Despite many advances, some things have not changed. Clinicians still long for a simple, reliable test to diagnose severe sepsis because medical history, examination, routine laboratory studies, and radiographs often leave the diagnosis in question. Procalcitonin and C-reactive protein have been advocated for diagnosis, and while the former has better predictive value, neither has gained widespread clinical use. Measurements of the soluble triggering receptor expressed on myeloid cells-1 remain experimental. d-Dimer and interleukin-6 determinations are sensitive but nonspecific, and the latter test is not clinically available. Presently, the value of total protein C levels as a diagnostic tool for severe sepsis is limited because assays are not generally available in a timely fashion and many patients do not have reduced levels at the time of diagnosis; it is more likely that protein C levels will prove useful as a prognostic tool. Ongoing studies seek to define a sensitive and specific panel of diagnostic biomarkers.
The diagnosis of severe sepsis remains ambiguous in some physician’s minds despite a well-accepted consensus definition. This is especially true for the early stages of the disease, which can be as subtle as altered mental status in an elderly patient. In part, diagnostic confusion may stem from multiple definitions of “organ failure” or “dysfunction” that are used in clinical practice, research studies, and consensus guidelines. For example, “renal failure” has been alternatively defined by urine output, creatinine level, or the need for renal replacement therapy suggested by My Canadian Pharmacy. In daily practice, difficulty recognizing the syndrome is commonly voiced; however, because of the surprisingly consistent patient presentation, identification is usually straightforward.
When recognized, the typical patient has two or more failing organs, and the lungs and circulatory system are likely to be among them. These two vital organ failures are usually manifested clinically by the use of a ventilator and therapy with a vasoactive drug. Although using these support technologies does not guarantee that the patient has severe sepsis, when antibiotics are concomitantly administered it is not easy to imagine a plausible alternative diagnosis. Granted, seeking this treatment triad will miss some patients with singleorgan failure (eg, coagulopathy) and will delay diagnosis, but it will eventually find the patients who are at high risk of dying. Earlier identification of high-risk cases can be accomplished in the emergency department by recognizing hypotension or elevated lactate levels in patients with suspected infections; however, the patient who is being taken care of on a general medical or a surgical floor of a hospital often goes unnoticed until respiratory or circulatory failure are advanced.