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MINISTRY OF HELTHCARE OF THE REPUBLIC OF UZBEKISTAN
TASKENT MEDICAL ACADEMY
APPROVED
Vice-rector for studying process
Senior Prof.
Teshaev O.R.
«_________» __________2011y
Uniform tutorial
Theme: Jaundice Syndrome
(Lesson 22)
Compiled by: senior lecturer of the department Arifzhanova Z.Sh.
Tashkent - 2011
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APPROVED
On conference in department of surgical diseases for general practitioners
Head of department___________________senior prof Teshaev O.R.
Text of lecture accepted by CMC for GP of Tashkent Medical Academy
Report №___________from____________2011 y
Moderator
senior professor Rustamova M.T.
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Exercise: number 22
Jaundice syndrome
Topic 7.2. Jaundice with liver diseases, bacterial and amebic abscess and liver cirrhosis. Parasitic
and non-parasitic liver cysts. Definition, causes, classification, methods of clinical, laboratory
and instrumental diagnostics. Clinical semiology and differential diagnosis, the tactics of GPs
and surgeons. Current aspects of treatment. Surgical traditional and complementary therapies.
Rehabilitation of patients, and prevention.
1. Venue activities and equipment: Hospital, Training Room, House of the hospital, dressing
room, operating. Case patients, hospital records and outpatient hospital patients, blood and urine
tests, the results of instrumental studies, guidelines, training manual on practical exercises, case
studies, test questions, algorithms, performance skills, scripts, interactive teaching methods,
standard protocols, handouts of Internet, slides, EMC, videos, training aids: slaydoskop, TV,
video.
2. Duration of training - 327 minutes.
3. Session Purpose:
3.1. Learning Objectives:
- Consolidate and extend knowledge about the clinic abscesses, cysts and liver cancer as the
cause of jaundice syndrome;
- The skills of clinical examination of patients with abscesses, cysts and liver cirrhosis;
- Create the ability to analyze data from laboratory and instrumental methods;
- Create the ability to carry out a differential diagnosis of liver diseases that occur with the
syndrome of jaundice;
- Learn basic principles and tactics of treatment of patients with liver disease;
- Adopt the tactics of GPs in charge of patients;
- To form the concept of minimally invasive treatments for liver disease;
- Learn basic principles of rehabilitation and prevention of liver diseases.
3.2. The student should know:
- Methods of examination of patients;
- Carrying out a differential diagnosis;
- The tactics of treatment of patients;
- Postoperative rehabilitation of patients;
- Prevention of liver diseases;
3.3. The student should be able to do:
- Sensing and gastric lavage;
- Determination of blood groups and blood transfusions conduct;
- Supervision of patient, professional and examination questions.
- Be able to palpate the abdomen.
- The imposition of the probe Blackmore;
- Be able to determine the technique simptokompleksov acute and elective surgical disease
requiring surgical intervention.
- Methodology for fistulografii and instrumental methods, and interpretation of laboratory,
radiologic and instrumental studies;
- The method of puncture of the abdominal cavity and letting ascites.
4. Motivation:
Jaundice is a symptom of diseases such as abscesses, cysts (parasitic, non-parasitic), cirrhosis of
the liver. GP routinely have to deal with diseases such as parasitic cysts of the liver, particularly
liver echinococcosis. The incidence of this disease is associated with a lifestyle most of the rural
population engaged in animal husbandry. Another disease syndrome manifested as
hepatomegaly, cirrhosis of the liver is. This disease is one of the regional pathology, due to the
high incidence of hepatitis. Therefore, general practitioner should know and be able to diagnose
these diseases, carry out a differential diagnosis, develop tactics for these patients.
5. Interdisciplinary communication and vnutripredmetnye:
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anatomy, regional anatomy, operative surgery, pathological anatomy, patfiziologiya, therapy,
infectious diseases, hematology, anesthesiology and resuscitation, clinical pharmacology.
The next stage of the pathological process: portal hypertension - increased pressure in the portal vein
caused by obstruction of the intra-or extrahepatic portal vessels. Portal hypertension, in turn, leads to
shunting of blood portokavalnogo, splenomegaly and ascites. Thrombocytopenia associated with
splenomegaly (increased deposition of platelets in the spleen), leukopenia, anemia (increased
hemolysis).
Ascites leads to restriction of mobility of the diaphragm (the risk of pulmonary atelectasis, pneumonia),
gastroesophageal reflux with peptic erosions, ulcers and bleeding from varices of the esophagus,
abdominal hernia, bacterial peritonitis, hepatorenal syndrome.
Patients with cirrhosis often have gepatogennye encephalopathy.
The leading place in the origin of primary biliary cirrhosis belong to genetic disorders immunoregulation.
For the initial changes include destruction of biliary epithelium with subsequent necrosis of the tubular
segments and in the later stage of the disease - their proliferation is accompanied by impaired excretion
of bile epithelium infiltrated by lymphocytes, plasma cells, macrophages. In the evolution of the disease
can be traced four stages: chronic nonsuppurative destructive cholangitis, duktulyarnoy proliferation
with destruction of bile ducts, scarring of the bile ducts with a reduction and the development of
cirrhosis and cholestasis SKD.
Pathogenesis of non-parasitic liver cysts. As a result sekrktsii abberantnyh epithelium of bile ducts in
them gradually accumulate fluid and they turn into cysts. Cysts are more common in the left lobe or in
the forefront of the right lobe of the liver.
Pathogenesis and pathology of the liver echinococcosis. Once in the gastrointestinal tract of human
parasite eggs under the action of digestive enzymes lose their outer shell and the released oncosphere
with hooks penetrates the mucous membrane of the stomach or intestines, from a current-carrying
venous blood and lymph is transferred to the portal system and is retained in the liver. Part
oncospheres, bypassing the liver capillaries, through the inferior vena cava, pulmonary heart of a small
circle of blood circulation to the lungs and accumulates in them. A small part of oncospheres,
penetrating through the arteriovenous anastomoses, enters the systemic circulation and may be
entered in any organ or tissue of the human body.
Settled in the tissues oncosphere for 5 months. turns into a larva - hydatid cyst with a diameter of 520 mm, depending on the structure of tissues, and which it develops. In lung tissue parasitic cysts grow
faster than in the liver and bones. Of great importance is sensitization of the host metabolic products of
E., which causes symptoms of intoxication (fatigue, reduced work capacity), and allergic reactions
associated with nicked the wall with small cysts. Complete ruptures larvotsist accompanied expiration
contents into the abdominal or pleural cavity as well as its breakthrough in the bronchi, bile inflows or
large vessels, often lead to severe anaphylactic shock, colonization of other organs and tissues and the
development of so-called secondary E.
The important role played by the mechanical action on tissue exerted by the growing cyst, which leads
to atrophy of the adjacent sections and expressed his body deformation, because can simultaneously
develop several larvotsist who are often on the surface, but there may be deep in the body. Hydatid cyst
of round shape and surrounded by a whitish thick fibrous capsule, which can be soldered to the
surrounding tissues, not belonging to the affected organ. In addition to atrophic changes in the tissues
of the body located around larvotsisty, inflammatory changes are observed - from minor to cirrhosis
formed. With the death of the parasite and the festering cyst develops a picture of acute purulent
inflammation of its walls and surrounding tissues.
6. The content of lessons:
6.1 Theoretical part:
Hepatophyma
Liver abscess - a limited collection of pus in the background section of the hepatic parenchyma destruction resulting
from penetration into the body of the microbial flora or parasites. Depending on the nature of the pathogen isolated
bacterial and parasitic abscess (amebic origin).
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Due to the success of diagnosis and treatment in most countries over the past decade the frequency of liver abscesses
was reduced by 5-10 times. In Europe and North America are more common bacterial abscesses, while in hot climates
(Asia, Africa, South America), almost 90% of patients reveal parasitic abscesses. A similar trend is observed in the CIS.
Thus, the population of the European territory of the Russian Federation, the most commonly observed bacterial
abscesses, while in the Caucasus, Central Asia, Kazakhstan and southern parts of Western Siberia is dominated by
parasitic abscess origin.
The paths of infection bacterial abscesses are divided into hematogenous (portal and arterial), holangiogennye,
contact, post-traumatic stress (ischemic) and cryptogenic when the source of infection can not be found. A separate
group of secondary abscesses appropriate cases to provide non-parasitic abscesses and hydatid cysts, foci of infection
with the collapse of benign and malignant liver tumors, and (rarely) the specific granulomas of the body - the
tubercular and syphilitic. This group of abscesses may be seen as a complication of various focal
liver disease not related to the primary suppurative diseases of the body.
Much less frequently hematogenous infection occurs through the hepatic artery in septic endocarditis, or any other
form of sepsis.
The main road is holangiogenny infection [Bergamini TM et al., 1987]. Most often it is observed in acute suppurative
cholangitis and obstructive jaundice due to gallstone disease and its complications (choledocholithiasis, stenosis of the
major duodenal papilla). Significantly less likely to Hal-giogennye abscesses occur against a background of jaundice
caused by pancreatic head cancer or a tumor of extrahepatic bile ducts. In general, recent years have witnessed an
increase in the number of patients with liver abscesses holangiogennymi.
Rarely develop abscesses caused by migration holangiogennyh into the lumen of the bile ducts of some species of
parasites (especially ascariasis, opisthorchiasis, Fasciola-se). Holangiogennye abscesses are usually multiple.
Hematogenous route of infection in patients with bacterial abscesses is also quite frequent. In this case the majority of
patients infected liver occurs through the bloodstream through the portal vein (portal route) in the presence of acute
destructive appendicitis, ulcerative colitis, diverticulitis complications of colon, pancreatic or common destructive
purulent peritonitis of different etiology.
Contact the penetration of infective usually observed at the break in the liver tissue of empyema of the gallbladder
and the penetration into it of gastroduodenal ulcers, as well as in open-traumatic lesions of the liver and
subdiaphragmatic abscesses of varying etiology.
Post-traumatic abscess developed after closed abdominal trauma. In some cases, become infected and fester
subcapsular or intraparenhimatoznyh (central) hematomas, in other similar process occurs in a restricted area of
tissue necrosis of the liver caused by its concussion. At the same microbial flora enters the zone of injury or biliary
hematogenous (portal) through.
