Chapter LV: Part 55
After death the serous pericardium is found to be opaque, somewhat thickened, and to have an anæmic appearance. The opacity is due either to interstitial deposit or to the swelling of the epithelium.
The DIAGNOSIS of hydropericardium is surrounded by similar difficulties to that of pericardial effusion. It presents the same physical signs as this disease, except the friction at the base, and can only be distinguished by the history of the case and the attending general features.
The PROGNOSIS depends upon the extent of the dropsy and the cause producing it; in point of fact, more upon the latter. The prognosis is apt to be unfavorable when the disease is occasioned by any of the exanthemata or by Bright's disease.
The TREATMENT is that of the disease occasioning it and of the dropsy of which it forms part.
Pyopericardium.
Pus may accumulate in the pericardium as a result of pericarditis, and this has been already described. Further, metastatic or pyæmic abscesses occur occasionally in the tissue of the heart, and may be sufficiently superficial to burst into the pericardium, provided the patient survive the constitutional disturbance long enough. Morgagni observed numerous small abscesses form in the pericardium in consequence of inflammation. Abscesses in the lung and pleura may rupture and discharge their contents into the pericardial sac, and the communication may heal. Thus, Balfour[32] records a case of a boy aged thirteen who had evidences of effusion into the pericardium. Paracentesis of the pericardium was performed, and thirty ounces of pus were drawn off. While there was no evidence of communication with an abscess external to the pericardium, yet an abscess was found at the base of the right lung which was partially adherent to the sac. A communication which was closed up by the subsequent pericarditis was believed to have existed. The quantity of pus does not often reach the amount just mentioned. The fact is, a small quantity may be attended by fatal consequence. There may be pus in the pericardium when death is occasioned by diseases involving the general system, as in scurvy, erysipelas, pyæmia.
[Footnote 32: _Diseases of the Heart_.]
The SYMPTOMS of pyopericardium are those of acute or chronic pericarditis, with marked depression. The physical signs are the same. Indeed, there is no certainty in the diagnosis. Where there is, the operation of paracentesis is strongly indicated. Free incision of the pericardium has been recently practised by Rosenstein and by Samuel West[33] for purulent pericarditis.
[Footnote 33: _The Lancet_, Dec., 1883.]
Pneumopericardium.
Pneumopericardium, or accumulation of air in the pericardial sac, is a very rare affection. Yet Laennec[34] has stated that in his opinion air as well as fluid accumulates in the pericardium in all diseases just prior to death. Pneumopericardium may be associated with fluid, and may or may not be attended with inflammation of the pericardium. As the pericardium is a closed sac, air does not readily gain entrance. But it may do so through perforations of the walls by stabs or gunshot wounds, or by openings communicating with the oesophagus, lung, or stomach. Air is then drawn into {791} the sac during the contractions of the heart. Cases are on record of perforation of the sac with a knife,[35] and through the oesophagus by means of a sword swallowed by a juggler.[36] Sometimes the perforations communicate with organs that contain gas, as the stomach or intestine or the oesophagus. Graves has recorded a case in connection with abscess of the liver. When the pericardial sac is intact, the distending gas may arise from decomposing fluid in the pericardium: it is supposed that it may even be secreted by the blood of the coronary vessels. Pure air, such as we breathe, is never developed in the sac.
[Footnote 34: _Traité de l'Auscultation mediate_, chap. xxiii.]
[Footnote 35: Flint, _Diseases of the Heart_.]
[Footnote 36: Walshe, _Diseases of the Heart_.]
The accumulation of air in the pericardium which is sometimes noticed after death has been declared by many to be the result of the death-struggle. But it most likely occurs shortly before life ceases. In such cases the source of the air or gas must be the blood, for it is well known that blood contains several gases which may leave the corpuscles and fluid in which they are held mechanically.
The DIAGNOSIS of the condition under consideration is difficult, since we must chiefly depend upon the signs elicited by percussion. The general indications are a feeling of oppression in the præcordia, a sense of suffocation, fluttering of the heart; these, however, would only point to some functional disturbance. Percussion shows a preternatural resonance over the heart, the area of cardiac dulness being restricted and indistinct in proportion to the amount of air or gas contained in the sac. Emphysema of the margins of the lungs which overlap the front of the heart may give the same resonant sound, but it is not likely that emphysema of the lungs would be confined to their margins only.
Uncomplicated pneumopericardium is not frequently met with, for the affection is usually associated with fluid accumulations, and with the percussion resonance there will be other phenomena presently to be noted. On auscultation the heart sounds have a ringing character.
Pneumo-hydropericardium.
This, too, is a disorder of great rarity, and may be considered one of the curiosities of clinical experience. It is indeed an unsolved problem whether pneumo-hydropericardium ever exists except as a result of the ingress of air from without the body or from an adjacent organ through an opening made into the pericardium. Nearly all the cases that have been reported have upon careful investigation exhibited the evidence of perforation either by mechanical means or by ulcerative action.
The SYMPTOMS of the accumulation of gas or air in the pericardium associated with fluid are largely, if not entirely, the same as in pericarditis with effusion. There is the same sense of oppression in the chest, irregular rapid action of the heart, pain in the præcordial region, difficulty of breathing, and there may be febrile excitement.
