Dolor de Espalda en Ancianos

8/8/2019 Dolor de Espalda en Ancianos

1/19

Back Pain in the Elderly

Joshua Broder, MD*, Jaime T. Snarski, MDDivision of Emergency Medicine, Department of Surgery,

Duke University Medical Center, Box 3096, Durham, NC 27710, USA

Back pain in the elderly is a complex chief complaint. Numerous life-

threatening or disabling diseases may present with acute back pain. Signs

and symptoms of these catastrophic illnesses are often similar to those of

more benign disorders. Understanding the limitations of the history and

physical examination in elderly patients who have back pain is essential to

avoid misdiagnosis and patient morbidity or mortality. This article describes

the presentation and evaluation of dangerous causes of back pain. Emphasis

is placed on vascular catastrophes, spinal cord compression (SCC) syn-

dromes, and infectious disease processes. Spinal compression fractures arediscussed briefly. Wherever possible, the authors refer to primary research

articles for information on disease presentations and the sensitivity of his-

torical, physical examination, laboratory, and imaging tests.

Epidemiology

Thirty percent of adults age 65 years or older report low back pain as

a significant complaint. Approximately 10% of all office visits for back

pain occur among elderly patients [13]. Although malignancy, heart dis-

ease, chronic lung disease, stroke, and diabetes are the leading causes of

death in the elderly, aortic aneurysm and aortic dissection (AD) are signif-

icant causes of mortality by the age of 65 years, accounting for nearly 1% of

deaths. These statistics remain static for each advancing decade [1,2,46].

Vascular catastrophes

Rupture of an abdominal aortic aneurysm (AAA) and AD account for anestimated 15,000 deaths annually in the United States and are consistently

* Corresponding author.

E-mail address: [email protected] (J. Broder).

0749-0690/07/$ - see front matter 2007 Elsevier Inc. All rights reserved.

doi:10.1016/j.cger.2007.01.011 geriatric.theclinics.com

Clin Geriatr Med 23 (2007) 271289
mailto:[email protected]:[email protected]


2/19

among the 15 leading causes of death according to the Centers for Disease

Control [46]. Both diseases may present initially with back pain. Rapid di-

agnosis and treatment of these two deadly disorders are essential. Unfortu-nately, the history and physical examination alone are limited in excluding

these diagnoses.

Abdominal aortic aneurysm

An AAA is defined as a dilated region of the aorta exceeding twice the

normal diameter (or approximately 3 cm). They occur in approximately

5% of the population above the age of 65 years [7]. Important risk factors

for AAA include male gender, family history of AAA, and cigarette smok-ing. Surprisingly, other risk factors for atherosclerosis, including hyperten-

sion, elevated cholesterol, and the presence of coronary artery or other

peripheral arterial disease, are more weakly associated with the risk for an-

eurysm formation [8]. In fact, for reasons that are not well understood, di-

abetes is negatively associated with the presence of AAA in large studies [8].

Risk of aneurysm rupture becomes substantial when the diameter rises

above 5 cm. Recent research, however, suggests that rupture may occur at

smaller diameters in women [9]. For patients presenting with AAA rupture,

mortality approaches 40% to 80% [10]. In contrast, elective AAA repair hasan operative mortality of approximately 4% [10]. Thus, early detection is es-

sential. At present, national guidelines recommend screening only in men

age 65 years or older [7,11].

Limitations of the history and physical examination for abdominal aortic

aneurysms

William Osler recognized the enigmatic presentation of aortic aneurysm,

stating, There is no disease more conducive to clinical humility than aneu-

rysm of the aorta [12]. Geriatricians always must consider AAA in anyelderly patient presenting with back pain. Although acute back pain may in-

crease suspicion for rupture, subacute or chronic presentations of AAA can

occur. In a case series of unruptured aneurysms, the duration of pain before

diagnosis ranged from 1 to 60 days, with a mean of 11.6 days [13]. In a series

of ruptured aneurysms, time from onset of symptoms to emergency depart-

ment presentation ranged from 44 minutes to 36 hours (Box 1) [14].

The difficulty of making this diagnosis is highlighted by the fact that 30%

to 60% of AAAs are misdiagnosed initially. The most common misdiag-

noses for AAA are renal colic, diverticulitis, and gastrointestinal hemor-rhage [15,16]. The reasons for misdiagnosis probably are multifactorial.

AAA may present with symptoms similar to those of more benign condi-

tions (eg, back pain mimicking renal colic, or left lower quadrant pain re-

sembling diverticulitis). Findings such as hematuria (present in 87% of

ruptured AAAs in one series) or heme-positive stools may confuse the diag-

nostic picture and delay diagnosis [17]. Moreover, in one series of

272 BRODER & SNARSKI


3/19

misdiagnosed AAA, hemodynamic shock was present in 57% of patients

and probably compromised the patients ability to provide a useful history

[15]. In addition, the classic finding of a pulsatile abdominal mass was noted

in only 26% of patients who initially were misdiagnosed; the absence of

a pulsatile abdominal mass probably obscured the diagnosis [15]. Delayed

presentations of disease, ranging from 10 hours to 14 days in one series,

also are common in patients who are misdiagnosed [16]. This delay may

reduce physicians suspicion of AAA, because the classic presentation is

one of more acute and severe illness.Physical examination is insensitive in identifying aortic aneurysms.

A normal examination never should exclude the diagnosis. Numerous stud-

ies have shown the sensitivity of abdominal palpation to detect a pulsatile

mass to be poor, reaching only 80% even in aneurysms up to 5 cm in size

[1820]. Smaller aneurysms are even less readily detected by examination.

Obesity further compromises examination sensitivity. Sensitivity of physical

examination for aneurysm rupture is not well studied.

