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M. Quadratus lumborum
41 Aetiology, Pathogenesis andAssessment ofChronic Pain After Inguinal Hernia Repair
T12
L1
399
M. Psoas
M. lliacus
1
2
4
3
5
3
4
L2
L3
L4
6
1
2
3
6
N.IIiohypogastricus (1)
N. llio-inguinalis (2)
N. Genitofemoralis (3)
N. Cutaneus femoris lat. (4
N. Femoralis (5)
N. Obturatorius (6)
Fig. 41.2 Neuroanatomy of the inguinal nerves
nerve is particularly at risk during a laparo- endoscopic procedure, as it runs on the bottom of the operative eld. Conversely, dam­age to ilioinguinal and iliohypogastric nerves is a frequent cause of pain following open inguinal hernia repair. Hence, a distinctive diagnostic and therapeutic approach for patients with CPIP is required depending on the repair technique (see Sect. 41.4). The risk of CPIP, however, may be reduced by meticulous identication of groin nerves during the hernia repair [8, 18].
Neuropathic pain caused by inguinal nerve damage, perineural scar tissue development or perineural brosis [17] may arise some weeks to months following the inguinal hernia repair. However, immediate postoperative neuropathic
pain may also occur, for instance, after a partial damage due to constricting ligatures. The under­lying mechanisms of this type of neuropathic pain differ from acute postoperative pain based on tissue damage. Furthermore, if a previous repair was mesh based, an ongoing inammatory response to the inserted mesh (Sect. 41.3.2.1) may result in CPIP by progressive nerve injury [19, 20]. One rabbit study investigating micro­scopic inguinal nerve reactions to insertion of a prosthetic mesh found nerve axonal dilation and mild-to-severe loss of myelinated axons in nerve fascicles [21]. Both mechanisms may be respon­sible for neuropathic CPIP evolving in the long term in patients. On the other hand, due to long­lasting compression, nerves may already have
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become damaged by the presence of the hernia for some time, resulting in myxoid histological changes of perineural oedema and an increased ratio of connective tissue to neural tissue [22].
41.3.1.2 Lower Intercostal Nerve
Following a laparo-endoscopic hernia repair, mechanical pressure following insufation of the preperitoneal space or abdominal cavity may lead to stretched endings of the lower intercostal nerves. Stretched nerves may result in a typical abdominal wall pain syndrome that is also referred to as anterior cutaneous nerve entrap­ment syndrome (ACNES) [23]. This pain syn­drome, which is often overlooked, may occur in patients after a variety of abdominal operations, although it frequently develops spontaneously. The same mechanism of injury may explain ACNES following open inguinal hernia repair, as pulling forces are exerted onto the abdominal wall during surgery. During physical examina­tion, a painful area of altered skin sensation that is often more proximally located, i.e. towards the umbilical area, may be found (Sect. 41.4).
41.3.1.3 Neuroma Formation
A neurectomy or partial nerve lesion may inci­dentally lead to a traumatic neuroma formation. A neuroma can be intraoperatively recognized as a shiny, white, oval or round, rm-elastic palpa­ble nodule at the proximal cut end of the nerve or at a damaged part along its course (Fig.41.3). Of note, the location of the neuroma depends on the
Fig. 41.3 Intraoperative view of a neuroma (*) of the
ilioinguinal nerve by compression caused by the placed mesh (arrow) that is elevated by the clamp
location of the lesion [
17]. Histopathological
examination of a potential neuroma is mandatory for verication. A neuroma develops by an inward migration and subsequent proliferation of broblasts and perineural cells and outward growth of axons [17]. In theory, inammation evoked by the inserted mesh may lead to the reac­tive proliferation of perineural cells in proximity to the mesh [24, 25]. This abnormal benign neu­ral proliferation may result in ectopic excitability of the concerning inguinal nerve, resulting in CPIP.
The incidence of traumatic neuromas in CPIP patients has been estimated between 12 and 14% [
2628], but proper studies have not been per-
formed to date. The question why some develop a neuroma after surgical nerve injury while others do not is largely unanswered. Earlier research has not fully unveiled its aetiology; hence, more research on the pathogenesis and how to avoid neuroma formation is desirable. When a neuroma is identied and removed, success rates of the remedial surgery may be increased [26].
