Anyone who wants to live to old age should familiarize themselves with the clinic of pancreatitis. Acute pancreatitis. Etiology. Pathogenesis. Clinic, diagnosis, treatment Pancreatitis clinic symptoms
Pancreatitis is a disease characterized by the development of inflammation in the pancreatic tissue.
Etiology and pathogenesis of acute pancreatitis
Factors contributing to the occurrence of acute pancreatitis:
alcohol abuse, bad eating habits (fatty, spicy foods);
· cholelithiasis;
virus infection (mumps, Coxsackie virus) or bacterial infection (mycoplasma, campylobacter);
Injury to the pancreas
Surgical interventions for other pathologies of the pancreas and biliary tract;
taking estrogens, corticosteroids, thiazide diuretics, azathioprine, etc. medicines with a pronounced pathological effect on the pancreas;
Congenital anomalies in the development of the gland, genetic predisposition, cystic fibrosis;
Inflammatory diseases of the digestive system (cholecystitis, hepatitis, gastroduodenitis).
In the development of acute inflammation of the pancreas, according to the most common theory, the main factor is cell damage by prematurely activated enzymes. Under normal conditions digestive enzymes are produced by the pancreas in an inactive form and are activated already in the digestive tract. Under the influence of external and internal pathological factors, the production mechanism is disrupted, enzymes are activated in the pancreas and begin digestion of its tissue. The result is inflammation, tissue edema develops, and the vessels of the parenchyma of the gland are affected.
The pathological process in acute pancreatitis can spread to nearby tissues: retroperitoneal tissue, omental bag, peritoneum, omentum, mesentery of the intestine and ligaments of the liver and duodenum.
A severe form of acute pancreatitis contributes to a sharp increase in the level of various biologically active substances in the blood, which leads to pronounced general disorders of life: secondary inflammation and degenerative disorders in tissues and organs - lungs, liver, kidneys, heart.
Classification of acute pancreatitis
Acute pancreatitis is classified according to severity:
mild pancreatitis occurs with minimal damage to organs and systems, is expressed mainly by interstitial edema of the gland, is easily treatable and has a favorable prognosis for a quick recovery;
a severe form of acute pancreatitis is characterized by the development of pronounced disorders in organs and tissues, or local complications (tissue necrosis, infection, cysts, abscesses).
Severe acute pancreatitis may be accompanied by:
acute accumulation of fluid inside the gland or in the peripancreatic space, which may not have granulation or fibrous walls;
Pancreatic necrosis with possible infection of tissues (a limited or diffuse zone of dying parenchyma and peripancreatic tissues occurs, with the addition of an infection, the likelihood of lethal outcome);
Acute false cyst (accumulation of pancreatic juice, surrounded by fibrous walls, or granulations that occurs after an attack of acute pancreatitis, is formed within 4 or more weeks);
pancreatic abscess (accumulation of pus in the pancreas or nearby tissues).
Symptoms of acute pancreatitis
Typical symptoms of acute pancreatitis.
Pain syndrome.
The pain can be localized in the epigastrium, left hypochondrium, be girdle in nature, radiate under the left shoulder blade. The pain is of a pronounced permanent nature, in the supine position it intensifies. Increased pain occurs after eating, especially fatty, spicy, fried, alcohol.
Nausea, vomiting. Vomiting may be indomitable, contains bile, does not bring relief.
Increase in body temperature.
Moderately pronounced yellowness of the sclera. Rarely - mild jaundice of the skin.
In addition, acute pancreatitis may be accompanied by dyspeptic symptoms (bloating, flatulence, heartburn), skin manifestations (bluish spots on the body, hemorrhages in the navel).
Diagnosis of acute pancreatitis
Diagnosis of pancreatitis by gastroenterologists is carried out on the basis of complaints, physical examination, identification of characteristic symptoms. When measuring blood pressure and pulse often note hypotension and tachycardia. Laboratory tests of blood and urine, MSCT and ultrasound of the abdominal organs, MRI of the pancreas serve to confirm the diagnosis.
In the study of blood in the general analysis, signs of inflammation are noted (ESR accelerated, the content of leukocytes is increased), in the biochemical analysis, an increase in the activity of pancreatic enzymes (amylase, lipase) is detected, hyperglycemia and hypocalcemia are possible. Also carry out the determination of the concentration of enzymes in the urine. There may be bilirubinemia and increased activity of liver enzymes.
When diagnosing acute pancreatitis, take biochemical analysis urine and determine the activity of amylase.
Visual examination of the pancreas and nearby organs (ultrasound, CT, MRI) allows you to identify pathological changes in the parenchyma, an increase in the volume of the organ, detect abscesses, cysts, and the presence of stones in the bile ducts.
Differential diagnosis of acute pancreatitis is carried out with:
acute appendicitis and acute cholecystitis;
Perforations of hollow organs (perforated ulcers of the stomach and intestines);
acute intestinal obstruction;
acute gastrointestinal bleeding (bleeding ulcer of the stomach and 12th intestine, bleeding from varicose veins of the esophagus, intestinal bleeding);
acute ischemic abdominal syndrome.
Treatment of acute pancreatitis
In acute pancreatitis, hospitalization is indicated. All patients were prescribed bed rest. The main goals of therapy are to relieve pain, reduce the load on the pancreas, and stimulate the mechanisms of its self-healing.
Therapeutic measures:
novocaine blockade and antispasmodics to relieve severe pain;
Hunger, ice on the projection area of the gland (creating local hypothermia to reduce its functional activity), parenteral nutrition is carried out, gastric contents are aspirated, antacids and proton pump inhibitors are prescribed;
Deactivators of pancreatic enzymes (inhibitors of proteolysis);
Necessary correction of homeostasis (water-electrolyte, acid-base, protein balance) with the help of infusion of saline and protein solutions;
detoxification therapy;
Antibiotic therapy (broad-spectrum drugs in high doses) as a prophylaxis of infectious complications.
Surgical treatment is indicated if:
stones in the bile ducts;
accumulation of fluid in or around the gland;
Areas of pancreatic necrosis, cysts, abscesses.
Operations performed in acute pancreatitis with the formation of cysts or abscesses include: endoscopic drainage, marsupialization of the cyst, cystogastrostomy, etc. When areas of necrosis are formed, depending on their size, necrectomy or resection of the pancreas is performed. The presence of stones is an indication for operations on the pancreatic duct.
Surgical intervention may also be resorted to in case of doubts about the diagnosis and the likelihood of missing another surgical disease requiring surgical treatment.
The postoperative period implies intensive measures for the prevention of purulent-septic complications and rehabilitation therapy.
