SPINAL INJURIES
Cauda equina syndrome:
principles of management
Niall Eames
Abstract
Cauda equina syndrome (CES) is a devastating condition for quality of
life which may lead to permanent loss of bladder, bowel and sexual
function with associated neurological pain affecting the patient, their
family and relationships. It is a time-sensitive syndrome, requiring
rapid and effective assessment, diagnosis and treatment if the best
possible outcome for the patient is to be achieved. Assessment and
diagnosis should be undertaken as an emergency. Surgery when it
is required must be performed at the earliest opportunity. Neverthe-
less, despite optimal medical care, many patients with CES will suffer
long-term symptoms with significant disability, which is often hidden
for the rest of their lives.
Keywords cauda equina syndrome; conus medullaris syndrome;
degenerative cascade; evolution of cauda equina syndrome; lumbar
disc protrusion; time-sensitive continuum; timing of surgery
Introduction
Cauda equina syndrome (CES) is a devastating condition for
quality of life which may lead to permanent loss of bladder,
bowel and sexual function with associated neurological pain
affecting the patient, their family and relationships. It is a time-
sensitive syndrome, requiring rapid and effective assessment,
diagnosis and treatment if the best possible outcome for the pa-
tient is to be achieved. The subsequent effects of this highly
disabling disorder can often lead to isolation and despair for
patients and their families who may struggle to comprehend the
complex and personal issues surrounding this often-invisible
condition.1
For the health service the legal implications of damages
settled for patients suffering from cauda equina syndrome is
enormous. Historically, delays in diagnosis and treatment have
led to poor outcomes for many patients and the resulting medical
negligence bill is massive. In England alone, 23% of litigation
claims relate to CES.2
The incidence of CES
Reported incidence rates vary widely. A retrospective review in
Slovenia found an annual incidence of CES resulting from
intervertebral disc herniation of 1.8 per million population.3 It is
estimated that CES occurs in approximately 2% of cases of her-
niated lumbar discs and is one of the few spinal emergencies.4
Most general practitioners are unlikely to see even one true
case caused by intervertebral disc herniation in their career.5
Niall Eames MD FRCS Orth Tr, Consultant Orthopaedic and Spine
Surgeon, Clinical Director, Belfast Health and Social Care Trust, UK.
Conflicts of interest: none declared.
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Whilst the majority of cases of CES are due to lumbar disc
protrusions, other causes of neurological compression such as
fractures, infections, and tumours may also cause the syndrome.
Traumatic injuries
The spinal cord ends between T12 and L2 in the conus medul-
laris. This area is the transition from the central to peripheral
nervous system and represents a dilatation of the spinal cord. It is
also a transitional area between the stiff thoracic spine and the
more flexible lumbar spine and it is an area with a proportionally
narrower anatomical spinal canal. It is therefore vulnerable to
trauma. Lesions above this level will present with upper motor
neurone signs, whereas below this lower motor signs will exist.
At this junctional level, patients may present with a mixture of
upper and lower motor neurone signs.
Similar signs and symptoms can occur when the conus
medullaris or distal portion of the spinal cord is compressed e a
conus syndrome. This is a type of often incomplete spinal pa-
ralysis and is difficult to differentiate clinically from CES. But the
compression is more proximal in the spinal canal. As well as
bladder symptoms, conus syndrome may be associated with a
flaccid or spastic paralysis of the lower limbs. It often results
from fractures compressing the thoraco-lumbar junction.
Whilst injury to the conus or cauda equina may obviously
occur at the time of injury, they may also evolve with time in an
unstable fracture. Therefore, repeated neurological assessment is
paramount in unstable fractures. When assessing fractures often
both CT and MRI imaging are required to evaluate bony integrity
and neurological compromise. The commonest injuries at this
level are compression fractures (A1 fractures) and burst fractures
(A3) (Figure 1). Burst fractures by definition involve retropulsion
of the posterior vertebral wall and it is this that can lead to
pressure on the conus medullaris. Such pressure should be rec-
ognised as a potential risk in such injuries and assessed fully.
Surgical stabilization with indirect decompression by liga-
mentotaxis of the posterior longitudinal ligament is usually
effective in decompressing the canal. But occasionally a formal
decompression of the area is required either by a posterior lam-
inectomy or indeed via an anterior vertebrectomy.
The prognosis for recovery in conus lesions is variable.6 If the
patient presents with a complete neurological injury, the prog-
nosis for recovery is extremely poor. The aim of surgery in these
patients realistically is to maximise rehabilitation potential.
