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_6032_Библиотеки_им_академика_М_И_Перельмана
.pdf
injection may obviate the need for surgery in some patients.
injection for cervicobrachialgia. Acta Anaesthesiol Scand 1993;37(6):562-566.
surgery for spinal pain: Systematic review and meta-analysis of randomized controlled
trials. Spine J 2015;15(2):348-362.
Epidural steroid injections have a small to moderate surgery-sparing effect (noted in up
to 50% of patients), at least in the short term (less than 1 year). Only studies using
surgery as the primary outcome demonstrated long-term effects of injection. Level of
evidence: II.
injections: Diagnostic and therapeutic value. Reg Anesth Pain Med 2015;40(6):674-680.
Registry analysis of 64 patients indicates that 70% of patients treated with cervical
transforaminal epidural steroid injections avoided surgery for cervical radiculopathy. Of
those who needed surgery, patients who had a positive initial response to an injection
tended to have more favorable surgical outcomes compared with those who did not
respond to the injection. Level of evidence: III.
pain: A systematic review. Spine (Phila Pa 1976) 2014;39(16):1314-1324.
Proven generalizable nonsurgical management for discogenic low back pain is lacking.
Level of evidence: II.
transforaminal epidural injection in patients with axial pain due to cervical disc
herniation. Medicine (Baltimore) 2016;95(4):e2568.
A study of 108 patients treated with interlaminar or transforaminal approaches to
manage axial pain reported an overall 53% rate of successful pain relief at 8-week
follow-up. Level of evidence: III.
Efficacy, safety, and predictors of intradiscal methylene blue injection for discogenic
low back pain: Results of a multicenter prospective clinical series. Pain Pract
2016;16(4):405-412.
Of 15 consecutive patients treated with intradiscal methylene blue injection for the
management of discogenic low back pain, 40% reported at least 30% pain relief 6
months after injection. Level of evidence: IV.
corticosteroids for chronic pain in the cervical zygapophyseal joints. N Engl J Med
1994;330(15):1047-1050.
2003;3(3 suppl):50S-59S.
Manip Ther 2008;16(3):142-152.
Randomized placebo-controlled study evaluating lateral branch radiofrequency
denervation for sacroiliac joint pain. Anesthesiology 2008;109(2):279-288.
the efficacy of lateral branch neurotomy for chronic sacroiliac joint pain. Pain Med
2012;13(3):383-398.
This study randomized 51 patients on a 2:1 basis to lateral branch neurotomy or sham
treatment. At 3-month follow-up, at least 50% reduction in pain was achieved in 47% of
the patients treated with neurotomy versus 12% in the patients who underwent sham
treatment. Level of evidence: I.
treatment of the lumbar dorsal root ganglion in patients with chronic lumbar radicular
pain: A randomized, placebo-controlled pilot study. J Pain Res 2014;7:47-55.
Outcomes at 3-month follow-up demonstrated small effect sizes of treatment compared
with placebo. Level of evidence: I.
plasma (PRP) injections: A prospective, double-blind, randomized controlled study. PM
R 2016;8(1):1-10, quiz 10.
In this trial of 47 patients treated with either intradiscal PRP or intradiscal injection of
contrast, mean improvement in pain and function and categorical improvement in
patient satisfaction was achieved in the treatment group at 8-week follow-up. Level of
evidence: I.
radicular pain: A minimum five-year follow-up. J Bone Joint Surg Am
2006;88(8):1722-1725.
disc herniation. Curr Orthop Pract 2012;23(3):203-208.
This review examined the available evidence on chymopapain injection for treatment of
symptomatic lumbar disk herniation. It was concluded that chymopapain is more
effective than placebo injection, but probably not more effective than surgery.
intradiscal methylene blue injection for the treatment of chronic discogenic low back
pain. Pain 2010;149(1):124-129.
injection for disc herniation. Int J Spine Surg 2014;8:17.
This retrospective review of 108 patients indicated that 75% of patients benefited from
the intervention. Of those patients who avoided surgery, improved outcomes persisted
in more than 80% 5 and 10 years after the intervention. Level of evidence: III.
medial branch radiofrequency neurotomy in New Zealand. Pain Med 2012;13(5):647-
654.
This high-quality study demonstrated successful outcomes in 61% to 74% of carefully
selected patients treated with RFN. Relief persisted 17 to 20 months after one treatment.
Repeat treatments were also effective in most patients. Level of evidence: IV.
in patients on antiplatelet and anticoagulant medications: Guidelines from the American
Society of Regional Anesthesia and Pain Medicine, the European Society of Regional
Anaesthesia and Pain Therapy, the American Academy of Pain Medicine, the
International Neuromodulation Society, the North American Neuromodulation Society,
and the World Institute of Pain. Reg Anesth Pain Med 2015;40(3):182-212.