These symptoms are thus not of much diagnostic value unless accompanied by the physical signs indicative of the disease. They are præcordial bulging, diminished cardiac impulse, and the sounds elicited by percussion and auscultation which show the presence of air and fluid. On percussion we have clear or tympanitic resonance in the cardiac region, somewhat modified, especially at the lower parts, by the dulness from the fluid, and very changeable with the altering postures of the patient. On auscultation the signs are variable. Laennec placed great reliance on fluctuation audible with the action of the heart and on deep inspiration, the heart sounds being heard at a distance. We may also find what has been called a splashing or a {792} churning splash, or the sounds of the heart may be extremely ringing, and even metallic; there may be a combination of sounds, as in the case recorded by Stokes,[37] where "they were not the rasping sounds of indurated lymph or the leather creak of Collin, nor those proceeding from pericarditis with valvular murmurs, but a mixture of various attrition murmurs with a large crepitating and gurgling sound, while to all these phenomena was added a distinct metallic character." In the case recorded by John F. Meigs[38] loud splashing or churning sounds were audible three or four feet distant from the heart; while Reynier[39] directs particular attention to an intermittent sound, at first metallic, and resembling a water-wheel.
[Footnote 37: _Diseases of the Heart and Aorta_.]
[Footnote 38: _Amer. Journ. Med. Sci._, Jan., 1875.]
[Footnote 39: _Arch. génér. de Méd._, Mai, 1880.]
In point of DIAGNOSIS we must be very careful not to confound the resonance transmitted from a distended stomach to the cardiac region with pneumo-hydropericardium. The rapid action of the heart and shortness of breath due to the gastric distension may further mislead, and the heart sounds may become sharply defined--the second more ringing. I have several times been called upon for an opinion in cases of the kind which were supposed to be pneumo-hydropericardium. Cavities situated near the heart may also present transmitted cardiac sounds of metallic timbre.[40]
[Footnote 40: Bauer, _Diseases of the Pericardium_.]
The PROGNOSIS is always very grave, yet cases of recovery have been reported in instances of traumatic origin.
The TREATMENT is that of pericarditis, with great attention to sustaining the action of the heart. This is chiefly effected by stimulants. Opium for its quieting effect is also indicated. In cases of marked cardiac pressure paracentesis has been recommended.
Cancer of the Pericardium.
Cancer of the pericardium is one of the rarest of all cancerous affections, never occurring as a primary disease, but consequent on cancer in some other part of the body, generally on cancer adjacent to the heart. It may be the result of direct extension of cancer or of secondary formations. In cancer of the pericardium the parietal layer of the sac is the one always attacked. The extension of the disease from the bronchi and mediastinal glands, from the lungs, pleura, oesophagus, and stomach, is the common cause. Cancer will under certain conditions produce lymphous exudation and adhesions and serous, hemorrhagic, and even purulent effusions. When lymph is thrown out friction sound exists and adhesions may follow. Serous effusion with little or no inflammation is generally present in cancer of the pericardium, and results from the obstruction in the vessels caused by pressure or by direct extension of the disease to the vessels. If the effusion be hemorrhagic, it can be attributed to the same cause. Pus is generally the result of erosion of vessels and membrane.
The DIAGNOSIS of cancer of the pericardium is practically impossible, for the physical signs are essentially the same as in pericarditis from other causes, the darting, lancinating pain excepted; yet even the pain may not be sufficiently typical to lead us to a correct conclusion. Therefore, as a rule, the existence of the disease can only be suspected, or regarded as very probable in consequence of the general features of the malady.
The rarity of this affection is seen in the summary given in _Ziemssen's Cyclopædia_. Köhler noted 6 cases of cancer of the pericardium in 9118 autopsies; Günsburg found 1 case of cancer in 1700 autopsies; and Willigk, 7 cases in 477 autopsies of persons dying of cancer.
Death, which is the result in all cases, is generally by exhaustion. Other {793} diseases of a nature allied to cancer also attack or involve the pericardium, such as lymphadenoma or lymphosarcoma in the mediastinum; the pathology is practically the same as that of cancer, and the general symptoms and the termination are alike.
Hydatids[41] give rise to growths which occasion a surmise of cancer; so do those white calcified bodies formed in concentric layers known as cardiliths. Neither has any diagnostic signs by which it can be distinguished.
[Footnote 41: See Rokitansky's _Pathological Anatomy_, and Klob, "Zeitschrift der K. K.," _Gesellschaft der Aertze zu Wien_, 1860.]
Tubercular Pericarditis.
Tubercular pericarditis is an exceedingly uncommon affection. Laennec only met with 2 instances of it, Louis with but 1 case. It is never primary, being always associated with tubercle in some other part of the body. Among the earlier records we find the case of Baillie,[42] who mentions "a case of two or three scrofulous tumors growing within the cavity of the pericardium." The case had tubercles in the lungs, and died with all the symptoms of phthisis, nothing indicating the presence of tumors in the pericardium prior to death.
[Footnote 42: _Morbid Anatomy_, 5th ed., London, 1818, pp. 11, 17.]
Tubercle in the pericardium may remain latent or excite inflammation which gives rise to the same physical signs and local phenomena as when the pericarditis is of idiopathic origin. The tubercle is mostly found beneath the serous layer of the pericardium, either cardiac or parietal, and sometimes in the adhesions, and bears a close resemblance to tubercular disease of the meninges, the peritoneum, and pleura. It must be understood, however, that pericarditis may happen in a tubercular person without being due to a deposit of tubercle in the pericardium; and a deposit may occur in the adhesions in a case of pericarditis in a tubercular person brought on by other causes than a tubercular development in the pericardium, as the instances reported by Burrows show.[43] Tubercular disease of the pericardium may be due, as Weigert has proved, to infection by contiguity from the lymphatic glands of the thorax. The pericardium may be free from tubercle, yet the purulent fluid in it be filled with tubercle bacilli.[44] Vaillard[45] declares the pericarditis to be dry in the majority of cases. The disease generally happens under forty years of age, but in Mickle's[46] case the patient died at the age of fifty-four.
