). Cancer of the pancreas. In V. T. Devita Jr., S. Hellman, & S. A. Rosenberg (Eds.), Cancer: Principles and practice of oncology (pp. 1409-1415). (6th ed.). Baltimore: Lippincott Williams & Wilkins.
Azathioprine Ifosfamide
Bleomycin Interleukin-2
Cisplatin L-asparaginase
Cyclophosphamide 6-mercaptopurine
Cytosine arabinoside Methotrexate
Didanosine Mitomycin-C
Doxorubicin Prednisone
Estrogens Vinblastine
5-Fluorouracil Vincristine

Medications: See Box 1-1.

Manipulation of ampulla of Vater/pancreas: Endoscopic retrograde cholangiopancreatography (ERCP), pancreatectomy, splenectomy, trauma, and placement of intrahepatic catheter (Friedman, 2005; Greenberger & Toskes, 2005).

Metabolic abnormalities: Tumor lysis syndrome (TLS), hyperlipidemia, hyperparathyroidism, hypercalcemia, and end-stage renal disease (Friedman, 2005; Yeo et al., 2005; Sinicrope & Levin, 2000).

Infection: Parasitic infection, adenoviruses, mumps, coxsackieviruses, Staphylococcus, scarlet fever, hepatitis B, Campylobacter, Mycoplasma, rubella, Epstein-Barr virus, cytomegalovirus, and human immunodeficiency virus (HIV) (Sekimoto et al., 2006; Friedman, 2005; Greenberger & Toskes, 2005).

Dietary: High-fat diet (leading to cholelithiasis) and long-term hyperalimentation (biliary sludge) (Sekimoto et al., 2006; Greenberger & Toskes, 2005; Turner, 2003).

Vascular problems: Ischemia, systemic lupus erythematosus and shock states (Friedman, 2005).

Miscellaneous: Post bone marrow transplant, graft-versus-host disease, ectopic pregnancy, pregnancy, ovarian cyst, hypothermia, hereditary pancreatitis, scorpion venom, perforated peptic ulcer, Crohn’s disease, and Reye’s syndrome (Sekimoto et al., 2006; Friedman, 2005; Greenberger & Toskes, 2005; Yahanda & Chang, 2005; Yeo et al., 2005).


The prognosis is determined through assessment of morphologic involvement, which may be seen as edematous interstitial pancreatitis or necrotizing fulminant pancreatitis. The mechanism of action that determines which form will predominate remains unclear. The edematous interstitial form is usually a mild case that is self-limiting. In 5% to 15% of all cases, the disease takes the fulminant course (Munoz & Katerndahl, 2006; Despins, 2005). Prognosis can be predicted by the morphologic type and the presence of the following systemic complications:
Oct 19, 2016 | Posted by in NURSING | Comments Off on 1. ACUTE PANCREATITIS

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