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Education/Training

CE Article: Back Pain in EMS, Part 1

This article is available on our LMS for CE credit.

Objectives

Upon conclusion of this course, students will be able to:

  • Understand the scope of the epidemic of back pain among EMS personnel;
  • Articulate the mechanical and biopsychosocial origins of low-back pain;
  • Describe how lifting, posture, and body position can give rise to chronic pain syndromes;
  • Understand the current evidence base surrounding EMS-specific back pain. 

EMS professionals experience the highest rate of on-duty injury of all public safety professions.1 The number who experience lost work time is estimated to be greater than 8 per 100 full-time workers—at least three times higher than the rates of other healthcare professionals and the national average.2–5 

Sprains and strains affecting the back or neck are the most commonly diagnosed injuries.5 These are often attributed to lifting patients and other physical aspects of EMS duties. Among EMS professionals, back injuries result in a disproportionately higher rate of lost workdays than injuries affecting other body areas.2

Nearly 8 out of 10 Americans will experience acute back pain in their life.6 The vast majority have a favorable natural history of spontaneous recovery within the initial 4–6 weeks, with a smaller fraction experiencing persistent symptoms beyond this period.7,8 Nonetheless, back pain remains the leading cause of disability worldwide.9 A 2010 survey illustrated the burden of back pain among EMS professionals, finding half of respondents had experienced back or leg pain within two weeks of answering the survey.10 

Persons experiencing low-back pain often seek a specific diagnosis and express a “strong desire for clear, consistent, and personalized information on prognosis, treatment options, and self-management strategies related to healthcare and occupational issues.”11  

Unfortunately, misconceptions about causes, prevention, and effective management strategies are common. Internet resources on low-back pain, even from reputable organizations, often provide inaccurate or unhelpful information.12 This two-part article will provide an evidence-based exploration of common misconceptions about pain and discuss the prevention and treatment of back pain with a focus on factors relevant to EMS professionals.

What Causes Back Pain?

The historical biomedical paradigm views the body as a machine composed of individual parts that are easily damaged or worn out with time and use. From this perspective, if an individual’s back pain started while lifting, it is assumed this pain reflects acute structural damage resulting from the mechanical forces placed upon the tissues. Similarly, if an individual experiences worsening pain over time, this is interpreted as evidence of progressive damage or use-related “wear and tear.” 

The available evidence reveals limitations to this view, principally that machines lack the essential feature of biological organisms: the ability to adapt to a variety of stimuli, including mechanical loading.13  

Most individuals experiencing low-back pain do not have a specific, identifiable source that can be confidently deemed to be a pain generator, even with the use of modern diagnostic technology.9 A number of findings that can be seen on radiologic imaging are often assumed to represent sources of pain, such as disk degeneration, disk herniation, and facet joint abnormalities.14 These findings may sound debilitating, particularly when presented to patients, but they are also common among asymptomatic individuals. A 2015 review found that among patients who had no back pain, more than 50% had evidence of disk degeneration by age 30, disk bulge by age 40, and facet degeneration by age 50.15 This suggests these radiographic changes may represent normal age-related findings 
rather than pathology. 

Given that these radiographic findings are so common in persons without symptoms, we should question the assumption of a direct causal relationship with back pain. Further, when these findings are present on imaging in persons without symptoms, they do not appear to reliably predict development of future symptoms.16  

Under the traditional assumption that such structural changes are the direct cause of pain, attenuating or excising these lesions would be expected to result in relief. However, contrary evidence continues to accumulate. For example, interventions including disk replacement surgery, spinal fusion, and radiofrequency ablation have failed to demonstrate clear efficacy for persistent low-back pain in trials.17–19 

The majority of persons with acute low-back pain experience significant improvement in symptoms by six weeks, even when structural findings on imaging remain unchanged.8 The presence or absence of abnormalities on MRI of the lumbar spine does not predict symptomatic recovery.20 Furthermore, among persons with sciatica, those who have MRI evidence of disk herniations have a higher rate of recovery than those who have normal disks,21 and in fact, a majority of herniations spontaneously heal on their own.22  

The sum of evidence suggests the vast majority of back pain cannot be reduced to an isolated structural or mechanical problem. Rather, it is a complex biopsychosocial experience that requires a broader clinical perspective.

