WHO-MONO-43-Part3-Eng.Pdf

700 CHOLERA considerable variations. Rapidly following evacuations may produce the dehydration and circulatory failure characteristic of the algid stage within as little as two hours, while, on the other hand, it may take 12 hours or even more before that stage has become fully developed. To what extent differences in the severity of the infection and in the individual susceptibility of the patients are responsible for these marked differences in the length of the evacuation period it is difficult to decide. Presumably, however, as a rule both these factors are of importance to a varying degree. Algid stage Even the full development of the algid or, as it is often called, the collapse stage of cholera gravis 1 does not necessarily lead to a disappear ance of the signs predominating during the first phase of the disease described above. The muscular cramps appearing in the evacuation stage may continue to torment .the collapsed cholera patients, or the cramps may even first become manifest in the algid stage. Sometimes vomiting may persist or, as is occasionally the case as early as the evacuation stage, may be replaced by retching. Moreover, as aptly stated by Macleod (1910): " Liquid colourless motions may still be occasionally passed involuntarily or the presence of watery material may be detected in the intestines by palpation or succussion." Rogers (1921) pointed out with much reason that " the lessened secretion by the bowel may be only due to the great failure of the circulation and concentration of the blood, and so be an unfavourable rather than a good sign. This view is borne out by the fact that intravenous injections of normal saline solution are commonly followed by renewed copious rice-water stools." Giving an excellent description of the algid stage of cholera gravis, Macleod (1910) stated that, though muscular cramps as well as lesser-scale bowel evacuations might persist, their continued presence is "overshadowed by the evidences of failing power: the pulse flickers and fails at the wrist, and is sometimes imperceptible in the brachial and almost so in the femoral arteries; the rate, always accelerated, may rise to 120 or 140, or even higher. The heart-sounds get less distinct, especially the first; in some cases murmurs and friction sounds are detected in this stage ... " "The capillary reaction ", Macleod continued, "becomes slow and feeble, the surface gets livid; respiration is quick and shallow; painful and often paroxysmal dyspnoea arises, compelling the sufferer to struggle for breath; the expired air is cold, and deficient in carbonic acid. The face presents the characteristic 1 Sticker (1912) was dissatisfied with both these designations and also pointed out tbat, as discussed already by Liebermeister (1896), the name of stadium asphycticum, used instead by some writers, since it refers merely to a state of pulselessness, was also inadequate. He recommended, therefore, the use of the term stadium para/yticum (already used by some earlier writers) to indicate " the extreme weakness of all vital functions " during the second stage of cholera gravis. Since, however, the designations of algid stage or collapse stage have been widely adopted and, moreover, as defined in the large dictionaries, they have a meaning quite similar to that of stadium paralyticum, no cogent reason exists to give them up in favour of the latter, unfamiliar designation which, in its turn, is somewhat misleading. SYMPTOMATOLOGY, DIAG"KOSJS, PROGNOSIS AND TREATMENT 701 choleraic expression-features pinched, skin drawn, eyeballs sunken and surrounded by a dark areola, lids half-closed, pupils contracted, mouth open, teeth covered with sordes, tongue cold, face apathetic. The general surface is cyanotic and clammy or bedewed with cold sweat; the fingers and toes are V. Tinkled. There is great restlessness and profound debility. The intelligence is clouded, the senses impaired, the muscular power diminished; in some cases sense and sensibility and capacity of movement are retained; in others coma or a semi-comatose state exists. The voice is husky and feeble, or the patient can speak only in faint whispers. Thirst is imperative, and a feeling of coldness is felt. The urine is suppressed; the bladder is generally emptied in the preceding stage, and no further accumulation of urine takes place. The temperature of the surface and mouth is greatly, and in fatal cases increasingly depressed, and may fall below 90°F. [32.2oC]; the tem perature of the axilla is higher, but below normal, readings of 95° [35°C] to 97°F. [36.1 oq being not uncommon in this stage; the rectal temperature may be slightly subnormal or normal, but in time it shews a tendency to rise above the normal." Fully adequate though the above description is in most