CHAPTER II.. Pericarditis.

PERICARDITIS.

Pericarditis consists in inflammation of the pericardial sac. It is attributable to different causes, varying in importance and in causation.

=Specific pericarditis= may be produced by the tubercle bacillus, or it may develop during an attack of contagious peripneumonia. Tuberculous or peripneumonic forms of pericarditis as a rule form only complications of chronic pulmonary tuberculosis or peripneumonia. They are very rarely primary in character, and, like the allied forms of pleurisy, assume a vegetative and adhesive form in tuberculous cases.

Moussu has never seen the true exudative form either in acute or chronic tuberculosis, but only vegetative and caseous forms.

=Simple acute pericarditis.= Cases of simple acute exudative pericarditis have been described, and have been referred to chills, wounds, or injuries in the region of the heart, and in a few cases to the rheumatic diathesis.

Such forms of pericarditis may occur, but probably are very rare, for Moussu has seen but two cases. As the symptoms correspond exactly to those of exudative pericarditis produced by a foreign body, it is unnecessary to describe them specially.

The only important detail to bear in mind with this disease is the possibility of cure by suitable treatment, such as the application of stimulants or vesicants to the cardiac zone, the administration of salicylate of soda or diuretics, and complete rest.

=The diagnosis=, moreover, should be confirmed by making an aseptic exploratory puncture with the capillary trocar. The nature of the liquid withdrawn will indicate whether the case is one of simple acute pericarditis or pericarditis due to a foreign body.

=Cancerous pericarditis= is generally secondary, and is caused by development of tumours on the pericardial serous membrane, and in the myocardium. Moussu, however, has seen one case of primary cancerous pericarditis, the tumours being found only on the periphery of the myocardium. The growth assumes a vegetative form with moderate exudation. The symptoms, however, so closely approach to those of exudative pericarditis due to foreign bodies that only the latter variety, which is by far the most frequent in animals of the bovine species, need be described.

EXUDATIVE PERICARDITIS DUE TO FOREIGN BODIES.

This condition has been erroneously described as traumatic pericarditis, but the latter term would suggest that the disease was due to an injury acting from without. It may be defined as a disease produced by the discharge into the pericardial cavity of some foreign body from the gastric compartments.

Boizy in 1858 described several cases of this kind of pericarditis. Hamon in 1866 gave an excellent table of symptoms. Roy in 1875 supplemented this with numerous observations showing clearly the possibility of recognising the disease by clinical examination. Pericarditis due to foreign bodies is to-day one of the best characterised diseases of the ox, and it is easy to diagnose.

Before approaching the etiological side of the question, it is necessary to recall in a few words the anatomical arrangement of the pericardium and its relations to neighbouring organs.

In the ox the diaphragm presents a marked concavity directed towards the abdomen. The pericardium, situated exactly in the median plane, is fixed by its point to the sternum. A fold of adipose tissue directly connects it with the anterior surface of the diaphragm. On the abdominal side the conical right compartment of the rumen is in free communication with the reticulum, which is closely applied to the posterior surface of the diaphragm on the median line opposite the spot occupied by the pericardium on the anterior surface (Fig. 176). As a result of this arrangement any object passing through the reticulum and diaphragm in the median plane would enter the pericardial cavity. These particulars indicate clearly how this form of pericarditis is produced.

=Causation.= One of the chief causes of pericarditis by a foreign body is connected with the way in which oxen feed. They rapidly swallow their food and any foreign bodies that may be concealed in it, submitting it later on to a second mastication in the course of rumination. This method of feeding results in bolting the food almost without mastication, hence the possibility of swallowing foreign bodies.

The proximity of the reticulum to the pericardium is also an important factor, because the foreign bodies fall into the reticulum as soon as the bolus of food begins to break up. It is important to notice, moreover, that pericarditis is commonest on farms where the oxen are attended by women, or in regions where sharp objects are to be found on roads or pastures frequented by the animals, such as the vicinity of needle, nail, and rivet factories.

The sole cause is the penetration of a foreign body into the pericardial sac.