41.3.1.4 Deaerentation
andCentralization ofPain
Another neuropathic CPIP entity is deafferenta­tion or postdissection pain leading to central sen­sitization [17, 29]. Patients with neuropathic postoperative pain following inguinal hernia repair who are unresponsive to all conservative and surgical treatments in the peripheral eld may have developed such type of pain. It can be considered as a type of phantom pain. This sort of pain results from a (complete or partial) disrup­tion of the afferent nerves. As a neurectomy or nerve injury interrupts the normal impulses from the afferent nerves, deafferentation pain is always looming.
Nerve lesions may further lead to molecular changes in nociceptive neurons (C-bres) and non-nociceptive neurons (Aδ- or Aβ-bres) by releasing growth factors [30]. These nerve growth factors were found to inuence neighbouring uninjured nerves, which react by an upgraded expression of certain receptors such as vanilloid receptors (trpV1 receptors, responding to nox­ious heat), adrenoceptors (adrenergic receptors,
41 Aetiology, Pathogenesis andAssessment ofChronic Pain After Inguinal Hernia Repair
401
responding to catecholamines) and upregulated sodium channels [3034]. By an upregulated expression of these receptors, hyperexcitability of initially normal surrounding nerves may ensue. Furthermore, a hyperexcitable state may result in an ongoing sensitization of the spinal cord dorsal horn neurons by releasing glutamate acting on postsynaptic N-methyl-D-aspartate (NMDA) receptors [30]. Both mechanisms may contribute to ectopic activity of the concerning nerves and consequent spontaneous pain [30, 35]. Since neighbouring, initially uninjured nerves have intact connections to the skin, pain is often expe­rienced at supercial groin areas [36] as also reected by a painful skin pinching test (Sect.
41.4). Why some patients develop deafferenta­tion pain while others do not is still unclear.
Long-lasting inguinal pain may result in cen­tral sensitization that can be extremely difcult to distinguish from other potential sources of pain. Centralized pain is independent of any peripheral drive [37] such as initiated by inguinal nerves and thus is refractory to peripherally directed treat­ments. Prolonged impulse stimulation along unmyelinated C-bre afferents may cause trans­neuronal morphologic changes to peripheral nerves (‘neuronal plasticity’). Peripheral nerve hyperexcitability may subsequently be caused by a lower threshold of nociceptor afferent periph­eral terminals, a phenomenon termed peripheral sensitization [30]. The extensive quantity and ongoing input resulting from peripheral sensiti­zation may lead to hyperexcitability of the spinal cord and morphological changes more proximal in the central nervous system and thus central sensitization [3841]. Patients with centralized pain should be excluded from remedial, peripher­ally oriented surgery [16, 42].
41.3.2 Non-Neuropathic Pain
Syndromes
41.3.2.1 Mesh-Related Pain
Non-neuropathic or nociceptive CPIP can be due to a mesh- or suture-induced inammatory reaction within the inguinal area. Theoretically, any foreign material has a potential of inducing an inamma-
tory reaction. Locoregional inammation is assumed critical for strengthening the hernia repair as formation of brosis is correlated to the intensity of inammation [43, 44]. Interestingly, lightweight meshes were found to induce less inammation and, as a consequence, less formation of brosis resulting in more hernia recurrences [44, 45].
The downside of mesh-related inammation is an occasionally occurring unfavourable effect of ongoing inammatory responses. Meshes that were explanted after 3 years were still demon­strating active foreign body reactions [46]. These ndings support the idea that inammation may go on for many years.
Inserted meshes may not only lead to an ongo­ing low-grade chronic inammatory reaction but may also exert mechanical pressure or irritation possibly contributing to pain. The ‘anatomy’ of inserted mesh may change as creasing, wrinkling and folding may occur. This slow process increases mechanical pressure and may lead to a foreign body feeling. This feeling is reported by patients as something that is constantly bothering them as if a ‘wrinkled handkerchief is sitting in their pocket’. Previous studies suggested that up to half of the patients with a sutured mesh-based hernia repair report some kind of foreign body feeling in the groin [15, 28, 47]. Trials comparing a standard and a lightweight mesh have demon­strated a signicantly lower rate of foreign body sensation in the latter group [20, 45, 47, 48]. The lesser formation of brosis may correlate with the reduced foreign body feeling. Moreover, adhesions to surrounding structures may contrib­ute to the sensation.
