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A liver cyst is formed when a connective tissue capsule within the liver is filled with a liquid or gel-like substance. The color of the fluid can be clear yellow but may also be mud colored depending on the etiology/cause of the cyst. The mud colored cysts occurs because of the accumulation of cholesterol, bilirubin within the cyst. The vast majority of cysts found in the liver incidentally are benign and do not require further workup.

within the liver cyst the liquid can become thick in consistency if fibrin, mucin predominates, and if the epithelium of the capsule of the cyst is exfoliated/sloughed off into the cyst. Inside the cavity/center of the cysts, parasites can also grow and begin their life cycle. Treatment of a liver cyst depends on its origin and form with most liver cysts being benign and filled with clear yellow fluid.

The consistency of cysts can change if there is infection or vascular involvement/bleeding into the cyst which can sometimes occur.  Active infections or growth of microbes within a cyst lead to the accumulation of viscous purulent fluid which can appear mass like at time especially by CT or ultrasound imaging.

Hepatic cysts can have several etiologies with the most common being benign idiopathic cysts following by the following parasitic, bilirubin, primary, and some metastatic lesions. Cancer cells which are brought to the liver by the bloodstream often from the bowel but from several other primary cancers can at times appear cystic but are generally easily evaluated for by Contrast liver mass protocol CT or ultrasound or liver mass protocol MRI.

The cyst of the right lobe of the liver occurs in half of the patients. In 35% of cases, localization is left-sided. 10-15% is occupied by a two-lobed form. Regardless of the side of localization, the cyst can grow inside the parenchyma or protrude beyond the stroma. The deeper the layer, the more difficult to treat or surgically remove.

Types of hepatic/liver cysts

Congenital non-parasitic cysts of the liver are found throughout the biliary tract, starting from the smallest intralobular tubules and ending with the intraduodenal portion of the common bile duct. Regardless of localization, the clinical manifestations of cysts can be divided into two broad categories. The first includes those that depend on the topography and size of the formations and determine the degree of compression of the surrounding tissues and adjacent organs. The second includes manifestations of biliary obstruction of varying degrees, often accompanied by cholangitis. In rare cases, with the development of hemorrhage in the cavity or rupture of the cyst with the outflow of contents into the abdominal cavity, a picture of an acute abdomen occurs, which requires surgical intervention. Cysts arising from small ducts that do not compress adjacent liver tissue

At the beginning of the 20th century, the diagnosis of intrahepatic cysts was carried out using radiography using contrast only in the presence of clinical symptoms, which caused a rare detection of pathology, which ranged from 0.14 to 0.17%, according to surgical interventions and autopsies. Therefore, in the world literature by 1949, less than 500 cases of various liver cysts were described, and by 1985 – about 900. Prior to the introduction of ultrasonography into practice, the correct diagnosis was established only in 30% of patients referred for surgery for volumetric liver pathology. With the widespread introduction of non-invasive instrumental (ultrasound, computed tomography, magnetic resonance imaging) and serological diagnostic methods into practice, the number of identified patients with volumetric liver lesions has increased,

The first description of a common bile duct cyst was made by AH Douglas in 1852. In 1865, F. Bristowe reported on a case of non-parasitic cystic liver disease, drawing attention to its combination with polycystic kidney disease. The observation was regarded by the author as a coincidence, since the combination of liver and kidney cysts was extremely rare.  Two weeks later, a meeting of the Society of Pathologists of London was held, at which S. Wilks presented a similar example of combined cystic lesions of the kidneys and liver, expressing doubt that these cysts are caused only by stagnation of bile. In 1857, N. Freidreich presented a description of an unusual histological type of solitary cysts – foregut hepatic cysts (ciliated anterior intestinal hepatic cysts – RPKK), the wall of which contained all the components of the intestinal wall, including the muscular layer. E. Moschcowitz summarized 85 observations of cystic liver lesions and, after analyzing the views of various researchers on the pathogenesis of cyst formation, came to the conclusion that liver cysts arise from aberrant bile ducts . In 1918, H. von Meyenburg described small groups of dilated small bile ducts in the liver tissue with cystic lesions, which were then called von Meyenburg complexes. In 1955, P. Melnick summarized data on 70 cases of polycystic liver disease over a thirty-year period. Cysts were found at autopsy with a frequency of 1 in 687 autopsies. In a series of articles on benign liver tumors, S. Henson et al. presented the results of 67 observations of single and multiple liver cysts: out of 38 patients with solitary cysts, 12 had reasonable indications for surgical treatment, polycystic disease was found in 29 patients during the study of postoperative material. J. Caroli et al. were the first to classify liver conditions in which cystic dilatations of the intrahepatic bile ducts are observed, and proposed the following classification of cystic liver lesions:

