Pediatric and adolescent back pain is a common complaint in the outpatient setting. Recent studies report that 17.8% of 9 to 12-year-old children had at least 1 episode of back pain in a 2-year observation period (14). Recent questionnaire studies have reported at least 1 lifetime episode of low back pain in 39% to 67% of European adolescents (4, 11). While most of these complaints are minor and self-limited, there are subsets of the pediatric and adolescent population that will present with a unique set of differential diagnoses.
In special populations, the differential diagnosis will guide evaluation. Patients with sickle cell disease can present with bone pain during a vasoocclusive crisis. Children under 5 years old are much more susceptible to discitis and vertebral osteomyelitis due to their unique anatomy (15). Back pain in children <5 years old is associated with a significant pathological diagnosis in up to 50% of patients, and further extensive work-up is indicated (6). Finally while individually rare, a number of pediatric cancers will present with low back pain, pain radiating to the back, or painful scoliosis (8).
In the adolescent sports medicine population, the etiology of low back pain is different from adults and is related in part to the rapid growth associated with adolescence (10). Injuries, both acute and chronic, occur when the spine and its supporting structures cannot accommodate the compression, distraction, or shear forces associated with activity. During growth, the vertebral bodies and neural arch are the weakest parts of the spinal column and are at the greatest risk of injury during force transfer (12). In late childhood, linear growth increases at a greater rate than bone mineral density (BMD), resulting in a relative decrease in bone density (1). This may result in an increased risk for fractures, both acute fractures from trauma, and stress fractures from repetitive activity (9). Following the early adolescent growth spurt, BMD increases more rapidly as vertical growth velocity slows, allowing for progress toward normal adult bone density (1). The lower lumbar pars interarticularis is particularly at risk for stress fractures. Adolescent athletes who engage in sports that involve axial loading of the spine, such as snowboarding, diving, and motor cross, also are at risk for vertebral body compression fractures since the bone density may be diminished transiently during rapid growth (2). Rapid growth also leads to decreased flexibility of the hamstrings and the hip flexors, increasing force demands on the low back muscles and supporting structures.
Common causes of back pain in the athletic adolescent population include spondylolysis (up to 47% in pediatric sports medicine clinics) and hyperlordosis (25%) (10). Athletes who participate in repetitive hyperextension activities, such as gymnastics, football, and dance are particularly at risk for each of these conditions. Disc pain (11%) does occur in this population, but unlike adults, disc herniation of the nucleus pulposus often does not occur through the annulus fibrosus. Instead, it herniates through the weaker cartilaginous end plate, resulting in either an apophyseal ring fracture (avulsion of the apophysis with the intact annulus attached) or a disc herniation into the vertebral body (limbus vertebrae) (7). Occasionally the discs can herniate through the inferior border of the vertebral body, creating a Schmorl node as seen in Scheuermann disease.
Tumors and infection are very infrequent causes of adolescent back pain. However their presentation often will mimic common back complaints (8). Lesions that involve the posterior column, including osteoid osteoma, osteoblastoma, and aneurysmal bone cysts, may mimic symptoms of spondylolysis. They generally are not associated with systemic symptoms or focal neurological deficits. Osteoid osteomas classically cause nighttime pain relieved by salicylates and some decrease in range of motion secondary to pain. Osteoblastomas usually cause dull pain and are not associated with nighttime pain. Both may cause painful scoliosis. Aneurysmal bone cysts generally cause pain secondary to expansion of the cyst or pathological fracture through the cyst similar to a spondylolytic lesion (8).
Malignant lesions of the spine include leukemia, metastatic lesions, and primary malignant tumors such as Ewing sarcoma and osteogenic sarcoma. Metastatic lesions are more common than primary tumors (3). Ewing sarcoma is the most common malignant spine tumor and often involves the pelvis, with sacral involvement being associated with lumbar back pain (3). Spinal cord lesions are rare and usually associated with worsening gait and bowel and bladder symptoms. Isolated back pain is a well-documented but rare presentation of leukemia (13).
