Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_754_Библиотеки_им_академика_М_И_Перельмана
.pdf
46 Inguinal Hernias: an Algorithmic Approach to Procedure Selection
479
open approach should always be considered in
this scenario if the surgeon is not completely
comfortable with laparoscopy, or if during laparoscopy there are dense and extensive adhesions
found. If a laparoscopic technique is used, a
urinary catheter is mandatory. The bladder can be
distended with methylene blue for easy identifi cation and protection. The surgeon can then
perform the laparoscopic dissection more safely.
Remember, the patient just wants his or her
hernia fi xed, and an open Lichtenstein repair
almost completely avoids the possibility of a
bladder injury.
Obesity (BMI > 35)
Signifi cant obesity can be a relative contraindication for a TEP, given the physical girth of the
lower abdominal wall or pannus. A TAPP repair
can be more straightforward than a TEP in these
patients. However, if the lower abdomen allows
entry into the retrorectus space, then an eTEP
repair may be utilized in standard fashion. This
decision can be made at the time of surgery.
Seroma minimization : Large cavernous
defects, both direct and indirect, run the risk of
forming large seromas. While these are selflimited, they can last many months and be uncomfortable for patients. Once trick to minimize these
is to take the redundant attenuated transversalis
fascia and pull it into the preperitoneal space and
fi xate it to the Cooper’s ligament with a permanent tack.
Conclusions
There are many surgical approaches that are
appropriate for repairing an inguinal hernia
depending on the patient. It is imperative to
understand the known outcomes of each, and
fi ne-tune or evolve one’s technique to minimize
postoperative chronic pain and recurrence rates.
Surgeons should stay in touch with the evolving
techniques and technology in order to provide
optimized outcomes. Learning the treatment
algorithms for the many different types of patients
presenting with inguinal hernias can help guide
surgeons toward this objective.
References
1. Fitzgibbons RJ, Giobbie-Hurder A, Gibbs JO, Dunlop
DD, Reda DJ, McCarthy Jr M, Neumayer LA, Barkun
JS, Hoehn JL, Murphy JT, Sarosi Jr GA, Syme WC,
Thompson JS, Wang J, Jonasson O. Watchful waiting
vs. repair of inguinal hernia in minimally symptomatic men: a randomized clinical trial. JAMA. 2006;
295(3):285–92.
2. Belyansky I, Tsirline VB, Klima DA, Walters AL,
Lincourt AE, Heniford TB. Prospective, comparative
study of postoperative quality of life in TEP, TAPP,
and modifi ed Lichtenstein repairs. Ann Surg. 2011;
254(4):709–14.
3. Scott NW, McCormack K, Graham P, Go PM, Ross
SJ, Grant AM. Open mesh versus non-mesh for repair
of femoral and inguinal hernia. Cochrane Database
Syst Rev. 2002;4:CD002197.
4. Langeveld HR, van’t Riet M, Weidema WF, Stassen
LP, Steyerberg EW, Lange J, Bonjer HJ, Jeekel
J. Total extraperitoneal inguinal hernia repair compared with Lichtenstein (the LEVEL-trial): a randomized controlled trial. Ann Surg. 2010;251(5):819–24.
5. Myers E, Browne KM, Kavanagh DO, Hurley
M. Laparoscopic (TEP) versus Lichtenstein inguinal
hernia repair: a comparison of quality of life outcomes. World J Surg. 2010;34(12):3059–64.
6. Eklund A, Montgomery A, Bergkvist L, Rudberg C.
Chronic pain 5 years after randomized comparison of
laparoscopic and Lichtenstein inguinal hernia repair.
Swedish Multicentre Trial of Inguinal Hernia Repair
by Laparoscopy (SMIL) study group. Br J Surg. 2010;
97(4):600–8.
7. Neumayer L, Giobbie-Hurder A, Jonasson O,
Fitzgibbons Jr R, Dunlop D, Gibbs J, Reda D, Henderson
W. Open mesh versus laparoscopic mesh repair of
inguinal hernia. N Engl J Med. 2004;350(18):1819–27.
8. Wake BL, McCormack K, Fraser C, Vale L, Perez J,
Grant AM. Transabdominal pre-peritoneal (TAPP) vs
totally extraperitoneal (TEP) laparoscopic techniques
for inguinal hernia repair. Cochrane Database Syst
Rev. 2005;25(1):cd004703.
9. Sevonius D, Gunnarsson U, Nordin P, Nilsson E,
Sandblom G. Recurrent groin hernia surgery. Br J Surg.
2011;98(10):1489–94.
10. Bringman S, Blomqvist P. Intestinal obstruction after
inguinal and femoral hernia repair: a study of 33,275
operations during 1992–2000 in Sweden. Hernia.
2005;9(2):178–83.
Evaluation and Treatment
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
of Postoperative Groin Pain
Martin F. Bjurstrom , Parviz K. Amid ,
and David C. Chen
Introduction
Chronic postherniorrhaphy inguinal pain (CPIP) is
today recognized as the most signifi cant severe
complication following inguinal hernia repair.