Apart from an uncomfortable sensation, a for­eign body feeling may possibly herald mesh­related pain. The results of previous studies that most mesh-related pain develops over a few years following hernia repair [28] support this hypoth­esis. Of note, not only the natural evolution of mesh-related pain but also insufcient knowl­edge of hernia surgeons and hesitance to refer patients to specialized centres contribute to this long diagnostic and treatment delay. Whether a foreign body feeling is also directly related to mesh shrinkage needs to be claried.
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Mesh-related pain may occur both after open and after laparo-endoscopic inguinal hernia repairs. In Western countries, laparo-endoscopic repairs such as TEP and TAPP are primarily rec­ommended, providing resources and expertise are available [49]. Approximately 15% of CPIP patients demonstrate a mesh-related pain after an open Lichtenstein repair [28]. The number of patients presenting with mesh-related pain is many times lower following laparo-endoscopic repairs [50]. An explanation for this difference is possibly provided by the position of the mesh in the preperitoneal space. This location is likely benecial not only in terms of evoking fewer cases of neuropathic pain [14, 51] but probably also for generating less mesh-related pain. It is thought, however, that the mesh may exert com­parable mechanical effects irrespective of mode of implantation, open or laparo-endoscopic [50].
Meshoma Formation
Meshes have the tendency to wrinkle, fold and shrink up to 30% over time [52], and if this pro­cess proceeds, a so-called meshoma may be formed (Fig.41.4). A meshoma is dened by the operating surgeon [53]. Different gradations may be present, varying from a mass-like density to more subtle effects of mesh wrinkling or brosis [53]. A meshoma results in CPIP by a volume effect or by mechanical pressure on surrounding structures in the inguinal region. Insufcient xa­tion or insufcient dissection to make adequate room for the prosthesis may increase the risk of meshoma formation [54].
A meshoma is increasingly recognized as an important factor contributing to CPIP [55]. A recent study on CPIP patients after open inguinal hernia repair observed an up to 17% incidence of a meshoma [26]. Interestingly, identication of this unique pathologic nding following laparo­endoscopic hernia repair is less frequently described [50]. It should be appreciated that a meshoma following initial laparo-endoscopic her­nia repair looks different compared to open repairs, as subtle effects as wrinkling or small folds of the preperitoneal mesh may create pressure and mass effects. The lower grade of folding of the mesh in the preperitoneal space is possibly related to a rel­ative limited grade of exing and extending forces when compared to the groin region.
The mesh, being a meshoma or not, may also invade the surrounding structures and organs, resulting in serious damage (for instance, to the vas deferens or bladder). A typical case of inva­sion of the appendix by a meshoma (Fig.41.5), leading to chronic visceral pain in epigastrium with nausea, was previously described [56]. After removal of this mesh, visceral complaints (besides the pain) that had been present for many years also disappeared.
41.3.2.2 Adductor Tendinopathy
Inguinal pain following hernia repair may result in a compensatory antalgic gait. If pain persists and an effective remedial therapy is postponed, such an ongoing antalgic gait can lead to a tendi­nopathy of the adductor muscles of the hip. This
Fig. 41.5 An appendix vermiformis rmly attached to a
Fig. 41.4 A surgically removed meshoma
plug that was previously used for inguinal hernia repair
41 Aetiology, Pathogenesis andAssessment ofChronic Pain After Inguinal Hernia Repair
403
(possibly latent) cause is not yet properly studied, whereas therapeutic options are limited and experimental. Moreover, persistent groin pain fol­lowing a successful neurectomy or meshectomy can be due to a persisting adductor tendinopathy. It is imperative that, prior to deciding on remedial surgery for CPIP, these patients should be coun­selled on the copresence of this pain syndrome. However, to our experience, this is difcult, espe­cially when the groin pain due to a neuropathic entrapment or meshoma is prevailing.
41.3.2.3 Periostitis Pubis
Another CPIP syndrome that is frequently encountered is periostitis of the pubic tubercle (also known as periostalgia pubis or pubalgia). This inammatory-related pain syndrome can develop after both open and laparo-endoscopic hernia surgeries. Periostitis of the pubic bone can evolve by a long-standing direct mechanical irri­tation by prosthetic material. Overlap of the inserted mesh onto the pubic tubercle may cause a periosteal reaction, as well as sutures or staples into the pubic bone. It is thought that the vector forces of the rectus and adductor muscle result in this intriguing pain entity. Surgery itself may also cause a painful local inammatory reaction, but this phenomenon is assumed to be self-limiting.
