Further contributions to our knowledge of the pernicious vomiting of pregnancy / by J. Whitridge Williams.

  • John Whitridge Williams
Date:
1912
Catalogue details

Licence: In copyright

Credit: Further contributions to our knowledge of the pernicious vomiting of pregnancy / by J. Whitridge Williams. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    days was eating the regular ward diet. She was discharged on the fourteenth day after admission in excellent condition, having gained 11 lb. The vomiting did not return, and she was delivered normally at term. The interpretation of this case is perfectly clear, as it is apparent that the patient was suffering from starvation dependent upon neurotic vomiting, and was cured by forced feeding and suggestion, while the high ammonia co-efficient was probably a manifestation of an acidosis. I feel confident that Cases ii and iii, as well as several others in my series, may be similarly explained. On the other hand, I am not prepared to admit that this is the only explanation for a high ammonia co-efficient, as will be shown more particularly when we consider in detail our cases of true toxsemic vomiting. In this connection, however, I wish to refer to the ammonia curve shown in Chart VI. This patient lived for more than a month following the interruption of pregnancy for supposed toxaemic vomit- ing, and during that period the ammonia co-efficient varied between 20 and 40 per cent. Upon three occasions an intravenous injection of 6 grams of sodium bicarbonate was given, with the result that the acid urine became neutral or alkaline in reaction, and remained so for from six to forty-two hours. Had the high ammonia been a manifestation of an acidosis such an effect could not have been obtained, as the amount of alkali employed lay within the range of normal tolerance, and was insignificant when compared with the quantity necessary to effect a similar change in acidosis complicating diabetes. Furthermore, Dr. Sellard, who was good enough to estimate upon several occasions the amount of acetone bodies contained in the urine, calculated that the increase in the ammonia co-efficient was many times greater than could be explained by their neutraliza- tion. Consequently, he concluded that in this case, at least, we had to deal with a primary disturbance in the proteid metabolism, and not with a starvation acidosis. Furthermore, the presence of large amounts of fat in the subcutaneous tissues at the time of autopsy indicated that death must be attributed to some other factor than mere starvation. In addition to the facts just adduced, certain negative evidence is available as tending to indicate that starvation is not necessarily the sole factor concerned in the production of a high ammonia co-efficient in vomiting of pregnancy. Thus, in Case ii of my monograph the ammonia co-efficient fell from 32 to 12 per cent, in the forty-eight hours following the induction of abortion, although the patient had taken no food. Consequently, it would seem, if inanition were the sole factor concerned, that the ammonia should have risen, but as it fell some other explanation must be invoked, and I am inclined to seek it in the rapid disappearance of the toxaemia following the emptying of the uterus. Furthermore, in