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pancreatitis

 
Medical Encyclopedia: Pancreatitis

Definition

Pancreatitis is an inflammation of the pancreas, an organ that is important in digestion. Pancreatitis can be acute (beginning suddenly, usually with the patient recovering fully) or chronic (progressing slowly with continued, permanent injury to the pancreas).

Description

The pancreas is located in the midline of the back of the abdomen, closely associated with the liver, stomach, and duodenum (the first part of the small intestine). The pancreas is considered a gland. A gland is an organ whose primary function is to produce chemicals that pass either into the main blood circulation (called an endocrine function), or pass into another organ (called an exocrine function). The pancreas is unusual because it has both endocrine and exocrine functions. Its endocrine function produces three hormones. Two of these hormones, insulin and glucagon, are central to the processing of sugars in the diet (carbohydrate metabolism or breakdown). The third hormone produced by the endocrine cells of the pancreas affects gastrointestinal functioning. This hormone is called vasoactive intestinal polypeptide (VIP). The pancreas' exocrine function produces a variety of digestive enzymes (trypsin, chymotrypsin, lipase, and amylase, among others). These enzymes are passed into the duodenum through a channel called the pancreatic duct. In the duodenum, the enzymes begin the process of breaking down a variety of food components, including, proteins, fats, and starches.

Acute pancreatitis occurs when the pancreas suddenly becomes inflamed but improves. Patients recover fully from the disease, and in almost 90% of cases the symptoms disappear within about a week after treatment. The pancreas returns to its normal architecture and functioning after healing from the illness. After an attack of acute pancreatitis, tissue and cells of the pancreas return to normal. With chronic pancreatitis, damage to the pancreas occurs slowly over time. Symptoms may be persistent or sporadic, but the condition does not disappear and the pancreas is permanently impaired. Pancreatic tissue is damaged, and the tissue and cells function poorly.

— Rosalyn Carson-DeWitt, MD



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Dictionary: pan·cre·a·ti·tis   (păng'krē-ə-tī'tĭs, păn'-) pronunciation
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n.
Inflammation of the pancreas.



Inflammation of the pancreas, associated with alcohol, trauma, or pancreatic-duct obstruction. Activated enzymes escaping into pancreatic tissues cause irritation and inflammation. If it does not subside, bleeding, tissue death and scarring, pus formation, and infection may occur. Symptoms include severe pain (worst when lying on the back), low fever, nausea, and hypertension. Acute cases are treated by controlling pain, preventing or relieving shock, inhibiting pancreatic-juice secretion (including eliminating oral intake of food), avoiding infection, and replacing lost fluids and salts. Chronic pancreatitis can destroy enough of the pancreas to cause pancreatic-juice deficiency and diabetes mellitus. Treatment may include a low-fat diet, avoiding overeating and alcohol, pancreatic extracts, and insulin.

For more information on pancreatitis, visit Britannica.com.

Dental Dictionary: pancreatitis
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n

Inflammation of the pancreas that may be acute or chronic, characterized by severe abdominal pain radiating to the back, fever, anorexia, nausea, and vomiting.

Definition

Pancreatitis is an inflammation of the pancreas, an organ that is important in digestion. Pancreatitis can be acute, beginning suddenly, usually with the patient recovering fully; or chronic, progressing slowly with permanent injury to the pancreas.

Description

The pancreas is located in the midline of the back of the abdomen, closely associated with the liver, stomach, and duodenum, the first part of the small intestine. The pancreas is considered a gland. A gland is an organ whose primary function is to produce chemicals that pass either into the main blood circulation (called an endocrine function), or pass into another organ (called an exocrine function). The pancreas is unusual because it has both endocrine and exocrine functions. Its endocrine function produces three hormones. Two of these hormones, insulin and glucagon, are central to the processing of sugars in the diet (carbohydrate metabolism or breakdown). The third hormone produced by the endocrine cells of the pancreas affects gastrointestinal functioning. This hormone is called vasoactive intestinal polypeptide (VIP). The pancreas's exocrine function produces a variety of digestive enzymes (trypsin, chymotrypsin, lipase, and amylase, among others). These enzymes are passed into the duodenum through a channel called the pancreatic duct. In the duodenum, the enzymes begin the process of breaking down a variety of food components, including, proteins, fats, and starches.