Globally over 20 million inguinal hernia repairs are
conducted every year, and in the USA alone about
800,000 procedures are performed [ 1 , 2 ]. The risk
of developing moderate-to-severe chronic pain for
those undergoing inguinal herniorrhaphy is
10–12% [ 3 ], and a conservative estimate of chronic
pain adversely affecting daily life or employment
(0.5–6.0%) [ 2 ] translates into 4,000–48,000 new
cases annually in the USA. Over the last decades,
herniorrhaphy techniques have been considerably
refi ned, which has resulted in open and laparoscopic tension-free approaches utilizing advanced
prosthetic mesh- material as the gold standard.
Consequently, hernia recurrence rates have
decreased dramatically (1–5%) [
pain remains a tangible challenge, and now constitutes the most relevant outcome measure. Chronic
postsurgical pain (CPSP) is defi ned as pain that
develops after a surgical procedure, and temporally
lasts more than 2 months, with other causes of pain
M. F. Bjurstrom • P. K. Amid • D. C. Chen (*)
Department of Anesthesiology , Lichtenstein Amid
Hernia Clinic at UCLA , Santa Monica , CA , USA
Department of Surgery , Lichtenstein Amid Hernia
Clinic at UCLA , Santa Monica , CA , USA
dcchen@mednet.ucla.edu
e-mail:
4 ], but chronic
4 7
excluded [ 5 ]. For CPIP, the duration of pain should
be at least 3 months, since postoperative meshrelated infl ammatory processes may take a few
months to subside [ 2 ]. CPIP patients suffer not only
from painful symptoms, but also detrimental psychological and physical consequences, and an
overall reduced quality of life [ 6 ]. The exact socio-
economic burden has not been calculated for CPIP,
but total annual direct and indirect costs may be
around US$40,000 per patient, as determined for
cases of severe postsurgical neuropathic pain [ 7 ].
Prevention and skilled treatment of this serious and
complex condition is of utmost importance.
Etiology and Clinical Presentation
Due to multiple pathophysiological mechanisms
underlying the development of CPIP, the clinical
presentation is complex and heterogeneous.
Iatrogenic damage or trauma to inguinal nerves is
generally considered the most important pathological mechanism with pain developing in the
sensory distribution of the affected nerve(s). The
major inguinal nerves vulnerable for damage
during or after inguinal herniorrhaphy are the
iliohypogastric nerve (IHN), the ilioinguinal
nerve (IIN), the genital branch of the genitofemoral nerve (GFN), and more rarely, the femoral
branch of the GFN or the lateral femoral cutaneous nerve. Intraoperatively, nerves can be
damaged by surgical manipulation, stretching,
crushing, electrical/thermal effects, partial or
Y.W. Novitsky (ed.), Hernia Surgery, DOI 10.1007/978-3-319-27470-6_47
481© Springer International Publishing Switzerland 2016
482
M.F. Bjurstrom et al.
complete transection, through entrapment in
suture during an open repair, or entrapment in
tacks, suture or fi xation during a laparoscopic
repair. Postoperatively, nerves can be damaged
due to envelopment within a meshoma [ 8 ], irrita-
tion secondary to an excessive fi brotic reaction,
or infl ammatory processes such as granuloma or
neuroma formation.
The symptomatology involves several types of
pain, including neuropathic, nociceptive (infl ammatory non-neuropathic), somatic and visceral
pain, which are overlapping in presentation and
often hard to discern clinically. The nonneuropathic pain is typically deep, dull, constant,
and localized over the entirety of the groin area,
while neuropathic pain can be either constant or
intermittent, and characterized by negative sensory
phenomena, dysesthesia, allodynia, or hyperalgesia. Neuropathic pain may radiate to the scrotum,
labium, and/or upper thigh, and occasionally a
trigger point can reproduce the neuropathic pain
symptoms. The symptoms are often aggravated by
ambulation, stooping, hyperextension of the hip,
and sexual intercourse, and can be decreased by
lying down, and fl exion of the thigh. Somatic pain,
characterized by maximum tenderness localized to
the pubic tubercle area, is most commonly caused
by deeply placed anchoring or periosteal anchoring
of the mesh near the pubic tubercle (periostitis
pubis) [ 9 ]. Finally, visceral pain may arise from
intestinal involvement with recurrence, incarceration, or mesh adherence or may be related to the
spermatic cord (funiculodynia) or other periurethral structures, including venous congestion of the
spermatic cord, dyssynergia of the ejaculatory
effector muscles, stricture of the spermatic duct, or
twisting of the spermatic cord. Visceral pain in
CPIP is generally related to sexual dysfunction or
ejaculatory pain in the region of the superfi cial ring
or the testicular/labial region.