The most common infectious agents of bacterial abscesses are Escherichia coli, staphylococcus, streptococcus, or their
associations. In some cases, the contents of the abscess at seeding the growth of bacteria is not detected (sterile pus).
In patients with liver abscesses caused by blood infection, usually staphylococcus and streptococcus are planted.
In recent years there have been reports of the presence in 30-45% of patients with liver abscess contents anaerobic
microflora, while dominated by Gram-negative bacteria nesporoobrazutoschie of bacteroids (for portal,
holangiogennom
and contact method of infection). It should be noted that such a high incidence of non-clostridial anaerobic bacterial
flora in the contents of abscesses associated with the use of special methods are currently the material of the fence
(without air) and subsequent cultivation of microbes in anaerobic culture apparatus. In this connection it must be
recognized it is expedient to regard different bacterial abscesses holangiogennogo, portal and contact of origin due to
a mixed anaerobic and aerobic flora, which requires a specific approach to determining the nature of the pathogen
and follow-up to conduct drug antibiotic therapy.
Parasitic (amebic) abscesses are caused by penetration into the liver tissue of the simplest organisms. Human infection
occurs through enteral. Amoebae embedded in the submucosal layer of the small intestine, where further migrate
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into the venous vessels of portal system. From the bloodstream, they reach the liver, where they cause necrosis of the
limited area of tissue with subsequent melting and the formation of solitary or (rarely) multiple abscesses. It must be
emphasized that some patients from the contents of the parasitic abscess planted microbial flora (often quantitativebacillary), while the amoebas are found in the abscess contents only in individual patients. The most common
parasites detected in the wall of the abscess.
Frequency of amebic liver abscess with intestinal amoebiasis varies widely - from 1 to 25% [De Bakey M. E., Iordan G.
L., 1977]. The disease usually occurs in people aged 20-40 years, men suffer 5-7 times more often than women.
Clinical manifestations of bacterial abs processes largely depend on their number, size, location and the nature of the
underlying disease which caused the suppurative process in the liver.
For large solitary abscesses (which tend to be localized in the right lobe of the liver) is characterized by a triad of
symptoms: pain in right hypochondrium, pyrexia, hepatomegaly. Pain is usually of a permanent character, and
sometimes the pain is preceded by a feeling of heaviness or a foreign body in the upper right quadrant of the
abdomen. Usually the patient can quite clearly define the localization of pain, which is probably due to the
inflammatory reaction adjacent parietal peritoneum. Characteristic of subserous localization of abscess is increased
pain when breathing or change of body position. When poddiaf ragmalnoy-localization of abscess pain radiating to the
right shoulder blade and shoulder girdle.
In addition to local pain, a very common symptom is hyperthermia, which usually reaches values of febrile (38 ° C and
above) and is permanent or intermittent. Against the background of massive antibiotic therapy, conducted at the main
inflammatory disease, which was a
cause of the abscess, the temperature reaction may be unexpressed. Almost half of patients with hyperthermia is
accompanied by chills and sweats torrential. Much more often, these symptoms occur in patients with abscesses that
have developed as a result of holangiogennogo and portal of infection.
One of the regular symptoms of bacterial abscess of the liver, which is found in many patients, are expressed general
weakness and malaise. In addition, patients reported frequently and a variety of dyspepsia: reduction of titanium
Annette, nausea and occasionally vomiting and weight loss.
Jaundice in solitary abscess is a rare and usually occurs as a result of toxic liver damage, or (more rarely) as a result of
compression of a large abscess of trunk and biliary tract. When jaundice is noted holangiogennyh abscesses in virtually
all patients and is parenchymal in nature.
Rare symptoms include ascites, and splenomegaly, which arise as a result of portal hypertension on the background of
acute portal vein thrombosis.
Approximately 15% of patients revealed a variety of pulmonary symptoms: cough with scanty sputum, mucus
(sometimes streaked with blood), shortness of breath, chest pain associated with compression of the sharp increase in
the liver, lungs and pneumonia or pneumonitis reactive.
An objective examination of most patients with determined hepatomegaly, palpation of the lower edge of the liver is
usually painful. Sometimes the enlargement of the liver can be very significant, and then observed asymmetry of the
anterior abdominal wall due to a bulging in the right upper quadrant. Rarely seen from the lower divisions note the
expansion of the right half of the chest, behind her in the respiratory movements. Percussion in these patients reveal
the extension of the upper border of the liver, a significant limitation of mobility edge of the right lung, the shortening
of percussion sound in the lower lung. Here are listened easing breathing and dry rales. In some patients, there is a
local muscle tension anterior abdominal wall in the right hypochondrium, which is due to involvement in the
inflammatory process surrounding areas parietal peritoneum.
On the surface (subserous) the location of the abscess in the right lobe of the liver may reveal local tenderness in the
intercostal spaces, with the area projection of an abscess (a symptom Kryukov).
In addition, the vast majority of patients present both subjective and objective signs of underlying disease, which was
the primary cause of liver abscess.
Among the complications of bacterial liver abscess is most common ulcer breakthrough in the free peritoneal cavity
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with widespread development of purulent peritonitis or abscess poddiaf-ragmalnogo. Considerably less is a
breakthrough in the contents of the abscess lumen of a hollow organ (stomach, colon), which initially appears to
improve the patient's condition, decrease pain, decrease in body temperature. Subsequently, additional infection with
abscess cavity intestinal flora leads to an increase in local and general symptoms of liver abscess. A break of abscess
contents into the pleural cavity developing acute empyema, is slightly more common form bronhobiliarnogo fistula,
which resulted in fairly quickly arise secondary lung abscess. All complications usually occur in patients with large liver
abscesses. If multiple small ulcers, they usually do not occur.
Clinical manifestations of amebic abscesses in many respects similar to the symptoms of bacterial liver abscess. They
are characterized by a more benign course, prone to chronic process with the gradual depletion of the patient, less
pronounced temperature reaction, the general condition of patients is disturbed to a lesser extent than in bacterial
abscesses. In secondary microbial infection of the parasitic abscess observed a significant increase in subjective and
objective manifestations of the disease. Typically, the interval from the time of clinical manifestations of amoebic
dysentery to the appearance of signs of liver disease is 2-6 months, although in rare cases it can be lengthened to
several years. Sometimes amoebiasis is asymptomatic. At the same time the first signs of parasitic invasion occurs only
in the development of amoebic hepatitis and abscess.
Local symptoms and complications of parasitic abscesses are the same as in patients with bacterial liver abscess.
Diagnosis, differential diagnosis. In patients with bacterial and amebic liver abscess in a general blood test is usually
observed mild anemia, leukocytosis with a shift to the left of the formula, the increase in ESR. Biochemical parameters
of liver function, as a rule, are within normal limits. Only patients with large and multiple abscesses observed elevated
levels of bilirubin in the blood and alkaline phosphatase. A moderate increase in activity of aminotrans-feraz observed
in 50-80% of patients. Nevertheless, it should be emphasized that changes in laboratory parameters are nonspecific
and are not pathognomonic for the disease. Some patients (especially at a young age) there is an increase in vitamin
Bi2 in the blood, due to necrosis of the adjacent intact paranhimy liver. In the septic nature of the abscess important
role in the diagnosis and subsequent treatment of the blood belongs to crops.
Among the instrumental methods commonly used gepatoskanirovanie, ultrasound, CT and angiography. The most
widely used ultrasound.
Gepatoskanirovanie informative in the diagnosis of abscesses of the liver in 75-89%. However, this method does not
differentiate abscess from other formations of focal liver, and therefore its diagnostic role is relatively small.
More informative are the ultrasound and CT scans, allowing the correct diagnosis in 85-95% of patients. Moreover,
recent research methods allow diagnosis at an early stage of the disease, so you can be successful in treating these
patients.
According to modern concepts CT is the method of choice in the diagnosis of focal hepatic lesions, including abscesses
of the liver. On CT scans of the liver abscess is visualized in the form of gene negomo of destruction of liver tissue
round or oval with a relatively clear, but irregular contours (Fig. 33). Relative X-ray density of the contents of the
abscess usually ranges from 15 to 30 conv. units., which is significantly lower than the relative density of normal liver
tissue (about 56 conv. sd..)
Approximately half of patients with X-rays can reveal changes in the thoracic cavity. The most frequently observed in
high standing and limited mobility of the right dome of the diaphragm, effusion in the right pleural cavity, atelectasis
and pneumonia signs in the basal segments of the right lung [Aliev, VM, 1985]. These symptoms are not
pathognomonic for abscess, however, they are indirect signs of acute inflammation in the liver tissue.
Only a single x-ray in patients can be identified in the liver projection chamber with a horizontal liquid level and gasbubble above it. This symptom is characteristic of patients with bacterial liver abscess, and usually does not occur in
the parasitic nature of the disease.
Sometimes, there are quite significant difficulties in the differential diagnosis of bacterial and amebic abscesses, given
the similarity of their clinical picture. In this regard, an important role belongs to the medical history (living in areas
endemic for amebiasis, amebic dysentery transferred earlier, the identification of diseases of internal organs, which
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were the cause of bacterial abscess), as well as serological tests for amoebiasis (latex-agtlyutinatsiya, gemagglyutination), which are positive in almost all patients with parasitic abscesses. In addition, patients with amebic abscess in
contrast to patients with bacterial infection occurs much less frequently jaundice, significantly less than the level of
leukocytosis, and general condition of suffering, to a lesser extent. In severe cases, the final method is to puncture the
differential diagnosis of abscess cavity under ultrasound or CT, followed by bacteriological examination of the
material.
Treatment. Treatment of bacterial liver abscess complex. The most important component of it is antibiotics.
At the same time prescribe broad-spectrum drugs that affect both aerobic and anaerobic microflora in [Kandel S,
1984]. In this regard, the most effective antibiotics were cephalosporin of the second (cefoxitin) and third (cefotaxime,
moksalaktam) generations. Very useful is the prescribing of metroiidazola having a selective effect on anaerobic
bacteria with minimal adverse reactions and good permeability in the cavity of the abscess.
For a long time the main method of treatment of bacterial abscesses of the liver is surgery, providing for opening and
drainage of abscess cavity through laparotomic access. Lethality in this method of treatment reached 20-30%, and in
the presence of complications (abscess breakthrough into the abdominal cavity or the pleural cavity) is doubled.
