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Low back pain is a common condition routinely managed by physical therapists and accounts for up to 53% of all client visits.1 It is also the fifth most common reason for all physician visits in the United States,19 with direct health care costs related

to the management of low back pain in the United States estimated

to be more than $85 billion annually.30 Unfortunately, despite increasing medi-cal expenditures, the prevalence of chron-ic, disabling low back pain continues to increase.30

Low back pain is most commonly caused by mechanical dysfunction, which

can be defined as symptoms that are re-lated to the musculoskeletal system and vary with movement.40 However, serious nonmechanical spinal disorders (eg, neo-plasm, infection, inflammatory arthritis, fracture) or visceral disease (eg, gastroin-testinal, genitourinary, vascular) may be

the cause of low back pain in a small per-centage of patients.22 Though mechanical dysfunction accounts for approximately 97% of low back pain cases, nonmechani-cal spinal disorders and visceral disease account for approximately 1% and 2% of low back pain cases, respectively.22

One type of visceral disease that may cause low back pain is an abdominal aor-tic aneurysm (AAA), which is an abnor-mal dilation in a weakened or diseased arterial wall.15 By convention, an infra-renal aorta that is 3 cm in diameter or larger is considered aneurysmal.12,26 The diameter of the infrarenal aorta is the strongest known predictor of risk for rup-ture,2 with the risk substantially increas-ing with infrarenal aorta diameters of 5.0 cm or greater.14,18

The etiology of an AAA is not com-pletely understood, but atherosclerosis, degeneration, and chronic inflammation have been identified as contributing to its development.39 Major risk factors for an AAA include hypertension, an age of greater than 60 years, male sex, past his-tory of smoking, atherosclerosis, coronary artery disease, family history of AAA, and use of statins (TABLE 1).2,7,12,13,26 Factors that are negatively associated with AAA include female sex, black race, and diabetes.2,7,13,24,25

The purpose of this resident’s case problem was (1) to describe the clini-cal reasoning and decision making in a patient referred with a diagnosis of me-chanical low back pain who had an AAA

TT STUDY DESIGN: Resident’s case problem.

TT BACKGROUND: The purpose of this report was to describe (1) the clinical reasoning that led a clinician to identify an abdominal aortic aneurysm (AAA) in a patient with low back pain requiring immediate medical referral, and (2) an evidence-based approach to clinical evaluation of patients with suspected AAA.

TT DIAGNOSIS: The patient was unable to identify a specific mechanism of injury for his low back pain, lacked aggravating/easing factors for his symptoms, and complained of night pain and an inability to ease his symptoms with position changes. While the patient’s symptoms remained unchanged during physical examination of the lum-bar spine and hip, abdominal palpation revealed a strong, nontender pulsation over the midline of the upper and lower abdominal quadrants. Due to concern for an AAA, the patient was immediately referred to his physician. Subsequent computed tomography imaging revealed a prominent AAA, which measured up to 5.5 cm in greatest dimen-

sion and extended from below the renal arteries to the bifurcation of the iliac arteries. The patient ini-tially deferred surgical intervention but eventually consented 6 months later, after repeat computed tomography imaging revealed that the AAA had progressed to 6.7 cm in greatest dimension.

TT DISCUSSION: It is essential for physical therapists to be familiar with a diagnostic pathway to help identify AAA in patients presenting with apparent musculoskeletal complaints. Knowledge of the risk factors for AAA, understanding how to screen for nonmusculoskeletal symptoms, and a basic competence in abdominal palpation and how to interpret findings will help with the clinician’s clinical decision making.

TT LEVEL OF EVIDENCE: Differential diagnosis, level 4. J Orthop Sports Phys Ther 2014;44(7):500-507. Epub 25 April 2014. doi:10.2519/jospt.2014.4935

TT KEY WORDS: abdomen, aorta, clinical reasoning, palpation

1Department of Physical Therapy, Charleston Air Force Base, Charleston, SC. 2Physical Therapy Department, Daemen College, Amherst, NY. 3Department of Physical Therapy, Fort McNair, Washington, DC. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the US Air Force or the Department of Defense. The authors certify that they have no affiliations with or financial involvement in any organization or entity with a direct financial interest in the subject matter or materials discussed in the article. Address correspondence to Dr Joshua J. Van Wyngaarden, 1311 Hitchcock Avenue, Charleston AFB, SC 29404. E-mail: josh.vanwyngaarden@gmail.com T Copyright ©2014 Journal of Orthopaedic & Sports Physical Therapy®

JOSHUA J. VAN WYNGAARDEN, PT, DPT1 • MICHAEL D. ROSS, PT, DHSc2 • BENJAMIN R. HANDO, PT, DSc3

Abdominal Aortic Aneurysm in a Patient With Low Back Pain

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requiring immediate medical referral, and (2) to describe an evidence-based ap-proach to clinical evaluation of patients with suspected AAA.