Acute pancreatitis occurs when the pancreas suddenly becomes inflamed but improves. Patients usually recover fully from the disease, and in almost 90% of cases, the symptoms disappear within about a week after treatment. The pancreas returns to its normal structure and functioning after healing from the illness. After an attack of acute pancreatitis, the tissue and cells of the pancreas typically return to normal. With chronic pancreatitis, damage to the pancreas occurs slowly over time. Symptoms may be persistent or sporadic, but the condition does not disappear and the pancreas is permanently impaired. Pancreatic tissue is damaged, and the tissue and cells function poorly.

Causes & Symptoms

There are a number of causes of acute pancreatitis. The most common, however, are gallbladder disease and alcoholism. These two diseases are responsible for more than 80% of all hospitalizations for acute pancreatitis. Other factors in the development of pancreatitis include:

  • certain drugs
  • infections
  • structural problems of the pancreatic duct and bile ducts (channels leading from the gallbladder to the duodenum)
  • injury to the abdomen resulting in injury to the pancreas (including injuries occurring during surgery)
  • abnormally high levels of circulating fats in the bloodstream
  • malfunction of the parathyroid gland, with high blood levels of calcium
  • complications from kidney transplants
  • a hereditary tendency toward pancreatitis (recent advances in gene mapping have led to the discovery that a mutation in the gene responsible for cystic fibrosis is associated with a greatly increased risk of pancreatitis)

Pancreatitis caused by drugs accounts for about 5% of all cases. Some drugs that are definitely related to pancreatitis include:

Some drugs that are probably related to pancreatitis include:

  • acetaminophen (Tylenol)
  • angiotensin–converting enzyme (ACE) inhibitors (Capoten, Vasotec)
  • erythromycin
  • methyldopa (Aldomet)
  • metronidazole (Flagyl, Protostat)
  • nitrofurantoin (Furadantin, Furan)
  • nonsteroidal anti–inflammatory drugs (NSAIDs) (Aleve, Naprosyn, Motrin)
  • salicylates (aspirin)

All of these causes of pancreatitis seem to have a similar mechanism in common. Under normal circumstances, many of the extremely potent enzymes produced by the pancreas are not active until they enter the duodenum, in which contact with certain other chemicals allows them to function. In pancreatitis, these enzymes become prematurely activated and actually begin their digestive functions within the pancreas. The pancreas, in essence, begins to digest itself. This process is known as autodigestion. A cycle of inflammation begins, including swelling and loss of function. Digestion of the blood vessels in the pancreas results in bleeding. Other active pancreatic chemicals cause the blood vessels to become leaky, and fluid begins to leak out of the normal circulation into the abdominal cavity. The activated enzymes also gain access to the bloodstream through the eroded blood vessels, and begin circulating throughout the body.

Pain is a major symptom of pancreatitis. The pain is usually quite intense and steady, located in the upper right hand corner of the abdomen, and often described as "piercing" or "boring." This pain is also often felt all the way through to the patient's back. The patient's breathing may become quite shallow because deeper breathing tends to cause more pain. Patients usually find some relief of pain by sitting up and bending forward; this postural relief is characteristic of pancreatic pain. Nausea and vomiting, and abdominal swelling are all common, as well. A patient will often have a slight fever, with an increased heart rate and low blood pressure.

Classic signs of shock may appear in more severely ill patients. Shock is a very serious syndrome that occurs when the volume (quantity) of fluid in the blood is very low. In shock, a patient's arms and legs become extremely cold, the blood pressure drops dangerously low, the heart rate is quite fast, and the patient may begin to experience changes in mental status.

In very severe cases of pancreatitis (called necrotizing pancreatitis) the pancreatic tissue begins to die and bleeding increases. Due to the bleeding into the abdomen, two distinctive signs may be noted in patients with necrotizing pancreatitis. Turner's sign is a reddish purple or greenish brown color in the flank area (the area between the ribs and the hip bone). Cullen's sign is the appearance of a bluish color around the navel.

