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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6033_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Foreword
- •Preface
- •Contents
- •2.1 Introduction
- •2.2 Lumbar Anatomy
- •2.2.1 Vertebra
- •2.2.2 Intervertebral Discs
- •1: History and Rationale for the Minimally Invasive Lateral Approach
- •1.1 Introduction
- •1.2 Historical Approaches to the Lumbar Spine
- •1.4 Validation of the Technique
- •References
- •2: Biomechanics of Lateral Spinal Reconstruction
- •2.2.3 Facets
- •2.2.4 Muscles and Ligaments
- •2.3.1 The Neutral Zone
- •2.3.2 Bending Moments and Load Carrying
- •2.3.3 Lumbar Lordosis
- •2.4 Biomechanics of Lumbar Pathology
- •2.4.1 Lumbar Surgery
- •2.5 Lateral Lumbar Fixation
- •References
- •3.1 Goals of Minimally Invasive Spine Surgery
- •3.2.1 Blood Loss
- •3.2.2 Decreased Infection Rates
- •3.2.4 Pain Control and Recovery
- •References
- •4: Costs and Economic Implications
- •4.1 Introduction
- •4.2 The Costs of Spine Surgery
- •4.3 Comparative Effectiveness of the MIS Lateral Approach
- •4.4 Cost-Effectiveness of the MIS Lateral Approach
- •4.5 Future Directions
- •References
- •5: Workup and Diagnostic Testing
- •5.1 Introduction
- •5.2 Patient History
- •5.3 Physical Examination
- •5.4 Adjunctive Tests
- •5.5 Preoperative Evaluation of the Pain Generator
- •5.6 Radiographic Studies
- •5.7 Summary
- •References
- •6: Literature Evidence of the MIS Lateral Approach
- •6.1 Adult Spinal Deformity
- •6.1.1 Studies
- •6.1.2 Treatment Characteristics
- •6.1.3 Clinical Outcomes
- •6.1.4 Fusion
- •6.1.5 Complications
- •6.1.7 Conclusion
- •6.2 Degenerative
- •6.2.1 Studies
- •6.2.3 Operative Time
- •6.2.4 Length of Stay
- •6.2.5 Clinical Outcomes
- •6.2.6 Fusion
- •6.2.7 Complications
- •References
- •7: Selecting the Proper Patient for Lumbar Lateral Interbody Fusion and Minimally Invasive Spinal Deformity Surgery
- •7.1 Indications for LLIF
- •7.2 The MISDEF Algorithm
- •References
- •8: Positioning and Safety
- •8.1 Introduction
- •8.2 Positioning the Patient
- •8.3.1 Pressure Ulcers
- •8.3.2 Peripheral Nerve Injury
- •8.3.3 Rhabdomyolysis
- •8.3.4 Postoperative Visual Loss
- •References
- •9: Intraoperative Electrophysiologic Monitoring
- •9.1 Introduction
- •9.2 Anatomic Considerations
- •9.3.2 Somatosensory Evoked Potentials (SSEP)
- •9.3.3 Spontaneous Electromyography (spEMG)
- •9.3.4 Triggered Electromyography (trEMG)
- •9.4 Patient Preparation and Anesthesia Requirements
- •9.6 Ongoing Monitoring
- •References
- •10: Motor-Based Monitoring During Minimally Invasive Lateral Spine Surgery
- •10.1 Introduction
- •10.3 Motor-Evoked Potentials
- •10.4 Electromyography
- •10.4.1 EMG Limitations
- •10.5 Mechanomyography
- •References
- •11: Frameless Navigation
- •11.1 Introduction
- •11.2 Technique
- •11.2.1 Positioning
- •11.2.2 Image Acquisition and Registration to CaSN
- •11.2.3 Surgical Approach and Cage Placement with CaSN
- •References
- •12.7 Retraction
- •12.8 Shallow Docking
- •12.9 Oblique Approach
- •References
- •12: Techniques for Avoiding Psoas Muscle and Lumbosacral Plexus Injury
- •12.1 Introduction
- •12.2 Anatomy
- •12.5 Retroperitoneal Dissection
- •12.6 Electromyography
- •13: Single Versus Dual Incisions for Lateral Retroperitoneal Approach
- •13.1 Single Incision
- •13.1.1 Surgical Technique
- •13.2 Dual Incisions
- •13.2.1 Surgical Technique [1]
- •13.2.2 Advantages and Disadvantages
- •References
- •14: Lateral Transpsoas Retractor Technology
- •14.1 Introduction
- •14.2 MaXcess® (NuVasive, Inc.)
- •14.3 Mars® 3V (Globus, Inc.)
- •14.5 Pipeline® (Depuy Synthes, Inc.)
- •14.6 Oracle® (Depuy Synthes, Inc.)
