MALARIAL FEVERS.
BY SAMUEL M. BEMISS, M.D.
In the medical nomenclature of this country the term malaria is synonymous with swamp or ague poison.
Malarial affections, therefore, comprise all those diseases or morbid manifestations which the swamp poison produces in the human organism.
This article is not designed to notice in a systematic manner any of these disorders which are not properly classifiable under the head of malarial fevers. It will, however, be necessary to make such references to the pathology of chronic malarial toxæmia as may serve to explain the influence this condition exerts in occasioning departures from type in the febrile attacks.
When a poison generated outside the human system obtains admission to it, and produces deleterious effects, three questions naturally arise: What is the essential character and natural history of this noxious agent? How does it obtain access to the human system? What is its mode of action when received?
In reference to the first of these questions, it must be admitted that the substantive essentiality of the malarial poison remains as yet undemonstrated. It is true, however, that the attempts at an objective study of this poison by means of the microscope and the cultivating retort point to the conclusion that it is an organism.
Its subjective or analogical study affords quite incontestable evidence in support of this conclusion. The leading features in the natural history of malaria are closely coincident with those of certain known organisms. It requires for its production suitable conditions of moisture, temperature, and a properly circumstanced breeding-place. Within certain bounds these conditions are requisite to the life and perpetuity of all organisms.
Again, when all the above-enumerated conditions correspond apparently in the most favorable degree, their continuous concurrence for a lapse of time is necessary before the poison manifests its presence. It is not improbable that this period of development may differ in different climates, but in this country we assume it to be about thirty days. If these facts related to some noxious organism visible to the eye, no doubt would be entertained that the presence of its germs in the places where it appeared was the indispensable condition. It would then follow that the concurrence of suitable meteorologic and telluric conditions with sufficient time for its growth and maturity were merely accessories to its perfect development. According to this theory, the coincidence of five circumstances is necessary before malaria can be fully matured—viz.: Its own specific germ; suitable soil or pabulum; suitable moisture; suitable temperature; sufficient time for its growth and development.
Certain physical qualities which pertain to the malarial poison can also be profitably made points of subjective study. These are very closely connected with the answer to the second question, or "How the malarial poison obtains access to the human system." They will therefore be briefly noticed in relation to the instrumentality of each in conveying malaria into the system.
The first to be mentioned is ponderability, which the following facts prove that malaria possesses:
Those different atmospheric states which affect the range of diffusion of known air-borne yet ponderable substances exert similar influences upon the malarial poison.
Altitude illustrates the ponderability of malaria by powerfully retarding its diffusion.
High readings of the barometer favor its aërial dissemination.
Fogs, smoke, dust, or floating particles presumably more buoyant than this poison may exert greater or less influence in overcoming the obstacle which ponderability attaches to malaria as an air-borne agent.
Currents of air passing continuously and steadily in one direction over the breeding-places of malaria increase the limits and intensity of toxic range.
The atmosphere is undoubtedly the medium by means of which malarial poison is most frequently brought into the human system. Liability to intoxication is increased in direct ratio to the proximity of points of exposure to places of development; to similarity of level; to situation in the line of prevailing winds which have traversed the breeding-ground; and, lastly, to the extent and fertility of the locality of production.
Whether malaria passes through the respiratory apparatus directly into the circulation, or is lodged upon the fauces and absorbed through some other surface, is not clearly ascertainable. It is certainly not deprived of its noxious qualities by stomach digestion, and therefore, sometimes at least, may reach the blood through the alimentary canal.
Malaria is miscible with water. It is capable of being carried by currents of water through distances and periods of time altogether undetermined, without losing either its toxic effects or, perhaps, the faculty of reproduction. It is more than likely that this means of conveyance has effected its distribution to continents and islands too widely separated to justify a belief that it was wind-wafted. No observations need be adduced to establish the water-borne habit of the malarial poison, or the positive liability to its toxic effects when received into the stomach through this medium. These facts have been well understood from the time of Hippocrates.
The matter of communicability of malaria by means of drinking water should not be dismissed without some allusion to the great probability that other fluids or solids are open to a similar charge. There is a widespread popular prejudice, especially notable in the southern part of the United States, that drinking milk occasions attacks of the endemic fevers. It is the usual custom to pour the evening supply of milk into broad uncovered pans, and allow it to remain exposed in the open air for consumption at the morning meal. This viscid fluid, so tenacious of ordinary air-borne particles, may well be suspected of entangling sufficient quantities of swamp poison to produce sickness if exposed where it is rife during a whole night.
A similar popular prejudice exists in regard to the muscadine grape, which flourishes best in swampy localities. The rough skin of this fruit, frequently covered with its own juice, offers favorable conditions for the adhesion of air-borne particles.
The malarial poison is not reproduced within the human system. This proposition is undeniable, since no intensification of the poison is produced by any degree of crowding of the sick which can be practised; neither do any conditions of contact with the sick ever impart malarial affections.
Malarial poison is specific. This allegation is sufficiently established by its specific effects on the human economy. There is no other agent known which is capable of originating morbid phenomena characterized by such marked diurnal periodicity.
It is not interchangeable with other specific poisons. This statement may be rested upon all fairly collected clinical observations.
There are no facts which justify the belief that malaria is capable of becoming mixed in the atmosphere, or outside the system, with any other specific morbific germ, so as to produce a third something which may give rise to compound forms of disease.
The answer to the second question which is best supported is, that the malarial poison is brought into the system principally by breathing an atmosphere impregnated with this miasm.
It is also ingested by being held in suspension in fluids used as drink or food; perhaps also by eating certain fruits or vegetables in their natural state whose external surfaces afford favorable conditions for its lodgment.
MORBID EFFECTS AND PHENOMENA WHICH FOLLOW ITS INTRODUCTION INTO THE HUMAN SYSTEM.—The discussion of the morbid process established by the malarial poison involves some difficult problems. A period of incubation must be admitted to follow the inception of the ague germs. But this period has no definitely marked limits. Perhaps it is a shifting one, according to the quantity or quality of the poison received, or the sudden or gradual manner in which it is received, or the state of receptivity of the system.
Certain facts seem to indicate very clearly that malarial poison is very slowly removed from a system which has been brought under its influence. These evidences of long systemic residence of the poison are principally displayed in those attacks which occur after long periods of removal from any surrounding where intoxication was possible. Vernal attacks may be classed in the same connection. In many instances the subjects of these long-delayed attacks have never suffered a paroxysmal seizure, and yet when some accidental derangement of health occurs, as from a fit of indigestion or a sudden wetting, they fall sick with one or another form of malarial fever.