Some of the complications of pancreatitis are due to shock. When shock occurs, all of the body's major organs are deprived of blood and the oxygen it carries, resulting in damage. Kidney, respiratory, and heart failure are serious risks of shock. The pancreatic enzymes that have begun circulating throughout the body (as well as various poisons created by the abnormal digestion of the pancreas by those enzymes) have severe effects on the major body systems. Any number of complications can occur, including damage to the heart, lungs, kidneys, lining of the gastrointestinal tract, liver, eyes, bones, and skin. As the pancreatic enzymes work on blood vessels surrounding the pancreas, and even blood vessels located at a distance, the risk of blood clots increases. These blood clots complicate the situation by blocking blood flow in the vessels. When blood flow is blocked, the supply of oxygen is decreased to various organs and the organ can be damaged.

The pancreas may develop additional problems, even after the pancreatitis decreases. When the entire organ becomes swollen and suffers extensive cell death (pancreatic necrosis), the pancreas becomes extremely susceptible to serious infection. A local collection of pus (called a pancreatic abscess) may develop several weeks after the illness subsides, and may result in increased fever and a return of pain. Another late complication of pancreatitis, occurring several weeks after the illness begins, is called a pancreatic pseudocyst. This occurs when dead pancreatic tissue, blood, white blood cells, enzymes, and fluid that has leaked from the circulatory system accumulates. In an attempt to enclose and organize this abnormal accumulation, a kind of wall forms from the dead tissue and the growing scar tissue in the area. Pseudocysts cause additional abdominal pain by putting pressure on and displacing pancreatic tissue, resulting in more pancreatic damage. Pseudocysts also press on other nearby structures in the gastrointestinal tract, causing more disruption of function. Pseudocysts are life-threatening when they become infected (abscess) and rupture. Simple rupture of a pseudocyst causes death 14% of the time. Rupture complicated by bleeding causes death 60% of the time.

As the pancreatic tissue is increasingly destroyed in chronic pancreatitis, many digestive functions become disturbed. The quantity of hormones and enzymes normally produced by the pancreas begins to seriously decrease. Decreases in the production of enzymes result in the inability to appropriately digest food. Fat digestion, in particular, is impaired. A patient's stools become greasy as fats are passed out of the body. The inability to digest and use proteins results in smaller muscles (wasting) and weakness. The inability to digest and use the nutrients in food leads to malnutrition and a generally weakened condition. As the disease progresses, permanent injury to the pancreas can lead to diabetes.

Diagnosis

Diagnosis of pancreatitis can be made very early in the disease by noting high levels of pancreatic enzymes circulating in the blood (amylase and lipase). Later in the disease, and in chronic pancreatitis, these enzyme levels will no longer be elevated. Because of this fact, and because increased amylase and lipase can also occur in other diseases, the discovery of such elevations are helpful but not mandatory in the diagnosis of pancreatitis. Other abnormalities in the blood may also point to pancreatitis, including increased white blood cells (occurring with inflammation and/or infection), changes due to dehydration from fluid loss, and abnormalities in the blood concentration of calcium, magnesium, sodium, potassium, bicarbonate, and sugars.

X rays or ultrasound examination of the abdomen may reveal gallstones, perhaps responsible for blocking the pancreatic duct. The gastrointestinal tract will show signs of inactivity (ileus) due to the presence of pancreatitis. Chest x rays may reveal abnormalities due to air trapping from shallow breathing, or due to lung complications from the circulating pancreatic enzyme irritants. Computed tomography scans (CT scans) of the abdomen may reveal the inflammation and fluid accumulation of pancreatitis, and may also be useful when complications like an abscess or a pseudocyst are suspected.

In the case of chronic pancreatitis, a number of blood tests will reveal the loss of pancreatic function that occurs over time. Blood sugar (glucose) levels will rise, eventually reaching the levels present in diabetes. The levels of various pancreatic enzymes will fall, as the organ is increasingly destroyed and replaced by nonfunctioning scar tissue. Calcification of the pancreas can also be seen on x rays. Endoscopic retrograde cholangiopancreatography (ERCP) may be used to diagnose chronic pancreatitis in severe cases. In this procedure, the doctor uses a medical instrument fitted with a fiber-optic camera to inspect the pancreas. A magnified image of the area is shown on a television screen viewed by the doctor. Many endoscopes also allow the doctor to retrieve a small sample (biopsy) of pancreatic tissue to examine under a microscope. A contrast product may also be used for radiographic examination of the area.