[Footnote 43: _Med.-Chir. Trans._, vol. xxx. p. 77.]
[Footnote 44: Kast, _Virchow's Archiv_, June, 1884; see also _Medical News_, Aug., 1884.]
[Footnote 45: _Journ. de Méd. de Bordeaux_, 1880, l. x.]
[Footnote 46: _London Lancet_, May 26, 1883.]
The differential DIAGNOSIS of tubercular pericarditis cannot be made, as there is no positive physical sign distinguishing this form from any other. If pericarditis either in its acute or advanced stage occur in a tubercular person, and if there be neither rheumatism, Bright's disease, nor pleuro-pneumonia, and if the person have not been subjected to any injury in the præcordial region, the pericardial affection may be presumed to be due to tubercle, but only an autopsy would afford certain proof.
The PROGNOSIS is always unfavorable.
The TREATMENT is that of chronic pericarditis, sustaining the failing nutrition as well as we can by cod-liver oil and other nutrients.
{794}
THE OPERATIVE TREATMENT OF PERICARDIAL EFFUSIONS.
BY JOHN B. ROBERTS, A.M., M.D.
The operative treatment of pericardial exudations and transudations has received a new impetus within the last fifteen or twenty years from the investigations of Trousseau,[1] Roberts,[2] Hindenlang,[3] Fiedler,[4] West,[5] and others. Reference to the works of these writers will furnish the reader with the history and statistics of such operations, and with those details that I have not deemed necessary to incorporate in the present article.
[Footnote 1: _Clinical Medicine_.]
[Footnote 2: _New York Med. Journ._, Dec., 1876, with analysis of 41 cases; also _Paracentesis of the Pericardium_, Philada., 1880; _Trans. Am. Med. Ass'n_, 1880; and elsewhere.]
[Footnote 3: _Deutsches Archiv für klinische Medicin_, 1879.]
[Footnote 4: _Samml. klin. Vortr._, No. 215, Leipzig, 1882.]
[Footnote 5: _Medico-Chirurgical Transactions_, 1883.]
In all cases of bloody, serous, purulent, or aërial effusions into the pericardium, that present dangerous symptoms of heart failure, operative interference should be undertaken as soon as it is evident that medication is not lessening the embarrassment of the central organ of circulation. It is bad practice to delay the operation, which will generally be aspiration, until exhaustion, pulmonary engorgement, pericardial changes, and degeneration of the cardiac muscle render permanent relief impossible. The tendency is to wait, instead of affording immediate relief of the distressing symptoms by prompt resort to pericardicentesis. Clinical experience has abundantly shown that when the pericardial fluid is evacuated, dyspnoea, cyanosis, irregularity of the pulse, and the other threatening symptoms are lessened; and usually at once.
The time for aspiration depends less on the amount of fluid than would at first be supposed, because the sudden effusion of a moderate amount of serum will exert more pressure upon the heart than a much larger quantity poured out in so gradual a manner as to allow the pericardium to become stretched. Aspiration should therefore be performed in all cases of pericardial effusion, in which dangerous symptoms of heart embarrassment occur, as soon as medication fails, and without regard to the supposed quantity of fluid. This should be the practice without regard to any other visceral lesion that may be present as a complication, except in the case of pleural effusion.
When pleural effusion of considerable amount coexists, the pleural sac should be aspirated first, because of the difficulty of discriminating between respiratory distress due to pulmonary pressure and that resulting secondarily from interference with cardiac action, and because the evacuation of the pleural effusion seems at times to lead to absorption of the fluid in the {795} pericardium without resort to operation. This rule applies to pleurisy of the right side as well as of the left.
In dropsy of the pericardium from renal disease I admit that the transudation is at times absorbed with great rapidity, and that aspiration does not directly affect the primary disease; but still, tapping should be done if the failure of circulation and respiration seems to be dependent on the effusion. Pepper's case[6] of recovery after pericardicentesis affords corroborative evidence of the propriety of this advice. Before operation the urine was albuminous and contained tube-casts, but these symptoms entirely disappeared in the course of a few weeks.
[Footnote 6: _Medical News and Library_, Philada., March, 1878; and _Am. Journ. Med. Sciences_, April, 1879.]
When the amelioration of symptoms following the operation is not permanent because reaccumulation takes place, repetition of the operative procedure is demanded. It is better, in my opinion, to vary somewhat the point of puncture, lest the heart be wounded at the second tapping because of adhesion of the parietal to the visceral pericardium at the original point of puncture. Should repeated tapping be required in serous effusions, I should at the time of the third operation inject into the sac, after removing the serum, a solution containing tincture of iodine, alcohol, or carbolic acid, with the purpose of modifying the secreting surface and producing pericardial adhesion. Universal pericardial adhesion has been found by examination subsequent to cure by aspiration; and in a number of cases intra-pericardial injections have been made without preventing, or apparently interfering with, recovery.
The fluid injected ought probably to be concentrated, as the object to be obtained is pericarditis of a grade that will furnish plastic exudation instead of serum. Undiluted but liquefied carbolic acid, such as is used in treating hydrocele of the vaginal tunic of the testicle, would be the proper agent were it not for the possibility that its contact with the heart-walls might induce dangerous cardiac spasm. The strength of the fluid to be injected, as well as its utility, will have to be determined by future observation. Aran used fifteen grammes of tincture of iodine (French), one gramme of iodide of potassium, and fifty grammes of distilled water, and his patient recovered. Malle injected a solution of tincture of iodine "five times weaker than that recommended for hydrocele operations," but suspended the operation quickly because of the excessive pain in the cardiac region produced by the injection. Violent inflammatory symptoms arose. The patient died of diarrhoea before the exact result of the injection could be determined, though the indications were that cure by pericardial adhesion was about to take place. The autopsy seemed to confirm this belief.[7] It must be remembered also that his operation was done by trephining the sternum, which may have had something to do with the inflammatory reaction, though the injection was not made until the sixteenth day after the original operation.