It does not appear to me that we are justified in assuming that such attacks as I refer to are to be ascribed to secondary changes produced in either the fluids or solids of the system by the malarial poison. In so far as the clinical phenomena are worth anything in demonstrating the presence and agency of the specific malarial poison in these deferred attacks, they are precisely similar to those observed in paroxysms arising after a few hours' or a few days' exposure to marsh miasm.
But we find further proofs of the long-continued and silent manner in which malaria exerts its pathological influences in those enlargements of the spleen which occur without specific attacks of sickness. The alterations of nutrition in this organ are so characteristic of malaria that they can scarcely be supposed to depend upon those chances which determine the nature of secondary blood-impurities.
Intermittent Fever—Simple Forms.
The clinical phenomena of intermittent fevers afford strong support to the opinion that this type of malarial attacks illustrates more strongly than any other the primary influence of the poison upon the human system. Fits of ague often occur very shortly after exposure in infected localities, and the persons thus suddenly attacked may present little or no evidence of cachexia before or after the paroxysm. Indeed, they frequently resume their ordinary avocations after the paroxysms, apparently as well as if they had not occurred.
It is therefore my opinion that the pathology of an intermittent fever does not necessarily involve an hypothesis that the attacks are the results of certain changes which the poison undergoes after its inception, nor, on the other hand, that certain perversions of systemic chemistry are required to inaugurate the paroxysms.
In accordance with these conclusions, it seems likely that the phenomena of intermittent malarial fever result from the primary effects of its specific poison exerted directly upon the fluids and solids of the system, and disturbing their functions, and especially the nerve-function.
Those malarial attacks which ensue almost immediately after exposure are principally manifested in persons exposed at points of unusually abundant evolution. The rule of malarial attacks in temperate latitudes is, that they require repeated exposure to infection for their production. The long residence of the poison in the system may render additional doses possible, until a point of saturation is reached which occasions paroxysmal explosions. In these cases the period of incubation is reckoned from the first date of exposure, thus forming the most striking contrast with the incubative periods of the cases occurring almost immediately after exposure.
Whether the quiescent period after exposure to malaria be long or short, attacks are seldom abrupt in their announcement. The symptoms which usually precede pronounced attacks consist, for the most part, in some derangement of the functions presided over by the organic nervous system. Derangement of digestion, vitiated taste, coating of the tongue, loaded urine, and sallow skin are ordinarily found among the prodromic symptoms. Next in succession come feelings of malaise, hot and cold flushes, and those neuralgias which precede and attend malarial paroxysms.
The symptoms of an ordinary or typical malarial paroxysm are so characteristic, as to be generally readily interpreted. Creeping, chilly, sensations over the surface, especially along the spine, yawning, livid coloration beneath the finger-nails, retreat of blood from superficial capillaries, and that consequent papillary elevation which is commonly called goose-skin, comprise the earliest symptoms. Then decided shiverings with chattering of the teeth come on, and the patient asks for blankets to be heaped upon him and hot applications to be made, even though the atmospheric temperature may be decidedly elevated.
Nausea and vomiting are frequent symptoms, no doubt due to the fact that the portal system of blood-vessels is so often the seat of congestion during a chill. No intelligent practitioner can watch a patient during the cold stage of a malarial paroxysm without realizing how important the attendant congestion is as a pathological state. It should first be considered that every chill necessarily implies a condition of congestion in some part of the system. The blood driven from the surface and extremities must be accounted for elsewhere; and the amount of blood which is lost from one part of the circulatory tree must correspond with that accumulated elsewhere. But in treating of the pernicious forms of malarial fevers this question will again receive notice.
In our present state of knowledge we are no more able to explain those perversions of the normal action of the physical forces of the system which occasion the phenomena of a chill than we are to explain how the altered circulation in the first steps of an inflammation is brought about. The theory which Cullen adopted is quite as explanatory and consistent as any which has been promulgated since his time. According to this, a state of spasm of the arterioles and capillaries causes the chill, while the fever is merely the rebound of functions held in abeyance during the chill.
After a variable length of time there occurs a change in these symptoms: the patient begins to remove the blankets which covered him; the face shows signs of returning circulation; the veins of the whole surface gradually fill again, apparently beyond their normal state. But the reaction goes far beyond any normal physiological state. The face becomes flushed and the eyes injected, and the patient complains of headache, thirst, dryness and heat of the surface; he will not permit any covering, and constantly shifts his place in the bed in the hope that some new position may afford him more comfort. Nausea and vomiting are commonly present. If the fever runs high, delirium is apt to occur. The thermometer seldom shows a temperature above 105°, but I have seen 106.5° recorded in the axilla in the hot stage of a paroxysm of simple intermittent fever.
The duration of the hot stage is different in different cases. According to Aitken, the mean duration is three to eight hours.
There is a very old and quite well-supported opinion, that the cold stage is shorter in the quotidian than in the tertian type, and also that the hot stage is longer in the former than in the latter. It may certainly be affirmed that in individual cases of either type there is no fixed relation between the duration of the chill and that of the hot stage.
The decline of the hot stage begins by the appearance of a gentle perspiration, limited at first to the forehead, face, and neck. This gradually extends itself over the surface and increases in quantity until the whole body is bathed in a profuse sweat. During this period the patient's symptoms, both subjective and objective, undergo wonderful mitigation, and, although this stage is usually short, it often happens that by the time it is concluded a restoration to ordinary health seems to have occurred.
The sweating stage terminates a malarial paroxysm. The intermission now begins, and lasts until the inauguration of another paroxysm. The intermission is longer or shorter accordingly, first, as the paroxysm occupies less or more time; and, second, as the interval may affect it. The interval is that period of time which reaches from the beginning of one paroxysm to the beginning of another. It therefore furnishes the basis of classification of simple intermittents into the following forms: quotidian, tertian, and quartan.
Statistics gathered from a great many sources and relating to many countries and climates indicate that quotidian intermittents are more common than tertian. It may then be assumed that the natural type of intermittents is that form characterized by diurnal paroxysms. It must be remarked, however, that if any natural law does exist establishing the quotidian as the typical form of intermittent fevers, it is very often set aside by unknown influences. In certain epidemics the tertian cases preponderate, and under all circumstances convertibility may be witnessed between the various forms.
