DIAGNOSTIC AND TREATMENT OF HEPATIC AND BILIARY SYSTEM DISEASES IN OUTPATIENT CONDITIONS. DIFFERENTIAL DIAGNOSIS OF JAUNDICE. PROPHYLACTIC MEDICAL EXAMINATION. SANATORIUM TREATMENT. MEDICAL AND LABOR EXPERTISE.

 

CHRONIC CHOLECYSTITIS

Cholecystitis (Greek, –cholecyst, “gallbladder”, combined with the suffix -itis, “inflammation”) is inflammation of the gallbladder, which occurs most commonly due to obstruction of the cystic duct with gallstones(cholelithiasis). Blockage of the cystic duct with gallstones causes accumulation of bile in the gallbladder and increased pressure within the gallbladder. Concentrated bile, pressure, and sometimes bacterial infection irritate and damage the gallbladder wall, causing inflammation and swelling of the gallbladder. Inflammation and swelling of the gallbladder can reduce normal blood flow to areas of the gallbladder, which can lead to cell death due to insufficient oxygen. Not everyone who has gallstones will go on to develop cholecystitis.

Actuality of problem. Disease of gall-bladder and bile ducts represent a widespread pathology of internal organs, that is observed in  10-15% of the population in the developed countries. Despite obvious success, achieved during last decades, in diagnosis and treatment of these diseases, still there are some unsolved questions and contradictions concerning their interpretation. First of all it touches upon the relations  between gall-stone diseases, chronic gall-bladder disease and diskinetics of bile ducts. That’s why studying the diagnostic criteria of gall-bladder diseases and bile ducts are actual.

CLINICAL ANATOMY OF BILE  DUCTS

Bile, produced by hepatic cells, enters intercellular bile channels, which are formed by bilious poles of two or more adjacent hepatic cells. The membrane of hepatic cells constitutes the wall of bile channels . Intercellular bile channels uniting at the periphery of hepatic particle, form larger perilobular bilious channels which fall in to interlobes bilious channels. These channels make shunt between each other, increase in their sizes, and turn into large lobe channels. On the lower liver surface, in the area of lumbar furrow, the left and right bile channels unite, and form general hepatic channel. Mirizi sphincter is located in the place of hepatic channels confluence. Mirizi sphincter regulates the bile reception into a gall-bladder and hinders its reverse flow into the liver. A general hepatic channel joins with gall-bladder, making-up a general bilious channel  (choledochus). Lyutcens’ sphincter is situated in the place of gall-bladder neck transition into  gall-bladder channel, and regulates the reception of bile from the gall-bladder into gall-bladder channel and choledochus. The distal part of general bilious channel is extended. In its wall there is the layer of smooth musculature – sphincter of hepato-pancreatis ampoule – sphincter Oddi, that resists bile flowing from a general bilious channel into a duodenum. Hepatic cells produce bile constantly, but into the duodenum it comes during digestion only (secretory pressure in the liver is constantly supported at a level not less than 300  mm of water post). Synchronous contraction and weakening of  the gall-bladder, sphincters and channels is one of key moments of bilious system function during reception meal.

 

The Fig. 1. Anatomy of bile ducts

1– Branches of hepatic duct.

2 – Common hepatic duct  and Mirizi sphincter/

3 – Cystic duct.

4 – Cystic duct.

5 – Common bile duct.

6 – Sphincter Oddi.

7 – Duodenum.

8 – Pancreatic duct.

P.S. :

·                        Common hepatic duct formed by junction of right and left hepatic bile ducts.

·                        Cystic duct connects common hepatic duct with gallbladder.

·                        Common bile duct formed by junction of cystic duct and common hepatic duct.

 

The Fig. 2. Gallbladder Anatomy

Regulation of bile excretion is carried out by hormones definite, such as gastrin, secretin, cholecystokinin which stimulate secretion of bile and empty the gall-bladder; somatostatin and vasoactive intestinal polypeptid  do the opposite.

 

Belong to the most important components of bile – Water (82%), bile acids (12%), letsetin and other fosfolipdi (4%), non-estherified cholesterol (0,7%), and other components: biliroubin, proteins, electrolytes, slime. Bile presents by itself  micellear solution. Bilious acids, cholesterol and fosfolipids, are components of micella. Concentration of bilious acids has to exceed the quantity of cholesterol in 10 times to ensure normal micellation. Bile acids in hepatic cells are     synthesized  from  cholesterol in presence of enzyme 7a-gidrocsilase. Two bile acids are synthesized from cholesterol in the liver – cholic and chenodesoxycholic  (“primary bilious acids”). Conjugation of primary bile acids with taourin and glycin, forming salts as a result takes place in hepatocytes. In the intestine salts of primary bilious acids turn into the secondary bilious acids ( desoxycholic and lithocholic). 90% bilious acids are absorbed from intestine into  blood and enter the liver again.

The Fig. 3. The bile travels through cystic duct into the common bile duct, then unites with the pancreatic duct to empty bile into the duodenum.

 

Evacuation of bile from the gall-bladder in time and absence of bile stagnation play an important role in prevention of violations of bile colloid stability.

 

Chronic without gall-stone holetcystitis is polyetiologic inflammatory disease of gall-bladder wall, accompanied by deteriotation of its motoric function and absorbing ability, structure and bile properties.

Chronic acalculous holetcystitis (CAC) is observed more frequently in  women than in men. Correlations, according to various authors ranges 1:3,- 1:4. CAC occurs  considerably, than it is diagnosed. The diagnosis of chronic cholecystitis in  most developed countries is put only in  case of  complicated gall-stone disease or obvious inflammatory process.

ETIOPATHOGENEZIS

To the basic causal factors of  SAS belong development:

1)    infection;

2)    impairment of bile outflow ;

3)    suppression of immune status;

4)    presence in  bile the agents, that irritate the mucous membrane of gall-bladder;

 Today an infectious factor is not the main factor. Pathogenic staphylococci, streptococci, intestinal stick and others are more frequent reasons of of acute cholecystitis development. Reduction of immunity, presence of of chronic infection focuses, period after viral hepatitis, stagnation of bile at hypotonic discinesis . assists the development of infection in bilious ways. An infection can get into the gall-bladder by contact (from an intestine), or limfogenic or gematogenic way from any focus of chronic inflammation in the organism (parodontoz, chronic tonsillitis, pielit, etc.).

An inflammatory process in a gall-bladder can be formed without participation of infection. Any temporal or permanent violations of outflow of bile lead to the increase of osmotic pressure in a gall-bladder. Dilatation and edema of its walls appear and there can be breaks and heart attacks with the secondary aseptic inflammation.

One of the principal reasons of chronic holetsistis origin is the irritation of mucous shells by different agents. The products of grilling fats, chemical food additions, belong to them, abuse by rich food, that results permanent receipt of bilious acids, especially desoxycholates, which irrilate the mucus shell of gall-bladder.

CLASSIFICATION

 

I. BASEDON DEGREE OF:                         II. ON PHASE OF   

                                                                  DISEASE SEVERITY:

1)    MILD FORM;                                     1) EXACERBATION   

2)    MODERATE;                                      2) ATTENUATION  

                                                                        EXACERBATION

3)    SEVERE.                                                 3) UNSTABLE REMISSION;

4)    STABLE   REMISSION.

 

III. ON PRESENCE OF COMPLICATIONS:

1)        UNCOMPLICATED;

2)        COMPLICATED BY PERICHOLECYSTITIS;

3)        COMPLICATED BY CHOLANGITIS   OR ANGIOHOLITIS;

4)        COMPLICATED BY HEPATITIS (PANCREATITIS,GASTRITIS, DOUODENIT IS ETC.).

IV. ON PRESENCE OF CONCOMITANT SYNDROMES:

 

1) NEURASTHENIC;                                              4) SOLAR;

2)     CARDIAC;                                                         5) OBESITY;

3)     HYPOTHALAMIC;                                            6) ALLERGIC.

CLINICAL MANIFESTATIONS

It is characterized by the presence of pain, dyspeptic syndrome and common displays.

(Algesic) Pain syndrome – is conditioned, mainly, by motive violations in the bilious system, and inflammatory process in the gall-bladder.

Characteristic pain in the right subcostal area with an irradiation  to the neck, shoulder, right shoulder-blade, back, in the area of heart; arises  after the reception of alcohol, rich, fried food and, is accompanied by nausea, bitter taste and dryness in the mouth.

At chronic acalculus choletcystitis, that runs on a background of hypertensive discinezis, pain is fit-like, the picture can be same like at colic, but intensity of pain and duration are less, than at bilious goal-stone illness. Hypotonic discinezis is observed in these patients more frequently. In these case the pain in the right subcostal area is  permanent, aching, nonintensive, strengthening at violation of diets and shaking ride.

Dyspeptic syndrome – patients complain on feeling of heaviness in the right subcostal area , epigastriс area, stomach swelling, nausea, bitter taste in the mouth, violation of excrements. The excretion of bile at interdigestive period can cause bilious reflux, nausea, bitter taste in the mouth. The decrease of maintenance in the bile of bilious acids leads to violation of digestion , especially  hydrolysis and suction of fats . Besides, bilious acids stimulate motoric of bowels, their deficit can be the reason of low pressured constipation, and excess of bilious acids – causes hologenic diarrhea.

The common   displays are  a weakness, headache, arising of  body temperature to the subfebril numbers, periodic fever, pain in joints, in the area of heart, tachycardia.

At the objective inspection –subicterus of the sclerar, soreness at palpation in   the projections of gall-bladder, positive Kerr’ symptom  (appearance or strengthening of pain at pat on height of inhalation in the gall-bladder  point – place of crossing of costal arc with the right direct muscle of stomach), Murphy’ symptom (pain at palpatsion in the right subcostal area during deep inhalation), phrenicus-symptom (symptom of Myusi — pain at pressure between the legs of right sterno-cleido-masteideus   muscle).   At   joining   of inflammation   in   bilious   channels positive Ortner’ symptom (pain at pat on the edge of right costal arc).

