Must Exclude Diagnoses of Back Pain
Infection (spinal epidural abscess)
Good data that a single lateral lumbo-sacral spine film is as good as three view series. One set of LS spine films gives the same amount of gonadal irradiation as 6 years of daily PA/LAT C-XRs (Br J Radiology 1990 Jul; 63(751))
Large randomized trial of MRI vs. radiographs showed no advantage to doing mri as initial test (JAMA. 2003;289:2810-2818.)
fever, unexplained weight loss, a history of cancer, neurologic deficits, alcohol or injection-drug abuse, an age of more than 50 years, or trauma. Failure of the pain to improve after four to six weeks should prompt radiography,”Red flags” that suggest a need for early imaging include major trauma, an age above 50, history of cancer, unexplained weight loss, fever, immune deficiency or suppression, injection drug use, active infection, saddle anesthesia, bladder or bowel incontinence, and/or a severe or progressive neurologic deficit
Leg pain>back pain, consider disc herniation
L4-extension of quads, squat and rise, knee jerk, sensory front of leg
L5-dorsiflexsion of great toe and foot, walk on heels, lateral of leg
S1-plantar flexion of toe and foot, walking on toes, ankle jerk, back of leg
the neurologic examination should focus on ankle and great-toe dorsiflexion strength (the L5 nerve root), plantar flexion strength (S1), ankle and knee reflexes (S1 and L4), and dermatomal sensory loss. The L5 and S1 nerve roots are involved in approximately 95 percent of lumbar-disk herniations.
Operating characteristics of medical history and physical examination findings for nontraumatic causes of lower back pain.
Etiologies of Back Pain Historical and Physical Exam Findings Sensitivity/Specificity, % LR+/LR− Cancer Age >50 y 77/71 2.7/0.3 Previous hx of cancer 51/98 25.5/0.5 Unexplained weight loss 15/4 0.2/21.3 No relief with bedrest 31/48 0.6/1.4 Pain duration >1 mo 50/81 2.6/0.6 Age >50 y, cancer hx, weight loss, or therapy failure 100/60 2.5/0.0 Compression fracture Age >50 y 84/61 2.2/0.3 Age >70 y 22/90 2.2/0.9 Trauma 30/85 2.0/0.8 Corticosteroid use 6/99 12.0/0.9 Spinal osteomyelitis IVDA or UTI or skin infection 40/NA na Herniated disc Sciatica 95/88 7.9/0.1 Spinal stenosis Pseudoclaudication 60/NA na Age >50 y 90/70 3.0/0.1 Ankylosing spondylitis Age of onset ≤40 y 23/82 1.3/0.9 Pain not relieved by supine 100/49 2.0/0.0 Morning back stiffness 64/59 1.6/0.6 Pain duration ≥3 mo 71/54 1.5/0.5 4 Of 5 positive responses 95/85 6.3/0.6
Hx, History; IVDA, intravenous drug abuse history; LR, likelihood ratio; na, not applicable; UTI, urinary tract infection.
Muscle strengthis tested by examining the:
- L2 nerve root (which supplies the iliopsoas muscle and is tested by hip flexion)
- L3 nerve root (quadriceps, tested by knee extension)
- L4 nerve root (tibialis anterior, assessed by evaluating ankle dorsiflexion and inversion at the subtalar joint)
- L5 nerve root (extensor hallucis longus and extensor digitorum longus, tested by asking the patient to dorsiflex the great toe, then the other toes)
- S1 nerve root (flexor hallucis longus, flexor digitorum longus, and tendoachilles, tested by asking the patient to plantar-flex the great toe, then the other toes, and then the ankle).
