Peritonitis

PERITONITIS, inflammation of the peritoneum; peritonitis is observed mostly as a complication of a disease of some organ in the abdominal or adjacent cavity, but sometimes it develops as a result of the introduction of infection via the bloodstream and from more distant organs. Primary inflammation of the peritoneum, the so-called idiopathic peritonitis, which was mentioned in isolated cases by old authors, is now described rarely, and the majority of clinicians and pathologists are inclined to deny the possibility of such a form of peritonitis altogether (Korte). Peritonitis is distinguished as acute or chronic depending on the nature and duration of the process, which are linked to the etiology of the inflammation (tuberculous, chemical, and similar non-bacterial processes). Peritonitis can be general or diffuse, and limited or local. General peritonitis is considered to be that in which the entire peritoneum is captured by the inflammatory process, whereas in limited peritonitis, the process is localized only in a specific place in the abdominal cavity. Between the healthy and inflamed sections of the peritoneum, initially more or less loose adhesions and synechiae develop. Limited peritonitis can, under appropriate conditions (increase in pressure in the limited cavity, melting of surrounding adhesions), turn from local into general. Some authors, in addition to general, also recognize diffuse peritonitis. Thus, according to Korte, by general peritonitis one must understand those cases of peritonitis where the entire peritoneum of all sections of the abdominal cavity is involved in the inflammatory process; in diffuse or free peritonitis, a significant part of the abdominal cavity is inflamed, and the process has a tendency to spread further. Etiology and pathogenesis. Inflammation of the peritoneum can be caused by mechanical and chemical factors, but most often by the penetration of bacteria into the abdominal cavity. Chemical and mechanical factors lead to peritonitis, which proceeds comparatively favorably, showing a tendency toward delimitation and the formation of adhesions, whereas peritonitis of bacterial origin, on the contrary, is accompanied by a severe clinical picture associated with the mechanism of the development of the process and pathological-anatomical changes. The cause of aseptic peritonitis can be the entry into the abdominal cavity of various irritating substances (strong antiseptic solutions, fluid from echinococcal cysts and ovarian cysts, as well as bile or urine free of microorganisms). Similar changes can be led to by the ligation en masse of significant sections of tissue in the abdominal cavity, twisting of tumors, volvulus of intestinal loops, etc. In the latter cases, the possibility of the penetration of microorganisms into the abdominal cavity through the walls of the intestines, which are compromised in their nutrition, is not excluded. Much greater importance is held by peritonitis caused by the penetration of pathogenic microorganisms into the abdominal cavity. The fact that the entry of microorganisms into a healthy peritoneum does not always lead to peritonitis has been known for a long time (Wegner); the quantity of microorganisms and their pathogenicity are of decisive importance. Kirschner explains this fact in the following way: the toxins of bacteria that have entered the abdominal cavity are neutralized by antitoxins partly in the blood and partly in the fluid of the peritoneum (transudation), which significantly retards the absorption of bacteria and their toxins. Furthermore, the liver, through which blood from the organs of the abdominal cavity passes, also possesses a neutralizing ability, whereas intravenously introduced microorganisms enter the blood directly. Through experiments on animals, Noetzel proved that the injection into the peritoneum of a tenfold dose of microorganisms, which is lethal upon intravenous injection, leads only to general malaise in the experimental animals. Obviously, some other factor is necessary in the form of mechanical or chemical moments that damage the cellular elements lining the peritoneum, which also possess bactericidal properties (Wolfsohn). The peritoneum of a human, in its biological properties, differs to a certain extent from the peritoneum of an animal, and therefore one cannot transfer the results of these experiments entirely to humans, especially since in humans, the absorption capacity, etc., are not identical and depend on a whole range of factors. However, experimental data still present some interest and provide certain indications when interpreting some facts in everyday practical work (Korte). In any case, in humans as well, a significant part of the bacteria perishes under the influence of the bactericidal properties of the peritoneum. The remaining part of the microorganisms is absorbed by lymphocytes or endothelial cells of the lymph and blood vessels (Kirschner). Thus, in inflammatory processes of the peritoneum, microorganisms rarely enter the blood, and if a part of them does enter, they in all probability perish there. Schottmüller is inclined to explain by this the fact that in peritonitis, it is very rarely possible to detect microorganisms in the blood. If the bacteria that have entered the abdominal cavity possess increased virulence, and the organism is at the same time weakened by some disease or other process, the microorganisms penetrate into the blood and lead to a general infection of a septic character (sepsis). As for the bacteriology of peritonitis in humans, in the vast majority of cases, one is dealing with a mixed infection with a predominance of aerobic bacteria and the presence of a significant quantity of Bacterium coli. Along with this, streptococci and diplococci of various characters and various virulence are often found. Staphylococci are discovered extremely rarely in peritonitis. The role of anaerobic microorganisms, which are difficult to isolate in peritonitis, has not yet been sufficiently studied. According to data from Runeberg, their significance is determined not so much by their pathogenicity as by the fact that their toxins are easily absorbed, noticeably worsening and complicating the entire course of the process. In women, the cause of peritonitis can be gonococci during the spread of the process from the genital organs and streptococci in peritonitis of a postpartum character. Pneumococci are observed most often in peritonitis in children. According to the collected statistics of Weil (cited by Korte), who collected 660 cases of peritonitis of appendicular origin, the following were discovered: only Bacterium coli in 60% of cases, Bacterium coli and streptococci in 19%, Bacterium coli and other bacteria in 4%, only streptococci in 9%, only diplococci in 3.5%, staphylococci in 1% (anaerobes are not included here). Pyogenic bacteria enter most often from organs located in the abdominal cavity and covered by the peritoneum, and sometimes from organs and tissues located in the vicinity of the abdominal cavity. The violation of the integrity of the peritoneum during trauma with the simultaneous introduction of microorganisms and during laparotomies can lead to the development of peritonitis, but most often the source of peritonitis is the gastrointestinal tract and the genital organs in women. The first place in terms of the frequency of the spread of infection to the peritoneum is occupied by the vermiform appendix. Most often, the inflammatory process is delimited in the form of local peritonitis, but sometimes the inflamed vermiform appendix perforates, the infection penetrates into the abdominal cavity, and general peritonitis ensues (see Appendicitis). Next in frequency follow perforations of peptic ulcers of the stomach and duodenum. Perforations of cancerous tumors of the stomach are observed significantly less frequently. Portals for the penetration of bacteria into the peritoneum from the small intestines are perforated typhoid or tuberculous ulcers, and from the large intestines—syphilitic and tuberculous ulcers. Foreign bodies during passage through the intestinal tract can also rupture the intestinal wall in some section. Changes in the walls of the intestines during strangulations, during the twisting of individual sections, the formation of ulcers with a tendency toward perforation during the stretching of the intestinal walls above the site of a stricture—all this can create favorable conditions for the penetration of bacteria into the cavity of the peritoneum. The female genital organs—the uterus, tubes, and ovaries—serve as a source of the penetration of infection into the peritoneum during the spread of postpartum and other corresponding inflammatory processes (see Pelviperitonitis). Perforative cholecystitis, micro-perforation of the gallbladder (Clermont, Haberer) in connection with the entry of an enzyme from the duodenum (Schönbauer), a ruptured bladder of a suppurating echinococcus of the liver or spleen, a ruptured abscess of the liver or spleen, suppuration during acute necrosis of the pancreas, a suppurated mesenteric gland, etc.—all this can be a cause of peritonitis. The spread of infection from adjacent serous cavities during pleurisy, pericarditis can also lead to the development of peritonitis. Finally, peritonitis can be in connection with an inflammatory process developing in the vicinity (phlegmon, erysipelas of the abdominal wall, etc.). The spread of infection via the bloodstream was mentioned above. The points of origin are distributed according to the autopsy material of Benda and Koch for 1,300 cases of peritonitis, cited by Korte, as follows: vermiform appendix—328, the remaining part of the intestine—307, female genital organs—242, stomach and duodenum—177, postoperative origin—42, gallbladder—40, urinary bladder, kidneys—23, pancreas—5, spleen—5, various other sources (phlegmons near the peritoneum, purulent periorchitis, proctitis, liver abscess, grippal pleurisy)—45, source unclear—76.

The development of peritonitis in connection with the penetration and multiplication of bacteria on the peritoneal covering is accompanied by a whole series of severe phenomena on the part of the entire organism as a whole and, first and foremost, on the part of the cardiovascular apparatus and the central nervous system.

In peritonitis, in the majority of cases, paresis of the intestine—paralytic obstruction—develops from the very beginning, and only in 3% (Kirschner) does the picture of inflammation of the peritoneum begin with diarrhea.

The mechanism of intestinal paresis has not yet been sufficiently studied. Whether toxins act directly on the intestinal musculature (Krehl), or on the nerve centers located in the wall of the intestine itself (Auerbach's plexus) (Hotz), or on the cerebral centers (Koenig, Matthes), or whether this paresis is a consequence of circulatory disturbance (Hotz)—is difficult to say (all the more so because all these factors are considered by the aforementioned authors in isolation).

Kirschner is more correct in pointing out that, in all likelihood, all these factors taken together are the cause of intestinal paresis. But in addition to this, the general state of the organism at the moment of the disease also has an undoubted influence.