It is probable that the statistics gathered by the medical staff of the United States Army during the late Civil War afford the most valuable data which we possess touching these points, in so far as they relate to this country. During three years of the war 724,284 cases of intermittent fever were recorded, tabulated as follows:
Quotidian, 370,401 cases, 388 deaths—equivalent to 1047 + deaths per 1,000,000 cases.
Tertian, 318,704 cases, 324 deaths—equivalent to 1007 + deaths per 1,000,000 cases.
Quartan, 35,179 cases, 79 deaths—equivalent to 2245 + deaths per 1,000,000 cases.
It has been remarked by several writers that quartan attacks have a smaller ratio in the Southern States than in other parts of the Union. My observations on this point have not been sufficiently well recorded to make them especially authoritative, but they support such a conclusion.
The morbid anatomy of malarial fevers is more properly discussed in treating of the graver forms, since the paroxysms of simple intermittent do not often occasion death.
TREATMENT.—This must necessarily vary with the stage of the paroxysm and condition of the patient at the time of the first visit.
Let us suppose this to be the incipiency of the paroxysm, or the early part of the cold stage. However little the danger to life from the paroxysm of a simple intermittent attack, the practitioner should not forget that whatever danger does exist is to be ascribed to damages suffered during or in consequence of the chill. There are few exceptions to this rule, and those will be noticed presently. With this fact in view the practitioner's duties are much simplified. He should first endeavor to remove any complications present which tend to aggravate the cold stage. If the chill has come on after a full meal or after eating indigestible food, the stomach should be promptly emptied; otherwise the cold stage will be prolonged and rendered more violent. Large draughts of warm water will frequently produce sufficient emesis. If this should fail, ipecacuanha may be added. The warm infusion of eupatorium perfoliatum answers well as an emetic, producing also a laxative effect. But it is disgusting to the palate, and sometimes prolongs its action beyond desired results. The effect of an emetic in abridging a chill by revulsive action are uncertain, and I avoid resorting to them for this purpose alone in simple intermittents.
The patient's subjective complaints of suffering should receive a due degree of attention. Additional blankets and warm applications should be allowed when solicited. I always discourage hot or heating drinks, except for the purpose just mentioned. I especially oppose alcoholic stimulants, because they seldom do any good in mitigating the chill, oftener aggravating the patient's symptoms during the hot stage, particularly the headache and vomiting, and sometimes directly occasioning perplexing perturbations. For example, I have seen convulsions speedily follow a strong brandy toddy given to shorten a chill.
While the removal of complications is imperatively indicated, it is also important to use promptly those means which are designed to modify and shorten the chill. It is a remarkable fact that all the agents found to be useful for this purpose are such as directly influence nervous function. Opium in some form enters into all prescriptions which I have found efficient in modifying a chill. It is quite efficacious when given alone, but I think its therapeutic energy and certainty are increased by the addition of other agents of the same class. I have often exhibited twenty to thirty drops of chloroform with an equal quantity of laudanum with excellent results. The tincture of opium may be combined with aromatic spirit of ammonia, or with bromide of potassium, or with chloral hydrate. In combination with either of the latter medicines it may be given by rectal injection. If the stomach is intolerant, or by preference because of facility of dosage and quickness of effect, the opiate may be given hypodermically. For this purpose one-sixth to one-quarter of a grain of morphia may be given, together with one-sixtieth to one-fortieth of a grain of atropia. It is rarely necessary to repeat the dose whichever form may be adopted.
After much experience in these methods of mitigating and abridging the chills of intermittent fever, I feel entitled to say that, whether the objects be achieved or not, no injurious consequences ensue.
The conditions of the circulatory and digestive organs are not favorable for the introduction of quinia or of any preliminary purgative which may be supposed to be necessary, and I therefore delay their exhibition. It may be excepted, however, that sometimes a very obstinately irritable stomach or exceedingly vitiated state of the fluids can be appropriately met by gr. x to xx of calomel.
The hot stage of a simple intermittent seldom calls for medical interference on account of excessive temperature. If the headache is very violent or the vomiting troublesome, a subcutaneous dose of morphia will bring speedy relief. The existence of high temperature does not contra-indicate its use.
I am in the habit of giving opium in the following combinations:
| Rx. | Morphiæ Acet. | gr. ss; |
| Liq. Ammon. Acet. | fl. oz. iv. M. |
S. Two tablespoonfuls every second hour.
Or, occasionally, the following:
| Rx. | Sodii Bicarb. | gr. xx. |
| Morphiæ Sulph. | gr. i; | |
| Aquæ Lauro-Cerasi, | ||
| Aquæ Menth. Pip. aa. | fl. drachm iv. M. |
S. Teaspoonful pro re nata.
I do not limit the use of opiates in the hot stage to old and infirm subjects, as Dickson suggests, but give them in all cases where vomiting, headache, or other neuralgias are excessive, or where unusual restlessness and jactitation are present.
The propriety of giving purgatives as a preliminary measure of treatment during the hot stage must be determined by symptoms connected with individual cases. In the majority of cases falling under my care purgatives are avoided. When regarded necessary, gentle purgation is solicited by administering bitartrate of potassium in lemonade or by combining mild mercurial doses with antiperiodics when these latter are resorted to during the fever. In some cases a very furred tongue, sallow skin, and costive bowels indicate more active purgatives, which may be exhibited during the febrile stage.
The most important question which relates to medication during the hot stage is in respect to the administration of antiperiodics. It may be safely stated that practitioners of this country were the first to adopt this method of procedure in malarial fevers. Here it has been well demonstrated that a competent dose of quinia, given during any part of the hot stage, is so often followed by the defervescence of the fever that it would be illogical to attribute the change to any other cause. Sometimes the remedy fails in producing this result; then excessive physiological disturbances may follow, and perhaps some general aggravation of the patient's symptoms.
There are four different circumstances, each of which, in my opinion, calls for the exhibition of quinia during the hot stage, whether the fever has reached its maximum point or not:
First. If the period which has elapsed since the beginning of the paroxysm is so considerable that further delay might prevent sufficient cinchonism to intercept the next accession.
Second. When the fever is so excessive that quinia should be given as an antipyretic.
Third. When apprehensions exist that the fever will occasion some complication or accident.
