ACUTE UNCOMPLICATED PANCREATITIS. CHOLECYSTOPANCREATITIS. ACUTE COMPLICATED PANCREATITIS (PANCREATITUOS PERITONITIS, PANCREONECROSIS, FALSE CYSTS OF THE PANCREAS). TACTICS OF TREATMENT.
ACUTE PANCREATITIS
Anatomy and function
The pancreas is an organ located in the abdomen. It plays an essential role in converting the food we eat into fuel for the body’s cells. The pancreas has two main functions: an exocrine function that helps in digestion and an endocrinefunction that regulates blood sugar.
Basic Anatomy: The pancreas is located behind the stomach and is surrounded by other organs including the small intestine, liver, and spleen. It is about six inches long and is shaped like a flat pear. The wide part, called the head of the pancreas, is positioned toward the center of the abdomen; the middle section is called the neck and the body of the pancreas; the thin end is called the tail and extends to the left side. Several major blood vessels surround the pancreas, the superior mesenteric artery, the superior mesenteric vein, the portal vein and the celiac axis, supplying blood to the pancreas and other abdominal organs.
Exocrine Function: The pancreas contains exocrine glands that produceenzymes important to digestion. When food enters the stomach, these pancreatic juices are released into a system of ducts that culminate in the mainpancreatic duct. The pancreatic duct joins the common bile duct to form theampulla of Vater which is located at the first portion of the small intestine, called the duodenum. The common bile duct originates in the liver and thegallbladder and produces another important digestive juice called bile. The pancreatic juices and bile that are released into the duodenum, help the body to digest fats, carbohydrates, and proteins.
Endocrine Function: The endocrine component of the pancreas consists of islet cells that create and release important hormones directly into the bloodstream. Two of the main pancreatic hormones are insulin, which acts to lower blood sugar, and glucagon, which acts to raise blood sugar. Maintaining proper blood sugar levels is crucial to the functioning of key organs including the brain, liver, and kidneys.
Acute pancreatitis
The basis of disease of pancreas is degenerative-inflammatory processes which are considered to be acute pancreatitis, the so called autolysis tissue by its own enzymes. In the structure of acute pathology of organs of abdominal cavity this disease takes the third place after acute appendicitis and cholecystitis. Women suffer from acute pancreatitis 3–3,5 times more frequently than men.
Pic. Pancreatic vascular supply.
Pic. Pancreatic Innervation
Pic. Ampullary Anatomy
Etiology and pathogenesis
Acute pancreatitis is a polyetiology disease. Its secondary forms, which arise on the background of pathologies of bile-excreting system and duodenum are closely associated with anatomic and functionally with pancreas, and are met in clinical practice.
Among the “starting” factors of origin of cholelithiasis disease (biliary pancreatitis) abuse by an alcohol and food overloads (fat and irritating products), traumas of pancreas, operating-room in particular, and also separate infectious diseases (parotitis, mononucleosis) are most frequent, especially infection of bilious ways. However, in 10–20 % of patients the reason of acute pancreatitis remains unknown (cryptogenic form).
In the basis of such damages of pancreas and enzymic toxemia lies mainly activating of pancreatic, and then the tissue enzymes (tripsin, lipase, amylase). Often the combination of the broken outflow of pancreatic secret and promoted secretion takes place, which provokes intraductal hypertension.
Among explanations of primary mechanisms of activating of pancreatic enzymes the most value belongs to: a) theory of “general duct” with reflux of bile in the ducts of pancreas; b) blockade of outflow of pancreatic juice with development of intraductal hypertension and penetration of secret in interstitial tissue; in) violation of blood flow of pancreas (vasculitis, thrombophlebitis and embolisms, cardiac insufficiency and others like that); g) toxic and allergic damages of gland. The role of alcohol in such situations can be dual: stimulation of secretion of pancreas and direct damaging action on its tissue.
Acute pancreatitis: Mechanisms
Pathomorphology
The process of acute inflammation of pancreas consistently passes the stages of edema, pancreatonecrosis and festering pancreatitis. In the stage of edema there is pancreas of hyperemic, increased in volume, with the shallow hearths of necrosis or, as it is in swingeing majority of cases, without them.
Pancreatonecrosis can pass with fatty or hemorrhagic character. In the first case, as a rule, pancreas is increased, dense, cut whity-yellow hearths are selected to necrosis. Increase of crimson-black pancreas with darkly-brown infiltrate on a cut is characteristic for hemorrhagic pancreatonecrosis.
Dystrophy of parenchyma is exposed microscopically, up to necrosis, hemorrhages, thromboses of vessels and signs of inflammatory infiltration.
Classification
(V All-russian convention of surgeons, 1978)
I. Clinico-anatomy forms:
1. Arching form.
2. Fatty pancreatonecrosis.
3. Hemorrhagic pancreatonecrosis.
II. Prevalence of necrosis:
1. Local (focus) damage of gland.
2. Subtotal damage of gland.
3. Total damage of gland.
III. Ran across: abortive, progressive.
IV. Periods of disease:
1. Period of hemodynamic violations and pancreatogenic shock.
2. Period of functional insufficiency of parenchymatous organs.
3. Period of degenerative and festering complications.
Symptoms and clinical passing
The disease begins suddenly, after the surplus reception of rich spicy food and use of alcohol. Pain, vomiting and phenomena of dynamic intestinal obstruction are considered the most characteristic signs of acute pancreatitis.
