Sepsis History

In the past, when medical hygiene was unknown, wound infections were a common and greatly feared complication of surgery. Wound putrefaction (sepsis) was blamed to be the cause.

Though the term Sepsis is linked closely to modern intensive care, the medical concept is rather older. The word "sepsis" was first introduced by Hippocrates (ca. 460-370 BC) and is derived from the Greek word sipsi ("make rotten"). Ibn Sina (979-1037 BC) observed the coincidence of blood putrefaction (septicaemia) and fever. This concept of sepsis which was introduced in classical antiquity was used until the 19th century. Only few examples of pathophysiological investigations are known. Herrmann Boerhave (1668-1738), a doctor in Leyden, thought that toxic substances in the air were the cause for sepsis. At the beginning of the 19th century, the chemist Justus von Liebig expanded the theory by claiming that the contact between wounds and oxygen was responsible for the development of sepsis.

Ignaz Semmelweis (1818-1865) was the first researcher who developed a modern view of sepsis. He was an obstetrician at the Vienna General Hospital at a time when the death of women in childbed from puerperal fever was a common complication. His department had an especially high mortality rate of ca. 18 %. Semmelweis discovered that it was common for medical students to examine pregnant women directly after pathology lessons. Hygenic measures such as handwashing or surgical gloves were not customary practice.

Semmelweis deducted that childbed fever was caused by "decomposed animal matter that entered the blood system". As a matter of fact, he succeeded in lowering the mortality rate to ca. 2.5 % by introducing handwashing with a chlorinated lime solution before every gynaecological examination. However, in spite of the clinical success, the hygienic measures were not accepted, and colleagues harassed him, forcing him to leave the city. It took him until 1863, more than 15 years after his findings, to publish his work "Aetiology, terminus and prophylaxis of puerperal fever" (Die Aetiologie, der Begriff und die Prophylaxis des Kindbettfiebers). The failure to achieve a professional reputation and the unrelenting opposition of the medical establishment may have facilitated the development of psychiatric symptoms. Semmelweis was eventually committed to a lunatic asylum where he died from a wound infection probably as a result of the beatings he underwent there. It is an irony of fate that he died from a disease that he dedicated his life to fight.

The French chemist Louis Pasteur (1822-1895) discovered that tiny single cell organisms caused putrefaction. He called them bacteria or microbes and correctly deducted that these microbes could be causing disease.

He also made the significant discovery that bacteria in fluids could be killed by heating. This meant that a fluid could be sterilised.


Joseph Lister (1827-1912) worked as a surgeon at Glasgow Royal Infirmary. At the time when he became chairman of the surgery department about 50 % of patients with amputations died of sepsis. Lister drew a correlation between Semmelweis' observations, Pasteur's findings and the deaths in his hospital. By almost modern scientific studies, first with animals, then with humans, he examined the effects of skin and instrument disinfection with carbolic acid (the so-called antiseptic method). By doing so, Lister was able to drastically reduce post-amputation mortality. Unlike Semmelweis, Lister managed to persuade his colleagues of the reasonableness of his antiseptic method. In 1887, Robert Koch (1843-1910) introduced steam sterilisation and thus refined Lister's techniques.


In Germany the physician H. Lennhartz, who worked as medical director at Eppendorf Hospital, initiated the change in the understanding of sepsis from the ancient concept of putrefaction to the modern view of a bacterial disease. It was, however, his student Hugo Schottmüller (1867-1936), who in 1914 paved the way for a modern definition of sepsis: "Sepsis is present if a focus has developed from which pathogenic bacteria, constantly or periodically, invade the blood stream in such a way that this causes subjective and objective symptoms." Thus, for the first time, the source of infection as a cause of sepsis came into focus. Schottmüller explained: "A therapy should not be directed against bacteria in the blood but against the released bacterial toxins (...)." With this thinking he was well ahead of his time.

Although antiseptic procedures meant a huge medical breakthrough, it soon became apparent that a number of patients still developed sepsis. . In this pre-antibiotic time, the death rate was very high. These patients often showed a very low blood pressure. This condition was called septic shock. Only with the introduction of antibiotics after WW II could the death rate of sepsis be reduced further. With technological progress, intensive care medicine started to develop and sepsis patients soon became the main patient fraction on intensive care units (ICU).

In 1967 Asbough and colleagues observed a severe lung disease which developed in intensive care patients with severe shortness of breath, loss of lung compliance, and diffuse alveolar infiltration. This disease was called Adult Respiratory Distress Syndrome (ARDS) and was frequently a fatal complication. It was soon understood that particularly sepsis patients suffered from this complication. Apart from that, it appeared that the development of ARDS was a result of an inflammatory reaction and thus caused by substances produced in the diseased body. In the 1980s it was discovered that this inflammatory reaction was not only apparent in the lungs but in the whole body. Hence it became clear that the onset of sepsis did not derive from an infectious focus alone, but that the host response against infection must in some way play a role.In 1989, US-American ICU specialist Roger C. Bone (1941-1997) offered a sepsis definition that is still valid until today: "Sepsis is defined as an invasion of microorganisms and/or their toxins into the bloodstream, along with the organism's reaction against this invasion."