Coma

COMA (from the Greek koma - deep sleep), or comatose state, is an unconscious state resembling deep sleep. Coma may occur suddenly or develop gradually. In the latter case, it is usually preceded by a so-called precomatose period, when loss of consciousness has not yet reached full development, and the patient still reacts to being called and can be awakened.-Comatose state is caused by injuries and poisonings as well as many diseases, including diseases of the nervous system (epilepsy, brain tumors, strokes, etc.). Mention should be made of infections (all types of typhus, malaria, pneumonia, especially during the crisis, severe dysentery) and some cases of botulism. Finally, comatose state is observed in some diseases of the liver, kidneys, and in diabetic coma. Coma is most often caused by intoxications acting directly on the nervous system. It has been proven that in cases of diabetic coma, acetone bodies accumulate in especially large quantities in the central nervous system. Whether something similar occurs in other types of coma (for example, uremic) has not yet been fully clarified. On the other hand, there are cases of coma in which marked anatomical changes are observed in the nervous system (strokes, capillary stasis in malaria, brain tumors, etc.). If coma developed as a result of a disease that was under a physician's observation, determining its origin usually does not present particular difficulties. On the contrary, if the patient comes under observation only at the time of full development of coma, it is not always possible to determine its etiology and the underlying condition. Different types of coma are united by the common feature of unconsciousness, but differ in details. To understand a case, it is necessary to pay attention to the following: whether the patient is constantly in a state of rest or periodically, without regaining consciousness, makes movements; whether there is pallor, jaundice, redness or blueness of the skin; temperature; rigidity, convulsions or twitching of muscles; symmetry of the muscular state on the right and left; condition of reflexes; whether there is involuntary urination or defecation; vomiting and hiccups, swallowing; bloating or abdominal distension; condition of the pupils and position of the eyeballs; character of breathing; integrity of the skin, bones, bruises, nosebleeds, burns of the oral mucosa, bites of the tongue. It is extremely important, if possible, to clarify the domestic circumstances and conditions under which the coma occurred.--Coma can pass into agony as the heart gradually weakens, but it can also end in recovery. The prognosis depends less on the depth of the unconscious state than on the cause that caused the coma. Of all types of coma, the greatest attention has been paid to diabetic coma (see Diabetes mellitus). This is explained by the fact that it has a number of characteristic symptoms that make correct diagnosis possible, as well as significant metabolic disturbance.-The term 'coma' is mainly applied to diabetic comatose state, while coma in kidney disease is usually included in the broader concept of uremia, and coma in liver diseases belongs to the group of cholemias.-The diagnosis of diabetic coma is based on the history, the presence of acetone bodies in the urine, characteristic breathing, and softness of the eyeballs. The sequence in which these signs appear is not entirely constant. 'Large breathing' of Kussmaul may sometimes already be observed in the precomatose period, when consciousness is still quite clear; but it more often develops after the onset of unconsciousness. 'Large breathing' is occasionally observed in uremic coma. Often instead of rare and deep sighs, there is frequent and shallow breathing. Sometimes there is a tendency to pauses of the Cheyne-Stokes or Biot type. Despite disturbed breathing, cyanosis does not occur. When unconsciousness has already reached full development, Kussmaul breathing is rarely absent.--Softness of the eyeball is a symptom that is not always present; it usually appears quite late and, having appeared, may pass again without improving the prognosis of coma. Pupillary reflexes are not disturbed in coma. The musculature is relaxed. Convulsions are not characteristic of coma. Sugar in the urine during coma does not always show a high percentage. If coma is prolonged, it may disappear from the urine altogether. A large amount of sugar remains in the blood. It is noteworthy that in strokes, sugar may also sometimes appear in the urine. Gerhardt's reaction for acetoacetic acid during coma is almost always sharply expressed. Sometimes a small amount of protein and peculiar short, broad