DIAGNOSIS

Chief Complaint

The patient was a 58-year-old Caucasian man referred to a physi-cal therapist with a primary com-

plaint of low back pain and a secondary complaint of abdominal pain. The pa-

tient was employed as a government contractor, and his job consisted primar-ily of desk work. The patient performed 30 minutes of cardiovascular exercise (elliptical machine) 7 days per week and weight training 6 days per week. He had continued this exercise schedule despite his low back and abdominal pain.

Symptom Location, Description, and BehaviorThe patient’s low back pain was located centrally at the L3 through L5 spinal

levels. He characterized the pain as a constant, deep, dull ache that varied in intensity, with intermittent throbbing sensations (FIGURE 1). During the physical therapist’s initial encounter, the patient rated his current resting pain as 3 on a verbal numeric pain rating scale ranging from 0 to 10, with 0 as no pain and 10 as the worst pain imaginable. Using the same pain rating scale, the patient rated his pain since the pain first presented as 3 at its lowest level and 7 at its typical maximum level.

The patient also reported abdominal pain that was centrally located, start-ing in the epigastric region and extend-ing inferiorly to the superior margin of the hypogastric region. He described his abdominal pain as a bloated feeling that progressed to a sharp, intense stabbing pain when aggravated. He currently rated his abdominal pain as 1; he also stated that 1 was the minimum pain he could feel, and the typical maximum pain was 4. The patient expressed that the low back pain and abdominal pain seemed to be related and increased proportionally; that is, when the low back pain increased, the abdominal pain increased as well.

Symptom BehaviorThe patient was unable to describe any specific aggravating factors for his low back or abdominal pain. More specifical-ly, he denied any difficulty or increase in symptoms with aerobic exercise, climb-ing stairs, lumbar flexion/extension ac-tivities, or resistance training. He also denied an increase in symptoms with coughing, sneezing, and taking a deep breath. Taking naproxen was the only easing factor the patient identified, and it would reportedly lessen both his low back and abdominal pain temporarily.

He had difficulty falling asleep at night, because the pain in his lower back would increase and be followed by an increase in abdominal pain. Once he fell asleep, he would typically wake at least once each night because of pain in his low back and abdomen. Position changes did not increase or decrease his symptoms.

TABLE 1Risk Factors Associated

With Abdominal Aortic Aneurysm and Their Corresponding Odds Ratios7,13

Risk Factor Odds Ratio*

Age 1.71 (1.61, 1.82) increase for every 7-y increase

Male sex† 2.66 (1.69, 4.20)

Hypertension† 1.44 (1.27, 1.63)

Smoking history

Past history† 1.5-2.4 (0.54, 6.75)

Current smoker 6.19-13.72 (2.86, 30.78)

Atherosclerosis† Not reported in literature

Family history 1.94 (1.63, 2.32)

Coronary artery disease 1.52 (1.37, 1.68)

Use of statins 3.77 (1.45, 9.81)

*Values in parentheses are 95% confidence interval.†Indicates the risk factors present in this patient.

FIGURE 1. Location and description of patient’s symptoms at the time of the initial physical therapy visit. Checkmarks denote symptom-free areas.

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To resume sleeping, he would typically have to lie in bed and wait 45 minutes to 1 hour until he fell asleep, or take one 500-mg naproxen.

History of Current ConditionThe patient reported that his pain began 8 days prior to his initial evaluation by the physical therapist. He denied a spe-cific mechanism of injury or trauma that preceded his symptoms. His symptoms came on suddenly while sitting in his ho-tel room when he was away on a business trip. He described his initial symptoms as a “sudden, severe pain” in his lower back and abdomen that forced him to lie su-pine for 30 minutes. Over the course of the next 8 days, the pain in his low back and abdomen slowly improved. The pa-tient denied a personal past history of low back or abdominal pain prior to this incident.

One day prior to being seen by the physical therapist, the patient was evalu-ated by his primary care physician and diagnosed with mechanical low back pain and abdominal pain that was related to the low back pain, both of which were deemed musculoskeletal in nature. Prior to referral to the physical therapist, plain-film radiographs were completed, which revealed mild degenerative changes of the L3 through S1 spinal levels. The phy-sician subsequently prescribed naproxen

(500 mg), to be taken twice daily for the next 10 to 14 days, and a physical therapy referral.

