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Table of Contents
REVIEW ARTICLE
Year : 2018  |  Volume : 1  |  Issue : 1  |  Page : 1-8

Inguinal neuroanatomy: Implications for prevention of chronic postinguinal hernia pain


Department of Surgery, Lichtenstein Amid Hernia Clinic, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

Date of Submission06-May-2018
Date of Acceptance09-May-2018
Date of Web Publication16-May-2018

Correspondence Address:
David C Chen
Lichtenstein Amid Hernia Clinic, David Geffen School of Medicine at UCLA, Los Angeles, CA
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijawhs.ijawhs_6_18

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  Abstract 


Inguinal hernia repairs represent one of the most common general surgery operations worldwide. Advances in the understanding of groin anatomy, operative technique, and prosthetics have improved the efficacy of these repairs with overall low recurrence rates and favorable outcomes. Chronic postherniorrhaphy inguinal pain has arguably become the most important and most frequent complication of inguinal hernia repair, with significant impact on patients' quality of life. Neuropathic inguinodynia may be caused by direct nerve injury, manipulation, entrapment, scarring, and interaction with mesh. Development of chronic postinguinal hernia repair pain is independent of the method of hernia repair as all inguinal hernia repair techniques may potentially cause injury. Understanding the neuroanatomy of the inguinal canal and the potential mechanisms for injury leads to lower rates of nerve injury and chronic pain and helps to guide prevention and treatment of inguinodynia. In this article, the neuroanatomy of the anterior inguinal canal and the prevention of nerve injury are addressed.

Keywords: Chronic postherniorrhaphy inguinal pain, inguinal neuroanatomy, inguinodynia


How to cite this article:
Graham DS, MacQueen IT, Chen DC. Inguinal neuroanatomy: Implications for prevention of chronic postinguinal hernia pain. Int J Abdom Wall Hernia Surg 2018;1:1-8

How to cite this URL:
Graham DS, MacQueen IT, Chen DC. Inguinal neuroanatomy: Implications for prevention of chronic postinguinal hernia pain. Int J Abdom Wall Hernia Surg [serial online] 2018 [cited 2021 Apr 20];1:1-8. Available from: http://www.herniasurgeryjournal.org/text.asp?2018/1/1/1/232497




  Introduction Top


Inguinal hernias are common with lifetime occurrence of 27% for men and 3% for women.[1] An estimated 20 million inguinal hernia repairs are performed each year worldwide. While most hernia repairs are performed with excellent outcomes and minimal morbidity, a small percentage of patients experience postoperative discomfort and pain that limit their activity and productivity, increase health care utilization, and diminish quality of life with both individual and societal ramifications.[2],[3],[4],[5] Chronic postherniorrhaphy inguinal pain (CPIP) is defined as pain persisting or arising at least 3–6 months following the index hernia operation after resolution of the acute postoperative inflammatory processes and mesh integration.[5] The estimated risk of chronic moderate-to-severe pain following inguinal hernia repair is 10%–12%, with pain affecting activities of daily life estimated to be 0.5%–6%.[2] Given the high burden of disease, even a low-frequency complication of inguinal hernia repair has a significant impact, resulting in 4000–48,000 new cases of CPIP each year in the US alone.[2],[3],[4],[5]

There are several etiologies of CPIP, including somatic, visceral, nociceptive, and neuropathic causes. Hernia recurrence, tissue inflammation, meshoma, and inguinal nerve injury or entrapment may all lead to CPIP. There is a significant overlap between these types of pain confounding both diagnosis and treatment. Neuropathic pain in CPIP is caused by damage to, trauma to, or scarring of the inguinal nerves. This typically manifests as pain and/or sensory disturbances in the dermatomal distribution of these nerves with negative sensory phenomena, dysesthesia, hyperesthesia, hypoesthesia, allodynia, or hyperalgesia. Although uncommon, affecting only a small subset of the CPIP population, severe chronic pain is a devastating complication and arguably a distinct neurologic disease entity.[6] In addition to pain, associated psychologic and affective disorders including depression, anxiety, cognitive impairment, somatic manifestations, and sleep deprivation exacerbate patients' subjective suffering.[7],[8],[9]