Guidelines for anticoagulant use around the time of spine interventions are presented,
indicating measurable increased cardiovascular risk associated with anticoagulant
cessation and the need for shared decision making with patients.
procedures. Pain Med 2008;9(suppl 1):S11-S34.
multifidus atrophy after successful radiofrequency neurotomy for low back pain. PM R
2009;1(8):719-722.
spine radiofrequency procedures in patients who have posterior spinal hardware. Pain
Med 2016;17(9):1634-1637.
Posterior spinal hardware can heat to dangerous levels during RFN. Temperature
monitoring with a probe on the hardware surface is recommended. Level of evidence:
IV.
systematic review of the current literature. Pain Med 2014;15(2):196-205.
The current body of evidence addressing the Minimally Invasive Lumbar
Decompression (mild) procedure is of low quality. High-quality studies independent of
industry sponsorship are needed.
decompression compared with fluoroscopy-guided transforaminal epidural steroid
injections for symptomatic contained lumbar disc herniation: A prospective,
randomized, controlled trial. J Neurosurg Spine 2010;12(4):357-371.
disorders. PM R 2015;7(4suppl):S19-S25.
Animal models support biologic therapies for degenerative spine conditions. Clinical
trials are beginning to address discogenic low back pain.
Section 4
Surgical Management of
Degenerative Spine Disorders
SECTION EDITOR:
Charles A. Reitman, MD
Chapter 15
Cervical Degenerative Disease
Patrick B. Morrissey, MD Alan S. Hilibrand, MD
Abstract
Cervical degenerative disease, the most common cause of spinal cord
impairment worldwide, affects up to 180 of every 100,000 people, and its
treatment comprises a large portion of surgical spinal pathology. Cervical
degenerative disease encompasses several pathologic processes such as
cervical disk derangement (herniated or protruding disks), spondylosis, and
ossification of the posterior longitudinal ligament; these processes can result
in symptomatic cervical radiculopathy and/or myelopathy. A wide range of
treatment options, both surgical and nonsurgical, exists for symptomatic
cervical degenerative disorders, depending on the specific compressive
pathology. Surgical treatment is typically recommended for patients with
myelopathy, and for those with persistent pain or worsening neurologic
findings. Cervical fusion, disk arthroplasty, and laminoplasty are all
commonly used, effective techniques, each with specific advantages and
disadvantages. Complications and sequelae of surgical intervention for
cervical degenerative disease are adjacent-segment disease, pseudarthrosis,
neurologic injury, postoperative kyphosis, and infection. It is important to
understand the epidemiology, pathophysiology, diagnosis, and management
of cervical degenerative disease and its complications.
Keywords: adjacent-segment disease; anterior cervical
diskectomy and fusion; C5 nerve palsy; cervical disk
replacement; cervical spondylosis; disk herniation; laminectomy;
laminoplasty; myelopathy; ossification of the posterior
longitudinal ligament; pseudarthrosis; radiculopathy
Dr. Hilibrand or an immediate family member has received royalties from
Aesculap/B. Braun, Amedica, and Biomet; has stock or stock options held in
Amedica, Benvenue Medical, Lifespine, Nexgen, Paradigm Spine, PSD, Spinal
Ventures, and Vertiflex; and serves as a board member, owner, officer, or
committee member of the American Academy of Orthopaedic Surgeons, the
Cervical Spine Research Society, and the North American Spine Society. Neither
Dr. Morrissey nor any immediate family member has received anything of value
from or has stock or stock options held in a commercial company or institution
related directly or indirectly to the subject of this chapter.
Introduction
Patients with degenerative disease of the cervical spine, the most common
cause of spinal cord impairment, comprise a large population of surgically
treated spine patients, both nationally and internationally. The term cervical
degenerative disease encompasses a wide variety of different pathologies.
Initial treatment is usually nonsurgical; however, in instances of spinal cord
or symptomatic nerve root compression, surgical management may be
recommended. Degenerative cervical myelopathy, commonly called cervical
spondylotic myelopathy (CSM), has an incidence of 605 per 1 million people
and accounts for 4.04 hospitalizations per 100,000 person-years.1 Cervical
radiculopathy is much more common, with incidences that range from 63.5 to
179 per 100,000 person-years; up to 26% of these patients ultimately require
surgical intervention.
2,3
It is important to understand the variety of
nonsurgical and surgical treatment techniques available to optimize patient
outcomes while minimizing patient risks.
Cervical Spondylotic Myelopathy and Cervical Radiculopathy
The pathoanatomy of CSM involves both static and dynamic components.