Hemodynamic stability should not be taken as a reassuring sign or as per-

mission to perform a less urgent evaluation. In a study of patients presentingto an emergency department with aneurysm rupture, 50% of patients who

died within 2 hours had initial heart rates less than 71 beats per minute

and systolic blood pressures greater than 110 mm Hg [14].

Fortunately, isolated back pain is a relatively rare presentation of aneur-

ismal rupture. In an emergency department study of patients who had rup-

tured AAA, isolated back pain constituted the chief complaint in only 4%,

Box 1. Key pearls and pitfalls: aortic disasters

Physical examination is inadequate to rule out an aorticcatastrophe.

A chest radiograph is inadequate to rule out aortic dissection.

In the office:

Obtain intravenous access.

Place the patient on a cardiac monitor.

Administer oxygen.

Arrange immediate emergency medical service transport to an

emergency department.

In the emergency department:Consult a surgeon immediately (before imaging) for unstable

patients.

Perform rapid bedside ultrasound to evaluate for AAA.

Consider initial noncontrast CT to evaluate for ruptured AAA.

Perform CT with intravenous contrast for definitive diagnosis

of AAA or aortic dissection.

273BACK PAIN IN THE ELDERLY


4/19

whereas the combination of abdominal and back pain occurred in 14% [14].

Back pain associated with syncope or near-syncope is an AAA rupture until

proven otherwise. In the same emergency department study of rupturedAAA, 20% had abdominal and back pain as well as collapse [14]. Rapid

evaluation for AAA should be considered in any elderly patient who has

acute nontraumatic back pain, because 12.5% of patients who have rupture

may die within 2 hours of presentation [14].

Diagnostic evaluation for abdominal aortic aneurysms

Imaging modalities used to diagnose an AAA include plain-film radiog-

raphy, ultrasound, CT, and MRI. Although an abdominal radiograph

sometimes may reveal a calcified aortic contour, the sensitivity for detectingAAA is not known. Therefore, plain films should not be used alone to ex-

clude AAA. In contrast, ultrasound has excellent sensitivity for the presence

of AAA (Fig. 1). Ultrasound has the advantage of being portable, noninva-

sive, and can be performed several times during the evaluation of an unsta-

ble patient. Unfortunately, ultrasound has limited sensitivity for AAA

rupture. In some studies, sensitivity for rupture has been as low as 4%

[21]. Nevertheless, an AAA seen on ultrasound in a symptomatic patient

should be treated as a rupture until proven otherwise.

CT has excellent sensitivity and specificity for AAA rupture [22]. Three-dimensional CT reconstructions of the aorta also are used to plan endo-

vascular repair and are thus of particular value (Fig. 2). Oral contrast is

contraindicated in CT conducted for aortic evaluation, because it may

limit the ability of computer algorithms to render three-dimensional views

of the aorta. Intravenous contrast is helpful in delineating aortic and

Fig. 1. Transverse ultrasound image of an abdominal aortic aneurysm. The aneurysm measures

4.75 cm by 4 cm. Ultrasound is highly sensitive for the detection of aneurysm but insensitive for

rupture. Ultrasound is the preferred modality for diagnosis of abdominal aortic aneurysms in

the unstable patient.



5/19

branch vessel anatomy, but aneurysm and even rupture can be detected

without contrast (Fig. 3) [2325]. In some settings, noncontrast CT is per-

formed as the test of first choice, allowing immediate evaluation for AAA

rupture before laboratory test results have returned [25].

MRI with gadolinium is a definitive test with excellent sensitivity and

specificity [26]. MRI is a poorer choice than CT for patients who have sus-

pected rupture because the test is more time consuming than CT. Also, the

high magnetic field, which precludes the presence of any ferromagnetic ma-terials, makes patient treatment and monitoring in the MRI suite more dif-

ficult. The use of MRI should be restricted to special circumstances, such as

patients who have poor renal function in whom iodinated contrast may

cause nephropathy. Even in these circumstances, the risk of contrast ne-

phropathy must be weighed against the potential for rupture resulting

from diagnostic delays.

Laboratory testing plays a limited role in the evaluation of possible AAA

rupture. A normal hemoglobin value should not be interpreted as a sign of

stability: in patients who died within 2 hours of emergency department ar-rival, 50% had an initial hemoglobin of 9.0 g/dL or greater [14].

When AAA rupture is suspected, definitive imaging must be conducted as

rapidly as possible. Unstable patients who have suspected ruptured AAA

require surgical consultation before imaging. Rapid emergency medical ser-

vice (EMS) transportation of patients who have suspected abdominal aortic

aneurysm rupture is necessary.

Fig. 2. Three-dimensional CT reconstruction of an abdominal aortic aneurysm. Reconstruc-

tions such as this CT with intravenous contrast are particularly helpful in planning endovascu-

lar repair. In an unstable patient, however, no delay should be incurred for imaging before

surgical consultation.



6/19

Aortic dissection

Limitations of the history and physical examination

AD, once thought to be the most common aortic catastrophe, is now be-

lieved to occur at a rate of 3.5 per 100,000, less often than AAA rupture [27].

Inhospital mortality for AD ranges from 13% to 43% [28,29]. The classic

presentation of AD is the sudden onset of tearing chest pain that radiates

to the back. In the elderly, however, classic symptoms of dissection are

less common. The International Registry of Aortic Dissection (IRAD)found abrupt onset of pain to occur in only 77% of patients age 70 years

or older, compared with 89% of those less than 70 years of age [28]. More-

over, neurologic deficits produced from carotid dissection, spinal cord ische-

mia, or peripheral ischemic neuropathy occur in 5% to 14% of patients age

70 years or older [28]. AD must be included in the differential diagnosis of

any patient who has back pain and neurologic signs or symptoms.