In the paralyzed intestine, its contents are retained, in which poisonous substances are formed, which are absorbed into the blood in the initial stages. Although experiments on animals (Clairmont and Ranzi, Enderlen and Hotz) have proven that absorption from the intestine occurs only in the first hours of its paresis, clinical observations give the impression that this absorption is of great importance.

In connection with increased excretion and the cessation of absorption, water metabolism is disturbed in the direction of fluid depletion of the entire organism.

Simultaneously with the paralysis of the intestinal walls, vascular disorders also develop in the portal system. Due to the distension of the intestine and the accumulation of fluid in the abdominal cavity, the abdominal walls are stretched and the diaphragm is raised upward, which exerts an influence on the activity of the heart and respiration; insufficient respiratory movements, in turn, affect the circulation in the inferior vena cava and in the portal system.

The large and small vessels of the abdominal cavity dilate and become engorged with blood. In the very first hours, paresis of the capillary network of the abdominal cavity is noted (Olivecrona), and then of the arterial and venous system as well, in connection with damage to the vasomotor center.

According to the data of Holzbach and Olivecrona, the paresis of the vessel walls in the organs of the abdominal cavity is not connected with the absorption of toxins into the blood and their action on the central nervous system, but with the direct effect of poisonous substances on the vessel walls, since the vasomotor center reacts well to stimulation even in far-advanced peritonitis.

All this leads to the fact that a significant amount of blood accumulates in the blood vessels of the portal system. Due to the stagnation of blood in the capillaries, the walls of the latter begin to allow fluid to pass through, which in turn contributes to a decrease in the amount of circulating blood in the organism.

All these circulatory disorders in the vascular system of the abdominal cavity initially exert an indirect influence on the heart, but subsequently, the work of the heart, given its insufficient blood filling and blood supply associated with the disturbance of blood distribution throughout the entire organism, ends in complete failure of cardiac activity.

As for the nervous system, in addition to the aforementioned disorder of the function of the vasomotor center, the fibers of the vagus nerve and the fibers of the splanchnic nerves turn out to be paralyzed due to direct contact with the pus bathing the intestine (Friedländer). In the opinion of Friedländer, irritation of the vagus nerve is accompanied by collapse, and irritation of the splanchnic nerve causes pain and intestinal paresis.

To what extent nerve fibers can exert an influence on the process of inflammation of the peritoneum has still not been clarified. Friedländer tried to sever both vagus nerves in animals and then infect the peritoneum; Strehl did the same. Neither author could note any peculiarities in the course of the inflammatory process.

According to the data of the laboratory of A. D. Speransky, the severing of the vagus nerves in rabbits immediately below the diaphragm has an undoubted influence on the course of peritonitis. The process becomes delimited, and a significant portion of the animals survive. Through experiments on animals, the question posed by the Speransky school is resolved only to a small degree. More definite data may be obtained in the clinic on humans, but here too a number of factors must be taken into account—the source and character of the infection, the moment of the severing, the condition of the patient, etc. This question deserves attention but is currently in the stage of research and study.

Pathological anatomy. Pathologically-anatomically and clinically, it is best to divide peritonitis: 1) by etiological factors and course—acute infectious and chronic, 2) by the character of the exudate, 3) by the degree of spread, or 4) delimitation.

The etiology, intensity, duration of the process, source of infection, and the state of the entire organism have a great influence on the spread and course of the inflammatory process of the peritoneum.

In the very earliest stages of peritonitis, hyperemia of the serous membrane is noted, mainly of the visceral peritoneum and the omentum, especially sharply expressed in the vicinity of the source of infection. Soon after this, a serous exudate appears in the abdominal cavity, in greater or lesser quantity depending on the character of the process.

A pure exudate, without fibrinous flakes, is observed only in the initial stages of peritonitis. With more significant deposition of fibrin on the serous membrane, one speaks of a serous-fibrinous exudate. This exudate is turbid, yellowish or greenish in color, with flakes and shreds of fibrin. Appearing initially in the form of a thin pellicle covering the serous membrane and easily peeled off, fibrin gives it a dull and rough appearance. At the places of contact of the serous membranes, thanks to the deposition of fibrin, adhesions form, and then synechiae and bands.

More significant quantities of fibrin are secreted in slowly progressing and less malignant cases of peritonitis. The accumulation of leukocytes in the exudate makes the latter more turbid, turning it into a serous-purulent-fibrinous or purely purulent effusion.

The effusion turns out to be putrid in those cases where there is a communication with the intestinal tract as a source of infection. In such cases, the purulent fluid turns out to be foul-smelling, grayish-dirty or brownish-red in color, and contains gas, due to anaerobic infection or in connection with the presence of an opening in some hollow organ.

In this pus, one often finds fecal stones from a perforated vermiform appendix, gallstones in the case of perforation of the gallbladder, etc. But not only the perforation of a hollow organ can lead to such a putrid peritonitis. The same pathological-anatomical changes can develop even without macroperforation, namely—during the passage of microorganisms (primarily anaerobes) through the gangrenously altered wall of the vermiform appendix, in gangrenous processes of the female genital organs, or during transfers from gangrenous foci of the liver, spleen, or other organs.

Pus can also have a fecal odor due to the seepage of gases through the intestinal walls. The exudate has a hemorrhagic character in cases of initial circulatory disturbance of the abdominal organs in the form of torsion, strangulation, intussusception, thrombosis, and embolism of the mesenteric vessels, as well as in hemorrhagic diatheses. A hemorrhagic effusion is also often found in tuberculous and cancerous peritonitis.

From a practical point of view, the source of infection has a definite significance; thus, peritonitis of appendicular, postpartum, typhoid, etc., origin is often limited, with a somewhat special clinical course. The character of the effusion is of equal importance, allowing the physician to judge macroscopically about the peculiarities of the infection and the course of the process.

For example, streptococcal pus is liquid with an insignificant content of fibrin; pneumococcal, on the contrary, is very rich in fibrin, and in individual cases is purely purulent; in peritonitis with anaerobic infection, a characteristic putrid odor is noted.

The character of the spread and delimitation of the process also has great clinical significance. Far from all diffuse peritonitis cases are general, involving the entire peritoneum. Much also depends on the initial source of infection.

When peritonitis develops in the upper section of the abdominal cavity above the transverse colon in cases of perforated ulcer of the stomach or duodenum, perforation of the gallbladder, etc., the inflammatory process may be delimited by this so-called supraomental section (pars supraomentalis; upper floor of the abdominal cavity according to Zernov) of the abdominal cavity.

In diseases of the vermiform appendix, intestine, and pelvic organs, that part of the peritoneum which is covered by the omentum (pars infra-omentalis; lower floor of the abdominal cavity according to Zernov) is involved in the process. Here, in turn, the mesentery of the intestine can separate the right half from the left.

In those cases where the inflammatory process is not limited to its initial localization and, by virtue of the character of the infection and the state of the organism, is inclined to spread further, the pus in the supraomental form can descend along the colon ascendens through the canalis lateralis dexter and break through into the infraomental part, turning into a general diffuse peritonitis with transition into all peritoneal folds, fissures, and recesses.

