Acute pancreatitis

 ICD9        = 577.0|

}} Acute pancreatitis is a rapidly-onset inflammationof the pancreas. Depending on its severity, it can have severe complications and high mortality despite treatment. While mild cases settle with conservative measures or endoscopy, severe cases require surgery (often more than one intervention) to contain the disease process.

Symptoms and signs

Common symptomsinclude:

• Severe abdominal painoften radiating through to the back.
• Nausea, vomitingand loss of appetite.
• Fever
• Shock, hemodynamic instability

Common signsinclude

• Grey Turner sign(hemorrhagic discoloration of the flanks), Cullen sign(hemorrhagic discoloration of the umbilicus)

• Recovery may be followed by development of pancreatic pseudocyst, pancreatic dysfunction(malabsorptiondue to exocrine failure) or diabetes mellitus.

Causes

Most common causes

A common mnemonicfor the causes of pancreatitis is: "I GET SMASHED"

• I - idiopathic
• G - gallstone. Gallstones that travel down the common bile ductand which subsequently get stuck in the Ampulla of Vatercan cause obstruction in the outflow of pancreatic juices from the pancreas into the duodenum. The backflow of these digestive juices causes lysis(dissolving) of pancreatic cells and subsequent pancreatitis.
• E - ethanol(alcohol)
• T - trauma
• S - steroids
• M - mumps(paramyxovirus) and other viruses (Epstein-Barr virus, Cytomegalovirus)
• A - autoimmune disease(Polyarteritis nodosa, Systemic lupus erythematosus)
• S - scorpionsting / snake bite
• H - hypercalcemia, hyperlipidemia/hypertriglyceridemiaand hypothermia
• E - ERCP(Endoscopic Retrograde Cholangio-Pancreatography - a form of endoscopy)
• D - drugs(SAND - steroids& sulphonamides, azathioprine, NSAIDS, diureticssuch as furosemideand thiazides, & didanosine) and duodenal ulcers

Less common causes

• pancreas divisum
• long common duct
• carcinomaof the head of pancreas, and other cancer
• ascarisblocking pancreatic outflow
• ischemiafrom bypass surgery
• fat necrosis
• pregnancy
• infectionsother than mumps
• repeated marathonrunning.

Causes by demographic

The most common causes of pancreatitis, are as follows :

• Western countries - chronic alcoholism and gallstones accounting for more than 85 % of all cases
• Eastern countries - gallstones
• Children - trauma
• Adolescents and young adults - mumps

Pathogenesis

The exocrinepancreas produces a variety of enzymes, such as proteases, lipasesand saccharidases. These enzymes contribute to food digestionby breaking down food tissues. In acute pancreatitis, the worst offender among these enzymes may well be the protease trypsinogenwhich converts to the active trypsinwhich is most responsible for auto-digestion of the pancreas which causes the pain and complications of pancreatitis.

Histopathology The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessels necrosis - hemorrhage. These are produced by intrapancreatic activation of pancreatic enzymes. Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. Necrotic fat cells appear as shadows, contours of cells, lacking the nucleus, pink, finely granular cytoplasm. It is possible to find calcium precipitates (hematoxylinophilic). Digestion of vascular walls results in thrombosis and hemorrhage. Inflammatory infiltrate is rich in neutrophils. Photos at: Atlas of Pathology

Investigations

• Blood Investigations - Full blood count, Renal function tests, Liver Function, serum calcium, serum amylase and lipase, Arterial blood gas
• Imaging - Chest Xray (for exclusion of perforated viscus), Abdominal Xrays (for detection of "sentinel loop" dilated duodenum sign, and gallstones which are radioopaque in 10 %) and CT abdomen

Amylase and lipase

• Serum amylaserises 2 to 12 hours from the onset of symptoms, and normalises within 1 week
• Serum lipaserises 4 to 8 hours from the onset of symptoms and normalises within 8 to 14 days.
• Serum amylase may be normal (in 10 % of cases) for cases of acute on chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia
• Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase) and macroamylasemia
• If Lipase level is about 2.5 to 3 times that of Amylase, it is an indication of pancreatitis due to Alcohol^{[{{fullurl:Template:FULLPAGENAME}}#endnote_1]}.

CT abdomen

CT abdomen should not be performed before the 1st 48 hours of onset of symptoms as early CT (<48 h) may result in equivocal or normal findings.

CT Findings can be classified into the following categories for easy recall :

• Intrapancreatic - diffuse or segmental enlargement, edema, gas bubbles, pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
• Peripancreatic / extrapancreatic - irregular pancreatic outline, obliterated peripancreatic fat, retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
• Locoregional - Gerota's fascia sign (thickening of inflamed Gerota's fascia, which becomes visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic ileus,

Balthazar scoring

Balthazar Scoring for the Grading of Acute Pancreatitis

• Grade A - normal CT
• Grade B - focal or diffuse enlargement of the pancreas
• Grade C - pancreatic gland abnormalities and peripancreatic inflammation
• Grade D - fluid collection in a single location
• Grade E - two or more collections and/or gas bubbles in or adjacent to pancreas

Classification by severity

Progression of pathophysiology

Acute pancreatitis can be further divided in mild and severe pancreatitis. Mostly the Atlanta classification (1992) is used. In severe pancreatitis serious amount of necrosis determine the further clinical outcome. About 20 % of the acute pancreatitis are severe with a mortality of about 20 %. This is an important classification as severe pancreatits will need intensive care therapy whereas mild pancreatits can be treated on the common ward.

