Downloaded from http://spcare.bmj.com/ on September 11, 2015 - Published by group.bmj.com

Case report

Unusual aetiology of malignant spinal cord compression Jason Boland,1,2 Adrienne Rennick1

1

Barnsley Hospice, Barnsley, UK Hull York Medical School, University of Hull, Hull, UK

2

Correspondence to Dr Jason Boland, senior lecturer and honorary consultant in palliative medicine, Hull York Medical School, Hertford Building, University of Hull, Hull HU6 7RX, UK; [email protected] Received 25 September 2012 Revised 8 February 2013 Accepted 7 March 2013

To cite: Boland J, Rennick A. BMJ Supportive & Palliative Care 2013;3:200–202.

200

ABSTRACT Malignant spinal cord compression (MSCC) is an oncological emergency requiring rapid diagnosis and treatment to prevent irreversible spinal cord injury and disability. A case is described in a 45-year-old male with renal cell carcinoma in which the presentation of the MSCC was atypical with principally proximal left leg weakness with no evidence of bone metastasis. This was due to an unusual aetiology of the MSCC as the renal carcinoma had metastasised to his left psoas muscle causing a lumbosacral plexopathy and infiltrated through the intervertebral disc spaces, initially causing left lateral cauda equina and upper lumbar cord compression, before complete spinal cord compression. This case illustrates the varied aetiology of MSCC and reinforces the importance of maintaining a high index of suspicion of the possibility of spinal cord compression.

INTRODUCTION Malignant spinal cord compression (MSCC) is a relatively common emergency seen by palliative medicine physicians and oncologists which requires rapid diagnosis and treatment to prevent irreversible spinal cord injury and disability.1 It is most often caused by haematogenous infiltration of the vertebrae and less frequently by direct tumour invasion into the spine or by deposition of tumour cells causing compression of the spinal cord. Metastases to the spinal column occur in 3%–5% of all patients with cancer and may cause pain, vertebral collapse and MSCC. In the USA, 3.4% of patients dying from cancer are hospitalised with MSCC.2 Presentation of MSCC is generally with spinal pain, which may be localised or radicular (including limb radiation), and can be accompanied by numbness or paraesthesia. Weakness might also occur, and in advanced stages bladder and bowel control can be lost (table 1). In a population-based data analysis of over 15 000 cases of MSCC from the USA, the most prevalent underlying diagnoses in

patients with MSCC were lung cancer (25%), prostate cancer (16%) and multiple myeloma (11%).2 A Scottish prospective observational study of 319 patients also showed breast cancer to be a common underlying diagnosis.1 In this study, the majority of patients diagnosed with MSCC already had an established diagnosis of cancer (77%), but in 23% of patients MSCC was the first presentation of malignancy.1 At diagnosis, 82% of patients with MSCC were unable to walk or needed assistance. In all, 94% had pain (84% severe pain), which was present for a median duration of 3 months, and had a nerve root distribution in 79%.1 We present and discuss a rare cause of MSCC in a patient with renal cell carcinoma, which metastasised to the psoas muscle and tracked through the intervertebral space to compress the lateral cauda equina and spinal cord.

CASE A 45-year-old male with renal cell carcinoma, lymph node and lung metastases diagnosed 6 months earlier was referred to the hospice with back pain and decreased mobility. Although he had a past medical history of chronic back pain this had significantly increased over the previous week. He was usually independently mobile but his mobility had decreased over the preceding 3 days to such an extent that on presentation he was bedbound. The pain was in his lower back which radiated to his left hip and anterior thigh and was worse at night. He reported that his legs felt cold, but denied pins and needles. There were no urinary symptoms and he had a long history of constipation which was unchanged. He had intermittent stabbing pain in his rectum, which was not related to defecation. Both legs had become increasingly swollen over the previous month.