Localized forms of peritonitis are most often localized at the initial source of inflammation—in the right iliac region or in the pouch of Douglas in cases of appendicitis, around the gallbladder, stomach, or under the diaphragm. The ability of the peritoneum to quickly form adhesions and synechiae (the so-called plastic property of the peritoneum) was studied as early as 1876 by Wegner. Thus, along with factors contributing to the rapid spread of the inflammatory process, there exist factors of an opposite nature that retard the development and spread of inflammation of the peritoneum. All these facts, obtained initially through experimental means, have been confirmed during autopsies and operations. Nevertheless, one should not transfer the conclusions of the aforementioned experiments entirely to clinical practice and pathology. For example, the plastic capacity of the peritoneum is by no means the same in all patients. In all cases of localized peritonitis, the initial pathological-anatomical changes, the character of the exudate, etc., differ little from those in generalized peritonitis. Subsequently, the purulent process may, under the influence of external factors (trauma) or the liquefying action of pus on the formed adhesions, spread to other areas of the abdominal cavity. Much more often, the formed adhesions turn out to be sufficiently dense, the inflammatory process subsides, the pus changes from liquid to thicker, and eventually is replaced by connective tissue, which can lead to the formation of bands and synechiae. Bacteria persist for a long time at the site of these resolved foci and can, in individual cases (contusion, a fall in the near future), serve as a source for a recurrent flare-up of inflammation, this time of a wider section, and sometimes of the entire peritoneum. Adhesions that have developed in connection with inflammatory processes bind the parietal peritoneum to neighboring organs—the stomach, the intestines. The resulting dense bands can lead to obstruction and strangulation of the intestine. In the presence of extensive adhesions, all organs of the abdominal cavity turn out to be tightly bound together; the omentum and mesentery are thickened and scarred. All such intraperitoneal adhesions mechanically disrupt the function of the intestine (perit. obliterans or deformans). In acute peritonitis, corresponding changes are noted in a number of parenchymatous organs. In the heart muscle, kidneys, and liver, phenomena of cloudy and fatty degeneration are found. Significant changes are also noted in the adrenal glands, expressed in their swelling, as well as depletion of chromaffin substance. Acute peritonitis. Symptomatology of generalized acute peritonitis. Given the diversity of etiological factors of generalized purulent inflammation of the peritoneum, the course of such peritonitis in different cases differs only in the character and intensity of the clinical manifestations of the disease. At the same time, it must be kept in mind that clinical phenomena do not always correspond to those pathological-anatomical changes that are discovered on the peritoneum. For example, cases are often observed where a severe pathological-anatomical picture of the inflammatory process of the peritoneum is accompanied by relatively weakly expressed symptoms of the disease, and vice versa. Here, obviously, the individual characteristics of the patient also have significance. The clinical picture, therefore, allows one to judge only to a certain degree about both the character of the exudate and the degree and form of the inflammation of the peritoneum. But nevertheless, in peritonitis, a number of characteristic general clinical phenomena are observed, allowing one to recognize the presence of inflammation of the peritoneum, the degree of its spread, etc. The general condition of patients with peritonitis is severe. The earliest and most characteristic symptom of peritonitis—intense pain—appears initially in the place where the infection penetrates into the peritoneal cavity; for example, in the case of perforation of a gastric ulcer—in the epigastrium, in the case of peritonitis of appendicular character—in the right iliac region, etc. (Great Medical Encyclopedia, vol. XXIV). Often, the pains are accompanied by collapse, which soon passes. The pains subsequently spread throughout the entire abdomen, and by the moment of the development of generalized peritonitis, they are equally intense in all sections of the abdominal cavity. The slightest touch to the abdomen, the most insignificant movements and shaking of the patient, the peristaltic movements of the intestine still present at the beginning—all this causes the most severe pain. The pain that appeared at the moment of the penetration of infection into the peritoneum causes a reflex contraction of the abdominal muscles, primarily at the site of perforation, and then in the remaining sections of the abdominal wall; in connection with this, the abdominal wall seems dense, and the entire abdomen retracted. With the development of the process, with the appearance of meteorism, the abdomen changes its configuration and becomes distended. At the moment of the penetration of infection into the abdominal cavity, the patient develops a fever, the temperature rises rapidly to 38–38.5°, only to drop somewhat after a short time, and sometimes almost to normal, and subsequently to show rises again. One should be guided by the temperature in peritonitis with maximum caution, since temperature fluctuations in peritonitis often do not reflect those severe changes and disorders that are playing out in the abdominal cavity. Madelung and Krogius recommend measuring the temperature in the axillary region and in the rectum, since the difference in peritonitis is more significant than under ordinary conditions. Characteristic is the expression of the face of patients with peritonitis, on which fear and anxiety are written. Subsequently, the face takes on an even more typical character (the so-called facies hippocratica): the eyes sink in, the cheekbones and nose stand out more sharply and become pointed, the skin of the face and the entire body loses its turgor and is covered with cold sweat. The tongue is dry and coated. The voice is quiet and suppressed; patients avoid and cannot speak loudly; subsequently, the voice weakens even more, becomes increasingly aphonic, and disappears completely. Such an appearance of the patient is observed already in the final stages of peritonitis, and waiting for this state, as many doctors did until relatively recently, is an error from the point of view of therapeutic intervention. The next cardinal symptom of peritonitis is vomiting, observed in almost all cases of acute inflammation of the peritoneum. Only in individual, rare cases of perforation of the stomach or duodenum can it be absent. Already from the very beginning of the disease, in many, upon the appearance of abdominal pain, nausea, eructation, and then vomiting of previously ingested food appear. With unceasing nausea, the patient continues to vomit remnants of food, and then bile. Vomiting movements increase the pain, all the more so because with an empty stomach, patients tense their abdominal muscles more strongly. Ingested liquid is immediately expelled shortly thereafter by vomiting along with bile. In individual cases, vomiting of blood is noted, which is a bad sign. With the spread of the inflammatory process along the peritoneum, the contents of the upper section of the intestine, in connection with the disorder of the work of the sphincters, penetrate into the stomach: fecal vomiting appears, which is distressing for the patient and those around them. In the last stage, the nose and extremities become cyanotic in connection with circulatory disorder and weakening of cardiac activity. The latter, as well as the character of the pulse, deserve special attention. At the moment of the entry of infection and the appearance of severe pain, the pulse immediately becomes frequent and small, only to become fuller after the first severe phenomena and the disappearance of the phenomena of shock, and in other cases to return to the initial state. With the further development of the inflammatory process in the abdominal cavity, the pulse becomes increasingly frequent, its filling gradually falls, and by the moment of a clearly expressed picture of the disease, when the facies hippocratica is already present, it becomes small, barely perceptible. Already from the very beginning of the inflammation of the peritoneum, patients begin to breathe superficially and frequently; the abdominal muscles become tense and no longer participate in the act of breathing. The entire type of breathing becomes exclusively "thoracic," costal. Initially, the abdominal muscles are excluded from the act of breathing reflexively, in connection with severe abdominal pain; subsequently, in connection with paresis of the intestine, general meteorism joins in, further disrupting the act of breathing. Frequent superficial breathing turns into convulsive "clicking" respiratory movements, often observed in the patient's last minutes. The function of the gastrointestinal tract is disordered, there is no appetite, the patients vomit copious dark masses, and in the intervals, the patients complain of intense thirst and incessantly demand drink, which further increases the vomiting. The intestine is paralyzed, strongly distended, there is no stool, gases do not pass, which, among other things, is an early sign of peritonitis. The stool observed at the beginning of the disease in some patients should be attributed to the passage of fecal masses that were in the lower sections of the descending part of the colon before the onset of inflammation of the peritoneum. In individual cases of appendicular and septic peritonitis, diarrhea is noted. A large loss of fluid by the organism leads to a significant decrease in the excretion of urine. In the urine, protein and indican are found. The reaction of the hematopoietic apparatus deserves attention. Already in the initial stages of peritonitis, leukocytosis begins to increase noticeably, reaching significant figures (15,000–20,000) depending on the character and course of the process. At the same time, the white blood cell picture also changes, in which neutrophilia and a decrease in the number of lymphocytes are noted. In severe forms of peritonitis, eosinophils disappear, and a shift to the left (according to Schilling) is noted in the neutrophilic blood. Consciousness continues to remain clear for a relatively long time, almost until the end.