The relative role of peripheral versus central
mechanisms in CPIP has not yet been elucidated,
but the mechanisms triggering and driving the
transition from acute to chronic pain may encompass intraoperative long-lasting, high frequency
injury discharge from damaged nerves, early
postoperative ectopic activity in injured nerves,
collateral sprouting from neighboring intact
nociceptive Aδ afferents, excitotoxic destruction
of antinociceptive inhibitory interneurons in the
spinal dorsal horn, neuroimmune alterations and
maladaptive neuronal plasticity [ 10 – 12 ]. CPIP is
also, importantly, infl uenced and modulated by
emotional, cognitive, social, and genetic factors.
Evidence from genetic research indicates an
important role of an individual’s genetic susceptibility to both generation and experience of pain,
and response to analgesics [ 13 ] .
Risk Factors
Several preoperative, perioperative, and postoperative factors related to the development and intensity of CPSP and CPIP have been identifi ed [ 3 , 14 ,
15 ]. Table 47.1 provides a complete list of risk
factors for CPIP [ 11 ]. A high magnitude of pre-
and postoperative pain consistently predicts future
chronic pain across CPSP conditions, and it is also
one of the strongest risk factors for development of
CPIP [ 3 , 10 , 16 ]. The optimal type of anesthesia
Table 47.1 Risk factors for chronic postherniorrhaphy
inguinal pain [
Preoperative factors
Young age
Female sex
High pain intensity level (inguinal/elsewhere)
Lower preoperative optimism
Impairment of everyday activities
Operation for a recurrent hernia
Genetic predisposition
Experimentally induced pain
High-pain intensity to tonic heat stimulation
Perioperative factors
Less experienced surgeon/not dedicated hernia
center
Open repair technique
Mesh type: heavyweight (open, laparoscopic)
Mesh fi xation: suture (open), staple (laparoscopic)?
IIN neurolysis in Lichtenstein repair
Postoperative factors
Postoperative complications (hematoma, infection)
High early postoperative pain intensity
Lower perceived control over pain
Sensory dysfunction in the groin
Note : ? = confl icting opinions/mixed evidence
IIN ilioinguinal nerve, HLA human leukocyte antigen
11 ]
47 Evaluation and Treatment of Postoperative Groin Pain
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
483
has not been extensively researched in connection
to CPIP, but it is not recommended to utilize
regional anesthesia (epidural, spinal) for inguinal
herniorrhaphy, especially among older patients,
due to an increased risk of urinary retention and
other rare, but severe, medical complications [ 17 ].
For open repairs, local infi ltration anesthesia is the
preferred method, providing advantages such as
early recovery and discharge, few complications,
and improved early pain relief [ 18 , 19 ]. However,
there are no published results regarding the role
of local anesthesia on the development of CPIP.
Although laparoscopic approaches may result in
less chronic pain [ 3 , 16 , 20 ], the incidence of sig-
nifi cant pain equilibrates over time, and pain after
laparoscopic repair remains a signifi cant challenge
due to positioning of the mesh and proximal injury
to the inguinal nerves [ 2 , 21 , 22 ].
Mesh is often implicated as a contributing
factor in CPIP. Systematic reviews and metaanalyses have demonstrated signifi cant reduction
of CPIP using lightweight mesh in both open and
laparoscopic settings [ 23 , 24 ]. This effect is likely
mediated through greater biocompatibility, less
infl ammatory response, and reduced foreign body
sensation through greater elasticity. While results
are mixed, it is a reasonable assertion that avoidance of sutures and tacks may reduce the incidence
of CPIP. In one meta-analysis, glue fi xation of
mesh in open repair reduced CPIP, hematoma,
acute postoperative pain, and time to return to
daily activities [ 25 ], but in another meta- analysis
only the latter and early CPIP (3–6 months) were
signifi cantly improved [ 26 ]. As concluded in two
other systematic reviews [ 27 , 28 ], glue mesh fi xa-
tion is an interesting alternative, but more data is
needed regarding several important end points, such
as CPIP and risk of recurrences in relation to size
and type of hernia. Based upon available publications,
self-gripping and sutured mesh demonstrate similar
CPIP rates [ 29 ] .
Evaluation
A detailed history and structured clinical examination are essential components of the diagnostic
evaluation of chronic groin pain. Imaging modalities,
such as ultrasonography, cross-sectional computed
tomography (CT) or magnetic resonance imaging
(MRI), are used to detect recurrence or meshoma,
and exclude a wide spectrum of differential diagnostic entities [ 30 , 31 ]. Currently, MRI is considered the
best valid diagnostic imaging tool for differentiating
causes of uncertain inguinal pain [ 32 , 33 ]. The
evaluation should aim to characterize the cause and
type of pain, and administration of validated pain,
function, and comorbidity assessment instruments
may contribute to the diagnostic process and future
research. Due to overlapping sensory innervations, it
is diffi cult to precisely ascertain which nerves are
involved in the neuralgic pain. Diagnostic peripheral
nerve block or paravertebral root block with a local
anesthetic are helpful for differentiating neuropathic
from non- neuropathic pain, but it is often inconclusive in identifying the specifi c neuralgias. When
results of nerve blocks are equivocal, needle electromyogram may provide additional information [ 34 ],
and magnetic resonance neurography may identify
peripheral nerve compression or injury [ 35 ].
