Drug-induced paraspinal myositis mimicking acute bilateral sciatica

Abstract

Although cocaine induced myopathy and myotoxicity are described in the literature, we report a rare case of cocaine induced paraspinal myositis presenting with acute sciatic symptoms. A 35-year-old man presented with acute left-sided sciatica and was discharged from the emergency department (ED). He subsequently attended ED the following day in severe pain and bilateral sciatic symptoms, but denied symptoms of neurogenic bowel/bladder disturbance. Clinical examination was limited by severe pain: focal midline lumbar tenderness was elicited on palpation, per rectal and limb examinations were within normal limits with no significant neurological deficit. He was admitted for observation and pain management. His blood tests revealed a leucocyte count of 21.5×10⁹/L, C reactive protein of 89 mg/L and deranged renal function with creatinine of 293 μmol/L. An urgent lumbar spine MRI was arranged to rule out a discitis or epidural abscess. Lumbar MRI did not demonstrate any features of discitis but non-specific appearances of paraspinal inflammation raised the suspicion of a paraspinal myositis. Creatinekinase (CK) was found to be 66329 IU/L and a detailed history revealed he was a cocaine user. Paraspinal muscle biopsy confirmed histological features compatible with myositis. Other serological tests were negative, including anti-GBM, ANCA, ANA, Rheumatoid factor, Hep B, Hep C, myositis specific ENA, Treponema pallidum, Borrelia burgdorferi, Rickettsia, Leptospira, EBV and CMV. There was good clinical response to treatment with prednisolone 20 mg OD with an improvement in renal function, CK levels and CRP. He had resumed normal activities and return to work at 6-week follow-up. A detailed social history including substance misuse is important in patients presenting to the ED—especially in cases of severe musculoskeletal pain with no obvious localising features. Drug induced myotoxicity, although rare, can result in symptomatic patients with severe renal failure.

Background

Cocaine is recognised as a cause of rhabdomyolysis, but it is very unusual for cocaine induced myotoxicity to present as a focal area of myositis. To our knowledge, there are no previous reported cases in the literature of cocaine induced paraspinal myositis.

Case presentation

A 35-year-old male office worker presented with a 24-hour history of lower back and progressive right sided buttock pain radiating down the posterior lower limb down to the sole of the foot. He had presented similarly the previous night on the contralateral side, diagnosed with acute left sided sciatica and discharged with analgesia and physiotherapy follow-up. His symptoms were now bilateral, associated with numbness and paraesthesia in the gluteal region and severe in nature, rendering him unable to mobilise. There was no history of trauma, arthropathy, preceding illness, foreign travel, constitutional symptoms including fever, night sweats, weight loss or localising symptoms of sepsis. As a teenager, he used to experience lower back spasms when jogging and had experienced a similar self-limiting episode 3 years ago. He had no other significant medical history or family history and no prior hospital admissions.

Clinically, the patient was apyrexial but in excruciating pain at rest. On physical examination, his cardio-respiratory and abdominal examinations were unremarkable. There was no renal angle tenderness but marked buttock, lumbar and paraspinal tenderness. Limb examination revealed intact distal pulses and capillary refill time <2 s. Pain precluded accurate assessment of neurological function, however the tone was symmetric and reflexes dull throughout. There was an impression of reduced knee extension (MRC 4/5) on the right. PR examination revealed intact anal tone and perineal sensation.

In the emergency department (ED), the patient was unable to pass urine. This remained the case following administration of 10 mg IV Morphine and a bladder scan showing a volume of 398 mL. Once on the ward, he required doses of oral opiates equivalent to 90 mg of oral Morphine during the first 24 hours of his admission in order to control his pain.

On detailed questioning, it later transpired that the patient had smoked crack cocaine 1 day prior to the onset of symptoms. He reported smoking approximately 4 g, however the exact chemical composition of the substance smoked cannot be confirmed. There was no history of overdose or loss of consciousness. He reported being an infrequent user of cocaine, using 2–3 times per year and last having used several months ago with no adverse effects. He also infrequently inhaled heroin nasally, but denied any other substance use including anabolic steroids, intravenous or oral recreational drugs.

Investigations

Urine dipstick test was positive for blood and protein. Initial blood tests showed Hb 151 g/L, MCV 86 fl, PLT 199×10⁹/L, urea 14.8 mmol/L, eGFR 21 mL/min, WBC 21.5×10⁹/L, neutrophils 18.7×10⁹/L, CRP 89 mg/L and creatinine 293 μmol/L, which peaked at 629 on day 3 of admission. A urinary toxicology screen was positive for cocaine and negative for methadone, amphetamines, MDMA and cannabis.