Past Medical HistoryThe patient had a history of hyperten-sion and atherosclerosis, for which he was currently taking amlodipine (5 mg), vytorin (10 mg), hyzaar (12.5 mg), and aspirin (81 mg) once daily. He indicated that he had smoked for 2 years in the early 1970s, amounting to 1 pack-year total, but has not used tobacco products since. He denied numbness and tingling in his upper and lower extremities, recent infection, fatigue, weight changes, fever, malaise, saddle anesthesia, pulsation in his abdomen, and pain with the Valsalva maneuver or coughing. Heartburn, in-digestion, changes in appetite, difficulty swallowing, and changes in bowel and bladder habit were also all denied. He denied a family history of hypertension, diabetes mellitus, cancer, coronary artery disease, and AAA.

Clinical Impression Post–History IntakeThe patient had a primary complaint of low back pain and a secondary complaint of abdominal pain that appeared to be re-lated. When considering the differential diagnosis, initial hypotheses were con-sidered in 3 categories: mechanical (eg, musculoskeletal condition), nonmechan-

ical (eg, neoplasm, infection, inflamma-tory arthritis, fracture), and visceral (eg, gastrointestinal, genitourinary, or vascu-lar). This approach to differential diag-nosis allowed the clinician to determine whether the patient’s condition was ap-propriate for physical therapist manage-ment or an additional physician consult was required.3

Mechanical dysfunction accounts for approximately 97% of low back pain cas-es, suggesting a high probability that the vast majority of patients with low back pain will have pain that is mechanical in nature. Lumbar dysfunction may also cause abdominal pain.10,23 From the pa-tient history, however, the physical ther-apist identified components suggesting that the patient’s symptoms might not be mechanical in origin, such as the patient’s inability to identify a specific mechanism of injury to the sudden onset of symp-toms, the inability to identify any aggra-vating or easing factors for his symptoms, and night pain with an inability to ease his symptoms with changes in position. Additionally, Sparkes et al37 developed 2 specific clusters of questions to be used in identifying patients with abdominal pain that is musculoskeletal in origin (TABLE

2). These question clusters have high specificity (96%), suggesting that this tool is most useful for ruling in a muscu-loskeletal cause of abdominal pain. The patient described in this report could not answer “yes” to either of the first 2 ques-tions of cluster 1, suggesting that he was negative for this question cluster, which decreased the likelihood for a musculo-skeletal origin of the patient’s abdominal symptoms.37 The sensitivity (0.67) and negative likelihood ratio (LR) (0.39) as-sociated with the cluster are relatively weak, suggesting that a musculoskeletal cause of the patient’s symptoms was still high. However, when considered in the context of the other historical findings, the fact that cluster 1 was negative gave the clinician added suspicion that the symptoms could be related to nonmus-culoskeletal pathology.

There were also components of the

TABLE 2Musculoskeletal Abdominal

Pain Questionnaire37

Cluster 1*

1. Does coughing, sneezing, or taking a deep breath make your pain feel worse? (yes)

2. Do activities such as bending, sitting, lifting, twisting, or turning over in bed make your pain feel worse? (yes)

3. Has there been any change in your bowel habit since the start of your symptoms? (no)

Cluster 2†

1. Does eating certain foods make your pain feel worse? (no)

2. Has your weight changed since your symptoms started? (no)

*A patient answering “yes” to either of the first 2 and “no” to the third question of cluster 1 suggests a high probability that abdominal pain is musculoskeletal in origin (sensitivity, 0.67; specificity, 0.84; positive likelihood ratio, 4.2; negative likelihood ratio, 0.39).†If the patient answers “no” to both questions in cluster 2, in addition to corresponding responses to the questions in cluster 1, there is an even greater probability that abdominal pain is musculoskeletal in origin (sensitivity, 0.67; specificity, 0.96; positive likelihood ratio, 16.8; negative likelihood ratio, 0.34).

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patient history that the physical therapist identified and assisted in determining if the patient’s symptoms were nonmechan-ical in origin. The incidence of cancer as a cause of low back pain in a primary care setting is 0.66%, or approximately 6 to 7 cases for every 1000 patients with low back pain.8 Therefore, while the probabil-ity of cancer as a cause of low back pain is low, evidence-based screening strate-gies suggest that cancer may be ruled out with 100% sensitivity as a cause of low back pain if there is no previous his-tory of cancer, the patient is improving with conservative medical treatment, the patient is younger than 50 years of age, and there is no unexplained weight loss.8 These 4 clinical findings also had high positive LRs when assessing the accu-racy of clinical findings for detecting the presence of cancer resulting in low back pain.8 The patient described in this report had 3 of the 4 findings that allow cancer to be ruled out with 100% sensitivity. Although cancer could not be ruled out with 100% sensitivity, it is a rare cause of low back pain, and the patient did not demonstrate any of the strong pre-dictive findings for cancer as a cause of low back pain.8 In addition, Henschke et al20 conducted a Cochrane review to as-sess the diagnostic accuracy of red flags in screening for spinal malignancy in patients with low back pain. This review found a previous history of malignancy to be a clinically meaningful finding for detecting cancer. Given these factors, in addition to the relatively benign findings on plain-film radiographs, it was believed that cancer was an unlikely cause of low back pain. Given that the patient did not report a fever, fatigue, or malaise, it was believed that an infection was also un-likely.3,22,31,41 Additionally, given the lack of constitutional symptoms and no re-ports of morning stiffness, the likelihood of inflammatory arthritis as a cause of the patient’s low back and abdominal pain appeared to be low as well.17,22,31,34,35 Final-ly, it was highly unlikely that the patient had a spinal fracture. Vertebral fractures are the most common serious pathology