Fourth. When the tongue is clean and the state of the system is favorable to absorption.
The hot stage is not usually favorable to absorption, and consequently the economical use of quinia must not be attempted. It should be given in doses varying from ten to twenty grains, preferably in solution. I may remark that I have seldom failed in getting good results from the powder or pills if lemonade or some fluid facile of absorption be given at the same time. The mixtures previously formulated answer this purpose very well, and at the same time mitigate the disagreeable physiological effects of the quinia.
Allusion has been made to certain symptoms occasionally connected with the hot stage which involve danger. Convulsions are among the most important of these. They occur most often among children, but occasionally with adults. They should be met by chloroform, cold to the head, hypodermic injection of morphia, and cupping or leeching if the face is flushed, the eyes injected, and the carotids pulsating forcibly.
The sweating stage may be classed with the intermission in respect to medication. No time should be lost in securing cinchonism. From the moment the sweating stage announces itself the fluids of the system begin to resume their normal physiological functions. Absorption from the intestinal surfaces is again restored, and remedies may be administered with confidence in their effects.
The question is now no longer whether antiperiodics should be administered, but how they shall be given. Many practitioners prefer exhibiting them in one large dose; others think it better to give them in repeated small doses. I have usually adopted the latter method. Beginning with the sweating stage, I give three grains of quinia every hour or two hours, until eighteen grains have been taken. This would occupy periods of five to ten hours to complete the doses, ordinarily quite a sufficient length of time to obtain cinchonism before the advent of another paroxysm. If the physician elects to give his antiperiodic in one or two large doses, he should not trust to so small an amount as eighteen grains. Allowance must be made for the loss incident to the probable over-taxation of the power to dissolve and receive a large amount into the circulation.
Purgation should not be induced to a sufficient degree to hurry the quinia off before absorption takes place. Some practitioners favor the employment of adjuvants to the quinia. Very few of these have appeared to me to be of service except opium. A very convenient formula is a solution of quinia in peppermint-water by addition of dilute sulphuric acid, in such proportions that fl. drachm j of the solution shall represent five grains of quinia and seven and a half drops of laudanum.
But, however we may boast of the efficacy of cinchona as the anceps remedium for malarial diseases, we are forced to admit that it is not certainly an immediate cure, and very commonly fails in producing a permanent curative effect. If we could in all cases discern and remove the impediments to its immediate or temporarily curative action, its claims to be regarded as a practical specific would be undeniable. It is probable that these impediments generally rest upon the fact that either the remedy does not gain admission to the circulation or that some complication exists not within the range of its therapeutic action.
The failure of cinchona to cure a malarial attack in such a permanent manner that it shall not be liable to return is probably owing to the incompetent action of the drug because of its transitory stay in the system as compared with that of the malarial poison. Some objections apply to this theory, because when the succession of intermittent attacks is broken by quinia and it is continuously administered afterward, the paroxysms occasionally recur in spite of its presence in the system. These objections may be answered by pleading that under these circumstances secondary blood-poisons precipitate the attacks, and cinchona should not be expected to cure these conditions.
The best methods of practice I know of to prevent a recurrence of intermittent fever after having interrupted the succession of attacks are, first, to continue the cinchona for at least forty-eight hours, giving at least three three-grain doses a day. After this no medicine need be given except such as may be required to correct chronic toxæmic states of the system or to act as blood-restoratives until such time as prodromes of another paroxysm may exhibit themselves. At the instant when these manifest themselves ten to fifteen grains of quinia in solution should be taken. In order that no loss of time should occur in applying this method, I always advise patients to keep a solution of quinia within immediate reach. The following prescription has sometimes appeared to effect a permanent exemption from recurrence of paroxysms:
| Rx. | Ferri Redacti | gr. xl; |
| Acid. Arseniosi | gr. j; | |
| Quiniæ Sulph. | gr. xl; | |
| Ol. Pip. Nigr. | gtt. x. M. | |
| Ft. pil. No. xx. |
S. One pill three times daily.
It seems sometimes to occur that intermittent attacks so impress the nervous system that they become, like epilepsy, more liable to recur because of an established habit. I have known chills to occur when the ears were ringing with quinia. Strychnia fails to arrest them; arsenic has more value, but frequently fails. Pure nitric acid, properly diluted, in doses of six to ten drops, given every four to six hours without regard to the stage of the paroxysm, succeeds more often than any medication I have ever resorted to.
Before dismissing the subject of the treatment of simple intermittent fever it may be proper to mention that I have made trials of cure by carbolic acid, administered by mouth and subcutaneously, and also of the sulphites, with no results worthy of recommendation.
Remittent Fever.
The difference in definition between the words remittent and intermittent expresses the clinical distinction between these two forms of fever in a very satisfactory manner.
Remittent fever exhibits oscillations of temperature regulated as to hours of recurrence by laws similar to those which govern the periodic returns of intermittent fever; but there is no complete defervescence of the fever. While the lowest angles of the fever curve approximate the normal body heat more or less closely, they never decline to a standard of apyrexia.
That remittent fever is a malarial disease, produced by a cause identical with that which produces intermittent fever, is well proven by the following facts:
First. Cases occur in close relation with cases of intermittent fever in populations similarly exposed to malaria, and at the same periods of the year.
Second. The two forms of disease are readily convertible, the one with the other.
In non-tropical countries remittent fever cannot be regarded as the natural type of malarial fevers. At least, it may be affirmed that the proportion of cases which begin as remittent attacks is so small that we are warranted in looking upon them as departures from type. In the United States army during the years 1861-66, inclusive, there occurred 286,490 cases of remittent fever. The fatal cases were 3853, being a mortality-rate of 13,450 per 1,000,000 cases. By comparing these statistics with those of intermittent fever recorded in a previous section it will be found that remittent fever is more than twelve times as fatal to life as the simple intermittent forms.
If we accept this view of the pathology of remittent fever, it is of interest to the sanitarian or practitioner to endeavor to arrive at the causes which occasion these departures from type. Some of these are undoubtedly extraneous to the system, and relate wholly to circumstances affecting the malarial poison as a disease-producing agent. Increased quantity of malaria is well understood to enlarge the ratio of remittent cases. There is also strong presumptive evidence supporting the hypothesis that different annual crops of malaria vary in respect to the noxious qualities of this agent. The same presumption relates to all crops produced in certain localities as contrasted with others. Other causes which determine remittent rather than intermittent attacks are personal to patients. They may be classed as follows:
First. Unusual personal receptivity or impressibility to malaria may exist, either because of some constitutional idiosyncrasy or of some state the system at the time of exposure.