A non-contrast enhanced CT of the abdomen and pelvis (figures 1–3) showed mild perinephric fat stranding with no evidence of hydronephrosis. Abdominal ultrasound was normal. Given the history and laboratory results, an inflammatory/infective spinal pathology including discitis or epidural abscess was suspected. An urgent MRI of the lumbar spine (figures 4 and 5) showed no evidence of discitis or cauda equina compression. There was, however, heterogeneous changes in the lumbar paraspinal muscles, with increased signal on STIR images, consistent with changes that can be seen in myositis. Subsequently, his creatine kinase was found to be 66 329 IU/L. Four sets of blood cultures were negative for micro-organisms. Serological tests were negative, including anti-GBM, ANCA, ANA, Rheumatoid factor, Hep B, Hep C, myositis specific ENA, Treponema pallidum, Borrelia burgdorferi, Rickettsia, Leptospira, EBV and CMV. Following MDT discussion, a paraspinal muscle biopsy was carried out which revealed necrosis and focal intense infiltration by macrophages associated with proliferation of myoblast forming multinucleated giant cells, consistent with a focal myositis.

Figure 1.

Non-contrast CT abdomino-pelvic scan. Axial cut at the level of the kidneys demonstrating mild perinephric stranding (red arrows) consistent with non-specific features of inflammation; this is an atypical finding in paraspinal myositis. ES, erector spinae; MF, multifidus.

Figure 2.

Non-contrast CT abdomino-pelvic scan. Axial cut at the level of the anterior superior iliac spine demonstrating extensive subcutaneous oedema (red arrows). Consistent with a non-specific inflammatory process or prolonged period in the supine position. This may have been secondary to extensive pain preventing sitting-up and mobilising (green arrow marks normal fascial appearances).

Figure 3.

Non-contrast CT abdomino-pelvic scan. Midline sagittal cut from inferior half of T9 superiorly to coccyx demonstrating vertical extent of diffuse midline subcutaneous oedema (red arrows).

Figure 4.

MRI lumbar spine. T2 weighted axial cut at the level of the L4 superior endplate. Abnormal increased T2 hyperintensity bilaterally in the paraspinal muscles consistent with non-specific diffuse paraspinal muscle inflammation. ES, erector spinae; MF, multifidus.

Figure 5.

MRI lumbar spine. Sagittal paramedian images (A+B) demonstrating abnormal STIR signal bilaterally in the paraspinal muscles and adjacent fascia (red arrows).

Differential diagnosis

Infective

Discitis, epidural abscess, pyomyositis.

Inflammatory

Idiopathic, dermatomyositis, polymyositis, inclusion body myositis.

Rheumatological

Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), sarcoidosis.

Muscular dystrophies

Limb-girdle muscular dystrophy, nemaline myopathy, dyferlinopathies.

Endocrine

Hypo/hyperthyroidism, hyperparathyroidism, Cushing’s syndrome (steroid myopathy), Addison’s disease, pituitary disorders, diabetic polyradiculopathy.

Malignancy

Myopathy and paraneoplastic syndromes.

Drug/toxin-induced myotoxicity

Alcohol, colchicine, statins, ezetimibe, anti-retrovirals, anti-malarials, immunosuppressive therapy (steroids, leflunomide, TNF-alpha inhibitors), voriconazole, d-penicillamine, vincristine.

Metabolic

Hypokalaemia/hypophosphataemia, metabolic myopathy.

Neurological

Myasthenia gravis, Eaton-Lambert syndrome.

Psychiatric

Generalised anxiety and depressive disorders.

Treatment

The patient was managed with increasing doses of opiate analgesia before being started on 20 mg of Prednisolone daily.

Outcome and follow-up

The patient was admitted under the care of the acute general medical team in collaboration with the nephrologists and rheumatologists providing input. A systemic inflammatory myopathy was initially considered, given the highly raised CK levels. However, there were no other signs on examination and other joint and muscle groups were spared. Given the lack of infective symptoms or preceding illness in the history and radiological or clinical evidence of infection, empirical antibiotic treatment for possible pyomyositis was not initiated. On day 4 of admission, a history of cocaine use was elicited and he was reviewed by a toxicologist several days later. Up until this stage, a viral cause of myositis had remained a consideration due to daily low grade fevers of 37.5°C–37.7° C. Common viral serology testing was arranged as per the above listed investigations. However, once the results of the relevant investigations were known a diagnosis of cocaine induced myositis was agreed by the specialist teams.

Paraspinal muscle biopsy was consistent with a drug-induced myositis. The patient’s renal function and inflammatory markers eventually improved and symptoms responded to analgesia and physiotherapy. He was discharged with a course of prednisolone, with an excellent clinical and biochemical response on 6-week review in rheumatology outpatients. The patient is now fully back to work as an office-worker.

Discussion

We have presented a case of acute onset lumbar back pain with bilateral sciatic symptoms, raised Creatinine and highly raised CK. Symptom onset was less than 24 hours after smoking cocaine and a diagnosis of cocaine induced myositis was agreed by a multidisciplinary team following extensive clinical, biochemical, serological, radiological and histological investigation.

