Lower
Back Pain
Case
Presentation
This presentation
addresses the anatomy and current methods for the diagnosis and treatment
of low back pain.
Lower
Back Pain
Introduction
Back
pain is one of the most common presenting complaints in the Emergency
Department. 60-90%
of the population will experience back pain in their lifetime.
Back pain is second only to upper respiratory infection as
a cause for lost work time.
Over 5 million people are disabled with low back pain which
makes it the number one disability for workers less than 45 years
old. The bad news is
that no definitive diagnosis will be found in over 80% of back pain
cases. The good news
is that over 90% of patients, even those with sciatica, will be
better in two months regardless of the type of therapy given.
Determining which patient with back pain is the “true emergency”
is one of the biggest diagnostic challenges that an emergency medicine
physician can face.
Anatomy
and Physiology
The
vertebra has three primary structures; the body, the neural arches
and the boney process. The
bodies are connected by inter-vertebral discs with supporting anterior
and posterior longitudinal ligaments.
The neural arches are joined by the zygoapophyseal joints.
The stability of the spine not only relies on the ligamentous
structures but also on the extensive muscular structures surrounding
it.
It
is important to remember that the cervical nerve roots, pass above
the same numbered vertebral body with the C8 nerve root passing
above the T1 vertebral body, and there after all nerve roots pass
below the same numbered vertebral body.
One should also note that the spinal cord ends at L1 and
that from this point on each nerve root runs as its own distinct
entity with the higher nerve roots being more lateral in the spinal
canal than the lower nerve roots (i.e. the L2 nerve root is more
lateral than the L5 nerve root).
Types
of Back Pain
There
are three primary types of back pain.
The first, is local pain.
This pain is caused by irritation to the structures in the
back including bone, muscles, ligaments and joints.
The pain is usually steady, sharp or dull, felt in the effected
area of the spine and may change with changes in position or activity. The second is referred
pain. Referred
pain can be pain caused by non-spinal pathology that is referred
to the back, such as an abdominal aortic aneurysm.
Referred pain can also be pain originating in the spine that
is felt in distant structures.
For instance upper lumbar pain is frequently felt in the
upper thighs, and lower lumbar pain is felt in the lower buttocks.
Sacroiliac joint pain is often referred to the inguinal and
antero-lateral thigh area.
Referred pain rarely extends below the knees, where as nerve
root pain can be felt in the calf or foot.
The third type of pain is radicular pain.
Radicular pain is caused by irritation of the nerve roots
usually caused by compression.
Radicular pain is usually more severe than referred pain
and has more distal radiation.
Radicular pain usually circumscribes the territory of innervation
of the given nerve root. In
addition, radicular pain is frequently exacerbated by any maneuver
that raises the pressure of cerebrospinal fluid, such as valsalva
or cough. Most patients with radicular back pain will recline on their
side with knee and hips flexed to decrease strain on the nerve root.
Increasing tension on the inflamed nerve root is what makes
the straight leg raising maneuver positive.
The straight leg raising maneuver is positive if radicular
pain is achieved before a 70 degree angle is made with the bed.
Further evidence of radicular pain is exacerbation of the
pain of straight leg raising with dorsi flexion of the foot, and
relief of the pain of straight leg raising with flexion of the knee.
Diagnosis
It
is beyond the scope of this discussion to describe the innervation
of each nerve root along the spinal cord.
However, since 90 % of all lower extremely radiculopathy
is caused by cord compression of either the L4-L5 or L5 S1
segments, these findings will be described.
L4 nerve root impingement
produces pain in the lateral back, antero-lateral thigh and
anterior calf, numbness
in the anterior thigh, weakness in the quadriceps and diminished
knee jerk reflexes.
A good screening exam is to have the patient squat and rise.
L5 nerve root impingement is characterized by pain in the
hip, groin, post-lateral thigh, lateral calf and dorsum of the foot.
Numbness is in the lateral aspect of the calf, weakness is
in the dorsiflexion of
the great toe. There
is no reliable change in reflexes for L5 nerve root impingement
. Heel walking is a
good test for L5 nerve
root impingement. Lastly,
S1, nerve root impingement
is characterized by pain in the midgluteal region, posterior
thigh, posterior calf to the heel and sole of the foot.
