1 Introduction

Acute presentation of LBP in a young adult may have varied aetiological reasons. Any mechanical or postural back pain is the one of the commonest benign causes in young adults.¹ The association of LBP with neurological deterioration due to SEA has been reported rarely.^2–4

A SEA has low incidence rate and has been presenting rarely.^4–6 However, with an increasing elderly age group, increasing spinal instrumentation, and increased risk factor association, the rate of SEA has also increased from 1/10,000 to 5.1persons/1000 patients.^1,3,5,7 The pyogenic pathogens are the common causative organisms.⁸

In developing countries, the spine affection by MBT presents commonly with chronic low back pain. The back pain with paraparesis due to MBT may manifest as one of the common causes for non-traumatic paralysis.⁸ MBT generally leads to bony destruction, abscess formation, intervertebral disc affection, vertebral collapse and kyphotic deformity.⁸ Acute on chronic presentation of MBT may present with diagnostic dilemma.

We present a case study in a young male presenting in the ED with an acute severe unbearable LBP of two days origin without any trauma, fever or significant past history. There was no neurological deficit at the time of presentation. During his short stay of few hours in the ED, he showed progressive neurological deterioration with weakness in the lower limbs. The orthopaedic team and emergency physicians were alerted to the developing emergency. A detailed secondary clinical and neurological assessment was done to identify an impending cauda equina. An MRI of the lumbar spine revealed and confirmed a SEA at the L4-S1 level. The uncommon presentation has serious implications. As clinicians, one needs to be aware of the rare presentations for acute LBP to manage the surgical emergency.

2 Case report

A 27-year-old male, presented to ED with a history of severe pain in back for two days. No past history of fever, trauma, cough, loss of weight or loss of appetite was available. The pain progressed and was not relieved by intravenous analgesics. Vital signs were stable, temperature of 98.4° Fahrenheit, and no neurological deficit was noted. However, the pain intensity increased during the next five to 6 ​h of the observation period and lead to an inability for him to stand and move his lower limbs. This presented as an acute crisis requiring consideration for the immediate management. On secondary clinical evaluation, an active bilateral straight leg-raising test was not possible. Motor sensory deficit was present in both lower limbs. On motor system examination both lower limbs had hypotonia and power graded as 2 out of 5 for muscles acting around hip joint, knee joint and ankle joint. Deep tendon reflexes were diminished. Early signs of an impending urinary retention and perianal hypo aesthesia were noticed. Investigations revealed 10.8 ​gm% haemoglobin, total leucocyte count of 9300 ​cells/cubic mm, erythrocyte sedimentation rate of 30 mm/hr, C reactive protein of 60mg/L, with liver and kidney function tests within normal limits. Patient tested negative for viral markers and his coagulation profile was within normal limits.

The magnetic resonance imaging (MRI) of lumbar spine showed large lobulated heterogenous lesion measuring approximately 1.6 (AP) x 2.1 (TR) x 4.1 (CC) cm lying in the dorsal side of the epidural space at the level of L4-L5 intervertebral disc space to the level of L5-S1 intervertebral disc space. It showed subtle iso to hyperintense signal on T1 and hypointense walls to hyperintense centre on T2W images with multiple thin linear septa (Fig. 1). Another similar lobulated heterogenous lesion was seen in the right posterior paraspinal soft tissues extending from L4 to S1 with oedematous changes in the adjoining soft tissues likely due to soft tissue collection (Fig. 2). There was severe narrowing of the thecal sac with anterior displacement and impingement of the cauda equina (Fig. 3). The right sided pedicles of L4 and L5 vertebra showed marrow hyperintensity. The findings confirmed a SEA, with non-specific appearance and a probable tubercular aetiology.

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Fig. 1 MRI T2W sequences show large lobulated heterogenous lesion on the dorsal side of the epidural space (a) at the level of L4-S1 intervertebral disc space with hypointense walls to hyperintense centre with multiple linear septa (marked with white arrow) and (b) posterior paraspinal soft tissue collection (marked with white arrow).

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Fig. 2 MRI T1W sequences show large lobulated heterogenous lesion in epidural space (a) at the level of L4-S1 intervertebral disc space with iso to hyperintense signal (marked with white arrow) and (b) posterior paraspinal soft tissue collection with pedicle involvement (marked with white arrow).

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Fig. 3 MRI T2W axial sequence shows (a) thecal sac compression with anterior displacement and impingement on the cauda equina at the level of L4-L5 intervertebral disc space (marked with white arrow) and (b) T1W axial sequence shows intrathecal collection (marked with white arrow).

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Emergency management with surgical spine decompression with laminectomy at L4-L5 level and evacuation of the spinal epidural abscess was done. Prone positioning with midline approach was used. Paraspinal collection was sent for biopsy and culture sensitivity. Soft tissue collection further guided to the lesion along the epidural space in relation to lumbar L4-L5 level. A unilateral laminectomy allowed further spinal decompression with abscess evacuation. A thorough lavage followed and a drain was kept in situ. An intensive care monitoring and observation for neurological deterioration followed. The acute pain settled to bearable proportions in the immediate postoperative period. The biopsy confirmed caseous granulomatous lesion of MBT aetiology (Fig. 4). A standard drug regime of antitubercular medications was initiated in dosages adjusted according to the body weight. Drugs were withdrawn in phases based on the clinical and biochemical marker evaluation in the regular follow up visit. He recovered neurologically to grade 4/5 power without any sphincter dysfunction in the next four months. Ability to ambulate without support or assistance was regained. At fourteen months follow up, clinical evaluation and biochemistry markers for inflammation were normal. MRI was advised for however, due to financial constraints no further imaging was possible.