Similar to AAA rupture, physical examination for AD has limited sensi-

tivity and specificity. Prospective studies do not validate traditional bedside

maneuvers, such as the measurement of bilateral upper extremity bloodpressures and palpation of pulse deficits. In fact, studies of asymptomatic

patients find large disparities in upper extremity blood pressures, creating

false-positive test results and a very low positive predictive value [30,31].

The sensitivity of blood pressure differences in dissection has not been val-

idated in any large clinical study, and the absence of a difference in upper

extremity blood pressures should not be used to exclude aortic disease. In

Fig. 3. Noncontrast abdominal CT showing a very large ruptured abdominal aortic aneurysm

(arrow). The calcified wall of the aorta appears white on this study. Blood has leaked into the

retroperitoneum on the patients left side (arrowheads). CT is very sensitive for detection of an-

eurysm and rupture, even without contrast. Noncontrast CT may be a good option for the rapid

diagnosis of a stable patient with a suspected abdominal aortic aneurysm, because no delay for

creatinine measurement is necessary.



7/19

addition, pulse deficits occur in only 20% to 30% of patients [28,29,32,33].

The diastolic murmur of aortic insufficiency occurs in only about 30% of

patients who have AD and when present does not increase the chance of dis-section significantly [34]. When dissection is suspected, definitive testing

must be performed rapidly.

Diagnostic imaging for aortic dissection

Imaging modalities used in the evaluation of suspected AD include chest

radiography (CXR), CT, MRI, and transesophageal echocardiography.

CXR is inadequate to exclude aortic dissection. According to IRAD data,

the CXR is normal in approximately 12% of dissections [35]. Additional

suggestive but nondiagnostic CXR findings, such as a widened mediasti-num, occur in only about 60% of cases (Fig. 4) [35]. Any patient suspected

of having AD should be transported rapidly to the closest emergency de-

partment, regardless of normal blood pressures, pulses, and CXR. Once

in the emergency department, CT with intravenous contrast, MRI with

gadolinium, and transesophageal echocardiography are all nearly 100%

sensitive for dissection [36,37].

Spinal cord compressive syndromes

SCC is a true emergency in which early diagnosis and intervention can

prevent further morbidity. Causes of SCC include spinal epidural

Fig. 4. (A). A normal chest radiography in a patient with back pain and a Stanford type A aor-

tic dissection, involving the ascending aorta, arch, and descending aorta. ( B) Coronal CT recon-

struction from the same patient. The dissection can be seen involving segments of the aorta in

both the chest and abdomen (arrowheads). The upper arrow points to a circular cross-section

through the aorta, showing a true lumen (lighter gray area) and a false lumen (darker gray

area) separated by an intimal flap. The lower arrow points to an elliptical aortic cross-section

showing the same features.



8/19

metastases, infectious processes such as spinal epidural abscess (SEA), and

spinal epidural hematoma (SEH). Of these, spinal epidural metastases ac-

count for the majority of cases [3840]. SEH typically occurs in patients re-ceiving oral anticoagulant medications [41]. It is important to have a low

threshold for rapid evaluation and treatment whenever cord compression

is suspected (Box 2).

Spinal cord compression caused by spinal epidural metastases

Four percent to 6% of patients who have cancer ultimately develop SCC,

and up to 80% complain of back pain before the onset of neurologic deficits

[42]. A retrospective study of patients diagnosed with cord compressionfound a median duration of symptoms of back pain of 3 months. In

many cases, patients experienced subtle sensory or motor symptoms up to

20 days before diagnosis. As a result of delays in diagnosis, more than

80% of patients in this study were unable to walk unassisted by the time

of diagnosis [43]. Back pain in a patient who has cancer should be con-

sidered a consequence of spinal metastatic disease until proven otherwise.

Once neurologic signs and symptoms have developed, the prognosis for re-

covery is grim. In patients who are unable to walk at presentation, only 15%

to 22% regain the ability to ambulate with treatment [44,45].

Box 2. Key pearls and pitfalls: spinal compressive syndromes

A normal neurologic examination does not rule out the

diagnosis.

Evaluation should precede the development of neurologic

abnormalities whenever possible, because deficits often areirreversible.

Plain-film radiographs are inadequate to rule out the diagnosis.

In the office:

Consider immediate steroid administration if neurologic

deficits are present.

Arrange immediate transport to an emergency department.

In the emergency department:

Consult a neurosurgeon and radiation oncologist immediately

(before imaging) for patients who have neurologic deficits.Administer steroids for patients who have neurologic deficits.

Perform definitive imaging with MRI with gadolinium

contrast.

In stable patients suspected of having infection, defer

antibiotics until CT-guided aspiration is performed.



9/19


A thorough history and complete neurologic examination are important,

but neither is sufficiently sensitive in detecting SCC. The majority of patientscomplain of back pain (37%82%) or radicular pain (41%) [42,45,46]. A

smaller percentage has subjective weakness (30%) or gross weakness with

inability to walk (16%67%) [4246]. Sensory loss and bowel and/or blad-

der dysfunction occur variably; in one series they were present in up to 90%

and 70% of cases, respectively [45]. Often these symptoms, once present, are

irreversible, so early suspicion in patients complaining of pain alone is war-

ranted. On physical examination, increased deep tendon reflexes (20%), ab-

normal plantar reflexes (20%), decreased rectal sphincter tone or distended

bladder (9%), spinal tenderness (35%), and objective weakness (41%) maybe noted [46]. As stated, none of these signs or symptoms is sufficiently sen-

sitive to rule out SCC.

