ACUTE CHOLECYSTITIS. CLINIC. DIAGNOSTIC. TACTICS.
CHRONIC CALCULOUS CHOLECYSTITIS. CHOLELITHIASIS, nCHOLANGITIS, MECHANICAL JAUNDICE.
ACUTE CHOLECYSTITIS
Acute cholecystitis is inflammation of gall-bladder. nAfter frequency this disease takes second place after appendicitis and makes nabout 10 % in relation to all acute surgical diseases of organs of abdominal ncavity.
Anatomy of the hepatoduodenal region: 1-А. gastrica sinistra; 2-А. splenica (lienalis); З — Rami oesophageales (r. A. gastrica sinistra); 4 — A. phreni-ca inferior (dextra et nsinistra); 5 — Aa. ngastricae breves; 6-А. splenica (lienalis) n(Endastre); 7-А. gast-roomentalis (epiploica); 8-А. pancre-atica dorsalis; 9-А. hepatica ncommunis; 10 — A. gastroomentalis (-epiploica) dextra; 11 — A. gastroduodenalis; 12 — A. npancreaticoduodenalis; 13-А, npancreaticoduodenal superior nposterior; 14 —A. supraduodenalis; 15—A. gastrica dextra; 16 — V. portae; 17 — Ductus choledochus; 18 — A. nhepatica propria; 19 — Ductus cysticus; 20 — A. cystica; 21 — Ramus dexter; 22— Ramus sinister; 23 — Truncus coeliacus; 24 — Aorta abdominalis; 25 — A. phrenica inferior (dextra et sinistra); 26 — Vesica fellea
Biliary Anatomy
Anatomy: vascular supply
Etiology and pathogenesis
In etiology of cholecystitis major factorsare nconsidered the following: infection, discoordination passage of bile and nmetabolic disturbance. All of them predetermine formation of concrement. Cholecystitis is often caused by cholelithiasis (the presence of ncholeliths, or gallstones, in the gallbladder), with choleliths most commonly blocking the cystic duct directly. This leads nto inspissation (thickening) of bile, bile stasis, and secondary infection by gut organisms, npredominantly E. coli and Bacteroides species. At bacteriological nexamination of maintenance of gall-bladder intestinal stick is sown, nstaphylococcus and enterococcus. Rarer there is streptococcus and other nmicroorganisms. The gallbladder’s wall nbecomes inflamed. Extreme cases may result iecrosis and rupture. nInflammation often spreads to its outer covering, thus irritating surrounding nstructures such as the diaphragm and bowel.
Considerably more frequently (70–80 %) women are ill nin whom during pregnancy the passage of bile in duodenum is always violated. It nis promoted by immobile way of life, “sedentary work” and other types of nhypodynamia.
Less commonly, in debilitated and trauma patients, the ngallbladder may become inflamed and infected in the absence of cholelithiasis, nand is known as acute acalculous cholecystitis. This can arise in patients with anorexia nervosa, as the lack of nstimulation of the gallbladder leads to an infectious process.
Stones in the gallbladder may cause obstruction and the naccompanying acute attack. The patient might develop a chronic, low-level ninflammation which leads to a chronic cholecystitis, where the gallbladder is nfibrotic and calcified.
Pathomorphology
The catarrhal develops at acute cholecystitis nfibrinogenous and festering inflammation. The wall of gall-bladder is thickened, nswollen, hyperemic with stratifications of fibrin and pus. Progress of process ncan bring walls over of gall-bladder to necrosis (gangrene).
Classification
Acute cholecystitis is divided into:
I. Acute calculous cholecystitis
II. Acute non-calculous cholecystitis
1. Catarrhal.
2. Phlegmonous.
3. Gangrenous.
4. Perforated.
5. Complicated:
a) Hydropsy;
b) Empyema;
c) Pancreatitis;
d) Icterus;
e) Hepatitis;
f) Cholangitis;
g) Infiltrate;
h) Abscess;
i) Hepatic-kidney ninsufficiency;
j) Peritonitis n(local, poured out, general).
Symptoms and clinical passing
The disease, as a rule, begins after violation of ndiet: reception of plenty of rich, meat food, especially in combination with nstrong drinks.
Pain syndrome. Characteristic for it is great arching pain in right nhypochondrium and epigastric area with an irradiation in right supraclavicular narea and right shoulder. If pain syndrome has the strongly expressed cramp-like ncharacter, it is named hepatic colic.
Cholecystitis usually presents as a pain ithe right upper quadrant. This is known as biliary ncolic. This is initially intermittent, but later usually presents as a nconstant, severe pain. During the initial stages, the pain may be felt in aarea totally separate from the site of pathology, known as referred pain. The pain is originally nlocated in the right upper quadrant but the referred pain may occur in the nright scapula region (Boas’ sign).
This may also present with the above mentioned pain after neating greasy or fatty foods such as pastries, pies, and fried foods.
Dyspepsia syndrome. Frequent symptoms which disturb a patient, are nnausea, frequent vomitting, at first by gastric maintenance, and later — with a ntouch of bile. Afterwards feelings of swelling of stomach, delay of emptying nand gases often join to them.
This is usually accompanied by a low-grade fever, ndiarrhea, and granulocytosis. The gallbladder may be tender and distended. More nsevere symptoms such as high fever, shock and jaundice indicate the development of ncomplications such as abscess formation, perforation or ascending cholangitis. Another ncomplication, gallstone ileus, noccurs if the gallbladder perforates and forms a fistula with the nearby small bowel, leading nto symptoms of intestinal nobstruction.
Examination. During examination almost in all patients subicterus nof sclera even at the normal passage of bile can be observed. Tongue, as a nrule, assesses by stratifications of whiter-grey colour. Patients complain for dryness nin mouth. In difficult cases the tongue is usually dry, assessed by white nstratification with a yellow spot in the center, that depends on passing of nattack of disease.
Increase of temperature of body is brief and ninsignificant (on the average to 37,2 0С) at catarrhal cholecystitis and more nproof (within the limits of 38 0 С) at its destructive forms.
Tachycardia to a certain extent testifies the degree of nintoxication. At first hours of disease the pulse, usually, is relevant to the ntemperature, and at progress of process, especially with development of nperitonitis, it becomes frequent and of weak filling.
During palpation painfulness in the place of crossing nof right costal arc with the external edge of direct muscle of stomach can be nobserved (the Kehr’s point). By superficial and deep palpation of right nhypochondrium, as a rule, painfulness, increased gall-bladder is exposed, that ncan be important as a symptom, and sometimes determining for the diagnosis.
The row of characteristic symptoms is determined ithe clinic of acute cholecystitis
Murphy’s symptoms is a delay of breathing during npalpation of gall-bladder on inhalation.
Kehr’s symptom is strengthening of pain at pressure othe area of gall-bladder, especially on deep inhalation.
Ortner’s nsymptom — painfulness at the easy pattering on right costal arc by the edge of npalm.
Mussy’s symptom — painfulness at palpation between the nlegs (above a collar-bone) of right nodding muscle.
Blumberg’s nsigns are the increases of painfulness at the rapid taking away of fingers by nwhich a front abdominal wall is pressed on. This symptom is not pathognomic for ncholecystitis but matters very much in diagnostics of peritonitis.
It is also needed to mark the importance of gradatioof expression of symptoms: acutely positive, poorly positive, doubtful, absent. n
Symptoms of acute cholecystitis can grow during 2–3 nhours, and then without some treatment, under act of hot-water bottle or only nafter the conservative treatment is begun, quickly go to the slump and ndisappear completely. It always means, that the reason which caused acute ninflammation is liquidated (a spasm disappeared, concrement passes by a duct, nthe ball of mucus moves up and others).
Destructive cholecystitis by the demonstration is the nmost difficult clinical picture. Thus, gangrenous cholecystitis as a rule, runs nacross with the acutely expressed phenomena of intoxication and is accompanied nby the clinic of bilious peritonitis. The perforation can complicate nphlegmonous or gangrenous cholecystitis and then the sudden worsening of the npatient’s condition comes on the background of the expressed clinic of ndestructive process. It shows up at the beginning the sudden strengthening of npain and rapid growth of the phenomena of peritonitis. But it is needed to mark nthat such clinical picture can develop only in case of perforated maintenance nof gall-bladder in free abdominal cavity.
Laboratory information. Leukocytosis within the limits of 10×109/L and more, nchange of leukocytic formula to the left, lymphopenia and increased ESR. Laboratory values may be notable for aelevated alkaline phosphatase, npossibly an elevated bilirubin (although this may nindicate choledocholithiasis), nand possibly an elevation of the WBC count. CRP (C-reactive nprotein) is often elevated. The degree of elevation of these laboratory values nmay depend on the degree of inflammation of the gallbladder. Patients with nacute cholecystitis are much more likely to manifest abnormal laboratory values, nwhile in chronic cholecystitis the laboratory values are frequently normal.
Sonographic examination of gall-bladder can expose the increase of its sizes, nbulge of walls, development of perivesical abscesses, presence or absence of nconcrement and their sizes. Sonography is a sensitive and nspecific modality for diagnosis of acute cholecystitis; adjusted sensitivity nand specificity for diagnosis of acute cholecystitis are 88% and 80%, nrespectively. The diagnostic criteria are gallbladder wall thickening greater nthan 3mm, pericholecystic fluid and sonographic Murphy’s sign. Gallstones are not part of the ndiagnostic criteria as acute cholecystitis may occur with or without them.
Sonography. nAcute calculous cholecystitis.
Sonography. nAcute calculous phlegmonous cholecystitis.
