Tropical Diseases/Chapter 14
CHAPTER XIV
BLACKWATER FEVER
Synonyms.— Hæmoglobinuric fever, melanuric fever, hæmaturic fever.
Definition.— An acute disease characterized by pyrexia— generally ushered in by severe rigor, bilious vomiting, icterus, hæmoglobinuria and, frequently, diminution or suppression of urine.
For a long time this disease, like kala-azar and several other tropical fevers, has been regarded as a form of malaria, and in earlier editions of this manual, in deference to general opinion, I described it, with some reservation, under that head. I have long entertained the idea that too much has been taken for granted in relegating black water to malaria, and thereby ignoring its possible individuality as a separate disease; an individuality strongly suggested not only by the symptomatology, but also by epidemiology and analogy. I have therefore now placed it by itself pending definite settlement of one of the most important problems still unsolved in tropical pathology. Such an arrangement, apart from other and more purely theoretical considerations, has its practical advantages.
Geographical distribution.— The geographical distribution of blackwater fever is very wide. Although it does not coincide with that of any of the known types of malaria, and although the endemicity of blackwater fever is not coextensive with that of malaria, it is only in localities in which malaria is very prevalent that blackwater fever can be acquired. Endemic concurrence, however, must not be looked on as conclusive of identity; the germ causes of very different diseases may have certain topographical requirements in common.
The prevalence of blackwater fever in various malarious countries is most unequal. It is common here and there throughout tropical Africa. It is found all along the West Coast from the Senegal to the Coanza, but principally on the Congo and on the deltas of the Niger and Gambia rivers. On the East Coast it is also widely spread, especially along the Zambesi, the lower Shire, and the shores of the Nyasa. It is far from uncommon in the Upper Niger, in British and German East Africa, in Uganda, in North and South Rhodesia, in Abyssinia, and in the valley of the Upper Nile. It is also common in some parts of Madagascar. But it is not found in the malarious regions of Lower Egypt, and it is rare in Algeria.
In America it extends over the Southern States of the Union, chiefly Florida, Georgia, Alabama, Mississippi, Arkansas, and Texas, but recently it has also been prevalent in North Carolina and Virginia. It is found, too, in Central America, on the plains of Venezuela and in the West Indies.
In Europe it is restricted to Greece, Sicily, and Sardinia. A few cases have been reported from Central Italy. It is extremely rare in the Roman Campagna, the classic land of malaria.
In Asia it is reported from Palestine (Zicron), Tonquin, the Malay Peninsula, Formosa, and lately it has been described as occurring in Assam, Burma, Darjeeling, the Terai, Meerut, and Amritsar. It occurs in many of the malarious islands Java, Solomon Islands, etc. of the Eastern Archipelago, and also in New Guinea.
Before 1885, strange to say, no Indian writer had mentioned hæmoglobinuria as a feature in the pyretology of Hindustan or of the East. Apart from the possibility of its having been overlooked, there may be another explanation for this singular silence: the disease may have been confounded with bilious remittent. It is difficult to believe, however, that the large number of acute observers who had studied Indian diseases so carefully and for so many years could have systematically ignored this striking disease. Possibly, therefore, it is of recent introduction into India. Such an idea is countenanced by the fact that certain medical men practising in Africa, good observers, declare that black water fever is of comparatively recent introduction there; and, moreover, that it is yearly becoming more common in that continent. In certain States of the American Union it seems to have been only recently introduced; Meek says it first appeared in Texas in 1886.
Topographical distribution.— Although black water fever has a wide general distribution, it is limited in its endemicity to low, swampy grounds; and although, as reported by several authors, it sometimes occurs at high altitudes, this does not prove that infection took place there. We know that the disease may remain latent for a considerable time, that those who have been infected may have relapses at long intervals, and that the clinical manifestations may appear for the first time far from the place in which the infection was contracted. It is a common belief among the older residents in British Central Africa that a change of district, particularly from one level to another, causes blackwater fever, an opinion based on the experience that many cases occur soon after such a change. Amongst Europeans in British Central Africa such changes of district are frequent, and, as it is only a day's journey from the lowlands to the highlands, it is reasonable to infer that the majority of the cases which occur on the highlands depend on infection contracted previously in the swampy regions at the foot of mountains, and in the season during which the conditions favouring infection are most prevalent.
