Managing a flare up

[Guest guest]

Inflammation of the pancreas can become a life-threatening emergency as the

pancreas literally digests itself. Here's how to cool the crisis before

irreversible damage occurs.

a.. Degrees of inflammation

a.. Many possible causes

a.. Assessing pain

a.. Sorting out laboratory findings

a.. Diagnosis and prognosis

a.. Setting nursing goals

a.. Managing drug therapy

a.. Abscesses and other complications

a.. Planning for discharge

a.. Using Ransom's criteria

You've just finished assessing your six patients when the charge nurse informs

you that a new patient is on her way up from the emergency department. The

diagnosis: acute abdominal pain, rule out pancreatitis.

Immediately you think, Alcohol abuse?... Salem sump... N.P.O.... lipase...

amylase... what else?

You know that this patient may need complex nursing care--- and it's been months

since you cared for your last patient with pancreatitis. Are you prepared to

take on another challenging patient today?

Unless you care for patients with pancreatitis routinely--- and most nurses

don't--- you could probably use a refresher on this often complicated and

dangerous disorder. Here, we'll provide the background you need to assess and

care for your emergency admission.

Degrees of inflammation

Located behind the stomach, the pancreas plays key exocrine and endocrine roles

in the body. Its exocrine function involves releasing a mixture of digestive

enzymes that flow into the pancreatic duct and, eventually, into the duodenum.

The pancreas also regulates carbohydrate metabolism by secreting the hormones

glucagon and insulin into the bloodstream--- an endocrine function. See

Examining the Pancreas from Head to Tail (108 KB jpg image) for more details.

Inflammation of this important gland can be either acute or chronic and varies

in severity from mild to severe. Mild pancreatitis is characterized by

interstitial edema of the pancreas. Severe or advanced pancreatitis is

associated with pancreatic hemorrhage and necrosis.

Acute pancreatitis doesn't usually lead to chronic pancreatitis unless

complications develop, such as strictures within the pancreatic duct. However,

chronic pancreatitis--- particularly alcoholic pancreatitis--- can cause acute

episodes when the disease flares up.

Whether acute or chronic, pancreatitis involves autodigestion. Pancreatic injury

or disruption of pancreatic ducts or acini permits enzymes to leak into

pancreatic tissue. The activated enzymes secreted by the pancreas--- chiefly

trypsin, elastase, and lipases--- break down tissue and cell membranes within

the organ and cause vascular damage, edema, hemorrhage, and necrosis.

Unchecked, pancreatitis ushers in a destructive cycle of events: As more

pancreatic cells are destroyed, more digestive enzymes are released, compounding

the damage. More inflammation results, affecting the surrounding peritoneum as

well as the pancreas. Drainage from damaged tissue may collect into abscesses,

which can eat through the bowel and trigger sepsis.

Meanwhile, fluid accumulation in the abdomen can account for tremendous

intravascular fluid losses--- 4 to 6 liters in the first 48 hours. Fluid

sequestration causes hypotension, hypovolemia, and electrolyte imbalances.

In severe acute pancreatitis, total autodigestion and pancreatic destruction may

lead to diabetic ketoacidosis, shock, coma, and death. But some patients live

with well-controlled chronic pancreatitis indefinitely: Mortality rates are

approximately 50% within 20 to 25 years.

Many possible causes

Pancreatitis was first documented in the medical literature in 1788. Over 200

years later, we still don't know exactly why it occurs, but we've identified

many possible triggers. An acute attack can be caused by:

a.. obstruction of the pancreatic ducts (for example, because of biliary

stones, bile stasis, or gallstones)

b.. biliary tract disease

c.. the toxic effects of alcohol and certain drugs, such as glucocorticoids,

sulfonamides, chlorothiazide, azathioprine, and didanosine (ddl)

d.. reflux of duodenal contents into the pancreatic duct

e.. transient obstruction of the common bile duct by gallstones located near

the pancreatic duct's orifice. Gallstones can intensify pancreatic pain and

contribute to acute attacks.

f.. trauma to the pancreas, either from abdominal injuries or surgery. For

example, acute pancreatitis can be a complication of endoscopic retrograde

cholangiopancreatography.