associated with low back pain.21 Red-flag questions that are useful in identifying spinal fracture include significant trauma (positive LR, 10.03; negative LR, 0.77), older age (positive LR, 11.19; negative LR, 0.52), and prolonged corticosteroid use (positive LR, 48.50; negative LR, 0.75).21,42 Henschke et al21 created a diag-nostic rule to identify vertebral fracture using the following variables: female sex, age greater than 70 years, significant trauma (major in young patients, minor in elderly patients), and prolonged use of corticosteroids. When at least 1 of these variables was positive, the positive and negative LRs were 1.8 and 0.24, respec-tively.21 With 2 positive features, the posi-tive and negative LRs increased to 15.5 and 0.39, respectively; 3 or more positive variables yielded a positive LR of 218.3 and a negative LR of 0.62.21 In addition to the absence of evidence of spinal fracture on plain-film radiographs, none of these variables were present in this patient, further decreasing the likelihood that a vertebral fracture was causing low back pain.

While mechanical dysfunction of the lumbar spine accounts for the vast major-ity of symptoms experienced by patients with low back pain, the majority of pa-tients with abdominal pain usually have a visceral cause, and in all patients with ab-dominal pain, visceral pathology should be ruled out.37 Furthermore, visceral dis-ease is a more frequent cause of low back pain compared to other nonmechanical spinal disorders.22 With regard to visceral disorders, initial screening questions for the gastrointestinal (eg, patient denied heartburn, nausea, indigestion, changes in appetite, difficulty swallowing, consti-pation, and changes in frequency of bowel movements) and genitourinary (patient denied pain with urination or changes in urinary frequency) systems were nega-tive.3 Although each of these findings does not necessarily rule out the presence of a gastrointestinal or genitourinary dis-order, the cluster of negative findings did suggest that the patient’s symptoms were most likely not related to these systems.

Considering vascular pathology, an AAA is a rare cause of low back pain, and in many cases patients experience no symp-toms at all.27 However, the patient in this case indicated that he had 4 of the 8 risk factors associated with increased preva-lence of AAA (TABLE 1).2,7,12,13,26

Physical ExaminationThe patient’s height was 188 cm, and he weighed 90.7 kg the day of the examina-tion (body mass index, 25.7 kg/m2). Vi-sual observation revealed a nonantalgic gait. A postural examination revealed a forward head and rounded shoulders, with a decreased lumbar lordosis. The iliac crests, anterior superior iliac spine, posterior superior iliac spine, and greater trochanters were level and in the same horizontal plane bilaterally.

Lumbar active range of motion and associated symptom responses were as-sessed with the patient in the standing position. The low back and abdominal pain remained unchanged during active range-of-motion testing, and all motions were within normal limits. Because the patient’s symptoms remained unchanged with active range-of-motion assessment, overpressure at the end range of active range of motion was applied to lumbar flexion, extension, and bilateral sidebend-ing. The low back and abdominal pain also remained unchanged during over-pressure assessment for each movement.

Seated hip active range of motion for flexion, internal rotation, and external ro-tation was within normal limits and pain free bilaterally. Passive range of motion with overpressure was then applied for hip flexion, internal rotation, and exter-nal rotation bilaterally, with the patient lying supine. Passive left hip flexion with overpressure slightly increased the pa-tient’s low back pain to 4 on the numeric pain rating scale, but the pain immedi-ately returned to the patient’s baseline pain level of 3 when his hip was taken out of the position of left hip flexion with overpressure. The patient did not note a change in his abdominal pain with hip range-of-motion assessment.

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With the patient positioned prone, spring testing through posterior-to-an-terior pressures over the spinous pro-cesses of T10 through L4 suggested mild hypomobility but no increase in the pa-tient’s symptoms. However, the patient did report a slight increase in low back pain with spring testing at the L5 level, and there was hypomobility noted at this level as well. A sacral spring test was then performed, which did not change the pa-tient’s symptoms. The patient denied any change in his abdominal pain with spring testing from T10 through S1.