Age-related disk degeneration, associated spondylosis, and hypertrophy of
the ligamentum flavum all contribute to static narrowing of the spinal canal
and compression of the spinal cord4 (Figure 1). The compressive effect of
these anatomic changes can be compounded further by segmental instability
secondary to degeneration of the facet joints and degradation of the
ligamentous stabilizers, particularly the posterior longitudinal ligament (PLL)
and ligamentum flavum. Chronic compression can result in cord ischemia
and a proinflammatory environment that activates apoptotic pathways and
Figure 1
triggers progressive neuronal cell death.
1
Illustration demonstrating pathoanatomic causes of
degenerative cervical spine disorders. PLL = posterior
longitudinal ligament, CSF = cerebrospinal fluid.
As with its myelopathic counterpart, cervical radiculopathy also involves
a substantial degenerative process, although the specific pathoanatomy is
slightly different. Degeneration of the intervertebral disks decreases the
height of the neuroforamen, and osteophytic formation at both the
uncovertebral and zygoapophyseal joints can further decrease space for the
exiting nerve roots. This compression results in an ischemic environment
that, when coupled with the release of multiple proinflammatory cytokines,
can result in sensitization and irritation of the nociceptive fibers within the
dorsal root ganglion and, with persistent insult, apoptotic death of these nerve
fibers.
2
Clinical Evaluation
Thorough and accurate clinical evaluation of the patient with degenerative
cervical disk disease is paramount in diagnosing these conditions. Initial
Figure 2
evaluation should consist of a detailed history, specifically focusing on
reports of progressive weakness, problems with fine motor tasks, gait and
balance disturbances, and bowel or bladder dysfunction. A complete
neurologic examination should be performed, with particular attention given
to the presence of upper motor neuron signs including hyperreflexia, the
Hoffman sign, the inverted radial reflex, the Babinski reflex, sustained
clonus, and gait ataxia because these suggest compressive myelopathy and
the need for surgical decompression. In addition, the presence of dermatomal
or myotomal neurologic changes should be documented and correlated with
relevant radiographic findings.
Radiographic Workup
The radiographic evaluation of degenerative cervical disease must only be
used to confirm the findings of the history and physical examination because
of the relatively high prevalence of radiologic abnormalities among
asymptomatic individuals. Workup should include plain radiographs of the
cervical spine, with flexion and extension views obtained to evaluate for
dynamic instability. Noncontrast MRI assists in the evaluation and
quantification of neural compression and is a necessary diagnostic tool. CT
myelography can be used in patients who are unable to undergo MRI. CT
also can provide additional information when treating patients with
ossification of the PLL or the ligamentum flavum, allowing better
quantification of these pathologies to assist in both patient counseling and
surgical decision making.
Graphs demonstrating the age-based incidence of cervical
disk bulges (A) and spinal cord compression (B) seen on
magnetic resonance images obtained from asymptomatic control
subjects. Asterisk indicates P <0.05. (Adapted and reprinted with
permission from Nakashima H, Yukawa Y, Suda K, Yamagata M, Ueta
T, Kato F: Abnormal findings on magnetic resonance images of the
cervical spines in 1211 asymptomatic subjects. Spine 2015;40[6]:392-
398.)
Although these studies contribute greatly to the evaluation of a patient,
care must be taken during their interpretation. Several studies have
highlighted the presence of abnormal imaging in asymptomatic individuals of
all ages
5-7
(Figure 2). Given the high rate of asymptomatic degenerative
findings, all abnormal imaging findings should be interpreted carefully in
conjunction with the patient’s history and examination when devising an
appropriate treatment strategy.
Surgical Intervention
Indications
Of patients with cervical radiculopathy secondary to degenerative disease,
more than 70% will respond to nonsurgical treatment modalities including
anti-inflammatory medications, physical therapy, and epidural steroid
injections. Surgical intervention is reserved for patients who do not improve
after 6 to 12 weeks of nonsurgical treatment, those with a progressive
neurologic deficit, and those with a persistent functionally limiting static
deficit.
Surgical intervention for patients with CSM is much more common, with
nonsurgical treatment reserved only for those with extremely mild symptoms
and no functional impairment or for those who are medically unsuitable for
surgical intervention. Since the 1950s, the natural history of CSM has been
recognized as a progressive, stepwise deterioration of neurologic function.
8
Therefore, individuals undergoing nonsurgical treatment should be counseled
appropriately regarding signs of disease progression to limit their potential
for neurologic morbidity. Surgical intervention should be recommended for
most patients with CSM. The urgency of treatment (“soon,” but rarely
emergent) is based on the severity of symptoms and the rapidity of disease
progression; acute declines in neurologic function should be treated sooner.
Соседние файлы в папке Библиотека им академика М.И. Перельмана