The pulse in relapsing fever is very rapid, and on the whole the rate corresponds with the movement of the temperature. It usually rises above 110, the limits being 90 and 140, the lower rate being noticed in the milder and uncomplicated cases and in subjects of phlegmatic constitution. The pulse rises rapidly at the invasion, and may reach 120 in the course of a few hours. Its maximum is usually noticed when the temperature is highest, shortly before the crisis; and when this actually begins the pulse may fall with a rapidity as remarkable as that of the decline of the temperature. Thus, within twenty-four hours it may fall from 152 to 80, or in even a shorter time from 140 to 54, or even as low as 48 (Obermeier) or 44 (Muirheid), or even 30 (Stillé). While this great fall is often noted, it is by no means constant. In our own cases it was frequently observed that the critical fall in temperature was not accompanied by a commensurate fall in pulse. Thus, at the close of a very severe initial paroxysm lasting nine days the temperature was 107°, and fell in the course of twenty-four hours to 99°, and in twenty-four hours more to 96°; during the first day of this fall the pulse was from 96 to 100, and during the second it fell to 76.
This want of correspondence was more marked at the close of the {383} relapse than of the primary attack; thus, in a well-marked case, where the maximum temperature (105.4°) occurred eighteen hours before the crisis of relapse, the temperature fell in four hours from 104.4° to 96.2°, while the pulse, which was 130, fell in twelve hours to 108, and in twelve more to 92. In another case, in a man aged twenty, the temperature at the close of the second relapse was 106.4°, with a pulse of only 100; after the crisis, as the temperature fell, the pulse rose to 120, and did not descend until the end of twenty-four hours; and later, at the close of thirty-six hours, the temperature was 98° and the pulse 72, lower than which it did not go. Carter states that in the Bombay epidemic it was invariably the case that the pulse did not decline to an extent corresponding with the temperature.
During the remainder of the intermission the pulse may be normal, or it may continue accelerated in consequence of some irritative condition; as the time for the relapse approaches it frequently again becomes abnormally slow. In either event it is found that any muscular exertion causes marked acceleration of the pulse.
During the paroxysm the character of the pulse is full and bounding, and there is considerable arterial tension. This is well shown in some of the sphygmographic tracings by Carter; while in one of our tracings from the right radial of a man æt. 32, taken on the fourth day of a severe initial paroxysm, the line of ascent is steep and the summit sharp. During the crisis, and for a day or two thereafter, the pulse may be weak, compressible, and dicrotic, and occasionally irregular.
The sounds of the heart and its impulse are weakened, except possibly during the first few days of the primary paroxysm. Blood-murmurs over the base of the heart and along the great vessels in relapsing fever were first noticed by Stokes, and have been frequently observed in subsequent epidemics. They were found in a large proportion of our cases, not rarely in both paroxysms, and during the early stage of convalescence when anæmia was marked; but during the intermissions they are rarely audible, and when the action of the heart was slow they were replaced by prolongation of the first sound.
It must be further noted that the pulse-rate is not a reliable indication of the danger in this disease, since, just as is the case with the hyperpyrexia, extreme rapidity of pulse may be present when the general symptoms denote no unusual danger, and when the patient ultimately recovers most satisfactorily.
There is a remarkable disproportion and dissimilarity between the cerebral and peripheral nervous phenomena in relapsing fever and those familiar to us in typhus and typhoid fevers. We have seen that patients almost invariably complain of headache. When prodromes are present it is commonly among them, and it may be the initial symptom to usher in each paroxysm. When the attack is fully developed headache is usually very severe, and no symptom is more bitterly complained of. It varies in seat and character. More commonly it is frontal or general; occasionally we found it occipital, and still more rarely it was unilateral, constituting hemicrania. It rarely continues during the relapse. Headache of an equally acute and violent character may be present in typhoid, but the headache of typhus is much more dull and contusive.
{384} The mental condition is only exceptionally affected, a circumstance which greatly increases the patient's perception of his sufferings. Delirium is not present in ordinary cases, even though very severe and attended with hyperpyrexia; or if present is limited to the period immediately preceding the crisis, when there may be violent and noisy delirium of transient character. In some of our cases forcible restraint was necessary under these circumstances.