The patient was then positioned su-pine, and an abdominal assessment was performed. Visual inspection of the pa-tient’s abdomen did not reveal any skin abnormalities, abdominal masses, or abnormal movement of the abdominal wall. Systematic palpation in each of the 4 abdominal quadrants did not provoke an increase in the patient’s symptoms. However, the clinician immediately no-ticed the presence of a very strong ab-dominal pulsation that lateralized from the midline bilaterally and was measured at approximately 5 cm in width. The pul-sation was palpable from the epigastric to the hypogastric regions. Following

this finding, the clinician elected to im-mediately stop the objective examination and contacted the patient’s primary care provider to discuss the findings from the evaluation.

Clinical Impression Post–Physical ExaminationThe patient’s low back and abdominal pain was not reproduced with any of the physical examination tests and measures performed, with the exception of a mild, temporary increase in low back pain with overpressure into hip flexion and L5 palpation. In the majority of patients with nonspecific mechanical low back pain, pain is reproduced with lumbar range-of-motion testing and/or lumbar palpation.4,5 Therefore, the absence of symptom reproduction during the physi-cal examination further elevated concern for the presence of visceral pathology, which led to a thorough palpation of the abdomen. During abdominal palpation, a very strong, nontender abdominal pulsa-tion at least 5 cm in width was detected, which was concerning for AAA.3,31

DiagnosisAfter discussing the case, the referring

physician immediately ordered an ultra-sound imaging study of the abdomen, which demonstrated dilation of the dis-tal abdominal aorta up to 5.5 cm wide (FIGURE 2). The physician subsequently ordered a computed tomography scan confirming the presence of a prominent AAA measuring 5.5 cm in greatest di-mension and an 80° angulation (FIGURE

3). The patient was immediately referred to a vascular surgeon. However, after a thorough discussion with the vascular surgeon, the patient decided to forgo immediate surgical intervention, believ-ing that the risks incurred from surgery outweighed the potential benefit. Given this decision, the patient was instructed to return biannually for repeat computed tomography scanning to determine if the AAA was progressing in size. The patient reported that his primary complaint of low back pain and secondary complaint of abdominal pain had completely sub-sided approximately 3 weeks after the initial onset of symptoms.

Six months following the initial di-agnosis of the AAA, repeat computed tomography scanning revealed that the

FIGURE 3. Initial computed tomography image, which demonstrated a prominent abdominal aortic aneurysm, which measured up to 5.6 cm in greatest dimension (line) and extended from below the renal arteries to the bifurcation of the iliac arteries. The aorta also buckled to the right, with approximately 80° of angulation present 1.3 cm distal to the left renal artery (arrow).

FIGURE 2. Initial ultrasound image demonstrating a 5.5-cm dilation of the distal abdominal aorta (region between the plus signs).

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aneurysm had increased by 1.2 to 6.7 cm in greatest dimension and to 90° of angulation (FIGURE 4). Interestingly, the patient reported that he did not have any further episodes of low back or abdomi-nal pain since the symptoms resolved ap-proximately 5 months earlier, despite the aneurysm’s progression. The average rate of expansion of the typical AAA is from 0.3 to 0.4 cm per year.14,18,29 Patients who have AAA expansion rates of 0.5 cm in a 12-month time frame are considered can-didates for elective surgical repair.16 Due to the rapid progression of the AAA, the patient accepted the risks of an open ab-dominal repair. The patient requested an endovascular repair, but the increasing angulation of the aorta and the weaken-ing aortic wall made an open repair the only viable option. TABLE 3 provides rela-tive dates of the patient’s medical visits and procedures.

Following surgery, the patient re-turned to walking 30 minutes to 1 hour daily. At 6 months following surgery, the patient was allowed to initiate a low-weight, high-repetition weight-training routine. At 9 months following surgery, the patient did not report any instances of low back or abdominal pain since the repair.

DISCUSSION

Identifying individuals with AAA is a challenging task for any clinician. There are no established algorithms

or clinical prediction rules to determine with reasonable certainty whether an AAA is present in a patient. Additionally, many AAAs are completely asymptom-atic, which further complicates the clini-cal picture.27 However, there is evidence in the peer-reviewed literature that can inform clinicians in their clinical reason-ing and thought process. Knowledge of the risk factors for AAA, systematic ap-plication of screening techniques for non-musculoskeletal symptoms, and a basic competence in abdominal palpation and how to interpret findings can help iden-tify AAA in a patient presenting with ap-parent musculoskeletal complaints.