Second. Want of timely medical treatment or of proper medical treatment may convert intermittents into remittents.
Third. The rapid occurrence of secondary blood infections, extraordinary in character or amount, may cause the fever to be continuous.
Fourth. The existence of complications, inflammatory in their nature, may change intermittent into remittent attacks.
However various or complex the causes may be which operate to convert intermittent attacks into remittent forms of fever, each one must be supposed to act by disturbing the functions of those centres which preside over the normal physiological and chemical changes of the system.
SYMPTOMS AND DIAGNOSIS.—Attacks of remittent fever are, as a rule, more abrupt in their advent than intermittents. When prodromic symptoms exist, they are similar to those which precede ordinary cases of ague.
The chill is seldom attended by such violent symptoms as the cold stage of intermittents. The duration of the cold stage is also more brief. In a small proportion of cases severe vomiting with large bilious ejections complicate the cold stage. The chill is quickly followed by the hot stage.
The mildest cases of remittent fever are not readily distinguishable from the intermittent forms. In these cases the temperature curves are marked by sharp angles and long tracings between the lowest and highest records. As cases become more decided in diagnosis, and consequently represent higher degrees of departure from the intermittent type, the angles of temperature curves become more obtuse and exhibit a more or less high average range. The accompanying temperature diagram (Fig. 23) shows the thermometric record of an unusually protracted and grave case. The patient was a near relative of my colleague, Prof. Logan, a leading practitioner of New Orleans, and the clinical records may be accepted as altogether accurate. It is somewhat to be regretted that the records of temperature were not begun at an earlier period, but the gravity of the case was not manifest until the continued type of fever was found to exist. The latter part of the diagram illustrates the lapse of the remittent fever into an intermittent. This is so commonly a mode of cure that the practitioner watches with solicitude for increasing oscillations of temperature to announce mitigations of severity in his gravest cases.
| FIG. 23. |
| Temperature chart showing the lapse of a remittent fever into an intermittent. |
| NOTE.—From the third to the fifteenth day after attack a half drachm of quinia was given daily. Observing no good result, it was omitted until the twenty-ninth day, on which date two doses of eight grains each were administered. On the morning of the thirty-fourth day eight grains were again given; on the thirty-fifth day one scruple was given. |
The differential diagnosis of intermittent and remittent fevers may be looked upon as practically unimportant. All cases so near the borderline as to make differential diagnosis a question should receive identical treatment.
There are, however, two other very grave forms of fever which are liable to give trouble in differentiation from remittent fever. These are typhoid and yellow fevers. The sanitary protection of communities exposed to cases of the latter, and also the practical treatment of the sick, call for early and correct differentiation.
But it is only in the early stages of the pathological processes of these affections that difficulties of diagnosis are liable to obtain. The facial expression of patients suffering with remittent is sufficiently characteristic to afford some diagnostic inferences. During the pyrexia the face is flushed and the eyes injected, but the redness is more vivid and the countenance more animated than in either typhoid or yellow fever. It would not be inaccurate to say that, however great may be the flushing or other alterations of the countenance in remittent fever, the natural facial expression is better preserved than in either of the fevers under comparison with it. Sallowness of the skin is an early and almost constant event in remittent fever. It comes on as a secondary manifestation, and appears in a large ratio of cases to bear some relation to the high temperature preceding its occurrence. The icteric hue is seldom intense, indeed very infrequently equalling the orange-yellow of jaundice resulting from obstruction. There is an exception to this statement in those cases in which remittent fever attacks a person already jaundiced. I have seen many cases in which the jaundice preceded the remittent fever, and became more strongly marked after its incursion, particularly in those persons who had remained for some time in a malarial region and suffered repeated attacks. In all cases of remittent fever it seems reasonable to ascribe the more or less jaundiced state to one or both of two factors, viz.—the accumulation of excrementitious material and bile constituents in the blood from primary derangement of its chemistry; and that excessive activity of the liver which the malarial poison appears to induce. Whether the latter mentioned factor results from some action of malaria directly affecting the nutritive processes of the liver, as it does those of the spleen, or whether the altered blood-currents during the paroxysms cause this supposed hypersecretion of bile, we certainly know that to malaria only can we ascribe those fevers which are marked by such peculiar symptoms of biliousness or superabundance of bile as to justify the prefix bilious fever or bilious remittent fever.
The state of the alimentary tract may properly receive notice after these remarks. In the early stages of remittent fever the tongue may be moist and large, and covered with a white or lead-colored or yellowish coat. The edges may be indented with imprints of the teeth. This is Osborne's malarial tongue, and its appearance is worth something in diagnosis.
Later in the progress of remittent fever the tongue may become dry, brown, cracked, and difficult of protrusion, but seldom showing the tremulousness of a typhoid-fever tongue, and differing also from the yellow-fever tongue in the fact that in this disease the appearance of the tongue is usually indifferent as a symptom, except that in advanced stages it is liable to be smeared with blood.
The stomach is irritable from the very beginning of an attack, and the acts of emesis are generally in striking contrast with those of typhoid or yellow fever, both in respect to their violence and to the relative amount of bile they eject.
The bowels are ordinarily costive, and when moved by purgatives the stools contrast strongly with those of typhoid or yellow fever by presenting evidences of the bile-coloring principles which attend all excretions in malarial fever, and are found in the urine, the perspiration, and occasionally the sputa.
Some unusually violent cases of malarial fever, which may become remittent, are inaugurated with convulsions, profuse diarrhoea, and coma.
Before closing the remarks concerning the digestive organs in remittent fever I should mention that in the long array of cases I have treated I cannot recall one solitary instance of black vomit. It is, however, true that I have observed hemorrhage from the bowels in quite a number of cases. These occurred late in protracted cases, and were sometimes the cause of death. Whether it be merely a coincidence I am unable to say, but it is true that the majority of these cases have been in young females just after the establishment of the catamenia.
Hemorrhage from the nose is frequent in remittent fever, but I have never seen a case with general tendency to hemorrhage.
The pulse in remittent fever differs from that of the typhoid or yellow fevers by being more synochal in character, firmer, and more resisting to pressure. The longer the duration of the case the less is this characteristic discernible.