DIAGNOSTICS (data of laboratory-instrumental methods )

At research of blood in the phase of exacerbation of chronic holetsistitis especially caused by pathogenic microflora, moderate leycotsitozis is exposed, neytrofilozis, insignificant acceleration of ESR. These changes are accompanied clinical by fever, and the positive results of bacteriological research of bile. There are  forms of holetsistitis without inflammatory process marks, with normal results of general blood test more frequently today.

Duodenal probing as a method of diagnostics of cholecystitis lost its value, because it was proved, that leucocytes in bile – indicators of inflammatory process- are very quickly collapse. It is possible to define the character of discinezis which supports the inflammatory reaction of mucous shell. Therefore at biochemical research, clotting of bile is marked up, its specific gravity grows, PH changes into the sour side, violation of bilious acids constant and is reduction is observed, then they annoy the mucous shell of gall-bladder. This method is used, mainly, for microbiological research of bile, determination of microflora, that caused inflammation, research of its sensitiveness to antibiotics, exposure of presence lamblia. But results require careful interpretation, because bile to collect in sterile conditions practically is not possible and more frequent sowed microflora enters to a test tube from oral cavity, thin bowel. The positive results of bacteriological research must be compared with the clinics of disease. It is necessary to take in to account the character of pain (has  permanent character, and appear after meals), rise of body temperature, the phenomena of intoxication, changes of general blood test (leycocytozis, increasing of ESR).

The Fig. 4. Duodenal probing

Real-time ultrasonography is the method of choice for diagnosing chronic holetcystitis.

 

The Fig. 5.  The ultrasonography gallbladder

The longitudinal cut of gall-bladder is pear-like. Normally gall-bladder in length is 8-10 cm and 3 cm in width. The contours of gall-bladder are clear. The thickness of walls does not exceed 3 mm. Cavity homogeneous. Signs of inflammatory process are: thickening of walls more than 3 mm, gyperechogenic of front wall, roughness, unclear contours, reduction of transparency of bile. In connection with wide introduction in practice of medical establishments  ultra-sound diagnostic (USD), X-ray methods are not practically used .

The Fig. 6.  USD gallbladder  (Normal)

The Fig. 7.  The ultrasonography of gates of liver: 1– cystic duct, 2 – common bile duct, 3 – portal vein, 4 –  gallbladder, 5 – hepatic artery.

 

The Fig. 8.  USD. Chronic acalculous holetcystitis   

Mild form of cholecystitis is characterised by short acute period for 2-3 days, is easily treated by diets. Substantial changes of functional violation of gall-bladder are absent.

Moderate form of chronic cholecystitis runs with the presence of clear acute periods and periods of remission. Acute period proceeds 2-3 weeks, which is confirmed by clinical, laboratory-instrumental data. The changes of functional tests of liver are exposed (increasing the activity of transaminase due to AlT, moderate rise of timole test, alkaline phosphatase). The changes of biochemical tests are absent during remission.

Severe form of chronic cholecystitis is characterized by nonstoping relapsing passing, by absence of clear long-term remission. The clinic of chronic hepatitis, pancreatitis joins to the clinic of chronic cholecystitis. At USD of gall-bladder expose a presence of the periprocesses, considerable thickening  of gall-bladder wall.

GALL-STONE DISEASE. CHRONIC CALCULOUS

Gall-stone disease (cholelythiasis) is  polietiological disease when in the gall-bladder (cholecystolitiasis), and sometimes in outflow channels (choledoholitiasis)  stones appear.

Gall-stones are crystalline structures which appear in abnormal bile. Stones are divided into cholesterol, pigmented and mixed. Cholesterol and mixed stones occur more frequently (in 90-95% of all cases of gall-stone disease) and consist  of cholesterol monohydrate, mixtures of  calcium salts, bilious acids and pigments. Pigmental stone consists of calcium bilirubinate .

 

The Fig. 9.  Location gall-stones in bile ducts

 

The Fig. 10.   Location of stone in cystic duct

 

The Fig. 11.   Location of stone in gallbladder and common bile duct

Risk factors

The     main risk factors of pigmental stone is demographic factor that is more frequently met at vegetarians and at persons, who live in countries with  hot climate, where is high-frequency of hemolytic anemia, malaria and other tropical diseases. Pigmented stone are more frequent observed in eastern people. Gall-stone disease in the countries of Europe, America and in our country is mainly presented by holesterine stone (genetic factor).

Obesity, high-caloric diet, medical treatment by clofibrate, hormonal contraceptives, starvation and diabetes mellitus became risk factors as a result of cholesterol excretion strengthening. Pregnancy influences on  concrements formation in the gall-bladder -progesteron increases the saturation of bile with cholesterol, decreases motoric of gall-bladder; also most pregnant women considerably add in  weight and it leads to the increasing of endogenous cholesterol synthesis. High frequency of cholesterol cholelitiasis is observed in patients with gyperlipidemia of IV type according to Fridrecson.

Decreasing  of bilious acids secretion is observed in women of mature age with liver diseases under the influence of female sexual hormones. The excretion of cholesterol totally depends on the liver function: decreasing or violation of bile formation can be the reason of hypercholesterolemia.

One of factors – is violation of water-salt exchange, tissue acidosis, decreasing of liquid using.

The important role in development of Gall-stone disease belongs to the gall-bladder, state of mucous shell and evacuation function. In inflammation there is the considerable excretion of mucous by the mucous shell of gall-bladder that contains big amount of mucopolisacharides, glycoproteins. It leads to bile clotting, forms the conditions for the delay of cholesterol on mucous, where in future the center of gall-stone will be formed. In literature mucopolisacharides,  glyocoproteins are known as factors of enucleating.

FACTORS, THAT ASSIST IN DEVELOPMENT OF GALL-STONE DISEASE

I. GENERAL FACTORS:

 FEMALE SEX

 OLD AGE,

GENETIC PREDISPOSITION

OBESITY

THE INCREASED CONSUMPTION OF LIPIDS,  

 EASILY ASSIMILATED PROTEINS,

 CARBOHYDRATES, CHOLESTEROL,

 DISTURBANCES OF LIPID’S EXCHANGE

  MEDICAL FACTORS (RECEPTION OF LIPIDO-REDUCING      PREPARATIONS, CONTRACEPTIVES), STARVATION

  DISTURBANCES OF WATER-SALT METABOLISM,

 

II. LIVER FACTORS:

-REDUCTION OF HOLATO-FORMATION FUNCTION OF LIVER,      

 –RISE  OF HOLESTEROL EXCREATION FUNCTION OF LIVER      

  -REDUCTION OF EXCRETION OF WATER AND ELECTROLYTES    BY EPITHELIUM OF INTERHEPATIC BILIOUS CHANNELS,     

  -VIOLATION OF MICELLA-FORMATION.

 

III. GALL-BLADDER FACTORS:

-HYPOTONIC-HYPOKINETIC DISKYNESIS OF GALL-BLADDER

-PRESENCE OF INFECTION IN GALL-BLADDER, INFLAMMATORY CHANGES OF MUCOUS SHELL OF GALL-BLADDER

-VIOLATION OF COLLOID STABILITY OF BILE.

Cholesterol is badly dissolved in water; and normally is in soluble state because of phospholipids and bilious acids. The lithogenisity of bile, its  possibility to form a gall-stone is conditioned by strengthening of synthesis of cholesterol, by the reduction  of bilious acids secretion and phospholipids. All risk factors of gall-stone disease assist to one or few mechanisms of rise of bile’s litogenisity increase.

CLASSIFICATION

I stage-physical and chemical;

II         stage – latent non symptomatic gall-stone carrier;

III        stage – clinical, complicated.

At I stage the diagnosis  is based on the results of  special research of bile- physical and chemical violation of bile (cholesterol “flakes” and precipitation). Clinical, eсhocardiograffic symptoms of the disease are absent. The II stage – is characterized by lythogenic physical and chemical changes of bile, formation of gall-stones in  bile outflow channels (more frequent in the gall-bladder),which do not show up clinically, and can be diagnosed at ultrasound research. III stage – symptomatic stage depends on  location of gall-stones, their size, composition and quantity, activity of inflammation, functional state of  bile out-flow system, and also on character and degree of other organs lesion.

ClinicAL HISTORY

The typical pictures of gall-stone disease are attacks of hepatic colic, as a result of moving concrements from gall-bladder to the channels. Pain is conditioned by spastic contraction of gall-bladder, rising pressure by in it. Pain arises up suddenly, localizes in the right subcostal area or very often in epigastric area, irradiates into the right hand, right shoulder-blade, is accompanied by nausea, repeated vomiting that does not bring facilitation. Pain is easily taken off by baralgin, spazmolgon. If temperature rises, it is possible to think about joining of inflammatory process. Soreness in the projection of gall-bladder is objectively determined and increased gall-bladder sometimes can be palpated. At inflammation there are positive symptoms of Merfi, Ker, Vasilenco, Schyotkin-Blyumberg. If stone even briefly obturates choledohus,   patients complain of darkening of urine after colic, and also excrements can be discolored. At dyspeptic form dyspeptic violations and dull pain are marked only in the right subcostal area, concrements can be exposed only at  planned inspection .

 

Fig. 12. This  image shows localization of pain at the gall-stone disease

1– Pancreatic area

2 – Gallbladder

3 – Shoulder area

 

COMPLICATIONS

 

Development of acute and chronic cholecystitis, secondary pancreatitis is the most frequent complication of gall-stone disease. Severe complication is hepatic icterus with following cholestasis. It arises up at obturation of general bilious channel by the stone. At valve stone icterus can have intermittent  character. In these case USR and ERCP are informative. Hydropsy of gall-bladder can develop as a result of obturation of gall-bladder’s channel. Then pain disappears, and at objective examination increased gall-bladder is palpated.