In many patients, following a severe subjective state, euphoria sets in; they stop complaining of pain, lie more quietly, and answer questions by saying that they are recovering, etc. At the same time, the patient does not stop regurgitating copious amounts of dark masses, facial features remain sharp, the pale face and the entire body are covered in cold sweat, the pulse weakens and becomes thready, the lips, nose, and extremities are cold and cyanotic, breathing becomes increasingly shallow, cardiac activity continues to weaken, and often, while the patient remains fully conscious and in an euphoric state, the heart stops beating, and the patient dies. Such is, in general, the typical picture of spreading general peritonitis. It was mentioned above that the intensity and nature of the process give a certain shade to the course of peritonitis, the clinical picture of which differs somewhat in certain details depending on the initial source of infection. For example, septic peritonitis, observed in puerperal diseases and often as a complication after laparotomies, proceeds with phenomena of general intoxication, a picture of septicemia, leaving the inflammatory process in the peritoneum to a certain extent in the shadows. A frequent pulse, decline in cardiac activity, shallow breathing, dry tongue, clouded consciousness—all these phenomena of a septic nature predominate and are always present, whereas pain, vomiting, etc., are expressed significantly more weakly. In perforated peritonitis, associated with the perforation of any hollow organ of the abdominal cavity, the picture of inflammation of the peritoneum predominates, on the contrary: intense pain at the site of perforation or trauma, vomiting, phenomena of severe shock, small pulse, slight chills, tense and retracted abdomen. All these acute phenomena gradually soften after a few hours, especially if morphine is injected into the patient, only to flare up again in connection with the progression of the inflammatory process and present the picture of general diffuse peritonitis. Similarly, in peritonitis of appendicular character, intense pain, rising from the right iliac region and spreading throughout the abdomen, becomes somewhat weaker, although muscle tension in this area does not disappear, and then, with the development and spread of the inflammatory process, the pain flares up again, vomiting repeats, and all other characteristic signs of peritonitis appear. Upon the transition of acute peritonitis into chronic, all symptoms of the disease become noticeably weaker, while examination of the abdominal cavity indicates the accumulation of exudate, pain sensitivity, etc. A similar course is often observed in pneumococcal peritonitis. The general phenomena of peritonitis, sometimes quite stormy, gradually, sometimes relatively quickly, subside if the inflammatory process is demarcated and becomes local. Diagnosis. The above-described severe picture of inflammation of the peritoneum is so typical and characteristic that it is not difficult to diagnose peritonitis when all phenomena are already present. But in this period of the disease, the condition of the patients is so severe, and the process has already spread so much, that there can hardly be any talk of any therapeutic measure. It is much more difficult to recognize peritonitis in the very initial stages of its onset and development. In this regard, it is necessary to emphasize a whole series of symptoms mentioned above, which must be taken into account when recognizing and differentially diagnosing peritonitis. In perforated peritonitis of appendicular, traumatic, or any other character, the patient may present at a moment when the initial acute phenomena have somewhat subsided, the pain has become weaker, the pulse has stabilized, etc., but examination of the abdomen and the entire patient will still provide certain indications of the developing inflammation of the peritoneum. By careful, gentle palpation, it is possible to determine clear muscle tension at the site of the initial appearance of pain. When palpating this area, the patient complains of significant pain, which intensifies at the moment of rapid cessation of palpation—the so-called Blumberg sign, who pointed out that in acute inflammations of the peritoneum, patients experience less pain upon pressure and significantly more at the moment of rapid removal of the palpating fingers. The pulse, although only slightly, is nevertheless somewhat accelerated, and the temperature is elevated by a few tenths. The presence of exudate in the abdominal cavity is also one of the characteristic signs of peritonitis. In the case of demarcation of the process, the exudate accumulates in the place where the infection began and where the peritonitis first began to develop, while with the spread of the process, the exudate accumulates in the lower-lying areas of the abdominal cavity. In the initial acute stages of peritonitis, it is very difficult to determine the presence of exudate by clinical examination. In later periods, when the process is already localized, it is possible to determine the presence of gas in the abdominal cavity by percussion (dull sound) and gentle palpation. Gases accumulating in the upper part of the abdomen are almost impossible to determine, as strongly distended loops of the intestines also rise upward. It is possible to diagnose the escape of air into the free abdominal cavity with the help of X-rays and during laparotomy. In all unclear cases, leukocytosis must be investigated, which begins to gradually increase even in the initial stages. Careful observation of the patient's general condition, accurate registration of the pulse during the first hours, examination per rectum (sensation of pain when pressing with a finger on the bottom of the Douglas pouch), and systematic blood examination every 2 hours allow in a number of cases to diagnose developing acute peritonitis. Meanwhile, the pulse becomes increasingly frequent, gradually rising to 96 or more beats per minute. Repeated, careful measurement of temperature is also of great importance. Anamnesis and careful examination of the patient allow in a number of cases to determine which specific organ is the source of infection. Along with this, there are patients in whom it is impossible to accurately diagnose the cause of peritoneal inflammation without laparotomy. In later stages of peritonitis, when the picture of the disease is generally quite clear, it is also not always easy to determine whether there is general peritonitis or local, and only after some time, when the process is already localized in a specific place in the abdominal cavity, can this question be resolved without difficulty. At the same time, it is necessary to keep in mind that the desire to accurately differentiate local peritonitis from general should not delay the moment of intervention. Peritonitis in the initial stages can be easily confused with a number of other diseases accompanied by acute severe pain, collapse, fainting simulating shock, vomiting, intestinal distension, and other general symptoms. Gallstone colic, kidney stones, acute intestinal obstruction, especially in its upper sections, intraperitoneal hemorrhages (ectopic pregnancy in women, rupture of the spleen), etc., sometimes give an unclear picture of the disease, which at first glance can be mistaken for peritonitis. In all these diseases, just as in acute peritonitis, acute pain comes to the fore, obscuring in a number of cases all other symptoms. (This, by the way, gave reason to designate such acute abdominal pain, accompanied by vomiting, collapse, etc., with the rather unfortunate term "acute abdomen".) In individual cases, incipient pleuropneumonia can, upon the spread of pain along the intercostal nerves, simulate peritoneal phenomena. The outcome of acute peritonitis depends on a whole complex of factors—the degree of spread of the process, the nature of the infection (peritoneal sepsis, pneumococcal or gonorrheal peritonitis), the stage of the disease, and the timeliness of surgical intervention. Preventive measures against acute peritonitis should be directed toward eliminating the possibility of perforation through the timely treatment of gastric and duodenal ulcers, cholecystitis, appendicitis, etc., and the fight against traumatism. At the same time, it should be emphasized that the etiology of a number of diseases (such as appendicitis, etc.) remains insufficiently studied to this day, gastric ulcers can proceed in general latently, and it is extremely difficult to foresee all these moments. Patients often seek help in a severe condition, when phenomena of acute peritonitis are already present, and the infection has a tendency to spread throughout the entire peritoneum. Treatment. In acute peritonitis, it is necessary first of all to put the patient to bed, thereby providing complete rest to the organs of the abdominal cavity and the organism as a whole, and then to eliminate or weaken the pain. The injection of 1 cm³ of 1% morphine noticeably reduces pain and improves the patient's well-being, but can at the same time obscure the picture of the disease. In view of this, it is recommended to inject morphine after the patient has been examined to such an extent that the picture of the disease will not be confused by the temporary improvement of his condition. Cold in the form of an ice pack on the abdomen or heat in the form of warm heating pads is to a certain extent analgesic. Not all patients tolerate cold and heat to the same degree, and therefore one has to reckon with the subjective sensations of the patients. It goes without saying that any laxatives are absolutely contraindicated. All these measures, carried out simultaneously with the examination of the patient, are preliminary, and they must be followed by active treatment.

The main goal of surgical intervention is the elimination of the source of infection, the evacuation of accumulated pus, and the creation of favorable conditions for better drainage of the forming purulent exudate. At present, there is no disagreement that the primary and most important task in the treatment of acute peritonitis must be the elimination of the source from which infection enters the peritoneal cavity: a ruptured gastric ulcer, a typhoid ulcer, a gunshot-perforated intestine, a ruptured urinary bladder, or an intestine must be closed. Real help in all such cases is the earliest possible surgical intervention. In America, the so-called conservative starvation treatment according to Ochsner enjoys a certain amount of attention, consisting of absolute rest, starvation, periodic gastric lavage, cold on the abdomen, and nutrient enemas. According to data from Runyan (1920), the results of such conservative treatment of patients with acute peritonitis 48 hours after the onset of the disease are quite favorable and are accompanied by a low (3%) mortality rate compared to the results of surgical intervention, in which, according to the materials of a number of surgeons, the mortality rate is supposedly equal to 10%. Among German surgeons, Pels-Leusden holds the same point of view and does not operate on patients arriving 48 hours after the onset of the disease. Regarding these conclusions, Kirschner notes that the figures for surgical treatment of acute peritonitis 48 hours after the onset of the disease do not correspond to the cited data, and therefore a doubt naturally arises as to whether one was truly dealing with acute peritonitis in all these cases. Each case of acute peritonitis must be individualized in connection with the source and nature of the infection. Gonorrheal peritonitis in women generally proceeds favorably and can end in recovery even without surgical treatment. A significant majority of the surgeons surveyed by Kirschner (27 out of 36), as well as he himself, believe that diagnosed gonorrheal peritonitis should be treated conservatively; the same applies to pneumococcal peritonitis in children; it is impossible to eliminate the source of infection in this case, especially since microorganisms are present in large quantities in the blood, and here it is more a matter of a general infection with a local focus on the peritoneum (Jensen). Surgical intervention in the early stages of pneumococcal peritonitis is accompanied by high mortality, while with an expectant method, the inflammatory process localizes and can subsequently be operated on, but with a significantly better outcome (Budde, Salzer). Kirschner also considers conservative treatment more appropriate and suggests that in cases where pneumococcal peritonitis is discovered during laparotomy, the abdominal cavity should be closed immediately. Surgical intervention also fails to achieve its goal in metastatic staphylococcal or streptococcal peritonitis. In acute peritonitis of appendicular origin, surgical intervention must be as early as possible and consist of the complete removal of the vermiform appendix, which proved to be the cause of the peritonitis. Only in very severe, neglected cases with extensive adhesions is the operation limited to the evacuation of pus. In peritonitis that has developed due to the perforation of a gastric or duodenal ulcer, the perforation should be closed and, if the patient's strength allows, an anastomosis between the stomach and the jejunum should be performed immediately. Recently, some surgeons (Yudin et al.) have recommended resecting such perforated ulcers, which, in the opinion of other authors, must to a certain extent complicate the surgical intervention (see Peptic ulcer) and is hardly feasible when general peritonitis is already present. The mortality rate for peritonitis in connection with perforated gastric and duodenal ulcers is high and equals 52.4% (Kirschner). Peritonitis from perforated typhoid ulcers must be operated on immediately if the patient is not yet dying. Shock, just as with perforated gastric ulcers, is not a contraindication to surgical intervention: patients under anesthesia recover and tolerate the operation satisfactorily, but the general condition of patients with typhoid fever is generally more severe, and therefore all manipulations must be performed as quickly as possible. In view of this, Escher recommends limiting the operation to suturing the ruptured ulcer into the abdominal wound, through which the intestinal contents will be discharged. In severe cases, this proposal deserves attention. The mortality rate is very high, from 40% to 75% (Krylov, Gasin). Peritonitis from ulcerative and traumatic perforations of the intestine still results in a high mortality rate despite surgical intervention—72% (Körte) and 74% (Kirschner). Repeat surgical intervention for postoperative peritonitis, mostly of a septic nature, which generally proceeds very severely, rarely leads to the goal. Only isolated cases of favorable outcomes are known after repeat laparotomies with aspiration of exudate, tamponade, and other measures. (The 'peritoneal irritation' observed after operations in the abdominal cavity is cured by appropriate therapeutic methods—gastric lavage, stimulation of intestinal peristalsis, and heat on the abdomen.) The evacuation of pus and, in general, the toilet of the peritoneum are of no less importance than the elimination of the source of infection. Purulent peritonitis must be treated in the same way as it is currently accepted to treat all acute abscesses, i.e., by opening the cavity filled with pus and evacuating the latter. The multitude of folds and pockets of the peritoneal sac and the vastness of the abdominal cavity make it impossible, with ordinary laparotomy incisions, not only to completely but even to sufficiently evacuate all the pus. Excessive eventration of the intestine is not indifferent to the patient and can lead to severe, fatal shock. In view of this, some surgeons (Anschütz, Braun, Schmieden, and many others) irrigate the abdominal cavity with significant amounts of physiological saline, while others (Garré, Clairmont, and others) prefer to wipe the peritoneum with gauze sponges or limit themselves only to an incision. Finally, a significant portion of surgeons individualize each separate case, sometimes irrigating, sometimes wiping, depending on the pathological-anatomical changes and features that are discovered at the moment of the operation. The latter point of view should be considered correct, as one or the other method has its positive and negative sides. It should be kept in mind that during irrigation, the stream of fluid can enter a section of the peritoneum that is not yet involved in the inflammatory process, but wiping with a gauze sponge irritates the peritoneal lining significantly more than irrigation. In any case, in general diffuse peritonitis, when all the fossae and pockets are filled with pus, it is better to irrigate, and in more limited cases, to wipe with sponges. Suction is very convenient, with the help of which it is possible to aspirate a significant amount of pus. In any case, the rule should be as follows: all food masses or intestinal contents that have entered the abdominal cavity during perforations of the stomach or intestines must be carefully removed, because, if they get stuck somewhere in the abdominal cavity, they can serve as a source of further infection. The removal of fibrinous films is pointless, as it yields nothing but trauma and tissue damage. Simultaneously with the evacuation of the purulent effusion, measures were undertaken to disinfect the peritoneum, as well as to delay the absorption of toxins from it. The injection of sterile Provence oil (Glimm, Borchard) or a 1% solution of camphor oil (Hirschel) into the abdominal cavity did not prove successful (Höhne, Pikin). Kuhn proposed injecting a 50-80% sugar solution into the abdominal cavity, which, in his opinion, should—similarly to hypertonic solutions in the treatment of infected wounds—induce transudation from the peritoneum and thereby protect against subsequent adhesions. Brutt speaks more or less favorably about this method, although in general, Kuhn's assumption did not prove successful (Kirschner). Morestin's suggestion to inject 60.0-100.0 of ether into the abdominal cavity during operations for acute peritonitis was met with a certain amount of attention from some surgeons, and many even began to far exceed the initially proposed dose, injecting patients with up to 100.0-500.0 of ether. These doses are very large and are essentially lethal. If patients do not die immediately from ether poisoning, it is only because the greater part of the ether evaporates immediately, without producing any significant effect. Schönbauer's proposal to inject hydrochloric acid pepsin into the abdominal cavity was based on the observation that with such gastric ulcers, peritonitis proceeds generally favorably, which, in his opinion, should be linked to the bactericidal property of hydrochloric acid, which is present in increased quantities in the stomach. The mortality rate for 109 perforated peritonitis cases at the Eiselsberg clinic using this method fell to 12.7%. In Kirschner's opinion, in perforated gastric ulcers, it is not so much the bactericidal action of hydrochloric acid that plays a role, but rather the fact that the acidic masses spilled from the stomach are, from the very beginning, more or less poor in microorganisms. All agents aimed at eliminating future adhesions and synechiae, in the form of oil injections or human fat (Humanol), did not lead to the goal. The process of adhesion formation is obviously connected, as was already indicated above, with the individual characteristics of each patient.