Light treatment forms of pancreatitis, as a rule, does not present difficulties, and positive dynamics is already noted within a week. Severe pancreatitis takes much longer to heal.
Chronic pancreatitis is a persistent inflammation of the pancreas leading to permanent structural changes with fibrosis and strictures of the pancreatic duct. These changes lead to a decrease in the endocrine and exocrine functions of the pancreas.
The main clinical manifestations of chronic pancreatitis
Abdominal pain and weight loss are the two most common clinical manifestations of chronic pancreatitis. Pain reduces patients' appetite and leads to food restriction, leading to weight loss and malnutrition. Abdominal pain is the most common indication for surgery in chronic pancreatitis.
Patients experience periodic bouts of severe pain in the epigastrium or left hypochondrium, and the pain may radiate to the back. More often, pain occurs one and a half to two hours after a rich, fatty or spicy meal. But often the pain appears 6-12 hours after the dietary error. An even longer "incubation" period is sometimes observed after drinking large doses of alcohol - it can reach 48 or even 72 hours. Less commonly, pain occurs in the next few minutes, especially after taking cold fizzy drinks. Sometimes the pain may not be related to food intake. Pain may occur at night.
The exact mechanisms underlying the onset of pain remain a matter of debate, but may be caused by inflammation of the pancreas, increased intrapancreatic pressure, neuroinflammation, or extrapancreatic causes such as common bile duct stenosis.
In approximately 20% of cases, a painless course of chronic pancreatitis is observed.
Weight loss initially occurs due to a decrease in the number of calories taken as a result of fear and anticipation of abdominal pain. Later, with the progression of pancreatitis, the patient develops malabsorption (maldigestion) as a result of pancreatic insufficiency (polyfaeces, steatorrhea).
Secondary diabetes develops when 80% of the pancreas is destroyed. Steatorrhea occurs when 90% of pancreatic function is lost.
Clinical variants of the course of chronic pancreatitis
1. Edema-interstitial (subacute) chronic pancreatitis.
According to the severity of clinical symptoms, the disease approaches acute pancreatitis, but in general the disease lasts more than 6 months, and after the first attack, residual effects are determined. In addition to intense pain, nausea and often vomiting are usually noted. Most patients have pain in the projection of the pancreas.
The severity of this variant of chronic pancreatitis is evidenced by the high rate of complications (30-40%).
2. Parenchymal (recurrent) chronic pancreatitis.
Exacerbations occur frequently - sometimes several times a year. Their frequency is usually associated not with gross changes in the pancreatic ducts, but with the repetition of alcohol and food (causing the passage of small gallstones) excesses.
Clinical manifestations are less pronounced than in interstitial chronic pancreatitis, an increase in amylase activity is less common (in 75-80% of patients) and not so significant.
This, the most common (more than 50% of patients), clinical variant is relatively rare (10-12%) leads to the development of complications. If the action of etiotropic factors stops, then in most cases the prognosis is quite favorable.
3. Fibrosclerotic (indurative) chronic pancreatitis.
In most patients, dyspeptic and especially pain syndromes are significantly pronounced and fairly stable.
Fibrosclerotic variant occurs in approximately 15% of inpatients with chronic pancreatitis. Often (almost 50% of patients) develop complications. The course of the disease is usually persistent.
4. Cystic chronic pancreatitis.
Of the clinical features, one can note the pain syndrome expressed during the period of exacerbation, the phenomena of general intoxication, and the most pronounced hyperamylasemia of all variants of chronic pancreatitis. In a significant proportion of cases, it is possible to palpate a painful or sensitive pancreas. During remission, both hyperamylasemia and pain may be absent.
This variant occurs in 6-10% of inpatients with chronic pancreatitis. Very often (almost 60%) develop complications.
5. Hyperplastic (pseudotumorous) chronic pancreatitis.
Significant severity of pain syndrome, often observed decrease in body weight, uneven local enlargement of the pancreas, detected by palpation, serve as the basis for suspecting carcinoma of the gland.
This variant of the disease occurs in 4-6% of inpatients with chronic pancreatitis. In some cases, the disease proceeds with mild or moderate clinical manifestations, but complications develop in almost 70% of patients.
Clinical diagnostics
Collection of anamnesis
When collecting an anamnesis, the nature of the pain syndrome and dyspeptic phenomena (nausea, vomiting, which does not bring relief) is clarified. Weight stability is assessed (if there is a decrease in body weight, it is specified how much the patient's weight has decreased and for how long). The nature of the stool is important - diarrhea, polyfecalia, steatorrhea, although constipation may occur at the onset of the disease. Duodenogastric reflux contributes to bad breath.
With severe exacerbations of chronic pancreatitis and acute pancreatitis, the abdomen is often moderately swollen. Chronic pancreatitis is characterized by "bloody tears" - purple formations towering above the skin of the abdomen with a diameter of 1-3 mm.
Palpation
With a mild course of chronic pancreatitis, an examination of the abdomen may not reveal pathology. Palpation of the gland is usually not very informative due to the very deep location of the organ. The pancreas can be clearly felt either in very malnourished patients, or through the divergence of the muscles in postoperative hernia. It is easier to feel a pathologically altered gland, especially with a significant increase in its size, which is observed primarily in cystic pancreatitis.
Soreness or painful resistance in the area of the gland can be established much more often than by probing the gland itself. With severe exacerbations of chronic pancreatitis, the abdomen is moderately swollen and muscle tension in the anterior abdominal wall is usually deceptively absent. Although a slight tension - "rubber belly" is often observed in severe forms of acute pancreatitis.
With thrombosis of the splenic vein, splenomegaly (enlargement of the spleen) can be observed.
Laboratory research
General blood analysis
In most patients with chronic pancreatitis, a complete blood count, both during the period of remission and at the time of exacerbation of the disease, is unchanged. Approximately a quarter of patients have an increased number of leukocytes and ESR. Leukocytosis more than 11 x 109 / l and ESR more than 30 mm / h are inherent in chronic pancreatitis with a severe course.
Glucose tolerance study
If, 2 hours after taking 75 g of glucose, its content in the blood exceeds 8 mmol / l, but not more than 11 mmol / l, then this indicates impaired glucose tolerance, and with a glucose content of 11.1 mmol / l or more, a diagnosis is made diabetes.
Enzyme research
Determination of α-amylase.
Determination of α-amylase saves importance in recognizing exacerbations of chronic pancreatitis.
α-amylase consists mainly of two fractions, two isoforms - S-salivary and P-pancreatic. With a pronounced exacerbation of chronic pancreatitis, the increase in the activity of P-isoamylase both in the blood and in the urine is so significant that this increase is quite well captured by the usual determination of the total activity of the enzyme.
