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A New Marker of Sepsis Post Burn Injury?*

Paratz, Jennifer D. PhD, FACP; Lipman, Jeffrey MBBCh, FCICM, MD; Boots, Robert J. PhD, FCICM; Muller, Michael J. MMedSc, FRACS; Paterson, David L. PhD, FRACP, FRCPA

Critical Care Medicine:
doi: 10.1097/CCM.0000000000000400
Clinical Investigations
Abstract

Objectives: Accurate diagnosis of sepsis is difficult in patients post burn due to the large inflammatory response produced by the major insult. We aimed to estimate the values of serum N-terminal pro-B-type natriuretic peptide and procalcitonin and the changes in hemodynamic variables as markers of sepsis in critically ill burn patients.

Design: Prospective, observational study.

Setting: A quaternary-level university-affiliated ICU.

Patients: Fifty-four patients with burns to total body surface area of greater than or equal to 15%, intubated with no previous cardiovascular comorbidities, were enrolled.

Interventions: At admission, a FloTrac/Vigileo system was attached and daily blood samples taken from the arterial catheter. Infection surveillance was carried out daily with patients classified as septic/nonseptic according to American Burns Consensus criteria.

Measurements and Main Results: N-terminal pro-B-type natriuretic peptide, procalcitonin, and waveform analysis of changes in stroke volume index and systemic vascular resistance index were measured within the first 24 hours after burn and daily thereafter for the length of the ICU stay or until their first episode of sepsis. Prevalences of stroke volume variation less than 12% (normovolemia) with hypotension (systolic blood pressure < 90 mm Hg) were recorded. Patients with sepsis differed significantly from “no sepsis” for N-terminal pro-B-type natriuretic peptide, systemic vascular resistance index, and stroke volume index on days 3–7. Procalcitonin did not differ between sepsis and “no sepsis” except for day 3. Area under the receiver operating characteristic curves showed excellent discriminative power for B-type natriuretic peptide (p = 0.001; 95% CI, 0.99–1.00), systemic vascular resistance index (p < 0.001; 95% CI, 0.97–0.99), and stroke volume index (p < 0.01; 95% CI, 0.96–0.99) in predicting sepsis but not for procalcitonin (not significant; 95% CI, 0.29–0.46). A chi-square crosstab found that there was no relationship between hypotension with normovolemia (stroke volume variation < 12%) and sepsis.

Conclusions: Serum N-terminal pro-B-type natriuretic peptide levels and certain hemodynamic changes can be used as an early indicator of sepsis in patients with burn injury. Procalcitonin did not assist in the early diagnosis of sepsis.

Author Information

1Burns, Trauma and Critical Care Research Centre, The University of Queensland, Brisbane, QLD, Australia.

2Department of Intensive Care Medicine, Royal Brisbane and Women’s Hospital, Brisbane, QLD, Australia.

3Department of Rehabilitation Sciences, Griffith University, Brisbane, Australia.

4Professor Stuart Pegg Burn Unit, Royal Brisbane and Women’s Hospital, Brisbane, QLD, Australia.

5University of Queensland Centre for Clinical Research, Brisbane, QLD, Australia.

* See also p. 2137.

Supported, in part, by Royal Brisbane and Women’s Hospital Research Foundation.

Dr. Paratz consulted for Edwards Lifesciences; is employed by University of Queensland; and received support for travel from Australian and New Zealand Intensive Care Society, South African Burns Society, and Australian Physiotherapy Association. Her institution received grant support from National Health and Medical Research Council (NIHMRC), Office of Health Medical Research, NHMRC Equipment grants, Royal Brisbane Hospital Research Foundation, and Office Medical Research; received provision of equipment from Edwards Lifesciences (equipment lent free of cost to ICU); and lectured for University of Queensland, Australian Catholic University. Dr. Lipman’s institution received grant support from the Royal Brisbane and Women’s Hospital Research Foundation; received provision of equipment from Edwards Lifesciences (equipment lent free of cost to ICU); served as board member for Bayer European Society Council Intensive Care Medicine Advisory Board; consulted for Merk Sharp Dohme (Aust) Pty Ltd, Pfizer Australia, and AstraZeneca; received grant support from AstraZeneca; and lectured for AstraZeneca and Pfizer Australia Pty Ltd. Dr. Boots’ institution received grant support from Royal Brisbane and Women’s Hospital Research Foundation and received provision of equipment from Edwards Lifesciences (equipment lent free of cost to ICU). Dr. Muller’s institution received grant support from Royal Brisbane and Women’s Hospital Research Foundation, received provision of equipment from Edwards Lifesciences (equipment lent free of cost to ICU), and received grant support from Royal Brisbane and Women’s Hospital Research Foundation. Dr. Paterson consulted for Merck, AstraZeneca, and Pfizer; and lectured for AstraZeneca.

For information regarding this article, E-mail: j.paratz@uq.edu.au

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