[Footnote 7: _De la Paracentèse du Péricarde_, par Michel Labrousse, Thèse No. 107, 1871, pp. 22, 27.]
When aspiration has shown the pericarditis to be purulent, a free incision should be made, an antiseptic drainage-tube of good size introduced, and the cavity washed out daily with antiseptic solutions of carbolic acid (1 to 40) or corrosive sublimate (1 to 2000). In fact, pericardial effusions should be managed exactly as pleural effusions by tapping, injection, or drainage, according to the character of the contents of the sac. I have advocated this course since 1876, and it has been justified by the cases of Villeneuve, Jürgensen, Viry, Rosenstein, West, Partzevsky,[8] and Savory. Although these operators did not all practise free incision, yet the study of their cases shows the absence from danger and the propriety of such incision. As far as I {796} know, no cases of purulent pericarditis have recovered after simple aspiration. The case of Rosenstein and that of West, however, did recover after incision and drainage; and in that of Villeneuve, which was originally serous, there remained a fistulous track discharging pus for nearly six months, when spontaneous closure and cure resulted. Gussenbauer has successfully treated pyopericardium following acute osteo-myelitis at the shoulder by resection of five ribs and washing out the sac with a thymol solution.[9]
[Footnote 8: See _Lond. Med. Rec._, Feb. 15, 1883.]
[Footnote 9: _Wien. med. Wochenschr._, Nov. 21, 1884, quoted in _Medical News_, Philada., Jan. 17, 1885.]
Pericardial fistules, due to spontaneous or operative evacuation, should be managed by dilatation, with compressed sponge, and irrigation of the cavity with astringent or disinfectant solutions. Some supposed pericardial fistules may be pleural fistules, or sinuses opening into small pockets between the parietal and visceral layers of an adherent pericardium, or entirely external to the pericardium in new tissue occupying the mediastinum. Such sinuses should be laid open with the scalpel, and compelled to granulate from the bottom. Sinuses dependent upon diseased rib, sternum, or cartilage should be laid open, and the necrotic or carious structure removed by burr or chisel.
Incision of the pericardium under antiseptic precautions may be useful, and is justifiable as a diagnostic procedure in grave cases when doubt exists between a large pericardial effusion and a dilated heart. The wound will scarcely increase the danger if the pathological condition be cardiac dilatation, and may save life if effusion be the cause of the threatening symptoms. The case of Vigla upon which Roux operated shows the value of such procedures.[10]
[Footnote 10: Trousseau's _Clinical Medicine_.]
Aspiration is the method to be employed at first in all instances of pericardicentesis. Incision is to be reserved for the second step in purulent pericarditis, for diagnostic purposes, and for the extraction of foreign bodies, and similar operative designs. The best point for aspiration is usually in the fifth interspace, just above the sixth rib, and about five or six centimeters (2-2¼ inches) to the left of the median line of the sternum. In a child it should be a little nearer the sternum. The point advised is outside of the line of the internal mammary artery, is in a wide portion of the intercostal space, corresponds with the notch in the border of the left lung, is low enough to preclude wounding the auricle, high enough to avoid the diaphragm, and does not approach the point where a cartilaginous band often joins the fifth and sixth costal cartilages. Both layers of the pleura will probably be pierced by the aspirating-needle at this point, but this is not an important complication, and can only be avoided with anything like certainty by going close to the sternum, which is objectionable on other grounds.
The aspiration may be performed by using the pump and the ordinary needle or trocar which is furnished by instrument-makers in the aspirator-case. In cases of emergency or for mere exploratory puncture the common hypodermic syringe and needle will answer the purpose. The puncturing instrument should be clean and anointed with carbolized oil, and in all cases the vacuum-chamber should be attached to the needle or trocar as soon as its point is buried beneath the skin, in order that a flow of fluid may indicate the moment at which the pericardial sac is entered. Abrasion of the heart, which may occur from contact with the needle-point when the fluid is almost entirely evacuated, is not very important, but should be avoided if possible by deflecting or partially withdrawing the needle, or by using Roberts's improved pericardial trocar or that suggested by Pepper. The instrument figured in my monograph on _Paracentesis of the Pericardium_ was too large {797} for use. The improved instrument here figured is no larger than a moderate-size aspirating-needle. It consists of such a needle, flattened at its upper extremity to give the surgeon a firm hold, within which slides a canula. The distal end of the canula, made flexible by a spiral, when thrust beyond the point of the needle curves downward, and thus prevents the point of the puncturing instrument injuring the heart when the sac is nearly emptied. During penetration of the thoracic wall the canula is retracted, so that the flexible end is contained within the needle, and the perforation at the end of the canula allows the fluid to escape as soon as the sac itself is punctured. The canula is then thrust forward until the sharp point of the needle is guarded. This movement brings a lateral fenestra in the canula opposite a similar opening in the needle, and thus provides a second orifice for the escape of fluid in case the terminal one becomes occluded. The external end of the canula has a square shoulder to prevent rotation within the needle, and should be tight enough at that point to preclude entrance of air. The canula finally terminates in a ground end for attachment to the aspirator-tube. The needle--or outer canula as it may be called--is marked on the surface to show the number of centimeters concealed in the tissues. If the inner canula is suspected to be clogged with shreds of lymph or with thick pus, it can be withdrawn without disturbing the needle. The attachment may then be made to the latter as if it were an ordinary aspirating-needle, or the inner tube being cleaned may be reinserted. This is an important element, gained by using a double aspirating-trocar; for plugging is not uncommon in pericardicentesis done for chronic inflammation of the sac.
