toneum secretes just sufficient material to lubricate its surfaces; but when congested or inflamed pours out an abundant serous exudate. Absorption is freely exercised, and this much more markedly in the upper than the lower abdomen; it is probably freest on the under surface of the diaphragm.

There is no reason to assume that the peritoneum differs from other lining membranes in being less liable to inflammation when unduly irritated; nor need it be supposed that inflammation when it attacks it differs in any material respect from similar processes elsewhere. Its becoming inflamed under any circumstances should be regarded as partially a protective process. It is Nature's effort to counteract and to inhibit the incursion and onslaught of invading forces which are inimical to the general welfare of the system as a whole.

The chief interest about an attack of acute peritonitis centers in the mode or source of infection. As far as is known, there is no such thing as an acute specific infection of the peritoneum, as a whole; that is, independently of any disease elsewhere; there is always a definite focus from which the inflammation starts. Further, everything tends to show that it is the presence of a particular microbe in the general peritoneal cavity that excites the inflammation; or, in many instances, the infection is mixed; that is to say, caused by two or more of the micro-organisms. The virulence of any attack will depend both upon the quantity and quality of the micro-organisms finding their way into the general peritoneal cavity; and probably also upon the resisting powers possessed by the host.

How do these micro-organisms gain access to the general peritoneal cavity? In the case of the female, they can easily do so by way of the Fallopian tubes; and it is by this route that such microbes as the gonococcus, the pneumococcus, and the pus-producing organisms probably do. Under all other circumstances, they must either make their

way through the unbroken surfaces of the peritoneum, or be ejected through some perforating lesion of a viscus. There is no difficulty in understanding the latter process, but in the former case we must assume that the serous coat has been damaged by an inflammatory process which has started from within; and, by extension outwards, impaired the protective properties of the membrane.

When inflammation arises from a gangrenous or ruptured appendix, or an inflamed bowel, it is usually the bacillus coli communis that is the infecting agent, although other micro-organisms are often associated in the process.

The infection which arises from a perforated gastric or duodenal ulcer is, as a rule, not acute in its inception, but rapidly becomes so after six hours or more. If any doubt existed as to the universality of a bacterial origin of all cases of acute general peritonitis, it would be in the case of a perforated gastric ulcer; for, except that the ulcer is itself probably septic, the extravasated material is not necessarily so; and the peritoneal inflammation might be chemical in origin, due to the acid gastric juices. It is certainly remarkable, sometimes, how often, after the closure of a perforated gastric ulcer, that much turbid fluid is left in the abdominal cavity, and yet the patient makes an uninterrupted recovery. However, it may be, after all, that the peritoneum is able, by its own powers of secretion and absorption, to neutralize all organisms that are not in excess; so that the limited number of those present in the escaped gastric contents are not beyond the power of the peritoneum to overcome and effectually dispose of.

Peritonitis, which follows upon operations within the abdomen, no matter what for, is unfortunately one of the most fatal forms of the disease we encounter. Why it should be so it is difficult to explain, except that the introduction of such micro-organisms as the staphylococcus pyogenes aureus, or the streptococcus pyogenes into a healthy and unprepared peritoneal cavity is more than that

lining membrane can withstand.

It has had no time to

prepare its forces of defense to combat the onslaught of the army of invasion.

It has been already pointed out that the virulence and rapidity of an attack depend upon the quality and quantity of the infecting material; so that while the symptoms may be comparatively slow in their progress in one case, they may be extremely rapid and acute in another. But taking the case at the earliest stage, when it is possible to be certain that acute peritonitis exists, we may expect to find fairly distinctive local and constitutional manifestations.

Before we take up the local and systemic symptoms, it would be well to consider the importance of obtaining a reliable history of the case; and this would bring us face to face with the well-known diseases that proceed or act as the direct etiological factor in the production of the peritonitis; necessitating a diagnosis of appendicitis, pus tubes, cholecystitis, gastric or duodenal ulcer. They are the four gross or most common sources of infection, named in the order of their causative frequency.