=Pathogeny.= All kinds of foreign bodies are swallowed by oxen, as is abundantly shown by post-mortem examinations. These indigestible bodies pass with the food into the rumen, and accumulate in the deepest portions of that receptacle. Owing to physiological contractions the lower wall of the rumen rises to the level of the orifice of communication with the reticulum, and so passes much of the material accumulated within it into this organ.

Soft foreign bodies fall towards the lower parts of the reticulum, but sharp objects may lodge in its walls. Very often the bodies penetrate in this way without causing reticulitis or grave inflammation. The functions of the reticulum are not impeded. The commonest of such objects are needles, pins, nails, or fragments of iron wire. On account of their form, needles are the most dangerous. The sharpness of one extremity ensures its passing readily through the tissues, and as the point is the part that offers least resistance, the needle continues gradually to penetrate.

If the foreign body becomes implanted vertically in the lower wall of the rumen or reticulum it may be expelled directly through the medium of an abscess. This is a favourable termination, though it usually results in permanent gastric fistula.

More often the objects penetrate the anterior wall of the reticulum and gradually work their way towards the diaphragm, impelled by the movements of the reticulum and the other digestive compartments. They perforate the muscle and pass into the thoracic cavity, either in the direction of the pericardium or of the pleural sacs.

First as to the penetration of the pericardium. The foreign body, whatever it may be, produces by its presence alone very marked irritation, and as in addition it is always infected in consequence of its having passed through the digestive compartments, inflammation is set up to a degree proportionate to the pathogenic qualities of the infective agent.

=Symptoms.= The early symptoms are those of indigestion, and not of pericardial disease, a fact which is easy to understand, because at first the whole mischief is in the abdominal cavity. The patients are dull, restless, and seem to be suffering from an obscure ailment. They remain standing more than usual, show more than ordinary deliberation in lying down, lose appetite, cease to ruminate regularly, and exhibit intermittent tympanites.

The cause of these symptoms is as follows: At first the reticulum is partly immobilised by the local inflammation, and at a later stage movement of the diaphragm is checked by reflex action when the sharp body has progressed far enough to touch it. The rhythmic movements of the reticulum and the diaphragm are interfered with, rumination is disturbed, eructation ceases, and tympanites appears.

The patient often utters slight groans, particularly when forced to move; but as this is a sign common to all grave diseases it can only give rise to a suspicion as to what has occurred. In ten to fifteen days this primary phase may have terminated; but it is impossible to say how long it lasts, for it varies with each animal as with each variety of foreign body, and it may be prolonged for months.

From the moment it reaches the thoracic cavity the foreign object makes its way towards the channel formed on either side by the ribs and below by the sternum, and therefore towards the point of the heart. This is the second phase of development.

The passage of the foreign body through the diaphragm occupies a more or less considerable time, depending on its length; the beginning of this second phase is characterised by relative immobility of the circle of the hypochondrium during respiration. The abnormal sensibility and pain impede contraction of the diaphragm.

Palpation of the region of the xiphoid cartilage then reveals abnormal sensibility, and sometimes causes the animal to resent being handled.

From this time the pericardial symptoms proper commence, the foreign body having come in contact with the pericardium. This phase, unlike those which precede it, presents well-defined symptoms. The irritation of the heart and its ganglionic system by a foreign body in the pericardium is shown by considerable acceleration of the heart beats even before there is any exudation into the pericardial sac. Instead of 60 to 70 beats, the normal number, the pulse may rise to 80, 90, 100, or even 110 beats per minute. The heart sounds are tumultuous, dull and ill-defined, while the pulse appears bounding and strong.

But this period of cardiac excitement while persisting is soon complicated by other symptoms. As soon as the foreign body penetrates the pericardial sac, there is infection, which produces an active form of inflammation and abundant exudation. From this time the pulse becomes weaker and weaker, until, under the steadily increasing pressure on the heart, it is almost imperceptible.

There is only moderate fever. As soon as the exudation becomes considerable, the symptoms of pericarditis grow very marked: they may be grouped in the following order, according to their importance.

