The complex of symptoms of severe inflammation in the abdominal area is often called Mondor's triad, in honor of the French surgeon. The disease is relatively rare, but doctors should be able to easily determine the type of ailment. With this description, a developed perforation of internal organs is assumed, also called a perforated ulcer. Problem organs are the stomach or duodenum.

What do the symptoms include?

Mondor's triad is described as a collection of acute conditions in the upper abdomen. A French surgeon examined critical conditions of patients requiring urgent resuscitation. You cannot hesitate in such cases; we are talking about saving a person’s life.

Mondor's triad in the works of a practicing surgeon-researcher (1885-1962) includes 3 types of clinical symptoms:

1. Acute unbearable malaise does not go away. There is also a discrepancy between the pulse and body temperature.
2. The effect of the platform in the abdominal area, a constrained state. Spasms often prevent you from breathing normally.
3. Symptoms of illness that accurately indicate the problem area - the stomach or duodenum.

Mondor's triad allows doctors to more accurately diagnose gastric ulcers. Based on clinical symptoms, they immediately proceed to surgical intervention, which reduces the time required to search for the causes of the ailment. Surgeons begin assistance immediately without additional tests.

Additional signs of illness

Mondor's triad is unstudied in relation to the formation of a critical condition in a patient. Scientists make only assumptions. The leading point of view is about disruption of the immune system, as a result of which the ulcerative process starts.

The formation of perforation can be easily confused with other complications with similar symptoms:

• developed cholecystitis;
• intestinal obstruction;
• renal colic;
• appendicitis.

If one of the listed complications is detected, a diagnosis of Mondor's triad is performed. If the latter condition occurs, the patient is urgently sent to the clinic. During the transportation process, situations requiring human rescue often arise. Therefore, the patient is carefully monitored in the ambulance.

Men are more prone to perforation, and the disease appears in an absolutely healthy person for no apparent reason. Complications are distinguished according to the location of the ailment: in the abdominal cavity, free area, damage to the walls of the stomach, retroperitoneal space.

Diagnosis of illness

During a differentiated examination, the listed complications are determined based on the studied symptoms. Thus, acute cholecystitis is determined by the initial signs: pain in the upper part of the stomach, which often radiates to the right upper part of the body. A sick person has a high body temperature and continues to vomit until bile is released. However, in the early stages, thickening of the abdominal wall muscles cannot be felt.

The symptom of acute pancreatitis has periodic repetitions. Vomiting and girdle pain are observed. The muscles are relaxed, the patient feels discomfort in the kidneys. With this complication, surgical intervention is not required; treatment is carried out with medication.

Intestinal obstruction is characterized by bloating of the abdomen and lower sections. There is a lack of feces and colic due to the accumulation of gases. Pain appears and disappears randomly.

Appendicitis occurs with sharp and dull pain on the right side. The elevated body temperature does not subside; when palpating the abdomen, the patient feels lumbago. The abdominal muscles are tense. Renal colic is comparable in symptoms to obstruction, but the patient experiences frequent bowel movements and vomiting.

Description of the development of clinical signs

Forms suddenly. It all starts with unbearable pain, which is difficult for even an adult man to endure. At this moment, any movement immediately affects the nerve endings, the abdominal muscles are overstrained, and the person is immobilized. Vomiting and severe weakness occur for about 6 hours, then it may improve. But not for long, after 12 hours everything repeats itself.

The calm phase often passes. If the attack occurs again, it will be difficult to help the patient on the road. The stage of inflammation is defined as peritonitis. The task of medical personnel is to overcome the consequences of such a complication.

Reasons for the development of critical condition

Mondor's triad in pancreatitis appears due to destruction in the walls of the internal organs of the digestive system. Peaks of inflammatory processes occur in the off-season. Ulcerative formations are considered to be the main sources of perforation.

The provocateurs of such conditions are:

• The walls of the internal organs suffer from increased intra-abdominal pressure due to injuries and physical training.
• An ulcer appears due to stress and psychological stress.
• Indigestion begins from hunger and poor nutrition.
• Medicines can thin the walls of the intestines and stomach.

How to deal with complications?

Acute perforation conditions, such as peritonitis, are managed in the operating room. The main task is to shorten the gap between the onset of an attack and the provision of first aid as quickly as possible. The most dangerous moments are when transportation to the hospital takes more than 3 hours.

The trapped contents are removed through the perforations using a special probe. It is strictly forbidden to rinse the stomach and move the patient under his own power. He is taken to the clinic on a stretcher. The surgeon needs complete information from emergency personnel about first aid procedures.