The causes of chronic pancreatitis are more insidious. Possibilities include

heavy alcohol consumption (a factor in more than half of cases), obstruction of

the pancreatic duct caused by posttraumatic ductal strictures, pseudocysts,

mechanical or structural changes of the pancreatic-duct sphincter, and

pancreatic tumors. Less-common causes include hyperparathyroidism, peptic ulcer

disease, and cystic fibrosis. It may also occur as a hereditary disease.

Tropical pancreatitis, another chronic form of the disease, may be caused by

protein deficiency or ingestion of a toxin. It's characterized by pancreatic

insufficiency, diabetes mellitus, and recurring pain.

Unless you know the patient's history, differentiating an exacerbation of

chronic pancreatitis from an acute episode isn't easy. However, the treatment

for both conditions is similar.

Abdominal pain is the number one symptom of pancreatitis. But it's not always a

reliable indicator because many patients complain only of nonspecific abdominal

pain--- and 10% to 20% of patients have no pain at all.

Your emergency admission is a typical example of a patient with pancreatic pain.

Assessing pain

Pamela Huber, 46, arrives in your unit with complaints of sharp abdominal pain

in the midepigastric area, nausea, and vomiting. When you take her history, she

describes herself as a social drinker who usually has a glass of wine with

dinner; she denies excessive alcohol use. Mrs. Huber tells you she's been having

this sharp pain for about 24 hours. She also says that her back often bothers

her after she eats a heavy meal.

Many patients with acute pancreatitis complain of knifelike pain in the

midepigastric area; it may radiate to the back (as in Mrs. Huber's case), left

flank, or left shoulder. Radiation to the back may be caused by the pancreas's

retroperitoneal location, and many patients mistake the sensation for orthopedic

pain.

Acute pain, which can persist for days or weeks, is caused by edema of the

pancreas, obstruction of the biliary tree, and release of pancreatic enzymes

into pancreatic and surrounding tissues. Chronic pain, which has a duller

quality, may last a few hours or persist for months.

Mrs. Huber exhibits abdominal tenderness, guarding, and hypoactive bowel sounds.

Her abdomen is slightly distended. You don't see Grey 's sign, a gray-blue

discoloration of the flank, or Cullen's sign, a gray-blue discoloration around

the umbilicus. Either could indicate pancreatic hemorrhage.

On further questioning, Mrs. Huber tells you that the pain begins abruptly,

usually after she drinks an alcoholic beverage or eats a large meal. She says

that the pain she's experiencing now is relieved when she shifts her body

position. Lying in a fetal position with her abdomen flexed eases her back pain.

She also complains of nausea and vomiting, which can be caused by hypermotility

or paralytic ileus secondary to the pancreatitis or peritonitis, a common

complication of pancreatitis.

Mrs. Huber's vital signs are: temperature, 100 F (37.8 C); pulse, 102;

respiratory rate, 24; and blood pressure, 98/54. Fever is a common symptom of

acute pancreatitis and may be caused by cholangitis, cholecystitis, peritonitis,

or intra-abdominal abscesses. Hypotension is also a common finding because of

fluid sequestration from vasodilation. Tachypnea can result from anxiety, pain,

and increased metabolic demands produced by compensatory mechanisms.

To determine the presence of steatorrhea (excessive excretion of fat in stools),

you'll need to obtain a stool specimen. Foul-smelling, fatty stools result from

pancreatic insufficiency and increased lipase release from damaged pancreatic

tissue.

In chronic pancreatitis, diabetes, jaundice, and malabsorption (which causes

steatorrhea) are common, as is weight loss when disease is advanced. Diabetes

and malabsorption may not arise until 80% or more of endocrine and exocrine

pancreatic tissue is destroyed.

Sorting out laboratory findings

Serum amylase and lipase levels are the keys to diagnosing acute pancreatitis.

These enzymes are released as pancreatic cells and ducts are destroyed, and

levels are usually elevated during the first 24 to 48 hours after the onset of

symptoms.

Normal serum amylase is 35 to 115 units/liter; a level above 300 units/liter

usually indicates acute pancreatitis. As a rule, serum amylase levels rise

within 12 hours after the onset of symptoms, peak in 20 to 30 hours, and return

to normal in 3 to 5 days.

But don't make the mistake of ruling out acute pancreatitis simply because serum

amylase is normal. Amylase is excreted in urine by the kidneys, so if the

patient has diuresed (for example, following fluid challenges or diuretic

administration), the amylase may be normal or even decreased despite

pancreatitis.