A stomach-ache is permanent and so strong, that can result in shock, localized in an epigastric area and left hypochondrium. Some patients feel pain in right hypochondrium with irradiation in the back, loin or breastbone.
Pain irradiation on acute pancreatitis
In a short period of time after appearance of pain there is a repeated strong vomiting, that does not facilitate the state of patient.
In general vomiting is considered a frequent and characteristic symptom. It is repeated or continuous and never brings facilitation. Vomit masses contain bile, as admixture, and at the difficult form of acute pancreatitis remind “coffee-grounds”.
Nausea, hiccup, belch and dryness in a mouth are attributed as less characteristic symptoms of this pathology.
During the examination the skin is pale, often subicterus. Some patients have cyanosys with a “marble picture” as a result of violation of microcirculation. Later the component of respiratory insufficiency can join it. At progressive general condition the patient quickly gets worse to passing of acute pancreatitis, intoxication grows. The skin takes shelter with sticky sweat.
The temperature of body of patients at the beginning of disease can be normal. It rises at resorption of products of autolysis tissue and development of inflammatory process in bilious ways.
The pulse in most cases is at first slow, then becomes frequent, notedly passing ahead the increase of temperature of body.
Arterial pressure goes down.
The tongue in the first hour of disease is moist, assessed by white and grey raid. At vomiting by bile the raid has yellow or greenish tint.
The abdominal is blown away, peristaltic noises are loosened. The signs of paresis of stomach and intestine demonstrate early. They need to be included in the pathological process of mesentery root of bowel. At palpation painfulness in an epigastric area and in right, and sometimes and in left, hypochondrium is marked. However, in spite of great pain in stomach, it remains soft for a long time. A little later there is moderate tension or resistance of muscles of front abdominal wall.
Poor local symptoms during heavy intoxication are characteristic for the early period of acute pancreatitis. Later there are symptoms of irritation of peritoneum, and at percussion dulling is marked in lateral parts of abdominal as a result of accumulation of liquid, and also the sign of aseptic phlegmon of retroperitoneal cellulose as slurred or edema of lumbar area is seen. For diagnostics of acute pancreatitis there is the row of characteristic symptoms which have different clinical value.
The Mondor’s symptom is violet spots on face and trunk.
The Lagermph’s symptom is acute cyanosys of person.
The Halsted’s Symptom is cyanosys of abdominal skin.
The Gray’s symptom is cyanosys of lateral walls of abdomen.
The Kullen’s symptom is the yellow colouring of skiear a belly-button.
The Korte’s symptom is painful resistance as a lumbar bar in a epigastric area on 6–7 cm higher belly-button.
The Voskresynskyy’s symptom is absence of pulsation of abdominal aorta in an epigastric area.
The Mayo-Robson’s symptom is feeling of pain at pressure by fingers in the left costal-vertebral corner.
The Rozdolskyy’s symptom — painfulness at percussion above pancreas.
The Blumberg’s symptom — in patients with acute pancreatitis more frequently is low-grade. Such feature of this sign of irritation of peritoneum needs to be explained by character of localization of pathological process, mainly in retroperitoneal spacious.
In clinical passing of pancreatonecrosis it is possible to select three periods (V.S. Saveljev, 1978).
The I period (hemodynamic violations and pancreatogenic shock) lasts during 2–3 days. Violation of central hemodynamics, diminishment of volume of circulatory blood and disorders of microcirculation, which at first arise as a result of angiospasm, are considered the most characteristic signs, and later as a result of joining of the intravascular rolling up and laying of elements of blood.
The II period (insufficiency of parenchymatous organs) lasts from 3rd to the 7th day of disease. Violation of functions of basic organs and systems, sign of cardio-vascular, hepatic and kidney insufficiency and growth of violations of breathing are thus observed. In this period there is possible damaging of the central nervous system, which is erected mainly to disorders of psyche, appearances of delirium and commas which in the eventual result are the main reasons of patients’ death.
The III period (postnecrosis dystrophic and festering complications) comes in 1–2 weeks after the beginning of disease. During it, on the background of progress of necrosis processes in pancreas, the regenerative changes develop, there are parapancreatic infiltrate and cysts, cystic fibrosis of pancreas. Aseptic retroperitoneal phlegmon which strengthens intoxication can also develop. There is festering pancreatitis at joining of infection. During this period such complications, as erosive bleeding, internal or external fistula, retroperitoneal phlegmon, can develop in patients.
From laboratory information leucocytosis which at the necrosis and hemorrhagic forms of pancreatitis sometimes arrives at 25-30 х 109, lymphopenia, change of leukocytic formula to the left and the increased ESR are characteristic. Growth of activity of amylase of blood and urine is very often marked, and is the important sign of pancreatitis. For estimation of the state of other organs maintenance of general albumen and its factions, glucose of blood, bilirubin, urea, electrolytes, acid-base equilibrium (ABE), and also the state of blood coagulation are determined. It is necessary to mark that the exposure of hypocalcemia is considered a bad predictive sign of heavy passing of acute pancreatitis.