A. =Cardiac symptoms.= On palpation of the cardiac zone on the left the impulse of the heart is no longer felt. Percussion, which under normal circumstances reveals only partial dulness, now seems to give pain, and indicates abnormal dulness distributed in a vertical plane. The pulmonary lobes between the pericardium and thoracic walls are thrust upwards. The distended pericardial sac approaches the parietal layer of the pleura and may adhere to it, hence the dulness. This dulness extends as far back as the xiphoid appendix of the sternum, and can be detected on both sides, marginated above by a convex line.

In rare cases the dulness is absent, being partially replaced by tympanitic resonance, due to the presence of gases in the distended pericardial cavity, which gases originate in the digestive reservoirs or result from putrid fermentation of the pericardial exudate.

Simple or double pleurisy, or even pneumonia of the cardiac lobes resulting from infection by contiguity, may complicate cases of rapid pericarditis. The dulness then appears modified, as do the signs observed on auscultation.

Auscultation furnishes valuable indications. From the outset it reveals acceleration of the heart. At a later stage, but only for a short time, it permits of the detection of the pericardial rubbing sound which precedes serous exudation, and which may persist for several days when large quantities of false membrane are produced.

If exudate is present in considerable quantities a liquid sound is heard at each heart beat. The heart appears to be beating in water, but the liquid note varies considerably. It has been termed the “claclaque” sound (Lecouturier, 1846), in allusion to the sound produced by the meeting of water ripples; “clapotement” sound (Boizy, 1858), with reference to the sound produced under the influence of a light breeze on the borders of a stream; “glou-glou” sound (Roy, 1875), suggested by the noise of liquid escaping from an inverted bottle into a resonant vessel, etc. It is important, however, to remember that cases occur (principally when the pericardium is greatly distended and entirely filled with liquid) where, with the animal at rest, these sounds are difficult to detect. To render them noticeable the patient must be walked for a few yards.

Vernant, again, has described a sound as of dripping water, of quite special character; he compared it to that resulting from the fall of drops of liquid on to a marble table or into a half-filled vessel. So far as can be ascertained this sound of dripping water greatly resembles that heard in pneumo-thorax, but it is less resonant and less prolonged.

It appears to be characteristic of the presence of air in the pericardial cavity, and its special quality varies with the quantity accumulated in the pericardium. Masked by these pericardial sounds the beating of the heart seems dull, badly defined, distant and stifled.

B. =Jugular symptoms.= The “jugular” symptoms are secondary, and result from the accumulation of liquid in the pericardial cavity. No intra-pericardial exudate can exist without exerting pressure on the heart, and as the auricles have very thin walls and are more compressible than the ventricles, this pressure immediately causes difficulty in the return circulation, whence venous stasis, varying in intensity, but clearly visible and appreciable on account of the distension of the jugulars.

The venous stasis is general, for the pulmonary veins are as much compressed as the posterior and anterior venæ cavæ, but it is only apparent in the large superficial veins. This stasis is accompanied by venous pulse, and particularly by peripheral or internal œdema, œdema of the lung, intestine, mesentery, etc., of the submaxillary space and of the dewlap and entrance to the chest. Œdema of the submaxillary space is specially characteristic, for it appears almost first amongst external signs. That of the dewlap follows at a later stage, and extends backwards as far as the umbilicus, rising above this point as high even as the entrance to the chest and the axillary region.

C. =Pulmonary symptoms.= The pulmonary symptoms result from difficulty in the return circulation and from the venous stasis. They are due to passive congestion and œdema of the lung or to hydro-thorax. At rest the respiration may appear fairly regular, but at the least movement it is accelerated, and may rise to 40 or even 60 per minute.

Percussion reveals lessened resonance of the parts, and in the case of hydro-thorax dulness marginated by a horizontal line, as in pleurisy.

On auscultation the vesicular murmur may sometimes have diminished or even disappeared, while the respiration may be blowing, as in active congestion, and in exceptional cases a tubal souffle may be observed. In most cases the animal has a paroxysmal, somewhat frequent cough, due to reflex irritability of the pneumo-gastric.