- •14.7 Aira® 3 (Stryker, Inc.)
- •14.8 Ravine® 3 (K2M, Inc.)
- •14.9 Veo® (Baxano, Inc.) [6]
- •References
- •15: Anterior to Psoas (ATP) Fusion of the Lumbar Spine
- •15.1 Introduction
- •15.2 Indications
- •15.3 Contraindications
- •15.4 Equipment
- •15.5 Surgical Technique
- •15.5.1 Patient Positioning
- •15.5.2 Incision
- •15.5.3 Exposure of the Disc
- •15.5.4 Discectomy and Endplate Preparation
- •15.5.4.1 ALL Release
- •15.5.5 Cage and Plate Insertion
- •15.5.5.1 L5/S1
- •15.6 Discussion
- •15.6.1 History
- •15.6.2 Cages
- •15.6.2.1 Clinical Results
- •15.6.3 Retractors
- •15.6.3.1 Neuromonitoring
- •15.6.4 Psoas Retraction
- •15.6.5 Levels
- •15.6.6 Vascular Injuries
- •15.6.7 Nerve Injuries
- •15.7 ALL Section
- •References
- •16: Thoracic MIS Retropleural Access
- •16.1 Introduction
- •16.2 Anterior-Based Approaches
- •16.3 Posterior-Based Approaches
- •16.4 Lateral-Based Approaches
- •16.5 Surgical Technique and Anatomic Considerations
- •16.5.1 Preoperative Planning
- •16.5.2 Preparation and Patient Positioning
- •16.5.3 Surgical Approach
- •16.5.4 Postoperative Care
- •16.6 Outcomes Using a Minimally Invasive Anterolateral Approach
- •16.7 Advantages of the Minimally Invasive Lateral Approach
- •16.8 Limitations of the Minimally Invasive Lateral Approach
- •16.9 Summary
- •References
- •17: Psoas Muscle Management
- •17.1 Introduction
- •17.3 Transpsoas Versus ATP
- •17.4 Traversing the Psoas Major
- •References
- •18: The Extreme Lateral Minimally Invasive Approach to Pure Degenerative Lumbar Disk Disease
- •18.1 Introduction
- •18.2 The Rome Experience
- •18.2.1 Surgical Technique
- •18.3 Results
- •18.3.1 Demonstrative Cases
- •18.3.1.1 Case 1
- •18.3.1.2 Case 2
- •18.3.1.3 Case 3
- •18.4 Discussion
- •References
- •19: Lateral Approach for Spondylolisthesis
- •19.1 Introduction
- •19.2 Treatment
- •19.3 Surgical Technique
- •19.4 Outcomes
- •19.5 Complications
- •References
- •20: Lateral Lumbar Interbody Fusion (LLIF) for the Treatment of Adult Spinal Deformity (ASD)
- •20.1 Introduction
- •20.2 MIS Treatment Algorithm
- •20.3 Surgical Technique
- •20.3.1 Patient and Bed Positioning
- •20.3.2 Fluoroscopic Imaging
- •20.3.3 Access to the Psoas
- •20.3.4 Transpsoas Approach and Retractor Docking
- •20.3.5 Preparing the Disk Space
- •20.3.6 Maximizing Correction
- •20.3.7 Approach Through the Concavity vs. Convexity
- •20.3.8 Sequence of LLIF Instrumentation
- •20.3.9 Wound Closure
- •20.4 Outcomes
- •References
- •21: Neoplasia
- •21.1 Introduction
- •21.2 Clinical Features
- •21.3 Diagnosis
- •21.4 Primary Vertebral Tumor
- •21.4.1 Aneurysmal Bone Cyst
- •21.4.2 Hemangioma
- •21.4.3 Osteosarcoma
- •21.4.4 Giant Cell Tumor
- •21.4.6 Meningioma
- •21.4.7 Nerve Sheath Tumor
- •21.5 Surgical Treatment for Primary and Metastatic Spine Tumors
- •21.5.1 Open Surgery
- •21.5.2 MIS Lateral Approach
- •References
- •22: Minimally Invasive Lateral Spine Surgery in Trauma
- •22.1 Introduction
- •22.3 Indications for the Anterior Approach
- •22.4 Complications Associated with the Open Anterior and Posterior Approaches
- •22.6 Lateral MISS Techniques
- •References
- •23: Lateral MIS Surgery for Spinal Column Infections
- •23.1 Introduction
- •23.2.1.1 Indications
- •23.2.1.2 Contraindication
- •23.2.2 Technique
- •23.2.2.1 Preoperative Preparation
- •23.2.2.2 Operative Procedure
- •23.2.2.3 Postoperative Treatment
- •23.3 Clinical Outcomes
- •23.4 Complications
- •23.4.1 Approach-Related Complications
- •23.4.2 Instrumentation-Related Complications
- •23.4.3 Infection-Related Complications
- •23.5 Case Studies
- •23.5.1 Case 1
- •23.5.2 Case 2
- •Further Reading
