Chronic pain after groin hernia repair

Since recurrence rates have been reduced to a few per cent with mesh repairs, outcome research in groin hernia repair has recently focused on chronic pain. Chronic pain adversely affects daily life for 5–10 per cent of patients1, and pain-related sexual dysfunction, including dysejaculation, occurs in about 2 per cent of young men2. Unfortunately, reports have used different methods of assessment, which hinders firm conclusions regarding pathogenesis, social consequences and treatment strategies. Recently, a sub-grouping of these patients has been proposed into neuropathic and somatic pain states3. This methodology, however, is questionable since the definition of neuropathic pain in other chronic pain conditions is unspecific except for requiring a nerve lesion. Sensory disturbances are apparent in many patients after groin hernia repair without chronic pain4 and so hypoesthesia and hypoalgesia have a low sensitivity in diagnosing chronic neuropathic pain. It is, however, plausible that nerve damage is a prerequisite for developing a chronic pain state1. Techniques such as magnetic resonance imaging, computed tomography and ultrasonography are required for a more detailed assessment to allow a more specific diagnosis and classification, and to exclude a recurrence. The main consideration for future research on the pathogenesis and treatment of chronic postherniorrhaphy pain is the role of patient-related factors versus surgeryrelated factors. Several studies have demonstrated preoperative pain, young age, pain at other sites of the body and psychosocial features to be predictive risk factors for postoperative pain1. In addition, recent genotype characterization has suggested that COMT genes are important for pain sensitivity1 and GTPcyclohydrolase is known to affect pain sensitivity and pain-related outcome after spinal surgery5. These findings emphasize the role of preoperative characteristics of the nociceptive system in the development of a chronic postoperative pain state. They may also help us to understand why the intensity of acute pain after herniorrhaphy is related to the risk of developing chronic postoperative pain1. Studies have also shown that preoperative pain response to a nociceptive stimulus correlates with the intensity of early postoperative pain1, again emphasizing the importance of the preoperative functional status of the nociceptive system. Clearly, large, well-defined, prospective studies that include all of the above variables of preoperative pain and psychosocial characteristics are needed to allow a proper understanding of the role of patient-related risk factors for the development of chronic post-herniorrhaphy pain. Most research on chronic postoperative pain has focused on factors related to surgical technique, such as nerve-handling (identification/preservation versus transection). However, the data so far are inconclusive, except for suggesting that nerve identification, presumably because it is associated with less neurological trauma, may reduce the risk of chronic pain6. However, it is noteworthy that nerve transection studies have focused on one nerve (iliohypogastric or ilioinguinal), despite all three nerves in the surgical field (iliohypogastric, ilioinguinal and genitofemoral) being at risk of injury. Clearly, the future studies referred to in the previous paragraph must also contain a welldesigned technical component if we are to understand the relationship of nerve handling to chronic postoperative pain1,4. Consideration must also be given to surgical expertise because many hernia centres claim very low incidences of chronic pain. Interpretation of such claims has so far been hindered by insufficient followup and lack of independent observation. Future studies require a complete and detailed follow-up, comparing technically experienced ‘‘centres of excellence’’ with results from regular general surgical activity. Nerve injury might be reduced by surgical expertise. The laparoscopic approach might reduce the risk of chronic pain1. However, most studies have been of poor design, lacking any assessment of preoperative risk factors or detailed appraisal of the intensity and consequences of the chronic pain state, including a full assessment of nerve damage. It has recently been claimed that the technique of mesh fixation is important7, as the use of staplers and tags is more likely to cause nerve injury than glue or no fixation at all. Non-fixation mesh techniques may also reduce the risk of chronic pain after open surgery, possibly by reducing nerve damage. These items again call for large-scale, welldesigned studies that include assessment of preoperative risk factors and