Pancreatitis

PANCREATITIS (pancreatitis), inflammation of the pancreas. To the present time, there is no firmly established classification of P. In reality, the detailed subdivision of P. (catarrhal, hemorrhagic, necrosis, etc.) has no significance, since clinically and patho-anatomically we often see the transition of one form into another, observing simultaneously hemorrhage, inflammation, and necrosis. It is probably more correct to speak of 'various stages, phases of the process, rather than of various forms of inflammation, which by the way often does not exist as such' (Ruffanov). Guleke, for example, proposes to call all acute forms 'acute necrosis of the pancreas'; Gessner believes that in ²/₃ of cases one can see the transition of one form into another; Seidel believes that in the first three days there are only hemorrhages, the following three days - hemorrhages and necroses, and later - only necroses of the gland. All these indications are meant to emphasize that the various forms of P. do not have sufficient demarcation from necrobiotic processes in the gland (see Fat necroses). On the other hand, it is still incorrect to classify these processes under the concept of P. only because they subsequently, in connection with the resorption of necrobiotic products, are combined with inflammatory processes: the leading pathological process here remains the necrobiosis of the gland, or hemorrhages into it. This must be kept in mind with the following, most accepted classification of P.: 1) acute hemorrhagic P. (acute necrosis of the pancreas); 2) acute suppurative P. (abscess of the pancreas); 3) chronic P. Acute hemorrhagic P. (acute necrosis of the pancreas). Factors predisposing to the development of acute hemorrhagic P. are considered to be obesity, prolonged severe dietary disturbance, especially abundant food with predominance of fatty dishes, syphilis, arteriosclerosis, obliterating endarteritis, embolisms, thrombi, and spasms, poisonings (lysol, phosphorus, etc.), pregnancy. Local contributing factors are considered to be injuries to the pancreas (open and closed) and all factors leading to angiospasms in it. Acute hemorrhagic P. is directly associated with diseases of the gastrointestinal tract (duodenitis, stomach ulcer), but most often with inflammatory processes in the biliary passages. Cases of acute hemorrhagic P. have been described as a result of ascarids entering the Wirsung duct, sometimes due to perforation of a stomach ulcer or its resection. Cammidge (1911) in 417 cases of acute hemorrhagic P. considered 13% to have a proven connection with diseases of the gastrointestinal tract and several times more - with inflammation of the biliary passages. Deaver (1916) in 132 cases of acute hemorrhagic P. had 19 cases of stomach ulcer and 12 of duodenal ulcer, and in 113 cases - cholecystitis and cholelithiasis. In the last 20 years, when this connection began to be studied more carefully, the number of cholecystopancreatitis cases has been increasing, and in most authors it reaches 60-90% (Haberer, Robson M., Nordmann, Guleke, etc.). Where this percentage is not high, it is more likely to assume incomplete or careless examination of the biliary passages and gallbladder. According to Ruffanov's collective case studies of 90 cases of acute hemorrhagic P., in 60 cases stones in the gallbladder were not found during operation, but were found on autopsy. Zopffel (1911) in 11 cases of acute hemorrhagic P. had stones in the biliary passages in 10 cases, and in half of these cases stones were found only on autopsy. This connection between pathological processes of the biliary passages and the pancreas is understandable, since both embryological data and the anatomical relationship of the excretory ducts of the pancreas and the common bile duct (see Gallbladder, fig. 1 and 16), and physiological relationships [the possibility of backflow and mixing with the enzymes of the pancreas of bile (especially infected) - an activator of trypsinogen] indicate the significance of diseases of the biliary passages in the origin of acute hemorrhagic P. The comparative rarity of acute hemorrhagic P. despite the widespread inflammation of the biliary passages is explained in part by the anatomical type of connection of the common bile duct with the Wirsung duct. Depending on whether they empty into the duodenum isolated or not isolated, the conditions for ascending infection or for mixing bile with the secretion of the pancreas, its backflow into the gland and activation of its enzymes are not the same. The presence of the Santorini duct - an accessory duct of the pancreas - is also of great