Seasonal prevalence.— In the Southern States of the American Union blackwater fever is reported to be especially frequent in late summer and in autumn. On the West Coast of Africa it seems to prevail at the close of the rainy season (August and September). For British Central Africa we have no definite information on this point. Like other infectious diseases, the acquisition of the germ cause of blackwater fever is directly or indirectly dependent on special meteorological conditions. The first clinical manifestations of the infection and relapses may occur at any season and in any place.
Epidemiology.— Blackwater fever at times assumes an epidemic form. It may not be seen for years in a district, and then numbers of cases may occur within a short time. Very often, as is the case in yellow fever, the magnitude of an " epidemic" may depend on the number of susceptible persons, possibly new arrivals, within the endemic region. It broke out amongst the labourers employed in making the canal through the Isthmus of Corinth; it attacked the Chinese labourers on the Congo railway; and in 1885, according to Dr. Wenyon, of Fatshan, China, " it ravaged like a plague the Chinese army on the Tonquin border of Kwangsi." In collective dwellings, such as barracks, hospitals, schools, it may attack several persons at the same time. In 1885 it broke out in a prison in Castiades, Sardinia, attacking 24 out of 800 convicts. Sometimes several cases may occur at intervals in the same house; such houses are known in British Central Africa as "blackwater fever houses."*[1]
Predisposing causes.— Individuals of all ages and both sexes are liable to blackwater fever, but they are not equally subject to it. It more commonly affects men about the middle period of life, obviously on account of their greater exposure either to its causative agent or to circumstances provocative of an attack.
At one time race was considered an important factor. In Africa, Europeans, Indians, and Chinese are attacked in great numbers, whilst the natives are said to enjoy an immunity. The immunity of the natives is probably not a racial immunity; more likely it is the immunity conferred by infection during childhood. In fact, negroes living in places which are free from blackwater fever contract the disease just like Europeans when they come within its reach. Plehn mentions a serious outbreak of blackwater fever among the blacks in the Cameroons, the disease especially attacking those who had come to the coast from the interior. Reynolds says that the disease occurs sporadically amongst the natives of Ashanti.
Among the circumstances which predispose to the active clinical manifestation of the blackwater-fever infection, debility from previous illness, bad food, or hardship have undoubtedly a powerful influence. It is usually in those who have suffered from subtertian infection, more rarely from tertian and quartan infections, or from dysentery, or who are "run down " from any cause, that blackwater fever appears, although cases of the disease in strong, healthy individuals of recent arrival have frequently occurred.
Length of residence.— It has been repeated again and again that Europeans are rarely attacked within the first year of residence in a blackwater-fever country, and great stress has been laid on this statement by those who believe that the hæmoglobinuria is not the special feature of a specific disease, but only a symptom of ordinary malaria in people who have previously suffered from several attacks of the prevailing intermittent fever. We know, however, that although in most cases attacks of the more widely spread subtertian may precede blackwater-fever infection, yet there are many cases on record in which blackwater fever occurred before any kind of "malaria" had manifested itself. Plehn, Scott, Ritchie, Cardamatis, Lynch, Hearsey, Daniels and others have reported cases of blackwater fever in robust individuals who were attacked within two or three months of their arrival in a blackwater-fever country. I have frequently been told by officers in the African colonial service that the attack of blackwater fever for which they were invalided suddenly developed while they appeared to be in perfect health and without any malarial antecedents. Daniels states that few cases occur during the first six months' residence, that they rapidly increase during the next six months, are most numerous during the second and third year, and become rare after five years' residence. This is exactly what might be expected to happen with any localized infectious disease. The relatively small number of cases within the first six months may be explained by non-exposure to the causative agents of the disease; indeed, many arrive in the endemic district at the end of the epidemic season. The progressive prevalence of cases during the first three years finds an obvious explanation in the accumulating chances of infection; the decrease in later years may be partly accounted for by the progressive diminution in the number of the older residents and by the weeding out of the most susceptible. Daniels states that the early cases of blackwater fever those under one year's residence are mainly (14 out of 21) in persons resident at or below the 1,500 feet level; and the majority (10 out of 14) of cases in persons having four years' residence are in persons residing principally in the highlands.