Beverley Robinson of New York has still further modified[11] my trocar. His additions may have improved the instrument if they do not unduly complicate it. Pepper, after operating upon his case, had made a delicate double canula, the inner tube of which was furnished with a fine needle-point. After introduction the inner tube was withdrawn until its point was sheathed.[12]
[Footnote 11: _New York Med. Record_, March 29, 1884.]
[Footnote 12: _Medical News and Library_, Philada., March, 1878.]
It is said that at the meeting of the Italian Medical Association at Pisa in 1878, Baccelli proposed a new method of puncture; but the account given by Severi[13] in speaking of Baccelli's cases indicates that his proposal referred not to a method of operating, but to a method of selecting the point of puncture.
[Footnote 13: _Lo Sperimentale_, Aprile, 1881, p. 392.]
It must also be remembered that failure to obtain fluid when pericardial effusion existed has occurred because the needle had been passed through a costal cartilage, and was thus plugged by a disk of cartilage. The manner in which the intercostal spaces are narrowed and changed in direction by the curving upward of the anterior portion of the ribs and by the curvature of the cartilages should be impressed upon the operator.
If failure to obtain fluid occurs, and the diagnosis remains quite certain from the symptoms, withdrawal of the needle and puncture in another position should be done or an incision of an exploratory kind made.
{798} In pericardicentesis care must be taken not to thrust the needle or trocar into the heart. This may happen even in quite careful hands. If the right ventricle is entered, venous blood will escape through the canula; if the needle is buried in the cardiac muscle, no fluid or blood can escape. The violent movements communicated to the needle will usually indicate that the needle is either in contact with the heart or thrust into its tissue. Of course such movements will occur from cardiac contact when most of the fluid has been withdrawn; but are not to be expected immediately after the introduction of the puncturing instrument unless the fluid is very small in amount, the needle deeply inserted, the pericardium adherent at the point of puncture, or the diagnosis of fluid an error.
Puncture of the heart has occurred accidentally during pericardial tapping without doing any harm, and has been suggested as a proper surgical procedure in certain cardiac conditions. Still, it is an accident to be avoided by the use of proper trocars and pumps, by the selection of a proper site of operation, by the adaptation of the suction power as soon as the point of the trocar or needle is buried beneath the skin, and by other precautions that will suggest themselves. In thick, oedematous, or fatty chest-walls no fluid will be reached perhaps until a depth of four or five centimeters (about two inches) has been attained by the point of the puncturing apparatus.
I must call attention to the fact that West[14] records a case of pericardial tapping occurring at St. Bartholomew's Hospital in 1874 where a trocar and a canula were introduced through the fourth left space near the edge of the sternum, and caused death in five minutes from hemorrhage into the pericardium, due to tearing of the right ventricle. The position chosen and the form of instrument may have had to do with this unfortunate result, of which the details are not given.
[Footnote 14: _Med.-Chir. Trans._, 1883, pp. 259, 275.]
A few words on cardicentesis, or intentional heart-puncture, may here be appropriate. It has been suggested as a means for rapid abstraction of blood from the right heart in intense pulmonary and cardiac engorgement, and for the abstraction of air after air-embolism has occurred from wounds of the large venous trunks. It has been known for years that aspiration and similar punctures of the heart are comparatively harmless. Roger accidentally withdrew 200 grammes of blood from the right ventricle of a boy of five years without doing harm. Hulke seemed to benefit a case of pleuro-pneumonia by accidentally aspirating the right heart. Cloquet, Bouchut, Steiner, and Legros and Onimus have made similar observations on the absence of danger from such wounds. Westbrook of Brooklyn, Corwin,[15] Dana,[16] and apparently Janeway of New York, have performed intentional cardiac aspiration in moribund patients without causing any noticeable harm. The contributions of Westbrook,[17] Roberts,[18] and Leuf[19] on this topic, as well as that of Senn[20] on air-embolism and its treatment, will interest those who wish further information.
[Footnote 15: _N.Y. Med. Record_, March 10, 1883, p. 263.]
[Footnote 16: _Ibid._, Feb. 3, 1883, p. 140.]
[Footnote 17: _Ibid._, Dec. 23, 1882.]
[Footnote 18: _Philada. Med. News_, Jan. 13, 1883.]
[Footnote 19: _Amer. Journ. Med. Sci._, Jan., 1885, p. 79.]
[Footnote 20: _Trans. Amer. Surg. Ass._, 1885, and _Annals of Surgery_, St. Louis, 1885.]
* * * * *
The results of operations for pericardial aspiration or incision are exceedingly good when the frequent postponement of the operation till the patient is almost moribund is recollected. Elaborate statistical tables would be out of place in this volume; and, besides, it seems almost impossible to get a complete collection of the cases. Hindenlang, West, and I have published {799} and analyzed long lists of cases collected from various sources, and I have now references to more, but this tabulation seems unnecessary, as the practical points to be derived from their study are well proved by the previous work done. In addition to the bibliographical notes already given, I add for the use of inquirers in this field two recent monographs--one by a German,[21] the other by a French writer.[22]
[Footnote 21: _Ueber Paracentese des Herzbeutels_, Gerhard Beck, Würzb., 1882, p. 33 (Thesis).]
[Footnote 22: _Contribution à l'Étude de la Paracentèse du Péricarde_, H. Ferraud, Bordeaux, 1883.]
{800}
DISEASES OF THE AORTA.
BY G. M. GARLAND, M.D.
Acute Aortitis.
