Inguinal hernia repair is a common procedure with infrequent postoperative morbidity, but it may be followed by complaints of chronic pain in 5%–30% of patients (1). However, most studies have not assessed chronic pain as the primary aim of the study; therefore, assessment of the functional consequences of chronic pain after inguinal herniotomy have only recently been reported (2–4). In these studies, approximately 10% stated that pain was interfering with work or leisure activity (2–4), thus emphasizing the importance of the problem.
The development of chronic pain after inguinal herniotomy has been attributed to several pathogenic mechanisms, including damage to the well defined sensory nerves in the groin area: the iliohypogastric nerve, the ilioinguinal nerve, and the genitofemoral nerve. Only two studies (5,6) have discussed the association between late postoperative cutaneous sensory disturbances and pain. However, in both these studies, the examination technique was not presented, and patients without pain were not examined, thereby hindering interpretation regarding the association between chronic pain and sensory dysfunction as an indicator of neuropathic pain. Therefore, the aim of this study was to evaluate in detail the association between chronic pain and sensory dysfunction in hernia repair patients with and without pain 6–12 mo after surgery.
After approval from the regional ethical committee, all patients were included who had undergone elective uncomplicated inguinal herniotomy by the Lichtenstein procedure 6–12 mo before the start of the study at our institution. Exclusion criteria were female sex, a bilateral procedure, surgery for recurrent hernia, age younger than 18 yr, chronic opioid medication, language barriers, cognitive dysfunction, or known neurological disease. Questionnaires with prestamped return envelopes were mailed to 171 patients (Fig. 1).
After verbal and written consent, the patients were asked to complete two questionnaires relating to pain and functional impairment (3). All patients were given detailed verbal instructions for correct completion. The first questionnaire is a modified Danish short form of the McGill Pain Questionnaire (3) that contains a visual analog scale (VAS; 0–100) for assessment of pain intensity, a list of adjectives describing pain quality, and an anatomical chart for depiction of pain localization. In the second questionnaire, the patients were asked to assess how the pain was interfering with daily living and leisure activity (3).
The quantitative sensory testing was performed with the patients resting in a comfortable semireclined position. To get the patients well acquainted with the testing paradigm, a preparatory testing sequence was performed at the patient’s forearm, followed by testing in the groin area. During the examination, the patient was asked to keep his eyes closed and to concentrate on the evoked sensations. The patient was unaware of the test results. The quantitative sensory testing was done by two investigators (TM and BL).
The actual sensory testing was performed starting in a reference area (25 × 50 mm) 4 cm cephalad for the incision. The reference area was used for all sensory thresholds and pain assessments in patients without any demonstrable skin hyperesthesia. In patients with hyperesthesia, a corresponding area (25 × 50 mm) was demarcated centrally in the hyperesthesia zone, taking care not to include scar tissue. This area and an area immediately outside were used for sensory thresholds and pain assessments.
Hypoesthesia was determined by stimulating with a von Frey monofilament (Senselab Aesthesiometer; Somedic AB, Sweden; No. 17; nominal buckling force, 468 mN) well outside the sensory testing area along eight linear paths angled at 45° and converging toward the center of the area. The patients were instructed to report a definite decrease in tactile sensation. Tactile allodynia was evaluated by gently stroking the skin with a soft brush perpendicular to the linear paths, and the patients were instructed to report any sensation of discomfort or pain.
Mechanical pain threshold was evaluated by stimulation with 11 progressively rigid calibrated von Frey monofilaments (No. 7, 2 mN; No. 8, 3 mN; No. 9, 6 mN; No. 10, 12 mN; No. 11, 22 mN; No. 12, 34 mN; No. 13, 58 mN; No. 14, 89 mN; No. 15, 212 mN; No. 16, 309 mN; and No. 17, 468 mN [calibrated at 23°C and a relative humidity of 35%]) as previously described (7). The mechanical pain threshold was defined as the least force that elicited a sensation of pain or discomfort. If von Frey filament No. 17 did not elicit a sensation of pain or discomfort, the observation was assigned a value of 18. Pain responses (VAS 0–100) to mechanical stimuli were assessed by five stimuli of a rigid von Frey filament (No. 17) with a stimulation rate of 0.5 Hz.