 

LABORATORY AND INSTRUMENTAL FINDINGS

 

The Duodenal sounding practically is not important, more over it is dangerous because may cause the attack of hepatic colic. If concrements are not present, but there is a suspicion on a lithogenisity of bile, the defined diagnostic value has biochemical research of gall-bladder bile. Research of maintenance of cholesterol, phospholipids, bilious acids is conducted.

USR is the method of direct diagnostics of gall-stone disease. Echographical concrements in gall-bladder are determined as hyperechogenic structures which make acoustic shades. Concrements are usually mobile; their position is changing when the possition of body is changed. It is considerably difficult to display concrements in bilious channels. Static B mode ultrasonography and oral cholecystography are also sensitive and specific.

Several diagnostic methods— Endoscopic retrograde cholangiopancreatography (ERCP).

Direct cholangiography by either ERCP or percutaneous transhepatic cholangiography has a small but definite incidence of sepsis and of failure. Ultrasound and computer tomography reliably detect ductal dilation as evidence of obstruction; however, obstructing stones often are associated with nondilated ducts.

Fig. 13. ERCP. Location of stone in common bile duct

Fig. 14. Cholecystitis can be seen on a cholangiogram. Radio-opaque dye is used to enhance the X-ray. Multiple stones are present in the gallbladder

 

Fig. 15. A cholecystogram in a patient with gallstones

 

Fig. 16. USD. Chronic cholecystitis . Location of stone in gallbladder

 

Fig. 17. Computed axial tomography (CAT) scan

Fig. 18. Cholecystolithiasis. CT scan of the upper abdomen showing multiple gallstones

VIDEO: Galblader ultrasound appearance

 in chronic  cholecystitis and multiple gallstones

DISKYNESIS OF GALL-BLADDER AND BILE DUCTS

 This is unpunctual, incomplete or excess contraction of gall-bladder and sphincters (Oddi, Lyutcens-Martinov, Miritsi).

Depending on an etiologic reason of the origins, there are two types of discinesis of gall-bladder and sphincters of bilious channels: primary and secondary.

Primary discinesis is caused by violation of the neurogumoral regulation  of gall-bladder and sphincters activity, conditioned by the presence of neurosis, neuroendocrinal violations, diseases of thyroid gland, by changes of ovaries in the period of the sexual maturing or in a climacteric, period, vegetative and vascular dystonus, diencephalic syndrome.

Development of secondary dyskinesis is related to the presence of pathological reflexes and violation of motoric and secretory function of other organs of digestion tract. Secondary dyskinesis arises up on a background of chronic gastritis, gastroduodenitis, ulcerous disease, chronic diseases of intestines, accompanies organic diseases of gall-bladder such as chronic cholecystitis, congenital defect and development  of gall-bladder, bilious channels.

Classification. Depending on the character of violations of gall-bladder motoric function and sphincter tone of hepato-pancreatic ampoule the following types of gall-bladder dyskinesis are distinguished:

1)    hypertensive-hyperkinetic;

2)    hypotensive-gypokinetic

3)    mixed.

Diagnosis. Hypertensive-gyperkinetic dyskinesis occurs more frequently is met in persons with advantage of parasympatic nervous system, hypotensive-gypokinetic- with advantage of sympatic nervous system.

Main clinical symptoms:

1.    Age of patient – more frequently are young women with mental and emotional lability.

2.    Asteno-vegetative syndrome.

3. Pain syndrome (the character of pain in the right under-costal area depends on the type of dyskinesis: dull, unsteady – at gypomotoric; periodic, paroxysm-like, that sometimes achieves a bilious colic – at hypertensive dyskinesis).

4.              Presence of dyspeptic syndrome (nausea, sometimes vomiting, feeling of bitter taste in the mouth, meteorism).

5.              Atonic constipation (at hypotensive dyskinesis).

6. Alternation of constipation and diarrhea (at hypertensive dyskinesis).
Diagnosis is based on:

1. Normal laboratory indexes.

2. Informative method is the multi-moment duodenal probing   that helps to delimit violation of motoric and evacuation function of gall-bladder and violation of sphincters of extrahepatic bilious channels.

Data of the multi-moment fractional probing   :

  a)   hypertensive-gyperkinetic type- lengthening   of period of first phase;lengthening of time of closed sphincter Oddi;   reduction of duration B-phase at normal volume of gall-bladder bile, or protracted, interruption  of portion B excretion;

б)  gypotonic–gypokinetic type – shortening  of closed sphincter Oddi phase, lengthening of phase B and increasing  of  gall-bladder bile volume.

At both dyskinesis microscopic research of bile does not show elements of inflammation are not shown.

Table 1

DATA of multi-moment duodenal probing

 

 

The mechanical irritation of duodenum attends opening sphincter Oddi and excretion of lightly-yellow bile from the common bilious channel to duodenum (choledochus-phase). After entering through the probe of 40 ml 33% solution of magnesium sulfate into the duodenum, sphincter Oddi closes (phase of closed sphincter Oddi). Then sphincter Oddi opens and excretes lightly—yellow bile (portion “A”). Opening of sphincter of Lyotcensa -Martinova is characterized by appearance of darkly-brown viscid gall-bladder’s bile. Probing is ending by opening of Miritsi sphincter and excreting of amber-colored bile (portion “C”).

2. Data of ultrasonic research of retraction power of gall-bladder:

a) The hypertensive type- 40 minutes after the bile-stimulating breakfast -gall-bladder retracts more than 2/3 of volume

б) Hypertensive type – stretched, increased gall-bladder is observed at USR, emptying less than 1/3 of volume  after 40 minutes of bile-simulative breakfast.

The Fig. 19.  The ultrasonography of gall-bladder with two bends

 

MEDICAL TREATMENT

Principles: it has to be directed for removing of pain, dyskinetic violations, influence on an infection and inflammation, correction of digestion and exchanges violations.

During the acute period a frequent (4-5 per day) diet is applied with reduction of volume and caloric content of meal (diet № 5, 5а according to Pevzner).

Medicinal medical treatment:

I removing of pain syndrome – anesthetics and spasmolytic preparations

parenteral (no-spa – 2 ml 2 % solution, papaverin hydrochloride-2 ml 1% solution, galidor – 2 ml 1% solution, platifilin gydrotartrat -2 ml 0,2 % solution; at expressed pain syndrome simultaneously entering  analgin – 2ml 50 % solution, baralgin – 5 ml, fortral – 1-2 ml 3 % solution, at necessity- promedol – 1ml 2 % solution.

II.        To prevent  vomiting and dyskinesis entering metoclopramid -2 to ml 0,05 % solution or
peroral domperidon (motilium)-10mg 3-4 times per  day before meal, tzizaprid (coordinacs,
prepoulsid) – 10 mg 3 -4 times per  day before meal.

III.       Antibacterial therapy is provided, taking in to account the sensitiveness of microflora (according to data of bile sowing). It is necessary to prescribe those antibacterial preparations which enter into the bile in high concentration. They are: half-synthetic penicillin (ampicillin, ocsatsilin, ampiocs) – 0,25-0,5 g 4 times per  day; cephalosporines (tsefalecsin – 0,25-0,5 g 4 times per  day, tsefobid – 1 g 2 times per day intramuscular, tseftriacson – 1 g 2 times per day intramuscular); preparations of hinoliniv (abactal – 0,4 g 2 times per day-time peroral during
 meal, tarivid-0,2 2 times per day); preparations of tetratsiclin (tetratsiclin  0,1 -0,25 g4 times per day, metatsiclin, rondomitsin  0,3 2 times per day, docsitsiclin or vibramitsin  0,1-0,5 g per day in combination with nistatinom) metranidazol 0,5g 3 times per  day or tinidazol  0,5-1 g 1 time per  day; at presence of staphylococcus infection in gall-bladder-
 claritromitsin  0,25-0,5 2 times per  day, eritromitsin  0,25 g 4 times per  day; derivative of nitrofouran (fouradonin, fourazolidon  0,1 g 4 times per  day after  meal), ocsihinolins (nitrocsolin  0,1 g 4 times per  day during meal); sulfanilamid’s preparations (biseptol  2 pills 2 times per  day after meal), Duration of antibacterial therapy is 7-12 days.

At parasitogenic lesion of bilious channels simultaneously to antibacterial preparations should be prescribed vermocs 1 pill 2-3 times per  day, hlocsil  2 g orally at a 1/2 glass of milk every 10 minutes 3-5  times during 2 days .

IV.      During intoxication – intravenous infusion 5% solution of glucose 200-400 ml,
polidez 250-450 ml.

V.       In acute phase, on height of inflammatory syndrome prescribing of holeretics is contra-indicated, and at hypertensive bilious dyskinesis – holicinetics is contra-indicated too.

In the attenuation of acute phase after cancellation of antibacterial preparations, holeretic preparations are prescribed:

1) that contain bilious acids (hologon  0,2-0,4 g 3 times per day after a meal , alohol 1-2 pills 3 times per day after a meal, holenzyme  2 pills 3 times per  day after a meal, liobil  0,2-0,4 g 3 times per  day after a meal, festal  1-2 pills 3 times per day after a meal);

2)              synthetic holeretics, that have anti-inflammatory and antibacterial  action (nicodin
  0,5 -1 g  3 times per   day  before meal, tsicvalon   0,1 g 3-4 times  before meal, ocsafenamid  0,25-0,5 3 times before meal

3)               holeretics of plant origin (holagogoum  1 capsoule 3 times per   day, febihol
  1-2 capsules 3 times per  day before   meal, holosas   1-2 tea -spoon 2-3 times per   day, flamin   0,05 g 3 times per   day  before  meal.