respects, it has to be pointed out that in the experience of most observers the intelligence of the algid cholera patients was not clouded. Thus Tao and colleagues (1948) stressed that "in spite of the severe prostration, preservation of a clear mentality was a striking feature". However, as Liebermeister (1896) put it, the sufferers are usually so apathetic as to evince little interest either in their environment or in their own condition. Probably, therefore, Liebermeister was right when asserting that " In general the subjective sensation of being ill [Krankheitsgefiihl] is usually much slighter than one would expect from the severe objective signs." [Trans.] Supplementary information on the symptomatology of the algid stage may be classified as follows: Dehydration According to El-Ramli (1948), the various clinical signs of dehydration were met with in the following order of frequency: "Weak or imperceptible pulse, low or not measurable blood pressure, cold skin, sunken eyes, cyanosis of nails and lips, diminished elasticity of the skin, oliguria, anuria, husky feeble voice, dry tongue, thirst, pinched nose, anxious look, washerwoman's hand, restlessness, muscular cramps, dyspnoea, pericardial rub and oppression in the chest." It is noteworthy, however, that Tao and colleagues (1948), who saw a far higher percentage of seriously affected cholera patients than El-Ramli, enumerated intense thirst (met with in 96.1% of their 687 patients) and signs of skin dehydration, characterized by loss of elasticity and wrinkling, the latter especially over the dorsum of the fingers (present in 81.2 %), among the most frequent signs of dehydration. Cyanosis was found to be present in but 35.5 ~,;; of the sufferers. As can be gathered from El-Ramli's study, the relation between the severity of the cholera attacks and the degree of dehydration was not quite constant: some of the patients who appeared to have been mildly affected, 702 CHOLERA their illness lasting not more than three days, were admitted in a severely dehydrated condition. Among the patients classified as suffering from moderately severe cholera (i.e., 4-6 days of illness with· but mild, if any, complications), some showed mild, but others marked, signs of dehydration. Further, though most of the patients classified as having severe cholera attacks were on admission in a bad condition, "some of them came to hospital in a fairly good condition with: a mild or moderate dehydration and then developed severe symptoms." Circulatory failure Though, as has been discussed in the previous chapter, the circulatory failure becoming maximal during the algid stage of cholera is primarily of an extracardiac origin, nevertheless, signs of a secondary involvement of the heart in this process are apt to become manifest. Griesinger (1857) noted in this respect a progressive weakening of the heart sounds, the second of which often became altogether inaudible, and also the occasional appear ance of systolic murmurs. He considered it possible, though unlikely, that the hypothetical cholera " poison " might exert an action on the heart, but ascribed far greater importance to " a kind of sympathetic action from the intestine", analogous to the depression of the cardiac activity occasion ally observed in patients with strangulated hernias. However, in Grie singer's opinion a most important role was played also by the stagnant circulation and the resulting metabolic deficiencies in the heart muscle, which thus, like the musculature in general, became extremely weakened. Propounding views similar to those of Griesinger, Liebermeister (1896) also maintained that the cardiac weakness observed in the algid stage was "in cases with marked blood concentration partly due to a deficient nutri tion of the cardiac musculature." The rapid, though sometimes only temporary, restoration of the blood circulation usually following even single saline infusions 1 leaves no room for doubt that the cardiac disturbances observed in the algid stage of cholera are as a rule of a functional nature only. That, however, this is not invariably the case, is proved by the occurrence of sudden deaths from heart failure in cholera convalescents. Interesting observations have been made in this connexion with the aid of electrocardiography. While Bien & Tung (1933), apparently the first to use this method for the examination of cholera patients, made no signi ficant findings, some have been more recently recorded by Weaver et al. (1948), Baligh (1948) and Godel (1948). According to Kamal, Messih & Kolta (1948), electrocardiographic tracings made during the 1947 cholera outbreak in Egypt by Weaver and colleagues "showed left axis deviation 1 It is of historical interest to note that Griesinger referred to

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