1. True polycystic liver disease. Cysts are located in the parenchyma along with von Meyenburg complexes, but there is no connection with the biliary system.

2. Mixed form of polycystic disease. The morphological picture is the same, but with attacks of cholangitis. Individual cysts contain bile and communicate with the biliary tree.

3. Cystic expansion of the intrahepatic bile ducts. There is bile in the gaps, patients suffer from bouts of pain and cholangitis. At the same time, there are no von Meyenburg complexes. Dilated segmental and/or lobar bile ducts.

4. Congenital fibrocystic disease. Microcysts are located in wide strands of connective tissue ( Hamartomes Biliaires Fibreux – bile hamartomas with fibrosis). There are no lesions of the biliary system, but there are signs of portal hypertension.

5. Multiple biliary cysts associated with fibrocystic changes are characterized by the presence of portal hypertension, cysts in the parenchyma, and signs of cholangitis [15].

In 1961, D. Kerr et al. suggested that congenital liver fibrosis is a condition that is associated with congenital liver cysts and is usually associated with polycystic kidney disease [16]. In an editorial, W. Foulk reported that congenital anomalies of the intrahepatic bile ducts in adults, in which diffusely located von Meyenburg complexes are found throughout the liver tissue, are accompanied by severe hypoplasia of the portal vein branches, and proposed calling this condition “congenital liver fibrosis” . If the tortuosity and dilatation of the intrahepatic bile ducts were the dominant features, and the clinical symptoms are associated only with an anomaly of these ducts, the term “congenital dilatation of the intrahepatic bile ducts” was used. W. Folk believed that,

Since the beginning of the active study of pathology, a fairly large number of various classifications have been proposed, which, however, have common features: subdivision into solitary cysts, polycystosis, true and false (traumatic) cysts. Clinical classifications also take into account the volume of the replaced liver parenchyma, which is a determining factor in choosing the tactics of surgical treatment [19, 20]. The modern classification of liver cysts can be considered proposed by P. Russo in 2007: parasitic, solitary (retention) non-parasitic cysts, ciliated anterior intestinal hepatic cysts, congenital (hereditary) liver cysts (congenital liver fibrosis, isolated dysontogenetic cysts; autosomal dominant polycystic liver disease and kidneys; isolated polycystic liver disease).

Polycystic liver diseases are a group of genetic diseases that mainly affect the bile ducts and often the epithelium of the renal tubules.

Autosomal dominant polycystic kidney disease (ADPKD) is a fairly common congenital pathology, found with a frequency of 1:400 to 1:1000 and is characterized by the formation of multiple cysts in the kidneys, liver, and often in the pancreas. And although the synthetic function of the liver is usually preserved, some complications of cysts (hemorrhage, infection or rupture), as well as their large number, can be considered as an indication for liver transplantation.

ARPKD (autosomal recessive polycystic kidney disease) and the liver-associated phenotypes Caroli disease (CD) and congenital liver fibrosis (CHF) are, on the contrary, rare pathologies with a prevalence of 1:20,000 newborns. CD and VFH are manifested by recurrent acute cholangitis and severe portal hypertension against the background of severe peribiliary fibrosis. Cases of malignancy have also been described. Even the very rare isolated polycystic liver disease (IPLD) is phenotypically similar to ADPLD, except that the kidneys are not involved. In all cases of cystic liver damage, the biliary epithelium is involved, which justifies the inclusion of this disease in the group of genetically determined cholangiopathy.