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 degeneration 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 connection with biliary system. Developmental anomalies, narrowing of the ductal system of the gland, disruption of innervation, and compression by neighboring organs are also important. An important role is played by systematic overeating, abuse of abundant, especially fatty, meat and spicy foods in combination with drinking alcoholic beverages. The effect of alcohol on the pancreas is complex and consists of several components: increased pancreatic secretion, disruption of the patency of the pancreatic duct due to edema of the mucous membrane of the duodenum and large duodenal nipple, 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.

An explanation for this was given back in 1901 by Opie. The “common channel” theory he developed explains the development of pancreatitis in cholelithiasis by the possibility of reflux of bile into the pancreatic ducts in the presence of stones in the ampulla common to 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 phase development of the 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 fat necrosis, after which the phase of melting and sequestration of dead areas of the pancreas and retroperitoneal tissue begins. Thus, these three phases create three periods of disease development.

Classification of acute pancreatitis

Forms of acute pancreatitis: I. Edematous (interstitial) pancreatitis.

II. Pancreatic necrosis sterile

by the nature of the necrotic lesion: fatty, hemorrhagic, mixed;

according to the extent of the lesion: small-focal, large-focal, subtotal;

by localization: capitate, caudal, with damage to 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 the retroperitoneal tissue: parapancreatic, paracolic, pelvic. 5. Arosive bleeding. 6. Obstructive jaundice. 7. Pseudocyst: sterile, infected. 8. Internal and external digestive fistulas.

Stages of development of destructive pancreatitis

1) Stage of hemodynamic disturbances and pancreatogenic shock– begins from the onset of the disease and lasts 3-5 days; at this time, symptoms of enzymatic toxemia, excessive formation and accumulation in the blood of biologically active substances (various kinds of kinins, breakdown products of protein bodies) in the gland itself and the surrounding fiber space prevail; 2) Stage of functional failure of internal organs when it is during this period of the clinical course of pancreatic necrosis that local signs of the disease are most clearly expressed, although symptoms of multiple organ failure predominate, which mainly depends on the area of ​​damage to the pancreas (starts from the third day); 3) Stage of local complications- parapancreatic infiltrate, “immature” pancreatic pseudocyst, abscess or phlegmon of the gland or retroperitoneal tissue, subphrenic abscess or widespread purulent peritonitis.

Phases of acute destructive pancreatitis

Acute destructive pancreatitis has a phase course, and each phase corresponds to a specific clinical form. Phase I - enzymatic, the first five days of the disease, during this period the formation of pancreatic necrosis of varying extent, the development of endotoxemia (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, with 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 incidence is 5%, mortality 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 is 95%, mortality is 2-3%. Pancreatic necrosis in this form of acute pancreatitis either does not form (swelling of the pancreas) or is limited in nature and does not spread widely (focal pancreatic necrosis - up to 1.0 cm). Non-severe acute pancreatitis is accompanied by endotoxemia, the severity of which does not reach a severe degree.

Phase II - reactive(2nd week of the disease), is characterized by the body’s reaction to the formed foci of necrosis (both in the pancreas and in the parapancreatic tissue). The clinical form of this phase is peripancreatic infiltrate. Phase III - melting 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 possible options for the course of 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 leaks, abscesses of the retroperitoneal space and abdominal cavity, purulent omentobursitis, purulent peritonitis, arrosive and gastrointestinal bleeding, digestive fistulas, sepsis, etc.) .

Pancreatitis occurs in three forms - acute, reactive and chronic. The most severe and serious form of the disease is acute, in which the disease develops rapidly and is complex. The causes of such pancreatitis are self-digestion of the pancreas, caused by the closure of the lumen of the gland or its spasm (sharp narrowing).

Most often, symptoms appear unexpectedly and are acute. The first thing patients complain about is severe pain in the pit of the stomach, in the right and left hypochondrium. The main symptoms of this period are vomiting of undigested gastric contents and flatulence. The combination of these three components in medicine is called Mondor's triad (a characteristic feature of pancreatitis). The pain is girdling in nature, pressure is felt at a level slightly above the navel (at the level of the pancreas). Most often, pain appears either in the evening or when the diet is not followed. The intensity of the pain does not subside; with prolonged severe pain, patients may lose consciousness. The pain reaches its greatest intensity in the midline of the abdomen, and then spreads throughout the entire abdomen. Radiation of pain is typical in the lower back, chest, hypochondrium. If the head of the pancreas is affected, then the symptoms resemble acute cholecystitis; if the body of the pancreas is affected, gastric diseases are observed; if the tail is affected, cardiac and renal pathologies are observed. Therefore, differential diagnosis is important in acute pancreatitis. In some situations, pancreatitis can give symptoms of shock - cold sweat, drop in blood pressure, tachycardia and a weak thread-like pulse. At the beginning of the process, the temperature may rise to high levels, after which a low-grade fever persists. Patients with pancreatitis are restless, often overly nervous, and ask for painkillers. In acute pancreatitis, cyanotic spots appear on the patient’s face and abdomen (in some cases, hyperemia)

Treatment of acute pancreatitis can be either conservative or surgical.