For further evacuation of pus in the postoperative period, surgeons for a long time (and many still do today) used copious tamponade (according to Mikulicz), and then began to insert drains into the abdominal cavity both through the laparotomy incision and through additional incisions in the abdominal wall. Rehn spoke out against such extensive drainage of the abdominal cavity, as in his opinion this must affect the restoration of intra-abdominal pressure, which is of great importance for the entire organism. He sutured the abdominal cavity tightly, leaving only a drain passed outward through the pouch of Douglas. At present, it can be asserted that neither tamponade nor drainage in ordinary peritonitis provides the expected effect: adhesions form rapidly around the tampons, and the inserted tubes—rubber or glass—do not drain the entire abdominal cavity, where adhesions and synechiae also form rapidly. Only in cases of localized, limited abscesses in the abdominal cavity is it possible to insert a drain or tampon through which pus will subsequently be discharged. A significant portion of surgeons prefers, after closing the source of infection and evacuating the purulent effusion as much as possible, to suture the abdominal cavity tightly in a number of cases. The outcomes of surgical intervention have not become worse from this and even seem, on the contrary, to have improved somewhat. The question of drainage or tight suturing is decided in each individual case depending on the degree of spread and the nature of the peritonitis, but still, the general correct guideline is the following position of Kirschner: 1. If surgical intervention succeeds in completely eliminating the source of infection and at the same time there is certainty that all factors for secondary infection are absent, the abdominal cavity can be sutured tightly even in severe infections; in such cases, the skin may not be sutured or the edges may be joined with one or two stitches. 2. If a possible source of primary or secondary infection or suppuration still remains in the abdominal cavity, be it necrotic tissues, extensive granulations, hematomas, insufficiently securely sutured hollow organs, etc., the abdominal cavity, or rather these areas, should be drained. According to the data of the same author, mortality with tight suturing and drainage is almost the same, but during recovery, the postoperative course in the former is significantly easier and shorter than in the latter. Lymphaticostomy (opening of the thoracic duct on the left side of the neck) for the purpose of diverting bacteria and their toxins absorbed from the abdominal cavity to the outside (Costain) is both theoretically unfounded and practically ineffective. The operation itself is only one of the stages of therapeutic intervention; a further measure is postoperative care, which after operations for acute peritonitis must be especially thorough. The general condition of the patient continues to remain severe in connection with postoperative shock. It is necessary to monitor the pulse and cardiac activity (camphor, caffeine, digalen subcutaneously); in case of restlessness and severe pain, 1 cm³ of 2% pantopon or 1% morphine is injected. Patients calm down and fall asleep, which best preserves their strength. By repeated subcutaneous infusions of physiological saline, one strives to compensate for the loss of fluid by the organism. Slow intravenous infusions of physiological saline over 25–30 minutes with 6–8 drops of adrenaline per 1 liter of fluid (Heidenhain) have a favorable effect on the cardiovascular apparatus. Drip infusions per rectum or intravenous drip infusions according to Friedländer are also appropriate. Such infusions can be repeated 1–2 times a day. To avoid shock and acidosis, Orator and Berezov recommend administering grape sugar with insulin intravenously. A valuable remedy is blood transfusion. Regarding the patient's position, at one time it was considered almost a rule to place the patient in bed in a semi-sitting position so that the effusion accumulating in the abdominal cavity would drain into the lowest located place, i.e., the pelvis, where a drain was inserted. Such a position of the patient in the postoperative period is called the Fowler position, named after the American surgeon who allegedly first reported this in 1904. German surgeons call this position the Rehn position (the latter reported on this in 1902), or the Fowler-Rehn position. For better outflow of venous blood from the lower extremities, Lennander advises placing patients in bed with the foot end elevated. It is best to place a severely ill patient after the operation so that they feel as comfortable and calm as possible, i.e., on their back with the head slightly raised and resting on a pillow, and a soft pillow is placed under the slightly bent knees. The patient is turned from side to side from time to time, and then, as soon as their condition becomes somewhat better, they are allowed to do this independently. Any movement of the limbs in a bedridden patient improves blood circulation. The patient is forced to breathe deeply despite the fact that initially deep breaths cause pain in the wound; the pain can be eliminated with pantopon. The respiratory apparatus must be given attention, all the more so because postoperative pneumonia is observed not infrequently in peritonitis. In peritonitis, thrombophlebitis of the femoral vein is sometimes observed, predominantly in the left leg. Septic thrombophlebitis in the portal vein, leading to the formation of an abscess in the liver, is also known. Pulmonary embolisms are observed very rarely in peritonitis, significantly less often than in aseptic laparotomies. It is hardly possible in such cases to speak of early mobilization as a method of combating thrombosis and embolism (postoperative parotitis, to which Seifert is inclined to attribute a stomatogenic character, is described relatively rarely in acute peritonitis). The state of the intestines deserves special attention in the postoperative period. Diarrhea, which is sometimes observed in pneumococcal, puerperal, and very rarely in other forms of peritonitis, is a bad sign. Already during the operation, especially in the later stages of the disease, it is not possible to replace the distended small intestines into the abdominal cavity without emptying them of gases and liquid contents by means of a corresponding puncture. In the earlier stages of peritonitis, one can manage without this. In the postoperative period, it is necessary to take measures to stimulate intestinal peristalsis as quickly as possible. Laxatives are of little use, especially since the patients are already nauseated. Enemas of warm water, oil, glycerin suppositories, etc., facilitate the passage of gas and the emptying of the large intestines, which noticeably improves the patients' well-being. Heating pads on the abdomen, subcutaneous administration of physostigmine, pituitrin two or three times at 1 cm³ per hour, Hypophysin, and other agents do not always lead to the goal. In cases where intestinal peristalsis cannot be induced, some surgeons suggest emptying it by puncture or by creating an intestinal fistula. When the intestine is punctured, gas is released, as a result of which the distended intestine collapses somewhat and the patient's well-being improves. This measure is permissible only in cases where the abdominal cavity is not sutured tightly and an intestinal loop is visible in the wound. The possibility of wound contamination and the short-lived nature of the effect limit the use of this technique. Significantly better results are obtained by creating an intestinal fistula, through which gases and intestinal contents are constantly emptied via a rubber tube. Heidenhain, Körte, Krogius, Spasokukotsky, and a number of other Russian surgeons use such a method of intestinal evacuation in the postoperative period. An emptying fistula should be placed if possible in the lower sections of the intestine, as one placed in the upper sections leads to rapid exhaustion of the patient's strength. Besides paralytic intestinal obstruction, there is also the possibility of intestinal blockage of mechanical origin, associated with extensive adhesions of intestinal loops to each other, which is often noted after the insertion of extensive tampons. In such cases, only a repeat laparotomy can eliminate the intestinal obstruction. Suppuration of the skin and subcutaneous tissue, often observed after operations for purulent peritonitis, must be recognized in time, the sutures removed, and the wound tamponed. Prophylactically, it is advisable to suture the skin only in places, with 2–3 stitches, or not to suture it at all. Recently, German surgeons and even more so French surgeons, simultaneously with surgical intervention, have been administering an appropriate serum aimed at eliminating the development of gas infection, the possibility of which always exists in connection with the presence of anaerobes in peritonitis of intestinal origin. This proposal undoubtedly deserves attention in our Union as well, in connection with the development of appropriate serums against gas phlegmons (Velikanov). The administration of such a serum during the operation of severe cases of peritonitis will possibly find its application. The outcome of the operation depends on the source of infection, on the time that has elapsed between the onset of the disease and the surgical intervention, on the virulence of the microorganisms, and finally on the state of the entire organism as a whole—an exhausted, weakened, or elderly patient tolerates the operation significantly worse. Mortality after surgical treatment of acute peritonitis still remains high—47.7% (Kirschner).