Etiology.— There are three theories as to the etiology of blackwater fever 1, the "malaria" theory; 2, the quinine theory; 3, the specific theory.
1. The malaria theory.— The prevalence of blackwater fever in malarious regions, the great frequency of its occurrence in persons who had previously suffered from one or other of the malarial fevers, the finding of malaria parasites and hæmozoin in the blood and organs, and the large mononuclear leucocytosis of hæmoglobin uric cases led to the belief that blackwater fever was an unusually severe form of "malaria." Against this theory is the fact that although blackwater fever is certainly co-endemic with one or other form of malaria in several regions, it is not so in all regions. It has its own peculiar distribution, and is absent or very rare in many places in which the various intermittent fevers are especially rife. It is exceedingly common amongst the few Europeans who live in tropical Africa; it is practically unknown amongst the many thousands of Englishmen who live in the fever haunts of India and elsewhere. It is quite true that blackwater fever generally occurs in persons who have previously suffered or are suffering from malaria; but this does not prove that it is a special manifestation of malaria. It may be concurrence merely. We do not believe tuberculosis to be a peculiar manifestation of enteric fever because it often follows in the wake of that disease. Mpreover, as already pointed out, blackwater fever frequently attacks people who previously had never had a single paroxysm of intermittent fever. The fact that malaria parasites are often found in the early stages of blackwater fever is not surprising when we consider that in many places malaria is exceedingly common and is co-endemic with blackwater fever. Although the tertian and quartan parasites have been found in the blood of blackwater-fever cases, the parasite which most frequently occurs is the subtertian, because it is that species of malaria parasite which is most common in the endemic regions of black- water fever. Yet of all the intermittent fevers, subtertian is the one that differs most, clinically, from blackwater fever. It is true that subtertian varies considerably in different cases; but the type of the disease does not alter, and the number and distribution of the parasites in the organs are always in perfect accordance with the intensity and nature of the various symptoms. In no case of subtertian, not even in the most pernicious, do we ever find the symptoms peculiar to blackwater fever. On the other hand, all cases of blackwater fever, however grave, however mild, always exhibit the same characteristic symptoms, with no difference other than as regards intensity and duration. Admitting the malaria theory of blackwater fever, we should have to consider a mild relapse of blackwater fever to be an unusually severe attack of subtertian an untenable paradox. When malaria parasites are found in cases of blackwater fever they may be very scanty and in no way proportional to the symptoms of the disease. But in many cases no parasites are found; or, what is still more striking, if there were a few parasites before the attack, they invariably completely disappear with the onset of blackwater fever, and may not return after recovery from the latter disease. In analogy with what is sometimes observed in pernicious cases of subtertian fever, some authors have suggested that the parasites, though scarce or even absent in the peripheral blood, may be numerous in some internal organ, particularly the brain. Against this a priori argument are the absence of cerebral symptoms during the attack, and the occasional negative evidence of post-mortem findings.
Much has been made of the large mononuclear leucocytosis present in this disease as a proof of its malarial nature. But we now know that a similar type of leucoeytosis occurs in several other forms of protozoal disease.
If blackwater fever be caused by any one of the known malaria parasites, this parasite must hare acquired its peculiarly powerful hsemolytic properties in a previous passage through an as yet unrecognized mammalian or insect host; or the subject of blackwater fever must have been exposed to some specific influence present in blackwater fever countries, but absent in other malarial districts.
