Sepsis: the rise of a global killer

The heightened fear reflects our evolving knowledge of life-threatening infectious diseases.

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When I qualified as a doctor in 1990, no one died of sepsis. Derived from the Greek verb “to make rotten”, back then it simply meant the presence of pus-forming bacteria such as one might find in an abscess. Pneumonia or peritonitis were infections that people died from – but sepsis didn’t kill; it wasn’t even a disease.

Fast-forward 30 years and, according to a new study from the University of Washington that was widely reported in the media, sepsis is now responsible for one in five deaths worldwide, making it more lethal than cancer.

Sepsis, it seems, is suddenly everywhere. Consulting rooms are festooned with stark red posters exhorting clinicians to “Think Sepsis”. The UK Sepsis Trust runs public information campaigns urging people to ask of their doctor: “Could it be sepsis?” Three years ago, no patient ever mentioned the word to me. Today it has superseded meningitis as the thing everyone most fears.

The transformation of sepsis from an arcane pathological process into a global killer is, on one level, no more than etymology: the word has acquired a profoundly different meaning. But the heightened fear of sepsis also reflects our evolving knowledge of life-threatening infectious diseases.

In the early years of my career, the syndrome had a variety of confusing synonyms: septicaemia (blood poisoning); septic shock (when blood pressure drops dangerously); disseminated intravascular coagulation (when spontaneous clots clog up arteries throughout the body); acute renal failure (when the kidneys begin shutting down); or multi-organ failure (when, as a result of the above, the body approaches near-certain death).

The unifying features of all of these were rapid progression and appalling outcomes; by the time one realised the syndrome was advancing, it was often too late to save the patient’s life.

This fulminant reaction can be caused by virtually any infection. Some bacteria – such as meningococcus, which is responsible for the most lethal form of meningitis – frequently provoke the syndrome, while it is a much rarer complication of those that cause pneumonia or infections of the skin. As such, the exact same bacterium that might cause one patient to die from multi-organ failure will in someone else produce nothing more than a bout of cystitis, readily treated with antibiotics.

The catastrophic reaction is best understood as a malfunction of our immune system: an infection triggers an aberrant immune response that, rather than attacking the bacteria, inflicts damage to our own tissues and organs. This occurs most commonly among those with impaired immunity: the very young, the very old, transplant patients, cancer patients undergoing chemotherapy and people with other debilitating long-term health conditions.

Research has illustrated the importance of identifying as quickly as possible patients who are developing this abnormal immune response. Detected early on, a cure is eminently possible; just 36 hours into the illness, the risk of mortality is high.

Yet early identification can be challenging. Patients who will quickly become moribund are initially indistinguishable from those who will simply shrug off their infection. Data analysis has identified thresholds in measures such as temperature and pulse rate that may suggest that a patient is developing problems. Even more important are markers that indicate organs are beginning to fail, such as altered consciousness-level, low blood pressure or raised respiratory rate.

Any one of these clinical findings, viewed in isolation, wouldn’t necessarily ring alarm bells. But patients who display a cluster of these vital signs are likely to be at risk of rapid deterioration. Clinicians are now trained to recognise the significance of these early warning indicators and to treat those patients swiftly while there is still a chance of a cure.

Key to improving sespis’s early detection has been defining the syndrome under a memorable and consistently used name. After international conferences in 1991 and 2001 produced conflicting results, today’s definition of sepsis was settled as recently as 2016. Now that it has a label and well-defined warning indicators, the push is on to save more lives.

Estimates vary, but in the UK sepsis certainly accounts for tens of thousands of deaths annually. This figure is increasing due to rising numbers of people in vulnerable groups, such as the frail elderly. But the spike in sepsis-related hospital deaths in the past few years (up by a third) principally reflects our heightened awareness; what might have previously been recorded as pneumonia is now being labelled as sepsis.

The Washington study should raise questions over antibiotic resistance – our overuse of such drugs for minor illnesses may eventually render them ineffective against sepsis. But the most significant lesson lies in that global statistic of one in five deaths. The vast majority of sepsis mortality occurs in low- and middle-income countries, where poor sanitation and overcrowding mean infectious diseases are rife; malnutrition and life stress impair immunity; and a lack of access to health care condemns too many to die from preventable causes. The true conclusion of the study should be shame at the inequality we allow to persist in our world.

Phil Whitaker is a GP and writes the New Statesman’s “Health Matters” column. His books include Chicken Unga Fever: Stories from the Medical Frontline (Salt)

This article appears in the 24 January 2020 issue of the New Statesman, Power to the people

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