Boland J, et al. BMJ Supportive & Palliative Care 2013;3:200–202. doi:10.1136/bmjspcare-2012-000373

Downloaded from http://spcare.bmj.com/ on September 11, 2015 - Published by group.bmj.com

Case report Table 1 Comparison of the main differentiating factors among spinal cord compression, cauda equina compression and peripheral lumbosacral plexopathy Spinal cord compression

Cauda equina syndrome

Lumbosacral plexopathy

Upper motor neurone: pressure on spinal cord Radicular pain at level of lesion, and sometimes below, sensory level

Lower motor neurone: pressure on spinal nerve roots

Tone

Increased

Normal or reduced

Clonus Reflexes

Sometimes Absent at level of lesion and increased below level (may be absent for few days after initial insult due to spinal shock) Extensor Sensory loss below level of affected dermatome Urinary and faecal incontinence: late

Absent Reduced or absent, may be asymmetrical (occasionally normal)

Lower motor neurone: pressure on L1–L4 and/or L5–S5 nerve roots Aching, pressure like or stabbing, unilateral: site depends on which roots affected Normal (occasionally reduced if extensive involvement) Absent Reduced or absent, may be asymmetrical (occasionally normal)

Aetiology Pain

Plantars Sensation Sphincter control

Low back, hip, thighs and legs, may be unilateral or bilateral (depending on site of lesion)

Flexor/absent Saddle anaesthesia in midline cauda equina lesions, dermatomal in lateral lesions Urinary and faecal incontinence early with midline cauda equina lesions (in lateral lesions, leg weakness and reduced reflexes occur before sphincter disturbance)

On examination he had tenderness over his upper lumbar spine. Neurological examination demonstrated normal tone in both legs and no clonus. His left leg was weak proximally with power 2/5 in his hip flexors and 2+/5 in his knee extensors. There was also a mild reduction in power (4/5) in his distal left leg and diffusely (4/5) in his right leg. The left knee reflex was absent and the left ankle reflex was reduced. The right lower limb reflexes were brisk. Both plantar responses were down going. Sensation to light touch was intact with no saddle anaesthesia. Review of previous chest, abdomen and pelvic CT scans 1 month earlier and a bone scan 3 months

Flexor/absent Unilateral lower limb sensory loss in radicular pattern Urinary and faecal incontinence uncommon for unilateral plexopathy

earlier showed no evidence of bony disease, but a left psoas metastasis, which along with the focal neurological signs made spinal cord compression an unlikely diagnosis. However, in view of the very high clinical suspicion, an urgent whole spine MRI scan was performed which showed diffuse malignant infiltration of the left psoas muscle, with penetration through the intervertebral disc spaces, causing compression of the spinal cord at L1 and also the left lateral aspect of the superior cauda equina (figure 1). As there was no surgical option he was administered 16 mg dexamethasone daily (commenced on presentation) and five fractions of radiotherapy (which started within 18 h

Figure 1 Spinal cord compression from malignant psoas muscle infiltration. (A) T1 sagittal MRI image showing tumour infiltration through the L1 and L2 intervertebral spaces; (B) T2 transverse (axial) MRI image showing the left renal cell carcinoma, psoas muscle metastasis and tumour invasion into the spinal cord.

Boland J, et al. BMJ Supportive & Palliative Care 2013;3:200–202. doi:10.1136/bmjspcare-2012-000373

201

Downloaded from http://spcare.bmj.com/ on September 11, 2015 - Published by group.bmj.com

Case report of presentation), but despite this his leg weakness steadily progressed, such that by a week later he had lost all power in both legs. These treatment modalities, along with polymodal pharmacotherapy, have been previously advocated.3 The back pain progressed to involve both legs and increased significantly in intensity. It was initially responsive to oxycodone, pregabalin and oral ketamine, but soon became so severe that he needed duloxetine, clonazepam and subcutaneous ketamine adding and titrating to achieve pain relief. He developed anaesthesia for light touch in the left L1 and L2 dermatomes which further progressed to involve the L3 and L4 dermatomes over the following 2 weeks. He also became incontinent of urine and faeces during this time and required catheterisation and regular bowel intervention.

The management options of spinal cord compression due to tumour penetrating through the intervertebral spaces include surgery, radiotherapy, steroids, opioids, non-steroidal anti-inflammatory drugs and adjuvant drugs for neuropathic pain; muscle relaxants such as benzodiazepines or baclofen may be needed to treat the muscle spasm.3 There has been a previous report of three patients with psoas muscle metastases in non-small cell lung cancer where radiotherapy was effective.5 In this rare cause of spinal cord compression, a detailed history and examination along with a high level of suspicion and urgent investigation enabled rapid diagnosis and treatment, which unfortunately, in this case, did not impact on the patient’s functional ability.