Understanding the risk factors for AAA can help identify patients who should be referred for further testing. The major risk factors and associated odds ratios for AAA are listed in TABLE

1. There is discrepancy in the literature as far as when patients should undergo medical screening for AAA.6,12,28 In obese male patients over the age of 60, Led-

erle et al28 recommended ultrasound screening examinations regardless of the physical examination findings. Flem-ing et al12 conducted a systematic review that looked at the benefits and harms of population-based AAA screening. They concluded that screening will reduce age-related mortality in men between the ages of 65 and 75 years.12 According to Cosford and Leng,7 an age of greater than 65 years, past history of smok-ing, male sex, and family history are the most significant AAA risk factors (TABLE

1).7,12 Therefore, if a male patient in his sixth decade of life has 1 or more addi-tional risk factors for AAA, a referral to the primary care provider with a recom-mendation for an ultrasound screening examination may be indicated.

In patients with complaint of abdomi-nal pain, the question cluster suggested by Sparkes et al37 can serve as a valuable clinical decision tool when determining whether a patient has symptoms of mus-culoskeletal origin (TABLE 2). Additional-ly, the characteristics of abdominal pain can provide insight into the structures responsible for symptoms. Abdominal pain of musculoskeletal origin may pre-sent as a deep, sharp, localized, cramping and aching pain.32 In comparison, pain

FIGURE 4. Computed tomography scan completed 6 months after the initial scan seen in FIGURE 3. This image demonstrated interval progression of the abdominal aortic aneurysm to 6.7 cm in greatest dimension (line). There was also significant angulation at the neck of the aneurysm, measuring at least 90° (arrow).

TABLE 3Relative Timing of the Patient’s

Medical Visits or Procedures

Date Medical Visits or Procedures

Day 1 • Initial physical therapy visit for a primary complaint of low back pain and a secondary complaint of abdominal pain

• Physical therapist informed the patient and the referring provider of the concern of an abdominal aortic aneurysm

• Ultrasound imaging and computed tomography scan completed, which confirmed the presence of an abdominal aortic aneurysm

• Initial vascular surgery visit

Day 17 • Second vascular surgery visit

Day 31 • Third vascular surgery visit• Decision made to forgo immediate surgical intervention of abdominal aortic aneurysm• Primary complaint of low back pain and secondary complaint of abdominal pain had completely

subsided• Patient instructed to complete repeat computed tomography scan in 6 mo

Day 204 • Fourth vascular surgery visit• Repeat computed tomography scan results evaluated, which demonstrated interval progression of

abdominal aortic aneurysm

Day 302 • Open vascular repair of abdominal aortic aneurysm

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[ resident’s case problem ]

REFERENCES

1. Battie MC, Cherkin DC, Dunn R, Ciol MA, Wheel-er KJ. Managing low back pain: attitudes and treatment preferences of physical therapists. Phys Ther. 1994;74:219-226.

2. Blanchard JF, Armenian HK, Friesen PP. Risk factors for abdominal aortic aneurysm: re-sults of a case-control study. Am J Epidemiol. 2000;151:575-583.

3. Boissonnault WG. Primary Care for the Physical Therapist: Examination and Triage. 2nd ed. St Louis, MO: Elsevier/Saunders; 2011.

4. Boissonnault WG, Bass C. Pathological origins of trunk and neck pain: part I—pelvic and abdominal visceral disorders. J Orthop Sports Phys Ther. 1990;12:192-207. http://dx.doi.org/10.2519/jospt.1990.12.5.192

5. Boissonnault WG, Bass C. Pathological origins of trunk and neck pain: part II—disorders of the cardiovascular and pulmonary systems. J Or-thop Sports Phys Ther. 1990;12:208-215. http://dx.doi.org/10.2519/jospt.1990.12.5.208

6. Chervu A, Clagett GP, Valentine RJ, Myers SI, Rossi PJ. Role of physical examination in detec-tion of abdominal aortic aneurysms. Surgery. 1995;117:454-457.

7. Cosford PA, Leng GC. Screening for ab-dominal aortic aneurysm. Cochrane Database Syst Rev. 2007:CD002945. http://dx.doi.org/10.1002/14651858.CD002945.pub2

8. Deyo RA, Diehl AK. Cancer as a cause of back pain: frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med. 1988;3:230-238.

9. Edwards JZ, Weiner SD. Chronic back pain caused by an abdominal aortic aneurysm: case report and review of the literature. Orthopedics. 2003;26:191-192.

10. Feinstein B, Langton JN, Jameson RM, Schil-ler F. Experiments on pain referred from deep somatic tissues. J Bone Joint Surg Am. 1954;36-A:981-997.

11. Fink HA, Lederle FA, Roth CS, Bowles CA, Nelson DB, Haas MA. The accuracy of physical exami-nation to detect abdominal aortic aneurysm. Arch Intern Med. 2000;160:833-836.