2. The quinine theory.— The quinine theory of blackwater fever arose in Greece. It was first suggested by Verétas in 1858, and soon became popular amongst Greek physicians. In 1874 it was upheld by Tomaselli in Italy, and more recently it received the support of Koch. The idea that quinine might produce blackwater fever originated from a misinterpretation of the fact that the administration of quinine, even in small doses, may provoke the manifestation of blackwater fever in a patient in whom the infection is latent. As quinine, even in toxic doses, never produces blackwater fever in healthy people or in malaria patients elsewhere, its peculiar action in Africa had to be explained by a peculiar hypothetical idiosyncrasy an idiosyncrasy— which, curiously enough, is found only in certain malarious countries and not in others. Thus, the connection between quinine and blackwater fever is not one of cause and effect, but merely one of coincidence. Blackwater fever was known long before the introduction of cinchona bark into Europe, indeed it was known in the days of Hippocrates. Besides, even recently, numerous cases of black water fever have been reported amongst Europeans who had never taken quinine. Cardamatis mentions thirty-two such cases. Then, again, a number of physicians have administered quinine in large doses for the treatment of blackwater fever and have greatly vaunted its beneficial action. Quinine, undoubtedly, provokes in some the clinical manifestation of blackwater-fever infection. So, and probably much more powerfully, do chill and fatigue. But no one will contend that the latter cause the disease. Why then attribute it to quinine, which, logically, has no stronger claim?
3. The specific theory.— In 1893, in a paper read before the Epidemiological Society, I stated that, on account of its peculiar symptoms and geographical distribution, I believed blackwater to be a disease sui generis. In 1898 Sambon suggested, because of the striking analogies that its distribution, course, symptoms and morbid appearances have with the hæmoglobinuric fevers of cattle, horses, dogs and sheep, that blackwater fever might be a form of babesiasis. This view, which has been adopted by Blanchard and others, deserves consideration. It is quite reasonable to expect to find in man parasites belonging to this genus of the hæmoprotozoa, so abundantly represented amongst the animals most intimately associated with him. Certainly, of all the diseases of man of which the etiology is still obscure, none could be more appropriately ascribed to this group of parasites. The analogies between the hæmoglobinuric fever of man and the hæmoglobinuric fevers of cattle are most striking. To explain the fact that as yet no babesia has been found in cases of blackwater fever, I might suggest that either the amœboid forms of the parasite have been mistaken for the early forms of the subtertian parasite, or that the parasite has escaped observation on account of diminutive size or anatomical habitat, or because it is not usually found in the peripheral blood.*[2]
Edington claims to have shown that when cattle, natives of the South African endemic regions of Texas fever, are inoculated with rinderpest, they develop hæmoglobinuria and the other symptoms of Texas fever, from which disease they might be supposed to be pathologically immune. The blood of immune cattle in Texas fever regions, we know, contains, in small numbers, the babesia. Edington's experiments show that the supervention of a second infection, rinderpest, determines the multiplication of the latent babesia, and the explosion of the characteristic symptoms. May this not be in strict analogy with what happens in blackwater fever? The infection of blackwater fever may remain latent for considerable periods, until provoked into activity by some special agency, as cold, shock, quinine, or some additional infection, especially malaria.
Cook has placed on record five cases of blackwater fever in which an attack of spirillum fever appeared to be the provocative agent.
Manifestly, the etiology of blackwater fever is not yet settled, and it is wise to preserve an open mind on this important subject.
Incubation period.— We know nothing definite as to the incubation period of blackwater fever. Scott, in British Central Africa, noticed that the attack usually occurred about eight days after exposure in certain low-lying districts. That the disease may remain in abeyance for a considerable time is proved by the facts that recurrences after long intervals months are very common, in fact the rule; and that in some cases the first attack may manifest itself in Europe several months after the patient has left the endemic regions. I have recently met with a case in England in which a severe attack, followed by a still more severe and prolonged relapse, was the first manifestation of a blackwater-fever infection which must have been acquired at least nine and a half months previously— the time that had elapsed since the patient left Africa.