Holicinetics (prescribed  with a purpose to stimulate excretion of bile   , to strengthening its outflow  via bilious channels, retractive of gall-bladder): magnesium the sulfate   20-25% solution  1   soupspoon inward on an empty stomach 3 times per   day; carlovar  salt   1  tea-spoon on glass of water at the 3O minutes before meal 3 times per   day; csilit, sorbit as a 10% solution on 50-100 ml 2-3 times per   day 20 minutes  before meal,oil, olive’s ,  sea-buckthorn’s oils  1  soupspoon 3 times per   day before   meal.

VI. Physical therapy   at attenuation of accute condition : at hypertensive discinezis-     electrophoresis;  at hypotensive –diodinamic current, impulsive current of low frequency, ultrasonic therapy, balneotherapy-     pearly, carbonic baths, at hypertensive discinezis- radon, coniferous, sulphuretted hydrogen).

VII. Mineral water prescribes  at attenuation of accute condition , and also during remission -“Borgomi”, “Trouscavetsca”, “Esentouci-17” – room temperature  0,5-1,5 glasses  3 times per   day, time of usage depends on  the gastric secretion.  Sanatoria and health   in the phase of remission- in balneological resorts of Trouscavets, Morshin, Gousyatin.

Duration of stationary medical treatment takes 12-14 days, ambulatory- not less than 2 months, and after that the patient is subjected to the clinical supervision.

MEDICAL TREATMENT OF GALL-STONE DISEASE

For patients declining surgical treatment or for whom surgical treatment is inappropriate, gallbladder calculi may sometimes be dissolved in vivo by giving bile acids orally for many months. Stones must not be calcified, the size of concrements should not exceed 20 mm,  demonstration of normal gallbladder function and bilious channels should be passable on oral cholecystography. Medical treatment by preparations of bilious acids is used for chemical dissolution of stones  – henodezocsiholev (HDHC) and ursodezocsiholev (UDHC). Preparations HDHC: henofalc, henohol. Preparations UDHC: oursofalc, oursodil, ourosan.  Ursodeoxycholic acid 10 mg/kg/day and henodezocsiholic acid 15 mg/kg/day reduces biliary secretion of cholesterol and decreases the cholesterol saturation of bile, resulting in gradual dissolution of cholesterol-containing stones in 30 to 40% of patients. Recurrence of stones is common after cessation of the drug. The duration of medical treatment should not exceed 2-3 years, and patient should be warned about this. Alternative methods of stone dissolution (methyl-tert-butyl ether) or stone fragmentation (extracorporeal shock wave lithotripsy) are now largely unavailable owing to greater patient acceptance of laparoscopic cholecystectomy.

 

The Fig. 20.  Papilosphincterotomy

 (chart)

Endoscopic retrograde sphincterotomy (ERS) is a therapeutic application of ERCP in which soft tissues and sphincter fibers of the papilla and intraduodenal duct are divided with electrocautery to permit release of ductal calculi into the duodenum. The duct is emptied successfully in 90% of attempted procedures. Mortality (0.3 to 1.0%) and morbidity (3 to 7%) rates are lower than those reported with surgical treatment. Immediate morbidity is caused by bleeding, pancreatitis, perforation, and cholangitis. Late complications include restenosis and reformed stones in open ducts.

The standard operation for gallbladder removal through a right subcostal or midline incision is open cholecystectomy. When performed electively during a period free of complications, the procedure is relatively safe, with a mortality rate of 0.1 to 0.5%. However, since its introduction in 1988, laparoscopic cholecystectomy has been the treatment of choice for symptomatic gallstones. This technique was popularized largely because of a shorter convalescence, decreased postoperative discomfort, and improved cosmetic results. The procedure entails the insertion of specialized surgical instruments and a video camera into the peritoneal cavity through multiple small incisions in the abdominal wall. After insufflation of the peritoneal cavity, the gallbladder is removed under video monitoring. Laparoscopic cholecystectomy is converted to an open procedure in approximately 5% of cases, usually because of an inability to identify the anatomy of the gallbladder or to manage a complication.

DURATION OF TREATMENT

1. Patients with dysfunctional disorders of biliary way should be treated and investigated ambulatory in average during 4 weeks.

EFFICIENCY  CRITERIA  AND REQUIREMENTS FOR TREATMENT RESULTS

 

1. Liquidation of clinical and laboratory-instrumental  displays of illness, improvement of life quality.

Clinical supervision

Patients with dysfunctional disorders of biliary way

 Not foreseen.

DURATION OF TREATMENT

chronic noncalculous cholecystitis

Duration of stationary treatment makes 12-14 days, ambulatory not less than 2 months, whereupon a patient is subject to a clinical supervision.

  EFFICIENCY  CRITERIA  AND REQUIREMENTS FOR TREATMENT RESULTS

Main criteria of efficiency of treatment are decreasing or disappearance of symptoms of biliar dyspepsia, improvement of life quality.

 

Table 2

Health center treatment of patients with chronic noncalculous cholecystitis

Table 3

Disability examination of patients with chronic noncalculous cholecystitis

 

Chronic liver pathology

Chronic liver pathology is  one of the burning problems of modern gastroenterology. According to statistic datum in Ukraine a huge increas of ill people wiht liver chronic pathology is observed from year to year.

CHRONIC HEPATITIS is taking an important place among disability and mortality reasons and they have tendention to increas. In patients with chronic hepatitis a big risk of this pathology transition in hepatocirrhosis or hepatocellular carcinoma exist. Hepatocirrhosis is one of the main reasons of inhabitants mortality. It takes 4 place in mortality reasons structure of men 40 years older.

It stipulates actuality of this pathology studying with aim of rapid prescription of etiological and pathogenical treatment and appearing of vital dangerous complications prevention.

   Anatomy of the liver and portal venous system

 

 VIDEO 1 VIDEO 2 (liver cellular structure)

 

 Anatomy of the liver and portal venous system

The Fig. 21.  Anatomy of hepatobile tract

Anatomy of the liver:

The liver is located in the upper right-hand portion of the abdominal cavity, beneath the diaphragm and on top of the stomach, right kidney and intestines.

Normal function of the liver:

The liver has a multitude of important and complex functions. Some of these functions are to:

· synthesize a number of proteins, including albumin;

· metabolize fats;

· the liver plays a major role in maintaining normal blood sugar levels;

· secrete bile that contains bile acids to aid in the intestinal absorption of fats and the fat-soluble vitamins A, D, E, and K;

· eliminate, by metabolizing and/or secreting, the potentially harmful biochemical products produced by the body;

· detoxify, by metabolizing and/or secreting, drugs, alcohol, and environmental toxins.

Chronic hepatitis – is an polyetiological inflammative liver disease, lasting longer than six months and characterized by progressive run, fibrosis developing  and could cause  hepatocirrhosis.

Etiological factors:

There are many possible causes including viruses infection, some drugs, alcohol, autoimmune hepatitis and metabolic disorders.

·                        Contagious viral hepatitis such as hepatitis B, hepatitis C and hepatitis D.

·                        Medicines.

·                        Toxins such as alcohol.

·                        Autoimmune hepatitis. This is a disease in which a number of liver cells are destroyed by the patient’s own immune system. Autoimmune hepatitis can also sometimes occur as acute hepatitis. The cause is unknown.

·                        Inborn metabolic disorders, such as Wilson’s disease (disorder of the body’s cooper metabolism) and haemochromatosis (disorder of the body’s iron metabolism).

Many cases are idiopathic, when unknown etiology.

   Hepatitis B virus (HBV) and hepatitis C virus (HCV) are major causes of chronic hepatitis; 5 to 10% of cases of hepatitis B (with or without hepatitis D virus co-infection) and about 75% of cases of hepatitis C become chronic. Infection with hepatitis A virus or hepatitis E virus is not the cause chronic hepatitis.

PATHOGENESIS

The mechanism of chronicity is uncertain, but a direct cytopathic effect of the virus appears to be only minor, especially with HBV infection; instead, liver injury is largely caused by an immune-mediated host reaction to the infection. The role of hepatitis G virus in chronic hepatitis is not clear.

Various drugs can cause chronic hepatitis, including isoniazid, methyldopa, nitrofurantoin, and possibly acetaminophen. The pathogenesis varies with the drug and may reflect an altered immune response, cytotoxic intermediate metabolites, or genetically determined metabolic defects.

The rare Wilson’s disease may present as chronic hepatitis and should be considered in children and young adults with the disorder. Occasionally, ₁-antitrypsin deficiency produces chronic hepatitis, although inactive cirrhosis is more common.

Overwhelming evidence points to immunologic mechanisms of hepatocellular injury in patients with autoimmune hepatitis, including coexisting clinical and serologic immune markers; an association with HLA-B8 and -DR3 haplotypes; extensive periportal infiltration with T lymphocytes and plasma cells; and positive response to therapy with corticosteroids or immunosuppressive drugs.

Chronic hepatitis classification (Los – Angeles 1994 )

According to etiology and pathogenesis:

1.                     Chronic viral hepatitis B

2.                     Chronic viral hepatitis D

3.                     Chronic viral hepatitis C

4.                     Indefinite chronic viral hepatitis (G)

5.                     Autoimmune hepatitis (type I – anti-sma and anti-ana; type II – anti-lkm-1;typeIII-anti-sla and etc.)

6.                     Drug-induced chronic hepatitis

7.                     Toxic hepatitis

8.                     Alcohol hepatitis

9.                     Cryptogenic hepatitis

According to clinical-biochemical and histological factors:

1.        Level of activity, which is determined by difficulties of necrotic and inflammative process:

mild; (when ALT exceeds a norm in 3-5 times)

moderate; -«- 5-10

severe. -«-    more 10

2.        Stage, which determines distribution of fibrosis and hepatocirrhosis developing:

 

0 – fibrosis is absent;

1 – hardly (mild) determined fibrosis;

2 – moderate fibrosis;

3 –  huge (severe ) fibrosis;

4 – hepatocirrhosis:

Note:

At viral hepatitis verification:

A-replication phase;

B-integration phase;

At unverificative hepatitis:

A-acute phase (cytolytic syndrome presence, cholestasis, autoimmune displays, liver insufficiency);

B-remision.