Sonography. nAcute calculous gangrenous cholecystitis
Sciagraphy survey of organs of abdominal cavity allows to nestablish the presence X-ray photography-positive of concrement with maintenance nof calcium in the projection of gall-bladder.
CT scan. The reported sensitivity and specificity of CT scan findings are in the range of 90–95%. CT is more nsensitive than ultrasonography in the depiction of pericholecystic inflammatory nresponse and in localizing pericholecystic abscesses, pericholecystic gas, nand calculi outside nthe lumen of the ngallbladder. CT cannot see noncalcified gallbladder calculi, and cannot assess nfor a Murphy’s sign.
Variants of clinical passing and ncomplications
Clinical passing of acute cholecystitis is various and ndepends on the row of reasons among which degree of violation of passage of nbile by a cystic duct and choledochus, virulence of infection, presence or nabsence of pancreato-cystic reflux (pelting of pancreatic juice) have the most nvalue. To this passing it is needed to add the preceding anatomic and nfunctional changes of gall-bladder and adjoining organs, and also the state of nprotective and regulator mechanisms of patient.
Features of passing of acute cholecystitis in the ndeclining and old-year patients. For them large frequency of development of ndestructive forms of cholecystitis and their complication by peritonitis are ncharacteristic. Thus, it is needed to state that such changes in gall-bladder ncan develop already in the first hour of peritonitis as a result of perforatioof bubble. Atipical passing in these patients shows up, mainly, by disparity of nclinical picture of disease to the pathomorphologic changes present igall-bladder. In clinical picture in patients with the first plan the symptoms nof intoxication come often forward, while pain and signs of peritonitis can be nnot acutely expressed.
Hydropsy of ngall-bladder is its aseptic inflammation, that arises up as a result of nblockade of cystic duct by concrement or mucus. The bile from a bubble is nsucked in, and on replacement transparent exudation accumulates in its nformation. During palpation increased and unpainfully gall-bladder is marked ipatients.
Empyema nof gall-bladder is unliquidated timely hydropsy, that nat repeated infection is transformed in a new form. Gall-bladder in such npatients is palpated as a dense, moderately painful formation, however, the nsymptoms of irritation of peritoneum, as a rule, are absent. The high ntemperature of body, chill are periodically observed. In blood high nleucocytosis with the change of formula of blood to the left is present.
Biliary npancreatitis. Worsening of the patient’s condition, nappearance of pain, frequent vomitting, signs of cardio-vascular insufficiency, nhigh amylasuria, presence of infiltrate in epigastric area and positive nVoskresensky’s and Mayo-Robson’s symptoms are its basic signs.
An icterus narises up at violation of passage of bile in duodenum as a result of obturatioof choledochus by concrement, by putty or through the edema of head of npancreas. Thus icterus sclera, bilirubinemia, dark urine and light unpainted nexcrement arise.
Cholangitis. nThe Sharko triad is characteristic for the patient with this pathology. Next to npain syndrome and icterus, the temperature of body rises to 38–39 0С, there is na fever, high leucocytosis and decline of sizes of functional tests of liver is nobserved.
Hepatitis nshows up by icterus, growth of the phenomena of general weakness, increase ithe blood of indexes of alanine aminotransferase and asparaginase and alkaline nphosphatase. Liver at this pathology during palpation is painful with acute nedges.
Infiltrate is na complication, that can arise on 3–4 days after the attack of acute ncholecystitis. Dull pain presence of dense tumular formation with unclear ncontours in right hypochondrium, increase of temperature of body to 37,5–38 0С nthat negative symptoms of irritation of peritoneum are characteristic for it.
Abscess. Patients nwith this pathology complain about high temperature, pain in the right overhead nquadrant of abdomen, where painful tumular formation is palpated, the fever, ngeneral weakness, absence of appetite, icterus, sometimes vomitting. nRoentgenologicly in right hypochondrium the horizontal level of liquid and gas nis observed above it. High leucocytosis with the change of leukocytic formula nto the left is present in blood.
Hepatic-kidney ninsufficiency often can arise at the most difficult forms of cholecystitis. nThe general condition of patient is difficult, acutely expressed intoxication, nexcitation, hallucinations, delirium, oliguria and anuria are observed.
Gall bladder nperforation (GBP) is a rare but life-threatening complication of nacute cholecystitis. The early diagnosis and treatment of GBP are crucial to decrease npatient morbidity and mortality.
Approaches to this complication will vary based othe condition of an individual patient, the evaluation of the treating surgeoor physician, and the facilities’ capability. Perforation can happen at the nneck from pressure necrosis due to the impacted calculus, or at the fundus. It caresult in a local abscess, or nperforation into the general peritoneal cavity. If the bile is infected, ndiffuse peritonitis may occur readily and rapidly and may result in death A nretrospective study looked at 332 patients who received medical and/or surgical ntreatment with the diagnosis of acute cholecystitis. Patients were treated with nanalgesics and antibiotics within the first 36 hours after admission (with a nmean of 9 hours), and proceeded to surgery for a cholecystectomy. Two patients died and n6 patients had further complications. The morbidity and mortality rates were n37.5% and 12.5%, respectively in the present study. The authors of this study nsuggests that early diagnosis and emergency surgical treatment of gallbladder nperforation are of crucial importance.
Peritonitis nis the most frequent complication during the perforation of gall-bladder ifree abdominal cavity and shows up by tormina and repeated vomitting. Patients nare covered with a death-damp, the skin is pale, arterial pressure falls, pulse nis frequent and of weak filling. During the objective inspection the tension of nmuscles of front abdominal wall is marked, positive guardian symptom in the nright half of abdomen or along it is observed.
Mirizzi’s syndrome is a rare complication in which a gallstone becomes nimpacted in the cystic duct or neck of the gallbladder causing compression of the common bile duct (CBD) or common hepatic duct, resulting in obstruction and jaundice. The obstructive njaundice can be caused by direct extrinsic compression by the stone or from nfibrosis caused by chronic cholecystitis (inflammation). A cholecystocholedochal fistula can occur.
Multiple and large gallstones can reside nchronically in the Hartmann’s pouch of the gallbladder, ncausing inflammation, necrosis, fibrosis and nultimately fistula formation into the adjacent common bile duct n(CBD). As a result, the CBD becomes obstructed by either scar or stone, nresulting in jaundice. It can be divided into four types.
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Type I – No fistula present |
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Type IA – Presence of the cystic duct |
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Type IB – Obliteration of the cystic duct |
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Types II-IV – Fistula present |
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Type II – Defect smaller than 33% of the CBD diameter |
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Type III – Defect 33-66% of the CBD diameter |
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Type IV – Defect larger than 66% of the CBD diameter |
The treatment of choice nis laparotomic surgical excision of the gallbladder, and reconstruction of the ncommon hepatic duct and common bile duct.
Diagnosis program
1. Anamnesis and nphysical methods of inspection.
2. Survey sciagraphy of norgans of abdominal cavity.
3. Sonography.
4. General analysis of blood and urine.
5. Diastase urines.
6. Biochemical blood test (bilirubin, amylase, alanine naminotransferase, asparaginase, alkaline phosphatase, remaining nitrogen, ncreatinine).
7. Coagulogram.
Differential diagnostics
Perforated ulcer. For this disease the Mondor’s triad (knife-like npain, tension of muscles of front abdominal wall and ulcerous anamnesis) and npositive Spizharskyy’s symptom are characteristic (disappearance of hepatic ndullness). During roentgenoscopy survey of organs of abdominal cavity in a npatient pneumoperitoneum as sickle-shaped strip under the right or left dome of ndiaphragm is exposed.
Kidney colic. Pain at right-side kidney colic also can be localized nin right hypochondrium. However, it is always accompanied by disorders of nurination, and at cholecystitis, it as a rule, is not present. Next to it, nkidney pain always irradiates downward after passing of ureter, in privy parts. nExcept, for this pathology micro- or macrohematuria, presence of concrement ia bud, exposed at sonography and on survey urogram, absence of function of bud nduring chromocystoscopy can be characteristic.
Acute appendicitis. It is needed always to remember, that the subhepatic nlocation of the pathologically changed appendix is also able to show up pain iright hypochondrium. However, for patients with acute appendicitis beginning of npain in epigastric area, absence of hepatic anamnesis, expressed dyspeptic nphenomena, inflammatory changes from the side of gall-bladder at sonography are ninherent.
Heart attack of myocardium. The so called cholecysto-cardial syndrome which quite noften imitates stenocardia pain and suspicion on possibility of origin of heart nattack of myocardium can develop. Electrocardiography examination is decisive nin establishment of diagnosis. However, laparoscopy is applied in doubtful ncases.
Pancreatitis. Acute pancreatitis is accompanied by the expressed npain in the epigastric area of belting character. At palpation in left ncostal-vertebral corner patients feel painfulness (the Mayo-Robson’s symptom), nand it is not at cholecystitis.
Tactics and choice of treatment method
Conservative treatment to the patients in default of nthe expressed signs of destructive or complicated cholecystitis and convincing ninformation which specify on a calculous process in them is expedient to napplication.