Numbness occurs on the posterior aspect of the calf.
Weakness occurs on plantar flexion of the great toe and foot,
the ankle jerk reflex may be diminished.
Having the patient walk on his toes is a good test of the
S1 nerve root.
There
are two specific syndromes of the lower spinal cord; conus medullaris
and cauda equina. The
conus medullaris is a lesion at the distal, sacral portion of the
spinal cord and its roots.
Patients with this syndrome present with bilaterally symmetrical
sensory loss. Root
involvement usually proceeds in an “inside-out” manner, with lower
levels affected earlier than upper levels resulting in the classic
“saddle” distribution of sensory loss.
Loss of sphincter tone occurs early, leading to urinary and
bowel incontinence. Motor
weakness is not a prominent finding, but if present, the L5 and
S1 nerve roots are the most likely to be involved.
The cauda equina syndrome involves the distal nerve roots
after the end of the spinal cord. The presenting symptoms include radicular pain that involves
the legs, buttocks, and perineal areas.
Motor deficits are common and are lower motor neuron in character.
Motor and sensory deficits are usually asymmetric.
Sphincter dysfunction is a late finding.
Because the cauda equina is made up of peripheral nerves
the prognosis for recovery is better than with conus lesions.
Spinal
Cord Compression
Patients
who present to the ED with acute spinal cord compression characterized
by back pain, focal neurological findings or both can have significant
morbidity if not aggressively evaluated and treated.
Four, nontraumatic etiologies for acute back pain and neurological
findings are epidural spinal cord compression from metastatic cancer,
disc herniation, spinal epidural abscess and spontaneous spinal
cord hematoma. All
four of these causes of spinal cord compression are partially or
completely treatable with excellent prognoses for recovery of neurological
function, if diagnosed early and treated aggressively.
Metastatic
epidural spinal cord compression (MESCC) usually occurs from the
hematogenous spread of tumor cells to the bone marrow of the vertebral
bodies. The enlarging
epidural tumor may not only compress the spinal cord but may compress
the vascular supply to the spinal cord leading to edema and infarction.
The six most likely primary malignancies to cause MESCC are
prostate, lung, breast, Non-Hodgkin’s lymphoma, multiple myeloma
and renal cell carcinoma.
MESCC is the initial presentation of a malignancy in 20%
of cases. The cervical,
thoracic and lumbar spine are effected in proportion to their vertebral
body volume, so the thoracic spine predominates. Back pain is present
in 95% of MESCC patients and usually precedes other symptoms by
1-2 months. The pain
is often non specific but can have features that may suggest malignant
origins such as, percussion tenderness, thoracic location and worsening
with lying down. Weakness is present in approximately 75% of patients by the
time the diagnosis is made.
Weakness is usually symmetric.
Sensory complaints are less frequent but common and usually
present as an ascending numbness and paresthesias.
Autonomic dysfunction, such as urinary retention, is common
but usually a late findings.
Plain
film spinal radiographs are helpful if they are positive.
Unfortunately, the false negative rate for plain radiography
for the diagnosis of MESCC is 10-17%.
In part, this may be due to the fact that 30-50% of the bone
must be destroyed before the radiograph is positive.
MRI and CT myelography are the current standards for diagnosing
soft tissue invasion of spinal structures and compression of the
spinal cord. MRI, if
available, has the advantages of providing greater detail of the
surrounding soft tissue structures and being non-invasive.
Treatment
of MESCC usually begins with corticosteroids because of the significant
edema which can be present.
One regimen uses high dose dexamethasone with a loading dose
of 20 to 100 mg., followed
by 4 to 24 mg four times daily. Though steroids help considerably with the pain of MESCC,
analgesics may be needed for patient comfort. Radiation therapy
is the mainstay of treatment and is usually begun within 24 hours
of diagnosis. Surgery
is usually reserved for patient unresponsive to radiation therapy
or acute neurological deterioration.