Injury or damage to the inguinal nerves may occur intraoperatively or postoperatively. Intraoperatively, surgical manipulation, overdissection, stretching, electrical or thermal damage, crushing, partial or complete transection, or fixation or entrapment in suture may damage the nerves. The susceptible nerves and mechanisms of injury will vary by repair type and location. Anterior tissue and mesh-based inguinal hernia repairs directly expose to the inguinal nerves as they traverse the same anatomic planes and operative field of the repair. Posterior minimally invasive approaches indirectly expose to the inguinal nerves which may be injured within the inguinal canal with the use of penetrating fixation with tacking devices and sutures or with overdissection of the retroperitoneal nerve structures found within the “triangle of pain” in the lateral preperitoneal space. Postoperatively, the nerves may become injured due to perineural scarring, irritation from excess fibrosis, entrapment in meshoma, inflammation, infection, recurrence, or granuloma/neuroma formation.

The inguinal nerves that are potentially affected in CPIP are iliohypogastric nerve (IHN), ilioinguinal nerve (IIN), and genital branch of the genitofemoral nerve (GFN) within the inguinal canal [Figure 1] and the GFN trunk and its femoral branch, lateral femoral cutaneous (LFC) nerve, and femoral nerve (FN) in the preperitoneal space [Figure 2].[10],[11],[12] There is a significant variation in the course of these nerves, and aberrant anatomy with shared, duplicated, cross-innervated, or absent nerves is common. While entry into inguinal canal and termination at their dermatomal distribution are relatively predictable, the individual pathways of these nerves are highly variable.[10],[12]
Figure 1: Neuroanatomy of the anterior inguinal canal

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Figure 2: Inguinal retroperitoneal neuroanatomy: IHN = Iliohypogastric nerve, IIN = Ilioinguinal nerve, GFN = Genitofemoral nerve. Courtesy of Reinpold et al.

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Given this anatomic complexity, placing nerves at risk or injuring nerves in inguinal hernia repair can never be completely avoided, which contributes to the clinical development of neuropathic CPIP. Despite this challenge, an in-depth understanding of the neuroanatomy of the inguinal canal and the potential mechanisms of nerve injury with each type of inguinal hernia operation significantly decreases the risk of nerve injury and the development of CPIP.[2],[5],[11],[12] Three-nerve identification in open inguinal surgery, however, is practiced by a minority of surgeons performing hernia repair. Multiple studies have shown that nerve identification can be simply, safely, and expeditiously performed.[5],[11] Directed review of the relevant neuroanatomy of inguinal hernia repairs quickly improved surgeons' ability to consistently identify the inguinal nerves and avoid subsequent injury.[13] This strategy of “nerve mindfulness” helps to avoid preventable nerve injury and will decrease an individual surgeon's personal rate of CPIP in their patient population.


  Anatomy of the Inguinal Canal Top


The inguinal canals are short pathways on each side of the lower abdomen that run cephalad and parallel to the inguinal ligament. The canals extend inferomedially allowing structures to pass obliquely through the layers of the abdominal wall from the intra-abdominal cavity to the external genitalia. The contents of the inguinal canal in males include the spermatic cord passing to the testes (including the vas deferens, spermatic and cremasteric arteries and veins, and the genital branch of the GFN enveloped in the cremasteric muscle) and the IIN and IHN. In females, the canal is narrower and contains the round ligament of the uterus which attaches to the labia majora, the accompanying genital branch of the GFN, and the IIN and IHN.

The inguinal canal is defined by two openings with a deep internal ring found at the midpoint of the inguinal ligament and a superficial external ring which lies just superior to the pubic tubercle. The posterior wall of the inguinal canal is defined by the transversalis fascia laterally and the conjoint tendon medially. The anterior wall is comprised of external oblique aponeurosis reinforced by the internal oblique muscle laterally. The roof of the canal includes the transversalis fascia, internal oblique, and transversus abdominis muscles. The floor is comprised of the inguinal ligament which is medially reinforced by the lacunar ligament. As a natural orifice that passes through the abdominal wall, the inguinal canal represents a potential site of weakness and clinically is a common site of hernia formation.