Boerger et al.7 performed a retrospective meta-analysis and
found that those patients with an incomplete neurological injury
treated surgically by stabilization and decompression have more
possibility of restoring neurological function than those patients
who did not undergo surgery. Surgery also has a role in a patient
with an evolving neurological injury by preventing further cord
compromise.
CES and ageing of the spine
The majority of cases of CES are due to lumbar disc protrusions.
To understand how these lead to CES clinically, we need to look
at the ageing process of the spine, the anatomy of the area and
what makes these nerves different. Firstly, the natural ageing
process of the spine.
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 SPINAL INJURIES

Figure 1 Burst (A3 type) fracture of L1. (a) Sagittal CT, (b) Axial CT showing retropulsion, (c) Sagittal MRI showing cord oedema with fracture site at
level of conus, (d) Axial MRI of normal section, (e) Axial MRI of compressed conus at fracture site.

The degenerative cascade
In the spine, ageing happens as a degenerative cascade,8 occur-
ring in everyone as a natural process from birth to death. If we
look at a ‘motion segment’ of the spine, we can see how this
natural process affects each area individually. A ‘motion
segment’ in the spine is defined as the two vertebral bodies either
side of a disc, the facet joints joining them together and the
associated supporting ligamentous structures.
In the disc, the major component is water. The disc is also
composed of proteins in the form of proteoglycans and glycos-
aminoglycans which imbibe water, providing the disc with
structure. With ageing, there is loss of distinction between the
nucleus and the annulus. We see an increase in the amount of
collagen within the disc and an overall decrease in the proteo-
glycan aggregates. A decrease in negatively charged proteoglycan
side chains occurs and this leads to a decrease in the overall
water content of the disc. Normally the water content of the disc
is approximately 80% but this reduces down to 70% with ageing.
In summary, the nucleus reduces its ability to imbibe water as
ageing occurs.
The nucleus is surrounded by the annulus. Within the
annulus a reduction in the number of cells and a consequent
reduction in the metabolic activity occurs. Similar to the nucleus,
we see a decrease in proteoglycans in the annulus. Larger
collagen fibrils begin to appear and overall there is decrease in
the amount of collagen with a shift to type 3 collagen. Structur-
ally, this presents itself as annular fissures, a normal part of the
aging process within the spine.
Within the facet joints we see all the normal features of
degenerative arthritis occurring. Subchondral sclerosis takes
place. Osteophytes form on the edge of the joints. These may
narrow the foraminae leading to foraminal stenosis. There is loss
of articular cartilage and overall there is joint laxity leading to
instability between the spinal segments. Within the endplates of
the motion segment calcification occurs which decreases further
the already poor supply of nutrients to an avascular disc.
Radiologically, these degenerative changes may be seen on
plain radiographs and CT scans. On MRI scans Modic has clas-
sified the changes occurring in and around the disc with ageing,
although debate exists as to whether these MRI Modic changes
relate to ageing or the magnetic properties of the scanners.9
So, what are the clinical consequences of the degenerative
cascade in the lumbar spine? As disc degeneration occurs, we see
annular fissures develop. Next, we see disc bulging and disc
protrusions occurring. Lumbar disc protrusions anatomically may
be described as a simple bulging, a protrusion or an extrusion of
the disc. If the fragment separates from the main body of the disc it
is known as a sequestrated fragment. A simple definition of a
protrusion anatomically is that the neck is wider than the head of
the disc protrusion. This is compared with an extrusion where the
neck is narrower than the head of the disc extrusion.
Back pain is a very common condition and is multifactorial in
its aetiology and pathophysiology. Disc protrusions are also
common and may lead to nerve root or radicular pain. The vast
majority of patients suffering from radicular leg pain due to disc
protrusions find their symptoms settle with conservative treat-
ment. Patients often require reassurance, analgesics, mobiliza-
tion and physiotherapy and possibly a nerve root injection to
ease their pain.10 If the pain fails to settle with maximal con-
servative treatment then surgery becomes an option for these
patients. Surgery is required for the minority of patients pre-
senting with a lumbar disc protrusion and radicular symptoms.
As the degenerative cascade continues, clinically we see
narrowing of the spinal canal presenting with spinal stenosis, a
rare cause of CES.11 With time, as the joints display increasing
degrees of incompetence due to ligamentous laxity and degen-
erative change, a sagittal plane deformity may occur leading to
degenerative spondylolisthesis. Finally, a deformity in the coro-
nal plane may present as degenerative scoliosis. Consequently,
this cascade may present at differing ages with diverse clinical
scenarios.