This figure was obtained from collected material of 11,000 cases that passed through a number of clinical and hospital institutions in Germany over the last 25 years. The curves compiled by the same author clearly demonstrate that mortality for all types of peritonitis is gradually falling, reaching its lowest figures in the last period (1920–24). There is reason to assert that for peritonitis of appendicular, perforative, etc., nature, the results of surgical treatment will continue to improve. A decisive role in this is played primarily by the fact that peritonitis began to be recognized earlier, and patients began to be referred for surgical help earlier. By this, i.e., by providing surgical help to patients in the early stages of the development of peritonitis in the first place, and by improving technique in the second, it was possible to reduce the mortality rate for appendicular peritonitis, for example, from 83.3% to 20.8%, for perforations of the stomach and duodeni from 100% to 42.2%, etc.

As for children, the younger they are, the worse peritonitis proceeds in them, and therefore Kirschner advocates that they should also be operated on as early as possible. Nehrkorn holds a completely different opinion, believing that surgical treatment of acute peritonitis in children yields worse results than conservative treatment, especially since pneumococcal peritonitis is encountered most often in children.

Symptomatology of acute circumscribed peritonitis. Circumscribed peritonitis can, just like general peritonitis, arise from any organ located in the abdominal cavity or in its vicinity. It was mentioned above that due to the plastic capacity of the peritoneum, adhesions and synechiae can form around the focus of inflammation between loops of the intestine, the omentum, the parietal peritoneum, as well as other organs located near the source of inflammation; thus, the inflammatory process is circumscribed and does not spread to the rest of the peritoneum. The effusion at the site of circumscribed peritonitis can be diverse—serous, fibrinous, purulent, and putrid—depending on the infection and the time of onset of the disease. Circumscribed peritonitis can reach significant sizes, but at the moment when the adhesions or synechiae rupture, pus penetrates into the rest of the abdominal cavity, and the inflammatory process spreads to the entire remaining peritoneum.

The clinical course of circumscribed peritonitis is significantly milder than that of general peritonitis. The initial symptoms are pain throughout the abdomen, vomiting, and intestinal distension. Pain can be very intense from the very beginning, depending on the proximity of the source of infection to the parietal peritoneum. But very soon it becomes clear that the intestinal distension is moderate and is limited more to the painful area. Despite the pain and recurring vomiting, the patient looks satisfactory: there is none of that anxiety of facial expression, that pallor, or cyanotic lips that are characteristic of general peritonitis; the patient breathes calmly, and consciousness is clear.

The pulse may be normal or slightly accelerated, of good filling. As with general peritonitis, one should carefully monitor the pulse, since the state of the cardiovascular system is also the best indicator here of the character and degree of spread of the infection. Temperature fluctuations are of less importance, since it is known that in circumscribed processes in the abdominal cavity, the temperature may remain without particular changes. A high temperature of a remittent type indicates a suppurative process. Upon palpation of the abdominal walls, tenderness, the Blumberg sign, and muscle tension are noted only at the site of inflammation; in the rest of the abdomen, the muscles are free and painless upon palpation. Percussion yields a dull sound at this same site. At the site of the effusion, if it has already reached certain dimensions and is easily palpable, it is sometimes possible to note fluctuation, indicating the presence of liquid pus.

In cases of circumscribed peritonitis developing in the lower part of the abdominal cavity, examination per rectum causes pain upon lifting the floor of the Douglas pouch. In women, incidentally, examination per rectum or per vaginam makes it possible to establish where the process originates—from the genital organs or from the intestine. Thus, for example, in cases of circumscribed appendicular peritonitis, the patient experiences severe pain upon lifting the floor of the Douglas pouch, while in an inflammatory process occurring around the genital apparatus, the pain is more intense upon lifting the uterus (I. Promptov).

As for the blood picture, there is leukocytosis. Its further increase indicates a suppurative process.

Circumscribed peritonitis proceeds in different ways. Serous and fibrinous exudates, even those that have reached significant sizes, can gradually be resorbed. Small abscesses also resorb, at the site of which yellowish dense masses, which are already sterile, are found between adhesions for a long time, but this does not always happen; much depends on the primary disease, the quantity and virulence of the bacteria, the size of the abscess, and the state of the entire organism. An abscess can, conversely, gradually increase and reach such dimensions that it will involve almost the entire right iliac region, the Douglas pouch, the pelvis, the subdiaphragmatic space, and other places in the abdominal cavity, while still remaining circumscribed and not spreading to the entire remaining peritoneum. Pus can rupture into one of the loops of the intestine, into the urinary bladder, the rectum, the vagina, occasionally through the abdominal walls, and into the retroperitoneal space (the latter is a serious complication, as the inflammatory process can spread along the retroperitoneal tissue to neighboring organs and lead to severe phlegmons). Finally, pus can penetrate into the mesenteric veins and lead to the formation of multiple abscesses in the liver.

Diagnosis. The anamnesis and clinical picture allow for the diagnosis of a local inflammatory process in a number of cases. It can sometimes prove difficult to differentiate the source of inflammation, especially in the initial stages of the disease, when the patient is unable to accurately characterize the pain and the place of its origin, and when the picture of the disease is obscured by phenomena of irritation of the entire peritoneum. Cases are known where a laparotomy was performed on the right in the iliac region, but the patient turned out to have an inflammatory process in connection with the perforation of a gastric or duodeni ulcer, and vice versa. In later stages of the disease, when an effusion accessible to examination has already formed, the differential diagnosis becomes easier. In the early stages of the disease, the differential diagnosis between acute peritonitis in the lower abdomen (in connection with appendicitis, for example) and ectopic pregnancy in women is of great importance. A thorough anamnesis, the general condition of the patient (pallor, pulse, respiration, temperature, etc.), local examination, and the increase and character of leukocytosis allow for a correct diagnosis.

Treatment. Circumscribed local peritonitis requires strict individualization. Gonorrheal and pneumococcal peritonitis are treated, as already mentioned, with conservative measures; they often resorb or turn into a local abscess (pneumococcal), which must subsequently be opened. Local peritonitis of other origins is treated depending on the source and stage of the inflammatory process. Existing circumscribed infiltrates, which become apparent approximately by the beginning of the 3rd day, can be treated with general therapeutic measures: bed rest, in the first days an ice pack on the painful area; the diet should be prescribed as predominantly liquid, avoiding dense food rich in fiber. It is necessary to monitor the function of the intestine; subsequently, when the temperature, pulse, and leukocytosis stabilize, a warming compress or a moderately warm pack is applied to the painful area of the abdomen. All these general instructions must be individualized, observing the patient all the time.

If the infiltrate changes from dense to soft and increases in size with simultaneous significant fluctuations in temperature, the question arises of draining the pus from the formed cavity. Surgical intervention consists only of opening the abscess through the abdominal walls, or per rectum in the case of an abscess of the Douglas pouch, and abundant loose tamponade or drainage. It is better not to touch the organ that served as the source of the inflammation of the peritoneum, because, in striving to isolate it, one simultaneously destroys synechiae and adhesions, which can turn local peritonitis into general peritonitis.