 

INTERNATIONAL  CLASSIFICATION  OF  DISEASES  OF  10^TH  REVISION

 

K73.2 Chronic active(lupoid hepatitis), non classified in other chapters

B 18 Chronic viral hepatitis

B 18.0 Chronic viral hepatitis B with d-antigen

B 18.1 Chronic viral hepatitis B without d-antigen

B 18.2 Chronic viral hepatitis C

K 70.0 Alcohol liver fat dystrophy

K 70.1 Alcohol hepatitis (acute, chronic)

K 70.2 Alcohol liver fibrosis and sclerosis

K 71.0 Toxic hepatitis

CHRONIC HEPATITIS CLINIC

The most commons syndromes and symptoms of chronic hepatitis

I.        PAIN:

·                     Periodic light pressure or pain below the right ribs – enlarged liver

II.     dyspepsia:

·                   nausea, poor appetite, changes in taste perception, belch, flatulence

III.  Jaundice:

·                   icterus; ictery of sclerae (the white portions of the eyes) and skin

   IV.   ASTENOVEGETATIVE DISORDERS (headache,

   lethargy, weakness)

IV. LOW–grade fever.   

V.    weight Loss

VI.  ARTHRALGIA (aching muscles) and MYALGIA

VII.              Hepatomegaly

VIII.           Splenomegaly

    X.     SYNDROME OF SMALL LIVER SIGNS

·                   spider-like blood vessels in skin (spider angioma)

              and palmar erythema (liver palms)

Clinical features vary. Many patients are asymptomatic, especially in chronic hepatitis C.

 

The Fig. 23. The liver palms 

In the autoimmune variant chronic hepatitis manifestations often occur, especially in young women. These can affect virtually any body system and include acne, amenorrhea, arthralgia, ulcerative colitis, pulmonary fibrosis, thyroiditis, nephritis, and hemolytic anemia.

A minority of patients develop predominant cholestatic features suggesting primary biliary cirrhosis.

Laboratory Findings

These include evidence of active hepatocellular inflammation, with predominant aminotransferase elevations and variable bilirubin and alkaline phosphatase values.

 In such cases, other laboratory clues to chronicity may aid the diagnosis (eg, low serum albumin and others).

Cholestatic laboratory features occasionally dominate.

Serologic “immune” markers are common in the autoimmune variant. HBV surface antigen or anti-HCV in serum indicates causation by HBV or HCV, respectively.

Table 4

Biochemical indexes of liver state during chronic hepatitis

 

Chronic viral B hepatitis has two phases, termed the replicative and integrative.

Table 5

Markers of chronic viral hepatitis

Immunological indexes:

AMA- antimitochondrial antibodies;

ANA- antinuclear antibodies;

ALKM- liver-kidneys microsomal antibodies;

ALM- antibodies to liver cells membranes;

SLA- antibodies to dissolve liver antigen;

SMA- smouthmuscle antibodies;

CIC- circulative immune complexes.

Histological criterion of chronic hepatitis is the combination of inflammative-cellular infiltration and various forms of hepatocellular degeneration and necrosis, presence of sclerotic changes. One can see widening of portal ways and its inflammative cellular infiltration.

 

 

The Fig. 24. The Histological criterion of chronic hepatitis: combination of inflammative-cellular infiltration and various forms of hepatocellular degeneration and necrosis.

The Fig. 25. The Histological criterion of chronic hepatitis: portal ways cellular infiltration

 

The Fig. 26. Echographic picture of normal liver.

Liver parenchyma structure is homogeneous with weak echosounds from its inner structures. Soundabsorption is normal. Innerliver  veins walls are not visible practically.

The Fig. 27. Echographic picture of chronic hepatitis. Echosound of parenchyma is increased and heterogeneous, which is caused by  large amount crossing of  increased echosound small areas and areas with less echosound.

The Fig. 28. Echographic picture of chronic hepatitis

VIDEO: liver ultrasound appearance in chronic hepatitis

Treatment

Medical diet № 5

I.                       Etiological:

Standart therapy is provided by recombinant ( which are made by gen engineering) interferons (IFN-a). One useof  such of preparations: aferon, velferon, intron, realdyron, reaferon, roferon.

Indications to interferon monotherapy :

1.                     Young age (not older than 40 years old).

2.                     Female

3.                     Normal weight

4.                     Increased level of GGTP, ALT in blood.

5.                     Presence of moderate active level of inflammative process and minimal level of fibrosis in liver bioptats.

6.                     The  begining of infection at old age.

7.                     Short duration of infection process.

8.                     Active viruse replication, at which one can find DNA HBV(PVR) and HbeAg, anti-HCV IgM.

9.                     Low DNA HBV level (less,than 200 by method of PCR)

10.                Not high RNA HBV level (determined by way of PCR)

11.                Infication of HCV genotype 2 or 3.

Unindications to IFN monotherapy:

1.                     Decompensative hepatocirrhosis (because of hepatitis exacerbation risk at 60 % sick)

2.                     Autoimmune hepatitis or other autoimmune diseases.

3.                     Endogenous or exogenous immunsuppression.

4.                     Depression or other psychic disorders.

5.                     Other liver diseases, such as Vilson disease, haematochromatosis, a-antitrypsyn deficit.

6.                     Epylepsy.

7.                     Leucopenia(<2·109/l), trombocytepenia(<50·109/l)

8.                     Pregnance.

Viral hepatitis C:

IFN is prescribed of 3 mln. IU 3 times on a week underskin

Standard combinated therapy needs subcutaneous injection 3 mln. IU 3 times for a week in combination with peroral use of rybaviryn (body weight <75kg – 1000 mg per 24 hours, means 2 pills for 200 mg in the morning and 3 pills for 200 mg in the evening, body weight>75kg – 1200 mg per 24 hours,means 3 pills for 200 mg in the morning and 3 pills for 200 mg in the evening)

 

Viral hepatitis B:

IFN is used for 5 mln.IU per 24 hours or 10 mln.IU 3 times per week subcutaneous.

For sick, to whom therapy with IFN was unsuccessful or which have little bit chance for good therapy by IFN (for sick with normal ALT level or with PRECORE- mutant (without Hbe Ag) HBV with prenatal infication, immunesuppresion, which is caused by HIV infection or ny organs transplantation) supposed to prescribed lamivudyn 100 mg per 24 hours per os during 1 year.

P.S. Priority of combinative therapy on monotherapy by lamivudyn wasn’t found.

II Pathogenetic therapy

Autoimmune hapatitis

Prednisolon 30 mg per os in a day, dose is lowered to 10-15 mg in a day during few weeks; azatiopryn is often prescripbed for 50 mg per os in a day, which allows to low dose of glucocorticoids and to avoid their side effects. It’s necessary to provide functional liver tests every month. It is possible soon to reduce the symptoms, but biochemical remision comes in few month, and histological – in 18-24 month. If we stop to give glucocorticoids – recidivation becomes at 50-90% cases and the demand to repeat treatment will appear. During often recidivations it is prescript small doses of glucocorticoids or asatyopryn per 24 hours.

III Symptomatic therapy

Hepatoprotectors:

I.                       Plant origin:

Flavonoids:

sylimaryn, sylobinin, sylibor, karsyl, legalon, darsil

hepabene;hepatofalk planta;hofitol

II.                    Preparations, which have essential phospholipids:

essentiale, essentiale H, forte H, lipin, lioliv

III.                 Preparations, which have aminoacids:

Heptral(ademiotynin), glutargin

IV.                Synthetic preparations:

tiatriazolin,tyoktacyd(tyoctov acid)

V.                   Preparations which have bile acids:

ursofalk, ursosan, ursohol.

DURATION OF TREATMENT

Duration of stationary treatment on the III – IV level of medical care makes 21-28 days with next treatment in C.R.H., ambulatory – during 3-6 month, up to the year,  whereupon a patient is subjected to a clinical supervision.

EFFICIENCY  CRITERIA  AND REQUIREMENTS FOR TREATMENT RESULTS

Main criteria of efficiency of treatment are normalization of the common state of patient, biochemical, immunological indexes, functional state of liver, patient’s transformation in the compensated state, absence of complications, improvement of life quality.

Table 7

Health center system of patients with chronic cryptogenic hepatitis

Table 8

Disability examination of patients with chronic cryptogenic hepatitis

 

Hepatocirrhosis

Hepatocirrhosis – it is chronic diffuse defect, which is characterized by violation of normal liver lobule architectonics due to fibrosis and  making of structure – unnormal knots of regeneration, that explains development of liver functional insufficiency and portal hypertension.

Table 9

    Causes of cirrhosis

Pathogenesis – unreturn process of fibrosis and pathological knots developing.

Classification

I.                       according to etiology:

viral

alcohol

toxic

conncted with born metabolism disorders

conncted with injury of

bileoutgoing ways

(primary and secondary biliar cirrhosis)

caused by vein outflow from liver (Badd – Chiari syndrome, veinocclusive disease, constructive pericarditis)

cryptogenic cirrhosis

II.                    according to morphological signs:

·                   active

nonactive

1.                micronodule

macronodule

mixed (micro-, macronodule).

III.                 according to run:

subsharp (hepatitis – cirrhosis)

fastprogressive(active)

slowprogressive(active)

latent.

IV.       Stage of disease ( according to Child-Pugh criterion)

           A-compensation,  B-subcompensation,  C – decompensation.

V.       Complications:

esophago-gastric bleeding

spontaneous bacterial ascites-peritonitis

trombosis of portak vein

hepatorenal syndrome

hepatocellular carcinoma.