Chemotherapy is used only in patient where the primary carcinoma
is known to be chemosensitive such as Non-Hodgkin’s lymphoma.
Recurrence of MESCC is less than 10%, but this is most likely
due to the poor prognosis of the primary carcinoma.
Intervertebral
disc herniation can occur from traumatic and non-traumatic causes.
The L4-5 and L5-S1 disc are the most frequently involved.
Thoracic and cervical spine herniations do occur.
Thoracic spine herniation can have a very abrupt onset of
symptoms with significant neurological deficits because the thoracic
spinal canal is the narrowest part of the entire spinal canal.
Therefore, very little herniation into the canal is needed
to cause symptoms. Patients
frequently present with unilateral
radicular back pain because the most common site of herniation
is the posterolateral aspect of the disc thus frequently impinging
one nerve root more
than the other. The
presenting symptoms and neurological deficits were previously described
in the Diagnosis section.
Plain film radiology is often not useful unless the herniation
is so significant that the volume of the disc has decreased and
so the two vertebrae surrounding the disc appear abnormally close
together. MRI is the
gold standard of disc herniation diagnosis.
It not only provides excellent anatomy of the disc involved
but also the extent of cord compression.
CT scan provides excellent detail of the boney structures
of the spine and when coupled with myelography can delineate cord
compression. Electromyograph allows for the localization of the specific
nerve root involved and helps to distinguish nerve involvement from
non-neurogenic disease.
Initial
treatment centers around decreasing the pressure on the nerve root.
This is accomplished by strict bed rest for up to 4 weeks
accompanied by non-steroidal anti-inflammatory medication.
Muscle relaxants are used when significant paravertebral
muscle spasm occurs. If
pain is severe narcotic analgesia may be necessary. There are multiple
surgical procedures that can be performed ranging from laminectomy
to laprascopic discectomy.
The timing of surgery is dependant on the severity of symptoms.
Absolute indications for laminectomy are significant muscular
weakness attributable to a nerve root or roots, progressive neurological
deficits despite absolute bed rest, and bladder or bowel dysfunction.
Relative indications for operative intervention are pain
unrelieved by complete bed rest and recurrent episodes of severe
pain and sciatica.
Spinal
epidural abscess (SEA) is a rare disease accounting for less than
1 case per 10,000 hospital admissions.
The major risk factors for SEA are intravenous drug abuse,
diabetes, trauma, prior spinal surgery, immune compromised host,
and a history of a spinal nerve block.
Back pain is the most common complaint followed by paresthesias,
motor deficit and fever. A peripheral white blood cell count may be helpful if elevated
but in one study by Rigamonti et al. was only elevated in 60% of
patients with SEA. Erythrocyte
sedimentation rate may also be elevated and in the Rigamonti study
was elevated in all 50 patients with SEA that were tested.
Plain spinal radiographs are only helpful if there is boney
involvement. MRI is
the test of choice because of the enhanced definition of soft tissue
structures. The most
frequently isolated organism is staphylococcus aureus with up to
15% being the methicillin resistant strain. Streptococcus, escherichia coli, pseudomonas, klebsiella,
acinetobacter and mycobacterium tuberculosis have also been found.
Surgery and antibiotics are the mainstay of therapy.
Surgery is dependant upon the severity of the neurological
deficits, the extent of the spine involved and the infecting organism,
if known. Patients
in whom non-operative management should be considered include: patients
with panspinal involvement, patients with lumbosacral SEA with a
normal neurological exam and patients with fixed neurological deficits
for greater than 48 hours.
Antibiotics should be started immediately after the diagnosis
is established. Initial therapy recommendations include vancomycin, because
of the high incidence of methicillin resistant
organisms and either on aminoglycoside or third generation
cephalosporin. The
antibiotic regimen is adjusted
once definitive culture and sensitivity are obtained.
Antibiotic treatment
usually lasts 4 to 6 weeks.
Spinal
epidural hematoma (SEH) is exceedingly rare with only approximately
300 cases being reported up to 1995.
The risk factors for SEH include coagulopathy, trauma, vascular
lesions, surgery or epidural injection.