Treatment
There is a paucity of high-quality, controlled,
randomized trials examining non-interventional,
pharmacological, and interventional pain management strategies in CPIP and the best current
conclusions are based on small CPIP studies,
case series, empiric evidence, and extrapolation
of evidence from other neuropathic and CPSP
conditions. Once established, CPIP is often
complex and refractory to treatment, necessitating
multidisciplinary and comprehensive pain management strategies.
Pharmacological Pain Management
At present, it is not possible to defi nitely rank the
pharmacological alternatives for the individual
patient, and it is thus important to choose treatment not only based on expected pain-reduction
effi cacy, but also potential side effects, concomitant treatments, drug interactions, risk of abuse,
and cost. Recent guidelines on pharmacological
484
M.F. Bjurstrom et al.
treatment of neuropathic pain provide systematic
analyses of treatment options based on randomized
clinical trials [ 36 – 39 ]. If basic analgesics (e.g.,
acetaminophen, non-steroid anti- infl ammatory
drugs) provide insuffi cient pain relief, either a
calcium channel α2-δ ligands (gabapentin or
pregabalin) or antidepressants with both norepinephrine and serotonin reuptake inhibition
(SSNRIs, e.g., duloxetine and venlafaxine, and
tricyclic antidepressants [TCAs]) may be started.
Opioids and tramadol are considered second-line
treatment alternatives for neuropathic pain, but can
be utilized as fi rst-line during episodic exacerbations of severe neuropathic pain, or during titration
of α2-δ ligands, TCAs or SSNRIs. There is often
a need for combination therapy, and the strongest
evidence supports TCA-gabapentin or gabapentin-opioids. There is no fi rm evidence to support
the use of lidocaine or capsaicin patches for CPIP
but these may be used adjunctively [ 40 , 41 ]. In
our practice, all patients considered for operative
remediation should have undergone a trial of
gabapentin, pregabalin, and/or an atypical antidepressant. A short trial of lidocaine patches may
be helpful for mild superfi cial neuropathic hypersensitivity, especially for patients that are sensitive to the systemic side effects of narcotics and
neuropathic agents.
Interventional Pain Management
Nerve blocks of the IHN, IIN, and/or GFN have
been used for diagnostic and therapeutic purposes for decades, but there is no robust scientifi c
evidence of analgesic effi cacy, or consensus
regarding best technique. Ultrasound guidance
enables direct visualization of peripheral nerves,
which improves accuracy and reduces intraperitoneal needle placement. Most evidence on
peripheral nerve blocks in CPIP is based on case
reports or case series, and there is only one
randomized, double-blind, placebo-controlled
study published to date, evaluating the effi cacy of
ultrasound- guided IIN/IHN blocks in the treatment of CPIP [ 42 ]. This study by Bischoff et al.
failed to provide evidence for analgesic effi cacy
of local anesthetic nerve block in CPIP. In our
experience, nerve blocks play an important role
in predicting the effi cacy of neurectomy for
patients with inguinodynia. Improvement with
blocks help to distinguish neuropathic pain from
nociceptive causes and helps patients to separate
these two entities. Failure of blocks to relieve
pain, however, is not necessarily predictive of a
lack of effect with neurectomy as there is signifi cant operator dependence with blocks and extensive individual neuroanatomic variability.
If nerve blocks provide signifi cant analgesia,
neuroablative techniques such as chemical neurolysis, cryoablation, and pulsed radiofrequency
(PRF) ablation may be considered for longerlasting effect. Cryoablation is neurodestructive
by means of Wallerian degeneration and selectively destroys axons and myelin sheaths while
leaving the epineurium and perineurium intact.
The affected axons treated with cryoablation are
very unlikely to form neuromas, and patients are
less likely to develop deafferentation pain, both
of which have been associated with neurectomy
or thermal non-PRF ablation. PRF delivers pulses
of electromagnetic energy in or near nerve
tissues, at the peripheral or vertebral level, which
allows for heat (typically 42 °C) to dissipate
during the latent phase so that neurodestructive
temperatures are not obtained, thus lowering the
risk of neuroma formation, neuritis-type reaction,
and deafferentation pain. It is hypothesized that
this moderate heating of nerve tissue temporarily
blocks nerve conduction. A systematic review of
PRF ablation for CPIP concluded that the current
evidence base is limited, and that the strength of
recommendation for this treatment modality is
weak to moderate [ 43 ]. Neuromodulation tech-
niques utilizing implantable devices, such as
peripheral nerve fi eld stimulation (PNFS), dorsal
root ganglion (DRG) stimulation, and spinal cord
stimulation (SCS) may also be considered when
all other conventional treatments have failed.
Case reports and case series provide promising
results [ 11 ], but the scientifi c evidence for these
treatments in CPIP is low quality at present.
