Pancreas

 

Most common causes of pancreatitis are gallstone and ETOH (worldwide it is parasitic)

Pulmonary effusion (usually l sided)

Amylase is at least 1.5x normal

Amylase sensitivity (Emerg Med J 20:550. Nov 2003)

 

 

Lipase At five times upper limit of normal: 60% sensitive, 100% specific Vissers RJ, et al. J Emerg Med. 1999 Nov-Dec;17(6):1027-37

 

Table 1. Standard Diagnostic Tests.Test Sensitivity Specificity CommentSerum enzymes high moderate > 3x normal increases specificity Ultrasound moderate high Best for gallstones CT moderate high Detects calcifications, fluid collections CT with pancreatic protocol and IV contrast moderate high Detects necrosis

Adapted from (3), www.gastroslides.org

 

Table 2B. Causes of Increased Serum Lipase.GI Related Non-GI RelatedAcute cholecystitis Diabetic ketoacidosis Bowel obstruction or infarction HIV Duodenal ulceration Macrolipasemia Pancreatic calculus Idiopathic Pancreatic tumors Drugs Post-ERCP/trauma

 

• Autoimmune
• Drug induced
• Iatrogenic
• IBD related
• Infections
• Inherited
• Metabolic
• Neoplastic
• Structural
• Toxic
• Traumatic
• Vascular

 

 

 

 

Calculations and Mortality Prediction Using CTSI

This scoring system (Table 5 and Figure 4) uses several CT observations including edema and fluid collections. Importantly, the estimates of the amount of necrosis of the gland, as determined by measuring the portion of the gland that perfuses with contrast injection, is highly predictive of necrosis and poor outcome. Stated simply, greater amounts of estimated necrosis are associated with greater rates of extrapancreatic organ failure and pancreatic infection occurring during the course of the episode.

Table 5. CT Severity Index.CT finding PointsGland enlarged 1 Peripancreatic inflammation 2 One fluid collection 3 Multiple fluid collections 4 Necrosis <30% 2 Necrosis 30 – 50% 4 Necrosis >50% 6

 

 

 

 

 

Admit Ranson’s-Age >55, WBC>16, Glucose>200, LDH>350, AST>250

In ICU-Decrease in Crit>10, Increase BUN>5, Ca<8,PaO2<60, Base Deficit>4, Fluid Sequestration>6L

Think hemorrhagic if crit is dropping

If the crit is elevated, portends worse prognosis and possible necrotizing pancreatitis (Am J Gastroenterol 2001; 96: 2081-2085)

Conservative treatment of necrotizing pancreatitis with antibiotics decreases mortality rate.  Get C-Reactive protein (values>150, point to necrotizing) All studies were done with Imipenem (1 g TID)  J Gastrointest Surg 2001 Mar-Apr;5(2), Ann Surg 2000 Nov;232(5), Arch Surg 1997 May;132(5) Cefuroxime and Norfloxacin have also shown benefit.

 

Uncomplicated acute pancreatitis is a 1 week disease

 

Complications

Pancreatic Necrosis

Infected Necrosis

Abscess

Pseudocyst

Infected Psuedocyst

 

First week: Inflammation

pancreas and adjacent structures are inflamed (phlegmon)

beer-like hemorrhagic exudate

 

Second Week: Necrosis

can be localized or spread to affect the entire retroperitoneum

this may resolve or become walled off as a pseudocyst

may become secondarily infected

 

Third Week: Infection

colonic bugs or superinfection with candida

Sterile and infected pancreatic necrosis are almost impossible to tell apart clinically

 

Fourth Week: Late phase

can be abscess formation

 

Severity of Illness

apache ii is better than ranson

>8 is severe

 

these folks do not need ct scan in the first week, they do need an abd uts if possibility exists for stone disease

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Necrosis

develops in 1/5 of the patients with Apache>8

get a CT at the end of the first week

parenchyma that does not pick up contrast is necrosed

you then must ask is it infected and is an operation indicated

Indications for necrosetomy

1. Infected necrosis

2. clinical deterioration after two weeks of supportive care

3. Suspicion of infection if >50% of the pancreas is necrotic

4. Extensive necrosis and prolonged ileus at least two weeks from onset

 

many current experts would precede with conservative management as long as possible until forced to operate by infection

 

 

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Pseudocyst

generally observed 6 weeks for maturation

If infected (FNA) then percutaneous drainage is usually the best choice

 

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Abcess

3rd gen and flagyl

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Cancer

gastrinoma-zollinger Ellison

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VIPoma

diarrhea and hypokalemia

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Carcinoid

flushing and diarrhea

 

Less common causes pancreatitis:  hypertrygliceridemia  (at least >1000 unless on estrogen), TTP, sickle cell, incomplete cystic fibrosis, Sjogren’s, Tylenol us

 

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Management of crit care pt with Pancreatitis

(Crit Care Med 2004;32(12):2524) maybe antibiotics in necrotizing but this article recommends against empirical jejunal enteral nutrition as soon as access can be obtained tight glycemic control FNA of necrotic pancrea to determine infection ERCP within 72 hrs of gallstone pancreatitis

 

A raised serum amylase activity is found in several different clinical contexts. In patients presenting with acute abdominal pain, acute pancreatitis is the most likely diagnosis, especially if amylase activity is markedly raised (> 10 times the upper limit of normal). Causes of more modest elevation include ruptured tubal pregnancy, perforated hollow viscus, small bowel obstruction, generalised peritonitis, diabetic ketoacidosis, and the administration of opiates (which cause spasm of Oddi’s sphincter). A different clinical scenario exists when the salivary glands are inflamed, most often with calculi or mumps; the resultant hyperamylasaemia is not usually a diagnostic problem. Asymptomatic hyperamylasaemia has several causes. Pancreatic pseudocysts may form during or after episodes of acute pancreatic necrosis. The amylase activity within these pseudocysts may be extremely high, and leakage into the blood may be associated with marked hyperamylasaemia. Sometimes amylase molecules combine with plasma proteins (usually immunoglobulins). The resultant complexes are so large that they can be precipitated by certain agents (such as polyethylene glycol) and cannot be cleared by the kidneys—in contrast with amylase, which has a relatively low molecular mass, doesn’t precipitate (much), and is readily excreted except in renal failure. Macroamylase is a well recognised phenomenon, at least by laboratory staff, and if suspected can be readily confirmed or excluded.1 In this patient, very high amylase activity was seen in urine (12 218 U/l), and only 9% of amylase activity precipitated (reference interval < 57%), thus excluding macroamylasaemia. Production of amylase (usually the salivary isoenzyme) has been documented with various kinds of ovarian neoplasm. Serous cystadenocarcinoma, mucinous tumour, surface papillary carcinoma, and endometrial adenocarcinoma of the ovary have all been implicated.2-5 Other malignancies reported to secrete amylase include gastric carcinoma, multiple myeloma, lung carcinoma, and phaeochromocytoma.6-9 The basis of amylase production by malignant tissue is unclear, although its secretion by tissues known to contain amylase might be activated through pathological processes such as inflammation or tumour formation.10

Pancreas March 2010 – Volume 39 – Issue 2 – pp 248-251

Conclusion: Total enteral nutrition is better than total parenteral nutrition in the prevention of pancreatic necrotic infection in severe acute pancreatitis.

 

 

 

 

 

 

 

 

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