- •25: Lateral Lumbar Interbody Fusion: A Review of the Current Clinical Outcomes of Different Supplemental Fixation Techniques
- •25.1 Introduction
- •25.2.1 Case Example
- •25.3 Interspinous Fusion
- •25.3.1 Case Example
- •25.4 Integrated Fixation Fusion
- •25.5 Simultaneous Combined Anterior and Posterior Fusion
- •References
- •26: Anterolateral Fixation in LLIF
- •26.1 Introduction
- •26.3 When? The Indications for Supplemental Fixation
- •26.3.1 Reduced Bone Density
- •26.3.2 Facet Arthropathy
- •26.3.3 Deformity
- •26.3.4 Instability
- •26.3.5 Pars Defects
- •26.3.6 Cage Width and Levels
- •26.3.7 Adjacent Segment Disease
- •26.3.8 Previous Surgery
- •26.4.1 Lateral Fixation
- •26.4.2 Posterior Fixation
- •26.4.3 Combination Lateral and Posterior Fixation
- •References
- •27: Anterior Column Realignment
- •27.1 Introduction
- •27.2 Applications
- •27.3 Regional Anatomy
- •27.4 Surgical Technique
- •27.5 Potential Pitfalls
- •27.6 Complications
- •References
- •28: Subsidence in LLIF
- •28.1 Introduction
- •28.3 Rates
- •28.4 Risk Factors
- •28.4.1 Caudal Endplate
- •28.4.2 Level
- •28.4.3 Bone Quality
- •28.4.4 Cage Size
- •28.4.5 Bone Morphogenetic Protein
- •28.6 Prevention/Recommendations
- •28.6.1 Standalone Cages/Supplemental Posterior Instrumentation
- •References
- •29: Osteobiologics
- •29.1 Introduction
- •29.2 Autografts
- •29.3 Allograft Bone
- •29.3.1 Demineralized Bone Matrix
- •29.4 Ceramics
- •29.5 Bone Morphogenetic Proteins
- •29.6 Bone Marrow Aspirate (BMA)
- •29.7 Platelet Gels
- •29.8 Summary
- •References
- •30: Indirect Decompression
- •30.1 Lumbar Stenosis
- •30.2 Lateral Interbody Fusion
- •References
- •31: Approaching a Deformity from the Concavity Versus Convexity
- •31.1 Introduction
- •31.2 Concavity Approach
- •31.3 Convexity Approach
- •31.4 The Importance of L4/L5
- •31.5 Additional Considerations
- •References
- •32: Awake Lateral Lumbar Fusion
- •33: Managing and Preventing Vascular Complications
- •33.1 Introduction
- •33.3 Incidence of Vascular Complications in Lumbar Spine Surgery
- •33.3.1 Posterior Approach
- •33.3.2 Anterior Conventional Approach
- •33.3.3 Lateral or Extreme Lateral Retroperitoneal Transpsoas Approach
- •33.4 Surgical Features in Lateral Retroperitoneal Transpsoas Interbody Fusion
- •33.5 Preventive Measures of Vascular Complications in Anterior Lumbar Spine Surgery
- •33.5.1 Preoperative Period
- •33.5.2 Operative Period
- •33.5.3 Postoperative Period
- •33.6 Management of Vascular Injuries
- •33.6.1 Venous Injury
- •33.6.2 Arterial Injury
- •References
- •34: Managing and Preventing Soft Tissue Complications
- •34.1 Introduction
- •34.3 Retroperitoneal Injuries
- •34.4 Management of Complications
- •34.5 Prevention of Complications
- •References
- •35: Ileus and Gastrointestinal Complications
- •35.2.1 Neural
- •35.2.3 Pharmacologic
- •35.6 Fiscal Consequences of POI
- •References
- •36: Lumbar Plexus Injury: Lateral MIS Spinal Fusion
- •36.1 Introduction
- •36.2 Sensory Complications
- •36.2.2 Ilioinguinal Nerve (L1): SDZ1
- •36.2.4 Lateral Cutaneous Nerve (L2, L3): SDZ2
- •36.3 Motor Complications
- •36.3.1 Femoral Nerve (Dorsal L2–L4)
- •36.3.2 Obturator Nerve (Ventral L2–L4) and Lumbosacral Trunk (L4, L5)
- •References
- •Index

2 Biomechanics of Lateral Spinal Reconstruction
13
of which leads to altered load sharing and transference of forces to the facets and the discendplate periphery. Together with decreased
bone mineral density and thinning of the cancellous trabecular architecture, weakened vertebral
bodies can fail under stress and lead to compression fracture [ 2 , 8 ].