  Neuroanatomy of the Inguinal Canal Top


The lumbar plexus

The lumbosacral plexus provides the nerve supply for the pelvis and lower extremities as well as the autonomic visceral innervation to the pelvic organs. This is subdivided into four parts: lumbar, sacral, pudendal, and coccygeal plexuses. The lumbar plexus which innervates the lower abdomen, inguinal region, and upper thigh is formed by the union of the anterior primary divisions of the lumbar nerves with overlap from the adjacent nerve roots and plexuses. Typically, the anterior rami of the first three lumbar nerves coalesce to form the plexus along with part of the fourth lumbar nerve and frequently a communicating branch from the subcostal (T12) nerve. This variability and cross-innervation leads to overlapping areas of nerve distribution rather than a typical segmental innervation.[14] The lumbar plexus is located in the posterior abdominal wall in front of the transverse processes of the lumbar vertebrae and posterior to or within the psoas muscle.

All branches of the lumbar plexus may be affected by inguinal hernia repairs, but the IHN, IIN, and GFN are at most risk within the inguinal canal due to direct exposure with anterior repairs. The LFC nerve and genitofemoral trunk traverse the preperitoneal plane and are most at risk with posterior repairs. The obturator nerve and FN may infrequently be injured along their course in the preperitoneal plane. Any portion of an inguinal hernia repair that penetrates the posterior boundary of the inguinal canal either from above or below can injure the nerves within the adjacent compartment. The inguinal nerves can be injured with posterior repairs using penetrating fixation, while the genitofemoral trunk and FN can be injured or entrapped with anterior fixation that penetrates too deeply. Understanding the likely location and course of these nerves, as well as the potential sites, and mechanisms of injury of these nerves helps to prevent these technical injuries during hernia repair.[5],[12]

Iliohypogastric nerve

The IHN is a mixed sensorimotor nerve and originates from the ventral ramus of L1 emerging from the upper lateral border of the psoas major.[12],[14] It travels over the quadratus lumborum muscle behind the lower renal pole and then enters the posterior part of the transversus abdominus muscle above the iliac crest. Between the transversus and internal oblique muscles, the IHN divides into a lateral and an anterior cutaneous branch. The lateral branch travels between the internal and external oblique muscles above the iliac crest and innervates the posterolateral gluteal skin. The anterior cutaneous branch runs between the transversus and internal oblique innervating both of these muscles. Approximately 2 cm medial to the anterior superior iliac spine (ASIS), the IHN exits the internal oblique muscle and passes inferomedially within the inguinal canal before exiting through the external oblique. It exits approximately 3 cm above the superficial external ring at the conjoined tendon, within the cleavage plane between the internal and external oblique.[11],[12],[14] This branch provides sensation to the medial suprapubic skin.

There is a significant variation in the IHN course from its origin at the L1 nerve root to its terminus in the dermatomal distribution of the suprapubic skin [Figure 3]. This anatomic variability increases as the nerve travels distally. The IHN may receive input from T12 and may give branches to the subcostal nerve and IIN. In a study from Anloague and Huijbregts, 20.6% of lumbar plexuses had an absent IHN.[14] Al-Dabbagh reported a common trunk of the IHN and IIN in 21.8% of cases.[16] The IHN may be replaced by the IIN and its entry into the inguinal canal is variable. In a study of the bilateral lumbar plexuses of 30 cadavers, Reinpold et al. found that the IHN is most consistent on the anterior surface of the quadratus lumborum.[12] The iliohypogastric entered the abdominal wall above the iliac crest in the majority of cases with considerable variation in the site of entry.[12] Within the inguinal canal, the course of IHN varies considerably [Figure 4]. In a study of anterior inguinal neuroanatomy, Wijsmuller et al. found that 89% of the time, the IHN could be identified entering lateral to the incision passing through the entire inguinal canal. In 11% of patients, the IHN entered the canal medially and ran a subaponeurotic course with variable entry into the canal. 17% of the time, there were two or three branches of the inguinal portion of the IHN [Figure 4]b.[11]
Figure 3: Anatomic variation of the upper lumbar plexus – iliohypogastric and ilioinguinal nerves: (a) Two separate trunks. (b) Two trunks bifurcate at L1. (c) Common trunk. (d) Adjacent but separate trunk