Blood can accumulate quickly in the closed spinal canal.
In one study by Lawton et al., they found that the average interval
from the onset of initial symptoms to the maximum neurological deficit
was 13 hours. The presenting
symptoms are similar to other cases of spinal cord compression,
back pain and neurological deficit. All segments of the spinal cord can be involved.
The diagnosis is made with MRI because of the soft tissue
involvement. Plain radiographs or CT scan are helpful in patients
with traumatic injury
and possible fractures or dislocations.
The treatment is surgical evacuation of the hematoma. Lawton’s study of 30 SEH cases found that immediate surgery
(within 12 hours of the onset of symptoms ) had a better neurological
outcome than those who had surgery after 12 hours of symptoms.
The
patient with back pain is seen frequently in the Emergency Department.
The cause is often local bone, joint or muscular irritation
that can be managed conservatively.
When radicular pain and/or neurological deficits are discovered,
diligence is required to find the cause.
The severity of spinal cord compression symptoms are related
to the force, duration and rate of compression.
The force and duration of MESCC, disc herniation and SEA may
produce symptoms requiring immediate therapy.
The force and rate of SEH also prompt immediate therapy, surgery.
Back pain always requires a thorough history and complete physical
exam so that the morbidity of spinal cord compression can be minimized.
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Lower
Back Pain
Reference
List
1.
Akalan N, Ozgen T.
Infection as a cause of spinal cord compression: a review
of 36 spinal epidural abscess cases.
Acta Neurochir.(Wien.) 2000;142.(1.):17.-23.
142:17-23.
2. Chen
CJ, Fang W, Chen CM, Wan YL.
Spontaneous spinal epidural haematomas with repeated remission
and relapse. Neuroradiology.
1997; 39:737-740.
3. Cormio
G, Colamaria A, Di Vagno G, De Tommasi A, Loverro G, Selvaggi L.
Surgical decompression and radiation therapy in epidural
metastasis from cervical cancer.
Eur.J Obstet.Gynecol.Reprod.Biol.2000.Mar.;89.(1.):59.-61. 89:59-61.
4. Flynn
DF, Shipley WU. Management
of spinal cord compression secondary to metastatic prostatic carcinoma.
Urol.Clin.North Am. 1991;
18:145-152.
5. Glick
TH, Workman TP, Gaufberg SV.
Spinal cord emergencies: false reassurance from reflexes.
Acad.Emerg.Med. 1998;
5:1041-1043.
6. Grossman
SA, Lossignol D. Diagnosis
and treatment of epidural metastases.
Oncology (Huntingt.) 1990;
4:47-54.
7. King
M. Spinal epidural
abscess: an elusive diagnosis. South.Med.J 1994; 87:288-289.
8. Komiyama
M, Yasui T, Sumimoto T, Fu Y.
Spontaneous spinal subarachnoid hematoma of unknown pathogenesis:
case reports. Neurosurgery
1997; 41:691-693.
9. Lord
GM, Mendoza N. Spontaneous spinal epidural haematoma: a cautionary tale.
Arch.Emerg.Med. 1993;
10:339-342.
10.
Manfredi PL, Herskovitz S, Folli F, Pigazzi A, Swerdlow ML.
Spinal epidural abscess: treatment options.
Eur.Neurol. 1998; 40:58-60.
11.
Martin RJ, Yuan HA. Neurosurgical care of spinal epidural, subdural, and intramedullary
abscesses and arachnoiditis.
Orthop.Clin.North Am. 1996;
27:125-136.
12.
Piccolo R, Passanisi M, Chiaramonte I, Tropea R, Mancuso P. Cervical spinal epidural abscesses. A report on five cases.
J Neurosurg.Sci. 1999;
43:63-67.
13.
Pousada L. Common
neurologic emergencies in the elderly population.
Clin.Geriatr.Med. 1993;
9:577-590.
14.
Quinn JA, DeAngelis LM.
Neurologic emergencies in the cancer patient.
Semin.Oncol.2000.Jun.;27.(3.):311.-21.
27:311-321.
15.