Ultrasonic examination of gall-bladder and pancreas often specifies the increase of their sizes, bulge of walls and presence or absence of concrement of gall-bladder and general bilious duct.
Pic. Sonography.
Computer tomography enables to describe in details the changes in pancreas and surrounding organs.
Pic. Computer tomography
At sciagraphy survey of organs of abdominal cavity gives a possibility to expose the unfolded “horseshoe” of duodenum, pneumatization, expansion of transverse colon (the Gobia’s symptom). On the 1st stage of diagnostics in the plan of differential diagnosis of acute destructive pancreatitis with other diseases of abdominal cavity, diagnostics of distribution of destructive damaging of different parts of pancreas and estimation of distribution of parapancreatitis is possible only by the method of computer tomography which depending on clinico-laboratory signs and weight of passing is needed to apply in a different period, and sometimes a few times in dynamics with interval of 4–5 days.
Laparoscopy and laparocentesis are often used for a doubtful diagnosis or necessity of taking away the exudation of abdominal cavity for biochemical or bacteriological examination.
Retrograde endoscopic cholangiopancreatography is used in case of mechanical icterus and suspicion of choledocholithiasis. The last methods are invasive and can if it is necessary transform from diagnostic to manipulation treatments: laparoscopic draining of abdominal cavity at pancreatogenic peritonitis and endoscopic papillotomy at choledocholithiasis and biliary pancreatitis.
Variants of clinical passing and complications
Clinical passing of disease can be abortive, slowly or quickly progressive. At abortive passing the process is limited to acute edema of pancreas with convalescence in 7–10 days.
Rapid progress is characteristic for pancreatonecrosis. In patients expressed toxemia, impregnation by exudation of retroperitoneal cellulose and development of fermentative hemorrhagic peritonitis can be seen. Strengthening of stomachache, continuous vomiting, proof paresis of intestine, positive symptoms of irritation of peritoneum and growth of hemodynamic violations are the clinical signs of necrosis of pancreas.
There is a formation of parapancreatic infiltrate at slow progress.
Among early complications of acute pancreatitis shock, peritonitis and acute cardiac, pulmonary, hepatic and kidney insufficiency can be distinguished.
Before later complications it is needed to deliver the abscesses of pancreas, subdiaphragmatic, interintestinal abscesses, pyogenic abscess omentum bag, phlegmons of retroperitoneal space and erosive bleeding.
In future formations of pseudocysts, fistula of pancreas, intestinal fistula and development of saccharine diabetes are possible.
Diagnosis program
1. Anamnesis and physical methods of inspection.
2. General analysis of blood and urine.
3. Biochemical blood test (amylase, bilirubin, sugar).
4. Analysis of urine on diastase.
5. Sonography.
6. Computer tomography.
7. Cholecystocholangiography.
8. Endoscopic retrograde cholangiopancreatography.
9. Laparoscopy.
10. Laparocentesis.
Physical Examination:
The following physical examination findings may be noted, varying with the severity of the disease:
· Fever (76%) and tachycardia (65%) are common abnormal vital signs; hypotension may be noted
· Abdominal tenderness, muscular guarding (68%), and distention (65%) are observed in most patients; bowel sounds are often diminished or absent because of gastric and transverse colonic ileus; guarding tends to be more pronounced in the upper abdomen
· A minority of patients exhibit jaundice (28%)
· Some patients experience dyspnea (10%), which may be caused by irritation of the diaphragm (resulting from inflammation), pleural effusion, or a more serious condition, such as acute respiratory distress syndrome (ARDS); tachypnea may occur; lung auscultation may reveal basilar rales, especially in the left lung
· In severe cases, hemodynamic instability is evident (10%) and hematemesis or melena sometimes develops (5%); in addition, patients with severe acute pancreatitis are often pale, diaphoretic, and listless
· Occasionally, in the extremities, muscular spasm may be noted secondary to hypocalcemia
A few uncommon physical findings are associated with severe necrotizing pancreatitis:
· The Cullen sign is a bluish discoloration around the umbilicus resulting from hemoperitoneum
· The Grey-Turner sign is a reddish-brown discoloration along the flanks resulting from retroperitoneal blood dissecting along tissue planes; more commonly, patients may have a ruddy erythema in the flanks secondary to extravasated pancreatic exudate
· Erythematous skiodules may result from focal subcutaneous fat necrosis; these are usually not more than
Rarely, abnormalities on funduscopic examination may be seen in severe pancreatitis. Termed Purtscher retinopathy, this ischemic injury to the retina appears to be caused by activation of complement and agglutination of blood cells within retinal vessels. It may cause temporary or permanent blindness.