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Figure 4: Anterior inguinal nerves. (a) Iliohypogastric nerve entrapped by anterior mesh. (b) IHN with duplicated branches passing to conjoined tendon (mesh folded medially). (c) Ilioinguinal nerve entrapped by mesh cephalad and lateral to internal ring near anterior superior iliac spine. (d) Genitofemoral nerve in preperitoneal space below split floor of inguinal canal (cephalad to internal ring)

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Given the highly variable nature and course of the IHN and its course, injury to the IHN is common especially if the course of the nerve is not identified. The mechanism of injury to the IHN in inguinal hernia repair is primarily within the inguinal canal [Figure 4].[2],[11],[16] The retroperitoneal course of the IHN is cephalad and lateral outside the field of both open anterior and posterior minimally invasive approaches. The inguinal segment, however, may be injured with both anterior and posterior inguinal hernia repairs. In anterior tissue based (Bassini, McVay, Shouldice) repairs, the inguinal portion of the nerve may be injured by dissection, traction, thermal or electric injury, inflammatory scarring, or entrapment by suture [Figure 4]a. In anterior (Lichtenstein) and open posterior (transinguinal preperitoneal [TIPP] and variations) mesh-based repairs, injury from mesh fixation, entrapment from mesh folding or meshoma, or inflammation and scarring from mesh integration may occur in addition to these mechanisms of injury. In minimally invasive laparoscopic and robotic inguinal hernia repair, the IHN is only at risk with penetrating fixation passing through the transversalis fascia, which can lead to injury, entrapment, or division of the nerve [Figure 5].
Figure 5: Injury to inguinal nerves from posterior mesh fixation: (a) Folded and tacked preperitoneal mesh. (b) Preperitoneal dissection with mesh and tacks. (c) Open dissection with tack penetrating ilioinguinal nerve through floor of inguinal canal. (d) Mesh and tack capturing ilioinguinal nerve

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Ilioinguinal nerve

The IIN is a mixed sensorimotor nerve arising from the first ventral lumbar ramus. It is typically smaller than the IHN and emerges from the superolateral border of the psoas muscle with or inferior to the IHN [Figure 3]. The IIN then travels over the quadratus muscle and upper part of the iliacus and enters the transversus abdominus muscle near the iliac crest.[12] The IIN at this point may reconnect with the IHN. The nerve innervates the internal oblique muscle and then pierces it lower than the iliohypogastric approximately 1 cm medial to the ASIS [Figure 4]c. There is considerable variability of the IIN in the inguinal canal, but the nerve will typically travel over the spermatic cord, exiting with the cord through the superficial external inguinal ring to supply the proximal medial skin of the thigh, inguinal crease, upper scrotum, and lateral base of the penis in males.[11],[16] In females, the IIN innervates the skin covering the medial thigh, mons pubis, and labia majora.

Similar to the IHN, there is a significant variation in the IIN from its origin at the L1 nerve root to its terminus in the suprapubic skin.[11],[12],[14] This anatomic variability increases as the nerve travels distally with multiple different potential pathways through or outside of the inguinal canal. The IIN may be duplicated or absent and will frequently be replaced, cross-innervated, or reconnected with the IHN. It may arise or receive accessory input from T12. It may terminate near the ASIS and then reconstitute with the IHN within the canal. It may be replaced by the IHN, GFN, or LFC. The IIN and IHN may arise as a common trunk in the retroperitoneum or anywhere along its course.[11],[12],[16] Reinpold et al. described that the course of the IIN from its exit at L1 passing over the quadratus is fairly consistent, but the entry point into the abdominal wall has great variability entering either above or below the iliac crest and lateral to the ASIS.[12] Wijsmuller et al. described the significant variability within the inguinal portion of the IIN.[11] In 60% of cases, the IIN lies ventral to the spermatic cord. Alternatively, it may travel posterior to, parallel to, or within the spermatic cord and may exist anywhere within the inguinal canal before piercing the external oblique aponeurosis.[11] Rab et al. found the IIN following an aberrant course in 43.7% of cases, illustrating the ubiquity of neuroanatomic variation.[10]