Apart from inammation, periostitis is also characterized by sclerosis in the pubic bone [57]. The diagnosis, however, is primarily based on physical examination (Sect. 41.4). The estimated incidence of this underreported cause of CPIP is less than 1% following open inguinal hernia sur­gery [20]. Together with adductor tendinitis, ongoing periostitis is the most frequent cause of persistent groin pain following successful reme­dial groin surgery for CPIP after nerve or mesh removal. Therefore, CPIP patients who are planned for a neurectomy or mesh removal must be informed on the issue of persisting periostitis after the operation.
41.3.2.4 Iliopectineal Bursitis
A seldom acknowledged and rare cause of CPIP is iliopectineal bursitis, which can also present spontaneously, that is, without any previous (her­nia) surgery. Injury and overstrain are the main causes of this pain syndrome, which results in
haemorrhage or uid retention in the bursa [58]. As a consequence, a sterile inammation of the iliopectineal bursa may occur. As previously mentioned, pain following CPIP may lead to an antalgic gait which occasionally leads to iliopec­tineal bursitis. Sometimes an enlarged bursa can be visualized using magnetic resonance imaging (MRI).
41.3.3 Combined Groin Pain Syndromes
41.3.3.1 Dysejaculation
Sexual complaints following inguinal hernia sur­gery are often ignored. Only a small portion of men spontaneously report sexual dysfunction after a standard mesh repair. Up to 3% of patients have a moderate to severe pain-related impair­ment of sexual activity following inguinal hernia repair [59]. Therefore, hernia surgeons should always check for the onset of sexual complaints when patients present with CPIP. Ideally, these issues must be discussed prior to hernia surgery.
Dysejaculation (pain just before, during or following ejaculation) is known to profoundly affect a patient’s sexual activities [60]. The inci­dence of dysejaculation is approximately 3–4% following inguinal hernia repair [5961] and may occur in male patients after both open and laparo­endoscopic repair techniques [60]. In one series of 100 men with CPIP, we encountered this phe­nomenon in some 30% [60]. The prevalence of ejaculatory pain is lower following laparo­endoscopic repair techniques compared to open repair [61].
The pathogenesis of dysejaculation involves injury to the vas deferens with or without damage to the inguinal nerves [59, 62, 63]. The vas may be compressed by the mesh or may be injured as a consequence of scar tissue. During ejaculation, peristalsis in the vas results in a post-obstructive dilation, triggering a spasm-related pain [64]. Mesh-related inammatory responses (Sect.
41.3.2.1) may also injure the vas deferens. Previous studies have identied a potential role of the three inguinal nerves at risk in dysejaculation following open mesh repairs [59, 62, 65, 66]. The relative contribution of these separate nerves
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regarding dysejaculation remains unknown. Successful effects of remedial surgery on sexual functioning, including a neurectomy (only), mesh removal and funicular release or a combination of these, support this mechanism of CPIP [60]. In one series, two out of three males reported serious improvement or disappearance of dysejaculation after these types of remedial surgery [60].
Mesh migrations due to insufcient xation or as a result of a foreign body reaction [67] are other etiologic factors contributing to dysejaculation. These reactions may lead to erosion of the sur­rounding tissue. The grade of erosion highly depends on the biocompatibility of the material [67, 68]. Other factors inuencing mesh biocom­patibility include the type of material, pore size and rigidity [68]. Irrespective of the mechanism of ero­sion, invasion of meshes into the vas deferens can cause dysejaculation by the described mechanism.
The analogue of dysejaculation in men is post­orgasm pain in women, seen of course in CPIP, but also after neuropathic pain in the so-called post-caesarean section pain syndrome. It is our experience that a pure neurectomy in these women can result in relieve of this specic sexual problem. Percentages of post-orgasm pain in women after hernia mesh repair are unknown.