A completely different approach is taken in the initial stages of peritonitis, i.e., in the first 24-48 hours from the moment of the disease. The clinical picture in the first 24 hours does not allow one to be absolutely certain that the inflammatory process will be circumscribed and will not turn into general diffuse peritonitis. In view of this, at the present time, every case of even apparently acute, circumscribed peritonitis of appendicular origin is preferred to be operated on in the early stages of the disease, in the first 2 days. The operation consists of removing the vermiform appendix, suturing the perforated ulcer of the stomach or intestine, etc.; this is followed by emptying the exudate and, if possible, a tight suture of the abdominal cavity (see above—treatment of general peritonitis).

The results of such surgical treatment are quite favorable; mortality is falling significantly, dropping lower and lower depending on the timeliness of the intervention.

As for appendicitis in children, early operation is possible only in the first 24 hours.

After this, it is better not to operate and to treat such patients conservatively (Nehrkorn). Regarding limited inflammation around the gallbladder, the opinions of surgeons differ. Recently, Anschütz, Stich, and others have taken the same position regarding acute inflammations of the gallbladder as they have regarding appendicitis, but not all surgeons agree with this. The anatomical relationships here are such that dense adhesions almost constantly form at this site, walling off the process, which can be managed conservatively; subsequently, when the infiltrate resolves, the question may arise of the operative removal of the source of a possible recurrence of peritonitis, i.e., an operation on the biliary tract. Only in those cases where the inflammatory process spreads from a ruptured purulent cholecystitis to the entire peritoneum should the patient be operated on as early as possible. Subdiaphragmatic abscesses proceed with a specific clinical picture and are recognized and treated accordingly (see Subdiaphragmatic abscess). Chronic peritonitis can be primary and secondary. Primary chronic peritonitis arises in the presence of a chronically acting infectious agent. Chronic peritonitis of a secondary nature develops upon the subsidence of an acute process and its gradual transition into a chronic form, which is most often observed in pneumococcal peritonitis. Periodic formation of effusions, traumatic injuries, chemical irritations, etc., can be a factor maintaining chronic inflammation of the peritoneum. Constant pressure on certain areas of the abdominal wall often causes chronic inflammation of the peritoneum corresponding to this area. In individuals suffering for a long time from the descent of viscera into a hernial sac, cicatricial thickenings are found on the omentum, mesentery, and other organs that have descended, in connection with constant injuries when attempting to reduce these organs into the abdominal cavity. At the site of repeated abdominal punctures for ascites, thickenings and cicatricial changes also form. Chronic peritonitis is observed in the form of exudative, similar to ascites, and adhesive, hyperplastic inflammations of the peritoneum. Exudative peritonitis is observed for the most part in young age and more often in women. The accumulation of serous fluid in the abdominal cavity occurs slowly, without any peritoneal phenomena. The clinical picture of these peritonitis cases very much resembles tuberculous inflammation of the peritoneum, especially when tumor-like formations are palpated in the abdominal cavity. Nevertheless, pathological-anatomical data allow one to reject the presence of a tuberculous infection. Trauma, severe chilling, and possibly some other, as yet unstudied causes are etiological moments of such chronic peritonitis. The accumulation of serous fluid in the abdominal cavity, along with its presence in the pleura and pericardium, is also observed in polyserositis. Significantly more often, adhesive peritonitis is observed, accompanied by the formation of extensive adhesions and dense cicatricial bands. Virchow already in 1853 drew attention to the practical significance that these limited areas of chronic inflammation of the peritoneum have, giving rise to extensive adhesions. Further pathological-anatomical observations on the cadaver and on the living during surgery indicated the diversity of these adhesions, localizing in various sections of the abdominal cavity and connected most often with those organs to which they are closest (see Perigastritis, Periduodenitis). Most often, such a form of chronic peritonitis is observed around the vermiform appendix, where chronic inflammation is constantly maintained by periodic attacks of appendicitis. Thanks to extensive adhesions with the formation of bands and bridges and the omentum, which is soldered and altered almost into the form of a tumor, the entire section of the abdominal cavity represents as if a solid mass. Such a form of chronic peritonitis is designated as fibroplastic peritonitis (peritonitis fibroplastica). All these changes can spread upward along the ascending part of the colon and simulate a tumor or tuberculoma (Bergmann, H. Braun, Körte, and others), especially in latent forms of appendicitis. Of the rarer forms of chronic peritonitis, one should point out peritonitis follicularis (Hauser), in which the peritoneum in the lower section of the abdominal cavity turns out to be studded with lymphatic nodules, similar to tuberculous ones. In peritonitis arenosa, on the peritoneum, besides traces of an old inflammation, one finds a series of multiple small flat elevations, in which, upon microscopic examination in old fibrous accumulations, there is noted a proliferation of endothelial cells of the lymphatic network of the serous membrane with the formation of hyaline more or less calcified layered bodies (Virchow, Borst, Gierke). Peritonitis can develop in the fetus even in the intrauterine period of its growth (peritonitis foetalis). The contents of the intestine and urinary tract remain sterile in the fetus, so that a rupture of the intestine or bladder in this period is accompanied only by mechanical and chemical irritation of the peritoneum. The cause of the rupture of the intestine is most likely atresia of the underlying section or overfilling of Meckel's diverticulum. These children are usually born dead or perish in the first days in connection with a defect in the development of the intestine or from an added bacterial peritonitis. The decisive moment for determining fetal peritonitis is, besides extensive adhesions and synechiae, which could be connected with embryonic underdevelopment, also the finding of clumps of meconium between the loops of the intestines. The clinical picture of chronic exudative peritonitis develops slowly. Patients are not in a condition to accurately indicate the beginning of the disease. Without any peritoneal phenomena, fluid begins to appear in the abdominal cavity, the quantity of which gradually increases and can reach significant dimensions. Temperature fluctuations are very insignificant and are observed rarely. Patients gradually lose weight, weaken, and feel generally unwell. The presence of fluid, tumors, and the clinical course allow one to make a diagnosis of chronic peritonitis, which is very difficult to differentiate from tuberculous peritonitis. Inoculation of the exudate into the abdominal cavity of a guinea pig decides the question of tuberculosis. Furthermore, one has to differentiate with ascites in cirrhosis of the liver, with congestive ascites, and cancerous peritonitis (see below). The prognosis is favorable, since with appropriate therapeutic measures, patients recover. Treatment is generally symptomatic. With the accumulation of a significant quantity of exudate in the abdominal cavity, one has to perform repeated punctures and drain the fluid. To improve the general condition, reinforced nutrition and appropriate medications are prescribed. Often, chronic serous peritonitis is confused with tuberculous, and such patients are operated on, limiting oneself to only a laparotomy. After such celiotomies, patients improve and often recover faster. The symptomatology of chronic adhesive and sclerosing peritonitis is not clearly enough expressed, all the more so because initially the disease proceeds secretly and unnoticeably. In later stages, when adhesions and scars of the peritoneum affect the emptying of hollow organs, on their function, the picture of the disease becomes clearer. Old processes in the pelvis of women with the formation of adhesions, synechiae, and scars change the position of the uterus, often causing great suffering. All these chronically proceeding peritonitis cases reflect on the general condition of the patients, noticeably lowering their working capacity. In individual cases, the course of the disease takes an acute form: around a band, scar, or adhesion, a kinking of a loop forms and acute intestinal obstruction develops, requiring emergency intervention. The diagnosis of chronic adhesive peritonitis is difficult. If, in the presence of corresponding complaints after a laparotomy, one thinks more often of postoperative adhesions, then in the presence of fibrous and adhesive peritonitis, the latter are often not recognized. The difficulties consist also in the fact that the clinical picture rarely corresponds to the existing pathological-anatomical relationships. At autopsies, one sometimes finds extensive adhesions and synechiae, which during life did not cause almost any suffering, and conversely, relatively small changes in a certain area are accompanied by a severe clinical picture, forcing one to resort to surgical treatment. X-ray examination does not give a full picture of the existing changes. The recently proposed pneumoperitoneum allows in a number of cases to orient oneself regarding adhesions and bands, but not always. Sauerbruch speaks out against pneumoperitoneum, considering it unsafe. As for the treatment of chronic adhesive peritonitis, in those cases where patients, due to severe pain, avoid eating, gradually fall in weight, and in connection with this fall into a severe psychic state, one has to resort to the operative separation of such adhesions. Unfortunately, there are no guarantees that in the place of the separated adhesions, synechiae will not appear again and all symptoms of the disease will not resume. The proposal to separate such adhesions not with a knife, but with Payr-Pregl solution to avoid recurrences (Oschmann) has not justified itself. The proposal of Kümmell to use humanol did not achieve the goal: the adhesions appeared again. The situation is even more complicated with fibroplastic peritonitis, in which surgical intervention always presents great technical difficulties.