Similarly, an elevated level can also be misleading. Although pancreatitis is

the most common cause, opiates, thiazide diuretics, and diagnostic dyes can also

raise amylase levels.

Because lipase is more specific to the pancreas than amylase and may remain

elevated for up to 14 days, it's a more accurate indicator of acute pancreatitis

and especially useful for a late diagnosis. Normal serum lipase ranges from 32

to 80 units/liter. An elevated level may indicate acute pancreatitis or a

pancreatic duct obstruction.

In response to the inflammatory process, white blood cell (WBC) elevation occurs

in 80% of all patients with pancreatitis. Serum glucose levels may also rise

(especially during a severe attack) because of damage to beta cells in the

pancreas. This damage impairs carbohydrate metabolism and may lead to diabetes

mellitus.

Finally, liver function tests, lactate dehydrogenase (LDH), and aspartate

aminotransferase (AST) may be elevated in the presence of alcoholic liver

disease and acute pancreatitis associated with cholelithiasis.

Diagnosis and prognosis

The most revealing assessment findings for Mrs. Huber include:

a.. serum amylase, 320 units/liter

b.. serum lipase, 220 units/liter

c.. WBC count, 17,000 mm3 (normal: 5,000 to 10,000 mm3)

d.. LDH, 365 units/liter (normal: 50 to 240 units/liter)

e.. AST, 90 units/liter (normal: 10 to 30 units/liter)

f.. serum glucose, 350 mg/dl (normal: 80 to 120 mg/dl).

An ultrasound examination is negative for gallstones.

On further questioning, Mrs. Huber admits to drinking three or more glasses of

wine a night. The physician diagnoses an acute exacerbation of chronic alcoholic

pancreatitis, based on clinical findings and her history of alcohol abuse. A

computed tomography scan is negative for fluid collection, abscesses, and

necrotic areas; abdominal X-rays rule out a perforated viscus and calcifications

in the pancreas.

How serious is Mrs. Huber's condition? Along with other clinical findings, the

physician may use Ransom's criteria (see box) to establish a prognosis. This

system, which is based on the patient's age and certain signs and symptoms over

the first 48 hours after the onset of acute pancreatitis, predicts morbidity and

mortality.

Mrs. Huber's condition meets 3 of 11 criteria listed: her WBC count is 17,000

mm3 , her serum glucose is 350 mg/dl, and her LDH is 365 units/ liter. This

places her in the 15% mortality rate category. With expert care, she stands a

good chance of recovering without complications.

Setting nursing goals

Your interventions for Mrs. Huber will aim primarily at limiting the severity of

pancreatic inflammation, keeping her comfortable, and preventing complications.

During the acute phase, monitor her vital signs closely. With her hypotension,

fever, and tachypnea, she may be dehydrated and have a fluid volume deficit, so

administer intravenous (I.V.) fluids as ordered. The physician may establish a

central line. Check her urine output hourly and keep accurate fluid intake and

output records. Check electrolyte levels daily.

If she becomes hemodynamically unstable, prepare her for transfer to the

intensive care unit for more-precise monitoring with a pulmonary artery (PA)

catheter and treatment with volume expanders, such as plasma or albumin. If her

PA pressure rises following treatment, she might need diuretics or a

vasodilating drug, such as I.V. nitroglycerin.

Along with vital signs and fluid status, also assess regularly for abnormal lung

sounds, such as crackles, wheezes, or decreased breath sounds. Respiratory

monitoring and support is essential in the acute phase because respiratory

failure can occur even in patients who are in no apparent distress. For all

patients, you should check arterial blood gases (ABGs) at the time of diagnosis

and at intervals of not more than 12 hours for the first 48 to 72 hours.

The need for respiratory support depends on the degree of pulmonary

insufficiency. In Mrs. Huber's case, her initial ABGs (pH, 7.35; Pao2, 68 mm Hg;

Paco2 , 50 mm Hg; HCO3 , 21 mEq/liter; Sao2 , 90%) are indications for oxygen at

4 liters/minute via nasal cannula. You'll monitor her respiratory status by

pulse oximetry continuously or every 2 hours for the first 12 hours; then have

another ABG sample drawn. If she experiences progressive pulmonary insufficiency

from acute respiratory distress syndrome (ARDS), a possible complication of

severe pancreatitis, she may need intubation and mechanical ventilation with

positive end-expiratory pressure.

