Types of postoperative pain

During surgery, cutting of the tissues and nerve fibers causes an intense burst of nociceptive pain.1

Once tissues have been damaged, the imperative is to promote healing. Local tissue damage activates nociceptor cells, which release inflammatory mediators. The tissue around the wound becomes flooded with acidic metabolites such as lactic acid.1,3

The resulting inflammatory pain increases sensitivity to the affected area and encourages patients to reduce movement of, or contact with, the injury until repair is complete to minimize further damage. Inflammation reaches its peak around 24 hours following surgery but continues to be high for 72 hours.1,4

Neuropathic pain is caused when the tissue trauma overloads the pain receptors that send messages to the spinal cord, which becomes overstimulated. In the resultant central sensitization, any stimulation becomes unpleasant; a patient may feel pain in movement or physical touch in locations far from the surgical site.1

The first 72 hours

Pain management in the first 72 hours after surgery is critical.

  • Postoperative pain has been shown to have a negative impact on physical activity, sleep, and cognitive function.5
  • Patients with higher postoperative pain at rest were significantly less likely to ambulate 72 hours following surgery and continued to show lower locomotion scores at 6 months.6
  • Inadequate management can delay discharge for patients.6
  • Increased pain severity has been associated with lower patient satisfaction.7

Graph of patient pain intensity over 72 hours; 75% of patients are still in moderate to severe pain 48 hours after surgery.Pain intensity is greatest during the first 72 hours postsurgery8

Managing Postoperative Pain

Learn more about some of the options currently available for treating postoperative pain.

Explore by specialty

Learn more about the postoperative pain management landscape as it applies to your area of expertise.

References: 1. Woolf CJ. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med. 2004;140(6):441-451. doi:10.7326/0003-4819-140-8-200404200-00010. 2. Berde CB, Strichartz GR. Local anesthetics. In: Miller RD, Cohen NH, Eriksson LI, Fleisher LA, Wiener-Kronish JP, Young WL, eds. Miller’s Anesthesia. Vol 2. 8th ed. Philadelphia, PA: Saunders; 2015:1012-1054.e4. 3. Basbaum AI, Bautista DM, Scherrer G, Julius D. Cellular and molecular mechanisms of pain. Cell. 2009;139(2):267-84. doi:10.1016/j.cell.2009.09.028. 4. Enoch S, Leaper DJ. Basic science of wound healing. Surgery (Oxford). 2007;26(2):31-37. doi:10.1016/j.mpsur.2007.11.005. 5. Aasvang EK, Luna IE, Kehlet H. Challenges in postdischarge function and recovery: the case of fast-track hip and knee arthroplasty. Br J Anaesth. 2015;115(6):861-866. doi:10.1093/bja/aev257. 6. Morrison RS, Magaziner J, McLaughlin MA. The impact of post-operative pain on outcomes following hip fracture. Pain. 2003;103(3):303-311. doi:10.1016/S0304-3959(02)00458-X. 7. Chan EY, Blyth FM, Nairn L, et al. Acute postoperative pain following hospital discharge after total knee arthroplasty. Osteoarthritis Cartilage. 2013;21(9):1257-1263. doi:10.1016/j.joca.2013.06.011. 8. Svensson I, Sjöström B, Haljamäe H. Assessment of pain experiences after elective surgery. J Pain Symptom Manage. 2000;20(3):193-201. doi:10.1016/S0885-3924(00)00174-3.