Acute Pancreatitis

A Look at Acute Pancreatitis

Pancreatitis is an inflammation of the pancreas. An accessory organ of the gastrointestinal (GI) tract, the pancreas lies in the left upper abdomen behind the stomach and between the spleen and duodenum. It functions as both an exocrine and endocrine gland, producing enzymes that promote digestion and hormones that aid in glucose balance. (See Functions of the pancreas.)

Adults of any age can develop acute pancreatitis; however, children rarely develop the disorder. It can occur in either edematous (interstitial) or necrotizing form. Both types cause inflammation that begins in the acinar cells. (See Edematous vs. necrotizing.) Most cases of acute pancreatitis are mild; however, about 15% of patients experience a severe form of the disease that can cause life-threatening complications, including fluid and electrolyte disturbances.

Acute pancreatitis that occurs on two or more occasions is classified as acute recurrent pancreatitis. When progressive recurring episodes of inflammation cause structural damage and loss of glandular function, pancreatitis becomes chronic. (See Chronic pancreatitis.)

How it happens

The two most common causes of acute pancreatitis are gallstones and alcohol consumption. Gallstones are the most common cause of acute pancreatitis. They pass into the bile duct and temporarily block the opening into the duodenum at the point where it's joined by the pancreatic duct. This obstructs pancreatic juices from flowing out of the pancreas into the duodenum. The backflow of these digestive juices causes lysis (dissolving) of pancreatic cells and subsequent pancreatitis. This typically mild type of pancreatitis resolves with the passage or removal of the gallstones.

Evil spirits

It's believed that ethyl alcohol, the second most common cause of acute pancreatitis, can cause the disease in several ways. Alcohol can affect the motility of the sphincter of Oddi, has direct toxic and metabolic effects on the pancreas, and forms protein plugs that obstruct small ducts in the pancreas. It's also believed that alcohol produces a temporary but significant reduction in blood flow to the pancreas. When these episodes occur repeatedly, they result in ischemic damage to the cells.

These effects can occur from long-term excessive consumption or from a single episode of binge drinking. A person sensitive to the effects of alcohol may have an attack of acute pancreatitis a few hours to a day or two after drinking; such a person may not need to drink very much alcohol to precipitate an attack. Alcohol typically results in a more severe type of pancreatitis because of the cell necrosis that occurs. With repeated attacks, pancreatitis becomes chronic.

Cause and exocrine effect

Acute pancreatitis can result from several other, less common, causes. (See Causes of acute pancreatitis.) But no matter what the cause, it's the exocrine functions that fail during acute pancreatitis. The enzymes that the pancreas normally excretes into the duodenum are instead activated within the pancreas or its ducts and begin to digest the pancreatic tissue itself. The inflammation that results causes intense pain, third-space shift of large volumes of fluids (which results in hypovolemia), pancreatic fat necrosis (with accompanying con sumption of serum calcium), and, occasionally, hemorrhage.

Imbalances caused by acute pancreatitis

Acute pancreatitis—whether mild or severe—can cause fluid and electrolyte imbalances, including hypovolemia, hyponatremia, hypocalcemia, hypomagnesemia, and hypokalemia.

Turn up the (blood) volume!

Hypovolemia is a major cause of death in patients with acute pancreatitis. Severe pancreatic damage triggers the release of systemic inflammatory mediators that produce increased capillary permeability and vasodilation. This, in turn, produces massive fluid shifts from the intravascular spaces to the interstitial spaces and the retroperitoneum, resulting in hypovolemia. Vomiting, diarrhea, excessive sweating, and, possibly, hemorrhage also contribute to hypovolemia.

The case of the lost electrolytes

Acute pancreatitis can also result in the loss of calcium, magnesium, and potassium. Vomiting and diarrhea can result in hyponatremia, hypokalemia, and (when severe) hypomagnesemia. Hyponatremia can also result from excessive sweating and increased antidiuretic hormone secretion caused by hypovolemia.