The patient is also asked to walk a few steps on the toes and then on the heels. Inability to toe-walk indicates S1 nerve root involvement; inability to heel-walk may indicate L4 or L5 involvement. If the patient cannot heelwalk, ask him or her to squat; inability to do so indicates L4 problems.6
10 cc .5% Bupi c 1 cc (40 mg) solumedrol, use 1 ¼ 25 g needle to inject at dimple just adjacent to sacrum or at point of maximal tenderness
Muscle Relaxants are Ineffective for Musculosckeletal Back Pain
Flexeril and NSAIDs was no better than NSAIDs alone (Annals EM 41:6, p.818), if you want to use it, use 5 mg (Borenstein DG et al: Efficacy of a low-dose regimen of cyclobenzaprine hydrochloride in acute skeletal muscle spasm: results of two placebo-controlled trials. Clin Ther 25:1056, 2003);
- Muscle relaxants are an option in the treatment of patients with acute low back problems. While probably more effective than placebo, muscle relaxants have not been shown to be more effective than NSAIDs. (Strength of Evidence = C.)
- No additional benefit is gained by using muscle relaxants in combination with NSAIDs over using NSAIDs alone. (Strength of Evidence = C.)
- Muscle relaxants have potential side effects, including drowsiness in up to 30 percent of patients. When considering the optional use of muscle relaxants, the clinician should balance the potential for drowsiness against a patient’s intolerance of other agents. (Strength of Evidence = C.) (Bigos, Stanley J et al. December 1994 (AHCPR Publication No. 950642). U.S. Agency for Health Care Policy and Research4. Acute Low Back Problems in Adults (Clinical Guide))
Cochrane review showed small benefit but may be overwhelmed by side effects (MUSCLE RELAXANTS FOR NONSPECIFIC LOW BACK PAIN: A SYSTEMATIC REVIEW WITHIN THE FRAMEWORK OF THE COCHRANE COLLABORATION van Tulder, M.W., et al, Spine 28(17):1978, September 2003)
The Relative Efficacy of Seven Skeletal Muscle Relaxants. An Analysis of Data From Randomized Studies. J Emerg Med. 2022 Jan 20;S0736-4679(21)00839-8. doi: 10.1016/j.jemermed.2021.09.
Ankylosing spondylitis is another important, though uncommon disease that presents with back pain. This inflammatory process usually affects young males and presents with slowly progressive back ache and stiffness that is worse in the morning and improves over the course of the day. Gradually, these patients develop diminished range of motion of the back. This is one of the HLA-B27-related inflammatory arthropathies that include psoriatic, Reiters, and inflammatory bowel disease-related syndromes. Physical examination reveals diminished excursion of the lumbar spine and chest. This is one situation in which plain films and the erythrocyte sedimentation rate (ESR) are helpful.
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Compression from Mets
Level of pain or symptoms doesn’t correlate with actual lesion level. Probably should MRI the entire spine.Back to top
Spinal Epidural Abscess
review article (NEJM 2006;355(19):2012)
anterior associated with vertebral body osteo or acute discitis
posterior is often from hematogenous spread
blunt trauma can cause a hematoma which is a nidus for infection
risk factors include AIDS/HIV, DM, ETOH, IVDA, cancer, steroid use, renal failure
staph aureus is the cause in more than 50% of cases, then strep and enteric anaerobes/aerobes. Actinomyces is a rare cause from dental sources.
Pain is the most common presentation along with fever and radicular symptoms. The symptoms may develop over days to weeks.
Progression is normally spinal ache » radicular pain » limb weakness » paralysis
CBC, ESR (average is ~77 in SEA), Blood CX
MRI is the 1st test of choice, though a combination of a CT and a myelogram should be reasonably sensitive.
CT c Contrast alone only detects 50% of cases.
Spinal epidural abscess (SEA) is a rare but feared complication of IDU. Difficulty arises from the facts that SEA may present simply as back pain, MRI generally is required for diagnosis, and diagnostic delay can be associated with sudden and irreversible neurological damage. The incidence of SEA in the general population is estimated at 0.2-1.0/10000 hospital admissions and is thought to be rising.69,70 While IDU is considered a major risk factor for SEA, no study specifically has addressed the incidence in this patient population.
