Acute pancreatitis in adults

Acute pancreatitis is an inflammation of the pancreas (and sometimes surrounding tissues) caused by the release of activated pancreatic enzymes. The main triggers of the disease are diseases of the biliary tract and chronic alcohol abuse.

The course of the disease varies from moderate (abdominal pain and vomiting) to severe (pancreatic necrosis and systemic inflammatory process with shock and multiple organ failure). The diagnosis of "acute pancreatitis" is based on clinical symptoms, determination of serum amylase and lipase levels. Treatment of acute pancreatitis is symptomatic, including IV fluid transfusion, analgesics and famine.

[1], [2], [3], [4], [5], [6], [7]

What causes acute pancreatitis?

Diseases of the biliary tract and alcoholism account for more than 80% of the etiological factors of acute pancreatitis. The remaining 20% is a consequence of various other reasons.

The exact mechanism of development of pancreatitis in the case of obturation of the sphincter of Oddi with a bile stone or microlithiasis (sludge) is not clear enough, but, most likely, this is due to an increase in intra-flow pressure. Long-term use of alcohol (> 100 g / day for> 3-5 years) can cause accelerated precipitation of the protein of pancreatic enzymes in the lumen of small pancreatic ducts. Obturation of the duct with these protein stoppers may be the cause of early activation of pancreatic enzymes. Alcohol abuse in such patients may be the cause of acute pancreatitis due to the activation of pancreatic enzymes.

A number of determining predispositions to pancreatitis of mutations have been established. The first is an autosomal dominant mutation of the cationic trypsinogen gene, which is the cause of pancreatitis in 80% of cases; thus the family history is traced. In other cases, mutations have less penetrance and are not always clinically traced, other than genetic studies. Genetic disorders are responsible for cystic fibrosis, which increases the risk of recurrence of acute pancreatitis.

Regardless of the etiology, pancreatic enzymes (including trypsin, phospholipase A2 and elastase) are directly activated within the gland. Enzymes damage the tissue, activate complement and trigger the inflammatory cascade, producing cytokines. This causes inflammation, swelling and sometimes necrosis. With moderate pancreatitis, inflammation is limited to the pancreas; mortality is less than 5%. In severe pancreatitis, there is marked inflammation with necrosis and hemorrhages in the gland and a systemic inflammatory response; the mortality rate is 10-50%. After 5-7 days, necrotic pancreatic tissue can be associated with intestinal infection.

Activated enzymes and cytokines that enter the abdominal cavity cause chemical peritonitis and fluid outlet into the abdominal cavity; enzymes that enter the systemic bloodstream cause a systemic inflammatory response that can lead to acute respiratory distress syndrome and kidney failure. Systemic effects are mainly the result of increased capillary permeability and a decrease in vascular tone. Phospholipase A2 is believed to damage the alveolar membranes of the lungs.

In approximately 40% of patients, the accumulation of enzyme-rich pancreatic fluid and tissue fragments is formed both in the pancreas and around it. In half the cases, the process is resolved spontaneously. In other cases, this pathological substrate becomes infected or pseudocysts are formed. Pseudocysts have a fibrous capsule without epithelial lining. Pseudocysts can be complicated by bleeding, rupture or infection.

Death for the first few days is usually associated with cardiovascular disorders (with severe shock and kidney failure) or respiratory failure (with hypoxemia and sometimes adult respiratory distress syndrome). Sometimes death is a consequence of secondary heart failure due to an unidentified myocardial suppressor factor. Death after a week of illness can be caused by pancreatic infection or rupture pseudocysts.

Symptoms of acute pancreatitis

Symptoms of acute pancreatitis consist in a constant, aching pain in the upper abdomen, usually quite strong, requiring large doses of parenteral opiates. The pain irradiates in the back in approximately 50% of cases; rarely pain first appears in the lower abdomen. With biliary pancreatitis, pain in the left side usually develops suddenly; with alcoholic pancreatitis, the pain develops within a few days. Pain syndrome usually persists for several days. In the sitting position and the torso of the trunk forward, pain can decrease, but coughing, active movements and deep breathing can strengthen it. Nausea and vomiting are characteristic.

