Hepatitis

HEPATITIS (from Greek hepar-liver), inflammation of the liver. Old pathology interpreted inflammation of the liver in a very broad sense, namely, it attributed to inflammation almost all diseases of this organ, especially those accompanied by pain. At the patient's bedside, the diagnosis was made very frequently, all the more so that with H. the afflictions of neighboring organs were often confused: right pleura, right kidney, stomach, etc. At present, in clinical practice, the term H. conditionally combines numerous inflammatory and degenerative processes localized in the liver—either in the parenchyma of the organ (parenchymatous H.), or in the interstitial tissue (interstitial H.), or finally, involving both tissues (mixed forms). For degenerative forms, some authors have proposed the name hepatoses (Geronne, Vichert). Although experimentally, by poisoning animals with special hepatic poisons—chloroform, phosphorus, toluenediamine, etc.—the indicated degenerative changes can be caused, however, the concept of hepatosis does not correspond to any definite clinical picture, therefore it is hardly necessary to introduce this new name and clutter an already complicated nomenclature. H. in the clinical sense is a collective concept, it includes many processes both inflammatory and non-inflammatory, which have acquired completely independent clinical and anatomical significance and are described under different names (see Jaundice, Cirrhosis of the liver, etc.). The basis of all changes in H., as experimental studies have shown, is the damage to the liver cell itself. The latter is extraordinarily sensitive not only to various infectious and toxic influences, but also to factors that disrupt the isotonicity of the blood flowing through the liver. The liver cell is easily damaged, but at the same time it is capable of regeneration and compensatory hypertrophy. Brief historical data. Descriptions of acute H. are already found in the works of ancient Greek physicians, and there they were also given a semiotic evaluation. Hippocrates (aphorism VII, 44) already speaks of opening liver abscesses with a hot iron, and in Celsus there is a remark that some doctors opened these abscesses with a knife. However, the beginning of a more precise acquaintance with H. was laid by path.-anat. studies of the XVI and XVII centuries. It should be noted that the largest casuistic material on purulent H. was collected by observations of doctors in hot countries, since this disease is observed incomparably more often there than in countries with a temperate climate. Information about chronic hepatitis, later called cirrhosis by Laennec (1813) (in view of the yellow color of the granulations—from Greek kirros-yellow), dates back at least to the IV century of the Christian era (Aurelianus, Vesalius). But this information is fragmentary, and only Morgagni in his famous 38th letter (1761) gave a brilliant description of chronic hepatitis in a rich Venetian senator who loved to drink a lot and eat tasty food. In this description we see both the clinical picture and the corresponding patho-anatomical substrate and indications of etiology. From the beginning of the XIX century, when morphological direction began to establish in medicine (see Internal diseases), an enormous number of works were devoted to H., and by the end of this century, through the work of French scientists (Laennec, Andral, Cruveilhier, Charcot, Hanot, Hutinel, Gilbert) and Germans (Virchow, Fre-richs, Ewald, Eppinger), the anatomical substrate and clinical picture of the disease forms united under the concept of H. were outlined in sufficient detail. The latest works are aimed at clarifying the pathogenesis and etiology and at illuminating the complex relationships between organs and systems that the polymorphic picture of these pathological processes gives. Etiology and pathogenesis. The complexity of the clinical picture and the diversity of pathological forms of H. are explained by two reasons. On the one hand, these processes are caused by numerous hepatotropic factors (toxins and poisons) affecting the liver cell, and on the other hand, the complex lobular structure of the liver with its special blood circulation provides several different paths for these hepatotropic influences. The most important and frequent route of infection and intoxication is through the portal vein. From this arise portal hepatitis, the final stage of which is the so-called Laennec's cirrhosis. In these cases, toxins penetrate from the side of the gastro-intestinal tract-enterogenous cirrhoses-hepatitis. It is necessary to point out that the processes acquire a special picture if hepatotropic harmful agents enter the liver from the splenic branch of the portal vein. This is the so-called hepatolienal diseases, or splenomegalic forms of cirrhosis. In these cases, hepatotropic toxins are carried from the spleen, which occurs in a number of infectious-parasitic diseases (malaria, leishmaniasis, syphilis, Banti's disease). These processes have a special picture, conditioned by the lesion of the reticulo-endothelial system, accompanied by destruction of blood—hemolysis and violation of pigment metabolism, and were isolated in a separate syndrome. From the side of the hepatic veins, the starting point for the development of H. can be a prolonged stagnation of blood as a result of weakening of the right heart's activity. In this case, the source of chronic intoxication for the liver tissue is the accumulation of carbon dioxide and other toxic metabolic products in the blood. It is well known that prolonged stagnation first leads to atrophy of the parenchymal elements of the liver (nutmeg liver), and then an interstitial process develops in it. Thus, harmful influences can act on the liver through veins from two sides—the portal vein and the hepatic veins, with portal H. in the initial stages, the growth of connective tissue occurs between the liver lobules, following the branches of the portal vein. In hepatic-vein H., on the contrary, the growth begins inside the lobule (central vein). However, in view of the fact that the interlobular branch of the portal vein anastomoses through the capillary network with the central hepatic vein, both venous H. (both portal and hepatic-vein) easily over time becomes mixed, bivenous. The arterial route less often becomes a source for the occurrence of H. However, through the arterial route, it is also possible for toxins circulating in the general bloodstream to penetrate the liver. This is especially the case