Cruzel in addition mentions a double respiratory movement like that produced in the horse by broken wind. This is really the result of hydro-thorax, and is not a constant symptom.

D. =General symptoms.= When the disease has lasted a certain time the patients show certain well-marked general symptoms: they remain standing in one position for long periods, with the head and neck extended, the front legs thrust outwards from the trunk and the body rigid, as though the least movement caused them pain. The general attitude expresses anxiety, the animals lie down with great care and seldom remain long in this position, which interferes with the functions of the heart and lung. In the last stages the animals remain constantly standing, appetite is almost entirely lost, and they waste rapidly.

=The course= of pericarditis due to foreign bodies is very variable. Sometimes death occurs in eight or ten days. In other cases the animal may survive for weeks, provided it is well tended. Everything depends on the rapidity with which the foreign body moves and on the character of the infectious organisms which it introduces into the pericardium. Death is the inevitable termination, and occurs as a consequence of cardiac and respiratory syncope. It may follow suddenly as the result of a simple forced movement, even when the animal still seems to retain some amount of strength. When the organisms introduced into the pericardium are of marked virulence, complications such as septic pleurisy and pneumonia may be observed, and death soon takes place.

It has been suggested that recovery might follow a return of the foreign body towards the reticulum. This view can only have been advanced as a consequence of errors in diagnosis, either as to the existence of pericarditis or as to its nature. Pericarditis due to cold or rheumatism sometimes becomes cured spontaneously.

Death, again, may suddenly occur by syncope when the foreign body penetrates the myocardium, passes through it, and enters the ventricular cavities.

The return of the foreign body is not conceivable, at all events after it arrives in the pericardial cavity. Up to that time the only disturbance is of a digestive character; no pericarditis exists. But when for example the disturbance is due to long fragments of iron wire which may extend from the reticulum as far as the pericardium, it is clear that the pericarditis is of a kind which cannot be cured without leaving traces. In our opinion, natural recovery is impossible.

=Diagnosis.= The diagnosis of pericarditis cannot be made until such pericarditis actually exists, i.e., until the disease has arrived at the third stage of development mentioned above.

As long as the symptoms point only to the first or second stage, the logical diagnosis is reticulitis produced by a foreign body. At this time the development of pericarditis, although possible, is not inevitable.

When, on the other hand, one knows how the digestive disturbance has originated and developed and thereafter notes signs of cardiac irritation, disappearance of the cardiac impulse, dulness of the heart sounds, venous stasis, etc., the diagnosis is easy even thus early.

Mistakes are not very likely. Only in some cases are they liable to occur, as in acute peripneumonia of the anterior pulmonary lobes, causing compression of the pericardium of the anterior vena cava and producing secondarily venous stasis and œdema of the dewlap. Cases of specific pericarditis due to peripneumonia also occur, and under such circumstances a mistake would be even more excusable. Nevertheless, the temperature curve in itself is a sure indication, for whilst in peripneumonia the fever is always very marked, it is scarcely noticeable in pericarditis due to a foreign body.

When the diagnosis of pericarditis has been arrived at it is desirable to determine the exact nature of the disease, for whilst cases of pericarditis due to foreign bodies are incurable and in the interest of the owner the animals should be slaughtered, pericarditis due to cold or rheumatism may be successfully treated. Rheumatism generally affects the synovial membranes even before it produces pericarditis, and this indication, supplemented by the history of the case usually ensures one against mistakes regarding the initial cause.

It is much more difficult to distinguish pericarditis due to a foreign body from pericarditis due to carcinoma and from the forms of pseudo-pericarditis produced by lesions in the neighbourhood of the heart. When considering the latter we shall deal with this particular point.

=Prognosis.= The prognosis is always fatal.

=Lesions.= When the foreign body is very thin and sharp, the reticulum may not become attached to the diaphragm. In such cases its passage has been rapid and the tissues have healed.

