Peer Reviewed

back pain

How Would You Triage This Patient’s Low Back Pain?

Eiyu Matsumoto, MB

Clinical Assistant Professor, Department of Internal Medicine, Division of Infectious Diseases, University of Iowa Carver College of Medicine, Iowa City, Iowa

Jennifer R. Carlson, PA-C
Iowa City Veterans Affairs Health Care System, Iowa City, Iowa

Matsumoto E, Carlson JR. How would you triage this patient’s low back pain? [published March 6, 2019]. Infectious Diseases Consultant.


A 67-year-old man presented to the emergency department (ED) with a 5-day history of nontraumatic low back pain (LBP). His multiple comorbidities included hypertension, hyperlipidemia, diabetes, obstructive sleep apnea, and pulmonary embolism for which he was on lifelong anticoagulation.

The patient stated that this was a new pain for him and that any spine movement elicited severe pain. The pain was on the midline of the upper lumbar spine, radiating to the bilateral posterior thighs. There had been no preceding event to the pain. He denied urinary tract symptoms such as dysuria and hematuria.

His vital signs included a blood pressure of 122/63 mm Hg, a heart rate of 95 beats/min, a respiratory rate of 18 breaths/min, a temperature of 36.0°C, and oxygen saturation of 95% on room air. Back examination revealed severe tenderness in the lumbar spine at L2-3. There was no costophrenic angle tenderness or skin lesions. Results of a straight leg raise test were normal bilaterally. He was neurologically intact.

Of note, this was his second visit to the ED. At the first visit 3 days prior, lumbar spine radiographs had been normal. He ultimately had been sent home with a short course of hydrocodone/acetaminophen.


Answer: D, inquire further into the patient’s history and symptoms.

LBP is a leading cause of disability worldwide, and its lifetime prevalence is nearly 80%.1 Spinal disorders are the fourth most common primary diagnosis for office visits in the United States.1,2 Most of those diagnoses (more than 85%) are for nonspecific back pain, meaning that the patient has back pain in the absence of a specific underlying condition that can be reliably identified.1 Most patients recover spontaneously in a few weeks.3 However, approximately 5% of cases are estimated to have serious systemic etiologies; the prevalence of compression fracture is 4%, nonskin cancer is less than 1%, ankylosing spondylitis is 0.3%, and infection is 0.01%.1

The differential diagnosis of LBP is broad. The first step is to identify medical (nonmusculoskeletal) diseases that may be responsible for a patient’s symptoms. These are usually categorized as neoplastic, inflammatory visceral, infectious, vascular, endocrine, or traumatic causes (Table 1).4

Table 1. Nonmusculoskeletal (Medical) Causes of LBP


Metastatic carcinoma, multiple myeloma, lymphoma, spinal cord tumors


Ankylosing spondylitis, psoriasis, rheumatoid arthritis, enteropathic spondylitis


Pancreatitis, endometriosis, prostatitis, nephrolithiasis


Osteomyelitis, epidural abscess, diskitis, herpes zoster, pyelonephritis


Aortic aneurysm, aortic dissection, sickle cell crisis


Osteoporotic fractures, Paget disease




Among these causes of LBP, spinal malignancy, epidural abscess, vertebral osteomyelitis, aortic dissection, aortic aneurysm, pancreatitis, and unstable compression fractures of the spine are particularly dangerous. A number of red flag signs can help detect these pathologies (Table 2).4 Although the sensitivity, specificity, and accuracy of red flag signs have been long debated,1 the only initial clues are derived from the history and physical examination findings.

Table 2. Some Red Flag Signs in Back Pain

Age >50 years or <20 years

Bowel/bladder incontinence


Major trauma

Pain worse at night

History of cancer


Intravenous drug use

Recent bacterial infection

Unexplained weight loss

Urinary retention

Unrelenting pain despite medication

Corticosteroid use


Recent surgical procedure

NEXT: Discussion (Continued)

Some clinicians may consider altering the pain medication regimen or adding physical therapy to the treatment course, but further interview to rule out other etiologies aside from musculoskeletal pain is necessary first. This was especially so in our patient’s case, given his refractory pain. Although aortic dissection should be in the differential diagnosis, this patient’s pain was localized to the lumbar spine, was reproduced by palpation, and was worse with body movement. Therefore, the pathology should be suspected in the spine system. Magnetic resonance imaging (MRI) would be the modality of choice for evaluation of the spine in this case.

Although he was afebrile in the ED, further questioning revealed that he had been experiencing chills and subjective fever over the past 5 days, which he had not mentioned previously. He also said that he had had a nonhealing lesion on the right great toe for the past 3 weeks for which he had not yet sought care (Figure 1).

fig 1
Figure 1. Further questioning elicited that the patient had had a nonhealing lesion on the right great toe for the past 3 weeks.


The positive red flag signs in this patient’s case included subjective fever and chills, intractable pain despite medication use, and old age. Laboratory testing revealed an elevated white blood cell count of 25,200/µL, an elevated C-reactive protein level of greater than 270 mg/L, and an elevated erythrocyte sedimentation rate of 52 mm/h. MRI findings were consistent with osteomyelitis/diskitis at the level of L2-3 (Figure 2). He was admitted to the hospital for management.

fig 2
Figure 2. Right: T1-weighted MRI image of the lumbar spine showing low intensity at the L2/3 disk/vertebral body. Left: T2-weighted image of the lumbar spine showing high intensity at the L2-3 disk/vertebral body. These findings were consistent with L2-3 vertebral osteomyelitis/diskitis.


Blood culture results later returned positive for methicillin-susceptible Staphylococcus aureus. Echocardiography findings were negative for vegetation. He was treated with 6 weeks of intravenous cefazolin with home infusion via a peripherally inserted central catheter. Our theory was that S aureus had been introduced into the bloodstream through the toe wound and ultimately was disseminated to the lumbar spine.


  1. Chou R. Low back pain. Ann Intern Med. 2014;160(11):ITC6-
  2. Centers for Disease Control and Prevention. National Ambulatory Medical Care Survey: 2010 Summary Tables. Atlanta, GA: Centers for Disease Control and Prevention; 2011. Accessed March 6, 2019.
  3. Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001;344(5):363-370.
  4. Hooten WM, Cohen SP. Evaluation and treatment of low back pain: a clinically focused review for primary care specialists. Mayo Clin Proc. 2015;90(12):1699-1718.