2.2.3 Facets
The facets are diarthrodial joints that extend bilaterally from the lamina to articulate with corresponding facets of the level above and below.
These osseous pillars have opposing cartilage surfaces and a synovial connective tissue lining that
provides lubrication to create a low friction environment [ 9 ]. A strong ligamentous capsule enve-
lopes the joint. The capsule resists deformation,
rotation, and translation, and a rich receptor innervation enables robust central nervous system communication to prevent joint overload or injury. The
facets not only increase in mass from L1 to L5, but
the orientation also progresses toward a more sagittal position with caudal descent (though the L5–
S1 facet abruptly assumes a coronal orientation).
Together they share in axial load bearing with the
intervertebral discs, with 25 % of the load transmitted through the facets in the normal spine and a
greater percentage with disc pathology or lumbar
extension [ 1 ]. The oblique lumbar joint geometry
means that they are excellent stops to rotatory,
translational, and lateral bending movements and
are less effective during fl exion [
ultimately guide and constrain movement at adjacent segments to prevent motions that could put
the disc and neural structures at risk [ 10 ].
9 ]. The facets
2.2.4 Muscles and Ligaments
Lumbar muscles are intimately involved with
coordinating the impressive degree of physiologic motion of the spine along with constraining
motion to qualities and quantities that do not put
anatomical structures at risk. Flexors include the
psoas muscle, as well as indirectly the rectus
abdominus muscle. The latter balances the long
extensors, as well as creating a rigid cylinder
around the spine by increasing intra-abdominal
pressure and tensing the lumbodorsal fascia [ 3 ].
The lumbar extensors consist of the upper erector
spinae (longissimus and iliocostalis lumborum)
and lumbar erector spinae muscles (multifi dus
and lumbar portions of the longissimus and iliocostalis). The upper erector spinae muscle arises
from the thoracic spine, spans the entire lumbar
region, and inserts on the sacrum and posterior
superior iliac spine. The lumbar longissimus and
iliocostalis muscles have an oblique orientation
which results in large posterior translation forces
during lifting, counteracting ventral shear forces.
The multifi dus muscle consists of multiple overlapping fi bers, with each fascicle arising from a
single tendon connected to a spinous process and
inserting on a caudal mammillary process,
sacrum, and iliac crest. Multifi dus muscle orientation and attachment points permit powerful
extension and rotation [ 11 ].
A series of vertically oriented ligaments span
dorsal and ventral vertebral segments. The posterior longitudinal ligament, supraspinous ligament, interspinous ligament, and ligamentum
fl avum resist hyperfl exion. This latter ligament is
infused with a high proportion of elastic fi bers
that resists buckling during extension. The anterior longitudinal ligament resists hyperextension
through a continuous attachment along the ventral vertebral bodies and fewer attachments to the
annulus fi brosus [ 4 ].
2.3 Lumbar Geometry
and Stability
The various anatomical elements of the lumbar
spine must interact seamlessly to ensure fl uid and
effi cient motion while protecting adjacent structures from injurious forces and motions. Spinal
stability, in essence, is the ability to safely engage
in such physiologic movements; conversely,
instability is defi ned by the inability to protect
neural and mechanical elements under physiologic loads, leading to neural decline, incapacitating pain, or deformity [ 12 , 13 ]. A stable lumbar
spine is expected to maintain a lordotic posture,

14
P. Porensky et al.
engage in effi cient energy expenditure during
movement, participate in force transfer to control
limb movement, and neutralize noxious forces. A
three-component system works to maintain stability: passive tensile forces such as osseous elements, ligaments, facets, and intervertebral discs;
active forces are the muscles and tendons that
work to maintain position within safe ranges of
motion; last is the system of peripheral to central
receptors and nerves that coordinate such safe
movement and attempt compensation for force
stresses [ 3 ].
2.3.1 The Neutral Zone
Spinal stability is better understood when considering displacement of lumbar elements while subjected to increasing loads. Neutral posture and
small but incremental load carrying is characterized by a zone of high laxity (fl exibility) with low
stiffness. The neutral zone (NZ) is manifest when
movements are highly energy effi cient, and ligaments, tendons, and muscles are under very little
tension [ 4 , 14 ]. As loads increase the terminus of
the NZ is reached and the spine begins to stiffen,
and individual spinal elements are placed under
tension. Hence, a region of linear increase on the
load-displacement curve known as the elastic
zone (EZ) is entered. The EZ in a stable spine
marks the end of pain and injury- free range of
motion. The biphasic lumbar load- displacement
curve, composed of the NZ followed by the EZ,
allows for the dual and contradictory goals of
movement and element protection (Fig.
two zones permit energy-conserved motion and
increase spinal stiffening near the terminus of
physiologic motion; additional forces beyond
these zones result in permanent deformation and
eventually complete failure. Active spinal forces
and central nervous system communication are
taxed with maintaining posture within this range
of motion [ 3 ].
