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A System of Practical Medicine. by American Authors. Vol. 1 · William Pepper — chapter 64 of 190 · ~2,804 words · public domain

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Wyss and Bock speak of enlargement of the mesenteric and retroperitoneal glands as of frequent occurrence, but we did not observe it, and Murchison states that these glands present no abnormal appearance.

Alterations of vascularity of the brain or its membranes are met with, but they are variable and bear no definite relation to the precedent symptoms. Ecchymoses of the membranes are occasionally observed, and in one of our cases extensive meningeal hemorrhage was found. Murchison reported a case in which embolism of the left femoral artery occurred, and subsequently of the left middle cerebral artery, inducing death. The suggestion may be hazarded that in some of the cases where there is severe delirium ending in stupor and death there has been multiple capillary embolism of the cerebral vessels.

There is occasionally the evidence of catarrhal inflammation of the upper air-passages, and in some epidemics diphtheritic exudation in the pharynx and larynx has been noted (Wyss and Bock); and Ponfick found acute oedema of the glottis in a considerable proportion of the fatal cases at Berlin. The lesions of pleurisy are met with in a small proportion of cases; in our own autopsies this complication was more frequent than in most epidemics.

The lungs may be normal, and Murchison concludes that they are more frequently so than in typhus. Still, they often present congestion or oedema, and subpleural ecchymoses, hemorrhagic infarctions, and pneumonic consolidation are not rare. Lobar pneumonia was present in 33 per cent. of our own autopsies, in 28 per cent. of Carter's, and in 20 per cent. of those conducted by Ponfick. The inflammation usually presents the regular stages, and is associated with a moderate degree of plastic pleurisy; but occasionally, as in one of our cases, it terminates in gangrene. In the instance referred to there was an area of gangrene about three inches square and one inch in depth, involving the pleura and a {414} superficial layer of lung on the antero-lateral aspect of the left lower lobe. In another remarkable instance, already referred to on account of the suppurative inflammation of one masseter muscle, the lungs, which were stained yellow throughout, presented numerous deep purplish patches, which on section altogether resembled the secondary metastatic deposits of pyæmia, with yellowish softening or even puriform centres surrounded by a rim of purplish livid discoloration. Very numerous similar patches, varying from the size of a pea to that of a hazel-nut, and presenting every stage of development, were found throughout both lungs. In a few instances we found the lesions of chronic phthisis, which had, of course, existed before the attack of relapsing fever. The bronchial glands were found swollen and infiltrated in cases where inflammatory processes in the lungs have existed.

Much interest attaches to the state of the genito-urinary organs in relapsing fever, but caution is required to distinguish lesions that have existed prior to the attack from those properly referable to it.

Owing to the intemperate and exposed lives of many of the patients, renal lesions might reasonably be expected in no small proportion. The comparative rarity of albuminuria (see p. 407), even in severe cases, is suggestive of the view that when it is present it may at least sometimes be due to pre-existing lesions aggravated by the acute infectious process, and further that the extreme gravity generally presented by such cases may be in part due to the impaired condition of the kidneys.

The morbid changes most frequently referable to the fever are moderate enlargement and congestion, occasionally very intense so that we find it described in our notes as deep blackish-purple or blue; ecchymoses of the capsule or of the mucous membrane of the pelvis; small hemorrhagic infarctions, usually in the cortex; and cloudy swelling of the glandular cells. Less commonly are found hemorrhagic infarctions, or small embolic patches advanced to various stages of disintegration, even to the formation of small puriform collections. In quite rare cases the lesions of acute nephritis are present, while caution must be used in interpreting other changes occasionally met with, such as pallor with granulo-fatty degeneration or other advanced alterations of the glandular cells, or hyperplasia of the intertubular connective tissue, with or without contraction of the kidneys.

The mucous membrane of the bladder, as already mentioned, may present ecchymoses, or, more rarely, croupous exudation (Wyss and Bock). The urine contained may be bloody, or, as in one of our cases where there had been total suppression of urine for over seventy-two hours before death, there may be but a small amount of almost pure blood, containing a few phosphate crystals, but no tube-casts. In this case there were also ecchymoses of the bladder and of the pelvis of the kidneys, with intense congestion and numerous small hemorrhagic infarctions of the kidneys.

The liver is constantly though variously affected. It is found enlarged in the great majority of cases, especially if death has occurred during the febrile stage. The ordinary degree of enlargement in our cases was from four to four and a half pounds, but in a few instances the liver weighed one hundred or one hundred and two ounces, though in most of these extreme cases the patients had been drunkards, and there was such advanced fatty alteration of the liver as to make it probable that the {415} organ had been diseased previously. These figures correspond with the results of other observers.