As with the IHN, the highly variable nature of the IIN increases the risk of injury, especially if the course of the nerve is not identified. During inguinal hernia repair, the IIN is most frequently injured within the inguinal canal.[10],[11],[12] The retroperitoneal course of the IIN is cephalad and lateral outside the field of both open anterior and minimally invasive posterior approaches. The inguinal segment of the IIN, however, may be injured with both anterior and posterior inguinal hernia repairs. In anterior tissue based (Bassini, McVay, Shouldice) repairs, the inguinal nerve may be injured by dissection, traction, thermal or electric injury, inflammatory scarring, or entrapment by suture. In anterior (Lichtenstein) and open posterior (TIPP and variations) mesh-based repairs, injury from mesh fixation, entrapment from mesh folding or meshoma, or inflammation and scarring from mesh integration may occur along with these mechanisms of injury.[2],[5] Similar to the IHN, in minimally invasive laparoscopic and robotic inguinal hernia repair, the IIN is only at risk with penetrating fixation passing through the transversalis fascia injuring, entrapping, or dividing the nerve [Figure 5].

Genitofemoral nerve

The GFN is a mixed sensorimotor nerve originating from the L1 and L2 ventral rami and forms within the psoas muscle [Figure 6]. It descends within the muscle and emerges on its medial border between the L3 and L4 level. It descends below the peritoneum overlying the psoas muscle, passes posterior to the ureter, and travels toward the inguinal ligament. The bifurcation into the genital and femoral branches ranges from separate genital and femoral trunks exiting the psoas muscle to a shared trunk continuing to the level of the inguinal ligament.[12],[16] The genital branch will typically pass over the external iliac artery and traverse the deep internal inguinal ring to join the cord structures or round ligament before entering the inguinal canal. In males, it provides motor innervation to the cremasters and sensation to the skin of the upper scrotum. In females, the genital nerve follows the round ligament and innervates the skin of the mons pubis and labia majora. The femoral branch descends lateral to the cord structures and iliac vessels passing underneath the inguinal ligament. It enters the femoral sheath lateral to the femoral artery and then pierces the femoral sheath and fascia lata to supply the skin of the upper anterior thigh over the femoral triangle.[12],[16]
Figure 6: Genitofemoral nerve: (a) Laparoscopic view of genitofemoral nerve over psoas muscle. (b) Open extended approach to genitofemoral nerve over psoas muscle. (c) Genital branch trapped by mesh plug with vas deferens. (d) Genitofemoral nerve Trapped by lap mesh at internal ring

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The variability of the GFN has been well documented in several anatomic studies, and the GFN is considered to be the most variable of the lumbar plexus nerves.[10],[12],[15] The GFN may arise from the lumbar plexus as completely separate genital and femoral branches. It occasionally may arise from L3. The GFN or either of its branches may be entirely absent with the genital branch being replaced by the IIN and the femoral branch covered by the anterior FN or LFC nerve.[16] Multiple genital and femoral branches of the GFN are common. Aasar studied 200 cadavers reporting a single trunk in 80% of cases.[15] Anloague reported an aberrant GFN course in 47.1% of cases. Reinpold et al. reported that genital branch entry into the inguinal canal and femoral branch passage into the lateral thigh is highly variable and could be classified only into relatively predictable ranges.[12] While the course of the GFN trunk and the genital nerve is highly variable in the retroperitoneal and preperitoneal spaces, the inguinal portion is quite consistent with almost uniform passage within the spermatic cord.[11] While the site of entry into the canal may slightly differ, the course through the canal is much more predictable.[11] Rab et al. reported that no genital nerve was identified in 28.1% of cases while Reinpold et al. reported that the genital branch could be identified in the spermatic cord in 97% of cases.[10],[12] This was confirmed in 100% of cases in Wijsmuller et al.'s study all with pathologic confirmation.[11]

Injury to the genital branch or femoral branch of the GFN in the preperitoneal space may occur after open preperitoneal (TIPP, bilayer mesh, plug and patch, plug) [Figure 6]c and laparoscopic preperitoneal repair due to overdissection of the lateral triangle of pain, thermal/electric injury, traction, irritation or scarring from mesh, entrapment within meshoma, or damage from fixation sutures or tacks [Figure 6]d. In open anterior tissue (Bassini, Shouldice, McVay) or mesh (Lichtenstein) repair, the genital nerve may be inadvertently injured by stripping the cremaster, disrupting the spermatic cord, overdissecting the cord structures, contacting the nerve with mesh, strangling the cord with a tight mesh internal ring, or through mesh folding, contraction, or meshoma formation.[5] In open anterior tissue or mesh repair, the femoral branch of the GFN is rarely at risk but may be injured with deep lateral suture fixation to the inguinal ligament used to suture the floor in tissue-based operations or the mesh to the inguinal ligament in anterior-based mesh repairs.