41.3.3.2 Orchialgia Versus Scrotal
Pain
Another CPIP syndrome with both neuropathic and non-neuropathic characteristics is orchialgia [69, 70]. Orchialgia is dened as an intermittent or constant, unilateral or bilateral testicular pain [69]. Sometimes orchialgia is accompanied by dysejaculation [64]. Its aetiology and innervation of the testis are complex. Pain in the testes and epididymides is mediated by the autonomic nerve bres that run along the internal spermatic ves­sels and on the surface of the vas deferens (so­called perivasal nerves), from the pelvic plexus originating in the Th10 to Th12 (testes) and Th12 to L1 segments (epididymides) [69, 70]. Since periprostatic application of local anaesthetics may relieve orchialgia, the idea is supported that the pelvic plexus supplies neural input to the tes­tes [69]. The perivasal nerves may be injured dur­ing hernia repair by various ways including dissection of the spermatic cord or entrapment of
the vas during open hernia repair techniques [70]. Injury due to the preperitoneal dissection or dis­ruption of the autonomic bres accompanying the vas can occur during laparo-endoscopic repairs, as well as placement of the mesh or addi­tional xation materials in proximity to these structures [54, 7072]. As mentioned before, orchialgia is a combined CPIP syndrome that can include both neuropathic and nociceptive charac­teristics. The nociceptive causes for orchialgia are diverse and include postherniorrhaphy testic­ular ischemia, oedema, brosis of the spermatic cord and infection [70].
Orchialgia is particularly complicating as a signicant overlap with inguinal and scrotal pain is present [70, 73]. However, since the testes themselves lack a somatic nerve innervation, it is essential to differentiate between true orchialgia and scrotal (skin) pain. Scrotal pain is neuro­pathic in origin and caused by the somatic genital branch of the genitofemoral nerve and/or the ilio­inguinal nerve. Localized diagnostic injections with local anaesthetics may help to distinguish between these two types of CPIP (Sect. 41.4.5).
Apart from dysejaculation, orchialgia and scrotal pain, other sexual CPIP syndromes have been described, although less frequently seen. Dyspareunia (pain during sexual intercourse) is one such symptom. Its occurrence ranges from less than <1 to 3%, and literature on this phenom­enon is scarce [59, 74, 75]. Pain in the penile shaft or glans is another such rare symptom [59].
41.4 Assessment
Concise history taking and an extensive physical examination provide the cornerstones in diagnos­ing inguinodynia. Clues for diagnosing the aeti­ology of CPIP are discussed below.
41.4.1 Patient’s History
41.4.1.1 Diagnostic Clues
forNeuropathic Pain
First, when a patient experiences excruciating pain immediately after inguinal hernia surgery, an acute reexploration is indicated. If postoperative
41 Aetiology, Pathogenesis andAssessment ofChronic Pain After Inguinal Hernia Repair
405
pain following a standard hernia repair develops later in the course of recovery or if pain persists after 3–6 months, a concise patient history and physical examination should indicate whether a patient suffers from neuropathic pain, from a nociceptive/inammatory pain (either mesh related or by other origins) or a combination of these or from pain due to a recurrent hernia. However, the differential diagnosis for groin pain in general is extensive, and not all CPIP does nec-
Table 41.1 The differential diagnosis of chronic postoperative inguinal pain
Hernia surgery Orthopaedics
Primary hernia Acetabular labral tears – Inguinal Avascular necrosis – Femoral Chondritis dissecans – Obturator Legg-Calve-Perthes disease Recurrent hernia Osteoarthritis Postherniorrhaphy Pelvic stress fractures – Neuropathic (including neuroma) Slipped femoral capsule epiphysis
• Iliohypogastric Snapping hip syndrome
• Ilioinguinal – Anterior
• Genitofemoral – Lateral
• Lateral femoral cutaneous Synovitis
• Lower intercostal nerve (Th12) Iliopectineal bursitis
• Deafferentation pain Spondylolisthesis
• Centralized pain Spondylolysis – Non-neuropathic
• Mesh related (including meshoma) Sports medicine
• Adductor tendinopathy Rectus strain
• Periostitis pubis (pubalgia) Adductor tendinopathy
• Iliopectineal bursitis Iliopsoas tendinopathy – Combined (non-)neuropathic Symphysiolysis/symphitis
• Dysejaculation Sportsman’s hernia (sports hernia)
• Orchialgia
Gynaecology Postvasectomy pain syndrome Post-Pfannenstiel Vas granuloma/brosis – Neuropathic Cystitis or urinary tract infection
• Iliohypogastric Epididymitis
• Ilioinguinal Prostatitis Cervical cancer Uro−/nephrolithiasis Endometriosis Torsion of the testis – Intra-abdominal – Round ligament of the uterus Gastroenterology – Pfannenstiel incision Appendicitis Adnex disorders (including torsion) Adhesions Uterus myomatosis Diverticulitis
Vascular Inammatory retroperitoneal phlegmon Hematoma Meckel diverticulitis Varices Granulomatous colitis
essarily have to be related to the previous surgery (Table41.1).