Differential diagnostics
· Acute Mesenteric Ischemia
· Acute Respiratory Distress Syndrome
· Bacterial Pneumonia
· Cholangitis
· Cholecystitis
· Choledocholithiasis
· Cholelithiasis
· Chronic Pancreatitis
· Colon Adenocarcinoma
· Colonic Obstruction
· Community-Acquired Pneumonia
· Duodenal Ulcers
· Gastric Cancer
· Gastroenteritis in Emergency Medicine
· Irritable Bowel Syndrome
· Myocardial Infarction
· Pancreatic Cancer
· Pancreatic Pseudocysts
· Viral Hepatitis in Emergency Medicine
Acute pancreatitis needs to be differentiated with the row of acute diseases of organs of abdominal cavity.
Acute mechanical intestinal obstruction. In patients with this pathology pain is of the alternated character and is accompanied by nausea, vomiting, delay of gases and emptying. It is possible to see the Klojber bowls on the sciagram survey of organs of abdominal cavity.
Acute cholecystitis runs with characteristic localization of pain and muscular defense, with presence of increased, painful gall-bladder or infiltrate in right hypochondrium. Often acute (especially lately) pancreatitis develops on the background of gallstone disease (biliary pancreatitis).
Thrombosis or embolism of mesenteric vessels. Both for pancreatitis and for the thrombosis of mesenteric vessels great pain at soft abdomen (absence of defense muscles of front abdominal wall), that precedes to development of peritonitis, is inherent. Yet from the beginning the disease gains heavy character of passing. In anamnesis in such patients a heart disease or heart attack of myocardium rheumatic is met. As a result of gangrene of intestine, the symptoms of peritonitis appear very quickly and intoxication grows. The fragments of mucus shell are found in flushing waters of intestine at the detailed examination, which have the appearance of ”meat flushing”.
A perforated gastric and duodenum ulcer is distinguished by the presence of dagger pain, defense of abdominal wall, ulcerous anamnesis.
Tactics and choice of treatment method
The conservative method is considered the basic one for treatment of acute pancreatitis, but in connection with that unsuccessful conservative treatment of patients with acute pancreatitis can often put a question about the necessity of operation, therefore patients must be in permanent surgical establishment. Thus acute pancreatitis with heavy passing is necessary to be treated under the conditions of separation of intensive therapy.
Before conservative treatment hunger, bed rest, fight against pain and enzymic toxemia, conducting of acid-base state, prophylaxis of festering infection and acute ulcers of digestive duct are to be entered .
Patient’s stomach is washed by cold soda solution and a cold on an epigastric area and left hypochondrium is used. Medicinal therapy is prescribed also: spasmolytics (papaverine, platyphyllin, no-shparum, baralgine, atropine); inhibitor of protease (contrical, trasilol, gordox, antagosan); cytostatic agent (5-fluorouracil, ftorafur). Positive action of inhibitor of protease is marked only in the first days of disease which are subject to conditioned application of large doses. Antibiotics of wide spectrum of action: a) tienam, which most effective in the prophylaxis of festering pancreatitis, as is selected by pancreatic juice; b) cephalosporins (kefzol, cefazoline); c) cefamizine (mefoxine).
Disintoxication therapy is conducted also (5 % but 10 % solutions of glucose, hemodes, reopolyhlukine, polyhlukine, plasma of blood, only from 3 to
For the improvement of rheological properties of blood heparine is prescribed (5 000 ODES every 4 hours).
If patients have the expressed pain syndrome and phenomena of general intoxication during all pain period plus 48 hours (by Bakulev), hunger is used. Such mode lasts on the average of 2–4 days. The parenteral feed of albuminous hydrolyzate is thus conducted, by the mixtures of amino acid and fatty emulsion. Alkaline water of to 1–2 l. and albuminous-carbohydrate diet are also appointed. Infusion therapy is complemented by plasma, by albumen, hemodes, reopolyhlukine. The improvements of microcirculation in pancreas are achieved due to introduction of reopolyhlukine, komplamine, trental and heparin 5000 ODES 6 times per days under the control the indexes of the coagulation system of blood. Anticholinergic drug (sulfate of atropine, methacin, platyphyllin), Н2-histamin blocker (cimetidine, ranisan, ranitidine, famotidine, omeprazol) are also applied. For the removal of pain: 1) sulfate of the atropine 0,1 % — 1 ml + promedol 2 % — 1 ml + papaverine 2 % — 2 ml + analgin 50 % — 2 ml; 2) isotonic solution of chloride of sodium — 500 ml + baralgine — 5 ml + diphenhydramine hydrochloride 1 % — 1 ml + papaverine 2 % — 2 ml + magnesium the sulfate 25 % — 5 ml + ascorbic acid — 5 ml + lipoic acid 0,5 % — 2 ml + novocaine 0,5 % — 10 ml. are used. From the first days by a nasogastral probe the permanent aspiration of gastric maintenance is conducted also. The Motility function of gastro-intestinal highway gets better at application of cerucal or primperane. With the same purpose forced diuresis (maninil, furosemide, aminophylline) is used on the background of intravenous introduction of plenty of liquid.
At uneffective conservative treatment of patients with acute pancreatitis of middle weight and heavy form it is expedient to apply surgical treatment.
Surgical treatment is carried out for patients with biliary pancreatitis (for a day long from the beginning of disease) in combination with the destructive forms of cholecystitis, at complications of acute pancreatitis by peritonitis, abscess of omentum bag or phlegmon of retroperitoneal cellulose.
