Paranephritis

PARANEPHRITIS, paranephritis (from Greek para- around and nephron-kidney), inflammation of the perirenal adipose tissue (fatty capsule - paranephron); first described in 1839 (Ray). In 1896, Küster (Kuster), based on the extensive case material he had collected, gave a comprehensive description of the clinical picture of acute suppurative P. Inflammation of the proper capsule of the kidney, rarely occurring as an independent disease, Küster called perinephritis (see). Against this nomenclature, Israel objected, proposing to call 1) inflammation of the proper capsule of the kidney - perinephritis, 2) inflammation of the perirenal adipose tissue - epinephritis, 3) inflammation of the retroperitoneal adipose tissue (massa pararenalis) (see Retroperitoneal space) - paranephritis. Most authors, however, adhere to Küster's classification. - The rich supply of lymphatic and blood vessels to the perirenal adipose tissue contributes to the development of inflammatory processes in it, some of which are constructed on the type of terminal vessels (rami perforantes interni from the group aa. capsulae renalis). Acute suppurative inflammation is most common. Initially, hyperemia and impregnation with serous fluid are noted, which then give way to the formation of a limited abscess with a rapidly developing dense infiltrate around it, sometimes reaching board-like hardness. The ability to form such infiltrates is characteristic of the perirenal adipose tissue (see below). For a considerable time, this infiltrate prevents the increase and spread of the abscess, which is also facilitated by the presence of dense fascial septa penetrating the perirenal adipose tissue in a radial direction. When the abscess is located directly near or not far from the capsula propria, a reactive thickening of it can develop with greater or lesser involvement of the renal parenchyma in the process. With further increase and spread of the abscess, the fascial septa are destroyed, and the abscess can eventually capture the entire perirenal adipose tissue and melt it down (phlegmona), forming within the fascia renalis a bag filled with pus. Further spread of the purulent process leads to the destruction of the fascia renalis and its transition to the surrounding tissues. The causative agent of P. in most cases (up to 70%) is staphylococcus, sometimes in combination with streptococcus, then E. coli (up to 6%), more rarely tubercle bacillus, gonococcus, diplococcus; individual cases of finding actinomycosis grains in pus have been described. The penetration of infection into the perirenal adipose tissue does not always lead to the formation of an abscess, but sometimes as a result of it, chronic inflammatory processes of a productive nature develop: 1) fibro-hyperplastic-sclerotic form and 2) fibro-lipomatous form (see Perinephritis). Acute suppurative P. can be a complication of many kidney and renal pelvis diseases: cortical abscess of the kidney (carbuncle, according to Israel), apostematous nephritis, pyelitis, pyelonephritis, kidney stone disease, tuberculosis, syphilis, echinococcus, and kidney neoplasms. The process spreads to the perirenal adipose tissue either directly (per continuitatem) or is carried into it through blood or lymphatic vessels. This transition often occurs after a previous injury to the renal area. However, not always in P. are visible changes in the kidneys found. As early as Reyer drew attention to cases of P. developing in apparently completely healthy kidneys. Küster, Tuffier and others isolated them into a special form of idiopathic P. Further observations showed that these P. can develop after a more or less long time after a past, sometimes insignificant purulent process far from the kidney, or any general disease; among them, furuncle, carbuncle, panaritium, abscess, phlegmona, angina, influenza, sepsis were most common. The studies of Riedel, Tuffier, Janusz, Blumenthal and others showed that both in operations and in autopsies (13 cases of Janusz) the kidneys in some cases of P. were completely normal both macroscopically and microscopically. Israel, Albrecht, Rehn, Stuckey and others were ardent opponents of the theory of metastatic extrarenal P. Israel asserted that even in these cases the kidney primarily becomes diseased, and P. is only a consequence of this process, which sometimes proceeds without objective symptoms. In his opinion, the most common cause of such P. is a metastatic cortical kidney abscess located subcapsularly and extending to the perirenal adipose tissue by perforation of the proper capsule of the kidney. These abscesses can be so insignificant that they either remain unnoticed during