Symptoms.— The onset of blackwater fever is usually sudden. A slight or, more generally, a very severe rigor is followed by intermitting, or remitting, or irregular fever with marked bilious symptoms. Earlier or later in the attack, usually during rigor, the patient becomes conscious of aching, perhaps severe, pain in the loins, in the region of the liver and spleen, and over the bladder; in exceptional instances these local pains are absent. In consequence of a somewhat urgent desire he passes water, when he is astonished to see that his urine has become very dark in colour, perhaps malaga - coloured or, possibly, almost black. The fever continues, though not necessarily very high. Very likely he suffers from epigastric pain and distress, bilious vomiting to an unusual extent, and, it may be, bilious diarrhœa; or he may be constipated. The pain in the loins and the liver-ache continue, and the urine becomes darker and darker. By and by the sufferer breaks into a profuse sweat and the fever gradually subsides. The urine, which hitherto may have been very abundant, or, perhaps, somewhat scanty, now flows freely; and, after passing through various paling shades, from dark brown to sherry red, becomes once more natural in appearance. Coincidently with the appearance of the dark colour in the urine, or even before this has been remarked, the skin and sclerse rapidly acquire a deep saffron-yellow tint. This icteric condition persists and even deepens during the progress of the fever, continuing for several days to be a striking feature in the symptoms. When the fever subsides the patient is conscious of a feeling of intense weakness from which he recovers but slowly. Fever, with or without rigor, may recur next day, or for several days; or it may cease; or it may be remittent, or almost continued in type. The hæmoglobinuria may recur with each rise of temperature; or there may be only one or two out- bursts; it may continue for an hour or two only; or it may persist off and on for several days or even weeks.
In the more severe forms of hæmoglobinuric fever there is usually a very great amount of bilious vomiting, of intense epigastric distress, and of severe liver-and loin-ache. The urine may continue copious and very dark in colour; or, continuing hæmoglobinous, it may gradually get more and more scanty, acquiring a gummy consistence, a few drops only being passed at a time. Finally, it may be completely suppressed.
In severe cases death is the rule. It appears to be brought about in one of three or four ways. The fever may assume the typho-adynamic type; or suddenly-developed cerebral, hyperpyrexial, or algide symptoms may supervene. Singultus is said to be a fatal symptom. In other cases the symptoms may be like those consequent on sudden and profuse hæmorrhage— jactitation, sweating, sighing, syncope. Or it may be that suppression of urine, persisting for several days, terminates, as cases of suppression usually do, in sudden syncope or convulsions and coma. Or, more rarely, nephritis may ensue and the patient die from uræmic trouble three or four weeks after all signs of hæmoglobinuria and fever have disappeared.
Recently I saw in London a case in which the fatal issue appeared to have been brought about by persistent hiccough— always a bad sign— hepatitis, and vomiting of blood,
The urine.— If the characteristic dark-brown, generally acid, urine of a hæmoglobinuric case be stood for some time in a urine glass, it will separate into two well-marked layers : an upper of a clear though very dark port- wine tint, and a lower—perhaps amounting to fine-half or one- third of the entire bulk— of a somewhat brownish-grey colour, and consisting of a sediment in which an enormous number of hyaline and hæmoglobin tube-casts are to be found, together with a large quantity of brownish granular material. Epithelium is also met with. Blood corpuscles may be entirely absent, or very few in number. With the hæmoglobin there is also an escape of the serum-globulin of the blood, for the urine, in many cases, turns almost solid on boiling; the coagulum so formed carries down with it as it subsides the dissolved and suspended hæmoglobin, leaving a pale-yellow supernatant urine. For some days after the urine has regained a normal appearance it will still contain albumin, though in gradually diminishing amount. Spectroscopic examination gives the characteristic bands of hæmoglobin, sometimes those of methæmoglobin.
Mortality.— This varies greatly in different epidemics, in the same and in different places, and even under the same treatment. Some cases are so mild and transient, amounting, perhaps, to a single emission of hæmoglobinous urine, with little or no fever, that they are unattended with risk; on the other hand, a practitioner may encounter a run of severe cases in which nearly all die. Some old residents in Africa have passed through ten or more attacks with impunity. Taking one with the other, the case -mortality in blackwater fever may be put down at about 25 per cent.
Post-mortem appearances. The kidneys.— If the kidneys of a fatal case are examined at an early stage of the disease, they are seen to be enlarged and congested, the tubules blocked with hæmoglobin infarcts, the cells laden with yellow pigment grains, and the capillaries most probably with a certain amount of malarial pigment. If the case survive for three or four weeks and then die of uræmia, the appearances are those of large white kidney.
The spleen is enlarged, congested, and usually contains malarial pigment.
The liver is enlarged, soft, of a dark -yellow colour. Microscopically it reveals evidence of cloudy swelling with a large amount of hæmosiderin in the liver cells. Hæmozoin may or may not be present.