A previously healthy 12-year-old boy who plays recreational baseball is referred to the Department of Orthopedics by his primary care physician for a 2-month history of lumbar and lower thoracic back pain and “muscle spasms.” The pain involves the midline and adjacent paraspinal areas of the lower thoracic and lumbar back. He describes the pain as sharp, episodic, and radiating to the calves bilaterally. Episodes occur sporadically and last only a few minutes. He reports that sometimes the pain is associated with running. It sometimes is relieved with stretching. Initially the pain only occurred about twice a week, but now, the episodes happen daily. Pain can be with activity or at rest. He is pain free and functions normally between the painful episodes.
There is no history of trauma or injury. He denies lower extremity numbness, tingling, and weakness. He has no bowel or bladder dysfunction. He has no fevers, painful nocturnal awakenings, or morning stiffness. There is no reported fatigue, pallor, or frequent infections. He has no allergies and takes no medications.
Family history is negative for autoimmune arthritis or back problems including disc disease. Of note, his father died from a myocardial infarction at the age of 32 years.
Well-developed male in no distress.
Vital signs: T, 37°C; Ht, 59 inches (50th percentile); Wt, 56 kg (90th percentile). Pain score: 0.
Head eyes ears nose throat: pupils equal round, reactive to light, no icterus, no lymphadenopathy.
Spine: full Cervical ROM without pain, normal contour, no cutaneous abnormalities. Adam’s forward bend test: no pain, no rib hump. No pain with side bending, rotation, or hyperextension.
The iliac crest is mildly tender to palpation bilaterally. There is full, pain-free range of motion at the hips, including internal or external rotation.
Strength is 5/5 and pain free upon resisted testing of the muscles about the hips and pelvis, but he is unable to hold a standard plank.
Thomas test is positive bilaterally.
Popliteal angle compliment is 45 degrees bilaterally.
Straight leg raise is negative.
Single-leg hop does not cause pain.
Deep tendon reflexes at the patellae and Achilles are normal.
He has normal, symmetric strength in the lower extremities with no atrophy.
He has normal light touch sensation and no clonus. His gait is normal.
- Muscle spasm
- Lumbar musculature strain
- Iliac crest apophysitis
Plain radiographs of the lumbar spine (Figs. 1, 2) are performed in the office on the day of presentation. Imaging is done to evaluate for possible spondylolisthesis or other conditions that potentially would cause lumbar muscle pain or spasms. These images are normal.
The initial presentation of deficits in core strength and flexibility (tight hamstrings, iliopsoas muscles), along with mild iliac crest tenderness and normal radiographs, is consistent with a muscular etiology of lumbar back pain and associated muscle spasm. There are no red flags of nocturnal pain, unexplained constitutional symptoms (fevers, poor appetite, weight loss, fatigue/lack of energy) or physical examination findings to suggest additional imaging is needed. He is prescribed physical therapy to address the biomechanical deficits found on the examination. The plan is for follow-up after 4 wk of therapy if the pain persists or sooner if symptoms become worse.
Three weeks after the initial visit, his mother calls with new concerns. There have been no interim injuries, but the painful episodes are more frequent, now up to three times a day despite physical therapy. The intensity of the pain has increased as well, with pain severe enough to “bring him to his knees.” His mother also reports that he has developed an intermittent rash this week that “looks like hives” and one episode of low-grade fever (100.5°F).
He is reevaluated in the office the day his mother calls. The physical examination is unchanged. He is afebrile and has no pain at the time of the examination. His skin appears normal with no rash or bruising. He has no lymphadenopathy or hepatosplenomegaly.
Given the new concerns, particularly the dramatic increase in pain, the unexplained rash, and a questionable fever, a new plan is developed. Diagnostic considerations remain similar to the initial differential, but there is a heightened level of concerns for occult infection or neoplasm. Blood work (complete blood count, erythrocyte sedimentation rate, and comprehensive metabolic panel) and magnetic resonance imaging (MRI) of the lumbar spine are ordered.