Treatment

Pancreatitis is a serious condition that requires medical diagnosis and treatment. Alternative therapies should be used only to complement conventional treatment.

Nutritional Therapy

Before taking nutritional supplements, patients should consult their doctors to make sure these supplements do not interfere with their overall treatment program. The following nutritional changes are recommended to help support pancreatic function and relieve pancreatitis symptoms:

  • Follow a diabetic diet and avoid alcohol consumption.
  • Limit intake of hydrogenated/saturated fats, sugar, and highly processed foods.
  • Increase intake of yellow and orange fruits and dark-green vegetables, which are good sources of betacarotene, whole foods, vitamin C, and other antioxidants.
  • Take high-potency multivitamin/mineral supplements.
  • Use chromium (300 mcg daily) supplements to help control blood sugar level and enhance insulin effectiveness.
  • Take lipotrophic agents (which increase bile flow to and from the liver), such as vitamin B6, vitamin B12, folic acid, choline, betaine, and methionine.
  • Take pancreatic enzymes at mealtime.

Other Therapies

Other alternative treatments such as acupuncture or relaxation techniques can help patients cope with painful symptoms associated with pancreatitis. Reduce stress by meditation, yoga, t'ai chi, or other relaxation techniques. Stress can stimulate pancreatitis attacks.

Allopathic Treatment

Treatment of acute pancreatitis involves quickly and sufficiently replacing lost fluids by giving the patient new fluids through a needle inserted in a vein (intravenous or IV fluids). Pain is treated with a variety of medications. In order to decrease pancreatic function (and decrease the discharge of more potentially harmful enzymes into the bloodstream), the patient is not allowed to eat. A thin, flexible tube (nasogastric tube) may be inserted through the patient's nose and down into his or her stomach. Oxygen may need to be administered by nasal prongs or by a mask.

Complications, such as infections that often occur in cases of necrotizing pancreatitis, abscesses, and pseudocysts, will require antibiotics administered intravenously. Severe necrotizing pancreatitis may require surgery to remove part of the dying pancreas. A pancreatic abscess can be drained by a needle inserted through the abdomen and into the collection of pus (percutaneous needle aspiration) or surgically removed, if necessary. Pancreatic pseudocysts may shrink on their own (in 25–40% of cases) or may continue to expand, requiring needle aspiration or surgery. When diagnostic exams reveal the presence of gallstones, surgery may be necessary for their removal.

Because chronic pancreatitis often includes repeated flares of acute pancreatitis, the same kinds of basic treatment are necessary. Patients receive IV replacement fluids, receive pain medication, and are monitored for complications. Treatment of chronic pancreatitis caused by alcohol consumption requires that the patient stop drinking alcohol entirely. As chronic pancreatitis continues and insulin levels drop, a patient may require insulin injections in order to be able to process sugars in his or her diet. Pancreatic enzymes can be replaced with oral medicines, and patients sometimes have to take as many as eight pills with each meal. Drugs can be used to reduce the pain, but when narcotics are used for pain relief, there is danger of the patient becoming addicted.

Expected Results

A number of systems have been developed to help determine the prognosis of an individual with pancreatitis. A very basic evaluation of a patient will allow some prediction to be made based on the presence of dying pancreatic tissue (necrosis) and bleeding. When necrosis and bleeding are present, as many as 50% of patients may die.

More elaborate systems have been created to help determine the prognosis of patients with pancreatitis. Ranson's signs, the most commonly used system, identifies 11 different signs that can be used to determine the severity of the disease. The first five categories are evaluated when the patient is admitted to the hospital:

  • age over 55 years
  • blood sugar level over 200 mg/Dl
  • serum lactic dehydrogenase over 350 IU/L (increased with increased breakdown of blood, as would occur with internal bleeding, and with heart or liver damage)
  • AST over 250μ (a measure of liver function, as well as a gauge of damage to the heart, muscle, brain, and kidney)
  • white blood count over 16,000 MUL

The next six of Ranson's signs are reviewed 48 hours after admission to the hospital. These are:

  • greater than 10% decrease in hematocrit (a measure of red blood cell volume)
  • increase in BUN (blood urea nitrogen, an indicator of kidney function) greater than 5 mg/dL
  • blood calcium less than 8 mg/dL
  • PaO2 (a measure of oxygen in the blood) less than 60 mm Hg
  • base deficit greater than 4 mEg/L (a measure of change in the normal acidity of the blood)
  • fluid sequestration greater than 6 L (an estimation of the quantity of fluid that has leaked out of the blood circulation and into other body spaces).