importance. According to Clairmont, the Santorini duct is absent in 44% and rudimentarily developed in 32%. It is understandable that the cessation of outflow of the gland's secretion (a necessary condition for the development of acute hemorrhagic P.) depends to a large extent on the number of its excretory ducts. Acute hemorrhagic P. is observed equally often in both men and women (according to some authors - more often in men). Age - most often 30-60 years. However, cases of acute hemorrhagic P. have been described at an earlier age. ^95 Pathological anatomy and pathogenesis. Depending on the stage and degree of the process, in initial, mild cases, a picture of minor circulatory disorders is observed - edema of the tissue ('prepancreatitis'), then its hardening, limited or widespread hemorrhages; finally, part or all of the pancreas may represent a necrotic mass, with dead parts of the gland floating in the resulting cavity with liquid bloody or dirty-brown contents. Most often, we have to deal precisely with this form of acute hemorrhagic P. The capsule of the gland itself is of a bluish-red color. In the abdominal cavity, a serous, more often bloody exudate is often observed, which does not contain bacteria but possesses great tryptic force. Sometimes infection is added, and with a slower course, a purulent peritonitis may develop. In the omentum, around the gland, and sometimes in distant areas of fatty tissue, fat necroses (see) are observed, which can occur at all stages of acute hemorrhagic P. Microscopically, edema between the lobules and in the connective tissue layers, dilatation, stasis, and thrombi in the smallest, small, and sometimes larger vessels of the gland with hemorrhages into the tissue itself are distinguished. Sometimes hemorrhages spread very far. The cells of the pancreas show a picture of necrobiosis. All these changes - in the blood vessels against the background of hemorrhages and necroses in the organ closely resemble hemorrhagic, or ischemic infarcts in connection with some acute circulatory disorders, possibly of angiospastic nature. Inflammatory-infiltrative processes are either completely absent or occupy only a minor place in the entire pathological process. Sometimes areas of chronic interstitial P. are noted, obviously preceding the acute hemorrhagic P. If the disease has a tendency to heal, a pseudocyst may develop (see Pancreas). Sometimes bleeding occurs due to erosion of large blood vessels. Large changes in the biliary passages are often found, more often stones in the ductus choledochus, obstructing the exit of secretions (bile and enzymes) in the ampulla. Sometimes the tissue of the gland is colored yellow due to backflow of bile through the ducts of the gland. Many experiments have been devoted to elucidating the pathogenesis of hemorrhagic P.: introduction of HCl, trypsin, bacteria, bile, etc. into the tissue of the gland; ligation of the pancreatic ducts with introduction of intestinal contents, etc. It has been experimentally confirmed that bile is a strong activator of trypsinogen, especially in combination with bacterial culture. It has been proven that the primary moment is not digestion, but sharp vascular-nervous changes, having as their effect a sharp disturbance of blood circulation in the tissue of the gland; in a number of cases the experiment succeeded if it was performed on a well-fed animal at the height of digestion, and conversely only small changes or chronic P. were obtained if the animal was hungry, which coincides with clinical data indicating that an attack of acute hemorrhagic P. more often occurs at the height of digestion in obese individuals who abuse fatty food. Some authors see the pathogenetic explanation for the development of acute hemorrhagic P. in the activation of the gland's enzyme, trypsinogen, before its excretion through the duct. Activators are intestinal juice, bile, bacteria (see Trypsin). It is more correct to think that the action of trypsin on the gland is manifested not in the direct digestion of the gland, but in a series of vasomotor disorders, damage to the nervous-vascular apparatus, in the strongest spasm of blood vessels with subsequent thromboses and hemorrhages. Subsequently, necrosis of the gland tissue occurs, and these necroses take on an extensive character precisely because the enzymes released during the initial necrosis act in a digestive manner on the latter tissue. The role of bacteria is rather to activate the process. In cases where the process does not have a stormy picture of toxemia, bacteria can change the character of the process, giving it a distinctly inflammatory, even purulent character.

