The term Eclampsia was first used to describe the sudden exaltation, flashing forth (eklampsis), of the vital faculties at puberty; later it was applied to convulsions, but now it is restricted to convulsions in pregnancy which sometimes begin suddenly, as in a flash. The disease is characterized by a series of violent convulsive movements, loss of consciousness, and coma, and is one of the most dangerous complications of gestation. All convulsions and comas in pregnancy, not due to hysteria, epilepsy, cervical tuberculosis, apoplexy, pneumonia, phosphorus, strychnia and like poisons, uremia, and meningitis, are commonly classed as eclamptic. When the symptoms of eclampsia are present with the exception of the convulsions, a rare condition, this state also is said to be eclampsia. Reineke[121] reported a case like this. After death the heart, kidneys, and liver showed all the signs of eclampsia.

The eclamptic attack may occur without warning, but almost always there are premonitory symptoms for from a few hours to some weeks. The preËclamptic symptoms are headache (commonly frontal), nausea and vomiting, vertigo, nervous excitement or somnolence, muscle twitching, occasional delirium, cramps in the calves, disturbances of sight, tinnitus, and pain in the epigastrium. Epigastric pain, headache, and disturbances of the optic tract are important symptoms. If these last signs are present in a woman who has some edema and nephritis, the eclampsia will certainly occur, if proper means to relieve the condition are not promptly taken. When the prodromata appear there is nephritis, as a rule, but exceptions are observed.

When the attack comes, if the patient is standing she falls unconscious. The pupils dilate, the eyes and head are turned to the side. She opens her mouth, and the jaw is pulled laterally. The woman stiffens, her face is distorted, her arms bent, and the whole body curves sidewise in a tonic spasm. After a few seconds her jaws chop, and if her tongue is between the teeth it is lacerated; twitching runs down from the face and ends in a violent convulsion of the whole body, which may toss the patient from the bed, and she may even fracture her skull or long bones in the fall. The breathing stops, the bloodshot eyes stick out, the face swells and darkens, the lips become purple. Gradually the convulsions wane, and the woman appears to be dying; but after deep sighing she begins to breathe stertorously; then she sinks into a coma, or, in favorable cases, revives.

After a few minutes to an hour or more another convulsion may befall her, or she may have no more than one. In very grave cases consciousness may never return after the first fit. The convulsions may run up into extraordinary numbers—a hundred or more. There is a pseudoeclampsia where the convulsions have been as many as two hundred. If there are many attacks in the first twenty-four hours with no clear evidence of subsidence, the woman nearly always dies. Fever begins in such cases, and goes up to 103 or even 107 degrees. In an untreated case Black found a temperature of 110 degrees before death. The average number of attacks in these cases is from five to fifteen, and the convulsions are from a half minute to two or three minutes apart. Olshausen had six patients who recovered after having had from twenty-two to thirty-six convulsions, but those who have above fifteen commonly die.

If the convulsions are severe the woman as a rule aborts, and often rapidly. After the child is delivered the eclamptic symptoms may subside, or they may come on again, even a week after labor. Often the fetus dies during the attack; rarely it survives and is carried to term; again, it may die and the eclampsia may subside, but the fetus remains in the uterus for some time.

If the woman is to die the eclamptic attacks usually increase in frequency and violence; the temperature runs up very high, or it sinks; the pulse becomes weak and running, edema of the lungs comes on, with rattling and cyanosis, and the urine ceases to flow. The woman may die in a convulsion from apoplexy or heart paralysis. At times the child is delivered, but the coma deepens and the woman dies. In other cases there are coma and death without convulsions. Rarely there is a condition akin to acute yellow atrophy of the liver, with delirium, twitchings, coma, and death.

Women who have chronic nephritis seldom have convulsions in pregnancy unless there happens to be cerebral hemorrhage as an effect, but they suffer the other results of chronic Bright's disease—dropsy, uremia, edema of the lungs, paralysis of the heart, and albuminuric retinitis; they also are inclined to premature labor, and to hemorrhages that loosen the placenta. When acute nephritis happens in pregnancy convulsions are quite common, and when there are convulsions as a result of either chronic or acute nephritis it is very difficult to differentiate between these convulsions and genuine eclampsia.

The real cause of eclampsia is unknown, but the most plausible explanation of this "disease of theories," as Zweifel of Leipsic called it, is that it is a toxemia which attacks the liver, and directly or indirectly the kidneys, and brings on convulsions by toxic action on the anterior cerebral cortex. The great difficulty is to explain how these toxins originate. One authority suggests that the poison comes from the liver; another, from the fetus; a third, from the placenta, the intestines, the general metabolism, disturbed glandular balance, bacteria, and so on, but nothing is certain as to the etiology except that it is an intoxication.