The existence of inflammation of the membranes of the aorta was mentioned by Galen and other early writers, but it was not until 1824 that a systematic treatise on this subject was published. Since that time the subject has received more attention, but the results obtained are unsatisfactory. There is grave doubt, according to many writers, as to the existence of acute aortitis independent of other lesions, although it is recognized that the aorta may participate in inflammation of the neighboring organs. Even then, as Powell says, "the aorta is very slow to share in such processes, and when it does so the inflammation is very chronic and limited, giving rise to no special symptoms." Peter treats the subject at length, and after enumerating certain so-called symptoms of acute aortitis, confesses that these symptoms are merely the ordinary phenomena of angina pectoris, and these two affections cannot be distinguished from each other. It must be concluded for the present, therefore, that acute aortitis is rare, and that we know of no symptoms which are characteristic of it.
Atheroma of the Aorta.
Atheroma of the aorta is the result of chronic endarteritis, and is always of slow development. The process may be limited to the intima or it may extend to the middle and outer tunics. Beginning with a thickening and softening of the wall, it finally develops plates of calcareous deposit. These plates are most numerous in the region of the aortic valves, and diminish in number as the artery proceeds from that point. The descending portion of the aorta is relatively free from these patches, but they reappear again near or at the bifurcation.
ETIOLOGY.--Atheroma is one of the ordinary products of old age, and is therefore one expression of senility. Heredity probably exerts some influence, and certain cachexias predispose to an early occurrence of the process. Gout and syphilis render one especially prone to it. High pressure and strain are also important factors. Continuous hard toil is more productive of atheroma, according to Allbutt, than intermittent work. The pre-albuminuric stage of Bright's disease, which is characterized by high arterial pressure, is frequently productive of atheroma.
SYMPTOMS.--When the inner coat alone is affected, there are no symptoms of this disease. According as the degeneration extends deeper and involves the middle and outer tunics, the aorta begins to dilate, and the symptoms may vary from the slightest feelings of discomfort upon exertion to the most violent attacks of palpitation and pain.
{801} Usually, at the beginning the symptoms are very obscure. A slight dyspnoea on exertion, or palpitation, or dyspeptic troubles are the chief complaint. The presence of these troubles in a man of fifty years or over, whose heart and kidneys present nothing abnormal, and in whom the smaller arteries of the extremities feel hard and calcareous, may excite the suspicion of atheroma of the aorta. There are no distinctive physical signs. Some writers speak of a short post-systolic murmur over the aorta beyond the valves, which may be audible only when the heart is acting strongly.
The aorta is almost invariably dilated, and Peter says that this dilatation may be traced by percussion. According to him, the normal aortic dull area measures from two to five centimeters transversely in the male, and from two to four centimeters in the female. He says that he has seen cases of atheroma where he was able to determine a dull aortic area of eight centimeters in diameter. If the inflammation extend from the aorta to the neighboring nerves, the patient may suffer from the ordinary symptoms of angina pectoris.
TREATMENT.--This disease cannot be cured by drugs. The physician's task is to regulate the habits of the patient, to remove so far as possible all conditions which tend to aggravate and increase the trouble, and to alleviate incidental symptoms of distress.
Thoracic Aneurism.
DEFINITION.--The origin of the term aneurism is buried in obscurity, and the theories which have been advanced regarding it are not very satisfactory. Montanus thought it was derived from _a_ privative, and _neuron_, a nerve. Oetius declares it is from _aneurisma_, an enlargement, from _eurumo_, I dilate. Coale thinks a ready origin is offered in the words _aneu_, without, _rusmos_, a series, course, or succession, from _ruo_, I flow.
Aneurism of the aorta is a local dilatation of that vessel. When all the arterial tunics persist unruptured in the tumor, it is a true aneurism. When one or more of the tunics are torn in the process of expansion, it becomes a false aneurism. When all the tunics of the artery rupture and the blood escapes into the neighboring cellular tissue, it becomes a diffuse false aneurism. The internal and middle coats of an artery may burst, and the blood escape into and coagulate in the space between the middle and external tunics, and this is termed a dissecting aneurism. In rare instances of this type of aneurism the blood finds a second opening, and returns into the artery again, thus forming a double tube for a short distance.
In former times great stress was laid upon the distinction of aneurism according to the number and combination of persistent tunics, and we read of the mixed internal and the mixed external type. These points have less clinical importance, however, than a proper appreciation of the size and shape of a tumor, because all aneurisms are false after they exceed a certain size. When an aneurism involves the entire periphery of the aorta, it may be cylindrical, fusiform, or globular in shape, and receive names accordingly. When it is a mere bulging on one side of the artery it is saccular in shape. Obviously, the opening into the fusiform aneurism is quite or nearly the entire length of the tumor, whereas in the false saccular type the orifice may be reduced to a mere puncture of the arterial wall. The size of the orifice is a matter of great importance, particularly in connection with the question of operative interference, and therefore it will be referred to later. The sacciform and fusiform aneurisms are often combined together, or, in other words, it is quite common to find a lateral bulging superimposed upon a local dilatation of the artery; but such grouping is not necessary, as either form appears {802} without the other. It is not uncommon also to find one bulbous aneurism superimposed upon another, the dependent aneurism in this case being of the false or diffuse type. The second aneurism often lies outside the chest-wall, and it is connected with the mother aneurism by a narrow opening or channel.
Varicose aneurism is a false aneurism formed by communication between the aorta and the vena cava, the pulmonary artery, the right auricle, or the right ventricle. It is almost without exception rapidly fatal and not amenable to treatment.
Occasionally the aorta will present alternate bulgings upon one side and the other, so that the vessel appears to wind in its course. This condition is called cirsoid aneurism, but it has nothing in common with external aneurism of the same name.
