Acute pancreatic necrosis

Acute pancreatitis is an inflammatory pancreatic disease of a wide range of severity – from mild to severe with signs of multiorgan failure or severe local complications such as abscesses, pseudocysts and pancreatic necrosis and adjacent tissues.

It is undoubtedly one of the most serious and prognostically worst sudden abdominal events.

Form interstitial edematous ( 70-80% )
It characterizes her edema interstitia, inflammation parenchyma, increase in concentration pancreatic enzymes in the pancreas and systemically. It is usually associated with pathology biliary systems.The course is light or moderate.

Form necrosis – sterile necrosis, infected necrosis
Within a few days, pancreatic cells will become massive and intra- and extrapancreatic adipose tissue necrosis will occur. Calcified fat forms necrosis (Balzer necrosis). The course determines the extent of necrosis, retroperitoneal involvement and bacterial contamination.

Pancreatic abscess
It is a late form that occurs about 3 – 6 weeks after necrotizing pancreatitis. It takes place under the image of a serious one septic state.

Pseudocysts
They develop several weeks after acute exposure. They are limited collections of fluid with a high concentration of enzymes.



Ethiology

 * Main reasons for origin


 * Gallbladder disease, bile ducts and Vater papillae ( = acute biliary pancreatitis );
 * alcoholism ( = acute ethyl pancreatitis );
 * postoperative pancreatitis, after ERCP ( = acute iatrogenic pancreatitis );
 * hyperlipidemic pancreatitis;
 * post-traumatic pancreatitis;
 * pancreatotoxic pancreatitis ( ATB – tetracyclines, diuretics – furosemide, immunosuppressants – cyclosporine, ACE inhibitors, etc. );
 * pancreas divisum ( embryonic development disorder – ventral and dorsal junction – is predisposing to acute pancreatitis in adulthood );
 * infection – parotitis virus, viral hepatitis.

Mnemonic: I Get Smashed. AND: idiopathic, G: gallstones, E: ethanol, T: tumorous, WITH: scorpion stings, M: microbiological / mumps, AND: autoimmune, WITH: surgery or trauma, H: hyperlipidemia, hypercalcemia, hypothermia, E: emboli or ischemia, D: drugs ( azathioprine, mercaptopurin, furosemide, estrogen, methyldopa, H2-blockers, antibiotics, salicylates, organophosphates, steroids )

Clinical picture

 * Acutely created pain in the abdomen, band-like character, radiate to the back;
 * they are accompanied by nausea and subsequent vomiting without feeling relieved, weakened peristalsis, meteorism, abdominal wall tension;
 * the condition gradually progresses to shock – tachypnoea, tachycardia, often hypotension, culminates in circulatory failure, kidneys, ARDS;
 * left-hand pleural effusion may also be present;
 * in biliary genesis – often signs jikteru.

Laboratory
Rise amylase, lipase and CRP in serum, increase glycemia, hypocalcemia, leukocytosis. However, there may not be deviations from the standard for the most difficult forms.

For differential diagnosis is the most important rise of amylase. If it rises to more than three times the standard, the diagnosis is almost certain. On the contrary, for prognosis the disease is a significant increase CRP. It is around 10 mg / l for light forms, and increases to values higher than 200 mg / l ( in severe forms, this signals necrosis infection ).

Hypocalcaemia is the result of uptake of calcium ions in fat necrosis ( so-called. Balzer necrosis, soap ).

More detailed information can be found on the page Acute pancreatitis ( laboratory diagnosis ).

Imaging methods

 * X-ray chest and abdomen


 * effusion in the left pleura;
 * so-called „ sentinel loop “ – air in the upper loops of the small intestine;
 * „ colon cut-off sign “ – level in the lienal bend of the columns.
 * USG


 * the best method is to monitor the course of ( resizing, onset of necrosis, concrement in the gallbladder, dilation of the bile ducts ).