12. Fleming C, Whitlock EP, Beil TL, Lederle FA. Screening for abdominal aortic aneurysm: a best-evidence systematic review for the U.S. Preventive Services Task Force. Ann Intern Med. 2005;142:203-211.

13. Forsdahl SH, Singh K, Solberg S, Jacob-sen BK. Risk factors for abdominal aortic aneurysms: a 7-year prospective study: the Tromsø Study, 1994-2001. Circulation. 2009;119:2202-2208. http://dx.doi.org/10.1161/CIRCULATIONAHA.108.817619

14. Glimåker H, Holmberg L, Elvin A, et al. Natural history of patients with abdominal aortic aneu-rysm. Eur J Vasc Surg. 1991;5:125-130.

15. Goodman CC, Snyder TEK. Differential Diagnosis in Physical Therapy. 3rd ed. Philadelphia, PA:

arising from visceral tissue is often de-scribed as dull, aching, cramping, throb-bing, burning, gnawing, or wave-like and is often poorly localized.32

Movement typically alters symptoms associated with musculoskeletal pain.4,5 In contrast, nonmusculoskeletal pain can be characterized as pain that cannot be provoked, alleviated, or eliminated by movement or position changes.4,5,15 If a patient is unable to identify specific ag-gravating and easing factors and the cli-nician is unable to reproduce symptoms with provocative testing, then a nonmus-culoskeletal origin of pain should be con-sidered and the case discussed with the referring physician.3,32

Abdominal palpation can play an im-portant role in identifying patients with AAA. However, the accuracy of palpation depends on the width of the aneurysm and the patient’s abdominal girth.11 Ab-dominal palpation has only a moderate overall ability in detecting smaller AAAs, but does appear very useful in identify-ing aneurysms large enough to warrant elective repairs.11,28,29 The sensitivity of palpation in patients with an abdominal girth less than 100 cm and an AAA 5.0 cm or greater is 100%.11 The patient in this case had a 95-cm waistline and had an AAA greater than 5 cm, resulting in a successful detection of the AAA during the palpation examination. Palpation of an AAA appears to be safe and has not been reported to precipitate rupture.27 If a palpable pulsation of 3.0 cm in width or greater is noticed, physician referral is indicated12; however, it’s important to re-member that aneurysms less than 5.0 cm are not as easily identifiable with palpa-tion. Therefore, sole reliance on abdomi-nal palpation is not recommended.11,24

It is important to note that the clini-cal examination plays a vital role in the recognition of AAAs, but should not be relied on to exclude their presence.29 If a referral to the primary care physi-cian for suspected AAA is indicated, the physician will likely order an abdominal ultrasound, as this can confirm the pres-ence or absence of an AAA (sensitivity,

0.97-1.0; specificity, 0.94-1.0; negative LR, 0-0.025; positive LR, 10.8 to infin-ity).28,33 Ultrasound screening is not only highly accurate in detecting AAAs33 but is also low cost and does not expose the patient to radiation.6,22,28 If the presence of an AAA is confirmed with ultrasound imaging, a computed tomography scan is the preferred imaging progression.16,38 While the sensitivity and specificity of computed tomography imaging of the ab-domen are lower than that of ultrasound imaging (sensitivity, 0.79-0.90; specific-ity, 0.77-0.91),36 it can detect additional aneurysms, evaluate the surrounding organs, and provide details on arterial-wall characteristics (dissection, rupture, or thickening).16 Computed tomogra-phy does have one major disadvantage: it exposes the patient to radiation.16,38 Magnetic resonance angiography yields similar results to those of computed to-mography without exposure to ionizing radiation, but high cost and limited avail-ability have prevented widespread adop-tion of this modality.16,38

CONCLUSION

Although the majority of indi-viduals with AAA are asymp-tomatic at the time of diagnosis,

some patients do present with a history and clinical presentation suggestive of AAA.9 This resident’s case problem de-scribed the decision making and clinical reasoning that led a clinician to cor-rectly identify the presence of an AAA in a patient referred from a primary care provider with a diagnosis of mechanical low back pain. Findings from the sub-jective interview and physical examina-tion led the clinician to suspect AAA as an explanation for the patient’s com-plaints. This suspicion was confirmed with a series of imaging studies, which led to expedited medical care and even-tual surgical intervention. t

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@ MORE INFORMATIONWWW.JOSPT.ORG

W.B. Saunders; 2000. 16. Gorski Y, Ricotta JJ. Weighing risks in abdominal

aortic aneurysm. Best repaired in an elective, not an emergency, procedure. Postgrad Med. 1999;106:69-70, 75-80.

17. Gran JT. An epidemiological survey of the signs and symptoms of ankylosing spondylitis. Clin Rheumatol. 1985;4:161-169.