The size of an aneurism is variable, like its shape, but in general the true aneurism rarely exceeds the size of an egg (Jaccoud). Beyond this size one or more of the coats give way, and the aneurism becomes false, in which condition it may grow as large as an adult's head if the patient lives long enough to allow such development. Balfour refers to two rare forms of aneurism--the intravalvular, which is situated within the aortic valves and above the ventricle, and the intervalvular, which is still more rare, and is situated between the valves themselves. The symptoms of these aneurisms are merely those of valvular lesion, and therefore present no differential points for diagnosis.
ETIOLOGY.--Local weakness of the aorta submitted to sudden strain is unquestionably the most frequent cause of aneurism. It is rare to find an aneurism in an otherwise healthy aorta, and some authors go so far as to assert that aneurism never occurs without preceding degenerative changes in the arterial wall. Naturally, strain is the physiological burden of the aorta, and this strain tends sooner or later to degeneration of the arterial tunics. Then, given a weakened spot, the ordinary occurrences of every-day life are sufficient to precipitate disaster. A sneeze, a cough, some sudden exertion of the body in lifting or moving, have been the starting-points of aneurism. All accumulated testimony indicates that sudden strain is more dangerous than prolonged uniform strain, and therefore some occupations are more productive of aneurism than others. Inasmuch as age, sex, occupation, and personal habits influence the development and nutrition of the aorta, it is obvious that they must exert an important influence upon the occurrence of aneurism.
All records agree that aneurism is pre-eminently a casualty of middle life, and a glance at the accompanying table, which I have prepared from an analysis of 69 reported cases, shows that the disease is most common between thirty and fifty years of age:
From 20 to 30 years of age, 4 cases.
" 30 " 40 " " 21 "
" 40 " 50 " " 29 "
" 50 " 60 " " 14 "
" 60 " 70 " " 1 case.
Youngest case, 20 years of age.
Oldest " 72 " "
Crisp analyzed 551 cases, and reports 398 between the ages of thirty and fifty.
Beneke has found in his records of arterial measurements that the pulmonary artery greatly exceeds the aorta in circumference up to the age of thirty. After that period the aorta begins to increase with relatively greater rapidity, until in the forties it exceeds the pulmonary artery in size, and it maintains its superiority from that time forward. The aorta continues to increase in circumference throughout life, but after the age of fifty this increase is considered a senile dilatation rather than an actual growth. It is interesting to {803} note that the era of greatest liability to aneurism coincides with that of most rapid aortic development.
Sex furnishes a distinction in the frequency of aneurism. In 82 cases I found that only a seventh were females; Crisp registers less than an eighth. The radically different occupations and habits of women may contribute somewhat to their relative immunity from aneurism, and their physiological development also seems in their favor. Beneke states that the blood-pressure during childhood is about the same for both sexes. From puberty onward it is greater in the male. This is due to the fact that after puberty the volume of the heart relative to the length of the body is less in the female than in the male, and at the same time the main arteries of the body relative to the length of the body are only a trifle narrower in women than in men. The pulmonary artery, indeed, is relatively a trifle wider in women than in men. It follows from this that the blood-tension in both the large vessels emerging from the heart is less in the female than in the male.
In general terms, it may be said that those people who are exposed to heavy labor, as mechanics, laborers, soldiers, porters, cabmen, etc., are more liable to aneurism than those who are less exposed to such straining efforts. Fixture of the chest during effort brings greater strain upon the heart and aorta, and therefore men who wield heavy hammers and sledges are especially liable to aortic disease. Constriction of the neck or forcible extension of the same during exertion is dangerous, because it thus happens that the arteries are stretched in their long diameter at the same instant that the blood-wave is expanding them laterally, and they are thereby subjected to double strain. I knew of a trotting horse which was killed by this very combination of strain upon the aorta. At the end of a trial of speed the animal refused to stop; whereupon a groom sprang forward, seized him by the bit, and threw his head strongly upward and backward. His carotids and aorta were thus stretched to full length at the moment when his heart was acting with great force. The horse dropped dead, and the autopsy revealed a rupture of the aorta.
The frequency of aneurism among the soldiers of the English army was long the subject of anxiety and thought to English surgeons. Finally, some bright man recognized one cause in the dress of the soldiers. They were obliged to wear a high stock, which constricted the neck and kept it stretched, and their trappings were adjusted so as to keep the body in a stiff and unnatural position. These objectionable details of the dress have been removed, and it is now claimed that aneurism is much less common in the army.
Syphilis and gout undoubtedly contribute to the formation of aneurism, because they both dispose to degenerative processes in the arterial tunics. Some writers, however, have laid too much stress upon syphilis. It was claimed that this disease was the cause of the great frequency of aneurism in the English army. Barwell, however, calls attention to the fact that aneurism has been 13½ times more frequent per 1000 men in the army than in the navy, and yet no one maintains that syphilis is more common in the army than in the navy.