The prerequisites for the development of acute hemorrhagic pancreatitis are the aforementioned factors: stagnation of secretions in the gland and retrograde (ascending) entry from the duodenum of contents (intestinal juice, bile, bacteria) through the Wirsung duct. Clinical picture, symptoms, diagnosis. There is no definite, clear symptom complex characteristic of acute hemorrhagic pancreatitis. In the diagnosis, individual symptoms are not as important as the presence of the overall clinical picture, which may only occasionally be characteristic. In the history, the gallstone symptom complex is noted in 60% of cases, the ulcer complex in 15%, and the absence of any characteristic data in 25%. General picture: with signs of shock, very frequent pulse, cyanosis, normal or subnormal temperature, sharp pains in the epigastrium (less often in the region of the cecum, in the lumbar region, pelvis) occur, intensifying when lying on the side. Unlike biliary colic, the pains have no intervals, do not yield to any therapeutic measures, continue for hours, and become unbearable ('pancreatic drama'). The abdomen is tender, especially in the region of the right rectus muscle 10 cm above the navel (point pancreatique Desjardins). Muscle tension is usually absent. Repeated vomiting, sometimes hiccups, retention of gas and stool, rarely diarrhea, bloating of the intestines, often isolated in the epigastrium. 'Sensitive resistance going across the epigastrium' according to Korte is a pathognomonic sign. Jaundice, noted in the history in 35% of cases of acute hemorrhagic pancreatitis, is observed at the time of the patient's consultation with the physician in no more than 20% of cases. Sometimes cyanosis of the abdominal walls is observed, bluish spots in the umbilical or lumbar region. The urine contains protein, diastase, sometimes blood (only with signs of severe toxemia). Sugar is rarely noted. Leukocytosis sometimes up to 30,000 and even 60,000 (Brugsch). A more gradual course of acute hemorrhagic pancreatitis is sometimes observed, when most of the cardinal symptoms are absent and the disease proceeds as cholelithiasis with digestive disturbances, sometimes with jaundice. In differential diagnosis, one must consider internal bleeding, perforative peritonitis, high ileus, thrombosis of mesenteric vessels. The diagnosis is helped by the absence of individual symptoms characteristic of each of the aforementioned diseases (absence of muscle tension, fecal vomiting, etc.). In general, the history is more helpful for diagnosis than any laboratory investigations. The Kemmidge reaction (see) is not characteristic. During operation, the diagnosis is facilitated by the presence of fat necroses of the omentum, sometimes of subcutaneous tissue, and bloody exudate in the abdominal cavity. According to the course, acute hemorrhagic pancreatitis can be divided into four clinical forms: 1) the most acute, 2) very acute, 3) acute, 4) subacute. Patients of the first group die within a few hours, lightning-fast, as in cholera, with signs of cyanosis, collapse, convulsions and severe toxemia (fecal vomiting, bloody urine, etc.). Patients of the 2nd group present the same symptoms of the disease but to a lesser degree, and give the impression rather of patients with high ileus or perforation. Most often they die within a day if not operated on in the first hours. Patients of the 3rd group resemble rather patients with a severe attack of gallstone disease and are often operated on under this diagnosis. Changes in the pancreas in the first two days do not reach great size. This group gives a significant percentage of recoveries. Patients of the 4th group present symptoms of a subacute process, often proceed as cases of ordinary biliary colic or catarrhal jaundice. It is possible that, if repeated, they may give the clinical picture of one of the previous groups. If these cases are operated on, they are often not recognized; in the abdominal cavity, serous exudate and swelling of the pancreas are sometimes found. The prognosis depends on the degree of damage to the gland. Hemorrhagic exudate worsens the prognosis. The presence of fat necroses does not always indicate the severity of the process, unless they are too widespread. The prognosis is poor when fat necroses extend to distant areas (epicardium, pleura). Softening of the gland, hemorrhages around it worsen the prognosis. The predominant presence of edema, hemorrhage or necrosis of the gland indicates one or another stage, and consequently the severity of the process. The age of the patient and the time of operation are of great importance for the prognosis: the earlier the patient is operated on, the sooner the abdominal cavity and the body are freed from toxins, the better the results. Jung, operating in the first day, had 22% mortality, in subsequent days up to 60%. In Seidel, operation on the first day of the disease gave 33% mortality, on the 3rd day-66%, later (5th-12th day)-100%. Patients with a gallstone history give the best results, worse with a gastric history, and poor in the absence of a characteristic history. The reason for this may lie in the repeated immunization of the gallstone patient with trypsin; animals immunized with trypsin in experiments were not prone to hemorrhagic necroses in a significant percentage of cases. The cause of death lies in poisoning by products of disintegration of the gland, activated by trypsin and formed soaps, which mechanically and chemically irritate the sympathetic plexus, causing the strongest shock. Treatment. The mildest cases of acute hemorrhagic pancreatitis sometimes can be eliminated without operation, but usually the treatment of acute hemorrhagic pancreatitis should be surgical. The described