Brush (dynamic) allodynia was evaluated by application of an electric toothbrush (Oral-B 4713; Braun, Germany; 127-Hz oscillations) on the skin for 30 s in the incisional area. Brush-induced pain or discomfort was evaluated by VAS ratings after 5 and 25 s of stimulation.
The mechanical pain threshold from deep somatic tissues was evaluated by pressure algometry (Bridge amplifier; Somedic AB, Sverige) with a circular probe (0.18 cm2) applied directly over the middle of the inguinal ligament. Pressure was applied at a constant rate (10 kPa/s), and the patient was instructed to press a button when a sensation of pain or discomfort appeared. Assessments were made in triplicate, with an interstimulus interval of 30 s, and the median value was used in the analysis.
Thermal thresholds were assessed by a computerized 25 × 50 mm contact thermode (Modular Sensory Analyzer; Somedic AB, Hörby, Sweden) applied in the incisional area. The patients were instructed to immediately push a button when a change of temperature was perceived. Assessments of warm detection threshold, cold detection threshold, and heat pain threshold (HPT) were made in triplicate with randomized interstimulus intervals of 4–6 s, starting from a baseline temperature of 32°C and with a ramp rate of ±1°C/s. The cutoff limits for warm and cold measurements were 50°C and 25°C, respectively. The cremaster reflex was elicited by stroking the inside of the thigh with a von Frey monofilament No. 18 (1584 mN), and retraction was noted.
The chronological order of testing was assessment of hypoesthesia and tactile allodynia, cold detection threshold, warm detection threshold, mechanical pain threshold (skin), HPT, mechanical pain response, brush allodynia, cremaster reflexes, and mechanical pain threshold (pressure algometry). All patients were examined clinically with palpation of both groin areas with the patient in the standing position, at rest, and during coughing.
Data were analyzed for normality by the Kolmogorov-Smirnov test (SPSS 10.0.7; SPSS Inc., Chicago, IL). Because several of the test data were not normally distributed, only nonparametric tests were used: the Mann-Whitney test for nonpaired data and Wilcoxon’s signed rank test for paired data. The χ2 test with Yates’ continuity correction or Fisher’s exact test, as appropriate (8), was used to assess differences in frequencies between groups. Values are median and interquartile range (25%–75%) unless otherwise stated. A P value <0.05 was considered to indicate statistical significance.
Between January 1 and December 31, 2000, 171 male patients had undergone elective primary inguinal herniotomy by the Lichtenstein procedure at our institution. Questionnaires with prestamped return envelopes were mailed to all patients (Fig. 1). The median age of the patients was 64 yr (interquartile range, 48–73 yr). The investigation period started April 3 and ended August 10, 2001, and the median follow-up time was 9.5 mo (7–13 mo).
Twenty (28%) of the 72 patients had experienced pain in the area, and 52 patients (72%) had not. Eleven (15%) of the patients with pain indicated that pain significantly interfered with work or leisure activity. The most commonly chosen descriptors of pain were pricking (13 of 20;Fig. 2), annoying/irritating (11 of 20), tender (10 of 20), and shooting/jolting (10 of 20). The number of descriptors was 4 (interquartile range, 3–8). The spontaneous VAS pain intensity in the pain group was 22 (interquartile range, 12–30).
Mechanical hypoesthesia or tactile allodynia in the incisional area was observed in 51% (37 of 72) of the patients. Three patients in the pain group and six patients in the nonpain group had areas with both hypoesthesia and tactile allodynia in the incisional area. The overall incidence of sensory dysfunction was not different among pain patients (14 of 20) compared with nonpain patients (23 of 52) (P > 0.3).