Diagnosis.— The diseases with which blackwater fever might be confounded are— 1, paroxysmal hæmoglobinuria; 2, bilious remittent malaria; 3, yellow fever; 4, icterus gravis. If it be borne in mind that rigor, hæmoglobinuria, pyrexia, are all in evidence at the outset in black water fever, and also that black water fever is acquired only in certain countries, an error in diagnosis is improbable.
As regards paroxysmal hæmoglobinuria occurring in the tropics, a diagnosis might be impossible. Both diseases have the same symptoms. Paroxysmal hæmoglobinuria, as a rule, is of a milder type. In bilious remittent malaria an examination of the urine will suffice to exclude one of the characteristics of blackwater fever, namely, the presence of hæmoglobin. Moreover, the malaria parasite will be present in the blood throughout the fever until quinine has been administered. In yellow fever the initial rigor is rarely severe, the appearance of icterus is a comparatively late event, the spleen and liver are not usually enlarged, the urine is albuminous, and if blood be present the erythrocytes are abundant. The same remarks apply to icterus gravis.
Treatment.— Having regard to the frequency with which hæmoglobinuric fever concurs with malarial infection, and the well-established fact that quinine may precipitate or determine a hæmoglobinuric attack, the question of the administration of that drug in hæmoglobinuria becomes an important point. Some practitioners of experience recommend the exhibition of the drug in heroic doses, giving it every two hours in divided doses to the extent of 120 gr. a day; this they keep up till convalescence is established. On the other hand, hæmoglobinuria may come on while the patient is cinchonized. The Plehns, Koch, and others, after trying quinine in these cases, and carefully comparing the results of treatment both with and without quinine, abandoned its use. So long as the hæmoglobinuria continued they treated the case symptomatically, cautiously resuming the specific if the case merged into and concluded as a simple intermittent. There can be no doubt that in large doses quinine exercises a certain amount of destructive action on the blood corpuscles, rendering their hæmoglobin unstable. When, therefore, its toxic influence is superadded to that of the specific cause of the hæmoglobinuric fever, it may be that it supplies the little that is required to determine an extensive liberation of hæmoglobin, which, had the quinine been withheld, might not have taken place. Bastianelli lays down the following sensible rules as to the use of quinine in hæmoglobinuric fever: (a) If hæmoglobinuria occurs during a malarial paroxysm and parasites are found in the blood, quinine should be given. (6) If parasites are not found in the blood, quinine should not be given, (c) If quinine has been already given before the hæmoglobinuria has appeared, and no parasites are found, its use should be suspended; but if parasites persist it should be continued.
Recommendations.— Patients who are suffering from or are threatened with hæmoglobinuria, or who have had this disease before, on the slightest indication of fever should go to bed at once, keep their skins warm and scrupulously protected from draughts, and take plenty of warm fluid if parasites are present in the blood, moderate doses— 5 gr.— of quinine every three or four hours (intramuscularly by preference) and a moderate dose of calomel should be given. Patients threatening blackwater should not be moved.
When the urine tends to be suppressed, diuretics must not be given with the idea of stimulating the kidneys. In these circumstances hot fomentations should be applied to the loins, plenty of bland diluents administered, and an exclusive milk diet ordered until all albumin has disappeared from the urine. Indeed, even in the mildest as well as the gravest cases, the free and frequent administration of fluid is a most important measure, whether the patient is thirsty or not, and should be insisted on from the beginning of the attack. When, owing to persistent vomiting, fluid cannot be retained by the stomach, enemata of warm physiological salt solution (much less irritating to the bowel, and thus far more likely to be retained than plain water) should be administered repeatedly, 6-8 oz. every half-hour or hour. If these are not retained, the salt solution (a teaspoonful to the pint of sterilized water), sterilized, may be slowly introduced into the subcutaneous connective tissue of the flank or elsewhere by means of a hollow needle attached by a rubber tube to some improvised reservoir placed one or two feet above the level of the patient. The water is rapidly absorbed, and cannot fail to be useful in washing out the hæmoglobin infarcts which plug the renal tubules and bring about, or at all events contribute to, suppression of urine. Marked restlessness may require minute doses of morphia (1/10 gr.); but this drug, of great use at times, must be employed with caution. This is the only rational and safe systematic treatment of hæmoglobinuric fever. Antipyretic drugs, as antipyrin and phenacetin, are dangerous.