ADPPD is caused by mutations in one of two genes, PKD1 (polycystic kidney disease 1) in 85–90% of cases or PKD2 in 10–15% of cases, encoding type 1 polycystin and type 2 polycystin, respectively. Polycystins play the role of mechano- and chemoreceptors and calcium channels, perceive changes in the apical current. ARPPD/CD and VFD are caused by mutations in the PKHD1 gene(polycystic kidney and hepatic disease 1), which encodes fibrocystin, a protein with insufficiently studied functions. Although the impact of ciliary dysfunction on cholangiocyte physiology is not fully understood, animal models deficient in ciliary proteins (polycystin, fibrocystin, and apical) have varying degrees of biliary dysgenesis. In the liver, both ADPBP and ARPBP/VFP/CD are morphologically represented by an aberrant state of the biliary epithelium, which retains an immature, duct-like, lamellar architectonics, followed by the formation of biliary microhamartomas, progressively transforming into macroscopically distinct cysts scattered throughout the liver parenchyma. ISPD is caused by mutations in the PRKCSH gene (chromosome 19), which codes for protein kinase C, also called hepatocystin, or in the geneSEC63. The SEC63 gene encodes a component of the molecular regulation of translocation and folding of synthesized membrane glycoproteins. Hepatocystin and SEC63 are not expressed in cilia, but in the endoplasmic reticulum; as a result, cystic liver diseases can be caused by defects in protein synthesis not only in cilia.

In embryogenesis, the liver tissue and the biliary system develop from the anterior part of the primary intestinal tube. Initially, a subpopulation of progenitor cells considered as precursors of epithelial cells of the bile ducts and hepatocytes is localized near the mesenchyme of the developing portal vessels, which, in turn, expresses bile-specific cytokeratins. From the 8th week, a layer of progenitor cells forms a continuous single-layer annular structure called the primary ductal lamina and surrounds the portal mesenchyme. From the 12th week of embryonic development, the ductal plate partially becomes two-layered. Local expansions of the ductal plate in places where it is two-layered give rise to the bile ducts . The rest of the ductal plate subsequently regresses. Remodeling of the ductal plate during fetal and postnatal development is a dynamic process of cell proliferation and apoptosis. Inhibition of maturation and defective remodeling lead to an excess of immature embryonic biliary structures, the violation of involution of which is one of the causes of the formation of liver cysts . However, in humans, cysts can form throughout life. In mice with conditional gene knockoutPKD1 or PKD2 , progressive liver and kidney cyst formation resembling human disease has been observed even when induction occurs several weeks after birth. This indicates that polycystin plays an important role in the maintenance of normal biliary architectonics in adulthood.

Persistence of unformed ductal elements stimulates fibrogenesis in the portal tracts of the liver, secondary cholangitis or portal hypertension and its associated complications develop. Long-term portal hypertension can lead to secondary portal vein thrombosis and to cavernous transformation of the portal veins (CVT) as a result. There is a point of view that CTPV is also one of the manifestations of embryogenesis disorders . It must be taken into account that the development of the bile ducts and the vascularization of the liver are interrelated processes. It has been established that malformation of the ductal plate is associated with malformation of the portal veins of the “apexless willow” type, which is characterized by the presence of a large number of venules closely located in the portal tracts. Depending on the severity of embryogenesis disorders, both small interlobular bile ducts (congenital liver fibrosis) and middle intrahepatic ducts (CD) can be involved in the process. Simultaneous pathological process in both structures is designated as Caroli’s syndrome. Depending on the characteristics of dysembryogenesis, morphogenetic differences are observed between ADPBP and ARPBP. In ADPPD, nascent cysts separate from the original duct and form autonomous structures that are not associated with the biliary tree; in ARPPD, communication between cysts and bile ducts is usually preserved. This is also the reason for the various clinical manifestations in ARPPD, CFD, CD, and ADPBP. Simultaneous pathological process in both structures is designated as Caroli’s syndrome. Depending on the characteristics of dysembryogenesis, morphogenetic differences are observed between ADPBP and ARPBP. In ADPPD, nascent cysts separate from the original duct and form autonomous structures that are not associated with the biliary tree; in ARPPD, communication between cysts and bile ducts is usually preserved. This is also the reason for the various clinical manifestations in ARPPD, CFD, CD, and ADPBP. Simultaneous pathological process in both structures is designated as Caroli’s syndrome . Depending on the characteristics of dysembryogenesis, morphogenetic differences are observed between ADPBP and ARPBP. In ADPPD, nascent cysts separate from the original duct and form autonomous structures that are not associated with the biliary tree; in ARPPD, communication between cysts and bile ducts is usually preserved. This is also the reason for the various clinical manifestations in ARPPD, CFD, CD, and ADPBP.