In any case, during operations for adhesive or fibrous peritonitis, it is necessary to remove the visible source of the inflammatory process. Most often, chronic inflammation is localized around the vermiform appendix, which, despite technical difficulties, must be removed. In individual cases, when there are kinks in the intestine due to extensive adhesions, the question may arise of creating an anastomosis between the corresponding loops of the intestines (Raug). Indications for surgical treatment in chronic adhesive and fibrous peritonitis should still be considered relative, except in cases where there are vital indications. In all other cases, therapeutic treatment, primarily of a symptomatic nature (elimination of pain, constipation, etc.), and physiotherapeutic measures improve the general condition of patients and restore their ability to work. Tuberculous peritonitis as a primary disease is encountered very rarely. For the most part, it develops secondarily and usually proceeds slowly. According to pathological-anatomical autopsy data, tuberculous peritonitis is found in nearly 3-5% of all cadavers. According to the same data, this disease is encountered equally often in men and women, although according to clinical material, tuberculous peritonitis is encountered somewhat more frequently in women, and in a significant portion of them, this process is associated with tuberculous inflammation of the genital apparatus. The organs that are primarily diseased and serve as foci of infection are the lungs, pleura, intestine, mesenteric and retroperitoneal lymph glands, neighboring tuberculous foci in the bones and joints (tuberculous coxitis), etc. The macroscopic picture of tuberculous peritonitis depends on the nature of the infection, the stage, and the duration of the process. For the most part, the peritoneum appears pale and dotted with miliary tubercles, or reddish spots of greater or lesser size are noted on the serous membrane [see separate table (Vol. IV, pp. 143-144), Fig. 2], up to the appearance of bloody ones. The exudate is often bloody, but for the most part, it is serous, serofibrinous, rarely seropurulent, and even more rarely purely purulent. Mononuclear elements, mainly lymphocytes, predominate in the exudate; it is often possible to detect tubercle bacilli only with great difficulty and only by inoculation into animals. In general, the following forms of tuberculous peritonitis are distinguished: 1) an exudative form with the formation of a significant amount of serous fluid; 2) the so-called dry form with the formation of extensive adhesions between the loops of the intestine [see separate table (Vol. IV, pp. 143-144), Fig. 3], adhesions of the omentum, with the formation of tumor-like tubercles and foci of caseous necrosis; 3) the so-called ulcerative-purulent form also with multiple adhesions, between which are located purulent and caseous foci of necrosis. Combinations between these forms of tuberculous peritonitis are possible. Thus, for example, along with extensive adhesions of individual loops of the intestine, there may be an effusion enclosed between these adhesions in the form of separate cysts filled with serous fluid, and in some cases, pus. Fibrinous deposits in the form of cloudy granularity up to cicatricial layers on various sections of the peritoneum lead to the formation of adhesions and synechiae between the loops of the intestines, as well as the intestines with the parietal peritoneum. These synechiae are essentially granulation tissue, in which there are, for the most part, caseously altered tubercles. Subsequently, this granulation tissue turns into dense connective tissue, encompassing a significant area of the abdominal cavity, and contributes to the dense adhesion of the intestine with neighboring organs and the parietal peritoneum. The mesentery can become so scarred, so thickened and shortened (mesenteriitis retrahens), that the intestine appears as if pulled to its root. In a number of cases, one can only be surprised at how such extensive dense synechiae and adhesions manifested themselves relatively little clinically. Symptoms. The patients' complaints boil down primarily to an increase in the volume of the abdomen and periodically recurring pains in it, which, however, do not reach the intensity as in acute peritonitis. As fluid accumulates in the abdominal cavity, patients begin to get short of breath when walking and complain of palpitations. At times, the temperature rises, although this may not happen. The general condition continues to worsen; patients become pale, lose weight, and often look cachectic. Vomiting is rarely observed. A disorder of intestinal activity is often noted due to cicatricial changes in the mesentery, extensive adhesions and synechiae, the formation of a stricture in the intestinal tube itself, etc. In the latter case, the pain can become very intense and constant. The fluid present in the abdominal cavity may turn out to be, as it were, encapsulated in separate closed cavities, simulating fluctuating tumors. The scarred omentum or enlarged mesenteric glands are often mistaken for nodular tumors. Diagnosis. All the described symptoms allow in some cases for the diagnosis of tuberculous peritonitis; the diagnosis becomes even more probable if a tuberculous process is simultaneously detected in the lungs or any other organ. Tuberculous peritonitis is difficult to distinguish from chronic serous [peritonitis]; the Pirquet reaction and the injection of exudate into a guinea pig contribute to clarifying the issue. The differential diagnosis between tuberculous and carcinomatous peritonitis is not always easy even at autopsy, but in the end, it is resolved by finding the primary malignant tumor. In ascites of a cirrhotic nature, the history, jaundice, and a noticeably enlarged spleen, which is very rarely palpable in tuberculous peritonitis, are typical. Treatment. As early as 1862, Spencer Wells performed a laparotomy for tuberculous peritonitis based on an erroneous diagnosis, which ended in recovery. Purely therapeutic treatment yielded poor results at that time, and therefore, at the end of the 19th and the beginning of the 20th century, following the suggestion of König, expressed as early as 1889, they began to operate widely for tuberculous peritonitis. The immediate results proved satisfactory in serous forms, somewhat worse in dry forms, and quite poor in caseous-ulcerative necrosis. An analysis of long-term results gave reason to take a critical attitude toward surgical intervention in tuberculous peritonitis, especially since modern methods of treating tuberculosis (improvement of living conditions, sanatorium-resort treatment, physiotherapeutic measures—X-ray, mountain sun) yield quite satisfactory results. Only in persistent cases of serous forms, when all these measures do not lead to the goal, should one proceed to surgical treatment. Repeated punctures of the abdominal wall and the release of fluid do not lead to the goal. Indicated is an operation consisting of only a laparotomy, which results in hyperemia of the serous membrane, acting as if analogous to the Bier congestion method and thereby exerting a beneficial influence on the course of the process (Hildebrand) (this explanation of the beneficial effect of laparotomy in tuberculous peritonitis is, however, not accepted by all surgeons). Contraindicated is any surgical intervention in advanced forms of tuberculosis of the lungs, intestine, or kidneys, in which a simple laparotomy, performed even under local anesthesia, can lead to a fatal outcome. The immediate results of the operation are generally seemingly favorable, but upon checking the long-term results, it turns out that many patients die due to a relapse or a tuberculous process in some other organ (Körte). Syphilitic peritonitis is characterized by the presence of gummatous formations on the peritoneum along with syphilitic lesions of other organs, although cases of isolated lues of the parietal peritoneum are known (Pick). Perforation of syphilitic ulcers of the intestine or rupture of the intestine stretched over a luetic stricture is accompanied by ordinary, nonspecific inflammation of the peritoneum. In congenital syphilis, inflammatory phenomena on the peritoneum, characterized by the deposition of fibrin, are found in stillborn children or children who have lived for some time around the enlarged spleen, liver, and in other areas of the abdominal cavity. It has not been possible to find spirochetes in these inflamed areas of the peritoneum and fibrin. Actinomycosis of the peritoneum is observed with the simultaneous disease of other organs of the abdominal cavity. The source of the spread of actinomycosis to the peritoneum is most often the intestine (cecum, vermiform appendix) and other organs of the abdominal cavity, as well as the spread of the process from the abdominal wall or female genital organs. Pathologically-anatomically, extensive dense adhesions, the formation of callous cords with separate accumulations of pus are noted. Characteristic is the formation of necrotic channels passing through this entire inflamed mass and connecting separate encapsulated abscesses, in which there are separate small grains, which turn out to be actinomycotic drusen upon microscopic examination. The clinical course of actinomycosis of the peritoneum is not very characteristic. Symptoms are concentrated for the most part around the organ that is the source of the spread of infection along the peritoneum. Periodically appearing pains are attributed to some organ of the abdominal cavity until a dense tumor appears in the abdominal integuments, which eventually ulcerates and discharges characteristic pus.

The disease can drag on for a very long time with apparent periodic improvements and even recoveries; but after some time, induration and suppuration reappear, and the condition of the patients deteriorates sharply. Treatment is the usual one for actinomycosis (see). Surgical treatment is only auxiliary—removal of the tumor, evacuation of pus, etc., but even those cases which ended in recovery (15-20% according to S. Brünner for abdominal actinomycosis) must still be attributed to therapeutic measures. Cancerous peritonitis as a primary disease is observed rarely. More often, cancer spreads to the peritoneum from other affected organs (stomach, intestine, ovary, etc.) and disseminates along the serous membrane in the form of small plaques and nodules, sometimes simulating tuberculous peritonitis. The tumor in the omentum and mesentery has the appearance of larger nodes. Among primary tumors of the peritoneum, gelatinous cancer, endotheliomas, and plexiform angiosarcoma have been described. Upon rupture of gelatinous tumors of the ovary, intestine, or vermiform appendix, pseudomyxoma of the peritoneum is sometimes discovered. Involvement of the peritoneum by a malignant tumor does not have great clinical significance, as these patients are incurable. In both primary and secondary cancerous peritonitis, a gradually increasing ascites is noted. In the clinical picture of the disease, general emaciation and decline of strength predominate, as a result of which patients soon perish. Treatment is purely symptomatic and boils down to periodic drainage of fluid from the abdomen, which provides only temporary relief.

V. Levit.