Lateral femoral cutaneous nerve

The LFC nerve is a purely sensory nerve with wide variability in its origin and course. It usually originates from the posterior division of second and third lumbar nerve roots but may also arise from a high L1/L2 or low L3/L4 origin. It may alternatively arise directly from the FN or from an independent branch from the lumbar plexus.[12],[14],[16] The nerve emerges from the lateral border of the psoas below the iliac crest and passes behind the peritoneum over the iliacus muscle obliquely toward the ASIS. It supplies sensory fibers to the parietal peritoneum in the iliac fossa. The nerve then passes behind or through the inguinal ligament approximately 1 cm medial to the ASIS halfway between the ASIS and femoral artery.[12],[16] The LFC then travels anterior to or through the sartorius muscle before dividing into anterior and posterior superficial branches. The anterior branch supplies the anterior and lateral thigh to the level of the knee and joins the peripatellar plexus. The posterior branch pierces the fascia lata higher than the anterior branch and divides to innervate the skin on the lateral thigh surface from the greater trochanter to the mid-thigh with occasional extension to the gluteal skin.[14],[16]

The LFC nerve, which is a purely sensory nerve, is highly variable with absent, duplicated, or numerous branches and significant cross-innervation [Figure 7]. Anloague reported aberrant anatomy in 17.6% of cases with variants arising from different nerve roots, bifurcation over the iliacus, and multiple branches.[14],[17] Bifurcation distal to the pelvis is very common. de Ridder et al. studied 200 cadavers and found that 51 (25.5%) demonstrated an abnormal anatomic course.[17]
Figure 7: Lateral femoral cutaneous nerve (3 branches) passing lateral to psoas muscle over iliacus. Genitofemoral nerve trunk over psoas

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Although there is considerable variability, LFC injury is uncommon during inguinal hernia repair and the LFC nerve is typically only at risk during posterior inguinal hernia repair approaches. Overdissection of the lateral compartment, thermal/electrical injury, mesh irritation/inflammation/entrapment, and fixation below the iliopubic tract with suture or tacks may injure the LFC as it crosses the iliacus lateral to the psoas [Figure 7]. In anterior inguinal repairs, the LFC is typically not at risk as it traverses cephalad and lateral to the operative field.

Femoral nerve

The FN is a mixed sensorimotor nerve and originates from the L2 to L4 ventral rami. It is located lateral to the psoas muscle and travels in the cleavage plane between the psoas and iliacus muscles [Figure 8]. It pierces the iliacus muscle and is covered by the iliac fascia separating it from the iliac vessels. It gives off branches to supply the iliacus and pectineus muscle and then is positioned lateral to the femoral artery and vein as it continues below the inguinal ligament.[14] The anterior division has two sensory branches that supplies the anteromedial thigh and two motor branches that supply the pectineus and sartorius muscles. The posterior division gives off a sensory branch, saphenous nerve, and motor branches to the quadriceps muscle with branches to the hip and knee joint.[14]
Figure 8: Femoral nerve passing lateral to psoas in groove between psoas and iliacus. Genitofemoral nerve on anterior surface of psoas muscle

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In one anatomic study, variations of the FN were demonstrated in 35% of lumbar plexuses.[14] The anterior cutaneous branch, which is the sensory component, may arise from the FN or directly from the lumbar plexus. It may partially or completely replace the femoral branch of the GFN. The medial cutaneous nerve may be small or absent and may overlap or be replaced by the obturator and saphenous nerve.[14]

Although infrequently seen as a complication of inguinal hernia repair, the FN may be injured with lateral dissection or fixation in the preperitoneal and retroperitoneal space during open or laparoscopic posterior inguinal hernia repairs, or it may be injured with deep penetrating fixation with sutures or tacks along the inguinal ligament lateral to the femoral vessels during open anterior repairs. Damage to the FN will result in atrophy of the anterior thigh muscles with resultant weakness of the quadriceps muscle and difficulty walking uphill or climbing stairs.[14] Accompanying sensory disturbances, such as pain or numbness in the anterior thigh distribution, may be found on dermatosensory mapping.