the operation, or by the time of the operation they heal, leaving behind an inconspicuous scar. The absence of pathological changes in the urine in such cases Israel also did not consider as proof of the extrarenal development of P., pointing out that small abscesses located far from the pelvis do not lead to the appearance of pus and other pathological impurities in the urine. Clinical experience and literary data of recent years (Riedel, Wilke, Janusz, Blumenthal and others) nevertheless allow one to assert categorically that in some cases (40-60%) paranephritis develops metastatically with a completely healthy kidney. The reason for the localization of the process precisely in the perirenal adipose tissue is its abundant vascularization with the development of anastomoses with the systems of large arterial and venous trunks. In addition to the inflammatory processes listed above in the anamnesis of P. patients (especially in its metastatic form), trauma to the renal area is often noted, sometimes very insignificant (light bruise, sharp tension of the back muscles when lifting heavy weights, awkward movement, etc.). An indirect confirmation of the importance of trauma in the pathogenesis of P. is the predominant disease of men, more often subject to trauma when awkwardly carrying heavy loads, etc. (according to Blumenthal up to 70%) or persons engaged in sports (observations of Muller in the German army). Inflammatory processes developing in organs connected with the perirenal adipose tissue by lymphatic pathways can also lead to P. These include appendicitis, postpartum parametritis, prostatitis, gonorrhea, etc. The importance of appendicitis in the etiology of P. is exaggerated by many authors, which apparently depends on incorrect recognition and confusion with the closely related paracolpitis (see), to which S. P. Fedorov drew attention. Of much less practical importance are P. from the direct transition of the inflammatory process from neighboring organs (pleurisy, perforated ulcer of the duodenum, abscess of the spleen). In addition to the forms of P. listed above, differing from each other in their pathogenesis and etiology, in almost all statistics there remains a number of cases whose etiology and pathogenesis cannot be explained. It should be assumed that these cases of so-called idiopathic P. should also be classified as the metastatic extrarenal form, all stages of which proceeded unnoticed for the patient until the appearance of the first symptoms of the abscess (Solovov). Finally, mention should be made of P. from the penetration of infection from the outside - from the surface of the body. These include the individual described cases of penetrating wounds - primary P. according to Fedorov. Most often P. develops behind the kidney - in the place most richly vascularized and most accessible to trauma. Next in frequency are P. at the upper pole, at the lower pole of the kidney and (rareest of all) in front of the kidney. Clinic of P. Paranephritis usually begins in the midst of complete health with a shaking chill with an increase in temperature (up to 40°) and the most severe pains in the kidney area; the temperature can remain high for a long time or after several days be replaced by subfebrile with periodic increases, often again accompanied by chills. Patients from the very beginning give the impression of being severely ill. General weakness, coated tongue, loss of appetite, constipation, abdominal bloating, slight defense, rapidly increasing leukocytosis indicate severe intoxication. Pains in the kidney area increase and intensify with the slightest movement. Patients assume a curved position with the convexity of the spine turned toward the diseased side. Pasternatsky's symptom (see) is sharply positive. The contours of the kidney, the palpation of which at first is only possible with difficulty due to pain and some tension of the anterior abdominal wall, gradually increase. Subsequently, a dense infiltrate develops, often occupying the entire corresponding half of the abdomen. The outlines of the back are smoothed out (disappearance of the "waist"); symptoms of psoitis (flexion of the leg in the hip joint) appear. Pathological impurities appear in the urine (protein, leukocytes, pus and granular cylinders), mostly absent in P. of extrarenal origin (differential diagnostic sign). Puncture of the abscess as an auxiliary diagnostic method is permissible only in exceptional cases provided that it is possible to proceed immediately after it to surgery, which is why it is best to perform the puncture already on the operating table. The classic symptoms of P. described now are by no means always present.