To date, the histogenesis of PBMC has not been studied in detail. According to the literature, cysts can arise from the embryonic anlage of the foregut (from which tissues of the oropharynx, esophagus, stomach, duodenum, liver, gallbladder, pancreas, tracheobronchial tree and lungs develop), extending from the oropharynx to the hepatic diverticulum. The lower respiratory tract begins to form at the end of the 3rd week of embryonic development in the form of a diverticulum of the ventral cranial anlage, from which the trachea, bronchial tree, and pulmonary buds develop. The hepatic bud begins to differentiate at week 4 and develops from endodermal cells that proliferate in the transverse septum and become hepatocytes. The section of mesoderm between the pericardial cavity and the umbilical-intestinal duct, called the transverse septum, is involved in the separation of the chest and abdominal cavities, which is incomplete. Due to this, pleuroperitoneal channels arise, which allow the growth of lung buds. The closure of these channels occurs at the 8th week due to the fusion of the pleuroperitoneal membrane with the transverse septum.

The rudiments of bronchioles have the ability to migrate from the chest cavity to the abdominal cavity through the pleuroperitoneal canal until it closes. Such abnormal bronchiolar “buds” can be incorporated into the transverse septum and then surrounded by endodermal cells of the hepatic diverticulum. In the process of intrauterine development, the left hepatic lobe has a large mass. Remodeling of the organ with an increase in the right lobe and regression of the left begins at 6–8 weeks, which may explain the predominant localization of PBMC in the left lobe . Starting from the 10th week, the columnar epithelium that forms the bronchial kidney can be replaced by a respiratory epithelium with ciliated cells, mucous cells, endocrine cells, and Clara cells, which is confirmed by immunohistochemical research methods.

Congenital liver cysts are often associated with fibrosis. A number of researchers have attempted to elucidate the pathophysiological mechanisms underlying the abnormal and excessive fibrotic response in VFD. Liver stellate cells (HSCs) play a key role in the development of fibrosis in liver diseases, including congenital liver fibrosis. Degradation of the basement membrane and components of the extracellular matrix, as well as their remodeling, play an important role in the pre- and postnatal periods of development. Basal lamina components such as laminin and type IV collagen, along with the coordinated expression of proteolytic enzymes, play an important role in the normal development of the intrahepatic bile ducts. Most of the proteolytic enzymes involved in these processes belong to the class of matrix metalloproteinases (MMPs) and serine proteinases, in particular plasminogen activators (AP)/plasmin system. Plasmin is known to promote the activation of MMP-9 and MMP-13, which play an important role in the degradation of basement membrane components, including type IV collagen. W. Sweeney and E. Avner believe that biliary overexpression of plasminogen and AP leads to the generation of excessive amounts of plasmin and subsequent plasmin-dependent lysis of extracellular matrix molecules, which can contribute to biliary dysgenesis in congenital liver fibrosis.

The overexpression of the osteoponin gene is also an important component in the pathogenesis of various variants of biliary atresia and congenital cholestatic syndromes – congenital liver fibrosis and CD. Osteoponin is an inflammatory stimulator, and its excessive synthesis is regulated by the presence of excessive amounts of regulatory factors (NF-κB and TGF-β1).

In a work devoted to the study of the relationship between an excessive number of poorly differentiated bile ducts and fibrosis, Y. Sato et al. demonstrated in a rat model that, in the presence of TGF-β1, cholangiocytes acquire the features of mesenchymal cells, mimicking fibroblasts; epithelial-mesenchymal transition (EMT) occurs. The authors suggested that overexpression of extracellular matrix molecules by these cells may be the cause of the progression of liver fibrosis.

