Pernicious Malarial Fever

Certain departures from the ordinary types of malarial fever are termed pernicious, because of their great tendency to inflict more than usual systemic damage and danger to life upon those who suffer such attacks. The word pernicious is used in its common English sense of being hurtful or injurious.

It is entirely unnecessary to enter upon a discussion respecting the propriety of employing this adjective to designate a class of cases of disease which are primarily due to the same poison which produces simple intermittent attacks. The extreme hurtfulness and danger of the attacks to be described in this section, and the awful suddenness with which they often occasion death, form striking contrasts with the more typical forms of malarial fever, and appear fully to justify the use of the qualifying adjective pernicious.

While all these various departures from type to be grouped under the term pernicious possess the quality ascribed to them, they nevertheless differ so widely in their modes of inflicting injury that it seems desirable to arrange them under distinct sub-classifications.

Some cases of pernicious malarial fever preserve the periodicity of simple attacks sufficiently well to enable one to classify them as intermittent or remittent in form. But more commonly it is impossible to determine this classification, and for practical purposes it is unimportant to attempt to make any such distinction.

The classification which appears to me most true to nature is the following:

First. The algid or congestive form;
Second. The comatose form;
Third. The hemorrhagic form.

The algid or congestive form occurs more frequently than either of the others. Its perniciousness is due to an aggravation or sheer exaggeration of the cold stage of an intermittent attack.

The following brief clinical histories of two cases will serve to illustrate the symptomatic phenomena of this form of pernicious malarial fever:

M. S., aged fourteen, had accompanied his father to a malarious locality in the country, and had remained with him during September and a portion of October. Shortly after his return I was asked to visit him because of some unusual symptoms attending a chill. I found him in a stupor, from which he was with difficulty aroused sufficiently to be able to swallow a dose of quinia combined with laudanum. His face was pallid and inexpressive; the skin cool and moist; extremities shrunken and cold; pulse small, easily obliterated by pressure, and irregular; tongue large and moist; and pupils rather dilated.

My second visit was at 12 M., one hour and a half later than the first. Patient was found in a deep stupor; surface cold; extremities and face shrunken and blue; pulse barely perceptible; large liquid and offensive stools occasionally escaped from the bowels without the consciousness of the patient. Death at 3 o'clock P.M.

Miss H., living in a malarious situation, complained about noon of September 19th of great cerebral fulness and unaccountable sleepiness and debility. She retired to her room, and after a few hours' sleep resumed her household occupations. On the 20th similar symptoms manifested themselves, but earlier in the day. She again slept for some hours, but complained of great prostration after the sleep. On the 21st, about 10 A.M., she complained of a return of the stupor, and while retiring to her room requested that I should be called if she did not awake in a better condition. At 1 P.M. she was found profoundly comatose, with cold extremities and surface and bathed in perspiration. When I reached her residence at 3 P.M. she had expired.

There is a common belief among non-professional people that the third congestive chill is necessarily fatal. There is no foundation for this opinion, except in the fact that when congestive chills are waxing in their perniciousness the subject is seldom able to survive the third recurrence if the second or first should not prove fatal.

It is difficult to account for the pathological dissimilarity between the simple and congestive types of malarial fevers. If we say that congestive chills are produced by an intensification of those causes which produce and govern an ordinary chill, we make an explanation which, however unsatisfactory, represents very nearly the full extent of our knowledge on this point.

It cannot be admitted that alterations of quantity or quality of the malarial poison exercise the sole influence in determining the occurrence of congestive cases. All experienced practitioners understand that certain constitutional conditions may pervert simple chills into congestive forms by producing prolongation or aggravation of the states of congestion always present in ordinary chills. Weakened cardiac function, from whatever cause, may be reckoned among these conditions. In these cases the feeble vis a tergo yields readily to those perturbations of vaso-motor influence which occasion passive blood-accumulations in the small veins and capillaries. I may say further, in speaking of the influence of the vaso-motor nerves in governing the phenomena of a chill, that we know that in congestive chills the cerebro-spinal system is much less the seat of symptomatic phenomena than in simple attacks. On the other hand, the organic system is far more profoundly affected.