It must include:
1. Bed rest.
2. Hunger of 1–3 days, in the following table № 5 by nPeuzner.
3. Cold on right hypochondrium.
4. Spasmolytics (sulfate of atropine, platyphyllin, npapaverine, ni-shparum, baralgin).
5. Antibacterial therapy:
а) semisynthetic penicillin (ampicillin, oxacilline, nampiox);
б) cephalospori(kefzol, klaforan);
в) nitrofurans n(nitrofurantoin, furazolidon);
g) sulfanilamides (biseptol, ethazzole, norsulfazole). n
6. Inhibitors of protease (contrical, trasilol, ngordox, antagosan).
7. Desensitizing preparation (dimedrole, pipolphen, ntavegile).
8. Disintoxication therapy (neohemodes, nreopolyglucine).
9. Vitamins (С, nВ1, В6, nВ12 vitamins).
Intensive pain in patients is taken off by morphine (1 n% – 1,0) together with introduction of atropine (0,1 % – 1,0). Less acute paiis halted by baralgin with platyphyllin and papaverine. If the patient’s ncondition from the conducted treatment does not get better, it is necessary to noffer urgent surgical interference.
Indication to surgical treatment. All forms of acute calculous cholecystitis, ndestructive and complicated forms of noncalculous cholecystitis (except for ninfiltrateу), and also acute catarrhal cholecystitis conservative treatment of nwhich was uneffective are subject to surgical treatment.
Overhead-middle laparotomy is considered the best nchoice. However, many surgeons give advantage to pararectal laparotomy, oblique n(by Koher) and angular (by Fedorov) accesses.
Methods of operative treatment. Most rational of operations at this pathology counts ncholecystectomy from the neck (retrograde). At its implementation the cystic nduct and artery are bandaged, and then gall-bladder is already deleted, sewing nup its bed. It is applicable at presence of shallow concrement in gall-bladder.
Cholecystectomy nfrom the bottom (antegrade) is applied in case of technical difficulties during nthe selection of elements of neck of bubble. It consists in deleting of bubble nfrom the bottom to the neck with the next bandaging of cystic duct, to the nartery and suturing of bed of gall-bladder.
Antegrade cholecystectomy
Retrograde cholecystectomy
Atipical ncholecystectomy. At this operative treatment gall-bladder is exposed after nits longitudinal axis, released from maintenance and under the control of the nfinger led in its lumen, position of neck is determined, and then deleted. nOperation is executed in case of widespread infiltrate and when accretions nsurround not only the bubble but also neck, cystic and bilious ducts. A surgeomust remember thus, that the searches of cystic duct and artery in such terms ncan be dangerous.
Atipical cholecystectomy
Laparoscopy ncholecystectomy. For its implementation it is drawn on complex nof special apparatus: operating laparoscop with a video camera and coloured nvideo monitor. After creation of pneumoperitoneum and introduction to the nabdominal cavity of laparoscope through the separate punctures of abdominal nwall instruments-manipulators are entered. With their help under the visual ncontrol in accordance with the image on video monitor, gall-bladder is deleted. nThus on stump of cystic duct and on an artery metallic clips are imposed.
Operating nRoom Set-Up
Trocars places
Exposing nthe Cystic Duct and Artery
Dissecting nthe Cystic Duct and Artery
Transecting nthe Cystic Duct and Artery
Dissecting nthe Body of the Gallbladder
Ideal cholecystolytotomy is operation that includes nopening of gall-bladder, deleting of concrement and its suturing. Applicable nfor patients with large single concrement in default of the expressed changes nfrom the side of wall of gall-bladder.
Cholecystostomy nis an operation, that is based on creation of external fistula of gall-bladder. nDuring this operation the bottom of the last is taken in a wound so that it was nisolated from abdominal cavity.
Laparoscopic ncholecystostomy is imposition of external fistula on gall-bladder under the ncontrol of laparoscope. It is the only operation, executed under the control of nlaparoscope.
video – ntechnic of the operation
video2 n
Cholecystectomy is applied, mainly, as the first stage nof operation in the very loosened patients for taking out the infected nmaintenance from bubble and ducts. This operation is palliative and often ithe future requires repeated operation for the removal of bilious fistula — ncholecystectomy.
It is needed to remember that during cholecystectomy nit is necessary to conduct the intraoperative revision of bilious ducts, which nmust include the examination, palpation and determination of diameter of nhepatico-choledochus (norm is to
Intraoperative ncholangiography is contrasting of bilious ducts by introductioiodine preparations (bilignost, cardiotrust, verigraphine in the concentratio30–33 %) in them through stump of cystic duct of soluble. Cholangiography nenables to define the width of ducts, presence or absence of concrement ithem, and also cone-shaped narrowing of terminal part of choledochus ncharacteristic of stenosis.
Cholangiomanometry is a method, that allows to expose the degree of nbilious hypertension in ducts by the water manometer of the Valdmann device. nNormal pressure is within the limits of 80–120 mm of waters. item (0,78–1,17 nkPa), and the higher testifies to bilious hypertension.
Debitomanometry nis a method of determination of amount of liquid at perfusion through the nFater’s papilla under permanent pressure for time unit (1 min). In patients nwith normal passing of bilious ducts the size to the debit of liquid at npressure
Choledochoscopy is a method of endoscopy examination of bilious ducts nby choledochoscope during choledochustomy.
The Choledochoscopy. Retrieving the CBD Stones
External draining of bilious ducts can be nexecuted by such methods:
1) by Pickovskyy – polyethylene catheter which is nentered through stump of cystic duct;
2) by Kehr — by Т-shaped latex drainage;
3) by Vyshnevsky — drainage to the gate of liver;
4) by Holsted.
Indication to external draining: 1) after diagnostic choledochustomy; n2) after choledocholytotomy; 3) at accompanying cholangitis, pancreatitis.
For internal draining of bilious ducts are applied by ntransduodenal sphincteroplasty or choledochoduodenostomy. At acute ncholecystitis these operations are executed under absolute indications. Such is nthe structure and tired out concrement of large duodenal papilla, multiple ncholedocholithiasis, presence of putty in ducts or their expansion.
The best method of renewal of normal outflow of bile nat stenosis and jammed concrement of large duodenal papilla is considered its ntransduodenal dissection. This method of internal draining allows to liquidate nthe reason of impassability of ducts and store the physiology passage of bile nin intestine.
At forming choledochodiodenoanastomosis most ndistribution acquired methods by Jurash, Flerken, Finsterer and Kirschner’s nmethods. The principle difference of them consists in correlations of directioof cut of choledochus and duodenum (longitudinal, slanting, transversal). The nwidth of anastomosis must be not less than 2,5–3 cm. It is thus needed to nremember, that imposition of choledochoduodenoanastomosis in the conditions of npresence of inflammatory process in abdominal cavity always needs to be nconnected with external draining of choledochus by Pikovskyy (double draining). n
n
OBTURATIVE ICTERUS
A obturative icterus is the type of icterus the reasoof which is violation of patency of bilious ways as a result of their nobstruction from within or external compression, or cicatrix narrowing.
Оbstructive njaundice, also called рost-hepatic jaundice, is caused by an interruptioto the drainage of bile in the biliary system. The most commocauses are gallstones in thecommon bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites nknown as “liver flukes” can live in the common bile duct, causing nobstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, cholangiocarcinoma, pancreatitis and pancreatic npseudocysts. A rare cause of obstructive jaundice is Mirizzi’s syndrome.
In complete obstructioof the bile duct, no urobilinogen is found in the urine, since bilirubin has no naccess to the intestine and it is in the intestine that bilirubin gets nconverted to urobilinogen to be later released into the general circulation. Ithis case, presence of bilirubin (conjugated) in the urine without nurine-urobilinogen suggests obstructive jaundice, either intra-hepatic or npost-hepatic.
The presence of npale stools and dark urine suggests an obstructive or post-hepatic cause as nnormal feces get their color from bile npigments. However, although pale stools and dark urine are a feature of biliary nobstruction, they can occur in many intra-hepatic illnesses and are therefore nnot a reliable clinical feature to distinguish obstruction from hepatic causes nof jaundice.
Patients also ncan present with elevated serum cholesterol, and often complain of severe nitching or “pruritus” because of the deposition of bile salts.
No single test ncan differentiate between various classifications of jaundice. A combination of nliver function tests is essential to arrive at a diagnosis.
Etiology and pathogenesis
Obstruction of external bilious ducts can arise for nmany reasons: as a result of inflammatory processes of surrounding organs n(pancreas, paracholedochus lymphatic knots), damage of walls of ducts during noperations. However, in most cases it is a gallstone disease, ncholedocholithiasis and related to them scar changes of large papilla of nduodenum. The second place among the reasons of obturation icterus is taken by ntumours of which the cancer of head of pancreas and large papilla of duodenum nis most widespread.
Disregarding the fact that each of the adopted ndiseases has special clinical passing, obturation of bilious ducts causes the nchanges which have general character. At complete blockade of external bilious nducts and growth of pressure higher than
Classification
(by О.О. Shalimov, 1993)
Obturation icteruses are ndivided into:
I. According to the nlevel of barrier:
1) obstruction of distal parts of general bilious nduct;
2) obstruction of supraduodenal part of general bilious nduct;
3) obstruction of initial part of general hepatic duct nand fork of hepatic ducts.
II. According to nthe etiologic factor:
1) conditioned by obturation by bilious concrement, nstrange bodies, grume of blood during hemobilia, parasite, iatrogenic influence nduring operation;
2) obstruction at the diseases of wall of bilious ways n— innate anomalies (hypoplasia, cysts and atresia), inflammatory diseases n(obstructing papillitis and cholangitis), scar strictures (posttraumatic and ninflammatory), bilious ways tumours of high quality;
3) obstruction caused by the out-of-ducts diseases, nthat pull them in the process (tubular stenosis of general bilious duct of npancreatic genesis, ulcerous disease of duodenum, paracholedocheal nlymphadenitis, peritoneal commissures).
Except that, according to the duration the disease nis distinguished:
1) acute obturative icterus, that to 10 days last;
2) protracted, that proceeds from 10 to 30 days;
3) chronic, that more than a month lasts.