Once a doctor determines how many of Ranson's signs are present and gives the patient a score, the doctor can better predict the risk of death. The more signs present, the greater the chance of death. A patient with less than three positive Ranson's signs has a less than 5% chance of dying. A patient with three to four positive Ranson's signs has a 15–20% chance of dying.

The results of a CT scan can also be used to predict the severity of pancreatitis. Slight swelling of the pancreas indicates mild illness. Significant swelling, especially with evidence of destruction of the pancreas and/or fluid buildup in the abdominal cavity, indicates more severe illness. With severe illness, there is a worse prognosis.

Surgical treatment of pancreatitis is frequently followed by complications because of the leakage of pancreatic enzymes from the remaining portion of the organ. A team of French surgeons has reported that treating patients with somatostatin-14, a hormone that inhibits pancreatic secretion as well as pancreatic blood flow, appears to be effective in lowering the rate of complications from pancreatic surgery. In spite of recent advances in surgical technique, however, the mortality rate following surgery for pancreatitis is still 3%–10%.

Prevention

Alcoholism is essentially the only preventable cause of pancreatitis. Patients with chronic pancreatitis must stop drinking alcohol entirely. The drugs that cause or may cause pancreatitis should also be avoided.

Resources

Books

Greenberger, Norton J., Phillip P. Toskes, and Kurt J. Isselbacher. "Acute and Chronic Pancreatitis." In Harrison's Principles of Internal Medicine, edited by Anthony S. Fauci, et al. New York: McGraw–Hill, 1998.

"Pancreatitis." In Reader's Digest Guide to Medical Cures & Treatments. Canada: The Reader's Digest Association, Inc., 1997.

"Pancreatitis." In Alternative Medicine: The Definitive Guide. Tiburon, CA: Future Medicine Publishing, Inc., 1999.

Periodicals

Amann, Stephen, et al. "Pancreatitis: Diagnostic and Therapeutic Interventions." Patient Care 31, no. 11 (June 15, 1997): 200+.

Goulliat, C., J. F. Gigot. "Pancreatic Surgical Complications—The Case for Prophylaxis." Gut 49 (December 2001): 32–39.

Le Marechal, C., O. Raguenes, I. Quere, et al. "Screening of Pancreatic Secretory Trypsin Inhibitor (PSTI) Mutations in Chronic Pancreatitis by DHPLC." American Journal of Human Genetics 69 (October 2001): 623.

Meissner, Judith E. "Caring for Patients with Pancreatitis." Nursing 27, no. 10 (October 1997): 50+.

"Mutations in the PSTI Gene Associated with Pancreatitis." Gene Therapy Weekly (December 27, 2001): 19.

Schlapman, Nancy. "Spotting Acute Pancreatitis." RN 64 (November 2001): 54.

Organization

National Digestive Diseases Information Clearinghouse. 2 Information Way, Bethesda, MD 20892-3570. .

[Article by: Mai Tran; Rebecca J. Frey, PhD]

Veterinary Dictionary: pancreatitis
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Inflammation of the pancreas.

  • acute hemorrhagic p. — a condition due to autolysis of pancreatic tissue caused by escape of enzymes into the substance, resulting in hemorrhage into the parenchyma and surrounding tissues. Seen most commonly in dogs, rarely in horses and pigs. Clinical signs include abdominal pain that may be severe and associated with cardiovascular shock, vomiting and diarrhea. Fatalities are not uncommon. In the longer term, the process may be slowly progressive, appearing clinically to be relapsing, often with eventual destruction of the islets of Langerhans that leads to diabetes mellitus. Called also acute pancreatic necrosis.
  • chronic p. — relapsing or continuing acute pancreatic necrosis. Called also relapsing pancreatitis.
  • focal p. — focal lesions discovered incidentally in patients dying of other disease, e.g. canine distemper, foot and mouth disease.
  • interstitial p. — inflammation of the interstitial tissue; may be acute or chronic.
  • necrotizing p. — see acute hemorrhagic pancreatitis (above).
  • relapsing p. — see chronic pancreatitis (see above).
Wikipedia: Pancreatitis
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Pancreatitis
Classification and external resources
ICD-10 K85., K86.0-K86.1
ICD-9 577.0-577.1
OMIM 167800
DiseasesDB 24092
eMedicine emerg/354
MeSH D010195