hyaline-granular cylinders appear in the urine. In characteristic cases, diagnosis does not present particular difficulties, but coma may not give sharp signs and especially in some stages may be atypical. Great difficulties arise if a diabetic simultaneously has nephritis, some nervous suffering, intoxication, etc. As soon as diabetic coma was described, it was noted that when it occurs, acetone bodies can be found in the urine and the urine reaction is sharply acidic. From this it was concluded that in the process of metabolism in these cases, bodies of sharply acidic nature are formed in large quantities (see also Acidosis). This conclusion remains correct to this day. This circumstance gave rise to compare diabetic coma in general with cases of poisoning by acids that do not burn in the body; since in these cases strong irritation of the respiratory center and symptoms similar to the Kussmaul phenomenon are also observed, such an explanation seemed quite suitable. The doctrine of acidic reaction and its connection with the concentration of hydrogen ions had not yet been developed at that time. When it was discovered that the pH of the blood is maintained with the greatest stability and barely shifts even in the most severe cases, the assumption of the exclusive significance of the acidic reaction of acetone bodies for diabetic coma could no longer be reconciled with the facts: coma can occur even with normal blood reaction. Nevertheless, the significance of the acidic nature of acetone bodies for metabolism (not for the clinical picture of coma) of course remains very important. Within the body, there are several adaptations by which the correct reaction of fluids and tissues is maintained. Acidic metabolic products are removed in large quantities by the kidneys with urine, by the lungs in the form of CO₂, and are also neutralized by ammonia and mineral bases. The abundant binding of cations by acidic valences formed in the process of metabolism causes increased excretion of ammonia, calcium, and magnesium with urine and leads to softening of the bones in severe diabetics. Bicarbonate salts of blood plasma give up a significant part of their CO₂ during breathing, and sodium is found bound with non-volatile acids in the form of sodium compounds: the reserve alkalinity of the blood, measured by the amount of CO₂ bound in the blood, is found to be significantly decreased during the comatose state compared to normal. When reserve alkalinity decreases, whatever its cause, one other phenomenon is always observed - a decrease in the tension of CO₂ in the alveolar air. Such a phenomenon occurs with any hyperventilation. Therefore, some authors believe that if increased breathing occurs during coma, it still needs to be proven that it depends on the acidic properties of metabolic products. It is possible that the Kussmaul phenomenon is caused by quite different properties of these products and only due to increased ventilation does the decrease in reserve alkalinity and low tension of CO₂ occur. If one continues to stand on the point of view that places coma in dependence on acetone bodies, then the question arises about the pharmacodynamic properties of these bodies, regardless of whether they have an acidic nature or circulate in the body in a neutralized state. Acetone, acetoacetic, and oximalic acids are derivatives of the fatty series, and therefore they have a narcotic effect on the nervous system. It has been proven that butyric acid affects the respiratory center both in the form of a salt and in the form of ethyl ester. Isobutyric acid does not have such an effect. Similar observations have been made in poisoning with oximalic acids. The poor success of treating coma with soda and the fact that coma can occur even with an alkaline reaction of urine from soda rather speak against than for the acidic origin of coma. It is interesting that the symptom of 'large breathing,' which was most often cited as proof of the acidic origin of coma, responds least to treatment with soda. Where, under the influence of soda infusions, the patient awakens, it remains debatable whether the same would have happened from an infusion of physiological NaCl solution, which has no neutralizing effect. The fact that very often severe ketonuria exists for years without giving any phenomena does not absolutely speak against the connection of acetone bodies with coma: what is important is not how much of these bodies are excreted with urine, but how much remains in the body and poisons the nervous system. Sometimes a slight harmfulness - fever, intestinal disturbance - is enough for a ketosis that has manifested itself in nothing to pass into coma.

