Infectious biomarkers in the critically ill

A study examining patterns of procalcitonin in a group of critically ill patients(1) showed some interesting findings:

Shock was associated with higher procalcitonin values independent of the presence of infection

Procalcitonin (PCT) levels were less in patients who developed infections later during their ICU stay compared with those who had infections when admitted to ICU.

The accompanying editorial(2) reminds us about commonly used inflammatory biomarkers.

White blood cells are influenced by almost every inflammatory stimulus, rendering them unhelpful in the management of severely ill patients.

Daily monitoring of CRP levels can identify ICU-acquired infections early, and some prognostic information can be provided by how rapidly CRP levels respond to treatment.

PCT rises early in severe sepsis, mainly by pneumonia and bloodstream infections, and can reflect the severity of the systemic inflammatory response syndrome to infection. PCT is more specific than CRP for infection compared with non-infectious causes of systemic inflammatory response syndrome. However PCT can also be increased in noninfectious diseases such as acute pancreatitis and cardiogenic shock.

1. Longitudinal changes in procalcitonin in a heterogenous group of critically ill patients
Crit Care Med. 2012 Oct;40(10):2781-2787
[EXPAND Click for Abstract]

OBJECTIVE: The utility of procalcitonin for the diagnosis of infection in the critical care setting has been extensively investigated with conflicting results. Herein, we report procalcitonin values relative to baseline patient characteristics, presence of shock, intensive care unit time course, infectious status, and Gram stain of infecting organism.

DESIGN: Prospective, multicenter, observational study of critically ill patients admitted to intensive care unit for >24 hrs. SETTING:: Three tertiary care intensive care units.

PATIENTS: All consenting patients admitted to three mixed medical-surgical intensive care units. Patients who had elective surgery, overdoses, and who were expected to stay <24 hrs were excluded.

INTERVENTIONS: Patients were followed prospectively to ascertain the presence of prevalent (present at admission) or incident (developed during admission) infections and clinical outcomes. Procalcitonin levels were measured daily for 10 days and were analyzed as a function of the underlying patient characteristics, presence of shock, time of infection, and pathogen isolated.

MAIN RESULTS: Five hundred ninety-eight patients were enrolled. Medical and surgical infected cohorts had similar baseline procalcitonin values (3.0 [0.7-15.3] vs. 3.7 [0.6-9.8], p = .68) and peak procalcitonin (4.5 [1.0-22.9] vs. 5.0 [0.9-16.0], p = .91). Infected patients were sicker than their noninfected counterparts (Acute Physiology and Chronic Health Evaluation II 22.9 vs. 19.3, p < .001); those with infection at admission had a trend toward higher peak procalcitonin values than did those whose infection developed in the intensive care unit (4.9 vs. 1.4, p = .06). The presence of shock was significantly associated with elevations in procalcitonin in cohorts who were and were not infected (both groups p < .003 on days 1-5).

CONCLUSIONS: Procalcitonin dynamics were similar between surgical and medical cohorts. Shock had an association with higher procalcitonin values independent of the presence of infection. Trends in differences in procalcitonin values were seen in patients who had incident vs. prevalent infections.

2. The many facets of procalcitonin in the critically ill population
Crit Care Med. 2012 Oct;40(10):2903-5

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