Symptoms and clinical passing
The clinical picture of obturative icterus is founded, nfirst of all, on the symptoms caused by violation of outflow of bile.
A pain syndrome is a characteristic accomponiment of gallstone disease nand choledocholithiasis, that run with the attacks of hepatic colic. However, npain syndrome at these pathologies can often be not acutely expressed or quite nabsent. Pain is often observed at stricture of bilious ducts, but it is not nquite typical of patients with the cancer of bile ducts.
An icterus is nan important sign of obstruction of bilious ways, speed of origin and intensity nof which depend on whether well-kept or broken passage of bile in intestine is. nFor choledocholithiasis with “valve” character of concrement transitional npassing of icterus is inherent, and for cancer it is more proof and nprogressive.
The itch of body is a frequent accomponiment of icterus, that arises up nas a result of action of bilious acids. It is thus needed to remember, that nunder the conditions of damage by tumour the itch which proceeds for a long ntime appears at first, only later there appears icterus. During examination the nyellowness of sclera, mucus shells and skin are observed. At the same time npatients specify urines and discolorations of excrement darkening (“argil”). nThe increase of temperature of body testifies the development of cholangitis, nmetastasis of tumors in liver is rarer.
In emaciated patients in right hypochondrium it is nsometimes possible to see formation, that moves during breathing, probably it nis a gall-bladder. If it is elastic, unpainful and it is accompanied by icterus n(the Courvoisier’s symptom), a patient then suffers from cancer of head of pancreas nor distal parts of general bilious ducts.
However, it is necessary to warn, that determinatioof character of icterus only on the basis of clinical signs to a great extent ncarries only conditional character. It must be connected to the fact that at nparenchymatous hepatitis expressed cholestasis often is observed, and at nobturation icterus damage of hepatic cells is characteristic. Therefore for nestablishment of diagnosis of obturative icterus, except for clinical ninformation, special methods of examination are necessary.
Laboratory information. For obturative icterus a cholestatic syndrome with nhigh bilirubinеmia mainly due to direct faction of bilirubin and bilirubinuria nis characteristic, by absence of urobilin in urine and stercobilin iexcrement, by high activity of alkaline phosphatase at the insignificantly npromoted transaminase activity and negative thymol test.
At growth of nhyperbilirubinemia this intercommunication changes in the side of increase of ndirect bilirubin. In general analysis of blood unsteady changes are which ndepend on the degree of intoxication or occult bleeding (in cancer patients).
Sonography examination allows to define the sizes of liver, gall-bladder, nstate of internal and external hepatic ducts, presence and degree of expansioor narrowing, presence or absence of concrement and new formation in hepatic nparenchyma.
Sonography nexamination
Duodenography in the conditions of artificial low blood pressure napply for the exposure of pathology of organs of pancreatoduodenal area.
Retrograde cholangiopancreatography enables to nexamine stomach, duodenum by endoscope, to conduct biopsy, to extract bile and npancreatic juice for examination, to get the roentgenologic image of ducts: nexternal and internal hepatic ducts and duct of pancreas, and in a number of ncases at presence of concrement to conduct endoscopic papillotomy and nextraction of them through papillotomic access.
Retrograde ncholangiopancreatography
Percutaneous ntranshepatic cholangioduodenography is used for the exposure of npathology of bilious ways. It to certain extent allows to expose both character nand localization of obturation in the area of hepatoduodenal area.
Laparoscopy is a ndiagnostic remedy that enables to define the sizes of liver, its colouring, ncharacter of surface, presence of metastases, size and degree of tension of ngall-bladder. Under the control laparoscope it is possible to execute puncture nof gall-bladder and conduct cholecystocholangiography and cholecystostomy.
The scanning of liver creates terms in which it is npossible to expose the primary and metastatic tumours of liver or other npathology of organ.
Variants of clinical passing and ncomplications
Clinical passing of icterus almost always depends othe reasons of obturation of bilious duct. In patients with tumours an icterus ngradually makes progress and results in complete and permanent obturation, ntogether with that, at presence of concrement in bilious ducts intensity of nicterus can vary. Its temporal, transitional character takes place at ncholedocholithiasis, acute cholecystitis or pancreatitis.
On this background in the case of joining of infectiocholangitis, abscess formation in liver and sepsis quickly develops. In other ncase there can be the bleeding (more frequent gastroduodenal) or hepatic-kidney ninsufficiency.
In some patients internal bilious fistula, which nclinically is proof cholangitis, appears as a result of inflammatory and nnecrosis processes. On the sciagram survey of organs of abdominal cavity isuch cases it is possible to see air in the hepatic ducts, the so called n“aerocholia”.
Diagnosis program
1. Anamnesis and nphysical methods of examination.
2. General analysis of nblood and urine.
3. Analysis of urine odiastasis.
4. Biochemical blood ntest (bilirubin, urea, albumin-globulin coefficient, blood on an australiaantigen, amylase, alanine aminotransferase, asparaginase, alkaline phosphatase). n
5. Coagulogram.
6. Sonography.
7. Endoscopy.
8. Retrograde ncholangiopancreatography.
9. Laparoscopy with nbiopsy.
10. Percutaneous transhepatic ncholangioduodenography.
11. Computer tomography.
Differential diagnostics
The main task of differential diagnostics of icterus nis a determination of surgical or unsurgical nature. In fact the decision of nthis question enables to take the amount of doubtful diagnostic laparotomy to nthe minimum.
Taking it into account, it is always needed to nremember, that among the diseases which can show up as icterus, viral hepatitis ntake a considerable place, mostly its cholestatic form, new formation of nhepatopancreatoduodenal area and gallstone disease.
Viral hepatitis is none of many clinical forms of viral infection the characteristic feature of nwhich is proof and protracted cholestasis. The disease carries the protracted ncharacter. For the pre-icteric period of hepatitis the inherent clinical triad nis the itch of skin, fever, arthralgia. Approximately in half of patients it is npossible to palpate a spleen and moderately increased liver. Laboratory the nincrease of activity of alanine aminotransferase and aspartate aminotransferase nand positive thymol test are determined. Also the reaction on bilious pigments, nbilious acids and urobilin in urine is positive.
Difficult from the point of view of verification of ndiagnosis it is needed to count combination of such diseases, as viral nhepatitis in patients with cholelithiasis or obturation by tumour in patients nwho suffer from alcoholism.
Taking into account information of previous methods, nonly successive application of sonography, endoscopic retrograde pancreatocholangiography nor percutaneous transhepatic cholangioduodenography and laparoscopy, allows nmaximally exactly to set diagnosis. Thus on the first stage it is needed to use nthe non-invasive methods of diagnostics (sonography), on the second useful are ninvasive methods of the direct contrasting of bilious ways (retrograde endoscopic ncholangiopancreatography, percutaneous transhepatic cholangiopancreatography) nwhich in the case of necessity can transform from diagnostic into medical n(endoscopic papillosphincterotomy at stenotic papillitis and ncholedocholithiasis, dilatation and endoprosthesis replacement of bilious ways nat cicatrix stricture and tumours of bilious ducts).
|
Table of diagnostic tests |
|||
|
Function test |
Pre-hepatic Jaundice |
Hepatic Jaundice |
Post-hepatic Jaundice |
|
Total bilirubin |
Normal / Increased |
Increased |
|
|
Conjugated bilirubin |
Normal |
Increased |
Increased |
|
Unconjugated bilirubin |
Normal / Increased |
Increased |
Normal |
|
Urobilinogen |
Normal / Increased |
Increased |
Decreased / Negative |
|
Urine Color |
Normal |
Dark (urobilinogen + conjugated bilirubin) |
Dark (conjugated bilirubin) |
|
Stool Color |
Normal |
Normal/Pale |
Pale |
|
Alkaline phosphatase levels |
Normal |
Increased |
|
|
Alanine transferase and Aspartate transferase levels |
Increased |
||
|
Conjugated Bilirubin in Urine |
Not Present |
Present |
|
|
Splenomegaly |
Present |
Present |
Absent |
n
n
Tactics and choice of treatment method
Final diagnosis, that maximally represents the character nof obturative icterus and volume of the most operative treatment, as a rule, is nset only during the intraoperative revision. At determination of medical ntactics and choice of method of surgical treatment of such icterus it is needed nalso to objectively estimate weight of general condition of patients. For this npurpose it is necessary to take into account the character of icterus, stage of nhepatic insufficiency keeping in mind the duration and intensity of ncholestasis, presence and character of cholangitis, weight and expression of naccompanying pathology, eyelids of patients.
Medical measures in preoperative period must be ndirected on correction of violations of homeostasis, hemocoagulatio(aminocapronic acid, vicasol, 10 % solution of chlorous calcium, one-group nfresh-frozen plasma, inhibitor of protease), improvement of microcirculation iliver (10 % solution of glucose with insulin, reopolyhlucine, nhepatoprotectors), deoxidation organism (neohemodes, enterosorbent), biliary ndecompression (percutaneous transhepatic cholangiopancreatocholangiostomy or ncholecystostomy), antibacterial therapy at the phenomena of cholangitis taking ninto account the character of sown microflora and its sensitiveness to the nantibiotics and vitamins.
In case of the gallstone disease complicated by ncholedocholithiasis and mechanical icterus, the volume of surgical interference nmust include: cholecystectomy, choledochuslithotomy and external or internal ndraining of general bilious duct. At presence of the special apparatus in case nof choledocholithiasis complicated by mechanical icterus, two-stage tactics of ntreatment is the method of choice — endoscopic papillosphincterotomy with nsubsequent extraction of concrement and their lithotripsy on the first stage nand cholecystectomy — on the second. Endoscopic papillosphincterotomy is the nmethod of choice at treatment of remaining (after cholecystectomy) ncholedocholithiasis.