47 Evaluation and Treatment of Postoperative Groin Pain
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
485
Surgical Pain Management
Despite advanced multimodal pain management
strategies, a minority of patients will still suffer
from intractable, refractory pain. Failure of conservative measures, is however not an indication
for further surgery, and successful outcomes are
entirely dependent upon choosing patients with
discrete, neuroanatomic problems that may be
corrected with surgery [ 1 , 2 , 44 ]. There is no
level 1 or 2 evidence and best available recommendations are derived from reviews of case
series and expert consensus [
Development of chronic inguinodynia is largely
independent of the method of hernia repair, but
an in-depth understanding of the causes of pain,
groin neuroanatomy, and technical aspects of the
initial operation are necessary to successfully
manage these patients, and determine the operative options [ 2 , 21 , 47 , 48 ].
The neuroanatomy of the groin is complex
and highly variable from the retroperitoneal lumbar plexus to the terminal branches exiting
through the inguinal canal. Understanding the
location of potential nerve injury is crucial [ 49 ].
2 , 45 , 46 ].
In front of the transversalis fascia, the IIN, the
visible and intramuscular segment of the IHN,
and the inguinal segment of the genital branch of
the GFN must be considered (Fig.
47.1 ). These
structures may potentially be injured during open
anterior repairs (tissue repair, Lichtenstein, PHS
[prolene hernia system], and plug) and from
mesh fi xation during laparoscopic repair (TEP
[totally extraperitoneal] and TAPP [transabdominal preperitoneal]). Behind the transversalis fascia within the preperitoneal space, the main trunk
of the genitofemoral and the preperitoneal segment of the genital branch of the GFN are at risk
(Fig.
47.2 ). These must be considered during
open preperitoneal repair (plug, PHS, and Kugel)
and laparoscopic repair (TEP and TAPP). Injury
to the nerves within the retroperitoneal space
including the main trunk of the GFN over the
psoas muscle and the lateral femoral cutaneous
nerve must also be considered after open and
laparoscopic posterior repair [ 47 , 50 ].
The recommended timing for surgical treatment of CPIP not responding to nonsurgical
management is a minimum of 6 months after the
original repair [ 1 , 2 ]. A systematic and thorough
Fig. 47.1 Inguinal
neuroanatomy : classic course
and location of the
ilioinguinal, iliohypogastric,
and genital Branch of the
Genitofemoral nerve within
the inguinal canal
486
Fig. 47.2 Retroperitoneal
neuroanatomy : normal course
of the iliohypogastric,
ilioinguinal, and genitofemoral
nerve trunks within the
retroperitoneal lumbar plexus
M.F. Bjurstrom et al.
preoperative evaluation is imperative, and should
always include review of prior operative reports
(specifi cally, type of repair, type of mesh used,
position of the mesh, method of fi xation, and
nerve handling), and response to prior interventions [ 2 ]. Neuropathic pain isolated to the ingui-
nal distribution, that was not present prior to the
original operation, and with improvement from
diagnostic and therapeutic nerve blocks, has the
highest likelihood of improvement with operative
neurectomy. In our practice, in the absence of
recurrence, infection, or an overt anatomic cause
for pain, we require all patients to be at least 6
months out from their initial operation. We ensure
that they have exhausted all appropriate conservative measures including pharmacologic management, physical therapy, and interventional
nerve blocks prior to consideration for operative
neurectomy.
Selective IIN, IHN, and GFN neurolysis or
neurectomy, removal of mesh and fi xation material, and revision of the prior herniorrhaphy are
common options for treatment [ 51 – 54 ]. Neurolysis
does not address ultrastructural changes of nerve
fi bers, and has limited effi cacy, and simple removal
of entrapping sutures or fi xating devices while
leaving the injured nerve behind is also inadequate
2 ]. Selective single or double neurectomy may be
[
effective for some patients but does not address
ultrastructural changes of seemingly normal
appearing nerves during reoperation, and discerning which nerve is involved can be extremely
diffi cult [
51 – 53 ]. The use of preoperative derma-
tomal mapping and clinical expertise may improve
the likelihood of success with selective neurectomy. Anatomically, the signifi cant variation and
cross-innervation of the inguinal nerves in the
retroperitoneum and inguinal canal make selective
neurectomy less reliable [ 2 , 49 ].
