Lane Library

Medical Care and Public Health 1800-1850

Treatment of Puerperal Fever

Before leaving the subject of puerperal fever we should further broaden our view of the practice of medicine in America by considering, as an example, the manner in which this devastating disease was being treated during the first half of the 19th century. We have already taken note of the controversies aroused by the views of Holmes and Semmelweis regarding its cause and prevention. With respect to its treatment, however, there appears to have been general agreement. No voice of authority seriously questioned either the benefit or the harm to the patient of the commonly employed regime of blood-letting, purging, mercury and opium. This in spite of the fact that there was no scientific evidence of the effectiveness of any of these remedies.


Blood-letting as a treatment for many diseases, but especially fevers, dates from antiquity. It was common practice among Greek physicians of the fourth century B.C. some of whom habitually applied it to almost every condition. Blood-letting continued in use as a therapy in the West throughout the Christian era and still had many adherents until near the end of the 19th century. Blood was withdrawn from the general circulation by venesection (phlebotomy), and from local tissues by leeches. [88]


In the mid 1800's prompt and copious blood-letting by venesection was the first and most important treatment in puerperal fever, and was sanctioned by virtually all European and American authors on midwifery. This procedure was perpetuated by the groundless theory that fevers were associated with a harmful accumulation or congestion of blood in the affected part. According to this theory an excess of blood was driven to the inflamed area by an overactive circulatory system and was highly detrimental.

In 1840 Professor Blundell of Guy's Hospital in London, an international authority on obstetrics, recommended repeated venesections in puerperal fever to remove 1200 to 1500 ml. of blood, on the average, and insisted that it should be removed within the first 24 hours for optimum effect. He stated that as much as 1800 ml. or more had sometimes been removed in anomalous cases "with apparent benefit." By way of caution, he advised against bleeding if the patient had already begun to "collapse." [89]

In 1842 Professor Meigs of Philadelphia graphically described what he believed to be the compelling reason for urgent venesection in puerperal fever: [90]

Nothing but the abstraction of blood can have an immediate and potent influence on the circulation, and reduce the momentum of the blood to such a degree of moderation, as may consist with a resolution of the inflammation. Nothing short of these venesections can diminish the force of the blows which the irritated, I might say, the infuriated ventricle strikes upon the columns of blood which it is driving like so many riving wedges into the (pelvic) tissues, to disorganize, to tear them to pieces, and overwhelm them with the torrent of circulation that it urges upon them, while their power to resist succumbs to every successive blow. . .

Dr. Gordon (of Aberdeen, Scotland) tells us, that it is not merely bleeding the patient that will save her. She must be bled copiously - so copiously as to give to the disease a definitive check. He tells us that where the woman is bled timidly, no available impression is made, that the disease advances and soon becomes indomitable. Twenty-five or thirty ounces (750-900 ml.) drawn from the arm, early in the attack, rarely fails to make so powerful an impression on the disorder, that the juvantia, such as calomel, opium, etc., hardly fail to effect the remainder of the cure.

All the experience I have had in regard to the course and treatment of this malady, leads me to concur fully with the instructions of Dr. Gordon on the subject. . .

To illustrate Professor Meigs's actual practice with respect to venesection, we can quote his comment on one of his own patients: [91]

This young woman (a 20 year-old primipara who developed puerperal fever on her fourth postpartum day) had a healthy and strong constitution. In her case I took away, between 11 and 6 o'clock on the first day of the attack, 52 ounces (1500 ml) of blood, without which, I think, she must have died. (I relate this case from my notebook) as a fair specimen of the mode of practice, in such attacks, which I have for years been in the habit of pursuing.

As Professor of Obstetrics at Jefferson Medical College, one of the largest and most prestigious American medical schools at the time, the influence of Dr. Meigs on the management of complications of pregnancy was enormous. As a brilliant and dramatic lecturer to hundreds of medical students, as well as a prolific writer, his denial of contagion in puerperal fever and his sanction of copious blood-letting in its therapy carried great authority, and resulted in corresponding ill effects on the practice of midwifery and the well-being of patients.