Instability is thus further defi ned by a decrease
in the capacity of spinal stabilizing systems to
maintain the neutral zone within physiologic
2.1 ). The
Physiologic range
of motion
Stress
Neutral zone Elastic zone
Strain
Fig. 2.1 A load-deformation curve illustrating the neutral
and elastic zones (deformation or strain on the x-axis, load
or stress on the y-axis) (With permission from Thieme
Publishing, New York, NY; in Biomechanics of the Spine
(editor/author: Edward C. Benzel), 2001)
ranges, that is, within quantitative and qualitative
ranges of motion that do not cause neurologic
dysfunction, pain, or deformity. The neutral zone
is naturally fl oppy. Rigidity for the maintenance
of the upright posture is sustained by active muscle contractions. The neutral zone is therefore
dynamic, with both physiologic and pathologic
behaviors augmenting its size. Stretching or ligamentous, disc, or other passive system injuries,
including destabilizing surgery, expand the zone.
The lumbar musculature stiffens the spine to prevent injury. Core strengthening (including the
strengthening of the lumbar musculature) shrinks
the neutral zone, as does surgical fi xation [ 12 , 14 ].
2.3.2 Bending Moments and Load Carrying
The maintenance of stability requires resistance
to deforming forces. These can be divided into

2 Biomechanics of Lateral Spinal Reconstruction
Fig. 2.2 Translation of the
IAR from preload ( a ) to a
more dorsal position ( b ) after
application of a ventral
bending moment (With
permission from Thieme
Publishing, New York, NY; in
Biomechanics of the Spine
(editor/author: Edward
C. Benzel), 2001)
15
component force vectors that have a well-defi ned
direction in space. To determine the effect of a
vector on an individual vertebral body functional
unit, the point at which the vertebral body pivots
at any given time (IAR, instantaneous axis of
rotation) and the orthogonal distance from the
IAR to the force vector (the moment arm) are
defi ned. When a spine segment moves, the IAR
typically passes through or close by the vertebral
body. The IAR is dynamic, moving dorsally with
fl exion in the sagittal plane and more ventral with
extension (Fig. 2.2 ). Its position can be predicted
with fl exion-extension radiographs. There are
twelve potential movements around each IAR,
encompassing both translation and rotation with
respect to the x / y / z axes [ 3 , 12 ]. To determine the
amount of force at a spinal level, one must calculate the force that a vector generates on the IAR
by means of torque on the “imaginary lever” of
the moment arm. The product of the moment arm
length ( D ) and the vector force ( F ) applied to the
moment arm is the bending moment ( M )
(Fig. 2.3 ).
DF M* =
12
[]
Fig. 2.3 ( a ) Force vector defi ned in three-dimensional
space; ( b ) a bending moment ( M ) is created when a force
( F ) is applied at a distance ( d ) from a fulcrum (the IAR)
(With permission from Thieme Publishing, New York,
NY; in Biomechanics of the Spine (editor/author: Edward
C. Benzel), 2001)

16
Fig. 2.4 The maximum
bending moment ( M , a
product of force ( F ) and
moment arm length ( D )) is at
the center of the circle created
by the radius of its arc. ( a )
Lateral view of vertebral body
failure from an excessive
bending moment; ( b )
anteroposterior view (With
permission from Thieme
Publishing, New York, NY; in
Biomechanics of the Spine
(editor/author: Edward
C. Benzel), 2001)
P. Porensky et al.
The bending moment results in rotation about the
IAR. Counteracting forces positioned to produce
bending moments equal in quantity though
opposite in direction result in zero net motion, in
keeping with Newton’s second law of motion.
The bending moments produced by forward
fl exion of the thoracic spine are counteracted by
extension bending moments in the lumbar spine.
2.3.3 Lumbar Lordosis
The lordotic curve of the lumbar spine is an
evolutionary adaptation to facilitate stability
during upright posture and bipedal gait. Humans
are born with a pan-kyphosis and assume cervical
and lumbar lordosis with ambulation. The curves
combine to center the trunk over the femoral
heads and increase the resistance to vertical loads
by deforming in ordered directions that are maintained by the active and passive spinal elements
[ 3 ]. The exaggerated lordosis of the lower lumbar
spine places the IAR in-line with major force
vectors, resulting in only small bending moments.