Most SEAs are due to hematogenous seeding of the vertebrae or epidural space. Common sources of bacteremia include skin and soft-tissue infections, dental infections, and urinary tract infections, as well as IDU.68,69 Interestingly, in a series of 18 cases of IDU-related SEA, no co-existing endocarditis was found.69S. aureus is the predominant pathogen in SEA, and is implicated in 50-65% of SEA cases overall and an even higher percentage of IDU-related cases.68,69,71 Pseudomonas and tuberculosis also have been isolated in IDU-related SEA. Epidural abscesses were associated with adjacent OM, diskitis, or psoas abscess in 14 of 18 cases, all involving IDU.69
There are two proposed mechanisms of cord injury in SEA, which may explain the wide variation in the time of onset of neurological deficits: direct compression and vascular ischemia. Compression due to mass effect is postulated to produce a subacute course, whereas thrombosis and vascular injury may result in a rapid paralysis.
While the classic presentation of SEA includes back pain, fever, and neurological symptoms, the presence of this triad is far from universal. Back pain is present in greater than 90% of patients, whereas fever is present in 60-76%, and neurological deficits are found at presentation in 57-70%.68,71 Neurologic findings include radicular pain, urinary incontinence, leg weakness, and paraplegia or quadraplegia. Patients occasionally may present with sepsis or encephalitis, further confounding and delaying the diagnosis.68
When faced with an IDU patient whose presentation is at all concerning for SEA, emergent imaging is required to exclude or establish the diagnosis. MRI now is the test of choice. With a sensitivity of 90%, it has come to replace the equally sensitive but more invasive CT-myelogram.68 In addition to revealing an abscess, MRI provides images of the cord itself, and may uncover an alternative diagnosis accounting for the patients symptoms.72 Plain x-rays cannot be relied upon to exclude the diagnosis of SAE, although they may be abnormal if there is associated vertebral OM. In such cases, end plate destruction or a narrowed disc space may be evident.
An ESR greater than 30 mm, while nonspecific, almost always is found in SEA. ESR also may be used to follow treatment efficacy. Some authors advocate ESR as a screening test for SEA in at-risk patients, such as injection drug users, who present with unexplained back pain.68,71 No prospective data exist to support this approach. Blood cultures are positive in greater than 60% of cases of SEA, and may provide an etiologic diagnosis if surgical cultures are unrevealing.68,69 Therefore, it is critical that blood cultures be obtained prior to beginning empiric antibiotics whenever the diagnosis of SEA is being entertained.
Spinal Cord Compression
Get MRI spinals survey
Pt with bone metastases can get vertebral fractures with resulting compression even with a recent negative MRI
Dex 10 mg then 4 mg Q6
Soft Tissue Thoracic
Less acute than LS spine pain, but takes longer to resolve
Lateral view through L4 sufficient as per study (see box)
Full series same dose of gonadal radiation as 6 yrs of daily C-XR
Get Films if <18, >50 or Trauma or >6 weeks duration or suspicion of occult cause
Cauda Equina-bowel/bladder incontinence or urinary retention/saddle anesthesia/decreased rectal tone
Spinal Stenosis-pain brought on by walking, relieved by rest but especially back flexion
Spondylolisthesis-slippage of 1 vetebrae over another
Fx-malignant or otherwise
Ankylosing Spondylitis-morning back pain relieved by exercise
Most Disk problems are L5 (Foot Dorsi) or S1 (Plantar Flex)
Straight Leg Raise-If crossover sign seen, very specific
Standing-walk on toes for S1
Acetabular Rotation-have patient stand with arms at his side, rotate him 30 degrees either way, should not hurt as done by hip, not back
Axial Loading-should not hurt when you push down on top of head
Knee Reflex-L3 and L4
Prone-contract buttocks (L1)
Complete cord transection
Spinal shock refers to the loss of muscle tone and reflexes with complete cord syndrome during the acute phase of injury. The intensity of the spinal shock increases with the height of the level in the spinal cord. Spinal shock typically lasts less than 24 hours but has been reported occasionally to last days to weeks. A marker of spinal shock is loss of the bulbocavernosus reflex, which is a normal cord-mediated reflex that may be preserved in complete cord lesions. The bulbocavernosus reflex involves involuntary reflex contraction of the anal sphincter in response to a squeeze of the glans penis or a tug on the Foley catheter. The termination of the spinal shock phase of injury is heralded by the return of the bulbocavernosus reflex; increased muscle tone and hyperreflexia follow later.