Hypocalcemia in acute pancreatitis usually results from concomitant hypoalbuminemia. Fat necrosis—caused by lipase necrosing the fat tissue in pancreatic interstitium and peripancreatic spaces—may result in the release of free fatty acids and intraperitoneal saponification, further decreasing serum calcium levels. Fat necrosis can also lead to hypomagnesemia because magnesium is deposited in areas of fat necrosis, which reduces serum levels. Because hypomagnesemia can contribute to hypocalcemia, hypomagnesemia should be corrected first.

What to look for

Often, the only symptom of mild pancreatitis is steady epigastric pain centered near the navel that's unrelieved by vomiting. In severe pancreatitis, the patient will likely report severe, persistent, piercing abdominal pain, usually in the midepigastric region, although the pain may generalize or occur in the left upper quadrant and radiate to the back or other areas. The abdominal pain is usually sudden in onset, and gradually becomes more severe until reaching a constant ache. The patient typically describes the pain as boring or penetrating and may report recent consumption of a large meal or alcohol. The pain may ease when the patient leans forward or lies on side with knees drawn toward the chest.

Sign language

Other possible signs and symptoms include nausea; vomiting; fever; mild jaundice; tachycardia; tachypnea; muscle spasms; and fatty, foul-smelling stools. Depending on the severity of the illness and degree of fluid loss and hemorrhage, the patient may also be hypotensive. Assessment may reveal Grey Turner sign (flank ecchymosis); Cullen sign (periumbilical ecchymosis); Chvostek and Trousseau signs (hypocalcemia); and abdominal distention, rigidity, and tenderness with hypoactive bowel sounds.

Pancreatitis can lead to severe, life-threatening complications. The patient will need close monitoring for signs and symptoms that may indicate such complications. (See Complications of acute pancreatitis.)

What tests show

Several types of diagnostic tests can help identify acute pancreatitis, including imaging and blood studies. Severity scoring can help predict the severity of the disease and the patient's prognosis.

Imaging studies

Chest X-rays show such pulmonary complications as atelectasis, pleural effusions (most commonly on the left side), or infiltrates that suggest adult respiratory distress syndrome.
Abdominal X-rays exclude other causes of acute abdominal pain and show bowel dilation and ileus.
ERCP should be done within 24 hours of admission for patients with concurrent acute cholangitis.
Magnetic resonance cholangiopancreatography may show stones in the common bile duct and necrosis; the test doesn't require an IV contrast medium.
Abdominal ultrasonography is the most useful test in determining the etiology of pancreatitis and is the technique of choice for detecting gallstones.
Acute pancreatitis can usually be diagnosed based on symptoms and laboratory findings. The American College of Gastroenterology states that contrast-enhanced computed tomography (CT) scanning and/or magnetic resonance imaging of the pancreas should be performed only in the absence of clinical improvement if the diagnosis is unclear. This is seldom done before 72 hours of symptom onset, usually to assess complications.

Blood studies

Elevated serum amylase levels (more than three times normal) almost always indicate pancreatitis, although amylase is not specific. Levels normally peak in 12 to 24 hours and return to normal within a few days.
Serum lipase levels are more specific to pancreatitis. They usually rise within 4 to 8 hours of the onset of symptoms and peak in about 24 hours. They typically return to normal in about 12 days.
Several other levels also rise, including glucose, triglyceride, bilirubin, aspartate aminotransferase, alanine amino transferase, lactate dehydrogenase, alkaline phosphatase, and blood urea nitrogen. Tests also show a prolonged prothrombin time and increased white blood cell count.
Hematocrit; partial pressure of arterial oxygen; and calcium, magnesium, potassium, and albumin levels all decrease.

Severity scoring

Several tools help predict the severity of acute pancreatitis and the patient's prognosis. It's crucial to use these tools early on because early recognition of severe pancreatitis can significantly improve the outcome. Tools include Ranson criteria, the acute physiology and chronic health evaluation (APACHE II) score, the multi organ system failure (MOSF) score, the modified Glasgow prognostic criteria, and the Balthazar score.