In the last decade, the main method of treatment of bacterial liver abscess is percutaneous puncture of the abscess
cavity under ultrasound and CT [Kuzin MI et al, 1986; Von T. Hau, Hartmann E., 1987]. This method allows not only to
evacuate the pus, but also to determine the sensitivity of the pathogen to other mi antibiotic for the purpose of
directed antibiotic therapy. Lethality in this method of treatment is typically 1-5% (in case of successful treatment of
diseases, which were the basis for the development of an abscess). When undeleted the source of infection in the
abdominal cavity showed operative treatment, and abscess puncture transparietalnaya can be performed as an
independent and less traumatic treatment for liver abscess. However, for this purpose can be made intraopera-tional
drainage cavity ulcer. If multiple small abscesses (usually holangiogennoy nature) of drainage is usually impossible. In
this situation, play a pivotal role in the massive antibiotic therapy combined with external drainage of extrahepatic
biliary tract, the elimination of acute suppurative cholangitis.
Treatment of uncomplicated amebic abscess is usually medication. For this purpose, commonly used emetine,
chloroquine and drugs of metronidazole (flags, metrodzhil, etc.). Intensive drug treatment is effective in most patients.
Transparietalnaya puncture the abscess is shown only when it is impossible on clinical grounds to differentiate amebic
abscess of bacterial. Surgical treatment is undertaken for failure of medical treatment, obstructive jaundice ^ as well
as the presence of complications (abscess break into the abdominal or chest cavity). The average postoperative
mortality with a planned treatment of 7-10%, while the complications it has significantly increased, reaching 20-40%
or more.
The prognosis of liver abscesses depends primarily on the etiologic factor. The highest fatality rates occur in patients
with biliary nature of the abscess. Prevention of hepatic abscess is early detection and treatment of diseases of
internal organs, causing abscesses
Non-parasitic liver cysts
The first description of non-parasitic liver cysts in the mid-XIX century. According to current views, non-parasitic liver
cysts (synonyms: true, innate, beat paired, simple, epithelial) are considered as violation of the formation of the
intrahepatic bile ducts during embryonic development of the fetus with the formation of cystic cavities lined by
epithelium that produces serous fluid.
Classification
In 1925, B. E. Linberg described six groups of non-parasitic liver cysts (NPC): true, false, Retention, dermoid,
okolopechenochnye and vascular (hemangioma, lymphangioma). SWHenson (1956) classified as congenital cysts
(solitary, cystic disease), traumatic, inflammatory, and neoplastic cysts.
Separation of true cysts of the liver based on the analysis of pathogenic origin, and therefore the most frequently used
in clinical practice, the classification of Petrovsky (1972):
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I. Cystic disease (polycystic liver) (with a lesion involving only the liver and kidneys and other organs).
II. Solitary, true liver cysts (simple, solitary, multi-chamber tsistadenoma, dermoid and retention cyst).
III. False cyst of the liver (traumatic, inflammatory).
IV. Okolopechenochnye cyst.
V. Cysts of the liver ligaments.
In the classification Ershov K. (1999), non-parasitic liver cysts (NPC) are distributed into 5 groups according to presence
or absence of clinical signs (symptomatic and asymptomatic); sizes - large (over 5 cm), small (3-5 cm), small (3 cm), the
dynamics of growth (do not change size, fast-growing), distribution (single, multiple, polycystic liver) sites (with an
indication of the affected segment, lobe of the liver and its ligaments), but, like several other authors, not includes
categories of cysts of large and giant size, making it difficult to determine their differential-diagnostic features and
rational choice of treatment strategy (D. Vishnyakov, 2003; WCBIonski et al., 2006).
Congenital liver cysts may be single, multiple or occur in the form of polycystic, often with cystic transformation of the
other organs, especially the kidneys. The likelihood of clinical detection of true liver cysts in children and young adults
is low due to the lack of complaints by small cysts (3-4 cm). In the future growth of cysts is accelerating, and the first
clinical manifestation of the disease usually occur at age 40-50 years, more often in women. Increasing the size of
cysts 7-10 cm, and more dramatically increases the risk of complications such as bleeding and / or zhelcheistechenie a
cyst, infection and abscess contents, spontaneous rupture cysts with bleeding into the abdominal cavity. Another type
of complication is atrophy of the pressure of growing cyst surrounding liver parenchyma, which leads to compensatory
hypertrophy of the rest of its mass to the development of hepato-megalith.
Precision study of the etiology of polycystic liver disease have shown that mutations in the genes PKD1, PKD2 and
protein kinase C substrate 80K-H (PRKCSH) lead to the development of various forms of polycystic liver with isolated
liver or combined cystic transformation of kidneys. The similarity of clinical manifestations and the development of
polycystic liver and congenital cysts, despite the molecular and genetic heterogeneity of "failures", determine the
relevance of search for "genetic analogy" in the justification of the latter (GTEverson, 2004).
Until the 70s of last century the frequency of detection of true cysts of the liver, mainly post-mortem, was 0,15-1,86%.
To date, detection of true cysts of the liver increased to 4-7% (mainly vivo), which is associated with the widespread
introduction of modern methods, like ultrasound and computed tomography.
Diagnosis
Prior to the survey instrument should not neglect the significance of clinical symptoms of the disease, most often
manifested in large cysts and giant size, diameter, according to our observations, is 97-119 mm and 120-260 mm, and
the volume from 400 to 999 ml of 1,000 to 5,500 ml, respectively. The views expressed in this clinical manifestations
observed in 85% of cases. Please be aware that such typical symptoms such as pain and / or heaviness in the right
upper quadrant or epigastric pain, a symptom of "satiation" associated with the location of large or giant cysts in the
left lobe of the liver, liver enlargement at physical examination, may be a manifestation of a number of similar
symptoms of diseases - liver, gallbladder, pancreas, stomach, intestines. Less common are complaints of weakness,
weight loss or abdominal circumference increased sharply, the yellowness of the skin, fever, shortness of breath, that
established the diagnosis of liver cyst can be suspected complicated course of the disease.
The diagnostic complex with cysts of the liver in the first place is an ultrasound, which is widely
known, popular and accessible method for noninvasive diagnosis.
Our experience of examination and surgical treatment of 95 patients with large and giant nonparasitic cysts of the liver allowed a comparison of the results of clinical, ultrasonic and
morphological studies of the contents of cysts highlight the basic criteria of the three options for
ultrasound cysts of large and giant sizes, which are the most neglected form of benign, in fact ,
disease.
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Thus, in the first (uncomplicated) form of flow, are more prevalent in 50% of cases determined
by the classical ultrasound picture: anehogennoe content, thin shell and the correct round or oval
shape. In 25% of cases occur variations in the minimum deviation from the above typical
echographic signs of congenital cysts. The contents of cysts, resulting in a puncture is always a
clear liquid watery consistency, slightly yellow. Cytology, it contains a moderate amount of
mucus, isolated red blood cells, neutrophils and epithelial cells lining the inner surface of the
cyst.
A complicated version of cysts ultrasound criteria vary in the direction of increasing
echogenicity and heterogeneity of cyst contents, increasing the wall thickness of the additional
intracavitary fibrous tissue or structures, the appearance of fine particulate matter, sometimes
forming sediment. The probability for this complication of the disease increases to 95-98%.
Vnutrikistoznaya fluid collected during the puncture, changing its color, clarity and consistency,
and according to cytology are often determined by red blood cells are able to lyse and
destruction of tissue detritus, inflammatory cells, mixed bacterial flora.
The use of modern ultrasound techniques, such as color duplex scanning and three-dimensional
reconstruction of the liver and adjacent vessels, and in difficult clinical cases, the correct
differential diagnosis of true cysts with other liquid benign and malignant diseases, and results
improve safety performance of a particular type of surgical treatment.
We consider it necessary for detection on the polyclinic stage of even a relatively small
congenital cysts of the liver, especially the progressive increase in size, to refer patients for
counseling in a medical institution having a branch surgery Hepatology, timely and competent
treatment.
Differential diagnosis: liver parasitic cysts, hemangioma, retroperitonealnmi tumors, tumors of
the intestine, mesentery, pancreas, gall bladder edema. There are three morphological types of
solitary liver cysts. Single wall with a dense, usually multi-chamber, delimited by partitions,
have malignant potential, with no epithelial lining, these cysts are filled with fibrin or
fibropurulent detritus. Complications:
hemorrhage in the wall of the brush;
festering cysts;
perforation of the cyst;
torsion of a cyst on the leg;
malignant degeneration.
Treatment
Until recently, the mainstay of treatment non-parasitic cysts of the liver was the only open
surgery, either opening and emptying of cysts (called their fenestration), or the removal of the
liver that is affected by a large cyst or multiple cysts drain.
The rapid growth of the number of identified true cysts of the liver, diagnosed primarily by
ultrasound, has led to what started the search of other, less traumatic and difficult, but no less
effective surgical techniques that treat benign disease.
Since the mid 70s in treatment policy for non-parasitic cysts of surgeons began to take root
technique liver sclerosis closed their cysts by puncture or puncture-chreskate Turn sclerosis.
Following this, as rapidly developing area - endoscopic surgery led to the possibility of a
combination of surgical techniques of partial excision of the cyst with sclerosing membrane
technology. With deep location of cysts in the liver parenchyma, pointing at them was carried
out using laparoscopic ultrasound issledovaniya.V now apply all these areas of surgical treatment
of congenital liver cysts (of course, under strict reading to them).
Surgical treatment
In choosing the indications for surgical treatment and determining the extent and nature of
surgical intervention in patients with polycystic liver must adhere to differentiated tactics, which
causes the size of cysts and their location, complications and associated diseases.
All operative interventions in cysts of the liver can be divided into radical, quasi-radical and
palliative.
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In polycystic liver radical surgery is liver transplantation.
Conditionally radical surgery:
husking the cyst with its shells, resection of the affected part of the liver, laparoscopic excision
of the cyst wall (domektomiya).
Palliative surgery:
opening and emptying of the cyst, the cyst marsupializatsiya; tsistoentero-,
tsistogastroanastomoz.
The survey and treatment of patients with non-parasitic cysts of the liver we proposed the
following classification of indications for laparoscopic surgical treatment.