Prolonged, almost constant hyperamylasemia, reaching large values, is usually observed only with the cystic form of pancreatitis.
Outside of an exacerbation or with a moderate exacerbation of chronic pancreatitis, the determination of the total activity of the P and S enzyme in the blood and in the urine usually gives a normal result or its decrease. The study of isoenzymes reveals a certain pattern: the activity of P-isoamylase in serum in the majority is reduced, which is explained by a decrease in the exocrine function of the pancreas. However, given the difficulty of determining pancreatic isoamylase, its study has found relatively little distribution. The main research method is the determination of the total activity of amylase.
An increase in the activity of amylase in the blood with normal activity of amylase in the urine can be observed in renal failure. In this case, if acute pancreatitis is suspected (exacerbation of chronic pancreatitis), it is recommended to investigate the "amylase creatinine ratio" equal to: amylase clearance / creatinine clearance in%. In acute pancreatitis (exacerbation of chronic pancreatitis), there is a predominant increase in the activity of urine amylase, the release of creatinine does not change. Values greater than 5.5% are considered characteristic of acute pancreatitis (exacerbation of chronic pancreatitis).
The study of amylase is rather nonspecific. Relatively naturally (due to enzyme isoforms) there is an increase in the total amylase activity of urine and especially blood serum in lung diseases, fallopian tubes, ovaries, prostate, salivary and lacrimal glands. Therefore, in the diagnosis of pancreatitis, more and more importance is attached to other enzyme tests, primarily the determination of elastase.
Determination of lipase activity.
The study of lipase (triacylglycerol-lipase) is determined by enzyme immunoassay, as well as by the titrimetric method. The first method is much more sensitive than the second. The determination of serum lipase in chronic pancreatitis is less sensitive than the amylase test, while in acute pancreatitis it is more reliable.
Determination of the activity of phospholipase A 2 .
The level of phospholipase A 2 naturally increases in acute pancreatitis. The method is increasingly used in the diagnosis of exacerbations of chronic pancreatitis.
Study of blood trypsin.
Serum trypsin in a biochemical study is a sensitive but insufficiently specific test. However, this does not apply to the diagnostic determination of trypsin by radioimmunoassay or enzyme immunoassay. In this way, the mass of the protein is determined, and not the enzymatic activity.
This approach eliminates the interference introduced by serum antiproteases. The determination of immunoreactive trypsin is a rather specific and sensitive test. Low levels of trypsin activity, as well as low levels of P-isoamylase, indicate a decrease in the exocrine function of the gland. This is usually observed against the background of steatorrhea and severe manifestations of chronic pancreatitis.
Study of blood elastase.
Serum elastase increases during exacerbation of chronic pancreatitis (acute pancreatitis), and this increase lasts longer than hyperamylasemia.
Methods for studying the exocrine function of the pancreas
Examination of feces
A person excretes an average of 250 g of feces per day under normal conditions. Polyfecalia, characteristic of exocrine gland insufficiency, is determined in cases where the weight of feces exceeds 400 g. Reliable results can only be obtained by weighing feces for three days. The bulkiness and inconvenience of the study hinders its wide application.
The definition of steatorrhea is not widely used. A normal indicator is the allocation of 7 g of fat per day on a diet containing 100 g of fat. Steatorrhea is observed in 30-35% of patients with chronic pancreatitis of moderate severity and in 65-75% of patients with severe forms of chronic pancreatitis.
Polyfecal and steatorrhea are not early manifestations of exocrine pancreatic insufficiency, since clear signs insufficiency of lipase production indicates the defeat of 70-90% of the parenchymal elements of the pancreas. In such a situation, weight loss is often observed. Thus, there are grounds for the use of pancreatic enzymes.
Direct tests for the study of exocrine function
Perhaps a direct study of external secretion using special probes, with two obturators that prevent leakage of gastric and intestinal juices.
Secretin-pancreozymin (or secretin-cerulein) test.
Due to the fact that pure cholecystokinin can cause side effects, octapeptide-cholecystokinin or cerulein is used for research purposes. In response to the administration of secretin and pancreozymin, the pancreas secretes pancreatic secretion of various characteristics. Therefore, only a combined study of both stimuli gives a complete picture of the exocrine function of the gland.
In chronic pancreatitis, enzyme secretion may decrease earlier than bicarbonate secretion. With pronounced clinical manifestations of exocrine pancreatic insufficiency, pathological changes in the secretin-pancreozymin test are observed in 85-90% of the examined. False positive results are observed with celiac disease, liver cirrhosis, cholestasis.
The invasiveness of the method, the high cost and complexity of acquiring secretin and pancreozymin limits the use of this informative test.
L U N D T - test.
Has become widespread. The stimulus used causes the production of endogenous secretin and pancreozymin. The study begins with the introduction of a duodenal probe. After reaching the duodenum, a solution of sorbitol is injected. Following the end of the flow of bile into the duodenum, at the moment when the probe is reliably in the duodenum, the patient drinks a mixture of the following composition: 13 g of soybean oil (or 18 g olive oil), 15 g milk powder, 45 g glucose, 15 ml fruit syrup, distilled water up to 300 ml.
Duodenal juice is collected within 120 minutes. Before the introduction of the stimulus for 30 minutes. juice is pumped out (basal secretion) and then for 90 minutes. after the introduction of the stimulus (stimulated secretion).
Usually, only trypsin is examined in the duodenal contents. The normal concentration of trypsin is 10-30 units/ml. A decrease to more than 8 units / ml indicates exocrine pancreatic insufficiency. Pathological results are recorded in 65-90% of patients.
False-positive results were noted in celiac disease, in persons with a resected stomach and diabetes mellitus.
Visualizing and instrumental studies
These methods of studying the pancreas have become of paramount importance, since they allow visualizing the gland, its ducts, and partly the duodenum.
Plain radiography of the abdominal organs
Ultrasound examination (ultrasound) of the pancreas
Computed tomography (CT) of the pancreas
Magnetic resonance imaging (MRI)
Magnetic resonance cholangiopancreatography (MRCP)
Endoscopic retrograde cholangiopancreatography (ERCP)
Endoscopic ultrasonography (EUS)
Endoscopy duodenum, stomach and esophagus
Angiography of the pancreas
Chronic pancreatitis refers to diseases with a tendency to relapse. With timely diagnosis and careful treatment in 2/3 of patients, the pathological process in the pancreas subsides.
Treatment objectives
Lifestyle changes (to reduce the impact of adverse factors on the pancreas).
Pain relief.
Replenishment of exocrine and endocrine functions pancreas.