Risk assessment for patients who have known cancers has been proposed

for selecting patients for diagnostic imaging. In women, breast cancer is the

most common cause of metastatic epidural SCC , and a study in this pop-

ulation identified four independent predictors of cord compression: bone

metastases for 2 or more years, metastatic disease at presentation with can-

cer, objective weakness on physical examination, and vertebral compression

fracture on spine radiograph. Unfortunately, although the presence of mul-tiple risk factors increases the risk of SCC, with 85% of those with SCC hav-

ing three or four risk factors, 12% of patients who had SCC had none of

these risk factors [46]. Moreover, approximately 2% of patients presenting

with SCC have an undiagnosed malignancy [45].

Diagnostic imaging for spinal cord compression caused by spinal

epidural metastases

Plain films of the spine are insensitive and nonspecific for the diagnosis of

SCC. The reported sensitivity is as low as 30% to 76% [46,47], and this sen-sitivity includes nonspecific findings such as spinal compression fractures.

Nuclear medicine imaging modalities also may yield false-negative results

in as much as 6% of cases [46,48]. By comparison, MRI with gadolinium

intravenous contrast is extremely sensitive for the diagnosis, nearing

100% [47,49]. As a result, emergent MRI should be obtained for any patient

when cord compression or spinal metastatic disease is suspected. For pa-

tients who cannot undergo MRI, CT myelography can be used [50].

Treatment of spinal cord compression caused by spinalepidural metastases

Urgent administration of steroids is recommended for suspected meta-

static SCC. Randomized trials have shown improvement in patients receiv-

ing adjuvant steroid therapy with dexamethasone in addition to radiation

therapy. The doses used are large (dexamethasone 96 mg intravenous bolus

followed by 96 mg orally for 3 days and then tapered) [51]. In some patients



10/19

who do not have motor deficits and in whom steroids are relatively contra-

indicated for reasons such as poorly controlled diabetes, radiation without

steroid therapy may be possible, although larger trials are needed [52].Single doses of steroids are unlikely to have deleterious effects, so immediate

administration of dexamethasone before imaging confirmation is appropri-

ate if SCC is suspected [53].

Radiation therapy with laminectomy is associated with better functional

outcomes than radiation alone. Recent randomized, controlled trials con-

firm that combination therapy results in better outcomes [5456]. Early con-

sultation with a radiation oncologist and neurosurgeon should be obtained.

Spinal cord compression caused by spinal infections: spinal epiduralabscess and vertebral osteomyelitis

Although uncommon, spinal infections remain a serious cause of morbid-

ity and mortality in patients presenting with back pain. SEA account for 0.2

to 2 cases per 10,000 hospital admissions and can affect patients of any age

[57,58]. A meta-analysis of 915 cases of epidural abscess from 1954 to 1997

demonstrated a mortality rate of approximately 15% [58,59]. The majority

of SEAs are caused by bacteria, with Staphylococcus aureus being the most

common organism. Infections caused by fungal, parasitic, and mycobacte-rial infections occur less commonly. In a significant number of cases, no or-

ganism is isolated. As in previously described back pain emergencies, initial

symptoms and signs are nonspecific and insensitive [59].


Back pain is the presenting symptom in 71% of patients who have SEA.

Fever is present in only two thirds of patients who have SEA [59]. Neuro-

logic deficits are relatively rare initial presenting symptoms. Twenty-five per-

cent of patients report muscle weakness, 25% report some degree ofincontinence, and 13% have sensory deficits [59]. Localized spinal tender-

ness is also unreliable, present initially in only 17% of patients [59].

Risk factors for SEA include immunocompromised states, trauma, sur-

gery, and infection. Immunocompromised states that increase the possibility

of SEA include malignancy, HIV infection, cirrhosis, steroid use, and diabe-

tes. Of these, diabetes is reported as an important risk factor for SEA, occur-

ring in 15% of cases in one series [59]. A history of intravenous drug abuse is

also a concerning risk factor, found in approximately 9% of cases [59]. Dis-

tant or contiguous infections constitute perhaps the largest risk factor, foundin more than 40% of cases [59]. A history of trauma is present in 10% of cases

[59]. Degenerative vertebral disease is reported as a risk factor in 6% of cases

[59]. Alcohol abuse has been reported in up to 5% of cases [59]. The precise

role and prevalence of these risk factors is unknown, because many of

the published reports on spinal infections come from inner-city populations

in which diabetes and injection drug use are particularly common [58].



11/19

Diagnostic evaluation for spinal epidural abscess

Laboratory findings are insensitive and unreliable in screening for SEA.

Leukocytosis is variable. Leukocyte counts in patients who have SEA rangefrom 1500 to 42,000 cells/mL, and normal white blood cell counts are found

in one fourth to one third of patients [59]. Never exclude the possibility of

SEA based upon a normal white blood cell count. The erythrocyte sedimen-

tation rate (ESR) is reportedly more sensitive for detecting SEA, with more

than 90% of patients having an ESR greater than 20 mm [59]. Subtle or

moderate elevations may occur, however, with approximately one third of

patients having an ESR below 60 mm [58].

Although plain-film radiographs may reveal destruction of vertebrae,

they are not helpful in the diagnosis of SEA (Fig. 5A) [60]. In contrast,MRI with gadolinium has a reported sensitivity of nearly 100% for epidural

abscess [61]. It is the imaging modality of choice when evaluating patients

for SEA (Fig. 5B). Single-photon emission CT and nuclear medicine bone

scanning with gadolinium-67 are also very accurate means of detecting ver-

tebral infection [6163].

Treatment of spinal epidural abscess

Antibiotic therapy should be started with a bactericidal agent effective

against Staphylococcus aureus, Streptococci, and gram-negative organisms.Antibiotics should be broad spectrum, able to penetrate bone, and have rel-

atively low toxicity because the duration of treatment will be 4 to 6 weeks.