Triple neurectomy of the IIN, IHN, and GFN,
pioneered in our institute in 1995, is currently a
universally accepted surgical treatment for neuropathic pain refractory to conservative measures
and is arguably the most effective option [ 2 , 21 ,
47 , 48 , 50 ]. Our experience has included over 700
patients, 650+ utilizing an open approach with an
over 85% success rate and 42 cases using a laparoscopic retroperitoneal approach with a 93%
success rate [ 50 ]. Operative neurectomy in con-
junction with removal of meshoma, when present,
provides effective relief in the majority of patients
with refractory inguinodynia [ 2 , 50 ]. Triple
neurectomy can be performed through an open
approach using the groin incision of the original
hernia operation or through a laparoscopic
approach particularly for pain after preperitoneal
47 Evaluation and Treatment of Postoperative Groin Pain
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
487
repair or after failed remedial surgery. With open
surgery, the IIN can be identifi ed lateral to the
internal ring, between the ring and the anterior
superior iliac spine. The IHN is identifi ed within
the anatomic cleavage between the external and
internal oblique aponeurosis. The nerve is then
traced proximally within the fi bers of the internal
oblique muscle to a point lateral to the fi eld of the
original hernia repair. Failure to do so may leave
the injured intramuscular segment of the nerve
behind. In those instances where the IHN has a
subaponeurotic course, the internal oblique
aponeurosis is split to visualize and address the
hidden nerve. The inguinal segment of the genital
branch of the GFN can be identifi ed between the
cord and the inguinal ligament and traced laterally
to the internal ring where it is severed.
Alternatively, the nerve may be visualized within
the internal ring through the lateral crus of the
ring. The nerves should be resected proximal to
the fi eld of original hernia repair. Although there
are no specifi c data available, we recommend
ligation of the cut ends of the nerves to avoid
neuroma formation and insertion of the proximal
cut end into the muscle to keep the nerve stump
away from the future scarring of the operative
fi eld [ 2 , 21 , 47 ]. Advantages of the open approach
are a single stage operation, simultaneous plug/
meshoma removal, repair of recurrent hernias,
extension if needed to include the GFN trunk, and
resection of paravasal nerves in case of orchialgia.
The disadvantage of the approach is its complexity
and technical diffi culty operating within the
scarred fi eld which places the spermatic cord,
testicle, and vascular structures at higher risk of
compromise.
Laparoscopic retroperitoneal triple neurectomy may be performed through a transabdominal or extraperitoneal approach [ 50 ]. The IIN and
IHN can be identifi ed within the retroperitoneal
space over the quadratus lumborum muscle and
the GFN over the psoas muscle proximal to the
scarred operative fi eld. Advantages of the laparoscopic approach are the ability to access the
nerves proximal to the mesh-material used during
the original herniorrhaphy, more consistent
neuroanatomy within the lumbar plexus, and its
technical simplicity. Disadvantages include not
being able to remove plugs, if any, not being able
to resect the lamina propria of the vas in case of
associated orchialgia, and potential laxity of the
abdominal muscles caused from proximal denervation. It is critical to clearly explain potential
benefi ts and consequences of operative intervention to manage patient expectations. In addition
to the usual operative risks, specifi c considerations include permanent numbness, the inability
to access or identify three nerves, abdominal wall
laxity from partial denervation of the oblique
muscles, testicular atrophy, numbness in the labia
in females that can interfere with sexual sensation, and loss of a cremasteric refl ex in male
patients [ 2 , 47 , 50 ]. Patients are specifi cally
advised of the potential for ongoing pain and
disability despite successful neurectomy due to
the nociceptive component of pain, maladaptive
neuroplasticity, and centralization of pain. The
development and course of deafferentation
hypersensitivity is unpredictable but typically
diminishes over time. These issues require
serious consideration and should be discussed
with the patient and adequately recorded.
Hernia recurrence and meshoma are obvious
anatomic pathologies amenable to surgical
correction. When recurrence is identifi ed, surgical correction is typically recommended using an
alternative approach (i.e., laparoscopic repair
after initial open repair or vice versa). However,
if accompanied by neuropathic pain, an anterior,
open approach allows for correction of the hernia
as well as access to the nerves [ 47 ]. Meshoma
may cause neuropathic pain from nerve entrapment, direct contact with mesh, or compressive
effects [ 8 ]. It may also cause nociceptive pain
from compression of adjacent structures and
foreign body sensation. Operative removal of the
meshoma is indicated with the need for simultaneous neurectomy directed by the type of mesh,
approach, symptoms, imaging, and anatomy. If
coexisting neuropathic pain is present, all nerves
within the reoperative fi eld should be addressed,
as neuropathy cannot be assessed visually, and
mesh removal will often compromise unaffected
nerves within the inguinal canal [ 2 ]. In patients
with groin pain associated with orchialgia, segmental resection of the lamina propria of the vas
488
M.F. Bjurstrom et al.
together with triple neurectomy has improved
outcomes and helped in the management of testicular pain [ 47 ]. In our experience, we have per-
formed vas neurolysis on over 40 patients with
refractory orchialgia in conjunction with triple
neurectomy with success in over 80% of patients.
Orchialgia, however, is a complex entity and
remedial surgery to correct it is less predictable
and less effective.
Our personal algorithm for operative remediation depends on whether the pain is neuropathic
or nociceptive and is tailored to the initial operation and potential pathologies associated with the
initial repair. Neuropathic pain without evidence
of recurrence or meshoma may be addressed with
triple neurectomy alone either through an open or
laparoscopic approach leaving the mesh and prior
repair intact. If the initial operation was performed
as an open anterior repair, we will typically offer
an open triple neurectomy via the inguinal canal.