There was no significant difference between the pain group and the nonpain group in mechanical pain thresholds for punctate stimuli (P > 0.4; Mann-Whitney test;Table 1). In contrast, the pain response to five repeated von Frey hair stimuli was significantly higher (P < 0.002) in the pain patients, but the VAS scores were very low (10 versus 2;Table 1). Pain to brush-evoked stimulation (5 and 25 s) was also more frequent in the pain group than in the nonpain group (P < 0.02 and P < 0.03; Mann-Whitney test;Table 1), but again with very low VAS scores, between 2 and 5 of 100 (Table 1). There was no difference in mechanical pain perception (von Frey or brush) among the pain patients with or without sensory dysfunction (P > 0.3).
Mechanical pain threshold assessed by pressure algometry in the incisional area did not differ between the pain and the nonpain groups (P > 0.1; Mann-Whitney test;Table 1). Warm detection, cold detection, and HPT did not differ between the pain group and the nonpain group (P > 0.6; Mann-Whitney test;Table 1).
The cremaster reflex was elicitable on the incisional side in 14 of 20 patients in the pain group and in 44 of 52 patients in the nonpain group (P > 0.2; χ2 Yates’ correction;Table 1). The physical examination did not reveal any recurrent or new hernias. Anatomical pain charts for the 20 pain patients are illustrated in Figure 3. In addition, two patients (Patients 29 and 52) spontaneously reported that they experienced severe ejaculatory pain that led to sexual dysfunction and impairment. Neither of these patients reported pain in the incisional area.
Post hoc statistical analysis showed that the power of the study (n = 72) ranged between 80% and 95% (α = 0.05; β = 0.05–0.20) in regard to detection of a 2.5× increased incidence of hypoesthesia or tactile allodynia, a 10% change in thermal thresholds, a 40% change in mechanical pain threshold (pressure algometry), or a 40% change in the incidence of elicitation of the cremaster reflex in the pain group compared with the nonpain group.
This study is the first to investigate chronic pain and sensory dysfunction by quantified sensory testing in hernia repair patients 6–12 months after elective uncomplicated surgery. A total of 28% of the patients reported pain, and 15% stated that the pain interfered with work or social activities; this is in agreement with previous follow-up studies (2–4,9). The quantitative sensory testing showed that sensory disturbances, i.e., mechanical hypoesthesia and tactile allodynia, were a common finding (37 of 72 patients; 51%) in the herniotomy area, but these sensory aberrations did not seem to occur more often in patients with pain than in patients without pain. Also, detailed, quantified sensory testing did not demonstrate differences between pain and nonpain patients except for minor, but significant, increased VAS responses in pain patients to von Frey and brush stimulation.
Chronic pain after herniotomy has primarily been assumed to be of neuropathic origin (1), and it has been hypothesized that the nerve injury could be attributed either to direct surgical trauma or to delayed injury caused by postoperative inflammatory changes. A previously observed relationship between chronic pain and late postoperative sensory dysfunction supports this interpretation (5,6), but in these studies no detailed sensory assessments were performed, and no information was provided from patients without pain. In the Cunningham et al. study (5), pain and sensory disturbances were followed up in 276 patients with 315 hernia repairs. At 12 months control, 31% of the patients reported numbness in the incisional area, and a significant correlation with pain was observed. On physical examination, 90% of patients with sensory impairment had hypoesthesia, whereas dysesthesia was uncommon and allodynia was not noted. In a large long-term follow-up questionnaire-based study, 8% of the patients indicated hypoesthesia and 2% indicated touch- or movement-related paresthesia in the incisional area (6).