Usually the reticulum, diaphragm and pericardium are united by a mass of fibrous tissue as thick as a man’s arm. It resembles a fibrous sleeve surrounded by an œdematous zone, usually of slight extent. This mass of new fibrous tissue is traversed by a sinuous tract resulting from the irritant action of the foreign body on the surrounding tissues. All writers describe this fibrous sleeve, which, however, only occurs in cases where a very long foreign body has occupied a considerable time in passing from the reticulum to the cavity of the chest.

In very exceptional cases the sinuous tract is ramified, possibly as a result of displacements of the foreign body.

The orifices of the tract are to be found, one in the reticulum, the other in the pericardium. On the side of the reticulum there is never more than one opening, and in many instances the tract is already closed on that side, either by exuberant granulations or by a cicatrix.

On the contrary, the fistula is more frequently open in the pericardial cavity. Its walls are of very varying appearance, depending on their age: they may be red, greyish, soft or hard, and when the lesion is of old standing they may have been converted into a sclerotic tissue.

The pericardium appears distended with a considerable quantity of liquid of a special character—sometimes sero-sanguinolent, sometimes almost or entirely purulent; sometimes yellowish, or greenish-grey; sometimes frothy, inodorous, or very fœtid.

These characters depend on the nature and number of the germs which have invaded the pericardial cavity. They also vary with the gravity and number of the hæmorrhages produced by the action of the foreign body on the myocardium.

The quantity of liquid also varies within very wide limits. There may be scarcely any exudation. In that case the pericarditis is of a partially adhesive character, with abundant false membranes. As a rule the quantity of fluid exudation varies between seven and eight quarts, but sometimes the quantity is much greater. Trasbot described an instance in which the united weights of the heart and pericardium exceeded 36 lbs. Hamon mentioned a case of pericarditis in which the liquid exudate exceeded twenty quarts.

“When inflammation is first set up the liquid is serous, yellowish, or reddish yellow. It contains fibrinous flocculi in suspension. Little by little this exudate becomes purulent, whilst the internal layers of the pericardial serous membrane undergo desquamation. These are next covered with false membranes of varying appearance; the fibro-albuminous exudation is wrinkled, villous and tufted. The two layers of serous membrane are connected at certain points by this exudation, the adhesions being sometimes very extensive. The pericardial sac properly so called becomes the seat of marked lardaceous thickening, due to inflammation. The heart appears entirely covered with a layer of greyish or earthy-coloured granulation tissue, which appears as though baked, and was compared by Hamon to the back of a toad. It is atrophied as a consequence of prolonged compression.

Under the influence of the eccentric pressure of the liquid the pericardial sac is distended and comes in contact with the walls of the chest, to which it may adhere. The foreign body, especially if small, is not always easy to find.

The myocardium often displays interesting lesions. At first there is thickening, or more commonly sclerous degeneration, of the superficial layers covering the ventricles, and then appears a crop of little miliary abscesses. Abscesses of considerable size have several times been detected in the walls of the ventricles and in the interventricular septum.

The foreign body, moreover, may not only injure the myocardium, but may even perforate it completely and produce ulcerative endocarditis (Cadéac). In this case infectious germs very rapidly invade the circulation and all the tissues, and the animal dies of pyæmia.

These essential lesions are accompanied by others of varying importance. Thus the lung is congested throughout, and by contiguity of tissue inflammation may extend from the pericardium to the lower part of the pulmonary lobes and to the pleura.

Interference with the return circulation induces lesions due to venous stasis: dropsy of the chief serous membranes, œdema of the connective tissue, pleural and peritoneal exudations, etc. If the hind limbs never become swollen it is because the skin covering them is very resistant and does not readily yield. The liver becomes hypertrophied, congested and engorged with blood, and when the animals live for some weeks, shows the appearances known as cardiac or nutmeg liver.

=Treatment.= The treatment of pericarditis due to the presence of foreign bodies is at present merely palliative. Often the only thing to be done is to slaughter the animal.

We need not go back to the methods formerly recommended. All are illusory or mischievous, such as the use of purgatives to arrest or reverse the progress of the foreign body, removal of the foreign body after opening the rumen, puncture of the pericardium, etc.

