Acute Pancreatitis.

Symptoms

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. After eating, especially fatty, spicy, fried, or drinking, there is an increase in discomfort. 

•    Nausea, vomiting . Vomiting may be indomitable, contains bile, does not bring relief.

•    Increase in body temperature .

•    Moderately pronounced yellowness of the sclera . 

 
In addition, acute pancreatitis may be accompanied by dyspeptic symptoms (flatulence , heartburn), skin manifestations (bluish spots on the body, hemorrhages in the navel).

Complications:

The risk of acute pancreatitis is the increased likelihood of serious consequences. When the inflamed gland tissue becomes contaminated with bacteria found in the small intestine, necrosis of the gland sites and the formation of abscesses are likely. Without prompt treatment (up to and including surgery), this illness can be deadly.

A state of shock and, as a result, multiple organ failure can occur in severe pancreatitis. After acute pancreatitis develops, pseudocysts (fluid accumulations in the parenchyma) can occur in the gland tissue, destroying the structure of the gland and bile ducts. Ascites happens when a pseudocyst ruptures and its contents spill out.
 

Causes

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);
•    Pancreatic injury;
•    surgical interventions for other pathologies of the pancreas and biliary tract;
•    Taking estrogens, corticosteroids, thiazide diuretics, azathioprine, other drugs with a pronounced pathological effect on the pancreas ( drug-induced pancreatitis );
•    Congenital malformations of the gland , genetic predisposition, cystic fibrosis ;
•    Inflammatory diseases of the digestive system (cholecystitis, hepatitis , gastroduodenitis ).

Pathogenesis:

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. The production process is hampered by internal and external pathogenic conditions, which also cause the pancreas's enzymes to get activated and start digesting its own tissue. Inflammation and tissue edoema occur, and the arteries of the gland's parenchyma are impacted.

Acute pancreatitis' pathogenic progression can affect adjacent tissues: 

Retroperitoneal tissue, the omental bag, the peritoneum, the omentum, the intestine's mesentery, and the liver and duodenum's ligaments. A severe case of acute pancreatitis causes the blood's level of several physiologically active molecules to spike dramatically, which triggers secondary inflammation and degenerative conditions in the lungs, liver, kidneys, and heart, among other tissues and organs.

Classification:

Acute pancreatitis is classified according to severity:

1.    A mild form proceeds 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;

2.    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 tissue infection (there is a limited or diffuse zone of dying parenchyma and peripancreatic tissues, with the addition of an infection and the development of purulent pancreatitis, the likelihood of death increases);

•    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).

Treatment

Hospitalisation is recommended in cases of acute pancreatitis. Bed rest was ordered for all patients. The main aims of treatment are to alleviate discomfort, lessen the stress on the pancreas, and boost the pancreas' self-healing capabilities.

Therapeutic measures:

•    Antibiotic treatment (broad-spectrum medicines in large doses) as a preventative measure against infection problems.Pancreatic enzyme deactivators (proteolysis inhibitors);

•    Antispasmodics with Novocaine Blockade to Reduce Severe Pain;

•     Hunger, application of ice to the gland projection region (producing local hypothermia to limit functional activity), parenteral feeding, aspiration of stomach contents, and administration of antacids and proton pump inhibitors;

•    Antibiotic treatment (broad-spectrum medicines in large doses) as a preventative measure against infection problems.Pancreatic enzyme deactivators (proteolysis inhibitors);

•    Corrective infusion of saline and protein solutions to assist restore homeostasis (water-electrolyte, acid-base, and protein balance);

•    Detoxification therapy;

Surgery:

Indication of surgery:

•    Stones in the bile ducts;
•    The accumulation of fluid in or around the gland;
•    Areas of pancreatic necrosis, cysts, abscesses.

Endoscopic drainage, marsupialization of the cyst, cystogastrostomy, etc. are among the procedures used in acute pancreatitis with the development of cysts or abscesses. Depending on their size, necrectomy or pancreatic resection is done when patches of necrosis arise. The presence of stones is a sign that the pancreatic duct needs to undergo surgery.