Fig. 5. (A) Abnormal plain-film radiograph in a patient who has an epidural abscess and ver-

tebral osteomyelitis. The patient has undergone resection of a damaged vertebral body, a risk

factor for infection. (B) Spinal epidural abscess. MRI shows bony destruction adjacent to an

area of epidural abscess. The epidural abscess (arrowheads, dark gray material) surrounds

and compresses the spinal cord (lighter gray material).



12/19

Blood cultures should be obtained to guide antibiotic treatment [5759]. In

addition to antibiotic therapy, laminectomy is performed traditionally, al-

though CT-guided percutaneous drainage may be effective in selected cases[64]. A retrospective review of patients undergoing antibiotic therapy and

percutaneous drainage found outcomes similar to those of patients undergo-

ing surgical decompression, although prospective, randomized trials are

needed to determine whether these therapies are truly equally effective [65].

Vertebral osteomyelitis

Vertebral osteomyelitis in the elderly is another rare but potentially dan-

gerous disease process. The risk factors, presentation, evaluation, and treat-ment are similar to those of epidural abscess. Compared with younger hosts,

elderly patients are more likely to be infected with gram-negative organisms,

particularly urinary tract organisms, and to have had recent surgery [66].

Staphylococcal species are the major infectious organism, although myco-

bacteria are also common organisms in some populations. Vertebral osteo-

myelitis is more common in older men [67].

Elevation of ESR and C-reactive protein is common, occurring in ap-

proximately 80% of cases [68]. Radiographic changes may occur in only

50% to 60% of cases (see Fig. 5A) [68]. MRI and CT are more helpful,showing abnormalities in 70% to 99% of cases [68]. Patients typically pres-

ent with back pain that has developed over weeks to months. The prognosis

is poor in patients who have neurologic dysfunction at diagnosis, chronic

debilitating diseases, and diagnosis delayed more than 8 weeks from the

start of symptoms [69]. Delay in diagnosis is common, exceeding 1 month

from symptom onset in one third of patients [68,69].

Once the diagnosis of osteomyelitis is made, a spine surgeon should be

consulted, and treatment with broad-spectrum antibiotics should be initi-

ated. Antibiotics should be given for 6 to 12 weeks and can be tailoredwith culture results. A CT-guided tissue biopsy should be performed, pref-

erably before antibiotic administration. Nonoperative management with an-

tibiotics and analgesia may be appropriate in patients who have a stable

spine and minor or no neurologic deficit; this strategy is effective in 60%

to 95% of such patients [70,71]. Surgical treatment with de bridement and

possible spinal reconstruction is indicated in patients with failure of medical

treatment, cord compression, and presence of a fluid collection [71].

Cauda equina syndrome

Cauda equina syndrome classically presents with perineal numbness and

urinary and fecal incontinence or retention. Sciatica may accompany these

neurologic deficits. Bilateral foot weakness and occasional weakness of

the quadriceps may occur also. Symptoms may progress rapidly over hours

in 85% of patients. Lumbar disc herniation is a common cause, although



13/19

infection and metastatic disease also may result in the syndrome. Delays in

diagnosis are common, occurring in roughly half of cases and are caused by

delayed patient presentation in 17% of cases and by physician-related delaysin the remaining 83% [72]. Delay in surgery of more than 48 hours has been

associated with poor clinical outcome, although no difference in outcome

has been shown in patients undergoing surgery within 5 hours compared

with those undergoing surgery within 24 hours of diagnosis [72,73]. Diag-

nostic evaluation with gadolinium-contrast MRI is recommended [74].

Spinal compression fractures

Spinal compression fractures are a common problem in the elderly andmay occur without preceding trauma. Although less time-sensitive than

the conditions previously described, these fractures have significant sequelae

including inability to perform activities of daily living, and need for analge-

sics, with a litany of medication side effects (eg, sedation and constipation

from opioids, gastrointestinal bleeding and renal insufficiency from nonste-

roidal anti-inflammatory agents). Proving the presence of a compression

fracture does not rule out the presence of other more ominous disease, be-

cause metastatic disease can result in compression fractures [75].

Diagnostic imaging for spinal compression fractures

Although plain-film radiographs may demonstrate the presence of com-

pression fractures, more advanced imaging modalities may provide useful

prognostic and therapeutic information. Patients who have risk factors for

malignancy-related fractures, such as past or current cancer, require MRI,

because plain films may not delineate fully the degree of pathology [75].

In fact, multiple myeloma has been diagnosed in patients being treated

for presumed osteoporotic compression fractures [76]. High-resolution CThas been shown in small studies to distinguish benign from malignant com-

pression fractures, based on a number of criteria including destruction of

bony elements and adjacent soft tissue or epidural masses [77].

When a compression fracture is found and is considered to be the sole

cause of the patients symptoms, treatment options exist, including vertebro-

plasty. Thus evaluating a patient for compression fracture serves multiple

purposes, including ruling out emergent pathology and establishing treat-

ment goals. Vertebroplasty has been shown to be safe and effective, with

demonstrated improvements in pain and quality of life [7881]. Unfortu-nately, up to a quarter of patients undergoing vertebroplasty experience

a second compression fracture within the first year after treatment, with

half of these fractures being symptomatic [82]. An association has been ob-

served between vertebroplasty and rapid subsequent fracture of adjacent

vertebral bodies, although studies are retrospective and do not prove

a causal relationship. Pain from spinal fractures may be significantly



14/19


15/19

dangerous causes of back pain. Physicians caring for elderly patients must

be vigilant in considering serious causes, including vascular disasters, com-

pressive spinal lesions, and serious infections. Awaiting overt signs andsymptoms may guarantee a poor outcome for many of these disease pro-

cesses. Advanced imaging may be necessary to avoid misdiagnosis and avert

patient morbidity and mortality (Box 3).