Beyond Mechanical Causes

The biological function of pain is an experience that reflects the apprehension of threat and motivates goal-directed behavior toward protection and survival.23,24  

The traditional model of pain holds that pain is transmitted directly from receptors in the tissue to the brain, where it is passively sensed in direct proportion to the intensity of the peripheral stimulus. In this way pain would represent an accurate reflection of current tissue status.25  

We have since learned that pain is far more complex than that. We now recognize the brain receives afferent input from tissue nociceptors (threat receptors) that can activate in response to chemical, mechanical, or thermal stimuli—although their sensitivity can be influenced by a variety of local and systemic factors. These signals are integrated with other sensory data, biological factors (such as immune and endocrine processes), and psychosocial factors such as beliefs, fears, behaviors, expectations, and past experiences. The system is regulated at multiple levels and exhibits features of adaptation and plasticity over time. The complex integration of these factors then relates to an emergent experience an individual labels as “pain.”

Under the traditional view treating tissue pathology is the only viable option to manage pain. Fortunately, our modern understanding of the complexity of pain provides us with a wide range of potentially modifiable targets. In the setting of a strong therapeutic alliance between patient and clinician, a collaborative approach can address these targets. Fatigue can be mitigated, beliefs can be challenged, fears can be confronted, and past experiences can be explored and better understood. Working through this process can alter an individual’s learned responses to the experience of pain. This is an active area of research.26  

Certain beliefs and behaviors are associated with poorer outcomes in acute musculoskeletal pain, including higher pain intensity and greater levels of pain-related disability, which are related to a higher risk of developing chronic pain.9 Two common factors influencing outcomes in back pain are catastrophizing, a belief that something is far worse than it actually is, and fear avoidance, avoiding an activity because of an expected negative outcome.27

In these ways the emotional significance of a pain experience and the meaning assigned to symptoms are critically important in driving behavioral responses. They are therefore also important to collaboratively explore and understand to modify behavioral responses in the face of pain.9  

Self-efficacy, a belief in the ability to influence events in one’s life—and specifically to manage pain symptoms—is strongly associated with intensity of pain, development of disability, level of distress, and pain severity.9,28  

Many of these psychological factors and behavioral responses are learned based on social interactions.29,30 Behavioral responses may also be learned from peers. The report of a negative experience with back pain from a partner may influence how an individual responds to back pain of their own. 

Recognition of these beliefs and behaviors is important. A person who does not assume the worst possible outcome or meaning of pain, who does not fear movement due to the possibility of pain, and who has confidence they will recover is likely to experience lower pain intensity and less pain-related disability and will be less likely to progress to persistent pain. 

References

1. Suyama J, Rittenberger JC, Patterson PD, Hostler D. Comparison of public safety provider injury rates. Prehosp Emerg Care, 2009; 13(4): 451–5.

2. Maguire BJ, Hunting KL, Guidotti TL, Smith GS. Occupational injuries among emergency medical services personnel. Prehosp Emerg Care, 2005; 9(4): 405–11.

3. Studnek JR, Ferketich A, Crawford JM. On the job illness and injury resulting in lost work time among a national cohort of emergency medical services professionals. Am J Industr Med, 2007; 50(12): 921–31.

4. Reichard AA, Jackson LL. Occupational injuries among emergency responders. Am J Industr Med, 2010; 53(1): 1–11.

5. Reichard AA, Marsh SM, Tonozzi TR, Konda S, Gormley MA. Occupational Injuries and Exposures among Emergency Medical Services Workers. Prehosp Emerg Care, 2017; 21(4): 420–31.

6. Rubin DI. Epidemiology and risk factors for spine pain. Neurol Clin, 2007; 25(2): 353–71.

7. Carey TS, Garrett J, Jackman A, et al. The outcomes and costs of care for acute low back pain among patients seen by primary care practitioners, chiropractors, and orthopedic surgeons. The North Carolina Back Pain Project. New Engl J Med, 1995; 333(14): 913–7.

8. Menezes Costa LD, Maher CG, Hancock MJ, et al. The prognosis of acute and persistent low-back pain: a meta-analysis. CMAJ, 2012 Aug 7; 184(11): E613–E624.

9. Hartvigsen J, Hancock MJ, Kongsted A, et al. What low back pain is and why we need to pay attention. Lancet, 2018; 391(10,137): 2,356–67.