Central in the neuropathic CPIP patient’s his­tory is a sharp, burning or shooting (electrical­shock- like) painful sensation which is progressive after repetitive stimulation. Paraesthesia (tin­gling, crawling ongoing non-painful sensations) and dysaesthesia (spontaneous or evoked unpleasant abnormal sensation) with radiation towards the associated skin area of the involved
Urology
a
Irritable bowel syndrome
b
(continued)
406
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Hernia surgery Orthopaedics
Pelvic congestion syndrome Postvein stripping Oncology Pseudoaneurysm (catheterization) Retroperitoneal neoplasm Iliac/femoral artery aneurysm Osseous metastasis pelvis/hip joint Iliac/femoral artery stenosis Thrombosis Infectious disease Vascular graft Herpes zoster Abdominal aortic aneurysm
Dermatology Psoas abscess Lymphadenitis Psoriasis/burn Neurology Sebaceous cyst Lumbosacral disorders Thrombophlebitis Neurobromatosis Cellulitis Disc disease Hidradenitis suppurativa Spinal injuries
Rheumatology Spinal inammation
Connective tissue disease Systemic lupus erythematosus
a
Entrapment genital branch of genitofemoral nerve
b
Pancreatitis
c
With compression of genitofemoral nerve
c
HIV/tuberculosis Lyme disease
Spinal tumours
Anterior cutaneous nerve entrapment syndrome (ACNES)
(inguinal) nerve are often reported. Depending on the affected nerve, pain may radiate towards the upper medial thigh (ilioinguinal nerve), the suprapubic region (iliohypogastric nerve) or the genitals or ventral upper leg (genitofemoral nerve, Fig.41.2). Some patients may spontane­ously complain of sensory disturbances in the groin area. It is known, however, that in clinical presentation a lot of overlap between these involved areas is possible.
Once it is decided to perform a surgical explo­ration for CPIP, it is important to consider the type of inguinal hernia repair, as the inguinal nerves at risk depend on the technique. During laparo-endoscopic hernia repair, a detailed explo­ration of both the ‘triangle of doom’ and the ‘tri­angle of pain’ is essential. Therefore, original operative reports of the primary repair should always be checked in detail, including intraoper­ative complications and identication of inguinal nerves. As a pragmatic neurectomy is recom­mended for inguinal nerves if considered at risk [49], the operative report may clarify on this issue. If a previous neurectomy was performed,
the occurrence of a traumatic neuroma should be considered. The use of sutures, tackers, staples and other prosthetic materials may indicate whether neuropathic pain is caused by injury from these.
The time after inguinal hernia repair may indi­cate possible neuropathic aetiologies of CPIP.As stipulated earlier, immediate pain may be due to direct intraoperative nerve injury of mechanical effects to the nerves from surgery, whereas pain manifestation after weeks to months suggests CPIP from scar tissue formation or mesh-based inammatory responses (Sect. 41.3.2.1). Of note, in patients with acute neuropathic postoperative pain following inguinal hernia repair who are unresponsive to all conservative and surgical treatments, deafferentation pain should be considered.
ACNES patients typically complain of a spe­cic localized pain, within the lateral border of the rectus muscle. In over 90% of the cases, local somatosensory disturbances are present. Compared to groin pain, the pain is often located more proximally, towards the umbilical area
41 Aetiology, Pathogenesis andAssessment ofChronic Pain After Inguinal Hernia Repair
407
corresponding the lowest Th10, Th11 and Th12 intercostal nerves.
Centralized pain is independent of any periph­eral drive. Distinction of centralized neuropathic pain cannot be done based on patient history only. Possibly, a spontaneous burning pain is more often present when pain is due to sensitiza­tion [76], but the same symptom may be present in other neuropathic pain syndromes.
41.4.1.2 Diagnostic Clues forNon-
Neuropathic Pain
Patients with a non-neuropathic CPIP usually report a throbbing or nagging pain located in a non-neuroanatomical area [77]. Once again, it is important to consider the type of inguinal hernia repair. Fixation methods and the inserted type of mesh are important clues associated with non­neuropathic pain syndromes. Studying previous operative reports is crucial. Moreover, the dura­tion of CPIP may contribute to the diagnosis.