The nervous system shows less ataxia. Delirium may occur in any stage of the disease, but differs from the delirium of typhoid and yellow fevers in showing a lessened degree of perversion of the reasoning faculties. The neuralgias have nothing special.
The urine is acid, high-colored, and scanty. I have never found much albumen in the urine of a case of remittent fever, unless there was some other cause to account for its presence. A small amount may be detected during excessive fever. Blood is a rare constituent.
Mild cases of remittent fever should terminate in recovery in from five to seven days. Fatal attacks usually end from the fifth to the tenth day. Many cases pursue a course which lasts from twenty to forty days. Under proper treatment the usual termination is in recovery, either directly or by conversion into the intermittent type.
POST-MORTEM APPEARANCES.—When death occurs in remittent fever the post-mortem changes generally consist of those which are principally due to chronic malarial toxæmia and those ascribable to the acute attack.
Under the former division are permanent enlargements of the spleen and liver, and pigmentary matter in the blood and deposited in various organs. Under the latter are to be classed hyperæmic or even inflammatory states of the stomach and intestines, and those degenerative changes which are the consequence of continuous hyperpyrexia. The post-mortem changes which are so uniformly found as to be most often appealed to in the establishment of diagnoses are enlargements of the liver and spleen. These may be due in part to hyperplasia and in part to blood-engorgement. The brown or slate color of an enlarged liver is strongly diagnostic of malarial affections. It contrasts strongly with the yellow and natural-sized liver of yellow fever and with the negative liver of typhoid fever.
The skin is generally yellow, sometimes quite intensely icteric, but seldom showing the ecchymotic extravasations of yellow fever. In remittent fever we never find the cadaver oozing blood from the nose and the mouth, nor are the stomach or intestines ever found to contain black vomit.
TREATMENT.—The indications of treatment in remittent fevers differ from those of intermittents in two leading essentials.
First. It is a far graver form of fever, and calls for more promptitude and energy in treatment for its successful management.
Second. The important pathological condition to be combated is the hyperpyrexia, and not the cold stage, as in intermittents.
But even with a clear realization of the practical importance of these facts in governing the treatment of remittents, the practitioner must still exercise care and self-control, lest he shall unconsciously adopt the doctrine that inflammatory lesions must be present to occasion such violent pyrexia as often exists. The physician who comes directly from a case of pneumonia or rheumatic fever and finds a patient suffering from remittent fever, with temperature higher and pulse more bounding than those of the patient he has just left, is pardonable for finding it difficult to realize that these furious symptoms are not also associated with inflammation.
Attempts to cure remittent fevers by an exclusively antiphlogistic treatment either result fatally or induce long periods of confinement and suffering before recovery is reached. The great indication is to secure cinchonism as promptly and completely as possible. Nothing should divert our attention from this object. The condition of the patient as it respects fever, delirium, or state of the tongue, should form no bar to the administration of quinia. There are no practitioners who have had much experience in treating these grave forms of malarial fever after this method who are not able to recall the numerous instances of most astonishing and gratifying amelioration of symptoms as soon as saturation with quinia was brought about. The dry tongue becomes moist, the skin is bathed in gentle perspiration, the delirium ceases, and the patient sinks into a quiet sleep.
The amount of quinia necessary to produce cinchonism must be estimated for each particular case according to the measure of its severity or to states of the system more or less favorable to its absorption. It must be borne in mind, however, that questions concerning the patient's safety are paramount to those of economy. In the mildest cases I never trust to a smaller amount than from twenty to thirty grains. In violent attacks I have administered scruple doses every fourth hour until a sufficient test had been made of its capability to arrest or modify the febrile paroxysm. I have never met with any of those exaggerated physiological effects which some observers teach us to fear from the exhibition of cinchona preparations during fever. Certainly, I can declare that no permanent deafness or other lasting lesion of nerve-function has ever occurred under my observation. I must also add that I know of no reasons why remissions afford more favorable conditions for the administration of quinia, beyond the fact that the system is in a better state for its absorption and assimilation. The quinia is preferably given in solution, but may be exhibited in the form of pills, or in powder suspended in black coffee, or in the thick mucilage of the slippery elm.
The considerations of treatment which are naturally connected with those just advocated relate to measures which it may be proper to associate with the quinia. The answers to the two following questions comprise all that is necessary to be said on this point—viz.:
Are conditions of the system present which may interfere with the specific treatment by quinia, and which are not, in themselves, curable by it?
Are any medicines to be given as succedanea to the specific remedy for the purpose of rendering its action more sure or prompt?
In regard to the first inquiry, it must be admitted that in quite a large proportion of cases of remittent fever specific treatment fails to cure. I suppose that may be a reasonable proposition which holds that in the majority of these cases the presence of secondary blood-impurities annuls the ordinary specific effects of cinchona. These must be gotten rid of by depurative medicines. The intestinal canal, the skin, and the kidneys are the emunctories through which elimination must be effected. It is therefore proper for the physician to endeavor to recognize cases where such impurities exist, and to so modify his treatment as to remove them. The indications for depurative treatment are jaundiced skin and eyes, furred tongue, costive bowels, and scanty, loaded urine. These are more or less positively expressed symptoms in a large majority of cases. It is therefore proper that in this large majority of cases of remittent fever depurative treatment should be conjoined with the specific treatment. In my opinion, no drugs meet this indication so well as mercurials and saline purges and diuretics. Calomel or blue mass may be given either simultaneously with the quinia or in alternate doses.
There are three very important rules to be observed in regard to cathartics: They should never be carried to such an extent that absorption of the quinine is interrupted. They should not be given in such large or repeated doses as to produce prolonged irritation, or it may be even inflammation, of the alimentary canal. Purgatives should be used for their depurative effects, and never as antiphologistics.
Opium exercises excellent effects in preventing local irritation or hypercatharsis, and in relieving derangements of nerve-function and insomnia. It is preferably given in small doses, combined either with purgatives or with the quinia.
I have found bitartrate of potassium the most grateful and efficient saline for depurative action. I have generally given it in lemonade in such amounts as to secure a gentle aperient and diuretic effect. I hold strongly to a conviction that all drugs as soluble as this facilitate the absorption of those less soluble—as, for example, of quinia.