Most often caused by hyperextension injury, especially in older folks c degenerative disease
Bilat motor paresis with effects on upper>lower and distal>proximal. May also feel burning sensation in upper extremities. (Burning hands syndrome)
Hemisection of the cord, usually from penetrating trauma. If from blunt, suspect fracture of lateral mass
Ipsilateral loss of motor and proprioception and contralateral heat/pain sensation loss
Loss of motor and pain/temp sensation with preservation of touch/proprioception
Hyperflexion inhuries are usually the etiology. Needs immediate neurosurg consultation as prompt treatment has good resultsBack to top
The cauda equina (horses tail) is the name given to the lumbar and sacral nerve roots that continue on within the dural sac caudal to the conus medullaris. The etiology of the cauda equina syndrome is usually a ruptured, midline intervertebral disk, most commonly occurring at the L4-L5 level. Tumors and other compressive masses may cause the syndrome as well. Like the conus medullaris syndrome, patients generally present with progressive symptoms of fecal or urinary incontinence, impotence, distal motor weakness, and sensory loss in a saddle distribution. Muscle stretch reflexes may also be reduced. The presence of urinary retention is the single most consistent finding, with a sensitivity of 90%. Low back pain may or may not be present.
Give DEX 16-96 mg divided Q6
A Babinski reflex suggests involvement of the conus medullaris, the lower part of the spinal cord which is in proximity to the nerve roots. Thus, injuries to this area often yield both upper and lower motor neuron signs (JEM, 11/06, pg. 381).
Pt must have both (hypoesthesia in the saddle or peri-anal–ask if it feels different, not can you feel this) and (bowel|bladder|sexual dysfunction)
by Rudy DR:
formation of the cauda equina
All physicians are familiar with the fact that the cauda equina forms as the embryonic and infantile spinal column grows faster and longer in time than the spinal cord, resulting in the nerve roots trailing downward to their corresponding intervertebral spaces before exiting to their areas of distribution. What many of us have forgotten is that the anterior and posterior rami descend the whole length of the distance to the intervertebral spaces before joining to form complete roots. We may also have forgotten that the dorsal roots carrying the preganglionic parasympathetic fibers and sensory fibers to the paravertebral ganglia descend along with their corresponding roots, and that the ganglia themselves appear virtually just proximal to or within the neural foramina spaces.
These preganglionic fibers are not supplied with neurilemmal sheaths. When they are damaged and undergo Wallerian degeneration, they do not regenerate as those so endowed are likely to do. When they are damaged in compression of the cauda equina they are less likely to recover. Thus, while somatic sensory and motor symptoms may or may not reverse with disc decompression, the bilateral loss of parasympathetic functions of the preganglionic roots involved, once damaged, can become quickly irreversible. If this occurs unilaterally, though, there may be few or no bowel or bladder symptoms.
red flags to watch for
The clinical red flags that should alert the practitioner to CES are increasingly severe and intractable radicular low back pain, combined with bilateral radicular symptoms and signs (which may not be symmetrical) or bladder or bowel control symptoms (or both).
Severe and increasing low back pain. By far the most common cause of CES is central or centrolateral herniation and extrusion of lumbar intervertebral discs, L4-5 or L5-S1 (or both). Rarely does CES present acutely without severe low back pain.