Myositis is an inflammatory myopathy that can result in rhabdomyolysis due to direct damage to muscle sarcolemma and consequent release of myoglobin and its toxic metabolites into the systemic circulation.¹ The differential diagnosis of an idiopathic inflammatory myopathy includes dermatomyositis, polymyositis and inclusion body myositis. However, the differential widens considerably when considering all causes of myositis. Myositis from infective disease can present with myalgia, acute weakness and rhabdomyolysis. Viral infections are the most common systemic infectious aetiology, with myalgia being the most common symptom.² ‘Overlap syndromes’ describe connective tissue diseases with associated inflammatory myopathies. These can occur in rheumatoid arthritis or systemic lupus erythematosus, however they are more commonly seen in less defined conditions such as mixed connective tissue disease.³ Endocrine causes include hypo/hyperthyroidism, hyperparathyroidism, Cushing’s syndrome (steroid myopathy), Addison’s disease, pituitary disorders and diabetic polyradiculopathy. These can present with myalgia and proximal muscle weakness, but are not commonly associated with a rise in CK. The exceptions are hypothyroidism and hypoparathyroidism, which raise CK levels due to prolongation of the muscle relaxation phase and sustained tetany.⁴

Malignancy can cause paraneoplastic effects through tumour produced hormones entering the bloodstream, or through the effects of antibodies produced by the body in response to the malignancy. These can manifest as myalgia and rapidly progressing muscle weakness, with an associated rise in CK. There is also a higher incidence of malignancy in patients with an idiopathic inflammatory myositis, particularly dermatomyositis.⁵

The most common drug-induced myopathies are from glucocorticoids and lipid lowering agents. Chronic glucocorticoid treatment causes proximal weakness accompanied by other manifestations of Cushing’s syndrome and the effects are dose/time dependant. CK values are usually normal. Myalgia and muscle tenderness from myotoxicity related to HMG-CoA reductase inhibitors (statins) is also dose/time dependant and due to increased release of calcium ions from muscle fibre mitochondria and the sarcoplasmic reticulum.⁶

Myopathies with elevated CK can be seen with recreational drugs such as cocaine, heroin and amphetamines. Intravenous self-administration can cause pain, haemorrhage, necrosis and local infection at the site of injection. Myotoxicity from cocaine can be due to several direct and indirect mechanisms. Cocaine directly inhibits the reuptake of nor-adrenaline at alpha adrenergic receptors, causing intracellular calcium levels to rise within muscle cells leading to cell damage.⁷ Cocaine also causes arterial vasoconstriction and subsequent muscle ischaemia that is potentiated by concomitantly increased sympathomimetic activity. Another mechanism of rhabdomyolysis following recreational drug use is direct muscle compression and ischaemia following long periods of immobilisation on a hard surface, due to acute intoxication and subsequent reduction in cognitive state. A review of 102 cases of sympathomimetic toxicity found that 42% developed rhabdomyolysis.⁸ Of the 39 cases of cocaine toxicity with associated rhabdomyolysis presenting to a Miami hospital over an 8-year period, a third of these patients developed acute renal failure and 6 of them died.⁹ The finding of perinephric fat stranding in the case presented here (figure 1), while commonly seen in conditions such as chronic kidney disease or obstructive uropathy, is a unique finding for a case of rhabdomyolysis with acute kidney injury and is likely due to a local inflammatory response.

Our case is unusual in that the patient’s symptoms and radiological signs were confined to a focal area of paraspinal myositis and were caused by a cocaine induced myotoxicity in the absence of any signs of localised infection. A similar case has been reported in the USA of cocaine induced rhabdomyolysis with acute renal failure and evidence of paraspinal muscle oedema on MRI.¹⁰ The patient in this case was a 50-year-old male who presented with acute, severe lower back pain on a background of degenerative lumbar stenosis and chronic lower back pain. He denied recreational drug use but his urine tested positive for cocaine. MRI demonstrated increased signal on T1 weighted images of the lumbar paraspinal muscles with associated reduction in T1 weighted signal. There were no other published cases in the literature identified on PubMed search of a cocaine induced focal myositis causing localised symptoms. One published case of lumbar paraspinal myositis with an associated L3 radiculopathy¹¹ was the result of a bacterial abscess causing a localised pyomyositis. Another case report describes an episode of paraspinal myositis in a Spanish patient following cocaine use,¹² however this was cocaine administered intravenously resulting in an infective pyomyositis due to pathogens associated with IV drug use. It is certainly possible in our case that, contrary to the reported history, the patient experienced a period of unconsciousness following recreational drug use, resulting in local muscle compression and ischaemia, accounting for his myositis.

Learning points.

• Sympathomimetic toxicity can result in significant rhabdomyolysis.

• Cocaine can cause a focal myositis in addition to a systemic rhabdomyolysis.

• When considering systemic causes for a focal presentation of myositis, prior physical insults to the area should be considered and a thorough social/drug history is imperative in all patients.