In the study by Cunningham et al. (5), three distinct types of pain were suggested but not analyzed: a somatic pain localized to the common ligamentous insertion to the pubic tubercle, a neuropathic pain referable to the ilioinguinal or genitofemoral nerve distribution, and a visceral, ejaculatory-related pain. In the anatomical chart (Fig. 3) in this study, 9 of the 20 pain patients indicated pain near the incision, 6 indicated discrete pain points near the inguinal ligament, and 6 indicated a more circumscribed pain area (Fig. 3). As previously mentioned, two patients reported ejaculatory pain. The discrete pain markings could represent a somatic pain component or a neuroma formation, whereas the circumscribed areas would seem to suggest involvement of one or more nerve branches. An anatomical study indicated a complex innervation pattern of the three cutaneous nerves supplying the groin area (10), and a detailed nerve lesion interpretation is therefore not possible. In support of a neuropathic component, we observed that 10 of the pain patients, including 3 of 6 patients with circumscribed pain areas, used a combination of 2 or more neuropathic pain descriptors (11–13), i.e., shooting, pricking, burning, or tender (Fig. 2). The most frequent pain descriptors belonged to the sensory or evaluative category (pricking, annoying/irritating, tender, and shooting/jolting), which is in close agreement with a previous study (3).
A number of studies have evaluated chronic cutaneous sensory impairment after tissue injury, by using quantitative testing methods: in postherpetic neuralgia (14–17), in neuropathy (18), in postmastectomy pain (19), in osteoarthritis (20), and in whiplash injury (21). In a prospective study of herpes zoster patients, the presence in the acute stage of brush-induced allodynia (gain of sensory function) and pinprick hypoesthesia (loss of sensory function) correlated with development of postherpetic neuralgia (15). In a recent study, it was suggested that two distinct mechanisms may be operational in neuropathic pain: central sensitization in patients with minor cutaneous sensory dysfunction (painful hyperalgesia) and partial nociceptive deafferentation in patients with major sensory dysfunction (painful hypoalgesia) (18). In this study of 20 pain patients, 14 had tactile allodynia or hypoesthesia, and 3 of these presented with a combination of allodynia and hypoesthesia.
In a study of postmastectomy pain, sensory abnormalities were studied with a quantitative sensory testing technique in pain patients (n = 15) and nonpain patients (n = 11). The inclusion criterion was abnormal sensitivity, painful (allodynia or dysesthesia) or nonpainful (hypoesthesia or dysesthesia), in or around the incisional area. Sensory thresholds to pin-prick and thermal stimuli were significantly increased on the operated side, with no difference between groups. There was no difference in HPT in the pain group, but a significant decrease was observed in the nonpain group in the hypoesthetic/dysesthetic area. The mechanical pain threshold for pinprick was significantly lower in pain patients on the operated side compared with control. Repetitive pinprick stimulation was associated with higher pain ratings in the pain group, indicating a prominent sensitization component. Data from this study corroborate these findings, bearing in mind that all pain patients in the study by Gottrup et al. (19) had an abnormal hypersensitivity in the incisional area. In this area we observed no difference in thermal detection thresholds and HPTs between pain and nonpain patients, but we did observe an increased pain response to pinprick and brush stimulation in patients with pain compared with those without pain, although these differences were quantitatively very minor (VAS <10 on a 100-point scale).
The lack of a clear relationship in sensory disturbances between pain and nonpain patients may at first seem surprising. However, sensory disturbances may be related to damage to the ilioinguinal and iliohypogastric nerves, and studies with intraoperative cryoanalgesia of these nerves have demonstrated sensory dysfunction but no effect on acute pain for up to four weeks after herniotomy (22). Therefore, chronic pain after inguinal herniotomy may be related to damage to deeper nerve structures (musculofascial layer) rather than damage to the nerves traversing the surgical field. Findings after herniotomy may therefore differ from those after herpes zoster and mastectomy, both of which include superficial tissue damage and therefore may be more closely related to cutaneous sensory disturbances.
In conclusion, we studied pain and sensory dysfunction in 72 patients 6–12 months after herniotomy with a quantitative sensory testing technique. The incidence of chronic pain was 28% (20 of 72) and that of sensory dysfunction was 51% (37 of 72), but there were no differences between the pain group and the non-pain group. Quantitative sensory testing had a low specificity for chronic pain after inguinal herniotomy. Future studies should therefore include a detailed assessment of all preoperative, intraoperative, and postoperative factors to elucidate the pathogenesis of chronic postherniotomy pain (23).