If the initial operation was an open or laparoscopic preperitoneal repair, the neurectomy is
best performed through a laparoscopic retroperitoneal approach. Neuropathic pain associated
with meshoma will require mesh removal at the
time of triple neurectomy and can be performed
through an inguinal re-exploration. This is
common for problems related to initial PHS and
plug and patch repair where mesh traverses both
the anterior and posterior planes. Pain caused by
an isolated plug may be removed open, laparoscopic, or at times via a hybrid approach to access
the mesh and nerves. Our preference to treat
neuropathic inguinodynia with triple neurectomy,
given the neuroanatomic considerations and
effi cacy rates. However, selective neurectomy is
appropriate at times with isolated nerve injuries
that do not overlap in dermatomal distribution,
such as an isolated lateral femoral cutaneous nerve
(lateral thigh) or femoral branch of the genitofemoral nerve (anterior thigh) injuries. While general
principles exist, remedial surgery for inguinodynia
remains a challenge and must be tailored for each
individual patient requiring creativity, a thorough
understanding of inguinal and retroperitoneal
neuroanatomy, and an armamentarium of different
open, laparoscopic, mesh, and tissue repairs.
Conclusion
Chronic pain after hernia repair is a dreaded,
heterogeneous pain syndrome representing a
substantial diagnostic and therapeutic challenge.
In-depth knowledge of groin neuroanatomy is
critical, as the best measure to address this debilitating pain state remains prevention by refi ning
the technique of hernia repair. Meticulous adherence to surgical principles with three nerve identifi cation, preservation, or pragmatic neurectomy
during open anterior repair decreases the incidence of CPIP. Avoidance of the preperitoneal
nerves below the iliopubic tract and limited or no
mesh fi xation decreases the risk of pain after
laparoscopic herniorrhaphy. Preventive analgesia
and anesthesia should be considered for patients
at high risk of developing CPIP. Evaluation by a
pain specialist is mandatory, and patients should
undergo multidisciplinary treatment, including
behavioral, pharmacological, and interventional
pain management modalities. For patients with
pain refractory to conservative measures, operative neurectomy, meshoma removal, and repair of
recurrence may provide relief. A multidisciplinary, logical, stepwise approach to CPIP will
afford patients the greatest opportunity to minimize symptoms, manage pain, decrease further
morbidity, and improve quality of life.
References
1. Aasvang E, Kehlet H. Surgical management of
chronic pain after inguinal hernia repair. Br J Surg.
2005;92:795–801.
2 . A l fi eri S, et al. International guidelines for prevention
and management of post-operative chronic pain following inguinal hernia surgery. Hernia. 2011;15:
239–49.
3. Aasvang E, Kehlet H. Chronic postoperative pain: the
case of inguinal herniorrhaphy. Br J Anaesth. 2005;95:
69–76.
4. Bittner R, Schwarz J. Inguinal hernia repair: current
surgical techniques. Langenbeck’s archives of surgery. Deutsche Gesellschaft für Chirurgie. 2012;397:
271–82.
5. Macrae WA, Davies HTO. Chronic postsurgical pain.
In: Crombie IK, Croft PR, Linton SJ, LeResche L,
Von Korff M, editors. Epidemiology of pain. Seattle:
IASP Press; 1999. p. 125–42.
47 Evaluation and Treatment of Postoperative Groin Pain
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
489
6. Kalliomaki ML, Sandblom G, Gunnarsson U, Gordh
T. Persistent pain after groin hernia surgery: a qualitative analysis of pain and its consequences for quality
of life. Acta Anaesthesiol Scand. 2009;53:236–46.
7. Parsons B, et al. Economic and humanistic burden of
post-trauma and post-surgical neuropathic pain
among adults in the United States. J Pain Res. 2013;6:
459–69.
8. Amid PK. Radiologic images of meshoma: a new
phenomenon causing chronic pain after prosthetic
repair of abdominal wall hernias. Arch Surg. 2004;
139:1297–8.
9. Loos MJ, Roumen RM, Scheltinga MR. Classifying
post-herniorrhaphy pain syndromes following elective inguinal hernia repair. World J Surg. 2007;
31:1760–5. discussion 1766-1767.
10. Katz J, Seltzer Z. Transition from acute to chronic
postsurgical pain: risk factors and protective factors.
Expert Rev Neurother. 2009;9:723–44.
11. Bjurstrom MF, Nicol AL, Amid PK, Chen DC. Pain
control following inguinal herniorrhaphy: current perspectives. J Pain Res. 2014;7:277–90.
12. Bjurstrom MF, Giron SE, Griffi s CA. Cerebrospinal
fl uid cytokines and neurotrophic factors in human
chronic pain populations: A comprehensive review.
Pain Pract . 2014.
13. Dominguez CA, et al. The DQB1 *03:02 HLA haplotype is associated with increased risk of chronic pain
after inguinal hernia surgery and lumbar disc herniation. Pain. 2013;154:427–33.