References

[1] National Center for Health Statistics. Health, United States, 2005 with chartbook on trends

in the health of Americans. Hyattsville (MD): 2005.

[2] Hing E, Cherry DK, Woodwell DA. National Ambulatory Medical Care Survey: 2004 sum-

mary. Advance data from vital and health statistics; no 374. Hyattsville (MD): National Cen-

ter for Health Statistics; 2006.

[3] Turner JA, LeResche L, Von Korff M, et al. Back pain in primary care. Patient characteris-

tics, content of initial visit, and short-term outcomes. Spine 1998;23(4):4639.

[4] Minin o AM, Heron MP, Smith BL. Deaths: preliminary data for 2004. National Vital Sta-

tistics Reports, vol. 53, no. 21. Available at: www.cdc.gov/nchs. Accessed June 28, 2005.

[5] Hoyert DL, Heron MP, Murphy SL, et al. Deaths: final data for 2003. National Vital Sta-

tistics Reports 2006;54(13):1120.

[6] Gillum RF. Epidemiology of aortic aneurysm in the United States. J Clin Epidemiol 1995;

48(11):128998.

[7] Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 practice guidelines for the man-agement of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and

abdominal aortic): a collaborative report from the American Association for Vascular Sur-

gery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interven-

tions, Society for Vascular Medicine and Biology, Society of Interventional Radiology,

and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop

Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed

by the American Association of Cardiovascular and Pulmonary Rehabilitation; National

Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society

Consensus; and Vascular Disease Foundation. Circulation 2006;113(11):e463654.

[8] Lederle FA, Johnson GR, Wilson SE, et al. The Aneurysm Detection and Management

Study screening program: validation cohort and final results. Aneurysm Detection and Man-agement Veterans Affairs Cooperative Study Investigators. Arch Intern Med 2000;160(10):

142530.

[9] Forbes TL, Lawlor DK, Derose G, et al. Gender differences in relative dilatation of abdom-

inal aortic aneurysms. Ann Vasc Surg 2006;20(5):5648.

[10] Wainess RM, Dimick JB, Cowan JA Jr, et al. Epidemiology of surgically treated abdominal

aortic aneurysms in the United States, 1988 to 2000. Vascular 2004;12(4):21824.

[11] Fleming C, Whitlock EP, Beil TL, et al. Screening for abdominal aortic aneurysm: a best-ev-

idence systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2005;

142:198202.

[12] Verma A, Lindsay TF. Regression of aortic aneurysms through pharmacologic therapy?

N Engl J Med 2006;354(19):20678.[13] Cambria RA, Gloviczki P, Stanson AW, et al. Symptomatic, nonruptured abdominal aortic

aneurysms: are emergent operations necessary? Ann Vasc Surg 1994;8(2):1216.

[14] Lloyd GM, Bown MJ, Norwood MG, et al. Feasibility of preoperative computer tomogra-

phy in patients with ruptured abdominal aortic aneurysm: a time-to-death study in patients

without operation. J Vasc Surg 2004;39(4):78891.

[15] Marston WA, Ahlquist R, Johnson G Jr, et al. Misdiagnosis of ruptured abdominal aortic

aneurysms. J Vasc Surg 1992;16(1):1722.

http://www.cdc.gov/nchshttp://www.cdc.gov/nchs


16/19

[16] Akkersdijk GJ, van Bockel JH. Ruptured abdominal aortic aneurysm: initial misdiagnosis

and the effect on treatment. Eur J Surg 1998;164(1):2934.

[17] Pomper SR, Fiorillo MA, Anderson CW, et al. Hematuria associated with ruptured abdom-

inal aortic aneurysms. Int Surg 1995;80(3):2613.

[18] Lederle FA, Simel DL. The rational clinical examination. Does this patient have abdominal

aortic aneurysm? JAMA 1999;281(1):7782.

[19] Fink HA, Lederle FA, Roth CS, et al. The accuracy of physical examination to detect

abdominal aortic aneurysm. Arch Intern Med 2000;160(6):8336.

[20] Venkatasubramaniam AK, Mehta T, Chetter IC, et al. The value of abdominal examina-

tion in the diagnosis of abdominal aortic aneurysm. Eur J Vasc Endovasc Surg 2004;27(1):

5660.

[21] Shuman WP, Hastrup W Jr, Kohler TR, et al. Suspected leaking abdominal aortic aneurysm:

use of sonography in the emergency room. Radiology 1988;168(1):1179.

[22] Hayter RG, Rhea JT, Small A, et al. Suspected aortic dissection and other aortic disorders:

multi-detector row CT in 373 cases in the emergency setting. Radiology 2006;238(3):84152

[Epub 2006 Feb 1].

[23] Sharma U, Ghai S, Paul SB, et al. Helical CT evaluation of aortic aneurysms and dissection:

a pictorial essay. Clin Imaging 2003;27(4):27380.

[24] Sprouse LR 2nd, Meier GH 3rd, Parent FN, et al. Is three-dimensional computed tomogra-

phy reconstruction justified before endovascular aortic aneurysm repair? J Vasc Surg 2004;

40(3):4437.

[25] Novelline RA, Rhea JT, Rao PM, et al. Helical CT in emergency radiology. Radiology 1999;

213(2):32139.

[26] Vosshenrich R, Fischer U. Contrast-enhanced MR angiography of abdominal vessels: is

there still a role for angiography? Eur Radiol 2002;12(1):21830 [Epub 2001 Aug 9].[27] Clouse WD, Hallett JW Jr, Schaff HV, et al. Acute aortic dissection: population-based inci-

dence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc 2004;79(2):

17680.

