Cardiac arrest patients have an impaired immune response, which is not influenced by induced hypothermia

• Published in: Critical care (London, England) Vol. 18; no. 4; p. R162
• Main Authors: Beurskens, Charlotte J, Horn, Janneke, de Boer, Anita M Tuip, Schultz, Marcus J, van Leeuwen, Ester Mm, Vroom, Margreeth B, Juffermans, Nicole P
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 30-07-2014; BioMed Central
• Subjects: Analysis of Variance; Body Temperature - immunology; Cardiac arrest; Cardiac patients; Care and treatment; Complications and side effects; Cytokines - blood; Cytokines - immunology; Development and progression; Female; Glasgow Coma Scale; Health aspects; Heart Arrest - immunology; Heart Arrest - therapy; Humans; Hypothermia, Induced - adverse effects; Hypothermia, Induced - methods; Inflammation - immunology; Intensive Care Units; Leukocytes - immunology; Lipopolysaccharides - blood; Lipopolysaccharides - immunology; Male; Medical research; Medicine, Experimental; Middle Aged; Mitogens; Netherlands; Patient outcomes; Prospective Studies; Risk factors; Toll-Like Receptors - blood; Toll-Like Receptors - immunology; Netherlands
• ISSN: 1364-8535; 1466-609X; 1364-8535
• DOI: 10.1186/cc14002

Induced hypothermia is increasingly applied as a therapeutic intervention in ICUs. One of the underlying mechanisms of the beneficial effects of hypothermia is proposed to be reduction of the inflammatory response. However, a fear of reducing the inflammatory response is an increased infection risk. Therefore, we studied the effect of induced hypothermia on immune response after cardiac arrest.
A prospective observational cohort study in a mixed surgical-medical ICU. Patients admitted at the ICU after surviving cardiac arrest were included and during 24 hours body temperature was strictly regulated at 33°C or 36°C. Blood was drawn at three time points: after reaching target temperature, at the end of the target temperature protocol and after rewarming to 37°C. Plasma cytokine levels and response of blood leucocytes to stimulation with toll-like receptor (TLR) ligands lipopolysaccharide (LPS) from Gram-negative bacteria and lipoteicoic acid (LTA) from Gram-positive bacteria were measured. Also, monocyte HLA-DR expression was determined.
In total, 20 patients were enrolled in the study. Compared to healthy controls, cardiac arrest patients kept at 36°C (n = 9) had increased plasma cytokines levels, which was not apparent in patients kept at 33°C (n = 11). Immune response to TLR ligands in patients after cardiac arrest was generally reduced and associated with lower HLA-DR expression. Patients kept at 33°C had preserved ability of immune cells to respond to LPS and LTA compared to patients kept at 36°C. These differences disappeared over time. HLA-DR expression did not differ between 33°C and 36°C.
Patients after cardiac arrest have a modest systemic inflammatory response compared to healthy controls, associated with lower HLA-DR expression and attenuated immune response to Gram-negative and Gram-positive antigens, the latter indicative of an impaired immune response to bacteria. Patients with a body temperature of 33°C did not differ from patients with a body temperature of 36°C, suggesting induced hypothermia does not affect immune response in patients with cardiac arrest.
ClinicalTrials.gov NCT01020916, registered 25 November 2009.