However we may account for the perversions of normal circulation underlying and producing congestive chills, the great degree of injury they are liable to inflict is so well understood as to awaken the most serious apprehensions whenever we are called upon to treat them. Congestion, however occasioned, may destroy life through abolishment of function by the sheer physical change of infarction, or, again, through those inevitable consequences which arrested circulation entails upon the blood. Blood-stasis is followed by separation of its constituents, and its disqualification as a circulatory fluid in a degree proportionate to the duration of the stoppage, and probably also to the actual extent of the passive engorgement. Thence result the formation of coagula in the congested vessels and deposits of pigmentary matter. If partial reaction should occur, portions of this blood-débris may be floated to various parts of the circulatory system, and give rise to greater or less important alterations of function.

Among the white soldiers of the United States army from May 1, 1861, to June 20, 1866, 13,673 cases were diagnosed as congestive intermittent fever. Of this number, 3370 died, being a mortality-rate of 23.91 per cent. The aggregate number of malarial cases returned was 1,255,623. It would therefore appear that 1 case in not quite 372 was congestive in its type, or 1.08 per cent. The late Dr. Cook of Washington, La., estimated 2 per cent. of his malarial cases to be of the congestive type. It can scarcely be doubted that the ratio of congestive attacks is greater in the more southern belts of latitude than in the middle or northern parts of the United States. Chronic malarial toxæmia and the enervating effects of long-continued heat upon the circulation must occasion an increased proportion of such attacks, but my own observations show slightly more than 1 per cent. of the cases treated in the Charity Hospital to have been of the congestive form.

The cure of a congestive chill is one of the most difficult problems the physician can possibly encounter. It is nothing less than the proposition to remove a perverted state of the blood-vessels which is dependent upon some influence exerted through a nervous apparatus whose therapeutics and experimental physiology are imperfectly understood. While a satisfactory solution of this problem will probably be a remote achievement in medicine, it was long ago empirically ascertained that certain agents exercised some degree of control over the cold stage of febrile attacks. For the most part, these agents are addressed to those perversions of nerve-function which constitute so important a part of the pathology of a chill. They are identically the same remedies whose aid we invoke to allay many other forms of perturbed nervous action. Opium, chloroform, belladonna, chloral hydrate, and bromide of potassium have proved more or less valuable, according to the idiosyncrasy of the patient or the circumstances under which they have been used. I consider opium the most valuable of these remedies. It should be given in moderate doses, and preferably combined with chloroform or ammonia, or, if more expedient to administer per rectum, combined with solutions of chloral hydrate or bromide of potassium. One-sixth of a grain of morphia, combined with one-fortieth or one-fiftieth of a grain of atropia, is an available and useful prescription when given hypodermically. Rubbing the extremities or the spine, or indeed the whole surface, with ice, is a mode of practice well worthy of attention. In the event of inability to procure ice, douches of cold water, followed by frictions with coarse towels, may be substituted. I have used nitrite of amyl by inhalation, but its effects are too transitory to prove serviceable.

Some practitioners speak highly of alcoholic stimulants. My own experience has not been favorable to their use. Perhaps their benefits are altogether restricted to those cases in which previously weakened heart-function existed. But it is important that alcohol be added in all those cases of pernicious malarial fever, whatever the type may be, where cardiac stimulation and improvement of nutrition are leading indications.

I am sure I have often derived benefit from enemas consisting of four ounces of well-prepared beef essence with a half ounce of whiskey or brandy and a half ounce of strong infusion of coffee.

The value of the hypodermic syringe in treating congestive chills must never be lost sight of. The suspension, or even reversal, of normal systemic currents is made evident by the serous vomiting and purging attending congestion of the abdominal cavity. Medicine placed in the stomach under these circumstances is virtually thrown away.