The absence of pain, which often occurs in the first days of the disease and is the main source of diagnostic errors, particularly complicates the correct diagnosis. In such cases, abdominal typhoid, prolonged influenza, pneumonia, malaria, tbc, etc., are most often diagnosed. Only the appearance of pain and swelling in the kidney area, leukocytosis, and other symptoms of an acute purulent process point to the correct path, sometimes after a prolonged period from the onset of the disease. In the absence of timely appropriate therapy, the P. abscess, increasing in size and involving neighboring organs and tissues in the process, can lead to a series of serious complications and cause death. The most frequent complication is inflammation of the pleura on the corresponding side. Pleurisy, initially serous and then often turning into purulent, is a reaction of the pleura to the developing neighboring process, but sometimes also the result of direct transfer of infection through lymphatic pathways penetrating the diaphragm. In left-sided P., perforation of the abscess through the diaphragm into the pleural cavity or (more often) into the lung tissue adhered to the diaphragm is observed. The anatomical features of the diaphragm area to which the upper pole of the kidney is adjacent - trigonum costo-lumbale (Bochdalekii) - facilitate this perforation. This area, devoid of muscle fibers, can easily be destroyed by the ever-growing abscess. Sometimes such abscesses can empty out with coughing, which can lead to self-healing (Svechnikov).-P. located in front of the kidney can perforate into the abdominal cavity or into the lumen of the adjacent large intestine, subsequently emptying out per vias naturales. Spreading downward, the abscess, descending along the ureter in its cellular tissue, can infiltrate the cellular tissue of the small pelvis and even rupture into the bladder. With properly conducted therapy, mortality from P. does not exceed 5-7%. Therapy is exclusively surgical - opening the abscess with a posterior oblique renal incision. After opening the abscess, its cavity is examined with a finger, destroying individual fascial strands to create one common abscess cavity. Finding and opening an abscess located at the upper pole of the kidney or in front of it can present significant difficulties. To drain these abscesses, it is sometimes necessary to remove the kidney. The operation is completed by the introduction of suction tampons. There are differences among authors regarding the timing of intervention. Some (Israel, Boeminghaus, Fedorov, etc.) are advocates of early intervention, pointing to the danger of waiting, which can lead to an increase in the abscess and its perforation into neighboring organs, while most authors (Maas, Simon, Riedel, Solovov, Blumental, etc.) adhere to the expectant method, opening the abscess only when there are clear signs of its localization and the formation of a delimiting granulation wall. The advantage of the expectant method lies in the shorter and more favorable postoperative course. After early operations, long-unhealing fistulas often remain. In cases of severe intoxication, changes in the white blood picture in the direction of a shift to the left in Schilling's formula, etc., early intervention is certainly indicated. During the waiting period - warmth (heating compress, hot-water bottles) and analgesics. Some authors, advocates of exclusively renal origin of P., consider it mandatory during the operation to carefully examine the kidney to detect the primary focus - the cause of P., but most object to such an examination, as it prolongs the operation and causes unnecessary trauma. These same authors object to one-stage nephrectomy in case of detection of a primary focus in the kidney, as according to Blumental it gives a mortality rate of 15 to 26%. In two-stage nephrectomy, the mortality rate is significantly lower (about 3-10%). Recovery after P. operation occurs on average in 2-4 decades. Often after the operation, long-unhealing fistulas remain, the cause of which may be insufficiently wide opening of the abscess and consequently insufficient outflow of pus. A secondary operation can lead to healing. In most cases, however, the presence of a long-unhealing fistula after the operation indicates a process in the kidney. In these cases, complete recovery occurs only after nephrectomy. Prevention of P. should proceed in two directions: early consultation and radical treatment of chronic kidney diseases, which are often the cause of P. The question of prevention in extrarenal P. is much broader. The fight against industrial trauma, the struggle for compliance with the rules of public and personal hygiene through mass health education and improvement of working and living conditions will lead to a reduction in cases of minor infectious processes on the skin, which are most often the entrance gates for infection leading to the formation of P.