In 1878 Bastin successfully opened the pericardium and extracted the foreign body through a window produced in the thoracic wall.

This operator recommends that after drawing the left limb forward and incising the skin and muscles, the operator, with his hand bound round with a cloth, should perforate the pleura, and then having found the foreign body, proceed to extract it. By this method it seems difficult to cause perforation of the pericardium, which would certainly lead to the production of pneumo-thorax complicated with fatal septic pleurisy.

It must be borne in mind that the two pleural sacs, right and left, descend as far as the sternum (Fig. 173), and that it is not possible to touch the pericardium directly without perforating the pleura.

Moussu has drained the pericardium through the pleura in the hope of relieving the pressure on the heart and facilitating the reabsorption of the œdema, in order to permit of the subsequent slaughter of the animal, but has had unsatisfactory results. Lastly, he has practised median trepanation of the sternum in the infra-pericardiac region. Here again the operation is difficult, because of the œdematous infiltration of all the substernal region, while it is so dangerous to the patient, which must be cast and may suddenly succumb, that it is of no use in ordinary practice.

There is probably only one condition in which it would be possible to attempt intervention with a fair chance of success, that is, when there exists a fibrous connection between the pericardium, lung, and wall of the chest on the right or left side.

In such cases aspiratory puncture or incision of the pericardium in an intercostal space might prove of service, because it would not expose the animal to the danger of pneumo-thorax.

The only difficulty lies in ascertaining beyond all question the existence of such an adhesion before attempting operation, and this is really very great, even having regard to the form of the dulness and the absence of all respiratory sound in the lower third of the thoracic cavity and cardiac zone. The pulmonary lobe between the heart and chest wall may be thrust upwards and be partially adherent to the pericardium and to the parietal pleura, and at the same time it may be impossible to avoid producing operative pneumo-thorax when the cartilages are resected to admit of incising the pericardium.

The only logical method seems to be puncture of the pericardium through the xiphoid cartilage, as described below.

The topographical anatomy of the thoracic viscera shows that the point of the pericardium extends along the sternum to a point close to the lower insertion of the diaphragm, and that the pericardial sac is only separated from the xiphoid region, or rather from the region of the neck of the xiphoid appendix of the sternum, by the fatty cushion at the point of the heart.

A glance at the annexed diagram (Fig. 177) will show this.

The diagram, carefully reproduced from an anatomical preparation of an animal which succumbed to pericarditis, shows that the distended pericardium extends close to the neck of the xiphoid cartilage.

=First stage.= Identify the three following anatomical guiding points:—

(1.) Xiphoid appendix and white line. (2.) Point at which the circle of the hypochondrium becomes attached to the sternum. (3.) Point at which the external mammary vein penetrates the abdominal wall (Fig. 178).

Lines uniting these three points enclose a right-angled triangle, which the operator must imagine to be bisected by a third line.

The incision, which should be about 8 inches in length, follows this bisecting line at an equal distance between the white line and the circle of the hypochondrium, to a point within about 8 inches of the anterior margin of the mamma. All these points are readily observable before the animal is cast.

The cutaneous incision affords exit to large quantities of fluid, and the pectoral muscles attached to the neck of the ensiform cartilage can then be divided with the bistoury. The area of operation is thus uncovered.

=Second stage.= The second phase comprises incision of the tissues opposite the neck of the ensiform cartilage, about 8 inches in front of the base of the triangle and at equal distances from the points Nos. 1 and 2; incision through the skin for a distance of 8 inches, and dissection of the muscles of the ensiform region exposed at the neck of the cartilage.

By means of the index finger or the index and middle fingers of the right hand the mediastinal space is explored, and the fatty masses round the base of the heart broken through. If the pericardium is greatly distended, the point of the sac can be felt with the tip of the finger, or its position can be recognised, even from a little distance, on account of the fluid contents transmitting the impulse of the heart. The sensation conveyed to the finger is very clear.