Pancreatitis is inflammation of the pancreas that can occur in two very different forms. Acute pancreatitis is sudden while chronic pancreatitis "is characterized by recurring or persistent abdominal pain with or without steatorrhea or diabetes mellitus."[1]

Contents

Causes

Excessive alcohol use is often cited as the most common cause of acute pancreatitis, yet gallstones are actually the most common cause. Less common causes include hypertriglyceridemia (but not hypercholesterolemia) and only when triglyceride values exceed 1500 mg/dl (16 mmol/L), hypercalcemia, viral infection (e.g. mumps), trauma (to the abdomen or elsewhere in the body) including post-ERCP (i.e. Endoscopic Retrograde Cholangiopancreatography), vasculitis (i.e. inflammation of the small blood vessels within the pancreas), and autoimmune pancreatitis. Pregnancy can also cause pancreatitis, but in some cases the development of pancreatitis is probably just a reflection of the hypertriglyceridemia which often occurs in pregnant women. Pancreas divisum, a common congenital malformation of the pancreas may underlie some cases of recurrent pancreatitis. Pancreatitis is less common in pediatric population.

The more mundane, but far more common causes of pancreatitis, as mentioned above, must always be considered first. However, the known porphyrinogenicity of many drugs, hormones, alcohol, chemicals and the association of porphyrias with autoimmune disorders and gallstones do not exclude the diagnosis of heme disorders when these explanations are used. A primary medical disorder, including an underlying undetected inborn error in metabolism, supersedes a secondary medical complication or explanation. As mentioned above, pancreatitis is less common in children but if seen, abuse or abdominal trauma should be suspected.

Autoimmune disorders, lipid disorders, gallstones, drug reactions and pancreatitis itself are not primary medical disorders.

It is worth noting that pancreatic cancer is seldom the cause of pancreatitis.[citation needed]

Type 2 diabetes subjects have 2.8 fold higher risk for pancreatitis compared to non diabetic subjects. [2] People with diabetes should promptly seek medical care if they experience unexplained severe abdominal pain with or without nausea and vomiting. [3]

Some of the causes of acute pancreatitis can be remembered by the acronym GET SMASHED

Gallstones; Ethanol; Trauma;

Steroids; Mumps; Autoimmune; Scorpion sting; Hypercalcaemia, hypertriglyceridaemia, hypothermia; ERCP; Drugs e.g. azathioprine, diuretics;

Porphyrias

Acute hepatic porphyrias, including acute intermittent porphyria, hereditary coproporphyria and variegate porphyria, are genetic disorders that can be linked to both acute and chronic pancreatitis. Acute pancreatitis has also occurred with erythropoietic protoporphyria.

Conditions that can lead to gut dysmotility predispose patients to pancreatitis. This includes the inherited neurovisceral porphyrias and related metabolic disorders. Alcohol, hormones and many drugs including statins are known porphyrinogenic agents. Physicians should be on alert concerning underlying porphyrias in patients presenting with pancreatitis and should investigate and eliminate any drugs that may be activating the disorders.

Still, notwithstanding their potential role in pancreatitis, the porphyrias (as a group or individually) are considered to be rare disorders. However, since there are no systematic studies to determine the actual incidence of latent dominantly-inherited porphyrias in the world population, there is DNA or enzyme evidence of high rates of latency of classic textbook symptoms in families where porphyrias have been detected and the technology is not developed to detect all latent porphyrias, the diagnosis of underlying inborn errors of metabolism impacting heme should not be routinely eliminated in pancreatitis.

Medications

Many medications have been reported to cause pancreatitis. Some of the more common ones include the AIDS drugs DDI and pentamidine, diuretics such as furosemide and hydrochlorothiazide, the anticonvulsants divalproex sodium and valproic acid, the chemotherapeutic agents L-asparaginase and azathioprine, and estrogen. Just as is the case with pregnancy-associated pancreatitis, estrogen may lead to the disorder because of its effect of raising blood triglyceride levels. Pancreatitis due to statins first started appearing in the medical literature as early as 1990. All statins currently in use reportedly can cause pancreatitis, a not surprising observation when one considers that all statins are reductase inhibitors and can be expected to have similar side effect profiles.