On an average, 20 per cent. of the women who have eclampsia die,—but statistics vary from 5.31 per cent. to 45.7 for the mother and from 30 to 42 per cent. for the child. Eclampsia occurring ante-partum has the worst mortality; intra-partum, less; post-partum, least. About half the children die from prematurity, toxemia, asphyxiation, narcotics administered to the mother, or injuries at birth.

If the patient's pulse remains full and hard and below 120, there is no immediate danger of death; but if faster, weaker, and running, the prognosis is bad. High fever is not necessarily fatal to the mother, but it is very dangerous to the fetus. Edema of the lungs is a very grave symptom, but recovery is possible. When the convulsions have gone beyond twenty the prognosis is bad, but there have been recoveries. Deep cyanosis, marked restlessness, anuria, and intense albuminuria are all bad symptoms. Apoplexy is nearly always fatal. After delivery the recovery of the woman is by no means certain. She may get pneumonia, sepsis, or another eclamptic attack. Hirst finds that if the diastolic pressure does not rise above a ratio of 1 to 3 times the pulse pressure (i. e., the difference between the systolic and diastolic pressures), the prognosis is good.

Every pregnant woman should be watched to prevent eclampsia, if possible, because all are liable to this outcome. The hygienic methods mentioned in the chapter on Abortion are most important here. The family history is of weight—if the women of the patient's family have been eclamptic, if her parents were alcoholic or insane, these facts increase her liability to the disease. If she has had eclampsia before, if her kidneys are acutely diseased,—especially if injured by infections,—if she is inclined to digestive disturbance, she is disposed to eclampsia. Albuminuria, diminishing amounts in the daily excretion of urine, and decrease in the total solids of the urine, casts or blood in the urine, are serious symptoms. If albumin increases and urea decreases, this is a grave sign.

The blood should be examined for the various anemias. If the thyroid gland is deficient or altered in activity, thyroid extract may be indicated—this acts also as a diuretic. Uterine malpositions should be corrected. Treatment should be given where there is any evidence of toxemia, as headache, altered secretion and excretion, neuralgia, mental eccentricity, increased vasomotor stimulation, high tension, disturbance in the sensory apparatus, obstinate constipation and jaundice. Toxemia is not necessarily renal in origin.

In any of these conditions the proteids should be kept low in the diet, so that the kidneys may not be overtaxed. To throw off toxins, the emunctories should be stimulated by laxatives, water for diuresis, tepid bathing. If the symptoms grow threatening, and the kidneys are involved, the woman should be put to bed, on water alone. After three days an absolute milk diet should be begun. As she improves, starches are added, then the vegetables containing proteid, vegetable oils, and butter. As the improvement goes on, the diet may be vegetables, fruit easy of digestion, and one egg a day. Later fish and chicken are used, but never a full meat diet. Beef, mutton, veal, and similar heavy meats are not to be eaten. The drink is to be water, buttermilk, or koumiss.

When the eclampsia is inevitable the question of inducing labor arises. If the child is not viable, abortion is out of the question, as has been proved in the chapter on Abortion and the general chapter on Homicide. If the child is viable, there are three opinions: one, that the premature delivery should be effected as soon as possible; a second, that this delivery should be delayed as long as possible; and a third, that it should not be attempted at all. Those who hold that the uterus should be emptied as soon as possible, induce labor at the first convulsion, rapidly and under deep narcosis. Chloroform is dangerous to the heart in such cases for full anesthesia; ether is better. Braun first observed that the convulsions cease or are lessened after delivery. DÜhrssen found these results in 93.72 per cent., Olshausen in 85 per cent., Zweifel in 66 per cent. Peterson said that in 615 cases of early delivery—as soon as possible after the first convulsion—the maternal mortality was 15.9 per cent., but 28.9 per cent. in the same maternities under the expectant method.

Olshausen was not in favor of forced delivery. Charpentier[122] held that forced delivery is dangerous and should be absolutely proscribed. His statistics of mortality are: after spontaneous labor, 18.96; after artificial labor, 30.04; after forced delivery, 40.74.