The patient's condition is heavy, the skin is covered with sweat. The heart rate is usually 100-140 beats per minute. Breathing is frequent and superficial. AD may be elevated or low with severe postural (orthostatic) hypotension. The temperature may be normal or even subnormal, but it can rise from 37.7 to 38.3 ° C for several hours.Consciousness can be confused, on the verge of a sopor.It is sometimes observed that the sclera is icteric.It can be reduced diaphragmatic lung excursion and there are signs of atelectasis .

Approximately 20% of patients have acute pancreatitis symptoms such as: bloating in the upper abdomen caused by bloating or stomach displacement by a pancreatic inflammatory process. The destruction of the pancreatic duct can cause ascites (pancreatic ascites). When palpation, tenderness is observed, most often in the upper abdomen. There may be moderate soreness in the lower abdomen, but with a finger examination the rectum is painless and feces without signs of latent blood. In the upper abdomen, muscle tension can be determined, from moderate to severe, but rarely tension is detected in the lower parts. Sometimes a pronounced irritation of the peritoneum leads to tension and a flaky abdomen. Peristalsis is reduced. Symptoms of Gray Turner and Cullen are ecchymoses on the lateral surfaces of the abdomen and in the navel region respectively and indicate extravasal hemorrhagic exudate.

The development of infection in the pancreas or in the pancreatic fluid is indicated by the phenomena of general intoxication with an increase in temperature and erythrocyte level or if the deterioration occurs after the initial period of stabilization of the course of the disease.

Diagnosis of acute pancreatitis

Acute pancreatitis should be suspected in the event of severe abdominal pain, especially in people who abuse alcohol, or in patients with diagnosed cholelithiasis. Similar symptoms of acute pancreatitis can be observed with a perforated ulcer of the stomach or duodenum, a mesenteric infarction, strangulation intestinal obstruction, exfoliating aortic aneurysm, biliary colic, appendicitis, diverticulitis, myocardial posterior infarction, abdominal wall abdominal injury and spleen injury.

The diagnosis is established by clinical examination, the determination of serum markers (amylase and lipase) and the absence of other causes that cause symptoms. In addition, a wide range of studies is performed, usually including a general blood test, electrolytes, calcium, magnesium, glucose, blood urea nitrogen, creatinine, amylase and lipase. Other standard studies include ECG and sequential studies of the abdominal cavity (thorax, abdominal cavity in horizontal and vertical position). Determination of trypsinogen-2 in urine has a sensitivity and specificity of more than 90% in acute pancreatitis. Ultrasound and CT, as a rule, do not have high specificity in the diagnosis of pancreatitis, but are often used to assess acute abdominal pain and their performance is indicated in the diagnosis of pancreatitis.

[8], [9], [10], [11], [12]

Laboratory diagnosis of acute pancreatitis

Amylase of serum and concentration of lipase in the blood increase on the first day of acute pancreatitis and return to normal after 3-7 days. Lipase is a more specific indicator for pancreatitis, but the level of both enzymes may increase with renal failure, as well as with other diseases of the abdominal cavity (eg, perforated ulcer, occlusion of mesenteric vessels, intestinal obstruction). Other causes of increased serum amylase include dysfunction of the salivary glands, macromyalasemia and tumors that secrete amylase. Levels of amylase and lipase may remain within normal limits in the event of destruction of the acinar tissue during previous episodes of the disease, which led to a decrease in adequate secretion of enzymes. The serum of patients with hypertriglyceridemia may contain a circulating inhibitor in the blood, which requires dilution to the detected increase in amylase in the serum.

The clearance of amylase / creatinine does not have sufficient sensitivity or specificity in the diagnosis of pancreatitis. This indicator is usually used to diagnose macromyalemia in the absence of pancreatitis. In macroamilasemia, amylase, associated with serum immunoglobulin, gives a false positive result by increasing the level of serum amylase.