DISCUSSION This patient had an atypical presentation of spinal cord compression which was caused by an unusual aetiology. The diagnosis could have been impeded as he did not have evidence of spinal metastases on recent imaging. By having a high level of suspicion, in view of the rapidly progressive weakness and severity of the back pain, exclusion of MSCC was paramount. Clear goals of care were established and reviewed with the patient and family, and after discussion with the radiologist and oncologist his management was optimised. The mixed clinical presentation and medical need for a definitive diagnosis had to be balanced with transferring a patient with severe pain to the nearest oncology centre. This is a rare presentation of spinal cord and cauda equina compression secondary to renal cell carcinoma metastasising to the left psoas muscle (causing a lumbosacral plexopathy) which then penetrated through the L1/L2 intervertebral spaces to compress the left lateral aspect of the superior cauda equina and lumbar spinal cord, before causing complete cord compression (table 1). Neoplastic lumbosacral plexopathy is caused by malignant infiltration of the L1–L4 and L5– S5 nerve roots as they traverse the psoas muscle, leading to pain and sensorimotor deficits. However, muscle involvement by cancer is rare as movement, high lactate and low pH inhibit neoplastic infiltration3 and there is only a very limited literature of psoas muscle metastasis from renal cell carcinoma.3 4

Acknowledgements The authors would like to

202

acknowledge Jane Alty, Neurology SpR, Leeds Teaching Hospitals NHS Trust and Ingrid Jolley, Consultant Radiologist, Sheffield Teaching Hospitals NHS Trust for their assistance with writing the case report. Contributors Both authors have made a substantial

contribution to this article. Competing interests None. Patient consent Obtained. Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES 1 Levack P, Graham J, Collie D, et al. Don’t wait for a sensory level—listen to the symptoms: a prospective audit of the delays in diagnosis of malignant cord compression. Clin Oncol (R Coll Radiol) 2002;14:472–80. 2 Mak KS, Lee LK, Mak RH, et al. Incidence and treatment patterns in hospitalizations for malignant spinal cord compression in the United States, 1998–2006. Int J Radiat Oncol Biol Phys 2011;80:824–31. 3 Stevens MJ, Atkinson C, Broadbent AM. The malignant psoas syndrome revisited: case report, mechanisms, and current therapeutic options. J Palliat Med 2010;13:211–16. 4 Camnasio F, Scotti C, Borri A, et al. Solitary psoas muscle metastasis from renal cell carcinoma. ANZ J Surg 2010;80:466–7. 5 Strauss JB, Shah AP, Chen SS, et al. Psoas muscle metastases in non-small cell lung cancer. J Thorac Dis 2012;4:83–7.

Boland J, et al. BMJ Supportive & Palliative Care 2013;3:200–202. doi:10.1136/bmjspcare-2012-000373

Downloaded from http://spcare.bmj.com/ on September 11, 2015 - Published by group.bmj.com

Unusual aetiology of malignant spinal cord compression Jason Boland and Adrienne Rennick BMJ Support Palliat Care 2013 3: 200-202

doi: 10.1136/bmjspcare-2012-000373 Updated information and services can be found at: http://spcare.bmj.com/content/3/2/200

These include:

References Email alerting service

This article cites 5 articles, 0 of which you can access for free at: http://spcare.bmj.com/content/3/2/200#BIBL Receive free email alerts when new articles cite this article. Sign up in the box at the top right corner of the online article.

Notes

To request permissions go to: http://group.bmj.com/group/rights-licensing/permissions To order reprints go to: http://journals.bmj.com/cgi/reprintform To subscribe to BMJ go to: http://group.bmj.com/subscribe/

Unusual aetiology of malignant spinal cord compression.

Malignant spinal cord compression (MSCC) is an oncological emergency requiring rapid diagnosis and treatment to prevent irreversible spinal cord injur...
129KB Sizes 3 Downloads 5 Views