Indications for surgical laparoscopic treatment of liver cysts.
1. Absolute: abscess, rupture, bleeding.
2. Conditional absolute:
Giant cyst of any location (more than 10 cm in diameter);
cyst from a central location at the gate of the liver (with compression of the biliary tract and / or
with signs of portal hypertension);
cyst with severe clinical features (persistent pain in the hypochondrium, dyspeptic symptoms,
emaciation, etc.).
3. Relative:
cysts of large size (from 3 to 10 cm in diameter);
isolated cyst segments III-IV;
recurrent cyst of the liver in case of failure of puncture by the method of treatment.
4. Patients with liver cysts with a diameter of 3 cm to be patient care.
Using the proposed classification allows to better define the indications and contraindications to
the laparoscopic method of surgical treatment of cysts of the liver and improve its results.
Echinococcosis - refers to one of the most severe parasitic diseases. In its development, he
always passes through the stage of formation of cysts. The causative agent of echinococcosis is a
tapeworm Echinococcus granulosus, which infests dogs. Intermediate hosts for the parasite - the
human and farm animals. Humans can be infected, stroking the dog from eating contaminated
vegetables. Echinococcus of the embryo develops slowly parent cyst, which is a bubble filled
with fluid. The wall of the cyst is composed of two layers: the outer cuticle (chitinous) and an
inner germinal (germ).
On the geographic spread of the disease may indicate that it is not found only in Antarctica.
Early diagnosis of the disease is often difficult, due to the lack of clear symptoms of the
disease (pain in the right upper quadrant in the middle of the abdomen, pain in the left upper
quadrant). This highlights the forefront of diagnostics visual research methods, the most
common and the leading of which is ultrasonography (U.S.). Method to diagnose echinococcosis
in a stage where parasitic cysts are small. Modern ultrasound machines with high-resolution,
color mapping, and the possibility of three-dimensional image reconstruction, allow experts to
identify itself cyst.
For small cysts is more informative magnetic resonance imaging MRI (in hard mode,
hydrography) that reveals the above-described characteristics of parasitic cysts, or computed
tomography (CT) imagers on the last generation.
Immunological methods in diagnosis of echinococcosis are of great, perhaps decisive. The
most informative are the reactions of latex agglutination (RLA), indirect hemagglutination
(Phragmites), immunoassay (Cay, ELIZA). They have practically no contraindications and can
be applied to detect echinococcosis and recurrences of the disease through their repeated
conduct. With the simultaneous use of several immunological diagnostic efficiency of more than
80%.
The most common treatment for patients with echinococcosis are still the traditional surgical
intervention. The most common variety of ehinokokkektomy.
The main problems that are solved in the development of professionals minimalnoinvazivnyh
surgical procedures were: the ability to remove fluid tight contact with the warning in her
12
abdominal cavity and colonization, antiparasitic treatment of cysts with a guaranteed loss of all
elements of echinococcus.
Application minimalnoinvazivnyh (benign) surgical techniques can improve the
effectiveness of treatment also have the most severe category of patients with combined
echinococcosis.
The application of effective germicide, compliance with ablastichnosti operations, the use of
perfect instruments are not fully exclude the possibility of relapse. So a huge impact on the
results of treatment has followed by chemotherapy. It is also necessary to influence the
screenings echinococcus small sizes are not available in modern methods of diagnosis.
Discoveries of recent years have dramatically changed the requirements for diagnosis and
treatment options of patients echinococcosis. Most effective in this regard were polipozitsionnoe
ultrasound ultrasound and magnetic resonance imaging MRI. All this makes it possible to judge
about the aggressiveness of the parasite and to choose the best method of treatment.
Parasitic cyst
Hydatidosis (echinococcosis) - bot of the group tsistodozov in which the liver, lungs or other organs and tissues are
formed cyst.
The most commonly found in E. Australia, New Zealand, South America, North Africa, southern Europe and
Mongolia. Observed in Southern Ukraine, Northern Caucasus, Kazakhstan, Transcaucasia, Moldova, Buryatia, Yakutia,
Chukotka, Siberia, western and mountain-taiga zone of the Far East.
Etiology. The causative agent is the larval stage of E. Band of the worm from the family chain. The life cycle of
Echinococcus granulosus (hydatid echinococcus synonym or a single-chamber), as well as a related type of pathogen
alveolar echinococcus, is committed to the change of the two hosts. Imaginal (mature) stage of the pathogen E. infests
the small intestine of carnivores (dogs, wolves, jackals, etc.), which are final (definitive) hosts of the parasite. It is a
small cestode white long 3,4-6,18 mm, width - 0,47-0,98 mm. E. granulosus consists of a head, neck and 3-4 segments,
of which the first two asexual, hermaphrodite but the third contains a system of organs (ovary, vitellarium, testes,
etc.). The last segment is sexually mature and has a uterus, which is from 400 to 800 eggs oval containing
shestikryuchny embryo - oncospheres.
Larval (bubble) the stage of the parasite - larvotsista (hydatid cyst) - vegetate in the tissues of animals (large and
small cattle, camels, horses, pigs, etc.) or wild herbivores (elk, deer, etc.), as well as human which are intermediate
hosts. Hydatid cyst consists of an inner germ (germinal) and the outer shell, cuticle, contains a colorless liquid, which
swim mature embryos - scolexes. When injected into the intestines of carnivores (definitive hosts) scolexes constitute
sexual maturity of the parasite, and in contact with human tissue and herbivores (intermediate hosts), a rupture of the
cyst to form new larvotsisty. Cyst may have a diameter of several millimeters to 35-40 cm and maintained in the
lumen of many small bubbles of subsidiaries, which, in turn, may be parasitic cysts grandchild. Under favorable
conditions of development, which is more often observed in the localization of hydatid cysts in the lung tissue, and
embryonic children Pupyrev scolexes missing, and these cysts are called acephalocyst.
Around the cyst in the reaction of host tissue is formed fibrous capsule, which prevents the increase in size
larvotsisty. Often in the thick fibrous capsule, calcium salts are deposited, in some cases calcification occurs
throughout the capsule. Echinococcus eggs have considerable resistance to adverse environmental factors, while
maintaining full viability in the wet and dry climate with an air temperature of -2 ° to 20 ° from 3 to 6 months.
Conventional disinfectants are not effective, just boil for 20 seconds causes the death of oncospheres.
Epidemiology. The source of infection of man is the infected animals: in the nature of carnivores (wolves, jackals,
etc.), a synanthropic foci - the dog. Mature segments E. granulosus, filled with eggs, break away from the body of the
parasite and during defecation or yourself crawl out of the vent outside, falling on the animal's hair and contaminating
the grass or water sources. Herbivores, including agricultural (cows, deer, goats, pigs), are infected by E., eating grass,
nagryaznennuyu feces of carnivores, which, in turn, eating meat and internal organs (especially liver and lungs) of
ungulates containing larvotsisty become infected with E. development Tape him stage, completing the life cycle of this
13
parasite development.
The generality of habitat and nutritional connection scheme predator - prey to the constant change of owners in the
community of wild ungulates and carnivores are responsible for the existence of natural foci of E. The person becomes
infected when handling the skins of wild carnivorous animals, contact with infected dogs, the coat which have
oncosphere, and the use of unwashed berries and herbs and vegetables from the gardens, frequented by infected
dogs, using raw water from contaminated water sources. So E. is more common among hunters and pastoralists,
especially when dogs are fed raw viscera of infected thermally domestic herbivores. Large and small ruminants may be
a mechanical carrier of Echinococcus eggs, wool for which they get from the grass contaminated pastures, so we must
be careful, for example, wash hands thoroughly after milking cows and shearing sheep.
The presence of natural foci, as well as mixed commensal and as a result of close contact with infected dogs or
eating unwashed fruits and vegetables from the gardens, frequented by these animals, causes a high percentage of
people with E.
Immunity. Resistant E. immunity is not formed, so there may be repeated reinvazii, but often relapse due to the
uneven growth of individual cysts and the duration of their development. Moreover, it is believed that the growth of a
cyst inhibits the growth of other larvotsist.
The clinical picture. Course of the disease regardless of the location of the lesion can be roughly divided into three
stages: latent, or asymptomatic - from the moment of penetration into the body oncosphere before the first
symptoms of illness, stage of onset of symptoms, stage of development of complications. In the first stage of the
patients did not complain, and hydatid cysts are detected incidentally during preventive examinations or during
surgery for other reasons
In the second stage of the disease, when the cyst reaches a considerable size and begins to squeeze the surrounding
tissue, there are relevant symptoms. E. When there is liver weight in the right upper quadrant pain and arching in the
epigastric region, there is an increase of the liver and palpation can reveal a dense rounded education in the right
upper quadrant or protruding edge of the liver. Clinical manifestations of E. lungs begin with hard dry cough,
hemoptysis, chest pain, especially when taking a deep breath. With the localization of hydatid cyst in the pelvis can be
dizuricheskie phenomenon. When placing larvotsisty kidney is characterized by hematuria. With the localization of
hydatid cysts in the brain appears focal neurological symptoms, signs of increased intracranial pressure.
The third stage is characterized by the development of complications: abscess of hydatid cyst, its gap with the arrival
of content called the pleural or peritoneal cavity, bronchi, bile ducts, major blood vessels, accompanied by pain, fever,
development of anaphylactic shock, hydrothorax, discharge of phlegm from the subsidiaries of bubbles and bits of
chitinous shell, obstructive jaundice, cholangitis, external appearance of pus and bile fistula or the formation of
internal biliodigestivnyh biliobronhialnyh or fistula. The death of the parasite is accompanied by a fibrous capsule
calcification, which can create significant difficulties for the surgical treatment.
The duration of each clinical stage of E. can not be accurately determined because time of infection is almost
impossible to establish. In addition, the duration of each stage depends on the localization of hydatid cyst, the
resistance of the host organism and the nature of the growth of cysts. Despite the slow increase in the size of cyst, E.
brain and muscles are diagnosed at earlier stages. Asymptomatic E. lungs are usually detected during preventive
radiological examination. In later stages the liver is detected E. and abdomen, and retroperitoneal organs.