Treatment Methods
Conservative treatment
Conservative treatment of chronic pancreatitis can be divided into three types:
1. Emergency care for a patient with severe exacerbation of edematous-interstitial chronic pancreatitis
Characteristic manifestations of the disease are usually persistent pain in the upper abdomen, often accompanied by vomiting and symptoms of general intoxication.
Principles of emergency care for patients with severe exacerbation of edematous interstitial chronic pancreatitis:
Reducing to a minimum the functional activity of the pancreas: hunger, removal of stomach contents with the help of constant suction through a nasogastric tube, taking antacids or H2-blockers of the second or third generation (ranitidine (Ranitidine, Ranisan), famotidine (Kvamatel, Gastrosidin, Famotidine)), proton pump blockers (omeprazole (Losek Maps, Ultop, Omez), rabeprazole (Pariet)), octreotide (Sandostatin).
The fight against edema of the pancreas and parapancreatic tissue (mannitol (Mannitol), furosemide (Lasix)).
Prevention of enzyme intoxication (aprotinin (Kontrykal, Gordox), octreotide (Sandostatin)).
Reducing the intensity of pain (solutions of paracetamol (Perfalgan UPSA), metamizole sodium (Analgin, Baralgin M) or promedol, often in combination with antispasmodics).
Correction of water and electrolyte balance (isotonic sodium chloride solution, Ringer's solution, low concentration glucose solutions).
Prevention or control of infectious complications (antibacterial agents).
2. Therapy for exacerbations of chronic pancreatitis that have not reached the degree of acute pancreatitis
The tactics of treatment for exacerbation of chronic pancreatitis is based on a combination of drug treatment and diet therapy.
AT drug treatment use anticholinergic and antispasmodic drugs with antacids and H2-blockers, analgesics, enzyme and anti-enzyme drugs.
After 3-10 days from the start of complex treatment, subject to diet and complete abstinence, in 65-70% of patients, the severity of pain and dyspeptic syndromes decreases.
Diet therapy.
Patients who often have relapses of pancreatitis are very sensitive to the nature of the diet. In case of severe exacerbations of chronic pancreatitis, usually occurring with night pains and vomiting, it is advisable to resort to fasting for 1-3 days, correcting the water and electrolyte balance by parenteral administration of Ringer's solution, glucose, etc. After reducing the severity of pain and stopping vomiting, they return to oral nutrition .
Medical treatment.
Analgesics and antispasmodics (pain relief).
Anticholinergic and antispasmodic drugs (atropine, platifillin (Platifillina g / t), pirenzepine (Gastrocepin), drotaverine (No-shpa), papaverine (Papaverine hydrochloride)) are used in medium doses orally and subcutaneously, as a rule, with pain forms of chronic pancreatitis .
A third of patients with chronic pancreatitis have persistent pain syndrome. They are prescribed paracetamol (Perfalgan UPSA), metamizole sodium (Analgin, Baralgin M). At the height of exacerbation, 2-5 ml of a 50% solution of analgin is administered intramuscularly 1-3 times a day or 2-3 ml of baralgin, as well as pentazocine (Fortral) at a dose of 30 mg intramuscularly. After the pain subsides, patients take the same drugs orally after meals, 2-3 tablets per day. The maximum daily dose of paracetamol should not exceed 4 g, and in persons with chronic alcohol intoxication, the dose should be reduced by at least 1/3.
In some cases, especially with intense pain, narcotic analgesics are prescribed: 1 ml of a 1-2% solution of promedol subcutaneously or intramuscularly 1-3 times a day, usually for no more than 3 days. For the same purpose, tramadol (Zaldiar) is used 1-2 ampoules (50 mg each) intramuscularly or intravenously (slowly) or 1-2 capsules (50 mg each) orally 1-3 times a day. Buprenorphine is also used at a dose of 300 mcg in an ampoule and 200 mcg in a tablet, small doses of stelazin (2 mg), melipramine (10 mg). Melipramine is also undesirable to use for more than 3-4 days because of the danger of addiction.
Antacids and antisecretory drugs
Almagel, Phosphalugel and other liquid alkaline mixtures are used as antacids. With severe pain syndrome, H2-blockers (ranitidine (Ranitidine, Ranisan), famotidine (Kvamatel, Gastrosidin, Famotidine)) and proton pump inhibitors (omeprazole (Losek MAPs, Ultop, Omez), rabeprazole (Pariet), etc.) are widely used.
Enzyme therapy.
In the regulation of pancreatic secretion, lipase and trypsin play an important role. In the lumen of the duodenum, the amount of trypsin capable of inhibiting pancreatic secretion according to the feedback law should be 150-300 mg for 1 hour, and to ensure the hydrolysis of neutral fat - lipase - at least 20,000 IU. Only microspherical enzyme preparations with a high content of lipase, amylase, protease and a special enteric coating (Creon 10000 and Creon 25000) have such properties.
Adequate enzyme therapy is applied immediately after the transfer of the patient to enteral nutrition. Assign Creon usually 2-3 capsules during or immediately after a meal. Doses of drugs are set depending on the need for lipase. For most patients, 20,000-40,000 IU of lipase per meal is sufficient. In especially severe forms of the disease with severe steatorrhea, the daily dose of the drug is increased to 50,000-60,000 IU per meal (Creon 25000). In severe steatorrhea, fat-soluble vitamins are additionally prescribed (vitamins A, D, E, K), as well as group B.
Reception of enzyme preparations can continue for years. In any case, experience shows that the subsidence of a pronounced exacerbation of chronic pancreatitis takes more often than 3-5 weeks, and the complete subsidence of the phenomena of exacerbations of chronic pancreatitis usually takes 6-12 months. It is desirable not to interrupt the whole period of enzyme therapy.
With exacerbations of the disease of moderate severity, exocrine pancreatic insufficiency plays an important role in the development of not only dyspeptic, but also pain syndrome. This is confirmed by the positive therapeutic effect of enzyme preparations.
Antibacterial therapy (with the development of peripancreatitis).
Often, exacerbations of chronic pancreatitis are accompanied by the development of peripancreatitis (detected during ultrasound) and cholangitis. In these cases, antibiotics are prescribed:
Ampioks 2-1.5 g 4 times a day intramuscularly for 7-10 days or
Cefoperazone (Cefobide) 1-2 g 2 times a day intramuscularly or intravenously or
Cefuroxime (Zinacef) 1 g 3 times a day intramuscularly or intravenously for 7-10 days.
In outpatient practice, doxycycline (Unidox Solutab) 0.1 g 1-2 times a day for 6-8 days or cefixime (Supraks) 0.05-0.1 g 2 times a day orally for 7-10 days is used. days.