Fractionation of total serum amylase by pancreatic type (p-type) and salivary type (s-type) of isoamylase increases the diagnostic value of the serum amylase level. However, the p-type level also increases in renal failure, as well as in other severe diseases of the abdominal organs, in which the clearance of amylase changes.

The number of white blood cells is usually increased to 12 000-20 000 / μL. The discharge of fluid into the abdominal cavity can significantly increase the hematocrit to 50-55%, thereby indicating a severe inflammation. There may be hyperglycemia. The concentration of calcium in the serum decreases on the first day of the disease due to the secondary formation of Ca "soap" as a result of the excess production of free fatty acids, especially under the influence of pancreatic lipase. Serum bilirubin increases in 15-25% of patients due to pancreatic edema and compression of the common bile duct.

Instrumental diagnosis of acute pancreatitis

Conventional radiography of the abdominal cavity can reveal calcification in the area of pancreatic ducts (indicative of previous inflammation and, consequently, phenomena of chronic pancreatitis), calcified gallstones or local intestinal obstruction in the left upper quadrant of the stomach or in mesogastrium ("swollen loop" of the small intestine, widening of the transverse guts or duodenal obstruction). Chest X-ray may reveal atelectasis or pleural effusion (usually left-sided or bilateral, but rarely only in the right pleural cavity).

If the studies are not informative, ultrasound should be performed for the diagnosis of cholelithiasis or dilatation of the common bile duct (which indicates the obturation of the biliary tract). Pancreatic edema can be visualized, but gas in the intestine often obscures the pancreas.

CT with intravenous contrast usually allows to identify necrosis, fluid accumulation or pseudocysts in case of pancreatitis diagnosis. This study is especially recommended in cases of severe pancreatitis or complications (eg, hypotension or progressive leukocytosis and fever). Intravenous contrasting facilitates the recognition of pancreatonecrosis, but this can cause pancreatic necrosis in areas with low perfusion (i.e., ischemia). Therefore, CT with contrast enhancement should be performed only after adequate fluid therapy and dehydration elimination.

If a suspected infection is indicated, a percutaneous puncture of the cyst, a zone of fluid accumulation or necrosis under the control of CT with fluid aspiration, Gram staining, and bacteriological sowing are indicated. The diagnosis of "acute pancreatitis" is confirmed by positive results of blood culture, and especially the presence of pneumatization of the retroperitoneal space with CT of the abdominal cavity. The introduction of MP cholangiopancreatography (MPGHP) into practice makes it possible to make instrumental examination of the pancreas more simple.

Treatment of acute pancreatitis

An adequate infusion therapy is important; sometimes it takes up to 6-8 l / day liquids containing the necessary electrolytes. Inadequate infusion therapy of acute pancreatitis increases the risk of developing pancreatic necrosis.

The exclusion of food intake has been shown to reduce the signs of inflammation (ie, the disappearance of pain and pain in palpation, the normalization of serum amylase, the appearance of appetite and subjective improvement). Hunger may be necessary for several days, with moderate pancreatitis, up to several weeks in severe conditions. To compensate for the absence of enteral nutrition in cases of severe disease, in the first few days, patients need to be transferred to full parenteral nutrition.

Treatment of pain in acute pancreatitis requires parenteral administration of opiates, which must be given in adequate doses. Despite the fact that morphine can cause spasm of the sphincter of Oddi, this is of questionable clinical importance. To facilitate vomiting, antiemetics should be prescribed (eg prochlorperazine 5-10 mg IV every 6 hours). In the case of persistent vomiting or symptoms of intestinal obstruction, nasogastric probing is required.

Assigned parenterally H ₂ blockers or proton pump inhibitors. Attempts to reduce pancreatic secretion with medications (eg, anticholinergics, glucagon, somatostatin, octreotide) have no proven efficacy.

Patients with severe acute pancreatitis require treatment in the DSM, especially in hypotension, oliguria, Ranson 3, APACHE II 8, or pancreatic necrosis> 30% according to CT. In the DIC, vital signs and diuresis should be monitored every hour; metabolic parameters (hematocrit, glucose and electrolytes) - to be determined every 8 hours; arterial blood gases are determined as needed; in the case of unstable hemodynamics or to determine the volume of the transfused liquid, the measurement of the linear central venous pressure or the Swan-Ganz catheter is performed every 6 hours. The total blood count, platelet count, coagulation index, total protein and albumin, blood urea nitrogen, creatinine, Ca and Mg are determined daily.