The term comatose is applied to certain cases of pernicious malarial fever because they present coma as a marked symptom. To appreciate the propriety of this classification, it must be well understood that the coma present is not due to cerebral congestion. Further than this one restriction upon the application of the word there is in its employment no declaration of any pathological views respecting the cases it is intended to define. While, therefore, the term is unquestionably liable to criticism, I suppose its use may still be admitted, provided it is accompanied by a satisfactorily explicit account of the symptoms and probable pathological conditions of the cases included under its caption.

There is a sharp line of distinction between the symptoms and conjectural pathology of comatose cases and of those of the congestive form of pernicious fever. The following notes of cases will sufficiently establish this statement:

C. L., fisherman, aged forty-four, brought into Ward 20, Charity Hospital, in an insensible condition, November 18, 1875. Temperature at time of admission 104.8°, pulse 120, respiration 40; able to swallow liquids placed far back in his mouth. Ordered scruple ij of quinia in solution, ten grains to be given every fourth hour. Nov. 19th, patient has taken and retained all the quinia ordered; is perspiring profusely; temperature 97.8°, pulse 88; more conscious; takes food and water when offered him. Ordered blue mass, comp. extr. colocynth., aa gr. v, to be taken at once. To drink through the day bitartrate potass. oz. j, dissolved in lemonade, until bowels are moved. Evening temperature 99.3°. Nov. 20th, temperature 98°; patient placed under convalescent treatment; discharged from hospital Nov. 29th.

Another comatose patient was admitted to Ward 19 on the 29th of October, entirely insensible. He was treated by large doses of quinia in solution per rectum, and by calomel gr. xx, sodii bicarb. gr. v, placed upon base of tongue, and caused to be swallowed by a tablespoonful of water trickled over the powder. As the patient began to recover it was noticed that his right arm was paralyzed. A history subsequently obtained showed that the patient was an engineer, and had been engaged in making some land surveys in a swampy portion of the State of Louisiana, and had been often obliged to wade or swim across the bayous and to sleep at night in the open air, sometimes without any protection from the weather. He had previously enjoyed good health, and was altogether unable to account for the paralysis of his arm. During convalescence he was treated with iron, strychnia, and preparations of cinchona, and by cold douches and frictions to the paralyzed arm. Convalescence was slow, but he was discharged, completely recovered, on November 20th.

In typical cases the differential diagnosis between the congestive form and the comatose is made without difficulty. In a congestive chill the surface is cold, blue, or livid, the pupils dilated, and the pulse generally slower than natural and irregular. In the comatose form the surface is preternaturally warm, of a muddy, semi-jaundiced hue, and the pulse and temperature both indicate the feverish rather than the algid state.

The subjects of attacks of the comatose form of malarial fever are for the most part persons who, having contracted attacks of fever in malarial regions, continue to reside in the same localities and yet use no proper medication, either for cure or for prophylaxis. We have in these cases accumulations of secondary blood-poisons quite sufficient to greatly impede brain-function, and the additional doses of the primary toxic agent must exercise more or less influence in determining the phenomena of the attacks.

Very little need be said of treatment, beyond a recommendation of the courses pursued in the cases cited. Hypodermic medication must be resorted to when necessary. Efforts to nourish the patient must never be relaxed. One must see many of these cases before he can realize how often they recover, from conditions apparently utterly hopeless, when promptly treated and properly nourished.

The hemorrhagic form of pernicious malarial fever can scarcely be regarded as an original type. Malaria is not a hemorrhage-inducing poison. Indeed, it may be positively stated that malaria never establishes the hemorrhagic diathesis as a primary effect; and it is only by changes effected in the human economy by its prolonged influence that it appears to become capable of doing so. The most experienced and accurate observers of malarial affections concur in the opinion that this rule is almost without exception.