In many cases, especially when death occurs early and during the febrile stage, the capsule and substance of the liver are congested, at times intensely so; and when ecchymoses are found elsewhere they are apt to be present here also, appearing as purplish patches dotted over the capsule and extending into the superficial layer of hepatic tissue. Not rarely, however, the liver substance is paler than normal, and presents a yellowish tinge, apart from the decided yellowish staining present in cases attended with jaundice. Carter describes a partial mottled paleness of the liver as having been frequently observed in his cases, the circumscribed pale areas presenting a corresponding localized degeneration of the cells, as though from some local interruption of circulation.

Cloudy swelling and fatty degeneration of the liver-cells are indeed very often present, and in some epidemics with preponderance of bilious symptoms are constantly found (Ponfick). The degree of the cell-alteration varies from a slight granulo-fatty change to an advanced fatty degeneration, even with a marked tendency, in rare cases, to disintegration of the cells, so as to produce lesions analogous to those of acute yellow atrophy (St. Petersburg epidemic).

The whitish deposits described by Küttner as due to albuminous or fibrinous infiltration are probably referable to transformed hemorrhagic infarctions, and the minute puriform collections that have been observed at the centre of the acini (Wyss and Bock) may have been metastatic in origin, or attributable to the disintegration of minute thrombi associated with irritative hyperplasia of the adjacent lymphoid elements. The consistence of the liver varies: when death occurs early and bilious symptoms have not been marked, it may be even firmer than normal, but more frequently it is softer, and it may be relaxed, flabby, and friable.

The condition of the bile-ducts is of great interest in view of the frequency of jaundice as a symptom in relapsing fever, and most authorities unite in saying that they present no lesions capable of explaining it.

The gall-bladder is usually found full of dark bile, but there is no such degree of inspissation, except in rare instances, as could interfere with its passage through the ducts. Murchison quotes the statement of Peacock that in some instances the bile was thick and viscid, so as apparently to cause obstruction, but all observations agree in showing that this is exceptional. The mucous membranes of the larger ducts may present evidences of slight catarrhal inflammation, but in nearly all cases where they have been carefully examined, even when jaundice had been marked, they have been found patulous and free, so that the jaundice cannot be regarded as due to obstruction of the larger ducts save in rare instances (Pastau). In further confirmation of this may be stated the fact that there is no want of bile in the duodenum and feces.

On the other hand, a careful consideration of the lesions of the substance of the liver will show that it would be most improbable that the minute biliary ducts in the areas most affected should escape implication. Münch, who investigated this subject carefully, found that there was a catarrhal state of the fine bile-ducts in every case of relapsing fever with jaundice; and Litten found the smallest ducts plugged with bile-stained pellets of mucus. It would appear, therefore, that in many cases at least {416} the jaundice is really obstructive in its origin, the seat of the obstruction being in the too-rarely examined minute bile-ducts, though further investigation of this interesting question is required.

The clinical bearing of these conditions has been fully discussed in the appropriate section.

The changes in the spleen are constant, and even more remarkable than those in the liver. It is enlarged with rare exceptions, and especially so if death has occurred during the febrile stage. Upon the subsidence of the fever the spleen probably returns to its normal size more rapidly than the liver. The more common extent of the enlargement in our own cases was from ten to eighteen ounces, though we found the spleen in one case weighing twenty-nine and a half ounces and in another forty-four and a half ounces. In neither of the latter instances was there any reason to suspect malarial complication. The most extensive enlargement we have found recorded is sixty-eight ounces in a case reported by Küttner.

There is usually a correspondence between the stage and extent of the splenic and hepatic lesions, but this is not invariable, and one or the other organ may present a far higher degree of enlargement or much more intense interstitial changes. It may be mentioned, moreover, that in some unusual cases the lesions of the lungs, such as ecchymoses and hemorrhagic infarctions, may be disproportionately marked as compared with those of either the liver or spleen.

The capsule of the spleen often presents a mottled look, with at times large purplish ecchymoses; it is apt to be more or less opaque, and local peritonitis, with thin layers of plastic exudation often forming friable adhesions with the abdominal wall, may exist.

In one of our cases the capsule presented a small perforation or rupture, with an exudation of plastic lymph over an area of four by six inches, and diffuse peritonitis, with effusion of bloody liquid with shreds of lymph throughout the abdominal cavity. This fatal termination is fortunately rare, but there are several other instances on record. The splenic pulp may retain its consistency and firmness, even in cases that have run a long course; but more frequently it is softened, and may be almost diffluent. The pulp is often swollen, so that when cut it projects above the section. The color is darker than normal, and often is of a deep maroon color. This swelling is due to enlargement of the blood-vessels, associated with great increase of the cellular elements of the pulp and with enlargement of the Malpighian corpuscles.