True recurrence resulting from E. reinvazii is rare and considered as a secondary disease. It develops many years
after surgical treatment in patients who continued to live and work in the same conditions. Since false relapse occurs
frequently, sometimes shortly after the operation. Usually it is caused by non-radical surgery, the presence of
undetected larvotsist, massive destruction, violation of ehinokokkektomii technology, resulting in a secondary
colonization of constructing tissue. In this regard, it is necessary (note the observance of certain principles when
examining patients with E. Thus, we can not perform research puncture of hydatid cysts. It is important to be careful
palpation of the abdomen and bimanual pelvic exam, in order not to provoke a rupture of cyst. Extreme caution
should be exercised when performing laparoscopy, t . since the introduction of trocar may damage the cyst located in
14
the abdominal wall or between the loops of the intestine, the more dangerous to make a biopsy of the fibrous
capsule, above the surface of the liver or spleen.
The diagnosis is mainly based on the data of instrumental studies and serological tests. Epidemiological history (the
patient stays in endemic foci, the occupation of herding or hunting) can only suspect the possibility of E. The clinical
picture is characterized by little and has a value only if there is complications of the disease. Therefore, upon detection
by palpation of the abdomen rounded education with a smooth surface or increase in the liver, especially in patients
previously operated on for IE, conducted a comprehensive survey using radiological, isotopic and ultrasound
techniques.
X-ray method of research is essential in E. lungs and is essential in the diagnosis of calcified cysts of E. liver and other
organs of the abdominal cavity, and E. bones. In the diagnosis of liver and E. of the abdominal cavity and
retroperitoneal space is crucial ultrasound and computed tomography. These methods allow us to determine the size
and location of cysts, as well as the presence of children Pupyrev, which is important in the differential diagnosis with
other abdominal formations. Much less diagnostic value of radionuclide scanning are the liver, which allows you to
install only the presence of filling defect in the liver without specifying the nature of the pathological process, and
angiography, allowing for the ousting of the characteristic vascular congestion and sickle radiopaque substance in the
fibrous capsule to establish the presence of hydatid cyst.
Of great importance in the differential diagnosis and prevention population surveys have immunologic latex
agglutination test, indirect hemagglutination, double diffusion in gel, as well as enzyme-linked immunosorbent
method (IPM - ELISA, Rem.) Serologic studies are based on immunological reaction of antibodies from human serum
specific antigen isolated from the fluid larvotsist human or sheep, which makes them completely safe for the patient
and allows more than once. Casoni reaction when injected intradermally in a sterile filtrate of hydatid fluid bales are
not currently used.
A complicated, E., with a breakthrough in the bronchi and bile ducts, to clarify the damage the bronchial tree or the
gallbladder, performed bronchography, retrograde puncture or cholangiography, cholecystography. These studies, in
some cases allow you to set message bronchi or bile duct to the cavity formed after draining the cyst, the latter can be
determined by X-ray survey of the liver or the lungs by the presence of the gas above the liquid level, however, this
pattern may be in purulent abscesses of these bodies.
The differential diagnosis is carried out with abscesses and benign non-parasitic cysts of the etiology, alveolar
echinococcosis, liver and lung tumors, as well as other parenchymal organs. The main value in this case have positive
serological tests and the presence of bubbles and subsidiaries chitinous shell which appear on ultrasound and
computed tomography. For the differential diagnosis of E. alveococcosis only suitable immunoassay method, as other
serological tests have high specificity and positive for both diseases.
Treatment. Conservative treatment of parasitic drugs are not effective in E. and is used to prevent contamination
during and after surgery, as well as in people in endemic foci with positive serological reactions, but the lack of hydatid
cysts with complete instrumental survey. The main type of treatment, regardless of the localization of parasitic cysts is
surgical. It should be possible at an earlier date, as over time the development of the parasite leads inevitably to the
prevalence of lesions, chronic toxicity, infectious complications, dysfunction of vital organs.
Surgery - ehinokokkektomiya - is to remove the cyst and its contents and shells. During the surgery requires careful
isolation of the operative field to avoid getting the contents of the cyst to the surrounding tissues, which use special
vacuum pumps that allow the puncture site distinguish a cyst from the surrounding tissue. After puncture and drain
the cyst in its clearance drugs are introduced, allowing it to neutralize remaining in scolexes (glycerol, 3%
formaldehyde solution in glycerine, etc.), and only then reveal a fibrous capsule and fluid are evacuated and chitinous
membrane from the lumen of the residual cavity, which repeatedly subjected to anti-parasitic treatment. For small
cysts or cysts located in the omentum, mesentery of the intestine may remove them with fibrous capsule with
resection of adjacent tissues. Light can be removed without opening the cyst parasitic shells after dissection of the
fibrous capsule, with the increase of pressure in their ventilation during general anesthesia.
15
Extensive resection of the bodies in E. are not shown due to the possibility of recurrence and the effectiveness of
antiparasitic treatment ehinokokkektomii with the residual cavity. The exceptions are multiple parasitic cysts of spleen
and calcification of the fibrous capsule with echinococcosis of the liver, because while leaving its current form longfestering and biliary fistula.
An integral element of operations for the elimination of residual E. is a cavity, as its abandonment leads to
suppuration and education, in essence, abscesses body. For this purpose, producing free edges excision and suturing
of the fibrous capsule cavity screw joints. In case of impossibility of its full closure in the remaining gap by introducing,
drainage tube, which is removed only after its complete elimination at the expense of growth of granulation tissue,
which occurs occasionally in a few months. Before removing the drain fistulografiyu perform control to ensure there
are no streaks and the residual cavity. In the untimely removal of drainage and suppuration of the residual cavity
closed resort to puncture them under ultrasound or CT scan with the introduction into the lumen of the drainage tube.
In multiple echinococcosis, when there is a lot of hydatid cysts in one area or organ of a person, as well as in
advanced and the combination of E., when the cysts are located simultaneously in different organs and regions of the
human body, surgical treatment is carried out in several stages, first removing the cyst, represent the greatest danger
to humans. The intervals between the operations ranged from 3 to 6 months., And the postoperative antibiotic
therapy is carried out to prevent the festering of the remaining cysts.
The prognosis for a timely and radical surgical treatment in patients with E. favorable. A complicated, multiple and
combination of E. prognosis depends on the distribution process and localization of hydatid cyst that causes a
relatively high postoperative mortality (3,5-16,2%). Self-healing is extremely rare, when it is small solitary calcification
of cyst.
Prevention of infection by E. humans and domestic animals is based on the activities carried out by veterinary and
health services. The task of the veterinary services include strict control and regular inspection of work and domestic
dogs to worms, especially in areas disadvantaged by E., treatment and disposal of stray dogs, as well as the monitoring
of meat at slaughter, culling and destruction (burning), to prevent feeding of infected E. dogs and other predators.
Sensitization of immune cells to their own tissues - an important factor in the pathogenesis and cirrhosis, developing
in patients with viral hepatitis B, C and D. The main target of the autoimmune reaction appears to hepatic lipoprotein
here. The dominant factor in the pathogenesis of congestive cirrhosis of the liver - hepatic necrosis associated with
hypoxia and venous stasis.
The next stage of the pathological process: portal hypertension - increased pressure in the portal vein caused by
obstruction of the intra-or extrahepatic portal vessels. Portal hypertension, in turn, leads to shunting of blood
portokavalnogo, splenomegaly and ascites. Thrombocytopenia associated with splenomegaly (increased deposition of
platelets in the spleen), leukopenia, anemia (increased hemolysis).
Ascites leads to restriction of mobility of the diaphragm (the risk of pulmonary atelectasis, pneumonia),
gastroesophageal reflux with peptic erosions, ulcers and bleeding from varices of the esophagus, abdominal hernia,
bacterial peritonitis, hepatorenal syndrome.
Patients with cirrhosis often have gepatogennye encephalopathy.
The leading place in the origin of primary biliary cirrhosis belong to genetic disorders immunoregulation. For the initial
changes include destruction of biliary epithelium with subsequent necrosis of the tubular segments and in the later
stage of the disease - their proliferation is accompanied by impaired excretion of bile epithelium infiltrated by
lymphocytes, plasma cells, macrophages. In the evolution of the disease can be traced four stages: chronic
nonsuppurative destructive cholangitis, duktulyarnoy proliferation with destruction of bile ducts, scarring of the bile
ducts with a reduction and the development of cirrhosis and cholestasis SKD.
Classification
World Association of hepatologists (Acapulco, 1974) and WHO (1978) recommended a simple morphological
classification of liver cirrhosis, based on minimum criteria according to which the distinction:
16
- Melkouzlovuyu or melkonodulyarnuyu (diameter of nodes from 1 to 3 mm);
- SKD, or makronodulyarnuyu (diameter of nodes greater than 3 mm);
- Incomplete septal;
- Mixed (in which there are various sizes of nodes) form.
According to the latest classification (Los Angeles, 1994) distinguish between cirrhosis etiology, degree of activity
determined by biochemical tests (ALT), morphological changes in the liver.
Depending on the etiology of liver cirrhosis are distinguished: viral, alcoholic, drug, secondary biliary, congenital
(hepatolenticular degeneration, hemochromatosis, a1-trypsin deficiency, tirozinoz, galactosemia, glycogen storage
disease), congestive (circulatory failure), disease and Budd-Chiari syndrome, metabolic -alimentary (overlay
enteroapocleisis, obesity, severe diabetes) and liver cirrhosis of unknown etiology (cryptogenic, primary biliary, an
Indian child).
Considered appropriate to share cirrhosis depending on the degree of hepatocellular failure (compensated,
subcompensated, decompensated), the degree of portal hypertension and activity of the process. Depending on the
activity of the process, which refers to the severity of inflammatory reactions, all of cirrhosis are divided into active
and inactive.
Hepatocellular function in cirrhosis assessed by the Child-Pugh (Table 2).
About compensated cirrhosis showed rates of group A, group rates, and C correspond to decompensated cirrhosis (a
technique using the criteria: an index of A is estimated at 1 point, the same rate in Group B two points, while in Group
C - 3 points). The proposed system is suitable to evaluate the prognosis, especially outside of a sharp aggravation of
cirrhosis and its complications. In recent years the prognosis for patients with CKD at the time of development of
complications such as gastrointestinal bleeding, coma, sepsis, etc., uses a system of criteria for SAPS (Simplifed Acute
Physiology Score), including the main physiological parameters, most of them not directly related with the state of the
liver. These include: age, heart rate and respiration, systolic blood pressure, body temperature, urine output,
hematocrit, number of white blood cells, the concentration of serum urea, potassium, sodium, and bicarbonate, the
stage of hepatic coma
The clinical picture
Cirrhosis is more common in men: correlation of patients, male and female averages 3:1. The disease occurs in all age
groups, but most often after age 40.