1. Perkins FM, Kehlet H. Chronic pain as an outcome of surgery: a review of predictive factors. Anesthesiology 2000;93:1123–33.
2. Callesen T, Bech K, Kehlet H. Prospective study of chronic pain after groin hernia repair. Br J Surg 1999;86:1528–31.
3. Bay-Nielsen M, Perkins FM, Kehlet H. Pain and functional impairment one year after inguinal herniorrhaphy: a nationwide questionnaire study. Ann Surg 2001;233:1–7.
4. Haapaniemi S, Nilsson E. Recurrence and pain three years after groin hernia repair: validation of postal questionnaire and selective physical examination as a method of follow-up. Eur J Surg 2002;168:22–8.
5. Cunningham J, Temple WJ, Mitchell P, et al. Cooperative hernia study: pain in the postrepair patient. Ann Surg 1996;224:598–602.
6. Gillion JF, Ganiez PL. Chronic pain and cutaneous sensory changes after inguinal hernia repair: comparison between open and laparoscopic techniques. Hernia 1999;3:75–80.
7. Pedersen JL, Kehlet H. Hyperalgesia in a human model of acute inflammatory pain: a methodological study. Pain 1998;74:139–51.
8. Altman DG. Practical statistics for medical research. London: Chapman & Hall, 1991.
9. Poobalan AS, Bruce J, King PM, et al. Chronic pain and quality of life following open inguinal hernia repair. Br J Surg 2001;88:1122–6.
10. Akita S, Niga S, Yamato Y, et al. Anatomic basis of chronic pain with special reference to sports hernia. Surg Radiol Anat 1999;21:1–5.
11. Boureau F, Doubrere JF, Luu M. Study of verbal description in neuropathic pain. Pain 1990;42:145–52.
12. Melzack R. The short-form McGill Pain Questionnaire. Pain 1987;30:191–7.
13. Melzack R, Katz J. Pain measurement in persons in pain. In: Wall PD, Melzack R, eds. Textbook of pain. London: Churchill Livingstone, 1999:1341–52.
14. Rowbotham MC, Fields HL. Post-herpetic neuralgia: the relation of pain complaint, sensory disturbance, and skin temperature. Pain 1989;39:129–44.
15. Haanpaa M, Laippala P, Nurmikko T. Allodynia and pinprick hypesthesia in acute herpes zoster, and the development of postherpetic neuralgia. J Pain Symptom Manage 2000;20:50–8.
16. Rowbotham MC, Fields HL. The relationship of pain, allodynia and thermal sensation in post-herpetic neuralgia. Brain 1996;119:347–54.
17. Pappagallo M, Oaklander AL, Quatrano-Piacentini AL, et al. Heterogenous patterns of sensory dysfunction in postherpetic neuralgia suggest multiple pathophysiologic mechanisms. Anesthesiology 2000;92:691–8.
18. Baumgartner U, Magerl W, Klein T et al. Neurogenic hyperalgesia versus painful hypoalgesia: two distinct mechanisms of neuropathic pain. Pain 2002;96:141–51.
19. Gottrup H, Andersen J, Arendt-Nielsen L, Jensen TS. Psychophysical examination in patients with post-mastectomy pain. Pain 2000;87:275–84.
20. Kosek E, Ordeberg G. Lack of pressure pain modulation by heterotopic noxious conditioning stimulation in patients with painful osteoarthritis before, but not following, surgical pain relief. Pain 2000;88:69–78.
21. Kasch H, Stengaard-Pedersen K, Arendt-Nielsen L, Staehelin JT. Headache, neck pain, and neck mobility after acute whiplash injury: a prospective study. Spine 2001;26:1246–51.
22. Callesen T, Bech K, Thorup J, et al. Cryoanalgesia: effect on postherniorrhaphy pain. Anesth Analg 1998;87:896–9.
23. Kehlet H, Bay-Nielsen M, Kingsnorth A. Chronic postherniorrhaphy pain: a call for uniform assessment. Hernia 2002;6:178–81.