The morbid conditions whose concurrence entails upon malarial fevers a tendency to hemorrhages may be classed together as follows: First. The blood-changes of chronic malarial toxæmia so alter the consistency of that fluid as to favor the occurrence of hemorrhage. Second. The long persistent states of malnutrition in chronic malarial cachexias produce textural weakening of the vascular walls and increased liability to their rupture. Third. There should be added to these one other factor, which is mainly operative during a malarial paroxysm—namely, the increased blood-pressure put upon the vascular walls by passive congestions.

Two of these factors, as above enumerated, are more or less general to the system, being the consequence of general cachectic states. The third factor acts in a purely dynamical manner in causing hemorrhages, and must necessarily have its area of influence confined to some certain portion or portions of the vascular tree, since the congestions of malarial paroxysms cannot by any possibility be general. It is an interesting fact that the influence of this last-mentioned factor is so frequently paramount in producing malarial hemorrhages. These hemorrhages occur in such immediate relation to chills that we are forced to the conclusion that while altered blood and weakened blood-vessels were previously present, yet some increase of pressure beyond the normal was required to precipitate the hemorrhage.

More than once in the presence of medical classes I have illustrated the influence of these various factors, respectively, by showing the arm of a patient suffering with chronic malarial cachexia, with no extravasation of blood, but upon which the slightest suction with the lips would produce exaggerated ecchymoses. This explains the fact that hemorrhages in malarial fevers are never general, but only manifest themselves upon those surfaces or into those structures which are the seats of congestion during the cold stage of an intermittent.

I do most earnestly assert that during a practice of almost half a century, nearly all of which has been passed in malarious localities, I have never once seen a malarial-fever patient with a general hemorrhagic tendency, if yellow fever and other hemorrhage-inducing diseases could be authoritatively excluded. The medical profession cannot be too watchful in guarding itself against erroneous entries upon mortuary records to account for deaths from fevers accompanied by hemorrhages from multiple surfaces of the body. Such aliases as hemorrhagic malarial fever, climatic fever, rice fever, hæmatemesic paludal fever, and many more of the same character, should receive the severest examination before approval and adoption.

When hemorrhage does attend malarial fevers, it may occur from one or another of a variety of surfaces or into shut cavities or in parenchymatous structures. Some years ago I visited a gentleman who was suffering from an attack of malarial fever, with hæmaturia. He made a rapid and, apparently, a complete recovery. Disobeying my injunctions, he returned to the intensely malarious locality where he had formerly resided. After a few weeks he was seized with a chill, followed by apoplectic symptoms, hemorrhage, and death on third day. It is hardly to be doubted that his death was caused by cerebral hemorrhage. But, however much in consonance with ascertained facts the foregoing remarks may appear to be, there are certain points of pathology connected with malarial hemorrhagic fevers not easy of explanation. Within the last score of years hæmaturia has been a far more common form of hemorrhage in malarial fevers than formerly. In many localities and during certain seasons it has been very prevalent.

In the present state of our knowledge it is not at all possible to explain why it is that different epidemics of malarial diseases should give rise to such a diversity of phenomena, so that one epidemic will be characterized by a peculiar train of symptoms which shall be absent in another, being there replaced by different symptoms equally distinctive of the second epidemic. Whatever may be the cause of these epidemical peculiarities, it must rest in a something which is capable of acting as a force upon the human system. We must think of that unknown agency which exercises this force and gives it some peculiar direction as possessing at least a conventional essentiality. It is not satisfactory to say that the renal blood-vessels are the first to give way, because they are accidentally more weakened than other parts of the vascular system, or accidentally more often the seat of congestion. When accidents become as numerous as these cases sometimes are, they acquire the authority of laws.