With severe peripancreatitis and insufficient effectiveness of antibiotic therapy, an assumption arises about the presence of microflora resistance, often in particular chlamydia. In these cases, treatment is carried out with pefloxacin (Abactal) and azithromycin (Sumamed).
antienzymatic therapy.
In relatively few patients, mainly with interstitial and parenchymal variants of chronic pancreatitis, occurring with pancreatic edema, as well as significant and persistent hyperamylasemia, there are indications for antienzymatic therapy. The drugs of this group are administered intravenously: aprotinin (Kontrykal) 1-2 times a day, 20,000 IU in 200-500 ml of isotonic sodium chloride solution (treatment course 7-10 days), aprotinin (Gordox) at a dose of 100,000 IU.
Allergic reactions to the introduction of these drugs occur in 7-10% of patients. The most severe complication is anaphylactic shock. These negative reactions significantly limit the use of antienzymatic drugs.
Correction of neuropsychiatric disorders.
Almost a third of patients with long-term chronic pancreatitis develop neuropsychiatric disorders. Their causes are different: long-term pain attacks of the disease, chronic "enzyme intoxication" (increased concentration of enzymes in the blood serum), insufficient absorption of vitamins. These patients are shown vitamin replacement therapy and psychotropic drugs. The most commonly used diazepam, medazepam, amitriptyline (Amitriptyline Nycomed), sulpiride (Eglonil). AT last years Sertraline (Zoloft) and ademetionine (Heptral) are also used.
3. Maintenance therapy after subsiding of a pronounced exacerbation of chronic pancreatitis
Maintenance therapy is especially important during the first 6-12 months after the exacerbation of chronic pancreatitis has subsided. It was during this period that the question of the next relapses of the disease was largely resolved. An important task of this period is the correction of living conditions, which must be carried out by a patient who has undergone a pronounced exacerbation of chronic pancreatitis. The question of changing the nature of work is for people who are constantly in contact with alcohol or who are constantly on business trips. In the first case, it is almost impossible to achieve an abstinence regime, in the second - the most modest dietary restrictions.
Persons who received psychotropic drugs during an exacerbation of chronic pancreatitis continue to take them for 1-3 months.
Enzyme therapy.
Maintenance therapy includes enzyme replacement therapy.
With a properly selected dose of Creon, patients' weight stabilizes or increases, diarrhea, flatulence, abdominal pain stop, steatorrhea and creatorrhoea disappear. Creon in chronic pancreatitis with exocrine insufficiency is prescribed for life. Doses may be reduced if strict diet with restriction of fat and protein and increase with its expansion.
Antisecretory drugs.
In case of severe pain, H2-blockers are indicated (ranitidine (Ranitidine, Ranisan), famotidine (Kvamatel, Gastrosidin, Famotidine)) and proton pump inhibitors (omeprazole (Losek MAPs, Ultop, Omez), rabeprazole (Pariet), etc.).
Insulin therapy (with endocrine insufficiency).
To eliminate endocrine insufficiency, fractional doses of simple insulin are used, daily requirement ranges from 20 to 30 units, depending on the nature of the diet, the amount of glucose administered, physical activity patient and baseline blood glucose levels. At the same time, it is extremely dangerous to lower the blood glucose level below 80 mg% (4.44 mmol / l), as this poses a great risk for the development of hypoglycemia. Oral hypoglycemic drugs usually ineffective.
Surgery
Indications for surgical treatment are set quite carefully. There are several indications for surgical treatment of patients with chronic pancreatitis:
Intractable pain that is not relieved by standard conservative therapy, including narcotic analgesics.
· Pseudocysts or blockage of the common bile duct that cannot be treated endoscopically.
Doubt in the diagnosis of chronic pancreatitis (it is necessary to exclude pancreatic cancer).
Persistent vomiting and progressive weight loss.
Etiology
- Diseases of the extrahepatic biliary tract (cholelithiasis, choledocholithiasis, spasm or stenosis of the Vater papilla, biliary dyskinesia, etc.).
- Exogenous intoxication (alcohol and its surrogates, some drugs, etc.).
- Diseases of the duodenum (duodenostasis, duodenal diverticula).
- Traumatic damage to the pancreas or Vater's nipple.
Clinical and morphological classification
- I. Acute mild pancreatitis.
- Edema form.
- Edematous form with accumulation of fluid (in the pancreas, parapancreatic fiber, stuffing bag).
- II. Acute severe pancreatitis.
- Pancreatic necrosis uninfected
(fatty, proteolytic,hemorrhagic, mixed):
- small focal
- mid-focal
- macrofocal
- total
- Pancreatic necrosis infected
- small focal
- mid-focal
- macrofocal
- total
III. Acute severe pancreatitis
Complicated:
- Parapancreatic infiltrate
- Necrotizing parapancreatitis (local,
common)
- uninfected
- infected
- Acute pancreatic cyst
- uninfected
- infected
- Peritonitis (local, diffuse, diffuse)
- enzymatic
- purulent
- Purulent abscesses of various localization
- sepsis
- Digestive and pancreatic fistulas
- Bleeding (gastrointestinal,
intra-abdominal)
- Functional organ failure
And systems:
- cardiovascular
- respiratory
- renal
- hepatic
- multiple organ
Clinic
The most constant symptom of acute pancreatitis is intense pain, usually expressed in the region of the epigastrium itself, along the pancreas, occurring suddenly, often appearing after a food overload, often radiating to the back, to the right, left or both shoulder blades, the left costovertebral angle , left shoulder girdle. Sometimes the pain increases gradually, has a cramping character and is not very intense.
The second most common (80-92% of patients) symptom of acute pancreatitis is recurrent vomiting that does not bring relief, which usually appears immediately after the pain (but may precede it) and is usually accompanied by constant nausea. Body temperature is initially normal or subfebrile. Characterized by "scissors" - the backlog of body temperature from the pulse rate.
Diagnosis of acute pancreatitis
In the diagnosis of acute pancreatitis, many clinicians great importance give a change in the color of the skin. Jaundice at the onset of the disease is rare. The most common is pallor of the skin. The acro- and general cyanosis that appears later is due to respiratory failure, toxic damage to the capillaries and is characteristic of severe forms of pancreatitis. Therefore, it always serves as a poor prognostic sign. Dryness of the tongue in acute pancreatitis, as in other acute surgical diseases of the abdomen, reflects the degree of dehydration of the body.
The abdomen is swollen at first only in the epigastric region, along the transverse colon (Bond's symptom), and later - all over.