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19. Hart LG, Deyo RA, Cherkin DC. Physician of-fice visits for low back pain. Frequency, clinical evaluation, and treatment patterns from a U.S. national survey. Spine (Phila Pa 1976). 1995;20:11-19.

20. Henschke N, Maher CG, Ostelo RW, de Vet HC, Macaskill P, Irwig L. Red flags to screen for malignancy in patients with low-back pain. Co-chrane Database Syst Rev. 2013;2:CD008686. http://dx.doi.org/10.1002/14651858.CD008686.pub2

21. Henschke N, Maher CG, Refshauge KM, et al. Prevalence of and screening for serious spinal pathology in patients presenting to primary care settings with acute low back pain. Arthritis Rheum. 2009;60:3072-3080. http://dx.doi.org/10.1002/art.24853

22. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med. 2002;137:586-597. http://dx.doi.org/10.7326/0003-4819-137-7-200210010-00010

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26. Lederle FA, Johnson GR, Wilson SE, et al. Rela-tionship of age, gender, race, and body size to infrarenal aortic diameter. The Aneurysm Detec-tion and Management (ADAM) Veterans Affairs Cooperative Study Investigators. J Vasc Surg. 1997;26:595-601.

27. Lederle FA, Simel DL. The rational clinical exami-nation. Does this patient have abdominal aortic aneurysm? JAMA. 1999;281:77-82. http://dx.doi.org/10.1001/jama.281.1.77

28. Lederle FA, Walker JM, Reinke DB. Selective screening for abdominal aortic aneurysms with physical examination and ultrasound. Arch In-tern Med. 1988;148:1753-1756.

29. Lynch RM. Ruptured abdominal aortic aneu-rysm presenting as groin pain. Br J Gen Pract. 2002;52:320-321.

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31. Mechelli F, Preboski Z, Boissonnault WG. Dif-ferential diagnosis of a patient referred to physical therapy with low back pain: abdominal aortic aneurysm. J Orthop Sports Phys Ther. 2008;38:551-557. http://dx.doi.org/10.2519/jospt.2008.2719

32. Rodeghero JR, Denninger TR, Ross MD. Abdomi-nal pain in physical therapy practice: 3 patient cases. J Orthop Sports Phys Ther. 2013;43:44-53. http://dx.doi.org/10.2519/jospt.2013.4408

33. Rubano E, Mehta N, Caputo W, Paladino L, Sin-ert R. Systematic review: emergency department bedside ultrasonography for diagnosing sus-pected abdominal aortic aneurysm. Acad Emerg Med. 2013;20:128-138. http://dx.doi.org/10.1111/acem.12080

34. Rudwaleit M, Metter A, Listing J, Sieper J, Braun J. Inflammatory back pain in ankylosing spon-dylitis: a reassessment of the clinical history for application as classification and diagnostic cri-teria. Arthritis Rheum. 2006;54:569-578. http://

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New criteria for inflammatory back pain in patients with chronic back pain: a real patient exercise by experts from the Assessment of SpondyloArthritis international Society (ASAS). Ann Rheum Dis. 2009;68:784-788. http://dx.doi.org/10.1136/ard.2008.101501

36. Silverstein MD, Pitts SR, Chaikof EL, Ballard DJ. Abdominal aortic aneurysm (AAA): cost-effectiveness of screening, surveillance of intermediate-sized AAA, and management of symptomatic AAA. Proc (Bayl Univ Med Cent). 2005;18:345-367.

37. Sparkes V, Prevost AT, Hunter JO. Derivation and identification of questions that act as predictors of abdominal pain of musculo-skeletal origin. Eur J Gastroenterol Hepatol. 2003;15:1021-1027. http://dx.doi.org/10.1097/01.meg.0000059173.46867.0c

38. Tang T, Boyle JR, Dixon AK, Varty K. Inflamma-tory abdominal aortic aneurysms. Eur J Vasc Endovasc Surg. 2005;29:353-362. http://dx.doi.org/10.1016/j.ejvs.2004.12.009

39. Thompson RW. Basic science of abdominal aor-tic aneurysms: emerging therapeutic strategies for an unresolved clinical problem. Curr Opin Cardiol. 1996;11:504-518.

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41. Waldvogel FA, Papageorgiou PS. Osteo-myelitis: the past decade. N Engl J Med. 1980;303:360-370. http://dx.doi.org/10.1056/NEJM198008143030703

42. Williams CM, Henschke N, Maher CG, et al. Red flags to screen for vertebral fracture in patients presenting with low-back pain. Cochrane Data-base Syst Rev. 2013;1:CD008643. http://dx.doi.org/10.1002/14651858.CD008643.pub2

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