If we can exclude any or all of these, then we consider the rarer cases; due to strangulation or obstruction from any cause, typhoid perforation, tubercular infection from the mesenteric glands, or by extension of any other infection process in the neighboring organs. We can't deal with peritonitis from any standpoint intelligently that does not take into consideration these lesions that form the focal point of infection; especially is it true when we come to the diagnosis, prognosis and treatment.

The local signs or symptoms are the following: the patient lies in bed in the dorsal position with the knees drawn up to relax the anterior abdominal wall; this attitude is significant, and there will be a general rigidity of the abdominal parietes, coupled with a feeling of tenderness to palpation in certain areas or all over the abdomen. The respiration will be costal, and any attempt to draw a

long breath will be checked by a sharp pain felt in the epigastrium and in the sides. The intestines being paralyzed, so in a state of paresis there will be in consequence neither passage of flatus nor of fæces; and as a consequence we have abdominal distention or tympanites. The temperature may, or not be raised, at the time of the examination; but the pulse is usually enfeebled and increased in frequency. There will be loss of appetite, and vomiting may or may not be present, but it usually is at some stage of the disease. The general appearance of the patient may suggest the gravity of the complaint, but often the facial aspect may be more or less natural. These four conditional symptoms-pains, rigidity, localized tenderness and rapid, weak pulse should be recognized and accepted to mean peritonitis, and should be treated as such. This is not true in every case perhaps, but it forms a safe working rule, and if you make a mistake it is not as fatal as it would be to fail to recognize this symptom complex as such.

When, however, a later stage is reached, these symptoms undergo considerable alteration, both locally and constitutionally. The abdomen may no longer be rigid; indeed it may convey a kind of dough-like impression to palpation, with great distention and complete absence of borborygmi or gurgling; pain may be inappreciable. In place of the abdominal parietes being flat and retracted, they may be distended and tympanitic. The face may assume the typical, so-called abdominal expression-the facies Hippocraticus; the complexion may have an ashen grey aspect; the eyes may be sunken, with dark, suborbital lines. The tongue may be brown, dry, and furred; and the vomiting of dark material may be constant. The patient's mental condition becomes lethargic, sometimes passing into unconsciousness and delirium. As the end approaches, the hands may become livid and cold, and the pulse uncountable. These later symptoms are usually regarded as toxic in character, indicating that the patient is gradually being

killed by the absorption into the system of toxins, the result of the increased development, multiplication, and extension of the bacilli.

We are often called in near the end to find a patient with an abdomen so distended as to render it absolutely impossible to outline anything in it. A patient so restless as to be unable to remain quiet for a minute, with hollow, sunken, tired, wide-awake eyes, from which sleep has been absent for many hours. A mind clear and active to all that transpires about him, with lips that are red, parched and hot, made doubly so by continually sucking and swallowing cracked ice, which is only adding insult to injury.

By his side is a bowl into which he vomits quantities of dark green, foul, offensive fluid, that seems to come from some inexhaustible source. But why describe it further? We are only too familiar with the picture, and as we sit quietly by, meditating and pondering over the lost opportunity and the hopelessness of the situation, and the patient dies with an overwhelming toxemia.

Treatment:-We have seen from an investigation of this subject that a rational treatment depends upon the recognition of the underlying causes, and when the primary lesion or focus can be determined, our treatment should be directed to the relief in so far as possible of the etiological factor. Our chief aim should be when a diagnosis is made to prevent the spread of the disease over the entire abdominal cavity, and assist nature as far as possible to localize the inflammatory process. This we can best accomplish by taking advantage of the principle of placing the parts at rest, by putting the patient in bed. We not only want to have bodily rest and quietude, but we want to control the normal peristalsis of the bowels; nature tries to splint that part of the alimentary tract, and keep it still till adhesion can be formed that walls off the infected area; and fluid or drink should be withheld, for the moment either is put into the stomach peristalsis is at once excited.