SYMPTOMS.--The diagnosis of aneurism of the aorta may be one of the easiest problems of clinical medicine, or it may present difficulties which defeat the most skilful diagnosticians. A large number of aneurisms utter no sign of their existence, and are only revealed by the manner of death or by an autopsy. Again, the so-called signs of aneurism are so indefinite in character, and so associated with other pathological conditions, that the greatest confusion often befogs their interpretation. Mistakes therefore arise in two ways: either aneurism is diagnosed as present when it is absent, or it is declared absent when present. Robin reports the case of a vigorous young man upon whom several of the most eminent clinicians of {804} Paris diagnosed aneurism of the aorta, and yet a rest of a few days sufficed to remove all symptoms of that disease. Three candidates for the diploma of the Royal College of Physicians and Surgeons in England recently declared a case of loculated pleurisy to be aneurism of the aorta, and B. W. Richardson says he has "seen at least seven persons suffering severe mental anxiety from the belief that they were fatally struck with aneurism," and yet they were free of such disease. Balfour says: "There is only one phenomenon positively characteristic of thoracic aneurism, and that is the existence in some part of the thorax of a pulsating tumor other than the heart, which beats isochronously with it, and at least as forcibly, and which at each pulsation expands in every direction." And yet simple dilatation of the aorta, combined with mental excitement, will so increase the thoracic pulsations as to simulate aneurism. It is necessary, therefore, that a patient during an examination should be as quiet as possible, both in mind and body, and if any doubt exist regarding the significance of the symptoms present, the patient should be kept in bed for a few days in order to allay the arterial excitement.
The phenomena produced by an aneurism are naturally divided into two groups: 1. The direct symptoms, which are confined to the limits of the tumor itself, and which are termed the physical signs. 2. The indirect symptoms, which are due to the influence of the tumor upon neighboring organs, and which present themselves often at remote points as signals of distress within. This influence of the tumor upon its environment is purely mechanical and due to pressure, and the resulting symptoms vary according to the particular organ or function involved. These symptoms are therefore classified as the physiological signs.
Pain is one of the earliest and most troublesome of the pressure symptoms of aneurism. It is due to a stretching of the nerve-filaments in the aortic wall and to the pressure of the tumor upon neighboring organs, especially the vertebral column and sternum. When due to nerve-stretching, the pain is neuralgic in character, and is not necessarily confined to the chest. It may appear in the back, and is intensified by coughing or sneezing. It may be rheumatic in type, and affect the arm and shoulders for several months before other aneurismal signs develop. In such cases the right arm and shoulder appear to be most often affected. Sometimes the pain cannot be located, but is referred indefinitely to the chest, or it may accompany acts of deglutition. As a rule--and this point is important--this form of pain from an aneurism exhibits wide variations of intensity and is usually intermittent. Exercise, coughing and sneezing, mental excitement, or anything which increases the activity of the circulation or raises the blood-tension, increases the pain. It may resemble angina pectoris in location and radiation, but it differs essentially otherwise. It is more continuous, and is associated with less anxiety, which is such a conspicuous element of angina.
When the pain is due to erosion of the vertebræ or sternum, it is more steady and gnawing. It is still liable to violent exacerbations, and excitement of all kinds increases it. Oftentimes the pain is so excessive that the sufferer cannot lie down or obtain relief in any position. This is especially the case with aneurism of the abdominal aorta. Bennet reports the case of a patient who poisoned himself to be free from the terrible pain, and deaths by exhaustion from pain and distress are not uncommon.
Numerous other accidents besides pain arise from pressure upon the neighboring veins. Balfour says that severe dyspnoea, vomiting, and flatulency are frequently caused by pressure of an aneurism upon the pneumogastric nerves, and that these symptoms may be relieved by gently rubbing the tumor. Hiccough and paralysis of one-half the diaphragm are caused by pressure upon the phrenic nerve. Occasionally destructive inflammations of {805} the lung and pleura occur with aneurism, and these have been attributed to pressure upon the pneumogastric nerves and the pulmonary plexus. Palpitation of the heart is likewise often produced in a similar manner. Sometimes the patient is conscious of a pulsation in the tumor itself. Pressure upon the intercostal nerves will produce herpes zoster, and cicatricial records of such attacks are found upon patients with aneurism. Implication of the sympathetic nerves produces modifications of the pupils according as the nerves are merely irritated or paralyzed. In the first case the radial muscles of the iris become permanently contracted and the pupil is dilated. In the second case the radial muscle becomes paralyzed and the pupil is contracted. Jaccoud says that this succession of changes is not rare, and he has watched cases progress through both pupillary stages. The nerves affected are those which emerge from the cilio-spinal region, which extends, according to Budge and Waller, from the sixth cervical to the sixth dorsal, or, according to Brown-Séquard, as low as the tenth dorsal vertebra. From the anterior roots of this region nerve-filaments pass through the cervical sympathetic to the iris. The difference in the pupils is often so slight that it requires very careful measurement to detect it. The application of atropia will assist in the examination, because that drug has very incomplete influence upon the affected pupil. The pupil is also much less sensitive to light, but it contracts more strongly than the normal eyes in its accommodation for near objects. Robertson cautions against conclusions based upon mere casual observance of the eyes, because 1 person in every 14 has one pupil naturally smaller than the other.
Myosis is not pathognomonic of aneurism. It denotes merely some trouble with the cilio-spinal nerves. The nature of that trouble must of course be determined by the other associated symptoms of the case. The contraction of the pupil is sometimes accompanied by paleness of the corresponding side of the face and neck, while at other times the same region may be swollen, oedematous, and perspiring. These symptoms are due to local vascular changes from interference with, and disorganization of, the vaso-motor nerves which govern these regions. Remote local paralysis sometimes utters the first warning of aneurism, and such cases are usually very striking. Paralysis of the recurrent laryngeal is the most frequent of this group of signs. Urquhart reports a case where for some months the chief symptom was a falling of the head on the breast, as if it had been forcibly drawn down by the sterno-cleido-mastoids. Another patient was supposed to have rheumatism, but he soon became paralyzed on the right side and lost his speech. He recovered somewhat, but died subsequently from bursting of the tumor into a pulmonary cavity. Tufnell says if an amaurosis occur suddenly look for valvular disease of the heart or for aneurism of the aorta.
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A system of practical medicine. By American authors. Vol. 3Chapter LV: Part 55
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