This protective factor results in a lower rate of
fracture with supranormal forces; fractures that
do occur here result in more pure axial loads and
a higher relative rate of burst fractures. In contrast, the straightening and slight kyphosis of the
thoracolumbar junction shifts the IAR dorsally
and increases the subsequent fl exion bending
moment, imparting signifi cant stress on the discs
and anterior vertebral bodies. Supranormal
vectors, as occurs during trauma or repetitive
fl exion, predispose to compression fracture and
disc degeneration [ 12 ] (Fig. 2.4 ). Lumbar hyper-
fl exion during lifting also shifts the IAR dorsally,
drastically increasing the fl exion bending
moment. Together with offl oading the facets onto
already stressed discs and vertebral bodies, such
posture considerably increases ventral shear
forces and the potential to damage spinal elements at lower compressive loads [ 11 ].
Maintaining lumbar lordosis, or augmenting
lordosis in the setting of a fl at back, decreases the
moment arm and ventral stress. Interbody lordotic cages or posterior osteotomies can achieve
this effect surgically [ 15 ]. Furthermore, a greater
fl exion moment arm must be counteracted by the
active and passive elements of lumbar extension

2 Biomechanics of Lateral Spinal Reconstruction
17
Fig. 2.5 The relative lever arm lengths of lumbar ligaments. ( a ) The moment arms of lumbar ligaments (yield-
ing fl exion or extension). ( b ) Ligament distance from the
IAR. ( Dot IAR, ALL anterior longitudinal ligament, PLL
posterior longitudinal ligament, LF ligamentum fl avum,
CL capsular ligament, ISL interspinous ligament) (With
permission from Thieme Publishing, New York, NY; in
Biomechanics of the Spine (editor/author: Edward
C. Benzel), 2001)
to maintain sagittal balance within the physiologic neutral zone. Posterior ligaments vary in
their capacity to resist fl exion based on their
intrinsic strength and their moment arm length
from the IAR. The supraspinous and intraspinous
ligaments have superior mechanical advantage
and a proportionally high bending moment compared to the PLL, and thus their disruption can
lead to progressive kyphosis. Capsular ligaments
have superior strength and a moderate-length
moment arm [ 12 , 16 ] (Fig. 2.5 ).
Lumbar muscular extensors are most effi cient
while in lordosis. Lumbar fl exion reduces the
lever arm length of the erector spinae and the
muscles must operate at a mechanical disadvantage
when resisting the forward fl exion of the trunk.
Sustained and more forceful contractions lead to
ineffi cient energy expenditure and back pain,
fatigue, and poor posture. Multifi dus loses optimal fascicle orientation with lumbar fl exion,
impairing its ability to resist fl exion, translation,
and shear forces [ 11 ].
2.4 Biomechanics of Lumbar Pathology
Common lumbar pathology, including stenosis,
degenerative disc disease, and spondylolisthesis,
results in anatomic changes that alter normal biomechanics. Furthermore, traditional surgical
interventions designed to treat these conditions
can themselves disrupt mechanics and lead to
progressive lumbar instability. Lumbar stenosis
is a progressive degenerative process defi ned by
canal, lateral recess, and foraminal narrowing. It
is frequently a result of ligamentous and osseous
hypertrophy in response to pathologic motion
within degenerative lumbar functional units [ 17 ].
Direct decompression of effected neural elements
is the treatment of choice, including laminectomy, laminotomy, and foraminotomy.
Degenerative disc disease (DDD) is one of the
most common causes of low back pain. Several
interrelated degenerative changes can lead to
derangement of normal biomechanics, including
annular tears, endplate fi ssuring and ossifi cation,
and loss of disc height through decreased water
content and proteoglycan degradation. These
degenerative changes increase the likelihood of
nucleus extrusion, decreased weight bearing by
the nucleus pulposus, and shifting of force carrying onto adjacent articular surfaces and facet
joints [ 7 ]. Therefore, facet joint degeneration is
almost always associated with or preceded by
degeneration of the intervertebral disc [ 9 ].
Furthermore, decreased hydrostatic pressure
diminishes tension along the longitudinal ligaments and inner annulus, compromising the ability of the disc to resist shear forces and forward
displacement [ 18 ]. The lumbar discs and vertebral
bodies are wedge shaped, and decreased disc
height together with osseous compression in

18
P. Porensky et al.
weakened cancellous bone yields a progressive
loss of lordosis. As described above, active and
passive lumbar extensors function most effi ciently
in physiologic lordosis. DDD not only results in
pain at the overloaded facets and deranged endplate but also from progressive kyphosis and the
biomechanical disadvantage of overburdened
lumbar extensor musculature. Surgical restoration
of disc height and reestablishment of a lordotic
curve addresses these pain generators.
Spondylolithesis describes the translational
motion of one vertebral body on another.
Classifi cation includes dysplasia from a congenitally incomplete neural arch, traumatic, pathologic, isthmic, and degenerative. Pathologic and
traumatic etiologies imply a localized trauma or
generalized osseous condition that permits forward
slip. Isthmic spondylolithesis is the result of pars
interarticularis incompetence (spondylolysis),
while a degenerative etiology is associated with
facet joint spondylosis and DDD [ 19 ]. The latter is
associated with an increased female prevalence
and most commonly occurs at the L4–5 level [ 6 ].