 * ERCP ± PST


 * especially if biliary genesis is suspected, we can perform papillosphinxotomy ( PST ) and improve the condition.


 * CT


 * monitoring the course of the disease and determining the stage, especially in obese people, where the USG does not tell us much;
 * angio CT – evidence of necrosis.

Differential diagnostics
Acute cholecystitis, gastroenteritis, biliary and left-hand renal colic, ileus, perforation ulcer, rupture aneurysm abdominal aorta, AIM, volvulus, embolism into mesenteric vessels.

Therapy

 * Initial phase – intensive conservative therapy with close monitoring of these parameters in the ICU.
 * The basis is effort reduce pancreatic activity – absolute carcass of oral supply of anything, gastric decompression with nasogastric tube ( aspiration of content ), the patient's nutritional options are two:
 * nasojeunal probe ( currently appears to be better – maintains the natural function of the intestine, which probably reduces the risk of infection with necrosis in the pancreas – does not overgrow bacteria ),
 * parenteral nutrition.
 * Intensive volumotherapy ( i.v. ) – starts at 1 l / h, later decreases to 0.5 l / h ( a total of a maximum of 10 – 15 l / day, provided that the patient's cardiovascular system can withstand ).
 * Analgesics – tramadol, ev. fentanyl (morphine increases the tone of Oddi's sphincter, they are KI).
 * ATB – are contraindicated tetracyclines ( are pancreatotoxic ), preferably cephalosporins, carbapenemy, metronidazole.
 * Monitoring CVT, diuresis,…

Indications for surgery
Currently surgical treatment is not at the acute stage of this disease preferred. The indications were limited to:


 * 1) failure of intensive conservative therapy ( patient in multiorgan failure, usually restrained – beware of high perioperative mortality );
 * 2) necrosis infection ( is detected by thin needle puncture ).

Necrectomy is performed.

Additional procedures are performed after successful conservative therapy ( elimination of necrosis, cysts, ... ) or in severe complications such as perforation or intestinal stenosis..

Operational therapy

 * Removal of necrotic tissue, evacuation and drainage of bacterially infected necrosis, evacuation of pancreatogenic tissue ascit;
 * basic rule – gently remove necrosis with maximum maintenance of functional tissue;
 * necrosectomy (debridement) associated with continuous postoperative lavage ornamental exchanges;
 * in the most severe cases – open-abdominal treatment (laparostomy);
 * resection technique is rarely used – are large blood losses, large lethality.

Systemic complications of pancreatitis

 * Pulmonary – atelectasis, pneumonia, hypoxia, ARDS;
 * KVS – tachycardia, hypotension, arrhythmia, shock;
 * renal – oliguria, azotemia;
 * hematological – DIC;
 * metabolic – hyperglycaemia, hypocalcemia, acidosis, hyperTAG;

prognosis – Ranson criteria – are determined by age, leukocytosis, glycemia, LDH and AST.

Related articles

 * Acute haemorrhagic pancreatic necrosis ( preparate )
 * Acute pancreatitis ( laboratory diagnosis )
 * Chronic pancreatitis
 * Chronic pancreatitis ( laboratory diagnosis )
 * Pancreatic tumors
 * Pancreatic cancer
 * Acute pancreatic necrosis / evidence

Literature used

 * ZEMAN, Miroslav, et al. Special surgery. 2nd edition. Prague: Galén, 2006. 575 p. ISBN 80-7262-260-9.
 * ZEMAN, Miroslav, et al. Special surgery. 2nd edition. Prague: Galén, 2006. 575 p. ISBN 80-7262-260-9.

Source

 * BENEŠ, Jiří. Study materials [ online ]. [ cit. 5/5/2010 ].
 * Incomplete citation of the site. . Medical State of Mind [ online ]. © 2012. Last revision 2012-11-15, [ cit. 2016-10-26 ]. < http://medicalstate.tumblr.com/post/35811751615/i-get-smashed-for-acute-pancreatitis >.