Both treatment tactics are characterized by several stages: 1. elimination of pain, 2. blood purification, 3. strict gentle diet, 4. treatment of symptoms of pancreatitis.

To relieve pain, both non-narcotic drugs and narcotic drugs (in especially severe cases) are used.

To cleanse the blood, infusion therapy is used - solutions are introduced that dilute the blood and thus lower the level of pancreatic enzymes in the blood. Pancreatic enzymes can be neutralized in patients using the drugs Trasylol, Gordox or Contrical.

To ensure rest for the pancreas, you need to fast for the first time and drink only water. The body's nutritional needs are met by administering special solutions intravenously. Throughout the fast, the body will be supported in this way. Typically, fasting is prescribed for three to six days, and then the patient is allowed to consume liquid food in small quantities.

To alleviate symptomatic signs, medications are given that suppress the gag reflex (especially if vomiting does not stop), increase the level of calcium in the blood, etc.

In some cases, the affected organ may become infected. To prevent this from happening, it is necessary to prescribe a course of antibiotics for the purpose of prevention.

Typically, conservative therapy is followed for about a week (unless urgent surgery is necessary). If the situation improves, treatment is continued further, and if the above methods do not help, then surgery is performed - laparotomy to remove the necrotic parts of the pancreas. The operation is performed under general anesthesia.

Surgical treatment of pancreatitis is used for necrotic pancreatitis or for serious complications (peritonitis, abscess, septic phlegmon). The nature of the operation can be organ-preserving (removing a necrotic part of an organ) or resection (complete removal of the pancreas). Confinement in a medical facility takes up to three weeks.

After removal of the pancreas or partial removal of one area, the patient must remember that he should then take enzymatic preparations, which to some extent will replace the functions of the pancreas. It is also worth remembering that without a pancreas, diabetes mellitus can develop - this situation is subject to medical control. Further nutrition is gentle, without foods that cause stress on the gastrointestinal tract.

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Clinical examination

The main symptoms of acute pancreatitis are: pain, vomit And flatulence(Mondor triad).
Pain appears suddenly, often in the evening or at night, shortly after an error in the diet (consumption of fried or fatty foods, alcohol). Its most typical location is the epigastric region, above the navel, which corresponds to the anatomical location of the pancreas. The epicenter of pain is located in the midline, but can shift to the right or left of the midline and even spread throughout the abdomen. Usually the pain radiates along the costal edge towards the back, sometimes to the lower back, chest and shoulders, to the left costovertebral angle. Often they are encircling in nature, which creates the impression of a tightening belt or hoop. If the head of the pancreas is predominantly affected, the localization of pain may resemble acute destructive cholecystitis; if its body is affected, it may resemble diseases of the stomach and small intestine; and if the tail is affected, it may resemble diseases of the spleen, heart, and left kidney. In some situations, severe pain is accompanied by collapse and shock.

Almost simultaneously with the pain, repeated, painful and non-relieving pain appears. vomit. It is provoked by eating or drinking water. Despite the repeated nature of vomiting, the vomit never has a stagnant (fecaloid) character.

The body temperature at the onset of the disease is often subfebrile. Hectic fever indicates the development of common sterile and various infected forms of pancreatitis. Based on the severity of the symptoms of a systemic inflammatory reaction, one can only roughly judge the nature and prevalence of the destructive process.

Cyanosis of the face and extremities is considered an important and early diagnostic sign of pancreatic necrosis. Cyanosis in the form of purple spots on the face is known as Mondor's sign, cyanotic spots on the lateral walls of the abdomen (peri-umbilical ecchymoses) - how Gray-Turner sign, and cyanosis of the peri-umbilical region - Grunwald's sign. In the later stages of the disease, cyanosis of the face may be replaced by bright hyperemia - "kallikrein face". The listed symptoms are based on rapidly progressing hemodynamic and microcirculatory disorders, hyperenzymemia and uncontrolled cytokinesis.

When examining the abdomen, note it bloating, mainly in the upper sections. With widespread pancreatic necrosis, the abdomen is evenly swollen and sharply sensitive even on superficial palpation. With deep palpation, the pain increases sharply and is sometimes unbearable. When palpating the lumbar region, especially the left costovertebral angle, sharp pain occurs ( Mayo-Robson sign). In the area of ​​increased sensitivity, detected during superficial palpation, rigidity of the muscles of the anterior abdominal wall is revealed, which indicates the presence of pancreatogenic effusion, rich in enzymes, and the phenomena of pancreatogenic peritonitis. Transverse painful resistance of the anterior abdominal wall in the projection of the pancreas is often observed ( Kerthe's sign).