Also check electrolyte values, keeping a close watch on her magnesium level

(normal is 1.8 to 2.1 mEq/ liter). If it drops, she may need I.V. magnesium

replacement.

Traditionally, clinicians expected many pancreatitis patients to have low

calcium levels and exhibit symptoms of hypocalcemia, such as tetany, muscle

cramps, and convulsions. But recent research suggests that symptoms and

complications related to hypocalcemia are uncommon. Even so, continue to monitor

calcium levels and initiate treatment, if indicated.

Patients with moderate to severe pancreatitis need gastrointestinal (GI)

decompression to limit pancreatic inflammation and secretions. For Mrs. Huber,

who has a moderately severe case, the physician orders nasogastric suctioning to

reduce vomiting and abdominal distension. However, nasogastric suctioning hasn't

been shown to be effective in patients with mild acute pancreatitis, especially

when it's associated with alcohol abuse.

A patient with acute pancreatitis won't tolerate oral feeding well, so Mrs.

Huber is kept N.P.O. for a few days. Administer I.V. D5W as ordered and adjust

the infusion as indicated according to daily electrolyte values.

Because nutritional depletion occurs rapidly in patients with pancreatitis, a

patient with a more severe case (or one who's N.P.O. for more than 2 days) needs

nutritional support. For most patients, standard total parenteral nutrition is

the most practical form of nutritional support once the patient's cardiovascular

status is stable. As bowel sounds return to normal, nasogastric suctioning can

be discontinued and the patient can start a clear liquid diet, then slowly

resume a normal diet.

Weigh Mrs. Huber daily and provide frequent oral care while she's N.P.O. Unless

complications develop, expect her to be back on a normal diet within a week.

What about enforced bed rest, a traditional strategy intended to help the

pancreas " rest " ? Although still sometimes suggested in nursing texts, the value

of bed rest has never been proved by research. However, your patient may be

lethargic--- especially when she's N.P.O.--- and want to stay put most of the

time. If so, pay particular attention to how she's positioned to preserve skin

integrity and relieve discomfort. Encourage chair rest and incentive spirometry

to help with lung inflation.

Managing drug therapy

To relieve symptoms and prevent complications, you may administer analgesics,

antibiotics, anticholinergics, antacids, and anticoagulants. Hold analgesics

until after initial laboratory blood specimens are drawn because these drugs may

elevate serum amylase and lipase.

Meperidine (Demerol) is the drug of choice for pancreatic pain; pentazocine

(Talwin) is an alternative for patients who can't tolerate meperidine.

Meperidine, which relaxes Oddi's sphincter, can be administered I.V. via a

patient-controlled analgesia device. Morphine is usually avoided because it's

associated with spasm of the ampulla of Vater.

Broad-spectrum antibiotics are commonly ordered to prevent or treat infection

associated with pancreatitis. These drugs may be an effective treatment for

gallstone-associated pancreatitis and severe necrotizing pancreatitis but less

effective for other types, such as mild alcoholic pancreatitis. Peritoneal

lavage with an isotonic electrolyte solution containing an antibiotic may be

considered in severe cases, although this treatment is controversial.

Parenteral anticholinergic drugs, such as atropine or propantheline, may be

ordered to decrease vagal stimulation, inhibit pancreatic enzyme secretion, and

relieve ampullary spasm. Use caution when giving an anticholinergic to a patient

with tachycardia and high fever--- it may exacerbate these symptoms.

Aluminum-magnesium antacids, such as magaldrate (Riopan), may be ordered for

pancreatitis with acute gastroduodenal ulceration and bleeding. In the case of

upper GI bleeding, histamine2-receptor antagonists (such as cimetidine) may be

given I.V.

In severe cases requiring surgical drainage of infected necrotic tissue and in

advanced pancreatitis with a risk of pulmonary embolism, the physician may order

I.V. heparin. However, this treatment is controversial because of the risk of

hemorrhage and disseminated intravascular coagulation (DIC). You'll need to

monitor platelet counts and fibrinogen levels closely.

Abscesses and other complications

Pancreatic abscesses are the most serious complication of pancreatitis---

untreated, they're always fatal. They develop when purulent drainage from

necrotic tissue drains and collects in pancreatic tissue. As they grow,

abscesses can erode through the retroperitoneum into the bowel, the mediastinum,

the pleural space, or the pelvis. Be alert for warning signs: a persistently

elevated temperature, increasing abdominal pain, and episodes of severe

vomiting.