individual cases of self-healing (discharge of gangrenous parts of the pancreas, formation of pseudocysts, scars) are rare. The first successful cases of operation belong to Korte (1895) and Razumovsky (1898). At present, there are already quite a number of successful operations for acute hemorrhagic pancreatitis. Complete unanimity has not been achieved on the question of the permissibility of waiting. If some authors (Nordmann) consider that waiting is permissible with violent phenomena, others (Dreesmann) believe that, on the contrary, cases with a benign course (pulse less than 100) can eliminate themselves spontaneously. Most authors, however, are inclined to operate on diagnosed or suspected acute hemorrhagic pancreatitis, if the patient is not in a state close to agony (1st group). The principle of the operation consists in the rapid freeing of the body from toxic products, in stopping the further destruction of the gland and in removing the source of acute hemorrhagic pancreatitis (gallstones in the ducts, ampulla or bladder). Technically, the operation is performed more often through an abdominal incision (less often transpleural or lumbar). Through the fig. hepato-gastricum, mesocolon transversum, more often through lig. gastro-colicum, access to the gland is obtained. The exudate is removed with tampons, the capsule is incised (possibility of bleeding), the disintegrated parts of the gland are removed, the cavity is drained and tamponed. If the source of acute hemorrhagic pancreatitis is the biliary tract, then cholecystostomy and choledochotomy, performed simultaneously, improve the results. Among postoperative complications, besides collapse and peritonitis, bleeding from large vessels, sometimes late, as well as persistent fistulas of the pancreas for a long time should be noted. In the postoperative period, it is recommended to watch the skin, grease it with fat to avoid the corrosive action of trypsin, to follow a specific (Wolgemuth) diet and to administer large amounts of physiological solution or glucose. The results of the operation, as indicated above, depend on a number of reasons. The average mortality is 60%. A careful study of the collected case histories gives interesting data. Dreesmann on 118 cases had 52% mortality. However, of these, rationally treated with tamponade were 40 cases and mortality in this group was only 20%. In other authors, a considerable part of the mortality could be attributed not to the severity of the process, but to incorrect diagnosis and irrational treatment. Analysis of the collected case histories of Ruffanov gives the following figures: of 40 non-operated, all died (100%), of 160 operated, 105 died and were autopsied (65%), recovered-55 (35%). Consideration of the causes of death shows that in 77 cases out of 105, errors, irrational therapy were made (stones left in ductus choledochus, abscesses not opened, only a trial laparotomy done, etc.). Early and correct recognition, early surgical intervention, correct orientation on the operating table, radical operation on the pancreas (tamponade, drainage), inspection and drainage of the biliary tract and postoperative struggle with shock, collapse and poisoning of the body will undoubtedly significantly improve the mortality statistics. As for prevention, it is recommended to remember that acute hemorrhagic pancreatitis is most often the result of gallstone disease; timely and correct therapeutic treatment, especially in obese individuals, or surgical, if there are indications for it (see Gallstone disease), to a large extent protects patients from the development of a severe complication-acute hemorrhagic pancreatitis. Acute purulent pancreatitis.

(pancreatitis acuta suppurativa) develops as a result of infection entering the pancreas 1) hematogenically, especially during epidemic parotitis (Simon in 652 cases of parotitis had 10 cases of pancreatic involvement), less frequently during typhoid fever, scarlet fever, influenza, phlebitis, etc.; 2) after traumatic injuries to the pancreas (open and closed); 3) through the excretory duct of the gland during inflammatory processes in the bile ducts (see above about acute hemorrhagic P.); 4) through lymphatic pathways, which are in close connection with the bile ducts (see Gallbladder); 5) during inflammatory processes of the gastrointestinal tract (duodenitis, ascariasis, etc.); 6) when a stomach ulcer adheres to the pancreas; 7) as a result of necrotic-degenerative forms (acute hemorrhagic P.), less frequently - chronic P. Abscesses sometimes occupy small areas of the gland, sometimes the entire organ turns into a continuous abscess, which, having ruptured the capsule, can cause a peri-pancreatic subphrenic abscess or descend into the lumbar region, forming a phlegmon, which can reach the inguinal region (Riese).-Usually, diffuse purulent inflammation (pancreatitis apostematosa) or isolated abscesses are distinguished, located more often in the head of the gland. The causative agents are most often staphylococci, streptococci, pneumococci, and the bacillus coli. Microscopically, there is a picture of edema, catarrhal process of the excretory ducts, infiltration in the vessel walls and interstitial tissue up to hemorrhages, necroses in entire lobules, purulently melted. Usually, swelling of the lymph glands is noted. The clinical picture of acute purulent P. is characterized, on one hand, by the symptoms of acute hemorrhagic P., but less severe, on the other hand - by the symptoms of a purulent process. Vomiting, pain in the epigastric region, constipation, abdominal bloating, resistance in the area of the pancreas, elevated temperature, chills - the main symptoms of acute purulent P. When the abscess compresses the d. choledochi, obstructive jaundice may occur. Sometimes a tumor can be palpated if the abscess has opened into the bursa omentalis. As with acute hemorrhagic P., rupture of large vessels can lead to fatal intra-abdominal bleeding, and rupture of the abscess into the free abdominal cavity can lead to peritonitis. Laboratory findings sometimes show sugar in the urine, diastase, fatty stool.