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Inguinal hernia is a common pathology, occurring in approximately 27% of men and 3% of women throughout their lives. Worldwide, operative repair of inguinal hernia is performed an estimated 20 million times annually. With the widespread adoption of tension-free, mesh-based techniques, and an ever-increasing variety of approaches to repairing inguinal hernias, recurrence rates have been reduced dramatically. The most significant morbidity still plaguing inguinal hernia repair is chronic postoperative inguinodynia, defined as pain that persists or arises after resolution of the acute postoperative inflammatory process and mesh integration following hernia repair (at least 3–6 months). Chronic, clinically significant discomfort or pain occurs in approximately 10%–12% of patients undergoing inguinal hernia repair, and activities of daily living are impacted in 0.5%–6.0%. Given the high prevalence of inguinal hernia, this accounts for up to 48,000 new cases of chronic post-herniorrhaphy inguinodynia in the United States annually. The affected patients may experience restricted activity, limited productivity, increased healthcare costs, and decreased quality of life.
Chronic post-herniorrhaphy inguinodynia may occur from varied causes, with numerous pain mechanisms including somatic, visceral, nociceptive, and neuropathic etiologies. Contributing factors may include inguinal nerve injury or entrapment, local inflammation, neuroma, meshoma, and hernia recurrence. These etiologies rarely occur individually and more commonly present as a complex combination of pain types, which increase diagnostic uncertainty and make treatment challenging. Neuropathic pain after inguinal hernia repair may result from direct injury or trauma to the inguinal nerves or from postoperative inflammation and scarring. The common manifestations of neuropathic inguinodynia include pain and sensory perturbations in the dermatomal distribution innervated by the inguinal nerves. Hyperalgesia, hyperesthesia, dysesthesia, hypoesthesia, and allodynia may be present. Concurrent associated syndromes include psychological and affective disorders such as depression, anxiety, cognitive impairment, and sleep deprivation.
The nerves of the groin may incur damage during hernia repair or in the postoperative period. Intraoperative trauma may arise from manipulation, over-dissection, stretching, crushing, transection, electrical or thermal contact, or fixation or entrapment in suture or mesh. While several common repairs have been standardized and optimized to maximize outcomes, there is no inguinal hernia repair technique that is immune to the development of chronic post-herniorrhaphy inguinodynia, and this pathology must therefore remain a consideration for any surgeon performing repairs. , , The nerves susceptible to injury depend on the approach, location, and prosthetic used for the repair. Inguinal herniorrhaphy performed via an anterior open approach results in direct exposure of the inguinal nerves as they course through the operative field. Posterior approaches, whether performed by a minimally invasive or open preperitoneal technique, render susceptible the preperitoneal and retroperitoneal nerves found within the “triangle of pain.” Minimally invasive approaches may also indirectly expose the inguinal nerves traversing the abdominal wall musculature to injury by fixating tacks or suture. In the postoperative period, nerve injury may occur due to inflammation, infection, recurrence, formation of perineural scar tissue, entrapment in a meshoma, or formation of a granuloma or neuroma ( Fig. 9.1 ).
Successful management of chronic post-herniorrhaphy inguinodynia requires a thorough understanding of the causative factors involved, neuroanatomy of the groin and abdominal wall, and technical details of the initial hernia repair. Only through careful analysis of these factors can the optimal medical and operative treatment strategy be determined. Effective management of chronic post-herniorrhaphy inguinodynia is paramount, given its dramatic effects on quality of life, productivity, and healthcare utilization.
The inguinal canals are passages that traverse the abdominal wall on both sides of the lower abdomen. Their course runs in an oblique inferomedial direction immediately superior and parallel to the inguinal ligament. The pathway created by the canal allows the passage of structures from the intra-abdominal cavity to the external genitalia obliquely through the layers of the abdominal wall musculature. The inguinal canal comprises two openings: the deep or internal ring located at the midpoint of the inguinal ligament, and the superficial or external ring, located over the superior aspect of the pubic tubercle. The anterior wall of the inguinal canal is the external oblique aponeurosis, which is reinforced by the internal oblique muscle laterally. The posterior wall is composed of conjoint tendon medially and transversalis fascia laterally. The roof of the canal includes fibers of the transversalis fascia, internal oblique, and transversus abdominis muscles. The floor is made up of the inguinal ligament, which is reinforced by the lacunar ligament along its medial aspect.
In males, the inguinal canal contains the spermatic cord (vas deferens, spermatic and cremasteric arteries and veins, and the genital branch of the genitofemoral nerve [GFN]) enveloped in the cremasteric muscle and the ilioinguinal nerve (IIN), which typically courses anterior to the spermatic cord. In females, the canal is narrower and contains only the round ligament of the uterus, the genital branch of the GFN, and the IIN. Because the inguinal canal represents an anatomic passage through the abdominal wall, it is an area of natural weakness and is subject to wear and loss of tissue strength and integrity over time. For this reason, it is a common site for the formation of hernias.