The evolution of CES
What makes a simple lumbar disc protrusion become CES?
Why do these nerves seem to react differently to other nerves?
Two significant factors exist. It is important to understand these
in order to comprehend the rationale behind the treatment of
CES.

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 SPINAL INJURIES
Firstly, the nerve roots of the cauda equina supply critical
functions. They control the important functions of the bladder
and the bowel. The nerve roots supply sensory innervation to the
saddle area and motor innervation to the sphincters, as well as
parasympathetic innervation to the bladder and large bowel. In
addition, they also have critical roles in sexual function. They
also have a high autonomic content. This combination makes
their role very important for normal human function.
Secondly, these nerve roots respond poorly to physical pres-
sure. Histologically these nerve roots are seen to have a poorly
developed epineurium. It is recognized that they tolerate trauma
poorly. This trauma may be physiological, it may be physical due
to pressure, it may be due to vascular occlusion or indeed due to
a combination of these factors. Olmaker et al.12 showed in a
porcine model that the venules and arterioles supplying these
sacral nerve roots are compressed at a very low blood pressure.
They therefore suffer relative hypo-vascularity under pressure
and once exposed to pressure display increased permeability
leading to oedema. The authors concluded, in an animal model,
that the magnitude, length and speed of obstruction to these
vessels were of importance. This is critical in understanding the
effects of CES in the clinical scenario.
So, in summary, we have vulnerable nerve roots which are
supplying critical functions and are susceptible to pressure. This
makes the nerve roots supplying bladder and bowel different to
the other nerve roots. When we add in to this scenario the
normal degenerative cascade, potentially leading to pressure on
these nerve roots we have the CES e a time-sensitive condition.
The anatomy of the lumbar spine
If we look at the anatomy of the nerve roots in relation to the
bony anatomy of the spine, we see how the nerve roots are
affected differently by different disc protrusions. If we look at a
coronal section of the spine (Figure 2), we are able to define a
central zone between the pedicles running down the middle of
the canal. Lateral to this, posterior to the facet joints, we have the
subarticular zone or lateral recess. Further lateral to this between
the pedicles we have the foraminal zone and lateral to this area
we have the extra-foraminal zone. The nerve roots exit directly
inferior to the pedicle within the lumbar spine. If we take as an
example the 4th lumbar vertebra, the nerve root exiting directly
beneath the pedicle is defined as the 4th lumbar nerve root. We
call this the exiting nerve root at this point. The nerve root that is
passing over the 4th lumbar vertebra and the L4/L5 disc to pass
beneath the L5 and exit subsequently is known as the traversing
Figure 2 Schematic coronal diagram of lumbar nerve root anatomy
and spinal zones.
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nerve root as it passes over the L4/L5 disc. This anatomical
relationship is extremely important clinically when correlating
clinical signs with radiological appearances and surgically during
dissection of the spine.
Disc protrusions occurring laterally under the facet joint in the
lateral recess may affect either the exiting or the traversing nerve
root or a combination of both. Disc protrusions occurring in the
foraminal zone will affect the exiting nerve root probably in
isolation. A disc protrusion occurring in an extra-foraminal or far
lateral zone will in all likelihood affect the nerve root that already
has exited the canal at the level above which is now outside the
canal passing laterally. In this example this would be the L3
nerve root. Most disc protrusions occur laterally due to the
presence of the posterior longitudinal ligament. When a disc
protrusion does occur centrally it will affect the central traversing
nerve roots passing through the central canal. It is damage to
these nerve roots (S2, S3, S4) that causes CES. The S2, S3 and S4
nerve roots lie in the central canal sitting posteriorly within the
dural sac in the lower lumbar spine (Figure 3a).
Initial presentation
The patient will often complain of back pain in addition to
radicular leg symptoms. Leg pain may be unilateral or bilateral.