Morphology:

A morphological change at hepatocirrhosis includes: hepatocytes necrosis and dystrophy, hepatocytes nodule regeneration, fibrosis, organs structure change, organs deformation.

 

The Fig. 29. Liver Lobule, Pig (Normal)

The Fig. 30. Shown is a mixed macronodular and micronodular cirrhosis.

                                                                                                                       Table 10

Criteria for Child-Pugh classification

 

Each index of  “A ” class is marked in 1 point ;    each index of “B” class is marked in 2 points; each index of “C” class is marked in 3 points.

Class “A” answers to 5-6 points; class”B” – 7-10 points; class”C”- >10 points.

ClinicAL HISTORY

1.                     Astenic syndrome

2.                     Dyspepsia

3.                     Pain syndrome

4.                     Icterus

5.                     Skin itching

6.                     Portal hypertension

7.                     Oedema-ascetic syndrome

8.                     Hemorrhage syndrome

9.                     Injury of endocrine system

10.                Increasing of body temperature

11.                Hepatosplenomegalia

12.                Small liver signs(vascular stars, liver palms)

 

Biochemical indexes of liver at cirrhosis – cytolitic, cholestatic, mesenchymal – inflammative, hepatodepresive  syndromes.

The Fig. 31. Spider naevus in liver cirrhosis

 

The Fig. 32. The   ascitis

Imaging Studies: abdominal ultrasonography, CT scan, or MRI.

                       The Fig. 33. Echographic picture of hepatocirrhosis. Echostructure of liver parenchyma uneven, caused by places of fibrosis, general echosound is increased soundconseption is not changed.

                       The Fig. 34. Echographic picture of hepatocirrhosis and presence of ascetic fluid in abdominal cavity

                       The Fig. 35. A CT scan of the upper abdomen showing cirrhosis of the liver

Treatment

Treatment of subcompensative hepatocirrhosis.

I.                       Specific therapy

a)                     at autoimmune and viral – corticosteroids (prednisolon 20-30 mg per 24 hours during 3-4 weeks with next low on 0,5 mg in every 3 days to support dose 7,5 – 10 mg per 24 hours; to 6 months). At viral hepatocirrhosis interferontherapy is used also.

b)                    Patients with autoimmune hepatocirrhosis (if there is no antiindications) imuran (asatiopryn) to 25 mg per 24 hours, metotrexat to 7,5 – 15 mg per 24 hours is prescribed.

c)                     At biliar hepatocirrhosis – ursodesoxycholiv acid (ursofalk) 15-20 mg/kg during 6 months and more; vit.D in dose 400 IU per 24 hours (osteoporosis)

d)                    At Vilson-Konovalov disease – D-penicylamin in connection with pyridoxine, antioxidants(vit.A, E, C, tokoferol-tryovit.)

e)                     At hematochromatosis – symptom bloodletting under patient selffeeling control, intramuscular injection of desferal – 500-1000 ml per 24 hours, preparations, which have Zn (gumet – 1 tablespoon 3 times per day.)

f)                      At a-antitrypsin insufficiency – hepatoprotectors and preparations, which make better breath function of lungs (aminophylin, ventolin).

II.  It doesn’t depend from cause of beginning you have to use:

a)                     vitamintherapy, such as balanced vitamin complexes; ryboxyn, essenciale H during 1-2 months with repeating 2-3 times per year.

b)                    Hepatoprotective therapy ;

Syndrome of malabsorbtion, maldigestion treatment, normal intestine microflora renewal. Normal intestine flora reimplantation: (bifidumbacteryn, bificol, laktobacteryn, bifi-form, acydofilus, symbiter);

 

c) Protein change correction: (anabolic steroids, albumin intravenous injection,clean aminoacids mixture: poliamin, alvezin, aminoplasmol, aminosol-600, 800).

Lipoid change correction: (essenciale, lipofundyn, intralipid-i/v)

Carbohydrate change correction: (i/v glucose)

d) desintoxication :

–  i/v glucose with vit. from group B, C, neodesis, polydesis;

–  enterosorbtion: enterodesis – 5g 3 times per 24 hours, enterosgel – 15g 3 times/24 hours

III at oedema-ascitis syndrome

–  bed regimen, sodium use – 0,5-2g/24 hours;

–  veroshpiron 75-200mg/24 hours;

–  at huge ascetic syndrome: veroshpiron 150-200mg/24hours + uregit 25-100 mg or furosemid 80mg – hypothyasid 100mg+ veroshpiron 200mg. If there is no effect – blood ultrafiltration.

IV for hypersplenism syndrome treating:

–  prednisolon 20-40mg/24 hours during 2-3 months with next dose low;

–  erythrocytes and thrombocytes mass transfusion.

V chronic liver encephalopathy therapy

–  using less of protein to 50g in food ration, mostly animal origin;

–  braking of amiakogen microflora in intestines (prescription of monomicin, canamicyn, metronidasol);

–  lactulose (dufalac, normaze) 30ml 3-5 times a day after meals;

–  hepasol 500ml i/v drops;

–  ornicetyl 2-6g/24 hours i/m or 2g 1-2 times/24 hours i/v;

–  glutamine acid i/v drops 300-500ml 1%solution or glutargin 50ml 2 times/24 hours i/v (2 pills 3-4 times a day per os

–  aminosol 600( 800,KEO 30ml/kg/24 hours);

–  metabolic acidosis correction (potassium diet, i/v 50-80ml 4% solution KCl in 500-100ml 5% solution of glucose;

VI Stop of bleeding from varicose extended veins

– severe bed regimen, ice on epigastria;

–  i/v drop 1-1,5 l poliglukin injection,200-400 ml of native plasma, 100ml 20% solution of albumin, 5% sol. of  glucose, isotonic solution of NaCl;

–  ¯ of portal pressure: vasopresyn 20 U in 100-200ml 5% sol. of glucose, if necessary – repeat every 4 hours; somatostatin i/v stream 1 dose 250mkg and than i/v drop 250 mkg during 24 hours (3 mg in 12 hours),treatment duration from 24 to 120 hours;

–  hemostatic therapy; i/v stream 400-600ml of  freshiced plasma;

–  decinon i/m or i/v 250-500mg; vikasol 1ml 1% of solution i/m;

–  antihemophil plasma 100-150 ml i/v drop;

–  CaCl or gluconat 10 ml 10% sol. i/v

Liver transplantation

With the dramatic improvement in results, liver transplantation became the recognized management for end-stage liver disease. A patient should be considered for liver transplantation when the diagnosis of irreversible end-stage liver disease is made. The selection of appropriate candidates out of a large number of patients with liver disease combined with the relative scarcity of available organs requires a strict individual assessment, which must to a certain extent be tailored to the cause of liver failure. Transplantation for hepatitis B remains controversial, and physicians should be aware of their transplant center’s policy when considering patients for referral. Exclusion of patients with contraindications to liver transplantation (Table ) allows the best use of scarce donor resources while maximizing patient benefit.

Liver transplantation: contraindications

 

DURATION OF TREATMENT

 

Duration of stationary treatment on the III – IV level of medical care makes 28 days with next treatment in C.R.H., ambulatory (according to necessity) – during month, whereupon a patient is subjected to a clinical supervision.

 

EFFICIENCY  CRITERIA  AND REQUIREMENTS FOR TREATMENT RESULTS

Main criteria of efficiency of treatment are improvement of the common state of patient, biochemical, immunological indexes, functional state of liver, patient’s improvement of life quality.

Table 11

Health center system of patients with chronic liver  cryptogenic cirrhosis

Table 12

Disability examination of patients with chronic liver cryptogenic cirrhosis

JAUNDICE

Jaundice (also known as icterus; from the Greek word ίκτερος, attributive adjective: icteric) is a yellowish pigmentation of the skin, the conjunctival membranes over the sclerae (whites of the eyes), and othe rmucous membranes caused by hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluid. Concentration of bilirubin in blood plasma is normally below 1.2 mg/dL (<25µmol/L). A concentration higher than 2.5 mg/dL (>50µmol/L) leads to jaundice. The term jaundice comes from the French word jaune, meaning yellow.

 

 

Hyperbilirubinemia could be caused by

·  increased bilirubin production

·  decreased uptake into the liver cells

·  impaired conjugation

·  interference with the secretion of conjugated bilirubin.

Here is a schematic diagram that represents normal bilirubin metabolism. Use this to compare with various abnormal states described below. Clicking on the diagrams will reveal larger versions of them.

 

Here are some examples of diseases in which hyperbilirubinemia is observed.

Hemolytic jaundice

 

·  results in increased production of bilirubin.

·  Here more bilirubin is conjugated and excreted thaormally, but the conjugation mechanism is overwhelmed, and an abnormally large amount of unconjugated bilirubin is found in the blood.

Gilbert’s disease

·  may be caused by an inability of the hepatocytes to take up bilirubin from the blood.

·  As a result, unconjugated bilirubin accumulates.

 

Physiological jaundice and Crigler-Najjar syndrome

 

 

·  are conditions in which conjugation is impaired.

·  Unconjugated bilirubin is retained by the body.

Dubin-Johnson syndrome

 

·  is associated with inability of the hepatocytes to secrete conjugated bilirubin after it has been formed.

·  Conjugated bilirubin returns to the blood.

 

 

Biliary obstruction

·  by (for example) biliary calculi causes backup and reabsorption of conjugated bilirubin.

·  Blood levels of conjugated bilirubin increase.

 

Jaundice is often seen in liver disease such as hepatitis or liver cancer. It may also indicate leptospirosis or obstruction of the biliary tract, for example by gallstones or pancreatic cancer, or less commonly be congenital in origin (e.g., biliary atresia).

Yellow discoloration of the skin, especially on the palms and the soles, but not of the sclera and mucous membranes (i.e. oral cavity) is due to carotenemia—a harmless condition^[4] important to differentiate from jaundice.

video

Signs and symptoms

The conjunctiva of the eye are one of the first tissues to change color as bilirubin levels rise in jaundice. This is sometimes referred to as scleral icterus.

