Clinical Review & Education

JAMA Pediatrics Clinical Challenge

A Case of Back Pain That Wakes a Child From Sleep

Arda Hotz, MD; Zachary Hena, MD; Elissa Gross, DO, MPH

A Radiograph of chest B Computed tomographic scan of chest

Figure. A, Radiograph of the chest reveals a right paravertebral mass (left arrowhead), destruction of the left seventh rib
(top right arrowhead), a compression fracture of T8 (middle right arrowhead), and bony erosion of L1 vertebra (bottom
right arrowhead). B, Computed tomographic scan reveals paravertebral abscesses (left arrowhead) with T8 compression
and destruction (right arrowhead).

An 11-year-old boy with a history of asthma and constipation presented with 6 weeks of
intermittent, worsening lower back pain. His pain was mild to moderate, woke him from WHAT IS YOUR DIAGNOSIS?
sleep, and limited his physical activity. He had previously been referred to orthopedics by
his pediatrician owing to multiple presentations for the same complaint. The patient de- A. Ewing sarcoma
nied recent trauma, fevers, weight loss, cough, rash, or sick contacts. He was born in the
United States with no recent travel. According to outpatient records, his height had been
B. Tuberculous spondylitis
unchanged for the last 2 years.
A physical examination showed a well-appearing young boy with unremarkable heart,
lung, and abdominal findings. There was mild tenderness to palpation of the lumbar spine, C. Discitis
and mild pain elicited with flexion and extension of his back. His strength was 4/5 in bilat-
eral lower extremities, with otherwise normal neurological examination findings. D. Pyogenic osteomyelitis
He had a white blood cell count of 6.2 × 103/μL (to convert to ×109 per liter, multiply
by 0.001), a hemoglobin level of 10.9 g/dL (to convert to grams per liter, multiply by 10.0),
and a platelet count of 611 × 103/μL (to convert to ×109 per liter, multiply by 1.0), with a nor-
mal peripheral smear result. The results of a complete metabolic panel were unremark-
able, and so were his lactate dehydrogenase and uric acid levels. He had an erythrocyte sedi-
mentation rate of 80 mm/h and a C-reactive protein level of 20 mg/L (to convert to
nanomoles per liter, multiply by 9.524).
In the emergency department, a radiograph of his chest (Figure, A) revealed a right para-
vertebral mass, destruction of left seventh rib, a compression fracture of T8, and bony ero-
sion of L1 vertebra. A computed tomographic (CT) scan (Figure, B) revealed paravertebral
abscesses with T8 compression and destruction. Mediastinal and hilar lymphadenopathy
was noted on imaging but are not shown.

jamapediatrics.com (Reprinted) JAMA Pediatrics November 2016 Volume 170, Number 11 1101

Copyright 2016 American Medical Association. All rights reserved.

 Clinical Review & Education JAMA Pediatrics Clinical Challenge

Diagnosis
B. Tuberculous spondylitis
Discussion
After reviewing the images, the orthopedic and neurosurgical
teams were concerned for spinal cord compression due to tuber-
culous spondylitis or malignancy. A CT-guided needle biopsy of L1
was performed, after which the patient was started on steroids
for spinal cord compression. His back pain quickly improved. Pre-
liminary results of the biopsy yielded granulomas and multinucle-
ated giant cells. Owing to high suspicion for tuberculosis (TB), the
patient was treated with rifampin, isoniazid, pyrazinamide, and
ethambutol (ie, RIPE therapy). Purified protein derivative (tuber-
culin) was used after initiation of steroids, and he had a 0-mm
induration at 48 hours; however, at 72 hours, he had an indura-
tion of more than 10 mm. The results of an interferon gamma
release assay were indeterminate. Three acid-fast bacterial Gram
stains of nasogastric aspirates were negative for TB; however, cul-
tures of the same samples and a culture from the biopsy con-
firmed pansensitive Mycobacterium tuberculosis 4 to 8 weeks
later. The boy’s treatment was changed to rifampin and isoniazid
for a total of 12 months of therapy.
Ultimately, the patient received a diagnosis of both tubercu-
lous spondylitis and miliary TB. A full investigation by the US
Department of Health revealed that a teacher at the child’s school
had received a diagnosis of the same strain of TB and is thought to
have been the source of infection.
Among children, back pain without a history of trauma is un-
common and always necessitates further evaluation.1 In the case of
this patient, the persistent focal back pain, the failure of expected
growth, and the pain waking him from sleep were all red flags. On-
cologic etiologies such as Ewing sarcoma and osteosarcoma were
considered because they can originate in the spine, although they
are rare.2 Osteomyelitis and discitis are unlikely given the appear-
ance of the bone and lung findings.
Tuberculous spondylitis (Pott disease) is the most common form
of skeletal tuberculosis, occurring in 1.7% of the world’s population.3
It can be a difficult diagnosis to make in children and often takes
weeks or months to confirm. Diagnosis is often delayed owing to the
subacute nature of symptoms, particularly in areas where TB is not
endemic.4 In cases for which there is high suspicion for TB, it is im-
portant to begin therapy as soon as possible. Tuberculous spondy-
litis is thought to be caused by the hematogenous spread of pri-
mary TB3 but can also occur from a contiguous disease or the
lymphatic spread of a nearby pleural disease. It typically presents
with lower thoracic and upper lumbar back pain,3,5 which is usually
present for weeks, months, or even years. Associated symptoms in-
clude muscle spasms, rigid or erect posture, weight loss, and fevers.3
The gold standard of diagnosis is a culture of infected tissue,
either by surgical biopsy or CT-guided needle biopsy.4,6 An inter-
feron gamma release assay is only 84% sensitive for skeletal tuber-
culosis, although it is 95% specific.7 Acid-fast bacterial stains are of-
ten negative for skeletal TB,7 although cultures are positive up to 75%
of the time.7 At the time of diagnosis of tuberculous spondylitis,
about 50% of patients have concomitant pulmonary TB.8 Tubercu-
lous spondylitis is treated medically with RIPE therapy,9 but surgi-
cal intervention may be warranted for patients with significant
kyphosis, spinal involvement, or neurological deficits.5,10
Patients with TB who are from endemic areas should be under
suspicion for having tuberculous spondylitis, but this diagnosis should
also be considered for children without known risk factors. For pa-
tients with tuberculous spondylitis, it is imperative to use a multi-
disciplinary approach (using the orthopedics, neurosurgery, and
infectious disease departments and the US Department of Health).

