Can we prevent acute pain becoming chronic?
With Professor Margarita Puig | 2 Mar 2015 | Print
Professor Margarita Puig is Director, Unidad de Investigación en Anestesiología, Hospital del Mar, UAB, Barcelona, Spain.
Acute and chronic pain are two distinct entities defined by their duration. However, the point at which pain is considered to be chronic can vary considerably. Some consider that any pain lasting more than 30 days has become chronic, others claim that pain must persist for longer than three to six months to be considered chronic. The burden of chronic pain is substantial, with 19% of the European adult population affected with a high socioeconomic cost. There is insufficient relief with existing treatments in approximately 40% of patients, and typically poor or no response to drugs that are useful to relieve acute pain.
The transition from acute to chronic pain has been shown to involve peripheral and central pain sensitization (changes in neuronal plasticity), enhanced descending facilitation from the rostral ventromedial medulla to the spinal cord and early glial cell activation. Life stressors and cognitive/affective factors have also been associated with an increased risk of chronic back pain one year after the acute injury,  suggesting that these may exert pain-modulating effects through enhanced descending facilitation and glial cell activation.
Preventing the transition from acute to chronic pain is one of the main goals in pain medicine, but efforts have been mostly unsuccessful. Multiple studies have reported predictive factors (Box) for the transition to chronic pain in different syndromes. It is of interest that psychological aspects and fear at baseline correlate with the progression to persistent pain indicating that life stressors and cognitive/affective factors play a key role in the transition from acute to chronic pain syndromes.
Box. Predicting factors for transition from acute to chronic pain[1-4]
The recognition that acute postoperative pain may become chronic in certain predisposed individuals is under active investigation in preclinical models and also in humans. Acute postoperative pain is followed by persistent pain in 10-50% of patients after common operations. There is evidence supporting an association with female sex, older age, previous exposure to opioids, high (pre- and post-operative) pain intensity and pre-injury anxiety or depression, with persistent pain outcomes, although some risk factors have been demonstrated only in certain types of surgeries.[8,9] Thus, predictive factors for the development of chronic postsurgical pain (CPSP) are comparable with those described for persistent pain after orthopedic trauma.
Preventive measures in surgical patients include an aggressive, multimodal, perioperative analgesic regimen that incorporates drugs that target the sensitization process. There is increasing evidence that perioperative administration of IV ketamine and/or oral gabapentin in some types of surgeries (thoracic, upper abdominal and orthopedic) may decrease a patient’s postoperative opioid requirement as well as the incidence of CPSP. However, optimal dosage regimens, timing or duration of administration, possible adverse effects and likely drug interactions have not been completely defined. Furthermore, the use of anti-hyperalgesic drugs to prevent the development of chronic pain after other types of injury, for example, trauma, has not been widely investigated.
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2. Wang CK, Myunghae JH, et al. Factors contributing to pain chronicity. Curr Pain Headache Rep 2009;13:7-11.
3. Clay F, Watson WL, et al. A systematic review of early prognostic factors for persisting pain following acute orthopedic trauma. Pain Res Manag 2012;17:35-44.
4. Casey CY, Greenberg MA, et al. Transition from acute to chronic pain and disability: a model including cognitive, affective, and trauma factors. Pain 2008;134:69-79.
5. Melloh M, Elfering A, et al. Predicting the transition from acute to persistent low back pain. Occup Med (Lond) 2011;61:127-131.
6. Romero A, Rojas S, et al. A ¹⁸F-fluorodeoxyglucose MicroPET imaging study to assess changes in brain glucose metabolism in a rat model of surgery-induced latent pain sensitization. Anesthesiology 2011;115:1072-1083.
7. Kehlet H, Jensen TS, et al. Persistent postsurgical pain: risk factors and prevention. Lancet 2006;367:1618-1625.
8. Shipton EA. The transition from acute to chronic post surgical pain. Anesth Intensive Care 2011;39:824-836.
9. Lavand’homme P. The progression from acute to chronic pain. Curr Opin Anaesthesiol 2011;24:545-550.
10. Weinbroum AA. Non-opioid IV adjuvants in the perioperative period: pharmacological and clinical aspects of ketamine and gabapentinoids. Pharmacol Res 2012;65:411-429.
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