Ranson criteria look at several factors on admission (such as the patient's age and laboratory values) and then again 48 hours later (laboratory values and systemic effects). If the patient meets three or more criteria, the criteria predict a severe course and an increased mortality risk. (See Ranson criteria.)

The APACHE II score uses a point score calculated from routine physiologic measurements to provide a statistical prediction of mortality. However, the scoring system is time-consuming—a minus for assessing severe acute pancreatitis.

Extra sensitive

More sensitive than Ranson criteria and the APACHE II, the MOSF score predicts the severity of the disease at admission and can be recalculated daily. It's typically used on intensive care units. The scoring system evaluates seven organ systems, with a higher score indicating more severe disease. All patients with an MOSF score greater than 3 have severe disease.

Similar to Ranson criteria but with fewer criteria, the modified Glasgow criteria allows for daily scoring. The Balthazar score uses CT scan results to arrive at a prognosis. (See The Balthazar score: A CT scan severity index.)

How it's treated

Medical management for acute pancreatitis is fairly straightforward. The patient stays nothing by mouth and IV fluid is given. Analgesics help with pain management. Antibiotics are generally not required.

Keep those fluids flowing

Patients with evidence of significant third-space fluid shift and those who have a large amount of fluid in the retroperitoneal space need aggressive fluid replacement. These fluid shifts deplete intravascular volume and may lead to tachycardia, hypotension, kidney failure, hemoconcentration, and generalized circulatory collapse. Patients who develop hemoconcentration are also at increased risk for pancreatic necrosis and organ failure.

Most cases of pancreatitis respond well to colloids or lactated Ringer solution to treat hypovolemia and shock. Patients require close monitoring for electrolyte abnormalities, particularly hypo calcemia, hypokalemia, and hypomagnesemia. Fluid replacement aims to correct these imbalances and replace volume. If a patient develops necrotizing pancreatitis or experiences a sudden, severe attack with hemorrhaging, the patient may also need packed red blood cells to maintain hemodynamic stability.

Pushing back at pancreatic pain

The severe pain that typically accompanies pancreatitis calls for pain relief. For mild to moderate pain relief, acetaminophen (Tylenol) is effective. Tramadol is an analgesic for moderately severe pain. It inhibits the ascending pain pathways, altering perception of and response to pain. Meperidine (Demerol) is a synthetic opioid narcotic analgesic for the relief of severe pain. It has multiple actions similar to morphine. Due to the depressing effects on the respiratory system with opioids, careful observation of patients must be maintained with the administration of any opioid. Positioning patients in the knee-to-chest position may also help relieve pain.

No food, please—just rest

Part of treatment includes letting the pancreas rest—and that means giving the pancreas a break from food, which stimulates enzyme secretion. Initially, the patient with pancreatitis should receive nothing by mouth. As pain subsides and the patient's condition improves, the patient can begin oral intake, with careful monitoring. The patient should at first receive small amounts low in fat and protein.

If needed, antacids can help neutralize gastric secretions, and histamine antagonists can decrease hydrochloric acid production. Anticholinergic medications can reduce vagal stimulation, decrease GI motility, and inhibit pancreatic enzyme secretion. If the patient has severe pancreatitis with significant pancreatic necrosis, the patient may need insulin to correct hyperglycemia.

A patient with recurrent vomiting, gastric distention, or intestinal ileus may need a nasogastric (NG) tube inserted. An NG tube with suctioning also suppresses pancreatic secretions by decreasing gastric fluids.

Although controversial, antibiotic therapy for acute pancreatitis is indicated if secondary infection or necrotizing pancreatitis is present.

The oral route is out

Until a patient with pancreatitis can tolerate oral intake, the patient must receive nutrition by an alternate method. In milder cases, food should be withheld for no more than 7 days. A patient with severe pancreatitis requires nutritional support because of the inherently high level of stress and hypercatabolism. Such a patient may receive total parenteral nutrition (without lipids if triglycerides are increased) or enteric feedings to maintain nutrition.

