A System of Midwifery

by Edward Rigby

Having drawn our information upon puerperal fevers from the same ample source, we willingly bear testimony to the accuracy with which they have described the different forms; and trust that in giving a detail of our own opinions and observations, it will be found that so far from differing from them, we have tended to confirm, reconcile, and carry out their views.

Nature and varieties of puerperal fever. The history of puerperal fevers at the General Lying-in Hospital, would of itself afford an excellent monograph on this class of diseases in all their varied forms. When we resided at the hospital in 1826, the cases were all of the inflammatory character; they appeared to occur sporadically, among the out as well as the in-patients; and were successfully relieved by bleeding, hot poultices, and a mercurial purge, and occasionally leeches. During the following years, an epidemic of a highly malignant character spread destruction rapidly among the patients, setting at defiance the treatment previously employed. Still more remarkable was the sudden change in the character of the disease noticed by Dr. Locock in 1822. “In the spring of 1822, puerperal fever existed in the lying-in hospital in two very different and well-marked forms, at an interval of about six weeks between the last case of the first epidemic and first case of the second. The early cases were of an active inflammatory character; the peritoneal covering of the uterus and intestines was chiefly affected; the albuminous and serous effusions in the fatal cases showed a sthenic state of the system, that is, the serum was clear, the coagulable lymph firm and white; the patients bore blood-letting, and other active treatment to a great extent, fairly, and with much advantage; the blood drawn was strongly cupped and highly buffed, and the fatal cases were few. Six weeks afterwards a very different epidemic was found to exist. The same remedies which had been so beneficial a few weeks before, were naturally at first tried, but their bad success confirmed the sagacious remark of Gooch, that ‘the effects of remedies form not only an essential but an important part of their history.’ (Gooch on Peritoneal Fevers, p. 35.) The fever was attended with marked oppression and debility; the local pain was comparatively slight; the pulse was extremely rapid from the first, with no force, and easily compressible. In many of the cases, purulent deposites took place in the joints and in the calves of the legs, and in one case there was destructive inflammation of the eye.” (Locock, op. cit. p. 349.)

The various forms and modifications under which puerperal fevers have appeared at different times, have produced an equal variety of arrangement in the classifications of authors. Thus, some who have attributed the disease to inflammation, have merely distinguished its varieties according to the different organs which have exhibited after death appearances of congested or injected vessels, or have been covered and imbedded in effusions of coagulable lymph, &c., or have had their structure more or less broken down and disorganized. Thus, for instance, Dr. R. Lee is of opinion, that “inflammation of the uterus and its appendages must be considered as essentially the cause of all the destructive febrile affections which follow parturition; and that the various forms they assume, inflammatory, congestive, and typhoid, will in great measure be found to depend on whether the serous, the muscular, or the venous, tissue of the organ has become affected.” (Med. Chir. Trans. vol. xv. part ii. p. 405, 1829.) He accordingly arranges “the principal varieties of inflammation of the uterus in puerperal women under the following heads, viz. 1. Inflammation of the peritoneal covering of the uterus, and of the peritoneal sac; 2. Inflammation of the uterine appendages, ovaria, fallopian tubes, and broad ligaments; 3. Inflammation of the muscular and mucous tissues of the uterus; 4. Inflammation and suppuration of the absorbent vessels and veins of the uterine organs.” (Cyc. Pract. Med. art. Puerperal Fever.) This arrangement is manifestly incorrect, and by giving so partial a view of puerperal fevers, must, if adopted, necessarily lead to serious errors in practice. “That these forms of inflammation are the proximate cause of the various febrile affections is most completely refuted by the detail of his own (Dr. Lee’s) experience, as relates to the varieties occurring under similar circumstances.” (Moore, on Puerp. Fever.) We may also add, that, according to our own experience, and that of our colleagues at the General Lying-in Hospital, in the worst forms of puerperal fever, the fewest traces of inflammation have been observed; and that in the severest and most rapidly fatal cases it has frequently happened, that not a single vestige of inflammation could be detected. In our review of Mr. Moore’s able work in the Brit. and For. Med. Rev. Oct. 1836, p. 483, we have made a similar remark, and quoted a striking passage from Dr. Stevens, when speaking of contagious fevers, that “there is not one symptom of inflammation during the fatal progress of the disease, nor one inflammatory spot to be seen after death, to mark its existence, or to induce us to believe that any thing but functional disease had existed in any of the solids; yet these are the very cases of all others which are the most fatal.” (On the blood, p. 179.)