When there are questions regarding the diagnosis and a chance that another surgical condition would go undiagnosed and untreated, surgical intervention may also be used. Intensive purulent-septic complication prevention measures and rehabilitative treatment are necessary throughout the postoperative period.

The majority of the time, mild pancreatitis is not difficult to treat, and within a week, a favourable trend has been observed. Healing from severe pancreatitis takes considerably longer.

Prognosis 

The prognosis is serious with the development of complications. Acute uncomplicated pancreatitis in children may have a favorable prognosis. With this form, mortality is about 10%, and in rare cases, with necrotizing or hemorrhagic pancreatitis, up to 90%. Recurrent episodes of acute pancreatitis lead to chronic pancreatitis.

Tests Required for Diagnosis

In the general blood test, nonspecific changes are noted: leukocytosis, neutrophilia, increased ESR.
Indicator (amylase, transaminases) and pathogenetic (lipase, trypsin) tests are both a part of biochemical research. Amylase activity in the blood increases significantly in acute pancreatitis. Diastase, the name for the form of amylase that is secreted in the urine, is similarly elevated, with mumps infection causing the highest levels of both.
Abnormalities in the lungs are evaluated based on the activity of phospholipase A2 in the blood serum, and the stage of acute destructive pancreatitis is determined by the amount of serum ribonuclease (RNase). An rise in bilirubin, transaminases, and alkaline phosphate are indicators that the biliary system is blocked.
Hypercoagulability, hypoproteinemia, and elevated urea levels are further biochemical indicators. Up to 25% of kids with pancreatitis experience hyperglycemia during an acute episode, and 15% of them experience hypocalcemia.
Unfavorable prognostic signs of acute pancreatitis:
•  Leukocytosis more than 15,000x10 9 /l;
•  Hypercoagulability (fibrinogen >6 g/l);
•  Amylaseemia >6 norms;
•  Amylosuria >4 norms;
•  Hyperbilirubinemia >4 norms;
•  Hyperglycemia >2 norms;
•  Increased urea >2 norms;
•  Hypoproteinemia <60 g/l.
An important diagnostic criterion is a test using monoclonal antibodies, which reveals a decrease in elastase-1 activity in feces. Indicators: normal - 200 mcg / g of feces and more; moderate, mild degree of exocrine insufficiency - 100-200; severe - less than 100 mcg / g of feces.
Instrumental diagnostics includes ultrasound of the pancreas (decreased echogenicity - edema, increased echogenicity - proliferation of connective tissue), MRI and CT. This method is superior to ultrasonography because it offers more accurate visualisation of the retroperitoneal structures and pancreatic tissue. It enables you to evaluate the degree of tissue metabolism, the existence of ischemia, the necrosis of pancreatocytes, fluid in the surrounding tissues of the pancreas in acute pancreatitis, and, for example, numerous calcifications in chronic pancreatitis.
Endoscopic examination of the upper gastrointestinal tract refers to additional instrumental research methods in acute pancreatitis and is used for differential diagnosis with diseases of the stomach and duodenum.
Laparoscopy helps you to diagnose pancreaticogenic peritonitis, parapancreatic infiltration, and simultaneous destructive cholecystitis, as well as define the shape and kind of the disease.
Pathomorphology
When there is pancreatic necrosis, the pancreatic tissue is completely absent - "minus tissue": there are no lobules, connective tissue septa, etc. (autolysis); interstitial edema, hemorrhages, fat and cellular necrosis. Massive leukocyte infiltration of the gland's stroma and a buildup of purulent masses in the lumen of the major excretory duct are symptoms of acute serous-purulent pancreatitis.
Differential Diagnosis:
The primary conditions that acute pancreatitis differs from are:

Myocardial infarction, acute appendicitis, acute cholecystitis, gastritis, food intoxication, perforated gastric and duodenal ulcers, acute appendicitis, intestinal blockage, and renal colic. The potential for mesenteric blockage, ectopic pregnancy (in teenage females), lower lobe pneumonia, and paranephritis must be considered.