Introduction

The pancreas is a gland with both external and internal secretion. It consists of three morphologically distinguishable parts: the head, body and tail of the pancreas. The endocrine part consists of islets of Langerhans, which produce insulin and glucagon. The exocrine part of the pancreas makes up 3/4 of the gland's volume. The basic unit is the acinus, a cluster of 4-6 acinous cells, from which the outlet emerges, the acin outlets join to form a lobe. The function of acinous cells is the production and secretion of pancreatic enzymes (proteolytic enzymes-trypsin, chymotrypsin, elastase, phospholipase A, carboxypeptidase; lipase and amylase). The outlet cells secrete minerals and water into the lumen. The pancreas in an adult produces about 1500 ml of pancreatic juice per day. This liquid is strongly alkaline, colorless. Its secretion is controlled nervously, humorally and hormonally. Secretion can be divided into three phases: 1. neural - reaction to olfactory, taste stimuli, but also the thought of ​​food, via n. vagus. 2. gastric - n. vagus, distension of the stomach, release of gastrin. 3. intestinal - release of enterohormones secretin (stimulates mainly bicarbonate and water component), cholecystokinin (secretion of digestive enzymes) and neurotensin (hydrogen carbonates and proteins). Exocrine function of the pancreas is essential for digestion and absorption, lipids, proteins and vitamins.

Definition

Acute pancreatitis is a sudden abdominal event, an acute condition that is accompanied by severe epigastric pain with varying radiation, increased levels of pancreatic enzymes in the blood and urine, increased leukocyte counts, or shock may develop. We know 2 forms: 1. Edematous form - inflammatory interstitial edema, no necrosis, reversible 2. Hemorrhagic-necrotic - the most severe form, self-digestion of pancreatic tissue occurs, Balzer's necrosis occurs as a result of lipase leakage into mesenteric fat and subsequent formation of calcium soaps, calcifications. Complications may occur: pancreatic abscess or pseudocyst.

 

Etiology

1. Choledocholithiasis (40-80 %) = acute biliary pancreatitis. Unconjugated bile acids and lecithin are toxic to pancreatic tissue, and pancreatic enzymes are also activated. 2. Alcohol abuse (35 %) = alcoholic form of acute pancreatitis. Alcohol is a substance toxic to pancreatic tissue, it also stimulates the production of HCl in the stomach and acidic muscle releases enterohormones and thus increases pancreatic secretion. The effect of alcohol on Oddi's animal is also described, it causes his spasm. 3. Idiopathic (15 %) without known cause. 4. Drugs - diuretics, B-blockers, ACE-inhibitors, methyldopa, estrogens, glucocorticoids, ATB (erythromycin, rifampicin, tetracycline), virostatics, anticonvulsants (valproate, NSAID, carbamazep) A, cytostatics et al. 5. Infection - viral (parotitis, coxsackie, hepatitis), leptospira infection. 6. Trauma - blunt abdominal injuries can lead to bruising and disruption of pancreatic tissue with subsequent leakage of pancreatic secretion into the environment after abdominal surgery, after ERCP. 7. Other - penetrating stomach/duodenum ulcer, dyslipidemia, hypercalcemia, ascarides, poisoning.

 

Pathogenesis

Premature intrapancreatic activation of digestive enzymes and their autolytic action. This process is caused by the reflux of duodenal contents or bile into the pancreatic duct and the concomitant accumulation of secretions. Phospholipase A cleaves lecithin and kephalin in the presence of bile acids into highly cytotoxic products that cause hemorrhage and necrosis. Lipase causes severe adipose tissue necrosis. The released fatty acids take up calcium and form calcium soaps. Calcifications also occur around the pancreas. Proteolytic enzymes disrupt capillaries and vessels and cause local coagulation disorders, intra and peripancreatic edema, bleeding and thrombosis. The products of autodigestion are washed away by the blood and can cause damage to more distant organs: lungs, kidneys, ... , in addition, they lower the pain threshold. With a very severe course, pancreatic shock can develop, the main cause of which is hypovolemia (fluid loss - edema, vomiting, paralytic ileus, intra and peripancreatic bleeding + the effect of kinins)