The complexity of early diagnosis of cirrhosis of the liver to a greater extent due to the diversity of its first clinical
manifestations. The most frequent clinical manifestations are common symptoms such as fatigue, reduced work
capacity, abdominal discomfort, dyspepsia, fever, pains in the joints. Frequently reported bloating, pain and heaviness
in the upper abdomen, weight loss, asthenia. On examination revealed an enlarged liver with compaction and
deformation of its surface, the edge of the liver pointed. In the initial stage observed even moderate increases in both
lobes of the liver, often prevails in a subsequent increase in the left lobe. Portal hypertension is manifested moderate
splenomegaly.
Period developed clinical picture is varied in its symptoms and reflects the involvement in the pathologic process of
nearly all body systems. The main characteristic of the symptoms associated with the presence of hepatocellular
failure and portal hypertension. The most frequent complaint - weakness, fatigue, decreased performance (abdominal
distension, poor tolerance of fatty foods and alcohol, nausea, vomiting, diarrhea), sleep disturbances, irritability.
Especially the case a feeling of heaviness or pain in the abdomen (mainly in the right upper quadrant), impotence,
itching skin, menstrual irregularities in women. The most common objective symptom appears hepatomegaly (70%).
The liver has a hardened consistency, sharp edge, little or painless. In 30% of patients with palpable nodal surface of
the body. In the terminal phase of illness in 25% of the marked decrease in liver size, splenomegaly in 50% of patients.
Often found the external symptoms of cirrhosis: palmar plantar erythema or, vascular "stars", has scant hair in the
underarm and pubic hair, white nails, gynecomastia in men. These changes are explained by the appearance on the
background of hepatocellular insufficiency symptoms giperestrogenemii. Characterized by weight loss, often masked
17
the simultaneous accumulation of fluid. About half of patients with increased body temperature. In most cases, fever
is subfebrile character and stored for several weeks. The temperature associated with necrosis of hepatocytes, often
accompanied by intense jaundice, increased aminotransferase activity and serum alkaline phosphatase, leukocytosis.
Rising temperatures associated with the passage through the liver intestinal bacterial pyrogens, which she was unable
to defuse it. Fever is not treatable with antibiotics and is only for improving liver function. Among the relatively late
symptoms of cirrhosis, characterized by severe hepatocellular insufficiency and portal hypertension are jaundice,
ascites, peripheral edema (swelling of the feet first), the external venous collaterals. Gepatolienalny syndrome is often
accompanied by hypersplenism, characterized by a reduction in the blood of blood cells (leukopenia,
thrombocytopenia, anemia) and an increase in cellular elements in bone marrow.
One of the most common signs of cirrhosis of the liver - varicose veins of the esophagus, stomach, intestine, including
duodenum, bleeding, of which at the rate of fatalities is the most serious complication of liver cirrhosis. Other venous
collaterals, including the mesenteric vessels, detectable only by angiography or surgical intervention, may cause
harmful bleeding to death. Bleeding are possible from the hemorrhoidal veins, but they are less frequent and less
intense.
Encephalopathies arise as against the background of hepatocellular and against the background of portal-hepatic
failure.
Etiologic variations of liver cirrhosis
Viral liver cirrhosis in most cases makronodulyarny. There are two variants of viral cirrhosis: a young, developing in the
first year after acute hepatitis (usually hepatitis A, which occurs with severe jaundice and cholestasis syndrome or
cytolysis), and the latter developing after long latent period (5-15 years).
The clinical picture resembles acute phase of viral hepatitis: jaundice, fever with chills, astenovegetativny and
dyspeptic syndromes. Jaundice is moderate, but persistent, hyperbilirubinemia remains constant, despite ongoing
therapy. Form of cirrhosis with cholestasis is accompanied by intense jaundice, persistent itching, high levels of
alkaline phosphatase. Peripheral abdominal collaterals do not have time to develop, telangiectasias are absent.
Hepatomegaly is combined with splenomegaly. Marker D-infection is the detection antidelta-IgM antibodies and IgG.
Late (more common) form of viral cirrhosis occurs slowly, slowly in the outcome of chronic hepatitis B and C. In
patients with anorexia appears, heaviness in the right upper quadrant, bloating, pain in muscles and joints,
nosebleeds, underweight, malnutrition of the muscles, dry skin. Develop hepatomegaly, splenomegaly with
hypersplenism, ikterichnost skin, sclera, vascular "stars" and palmar erythema, portal hypertension and
encephalopathy. Functional liver failure appears early and coincide with periods of exacerbation of the disease. In the
stage of cirrhosis, there are formed veins of the esophagus and hemorrhage. Ascites joins in the later stages of the
disease.
Alcoholic cirrhosis develops in approximately 10% of persons abusing alcohol in a period of 5 to 20 years. Increasingly
ill men.
In the developed stage is dominated by diarrhea complaints - loss of appetite, vomiting, diarrhea. Dyspeptic symptoms
due to concomitant gastritis and alcoholic pancreatitis. Much earlier than in viral cirrhosis, revealed signs of
malnutrition and vitamin deficiency. Systemic effects of chronic alcohol intoxication cause polyneuritis, myopathy,
muscle atrophy, contracture Dipyuitrena, an increase in the parotid glands, hair loss and atrophy of the testicles. In
addition, alcohol causes damage to the kidneys, heart, and moderate hypertension.
Secondary biliary cirrhosis develops due to long-term violations of the outflow of bile on the level of large intra-and
extrahepatic bile ducts: obstruction of bile ducts stones, scars, benign tumors, is also observed in primary sclerosing
cholangitis, choledochal cysts, limfogranulomatoze. The main pathogenetic links: initial cholestasis perilobulyarny
fibrosis, cirrhosis. Due to the mechanical obstruction of the biliary tract occurs biliary hypertension and noted receipt
of the components of bile in periduktalnye space. The elimination of cholestasis promotes regression of the process.
Biliary cirrhosis characterized by pain, fever, chills, leukocytosis, hepatomegaly, splenomegaly, cholestasis syndrome itchy skin, jaundice, severe, hyperbilirubinemia, elevated cholesterol, bile phosphatase, bile acids.
18
Primary biliary cirrhosis. The etiology of most cases is unknown.
The prevalence is 23-50 per 1 million adults, of all cirrhosis is 6-12%. Ill mostly women in menopause.
This is gradually beginning a progressive liver disease characterized by granulomatous nonsuppurative destructive
cholangitis with development of fibrosis, cirrhosis. The first sign of disease is pruritus, which is due to higher blood bile
acids. Jaundice appears after a few years after the start itching. Characterized by skin pigmentation, xanthoma,
xanthelasma, scratching. The liver is enlarged moderately, splenomegaly is determined at a later stage of the disease.
During prolonged jaundice revealed systemic osteoporosis: changes in the pelvis, skull, spine, ribs. Signs of portal
hypertension (esophageal varices, etc.) appear later than the common forms of liver cirrhosis. Of biochemical tests
most diagnostic value has a high level of IgM and alkaline phosphatase in serum, hypercholesterolemia,
hypertriglyceridemia. In 90% of cases are reported antibodies to mitochondria.
Complications of cirrhosis
The most severe complication of cirrhosis: hepatic coma, bleeding from varices of the esophagus (at least - the
stomach, intestines), thrombosis in the portal vein, hepatorenal syndrome, a form of liver cancer. Often, especially in
alcoholic cirrhosis, observed infectious complications - pneumonia, "spontaneous" peritonitis with ascites (assume
that in its development an important role to play pathogenic intestinal bacterial flora - under the influence of edema
resulting from intestinal loops lymphostasis and immunity disorders penetrates the intestinal flora in the free
abdominal cavity and becomes clear pathogenic properties), sepsis.
Diagnosis of liver cirrhosis
Medical history - alcohol abuse, viral hepatitis, carried B, C or D. Typical complaints of epistaxis, dyspeptic disorders,
fatigue, abdominal pain, and others allow the formation of suspicion in patients with cirrhosis of the liver.
An objective study draw attention to themselves the following indicators: telangiectasia in the shoulder girdle and
face, finger and palmar erythema elevations, paleness of nails, the phenomenon of hemorrhagic diathesis, the decline
of power and atrophy of skeletal muscles, grayish-white tinge to the skin or moderate ikterichnost sclera, compacted
liver with a sharp lower edge, splenomegaly, endocrine disorders.
These laboratory and instrumental methods include blood analysis, leykotrombotsitopeniya, anemia, and biochemical
changes characteristic: the hyper-g-globulinemiya, hypoalbuminemia, elevated transaminases, hyperbilirubinemia due
to conjugated fraction of pigment, etc., decrease in prothrombin index, other indicators of coagulation the blood
system. Immunological methods of investigation of blood serum is used to confirm one way or another etiologic forms
of cirrhosis. Concentrations of immunoglobulins in active cirrhosis usually raised for alcoholic cirrhosis is characterized
by increased levels of IgA, mainly for the virus - IgG u IgM. Particularly significant increase in IgM concentration
observed in patients with primary biliary cirrhosis. In this case, the serum antibody to the mitochondria. Among
antimitochondrial antibodies identified a number of factions, such as M-2 and M-9, the latter has a special role in the
early diagnosis of primary biliary cirrhosis.
The importance of instrumental methods of investigation in this disease is different.
Liver ultrasound to determine the size of organs - the liver and spleen, the density of the parenchyma, to visualize the
presence of knots and distribution process, identify the signs of portal hypertension.
Computed tomography - a more informative method, especially in patients with ascites and severe flatulence,
provides information about the density, the homogeneity of liver tissue, well caught by even small amounts of ascites.
Radionukleidnoe scan. Studies conducted with colloidal 197Au therapy and 99mTc. Liver cirrhosis observed a diffuse
decrease in the absorption of the isotope in the liver. Maloinformativen method.