10. Studnek JR, Crawford JM, Wilkins JR 3rd, Pennell ML. Back problems among emergency medical services professionals: the LEADS health and wellness follow-up study. Am J Industr Med, 2010; 53(1): 12–22.

11. Lim YZ, Chou L, Au RT, et al. People with low back pain want clear, consistent and personalised information on prognosis, treatment options and self-management strategies: a systematic review. J Physiotherapy, 2019; 65(3): 124–35.

12. Ferreira G, Traeger AC, Machado G, O’Keeffe M, Maher CG. Credibility, Accuracy, and Comprehensiveness of Internet-Based Information About Low Back Pain: A Systematic Review. J Med Internet Res, 2019; 21(5): e13357.

13. Thielke S, Sale J, Reid MC. Aging: are these 4 pain myths complicating care? J Fam Pract, 2012; 61(11): 666–70.

14. Lutz GK, Butzlaff M, Schultz-Venrath U. Looking back on back pain: trial and error of diagnoses in the 20th century. Spine, 2003; 28(16): 1,899–905.

15. Brinjikji W, Luetmer PH, Comstock B, et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. Am J Neuroradiology, 2015; 36(4): 811–6.

16. Steffens D, Hancock MJ, Maher CG, et al. Does magnetic resonance imaging predict future low back pain? A systematic review. Eur J Pain, 2014; 18(6): 755–65.

17. Louw A, Diener I, Fernández-de-las-Peñas C, Puentedura EJ. Sham Surgery in Orthopedics: A Systematic Review of the Literature. Pain Medicine, 2017; 18(4): 736–50.

18. Mannion AF, Brox JI, Fairbank JC. Comparison of spinal fusion and nonoperative treatment in patients with chronic low back pain: long-term follow-up of three randomized controlled trials. Spine J, 2013; 13(11): 1,438–48.

19. Bagg MK, McAuley JH, Moseley GL, Wand BM. Recent data from radiofrequency denervation trials further emphasise that treating nociception is not the same as treating pain. Br J Sports Med, 2019; 53(13): 841–2.

20. de Schepper EI, Koes BW, Oei EH, et al. The added prognostic value of MRI findings for recovery in patients with low back pain in primary care: a 1-year follow-up cohort study. Eur Spine J, 2016; 25(4): 1,234–41.

21. el Barzouhi A, Vleggeert-Lankamp CL, Lycklama à Nijeholt GJ, et al. Magnetic resonance imaging in follow-up assessment of sciatica. New Engl J Med, 2013; 368(11): 999–1,007.

22. Chiu CC, Chuang TY, Chang KH, et al. The probability of spontaneous regression of lumbar herniated disk: a systematic review. Clin Rehab, 2015; 29(2): 184–95.

23. Cohen M, Quintner J, van Rysewyk S. Reconsidering the International Association for the Study of Pain definition of pain. Pain Rep, 2018; 3(2): e634.

24. Baliki MN, Apkarian AV. Nociception, Pain, Negative Moods, and Behavior Selection. Neuron, 2015; 87(3): 474–91.

25. Chen J. History of pain theories. Neurosci Bull, 2011; 27(5): 343–50.

26. O’Sullivan PB, Caneiro JP, O’Keeffe M, et al. Cognitive Functional Therapy: An Integrated Behavioral Approach for the Targeted Management of Disabling Low Back Pain. Phys Ther, 2018; 98(5): 408–23.

27. Vlaeyen JWS, Crombez G. Behavioral Conceptualization and Treatment of Chronic Pain. Ann Rev Clin Psych, 2020; 16(1): 187–212.

28. Menendez ME, Ring D. Factors Associated with Greater Pain Intensity. Hand Clinics, 2016; 32(1): 27–31.

29. Kraljevic S, Banozic A, Maric A, et al. Parents’ pain catastrophizing is related to pain catastrophizing of their adult children. Int J Behav Med, 2012; 19(1): 115–9.

30. Palermo TM, Valrie CR, Karlson CW. Family and parent influences on pediatric chronic pain: a developmental perspective. Amer Psych, 2014; 69(2): 142–52.

Michael W. Supples, MD, NRP, is an academic emergency medicine physician and EMS fellow at the Indiana University School of Medicine and a deputy medical director in Indiana. 

Austin N. Baraki, MD, is an academic internist and assistant professor of medicine at Brooke Army Medical Center in San Antonio, Tex.

 

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