Obturator nerve

The obturator nerve is a sensorimotor nerve arising from the anterior division of the second to fourth lumbar ventral rami and supplies the medial compartment of the thigh. The obturator nerve descends through the psoas major and emerges from the medial border at the pelvic brim, crosses the sacroiliac joint posterior to the iliac vessels, and runs along the lateral pelvic wall medial to the obturator internus and anterosuperior to the obturator vessels.[14] It then exits the obturator foramen to supply the upper thigh, providing motor innervation to the adductor and obturator muscles and sensation to the medial thigh. Variations of the obturator nerve include a high form originating from L1 to L4 and a low form from L2 to L5 as well as a highly variable cutaneous sensory distribution.[14]

Injury to the obturator nerve is extremely uncommon in inguinal hernia surgery. Open anterior preperitoneal repairs (TIPP, plug and patch, plug, bilayer mesh) may potentially injure the nerve with medial mesh placement or blind medial dissection. More likely, in minimally invasive posterior repairs, overdissection of the obturator foramen, mesh folding or irritation, or malpositioned mesh fixation with tack or sutures may potentially, however infrequently, injure the obturator nerve. The resultant injury may clinically present as atrophy of the medial thigh, numbness or pain in the cutaneous distribution along the distal medial thigh, or weakness/paralysis of hip adduction.[14]


  Discussion Top


CPIP may develop after all methods of hernia repair and is independent of technique.[2] The neuroanatomy of the inguinal canal is complex and highly variable from the retroperitoneal lumbar plexus to the terminal branches exiting through the inguinal canal.[10],[11],[12],[13],[14],[15],[16] Neuropathic pain from nerve injury or entrapment is a common mechanism. While it is not possible to completely prevent injury due to the considerable neuroanatomic variability and inevitability of postoperative scarring, nerve injury is often technical and related to inadvertent iatrogenic damage. Multiple studies have demonstrated the feasibility of routine nerve identification, the benefit of focused neuroanatomic teaching, and the efficacy of nerve sparing in the reduction of CPIP. An in-depth understanding of groin neuroanatomy and potential causes of pain unique to each operative technique allows for a “nerve-mindfulness” approach that increases nerve identification and preservation, decreases injury, and improves patients outcomes.[5],[11],[17]

The nerves most commonly affected in CPIP are the iliohypogastric, ilioinguinal, and genital branch of the GFN. In open anterior tissue and mesh repairs, techniques such as three-nerve identification, local anesthesia infiltration, preservation of the investing fascia around the inguinal nerves, meticulous avoidance of nerve injury during suture repair of the canal or fixation of the mesh, lightweight mesh usage, and pragmatic neurectomy of nerves deemed to be injured or at risk during the primary operation all help to decrease the risk of CPIP.[2],[5] In laparoscopic and minimally invasive repair, techniques such as preserving the transversalis fascia to prevent overdissection of the inguinal nerves, judicious use or avoidance of penetrating mesh fixation, avoidance of posterior suturing of the myopectineal orifice, and careful deployment and positioning of mesh prostheses all help to prevent technical complications that may lead to nerve injury. Although infrequent, the LFC nerve, femoral branch of the GFN, FN, and obturator nerve may also be injured in the preperitoneal space and similar avoidance of overdissection, limited or no penetrating fixation, and meticulous mesh placement will help to limit the risk of these infrequent injuries.


  Conclusions Top


Prevention is the most important measure in mitigating neuropathic CPIP. Recognizing the typical neuroanatomy of the lumbar plexus, the highly variable nature of these nerves, and the operation-specific mechanisms for nerve entrapment will limit the potential for injury and improve outcomes in inguinal hernia repair.

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Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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