-^Diagnosis of acute purulent P. is not difficult in those rare cases when metastasis of the abscess to the pancreas during any infectious disease gives a local picture of the process (resistance, pain, sometimes jaundice, disturbance of secretion). In other cases, the diagnosis is very difficult, and sometimes impossible.-The prognosis is more favorable than in acute hemorrhagic P. The mortality rate is 47-50%. The most favorable outcome is given by encapsulated abscesses and the unfavorable outcome is given by diffuse phlegmons. Spontaneous "self-healing" occurs when the abscess ruptures into the gastrointestinal tract. Mild forms of catarrhal-purulent P. may pass, leaving as a consequence interstitial P. Treatment-surgical: opening of the abscess. The best route is a lumbar incision, but this is possible only in late stages, when the diagnosis is made, in most cases of undiagnosed condition, it is necessary to make an intraperitoneal incision. Drainage is better done extraperitoneally. For an isolated abscess, incision and tamponade are performed, for diffuse - incision and splitting of the pancreatic tissue containing abscesses or purulent infiltration. A feature of the organ is its high sensitivity to injury. For deep abscesses, puncture and opening of the abscess with a blunt instrument, tamponade and drainage are recommended. The bile ducts should be examined and measures taken to eliminate the primary focus, if such exists. Tamponade is prolonged. In case of favorable outcome, as in the hemorrhagic form, it is recommended to remember possible disturbances of external and internal secretion of the pancreas and the need to choose an appropriate dietary regimen. Chronic P. (p.chronica) has various etiology and pathogenesis (syphilis, tuberculosis, catarrh of the excretory ducts of the gland, infection of them or lymphatic pathways). The entire gland can be involved in the process or only the head of the gland can be affected. The latter form (P. of the head) is now increasingly noted as a complication of gallstone disease (50% - Kehr, 60% - Robson, 81% - Mayo). Experimentally, P. has been obtained by a number of authors (Korte, Polya, Hess, Martynov, Ruffanov, etc.). Another source of chronic P. is the outcome of various forms of acute hemorrhagic and acute purulent P. or the introduction of infection through the gastrointestinal tract.-Patho-anatomically, two forms are distinguished: hypertrophic and atrophic. The development and growth of connective tissue between the lobules leads to their compression and atrophy (cirrhosis of the pancreas). Both interlobular and intralobular forms are observed. The development of connective tissue in the head of the gland gives the impression of a dense and sometimes hard tumor. The interlobular form leads to disturbance of only external secretion, little affecting internal secretion. The intralobular form leads to the death of the Langerhans islets, which is manifested by disturbance of internal secretion. Sometimes there is an expansion of the smallest ducts, creating the impression of small-cystic degeneration of the gland. Microscopically, sclerosis and atrophy of the glandular tissue are noted.--Clinically, complaints come down to pain in the epigastrium with radiation to the sacrum, right shoulder, left scapula, kidney. Sometimes the pain is dull, sometimes of colic nature, associated with food intake, sometimes dyspepsia, cachexia, weight loss, disturbance of bowel movements (diarrhea, constipation) appear. If an inflammatory tumor of the head forms, then obstructive jaundice develops. When the insular apparatus is affected, sugar appears in the urine. Objectively-tenderness, sometimes a tumor in the epigastrium or to the right of the midline, fatty stool, undigested muscle fibers in the stool.--Diagnosis at the beginning of the process is difficult. During surgery, the tumor of the head of the pancreas is sometimes not easy to distinguish from cancer. In the presence of cholecystitis and stones, chronic P. can be confused with a stone in the d. choledochi. Since P. of the head most often develops on the basis of diseases of the bile ducts, the gallbladder is usually changed, and the Courvoisier symptom is not observed (difference from cancer of the head of the gland). Treatment in the initial stages of chronic P., not causing obstructive jaundice, consists in the application of heat, alkaline waters (Carlsbad). Some recommend potassium iodide and an appropriate diet. For P. of the head, not accompanied by obstructive jaundice and being a consequence of gallstone disease, removal of stones, diversion of infected bile and drainage of the hepatic pathways are recommended, whereby further compression of the d: choledochi by the inflammatory tumor of the head of the pancreas can be prevented. When it is compressed and obstructive jaundice occurs, prolonged diversion of bile can lead to exhaustion. In such cases, anastomosis of the gallbladder, if it is not changed, with the stomach or duodenum is recommended; for a shrunken gallbladder-choledochoduodenal anastomosis. This operation is increasingly being used; the mortality rate is 3-10%.-Since more than 80% of cholecystitis and cholelithiasis are complicated by chronic P., prophylactically, treatment of inflammatory processes of the gallbladder, timely surgery and an appropriate dietary regimen are recommended.