The patient will often complain of loss or altered perianal sensa-
tion. They will have altered bladder function which may range
from irritability at passing urine to frank incontinence of urine or
full-blown retention of urine. They may also have altered bowel
function. Often no preceding history of back symptoms exists. A
full neurological assessment of the patient is mandatory, including
recording of power, tone, sensation and reflexes. Perianal sensa-
tion should be assessed and clearly documented. Debate exists as
to the role of rectal (PR) examination. The sensitivity of anal tone
as a means to predict CES is low at 52.9%.13 Peri-anal numbness
(either unilateral or bilateral) has sensitivity of 82.3% and nega-
tive predictive value of 92%. Repeated PR examinations of a pa-
tient are unnecessary and inappropriate given these findings but a
PR examination should be documented during a patient journey.14
Imaging
MRI scanning is the examination of choice for suspected CES
(Figure 3).15,16 It is most effective time management for the
patient if an MRI scan is performed in the referring hospital
prior to transfer for definitive management. A high-quality CT
scan may be performed if MRI is contraindicated. Consideration
should be given to a sagittal T2 screen of the whole spine if no
significant cauda compression exists in a patient with bladder
symptoms.
When scanning patients with suspected CES it is to be ex-
pected that the pick-up rate of positive scans will be low
compared to a high pick-up rate for positive scans in patients
presenting with CES with retention.17 It must be remembered
however that the cost for the patient in terms of a missed diag-
nosis, as well as the medicolegal consequences by not scanning a
patient are devastating and far outweigh the cost of performing
multiple scans with a low pick-up rate.
Post-micturition ultrasound scanning of a patient’s bladder
has been put forward as a means to help in the diagnosis of CES.
The rationale is that if the patient is able to empty their balder
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 SPINAL INJURIES

Figure 3 Typical MRI scans. (a) Suspected cauda equina syndrome (CES) showing S2, S3 and S4 nerve roots. (b) CES incomplete. (c) CES
retention. Reproduced from reference 17 with permission. Ó Copyright the British Editorial Society of Bone & Joint Surgery.

effectively, they do not have CES at that time. This has proven to
be a useful technique. Bladder scanning has been shown to be a
useful adjunct in the diagnosis of CES with a better negative
predictive value than physical examination.13 The optimal
bladder volume cut-off for predicting CES is 200 ml for post-
void residual (PVR) volume. A PVR of <200 ml gives CES
probability of 3.6%. If >200 ml, then the probability of having
CES is 43% (p < 0.001). A PVR <200 ml has a negative pre-
dictive value of 97%. It is a useful technique which can be per-
formed in an outpatient setting at relatively low cost. It must be
remembered however that whilst the bladder function may be
adequate at the time of scanning, the syndrome may be evolving
and it is a useful adjunct to the diagnosis of CES.
Treatment
Surgical decompression is the treatment of choice for CES. Whilst
a simple microdiscectomy may suffice in some cases, often the
dura is under significant pressure and consideration should al-
ways be given to a central approach with as wide decompression
as is required to safely remove the disc protrusion. It is important
to remember that surgical intervention has the potential to
exacerbate the situation by placing further pressure on already
critical nerve roots. When consenting before surgery this must be
clearly explained to the patient and documented.15
Timing of surgery
Confusion exists in describing both definitions and outcomes
through the literature in relation to CES. Most studies are retro-
spective with reliance being placed on various meta-analyses. As
a consequence, it is difficult to draw definitive conclusions.
However, some salient facts can be drawn from a review.
As early as 1959, Shepherd et al.18 advocated early decom-
pression due to improved results. Tay and Chacha19 in 1979
reviewed 8 CES patients who underwent surgical decompression
ranging from 1 to 14 days. Seven patients recovered full bladder
control at 5 months. Overall motor recovery was good but all
patients had poor sensory and sexual function recovery. The
outcome was poor if surgery was delayed by days. Kostuik

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 SPINAL INJURIES

et al.20 reviewed a group undergoing surgery within 48 hours and A time-sensitive continuum
those with a more insidious onset undergoing surgery within 5
It is useful to look at CES as a continuum of clinical events with
days; 50% of the acute onset patients and 10% of the insidious
time as a critical variable.17 Three subtypes of CES are recog-
onset group had residual bladder dysfunction. Whilst at 2 years
nized. CES suspected, incomplete and with retention. We can
27% of the patients had residual sexual dysfunction, 10% had
demonstrate this graphically in Figure 4.
residual weakness and 20% had residual sensory changes; their
CES suspected is the scenario when a patient presents with
results gave weight to the premise that the outcome is worse for
urinary symptoms, usually bladder irritability, associated with
CES retention patients than for CES incomplete.