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Fig. 4 Histopathological microscopic examination show caseating granulomatous lesion comprising of langerhans giant cells, epitheloid cells, lymphocytes and plasma cells with necrosis.

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3 Discussion

An acute LBP may be one of the commonest orthopaedic presentation in the outpatient clinics. An emergency presentation of acute LBP may be more commonly due to trauma, pyogenic infection, mechanical or postural, and neoplastic aetiology.⁵ Normally, the young adults are more tolerant to pain as compared to an elderly. They may present late to the clinicians as their threshold for pain may be high. A young adult may rather present commonly with LBP of chronic onset or pain associated with the advanced or late stages of the disease presentation.⁸ In ED, an acute LBP presentation in a young adult without any associated symptoms require close observation and careful diagnostic evaluation. Any persistence of pain or deterioration of neurological status should raise an alarm for the emergency physician and orthopaedic clinicians.

An acute SEA with pyogenic abscess may commonly develop due to either Streptococcus, Staphylococcus, Brucella, Salmonella, Klebsiella and/or Haemophilus species variants.^1–3,8–12 Aetiological factors are associated uncommonly with acute on chronic presentation of SEA due to MBT, and rarely due to Pasteurella multocida following bites caused by cats and dogs.^11,13 The MBT has been reported as a causative organism in two out of eleven SEA cases but with a gradual onset presentation in an elderly age group associated with medical comorbidities.¹¹ An immune-compromised state due to AIDS affection presented with SEA of MBT aetiology with history of LBP of three months duration and fifteen days of paralysis.¹⁴ Review article suggest <1% MBT induced SEA.¹ An acutely developing SEA due to MBT without any known risk factors or any past history of significance has been rarely reported.

The predisposing risk factors need to be identified. They may include diabetes mellitus, immunocompromised states, local or systemic infection, intravenous drug abusers, trauma, or surgical intervention.^{3,4,6,8,9,11,13,14} Around 20% may be idiopathic in nature.^4,5 The spread of infection to epidural space is hematogenous in 50%, contiguous spread 33% and unrecognised in other cases.^1,5,13

The triad of low back pain, fever and neurological deficit characterizes the common symptoms associated with SEA.¹ However, the triad may present only in 20% of the cases and in early phases of disease their absence may mislead the clinicians. Our case had an acute onset LBP in a young adult with no known identifiable risk factors with progression to neurological deficit within few hours of the presentation in the ED. ESR and CRP have been identified as highly sensitive and moderately specific for the workup and diagnosing of SEA.¹⁵ In the study on 86 patients (55 in control group and 31 in study group after diagnostic guideline implementation), authors observed that motor deficit was present in 81.8% cases of the control group and 19.6% cases in the study group after early detection guideline implementation. Diagnostic delays were observed in 83.6% in the control group of 55 patients and much less up to 9.7% in the study group of 31 patients after the diagnostic guideline implementation.¹⁵

Conservative measures and medication alone have a limited role. Treatment for an acute paraparesis induced due to SEA require emergency spine decompression and abscess evacuation with adjuvant intravenous empirical antimicrobial antibiotic coverage.^2,3,6,10 Poor medical condition, children, and/or debilitated unfit medical status cases of SEA, have been occasionally treated by percutaneous fluoroscopic drainage of the abscess.¹⁰ The biopsy confirmation and culture sensitivity may guide further regarding the long-term definitive use of the antimicrobial regime.⁸ In our case, the MBT aetiology responded to the standard antitubercular drug regime to give us a favourable clinical outcome.

An increasing LBP, motor deficit, dorsal located SEA are independent poor outcome factors.⁷ The prognosis should be guarded for any neurological recovery in SEA of late or undiagnosed nature.^4,5 The severity and duration of preoperative neurological deficit are important predictors of functional outcomes with diagnostic delays presenting with poor outcomes.¹ High mortality rates up to 7%–20% have been associated with SEA.^3,5,7

4 Conclusion

The clinicians should consider SEA in the differential diagnosis for the acute onset LBP compounded with a developing acute paraparesis on presentation. Any missed or late diagnosed SEA may have poor outcomes and high mortality. MBT may respond to the standard antitubercular drug regime.

The case highlights the need to address an unexplained presentation of acute LBP minus the neurological deficit at first contact with a thorough clinical and radiological assessment in the ED to avert an emergency life threatening scenario.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Consent for publication

The patient was informed that data from the case would be submitted for publication and the patient gave written consent. The patient understands that his name and initials will not be published, and due efforts will be made to conceal his identity but anonymity cannot be guaranteed.

Ethic approval

Ethical approval was not required for this study in accordance with local guidelines.

Authors contribution and declaration

LT and GG contributed to the study conception, design, investigation and methodology.

GG and PD performed data collection and interpretation.

GG performed the literature search and prepared the original draft of the manuscript and reviewed the subsequent version with editing of the manuscript.

LT and PD did review analysis.

All authors commented on the previous versions of manuscript.

All authors read and approved the final version of manuscript.