[28] Mehta RH, OGara PT, Bossone E, et al, International Registry of Acute Aortic Dissec-

tion (IRAD) Investigators. Acute type A aortic dissection in the elderly: clinical charac-

teristics, management, and outcomes in the current era. J Am Coll Cardiol 2002;40(4):

68592.

[29] Suzuki T, Mehta RH, Ince H, et al. International Registry of Aortic Dissection. Clinical

profiles and outcomes of acute type B aortic dissection in the current era: lessons from

the International Registry of Aortic Dissection (IRAD). Circulation 2003;108(Suppl 1):

II3127.[30] Singer AJ, Hollander JE. Blood pressure. Assessment of interarm differences. Arch Intern

Med 1996;156(17):20058.

[31] Pesola GR, Pesola HR, Lin M, et al. The normal difference in bilateral indirect blood pres-

sure recordings in hypertensive individuals. Acad Emerg Med 2002;9(4):3425.

[32] Teece S, Hogg K. Best evidence topic report. Peripheral pulses to exclude thoracic aortic dis-

section. Emerg Med J 2004;21(5):589.

[33] Bossone E, Rampoldi V, Nienaber CA, et al, International Registry of Acute Aortic Dissec-

tion (IRAD) Investigators. Usefulness of pulse deficit to predict in-hospital complications

and mortality in patients with acute type A aortic dissection. Am J Cardiol 2002;89(7):

8515.

[34] Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA 2002;287(17):226272.

[35] Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute

Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283(7):

897903.

[36] Moore AG, Eagle KA, Bruckman D, et al. Choice of computed tomography, transesopha-

geal echocardiography, magnetic resonance imaging, and aortography in acute aortic



17/19

dissection: International Registry of Acute Aortic Dissection (IRAD). Am J Cardiol 2002;

89(10):12358.

[37] Sommer T, Fehske W, Holzknecht N, et al. Aortic dissection: a comparative study of diag-

nosis with spiral CT, multiplanar transesophageal echocardiography, and MR imaging.

Radiology 1996;199(2):34752.

[38] Hentschel SJ, Woolfenden AR, Fairholm DJ. Resolution of spontaneous spinal epidural

hematoma without surgery: report of two cases. Spine 2001;26(22):E5257.

[39] Joseph AP, Vinen JD. Acute spinal epidural hematoma. J Emerg Med 1993;11(4):43741.

[40] Parman SC. Spontaneous spinal epidural hematoma. Ann Emerg Med 1980;9(7):36870.

[41] Seet RC, Lim EC, Wilder-Smith EP, et al. Spontaneous epidural haematoma presenting

as cord compression in a patient receiving clopidogrel. Eur J Neurol 2005;12(10):

8112.

[42] Pedersen AG, Bach F, Melgaard B. Frequency, diagnosis, and prognosis of spinal cord com-

pression in small cell bronchogenic carcinoma. A review of 817 consecutive patients. Cancer

1985;55(8):181822.

[43] Levack P, Graham J, Collie D, et al. Scottish Cord Compression Study Group. Dont wait

for a sensory levellisten to the symptoms: a prospective audit of the delays in diagnosis of

malignant cord compression. Clin Oncol (R Coll Radiol) 2002;14(6):47280.

[44] Bach F, Larsen BH, Rohde K, et al. Metastatic spinal cord compression. Occurrence, symp-

toms, clinical presentations and prognosis in 398 patients with spinal cord compression. Acta

Neurochir (Wien) 1990;107(12):3743.

[45] Bach F, Agerlin N, Sorensen JB, et al. Metastatic spinal cord compression secondary to lung

cancer. J Clin Oncol 1992;10(11):17817.

[46] Lu C, Stomper PC, Drislane FW, et al. Suspected spinal cord compression in breast cancer

patients: a multidisciplinary risk assessment. Breast Cancer Res Treat 1998;51(2):12131.[47] Husband DJ, Grant KA, Romaniuk CS. MRI in the diagnosis and treatment of suspected

malignant spinal cord compression. Br J Radiol 2001;74(877):1523.

[48] Portenoy RK, Galer BS, Salamon O, et al. Identification of epidural neoplasm. Radiography

and bone scintigraphy in the symptomatic and asymptomatic spine. Cancer 1989;64(11):

220713.

[49] Li KC, Poon PY. Sensitivity and specificity of MRI in detecting malignant spinal cord com-

pression and in distinguishing malignant from benign compression fractures of vertebrae.

Magn Reson Imaging 1988;6(5):54756.

[50] Carmody RF, Yang PJ, Seeley GW, et al. Spinal cord compression due to metastatic disease:

diagnosis with MR imaging versus myelography. Radiology 1989;173(1):2259.

[51] Sorensen S, Helweg-Larsen S, Mouridsen H, et al. Effect of high-dose dexamethasone in car-cinomatous metastatic spinal cord compression treated with radiotherapy: a randomised

trial. Eur J Cancer 1994;30A(1):227.

[52] Maranzano E, Latini P, Beneventi S, et al. Radiotherapy without steroids in selected

metastatic spinal cord compression patients. A phase II trial. Am J Clin Oncol 1996;

19(2):17983.

[53] Wessling H, de las Heras P. Cervicothoracolumbar spinal epidural abscess with tetraparesis.

Good recovery after non-surgical treatment with antibiotics and dexamethasone. Case

report and review of the literature. Neurocirugia (Astur) 2003;14(6):52933.

[54] Sorensen S, Borgesen SE, Rohde K, et al. Metastatic epidural spinal cord compression.

Results of treatment and survival. Cancer 1990;65(7):15028.

[55] Lewis S. Direct decompressive surgery and radiation therapy improved walking ability inmetastatic epidural spinal cord compression. J Bone Joint Surg Am 2006;88(5):1169.