back pain and radicular leg pain. Due to the presence of bladder
Shapiro21 retrospectively reviewed 14 patients on the basis of
symptoms we assume the patient has compression of the cauda
48 hours being the critical time for decompression. Of those un-
equina nerve roots and therefore requires a rapid MRI scan for
dergoing surgery after 48 hours, only 2 of 6 regained continence, 3
diagnosis. The majority of patients presenting in this manner will
of 7 had permanent weakness requiring assistance for ambulation
not have CES. The pick-up rate for the MRI scan will be low. The
and 2 of 7 had chronic sciatica. Shapiro22 further looked at a group
MRI scan will for the majority of patients with these symptoms
of 20 patients retrospectively and found that those decompressed
demonstrate no significant cauda equina compression and may
within 24 hours did better than those decompressed between 24
well demonstrate a simple lateral disc protrusion (Figure 3a) or
and 48 hours and they in turn did better than those decompressed
indeed no pressure on any nerve roots. If no compression is
after 48 hours.
demonstrated on MRI of the lumbar spine, consideration should be
In 2003, Hussain et al.23 reviewed 20 patients who presented
given to a sagittal screen of the rest of the cervical and thoracic
within 48 hours of symptoms. There was no significant differ-
spine in-case other undiagnosed compressive pathologies exist.
ence in urological outcome or overall quality of life between
Pain may be the cause of the bladder symptoms. Those pa-
patients who were decompressed within 48 hours and those who
tients without CES confirmed on MRI, once the correct diagnosis
were decompressed after 48 hours. Qureshi and Sell24 concluded
is established and appropriate treatment given will find that the
that the severity of bladder dysfunction at the time of surgery
urinary symptoms will settle (Figure 5a). If they do not, another
was the dominant factor in recovery of bladder function.
cause outside the spinal canal should be sought.
Ahn et al.25 conducted a large meta-analysis of 322 patients. No
Compare this to patients who present with back pain and uni
difference was found in outcome for those patients undergoing
or bilateral leg pain often for only a short duration (Figure 5b).
decompression more than 48 hours after symptoms. Kohles et al.26
They may also have bladder irritability lasting for some hours
re-analysed Ahn’s data and concluded that the risk for poor out-
and they may have altered perianal sensation. A post-micturition
comes increases continuously with time. Similarly, Todd27 per-
bladder scan will probably show a low volume of retained urine
formed another meta-analysis and concluded that there was
but this may approach or pass the residual volume threshold of
stronger evidence for a 24-hour rather than 48-hour window of
200 ml. Again, these patients require a rapid MRI scan to di-
opportunity.
agnose if pressure is actually occurring on the cauda equina
So, the literature is not clear and concise, but as Todd
nerve roots. Once the MRI scan has been performed if the scan
concluded in 2015 damage to the nerve roots occurs in a
confirms significant pressure on the cauda equina nerve roots,
continuous and progressive fashion.28 The evidence points to the
then the patients require surgical decompression rapidly
fact that if treatment is delayed, the prognosis is extremely
(Figure 3b). They are presenting with an incomplete neurological
poor.29 It also points to the evolution of symptoms with time for
deficit of the cauda equina nerve roots and require rapid
the majority of patients in whom rapid treatment can be effec-
decompression of those nerve roots if permanent damage is to be
tive. This has led to the description of CES as a continuum.17
avoided. The potential exists for their bladder symptoms to
CES has led to multiple papers describing the various clinic
deteriorate without treatment. If we can treat these patients
settings and has led to debate for many years as to the timing of
appropriately and rapidly when they present with CES incom-
appropriate intervention for patients suffering from CES. The key
plete, the majority will find that their symptoms do improve
message for patients suffering from CES is that the clock is
following surgery. This is not always happening but it is the case
ticking. As their symptoms develop, damage occurring to the
with the majority of patients. These are the patients we want to
nerve roots occurs in a continuous and progressive fashion.28
find and treat. We can make a significant difference to the
This means that rapid diagnosis and treatment are essential. It
outcome for these patients. Delays with failure to appropriately
is the recognition of this principle that often leads to problems
diagnose, transfer and operate in this group are a failure of
encountered by the patients and clinicians.
medical care. The clock is ticking and it is our responsibility to
act rapidly in order to allow maximal opportunity for recovery.