Ruiz A, Post MJ, Sklar EM, Holz A.
MR imaging of infections of the cervical spine.
Magn.Reson.Imaging Clin.N.Am.2000.Aug.;8.(3.):561.-80.
8:561-580.
16.
Sampath P, Rigamonti D.
Spinal epidural abscess: a review of epidemiology, diagnosis,
and treatment. J Spinal.Disord.
1999; 12:89-93.
17.
Schiff D, Batchelor T, Wen PY.
Neurologic emergencies in cancer patients.
Neurol.Clin. 1998; 16:449-483.
18.
Sillevis SP, Tsafka A, van den Bent M, de Bruin H, Hendriks
W, Vecht C, et al. Spinal
epidural abscess complicating chronic epidural analgesia in 11 cancer
patients: clinical findings and magnetic resonance imaging.
J Neurol. 1999; 246:815-820.
19.
Varalakshmi V, Idowu A, Jeevan S.
Spinal tumour: a diagnostic lesson.
J Accid.Emerg.Med. 1998;
15:199
20.
Vilke GM, Honingford EA.
Cervical spine epidural abscess in a patient with no predisposing
risk factors. Ann.Emerg.Med.
1996; 27:777-780.
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Lower
Back Pain
Annotated
Bibliography
1)
Tawney, PJW; Siegel, CB; LaBan, MM; Thoracic and Lumbar Pain Syndromes,
in Emergency Medicine, A Comprehensive Study Guide, 5th
edition; editors Tintinalli, JE; Kelen, GD; Strapczynski, JS; McGraw-Hill,
New York, 1999.
This
is a good chapter with a nice overview of the various pain syndromes
associated with back pain.
The physical exam, specifically a screening neurological
exam is well described with specific attention to the L4, L5 and
S1 nerve roots. Though
specific diagnoses are not covered in detail their is a nice review
and plan for the treatment of sciatica and back pain in general.
Overall, this is a good review of back pain.
2)
Bigos, S; Bowyer, O; Braen, G; et al.: Acute Low Back Problems in
Adults. Clinical Practice Guideline No.
14 Rockville, MD: Agency for Health Care Policy and Research,
Public Health Service, US department of Health and Human Services,
December 1994. AHCPR
Publication No. 95-0642.
This
is a long and dry necessary evil.
It is very general guideline to the assessment and treatment
of acute back pain, where acute is defined as less than three months. There is a shorter Quick Reference Guide which is worth while
and gives the essential parts of the longer version. The best part of this guideline is the breakdown of low back
problems into three categories; potentially serious spinal conditions,
sciatica, and nonspecific back symptoms. There is a nice table of
the red flags for the potentially serious conditions and physical
findings that correlate to the diagnoses.
3)
Rigamonti D, Liem L, Sampath P, Knoller N, Namaguchi Y, Schreibman
DL, et al. Spinal
epidural abscess: contemporary trends in etiology, evaluation, and
management. Surg.Neurol. 1999; 52:189-196.
This
is the best overall review of the SEA currently available.
Most of the literature available is case reports and small
case series (25 or less).
This is a review of 75 cases which showed an increase in
the incidence of SEA, particularly in the late 1980s and early 1990s.
This review found that the three biggest risk factors for
SEA are intravenous drug abuse, diabetes, and multiple medical illnesses.
Staphylococcus aureus was the predominant organism in 67%
of cases with methicillin-resistant staphylococcus being found in
15%. Back pain, paraplegia
and fever were the top three signs and symptoms.
Finally, regarding treatment, the authors agree with the
concept that surgery is the mainstay of therapy for SEA, but they
also have a group of patients in whom nonoperative management should
be considered.
4)
Sorensen PS, Helweg-Larsen S, Mouridsen H, Hansen HH; Effect of
high-dose dexamethasone in carcinomatous metastatic spinal cord
compression treated with radiotherapy: a randomized trial.
Eur. J. Cancer, 1994, 30A: 22-27.
This
is a trial that proves the
effectiveness of high dose glucocorticoid therapy as the initial
treatment of spinal cord compression from metastatic cancer.