Sternberg's mixture of bichloride of mercury and sodium bicarbonate (p. 268) has come into favour lately, especially in Central Africa.
Calomel in large doses— 20 to 30 gr. is with some a favourite remedy for hæmoglobinuric fever. Formerly it was used systematically in Africa in these cases. I have heard of its being given there by the teaspoonful. I know of cases which recovered perfectly without a grain of calomel or of quinine. Severe stomatitis may arise from the former; it should therefore be employed with great caution, and in reasonable dose.
Quennec has advocated the administration, of small doses of chloroform in hæmoglobinuric fever. His formula is chloroform 4 grin., powdered gum q.s., sweetened water 250 c.c.: of this a tablespoonful is given every ten minutes until a certain degree of chloroform intoxication is produced. Thereafter the effect is kept up by enemata of chloral. In twenty-two successive cases Quennec had no death.
Tannic acid is another drug which enjoys a certain reputation in the treatment of malarial fevers that have resisted quinine, and also in hæmoglobinuric fever. It is given, well diluted, in 15-gr. doses every two hours for four or five times, the dosing being repeated on the third and sixth days to the extent of two doses each day. Salicylate of soda, boric acid, chloride of calcium, potash, preparations of Beereana, are used by some medical men in West Africa at the present time, and, it is said, as of many other drugs, with good results.
Transfusion of blood has been successfully practised in high degrees of anæmia in some cases. Oxygen inhalations are indicated, but are rarely available. Intravenous injection of normal saline, of hypertonic saline, of neo-salvarsan, have each in certain cases been followed by recovery. Burkitt, finding acetone in the urine, has had good results from an active alkaline treatment with potassium and sodium bicarbonate and calcium chloride.
In desperate cases of suppression of urine, Stannus suggests, and has practised with temporary success in one case, incision of the kidney; Sorel has employed intravenous injection of isotonic solution of sugar in six cases with success.
Nursing is. a most important element in the man-agement of blackwater fever. If the stomach will retain food this should be given in a bland and fluid form, but there should be no attempt to force feeding, especially with rich and indigestible viands. One precaution against syncope must be sedulously enforced: the patient must not be allowed to sit up, much less to get out of bed, until food has been retained and assimilated, and the risk of sudden death from syncope has passed.
If possible, the subject of a hæmoglobinuric attack should quit the endemic area, and never return to it, or to any malarial locality; a severe attack, or a second attack, implying as they would special liability, should be regarded as imperative indications to this effect.
Prophylaxis.— All depressing and predisposing causes must be carefully avoided, more especially chill, fatigue, and malaria, and also irregular dosing with quinine. In blackwater regions those who are the subjects of malarial infection should take quinine systematically, never irregularly, and should be especially careful to continue its use, in the accustomed doses and at the accustomed intervals, for at least six months after arrival in Europe. Most of the cases of blackwater I have seen in this country were, I believe, attributable to neglect of this precaution and to a big dose of quinine taken for a relapse of a malarial infection supposed to have died out. Those who have had blackwater should gradually habituate themselves to quinine, beginning with minute doses— ½ gr.— slowly increased to 5 gr., which dose they should take daily while under the endemic influences, and at least for six mouths afterwards.
- ↑ * Some years ago I saw a lady suffering from blackwater fever. She with her husband and child had recently returned to England from the Upper Zambesi district. She died. I was struck with the anæmic appearance of her husband and examined his blood. He had blackwater infection. A few days after his wife's death he got subtertian fever. He was very ill but recovered. The child escaped.
- ↑ * Leishman has recently described certain minute and somewhat ill- defined bodies in mononuclear corpuscles in the blood of a number of cases of blackwater fever. He does not claim that these bodies are parasites, but he does not deny that they may be of that nature. He also describes peculiar cells; he calls them "chrome cells " in the blood of such cases. Balfour has found similar cells in blackwater. Low, "Wenyon, and Schilling Torgau have found similar bodies in other diseases.