One of the signs of destructive pancreatitis is the phenomenon of absence of pulsation of the abdominal aorta due to an increase in the size of the pancreas and edema of the retroperitoneal tissue - Voskresensky's symptom.

When the process is localized in the omental bursa, muscle tension is detected mainly in the epigastric zone; when inflammation spreads beyond its limits (to the pericolic and pelvic tissue, as well as to the peritoneum), pronounced muscle tension and positive Shchetkin-Blumberg symptom. It must be remembered that when the necrotic process is localized in the tail of the pancreas, the symptoms of peritoneal irritation may be mild, which is associated with the predominantly retroperitoneal localization of the process and the absence of peritonitis. When the head is affected, the rapid development of jaundice syndrome and gastroduodenal paresis is typical.

Dullness of percussion sound in sloping areas of the abdomen indicates the presence of effusion in the abdominal cavity. Auscultation of the abdomen reveals weakening or absence of bowel sounds due to the development of paralytic ileus and pancreatogenic peritonitis.

Laboratory diagnostics

The main manifestation of acute pancreatitis is functional disorders of the pancreas, in particular hyperenzyme phenomenon . This feature of the pathogenesis of acute pancreatitis has been traditionally used for many decades in differential diagnosis with other emergency diseases of the abdominal organs. Determination of amylase activity in blood plasma (less commonly, lipase, trypsin, elastase) is a diagnostic standard. The most common in clinical practice is the determination of amylase and lipase activity in the blood. An increase in the activity of total and pancreatic amylase by 4 times and lipase by 2 times relative to the upper limit of normal indicates the phenomenon of pancreaostasis.

The maximum values ​​of serum amylase activity are typical for the first day of the disease, which corresponds to the period of hospitalization in the majority of patients with acute pancreatitis. Determination of lipase activity in the blood is a significant diagnostic test at a later date from the onset of the disease, since its activity in the blood of a patient with acute pancreatitis persists for a longer time than the values ​​of amylasemia. This phenomenon determines the higher sensitivity and specificity of the lipase test relative to the amylase test.

In domestic clinical practice, the determination of amylase in urine is traditionally used. An additional test is the study of amylase activity in peritoneal exudate during laparoscopy (laparocentesis). When using the Wolgemut method (determining the total amylolytic activity of urine), according to which the normal activity of amylase in urine is 16-64 units, one can detect various levels of its increase - 128-1024 units. and more. The Wohlgemuth method is not specific enough for pancreatic α-amylase, since it reflects the total activity of glycolytic enzymes contained in the biological medium sent for research.

Determination of trypsin and elastase activity in the blood in the diagnosis of acute pancreatitis has less clinical use than laboratory monitoring of amylase (lipase) due to the labor-intensive and expensive methods.

Hypreamylasemia in the dynamics of the disease, it is an important marker of preserved pancreatic function in conditions of pancreaostasis, which is typical for interstitial pancreatitis or focal (capitate) pancreatic necrosis in the first days of the disease. Dysfermentemia(violation of the ratio of amylase and blood lipase) indicates pancreatic necrobiosis, while the normal level of amylase in the blood, hypoamylasemia(and even afermentemia) are most characteristic of pancreatic necrosis, indicating the widespread nature of the destruction of the pancreas and the loss of its excretory function.

There is no direct relationship between the level of amylasemia (amylasuria), the prevalence and form of pancreatic necrosis (interstitial, fatty, hemorrhagic). The results of studies of the enzyme spectrum of blood should always be considered only in conjunction with data from other clinical, laboratory and instrumental methods of examining a patient with acute pancreatitis.

Changes in clinical blood tests in acute pancreatitis do not have strict specificity. In this regard, the significant difficulties in laboratory differential diagnosis of aseptic and infected forms of pancreatic necrosis are widely known, which is extremely important from the standpoint of timely surgical treatment. An increase in these indicators in the dynamics of the disease by more than 30% of the initial level, together with other clinical and laboratory data, reliably confirms the development of a pancreatogenic infection, but, as a rule, 2-3 days remain missed. The most convincing evidence in favor of the infected nature of pancreatic necrosis is the threshold numbers of blood leukocytes above 15x10 9 / l and the leukocyte intoxication index of more than 6 units.

Indirect signs infections are considered thrombocytopenia, anemia And acidosis, they must be taken into account in the totality of clinical and instrumental data.

