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There are different forms of pancreatitis, which are different in causes and symptoms, and require different treatment:
Acute pancreatitis is an acute episode of pancreatitis.
Chronic pancreatitis is the "inflammation of the pancreas that is characterized by recurring or persistent abdominal pain with or without steatorrhea or diabetes mellitus"
The most common cause of acute pancreatitis is gallstones. Excessive alcohol use is often cited as the second most common cause of acute pancreatitis. 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.
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.
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.
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.
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. A number of homeopathic medicines have been mentioned as effective in some cases, when prescribed according to strict homeopathic principles. They include: achy., agar., aran-ix., Bell., beryl., but-ac., butho-t., calc-f., Con., cortiso., hep., Iod., Iris, lept., phos., plb., podo., Puls., Rhus-t., SPONG., tity-s., tity-t. (Self prescribing is unwise and usually fails.)[ Repertorium Universale V]
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: Trypsinogen mutations, Cystic Fibrosis Transmembrane Conductance Regulator Gene (CFTR) mutations and SPINK1 which codes for PSTI - a specific trypsin inhibitor.
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.
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."
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. 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.
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.
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 . In addition, CT contrast may exacerbate pancreatitis, although this is disputed. See acute pancreatitis.
There are several scoring systems used to help predict the severity of an attack of pancreatitis. The Apache II has the advantage 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.
1. age in years >55years 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
* 1. Haematocrit fall > 10% * 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 > 4Meq/L * 6. Estimated fluid sequestration > 6L
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.
* If the score >=3, severe pancreatitis likely. * If the score < 3, severe pancreatitis is unlikely
* 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'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).
Acute (early) complications of pancreatitis include
The treatment of pancreatitis will, of course, depend on the severity of the pancreatitis itself. Still, general principles apply and include
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Pancreatitis". A list of authors is available in Wikipedia.|