Some experimental and clinical studies indicate that proliferating cholangiocytes actively respond to hormones, neuropeptides, growth factors, cyto- and chemokines, secreting, in turn, a large number of different agents that, through autocrine regulatory mechanisms, reinforce the proliferation system, inhibit apoptosis and contribute to “excessive” communication with other types of liver cells (hepatocytes, stellate and endothelial cells). Among these substances, estrogens and insulin-like growth factor type 1 play a crucial role in maintaining the proliferative activity of rat and human cholangiocytes by acting on specific receptors. They enhance the proliferative effect on the receptor and post-receptor levels, through which the “survival pathways” are activated. “Reactive” or “activated” cholangiocytes are formed from progenitor cell compartments located as close as possible to the terminal cholangiols in the tubules of Hering. They can initiate the proliferation of inflammatory and mesenchymal cells and the synthesis of the latter components of the extracellular matrix [48]. Although mesenchymal cells are considered to be the promoters of fibrosis, reactive cholangiocytes are called the “pacemakers of liver fibrosis”. The list of factors on the basis of which intercellular interaction occurs is constantly expanding: interleukin-6, interleukin-8, tumor necrosis factor α, interferon gamma, monocytic chemotactic factor type 1, cytokine-induced neutrophil chemoattractant and nitric oxide, which regulates the immune activity of lymphocytes and polymorphonuclear cells.

In addition to establishing a paracrine connection with mesenchymal cells, cholangiocytes can be involved in the generation of liver fibrosis through EMT. EMT is a cellular reprogramming process in which epithelial cells acquire some of the phenotypic and functional characteristics of mesenchymal cells, such as the expression of fibroblast-specific markers (fibrin-1 degradation products, vimentin), the ability to migrate by local dismantling of the base of the membrane on which the epithelial layer is located. , and the ability to generate various components of connective tissue (fibronectin, collagen, elastin, tenascin). Thus, EMT may contribute to the accumulation of activated fibroblasts due to the loss of bile ducts. This biological process has also been described in the pathogenesis of organ fibrosis in the kidneys and lungs . Recent studies show that EMT is also involved in liver fibrosis through active synthesis of TGF-β2 HSC. HSC activation is primarily initiated by TGF-β1 derived from Kupffer cells. It is generally accepted that TGF-β2 is a potent growth inhibitor and profibrotic cytokine that plays a major role in the physiological processes of wound healing and the pathogenesis of fibrosis in various organs. Under pathological conditions, this leads to the accumulation of the fibrous matrix, and in the process of reparative regeneration, to the optimal formation of scar tissue [48, 49]. which plays a major role in the physiological processes of wound healing and the pathogenesis of fibrosis in various organs. Under pathological conditions, this leads to the accumulation of the fibrous matrix, and in the process of reparative regeneration, to the optimal formation of scar tissue. which plays a major role in the physiological processes of wound healing and the pathogenesis of fibrosis in various organs. Under pathological conditions, this leads to the accumulation of the fibrous matrix, and in the process of reparative regeneration, to the optimal formation of scar tissue.

In response to injury, reactive cholangiocytes acquire a phenotype similar to neuroendocrine cells and are able to respond to neuroendocrine stimuli. Cells receive β1 and β2 adrenergic receptors, M3 acetylcholine receptors, and serotonin 1A and 1B receptors. In the case of cholestasis, cholangiocytes can also secrete serotonin directly, limiting bile duct growth with an additional autocrine inhibitory loop.

The morphological picture, both in solitary cysts and in polycystic liver disease, is represented by a fibrous capsule of various thicknesses, often with angiomatosis, the presence of poorly differentiated biliary structures and islets of hepatocytes. A single-layered biliary-type cuboidal epithelium or prismatic epithelium lines the cysts . The structure of the RPC wall differs from simple solitary cysts. Their wall is four-layered: cylindrical ciliated epithelium, loose connective tissue, bundles of smooth muscle cells of various thicknesses, nerve trunks, and fibrous capsule . The presence of cilia is confirmed by electron microscopy. The contents of the cysts may be mucus, bile, or serous fluid. In case of suppuration in the thickness of the wall and lumen of the cyst, accumulations of neutrophilic granulocytes are noted,

Hemorrhages in the walls of cysts can be caused not only by surgical intervention associated with the method of removal and treatment of cysts, but also by the presence of vessels with obvious signs of dysplasia in their walls. In the wall, the formation of multi-row structures with proliferation, represented by poorly differentiated (so-called reserve) cells, is possible.