Plain X-rays, an MRI, and a bone scan should clarify the possibility of a malignant cause. Metastatic lung, breast, and prostate cancers are high on the list, followed by lymphoma, multiple myeloma, and less common tumors such as melanoma. However, unless such tumors develop in the region of the cauda equina, they do not result in CES; in addition, they occur with far less frequency than lumbar disc herniations. Spinal epidural abscess, trauma, and, in children, various congenital anomalies can also cause CES.
In any event, if the pain is associated with radicular symptoms and signs, then the first questions to be addressed are: Is the involvement bilateral? Is there saddle area sensory loss? Is there bladder or bowel dysfunction?
Bilateral evidence of radiculopathy. With lateral disc herniation, only one side of the cauda can be affected. The parasympathetic functions remain virtually intact under such circumstances, and other manifestations of radiculopathy are unilateral. With central herniation, however, at a certain point symptoms and signs begin to appearperhaps quicklyon both sides. Thus, you may find low back pain radiating into the lower extremity or extremities, a positive straight leg raising test, decreased amplitude of the deep tendon reflexes in the quadriceps or Achilles tendon (or both), or weakness with toe- or heel-walking.
These findings are not likely to be symmetrical. For example, there may be pain radiating down the right posterior thigh and into the leg and foot, a positive straight leg raising test on the left, or a diminished ankle jerk and a weak toe with walking on the left.
Bladder or bowel control symptoms. Last comes evidence of involvement of the parasympathetic functions affecting bladder or bowel control. The first symptom may be loss of the sensation of bladder fullness, poor urinary stream, or the conscious need to strain to micturate. This has been referred to as incomplete CES and is thought to be reversible with timely surgical correction.
Further progression results in total loss of the sensation of bladder fullness and awareness of the need to void, leading to dribbling overflow incontinence, or what is called CES with retention. Bladder atony is a result of loss of detrusor muscular sensitivity. At this stage, a conscious effort must be made to accomplish voiding by straining or applying pressure to the suprapubic area. Testing for post-voiding residual urine by catheter can provide an objective measurement of bladder function. A positive finding is a residual urine volume of 100 ml or more.
Early in the progression of CES, saddle anesthesia (including numbness in the genitalia) often develops, which suggests a worse prognosis. The patient loses rectal sphincter tone, a more certain sign of CES than the symptom of difficult bowel movements, which are subject to the vagaries of habit, nonspecific effects of lower body pain, and variability among patients.
To test rectal sphincter tone, ask the patient to squeeze down on the examining digit or simply test the external sphincter for resistance at the onset of the digital examination. Adjunctively, the anus may be observed for the so-called wink when the perianal skin is stroked in the same manner as in obtaining the abdominal and cremasteric reflexes. In terms of medicolegal implications, checking for saddle hypesthesia and anesthesia and performing a rectal examination to assess sphincter tone have become the standard of care for patients with low back pain and bilateral evidence of radiculopathy.
Most patients do not present with all the characteristic features of CES. Sacral sensory loss is a sensitive and relatively specific sign for diagnosing CES. (Emerg Med J 2007;24:33–34.)Back to top
Spinal Subarachnoid Hemorrhage
usually from AVMsBack to top
The classic pattern of sensory deficit is a loss of pain and temperature sensation in the upper extremities, with preservation of proprioception and light touch. This phenomenon is described as a disassociative anesthesia because of the discrepant loss of sensory modalities. The sensory deficit is often described as being in a cape-like distribution over the shoulders and arms. The anatomic basis for the neurologic findings of syrinx is due to its central location near the central canal. Here it may compress the crossing fibers of the lateral spinothalamic tract that carry pain and temperature fibers. Crude touch, position, and vibratory sensation are typically unaffected. Sensory fibers from the lower limbs are similarly spared.Back to top
Spinal Epidural Hematoma
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Order MRI C/T/L spine or at the least T&L
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