Overhead-middle laparotomy, which allows to estimate the state of pancreas, bilious ways and other organs of abdominal cavity, is the best access in this situation. In case of destructive pancreatitis the possible use of lumbar laparotomy from left to right hypochondrium through a mesogastric area is useful.
Cholecystectomy is executed at calculous cholecystitis, phlegmonous inflammation of walls of gall-bladder and biliary pancreatitis. If there are more than
Transduodenal sphincteroplasty is shown at fixed concrement of large duodenal papilla, if they are diagnosed intraoperative, and also in the cases of papillotomy with extraction of concrement when there is no possibility to execute endoscopic operation .
Omentopancreatopexy. After laparotomy and cutting of gastro-colon and gastro-pancreatic ligament mobile part of large omentum through opening in gastro-colon ligament is conducted and fixed by separate stitches to the peritoneum along the overhead and lower edges of pancreas. Such operatioeeds to be considered rational at the expressed edema of pancreas and presence of necrosis in it.
Abdominisation of pancreas. A cellulose round pancreas (along the lower and overhead edges of body and tail) is infiltrated by solution of novocaine, after it parietal peritoneum is cut. Under the body and tail glands free end of omentum is conducted and is bundled by a gland. This operation is able to warn the hit of enzymes and products of disintegration in retroperitoneal space.
Sequestrectomy is deleting of necrosis part of gland within the limits of nonviable tissue. Operation is executed in a dull way.
Necrectomy (deleting of necrosis part of gland within the limits of healthy tissue) is executed by an acute way: tissue of gland is cut on verge of necrosis and bleeding vessels are carefully bandaged.
The resection of pancreas is deleting the part of organ with its transversal cutting within the limits of the unchanged (ad осulus) tissue of gland. The resections of tail and body of pancreas are distinguished.
Pancreatectomy is a complete deleting of pancreas. Operative treatment is applied infrequently. After the resection of pancreas adequate draining of its bed is very responsible.
The prognosis of disease depends on character of morphological changes of parapancreatic to the cellulose in pancreas. The more difficult destructive changes, the worst the prognosis.
CYSTS OF PANCREAS
Cyst of pancreas is a cavity, filled by liquid (pancreatic juice, exudation, pus), intimately soldered with head, body or tail of organ, is limited by capsule, which has epithelium on internal surface.
Pseudocyst (unreal cyst) is a cavity in pancreas which appears as a result of its destruction, limited by capsule, that does not have epithelium on internal surface.
Etiology and pathogenesis
Acute or chronic pancreatitis or abdominal trauma causes pseudocysts. If no history of pancreatitis or trauma exists, the diagnosis must be carefully confirmed. The reasons of pseudocysts are destructive pancreatitis, traumas of pancreas, oklusion of Wirsung’s duct by parasite, concrement, tumors, innate anomalies of development.
To the real cysts belong: innate (dysontogenetic) cysts which are anomalic in development; acquired retention cysts which develop as a result of difficult outflow of pancreatic juice, cystadenoma and cystadenocarcinoma (by mechanism the origins belong more frequently to proliferative, sometimes — degenerative cysts).
The mechanism of development of pseudocysts consists in the focus necrosis of gland, difficult normal outflow of its secret, there is a destruction of walls of pancreatic ducts with overrun of pancreatic juice gland that causes reactive inflammation of peritoneum of surrounding organs which form the walls of pseudocyst.
Pancreatic pseudocysts can be single or multiple. Multiple cysts are more frequently observed in patients with alcoholism, and they can be multiple in about 15% of cases. Size varies from 2-
The pathogenesis of pseudocysts seems to stem from disruptions of the pancreatic duct due to pancreatitis and extravasation of enzymatic material. Two thirds of patients with pseudocysts have demonstrable connections to the pancreatic duct. In the other third, an inflammatory reaction is supposed to have sealed the connection so that it is not demonstrable. The cause of pseudocysts parallels the cause of acute pancreatitis; 75-85% of cases are caused by alcohol or gallstone disease–related pancreatitis. In children, pseudocysts and trauma are frequently associated.
Pathomorphology
Morphologically the cysts of pancreas are divided into: pseudocysts retention to the duct are innate, single and multiple.
Pseudocysts are fresh and old. The internal surface of fresh pseudocyst is rough, granulating, grey-red. The table of contents is alkaline, grey or with a brown tint. In an old pseudocyst the wall is smooth and shiny, pale-grey. The table of contents is lighter. Epithelium pseudocysts is absent. More frequently they are met in body and tail of gland and are not connected with ducts.
Retention cysts connected with an obturated duct. The cavity has smooth, grey-white surface, maintenance is transparent, watery or mucous-like. Innate cysts are mainly multiple and shallow. A simple retention cyst differ from those that are always connected with the anomalies of development of ducts and are unite with polycystosis buds and liver.
Rarely there are echinococcus cysts, which have a clear chitinous shell, liquid in cavity and daughter’s blisters. They are localized in the area of head of pancreas.
