A system of practical medicine. By American authors. Vol. 1

by Unknown

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 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. Carter¹⁴ states that in the Bombay epidemic it was invariably the case that the pulse did not decline to an extent corresponding with the temperature.

¹⁴ Op. cit., p. 140.

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;¹⁵ 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.

¹⁵ Op. cit., p. 103.

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.

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.