For declining patients with heavy accompanying npathology combination of extracorporal shock-wave lithotripsy with endoscopic nsanation of hepaticocholedochus is an effective method. For some of them at the nhigh risk of operative treatment and small concrement of general bilious duct n(by the diameter of to
At malignant new formations of bile-excreting ways nwith a obturative icterus, depending on distribution of tumour process, radical nor palliative operative treatment are executed.
For patients with the tumours of head of pancreas, nlarge papilla of duodenum and terminal part of choledochus, that is exposed to nradical operation, a pancreatoduodenal resection is performed, thus in the case nof high icterus on the first stage of treatment bilious decompression of the nhepatobiliary system is performed (percutaneous hepaticocholangiostomy, forming nof biliary-enteric anastomosis). A pancreatoduodenal resection is executed othe second stage, in 30–35 days after imposition of bile-excreting anastomosis nand liquidation of icterus.
Palliative bile-excreting operations at the neglected ntumours are mainly directed on liquidation of obstruction of bilious ducts. Isuch patients, as a rule, roundabout biliary-enteric anastomosis is imposed: ncholecystoentero- or hepaticojejunostomy. If through technical difficulties and nbad general condition of patients it is impossible to execute this, external ndraining of bilious ways is applied.
ACUTE PANCREATITIS
The basis of disease of pancreas is ndegenerative-inflammatory processes which are considered to be acute npancreatitis, the so called autolysis tissue by its own enzymes. In the nstructure of acute pathology of organs of abdominal cavity this disease takes nthe third place after acute appendicitis and cholecystitis. Women suffer from nacute 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 ndisease. Its secondary forms, which arise on the background of pathologies of nbile-excreting system and duodenum are closely associated with anatomic and nfunctionally with pancreas, and are met in clinical practice.
The pathogenesis of acute npancreatitis has not beeot fully understood. The mechanism by which the npassage of gallstones induces pancreatitis is unknown. Suggested possible ninitiating events in gallstone pancreatitis include the reflux of bile into the npancreatic duct due to transient obstruction of the ampulla during passage of ngallstones. In the past two decades there has been much interest about early nremoval of retained CBD stones and how beneficial it would be for patients with nacute biliary pancreatitis. Many years later it was found that over 85% of npatients with so called gallstone pancreatitis spontaneously passed stones that nwere recoverable in the stool.
This discovery supported the n’common channel theory’. Subsequently, it was demonstrated that sterile bile ndoes not result in pancreatitis. However, infected bile is capable of nactivating pancreatic enzymes leading to auto digestion of the gland. These two concepts: (a) reflux of infected bile into the npancreas activating a cascade of proteolytic enzymes, and (b) obstruction of npancreatic duct causing acinar disruption from raised pressure, are the favored nexplanations for the triggering of gallstone pancreatitis. A potentially nunifying, yet unproven, hypothesis advanced by Moody in 1993 states that ngallstones initiate pancreatitis through obstruction of the pancreatic duct and nthat progression to necrosis and severe pancreatitis requires the reflux of nbile.
Among the “starting” factors of origin of ncholelithiasis disease (biliary pancreatitis) abuse by an alcohol and food noverloads (fat and irritating products), traumas of pancreas, operating-room iparticular, and also separate infectious diseases (parotitis, mononucleosis) nare most frequent, especially infection of bilious ways. However, in 10–20 % of npatients the reason of acute pancreatitis remains unknown (cryptogenic form).
In the basis of such damages of pancreas and enzymic ntoxemia lies mainly activating of pancreatic, and then the tissue enzymes n(tripsin, lipase, amylase). Often the combination of the broken outflow of npancreatic secret and promoted secretion takes place, which provokes nintraductal hypertension.
Among explanations of primary mechanisms of activating nof pancreatic enzymes the most value belongs to: a) theory of “general duct” nwith reflux of bile in the ducts of pancreas; b) blockade of outflow of npancreatic juice with development of intraductal hypertension and penetratioof secret in interstitial tissue; in) violation of blood flow of pancreas n(vasculitis, thrombophlebitis and embolisms, cardiac insufficiency and others nlike that); g) toxic and allergic damages of gland. The role of alcohol in such nsituations can be dual: stimulation of secretion of pancreas and direct ndamaging action on its tissue.
Acute pancreatitis: Mechanisms
Pathomorphology
The process of acute inflammation of pancreas nconsistently passes the stages of edema, pancreatonecrosis and festering pancreatitis. nIn the stage of edema there is pancreas of hyperemic, increased in volume, with nthe shallow hearths of necrosis or, as it is in swingeing majority of cases, nwithout them.
Pancreatonecrosis can pass with fatty or hemorrhagic ncharacter. In the first case, as a rule, pancreas is increased, dense, cut nwhity-yellow hearths are selected to necrosis. Increase of crimson-black npancreas with darkly-brown infiltrate on a cut is characteristic for nhemorrhagic pancreatonecrosis.
Dystrophy of parenchyma is exposed microscopically, up nto necrosis, hemorrhages, thromboses of vessels and signs of inflammatory ninfiltration.
Classification
(V All-russian convention of surgeons, n1978)
I. Clinico-anatomy nforms:
1. Arching form.
2. Fatty pancreatonecrosis.
3. Hemorrhagic pancreatonecrosis.
II. Prevalence of nnecrosis:
1. Local (focus) damage of gland.
2. Subtotal damage of gland.
3. Total damage of gland.
III. Ran across: nabortive, progressive.
IV. Periods of disease:
1. Period of hemodynamic nviolations and pancreatogenic shock.
2. Period of functional ninsufficiency of parenchymatous organs.
3. Period of degenerative and nfestering complications.
Symptoms and clinical passing
The ndiagnosis of gallstone pancreatitis should be suspected if the patient has a nprior history of biliary colic. Although ngallstone pancreatitis is the most common cause of pancreatitis, other netiologies must be considered, prior to initiating treatment, like moderate to nheavy alcohol consumption over a period of years. Other causes include nmedication, genetic diseases, infectious agents, postoperative states, nendoscopic procedure involving pancreatic and bile ducts and other types of ninjury to pancreas. It goes nwithout saying that a detailed history and careful physical examination are the nfirst step towards making the diagnosis. Laboratory nand radiological investigations are critical for diagnosis as well as prediction of prognosis when a npatient presents with gallstone pancreatitis. Documenting an elevated serum namylase and/or lipase is helpful in diagnosing pancreatitis. Serum amylase is nelevated in at least 75% of cases of acute pancreatitis and remains elevated nfor 5-10 days in most patients. However, amylase lacks specificity for pancreatitis because nit can be elevated in other disorders. Lipase is more specific for npancreatitis, but both enzymes may be increased in renal failure and various nabdominal conditions (e.g., perforated ulcer, mesenteric vascular occlusion and nintestinal obstruction). Other causes of increased serum amylase include nsalivary gland dysfunction, macro amylasemia, and tumors that secrete amylase. Serum nlipase has a longer half life than amylase and therefore tends to remaielevated for longer. Using a cut-off of three times the upper limit of normal, nthe sensitivity of serum lipase for pancreatitis approaches 90% in patients npresenting with abdominal pain. A urine dipstick for trypsinogen-2 has sensitivity and specificity of nmore than 90% for acute pancreatitis.
The disease begins suddenly, after nthe surplus reception of rich spicy food and use of alcohol. Pain, vomiting and nphenomena of dynamic intestinal obstruction are considered the most ncharacteristic signs of acute pancreatitis.
A stomach-ache is permanent and so nstrong, that can result in shock, localized in an epigastric area and left nhypochondrium. Some patients feel pain in right hypochondrium with irradiatioin the back, loin or breastbone.
Paiirradiation on acute pancreatitis
In a short period of time after nappearance of pain there is a repeated strong vomiting, that does not nfacilitate the state of patient.
In general vomiting is considered a nfrequent and characteristic symptom. It is repeated or continuous and never nbrings facilitation. Vomit masses contain bile, as admixture, and at the ndifficult form of acute pancreatitis remind “coffee-grounds”.
Nausea, hiccup, belch and dryness ia mouth are attributed as less characteristic symptoms of this pathology.
During the examination the skin is npale, often subicterus. Some patients have cyanosys with a “marble picture” as na result of violation of microcirculation. Later the component of respiratory ninsufficiency can join it. At progressive general condition the patient quickly ngets worse to passing of acute pancreatitis, intoxication grows. The skin takes nshelter with sticky sweat.
The temperature of body of patients at the beginning of disease can be normal. nIt rises at resorption of products of autolysis tissue and development of ninflammatory process in bilious ways.
The pulse in most cases is at first nslow, then becomes frequent, notedly passing ahead the increase of temperature nof body.
Arterial pressure goes down.
The tongue in the first hour of ndisease is moist, assessed by white and grey raid. At vomiting by bile the raid nhas yellow or greenish tint.
The abdominal is blown away, nperistaltic noises are loosened. The signs of paresis of stomach and intestine ndemonstrate early. They need to be included in the pathological process of nmesentery root of bowel. At palpation painfulness in an epigastric area and iright, and sometimes and in left, hypochondrium is marked. However, in spite of ngreat pain in stomach, it remains soft for a long time. A little later there is nmoderate tension or resistance of muscles of front abdominal wall.
