Acute pancreatitis

Acute pancreatitis is a disease based on the autolysis of the pancreas, caused by the activation of enzymes in the ducts.

Etiology. Diseases of the bile ducts are noted in 60% of cases, however the theory of the general Oddy channel is confirmed only in 1-2% of cases; More often such etiologic dependence is explained by close connections of lymphatic collectors and transition of an inflammation on lymphatic vessels. Causes of acute pancreatitis include alcohol intake, excessive intake of fat-rich foods, cholecystitis and choledocholithiasis, duodenal diverticulitis, etc.

Pathogenesis. As a result of increased pressure in the pancreatic ducts (stimulation in conjunction with an outflow disturbance), cells are damaged, cytokinase activates trypsinogen, which turns into trypsin. The latter is the activator of most of the proenzymes: chymotrypsin, elastase, collagenase, phospholipase A. It is the phospholipase A that releases from the phospholipids of the cell membranes lyuletsitin and liieo-phalin, which have a strong cytotoxic effect. Trypsin also releases polypeptides and quinines from the kininogen of tissues and blood. Activated quinines cause pain and generalized vasodilation, which is one of the causes of hypovolemic shock. Active lipases, splitting cell fats for glycerol and bile acids, lead to the development of severe dystrophic changes in tissues, promote the formation of areas of fatty necrosis (steatonecrosis) directly into the gland tissue, cellulose, surrounding the gland, distant tissues and organs.

Active kinins cause a sharp increase in the permeability of capillaries, stasis, microcirculatory block with complete cessation of perfusion through capillaries, ischemia, hypoxia, acidosis, violation of hemocoagulation with disseminated intravascular coagulation and subsequent consumption coagulopathy.

Symptoms, course. Women are more often ill at the age of 30-60 years. The disease begins more often after a plentiful meal. Suddenly, there is a pain of a bursting nature, usually very intense. The localization of pain is diverse and depends on the main localization of pancreatic changes: epigastrium, hypochondrium, more often the pain is shrouded in nature. Vomiting uncontrollable, not bringing relief. At the beginning of the disease, the temperature is normal or subfebrile. The position of the body is forced - with the legs brought to the abdomen. There is cyanosis of the skin, there may be hysteria, tachycardia, lowering blood pressure. Sometimes there is limited cyanosis in the lateral parts of the abdomen (a symptom of Gray Turner) or in the navel (Cullen's symptom) due to the proliferation of quinine systems in the retroperitoneal tissue or the round ligament of the liver. The tongue is covered with white bloom, dryish. The abdomen is slightly inflated. At the beginning of the disease the abdomen is soft, there may be slight muscle tension in the epigastrium and tenderness along the pancreas (Kurt's symptom). Quite often, soreness is detected in the left costal-vertebral corner (Mayo-Robson syndrome). Symptoms of irritation of the peritoneum become positive in the development of pancreatic necrosis (fermentative peritonitis) or purulent complications.

In the blood - high leukocytosis with a shift of the formula to the left, increase of hematocrit (dehydration), increase of amylase (diastase) of serum in urine. A sharp decrease in the numbers of blood amylase in combination with worsening of the patient's condition indicates the development of pancreatic necrosis. In 10-20% of patients develop hepatic-renal failure. A poor prognostic sign is increased blood sugar and urine, a decrease in serum calcium is below normal.

Radiographically determined high standing of the left dome of the diaphragm, in the pleural cavity to the left may be the level of fluid, in the lung - atelectasis. With an overview radiographic examination of the abdominal cavity, signs of paralytic intestinal obstruction, a developed loop of the duodenum, are revealed.

The diagnosis is based on history, objective research, abdominal ultrasound, laparoscopy (at the same time it can be of a therapeutic nature), computed tomography.

Treatment. From the very beginning, complex therapy is carried out: fighting with pain, enzyme toxemia, correction of hydroionic disorders, acid-base state. To combat enzyme toxemia, use: 1) suppression of the exocrine function of the gland by aspiration of gastric contents and gastric lavage with cold soda solution, atropinization (carefully, psychoses are possible in alcoholics patients), intragastric hypothermia; 2) the introduction of antispasmodics, which ensures the evacuation of enzymes naturally; 3) removal of enzymes trapped in the bloodstream: forced diuresis, lymphosorption, plasmapheresis; 4) inactivation of enzymes by protease inhibitors (countercranol, trazylol, etc.), however they are active only in the first hours of the disease; It is necessary to introduce very large doses, when necrosis of the gland tissue occurs, their use is nonsensical.

To prevent and treat secondary inflammatory changes, antibiotics of a wide spectrum of action are prescribed. Surgical treatment is indicated: with pancreatitis combined with acute destructive cholecystitis, with pancreatogenic peritonitis and inability of laparoscopic drainage of the abdominal cavity, with complications of acute pancreatitis (abscess of gland bag, retroperitoneal phlegmon).

Complications. A frequent complication is the formation of an abscess of the gland bag. After the enzyme toxemia subsides, the patient's condition worsens again: high fever, pain intensification, abdomen soft, painful in epigastrium and lumbar region, often the palpable infiltration, respectively, the localization of the abscess. The diagnosis is clarified by repeated radiographic examinations of the abdominal cavity: gastric pressure, fluid accumulation in the left pleural cavity, liquid level under the diaphragm. With ultrasound examination of the abdominal cavity, a compaction is observed in the pancreas and cavity formation. Treatment operative - opening the asbestos and draining it through the lumbotomy section. Other complications: bleeding, sepsis, shock, pleuropulmonary syndrome, compression of the common bile duct with the development of mechanical jaundice, peritonitis.

Pancreatic pseudocyst is a late complication of acute pancreatitis, which sometimes occurs several months or years after acute pancreatitis or pancreatic injury. The walls of the cyst are dense fibrous tissue and the walls of neighboring organs. Symptoms: a feeling of heaviness and a distending pain in the abdomen, an increase in the size of the abdomen and visible formation of the eye, with palpation dense and almost immobile, painless. The temperature is normal, if there is no suppuration of the cyst. In contrast radiographic examination of the abdominal cavity organs, it is possible to determine the excision of neighboring organs and the location of the cyst. Help is provided by ultrasound. The use of retrograde pancreatography is inexpedient in connection with the possibility of suppuration of the brush. Treatment is operative (but not earlier than 2 months after acute pancreatitis): more often, cystoanthroanastomosis is produced in the bowel loop that is turned off on the Roof. Remove the cyst is rarely possible due to intimate adhesion with neighboring organs. The prognosis is favorable.