ARTICLE INFORMATION
Author Affiliations: Children’s Hospital of
Montefiore, Bronx, New York (Hotz, Hena, Gross);
Albert Einstein College of Medicine, Bronx,
New York (Hotz, Hena, Gross).
Corresponding Author: Elissa Gross, DO, MPH,
Children’s Hospital of Montefiore, 3415 Bainbridge
Ave, Bronx, NY 10467 (egross@montefiore.org).
Section Editor: Samir S. Shah, MD, MSCE.
Conflict of Interest Disclosures: None reported.
Additional Contributions: We thank the patient’s
family for granting permission to publish this
information.
2. Graham GN, Browne H. Primary bony tumors of
the pediatric spine. Yale J Biol Med. 2001;74(1):1-8.
3. Fuentes Ferrer M, Gutiérrez Torres L, Ayala
Ramírez O, Rumayor Zarzuelo M, del Prado
González N. Tuberculosis of the spine: a systematic
review of case series. Int Orthop. 2012;36(2):221-231.
4. Nussbaum ES, Rockswold GL, Bergman TA,
Erickson DL, Seljeskog EL. Spinal tuberculosis:
a diagnostic and management challenge. J Neurosurg.
1995;83(2):243-247.
5. Vadivelu S, Effendi S, Starke JR, Luerssen TG, Jea
A. A review of the neurological and neurosurgical
implications of tuberculosis in children. Clin Pediatr
(Phila). 2013;52(12):1135-1143.
7. Kumar R, Das RK, Mahapatra AK. Role of
interferon gamma release assay in the diagnosis of
Pott disease. J Neurosurg Spine. 2010;12(5):462-466.
8. Cruz AT, Starke JR. Clinical manifestations of
tuberculosis in children. Paediatr Respir Rev. 2007;
8(2):107-117.
9. Committee on Infectious Diseases. Red Book:
2012 Report of the Committee on Infectious Diseases.
29th ed. Elk Grove Village, IL: American Academy of
Pediatrics; 2012.
10. Varatharajah S, Charles YP, Buy X, Walter A,
Steib JP. Update on the surgical management of
Pott’s disease. Orthop Traumatol Surg Res. 2014;
100(2):229-235.

REFERENCES 6. Kumar M, Kumar R, Srivastva AK, et al. The

efficacy of diagnostic battery in Pott’s disease:
1. Sponseller PD. Evaluating the child with back a prospective study. Indian J Orthop. 2014;48(1):
pain. Am Fam Physician. 1996;54(6):1933-1941. 60-66.

1102 JAMA Pediatrics November 2016 Volume 170, Number 11 (Reprinted) jamapediatrics.com

Copyright 2016 American Medical Association. All rights reserved.

Copyright of JAMA Pediatrics is the property of American Medical Association and its
content may not be copied or emailed to multiple sites or posted to a listserv without the
copyright holder's express written permission. However, users may print, download, or email
articles for individual use.