Poor local symptoms during heavy nintoxication are characteristic for the early period of acute pancreatitis. nLater there are symptoms of irritation of peritoneum, and at percussion dulling nis marked in lateral parts of abdominal as a result of accumulation of liquid, nand also the sign of aseptic phlegmon of retroperitoneal cellulose as slurred nor edema of lumbar area is seen. For diagnostics of acute pancreatitis there is nthe row of characteristic symptoms which have different clinical value.
The nMondor’s symptom is violet spots on face and trunk.
The nLagermph’s symptom is acute cyanosys of person.
The nHalsted’s Symptom is cyanosys of abdominal skin.
The Gray’s nsymptom is cyanosys of lateral walls of abdomen.
The nKullen’s symptom is the yellow colouring of skiear a belly-button.
The nKorte’s symptom is painful resistance as a lumbar bar in a epigastric area non 6–7 cm higher belly-button.
The nVoskresynskyy’s symptom is absence of pulsation of abdominal aorta in aepigastric area.
The nMayo-Robson’s symptom is feeling of pain at pressure by fingers in the left ncostal-vertebral corner.
The Rozdolskyy’s nsymptom — painfulness at percussion above pancreas.
The nBlumberg’s symptom — in patients with acute pancreatitis more frequently is nlow-grade. Such feature of this sign of irritation of peritoneum needs to be nexplained by character of localization of pathological process, mainly iretroperitoneal spacious.
In clinical passing of pancreatonecrosis nit is possible to select three periods (V.S. Saveljev, 1978).
The I period (hemodynamic violations nand pancreatogenic shock) lasts during 2–3 days. Violation of central nhemodynamics, diminishment of volume of circulatory blood and disorders of nmicrocirculation, which at first arise as a result of angiospasm, are nconsidered the most characteristic signs, and later as a result of joining of nthe intravascular rolling up and laying of elements of blood.
The II period (insufficiency of nparenchymatous organs) lasts from 3rd to the 7th day of disease. Violation of nfunctions of basic organs and systems, sign of cardio-vascular, hepatic and nkidney insufficiency and growth of violations of breathing are thus observed. nIn this period there is possible damaging of the central nervous system, which nis erected mainly to disorders of psyche, appearances of delirium and commas nwhich in the eventual result are the main reasons of patients’ death.
The III period (postnecrosis ndystrophic and festering complications) comes in 1–2 weeks after the beginning nof disease. During it, on the background of progress of necrosis processes ipancreas, the regenerative changes develop, there are parapancreatic infiltrate nand cysts, cystic fibrosis of pancreas. Aseptic retroperitoneal phlegmon which nstrengthens intoxication can also develop. There is festering pancreatitis at njoining of infection. During this period such complications, as erosive nbleeding, internal or external fistula, retroperitoneal phlegmon, can develop nin patients.
From laboratory informatioleucocytosis which at the necrosis and hemorrhagic forms of pancreatitis nsometimes arrives at 25-30 х 109, lymphopenia, change of leukocytic formula to nthe left and the increased ESR are characteristic. Growth of activity of namylase of blood and urine is very often marked, and is the important sign of npancreatitis. For estimation of the state of other organs maintenance of ngeneral albumen and its factions, glucose of blood, bilirubin, urea, nelectrolytes, acid-base equilibrium (ABE), and also the state of blood ncoagulation are determined. It is necessary to mark that the exposure of nhypocalcemia is considered a bad predictive sign of heavy passing of acute npancreatitis.
Several ntests can help differentiate biliary pancreatitis from other causes of npancreatitis. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), nalkaline phosphatase and serum bilirubin are the so-called liver functiotests; they should be reviewed before making a confident diagnosis.
In a nrecent study, the specificity of a serum ALT level of more than 150 IU/L for ndiagnosing gallstone pancreatitis was 96%. Unfortunately, nthe sensitivity was only 48%. This means that if the patient has a serum high nALT in the appropriate setting one can be fairly sure that the etiology of npancreatitis is biliary, but a normal AL T does not exclude gallstones as a ncause. Experimental biochemical nmarkers that may hold promise for assessing the severity of disease include trypsinogeactivation peptide, interleukin-6, interleukin-10, procalcitonin, phospholipase nA2 and C-reactive protein levels. Currently, nthese markers have limited clinical availability, but there is significant ninterest in better understanding markers of immune response and pancreatic ninjury because these could be valuable tools for reliably predicting the nseverity of acute pancreatitis and supplementing imaging modalities.
Ultrasonic examination of ngall-bladder and pancreas often specifies the increase of their sizes, bulge of nwalls and presence or absence of concrement of gall-bladder and general bilious nduct.
The nfinding of gallstones and dilatation of the extra hepatic biliary tree ocross-sectional abdominal imaging lends further support to the diagnosis of ngallstone pancreatitis. However, the sensitivity for detection of dilated bile nducts from biliary obstruction ranges in various studies from 55 to 91% . Trans abdominal ultrasonography seldom visualizes the npancreas in patients with acute pancreatitis due to air in the distended loops nof the small bowel.
Pic. Sonography.
Computer tomography enables to describe in details the changes in pancreas nand surrounding organs.
Pic. Computer ntomography
Helical computerized ntomography (CT) is one choice for accurate imaging diagnosis and staging of npancreatitis. A CT allows identification of pancreatic edema, fluid or cysts, nand the severity of pancreatitis to be graded, detects complications including ndevelopment of pseudocysts, abscess, necrosis, hemorrhage, and vascular nocclusion.
The CT criteria for diagnosis of pancreatic necrosis are ndependent on the detection of areas which lack glandular enhancement, which may nbe focal or more diffuse. Balthazar et al. showed that there was close correlation between the npresence and extent of necrosis and course of hospitalization including nmorbidity and mortality. Based on this work a CT severity index was developed nwhich attempted to use CT as a numeric grading system for the radiological ngrading of pancreatitis. The system provides a score between 0 and 10 with nhigher morbidity and mortality found with higher scores. A severity score of n7-10 had 92% complication rate and 17% mortality rate while a score of 0-1 had nnil morbidity or mortality.
Caution in defining pancreatic necrosis is important as nareas of peri pancreatic fluid can simulate areas of necrosis. Pancreatic nnecrosis is ideally detected on scans performed 48-72 hours after the onset of nan attack of acute pancreatitis. Scans done within the first 24 hours may be nfalsely negative or equivocal. Although scans are commonly done at time of nadmission, the need for a second study should be kept in mind for patients nwithout rapid improvement initially.
The CT finding of CBD stones may have sensitivity as high nas 80%, as noted by Baron et al, . who reviewed 69 patients with biliary obstruction, n12 of whom subsequently proved to have CBD stones (10 identified by the CT nscan). However, according to experiences of many gastroenterologists, CT is noften less sensitive than trans abdominal ultrasound. Contrast-enhanced CT nscans are more valuable thaoncontrasted ones for assessing the severity of nacute pancreatitis. CT scans can be normal in 15-20% of patients with mild npancreatitis. Not all patients with acute pancreatitis require a CT scan. This ncan be reserved when the diagnosis is in doubt, severe pancreatitis is nsuspected or conservative management fails.
At sciagraphy survey of organs of abdominal cavity gives a possibility to nexpose the unfolded “horseshoe” of duodenum, pneumatization, expansion of ntransverse colon (the Gobia’s symptom). On the 1st stage of diagnostics nin the plan of differential diagnosis of acute destructive pancreatitis with nother diseases of abdominal cavity, diagnostics of distribution of destructive ndamaging of different parts of pancreas and estimation of distribution of nparapancreatitis is possible only by the method of computer tomography which ndepending on clinico-laboratory signs and weight of passing is needed to apply nin a different period, and sometimes a few times in dynamics with interval of n4–5 days.
Laparoscopy and nlaparocentesis are often used for na doubtful diagnosis or necessity of taking away the exudation of abdominal ncavity for biochemical or bacteriological examination.
Retrograde endoscopic ncholangiopancreatography is used icase of mechanical icterus and suspicion of choledocholithiasis. The last nmethods are invasive and can if it is necessary transform from diagnostic to nmanipulation treatments: laparoscopic draining of abdominal cavity at npancreatogenic peritonitis and endoscopic papillotomy at choledocholithiasis nand biliary pancreatitis.
Variants of clinical passing and complications n
Clinical passing of disease can be abortive, slowly or nquickly progressive. At abortive passing the process is limited to acute nedema of pancreas with convalescence in 7–10 days.
Rapid progress is characteristic for npancreatonecrosis. In patients expressed toxemia, impregnation by exudation of nretroperitoneal cellulose and development of fermentative hemorrhagic nperitonitis can be seen. Strengthening of stomachache, continuous vomiting, nproof paresis of intestine, positive symptoms of irritation of peritoneum and ngrowth of hemodynamic violations are the clinical signs of necrosis of npancreas.
There is a formation of parapancreatic infiltrate at slow nprogress.
Among early complications of acute pancreatitis shock, nperitonitis and acute cardiac, pulmonary, hepatic and kidney insufficiency cabe distinguished.
Before later complications it is needed to deliver the nabscesses of pancreas, subdiaphragmatic, interintestinal abscesses, pyogenic nabscess omentum bag, phlegmons of retroperitoneal space and erosive bleeding.
In future formations of pseudocysts, fistula of npancreas, intestinal fistula and development of saccharine diabetes are npossible.
Diagnosis program
1. Anamnesis and nphysical methods of inspection.
2. General analysis nof blood and urine.
3. Biochemical nblood test (amylase, bilirubin, sugar).
4. Analysis of nurine on diastase.
5. Sonography.
6. Computer ntomography.
7. nCholecystocholangiography.