When death occurred early in the disease we found these bodies grayish or grayish-yellow in color and of the size of hempseed, so that the section very thickly studded with them closely resembled shad-roe, and this stage of the lesion is frequently described in our notes as the shad-roe spleen. Subsequently, the Malpighian bodies enlarge still more, and stand out above the section a line or more in diameter, and of a lighter color; not rarely, several of them come in contact, and thus form a considerable mass of irregular shape, resembling the infarctions described below. It is probable that central softening may occur later in the {417} Malpighian bodies, though we are inclined to regard the puriform collections frequently found as chiefly due to the disintegration of hemorrhagic infarctions or of embolic patches. Of these, hemorrhagic infarctions are by far the most common and present the familiar appearances. They may be quite numerous, superficial, or deep-seated, and of variable shape and size. At first dark reddish, firm, and sharply separated from the surrounding pulp, they grew reddish-yellow or yellowish later, softened in the centre, and eventually were transformed into puriform collections. Doubtless, in a large proportion of cases that recover such infarctions exist and are slowly absorbed. Ponfick has shown that these are venous infarctions, the arterioles leading to them being patulous. True arterial embolism does, however, occur, though much more rarely (Ponfick, Murchison), giving rise to firm, wedge-shaped infarctions at the periphery of the spleen, which may undergo degenerative changes similar to those above described. The resulting abscesses may burst into the peritoneum, pleura, lung, or bowel. The microscopic appearances have been most fully described by Ponfick, our own comparatively meagre observations having accorded entirely with his subsequent accurate description. The cells of the swollen pulp contain red blood-discs and pigment, and some present collections of bright granules. The lymphoid cells of the Malpighian corpuscles are at first in a state of cloudy swelling with multiplication of their nuclei, and later show marked granular fatty degeneration.

The lymphatic glands present no lesions, and the pancreas is normal.

The peritoneum is not affected as frequently as other serous membranes in this disease. Superficial ecchymoses are, however, quite common, especially so over the solid viscera; and more rarely effusions of blood have been found in the subperitoneal connective tissue, involving the muscular or glandular tissues beneath. We have already mentioned (p. 406) the occasional occurrence of local peritonitis, most frequently of the splenic capsule, and also the rare accident of diffuse inflammation from rupture of the spleen.

The marrow of the bones was carefully examined by Ponfick, who first called attention to the presence of important changes in relapsing fever, which have since been confirmed by other observers. These changes consist in proliferation and subsequent degeneration of the lymphoid cells of the marrow, with multiplication of the nuclei in the walls of the minute vessels and fatty degeneration of their coats. As a result of these changes, spots of puriform softening may form, chiefly in the cancellous tissue of the extremities of the long bones, with the production of localized necrosis, and possibly with extension of inflammation to the neighboring articular cavity.

Considerable space has been devoted to the detailed consideration of the pathological changes in relapsing fever, partly because we believe the fact has not been sufficiently recognized that the disease is constantly attended with important and characteristic lesions. These consist, in brief, of remarkable changes in the blood; of widespread ecchymoses and infarctions, which not rarely undergo puriform disintegration; of hyperplasia and subsequent degeneration of the Malpighian corpuscles of the spleen, with changes in the cellular elements of the splenic pulp; of cloudy swelling of the gland-cells of the liver and kidneys, with a {418} marked tendency to fatty degeneration; of changes in the marrow of the long bones; and, finally, of granulo-fatty degeneration of the muscles, and especially of the heart.

DIAGNOSIS AND RELATION TO OTHER DISEASES.--The entire question of the diagnosis of relapsing fever is dominated by that of spirillar infection. Before Obermeier's discovery the differential diagnosis of the initial paroxysm, and to a less extent that of the subsequent events of a case of relapsing fever, was attended with considerable difficulty. But if, as now seems established, immediately before and throughout the initial paroxysm and subsequent relapses a characteristic spirillum is to be detected in the blood upon proper examination, while it rapidly disappears after the crisis, it is evident that as soon as a suspicion is aroused as to the possible presence of relapsing fever the question may be settled conclusively by the microscope.

None the less is it important to consider carefully, but briefly, the symptoms by which relapsing fever is to be distinguished from various affections which may simulate it, because even the most experienced observers admit that the spirillum cannot be invariably detected; because it is not yet known that a similar organism may not be found in some other affections; and, finally, because on the outbreak of an epidemic of relapsing fever, especially in America, where its occurrence has hitherto been so rare, there is strong probability that the nature of the early cases will not be even suspected until the relapse occurs.

Typhus fever often prevails in an epidemic form simultaneously with relapsing fever, so that it was inevitable they should have been for a time confused. Their essential non-identity is, however, now too well recognized to require any lengthy demonstration. The following statement of the heads of the argument may therefore suffice.

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