Tension of the muscles of the abdominal wall is initially localized only in the projection of the pancreas (Kert's symptom).
Participation in the protective reaction of the muscles of the entire abdomen indicates a complication of pancreatitis with enzymatic and then purulent peritonitis, in which Shchetkin-Blumberg's symptom is also positive.
The Grekov-Ortner symptom confirms the involvement of the gallbladder in the pathological process and is positive in about 32% of patients.
In the study of peripheral blood in 61-80% of patients, an increase in the number of leukocytes and a shift in the white blood formula to the left are revealed, and in 54-82% - lymphopenia.
Much less often there are changes in the red blood. Anemia is associated with the release of erythrocytes into the interstitial space with an increase in the permeability of the vascular wall, their destruction under the influence of proteolytic enzymes. It is mandatory to determine the daily diuresis (if necessary, hourly), the indicators of which may indicate the degree of intoxication. In the urine, proteinuria, microhematuria, cylindruria and other pathological impurities are detected.
special diagnostic value have biochemical studies, and above all - the determination of the activity of pancreatic enzymes. Since not all patients are admitted to the hospital in the first hours of the disease, the increased activity of these enzymes is found in 82.5-97.2% of cases. That's why normal performance blood and urine enzymes do not exclude the presence of acute pancreatitis. With an increase in the duration of the disease, the frequency of hyperenzymemia decreases. Of certain importance is the determination of quantitative and qualitative indicators of bilirubin in the blood.
An important role in the diagnosis of acute pancreatitis belongs to plain radiography and fluoroscopy of the chest and abdominal cavity, with the help of which it is possible to exclude a number of common surgical diseases organs of the abdomen and detect signs of damage to the pancreas. Often there is swelling of the transverse colon - a symptom of Bonde - and other parts of the intestine, an increase in the distance between the greater curvature of the stomach and the transverse colon. X-ray examination of the gastrointestinal tract allows you to catch indirect signs of pancreatitis: the deployment of a horseshoe and compression of the descending loop of the duodenum 12, compression and displacement of the stomach and duodenum 12, and a significant violation of their evacuation (12.6%).
Selective angiography
(mesenteric and ciliacography) makes it possible to identify direct signs of acute pancreatitis even when patients are admitted late in the disease, when the activity of blood and urine enzymes becomes normal. In addition, with the help of angiography, complications such as thrombosis of large arterial and venous trunks, etc. are detected.
Scanning of the pancreas
allows you to determine the degree of damage to the function of acinar cells and to identify the deformation and enlargement of the organ itself. With the introduction of endoscopic and non-invasive research methods into the practice of surgery, the importance of the last two methods has noticeably decreased.
Fibrogastroduodenoscopy
plays a supporting role in the diagnosis of acute pancreatitis. The most characteristic endoscopic signs are bulging of the posterior wall of the stomach and a picture of acute gastroduodenitis. In severe pancreatitis, erosive and hemorrhagic gastroduodenitis, papillitis and signs of reflux pyloritis are more often detected. Laparoscopy provides clinicians with enormous diagnostic possibilities. Direct signs of acute pancreatitis are: plaques of fatty necrosis on the peritoneum, omentum, hemorrhagic effusion, swelling of the omentum, intestinal mesentery, tissue, hyperemia and imbibition of the peritoneum. Among indirect signs note: paresis of the stomach and transverse colon, congestive gallbladder. High activity of pancreatic enzymes in peritoneal effusion at laparoscopy fully confirms the diagnosis of acute pancreatitis.
Treatment
Modern conservative therapy of acute pancreatitis solves the following problems:
- Elimination of pain and spasm, improvement of microcirculation in the gland;
- Fighting shock and restoring homeostasis;
- Suppression of exocrine secretion and activity of gland enzymes;
- Fight against toxemia;
- Normalization of the activity of the lungs, heart, kidneys, liver;
- Prevention and treatment of complications.
In different phases and periods of development of acute pancreatitis, various surgical interventions are justified, pursuing two main goals:
Stop an acute attack of the disease and prevent death;
Prevent recurrence of acute pancreatitis after the patient is discharged from the hospital.
For the best solution of the main issues of surgical treatment and surgery in patients with acute pancreatitis (depending on the phase of development and the period of the course of the disease) are divided into 3 groups:
Early, performed in the first hours and days of the disease in the acute period of development of edema or necrosis of the gland. Indications for early surgery:
Difficulty in making a diagnosis;
Diffuse enzymatic peritonitis with symptoms of severe intoxication;
The combination of pancreatitis with destructive cholecystitis;
Obstructive jaundice.
After the introduction of urgent surgery laparoscopy into practice, which allows determining the form of pancreatitis and determining the state of the biliary system, the number of early operations has decreased. In addition, laparoscopic lavage can be used as a preoperative preparation of the patient. Under certain indications, early operations end with resection of the pancreas and sanitation of the biliary system.
Operations in the phase of melting and sequestration of necrotic foci of the pancreas and retroperitoneal tissue, which are usually performed on the 2-3rd week from the onset of the disease. When treating patients in this phase, it is possible to remove dead tissues of the gland and retroperitoneal tissue in time, that is, they will perform necrectomy (after the 10th day of the disease) or sequestrectomy (on the 3-4th week from the onset of the disease) in a timely manner.
Late (delayed) operations, carried out in a planned manner during the period of subsiding or complete elimination of pathological changes in the pancreas. These operations are indicated for those diseases of the abdominal organs that can cause pancreatitis or contribute to its development (cholelithiasis, cholecystitis, gastroduodenal obstruction, duodenostasis, duodenal diverticulum, obstruction of the pancreatic duct, etc.). They are aimed at preventing the recurrence of acute pancreatitis by surgical sanitation of the biliary tract and other digestive organs, as well as the pancreas itself.
The main task of pancreatic surgery is to create conditions that exclude the development of hypertension in the pancreatic ducts.
Acute pancreatitis is a degenerative-inflammatory lesion of the pancreas caused by various causes. The disease is based on autolysis of pancreatic tissues due to the impact on it of its own activated proteolytic enzymes - this is an enzymatic-chemical process, which can be secondarily joined by an infection.
Activation of enzymes can contribute to:
I / Increased pressure in the biliary tract - biliary hypertension (considered the main cause), which may be based on diseases of the gallbladder, which in 63% of cases are accompanied by spasm of the sphincter of Oddi, especially calculous "process - gallbladder and choledochal stones, choledochal stricture. If present common ampulla of the choledochus and the Wirsung duct, bile is thrown into the latter - biliary reflux, causing the activation of trypsinogen and its transition to trypsin, followed by autolysis of the pancreatic tissue - "tubular theory", the theory of the common channel. Pancreatitis of this genesis in accordance with the decision of the conference in Kyiv in 1988 are called biliary pancreatitis, they account for about 70% of all acute pancreatitis.All other pancreatitis are called idiopathic.