14. Kehlet H, Jensen TS, Woolf CJ. Persistent postsurgical pain: risk factors and prevention. Lancet. 2006;
367:1618–25.
15. Aasvang EK, et al. Predictive risk factors for persistent postherniotomy pain. Anesthesiology. 2010;112:
957–69.
16. Kalliomaki ML, Meyerson J, Gunnarsson U, Gordh T,
Sandblom G. Long-term pain after inguinal hernia
repair in a population-based cohort; risk factors and
interference with daily activities. Eur J Pain. 2008;12:
214–25.
17. Bay-Nielsen M, Kehlet H. Anaesthesia and postoperative morbidity after elective groin hernia repair:
a nation-wide study. Acta Anaesthesiol Scand.
2008;52:169–74.
18. Kehlet H, Aasvang E. Groin hernia repair: anesthesia.
World J Surg. 2005;29:1058–61.
19. Nordin P, Zetterstrom H, Gunnarsson U, Nilsson
E. Local, regional, or general anaesthesia in groin hernia repair: multicentre randomised trial. Lancet. 2003;
362:853–8.
20. Nienhuijs S, et al. Chronic pain after mesh repair of
inguinal hernia: a systematic review. Am J Surg.
2007;194:394–400.
21. Amid PK, Hiatt JR. New understanding of the causes
and surgical treatment of postherniorrhaphy inguinodynia and orchalgia. J Am Coll Surg. 2007;205:381–5.
22. Kalkman CJ, et al. Preoperative prediction of severe
postoperative pain. Pain. 2003;105:415–23.
23. Sajid MS, Leaver C, Baig MK, Sains P. Systematic
review and meta-analysis of the use of lightweight
versus heavyweight mesh in open inguinal hernia
repair. Br J Surg. 2012;99:29–37.
24. Sajid MS, Kalra L, Parampalli U, Sains PS, Baig
MK. A systematic review and meta-analysis evaluating the effectiveness of lightweight mesh against
heavyweight mesh in infl uencing the incidence of
chronic groin pain following laparoscopic inguinal
hernia repair. Am J Surg. 2013;205:726–36.
25. Colvin HS, Rao A, Cavali M, Campanelli G, Amin
AI. Glue versus suture fi xation of mesh during open
repair of inguinal hernias: a systematic review and
meta-analysis. World J Surg. 2013;37:2282–92.
26. de Goede B, et al. Meta-analysis of glue versus
sutured mesh fi xation for Lichtenstein inguinal hernia
repair. Br J Surg. 2013;100:735–42.
27. Ladwa N, Sajid MS, Sains P, Baig MK. Suture mesh
fi xation versus glue mesh fi xation in open inguinal
hernia repair: a systematic review and meta-analysis.
Int J Surg. 2013;11:128–35.
28. Sanders DL, Waydia S. A systematic review of randomised controlled trials assessing mesh fi xation in
open inguinal hernia repair. Hernia. 2014;18:165–76.
29. Zhang C, et al. Self-gripping versus sutured mesh for
inguinal hernia repair: a systematic review and metaanalysis of current literature. J Surg Res. 2013;185:
653–60.
30. Ferzli GS, Edwards ED, Khoury GE. Chronic pain
after inguinal herniorrhaphy. J Am Coll Surg.
2007;205:333–41.
31. Bradley M, Morgan D, Pentlow B, Roe A. The groin
hernia—an ultrasound diagnosis? Ann R Coll Surg
Engl. 2003;85:178–80.
32. van den Berg JC, de Valois JC, Go PM, Rosenbusch
G. Detection of groin hernia with physical examination, ultrasound, and MRI compared with laparoscopic fi ndings. Invest Radiol. 1999;34:739–43.
33. Aasvang EK, Jensen KE, Fiirgaard B, Kehlet H. MRI
and pathology in persistent postherniotomy pain. J Am
Coll Surg. 2009;208:1023–8; discussion 1028–1029.
34. Knockaert DC, Boonen AL, Bruyninckx FL, Bobbaers
HJ. Electromyographic fi ndings in ilioinguinaliliohypogastric nerve entrapment syndrome. Acta
Clin Belg. 1996;51:156–60.
35. Filler A. Magnetic resonance neurography and diffusion tensor imaging: origins, history, and clinical
impact of the fi rst 50,000 cases with an assessment of
effi cacy and utility in a prospective 5000-patient study
group. Neurosurgery. 2009;65:A29–43.
36. Dworkin RH, et al. Pharmacologic management of
neuropathic pain: evidence-based recommendations.
Pain. 2007;132:237–51.
37. Attal N, et al. EFNS guidelines on pharmacological
treatment of neuropathic pain. Eur J Neurol. 2006;
13:1153–69.
38. Attal N, et al. EFNS guidelines on the pharmacological treatment of neuropathic pain: 2010 revision. Eur
J Neurol. 2010;17:1113–88.
Соседние файлы в папке Библиотека им академика М.И. Перельмана