In the liver tissue, hepatocyte dystrophy, intracellular or canalicular cholestasis, moderate or severe fibrosis of the portal tracts, capillarization of the sinusoids, perivenular sclerosis are noted, which causes the development of portal hypertension. Moreover, poorly differentiated biliary structures, partially cystically dilated, are often detected. Interlobular arterioles and venules often form conglomerates in the portal tracts. The described changes can be both congenital and acquired. Congenital changes are characterized by dysplasia of various structures of the liver tissue – hypoplasia of the lobules, dysplasia of the venous and arterial vessels and bile ducts. In the walls of the cysts, there are also signs of tissue dysplasia – immature biliary structures (Meyenburg complexes), islets of hepatocytes, conglomerates of arterial and venous vessels. Often there are strands of biliary epithelial cells, consisting of persistent elements of the embryonic ductal plate and accumulations of poorly differentiated cells of the biliary epithelium .

Etiology, pathogenesis, classification 

The disease usually manifests clinically between the ages of 30 and 50 and occurs 35 times more often in women than in men. There are true and false cysts of the liver. The former have a cover on the inner surface of the cavity, consisting of the epithelium of the bile ducts. It is believed that they are formed due to changes in the ducts in embryogenesis, followed by their disconnection from the common bile tree. False cysts are more often the result of trauma. The basis of the wall of the false cyst is the fibrous-altered liver tissue at the site of damage or inflammation. 

The fluid contained in the cysts of the liver, most often transparent, light or slightly yellowish, in rare cases – has an admixture of blood or bile. 

What are the symptoms of the disease?  

Symptoms are associated with the growth of formations, their number, the location of the cyst (cysts) in the organ, as well as compression of adjacent organs. An increase in the size of the formation leads to pressure on the tissues and vessels of the liver, impaired blood circulation and atrophy of the compressed areas. In addition, there is pressure on the stomach, duodenum and diaphragm. This causes pain in the stomach area, there is a constant heaviness in the right hypochondrium, eating is accompanied by discomfort, a person is quickly satiated. Then nausea joins, appetite is lost, weakness increases, jaundice is possible due to compression of the bile ducts. Some patients develop liver fibrosis and liver dysfunction. On examination and palpation of the liver, it is possible to detect a smooth, dense, tense mass associated with the liver. Often there is pain when feeling the cyst. An experienced doctor will describe the cyst as “an elastic, fluctuating (oscillating, iridescent) formation.” Rarely, single large cysts appear in the left lobe, protruding beyond the borders of the liver, which can be mobile. But still, it is not always possible to probe even large formations because of their location.

When a liver cyst is detected, it is required to clarify its nature and find out if it is parasitic. For this purpose, laboratory blood tests (serological reactions) are performed for the presence of echinococcus in the body. It is also necessary to carry out differential diagnostics with various tumors of both the liver itself and the intestines, retroperitoneal space, pancreas, formations or dropsy of the gallbladder.

Despite the fact that the cyst grows very slowly and may not cause any complaints, this problem should be taken seriously. The development and progression of the cyst often leads to formidable complications. Violation of the movement of food through the stomach and small intestine due to compression of these organs by a large cyst can cause not only food absorption disorders, but also hepatic or renal colic. The cyst, squeezing the bile ducts, can contribute to their inflammation, lead to obstructive jaundice. In addition, suppuration of the cyst, hemorrhages in it, ruptures into the abdominal cavity with subsequent bleeding are possible. If the cyst is on a leg, then its torsion occurs, which causes symptoms of an acute abdomen. Cases of transformation of cysts into malignant neoplasms are described. 