Blood-letting by leeches was recommended by many experts on puerperal fever as an optional adjunct to venesection. According to Professor Wood of the University of Pennsylvania, whose Treatise on the Practice of Medicine was published in 1847 and contained a section on puerperal fever and peritonitis, leeches should be placed on the abdomen immediately after venesection. For example, after one or two large bleedings, from 50 to 150 American leeches should be applied at once in the areas of greatest pain and tenderness, the procedure to be repeated if indicated by persisting symptoms. Professor Meigs had these words of approval for the practice: "While I profess in the strongest terms to confide in the lancet as the first and chief remedy, I would not pretermit any mention of leeches, which, as a secondary and subservient prescription, will be found of the greatest utility in the management of the cases." [92] [93]

Leeches are efficient and painless blood-letters and capable of removing many ounces of blood because they inject an anticoagulant into the tissues where they bite. The application of leeches to the abdominal wall was based on the notion that their proximity to the inflamed pelvis would enable them to "decongest" that region more directly of its excess blood. Leeches had several disadvantages. They were loathsome to the patient and on rare occasion their bites could be lethal by continuing to bleed after removal of the leeches, resulting in exsanguination of the patient. There were reports of patients who, being left unattended for a period of much-needed rest after removal of leeches and application of an abdominal poultice, were later found dead in bed, lying in a pool of blood.

We shall return to the subject of "leeching" when we discuss the various "medical systems" in vogue during the early 1800's.

Mercury and Purging

Immediately following the first venesection, the second or medicinal phase of treatment of puerperal fever was begun This phase consisted of giving drugs that presumably led to the further "depletion" of the congested circulatory system. [94]

Calomel (mercurous chloride), a mild laxative, was considered the most important drug in puerperal fever and other inflammatory disorders. It was started after the first venesection and continued in serious cases to the point of toxicity as indicated by salivation. It was thought, erroneously, that mercury had a specific anti-inflammatory effect and that salivation was a sign of depletion.

Purging (by such cathartics as castor oil, sulfate of magnesia, and infusion of senna) was, like calomel, begun early in order to assure complete evacuation and thorough decongestion of the gastrointestinal tract.

Emetics once had a great, but fortunately evanescent, reputation as a treatment for puerperal fever, ipecacuanha being the drug of choice for inducing vomiting. The most distinguished advocate of this agent was Doulcet of France who In 1782 observed that puerperal fever often commenced with vomiting: [95]

He viewed this as an indication of nature, and he assisted her efforts by giving 15 grains of ipecacuanha, which he repeated the next day. The patient recovered. This unexpected success led him to try it on all of the rest of his patients (during an epidemic of puerperal fever) and 200 were saved, while six, who refused to take the emetic, died. . . The previous devastation of the malady, and the consequent despondency in the practitioners of France, caused the news of Doulcet's success to be hailed with enthusiasm throughout the kingdom. The government compensated the discoverer largely. The Faculty of Medicine drew up minute instructions for this mode of treatment, and distributed them gratuitously over the whole of France. On the following year the malady was once more epidemic, and the remedy of Doulcet resorted to in full and earnest faith, but this time quite unsuccessful.

Other medicaments including antimony, arsenic and oil of turpentine were tried as therapy but fortunately never came into common use.

Opium, mercifully, was administered freely for analgesia and sedation and represented the only element of the entire therapeutic regimen with a positively beneficial effect when properly administered. [96]


Treatment of Autumnal Fever (Malaria)

In the mid 1800's it was assumed that both puerperal fever and autumnal fever, and many other "inflammatory" conditions as well, were associated with an overstimulated and aroused circulatory system as described by Professor Meigs. Theoretically, this hyperdynamic and congested state could be mitigated by "depletion" of the circulation through a combination of blood-letting, purging and mercury - a so-called antiphlogistic (anti-inflammatory) regime. Accordingly, we find that Drake's therapy for autumnal fever consisted of venesection, purging and calomel, with one noteworthy addition: the sulfate of quinine. [97]

Quinine is an alkaloid isolated from the bark of a species of the cinchona tree, native to Peru. As early as 1600 the Jesuits in Peru knew of the bark's curative effect on intermittent fever but it was not until the mid 1600's that its remedial properties were "certified" by the Pope's physician in Rome where malaria was rampant and where, by 1650, the Peruvian bark had become a popular remedy. Nevertheless, because effectiveness of the bark in malaria was considerably obscured by its indiscriminate use for all fevers, there was resistance to its use by the generality of physicians who remained committed to bleeding and purging. Thus, for the next 150 years, and until isolation of the bark's active principle, quinine sulfate, by French chemists in 1820 made it available in this more usable form, quinine was slow to gain wide acceptance by the medical profession. Finally, by 1850 quinine was in general use as a remedy for the syndrome we now know as malaria. The specificity of quinine's effect exclusively on malaria made it possible to begin the objective differentiation of malaria from other fevers. Although the emerging recognition of quinine as a specific for malaria tended to undermine the antiphlogistic regime, Drake could not bring himself to abandon the old order. He insisted that bleeding, purging and mercury were essential "preparation" of the patient before administration of quinine sulfate. [98] [99]