However, the sclera themselves are not “icteric” (stained with bile pigment) but rather the conjunctival membranes that overlie them. The yellowing of the “white of the eye” is thus more properly termed conjunctival icterus. The term “icterus” itself is sometimes incorrectly used to refer to jaundice that is noted in the sclera of the eyes, however its more common and more correct meaning is entirely synonymous with jaundice.

Jaundice is a sign of an underlying disease process. .

Common signs and symptoms seen in individuals with jaundice include:

·  yellow discoloration of the skin, mucous membranes, and the whites of the eyes,

·  light-colored stools,

·  dark-colored urine, and

·  itching of the skin.

The underlying disease process may result in additional signs and symptoms. These may include:

·  nausea and vomiting,

·  abdominal pain,

·  fever,

·  weakness,

·  loss of appetite,

·  headache,

·  confusion,

·  swelling of the legs and abdomen,

·  newborn jaundice.

Iewborns, as the bilirubin level rises, jaundice will typically progress from the head to the trunk, and then to the hands and feet. Additional signs and symptoms that may be seen in the newborn include:

·  poor feeding,

·  lethargy,

·  changes in muscle tone,

·  high-pitched crying, and

·  seizures.

Differential diagnosis

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When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:

Types of jaundice

 

 

Pre-hepatic

 

Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). In tropical countries, malaria can cause jaundice in this manner. Certain genetic diseases, such assickle cell anemia, spherocytosis, thalassemia and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such ashemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also present as jaundice, as in Gilbert’s syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population) and Crigler-Najjar syndrome.

In jaundice secondary to hemolysis, the increased production of bilirubin, leads to the increased production of urine-urobilinogen. Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble, so, the combination of increased urine-urobilinogen with no bilirubin (since, unconjugated) in urine is suggestive of hemolytic jaundice.

Laboratory findings include:

·  Urine: no bilirubin present, urobilinogen > 2 units (i.e., hemolytic anemia causes increased heme metabolism; exception: infants where gut flora has not developed).

·  Serum: increased unconjugated bilirubin.

·  Kernicterus is associated with increased unconjugated bilirubin, neonates are especially vulnerable to this due to increase permeability of the blood brain barrier.

Hepatocellular

Hepatocellular (hepatic) jaundice can be caused by acute or chronic hepatitis, hepatotoxicity, cirrhosis, drug induced hepatitis and alcoholic liver disease. Cell necrosis reduces the liver’s ability to metabolize and excrete bilirubin leading to a buildup of unconjugated bilirubin in the blood. Other causes include primary biliary cirrhosis leading to an increase in plasma conjugated bilirubin because there is impairment of excretion of conjugated bilirubin into the bile. The blood contains abnormally raised amount of conjugated bilirubin and bile salts which are excreted in the urine. Jaundice seen in the newborn, known as neonatal jaundice, is common iewborns  as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age. Rat fever (leptospirosis) can also cause hepatic jaundice. In hepatic jaundice, there is invariably cholestasis.

Laboratory findings depend on the cause of jaundice.

·  Urine: Conjugated bilirubin present, urobilirubin > 2 units but variable (except in children). Kernicterus is a conditioot associated with increased conjugated bilirubin.

·  Plasma protein show characteristic changes.

·  Plasma albumin level is low but plasma globulins are raised due to an increased formation of antibodies.

Bilirubin transport across the hepatocyte may be impaired at any point between the uptake of unconjugated bilirubin into the cell and transport of conjugated bilirubin into biliary canaliculi. In addition, swelling of cells and oedema due to inflammation cause mechanical obstruction of intrahepatic biliary tree. Hence in hepatocellular jaundice, concentration of both unconjugated and conjugated bilirubin rises in the blood. In hepatocellular disease, there is usually interference in all major steps of bilirubin metabolism—uptake, conjugation and excretion. However, excretion is the rate-limiting step, and usually impaired to the greatest extent. As a result, conjugated hyperbilirubinaemia predominates.

The unconjugated bilirubin still enters the liver cells and becomes conjugated in the usual way. This conjugated bilirubin is then returned to the blood, probably by rupture of the congested bile canaliculi and direct emptying of the bile into the lymph leaving the liver. Thus, most of the bilirubin in the plasma becomes the conjugated type rather than the unconjugated type, and this conjugated bilirubin which did not go to intestine to become urobilinogen gives the urine the dark color.

Post-hepatic

Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as “liver flukes” can live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, cholangiocarcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi’s syndrome.

In complete obstruction of the bile duct, no urobilinogen is found in the urine, since bilirubin has no access to the intestine and it is in the intestine that bilirubin gets converted to urobilinogen to be later released into the general circulation. In this case, presence of bilirubin (conjugated) in the urine without urine-urobilinogen suggests obstructive jaundice, either intra-hepatic or post-hepatic.

The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments. However, although pale stools and dark urine are a feature of biliary obstruction, they can occur in many intra-hepatic illnesses and are therefore not a reliable clinical feature to distinguish obstruction from hepatic causes of jaundice.

Patients also can present with elevated serum cholesterol, and often complain of severe itching or “pruritus” because of the deposition of bile salts.

No single test can differentiate between various classifications of jaundice. A combination of liver function tests is essential to arrive at a diagnosis.

 

Neonatal jaundice

Main article: Neonatal jaundice

Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births. Typical causes for neonatal jaundice include normal physiologic jaundice, jaundice due to breast feeding, and hemolytic disorders that include hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, pyruvate kinase deficiency, ABO/Rh blood type autoantibodies, or infantile pyknocytosis. Serum bilirubiormally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In cases where bilirubin rises higher, a brain-damaging condition known as kernicterus can occur, leading to significant lifelong disability; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia. A Bili light is often the tool used for early treatment, which often consists of exposing the baby to intensive phototherapy. However, in third world countries where procuring such treatment is prohibitively expensive, parents often subject their children to regular daily sunbathing. Bilirubin count is lowered through bowel movements and urination so regular and proper feedings are especially important.^]

Pathophysiology

Jaundice itself is not a disease, but rather a sign of one of many possible underlying pathological processes that occur at some point along the normal physiological pathway of the metabolism of bilirubin in blood.

When red blood cells have completed their life span of approximately 120 days, or when they are damaged, their membranes become fragile and prone to rupture. As each red blood cell traverses through the reticuloendothelial system, its cell membrane ruptures when its membrane is fragile enough to allow this. Cellular contents, including hemoglobin, are subsequently released into the blood. The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, a protein, is degraded into amino acids and plays no role in jaundice. Two reactions then take place with the heme molecule. The first oxidation reaction is catalyzed by the microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron and carbon monoxide. The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is “unconjugated,” “free” or “indirect” bilirubin. Approximately 4 mg of bilirubin per kg of blood is produced each day.^[13] The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. However approximately 20 percent comes from other heme sources, including ineffective erythropoiesis, and the breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.

Hepatic events

The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to serum albumin. Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just “conjugated bilirubin”) to become more water soluble. The reaction is catalyzed by the enzyme UDP-glucuronyl transferase.

This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen. From here urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the feces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. Stercobilin and urobilin are the products responsible for the coloration of feces and urine, respectively.

Diagnostic approach

Biliary tract dilation due to obstruction as seen on CAT scan

 

Biliary tract dilation due to obstruction

Most patients presenting with jaundice will have various predictable patterns of liver panel abnormalities, though significant variation does exist. The typical liver panel will include blood levels of enzymes found primarily from the liver, such as the aminotransferases (ALT, AST), and alkaline phosphatase (ALP); bilirubin (which causes the jaundice); and protein levels, specifically, total protein and albumin. Other primary lab tests for liver function include gamma glutamyl transpeptidase (GGT) and prothrombin time (PT).

The gallbladder is a small, pear-shaped pouch that lies beneath the liver, in the upper abdomen. It stores bile. This fluid, produced by the liver, helps digest fat. The gallbladder releases bile into the small intestine through the bile duct. This thin tube connects the liver and gallbladder to the small intestine. Cancer develops when abnormal cells in these structures multiply and grow rapidly.

 

Most gallbladder and bile duct cancers are adenocarcinomas—cancers of cells that line the glands and ducts. Bile duct adenocarcinoma forms from the mucus glands that line the duct. It can develop in any part of the bile duct.

Gallbladder and bile duct cancers are rare. Gallbladder cancer is more common in women than in men. People with gallstones have a slightly higher risk of developing gallbladder and bile duct cancer. These cancers also have been linked to infections with the liver fluke parasite. They have also been tied to sclerosing cholangitis, ulcerative colitis, and cirrhosis. These diseases can cause inflammation and scarring of the bile duct, colon, or liver.

Symptoms

Early on, gallbladder and bile duct cancers may cause no symptoms. Nor can they be seen or felt during a routine physical exam. Rather, many of them are found when the gallbladder is removed as a treatment for gallstones. There are no screening tests for these cancers.

When symptoms occur, they can include

·  jaundice

·  abdominal pain or swelling

·  nausea and/or vomiting

·  lack of appetite

·  losing weight for no reason

·  itching

·  fever that doesn’t go away.

Jaundice is the most common symptom of bile duct cancer, and nearly half of all people with gallbladder cancer have jaundice when they are diagnosed. Jaundice makes the skin and the whites of the eyes look yellow. This happens when the liver cannot get rid of bile. Levels of bilirubin (a dark yellow chemical in bile) then rise in the bloodstream. Bile and bilirubin can also cause itching.

Although many people with gallbladder and bile duct cancers have jaundice, the most common cause of jaundice is hepatitis, not cancer. Having a gallstone lodged in the bile duct can also cause jaundice; it can prevent bile from flowing into the small intestine. This is a noncancerous condition.