Blood work returns 2 d later with white blood cells 3,400 μL−1 (2% polymorphonuclear leukocytes, 98% lymphocytes, 12 atypical lymphocytes, no blasts, absolute neutrophil count 68), hemoglobin 8.1 mg·dL−1, hematocrit 22.6%, and platelets reported as clumped. His CMP is normal including calcium, alkaline phosphatase, and uric acid. ESR is 22 mm·h−1. He is contacted immediately upon receipt of these results and advised to proceed to the emergency department for urgent evaluation of anemia and neutropenia. He is admitted to the oncology service. Their work-up includes a bone marrow biopsy that reveals hypercellularity with greater than 95% blasts, consistent with leukemia. MRI of the entire spine is performed shortly after admission and revealed diffuse marrow signal abnormality (T1 hypointensity and short TI inversion recovery hyperintensity) throughout the vertebrae and other visualized osseous structures. There is no spinal cord compression or vertebral fractures. Radiologist report notes that “while this may represent red marrow conversion related to underlying anemia, the appearance is concerning for leukemic or other marrow infiltration.” He is diagnosed ultimately with acute myeloid leukemia (AML).
The young adolescent patient in our case presents with low back pain in association with relative core weakness and lower extremity muscle tightness, a common scenario in the sports medicine clinic. Despite a presumably appropriate course of action, he develops atypical features that are worrisome in this setting. Of particular concern are the unexplained increase in pain and the reported fever and rash. Immediate follow-up after this clinical update again demonstrated a pain-free physical examination, but the clinical course was not progressing as expected and his pain seemed out of proportion to the examination. Given this information, the initial differential diagnosis needed to be reprioritized and additional evaluation for occult infection and neoplasm is initiated.
Imaging studies remain a cornerstone of the work-up for back pain. Plain radiographs are generally adequate imaging studies for initial diagnostic work-up. If the initial plains films are concerning for potential bony abnormality, then direct consultation with the reading radiologist or with an orthopedic surgeon experienced in treatment of bony tumors may be warranted to elucidate an appropriate differential. Advanced imaging may be indicated if the diagnosis is in question, particularly in patients with worrisome signs and symptoms. MRI, typically without contrast, is the most appropriate approach to the broad work-up of atypical adolescent back pain, especially in the setting of normal plain radiographs. Bone scan is an alternative but has the disadvantage of radiation exposure and less tissue detail. If a specific bony lesion has been identified on plain radiography, contrast MRI or computed tomography (CT) scan may be the preferred imaging modality. CT scans can accurately define osseous lesions and can be completed rapidly in urgent situations. However they may expose children to unnecessary radiation and are less adept at defining soft tissue disorders.
Blood work should be directed by the differential diagnosis. The red flags that may alert a clinician to consider blood work are similar to those that guide decisions to obtain advanced imaging. Unexplained constitutional symptoms (fever, chills, weight loss, fatigue, and rash), increasing pain despite follow through with prescribed interventions, nocturnal awakenings due to pain, and pain out of proportion to the suspected etiology should raise clinical suspicion, and blood work needs to be considered. Screening laboratories may include CBC with differential and inflammatory markers (ESR, c reactive protein). Situations more concerning for malignancy may warrant more extensive metabolic panels that include lactate dehydrogenase and uric acid as well as liver function tests. Concern for autoimmune disorders and spondyloarthropathy are evaluated with screening ANA titers, RF and HLA-B27 assessment.
This case is a unique presentation of AML presenting as adolescent back pain. It is similar to previously reported presentations of acute lymphoblastic leukemia (ALL). A small percentage of ALL cases (less than 1%) present with extensive skeletal involvement prior to overt symptoms. With this presentation, there is no organomegaly or adenopathy, no blasts in the peripheral blood, and only moderate anemia. Bone metabolic parameters are usually normal, although hypercalcemia may be seen (13). During this process the hypercellular marrow replaces the bony architecture of the spine. This may result in osteopenia and vertebral body compression fractures. While extensive osteopenia and spinal compression fractures may be observed 1 month after induction of chemotherapy, the overall prognosis in ALL is generally favorable with this presentation. In the skeletally immature population, vertebral body remodeling is possible and many regain normal spinal body height (4).