Classification
(by A.N. Bakulev and V.V. Vinogradov, 1952)
I. Innate cysts of pancreas:
1. Dermoid cysts.
2. Teratoid cysts.
3. Innate adenomas.
4. Fibrocystic degeneration.
5. Polycystic degeneration.
II. Inflammatory cysts:
1. Pseudocysts.
2. Retention cysts.
III. Traumatic cysts:
1. As a result of direct damage of gland.
2. As a result of indirect damage of gland.
IV. Parasite cysts:
1. Echinococcosis glands.
2. Cysticercosis glands.
V. Neoplasty cysts:
1. Cyst-adenoma.
2. Cyst-adenocarcinoma.
3. Cavernous hemangioma.
4. Cystic epithelioma.
Pathomorphologyо cysts are divided on:
1. The true cyst.
2. Pseudocysts.
According to clinical passing pseudocysts are divided into acute, subacute and chronic.
According to weight of passing — into simple (uncomplicated) and complicated.
Symptoms and clinical passing
In patients with the cystic damaging of pancreas there can be pain of different character and intensity (dull, permanent, cramp-like and belting). It is localized more frequently in right hypochondrium, epigastric area (cyst of head and body of gland), left hypochondrium (cyst of tail of pancreas). Pain is irradiated in the back, left shoulder-blade, shoulder and spine.
Dyspepsia violations are characteristic. Nausea, vomiting and belch are observed.
The syndrome of functional insufficiency of pancreas shows up by disorders of exocrine and endocrine insufficiency and depends on the degree of damage of organ. The unsteady emptying, replacement of diarrhea of constipation, steatorrhea and creatorrhea, development of the second diabetes are marked.
Compression syndrome. Arises as a result of compression of neighbouring organs. Clinically the compression of organs of gastro-intestinal highway shows up by complete or partial obstruction of general bilious duct (mechanical icterus), vein (portal hypertension) gate, splenic vein (splenomegaly).
Physical:
· The sensitivity of physical examination findings is limited.
o Patients very frequently have a tender abdomen.
o Patients occasionally have a palpable mass in the abdomen.
· Peritoneal signs suggest rupture of the cyst or infection.
· Other possible findings include the following:
o Fever
o Scleral icterus
o Pleural effusion
Diagnosis program
1. Anamnesis.
2. Biochemical blood test (amylase, sugar, bilirubin).
3. Analysis of urine on diastase.
4. Coprograma.
5. Sonography.
6. Contrasting sciagraphy of stomach and duodenum (relaxation duodenography).
7. Retrograde pancreatocholangiography.
8. Computer tomography.
X-ray examination. Shift the stomach to the left
During the examination patients with large cysts are marked by asymmetry of abdomen in epigastric and mesogastric areas. At palpation of abdomen tumular formation of elastic consistency with an even, immobile surface is found.
Abdominal ultrasound: Sonography examination shows echo-free formation with a clear capsule, determines localization and sizes of cyst. While cystic fluid collections in and around the pancreas may be visualized via ultrasound, the technique is limited by the operator’s skill, the patient’s habitus, and any overlying bowel gas. As such, ultrasound is not the study of choice to establish a diagnosis.
Sonography
Contrasting roentgenologic examination of stomach and duodenum with the sulfate of barium at the cyst of head of pancreas exposes moving of pyloric part of stomach upwards and breeding of ,,horseshoe” duodenum (at relaxation duodenography in the conditions of low artificial blood pressure). If a cyst is localized in the area of body of gland, displacement of stomach is marked forward and upwards or downward, rapprochement of its walls, moving of duodenal transition and loops of thin bowel downward and to the right; at lateral projection the distance between stomach and spine is increased. The cyst localized in the area of tail of gland, displaces the stomach forward and upwards, to the left or to the right.
Cholecystocholangiography exposes calculous cholecystitis and cholelithiasis.
Retrograde pancreatocholangiography exposes the changed and deformed, infrequently extended pancreatic duct, occasionally there can be filling of cavity of cyst by the contrasting matter.
Abdominal CT scan: Computer tomography shows accumulation of liquid limited by the capsule of different closeness and thickness.
CT Scan. Cyst of the pancreas
· CT scan is the imaging criterion standard for pancreatic pseudocysts. It has a sensitivity of 90-100% and is not operator dependent.
· The usual finding on CT scan is a large cyst cavity in and around the pancreas.
· Multiple cysts may be present.
· The pancreas may appear irregular or have calcifications.
· Pseudoaneurysms of the splenic artery, bleeding into a pseudocyst, biliary and enteric obstruction, and other complications may be noted on CT scan.
· The CT scan provides a very good appreciation of the wall thickness of the pseudocyst, which is useful in planning therapy.
Endoscopic retrograde cholangiopancreatography:
· Endoscopic retrograde cholangiopancreatography (ERCP) is not necessary in diagnosing pseudocysts; however, it is useful in planning drainage strategy.
· A study by Neil et al investigated the use of ERCP and the treatment of pseudocysts and acute pancreatitis and reported that a change in management occurred 35% of the time after the ERCP findings in pseudocysts were evaluated. Therefore, many authors recommend performing an ERCP before contemplated drainage procedures.
