straight-leg raise (reproduction of the patient's radicular
symptoms between 30 and 70 degrees of leg elevation) has
a relatively high sensitivity ( 9 1%), but a low specificity
Evaluate strength for nerve root dysfunction by testing knee
strength (IA nerve root), great toe/foot dorsiflexion (LS
nerve root), and foot plantartlexion (S1 nerve root). Sensory
deficits in radiculopathy include decreased sensation
between the first and second toes (LS nerve root) and
decreased sensation on the lateral aspect of the foot (S1
Lastly, assess the pulses and palpate the abdomen for
possible vascular causes of the pain, including aortic
Laboratory testing generally plays a limited role in the
evaluation of low back pain. Obtain a urine pregnancy test
in females of reproductive age to exclude ectopic pregnancy
and guide future decisions regarding imaging. A urinalysis
may also be helpful to evaluate for nephrolithiasis or
pyelonephritis as potential causes of low back pain.
Although erythrocyte sedimentation rates and C-reactive
protein may be elevated in some patients with back pain
( eg, epidural abscess, malignancy), these studies are
nonspecific and should not be routinely ordered as part of
Patients presenting with nonspecific low back pain with
none of the high-risk features discussed previously do not
warrant routine radiographic evaluation. Prompt
evaluation with magnetic resonance imaging (MRI) or
computed tomography (CT) is recommended when severe
or progressive neurologic deficits are present or when
serious underlying conditions are suspected on the basis of
history and physical exam. If available, MRI is preferred
over CT because it provides better visualization of soft
tissues, vertebral marrow, and the spinal canal.
In patients suspected of a vertebral compression
fracture (eg, osteoporosis, chronic steroid use), plain
radiography is recommended (Figure 92-1). A CT should
be considered if there is significant loss of height of the
vertebral body or if any neurologic symptoms are present.
Patients with an underlying malignancy with acute back
pain should have an MRI on an urgent basis (within
24 hours) when no neurologic deficits are present. When
neurologic deficits are present, the MRI is performed
emergently. For patients with low back pain associated
with radiculopathy, MRI (preferred) or CT are only
recommended if the patient is a candidate for surgery or
Figure 92-1. T1 2 compression fracture.
epidural steroid injection, as the natural course of lumbar
disc herniation with radiculopathy is improvement within
The history and physical exam serve as the cornerstones in
the evaluation of low back pain. Eliciting risk factors
indicative of a serious underlying condition ( eg, urinary
retention concerning for cauda equina syndrome) or
identifying neurologic deficits on exam should prompt
advanced imaging. In the absence of risk factors, neurologic
deficits, or symptoms suggestive of a potentially serious
cause, the source of the low back pain is most likely benign,
and reassurance and symptomatic management with
outpatient follow-up is recommended (Figure 92-2).
The treatment of low back pain varies depending on the
identified etiology. For those patients with nonspecific low
back pain, symptomatic therapy should include advice to
remain active and application of heat as needed.
Acetaminophen and nonsteroidal anti-inflammatory drugs
(NSAIDs) have shown short-term benefits. One must weigh
the potential analgesic benefit from NSAIDs with the known
risks of their use. Opioid analgesics or tramadol are an
option for patients with severe, debilitating pain that is not
controlled with acetaminophen or NSAIDs, but again, they
for abuse. Musculoskeletal relaxants are approved by the
Perform a focused history & physical exam for:
• Risk factors for potentially serious cond itions
• Symptoms suggestive of radiculopathy or spinal stenosis
• Presence & severity of neurologic deficits
Perform diagnostic studies (x-ray,
CT, MRI) to identify specific cause
No specific cause identifiedsymptomatic treatment with
Figure 92-2. Low back pain diagnostic algorithm. CT, computed tomography; MRI,
short-term use in acute low back pain.