Eradicating infections

An inactive bowel allows intestinal flora to cross the colonic wall and infect the pancreas, particularly necrotic areas, which are the most vulnerable to infection.

Antibiotics can help prevent infection or treat one that's already present. If infected pancreatic necrosis arises, the patient may need surgical debridement and drainage. The health care provider may also use a CT scan to guide aspiration of necrotic areas. This allows identification of the infecting organism, leading to more effective treatment.

Memory Jogger

To remember some of the key treatments for acute pancreatitis, just think of the word PANCREAS:

Pain control

Arresting shock with IV fluids

Nasogastric intubation

Calcium monitoring

Renal evaluation

Ensuring pulmonary function

Antibiotic administration

Surgery or special procedures as needed.

Coping with complications

To prevent the disease from progressing, the patient may need surgery or ERCP to remove gallstones or other biliary tract obstructions. A patient with a pancreatic abscess or pseudocyst may need surgical drainage. If a patient develops complications in the cardiovascular, renal, pulmonary, GI, or neurologic system, the patient will need treatment for the specific complication.

How you intervene

Patients with acute pancreatitis need careful monitoring, thorough assessments, and diligent nursing care. Follow these guidelines:

Teach the patient and family about acute pancreatitis and include them whenever possible in care planning.
Ensure a patent airway and assess the patient's respiratory status at least every hour or as ordered. Assess for adventitious or diminished breath sounds. Check oxygen saturation levels and arterial blood gas results as ordered.
Closely monitor the patient's cardiac and hemodynamic status at least every hour or as ordered.
Monitor the patient's vital signs at least every hour or as ordered.
Place the patient in a comfortable position that minimizes pain such as sitting and leaning forward, lying on side with knees bent, or sitting with knees flexed toward the chest.
Allow for periods of rest to reduce metabolic stress.
If the patient develops acute respiratory syndrome, anticipate the need for additional therapies such as prone positioning.
Provide supplemental oxygen as ordered.
Initiate IV fluid replacement therapy as ordered. Assess for signs of fluid overload, including dyspnea, edema, and crackles.
Monitor serum laboratory values (hematology, coagulation, and chemistry) for changes.

Dangerous drop-offs

Watch closely for signs and symptoms of hypokalemia (hypotension, muscle weakness, apathy, confusion, and cardiac arrhythmias), hypomagnesemia (hypotension, tachycardia, confusion, tremors, twitching, hypoactive deep tendon reflexes, and confusion), and hypocalcemia (positive Chvostek and Trousseau signs, tetany, seizures, and prolonged QT intervals on an electrocardiogram). Have emergency equipment readily available.
Assess for Cullen and Grey Turner signs, which indicate hemorrhagic pancreatitis.
Monitor the patient's intake and output closely, and notify the practitioner if the patient has a urine output of less than 0.5 ml/kg/hour. Weigh the patient daily.
Monitor the patient's neurologic status, noting confusion or lethargy.
Maintain the patient in a normothermic state to reduce the body's demand for oxygen.
Assess the patient's pain level, and administer medications as ordered.
Administer antibiotics as ordered, and monitor serum peak and trough levels as appropriate.
Withhold all oral fluids and food as ordered to prevent stimulation of pancreatic enzymes.
Insert an NG tube as ordered. Check placement at least every 4 hours. Irrigate with normal saline solution to maintain patency. Monitor drainage for frank bleeding and watch for bleeding in vomitus and stool.
Assess the patient's abdomen for distention and for diminished or absent bowel sounds; measure the abdominal girth.
As ordered, administer stool softeners to relieve constipation caused by immobility and opioid use.
Administer parenteral nutrition therapy or enteral feedings as ordered. Monitor blood glucose levels. Administer insulin as ordered.
When bowel sounds become active and the patient's condition improves, anticipate switching to low-fat oral feedings after 1 or 2 days on clear liquids.
Perform range-of-motion exercises to maintain joint mobility.
Perform meticulous skin care.
Provide emotional support to the patient and family, and encourage them to express their feelings.
Prepare the patient for surgery as indicated.
Document your assessments and interventions.

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