Occasionally one statin will have a somewhat greater tendency for a side effect than another, like Baycol, removed from the market because of excess rhabdomyolysis deaths, but all statins cause this condition. The total rhabdomyolysis deaths seen today far exceed the 100 or so attributed to Baycol.[4]

Genetics

Hereditary pancreatitis may be due to a genetic abnormality that renders trypsinogen active within the pancreas, which in turn leads to digestion of the pancreas from the inside.

Pancreatic diseases are notoriously complex disorders resulting from the interaction of multiple genetic, environmental and metabolic factors.

Three candidates for genetic testing are currently under investigation:

Virus infection

Viruses can cause profound inflammation in, and destruction of, the pancreas. This is true of several viruses in the coxsackievirus group.

Symptoms and signs

Severe upper abdominal pain, with radiation through to the back, is the hallmark of pancreatitis. Nausea and vomiting (emesis) are prominent symptoms. Findings on the physical exam will vary according to the severity of the pancreatitis, and whether or not it is associated with significant internal bleeding. The blood pressure may be high (when pain is prominent) or low (if internal bleeding or dehydration has occurred). Typically, both the heart and respiratory rates are elevated. Abdominal tenderness is usually found but may be less severe than expected given the patient's degree of abdominal pain. Bowel sounds may be reduced as a reflection of the reflex bowel paralysis (i.e. ileus) that may accompany any abdominal catastrophe.

Diagnosis

The diagnostic criteria for pancreatitis are "two of the following three features: 1) abdominal pain characteristic of acute pancreatitis, 2) serum amylase and/or lipase ≥3 times the upper limit of normal, and 3) characteristic findings of acute pancreatitis on CT scan."[6]

Laboratory tests

Most frequently, measurement is made of amylase and/or lipase, and often one, or both, are elevated in cases of pancreatitis. Two practice guidelines state:

It is usually not necessary to measure both serum amylase and lipase. Serum lipase may be preferable because it remains normal in some nonpancreatic conditions that increase serum amylase including macroamylasemia, parotitis, and some carcinomas. In general, serum lipase is thought to be more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis".[6]
Although amylase is widely available and provides acceptable accuracy of diagnosis, where lipase is available it is preferred for the diagnosis of acute pancreatitis (recommendation grade A)".[7]

Most,[8][9][10][11][12] but not all[13][14] individual studies support the superiority of the lipase. In one large study, there were no patients with pancreatitis who had an elevated amylase with a normal lipase.[8] Another study found that the amylase could add diagnostic value to the lipase, but only if the results of the two tests were combined with a discriminant function equation.[15]

Conditions other than pancreatitis may lead to rises in these enzymes and, further, that those conditions may also cause pain that resembles that of pancreatitis (e.g. cholecystitis, perforated ulcer, bowel infarction (i.e. dead bowel as a result of poor blood supply), and even diabetic ketoacidosis.

Imaging

Although ultrasound imaging and CT scanning of the abdomen can be used to confirm the diagnosis of pancreatitis, neither is usually necessary as a primary diagnostic modality[16] . In addition, CT contrast may exacerbate pancreatitis,[17] although this is disputed.[18] See acute pancreatitis.

Prognosis

There are several scoring systems used to help predict the severity of an attack of pancreatitis. The Apache II has the advantage of being available at the time of admission as opposed to 48 hours later for the Glasgow criteria and Ranson criteria. However, the Glasgow criteria and Ranson criteria are easier to use.

APACHE II

Ranson criteria

At admission:

  1. age in years > 55 years
  2. white blood cell count > 16000 /mcL
  3. blood glucose > 11 mmol/L (>200 mg/dL)
  4. serum AST > 250 IU/L
  5. serum LDH > 350 IU/L

After 48 hours:

  1. Haematocrit fall > 11.3444%
  2. increase in BUN by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
  3. hypocalcemia (serum calcium < 2.0 mmol/L (<8.0 mg/dL))
  4. hypoxemia (PO2 < 60 mmHg)
  5. Base deficit > 4 Meq/L
  6. Estimated fluid sequestration > 6 L

The criteria for point assignment is that a certain breakpoint be met at anytime during that 48 hour period, so that in some situations it can be calculated shortly after admission. It is applicable to both biliary and alcoholic pancreatitis.