The right index finger is then replaced by the left, and, a trocar about 10 inches long and ¼ inch in diameter being introduced along the index finger used as a director, the pericardial sac is reached. The exudative fluid transmits the impulse due to the beating of the heart, and the pulsations can be clearly distinguished when grasping the handle of the trocar.

=Third stage.= Digital exploration of the course of the puncture and fatty cushion at the base of the heart, with the object of discovering the position of the pericardium.

=Fourth stage.= Puncture with a trocar about 10 to 12 inches in length, puncture of the pericardium, irrigation and dressing.

The trocar is inclined in a slightly oblique direction from without inwards and forwards towards the median plane, in order that the point may not deviate towards the left pleural sac; the left index finger is then withdrawn, and by a sharp thrust of the right hand the trocar is pushed forward about 1 to 1½ inches and the pericardial sac is entered.

The position of the canula should not be altered whilst liquid is escaping, for if it is thrust in too far a considerable quantity of fluid may remain in the deepest portion of the sac.

The cavity having been drained, a long strip of iodoform gauze is introduced into the track and a protective surgical dressing applied over the incision in order to prevent infection by the litter.

In consequence of the introduction of the fingers into the track caused by puncture and the escape of pericardial liquid along the canula or after removal of the canula, the operative wound is necessarily infected; but this is of little importance, because the opening is inclined downwards, and also because it is impossible to hope for aseptic healing.

The dressing is renewed after forty-eight hours, and every three or four days afterwards.

The œdematous infiltration about the front portion of the body disappears rapidly in two to three days, and should the animal be slaughtered the meat is quite sound in appearance.

This operation does not aim at effecting a cure, but is simply for the purpose of allowing animals which would otherwise be valueless to be slaughtered and sold.

CHRONIC PERICARDITIS.

Pericarditis when due to tuberculosis may assume the chronic form. Tuberculous pericarditis, at least in a large number of cases, is only accompanied by slight exudation, which might remain unnoticed unless the animals were carefully examined; but it causes the internal surface of the pericardial sac and the surface of the myocardium to become covered with exuberant vascular growths, which by setting up adhesions lead to partial or generalised union of the heart and pericardial sac. Between these adhesions, which form partitions, are found little cavities filled with sero-sanguinolent, grumous, or caseous liquid. In time the adhesions increase in number, pericarditis obliterates the free space, and the heart becomes wholly adherent to the pericardium.

As in acute pericarditis, the fibrous layer undergoes thickening and hardening processes. The superficial layers of the myocardium undergo sclerous transformation, and the tissues forming the adhesions themselves may assume the characters of fibrous tissue.

In one solitary case Moussu saw another form of chronic pericarditis with complete adhesion of the heart and pericardial sac, without any exudation and almost without any false membranes. He was unable to determine the exact cause, but was strongly inclined to regard the disease as having followed pericarditis à frigore or pericarditis of a rheumatic character.

Adhesions between the heart and pericardial sac are also said to be the inevitable though delayed result of all punctures of the pericardium through the ensiform cartilage in cases of pericarditis due to a foreign body.

=Symptoms.= If the chronic pericarditis is limited to a few partial adhesions, it remains unnoticed; but when it is more marked it offers certain signs of acute pericarditis, such as partial dulness of the cardiac area, which is more extensive than usual, disappearance of the cardiac shock, weakening of the sounds, feebleness of the pulse, very marked venous pulse, moderate stasis, extremely rapid and aggravated dyspnœa when the animal is forced to walk, threatened asphyxia if exercise is prolonged, and complete asystole.

All these symptoms are due to the existence of adhesions between the heart and pericardium, which, by destroying the interpericardial space, interfere with diastole while preventing regular systole.

Sudden death is a frequent consequence.

The =diagnosis= of chronic pericarditis is very difficult. The =prognosis= is extremely grave, and we do not possess any means of dealing with the condition.

PSEUDO-PERICARDITIS.