MRI:
· MRI is not necessary to establish a diagnosis of pseudocysts; however, it is useful in detecting a solid component to the cyst and in differentiating between organized necrosis and a pseudocyst.
· A solid component makes catheter drainage difficult; therefore, in the setting of acute necrotizing pancreatitis with resultant pseudocyst, an MRI may be very important before a planned catheter drainage procedure.
Endoscopic ultrasound:
· Endoscopic ultrasound (EUS) is not necessary to establish a diagnosis but is very important in planning therapy, particularly if endoscopic drainage is contemplated.
· A gastric wall with a thickness greater than
· EUS may also be helpful in detecting small portal collaterals from otherwise undetected portal hypertension that may increase bleeding risks with transmural drainage.
· Transmural drainage may be performed only when the symptomatic pseudocyst is positioned next to the gut wall.
Laboratory examinations exposes hyperamylasemia, steatorrhea and creatorrhea, sometimes — hyperglycemia and glycosuria.
Laboratory Studies:
· Serum tests have limited use.
o Amylase and lipase levels are often elevated but may be within reference ranges.
o Bilirubin and liver function test (LFT) findings may be elevated if the biliary tree is involved.
· Analysis of the cyst fluid may help differentiate pseudocysts from tumors. Attempt to exclude tumors in any patient who does not have a clear history of pancreatitis.
o Carcinoembryonic antigen (CEA) and carcinoembryonic antigen-125 (CEA-125) tumor marker levels are low in pseudocysts and elevated in tumors.
o Fluid viscosity is low in pseudocysts and elevated in tumors.
o Amylase levels are usually high in pseudocysts and low in tumors.
o Cytology is occasionally helpful in diagnosing tumors, but a negative result does not exclude tumors.
o A CEA level of greater than 400 ng/mL within the cyst fluid strongly suggests malignancy.
Clinical passing of cysts of pancreas depends on their kind, localization, size, stage of forming and complications.
Four stages of forming of pseudocyst are distinguished (Р.G. Karaguljan, 1972).
I stage (1–1,5 months last) — in the center of inflammatory process the cavity of disintegration, which takes surrounding tissue, appears in an omentum bag.
The II stage (2–3 months) is characterized by the beginning of forming of capsule of pseudocyst. Cyst is magnificent, unformed, acute inflammatory phenomena calms down.
The III stage (3–12 months) is completion of forming of capsule of pseudocyst. Last accretes with surrounding organs.
The IV stage (begins an in year from the origin of cyst) is a separated cyst. The cyst is mobile, easily selected from connections with surrounding organs.
Retention cysts arise at closing of lumen of pancreatic duct (concrement, sclerosis). The internal surface of cyst is covered with epithelium. Pain syndrome, violation of exocrine function of gland are characteristic.
Traumatic cysts belong to the pseudocysts with similar passing and clinic, as well as inflammatory pseudocysts.
Parasite cysts (to echinococcus, cysticercotic) are met as casuistry. In such patients Kaconi test and serological Weinberg’s reaction are positive.
The variants of clinical passing of the real and unreal cysts depend on their complications.
Perforation in free abdominal cavity. Clinic of the poured peritonitis is characteristic. Tormina, positive symptoms of irritation of peritoneum, possible shock state as a result of irritation of peritoneum by pancreatic juice arise.
Perforation in stomach, duodenum, small, rarer in large intestine is accompanied by diminishment of cyst in sizes or complete disappearance, sometimes diarrhea appears.
Suppuration of maintenance of cyst is accompanied by pain which becomes more intensive, temperature rises, leucocytosis grows.
The erosive bleeding appears suddenly and is accompanied by the symptoms of internal bleeding (expressed general weakness, dizziness). The pallor of skin and mucus shells, sticky death-damp, tachycardia and anemia are observed.
Mechanical icterus arises as a result of compression of cyst on the terminal part of choledochus. The icterus of skin and mucus shells, acholic excrement, dark urine, hyperbilirubinemia, increase of the AlT and AsT level are exposed.
Portal hypertension develops as a result of compression of portal vein. Ascites, varicose expansion of veins of esophagus and stomach, moderate icterus are diagnosed.
Reactive exudation pleurisy more frequently arises in left pleura cavity, where roentgenologic exudation is diagnosed with high maintenance of amylase.
At malignization the walls of cyst specific symptoms are absent, a diagnosis is set during operation (surgical biopsy of cyst wall).
Differential diagnostics
· Pancreatic Cancer
· Pancreatic Necrosis and Pancreatic Abscess
· Pancreatic Pseudoaneurysm
· Pancreatitis, Acute
· Pancreatitis, Chronic
· von Hippel-Lindau Disease
The cysts of pancreas are differentiated with the tumors of abdominal cavity and of retroperitoneal space.
Cancer of pancreas. For the cancer tumor of pancreas syndrome of “small signs” (discomfort in epigastric area, loss of appetite, general weakness), permanent dull pain, unrelated with the reception and composition of meal, icterus (cancer of head of gland), Courvoisier’s symptom (increased, unpainfully gall-bladder) are characteristic. Inconstant pain at cysts of pancreas is more frequently related to faults in a diet; in anamnesis destructive pancreatitis, traumas of gland are carried. Sonography examination, retrograde pancreatocholangiography and computer tomography help in establishment of diagnosis.