Diagnosis

Your doctor will ask about your medical history and examine you, focusing on your abdomen. He or she will check for masses, tender spots, fluid build-up, and enlarged organs. In addition, your doctor will check your skin and eyes for jaundice and feel lymph nodes for swelling.

Next, you will have blood tests. These tests can measure the levels of liver and gallbladder enzymes, and of bilirubin. Too much bilirubin in the blood may mean that your bile duct is blocked or that you have gallbladder or liver problems. An elevated level of an enzyme called alkaline phosphatase also can point to a blocked bile duct or gallbladder disease. A substance called CA 19-9 may be elevated in people with bile duct cancer.

But blood tests cannot determine why levels of these substances are elevated. To do that, your doctor may order one or more of these tests:

·  Ultrasound — Ultrasound uses sound waves to make pictures of internal organs. It can detect about half of gallbladder cancers. It can also help find a bile duct obstruction or tumor, if it’s large enough.
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Ultrasound can be combined with endoscopy and laparoscopy. During endoscopy, your doctor inserts a flexible viewing tube (an endoscope) into your mouth. He or she then feeds the tube through the stomach and into the first part of the small intestine, where the bile duct empties. Laparoscopy is a limited type of surgery. It involves placing a surgical instrument called a laparoscope through a small cut on the side of the body. Both procedures allow the ultrasound transducer to be placed closer to the gallbladder. This placement produces more-detailed images than a standard ultrasound.

·  Computed tomography (CT) —  video

This test uses a rotating x-ray beam to make detailed, cross-sectional images of the body.

A CT

scan can identify a tumor inside the gallbladder or one that has spread outside of it. It also can help to determine whether the tumor has spread to the bile duct, liver, or nearby lymph nodes.

·  Magnetic resonance imaging (MRI) — These scans also create cross-sectional images of internal organs. However, they use radio waves and powerful magnetic fields instead of radiation. They can make more detailed images than ultrasounds and CT scans. That’s why they are effective in showing whether a tumor is only in the gallbladder or has invaded the liver. A special type of magnetic resonance imaging — magnetic resonance cholangiopancreatography (ko-LAN-gee-o-PAN-cree-a-TOG-ruh-fee) (MRCP) — creates pictures that make the bile duct stand out. It’s among the best noninvasive ways to check for bile duct cancer.

·  Endoscopic retrograde cholangiopancreatography (ERCP) — In this procedure, a flexible tube is passed down the throat, through the esophagus and stomach, and into the common bile duct. A small amount of contrast dye is used to help outline the bile duct in x-ray images. These pictures can show if the bile duct is narrowed or blocked. The advantage of ERCP is that it can be used to take biopsies of a blocked area and relieve the blockage. To do this, the doctor places a wire-mesh tube, called a stent, in the bile duct to keep it open. Sometimes, inserting a stent eliminates the need for surgery.

·  Surgery — Sometimes surgery must be done to determine if there is cancer in the gallbladder or bile duct.

·  Biopsy — To be certain of the diagnosis, a tissue sample will be taken from the tumor or mass and examined in a laboratory. Bile may be taken to see if it contains cancer cells. Tissue and bile samples can be taken during an ERCP, with a needle guided by a CT scan, by scraping the lining of ducts with a small brush, or during surgery.

Expected Duration

Gallbladder and bile duct cancers will continue to grow unless treated.

Prevention

There is no way to prevent gallbladder or bile duct cancers. However, you can lower your risk of gallbladder cancer by maintaining a healthy weight and avoiding tobacco.

Preventing and treating liver fluke infections may help to reduce the risk of bile duct cancer. To do this,

·  Cook or freeze freshwater fish from Asia before eating it.

·  Purchase shellfish only from reputable stores.

·  Take medication as prescribed if you are diagnosed with a liver fluke infection.

Preventing hepatitis may also reduce the risk of bile duct cancer. To do this

·  Practice safer sex by using condoms.

·  Do not inject illegal drugs. If you do, never share needles with anyone.

·  Ask your doctor about getting vaccines against hepatitis A and B. There is no vaccine against other forms of hepatitis.

If you have been exposed to someone with hepatitis A or B, talk to your doctor about getting the vaccine or an immunoglobulin shot as soon as possible.

If you have an inflammatory bowel disease, such as ulcerative colitis, you have an increased risk of gallbladder and bile duct cancers. Your doctor may evaluate you for these cancers during routine exams.

Treatment

Treatment will depend on

·  the type, location, and extent of your cancer

·  your overall health

·  the chances of curing the disease, extending your life, or relieving symptoms.

Because gallbladder and bile duct cancers are rare, get a second opinion before deciding on a treatment. Seek treatment at a medical center with a staff that is expert in treating your type of cancer.

Surgery is the main treatment for gallbladder and bile duct cancers. Surgery is the only possible way to cure the disease, but opinions vary as to how advanced a gallbladder or bile duct cancer can be and still be curable. Because there usually are no symptoms early on, these cancers are often fairly advanced when they are discovered. Surgery for gallbladder and bile duct cancer is difficult for both doctors and patients. Unless there is clear evidence that the procedure is likely to significantly extend your life or improve your quality of life, it may not be the best option.

However, surgery sometimes can help to relieve pain or prevent complications. This type of “palliative surgery” includes a biliary bypass. This procedure restores the flow of bile. The surgeon can insert a biliary stent or catheter (tube) to release bile into the small intestine or externally. Biliary stents also can be placed without surgery. A doctor can guide an endoscope from your mouth into your stomach and small intestine, where the bile duct opening can be reached.

Radiation therapy also can be used to treat gallbladder and bile duct cancers. There are two types of radiation therapy:

·  External beam radiation directs x-ray beams at the cancer from a machine outside the body.

·  Brachytherapy involves putting radioactive material in the body, near the tumor.

Radiation may be used after surgery to kill any remaining cancer cells. If the cancer has spread too far to be removed completely, it may be the primary treatment. However, radiation therapy cannot cure these cancers.

For advanced cases, radiation also may be used as palliative therapy. That means the goal is not to cure the cancer, but to reduce pain or other symptoms by shrinking the tumor.

If you have bile duct cancer, your doctor might also recommend chemotherapy. Chemotherapy involves the use of drugs—taken by mouth or injected into a vein—to kill cancer cells. Chemotherapy can help shrink a bile duct tumor before surgery. It can also help control symptoms when surgery is not recommended or the tumor has advanced despite other treatments.

Gallbladder cancer does not respond very well to chemotherapy.

In advanced stages of gallbladder cancer, treatment response can sometimes be assessed with tumor markers. Blood tests for CA 19-9 and CEA can be done prior to starting treatment. If one or both levels are high and decrease after cancer therapy, this usually indicates shrinking of the cancer.

When To Call a Professional

You should see your doctor if you have

·  jaundice (yellowing of the skin and whites of the eyes)

·  persistent itching

·  persistent abdominal pain

·  weight loss for no known reason

·  a fever that won’t go away.

All of these symptoms can be related to noncancerous diseases. But you should visit your doctor so that your condition can be diagnosed and treated as soon as possible.

Prognosis

The outlook depends on your general health, how far the cancer has spread, and the type of treatment. In the earlier stages of gallbladder and bile duct cancer, when surgery can be done, between 15 percent and 50 percent of patients survive at least five years. When the tumor is advanced and surgery is not possible, the five-year survival rate is much lower. Unfortunately, this is when many gallbladder and bile duct cancers are diagnosed.

 

Some bone and heart disorders can lead to an increase in ALP and the aminotransferases, so the first step in differentiating these from liver problems is to compare the levels of GGT, which will only be elevated in liver-specific conditions. The second step is distinguishing from biliary (cholestatic) or liver (hepatic) causes of jaundice and altered laboratory results. The former typically indicates a surgical response, while the latter typically leans toward a medical response. ALP and GGT levels will typically rise with one pattern while aspartate aminotransferase (AST) and alanine aminotransferase (ALT) rise in a separate pattern. If the ALP (10–45 IU/L) and GGT (18–85) levels rise proportionately about as high as the AST (12–38 IU/L) and ALT (10–45 IU/L) levels, this indicates a cholestatic problem. On the other hand, if the AST and ALT rise is significantly higher than the ALP and GGT rise, this indicates an hepatic problem. Finally, distinguishing between hepatic causes of jaundice, comparing levels of AST and ALT can prove useful. AST levels will typically be higher than ALT. This remains the case in most hepatic disorders except for hepatitis (viral or hepatotoxic). Alcoholic liver damage may see fairly normal ALT levels, with AST 10x higher than ALT. On the other hand, if ALT is higher than AST, this is indicative of hepatitis. Levels of ALT and AST are not well correlated to the extent of liver damage, although rapid drops in these levels from very high levels can indicate severe necrosis. Low levels of albumin tend to indicate a chronic condition, while it is normal in hepatitis and cholestasis.

Lab results for liver panels are frequently compared by the magnitude of their differences, not the pure number, as well as by their ratios. The AST:ALT ratio can be a good indicator of whether the disorder is alcoholic liver damage (10), some other form of liver damage (above 1), or hepatitis (less than 1). Bilirubin levels greater than 10x normal could indicate neoplastic or intrahepatic cholestasis. Levels lower than this tend to indicate hepatocellular causes. AST levels greater than 15x tends to indicate acute hepatocellular damage. Less than this tend to indicate obstructive causes. ALP levels greater than 5x normal tend to indicate obstruction, while levels greater than 10x normal can indicate drug (toxic) induced cholestatic hepatitis or Cytomegalovirus. Both of these conditions can also have ALT and AST greater than 20× normal. GGT levels greater than 10x normal typically indicate cholestasis. Levels 5–10× tend to indicate viral hepatitis. Levels less than 5× normal tend to indicate drug toxicity. Acute hepatitis will typically have ALT and AST levels rising 20–30× normal (above 1000), and may remain significantly elevated for several weeks. Acetaminophen toxicity can result in ALT and AST levels greater than 50x normal.