This case demonstrates a number of useful points for sports medicine clinicians. In adolescent back pain, an atypical course such as nighttime pain, increasing severity of pain, particularly if out of proportion to the suspected injury or etiology, or pain with subsequent development of unexplained constitutional symptoms should prompt the clinician to look for unusual causes of pain. These atypical causes of pain may mimic spondylolysis and include posterior column lesions such as osteoid osteoma, osteoblastoma, and aneurysmal bone cysts. Unusual causes of pain that mimic functional back pain include spinal compression fractures or bone pain due to infiltration of tumor cells including leukemia and metastatic lesions. Ultimately this case illustrates the need for the sports medicine clinician to maintain a broad differential diagnosis and to be prepared to escalate diagnostic investigation when presented with new clinical information.
The authors declare no conflicts of interest and do not have any financial disclosures.
1. Bailey DA, Wedge JH, McCulloch RG, et al. Epidemiology of fractures at distal end of radius in children as associated with growth. J. Bone Joint Surg. Am
. 1989; 71A: 1225–31.
2. Baranto A, Hellstrom M, Cederlund CG, et al. Back pain and MRI changes in the thoracolumbar spine of top athletes in four different sports: a 15-year follow-up study. Knee Surg. Sports Traumatol. Arthrosc
. 2009; 17: 1125–34.
3. Binning M, Klimo P, Gluf W, Goumnerova L. Spinal tumors in children. Neurosurg. Clin. N. Am
. 2007; 18: 631–58.
4. Bjeregaard LL, Rosthoøj S. Vertebral compression and eosinophilia in a child with acute lymphatic leukemia. J. Pediatr. Hematol. Oncol
. 2002; 24: 313–5.
5. Drozda K, Lewandowski J, Garski P. Back pain in lower and upper secondary school pupils living in urban areas of Poland. Ortop. Truamatol. Rehabil
. 2011; 13: 489–503.
6. Hasler CC. Back pain during growth. Swiss Med. Wkly
. 2013; 143: w13714.
7. Haus BM, Micheli LJ. Back pain in the pediatric and adolescent athlete. Clin. Sports Med
. 2012; 31: 423–40.
8. Kim HJ, Green DW. Adolescent back pain. Curr. Opin. Pediatr
. 2008; 20: 37–45.
9. Krabbe S, Christiansen C. Effects of puberty on rates of bone growth and mineralization: with observations in male delayed puberty. Arch. Dis. Child
1979; 54: 950–3.
10. Micheli LJ, Wood R. Back pain in young athletes: significant differences from adults in causes and patterns. Arch. Pediatr. Adolesc. Med
. 1995; 199: 15–8.
11. Pellisa F, Balagua F, Rajmil L, et al. Prevalence of low back pain and its effect on health-related quality of life in adolescents. Arch. Pediatr. Adolesc. Med
. 2009; 163: 65–71.
12. Salter RB, Harris WR. Injuries involving the epiphyseal plate. J. Bone Joint Surg. Am
. 1963; 45: 587–622.
13. Samuda GM, Cheng MY, Yeung CY. Back pain and vertebral compression: an uncommon presentation of childhood acute lymphoblastic leukemia. Arch. Dis. Child
. 1977; 52: 503–3.
14. Szapalski M, Gunzburg R, Balague F, Nordin M, Melot C. A 2-year prospective longitudinal study on low back pain in primary school children. Eur. Spine J
. 2002; 11: 459–64.
15. Ring D, Johnston CE II, Wenger DR. Pyogenic infectious spondylitis in children: the convergence of discitis and vertebral osteomyelitis. J. Pediatr. Orthop
. 1995; 15: 652–60.