From a biomechanical perspective, forward fl exion increases shear stress on the ventral disc,
which is counteracted by extensor muscles and
ligaments. The application of these force vectors
places a maximum amount of stress along the pedicle and pars, ventral disc, and facet; eventual failure of one or all of these structures results in
translation of one vertebral functional unit over
another. Progression of spondylolithesis is associated with disc degeneration and is highly correlated with loss of disc height [
18 ]. Spondylolithesis
is clinically manifest most commonly by mechanical back pain, and displacement of the neural arch
can lead to compression of nerve roots and the thecal sac. Surgical intervention targets decompression and fi xation/fusion to arrest and possibly
correct listhesis.
2.4.1 Lumbar Surgery
Many biomechanical considerations should be
appreciated during a posterior approach to the
lumbar spine for decompression and posterolateral fi xation and fusion [ 20 ]. Extensive soft- tissue
dissection during exposure risks muscle denervation and disruption of the active stabilizing systems. Resection of the interspinous ligaments
weakens the passive extensor stabilizers and
diminishes their large bending moments that
counteract fl exion vectors. Facet capsules, associated with strong ligamentous complexes with
moderate moment arms, resist fl exion and are
easily injured during exposure and decompression. The facet joints themselves are important
for guiding and constraining motion as well as
for axial load bearing. Excessive facet joint resection places increased loads on adjoining joints
and discs and results in accelerated degeneration.
Aggressive resection of the pars interarticularis
disassociates functional units and increases shear
stress on ventral structures, leading to iatrogenic
spondylolisthesis (Fig. 2.6 ).
Because anterior column degeneration is a primary cause for spondylolisthesis, surgical management is aimed at restoration of anterior
column support. Insertion of interbody spacers
allows tensile strain restoration, disc height augmentation, correction of anterior column alignment, and subluxation reduction [ 21 ]. Indirect
decompression of the neural foramen may also
occur [ 22 ]. If posterior elements are also affected,
as with isthmic spondylolysis, anterior interbody
instrumentation must be followed by posterior
instrumentation.
Traditional treatment options for lumbar
interbody fusion include anterior lumbar interbody fusion (ALIF), transforaminal lumbar interbody fusion (TLIF), and posterior lumbar
interbody fusion (PLIF). PLIF and TLIF use a
posterior approach and therefore the biomechanical considerations of a posterior approach must
be considered. Facet joint resection mandates
posterolateral fi xation and fusion to ensure stability. The ALIF approach spares the posterior elements, though sacrifi ces the anterior longitudinal
ligament (ALL) when creating a ventral annulotomy. The ALL is a strong tension band in extension [
4 ]. After disruption of this ligament, the
PLL and dorsal elements alone must recreate this
tension band effect, although placement of an
anterior plate restores stability in extension [ 23 ].
Stand-alone interbody spacers risk over

2 Biomechanics of Lateral Spinal Reconstruction
Fig. 2.6 Iatrogenic progressive L4/5 spondylolisthesis after lumbar laminectomy. ( a ) T1-weighted MRI prior to lami-
nectomy; ( b ) T2-weighted MRI post-laminectomy
19
distraction of the facet joints, leading to shifting
of load sharing ventrally and impaired resistance
to forward fl exion.
2.5 Lateral Lumbar Fixation
A lateral lumbar approach avoids many of the
destructive changes that accompany anterior or
posterior approaches [ 24 ] and may offer further
biomechanical advantage by nature of the interbody graft and fusion. All three major tensile
ligaments, including the ALL, PLL, and interspinous ligament complex, are left intact during
dissection and discectomy, maintaining inherent
stability. Denervation of the erector spinae
muscle is circumvented, though the transpsoas
technique does place temporary traction on a
major lumbar fl exor, the psoas muscle. The facet
joint and capsule are not disturbed, thus avoiding
iatrogenic instability from posterior bony element
resection.
Lumbar spine biomechanics are augmented in
several ways by the lateral interbody method.
Placement of a large intervertebral graft with
accompanying disc space distraction permits
indirect decompression of the foramen and spinal
canal via ligamentotaxis and unbuckling of the
PLL and ligamentum fl avum. Restoration of
anterior column height and tensioning of the ligaments may reduce spondylolisthesis and restore
physiologic lordosis [ 18 , 21 ]. Correction of sagit-
tal kyphotic deformity places each element of the
vertebral functional unit into the most effi cient
orientation for maintenance of stability within
the neutral zone; it also may reduce the incidence
of adjacent level disc degeneration [ 11 , 15 , 25 , 26 ].