Lichtenstein[123] reported, from Zweifel's clinic in Leipsic, the results of 400 cases of eclampsia, and he found that the eclamptic convulsions cease in only one-third of the cases after any form of delivery. He says the mortality of induced labor is no better than that after forced delivery, and that the mortality of both methods does not materially differ from the mortality of a long series of cases where there was no such intervention. The difference in the mortality between eclampsia without delivery or with delivery seems to depend on the relative loss of blood. In 40 per cent. of eclamptic cases operated upon, the loss of blood was 500 c.c. above the loss in cases of spontaneous delivery. The loss of blood tends to produce collapse when the blood comes from the uterus, although it may be beneficial if removed by venesection before delivery. Five hundred c.c. of blood is one-eighth to one-ninth of the entire blood supply of the body in a woman of average size. If 500 c.c. of blood is withdrawn before the shock of forced delivery and replaced by an equal quantity of normal salt solution, the toxin is thus reduced by one-fourth or one-third and then diluted by the normal salt solution, so that it has less poisonous effect.

Lichtenstein[124] describes the expectant treatment by phlebotomy and narcotics to replace operative interference, and this method has revolutionized the mortality of the treatment of eclampsia. In ninety-four cases of eclampsia his mortality was only 5.3 per cent., and none of the deaths could be ascribed to the treatment. The infant mortality was 37.3 per cent., as against his 38.8 per cent. in active operative interference during preceding years. Werner, in the Second Gynecological Clinic in the University of Vienna,[125] by this new method in thirty-eight cases of eclampsia had a maternal mortality of 5.2, as Lichtenstein had, but his infant mortality was only 14.65 per cent., an enormous advance for the better. Formerly the mortality in the Viennese clinic was 15.8 for the women and 44.3 for the children, in a series of 120 cases of eclampsia. A mortality of 50 per cent. in the children is common in the old method. In Lichtenstein's cases there were mental disturbances in 2.1 per cent. of the women, as against 6.75 per cent. in the old method. Eclamptics may go insane and kill the child after delivery. Lichtenstein treated 74 consecutive cases without a single death. In 54 per cent. of his cases the convulsions ceased after one venesection, and 42 per cent. of the women with ante-partum attacks recovered before labor came on. Engelmann[126] reported a case where a woman who had had 188 convulsions recovered after the third venesection.

In this method the woman is put in a dark, quiet room; 400 to 600 c.c. of blood are withdrawn by venesection, and 0.002 gm. morphine is injected; two hours later 3 gm. chloral is given in an enema. If the fetus presents in a position for prompt delivery it is removed with forceps, or by expression to spare the mother; but expression is a dangerous process always.

Zinke[127] of Cincinnati has a method which reduces the maternal mortality, but it has an enormous infantile mortality. He depresses the maternal pulse by veratrum viride, and this depression is probably the cause of the infantile mortality through asphyxia. Veit introduced the use of morphine in eclampsia, and Winckel the use of chloral. It has been found that narcotics check the action of toxins on the nuclei of cells, and in eclampsia the action of narcotics may be of this nature. Baker of Alabama in 1859 first gave veratrum viride in eclampsia. The drug lowers arterial tension by depressing the vasomotor centres and the heart itself. In eclampsia it diverts blood from the brain and depresses the motor neurons of the spinal cord. Aconite has the same effect in acute cerebral congestion without depressing the vasomotor centres or irritating the stomach as veratrum viride does.

Cesarean delivery is used frequently of late in eclampsia. The mortality of the children is lowered somewhat by a cesarean section, but the mortality of the mothers is much worse than in the expectant method described by Lichtenstein. Eclamptic women usually have badly affected kidneys, and the anesthetic used in the section may be a cause of the raised mortality. Peterson reviewed 500 cases of cesarean section for eclampsia[128] done by 259 operators in various countries. Up to 1908 the maternal mortality was 47.97 per cent. in 198 cases; from 1908 to 1913 it was 25.79 per cent. in 283 cases. Convulsions ceased in only 54.92 per cent. of the women after cesarean delivery, and in those cases in which the convulsions continued the mortality was 31.53 per cent. In 146 cases where the convulsions ceased the mortality was still 19.8 per cent. for the mothers. The fetal mortality was 10.69 per cent., counting all children who died within three days after delivery by section. The maternal mortality after cesarean section increases with the age of the patient. The cesarean delivery, then, has a maternal mortality of late of 25.79, with a tendency to increase as unskilled men attempt it; the expectant method has a maternal mortality of only 5.3 per cent. The cesarean delivery has a fetal mortality of 10.69 per cent.; the expectant, 14.65 per cent. The expectant method is preferable.