The following notes of two cases of malarial hemorrhagic fever may be found of interest:

C. E., aged twenty-six years, was admitted to Ward 19, Charity Hospital, Nov. 18, 1872. Had been in America more than a year, and for several months had been working in an intensely malarial district preparing the bed of a railroad; has had malarial diseases for several months, and suffered a severe chill the day before admission. A few hours after admission temp. 103°, pulse 120, respiration 29; effusion in both thoracic cavities, and very marked in abdominal cavity; lower lobe of right lung oedematous, legs anasarcous, pitting greatly on pressure, with several ulcers of long standing. Urine loaded with albumen and showing under the microscope abundant blood-corpuscles; considerable jaundice present, which the patient states to have occurred suddenly. Ordered five grains each of calomel and bicarbonate of sodium, to be followed after catharsis with ten grains of quinia in solution every two hours. Nov. 22d, patient has taken and retained one hundred and eight grains of quinia; secretion of urine abundant; no blood present, and only a trace of albumen; ordered twenty drops of tincture of chloride of iron three times daily. Discharged cured December 12th. The above comprises the whole treatment in this case, except one important measure, which consisted in determined and persistent efforts at forced nutrition. Meat essences, milk, eggs, and milk-punch were given as methodically as drugs.

H. K., fifteen years of age, was admitted to Charity Hospital Sept. 15, 1872; has a history of malarial poisoning for several months; was considerably jaundiced at time of admission, with anasarcous legs. Under the administration of a mercurial, followed by quinia and iron, he improved so greatly that he was discharged from my wards and placed upon some duty in the hospital. Dec. 19th, at 11 A.M., had a chill which lasted several hours; this was followed by violent fever, with rapid but compressible pulse; much jactitation; incessant vomiting of a greenish-black fluid; urine loaded with blood; and sudden supervention of intense jaundice. Ordered quinia gr. xij by hypodermic injection; small doses of calomel and soda to be placed upon the base of the tongue and washed down with ice-water. Secretion of urine ceased on the morning of the 20th, followed by death at 11 P.M. Autopsy showed both kidneys dark-colored and swollen from complete blood-engorgement.

The treatment of hemorrhagic malarial fevers may be included under the following indications:

First, to secure cinchonism as early as possible;

Second, to arrest the extravasation of blood;

Third, to sustain the patient's strength, and to preserve the systemic fluids at as near a healthy standard as may be possible.

The first-mentioned indication is certainly the first in importance. If the hemorrhage originates during a chill, or exhibits degrees of aggravation in such close relation to the cold stage of malarial paroxysms as to point to a relation of cause and effect, then that course of treatment which breaks the recurrence of paroxysms will at the same time mitigate the hemorrhage, if, in truth, it should fail to stop it entirely. Quinia should be given in large doses by the mouth or rectum, or both, or subcutaneously if demanded by the urgency of the symptoms. I have generally used carefully prepared solutions of the sulphate for hypodermic injections, but many practitioners prefer solutions of the hydrobromate for this mode of exhibition. I have never witnessed any symptoms following the administration of cinchona salts which justified a belief that they increased the hemorrhage. My rule of practice has invariably been to endeavor to prevent the occurrence of another paroxysm, without regard to this very questionable charge.

In regard to the second indication, it may be stated that patients are not likely to die from actual loss of blood in any form of hemorrhagic malarial fever. The blood which is poured out on free surfaces and escapes by some outlet is seldom so much as to endanger life, but the hemorrhagic process is likely to involve deeper-seated vessels. This is especially true in malarial hæmaturia. Hemorrhages into the stroma of the kidneys, the Malpighian tufts, and the uriniferous tubules arrest urinary secretion, and thus entail death. In order to prevent these results hæmostatics should be resorted to as often as attendant circumstances will permit. Generally these are such as to admit of the use of hæmostatics without prejudicing the effects of other remedies. In my experience ergot in combination with gallic acid and dilute sulphuric acid has been very efficient. The following prescription has been usually given:

Rx. Ext. Ergot. Fluid. fl. drachm iv;

Acid. Gallic. gr. xl;

Acid. Sulphuric. dil. fl. drachm j;

Syr. Zingiber. fl. drachm iij;

Aquæ q. s ad fl. oz. ij. M.