Biochemical changes in the blood indicate the development of hyper- and dysmetabolism syndrome, which is most pronounced in destructive forms of pancreatitis. In these situations, the most significant changes in the biochemical spectrum of blood are dysproteinemia, hypoprotein and hypoalbuminemia, hyperazotemia and hyperglycemia. Persistent hyperglycemia indicates extensive necrosis of the pancreas, and its value more than 125 mg/dl (7 mmol/l) is an unfavorable prognostic factor. In the blood lipid spectrum, hypertriglyceridemia, hypocholesterolemia, deficiency of high-density lipoproteins, and an increase in the concentration of fatty acids are recorded.

C-reactive protein along with haptoglobin and α 1 -antitrypsin - a protein of the acute phase of inflammation. In acute pancreatitis, a C-reactive protein content of more than 120 mg/l in the patient’s blood indicates necrotic damage to the pancreas. The concentration of C-reactive protein reflects the severity of the inflammatory and necrotic processes, which allows this test to be used to determine, on the one hand, edematous pancreatitis or pancreatic necrosis, and on the other, the sterile or infected nature of the necrotic process.

Application procalcitonin test in various forms of acute pancreatitis showed that in patients with infected pancreatic necrosis the concentration of procalcitonin is significantly higher than in a sterile destructive process.

The threshold for widespread pancreatic necrosis is considered to be a concentration of C-reactive protein of more than 150 mg/l, and of procalcitonin - more than 0.8 ng/ml. A common pancreatogenic infection is characterized by concentrations of C-reactive protein in the patient’s blood greater than 200 mg/l and procalcitonin greater than 2 ng/ml.

Among other biochemical markers characterizing the severity of acute pancreatitis, promising studies are the catalytic activity of phospholipase A 2, trypsinogen, urotrypsinogen-2, trypsin-activated peptide, pancreatitis-associated protein, interleukins 1, 6 and 8, tumor necrosis factor and neutrophil elastase. It has been established that the concentration of trypsin-activated peptide in the urine correlates with the concentration of C-reactive protein and interleukin 6. The concentration of this metabolite in the peritoneal fluid is directly proportional to the degree of pancreatic necrosis.

Despite the fact that the content of most biochemical substances sharply increases in the blood of patients with pancreatic necrosis already in the short term (24-48 hours) from the onset of the disease, the use of these markers in the clinical practice of emergency surgery is limited by the high cost of the techniques and the lack of a reliably known minimum threshold level. Determining the concentration of C-reactive protein in any biochemical laboratory seems to be a kind of compromise in the current material and technical conditions.

Hemoconcentration most typical for destructive forms of acute pancreatitis. A hematocrit of more than 47% at the time of hospitalization of the patient and the absence of its decrease within 24 hours of intensive care indicates the development of pancreatic necrosis.

Study of the spectrum of liver enzymes in patients with acute pancreatitis, complicated by the development of hepatic cell failure, characteristic of pancreatic necrosis, allows us to detect high activity of alanine and aspartic aminotransferases. A significant increase in lactate dehydrogenase activity reflects large-scale damage to pancreatic cells. From the standpoint of differential diagnosis, it must be remembered that similar changes are characteristic of acute myocardial infarction, extensive intestinal infarction and hepatitis of various etiologies.

In biliary pancreatitis due to choledocholithiasis, as well as with predominant damage to the head of the pancreas, cholestasis syndrome is characteristic, expressed by hyperbilirubinemia with a predominance of the direct (bound) bilirubin fraction, high activity of aspartate amine transferase and alkaline phosphatase.

ABOUT pronounced changes in water-electrolyte balance indicate hemoconcentration, deficiency of potassium, sodium, calcium. At common forms of pancreatic necrosis a decrease in the concentration of calcium in the blood plasma is due to its deposition in the foci of steatonecrosis in the form of bile salts.

B.C. Savelyev, M.I. Filimonov, S.Z. Burnevig

For quotation: Luzganov Yu.V., Ostrovskaya N.E., Yagubova V.A., Shkirya K.S. Differential diagnosis and principles of treatment of various forms of pancreatitis and pancreatic necrosis // RMZh. 2005. No. 27. S. 1842

Currently, in the structure of emergency surgical pathology, there is a tendency towards an increase in the number of acute pancreatitis, including destructive and complicated forms. Acute pancreatitis is the most severe and costly pathology of emergency surgery. Inflammatory and necrotic processes vary from interstitial pancreatitis to the development of complicated forms of sterile and infected pancreatic necrosis.