It has been noted that chloroforming and the use of ether can cause C. in a diabetic. In this, one can see as it were a summation or superposition of the narcotic effect of acetone bodies and medicinal substances. Theories explaining diabetic C. by the presence of acetone bodies are unsuitable for explaining those cases where C. occurs without ketonuria or when acetone bodies appear only with fully expressed comatose phenomena. Meanwhile, sufficient observations of typical diabetic C. without the excretion and without the retention of acetone bodies in the blood have accumulated that the fact itself can be considered fully established. To explain it, a new viewpoint is proposed, according to which ketosis is not an indispensable condition for the development of C. Coma is considered as the result of a progressively worsening carbohydrate metabolism until the final inability to assimilate and break down glucose. This theory is supported by the constant absence of glycogen in the liver and muscles with a high level of sugar in the blood in comatose patients. The same is indicated by the excellent effect of insulin in the comatose and precomatose periods. Thus, a completely satisfactory interpretation of diabetic C. does not exist. Since the introduction of insulin into the treatment of diabetes, attention has again been drawn to the fact that along with the classical C., accompanied by Kussmaul's breathing, in diabetes mellitus, a phenomenon of another kind is sometimes observed: unconsciousness or a semi-conscious state with a simultaneous extremely sharp drop in blood pressure and pulse filling. This picture was called cardiovascular C. Since the introduction of insulin, cases of cardiovascular C. have become more frequent. The ordinary ketonuric form of C. yields to insulin treatment; consciousness clears up, breathing improves, the softness of the eyeball disappears, but the patient continues to remain in a state of cardiovascular C. in complete prostration for several hours or days and finally dies. Insulin has no effect on these cases, and there is often no excess of sugar in the blood. The picture of the disease indicates deep and irreversible relaxation of the vasomotor peripheral tone and to a lesser degree cardiac weakness, similar to what is observed in unfavorable courses of infections. If symptoms from the respiratory center appear in ordinary C., then cardiovascular C. is the result of poisoning of the vasomotor center. Insulin, saving the patient from dyspneic C., enables him to live until cardiovascular collapse, against which it proves powerless. Measures against diabetic C. must first be preventive. Very great importance is attached to the proper management of dietary treatment without rapid transitions from carbohydrate-rich food to purely protein food; one should also avoid the sudden withdrawal of insulin from a ketonuric diabetic. But even diabetes without ketonuria, under unfavorable circumstances (fever, intestinal poisonings, emotions, etc.), can in a short time give rise to C., passing through a period of more or less sharp excretion of acetone bodies.-To some authors, bicarbonate of soda for preventing C. is of no importance; others see in it a means promoting the excretion of acid metabolic products and give it in doses of 20-30 g daily. With these measures in many, but far from all cases, it is possible to prevent the onset of coma.-Developed C. and even precomatose state before the discovery of insulin gave an almost invariably bad prognosis. At present the prognosis is much better. The earlier the comatose patient is subjected to insulin treatment, the greater the chances of a favorable outcome of C. Severe cases of C. do not respond to insulin treatment. As soon as precomatose phenomena are detected, the patient is given easily assimilable carbohydrates-glucose, fruit and cane sugar, orange juice and fruits. The diet, if the patient is still able to take food, should not be abundant and should contain little protein and fat. The introduction of insulin in amounts of 20-100 units is begun immediately. If insulin has a favorable effect, there is no need to strive to introduce as many units as possible. If necessary, 150 and 200 units per day can be administered. It is possible that careless doses of insulin can even harm the patient, and therefore, especially if C. is prolonged, it is desirable to control the sugar content in the blood. It is difficult to say how much stronger the intravenous administration of insulin is compared with the subcutaneous. Along with insulin, it is advisable to administer subcutaneously 200-300 cm³ of a glucose solution (4-5%). It is necessary from the very beginning to monitor the state of circulation (camphor, caffeine, digenal, adrenaline). Infusions of a solution of bicarbonate of soda into the vein (not subcutaneously!) 200-400 cm³ of a 4-5% solution, prepared ex tempore from freshly sterilized water, cooled to body temperature (the solution cannot be sterilized), are useful.-In recent years, along with the introduction of insulin, the question has arisen about the possibility of another type of C.-hypoglycemic. The material available in the literature does not yet allow a final statement to be made as to whether such a phenomenon exists as an independent disease. The most convincing are cases in which cancerous lesions of the Langerhans islands with metastases were observed. The clinical picture manifests itself with signs of extreme weakness, reaching periodically to the state of fainting, with convulsive twitchings. The sugar in the blood at this time drops to 0.03 mg% and below; blood pressure is not always below, and sometimes even above normal. Especially convincing is the fact that all the phenomena of hypoglycemia disappear after the introduction of sugar. Lat.: Virshubsky A., On the question of coma neoplasmaticum, Prakt. vrach, 1926, № 5; Klinkovstein I., Modern teaching on acidosis, coma and their therapy, Klin. med., vol. V, № 19, 1927 (lit.); Magazanik G., Treatment of diabetic coma, Kazan med. zh., 1927, № 8 (lit.); Fischer O., Treatment of diabetic coma, Klin. med., vol. III, № 8-9, 1925; Elias H., On the significance of the acid-base balance and its disorders, Erg. d. inneren Med., B. XXV, 1924. See also lit. to art. Diabetes. E. Fromhold.