Tumors of retroperitoneal space are passed asymptomatic, clinic shows up by a considerable compression oeighbouring organs. Nausea, vomit, chronic intestinal obstruction, dysuric disorders arise. Clinic of cysts of pancreas, on the opposite, are expressed on early stages. Pain, dyspepsia syndromes, syndrome of exocrine and endocrine insufficiency of pancreas are characteristic. Pain is related to the reception of meal and alcohol.
Aneurism of abdominal aorta. Dull, indefinite pain in abdomen which is unrelated with the reception of meal, pulsation and pulsating formation in abdomen are characteristic, auscultatory is systolic murmur. Aortography allows to confirm a diagnosis.
The cyst of mesentery of thin bowel has painless passing, at palpation it is mobile, easily changes position in abdomen. The cysts of pancreas are practically immobile, pain, anamnesis and laboratory information are characteristic.
The cyst of liver has protracted asymptomatic passing. Pain appears at infection of cyst. For this pathology symptoms which take place at the cysts of pancreas are not typical (pain related to the reception of rich food, alcohol, hyperamylasemia). Topic diagnostics is carried out at ultrasonic examination, scintigraphy, computer tomography.
Tactics and choice of treatment method
Conservative treatment. Treatment of acute or chronic pancreatitis is conducted in accordance with principles. At the unfavorable dynamics of passing the diseases hunger with the permanent sucking of gastric maintenance, parenteral feed and intravenous introduction of liquids are appointed. Puncture of cysts is used through abdominal wall under sonography control with aspiration of maintenance.
Peripancreatic fluid collections persisting for more than 4 weeks are referred to as acute pseudocysts. Pseudocysts lack an epithelial layer and thus are not considered true cysts. They also differ from true cysts in that they are usually filled with necrotic debris rather than fluid. Accordingly, pseudocysts may be better described by the term organized necrosis.
Surgical treatment is the method of choice of treatment of cysts of pancreas. The choice of treatment method depends on the stage of forming of pancreas cysts.
In selected patients with very large fluid collections, percutaneous aspiration of pancreatic pseudocysts is a reasonable approach. Even though treatment failures are common when the pseudocyst communicates with the pancreatic ductal system, percutaneous drainage serves as a temporizing measure that may later lead to successful endoscopic or surgical intervention. Often, an infected pseudocyst (which by definition is regarded as a pancreatic abscess) can be successfully managed by means of percutaneous drainage.
Pseudocysts may also be managed endoscopically with transpapillary or transmural techniques. Transpapillary drainage requires the main pancreatic duct to communicate with the pseudocyst cavity, ideally in the head or body of the gland. The proximal end of the stent (which should be smaller than the diameter of the pancreatic duct) is placed into the cavity. The technical success rate is 83%, the complication rate 12%. Generally, however, pancreatic stents are difficult to monitor and prone to obstruction and carry an increased risk of infection and ductal injury.
Some noncommunicating pseudocysts may be amenable to transmural enterocystostomy. Technical success requires a mature cyst that bulges into the foregut, and the distance from the lumen to the cyst cavity should be less than
On the basis of prospective data from the 1970s, surgery was recommended for persistent large (>
On the I stage operation is not used, conservative treatment of pancreatitis is conducted. On the II stage it is used at suppuration of pseudocyst (external draining of cyst). On the III — internal draining of cyst is used.
More frequently cystojejunostomy on the eliminated loop of thin bowel by Roux, cystojejunostomy with entero-entero anastomosis by Brawn and closing of afferent loop by Shalimov. Cystogastrostomy are executed and cystoduodenostomy is now not applied because of possible complications (infection of cyst, erosive bleeding). Marsupialization (opening and sewing down of cyst to the parietal peritoneum and skin) is used infrequently (at suppuration of cyst is seriously patientsing with the septic state). On the IV stage external and internal draining of cyst and radical operations are applied: a) enucleation of cysts (executed very rarely); b) distal resection of pancreas with a cyst.
Cystoejunostomy
Complications:
· Bleeding is the most feared complication and is caused by the erosion of the pseudocyst into a vessel.
o Consider the possibility of bleeding in any patient who has a sudden increase in abdominal pain coupled with a drop in hematocrit level or a change in vital signs.
o Therapy is emergent surgery or angiography with embolization of the bleeding vessel.
o Do not perform a percutaneous or endoscopic drainage procedure under any circumstances in patients with suspected bleeding into a pseudocyst.
· Consider the possibility of infection of the pseudocyst in patients who develop fever or an elevated WBC count. Treat infection with antibiotics and urgent drainage.
· GI obstruction, manifesting as nausea and vomiting, is an indication for drainage.
· The pseudocyst can also rupture.
o A controlled rupture into an enteric organ occasionally causes GI bleeding.
o On rare occasions, a profound rupture into the peritoneal cavity causes peritonitis and death.
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Prepared ass. Romaniuk T.