in syphilis and tbc. Much more often hepatitis spreads along the bile ducts. As a result of obstruction (e.g., by a stone) of the large bile ducts, infection easily occurs, carried from the intestine. It spreads upward to the intrahepatic branches of the bile ducts, and thus, cholangitis easily occurs with degenerative processes in the liver cells (biliary H.). Finally, less often the starting point for the development of H. is perihpatitis. In these cases, infection goes from the peritoneal cover along lymphatic paths, penetrating into the liver parenchyma. Similar processes are sometimes observed in polyserositis, adhesive pericarditis, and their appearance is facilitated by the presence of venous stagnation in the liver on the basis of weakening of cardiac activity. Thus, we see five paths (two venous, arterial, biliary and lymphatic through the liver capsule), along which harmful factors can influence the liver. It must be borne in mind that these harmful factors often can go along several paths simultaneously, and then, of course, the result of this action occurs faster, and before us develops the picture of a mixed symptomocomplex. Before we stop closer at the causes and course of H., it is necessary to point out that there is no single cause of these processes, and the causes are always numerous and complex. Not to mention that in the origin of these diseases, internal predisposing moments have significance, such as general weakness of the body, heredity and individual instability of the liver, along with weakening of many protective adaptations, it must be borne in mind that external causes, such as infection and intoxication, must be influences that are prolonged and often repeated.—Among hepatotropic infections in the origin of chronic H., three are of particular importance: syphilis, tbc and malaria, and for acute H.—dysentery and typhoid fever. It is known that syphilis is such an infection that easily causes sclerosing processes. However, one should not think that in this disease, in which perivascular scleroses are so frequent, scleroses of vascular origin are always observed. Just as cirrhosis of the liver is the result or final stage of hepatitis, syphilitic sclerosis is a direct consequence of the developed infectious process, ending in scarring.—The etiological role of tbc in chronic H. or in cirrhosis has been established by numerous path.-anat. works, namely, in autopsies of tuberculous patients, besides fatty degeneration, interstitial changes in the liver are very often found, sometimes along with miliary tubercles. Some authors (Lie-bermeister, Husse) succeeded by inoculating pieces of liver taken from patients who died from tbc, to prove the tuberculous nature of such processes where, despite careful histological examination, it was not possible to detect bacilli.

On the other hand, some authors experimentally induced interstitial hepatitis in animals by inoculating them with tuberculous material (Stern, Gano, Gilbert). In the second, very prolonged and often latent, stage of tuberculosis (Ranke), one can consider the possibility of hematogenous spread of infection to various organs and primarily to the liver (Gausman).-It is known that malaria, as a chronic infection with relapses, causes liver damage; in this case, hypertrophic and pigmentary hepatitis are more often observed than atrophic forms.-In the etiology of acute hepatitis, dysentery and typhoid fever are particularly important. These hepatitis often end in suppuration and give a clinical picture of liver abscess. Classification of hepatitis. From the clinician's point of view, the classification can be based on two points with some reservations: the predominant localization of the process in one or another part of the liver and the acuteness or chronicity of its course. Thus, a distinction is made between parenchymal hepatitis, if the process is localized predominantly in the liver cells themselves, and interstitial hepatitis-when the intermediate connective tissue is predominantly affected. In the first case, there is a degenerative process, and in the second, an inflammatory one; since usually both tissues are affected, mixed forms are more common. All three of the above forms can have acute, subacute, and chronic courses.-Acute parenchymal hepatitis corresponds to various clinical syndromes: phosphorus poisoning and other toxic jaundices, icterus gravis, acute yellow atrophy of the liver, yellow fever and infectious jaundices. The latter, depending on the nature and strength of the infection, can have acute and subacute courses (the former concept of catarrhal jaundice). The outcome of acute hepatitis-either complete recovery with restoration of normal structure and function or necrosis and unstoppable death of liver tissue (acute yellow atrophy of the liver).-Chronic parenchymal hepatitis can include hypertrophic cirrhosis of Gano, however, in this cirrhosis, in addition to the parenchyma, the interstitial tissue is also affected, so in terms of its localization, it should be considered a mixed form.-Acute interstitial hepatitis includes purulent inflammation of the liver and liver abscesses (see Liver-abscess).-Chronic hepatitis to a large extent correspond to the former concept of cirrhosis, and the latter should rather be considered as the final stage or scarred stage of chronic hepatitis. Taking into account the teaching of Kretz, according to which in liver cirrhosis, degenerative changes in the parenchyma go hand in hand with parallel changes in the intermediate connective tissue, it must be recognized that cirrhosis is the result of chronic, mixed (parenchymal-interstitial) hepatitis. Such a view of cirrhosis as a result of hepatitis corresponds to the fact that cirrhosis does not occur immediately. Under the influence of a number of hepatotropic toxins, a so-called pre-cirrhotic stage can be observed in the liver, which is expressed by an increase in the organ due to active hyperemia, and if the influence of toxins continues, the organ decreases and the process ends in cirrhosis. Thus, it is clear that the concept of hepatitis in the above sense is a collective concept, conditionally uniting a large number of pathological processes of different nature and localization, with different courses and far from identical clinical pictures. A significant part of these processes does not belong to the manifestation of inflammation in the liver and, strictly speaking, does not deserve the name hepatitis. Description of individual clinical forms-see Jaundice, Cirrhosis of the liver.