If the first efforts to break the febrile paroxysms fail, it is better to discontinue the quinia and place the patient under symptomatic treatment, and await conditions of the system more favorable for its repetition. Of course the high temperature is generally the symptom requiring most care and attention.
Vomiting is one of the troublesome symptoms of remittent fever. As internal medication minute doses of morphia, dry upon the tongue or in solution in cherry-laurel water, or in combination with eight or ten drops of chloroform, are generally efficacious. Swallowing pellets of ice or frequently taking iced effervescing mixtures are good measures of treatment. Occasionally, a mild emetic, such as warm chamomile infusion, or warm water alone, will arrest the vomiting temporarily. It is doubtful, however, whether this relief is secured by the ejection of any offending matter from the stomach. It is more than probable that the forced dilatation of the stomach has arrested the spasms, for filling this viscus with cold drinks to repletion will often effect the same result.
Of all applications to the epigastrium, a cold wet towel occasionally sprinkled with chloroform is the best.
A tympanitic or tender abdomen requires stupes wrung from warm water. They may be dashed with turpentine at first, and afterward consist of warm water with whiskey. I have occasionally given two or three doses of turpentine emulsion with benefit, but from much observation I am forced to protest against the turpentine treatment, as it is called, which is to give twenty drops of turpentine every two to four hours as a curative agent.
Hemorrhage from the bowels must be met by hæmostatic treatment—preferably, in my experience, by the use of five grains of gallic acid in half an ounce of camphor-water every two hours, of morphia subcutaneously, and of cold cloths over the bowels. As in all diseases liable to cause death from exhaustion, careful attention must be paid to the nutriment, and stimulants must be administered as required.
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.
Typho-Malarial Fever.
The prefix typho- is properly applicable to a class of malarial fevers which are complicated by the specific poison which produces typhoid fever.
This term was introduced into medical nomenclature by Surgeon J. J. Woodward of the United States Army. His classical paper on this subject has been published in the Transactions of the International Medical Congress at Philadelphia in 1876. The following extract from the proceedings of this congress will show the interpretation of this term by Woodward:
"On motion of Dr. Woodward, seconded by Dr. Pepper, the following was adopted as expressing the opinion of the section: Typho-malarial fever is not a specific or distinct type of disease, but the term may be conveniently applied to the compound forms of fever which result from the combined influence of the causes of the malarious fevers and of typhoid fever."
It follows, therefore, that the term should be so restricted as to define a disease compounded of the two pathological factors which when acting separately produce either typhoid or malarial fever.
When understood in this sense, and carefully employed, the term appears to me unobjectionable. Perhaps, indeed, it may be a convenient addition to medical nomenclature. If such a name had not been introduced, we would be forced to speak of these cases of compound disease as complications. As it is customary to regard the minor or less important affection as the complicating disorder, we would often have confusion in determining whether the case should be typhoid fever complicated by malaria or malarial fever complicated by typhoid. This term leaves all questions of precedence or predominance in abeyance.
There are no facts, however, which support a conclusion that the malarial poison is capable of forming combinations with the particular poisons of other specific fevers and give birth to a new special poison, which may be perpetuated by successive generations, and thus produce epidemics of a new but compound disease.
The importance of a proper use of the term typho-malarial implies co-ordinate care in diagnosing the true nature of the malady it should define.
It may be said, in brief, that the diagnosis of typho-malarial fever must rest upon the blending of the symptomatic phenomena peculiar to each one of the two fevers which enter into combination. In other words, if the differential diagnosis between the two diseases when they are distinct is made by contrasting the symptoms peculiar to each, the compound disease is to be recognized by more or less positive combinations of these symptoms.
These blended symptoms should not be expected to exhibit the results of a copartnership in which each member exerts equal influence. It is well understood that when two diseases coincide, that one which is more violent or excessive in its morbid process holds so much sway as in some cases almost to extinguish the symptoms of the weaker member of the combination. Consequently, in typho-malarial fever, the typhoid, being the graver of the two forms of disease, ordinarily rules the pathology.
The following notes, accompanied by a temperature chart, will illustrate the clinical course of a case of typho-malarial fever:
J. L., aged thirty years, of French nativity, but a resident of New Orleans for three years, was admitted to Ward 21, Bed 311, Charity Hospital, on the night of December 10, 1881. Had been ill some days with ague. The house-surgeon administered gr. x. of quinia in solution and gtt. xv. of tincture of opium.
The records and temperature date from the 12th of December. During the 11th he took drachm ij sulph. cinch. in solution.
| FIG. 24. |
|
PART I., showing the temperature curve from
December 12th to 31st, inclusive, during which time the more
characteristic typhoid symptoms predominated. |
| PART II., showing the temperature curve in same case from January 1st to 20th, inclusive, during which the influence of the associated malarial poison was prominent. |
Dec. 13th, tenderness and gurgling in ileo-cæcal region; epistaxis; rose spots on abdomen; deafness and ataxia; no stools since 11th. Ordered
| Rx. | Acid. Sulphuric. dil., | |
| Syr. Aurantii Cort. aa. | fl. drachm ij; | |
| Tinct. Cinchonæ Co. | fl. oz. j. M. |
S. Teaspoonful in water every four hours.
Also ordered beef-essence, milk-punch, and milk.
Dec. 13th, two very offensive liquid stools; ataxia greater; skin yellow and countenance dull and listless. Dec. 14th, fresh rose spots; tongue brown and dry; three stools; much jactitation. Dec. 15th, more ataxia; some delirium; pulse 100, weak. Gave gr. iiss quinia in solution, with tincture opium gtt. iii, every two hours. Dec. 16th, pulse 128, weak; delirious. Dec. 17, new rose spots; belly tympanitic; tongue brown, dry; sordes on teeth and lips; eyes injected; very delirious. Treatment continued; nutrition and stimulants given methodically. From 17th to 22d but little change in condition or treatment. Diet and stimulants administered regularly. Dec. 22d, coma vigil; completely delirious. Ordered
| Rx. | Liq. Morphiæ Sulph., | |
| Tinct. Digitalis aa. | fl. drachm iij; | |
| Spts. Æther. Nitrosi | fl. drachm ij; | |
| Liq. Potass. Citrat. | fl. oz. iij. M. |
S. Tablespoonful every three hours.
As the oscillations of temperature became more marked, quinia was resorted to, apparently with good effect. The patient was discharged from the hospital Feb. 8, 1882.