Diagnosis

1. Pain - the main symptom is pain in the epigastrium, sometimes in the right or left hypogastrium, rarely elsewhere. It can shoot into the back, many patients describe the so-called waist pain. Tension of the abdominal wall is also characteristic. History - when it started, causing factor, duration, relief positions, gallstones. 2. Nausea and vomiting. 3. Meteorism, paralytic ileus, ascites. 4. Fever. 5. Hypotension, tachycardia, signs of shock. 6. Pleural discharge, jaundice, flushing of the face, ...

 

Laboratory diagnostics

Amylase - total amylasemia has no diagnostic value, it consists mainly of salivary glands (isoenzyme S). Thus, isoenzyme P and their mutual ratio are determined. Pancreatic lipase and elastase - less frequent examinations, the increase in concentration occurs later. Examination of minerals - K, Ca. In necrotizing forms - CRP, LDH, PMN-elastase, phospholipase A. In obstruction of the ductus choledochus GMT, ALP, and direct bilirubin. Other changes - hyperglycemia, hypocalcemia, leukocytosis, rise in urea and creatine, Hb, coagulation factor levels (platelet count, factor V, VIII, fibrinogen and antithrombin), blood gas analysis (metabolic acidosis).

 

Imaging methods

1. Endo/sonography - edema, blurred border, effusion, necrosis, abscesses, stones. 2. Native X-ray of the abdomen + chest - calcifications, or effusion. 3. CT. 4. ERCP - also therapeutic. 5. Thin puncture needle under CT control - evidence of secondary infection. 6. MRCP.

 

Diff. Dg.

Other sudden abdominal events should be distinguished: renal colic, biliary colic, ulcer perforation, colon perforation, mechanical ileus, acute appendicitis, mesenteric infarction, extrauterine pregnancy, and other diseases that may have a similar picture: acute exacerbation of chronic pancreatitis, myocardial infarction, pulmonary embolism, dissecting abdominal aortic aneurysm.

 

Complications:

1. Abscesses and pseudocysts - worsening of symptoms, pain, increase in enzymes, temperature

2. Acute renal failure

3. Respiratory insufficiency

4. Bacterial infection of necroses

5. Circulatory failure, shock

 

Therapy:

1. Conservative

A. Monitoring the patient's clinical condition - circulatory parameters, fluid intake and output, electrolytes, laboratory parameters, control sono, X-ray

B. Prohibition of food intake or aspiration of stomach contents

C. Parenteral fluid and electrolyte replacement

D. Pain relief - mild pain e.g. Procaine 0.5% severe pain e.g. 50 mg Pethidin i.v., other morphine derivatives are contraindicated (cause Vater papilla spasm)

E. Prophylaxis of stress ulcer - e.g. H2-blocker

F. ATB - only in necrotizing or biliary form

G. Treatment of complications

 

2. Minimally invasive choledocholithiasis: endoscopic papillotomy, stone extraction - ERCP. Pseudocysts: transpapillary drainage or endoscopic transgastric drainage. Pancreatic abscess: puncture drainage, lavage

3. Surgical-necrectomy, lavage. Indications: failure of conservative treatment, especially in pancreatic necrosis infection, signs of sudden abdominal event, sepsis, multiorgan failure, ...

Prognosis

depends on early detection and adequate therapy of necrotizing pancreatitis and its complications - lethality depends on the severity of the disease - the most common cause of death are septic complications of necrotizing pancreatitis.

 

Prophylaxis

removal of possible causes: bile duct remediation, alcohol abstinence, treatment of hyperlipidemia, hyperparathyroidism, exclusion of drugs damaging the pancreas.