Under this title we purpose grouping a certain number of pathological accidents due to different causes, but manifesting themselves by identical symptoms, which symptoms offer so marked a resemblance to those of pericarditis produced by foreign bodies as to suggest the presence of that disease. This refers to accidents by which the foreign body closely approaches, without actually touching, the pericardium, the lung or the pleural sacs, but in which it causes purulent collections which displace the pericardium, indirectly compress the heart, and finally cause symptoms of an apparently pericardial character.

=Causation.= During the development of pericarditis the foreign body perforates the reticulum and diaphragm, passing along the middle line of the body, without which it would not come in contact with the pericardium. If the perforation, however, occurs to the right or left of the median plane, the foreign body moves forward just as easily, but it misses the pericardium and passes either into the lung, where it causes fatal pneumonia; or the pleura, where either it sets up septic pleurisy in the subpleural connective tissue or produces an abscess.

The abscess is generally lateral, situated in the right subpleural region, or it may develop below the pericardium. These are the two varieties of pseudo-pericarditis seen by Moussu.

There is, however, a third variety, which might be called “parasitic pseudo-pericarditis.” It is extremely rare, and Moussu has only seen one case. It was due to the presence of an enormous hydatid cyst of the right lung as large as a man’s head, which was situated towards the mediastinal plane of the lung and pressed on the supero-posterior surface of the heart and pericardium. In consequence of the permanent downward pressure which it exercised it interfered seriously with the heart’s action and caused symptoms of pseudo-pericarditis.

=Symptoms.= The general and external symptoms are those of pericarditis—viz., dulness, diminution in appetite, irregular rumination, wasting, œdema of the dewlap, distension of the jugulars, marked venous pulse, great anxiety and dyspnœa when the patients are forced to move, etc.

But the cardiac symptoms differ notably, and moreover vary, according to the nature of the lesions. Speaking generally percussion reveals complete dulness on one or both sides, and auscultation always indicates the absence of sounds due to extravasated fluid in the pericardial sac.

When the abscess is situated below the pericardium, a condition difficult to diagnose, the dulness seldom extends very high on either side of the chest, and the sounds heard over the cardiac area, while much weaker than usual, are audible above the normal points.

An abscess developing beneath the pleura on one side displaces the heart in the opposite direction. The cardiac beat is weakened by the compression, but, nevertheless, transmits an impulse to the purulent fluid, which in its turn conveys it outwards through the intercostal spaces in the form of movements corresponding in rhythm with the beating of the heart, so that at first glance one might imagine an aneurism existed at the base of the large arterial trunks. The lower pulmonary lobe is thrust upwards, and over the area of dulness pulmonary sounds completely disappear.

When the heart is compressed by a large hydatid cyst or other lesion, the general and external symptoms are similar to those above described.

Finally, one last symptom, which appears of some importance, may be mentioned. When animals suffering from pericarditis due to a foreign body are forced to move, the heating of the heart becomes so tumultuous that it can no longer be counted, and even in a state of rest it may rise to 140 or 150 beats per minute. In cases of pseudo-pericarditis it rarely rises above 90 or 110.

=Diagnosis.= The attempt to diagnose this condition accurately must not be regarded merely as a result of scientific curiosity. Under certain circumstances the diagnosis may be of very great importance. While the patient affected with pericarditis due to a foreign body is beyond all hope of recovery, certain cases of pseudo-pericarditis appear amenable to treatment.

The diagnosis, therefore, is of great importance, and the practitioner should spare no effort to confirm it, bearing in mind the symptoms enumerated, and remembering that the normal sounds of the heart never completely disappear.

An aseptic exploratory puncture with a long, fine needle will sometimes prove of great assistance.

=Prognosis.= Although grave, the prognosis is less so than in true pericarditis.

=Treatment.= If clearly recognised, both subpleural and subpericardial abscesses seem curable. By freely puncturing the pus-filled cavity through an intercostal space, the liquid may be evacuated and recovery may occur. Healing is favoured by carefully washing out the cavity with a non-irritant disinfectant.

The only precaution required in making such punctures is to avoid the internal thoracic artery and vein, the intercostal artery, and the lower cul-de-sac of the pleura.