8. Endoscopic nretrograde cholangiopancreatography.
9. Laparoscopy.
10. Laparocentesis.
Differential diagnostics
Acute pancreatitis needs to be differentiated with the nrow of acute diseases of organs of abdominal cavity.
Acute mechanical intestinal obstruction. In patients with this pathology pain is of the nalternated character and is accompanied by nausea, vomiting, delay of gases and nemptying. It is possible to see the Klojber bowls on the sciagram survey of norgans of abdominal cavity.
Acute cholecystitis runs with characteristic localization of pain and nmuscular defense, with presence of increased, painful gall-bladder or ninfiltrate in right hypochondrium. Often acute (especially lately) pancreatitis ndevelops on the background of gallstone disease (biliary pancreatitis).
Thrombosis or embolism of mesenteric vessels. Both for pancreatitis and for the thrombosis of nmesenteric vessels great pain at soft abdomen (absence of defense muscles of nfront abdominal wall), that precedes to development of peritonitis, is ninherent. Yet from the beginning the disease gains heavy character of passing. nIn anamnesis in such patients a heart disease or heart attack of myocardium nrheumatic is met. As a result of gangrene of intestine, the symptoms of nperitonitis appear very quickly and intoxication grows. The fragments of mucus nshell are found in flushing waters of intestine at the detailed examination, nwhich have the appearance of ”meat flushing”.
A perforated gastric and duodenum ulcer is ndistinguished by the presence of dagger pain, defense of abdominal wall, nulcerous anamnesis.
Tactics and choice of treatment method
The conservative method is nconsidered the basic one for treatment of acute pancreatitis, but in connectiowith that unsuccessful conservative treatment of patients with acute pancreatitis ncan often put a question about the necessity of operation, therefore patients nmust be in permanent surgical establishment. Thus acute pancreatitis with heavy npassing is necessary to be treated under the conditions of separation of nintensive therapy.
Before conservative treatment nhunger, bed rest, fight against pain and enzymic toxemia, conducting of nacid-base state, prophylaxis of festering infection and acute ulcers of ndigestive duct are to be entered .
Patient’s stomach is washed by cold nsoda solution and a cold on an epigastric area and left hypochondrium is used. nMedicinal therapy is prescribed also: spasmolytics (papaverine, platyphyllin, nno-shparum, baralgine, atropine); inhibitor of protease (contrical, trasilol, ngordox, antagosan); cytostatic agent (5-fluorouracil, ftorafur). Positive naction of inhibitor of protease is marked only in the first days of disease nwhich are subject to conditioned application of large doses. Antibiotics of nwide spectrum of action: a) tienam, which most effective in the prophylaxis of nfestering pancreatitis, as is selected by pancreatic juice; b) cephalosporins n(kefzol, cefazoline); c) cefamizine (mefoxine).
Disintoxication therapy is conducted nalso (5 % but 10 % solutions of glucose, hemodes, reopolyhlukine, polyhlukine, nplasma of blood, only from 3 to
For the improvement of rheological nproperties of blood heparine is prescribed (5 000 ODES every 4 hours).
If patients have the expressed paisyndrome and phenomena of general intoxication during all pain period plus 48 nhours (by Bakulev), hunger is used. Such mode lasts on the average of 2–4 days. nThe parenteral feed of albuminous hydrolyzate is thus conducted, by the nmixtures of amino acid and fatty emulsion. Alkaline water of to 1–2 l. and nalbuminous-carbohydrate diet are also appointed. Infusion therapy is ncomplemented by plasma, by albumen, hemodes, reopolyhlukine. The improvements nof microcirculation in pancreas are achieved due to introduction of reopolyhlukine, nkomplamine, trental and heparin 5000 ODES 6 times per days under the control nthe indexes of the coagulation system of blood. Anticholinergic drug (sulfate nof atropine, methacin, platyphyllin), Н2-histamin blocker (cimetidine, ranisan, nranitidine, famotidine, omeprazol) are also applied. For the removal of pain: n1) sulfate of the atropine 0,1 % — 1 ml + promedol 2 % — 1 ml + papaverine 2 % n— 2 ml + analgin 50 % — 2 ml; 2) isotonic solution of chloride of sodium — 500 nml + baralgine — 5 ml + diphenhydramine hydrochloride 1 % — 1 ml + papaverine 2 n% — 2 ml + magnesium the sulfate 25 % — 5 ml + ascorbic acid — 5 ml + lipoic nacid 0,5 % — 2 ml + novocaine 0,5 % — 10 ml. are used. From the first days by a nnasogastral probe the permanent aspiration of gastric maintenance is conducted nalso. The Motility function of gastro-intestinal highway gets better at napplication of cerucal or primperane. With the same purpose forced diuresis n(maninil, furosemide, aminophylline) is used on the background of intravenous introductioof plenty of liquid.
At uneffective conservative ntreatment of patients with acute pancreatitis of middle weight and heavy form nit is expedient to apply surgical treatment.
Surgical treatment is carried out nfor patients with biliary pancreatitis (for a day long from the beginning of ndisease) in combination with the destructive forms of cholecystitis, at ncomplications of acute pancreatitis by peritonitis, abscess of omentum bag or nphlegmon of retroperitoneal cellulose.
Overhead-middle laparotomy, which nallows to estimate the state of pancreas, bilious ways and other organs of nabdominal cavity, is the best access in this situation. In case of destructive npancreatitis the possible use of lumbar laparotomy from left to right nhypochondrium through a mesogastric area is useful.
Cholecystectomy is executed at ncalculous cholecystitis, phlegmonous inflammation of walls of gall-bladder and nbiliary pancreatitis. If there are more than
Transduodenal nsphincteroplasty is shown at fixed concrement of large duodenal papilla, if nthey are diagnosed intraoperative, and also in the cases of papillotomy with nextraction of concrement when there is no possibility to execute endoscopic noperation .
Omentopancreatopexy. nAfter laparotomy and cutting of gastro-colon and gastro-pancreatic ligament nmobile part of large omentum through opening in gastro-colon ligament is nconducted and fixed by separate stitches to the peritoneum along the overhead nand lower edges of pancreas. Such operatioeeds to be considered rational at nthe expressed edema of pancreas and presence of necrosis in it.
Abdominisatioof pancreas. A cellulose round pancreas (along the lower and noverhead edges of body and tail) is infiltrated by solution of novocaine, after nit parietal peritoneum is cut. Under the body and tail glands free end of nomentum is conducted and is bundled by a gland. This operation is able to warthe hit of enzymes and products of disintegration in retroperitoneal space.
Sequestrectomy nis deleting of necrosis part of gland within the limits of nonviable tissue. nOperation is executed in a dull way.
Necrectomy n(deleting of necrosis part of gland within the limits of healthy tissue) is executed nby an acute way: tissue of gland is cut on verge of necrosis and bleeding nvessels are carefully bandaged.
The resectioof pancreas is deleting the part of organ with its transversal cutting withithe limits of the unchanged (ad осulus) tissue of gland. The resections of tail nand body of pancreas are distinguished.
Pancreatectomy nis a complete deleting of pancreas. Operative treatment is applied infrequently. nAfter the resection of pancreas adequate draining of its bed is very nresponsible.
The prognosis of disease depends ocharacter of morphological changes of parapancreatic to the cellulose ipancreas. The more difficult destructive changes, the worst the prognosis.
CYSTS OF PANCREAS
Cyst of npancreas is a cavity, filled by liquid (pancreatic juice, exudation, pus), nintimately soldered with head, body or tail of organ, is limited by capsule, nwhich has epithelium on internal surface.
Pseudocyst n(unreal cyst) is a cavity in pancreas which appears as a result of its ndestruction, limited by capsule, that does not have epithelium on internal nsurface.
Etiology and pathogenesis
The reasons of pseudocysts are ndestructive pancreatitis, traumas of pancreas, oklusion of Wirsung’s duct by nparasite, concrement, tumors, innate anomalies of development.
To the real cysts belong: innate n(dysontogenetic) cysts which are anomalic in development; acquired retentiocysts which develop as a result of difficult outflow of pancreatic juice, ncystadenoma and cystadenocarcinoma (by mechanism the origins belong more nfrequently to proliferative, sometimes — degenerative cysts).
The mechanism of development of pseudocysts consists nin the focus necrosis of gland, difficult normal outflow of its secret, there nis a destruction of walls of pancreatic ducts with overrun of pancreatic juice ngland that causes reactive inflammation of peritoneum of surrounding organs nwhich form the walls of pseudocyst.
Pathomorphology
Morphologically the cysts of pancreas are divided ninto: pseudocysts retention to the duct are innate, single and multiple.
Pseudocysts are fresh and old. The internal surface of nfresh pseudocyst is rough, granulating, grey-red. The table of contents is nalkaline, grey or with a brown tint. In an old pseudocyst the wall is smooth nand shiny, pale-grey. The table of contents is lighter. Epithelium pseudocysts nis absent. More frequently they are met in body and tail of gland and are not nconnected with ducts.
Retention cysts connected with an obturated duct. The ncavity has smooth, grey-white surface, maintenance is transparent, watery or nmucous-like. Innate cysts are mainly multiple and shallow. A simple retentiocyst differ from those that are always connected with the anomalies of ndevelopment of ducts and are unite with polycystosis buds and liver.
Rarely there are echinococcus cysts, which have a nclear chitinous shell, liquid in cavity and daughter’s blisters. They are nlocalized in the area of head of pancreas.