S. Dessertspoonful every four hours, diluted with water.

Some practitioners place a very high estimate upon the hæmostatic effects of turpentine. This is undoubtedly a most valuable and accessible remedy. Dr. Schnell of Plaquemine Parish, La., has found the tincture of chloride of iron the best hæmostatic. He places fl. drachm ij in fl. oz. iv of water, and directs a dessertspoonful every hour as long as the hemorrhage continues. In a great majority of cases of malarial hæmaturia occurring under my observation solutions of bitartrate of potassium have been given with great apparent benefit. Its action is certainly not that of a direct hæmostatic, but by setting up currents through the kidneys, and perhaps by some solvent power over exudations in the uriniferous tubules, it has acted as a renal deobstructive.

In the arrest of renal secretion diuretics, cupping over the lumbar region, and large injections of warm water into the bowels may be resorted to. Some practitioners state that they have found buchu beneficial.

The third indication involves a twofold duty. One relates to judicious and vigilant attention to the patient's nutrition; the other relates to such measures for depuration as may be called for in each particular case.

It must be admitted that there is a degree of antagonism in the measures of practice proper to effect these two purposes, which renders their coincident exercise a difficult practical question. In many cases of hemorrhagic malarial fever a competent supply of properly prepared foods is sufficient. In other cases—and this is especially true of malarial hæmaturia—depurative medication becomes paramount. A person suffering under the effects of chronic malarial poisoning is seized with a chill; this is followed by bloody urine, and in the course of four or five hours intense jaundice appears. Incessant vomiting, delirium, and jactitation also occur. The experienced physician is at once brought to the conclusion that he has to deal with a case of blood-poisoning bearing a close resemblance in symptoms to uræmia. To render this conclusion still more absolute, he has only to recall the suddenness of the occurrence of the jaundice and to inquire what has occasioned it. Its appearance is too rapid to permit us to ascribe it to obstruction. It is altogether improbable that it is due to sudden hypersecretion in such pathological states of the system as are present. If, however, we account for it by saying that the addition of a new toxic constituent, urea and its congeners, to an already profoundly poisoned fluid suddenly arrests those processes which dispose of bile in physiological conditions of the system, it seems to me that we adopt the most rational theory. It is then jaundice from lack of consumption. The mere probability of truth in this theory will impress the practitioner with the great importance of eliminant practice in these conditions.

Calomel has been the medicine to which I have principally trusted. I give it merely as a depurative, and not as an alterative. Doses of from two to ten grains may be repeated at suitable intervals until catharsis has been produced. Bitartrate of potassium, Seidlitz powders, or solutions of citrate of magnesia may be also administered if indicated. After purgation the vomiting is mitigated, if not altogether relieved. On this account, and because of bettered states of the system for absorption and assimilation, the way is now clear to the physician. He can ply his antiperiodics, his properly prepared sustenance, and his alcoholic stimulants according to the exigencies of each particular case.

The following propositions may seem not inappropriate in closing this section:

1st. Attacks of pernicious malarial fever are attended by more danger to life or subsequent health than simple attacks; therefore more prompt and energetic efforts should be made to cut them short by cinchonism.

2d. The blood depravations of pernicious malarial fevers far exceed those of simple cases; and therefore it becomes a leading indication of treatment to correct faulty conditions of this fluid as early as possible. In endeavoring to secure this end assimilable foods, stimulants, and depurants must have a shifting scale of value according to the exigencies of each particular case.

3d. The complications of attacks of pernicious fever are far more important than those of simple forms; and therefore symptomatic treatment is often urgently required.

4th. Attacks of pernicious fever may be greatly diminished in number by properly directed treatment of chronic malarial toxæmia, and especially also by the removal of persons suffering under this cachexia to non-malarious localities.