Compared to other techniques, a larger interbody
cage can be used that covers the entire transverse
dimension of the endplate and creates a larger
area for fusion [ 27 ]. Larger implants that cover
greater endplate surface area may also reduce the
rate of cage subsidence and the risk of ventral
loss of height [ 28 ].
Restoration of disc height and fusion with a
large interbody implant may be suffi cient for correction of degenerative spondylolisthesis [ 21 ].
Conversely, an incompetent posterior ligamentous or osseous complex (i.e., spondylolysis)
must be supplemented with dorsal fi xation in
order to avoid progressive instability [ 18 , 20 ].
Cage shape, bone density, and simultaneous use

20
P. Porensky et al.
of dorsal instrumentation determine compressive
strength of cages used in interbody techniques
[ 20 ]. Cylindrical cages provide less implant-
endplate contact area than rectangular grafts and
therefore resist motion to a lesser extent than
rectangular grafts [ 27 , 29 ]. Since larger grafts
create a larger surface area for fusion and provide
more stability, rectangular grafts are preferred.
As mentioned earlier, excessive disc space
distraction with an oversized interbody implant
risks facet joint distraction and a diminished ability to resist fl exion. Care must be taken to avoid
this potentially destabilizing maneuver, and the
goals of indirect foraminal decompression and
disc height restoration must be balanced with the
integrity of the facet joints. Supplemental posterior fi xation should be considered to ensure a
high rate of fusion [ 30 , 31 ].
Conclusions
The lumbar spine relies on a complex interplay
among ligamentous, osseous, and muscular
structures to coordinate physiologic motion
while maintaining stability. While many
degenerative conditions alter normal anatomy
and disrupt spinal biomechanics, surgical
interventions can themselves accelerate insta-
bility during dissection and through aggressive
decompression. Lateral lumbar exposures cir-
cumvent many of the lumbar stabilizing ele-
ments, thus avoiding much of the iatrogenic
biomechanical morbidity of posterior and
anterior approaches. Moreover, lateral recon-
struction may offer further advantage through
robust disc height restoration, reestablishment
of lordosis through ventral lengthening, and a
large surface area for fusion across the
endplates.
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Physiologic Benefi ts and Impacts
of Minimally Invasive Spine
Surgeries
Gisela Murray , Chun-Po Yen , and Juan S. Uribe
3
3.1 Goals of Minimally Invasive Spine Surgery
Minimally invasive spine surgeries (MIS) are
percutaneous or mini-open techniques utilized for
spine decompression, fusion, instrumentation, or
malalignment correction akin to their open counterparts with the benefi ts of reducing intraoperative blood loss, postoperative pain, infection, and
complications. MIS surgery achieves these goals
through minimizing dissection and crush injury to
the paraspinal musculature and preserving posterior tension band. Introduction of tubular or
expandable retractors and refi nement of long and
bayoneted instruments allow the spine surgeons
not only able to perform the routine posterior
decompressive procedures but also posterior lumbar interbody fusion (PLIF) or transforaminal
lumbar interbody fusion (TLIF) [
Another innovative breakthrough in the past
decade is the minimally invasive lateral approach
to the thoracic and lumbar spine utilizing the
natural retroperitoneal or retropleural corridors
[ 3 , 4 ]. Originally used for degenerative spinal
G. Murray , MD • C.-P. Yen , MD
Department of Neurological Surgery ,
University of South Florida ,
Tampa , FL 33606 , USA
J. S. Uribe , MD (*)
Department of Neurological Surgery , University of
South Florida , Tampa , FL , USA
juansuribe@gmail.com
e-mail:
1 , 2 ].
disorders, the lateral approach has expanded its
indications to treat pathologies involving anterior
and middle column of the spine such as trauma,
neoplasm, and deformity. It replaces more morbid
procedures, which often involve thoracotomy, laparotomy, or extensive posterolateral dissection
[ 5 – 8 ]. Percutaneous pedicle screws and rods have
been another powerful addition in the MIS spines
surgeons’ armamentarium to stabilize and realign
the spine [ 9 ].
3.2 Physiological Benefi ts
Many physiological benefi ts have been described
for MIS in general. The most important are
reduced blood loss, lower infection rates, and soft
tissue envelope preservation.
3.2.1 Blood Loss
This has been the most consistent benefi t of the
MIS. In a prospective study of 61 patients undergoing single level PLIF through MIS or open
approach, the authors found no clinical or radiological difference between the groups at 1 year
minimum follow-up. However, there was signifi cantly less blood loss and a lower transfusion rate
in the MIS group [ 10 ]. In our experience, the
average blood loss for a single level lateral
interbody fusion (LIF) is approximately 50 ml
© Springer International Publishing Switzerland 2017
M.Y. Wang et al. (eds.), Lateral Access Minimally Invasive Spine Surgery,
DOI 10.1007/978-3-319-28320-3_3
23
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