Classification
(by A.N. Bakulev and V.V. Vinogradov, 1952)
I. Innate cysts of npancreas:
1. Dermoid cysts.
2. Teratoid cysts.
3. Innate adenomas. n
4. Fibrocystic ndegeneration.
5. Polycystic ndegeneration.
II. Inflammatory cysts:
1. Pseudocysts.
2. Retention cysts. n
III. Traumatic cysts:
1. As a result of ndirect damage of gland.
2. As a result of nindirect damage of gland.
IV. Parasite cysts:
1. Echinococcosis nglands.
2. Cysticercosis nglands.
V. Neoplasty cysts:
1. Cyst-adenoma.
2. nCyst-adenocarcinoma.
3. Cavernous nhemangioma.
4. Cystic nepithelioma.
Pathomorphologyо cysts nare divided on:
1. The true cyst.
2. Pseudocysts.
According to clinical passing npseudocysts are divided into acute, subacute and chronic.
According to weight of passing — ninto simple (uncomplicated) and complicated.
Symptoms and clinical passing
In patients with the cystic damaging nof pancreas there can be pain of different character and intensity (dull, npermanent, cramp-like and belting). It is localized more frequently in right nhypochondrium, epigastric area (cyst of head and body of gland), left nhypochondrium (cyst of tail of pancreas). Pain is irradiated in the back, left nshoulder-blade, shoulder and spine.
Dyspepsia violations are ncharacteristic. Nausea, vomiting and belch are observed.
The syndrome of functional ninsufficiency of pancreas shows up by disorders of exocrine and endocrine ninsufficiency and depends on the degree of damage of organ. The unsteady nemptying, replacement of diarrhea of constipation, steatorrhea and creatorrhea, ndevelopment of the second diabetes are marked.
Compression syndrome. Arises as a result of compression of neighbouring norgans. Clinically the compression of organs of gastro-intestinal highway shows nup by complete or partial obstruction of general bilious duct (mechanical nicterus), vein (portal hypertension) gate, splenic vein (splenomegaly).
X-ray examination. Shift the stomach to the left
During the examination patients with nlarge cysts are marked by asymmetry of abdomen in epigastric and mesogastric areas. nAt palpation of abdomen tumular formation of elastic consistency with an even, nimmobile surface is found.
Sonography examination shows necho-free formation with a clear capsule, determines localization and sizes of ncyst.
Sonography
Contrasting roentgenologic nexamination of stomach and duodenum with the sulfate of barium at the cyst of nhead of pancreas exposes moving of pyloric part of stomach upwards and breeding nof ,,horseshoe” duodenum (at relaxation duodenography in the conditions of low nartificial blood pressure). If a cyst is localized in the area of body of ngland, displacement of stomach is marked forward and upwards or downward, nrapprochement of its walls, moving of duodenal transition and loops of thibowel downward and to the right; at lateral projection the distance betweestomach and spine is increased. The cyst localized in the area of tail of ngland, displaces the stomach forward and upwards, to the left or to the right.
Cholecystocholangiography exposes ncalculous cholecystitis and cholelithiasis.
Retrograde pancreatocholangiography nexposes the changed and deformed, infrequently extended pancreatic duct, noccasionally there can be filling of cavity of cyst by the contrasting matter.
Computer tomography shows naccumulation of liquid limited by the capsule of different closeness and nthickness.
CT Scan. nCyst of the pancreas
Laboratory examinations exposes nhyperamylasemia, steatorrhea and creatorrhea, sometimes — hyperglycemia and nglycosuria.
Clinical passing of cysts of npancreas depends on their kind, localization, size, stage of forming and ncomplications.
Four stages of forming of pseudocyst nare distinguished (Р.G. Karaguljan, 1972).
I stage (1–1,5 months last) — in the ncenter of inflammatory process the cavity of disintegration, which takes nsurrounding tissue, appears in an omentum bag.
The II stage (2–3 months) is ncharacterized by the beginning of forming of capsule of pseudocyst. Cyst is nmagnificent, unformed, acute inflammatory phenomena calms down.
The III stage (3–12 months) is ncompletion of forming of capsule of pseudocyst. Last accretes with surrounding norgans.
The IV stage (begins an in year from nthe origin of cyst) is a separated cyst. The cyst is mobile, easily selected nfrom connections with surrounding organs.
Retentiocysts arise at closing of lumen of pancreatic duct (concrement, sclerosis). The ninternal surface of cyst is covered with epithelium. Pain syndrome, violatioof exocrine function of gland are characteristic.
Traumatic ncysts belong to the pseudocysts with similar passing and clinic, as well as ninflammatory pseudocysts.
Parasite ncysts (to echinococcus, cysticercotic) are met as casuistry. In such patients nKaconi test and serological Weinberg’s reaction are positive.
The variants of clinical passing of nthe real and unreal cysts depend on their complications.
Perforation in free abdominal ncavity. Clinic of the poured peritonitis is characteristic. Tormina, positive nsymptoms of irritation of peritoneum, possible shock state as a result of nirritation of peritoneum by pancreatic juice arise.
Perforation in stomach, duodenum, nsmall, rarer in large intestine is accompanied by diminishment of cyst in sizes nor complete disappearance, sometimes diarrhea appears.
Suppuration of maintenance of cyst nis accompanied by pain which becomes more intensive, temperature rises, nleucocytosis grows.
The erosive bleeding appears nsuddenly and is accompanied by the symptoms of internal bleeding (expressed ngeneral weakness, dizziness). The pallor of skin and mucus shells, sticky ndeath-damp, tachycardia and anemia are observed.
Mechanical icterus arises as a nresult of compression of cyst on the terminal part of choledochus. The icterus nof skin and mucus shells, acholic excrement, dark urine, hyperbilirubinemia, nincrease of the AlT and AsT level are exposed.
Portal hypertension develops as a nresult of compression of portal vein. Ascites, varicose expansion of veins of nesophagus and stomach, moderate icterus are diagnosed.
Reactive exudation pleurisy more nfrequently arises in left pleura cavity, where roentgenologic exudation is ndiagnosed with high maintenance of amylase.
At malignization the walls of cyst nspecific symptoms are absent, a diagnosis is set during operation (surgical nbiopsy of cyst wall).
Diagnosis program
1. Anamnesis.
2. Biochemical nblood test (amylase, sugar, bilirubin).
3. Analysis of nurine on diastase.
4. Coprograma.
5. Sonography.
6. Contrasting sciagraphy of stomach nand duodenum (relaxation duodenography).
7. Retrograde npancreatocholangiography.
8. Computer ntomography.
Differential diagnostics
The cysts of pancreas are differentiated with the ntumors of abdominal cavity and of retroperitoneal space.
Cancer of pancreas. For the cancer tumor of pancreas syndrome of “small nsigns” (discomfort in epigastric area, loss of appetite, general weakness), npermanent dull pain, unrelated with the reception and composition of meal, nicterus (cancer of head of gland), Courvoisier’s symptom (increased, nunpainfully gall-bladder) are characteristic. Inconstant pain at cysts of npancreas is more frequently related to faults in a diet; in anamnesis ndestructive pancreatitis, traumas of gland are carried. Sonography examination, nretrograde pancreatocholangiography and computer tomography help iestablishment of diagnosis.
Tumors of retroperitoneal space are passed nasymptomatic, clinic shows up by a considerable compression oeighbouring norgans. Nausea, vomit, chronic intestinal obstruction, dysuric disorders arise. nClinic of cysts of pancreas, on the opposite, are expressed on early stages. nPain, dyspepsia syndromes, syndrome of exocrine and endocrine insufficiency of npancreas are characteristic. Pain is related to the reception of meal and nalcohol.
Aneurism of abdominal aorta. Dull, indefinite pain in abdomen which is unrelated nwith the reception of meal, pulsation and pulsating formation in abdomen are ncharacteristic, auscultatory is systolic murmur. Aortography allows to confirm na diagnosis.
The cyst of mesentery of thin bowel has painless npassing, at palpation it is mobile, easily changes position in abdomen. The ncysts of pancreas are practically immobile, pain, anamnesis and laboratory ninformation are characteristic.
The cyst of liver has protracted asymptomatic passing. nPain appears at infection of cyst. For this pathology symptoms which take place nat the cysts of pancreas are not typical (pain related to the reception of rich nfood, alcohol, hyperamylasemia). Topic diagnostics is carried out at ultrasonic nexamination, scintigraphy, computer tomography.
Tactics and choice of treatment method
Conservative treatment. Treatment of acute or chronic pancreatitis is conducted nin accordance with principles. At the unfavorable dynamics of passing the ndiseases hunger with the permanent sucking of gastric maintenance, parenteral nfeed and intravenous introduction of liquids are appointed. Puncture of cysts nis used through abdominal wall under sonography control with aspiration of nmaintenance.
Surgical treatment is the method of nchoice of treatment of cysts of pancreas. The choice of treatment method ndepends on the stage of forming of pancreas cysts.
On the I stage operation is not nused, conservative treatment of pancreatitis is conducted. On the II stage it nis used at suppuration of pseudocyst (external draining of cyst). On the III — ninternal draining of cyst is used. More frequently cystojejunostomy on the neliminated loop of thin bowel by Roux, cystojejunostomy with entero-entero nanastomosis by Brawn and closing of afferent loop by Shalimov. Cystogastrostomy are executed and cystoduodenostomy is nnow not applied because of possible complications (infection of cyst, erosive nbleeding). Marsupialization (opening and sewing down of cyst to the parietal nperitoneum and skin) is used infrequently (at suppuration of cyst is seriously npatientsing with the septic state). On the IV stage external and internal ndraining of cyst and radical operations are applied: a) enucleation of cysts n(executed very rarely); b) distal resection of pancreas with a cyst.
Cystoejunostomy
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Prepared ass. nRomaniuk T.
