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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