Angiography - tseliakografiya and hepatosplenography. Used to visualize blood vessels and determine the presence
and degree of development of portal hypertension.
Needle biopsy of the liver - the most informative procedure, because it allows to carry out histological biopsy, to
determine the type of pathological process and its stages.
Laparoscopic examination of the abdomen, despite the trauma in these patients can get more information about the
state of the abdominal organs and vessels.
19
Treatment
Therapeutic and preventive measures in patients with CKD secondary prevention begins with:
- Prevention of infection with acute viral hepatitis, which, according to statistics, leading to death 50-60% of patients
within the first year of its development;
- Categorical rejection of alcohol, which can significantly improve the prognosis and life expectancy of patients;
- Protection of hepatotoxic drugs.
Causal treatment for most forms of CKD at the moment.
Appoint a full-balanced 5 to 6 meals a day for better drainage of bile, a regular chair (diet within the table number 5).
When receiving encephalopathy protein is reduced to a level at which no symptoms of ammonia intoxication. Table
salt limit, with ascites prescribe salt-free diet, supplementing the diet of foods rich in potassium. Itch and bradycardia
reduces the amount of meat protein, legumes, contain tryptophan, tyrosine, cystine and methionine, which are
sources of toxic metabolites and ammonia.
Patients in the inactive stage of compensated cirrhosis of the liver in drug therapy do not need. They are periodically
administered vitamin complex for oral administration.
In cirrhosis of the liver mean activity to improve the exchange of liver cells are recommended medications, which
include vitamins (vitamins B6 and B12, co-carboxylase, rutin, riboflavin, ascorbic acid, folic acid), lipoic acid, milk thistle
extract. Courses of therapy are designed for 1-2 months. The increasing importance of this group of drugs get herbal
medicinal products. The purified dry extract obtained from the fruit of milk thistle containing flavolignany and
flavonoids - the drug has a strong hepatoprotective Silimar action: inhibits the growth of the indicator enzyme,
stabilizing the cell membrane of hepatocytes, hinders the process of cytolysis, prevents the development of
cholestasis. It exhibits antioxidant and radioprotective properties, enhances detoxification and exocrine function of
the liver, has antispasmodic and a slight anti-inflammatory effect. Proved significantly improve the clinical
manifestations in the form of reduction of subjective complaints from patients, reducing the biochemical activity of
the process in the liver. According to the experiment, the following characteristics: a 7-day growth inhibition activity
for AST and ALT was 54.8% on day 14 - 66% of the original background of ALT and a slightly smaller delay for the ACT, a
clear (to 33-60%) dose-dependent decrease in activity of GGT in the serum. These changes were recorded in both the
acute and in chronic experiments. Choleretic function of the drug is clearly discernible at a minimum dosage of 50 mg
per kg for 1 and 2 hours of research and discovered it increased by 31.6% and 26.3% respectively. Such indicators of
cholestasis syndrome such as cholesterol, triglycerides, alkaline phosphatase fully come to normal, and bilirubin and gglutamintranspeptidaza down to numbers that exceed the rate of 1.4 and 2.1 times, and initially they exceeded the
norm by 3.1 and 5 4 times. In addition, in clinical trials marked a distinct normalization function of the gallbladder in
patients with manifestations gipomotornoy dyskinesia. It is these moments can be used Silimar patients with lesions of
the liver against the cholestatic syndrome, unlike its counterparts. The drug is used in the course of any age from 25
days to 1.5 months, 1-2 tablets 3 times a day for 30 minutes before eating.
In decompensated cirrhosis with encephalopathy, ascites or severe haemorrhagic syndrome dose of lipoic acid or
lipamida increased to 2-3 g per day, the treatment course of 60-90 days. Ingestion is combined with parenteral
administration of drugs for 10-20 days. Similarly, a treatment essentiale: orally, 2-3 capsules 3 times a day and an IV
drip of 10-20 ml 2-3 times a day for an isotonic solution. Course of combined treatment for 3 weeks to 2 months. As
these phenomena hepatocellular failure to receive the pass inside the capsule. The total duration of treatment up to 6
months.
In viral liver cirrhosis secondary activity to the presence of serum markers of HBV, HCV shows the use of prednisolone
at a daily fraction of 30 mg per day. Severe cytopenia is also an indication for. Gradually reduce the dose of 2.5 mg
every 2 weeks. Maintenance dose - mg 15-7,5 selected individually and taken for 2-3 years. The high degree of activity
and quickly progressing within require high doses - from 40 to 60 mg. Use of corticosteroids in dekompensirovannnoy
stage of the disease has not been shown because they contribute to the adherence of infectious complications and
sepsis, ulceration of the gastrointestinal tract, osteoporosis, catabolic reactions that lead to renal failure and hepatic
20
encephalopathy.
Treatment of patients with ascites is carried out by combining a diuretic drugs: aldosterone antagonists and thiazide
drugs row. Effective combination of spironolactone - ethacrynic acid, spironolactone - triampur, spironolactone furosemide. The daily urine should not exceed 2.5-3 liters avoid significant electrolyte imbalance. With the advent of
powerful diuretics paracentesis virtually ceased due to the arising in its loss of protein and the risk of introducing
infection.
Effective treatment of primary biliary cirrhosis is not. Corticosteroids should not significantly affect the course of the
disease, but slows its progression. D-penicillamine inhibits inflammation of the connective tissue, fibrosis, reduces the
amount of immunoglobulins, the level of copper in the hepatocytes. Noticeable effect is observed only with prolonged
use it (1.5-2 years). Ursodeoxycholic acid at a dose of 10-15 mg per kg of duration from 6 months to 2 years, resulting
in improved blood biochemical parameters with the disappearance of itching, weakness, anorexia. Temporary relief
brings plasmapheresis. Spend a liver transplant.
Indications for surgical treatment of CP are - in terms of portal hypertension, varicose veins, esophageal bleeding
suffered from varicose veins of the esophagus without bleeding, and if found dramatically enhanced coronal Vienna
stomach in combination with high portal hypertension, hypersplenism, indicating a history of esophageal bleeding or
with its threat. Use different types of anastomoses portokavalnyh: mesocaval, splenorenal, combined with or without
splenectomy. Contraindications for surgery are progressive jaundice and age over 55 years.
Forecast
The longevity of more than 5 years from diagnosis is noted in 60% of patients with alcoholic cirrhosis, in patients with
viral cirrhosis - 30%. In primary biliary cirrhosis, the life span of 5-15 years. Very marked effect on the prognosis of the
degree of compensation of the disease. Approximately half of patients with compensated cirrhosis is home to over 7
years. With the development of ascites, only a quarter of patients undergoing 3 years. Even more adverse prognostic
significance has encephalopathy, in which patients are in most cases die within a year. Leading causes of death hepatic coma (40-60%) and bleeding from the upper gastrointestinal tract (20-40%), other causes - cancer of the liver,
intercurrent infection, hepatorenal syndrome.
Used in this lesson, new educational technologies:
Interactive game "Brain Attack."
6.2. The analytical part.
Supervision and examination of patients.
The teacher divides the group into two subgroups. A subgroup of patients with supervising echinococcus of the liver, 2
- subgroup of supervising the patient with liver cirrhosis complicated by esophageal bleeding. Students are given time
for independent supervision of patients and study the data of laboratory and instrumental research. Then the teacher
conducts an analysis of patients, interpretation of laboratory and instrumental investigation of the differential
diagnosis of treatment options. In the course of parsing the patients performed the practical skills.
During the parsing of supervised patients with liver disease should consider the following issues:
- Tactics GPs: to establish the presence of jaundice syndrome on the basis of the collection of complaints, medical
history, objective, and laboratory data and send the patient to the specialist. facility for instrumental methods of
diagnosis and treatment.
- Tactics surgeon: Traditional treatments for liver abscess: abscess drainage traditional operative method. Alternative
treatment: minimally invasive methods of drainage of abscess of the liver under ultrasound guidance.
Traditional methods of treatment of echinococcosis of the liver: a traditional ehinokokkektomiya.
Alternative treatment of echinococcosis of the liver: fine needle puncture and cyst puncture with drainage of cysts
after antiparasitic therapy.
- Rehabilitation of patients after surgical treatment with an abscess, echinococcosis of the liver: restoration of
hepatotropic therapy;
21
- Prevention of liver abscesses: Modernization of foci. Prevention of echinococcosis of the liver: san. Educate the
population, treatment of infected animals echinococcosis.
Prevention of cirrhosis of the liver: a timely diagnosis and treatment of acute and chronic hepatitis.
Case Problem 1
The patient, aged 24, had suffered in the recent past, amoebic dysentery and treated with a subsequent recovery,
there were growing pretty intense pain in right hypochondrium, aggravated by breathing. Fever and began to carry
intermittent. There were harassing chills. The patient became progressively lose weight. On examination revealed a
painful greatly increased heating. Stool and urine are normal. Leukocytosis 1700.
Your diagnosis and treatment strategy.
Answer:
Amebic liver abscess.
Surgical treatment - puncture of abscess cavity and rehabilitation or conventional surgery - opening the abscess.
Case Problem 2
The patient, 41god, hunter, and complains of heaviness in the right hypochondrium. Others had no complaints. A
history of unexplained hives a year ago and itchy skin. When viewed from a liver edge palpable 3 cm below the costal
to the arc, it is rounded, painless. Other pathology on physical examination the patient could not be found.
Temperature is normal. In the X-ray examination revealed protrusion of the right dome of the diaphragm
hemispherical shape.
1. What kind of disease should not think in this case?
2. What additional methods of investigation may help in diagnosis?
3. What kind of research will determine exactly from which a protrusion?
4. How to treat a patient?
Answers:
1. Echinococcus of the liver
2. KLA-eosinophilia, serological tests
3. Ultrasound, CT
4. Antiparasitic conservative treatment followed by a puncture and the readjustment of hydatid cavity, or surgical
treatment, ehinokokkektomiya.
Case Problem 3
The patient, 44 years old, was admitted to hospital in order emergency assistance. Suddenly fell ill. There was profuse
hematemesis. The patient dramatically weakened. Of history was revealed that he had abused alcohol for many years.
On examination the patient drew the attention of large dense spleen. Liver not palpable.