In many of the worst cases which have come under our notice, there has neither been time nor power sufficient to produce either a symptom or a trace of inflammation; the powers of life have from the very commencement sunk under the deadly influence of the disease, without a single effort to establish even a temporary reaction in the system: hence, in most instances, we are led to the necessary conclusion, that inflammation, when it does appear, is the result of disease, not the disease of inflammation. “For,” as Dr. Ferguson observes, “if any or more of these (phlebitis, peritonitis, &c.) be assumed as constituting the essence of puerperal fever, abundant examples may be found of puerperal fever, in which the cause fixed on is absent. Thus to believers in the identity of peritonitis and puerperal fever, we can show puerperal fever with a perfect healthy peritoneum. To those who insist on inflammation of the uterine veins, as constituting puerperal fever, we can show the genuine disease without this condition.” (Essays on the most important Diseases of Women, part i. Puerperal Fever, p. 81.)

The vitiation of the blood has long been a subject which has excited our deepest interest, and the admirable researches of Dr. Stevens upon the condition of this fluid under the effects of malignant fevers, have tended to disclose the real nature of the diseases under consideration. We have long been convinced that one of the causes of puerperal fever is the absorption of putrid matters furnished by the coagula and discharges which are apt to be retained in the uterus and passages after parturition,—a view which has been adopted by Kirkland, C. White, and other older authors. It is with sincere pleasure that we now find ourselves supported by the able author, from whom we have just quoted, in this opinion. Dr. Ferguson’s three positions respecting “the source and nature of puerperal fever” are highly valuable, for they have been deduced from careful physiological experiments, and not less sound physiological reasoning; they are as follows:—

1. The phenomena of puerperal fever originate in a vitiation of the fluids.

2. The causes which are capable of vitiating the fluids are particularly rife after childbirth.

3. The various forms of puerperal fever depend on this one cause, and may readily be deduced from it.

We do not agree with him in supposing that every form of puerperal inflammation is produced by vitiation of the circulating fluids, because in one species of uterine phlebitis, which occurred sporadically, and prevailed a good deal from 1829 to 1832, it was, in our opinion, evidently produced directly by the absorption of putrid matter into the uterine veins and lymphatics, exciting inflammation in these vessels: the same cause, when only carried to a certain extent, produces a local inflammation, which, when affecting the general circulation, is followed by fever. Thus, then, we may have in the same case uterine phlebitis followed by the typhoid malignant puerperal fever—the local and constitutional disturbance arising from the same cause, imbibition or absorption of putrid matter; the one being the local, the other the general effect, but not the one resulting from the other. The doctrine of the vitiation of the blood from its admixture with pus secreted by the lining membrane of an inflamed vein, though very plausible, still requires farther confirmation, for it is doubtful if the introduction of pure healthy pus into the circulation produces any of those dangerous effects which result from the absorption of putrid matters, whether purulent, sanious, mucous, &c. It is the introduction into the circulation of an animal poison generated by putrefaction, which destroys the vitality of the blood, and renders it unfit for maintaining the vital powers.

Few have expressed this opinion more strikingly than Dr. Kirkland, although so long ago as 1774; and it has often created our surprise, that amid all the numerous writings on this subject, which have excited attention during later years, so little notice should have been taken of his observations. We consider that Dr. Kirkland is one of the earliest authors who has shown that puerperal fever is not the result of inflammation, but that it may be produced by the introduction of an animal poison into the circulation. “There are other causes beside inflammation which bring on a puerperal fever; for it sometimes happens that coagulated blood lodges in the uterus after delivery, and putrefying from access of air, forms a most active poison, is in part absorbed, and brings on a putrid fever. In this case the discharge which should immediately follow delivery is not sufficiently large, making allowance for the difference which happens to different women in this respect: small clots of blood make part of the lochia, which are less in quantity than they ought to be; but the patient has not any other sort of complaint for three or four days till the retained blood begins to putrefy. A fever then first makes its appearance, followed by a quick weak pulse, thirst, pain in the head, want of sleep, sighing, load at the præcordia, restlessness, great weakness, dejection of spirits, either wildness or despair in the countenance, and the white of the eyes is often a little inflamed.” (A Treatise on Childbed Fevers, by Thos. Kirkland, M. D. p. 70.)