Evaluating the SIRS response in transplant and non-transplant patients
Background
The clinical signs of sepsis, which include pyrexia, tachycardia,
tachypnea, and leukocytosis, are collectively termed systemic
inflammatory response syndrome (SIRS). In organ transplant patients,
signs of infection are often attenuated. This could put them at risk
of delayed therapy. Studies have shown that procalcitonin is a
specific marker for bacterial infections. However, many of the studies
involving procalcitonin-guided therapy excluded transplant patients.
This study examined the relationship between the probability of
exhibiting SIRS signs, and the concentration of serum procalcitonin. We
studied this relationship in transplant and non-transplant patients.
Methods
A dataset of 2847 procalcitonin measurements was constructed from
transplant and non-transplant patients hospitalized in the Fairview
Health System between November 2011 and December 2013. This dataset
also included the maximum ‘SIRS score’ achieved on the day of the
procalcitonin measurement. Patients were divided into categories
based on the range of procalcitonin values, and the calculated
log-likelihood of having SIRS was calculated for each category.
Results
A mean log-likelihood ratio was 1.2 (CI 0.5-1.2) in the patients in the lowest procalcitonin range
(log(procalcitonin) <=-1) and increased to a mean log-likelihood ratio of 2.1 (CI 1.1-2.3) in the
highest procalcitonin range (log(procalcitonin) >=1) (p<0.001) in the non-transplant patients.
However, this increase in the probability of exhibiting SIRS signs was not seen in the transplant
patients, where the mean log-likelihood ratio did not increase over a wide range of procalcitonin
values (log-likelihood of 1.4 and 1.2 in the lowest and highest ranges of procalcitonin).
Moreover, in the highest procalcitonin range, the non-transplant patients had a significantly
higher likelihood of exhibiting a SIRS response (LR 2.1, CI 1.8-2.3) than the transplant patients
(LR 1.2, CI 0.7-1.8) (p<0.001).
Conclusions
Previous studies have described that individual signs of SIRS are
often attenuated in transplant patients. However, these studies did not
examine the SIRS score. To our knowledge, these results are the first
to demonstrate the attenuation of the SIRS response in transplant
patients. Our results show that as expected, non-transplant patients have a
higher likelihood of having SIRS signs with a progressive increase in
procalcitonin values. However, this increase in the probability of
having SIRS does not occur in transplant patients as serum
procalcitonin levels increase.