Pancreatitis

[edit] Americola's celebrity biographies are provided by AmericolaWiki, a celebrity wiki. You can help contribute to Americola and edit this article.

Pancreatitis
Classification & external resources

ICD-10	K85., K86.0-K86.1
ICD-9	577.0-577.1
eMedicine	emerg/354

Pancreatitis is inflammation of the pancreas. See also acute pancreatitis and chronic pancreatitis for more details.

Contents 1 Causes 2 Symptoms and Signs 3 Diagnosis 3.1 Laboratory tests 3.2 Imaging 4 Genetic Testing 5 Complications 6 Treatment 7 Types 8 References 9 External links

Causes

The most common causes of acute pancreatitis are gallstones and excessive consumption of alcohol (together accounting for more than 80% of cases). 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 Cholangio-Pancreatography), 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.

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 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 to raise blood triglyceride levels.

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.

It is worth noting that pancreatic cancer is seldom the cause of pancreatitis.

Idiopathic pancreatits is the term used to denote pancreatitis of undetermined cause - representing approximately 25 to 30 percent of cases.

Symptoms and Signs

Severe upper abdominal pain, with radiation through to the back, is the hallmark of pancreatitis. Traditionally it is stated that the pain of pancreatitis is relieved by bending forward. Nausea and vomiting 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. Often, in more severe cases, there is evidence of a pleural effusion (i.e. water on the lung). 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. If there has been severe internal bleeding, the skin around the umbilicus or the flanks may be discolored with a dark reddish or purple hue (so-called Cullen's sign and Grey-Turner's sign respectively). The discoloration is blood which has tracked along the retroperitoneal fascial plane.

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."^[1]

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"^[1]

"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)"^[2]

Two notable scoring systems are used to help predict the severity of an attack of Pancreatitis, this is the Glasgow criteria and Ranson's scoring. They are similar and overlap in their criteria but help differentiate patients who may require high dependancy care.

Glasgow's criteria: 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).

Parameters used:

(1) age in years >55years = 1

(2) serum albumin < 3.2 g/dL = 1

(3) PaO2 on room air < 60 mm Hg = 1

(4) serum calcium < 8 mg/dL = 1

(5) blood glucose > 180 mg/dL = 1

(6) serum LDH > 600 U/L = 1

(7) BUN > 45 mg/dL = 1

(8) WBC count > 15,000 per µL = 1

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:

• minimum score 0

• maximum score 8

• If the score >=3, severe pancreatitis likely.

• If the score < 3, severe pancreatitis is unlikely

Most (PMID 15943725, PMID 11552931, PMID 2580467, PMID 2466075, PMID 9436862), but not all (PMID 11156345, PMID 8945483) 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.^[3] 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.^[4]

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^[5] . In addition, CT contrast may exacerbate pancreatitis,^[6] although this is disputed.^[7] See acute pancreatitis.

Genetic Testing

Pancreatic diseases are notoriously complex disorders resulting from the interaction of multiple genetic, environmental and metabolic factors. Three candidates for genetic testing are currently investigation: Trypsinogen mutations, Cystic Fibrosis Transmembrane Conductance Regulator Gene (CFTR) mutations and SPINK1 which codes for PSTI - a specific trypsin inhibitor.^[8]

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). 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 of pancreatitis 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 (with morphine, contrary to earlier pronouncements, being the agent of choice), 2. provision of adequate replacement fluids and salts (intravenously), 3. limitation of oral intake (with dietary fat restriction the most important point), and 4. monitoring and assessment for, and treatment of, the various complications listed above. When necrotizing pancreatitis ensues and the patient shows signs of infection it is imperative to start antibiotics such as Imipenem due to its high penetration of the drug in the pancreas.

Types

There are three forms of pancreatitis, which are different in causes and symptoms, and require different treatment:

• Acute pancreatitis: One-time occurrence
• Chronic pancreatitis: Persists even after the cause has been removed
• Hereditary pancreatitis: - A genetic abnormality leads to activation of enzymes. 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.

References

1. ^ ^{a b} Banks P, Freeman M (2006). "Practice guidelines in acute pancreatitis". Am J Gastroenterol 101 (10): 2379-400. DOI:10.1111/j.1572-0241.2006.00856.x. PMID 17032204. 
2. ^ UK Working Party on Acute Pancreatitis (2005). "UK guidelines for the management of acute pancreatitis". Gut 54 Suppl 3: iii1-9. DOI:10.1136/gut.2004.057026. PMID 15831893. 
3. ^ Smith R, Southwell-Keely J, Chesher D (2005). "Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis?". ANZ J Surg 75 (6): 399-404. DOI:10.1111/j.1445-2197.2005.03391.x. PMID 15943725. 
4. ^ Corsetti J, Cox C, Schulz T, Arvan D (1993). "Combined serum amylase and lipase determinations for diagnosis of suspected acute pancreatitis". Clin Chem 39 (12): 2495-9. PMID 7504593. 
5. ^ Fleszler F, Friedenberg F, Krevsky B, Friedel D, Braitman L (2003). "Abdominal computed tomography prolongs length of stay and is frequently unnecessary in the evaluation of acute pancreatitis". Am J Med Sci 325 (5): 251-5. PMID 12792243. 
6. ^ McMenamin D, Gates L (1996). "A retrospective analysis of the effect of contrast-enhanced CT on the outcome of acute pancreatitis". Am J Gastroenterol 91 (7): 1384-7. PMID 8678000. 
7. ^ Hwang T, Chang K, Ho Y (2000). "Contrast-enhanced dynamic computed tomography does not aggravate the clinical severity of patients with severe acute pancreatitis: reevaluation of the effect of intravenous contrast medium on the severity of acute pancreatitis". Arch Surg 135 (3): 287-90. PMID 10722029. 
8. ^ D. Whitcomb (2006). Genetic Testing for Pancreatitis.

Wikipedia information about Pancreatitis This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Pancreatitis". It may not have been reviewed by professional editors (see full disclaimer). Help contribute to Americola and edit this article.