It is necessary to distinguish the formation of single liver cysts from polycystic. Polycystic is a hereditary disease that is characterized by the development of multiple cysts in the liver and other parenchymal organs – the kidneys, pancreas, ovaries. Such a disease has a favorable course for a long time. Only when the organ is damaged is more than 50%, symptoms associated with an enlarged liver appear: dyspeptic disorders, a feeling of heaviness, dense tuberous liver tissue is detected on palpation. Violations of liver function appear only with a far advanced process – the synthesis of albumin, prothrombin, etc. decreases. Later, when there are few working liver cells, liver failure increases, which can lead to death.

Algorithm for examining patients with liver cysts

Examination of patients with idiopathic liver cysts, in addition to general issues, should solve the following specific tasks: 

  • Detection of the exact location of the cyst in the organ, determination of its size.
  • Differential diagnosis with other focal liver diseases (parasitic cysts, abscesses, hemangiomas, etc.) or cysts of perihepatic localization. 
  • Assessment of the functional state of the liver. 

The diagnosis of a non-parasitic liver cyst is based on the results of a comprehensive study, including the clinical picture, data from laboratory and serological studies, various methods of radiation diagnostics (X-ray, ultrasound, CT, MRI, SCG), and, if necessary, supplemented by immunological tests and angiographic studies.

X-ray studies reveal only some indirect signs of the disease in the form of changes in the contours of the liver, displacement of the diaphragm, displacement of hollow organs, in rare cases, the cyst becomes visible due to the deposition of salts in its wall. 

Ultrasound is a very valuable method in the diagnosis of focal liver diseases. 

Liver cysts are fluid-filled cavities delimited by a thin wall (1-2 mm); their shape can be round or oval. If there is an internal septum, liver cysts may have a patchy pattern. Sometimes, for differential diagnosis, it is necessary to perform a percutaneous puncture of the cyst to obtain its contents in order to conduct a cytological and bacteriological examination of the material. This procedure is performed under ultrasound guidance. 

CT scan 

This type of study allows you to detect any asymptomatic non-parasitic liver cysts. They look like homogeneous foci of a rounded shape, with clear and even contours. The wall of the “true” cyst, as a rule, is not visible. In order to distinguish a cyst from another mass of the liver, computed tomography is used with the “amplification” technique, i.e. intravenous administration of a radiopaque preparation. This technique also makes it possible to distinguish between complicated and uncomplicated, parasitic (Echinococcus) and non-parasitic liver cysts.

Based on the results of the examination, the following questions of medical tactics are solved: 

  • Indications for surgical treatment. 
  • Method and volume of surgical intervention.
  • Access and type of operation. 

Conventional Treatments for Nonparasitic Liver Cysts 

The size and localization of liver cysts are the determining parameters for choosing a method of surgical treatment. Identified asymptomatic small liver cysts of stable size are subject to observation in dynamics, except when they are localized in the region of the liver gate and create biliary stasis. 

The most radical method of surgical treatment is liver resection. However, the risk of organ resection is quite high and, in comparison with the therapeutic need, is justified only in the presence of multilocular cystadenoma or huge cysts with a potentially high degree of malignancy. 

The leading role in liver cyst surgery belongs to organ-preserving operations. These include partial resection of the cyst wall or opening of the cyst with drainage of the remaining cavity. 

Fenestration of cysts is technically simple, gives significantly fewer complications, allows you to save liver tissue, creates effective decompression and drainage of cysts that lie deep in the parenchyma of the organ. The essence of the method is to open the formation cavity, evacuate the contents, remove part of the wall and coagulate the remaining part. As a rule, they are performed with total polycystic disease. Also, with polycystic, you can use percutaneous puncture and sclerosis of rapidly growing cysts. 

Commonly diagnosed liver cysts

A biliary cyst of the liver from its own ducts appears in the prenatal period. The provoking factor is inflammation of the biliary tract at the stage of embryogenesis. There is a failure in the division of tissues, due to which both benign and malignant neoplasms appear.

The solitary cyst of the liver is represented by a single chamber with serous contents. Does not affect hepatobiliary function, but requires dynamic monitoring. Dermoid develop from the epithelium. Retention provokes a violation of the outflow of bile.

Acquired single cysts are also dangerous. Their reasons include: surgery, abdominal trauma. In such cases, a rupture of the vascular wall occurs. A large hematoma may burst, small ones suppurate.