Interpretation

  • If the score ≥ 3, severe pancreatitis likely.
  • If the score < 3, severe pancreatitis is unlikely

Or

  • Score 0 to 2: 2% mortality
  • Score 3 to 4: 15% mortality
  • Score 5 to 6: 40% mortality
  • Score 7 to 8: 100% mortality

Glasgow criteria

Glasgow's criteria[19]: The original system used 9 data elements. This was subsequently modified to 8 data elements, with removal of assessment for transaminase levels (either AST (SGOT) or ALT (SGPT) greater than 100 U/L).

On Admission

  1. Age >55 yrs
  2. WBC Count >15 x109/L
  3. Blood Glucose >200 mg/dL (No Diabetic History)
  4. Serum Urea >16 mmol/L ( No response to IV fluids)
  5. Arterial Oxygen Saturation <76 mmHg

Within 48 hours

  1. Serum Calcium <2 mmol/L
  2. Serum Albumin <34 g/L
  3. LDH >219 units/L
  4. AST/ALT >96 units/L

Complications

Acute (early) complications of pancreatitis include

  • shock,
  • hypocalcemia (low blood calcium),
  • high blood glucose,
  • dehydration, and kidney failure (resulting from inadequate blood volume which, in turn, may result from a combination of fluid loss from vomiting, internal bleeding, or oozing of fluid from the circulation into the abdominal cavity in response to the pancreas inflammation, a phenomenon known as Third Spacing).
  • Respiratory complications are frequent and are major contributors to the mortality of pancreatitis. Some degree of pleural effusion is almost ubiquitous in pancreatitis. Some or all of the lungs may collapse (atelectasis) as a result of the shallow breathing which occurs because of the abdominal pain. Pneumonitis may occur as a result of pancreatic enzymes directly damaging the lung, or simply as a final common pathway response to any major insult to the body (i.e. ARDS or Acute Respiratory Distress Syndrome).
  • Likewise, SIRS (Systemic inflammatory response syndrome) may ensue.
  • Infection of the inflamed pancreatic bed can occur at any time during the course of the disease. In fact, in cases of severe hemorrhagic pancreatitis, antibiotics should be given prophylactically.

Late complications

Late complications include recurrent pancreatitis and the development of pancreatic pseudocysts. A pancreatic pseudocyst is essentially a collection of pancreatic secretions which has been walled off by scar and inflammatory tissue. Pseudocysts may cause pain, may become infected, may rupture and hemorrhage, may press on and block structures such as the bile duct, thereby leading to jaundice, and may even migrate around the abdomen.

Treatment

The treatment of pancreatitis will, of course, depend on the severity of the pancreatitis itself. Still, general principles apply and include:

  1. Provision of pain relief. In the past this was done preferentially with meperidine (Demerol), but it is now not thought to be superior to any narcotic analgesic. Indeed, given meperidine's generally poor analgesic charactersitics and its high potential for toxicity, it should not be used for the treatment of the pain of pancreatitis. The preferred analgesic is morphine for acute pancreatitis.
  2. Provision of adequate replacement fluids and salts (intravenously).
  3. Limitation of oral intake (with dietary fat restriction the most important point). NG tube feeding is the preferred method to avoid pancreatic stimulation and possible infection complications caused by bowel flora.
  4. Monitoring and assessment for, and treatment of, the various complications listed above.
  5. ERCP if gallstone pancreatitis

When necrotizing pancreatitis ensues and the patient shows signs of infection, it is imperative to start antibiotics such as Imipenem due to the high penetration of the drug in the pancreas. Floroquinolone + metronidazole is another treatment option.

References

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  10. ^ Steinberg WM, Goldstein SS, Davis ND, Shamma'a J, Anderson K (May 1985). "Diagnostic assays in acute pancreatitis. A study of sensitivity and specificity". Ann. Intern. Med. 102 (5): 576–80. PMID 2580467. 
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