There are numerous instances on record showing the abruptness with which noisy, demonstrative, or even destructive delirium may appear, and the equal suddenness with which in the course of a few hours, or even of fifteen minutes, the patient may become rational and composed. Such attacks resemble hysteroidal spells, and probably occur more readily in patients of a nervous or hysterical temperament. They were certainly more common when the patients had been of intemperate habits; and, further, we had opportunities of noting that the occurrence of relapses in habitual drunkards who had previously suffered with delirium tremens was apt to develop a form of delirium which was to all appearance of that nature.
Delirium of a different and much more grave type may appear in connection with the symptoms of the typhoid state. In some cases this results from the presence of serious complications which induce a state of great prostration, while in others it is associated with great diminution or entire suppression of urine. The delirium under these circumstances is apt to be low and muttering, with a tendency to pass into stupor or profound coma.
Vertigo is present more frequently and in a more persistent form than in any other febrile disease. It was noticed as among the occasional prodromes, and was especially severe for the first few days of the initial paroxysm, though it often continued throughout this stage and recurred with the relapse. Occasionally it was complained of in the recumbent position, but usually it was excited only by a change of position.
Wakefulness was one of the most distressing symptoms in all cases, and appears to have been noted in all epidemics. Although the severity of the pain in various parts of the body and the absence of blunting of the perceptions would naturally cause much loss of sleep, the degree of the insomnia and the obstinate resistance it offers to the action of anodynes are apparently far in excess of what could thus be accounted for. Parry found that several of his patients could take as much as three grains of opium every second hour throughout the afternoon and night without either inducing sleep or causing contraction of the pupils.
Convulsions are rare and of very grave import. They may occur at the period just preceding crisis, when the nervous irritation is most intense, and are then somewhat less indicative of a fatal result than if occurring in the course of the paroxysm, when they are apt to be associated with extreme prostration of the nervous centres, with a tendency to subsequent fatal coma. No connection has been observed between their occurrence and the presence of albumen in the urine.
General tremor is rare, and was observed only in those of our cases where there had been habitual intemperance, with presumably a tendency to delirium tremens. Muscular rigidity was noticed occasionally, but may have been only apparent, being induced by the hyperæsthesia and {385} soreness which were marked in some cases. The hyperæsthesia which was observed was both cutaneous and muscular, and was attended with tenderness of the body of the muscle, and also of the nerve-trunk supplying it. Meschede speaks of opisthotonos as a rare complication in his cases.
Motor paralysis involving single muscles or groups of muscles is occasionally noticed, as of the deltoid or of one arm (Meschede). Parry observed transient loss of power of the extremities in several cases, chiefly during the intermission or the period of convalescence. In one of our cases temporary hemiplegia occurred, with partial loss of sensation on the affected side.
The bladder and rectum are rarely affected, except in cases where the typhoid state with tendency to coma is present. Disorders of sensation are, however, much more common. When motor palsy occurs the affected part may also be the seat of impaired sensibility, while in a large proportion of all cases numbness of the extremities, with or without a sense of tingling, is complained of; out of 182 cases we noted this symptom in 94, affecting the fingers alone in 62, the feet alone in 6, and all the extremities in 25 cases. Cutaneous hyperæsthesia or partial anæsthesia are also occasionally observed. But the most noteworthy and constant symptom of this class are the pains in the muscles and joints which are bitterly complained of by nearly all patients with relapsing fever. They constitute, indeed, one of the highly characteristic features of the disease, and possess a diagnostic value. They may occur among the rarely present prodromes, but usually they appear with the chill and increase in intensity during the paroxysm; they may persist with even greater severity during the intermission, or, if they have then subsided, recur with the relapse, and may constitute one of the most troublesome hindrances to convalescence. It will thus be seen that in frequency, severity, and persistency they differ widely from the aching pains in the extremities complained of in typhus and other specific fevers. They are one of the most potent causes of the extreme insomnia, and are apt to dwell in the mind of the patient so vividly that he dreads each relapse on this account, and consequently looks back upon his attack of relapsing fever as a terribly painful experience. These pains are usually described as rheumatic in character, and several times patients presenting themselves at the hospital on the second or third day of the initial paroxysm stated that they had inflammatory rheumatism. As a fact, we observed the utmost intensity of these pains in a few cases where the patients were of marked rheumatic diathesis. The nape of the neck, the muscles of the trunk or extremities, or the large or small joints, or lower parts of the spinal region, may be the seat. At times they extend along the course of nerve-trunks. In character they are described as a deep intense aching, with occasional severe or excruciating, sharp, lancinating pains. Pressure or movement increases them. The joints are not red or swollen (though swelling may appear as a sequel), and the pains seemed to us rather to be referred to the joints than to be caused by any local irritation therein. As already stated, there is often tenderness of the body of the muscles, and this was especially marked in many of our cases on pressure along the course of the nerve-trunk.