Delays in treatment
If we compare this to the disastrous scenario (Figure 5c) of a
Delays in treatment are well recognized. Shapiro30 described young person presenting with a 3-day history of leaking bladder
three areas of delay in surgical decompression occurring. Firstly, incontinence and a residual post-micturition scan volume of 1000
there may be a delay on the part of the general practitioner or ml, for example, loss of perianal sensation and a lax PR on ex-
primary care physician in diagnosing CES or seeking specialist amination by the time this patient presents to medical care they
consultation. Secondly, there may be a delay in obtaining a are displaying the features of a complete lesion. These patients
diagnostic study, mainly an MRI. Thirdly, the surgeon may delay have CES with retention. Even with the MRI scan being per-
decompression for a more convenient setting e for example a formed rapidly (Figure 3c), pressure damage already has
non-emergency setting in which more qualified staff is available. occurred to these critically important nerve roots. Despite

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 SPINAL INJURIES
Figure 4 The evolution of cauda equina syndrome. Reproduced from
reference 17 with permission. Ó Copyright the British Editorial Society
of Bone & Joint Surgery.
Figure 5 Cauda equina syndrome subtypes. Reproduced from
reference 17 with permission. Ó Copyright the British Editorial Society
of Bone & Joint Surgery.
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operating on this group of patients rapidly, only a minority will
find that their bladder and bowel symptoms recover. This leads
to the devastating consequences that CES produces. The key in
this situation is that it is often too late for the nerve roots to
recover. This is the situation we must try and avoid at all costs if
at all possible. A minority of patients may find that their symp-
toms do improve after surgery, but this is sadly a limited number
of patients. Nevertheless, we must treat all patients in this cate-
gory rapidly to give them the best possible opportunity for re-
covery, even though it is small (Figure 6). Compare this with CES
incomplete where a significant potential for recovery exists.
As a profession, it is our role to rapidly diagnose patients with
CES and offer timely and appropriate treatment. The disaster
scenario is if we allow a CES incomplete to develop into CES
retention under our care. We must strive to reduce delays once
patient presents to us but only education of wider society in
general will reduce the delays in presentation to medical care in
the first place. The utilisation of wallet-sized alert cards for pa-
tients is one example of how we can make a difference here.31
Rehabilitation
It is vital to recognize that even after surgery patients will often
not have normal return of bladder and/or bowel function. In
addition, they may have altered sensation in their limbs leading
them prone to pressure ulceration. They will have been going
through a very significant and traumatic life event and will be
extremely frightened regarding the future.
Consequently, patients postoperatively who have residual
symptoms should be referred to a rehabilitation consultant. It is
crucial in the early postoperative period that proper attention is
paid to bladder residual volumes. The bladder is vulnerable to
stretching and subsequently infections which must be
prevented by proper catheterization techniques. It may be
necessary to teach the patient the technique of intermittent
self-catheterization to allow return to home.
Similarly, the patients will require counselling if erectile
dysfunction has occurred. They will require advice, reassurance
and support at this very distressing time. Sympathetic and sup-
portive multidisciplinary postoperative management over many
months may be necessary with the help of a spinal injuries’ unit,
Figure 6 The potential for recovery in cauda equina syndrome.
Reproduced from reference 17 with permission. Ó Copyright the
British Editorial Society of Bone & Joint Surgery.
253 Crown Copyright Ó 2020 Published by Elsevier Ltd. All rights reserved.
 SPINAL INJURIES
a urologist and/or gynaecologist, a specialist gastroenterologist
and social services.32 Approximately 75% of all CES patients
will eventually have acceptable urological function,33 though
frequently with chronic back pain and some motor and sensory
deficits in the perineum and lower limbs.
Conclusion
CES is a devastating condition which may lead to misery for
affected patients. Any patient presenting with acute symptoms or
an exacerbation of pre-existing symptoms, including back and/or
leg pain with the suggestion of a disturbance of their bladder/
bowel function and or saddle sensory disturbance should be
considered to have CES.15 An MRI scan should be undertaken as
an emergency. Surgery when it is required must be performed at
the earliest opportunity. It is important to remember to counsel a
patient that surgery may make symptoms worse. The disaster
scenario of allowing a patient who presents with CES incomplete
to progress to CES with retention whilst under medical care must
not be allowed to happen. Nevertheless, despite optimal medical
care, many patients with CES will suffer long-term symptoms
with significant disability, which is often hidden for the rest of
their lives. A
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lesions. Muscle Nerve 2007; 35: 529e31.
4 Gitelman A, Hishmeh S, Morelli B, et al. Cauda equina syndrome:
a comprehensive review. Am J Orthoped 2008; 37: 556e62.
5 James L, Wilson-Macdonald J, Fairbank J. Cauda equina syn-
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