It is relevant to our evaluation of Drake's vegeto-animalcular hypothesis of the cause of malaria to point out that the elusive plasmodia of the malarial parasite were not found in the blood of malarial patients until 1880. The discovery was made by Alphonse Laveran (1845-1922), a French military medical officer working in a military hospital in Constantine, Algeria. He suspected that the parasite was probably transmitted by a mosquito, but could not prove it. [100] Sir Ronald Ross (1857-1932), a British army surgeon working in India, identified plasmodia in the stomach wall of Anopheles mosquitoes which had fed on the blood of malarial patients (1897). He also found that sporozoites of the parasite were concentrated in the mosquito's salivary gland. He concluded that they were injected from there into the blood stream of the human host. For this work, which led to effective methods to control mosquitoes and prevent malaria, he was awarded the Nobel Prize in 1902. [101] By this time clearing of land, drainage of swamps and improved housing had resulted in the control of mosquitoes and the end of malaria as the scourge of the Northwest.

In retrospect, Drake's hypothesis regarding the etiology of malaria was about as close to the mark as was reached until Pasteur and Koch demonstrated the microbial origin of infectious disease; laid to rest the theories of their atmospheric, constitutional or spontaneous origin; and set off an intensive search for specific agents of infection.

As we have seen, malaria was the commonest infectious disease in the Northwest. It was so widely prevalent and unavoidable that it was tolerated stoically by those who could not move to more healthful locations away from the low or "bottom" lands where it was known to be an almost universal complaint. Although malaria was the major cause of recurrent illness and was not infrequently lethal, especially among the very young, it is important to keep in mind that the principal causes of death in the region in the 1850's were a host of other infectious diseases: infant diarrhea; exanthemata in childhood, particularly scarlet fever; diphtheria; pulmonary tuberculosis; lobar pneumonia; typhoid fever; and bacillary dysentery. These nineteenth century destroyers, now well controlled in developed countries, were then a dreaded menace to every family.

To these endemic afflictions were added the periodic visitations of Asiatic Cholera, the most feared of all diseases in the 19th century. This pestilence followed trade routes across the Atlantic and invaded North America for the first time in June 1832. It was carried from Europe to Quebec and Montreal by Irish immigrants fleeing the cholera epidemic in Ireland. Between June 9 and September 2 there were 2127 deaths from cholera in Quebec City. Between June 10 and July 14 there were 1220 deaths from cholera in Montreal. It appeared within the next few months in the New York, Philadelphia, Maryland, Virginia, Kentucky and the Ohio Valley.

By July 1832 the epidemic had already crossed the Great Lakes from Canada into Northern Illinois where the Black Hawk War was in progress. On July 2 General Winfield Scott was dispatched from Buffalo with troops aboard two lake vessels to put down the Indian uprising. General Scott never engaged Black Hawk who was defeated before his arrival in Northern Illinois. Instead, the General encountered cholera which broke out aboard the vessels, disorganizing his expedition and costing the lives of 500 men. [102]

The plague returned to Northern Illinois in 1866 and attacked Chicago where there were 1581 cases of cholera in that year with 970 deaths, including that of Professor Daniel Brainard of Rush Medical College. Brainard died within less than 24 hours from the onset of the disease. Because of its rapid progress and high mortality rate, cholera struck terror wherever it appeared. It was well-known in some cases to begin in the morning with mild gastrointestinal symptoms and copious watery diarrhea and terminate with dehydration, collapse and death by nightfall. Crowded, unwashed populations living amidst filth and pollution with fecally contaminated water and food supplies were seen to be more susceptible to cholera and typhoid than those living under opposite conditions. This observation, even though the nature of the contagion was unknown, stimulated the inception during the first half of the 19th century of the modern public health movement known as "The Great Sanitary Awakening," devoted to sanitary reform throughout the world. [103] [104] [105]

Finally, as a rough measure of social and medical progress over the past century and a half we see that the death rate in the nation is now half that in the mid 1800's and life expectancy is twice as long: [106] [107]

  Deaths per 1000 Population Life Expectancy at Birth
Massachusetts 19 (1860) [108] 39 Years (1850)
All USA 9 (1990) 75 Years (1990)
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