Infected pancreatic necrosis is the most dangerous complication of this pathology, the mortality rate of which reaches 40% [B.R. Gelfand, F.I. Filimonov, 2002]. Destructive forms of pancreatitis develop in 30% of patients with inflammation of the pancreas [V.K. Gostishchev, V.A. Glushko, 2003]. Pancreatic necrosis with the addition of infection is a substrate for the development of purulent complications, such as pancreatogenic abscess, retroperitoneal phlegmon, purulent peritonitis. Despite the prevalence of the disease, there are still many controversial issues in treatment tactics: there is no unified concept regarding the indications and scope of surgical treatment, and there are no generally accepted conservative treatment regimens.
Materials and methods
During the period from January 2002 to December 2004, 89 patients with various forms of pancreatitis were treated at the Main Clinical Hospital of the Ministry of Internal Affairs of the Russian Federation. The average age was 34 years, the majority of patients were men (84%), women – 16%.
Upon admission to the hospital, all patients underwent the following studies:
l a-pancreatography with intravenous contrast using CT - on the 1st and 5th day. The size of the pancreas, the degree of change in perfusion and the depth of tissue damage, the state of parapancreatic tissue, the presence of fluid in the pleural cavities, and the presence and location of fluid collectors in the free abdominal cavity were assessed.
The probability of infection was assessed by the decrease in echogenicity of the signal and fluid density in fluid formations.
l Dynamic ultrasound of the abdominal cavity (also from the first day) was performed to assess the condition of the abdominal organs and timely detect biliary hypertension, determine the size of the pancreas and its structural changes.
Laboratory diagnostics do not have strict specificity for verifying the stage of the disease. As M. Sashi points out: “If in the future someone proposes a system capable of distinguishing between edematous and necrotizing forms of acute pancreatitis based on one or more laboratory parameters, this will mean a solution to the classification problem.” Nevertheless, in the first 48 hours from the onset of the disease, strict laboratory monitoring of indicators specific to this pathology is carried out: blood amylase; urine diastasis; leukocytes, formula; bilirubin and its fractions; transaminases; hemoglobin, hematocrit; blood glucose, total protein, fractions; electrolytes. The only objective criterion for the level of pancreatic damage was computed tomography data.
Many classifications of acute pancreatitis have been proposed, reflecting anamnestic data, morphological changes in the pancreas and parapancreatic tissue, the level of metabolism, the degree of compensation of the cardiovascular and respiratory systems of the body.
We based the classification of patients with acute pancreatitis on morphological changes in the pancreas and the presence of complications. According to this principle, patients were divided into three groups:
1. Interstitial pancreatitis – 41%.
2. Destructive – 38%:
- aseptic uncomplicated pancreatic necrosis – 23%;
- aseptic complicated pancreatic necrosis (pancreatogenic peritonitis, reactive pleurisy, parapancreatitis) – 15%.
3. Infected pancreatic necrosis – 21%.
This classification was the basis for the principles of therapy and determined various treatment tactics for patients in the above groups.
Interstitial pancreatitis
The clinical picture was characterized by an acute onset, lasting 24-48 hours from the onset of the disease, Mondor's triad (pain, vomiting, flatulence), hemodynamic disorders: arterial hypertension, tachycardia. Laboratory tests showed hemoconcentration, leukocytosis without a shift of the leukocyte formula to the left, increased blood amylase and urine diastase, no electrolyte disturbances were noted, the levels of bilirubin, creatinine, and urea nitrogen were within normal limits, the level of transaminases was increased 2-3 times.
According to CT data on the first day: swelling and an increase in the size of the pancreas (15-30%) were noted without signs of destruction of glandular tissue and parapancreatic tissue, the absence of fluid collectors in the free abdominal cavity and fluid in the pleural cavities. According to ultrasound data, the sizes of the head, body and tail of the pancreas were increased, swelling of the parapancreatic tissue was noted, and there were no signs of biliary hypertension.
Destructive pancreatitis
Aseptic small-focal uncomplicated: It was distinguished by the appearance of foci of destruction of pancreatic tissue.
Clinically, an acute onset, disease duration of more than 48 hours, Mondor's triad, arterial hypertension, tachycardia, and hyperthermia of a predominantly hectic nature were noted. Laboratory parameters were characterized by the presence of hemoconcentration, leukocytosis with a moderate shift of the leukocyte formula to the left, increased amylasemia, diastasuria, while the level of bilirubin, nitrogenous wastes, and electrolytes remained within normal limits.