When an abscess (or pseudocyst) is incised or drained, the surgeon may insert a

drainage tube, suture it in place, and attach it to low suction to prevent

tissue contact with the drainage and further necrosis.

Fluid sequestration, a hallmark of pancreatitis, can also complicate your

patient's condition by causing hypotension, hypovolemia, and electrolyte

imbalances. Closely monitor her vital signs, electrolyte values, and cardiac

rhythm. Be especially vigilant for these electrolyte imbalances:

a.. Hypocalcemia (calcium less than 8 mg/dl). Assess the patient for tingling

sensations (neuromuscular irritability), spasms (tetany), or tremors. You can

also assess for hypocalcemia by lightly tapping her cheek to elicit spasms

(Chvostek's sign) or by applying pressure over the large arteries and nerves in

her upper arm to elicit spasms (Trousseau's sign).

b.. Hypokalemia (potassium less than 3.5 mg/dl). Monitor for arrhythmias,

muscle weakness, and hypotension.

c.. Hypomagnesemia (magnesium less than 1.4 mg/dl). Like hypokalemia,

hypomagnesemia can lead to life-threatening arrhythmias.

In severe cases of fluid sequestration, hypo-volemia can lead to decreased renal

perfusion and acute renal failure. Hypovolemia induces the release of renin,

angiotensin, and aldo-sterone, which leads to constriction of blood vessels and

retention of sodium and water. Also responding to hypovolemia, the posterior

pituitary gland releases antidiuretic hormone, which contributes to sodium and

water retention. To prevent renal complications, carefully monitor fluid balance

and electrolytes and maintain urine output at more than 30 ml/hour.

Pulmonary complications range from hypoxia to ARDS. Deep breathing may be

painful, so patients often splint the painful areas and breathe shallowly---

responses that decrease tidal volume and may lead to atelectasis. Respiratory

complications can also occur as a result of pancreatic enzyme release and

exudate crossing the diaphragm and entering the pleural space via the lymphatic

channels. If you hear bronchial breath sounds, your patient could be developing

a pleural effusion.

A patient like Mrs. Huber is also at risk for bleeding and DIC. Pancreatic

inflammation prevents vitamin K, a key element in coagulation, from being

absorbed through the GI tract. So monitor your patient for bruising and other

signs of bleeding. Test stools for occult blood and carefully monitor her

platelet count, prothrombin time, and activated partial thromboplastin time.

Some patients develop pseudocysts, so named because they lack the epithelial

lining that characterizes true cysts. They're formed from pancreatic juices that

collect near the pancreas and are encapsulated. They can be diagnosed by

ultrasound or computed tomography scan. Clinical signs include a persistent

elevation of serum lipase.

Unlike abscesses, pseudocysts may resolve spontaneously. Large cysts (5 cm or

more) that persist for more than 6 weeks may be drained or removed

percutaneously, endoscopically, or surgically.

Planning for discharge

Because Mrs. Huber was diagnosed with an acute episode of chronic alcoholic

pancreatitis, your discharge planning includes teaching her about the

relationship between pancreatitis and alcohol use so she can avoid future

flare-ups. Social services initiates a referral for counseling related to

alcohol abuse.

Arrange for a consult with a nutritionist as soon as possible after admission.

Make sure Mrs. Huber gets written instructions for a low-fat, high-protein diet

containing moderate amounts of carbohydrates and tell her to avoid alcohol,

spices, caffeine, and nicotine. Reinforce dietary guidelines until discharge.

If she's discharged with a pancreatic enzyme replacement such as pancrelipase

(Viokase), make sure she understands what it's for, how to take it, what

benefits to expect, and what possible adverse reactions to watch for.

Other patients might need other specialized teaching before they go home. For

example, if diabetes is a factor, you'd want to teach the patient how to monitor

and manage her blood glucose levels.

Fortunately, Mrs. Huber's acute pancreatitis resolved without complications. But

she faces the threat of flare-ups for the rest of her life. Your discharge

planning can lay the foundation for successful management of her chronic

condition.

Mark E. Armstrong

www.top5plus5.com

Oregon State Chapter Rep

Pancreatitis Association, International