[56] Patchell RA, Tibbs PA, Regine WF, et al. Direct decompressive surgical resection in

the treatment of spinal cord compression caused by metastatic cancer: a randomised trial.

Lancet 2005;366(9486):6438.

[57] Hlavin ML, Kaminski HJ, Ross JS, et al. Spinal epidural abscess: a ten-year perspective.

Neurosurgery 1990;27(2):17784.



18/19

[58] Grewal S, Hocking G, Wildsmith JA. Epidural abscesses. Br J Anaesth 2006;96(3):292302

[Epub 2006 Jan 23].

[59] Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: a meta-analysis of 915 patients.

Neurosurg Rev 2000;23(4):175204 [discussion: 205].

[60] An HS, Seldomridge JA. Spinal infections: diagnostic tests and imaging studies. Clin Orthop

Relat Res 2006;444:2733.

[61] Ledermann HP, Schweitzer ME, Morrison WB, et al. MR imaging findings in spinal infec-

tions: rules or myths? Radiology 2003;228(2):50614 [Epub 2003 Jun 11].

[62] Love C, Patel M, Lonner BS, et al. Diagnosing spinal osteomyelitis: a comparison of bone

and Ga-67 scintigraphy and magnetic resonance imaging. Clin Nucl Med 2000;25(12):

96377.

[63] Concia E, Prandini N, Massari L, et al. Osteomyelitis: clinical update for practical guidelines.

Nucl Med Commun 2006;27(8):64560.

[64] Lyu RK, Chen CJ, Tang LM, et al. Spinal epidural abscess successfully treated with

percutaneous, computed tomography-guided, needle aspiration and parenteral antibiotic

therapy: case report and review of the literature. Neurosurgery 2002;51(2):50912 [dis-

cussion: 512].

[65] Siddiq F, Chowfin A, Tight R, et al. Medical vs surgical management of spinal epidural ab-

scess. Arch Intern Med 2004;164(22):240912.

[66] Belzunegui J, Intxausti JJ, De Dios JR, et al. Haematogenous vertebral osteomyelitis in the

elderly. Clin Rheumatol 2000;19(5):3447.

[67] Nather A, David V, Hee HT, et al. Pyogenic vertebral osteomyelitis: a review of 14 cases.

J Orthop Surg 2005;13(3):2404.

[68] Beronius M, Bergman B, Andersson R. Vertebral osteomyelitis in Goteborg, Sweden:

a retrospective study of patients during 199095. Scand J Infect Dis 2001;33(7):52732.

[69] Solis Garcia Del Pozo J, Soto MV, Solera J. Vertebral osteomyelitis: long-term disability as-

sessment and prognostic factors. J Infect 2007;54(2):12934.

[70] Carragee EJ. Pyogenic vertebral osteomyelitis. J Bone Joint Surg Am 1997;79(6):87480.

[71] Nakase H, Matsuda R, Tamaki R, et al. Two-stage management for vertebral osteomyelitis

and epidural abscess: technical note. Neurosurgery 2006;58(6):E1219.

[72] Shapiro S. Medical realities of cauda equina syndrome secondary to lumbar disc herniation.

Spine 2000;25(3):34851 [discussion: 352].

[73] Hussain SA, Gullan RW, Chitnavis BP. Cauda equina syndrome: outcome and implications

for management. Br J Neurosurg 2003;17(2):1647.

[74] Coscia M, Leipzig T, Cooper D. Acute cauda equina syndrome. Diagnostic advantage ofMRI. Spine 1994;19(4):4758.

[75] Ho CS, Choi WM, Chen CY, et al. Metastasis in vertebra mimicking acute compression frac-

tures in a patient with osteoporosis: MRI findings. Clin Imaging 2005;29(1):647.

[76] Togawa D, Lieberman IH, Bauer TW, et al. Histological evaluation of biopsies obtained

from vertebral compression fractures: unsuspected myeloma and osteomalacia. Spine 2005;

30(7):7816.

[77] Kubota T, Yamada K, Ito H, et al. High-resolution imaging of the spine using multidetector-

row computed tomography: differentiation between benign and malignant vertebral com-

pression fractures. J Comput Assist Tomogr 2005;29(5):7129.

[78] Kumar K, Verma AK, Wilson J, et al. Vertebroplasty in osteoporotic spine fractures: a qual-

ity of life assessment. Can J Neurol Sci 2005;32(4):48795.[79] Cheung G, Chow E, Holden L, et al. Percutaneous vertebroplasty in patients with intractable

pain from osteoporotic or metastatic fractures: a prospective study using quality-of-life as-

sessment. Can Assoc Radiol J 2006;57(1):1321.

[80] Do HM, Kim BS, Marcellus ML, et al. Prospective analysis of clinical outcomes after per-

cutaneous vertebroplasty for painful osteoporotic vertebral body fractures. AJNR Am J

Neuroradiol 2005;26(7):16238.



19/19

[81] Liliang PC, Su TM, Liang CL, et al. Percutaneous vertebroplasty improves pain and physical

functioning in elderly osteoporotic vertebral compression fracture patients. Gerontology

2005;51(1):349.

[82] Voormolen MH, Lohle PN, Juttmann JR, et al. The risk of new osteoporotic vertebral com-

pression fractures in the year after percutaneous vertebroplasty. J Vasc Interv Radiol 2006;

17(1):716.

[83] Lyritis GP, Ioannidis GV, Karachalios T, et al. Analgesic effect of salmon calcitonin sup-

positories in patients with acute pain due to recent osteoporotic vertebral crush fractures:

a prospective double-blind, randomized, placebo-controlled clinical study. Clin J Pain

1999;15(4):2849.


Documents

Dolor de Espalda en Ancianos