2/ Congestion in the upper sections digestive tract; gastritis, duodenitis, duodenostasis contribute to insufficiency of the sphincter of Oddi and the casting of intestinal contents containing enzymes into the pancreatic duct - duodenal reflux, which also contributes to the activation of trypsinogen with the development of OP - the theory of duodenal reflux.
3/ Disorders of metabolism, especially fat, overeating - lead to disturbances in the system of proteolytic enzymes and their inhibitors. With age, the activity of inhibitors decreases, which, with provocative moments (overeating, diet violations), leads to activation of the trypsin gene - a metabolic theory. Hence the name OP - "the disease of gluttons", the disease of "well-fed life." During the war years, during the Leningrad blockade, there were almost no pancreatitis; they appeared after the blockade was broken, primarily among the suppliers, head. canteens.
4/ Circulatory disorders in the gland, ischemia of the organ, most often due to atherosclerotic changes, hypertension, diabetes, alcoholism, also lead to imbalance in the "enzyme-inhibitor" system. In pregnant women, circulatory disorders may be associated with the pressure of the pregnant uterus on the vessels. - vascular theory.
5/ Food and chemical poisoning - alcohol, acids, phosphorus, drugs (tetracycline series, steroid hormones), helminthic infestations also contribute to the activation of enzymes - toxic theory.
6 / General and local infection, especially of the abdominal cavity - biliary tract, with peptic ulcer, especially with penetration of ulcers - infectious theory.
7/ Injuries of the pancreas - directly with wounds, blunt trauma, as well as operating room (during operations on the duodenum, biliary tract) can also lead to acute pancreatitis. The frequency of postoperative pancreatitis reaches 6 - 12% (Zhidkov, Tkachenko) - a traumatic theory.
8 / Allergic theory - especially a large number of supporters has in recent years. When using various serological reactions in patients with OP, many researchers found antibodies to the pancreas in the blood serum, which indicates autoaggression.
Almost more often there is a combination of several of the listed causes with the prevalence of any, so acute pancreatitis should be considered a polyetiological disease.
According to the nature and degree of changes in the pancreas, 4 forms of acute pancreatitis are distinguished:
I/ catarrhal - acute pancreatic edema -78%
2/ hemorrhagic - hemorrhagic impregnation
3/ necrotic - nested or total necrosis - 12%
4/ purulent - abscess formation or complete purulent fusion of the gland -10%.
The first 2 forms usually correspond to the 1st phase of the process flow, the second two - to the second phase.
It is very diverse depending on the form of the lesion, the localization of the process, the reactivity of the organism.
I/ Pain - in localization correspond to the location of the pancreas - in the epigastrium (99 - 100%); radiate more often to the back (48%), more to the left (68%), with cholecystopancreatitis - to the right; shingles (50%), There may be irradiation to the region of the heart, simulating angina pectoris and even a heart attack, Usually the pain is intense, sometimes very intense, begins suddenly. The intensity of pain does not always correspond to the degree of damage to the pancreas, with pancreatic necrosis there is a tendency to reduce the intensity of pain.
2/ Vomiting is an almost constant symptom, appears after the onset of pain and does not relieve them, repeated (82%), does not bring relief. Belching is observed in 75% of cases.
3 / Delay in the passage of gases and feces, bloating as a result of paralytic obstruction (center in the zone n. splanchnici).
4/ Pallor or yellowness of the skin (mechanical or toxic jaundice).
5/ B severe cases- cyanosis - (cyanosis of the face - Mondor's symptom, navel - Kulen's symptom, lateral parts of the abdomen - Gray-Turner) - as a result of the action of proteolytic enzymes on the vascular wall and pulmonary insufficiency).
6/ Tongue - lined, dry.
7/ The smell of acetone from the mouth.
8/ Body temperature is normal or subfebrile, subnormal in severe cases.
9/ BP at first normal, in severe cases reduced, up to collapse.
10/ Pulse - first bradycardia, then tachycardia, weak filling,
II / Psycho-somatic disorders - delirium (differentiate with delirium alcoholic!!!).
12/ Decreased diuresis, up to acute renal failure; other signs of PON.
13/ In the anamnesis - errors in the diet - fatty foods, alcohol, food poisoning, as well as cholecystitis, peptic ulcer, gastritis, pregnancy.
Examination of the abdomen: I / bloating, more in the epigastrium - swollen transverse colon (Bondé's symptom), often simulates intestinal obstruction,
2/ cyanosis of the umbilical region - Kulen's symptom, lateral sections - Gray-Turner's symptom (7%).
3/ Palpation is painful in the projection of the pancreas, muscle tension is insignificant or absent (retroperitoneal location). Soreness of the point under the xiphoid process (symptom Kamenchik), 6-7 cm above the navel - a symptom of Kerte. Soreness in the left costovertebral angle - a symptom of Mayo-Robson,
4/ Absence of pulsation of the aorta during palpation in the projection of the pancreas - a symptom of Voskresensky.
5 / Peritoneal phenomena are absent at first, when the process goes beyond the omental bag, they are positive throughout the abdomen.
5 / Dullness in the lateral parts of the abdomen - with peritonitis.
7/ Disappearance of peristaltic noises "silent belly"
8/ Symptoms of PON.
Additional Research
I/ Complete blood count - high hematocrit (hemoconcentration), leukocytosis, shift to the left, increased ESR.
2/ Serum amylase is increased (more than 7 mg/s/l), absent in pancreatic necrosis.
3/ Amylase (diastase) urine more than 26 mg/s/l.
4/ Blood transaminases are elevated, which is very characteristic (ASAT more than 125, ALAT more than 189).
5/ Bilirubin (norm up to 20.5 mg/l); sugar more than 5.5 mmol / l, 6 / Urea and residual nitrogen in the blood - increased.
7/ Heminic compounds in serum are sharply increased (up to 30-40 units at N - 9 - II),
8/ Prothrombin index - increased especially in the elderly,
9/ Blood calcium decreases (N 2.24 - 2.99 mmol / l), especially in severe forms,
10/ Ionogram - decrease in K, chlorides,
II / Analysis of peritoneal exudate - an increase in the content of amylase,
12/ X-ray examinations: a/ increase in the shadow of the pancreas (soft rays) - a direct sign b/ deployed horseshoe duodenum c/ reactive effusion in the sinus, d/ distension of the transverse colon, ^ indirect e/ limitation of diaphragm mobility, / signs e/ blurring contours of the left.b.clar.muscle (symptom of Pchelkina)
13 / Ultrasound diagnostics - changes in the size of the gland, its departments (currently considered the leading additional study).