According to CT data, on the first day there was also an increase in the size of the pancreas, swelling and infiltration of the parapancreatic tissue, significant accumulations of fluid in the retroperitoneal tissue, the abdominal cavity was not detected, and no fluid was noted in the pleural cavities. According to ultrasound data, a picture of acute destructive pancreatitis was observed with foci of destruction mainly in the area of ​​the head and (or) body of the pancreas. There are no signs of biliary hypertension.
Aseptic small-focal complicated pancreatic necrosis: accompanied by the addition of reactive changes in the abdominal and pleural cavities, parapancreatic tissue. (pancreatogenic peritonitis, reactive pleurisy, parapancreatitis). The clinical picture was characterized by a duration from the onset of the disease of more than 48-72 hours, the presence of Mondor's triad, hemodynamic changes: arterial hypotension, tachycardia. Laboratory tests revealed anemia, leukocytosis with a moderate band shift of the leukocyte formula to the left, amylasemia, diastasuria, nitrogenous wastes and electrolytes remained within normal limits, the bilirubin level was increased due to the direct fraction.
The following were also noted: hypoproteinemia and increased levels of transaminases (AST, ALT).
According to CT data, a picture of focal infiltrative necrotic pancreatitis without signs of sequestration of gland fragments, unilateral compaction of Gerota's fascia depending on the location of the lesions, and dilation of the Wirsung duct were observed. Liquid collectors were identified in the parapancreatic tissue, abdominal cavity (mainly in the omental bursa), and reactive right-sided pleurisy. The scale of destructive changes is 30-50%.
According to ultrasound data, a picture of acute destructive pancreatitis with diffuse changes in the pancreas, the presence of local destructive foci, and signs of biliary hypertension was observed.
Infected macrofocal
pancreatic necrosis
It was determined by the presence of purulent inflammation of the gland tissue and extrapancreatic fluid collectors.
This form of the disease was characterized by: duration from the onset of the disease of more than 72 hours, the presence of Mondor's triad, hectic hyperthermia, changes in hemodynamic parameters: (arterial hypotension, tachycardia). Laboratory tests noted: anemia, leukocytosis with a pronounced band shift of the leukocyte formula to the left, amylasemia, reduced diastasuria, hyperkalemia, increased bilirubin levels due to direct and indirect fractions, increased levels of nitrogenous waste (creatinine, urea nitrogen), increased levels of transaminases (AST, ALT) .
According to CT data, the following were noted: heterogeneity of the structure of the pancreas with increased echogenicity, edema, infiltration of the gland itself and parapancreatic tissue, the presence of necrotic foci in the pancreatic tissue (the scale of necrotic changes is more than 50%). Fluid in the omental bursa, fluid collectors in the free abdominal cavity of increased density, and the presence of fluid in the pleural cavities were determined. Ultrasound visualized the heterogeneity of the structure of the pancreas, fluid formations in the projection of the head, body and tail of the pancreas with reduced echogenicity, the presence of biliary hypertension, fluid in the free abdominal cavity, and pleural cavities.
Treatment
Basic therapy for all forms of pancreatitis included: total parenteral nutrition using highly concentrated glucose solutions (20-40%), solutions of amino acids and fat emulsions, dipeptivene. Intensive intravenous infusion therapy and intra-arterial in selectively installed catheters in the celiac trunk. Extracorporeal detoxification methods were actively used: plasmapheresis with 100% plasma replacement. In the early stages of treatment, with high secretory activity of the pancreas, for the purpose of pharmacological blockade of its exocrine function, synthetic analogues of somatotropic hormone were used: octreotide, sandostatin in dosages of 0.6 to 1.2 g per day. Combined antisecretory therapy included an infusion of 80 mg per day of omeprazole (Losec IV), which had a positive effect on reducing gastric secretion, while simultaneously protecting the patient from the development of stress damage to the stomach.
In extremely severe cases with the development of ARDS, patients were transferred to artificial ventilation.
In complicated forms of pancreatic necrosis, timely surgical treatment is necessary with the maximum possible use of laparoscopic technology.
In the presence of purulent complications, before obtaining the results of a microbiological study, antibacterial therapy was carried out according to the principles of de-escalation therapy with carbapenems, followed by a transition to antibiotics of a narrower spectrum of action, depending on the results of the sensitivity of the microflora. The use of antifungal drugs (fluconazole 400 mg per day) was mandatory.
One of the most important components of complex therapy for patients with acute pancreatitis is adequate relief of pain, since intractable pain triggers a cascade of pathophysiological reactions that ultimately accelerate the development of multiple organ failure. Considering, on the one hand, the ineffectiveness of metamizole-containing analgesics, and on the other, the worsening of intestinal paresis under the influence of narcotic analgesics, prolonged epidural analgesia became the method of choice.