When a specific etiology for low back pain is identified, the
treatment varies depending on the underlying pathology. Low
recover without surgery. Patients diagnosed with vertebral
osteomyelitis require intravenous (N) antibiotics, whereas an
epidural abscess is treated with neurosurgical evaluation
for potential drainage as well as parenteral antibiotics.
Neurosurgical consultation should also be obtained immedi
ately for patients with cauda equina syndrome. In patients
compression is advised. The administration of corticosteroids
(dexamethasone 10 mg N) for acute spinal cord compression
should also be considered in consultation with neurosurgery.
The patient disposition depends primarily on the etiology
of the back pain as well as analgesic control of symptoms.
Patients found to have a serious underlying etiology of low
back pain (eg, cauda equina syndrome, epidural abscess)
should be admitted in consultation with neurosurgery. It is
also reasonable to consider observation for patients with
nonspecific low back pain (with or without radiculopathy)
when pain control cannot be achieved in the ED.
Patients with nonspecific low back pain or back pain with
radiculopathy in whom pain is reasonably controlled can
be discharged with outpatient follow-up. All patients
should receive patient education regarding self-care and
treatment for low back pain as well as indications to
return to the emergency department ( eg, development of
neurologic deficit, change in urinary or bowel functions) .
Chou R, Huffman LH. Medications for acute and chronic lower
back pain: A review of evidence for an American Pain Society/
American College of Physicians clinical practice guideline. Ann
Intern Med. 2007;147:505-5 14.
Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low
back pain: A joint clinical practice guideline from the American
College of Physicians and the American Pain Society. Ann
Frohna WJ, Della-Giustina D. Neck and back pain. In: Tintinalli
JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.
Tintinalli's Emergency Medicine: A Comprehensive Study Guide.
7th ed. New York, NY: McGraw-Hill, 20 11, pp. 1885-1 893.
• Compartment syndrome occurs when tissue pressure in
a closed space rises, compromising perfusion to nerves
• The leg and forearm compartments are most commonly
involved, but compartment syndrome can also occur in the
upper arm, thigh, hand, foot, gluteal region, or abdomen.
Acute compartment syndrome is a surgical emergency. If
unrecognized and untreated, it can lead to tissue ischemia,
necrosis, and long-term functional impairment. Volkmann
ischemic contracture is the end result of an ischemic injury
to the muscles and nerves of a limb. Compartment syndrome
is seen most commonly in the setting of trauma, including
long bone fractures, crush injuries, and circumferential
burns to the extremities. Males and young people are
affected more commonly than females and elderly.
The pathophysiology of compartment syndrome
involves increased pressure in a muscle compartment that is
enclosed by a fascial structure with limited ability to expand.
This increased pressure is caused by edema or bleeding,
from compression of the compartment by a circumferential
burn or a constricting cast, or a combination of both.
Increased pressure leads to decreased venous outflow from
the compartment, causing a decrease in the arteriovenous
pressure gradient and ultimately cellular ischemia and tissue
Cardinal signs and symptoms include severe pain over
the involved area, pain with passive stretch of the muscles
in the affected compartment, weakness, and paresthesias.
Although commercially available devices can be used to
• Compartment syndrome is usually associated with long
bone fracture, crush injuries, circumferential burn, or
• Acute compa rtment syndrome is a surgical emergency,
treated by fasciotomy to relieve pressure and restore
measure compartment pressures, the diagnosis is often
made on clinical grounds alone. Early recognition and
orthopedic consultation are essential in preventing t issue
Acute compartment syndrome is seen most commonly in
the setting of trauma or long bone fracture. Significant
blunt trauma or crush injury can lead to compartment
syndrome, even in the absence of fracture. Symptom onset
is usually within hours of injury, but can pres
ical consultation should also be obtained immedi
ately for patients with cauda equina syndrome. In patients
compression is advised. The administration of corticosteroids
(dexamethasone 10 mg N) for acute spinal cord compression
should also be considered in consultation with neurosurgery.
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