Congenital multiple liver cysts is a hereditary polycystic disease that progresses with age, making the liver multilocular. Genetic pathology is accompanied by polycystic kidney disease. There are combinations with an aneurysm (risk of stroke), weakness of the bicuspid valve (heart failure).

Parasitic cysts appear with helminthic invasion. Liver parasites include: alveococcus, echinococcus, opisthorch, roundworm. The latter are in the liver at the stage of the larva. After maturation, they descend into the intestines.

Symptoms of hepatic cysts

Small cysts on the liver are asymptomatic or with mild discomfort in the hypochondrium. The larger their size and number, the more significant functional disorders. The clinical picture unfolds with the following signs of varying intensity:

  • pain in the right hypochondrium
  • stomach discomfort
  • dyspepsia: nausea, vomiting, belching, flatulence, constipation
  • asymmetry of the abdomen with an enlarged liver (hepatomegaly)
  • violation of the outflow of bile – the skin and sclera become icteric
  • general malaise: subfebrile temperature, loss of appetite, sweating
  • shortness of breath on exertion

A small cyst of the liver with echinococcosis is calcified. With a prolonged course, they become more, liver failure occurs. A specific sign of a parasitic invasion is a rash. The bile ducts are often clogged, which is manifested by obstructive jaundice, skin itching.

Common Complications

An avascular cyst of the liver is devoid of blood supply, distinctive of cancerous tumors. They do not regenerate, but carry other health risks:

  • indigestion
  • inflammation of the gastrointestinal tract
  • liver failure
  • infection

Left untreated, the digestive system suffers. New diseases join: gastritis, pancreatitis, cirrhosis, enterocolitis, cholelithiasis.

An infectious liver cyst suppurates, causing tissue necrosis. Its rupture is complicated by septic inflammation of the abdominal cavity – peritonitis.

Stagnation and thickening of bile leads to the appearance of stones. Stones block the ducts, stretch the walls. Perforation can be fatal.

The solitary cyst on the leg has blood vessels, so when it is twisted, acute ischemia occurs. The death of tissues is accompanied by a purulent-septic process.

Diagnosis of a liver cyst

The subcapsular cyst of the liver is easily determined by ultrasound. Cells of different sizes, shapes, partitions are visualized. Echoes reflected from the organ also convey the nature of the contents: serous, purulent, bloody.

If during the examination there was a question about suspicion of hemangioma, tumor, dropsy of the gallbladder, additional methods are used:

  1. CT scan.
  2. Scintigraphy.
  3. Laparoscopy.
  4. Angiography.

To exclude a malignant process, a diagnostic puncture is prescribed. The resulting material is sent for cytology. With the accumulation of parasites in the parenchyma, serological tests are taken. Blood is examined for antibodies to worms (echinococcus, alveococcus).

Treatment methods for liver cysts

A single cyst of the left lobe of the liver up to 3 cm is not removed. Patients are subject to periodic follow-up ultrasound. To prevent its growth, improve well-being, maintain hepatobiliary function, drug treatment is carried out:

Medicinal herbs slow down the growth of cysts, promote its resorption. This effect is possessed by decoctions and infusions from the roots of burdock, wild rose, and initial letters. They stay fresh throughout the day when stored in a cool place. Reception should be regular, dosed.

The parenchymal cyst of the liver with helminthic invasions is treated etiotropically. Albendazole is used as an antiparasitic agent. It has low toxicity and is not inactivated in the gastrointestinal tract. Well absorbed, concentrated in bile and hepatocytes, destroys larvae.

Surgical treatment is indicated for cysts larger than 4-5 cm, complications, polycystosis. A sparing operation includes drainage followed by the introduction of a sclerosing agent. Bonding the cavity prevents re-accumulation of fluid. Marsupialization involves emptying the capsule, but its edges are sutured to the parietal peritoneum.

Enucleation is rarely used, since husking is a traumatic operation. A simple liver cyst is safely removed by excising its walls. If they are grouped in one lobe, resection will be required. Giant cysts of 20-25 centimeters are treated palliatively. For their drainage, an artificial anastomosis is created between the liver and the stomach or intestines.

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