Necrosis will be followed by an systemic inflammation response syndrom (SIRS) and will determine the immediate clinical course. The further clinical course is then determined by bacterial infection. SIRS is the cause bacterial translocation from the patients colon.

There are several ways to help distinguish between these two forms. One is the above mentioned Ranson Score.

Prognostic indices

Important biochemical markers for pancreatitis are serumamylaseand lipaselevels. Amylase and lipase levels can rise to more than a hundred times normal levels in cases of acute pancreatitis.

In addition, in predicting the prognosis, there are several scoring indices that have been used as predictors of survival. Two such scoring systems are the Ranson and APACHE (Acute Physiology, Age and Chronic Health Evaluation) II indices.

Ranson

Ranson's Criteria on Admission :

• age greater than 55 years
• a white blood cell count of > 16,000/µL
• blood glucose > 11 mmol/L (>200 mg/dL)
• serum LDH > 400 IU/L
• serum AST >250 IU/L

Ranson's Criteria after 48 hours of admission :

• fall in hematocrit by more than 10 percent
• fluid sequestration of > 6 L
• hypocalcemia (serum calcium < 1.0 mmol/L (<8.0 mg/dL)
• hypoxemia (P_O2 < 80 mmHg
• increase in BUN to >1.98 mmol/L (>5 mg/dL) after IV fluid hydration
• hypoalbuminemia (albumin <32 g/L (<3.2 g/dL) in the first 48 hours of admission
• base deficit of >4

The prognostic implications of Ranson's criteria are as follows :

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

APACHE

"Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 12 points

• Hemorrhagic peritoneal fluid
• Obesity
• Indicators of organ failure
• Hypotension(SBP <90 mmHG) or tachycardia> 130 beat/min
• PO₂ <60 mmHg
• Oliguria(<50 mL/h) or increasing BUNand creatinine
• Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>

Treatment

General measures

• Antibioticsfor infected necrosis and severe pancreatitis improves outcome. The drug of choice is imipenem.
• Supportive for shock.
• Pain relief

The following have no role in the management of acute pancreatitis

• Enzyme inhibitors are not proven to work.
• The use of octreotidehas not been shown to improve outcome.

In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving him or her nothing by mouth, giving intravenousfluids to prevent dehydration. As the pancreas is stimulated to secrete enzymesby the presence of food in the stomach, having no food pass through the system allows the pancreas to rest.

Recently, there has been a shift in the management paradigm from TPN (total parenteral nutrition) to early enteral feeding. The advantage of enteral feeding is that it is more physiological, prevents gut mucosal atrophy, and is free from the side effects of TPN.

ERCP

Early ERCP (endoscopic retrograde cholangiopancreatography), performed within 24 hours of presentation, is known to reduce morbidity and mortality. The indications for early ERCP are as follows :

• Clinical deterioration or lack of improvement after 24 hours
• Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on CT abdomen

The disadvantages of ERCP are as follows :

• ERCP precipitates pancreatitis, and can introduce infection to sterile pancreatitis
• The inherent risks of ERCP i.e. bleeding

It is worth noting that ERCP itself can be a cause of pancreatitis.

Surgery

Surgery is indicated for (i) infected pancreatic necrosis and (ii) diagnostic uncertainty and (iii)complications. The most common cause of death in acute pancreatitis is secondary infection. Infection is diagnosed based on 2 criteria

• Gas bubbles on CT scan (present in 20 to 50 % of infected necrosis)
• Positive bacterial culture on FNA (fine needle aspiration, usually CT or US guided) of the pancreas.

Surgical options for infected necrosis include:

• Conventional management - necrosectomy with simple drainage
• Closed management - necrosectomy with closed continuous lavage
• Open management - necrosectomy with planned staged reoperations at definite intervals (up to 7 reoperations in some cases)

Complications

Complications can be systemic or locoregional.

• Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia(from fat saponification), hyperglycemiaand insulin dependent diabetes mellitus(from pancreatic insulin producing beta celldamage)
• Locoregional complications include pancreatic pseudocyst and phelgmon / abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis

Epidemiology

• Annual incidence in the USis 17 per 100,000 population. [1]
• Prevalence in the US is 80,000 cases per year.

See also

• Chronic pancreatitis

Reference

• ^  Gumaste VV, Dave PB, Weissman D, Messer J. Lipase/amylase ratio. A new index that distinguishes acute episodes of alcoholic from nonalcoholic acute pancreatitis. Gastroenterology 1991;101:1361-6. PMID 1718808.

External links

• Pancreatitis

fr:Pancréatite it:Pancreatite acuta nl:Pancreatitis pt:Pancreatite

This article is licensed under the GNU Free Documentation License.
It uses material from the http://en.wikipedia.org/wiki/Acute+pancreatitis Wikipedia article Acute pancreatitis.