1. What do you think might be a source of bleeding?
2. Between what diseases should be differentiated?
3. Tactics GPs
Answers:
1. Esophageal varices
2. Ulcer bleeding syndrome Melora-Weiss, a disintegrating tumor of stomach
3. First aid - to set the probe Blackmore, to direct the surgical department
6.3. The practical part.
Definition of symptoms of obstructive jaundice syndrome, technology insertion probe Blackmore.
1. Definition of symptoms of obstructive jaundice syndrome
22
Not performed Fully executed correctly
(0 points)
(10 points)
№
Action
1
The general approach to the patient on the right.
10
2
Defining characteristics of jaundice (skin and mucous
membranes, urine and feces).
10
3
Examination of language and definition of plaque.
10
4
Superficial palpation of the abdomen to determine the
areas of pain.
10
5
Deep palpation the abdomen:
definition of painless enlarged gallbladder (Courvoisier sign).
15
6
Determination of hepatomegaly, consistency of the liver,
the liver edge.
15
7
Percussion: Sizing liver Kurlov.
15
8
Definition of stupidity in the sloping ground belly.
15
In all :
100
7. Form of control knowledge, skills and abilities:
- Oral;
- Writing;
- GST;
- The case of the problem;
- OSKE.
8. Criteria for evaluating the current control:
23
№
1
2
3
4
%
96-100%
91-95%
86-90%
81-85%
Mark
Criterias
Very well “5”
Complete the correct answer to the questions on the anatomy and
physiology of the liver, jaundice syndrome concept, classification,
diagnosis, Diff. Diagnostics, Diagnostic, treatment of jaundice in liver
diseases, bacterial and amebic abscess, liver cirrhosis, non-parasitic cysts
of the liver. Summarizes the correct decision. Creative thought.
Independently analyzed. Self-supervised patients correctly perform
practical skills in an objective examination of the patient, correctly
interprets the data from clinical and biochemical tests and instrumental
research. Independently and competently determine the tactics of the
patients. Actively involved in interactive games. Solve situational
problems correctly with a creative approach with a full justification for the
answer.
Very well “5”
Complete the correct answer to the questions on the anatomy and
physiology of the liver, jaundice syndrome concept, classification,
diagnosis, differential. Diagnostics, Diagnostic, treatment of jaundice in
liver diseases, bacterial and amebic abscess, liver cirrhosis, non-parasitic
cysts of the liver. Summarizes the correct decision. Creative thought.
Independently analyzed. Self-supervised patients correctly perform
practical skills in an objective examination of the patient, correctly
interprets the data from clinical and biochemical tests and instrumental
research. Independently and competently determine the tactics of the
patients. Actively involved in interactive games. Solve situational
problems correctly with a creative approach with a full justification for the
answer. Allowed one mistake in the interpretation of biochemical tests
Very well “5”
Complete the correct answer to the questions on the anatomy and
physiology of the liver, jaundice syndrome concept, classification,
diagnosis, differential. Diagnostics, Diagnostic, treatment of jaundice in
liver diseases, bacterial and amebic abscess, liver cirrhosis, non-parasitic
cysts of the liver. Summarizes the correct decision. Creative thought.
Independently analyzed. Self-supervised patients correctly perform
practical skills in an objective examination of the patient, correctly
interprets the data from clinical and biochemical tests and instrumental
research. Independently and competently determine the tactics of the
patients. Actively involved in interactive games. Solve situational
problems correctly with a creative approach with a full justification for the
answer. 02.03 admitted inaccuracies in solving situational problems, but
with the right approach.
Well “4”
The correct full coverage of the issue. The student knows the anatomy
and physiology of the liver, the concept of the syndrome of jaundice,
symptoms of jaundice, diagnosis, differential. diagnosis of jaundice with
liver diseases, bacterial and amebic abscess, liver cirrhosis, non-parasitic
cysts of the liver, classification, causes, clinical picture, diagnosis, tactics,
the introduction of patients into practice properly perform practical skills
24
in the supervision of patients with the syndrome of jaundice, correctly
interprets the data from clinical and biochemical and instrumental
examinations, but there are 3.2 errors or inaccuracies. Solve situational
problems correctly, but the rationale for not fully answer.
5
6
7
8
76-80%
71-75%
66-70%
61-65%
Well “4”
Proper lighting is not a complete question. The student knows the liver
accompanied by jaundice syndrome, diagnosis, differential. diagnosis of
jaundice with liver diseases, bacterial and amebic abscess, liver cirrhosis,
non-parasitic cysts of the liver, the tactics of the introduction of patients,
understands the issue, says confidently, is the exact representation on
case studies give an incomplete solution, has been active in interactive
games.
Well “4”
Proper lighting is not a complete question. Student knows, liver disease,
accompanied by jaundice syndrome, the diagnosis, but not complete lists
dif.diagnostiku jaundice with liver diseases, bacterial and amebic abscess,
liver cirrhosis, non-parasitic cysts of the liver, knows the reason, the
diagnosis, but more difficult to determine the tactics of the patients.
Understands the issue, says confidently, takes practice. However, when
the practical skills makes mistakes, the case studies give an incomplete
description.
Satisfactory
“3”
Correct answers half the questions. The student knows the essence of the
syndrome of jaundice, liver disease, accompanied by a syndrome of
jaundice, the cause, but confused in the methods of study patients and
differentiation. diagnosis of jaundice with liver diseases, bacterial and
amebic abscess, liver cirrhosis, non-parasitic cysts of the liver. Has a
faithful representation only individual issues topics. Situational problems
decides correctly, but there is no justification for an answer. Into practice,
but does not properly take into account some practical skills.
Satisfactory
“3”
Correct answers half the questions. The student knows the essence of the
syndrome of jaundice, but confused in the liver accompanied by jaundice
syndrome classification reasons. Poorly versed in the differential.
diagnosis of jaundice with liver diseases, bacterial and amebic abscess,
liver cirrhosis, non-parasitic cysts of the liver and the algorithm of
treatment. Says uncertainly is accurate representations only on individual
issues topics. Into practice, but does not properly perform practical skills.
Mistakes in solving situational problems.
25
9
55-60%
Satisfactory
“3”
10
54 and
below
Unsatisfactory
“2”
Correct answers to half of the questions, make mistakes in defining the
syndrome, classification, diagnosis, differential. diagnosis and treatment
algorithm of jaundice with liver diseases, bacterial and amebic abscess,
liver cirrhosis, non-parasitic cysts of the liver and the algorithm of
treatment. Says uncertainly. Has a partial view on the subject. Into
practice, but admits a lot of mistakes in the performance of practical skills.
Situational problems decides not true.
The student does not have an exact representation of the syndrome, do
not know the classification, diagnosis, differential. diagnosis, patients
tactics. Does not apply in practice.
9. Chronological map of classes.
№
1
Stages of class topics and key issues
form class
Lead-in tutor (study subjects)
2
Discussion threads symptoms of jaundice, check the
source of knowledge
3
Summing up the discussions
Duration of
classes 327
minutes
10
Survey ECV, case
studies, the method of
"brainstorming", the
slides
60
15
4
Giving students tasks to perform practical work.
self-Supervision
Distribution of
patients, instructing.
Algorithms
"incremental" The
hands-on skills
5
Individual practical work of students: Supervision of
patients with liver abscess, liver cirrhosis, liver cyst
(questions, inspection, palpation, percussion),
dressing patients, sensing and gastric lavage
Medical history, the
work of dressing,
manipulative
60
6
Data interpretation of clinical and instrumental
study of patients with syndrome of jaundice, diff.
Diagnosis of diseases occurring with the syndrome
of jaundice. Determination of the tactics of
treatment.
Working in the offices
of ultrasound and xrays, clinical data
analysis,
ultrasound
and cholangiogram
60
7
Talk degree goal classes at the base of the
developed theoretical knowledge and practical
experience on the result of students
Oral questioning, case
studies, discussions,
and
"academic
60
42
26
controversy."
8
Conclusion of the teacher on this lesson.
Assessment of the students on a 100 point system
and its publication. Cottage tasks to prepare for the
next lesson (a set of questions).
Information, questions
for self-study
20
10. Control questions:
1. Classification of liver abscesses;
2. Clinics and symptoms of liver abscesses;
3. Classification of cysts of the liver;
4. Diagnosis and difdiagnostika liver cysts, treatment;
5. Echinococcosis of the liver, treatment;
6. Etiopathogenesis of cirrhosis of the liver;
7. Clinic liver cirrhosis;
8. Complications of cirrhosis.
9. Treatment and prevention of liver cirrhosis.
11. Recommended Reading
1.Aripov UA, Karimov SH.I. Қorin bўshliғi azolarining oshiғich zharrohligi.T.1991 th.
2. Karimov SH.I. Hirurgik kasalliklar.T.2005y.
3. . Karimov SH.I Surgical bolezni.T.2005g.
4. Kuzin MI Surgical bolezni.M.1987g.
5. YM armor Clinical Surgery, Moscow, 1998
6. J. Mert "Handbook of general practitioner," translated from English. M. 1998
7. OKP on obstructive jaundice;
8. Standard protocols for the subject;
9. Saveliev VS Manual emergency surgery of abdominal polosti.M.2004g.
10. Savel'ev VS, Kiriyenko AI Surgical Diseases (2 volumes). M.2006, the
11. Clinical guidelines for practitioners based on the evidence, the meditsine.M.2002
12. Shevchenko YL Private surgery. M.2000, the
13. Algorithms for diagnosis and treatment of major syndromes for training GPs. T. 2003.
14. Algorithms for diagnosis and treatment of surgical. T. 2003
15.Borzyak EI, Bocharov VY, Volkova, LI; / Ed. MR SAPINA. Human anatomy. In 2 volumes. T. 2, Moscow:
Medicine, 1986
16.Zabrodskaya VF Zatolokin VD On the topography of the hepatic veins. In the book.: Proceedings of the
third thematic conference. Ivano-Frankivsk, 1967 p. 221-223
17.Maisaya K. Mizandari M. Mtvaradze A. Urushadze, O., F. Todua Features arterial hemodynamics of the
internal organs in liver cirrhosis. / / Medical imaging. 2001 № 2 p. 59-61
18.Ostroverhov GE, Lubotsky D. N. Bomash M. Operative surgery and topographic anatomy. Moscow:
Medicine 1972
19. http://medicall.ru/