In hypoxemia, acute pancreatitis is treated with moistened oxygen through a mask or nasal tubes. With the preservation of hypoxemia or the development of adult respiratory distress syndrome, auxiliary ventilation is shown. In the case of an increase in glucose levels of more than 170-200 mg / dl (9.4-11.1 mmol / l), careful subcutaneous or IV insulin administration with careful monitoring is indicated. Hypocalcemia does not require any treatment if neuromuscular irritability does not develop; 10-20 ml of a 10% solution of Ca gluconate in 1 liter of intravenous fluids are administered for more than 4-6 hours. Chronic alcoholics and patients with hypomagnesemia identified should receive Mg sulphate 1 g / l of transfused liquid, a total of 2-4 g prior to the normalization of the electrolyte level. With the development of renal failure requires constant monitoring of serum Mg and careful intravenous injection of Mg. With the restoration of normal levels of Mg levels, serum Ca levels return to normal.

Prerenal azotemia requires increased infusion therapy. With the development of renal failure, dialysis (usually peritoneal) is indicated.

Antibiotic prophylaxis with imipenem can prevent infection of sterile pancreatic necrosis, although its effect on mortality is not specified. Infected areas of pancreatic necrosis require surgical sanitation, but infected fluid accumulations around the pancreas can be drained percutaneously. Pseudocysts with rapid filling, infection, bleeding or the risk of rupture require drainage. The choice of the method of drainage (percutaneously, by surgical intervention or endoscopically) depends on the localization of the pseudocyst and the possibilities of the hospital. Peritoneal lavage to remove activated pancreatic enzymes and inflammatory mediators has no proven efficacy.
Surgical treatment of acute pancreatitis during the first few days is justified with severe closed or penetrating trauma and progressive biliary pathology. Although more than 80% of patients with biliary pancreatitis stone is displaced spontaneously, ERCPH with sphincterotomy and removal of the calculus is indicated in patients who do not improve after 24 hours of treatment. Patients in whom the process is resolved spontaneously, require elective laparoscopic cholecystectomy. Elective cholangiography remains a controversial method.

What prognosis does acute pancreatitis have?

Oedemic acute pancreatitis has a lethality of less than 5%. With necrotic and hemorrhagic pancreatitis, the mortality rate reaches 10-50%. In case of infection, without extensive surgical treatment or drainage of the infection zone, mortality usually reaches 100%.

The data obtained during CT scan correlate with the prognosis. If CT changes are not detected or CT indicates only moderate pancreatic edema (class A or B by Balthasar), the prognosis is favorable. Patients with peripancreatic inflammation or fluid congestion in one region (class C and D) form an abscess in 10-15% of cases; when fluid accumulates in two or more areas (class E), the risk of abscess formation is more than 60%.

Prognostic signs of Ranson help predict the course of acute pancreatitis. Five signs of Ranson can be determined at hospitalization: age over 55, serum glucose> 200 mg / dl (> 11.1 mmol / L), serum LDH greater than 350 MED / L, ACT greater than 250 U, and white blood cell count greater than 16,000 / / RTI & gt; The remaining parameters are determined within 48 hours after hospitalization: a decrease of Hct> 10%, an increase in blood urea nitrogen> 5 mg / dL (> 1.78 mmol / l), Ca serum <8 mg / dl (<2 mmol / l), pO2 <60 mmHg (<7.98 kPa), a base deficit> 4 meq / l (> 4 mmol / l) and an expected fluid sequestration> 6 liters. Acute pancreatitis has a different risk of mortality, which increases with the number of positive symptoms: if less than three signs are positive, the mortality rate is less than 5%; if three or four are positive, mortality can be 15-20%.

The APACHE II, calculated on the 2nd day after admission, also correlates with the prognosis of acute pancreatitis.