How can pain persist after mesh removal?


Serious hernia mesh pain persists in 25% of patients after mesh removal. No treatment helps this persistent pain. This is why hernia mesh pain is such a serious complication of mesh hernia repair.

The term neuropathic pain is commonly misused by hernia surgeons describing groin pain associated with hernia mesh. The correct usage of neuropathic pain is any pain that is not nociceptive, that is, due to direct stimulation of pain receptors (nociceptors). This includes Central Pain Sensitization and Peripheral Neuropathy.

Central pain sensitization is an underappreciated form of neuropathic pain. It is the key feature of all chronic pain. Clinically it can be identified by unique symptoms of allodynia, hyperalgesia and widening of the pain field. It is resistance to narcotic pain medication and neurectomy.

Neuromas are not pain generators per se. They are sensitive to mechanical and chemical stress and will cause pain if unprotected. In limb amputation surgery retraction and high division of the nerves, burying them in the muscle is done. This does not prevent neuroma formation but it keeps them asymptomatic by protecting them from mechanical stress.

Patients with hernia mesh pain typically have mixed central pain sensitization, peripheral neuropathic pain and nociceptive pain. Hernia mesh causes chronic inflammation which stimulates nociceptors and damages nerves and leads to central pain sensitization.

The primary lesion in mesh associated groin pain is chronic inflammation. It is not the tacks. Removing mesh removes the primary source of the pain but the pain may persist because of central sensitization and peripheral neuropathy. Neurectomy may relieve the pain of peripheral neuropathy but does nothing for and may worsen central pain sensitization.

There is condition known as Complex Regional Pain Syndrome (CRPS) Type 1 and Type 2 where nerve trauma leads to severe and disabling pain of an entire limb. In type 1 the injury is relatively minor with no visible evidence of injury. Type 2 has visible evidence of the nerve injury. Type 1 responds to ketamine infusion therapy indicating the dominant role of central pain sensitization. Many cases of CRPS simply get better over time.

It is my guess that pain persists after mesh removal in some patients because of central pain sensitization. Different patients have different susceptibility to central pain sensitization and this may explain why the vast majority of patients with hernia mesh do not develop chronic pain to begin with. In persistence of pain after mesh removal peripheral neuropathy may play some role but I do not believe it is the primary lesion.


Central pain

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