The inguinal nerves that may be implicated in neuropathic chronic post-herniorrhaphy pain are the iliohypogastric nerve (IHN), IIN, genital branch, femoral branch, or common trunk of the GFN, lateral femoral cutaneous nerve (LFCN), and femoral nerve. While certain anatomical characteristics of these nerves are relatively predictable, such as entry into the inguinal canal and terminal dermatomal distribution, the course of these nerves remains highly variable. Additionally, aberrant anatomy is common, including duplicated, shared, cross-innervated, or absent nerves. , Understanding the anatomy of these nerves is crucial to avoiding injury during inguinal hernia repair and to successful surgical remediation for chronic post-herniorrhaphy pain.
The lumbosacral plexus innervates the pelvis and lower extremities and provides the autonomic visceral innervation to the pelvic organs. The lumbosacral plexus comprises four individual plexuses: the lumbar, sacral, pudendal, and coccygeal plexuses. The lumbar plexus is formed by the merging of the anterior primary divisions of the lumbar nerves and includes overlap from the adjacent nerve roots and plexuses. It serves as the nerve supply to the lower abdomen, inguinal region, and upper thigh. Classically, the lumbar plexus originates from the anterior rami of L1-L3, with partial contribution from L4 and the subcostal nerve (T12). The resulting variability and cross-innervation cause significant overlap in nerve distribution rather than a purely segmental innervation pattern. The lumbar plexus resides in the posterior abdominal wall, anterior to the transverse processes of the lumbar spine, and posterior to or within the psoas muscle.
The lumbar plexus has many branches, any of which may be injured or irritated during inguinal hernia repair ( Fig. 9.2 ). Anterior inguinal hernia repairs, such as the Lichtenstein or Shouldice repairs, directly expose the IHN, IIN, and genital branch of the GFN, placing these nerves most at risk. It is possible to injure the femoral branch or common trunk of the GFN, the LFCN, or the femoral nerve with the use of anterior fixation that penetrates into deeper tissue. Similarly, the nerves most at risk during posterior repairs are the nerves found in the “triangle of pain,” namely the GFN and its branches and the LFCN. The obturator nerve and femoral nerve also course through the preperitoneal plane and infrequently may be at risk with these repairs. Although not directly exposed, the IHN and IIN can likewise be injured during a posterior repair with penetrating fixation. Therefore, the best means of preventing injury to these nerves is to understand their likely location and course and to be aware of potential sites and mechanisms of injury. ,
The IHN has both sensory and motor function. It arises from the ventral ramus of L1 at the superolateral border of the psoas major. , The course of the IHN runs anterior to the quadratus lumborum muscle, posterior to the lower pole of the kidney, and penetrates the posterior aspect of the transversus abdominus muscle superior to the iliac crest. From there, it courses between the transversus abdominus and internal oblique muscle layers, where it splits into two cutaneous branches, the lateral and anterior. The lateral cutaneous branch runs between the internal and external oblique muscles and terminally innervates the skin of the posterolateral gluteal region. The anterior cutaneous branch courses anteriorly in the plane between the transversus abdominus and internal oblique and provides the innervation to both of these muscles. The IHN exits through the internal oblique muscle at an area typically a few centimeters anterior to the anterior superior iliac spine, traverses in an inferomedial direction through the inguinal canal for a short distance before passing through the cleavage plane between the internal and external oblique muscles, and ultimately penetrates anteriorly through the external oblique. The terminal branches of the anterior cutaneous branch provide sensory innervation to the skin of the medial suprapubic region.
There is significant variation in the composition and course of the IHN ( Fig. 9.3 ). In addition to its primary contributions from L1, it may receive fibers from the subcostal nerve (T12). It may have overlap or give off branches that join the subcostal nerve or IIN. The midportion of the nerve’s course on the anterior surface of the quadratus lumborum muscle is a relatively consistent location at which to identify the nerve. The distal IHN is again subject to significant anatomic variability. The IHN and IIN may travel as a common trunk for part or all of their length; this has been reported in approximately 22% of subjects. The inguinal portion of the IHN may be duplicated, appearing as two or three terminal branches in approximately 17% of cases. Alternatively, the inguinal segment of the IHN may be absent in up to 20% of patients.
The IHN may suffer direct injury during anterior approaches, especially if the nerve is not identified. From a posterior approach, it may be injured along its course within the layers of the abdominal wall by penetrating fixation material ( Fig. 9.4 ). Injury to the retroperitoneal portion of the IHN is uncommon with inguinal repair, as this lies superolateral to the operative field during both anterior and posterior repairs.
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