Mesh-related CPIP is suspected when patients complain of a foreign body sensation or feeling of tightness in the groin area [28]. The pain is often aggravated during car driving or leg cross­ing (pressurizing the groin), whereas a supine position relieves mesh-related pain [28]. The same set of nociceptive pain characteristics are present in patients with a meshoma.
When patients or their partners notice an abnormal gait, musculoskeletal origins such as adductor tendinopathy or periostitis pubis (pubal­gia) should be considered. Adductor tendinopa­thy typically relieves during rest and increases during physical activity when using the hip adductor muscles (in particular climbing stairs). The chance on these syndromes increases with the duration of CPIP. Excluding other disorders may lead to the diagnosis of more rare pain syn­dromes such as iliopectineal bursitis.
On the other hand, sexual complaints includ­ing dysejaculation are solely diagnosed on the basis of patient history taking since no physical ndings can be noted. An intense burning, pain­ful sensation that occurs just before, during or after ejaculation [64] conrms the diagnosis of dysejaculation. Orchialgia is experienced as an intermittent, squeezing, deep ache in the testis
‘like the sensation the day after you got kicked there’ [69, 78]. Sometimes the patient reports that it feels as if the testicle is pinched in the crotch of the underwear but trouser readjustment does not help. The onset of pain is commonly related to particular activities such as long car journeys or unsupported seating posture [69, 78].
41.4.1.3 Diagnostic Questionnaires
The French Neuropathic Pain Group developed a questionnaire (DN4) discriminating between neuropathic and non-neuropathic pain syndromes [79]. The DN4 questionnaire consists of both sensory descriptors and characteristics during physical examination [79]. This questionnaire was tested in a variety of neuropathic pain syn­dromes and demonstrated to be valid. Whether the questionnaire is also usable for distinguishing neuropathic from non-neuropathic CPIP patients needs to be investigated.
41.4.2 Physical Examination
41.4.2.1 Tests forDiagnosing Sensory Disturbances
All of the CPIP pain syndromes are characterized by distinct clinical signs and symptoms that can be used to differentiate between them. First, the presence of sensory disturbances is a key diag­nostic feature for neuropathic CPIP and generally lacking in non-neuropathic pain.
An area of sensory decit can be assessed by touching the skin of the alleged painful area with a cotton swab or gauze (Fig.41.6). If the patient experiences a normal sensation in the area of pain, as compared to the contralateral side, neu­ropathic pain becomes less likely. Hypoaesthesia (reduced response to non-painful stimuli) is pres­ent if a reduced perception or numbness is expe­rienced. This by itself can of course be present in any groin scar after hernia surgery. Nevertheless, patients with groin pain and hypoaesthesia expe­rience this type of numbness as (very) annoying. Conversely, hyperaesthesia is present when an increased sensation to non-painful stimuli is reported. Allodynia can be tested likewise, but the stimulus evokes severe pain. When a sharp,
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W. A. R. Zwaans et al.
c d
Fig. 41.6 Physical examination for sensory disturbances
and identication of trigger points. Testing of sensory dysfunctions by touching the skin with a cotton swab (a), pinching of the skin (b), altered cold sensation assessed by a gauze soaked in liquid disinfectants (c). Results of the sensory mapping by these tests as illustrated by the
burning and supercial pain in the primary affected zone is spreading into unaffected skin areas, allodynia is likely [30].
Pain sensation following pinching of the skin (Fig. 41.6) may be disproportionally painful (hyperalgesia). Positive sensory abnormalities such as hyperalgesia and hyperpathia (abnormally painful reaction to a stimulus, especially a repeti-
drawing (d): decreased sensation (), increased sensation (+), normal sensation (0). Identication of circumscriptive pain points using the index nger (e). End result of the sensory mapping in the inguinal region with a diagnostic local nerve block with 5 cc lidocaine 1% placed at the point of maximum pain (f)
tive stimulus, as well as an increased threshold) can both point towards at neuropathic CPIP [30]. Moreover, negative neurophysiologic phenomena including hypoaesthesia and hypoalgesia (dimin­ished pain in response to a normally painful stim­ulus) also contribute to the picture [30].
Cold sensation can be assessed by the response
to a gauze soaked in ethanol or other liquid disin-