Murchison suggests that they are due to the circulation in the blood of an {386} abnormal substance, such as uric, lactic, or phosphoric acid; but it appears to us altogether probable that they are rather to be connected with states of congestive irritation of the sheaths of the nerve-trunks (early stage of perineuritis), or possibly in some cases of the spinal membranes also. It is true that they are sometimes shifting in their seat and fluctuating in their severity, but this is not inconsistent with the above suggestion, while the widespread irritative processes found in this remarkable disease, the resemblance of these pains and the frequently attendant numbness and tingling to the sensations caused by other forms of perineuritis, and the occasional development of local palsies of a single muscle or group of muscles, all are in its support.
The special senses are acute, sometimes painfully so. The eyes are watery and occasionally injected, but this latter condition is rare and slight in relapsing as compared with typhus fever. At the crisis and for a few days subsequently wide dilatation of the pupils is not infrequently observed. Dulness of hearing was present during the paroxysm in 14 of our cases, and a few patients complained of tinnitus; but these symptoms are not at all common in the disease, although it will be seen hereafter that affections of the middle ear are among its sequelæ.
Debility is not such a prominent symptom as in typhus and typhoid fevers. Patients manage to drag themselves about for several days during the initial paroxysm with all the symptoms fully developed, and after admission to the hospital will often be able to help themselves, or even to rise from bed, unless prevented by the severe pains or the vertigo. Still, there are many cases, not necessarily of very grave type, in which there is a marked sense of weariness and exhaustion, and of course in all cases of typhoid character the prostration is great. It must constantly be borne in mind that even when the patient feels or seems able to sit up he must on no account be permitted to do so, since the occurrence of sudden and fatal syncope is one of the accidents constantly to be apprehended. It is not only during the pyrexia that this precaution must be enforced; we meet with extreme debility during the intermission in some cases, and syncope has followed exertions made at that period as well as at others.
During the paroxysms the respirations are much accelerated, at times to a greater degree than would correspond with the pulse-rate, while at others extreme rapidity of pulse may be associated with moderate elevation of the rate of respirations.
As examples of the relation between temperature, pulse, and respirations we quote the following from our records of adult cases:
(a) Temperature, 108°; pulse, 124; respiration, 40. In the relapse; no chest trouble.
(b) Temperature, 107.5°; pulse, 120; respiration, 28; falling to temperature, 96°; pulse, 68; respiration, 18, within twelve hours, during which crisis occurred.
(c) Temperature, 107°; pulse, 144; respiration, 31. In the relapse.
(d) Temperature, 107°; pulse, 108; respiration, 44. Initial paroxysm; no pulmonary congestion.
Temperature, 106°; pulse, 116; respiration, 28. Relapse; no pulmonary congestion.
Temperature, 97°; pulse, 76; respiration, 24. Critical fall; cough, {387} congestion of lungs posteriorly, and left one relatively dull on percussion, but pneumonia did not develop.
In many epidemics bronchitis, hypostatic congestion, and pneumonia are of rare occurrence, while in others, as in Philadelphia in 1870, they are comparatively frequent and lead to serious respiratory symptoms. While the pyrexia was high there was very frequently an irritative dry cough, with the fine crepitant and subcrepitant râles attending congestion and imperfect expansion of the lungs heard at the middle and lower portions of the chest posteriorly. In numerous instances the râles would disappear entirely after a few full inspirations in the sitting posture, just as in the corresponding condition in typhoid fever. But in a considerable proportion of all the cases (fully 35 per cent.) there was more troublesome bronchial cough, associated with sonorous, sibilant and subcrepitant râles, with mucous or muco-purulent expectoration.
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