14/ Computed tomography (if possible).
15/ Laparocentesis with the study of the contents of the abdominal cavity for enzymes.
16/ Laparoscopy - spots of stearic necrosis, bile impregnation, exudate for enzymes. The differential diagnosis is carried out with acute gastritis, food poisoning, ulcer perforation, intestinal obstruction, thrombosis of mesenteric vessels, myocardial infarction, ectopic pregnancy.
With the correct diagnosis, only about a third of patients enter the hospital.
Acute pancreatitis is an acute aseptic inflammation of the pancreas of the demarcation type, which is based on necrobiosis of pancreatocytes and enzymatic autoaggression, followed by necrosis and dystrophy of the gland and the addition of a secondary purulent infection.
Etiology and pathogenesis of acute pancreatitis
Acute pancreatitis is a polyetiological disease. Predisposing factors primarily include features of the anatomical structure of the pancreas and a close relationship with biliary excretory system. Anomalies of development, narrowing of the ductal system of the gland, impaired innervation, and compression by neighboring organs are also important. An important role is played by systematic overeating, the abuse of plentiful, especially fatty, meat and spicy foods in combination with the intake of alcoholic beverages. The effect of alcohol on the pancreas is complex and consists of several components: increased pancreatic secretion, impaired patency of the pancreatic duct due to edema of the mucous membrane of the duodenum and major duodenal papilla, which leads to increased pressure in the pancreatic ducts. The most common cause of acute pancreatitis is cholelithiasis. The presence of stones in the bile ducts or gallbladder is detected in 41-80% of patients with pancreatitis.
The explanation for this was given back in 1901 by Opie. The theory of the “common channel” developed by him explains the development of pancreatitis in cholelithiasis by the possibility of bile reflux into the pancreatic ducts in the presence of calculi in the common ampulla for the pancreatic duct and the common bile duct.
Currently, most scientists adhere to the enzymatic theory of the pathogenesis of acute pancreatitis.
Acute pancreatitis is characterized by a phase development of a local pathological process. With progressive forms of pancreatitis, the initial phase of serous and then hemorrhagic edema is replaced by a phase of parenchymal and fatty necrosis, after which the phase of melting and sequestration of dead areas of the pancreas and retroperitoneal fat begins. Thus, these three phases create three periods of development of the disease.
Classification of acute pancreatitis
Forms of acute pancreatitis: I. Edema (interstitial) pancreatitis.
II. Pancreatic necrosis sterile
by the nature of the necrotic lesion: fatty, hemorrhagic, mixed;
according to the prevalence of the lesion: small-focal, large-focal, subtotal;
by localization: capitate, caudal, with lesions of all parts of the pancreas.
III. Infected pancreatic necrosis. Complications of acute pancreatitis: 1. Parapancreatic infiltrate. 2. Pancreatic abscess. 3. Peritonitis: enzymatic (abacterial), bacterial. 4. Septic phlegmon of retroperitoneal tissue: parapancreatic, paracolic, pelvic. 5. Arosive bleeding. 6. Mechanical jaundice. 7. Pseudocyst: sterile, infected. 8. Internal and external digestive fistulas.
Stages of development of destructive pancreatitis
1) Stage of hemodynamic disorders and pancreatogenic shock- begins with the onset of the disease and lasts 3-5 days; at this time, the symptoms of enzymatic toxemia, excessive formation and accumulation of biologically active substances in the blood (various kinds of kinins, breakdown products of protein bodies) in the gland itself and the surrounding cellular space prevail; 2) Stage of functional insufficiency of internal organs when it is during this period of the clinical course of pancreatic necrosis that local signs of the disease are most pronounced, although symptoms of multiple organ failure predominate, which mainly depends on the area of the pancreas lesion (starts from the third day); 3) Stage of local complications- parapancreatic infiltrate, "immature" pseudocyst of the pancreas, abscess or phlegmon of the gland or retroperitoneal tissue, subphrenic abscess or widespread purulent peritonitis.
Phases of the course of acute destructive pancreatitis
Acute destructive pancreatitis has a phase course, and each of its phases corresponds to a certain clinical form. I phase - enzymatic, the first five days of the disease, during this period there is the formation of pancreatic necrosis of various lengths, the development of endotoxicosis (the average duration of hyperenzymemia is 5 days), and in some patients, multiple organ failure and endotoxin shock. The maximum period for the formation of pancreatic necrosis is three days, after this period it does not progress further. However, in severe pancreatitis, the period of formation of pancreatic necrosis is much shorter (24-36 hours). It is advisable to distinguish two clinical forms: severe and non-severe acute pancreatitis.
Heavy acute pancreatitis. The frequency of occurrence is 5%, lethality is 50-60%. The morphological substrate of severe acute pancreatitis is widespread pancreatic necrosis (large-focal and total-subtotal), which corresponds to severe endotoxicosis.
Not heavy acute pancreatitis. The incidence rate is 95%, lethality is 2-3%. Pancreatic necrosis in this form of acute pancreatitis either does not form (pancreatic edema), or is limited and does not spread widely (focal pancreatic necrosis - up to 1.0 cm). Mild acute pancreatitis is accompanied by endotoxicosis, the severity of which does not reach a severe degree.
II phase - reactive(2nd week of the disease), characterized by the reaction of the body to the formed foci of necrosis (both in the pancreas and in the parapancreatic tissue). The clinical form of this phase is a peripancreatic infiltrate. III phase - meltdown and sequestration(starts from the 3rd week of the disease, can last several months). Sequesters in the pancreas and retroperitoneal tissue begin to form from the 14th day from the onset of the disease. There are two possibilities for this phase:
aseptic melting and sequestration- sterile pancreatic necrosis; characterized by the formation of postnecrotic cysts and fistulas;
septic meltdown and sequestration- infected pancreatic necrosis and necrosis of parapancreatic tissue with further development of purulent complications. The clinical form of this phase of the disease is purulent-necrotic parapancreatitis and its own complications (purulent-necrotic swells, abscesses of the retroperitoneal space and abdominal cavity, purulent omentobursitis, purulent peritonitis, arrosive and gastrointestinal bleeding, digestive fistulas, sepsis, etc.) .
- Dignities and clothes of Orthodox priests and monasticism
- Healers and fortune tellers - why do people go to them?
- During confession. Preparing for confession. List of sins for confession. How to dress for confession
- Praise of the Most Holy Theotokos Praise of the Mother of God with an akathist what they pray for