We used the following technique: after caterterization of the epidural space, 1% ropivacaine 6-8 ml was administered as a bolus, then ropivacaine 0.2%, 100 ml was added at a rate of 6-12 ml per hour using an infusion pump. Continuous epidural analgesia was carried out from 3 to 7 days and had the following advantages:
– sufficient level of analgesia with good controllability depending on the rate of administration;
- absence of hemodynamic disorders, orthostatic reactions, resorptive effect;
- good muscle tone combined with a sufficient level of analgesia allowed for early activation of patients.
For interstitial pancreatitis, we limited ourselves to infusion therapy, without parenteral nutrition. Infusion volume: 45-50 ml/kg/day. Crystalloid solutions 52%, colloid – 44%, protein preparations (albumin 20%) – 4%. To suppress the secretory function of the pancreas, octreotide or sandostatin were used: during the first two days at a dosage of 0.6 mg/day. subcutaneously With a decrease in the level of blood amylase, urine diastase, and a decrease in leukocytosis in the next three days, the dosage of octreotide was reduced to 0.3 mg/day. To avoid “withdrawal syndrome”, the drug was administered at a dose of 0.2 mg/day up to 9 days from the onset of the disease.
Long-term epidural analgesia was carried out with ropivacaine 0.2% at a rate of 6-12 ml/h for up to 7 days.
For aseptic small-focal uncomplicated forms of destructive pancreatitis: from the first day, parenteral nutrition was administered using concentrated glucose solutions, amino acid solutions and fat emulsions (Lipovenosis, Intralipid 10%, 20%). The volume of infusion therapy is 50 ml/kg/day. Crystalloid solutions - 48%, colloid - 48%, protein solutions - 4-6%. Octreotide was used at a dose of 0.6 mg for 3-5 days. Then, when blood amylase and urine diastase levels normalized, the dosage was reduced to 0.3 mg/day. within 7-10 days. In case of existing enzyme toxemia in conditions of increased vascular permeability, a protease inhibitor (aprotinin 400-800 thousand per day) was used for 5-7 days.
All patients received epidural analgesia with ropivacaine 0.2% for 7 days in the above dosages. During the first 2-3 days, against the background of severe intestinal paresis, gastric contents in a volume of 600 ml to 1800 ml were evacuated twice a day through a nasogastric tube.
In this regard, we consider it inappropriate to place a nasojejunal tube in the early stages for enteral nutrition, since the presence of a foreign body in the stomach provokes gastric secretion.
For complicated forms of small-focal pancreatic necrosis: laparoscopic drainage surgery was performed - cholecystostomy for the purpose of decompression of the biliary tract, application of an omentobursostomy, drainage of the abdominal cavity. On the first day, the aorta (celiac trunk) was selectively catheterized for infusion and antibacterial therapy. Plasmapheresis with 100% plasma replacement was carried out on days 1-3. From the first day, parenteral nutrition was used. The volume of infusion therapy is 50-55 ml/kg/day. Octreotide was administered in maximum dosages of 1.2 mg/day. intravenously for 3-5 days. Combination antibacterial therapy included 3rd generation cephalosporins in maximum (up to 8 g per day) dosages in combination with aminoglycosides and metronidazole. An auxiliary method of treating acute pancreatitis (interstitial and destructive aseptic forms) was hyperbaric oxygen therapy, carried out from the 2nd day of the patient’s stay in the intensive care unit every day for 5-7 days.
For infected pancreatic necrosis: laparotomy, cholecystostomy, omentobursostomy, necrosequestrectomy, drainage of the abdominal cavity and retroperitoneal space were performed. Programmed rehabilitation operations with necrosequestrectomy. Selective catheterization of the celiac trunk. Plasmapheresis with 100% plasma replacement on days 1-3-5. Mandatory prolonged epidural analgesia with 0.2% ropivacaine. The volume of infusion therapy varied from 50 to 60 ml/kg/day. Octreotide (Sandostatin) - in maximum dosages of 1.2 g intra-aortically for 5-7 days with a reduction in dosage to 0.6-0.3 g/day. within 10-12 days. The criteria for discontinuation of the drug were normalization of fermentemia, diastasuria, clinical picture of the disease and dynamic changes in the condition of the pancreas and parapancreatic tissue according to computed tomography. Before receiving the results of the microbiological study, initial empirical antibacterial therapy was carried out with carbapenems (meropenem) 3 g/day, in combination with vancomycin 2 g/day. The transition to narrow-spectrum antibiotics was carried out depending on the results of microflora sensitivity.
Conclusions
1. The most reliable method for determining the severity of acute pancreatitis is CT.
2. The proposed classification allows us to standardize the treatment of various forms of acute pancreatitis.
3. A standardized approach to therapy makes it possible to timely assess the degree of damage to the pancreas and correct developing complications.
A systematic approach to the treatment of acute pancreatitis allowed in 2002-2004. avoid deaths in groups of uninfected pancreatic necrosis, and when phlegmon of retroperitoneal tissue is formed, mortality did not exceed 10%.

Literature
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