There were two treatment groups.
One received 96 mg of dexamethasone for four days and then
a taper, and the other group received placebo.
Both groups received radiation therapy.
There were 57 patients in this study. Successful treatment
was defined as the ability to walk.
81% in the steroid group were able to ambulate at discharge
compared to 63% in the control group.
At six months 59% in the steroid group could walk and only
33% in the control group.
This is one trial, though small, that confirmed that the
use of glucocorticoids in patients with spinal cord compression
secondary to metastatic cancer is beneficial.
5)
Grant R, Papadopoulos SM, Sandler HM, Greenberg HS, Metastatic epidural
spinal cord compression: current concepts and treatment.
J. Neuro-Onc. 1994, 19:79-92.
This
is an excellent review of the diagnosis and treatment of spinal cord
compression caused by metastatic cancer.
There is good review of the epidemiology and presentation which
includes the fact that though back pain may have been present for
one to two months prior to presentation, approximately 80% of these
patients present with weakness.
There is also a section on prognostic indicators such as, 80
% of those that are ambulatory at presentation will remain ambulatory
and only 5% of those that have no antigravity proximal function will
walk again. Lastly, there
is a nice flow diagram for the assessment and treatment of patients
with metastatic epidural spinal cord compression.
6)
Lawton MT, Porter RW, Heiserman JE, Jacobowitz R, Sonntag VK, Dickman
CA. Surgical management of spinal epidural hematoma: relationship
between surgical timing and neurological outcome. J Neurosurg. 1995; 83:1-7.
Since
SEH is such a rare diagnosis it is hard to find articles with more
than a handful of patients in a case series.
This is one of the largest case series with 30 cases. The
most important concept in this paper is that time is critical.
The average interval from the onset of symptoms to maximum
neurological deficit was 13 hours.
The average interval from the onset of symptoms to surgery
was 23 hours. Patients
taken to the operating room for evacuation of the hematoma within
12 of symptom onset had better neurological outcomes than those operated
on after 12 hours of symptom onset.
7)
Reinus WR, Strome G, Zwemer FL.
Use of lumbosacral spine radiographs in a level II emergency
department. Am.J Roentgenol. 1998;
170:443-447.
This
is a study looking at the indications for plain lumbosacral spine
x-rays in emergency department patients complaining of low back pain.
482 patients were studied.
The authors found that 86% of the films ordered had a reading
of normal or spondylosis. The two groups in which these films were helpful were trauma
patients and the elderly with a history of cancer. Overall, plain x-rays provide no clinically useful information
in patients with an isolated complaint of low back pain.
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Lower
Back Pain
Questions
1)
First line of therapy for epidural spinal cord compression from
metastatic cancer is:
a)
Radiation therapy
b)
Surgery
c)
Corticosteroids
d)
Chemotherapy
2)
The most common site of epidural spinal cord compression from metastatic
cancer is:
a) Cervical spine
b) Thoracic spine
c) Lumbar spine
d) Sacral spine
3)
All of the following are indications for non-operative treatment
of spinal epidural
abcesses except:
a) Panspinal involvement
b) Lumbosacral SEA and normal neurological
exam
c) Fixed neurological deficits for greater
than 48 hours
d) Urinary incontinence and sensory deficit
4)
All of the following contribute to the severity of spinal cord compression
except:
a)
Force of compression
b) Length of spinal cord compressed
c) Duration of compression
d) Rate of compression
5)
The most common organism cultured in spinal epidural abcesses is:
a) Streptococcus
b) Pseudomonas
c) Staphylococcus aureus
d) Klebsiella
e) Mycobacterium tuberculosis
Answers
1)
C. Corticosteroids are the fastest way to decrease the edema surrounding
the spinal cord prior to radiation therapy.
2)
B. Thoracic spinal bodies have the largest overall space compared
to other spinal bodies.
3)
D. Urinary incontinence and sensory deficits are indications for
surgical therapy.
4)
B. The length of the spinal cord compressed matters little since
the point of maximum compression is the site of the neurological deficits.
5)
C. Remember 15% is MRSA.
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