American Journal of Medical and Biological Research
ISSN (Print): 2328-4080 ISSN (Online): 2328-4099 Website: Editor-in-chief: Apply for this position
Open Access
Journal Browser
American Journal of Medical and Biological Research. 2017, 5(2), 13-17
DOI: 10.12691/ajmbr-5-2-1
Open AccessArticle

The Analysis of Prostaglandin E2 (PGE2), Pain Pressure Threshold (PPT), and Critical-Care Pain Observation Tools (CPOT) of Systemic Inflammatory Responses Syndrome (SIRS) Patients in Intensive Care Unit

Dwi Pantja Wibowo1, , Suryani As’ad2, Fransiscus Suhadi1, I Wayan Suranadi3, Ilhamjaya Patellongi4, Irawan Yusuf4, Mohammad Ramli Ahmad5, Syafrie Kamsul Arif5 and Andi Husni Tanra5

1Anesthesiology and Intensive Care Department, Bintaro Premier Hospital, Banten, Indonesia

2Clinical Nutrition Department, Hasanuddin University, Makassar, Indonesia

3Anesthesiology and Intensive Care Department, Udayana University, Denpasar, Indonesia

4Physiology Department, Hasanuddin University, Makassar, Indonesia

5Anesthesiology and Intensive Care Management Department, Hasanuddin University, Makassar, Indonesia

Pub. Date: July 20, 2017

Cite this paper:
Dwi Pantja Wibowo, Suryani As’ad, Fransiscus Suhadi, I Wayan Suranadi, Ilhamjaya Patellongi, Irawan Yusuf, Mohammad Ramli Ahmad, Syafrie Kamsul Arif and Andi Husni Tanra. The Analysis of Prostaglandin E2 (PGE2), Pain Pressure Threshold (PPT), and Critical-Care Pain Observation Tools (CPOT) of Systemic Inflammatory Responses Syndrome (SIRS) Patients in Intensive Care Unit. American Journal of Medical and Biological Research. 2017; 5(2):13-17. doi: 10.12691/ajmbr-5-2-1


Sepsis is one of the major health problems with very high costs, a number of patients who survived sepsis developed long-term complications such as persistent pain. Studies found correlation of persistent pain and PGE2 level. Aims of this study were to investigate the changes in the prostaglandin E2 levels from patients with systemic inflammatory responses syndrome (SIRS) that affect pain intensity changes with the marked increase of critical-care pain observation tools (CPOT) and decreased of the pain pressure threshold (PPT). A cross-sectional analysis to compare the values of PGE2, CPOT, and PGE2 of SIRS patients and patients without SIRS. Of the 46 patients who were the subjects of the study, there were 21 SIRS patients and 25 patients, not SIRS. Patients with SIRS had higher CPOT values and PGE2 levels than patients without SIRS; CPOT values (3.3 vs. 1.2)) and PGE2 levels (6195.81 vs. 2728.67). The PPT scores of patients with SIRS were lower than those without SIRS (4.24 vs. 7.37). The CPOT was significantly correlated (p <0.05) with PGE2 (r = -0.624). We conclude that in SIRS patients there is an increase PGE2, which in turn leads to decreased pain threshold (PPT) and increased pain score (CPOT).


Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit


[1]  Shankar, Ravi, Kurt A Melstrom, and Richard L Gamelli. “Inflammation and Sepsis: past, present, and the future.” Journal of Burn Care & Research 28, no. 4 (July 2007): 1-6.
[2]  Singer, M, C S Deutschman, and C W Seymour. “The Third International Consensus Definitions for Sepsis and Septic Shock (2016) (Sepsis - 3).” JAMA 315, no. 8 (2016): 801-810.
[3]  Shankar-Hari, M, G S Phillips, and M L Levy. “Developing a new definition and assessing new clinical criteria for septic shock: for the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).” JAMA 315, no. 8 (2016): 775-785.
[4]  Seymour, C W, V X Liu, and T J Iwashyna. “Assessment of clinical criteria for sepsis: for the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).” JAMA 315, no. 8 (2016): 762-774.
[5]  Torio, C M, and R M Andrews. “National inpatient hospital costs: themost expensive conditions by payer.” Healthcare Cost and Utilization Project (HCUP) Statistical Briefs. August 2013.
[6]  Global Sepsis Alliance. GSA. 2016.
[7]  Rhodes, Andrew, et al. “Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016.” Intensive Care Med, 2016.
[8]  Dowdy, David W, et al. “Quality of life in adult survivors of critical illness: A systematic review of the literature.” Intensiva Care Medicine 31, no. 5 (May 2005): 611-620.
[9]  Marx, G, A Zimmer, J Rothaug, S Mescha, K Reinhart, and W Meissner. “Chronic pain after surviving sepsis.” Critical Care 10, no. Suppl (2006): P421.
[10]  Park, Giburm, Chan Woo Kim, Si Bog Park, Mi Jung Kim, and Seong Ho Jang. “Reliability and usefulness of the pressure pain threshold measurement in patients with myofascial pain.” Ann Rehabil Med 35, no. 3 (June 2011): 412-417.
[11]  Nussbaum, Ethne L, and Laurie Downes. “Reliability of clinical pressure-pain algometric measurements obtained on consecutive days.” Physical Therapy 78 (1998): 160-169.
[12]  Obenholzer, A, C Oberholzer, and L L Moldawer. “Sepsis syndrome: understanding the role of innate and acquire immunity.” Shock 16 (2001): 83-96.
[13]  Nurnberg, D, F Sabonchi, PV Sackey, and G Bjorling. “A preeliminary validation of Swedish version of the critical-care pain observation tool in adults.” Acta Anaesthesiologica 55, no. 4 (2011): 379-386.
[14]  Ji, R R, T Kohno, K A Moore, and C J Wolf. “Central sensitization and LTP: Do pain and memory share similar mechanisms?” Trends Neurosci 23 (2003): 696-705.
[15]  Herridge, M S. “One-year outcomes in survivors of the acute respiratory distress syndrome.” N Engl J Med 348 (2003): 683-693.
[16]  Gelinas, C, L Fillon, K A Puntilo, C Viens, and M Fortier. “Validation of the critical-care pain observation tool in adult patients.” American Journal of Critical Care 15, no. 4 (2006): 420-442.
[17]  Kawasaki, Y, L Zhang, Jen Kun Cheng, and Ru Rong Ji. “Cytokine mechanisms of central sensitization : distinct and overlapping role of interleukin-1β, interleukin-6, and tumor necrosis factor-α in regulating synaptic and neuronal activity in the superficial spinal cord.” The Journal of Neuroscience 28, no. 20 (2008): 5189-5194.
[18]  Bone, R C. “Sir Isaac Newton, sepsis, SIRS, and CARS.” Crit Care Med 24 (1996): 1125-1128.
[19]  Obenholzer, A, C Obenholzer, and L L Moldawer. “Sepsis syndrome: understanding the role of innate and acquire immunity.” Shock 16 (2001): 83-89.
[20]  Carson, William F, and L Kunkel Steven. “Immune cell dysfunction as a consequence of severe sepsis.” In Killer, Severe Sepsis and Septic Shock - Understanding a Serious, by Richardo Fenrnandez, 125-154. Michigan: Intech, 2012.
[21]  Woolf, CJ, and Q Ma. “Nociceptors-noxious stimulus detectors.” Neuron 55, no. 3 (2007): 353-364.
[22]  Woolf, Clifford J, and Mun Seng Chong. “Preemptive analgesia - Treating post operative pain by preventing the establishment of central sensitization.” Anesthesia Analgesia (IARS) 77 (1993): 362-379.
[23]  Battle, Ceri E, Simon Lovett, and Hayley Hutchings. “Chronic pain in survivors of critical illness: a retrospective analysis on incidence and risk factors.” Critical Care 17, no. R101 (2013): 1-8.
[24]  Bergbom-Engberg, I, and H Haljamae. “Assessment of patients' experience of discomforts during respiratory therapy.” Crit Care Med 17 (1989): 1068-1072.
[25]  Puntilo, K A. “Pain experiences of intensive care unit patients.” Heart Lung 19, no. 5 Pt 1 (1990): 526-533.
[26]  Lee, M, S Silverman, H Hansen, V Patel, and L Manchikanti. “A comprehensive review of opioid-induced hyperalgesia.” Pain Physician 14 (2011): 145-161.
[27]  Mattia, C, G Savoia, F Paeletti, O Piazza, D Albanese, and B Amantea. “SIAARTI recommendations for analgo-sedation in intensive care unit.” Minerva Anestesiol 72 (2006): 769-805.
[28]  Ching, Tang. “The effect of epidural clonidine on perioperative cytokine response, postoperative pain and bowel function in patient undergoing colorectal surgery.” Anesth Analg 99 (2004): 502-507.
[29]  McMahon, S B, W B Cafferty, and F Marchand. “mmune and glial cell factors as pain mediators and modulators.” Exp Neurol 192 (2005): 444-462.
[30]  Verri, W A, T M Cunha, C A Parade, S Poole, F Q Cunha, and S H Ferreira. “Hypernociceptive role of cytokines and chemokines: targets for analgesic drug development?” Pharmacol Ther 112, no. 1 (Oct 2006): 116-138.
[31]  Rapanos, T, P Murphy, J P Szalai, L Burlacoff, J Lam McCulloch, and J Kay. “Rectal indomethacin reduces postoperative pain and morphine use after cardiac surgery.” Can J Anaesth 46 (1999): 725-730.
[32]  Hynninen, M S, D C Cheng, I Hossain, J Carrol, S S Aumbhagavan, and R Yue. “Non-steroidal anti-inflammatory drugs in treatment of postoperative pain after cardiac surgery.” CanJ Anaesth 47 (2000): 1182-1187.
[33]  Pandey, C K, N Bose, G Garg, N Singh, A Baronia, and A Agarwal. “Gabapentin for the treatment of pain in Guillain-Barré syndrome: a double-blinded, placebo-controlled, crossover study.” Anesthe Analg 95 (2002): 1719-1723.
[34]  Pandey, C K, M Raza, M Tripathi, D V Navkar, A Kumar, and U K Singh. “The comparative evaluation of gabapentin and carbamazepine for pain management in Guillain-Barrésyndrome patients in the intensive care unit.” Anesth Analg 101 (2005): 220-225.
[35]  Pandey, C K, et al. “Gabapentin provides effective postoperative analgesia whether administered preemptively or post-incision.” Can J Anesth 52 (2005): 827-831.
[36]  Joly, V, R Richebe, B Guignard, D Fletcher, P Maurette, and D I Sessler. “Remifentanil-induced postoperative hyperalgesia and its prevention with small-dose ketamine.” Anesthesiology 103 (2005): 147-155.
[37]  Woolf, Clifford J. “What is this thing called pain?” J Clin Invest 120, no. 11 (Nov 2010): 3742-3744.
[38]  Meier, Karin, Dieter Steinhiber, and Ewgenji Proschak. “Inhibitors of the Arachidonic Acid Cascade: Interfering with Multiple Pathways.” Basic & Clinical Pharmacology & Toxicology 114 (2014): 83-91.