It should be observed that after the 14th of December the patient's bowels were rather costive, and the stools occasionally moulded and very dark in color. On the forty-fifth day after admission the patient had a severe chill, followed by a rise of temperature to 104°. This yielded to competent doses of sulphate of cinchonidia.
This was a typical case of typho-malarial fever. The blended symptoms, as well as those special to each disease, are sufficiently exhibited in the clinical account. The presence of typhoid fever was established by the rose spots and the marked nervous symptoms. The typhoid process seems to have been unusually mild in so far as evidence of bowel lesions were made manifest.
The history of the patient before admission, the color of his skin and stools, and the temperature curves gave abundant proofs of the malarial element in the pathology of the case.
Perhaps nothing need be added on the subject of diagnosis. I may, however, remark that I am very cautious in asserting the diagnosis of typho-malarial cases unless the nervous symptoms, positively-marked bowel symptoms, or rose spots are present to vindicate such a decision. The presence of malarial poison may be determined with less difficulty from the previous history of the case and its special symptoms in the early stages of an attack. But if the morbid processes of the typhoid poison are violent, there are likely to be stages of the disease when it is not possible to detect symptoms which indicate the presence of malaria. On the other hand, it is unquestionably true that the typhoid condition, as it is termed, which so often complicates malarial fevers, can very generally be differentiated from true typhoid fever. While certain cases, or even epidemics, of malarial fevers are attended by remarkable adynamia, often manifesting itself from the very incipiency of attacks, it differs widely from that utter nervous ataxia which characterizes typhoid fever. Again, the adynamia of malarial attacks is generally ascribable to some cause not essential to those affections. Imperfect reaction from a chill, long persistent hyperpyrexia, diarrhoea or vomiting, or chronic paludal cachexia, or, it may be, some epidemic influence, may produce it. The ataxia of typhoid fever is part of its morbid process.
Woodward's statistics show that 49,871 cases of fever diagnosed as typho-malarial occurred among the white forces of the United States during the late Civil War. Of this number, 4059 proved fatal, a mortality-rate of 8.13 + per cent. Among the colored troops 7529 cases occurred, with 1301 deaths, a mortality-rate of 17.27. Statistics borrowed from the same excellent authority give the number of cases of unmixed typhoid fever (or fever classed as typhoid without reference to any complication) as 75,368 among the white troops, with 27,056 deaths, a mortality-rate of 35.89. Among the colored troops 4094 cases occurred, and 2280 died, a mortality-rate of 55.68. These figures show very singular comparative results. They prove that typhoid fever as an uncomplicated malady, was four and a half times as fatal among the whites as the same disease when in combination with malarial poison. Among the colored troops typhoid fever was three and a half times more fatal than typho-malarial fever.
It is highly probable that inaccuracies exist in statistics gathered in the confusion of a great civil war, but I am not prepared to say that the conclusions they point to are incorrect. When an acute inflammation is complicated by malaria, its prognosis is rendered more grave. This, no doubt, is due in part to degradations of the fluids of the system by the malarial poison, and in part to the revulsions of circulation during paroxysms. But it does not follow from this fact that the presence of malaria in the blood, or its effects upon that fluid, exercise an unhappy influence upon diseases due to other specific poisons. It may, on the contrary, be ascertained in the future that it modifies the typhoid process, so as to deprive it of some of its most dangerous features.
Further investigations are required to determine the facts in regard to these questions. But it may be premised that if such a conclusion shall ever be reached, it will influence our expectations of cure rather than our practice. If the malarial poison is capable of modifying the toxic effects of the typhoid poison, it must do so in the very formative stages of that affection, if not in its incubative period, so that, having accomplished all the good it is capable of effecting, we may proceed at once to rid ourselves of its presence.
In entering upon the treatment of two diseases compounded in the same patient, if one should ordinarily be amenable to specific treatment, it must certainly be wise practice to endeavor to simplify the case by subtracting that one from its composition. This is more especially true if the treatment does not affect the course of the other disease in any injurious manner. It is therefore proper to begin the treatment of a case of typho-malarial fever by administering large doses of quinia. A scruple may be given every fourth hour, until its effects in eliminating symptoms ascribable to malaria, and also as an antipyretic, have been sufficiently tested. In the early stages of typho-malarial attacks the febrile exacerbations conform to those laws of periodicity which govern uncomplicated malarial fevers. After the first week, or when the typhoid process has become well established, periodic returns of the fever are less plainly observable. It is possible that in some cases in which the typhoid process manifests itself with great severity the temperature curves may be very characteristic of that disease. I am satisfied that the indications for giving quinia to eliminate the malarial element must be based upon the fever curves which mark the case. Perhaps a more frequent application of the thermometer would often exhibit malarial periodicity where it may otherwise remain unsuspected. I know this to be very often the case in pneumonia complicated by a malarial fever.
Whether thorough cinchonism in the early progress of the attack rids the case of symptoms due to malaria or not, only a very few days are likely to elapse before oscillations of temperature call for its repetition.
The typhoid processes require very much the same measures which are applicable in uncomplicated cases of that disease. The stools of the early stages of attacks should not be checked unless excessive, and mercurials and laxatives should be more freely used than in simple typhoid fever. The effects of the malarial fever and of the hyperpyrexia of typhoid fever, when combined, must almost necessarily entail more accumulation of excrementitious material in the blood than would occur either disease existing separately. On this account eliminating treatment is an important indication. When it becomes necessary to check the diarrhoea because excessive or on account of failing strength, diuretics subsequently prove serviceable. Effervescing solutions of potassium or ammonium, lemonade, Apollinaris water, iced tea, strawberry, mulberry, or raspberry juice, are grateful beverages and increase renal activity. The mineral acids may be given during the ulcerative periods of the disease. Insomnia must be relieved by opiates, chloral hydrate, or other hypnotics.
Tympanites should be met by warm stupes, large enemas of warm water with fl. drachm j tincture of asafoetida or fl. oz. j of whiskey. Small doses of turpentine in emulsion are often beneficial.
In the early progress of cases the diet should consist of farinaceous foods, with milk and the pulps or juices of fresh fruits, given either cooked or in their natural state as the physician may determine for each patient. Methodical and forced nutrition becomes necessary at more or less early periods in different cases.
The stools and all ejecta of the sick should be disinfected and disposed of with the same care and for the same purpose as those of unmixed typhoid fever.