Back Pain

Question 1

What is spinal cord compression?

Answer 1

Acute spinal cord compression is a neurosurgical emergency.

Rapid diagnosis and management are essential to have the highest chances of preventing permanent loss of function.

Question 2

Causes of spinal cord compression

Answer 2

Trauma 
Tumours 
Prolapsed disc 
Epidural or subdural haematoma 
Inflammatory disease
Infection 
Cervical spondylitis myelopathy 
Spinal manipulation

Question 3

Features of trauma causing spinal cord compression

Answer 3

Trauma (including car accidents, falls and sports injuries):
o There is usually either vertebral fracture (most common in cervical vertebrae) or facet joint dislocation.
o Complete transection of the spinal cord can occur.
o Hemisection of the spinal cord can occur and is known as Brown-Séquard’s syndrome. It is usually caused by a penetrating trauma.

Question 4

Features of tumours causing spinal cord compression

Answer 4

o These can include bone tumours, primary or metastatic tumours, lymphomas, multiple myeloma and neurofibromata.

o Acute myelopathy in patients with cancer can also be caused by irradiation, paraneoplastic necrotising myelitis, ruptured intervertebral disc and meningeal carcinomatosis with spinal cord involvement.

Question 5

Features of prolapsed intervertebral disc causing spinal cord compression

Answer 5

o L4-L5 and L5-S1 are the most common levels for disc prolapse. Large disc herniations can cause cauda equina syndrome

o Cervical disc herniation can also occur.

Question 6

Features of inflammatory disease causing spinal cord compression

Answer 6

• Inflammatory disease, especially rheumatoid arthritis:

o In rheumatoid arthritis there is often considerable weakness of the ligament that holds the odontoid peg. If this rupture, the atlas can slip forward on the axis and compress the high cervical spine.

Question 7

Features of epidural or subdural haematoma causing spinal cord compression

Answer 7

• An epidural or subdural haematoma:

o There may be a history of trauma, a recent spinal procedure and/or the patient may be on anticoagulant therapy.

Question 8

Features of infections causing spinal cord compression

Answer 8

• Infection:
o Spinal infections can be acute or chronic.

o Acute infections are usually bacterial; chronic infections are usually due to tuberculosis or fungal infection.

o Vertebral osteomyelitis, discitis or haematogenous spread of infection can lead to an epidural abscess.

Question 9

Features of cervical spondylitis causing spinal cord compression

Answer 9

o The ageing process can lead to narrowing of the spinal canal due to osteophytes, herniated discs and ligamentum flavum hypertrophy.

o In advanced stages, it can cause spinal cord compression.

Question 10

Features of spinal manipulation causing spinal cord compression

Answer 10

o Damage to the spinal cord may be a very rare complication of chiropractic or osteopathic manipulation of the neck.

Question 11

Red flag signs suggesting spinal compression?

Answer 11

• Red flags that suggest spinal compression include:

o Insidious progression.

o Neurological symptoms: gait disturbance, clumsy or weak hands, or loss of sexual, bladder, or bowel function.

o Neurological signs:

• Lhermitte’s sign: flexion of the neck causes an electric shock-type sensation that radiates down the spine and into the limbs.
• Upper motor neurone signs in the lower limbs (Babinski’s sign: up-going plantar reflex, hyperreflexia, clonus, spasticity).
• Lower motor neurone signs in the upper limbs (atrophy, hyporeflexia).
• Sensory changes are variable, with loss of vibration and joint position sense more evident in the hands than in the feet.

Question 12

Presentation of spinal cord compression

Answer 12

• Clinical features depend upon the extent and rate of development of cord compression.

o Motor symptoms can include ready fatigue and disturbance of gait.

o Cervical spine lesions can produce quadriplegia. Injury above the level of C3, C4, C5 (the segmental level of the phrenic nerve) cause paralysis of the diaphragm and artificial ventilation is required.

o Sensory symptoms can include sensory loss and paraesthesia. Light touch, proprioception and joint position sense are reduced.

o There can be root pain in the legs.

o Tendon reflexes are typically:
Increased below the level of injury and/or compression.
Absent at the level of injury and/or compression.
Normal above the level of injury and/or compression.

o Sphincter disturbances - late features of cervical and thoracic cord and/or compression.

o There may be loss of autonomic activity with lack of sweating below the level, loss of thermoregulation and drop in peripheral resistance causing hypotension.

Question 13

Investigations for spinal cord compression

Answer 13

• Haemoglobin and haematocrit levels should be measured initially and monitored serially to monitor blood loss.

• Blood tests:
o FBC – bone marrow infiltration can lead to bone marrow suppression with anaemia and thrombocytopenia
o Bone profile – hypercalcaemia can occur with bone metastases and may be asymptomatic
o U&Es – especially important if hypercalcaemia is found
o LFTs – as a marker for other sites of metastatic disease

• Renal function and electrolytes: dehydration.
• MRI scan of the whole spine.
• CT scan and CXR to look for signs of metastasis in metastatic spinal cord compression (MSCC)

Question 14

How is early detection of MSCC facilitated?

Answer 14

• Inform patients at high risk of developing bone metastases, patients with diagnosed bone metastases, or patients with cancer who present with spinal pain about the symptoms of MSCC.
• Offer information (for example, in the form of a leaflet) to patients and their families and carers which explains the symptoms of MSCC, and advises them (and their healthcare professionals) what to do if they develop these symptoms.

Question 15

When should the GP contact the MSCC coordinator regarding a cancer patient?

Answer 15

• Contact the MSCC coordinator urgently (within 24 hours) to discuss the care of patients with cancer and any of the following symptoms suggestive of spinal metastases:
o pain in the middle (thoracic) or upper (cervical) spine
o progressive lower (lumbar) spinal pain
o severe unremitting lower spinal pain
o spinal pain aggravated by straining (for example, at stool, or when coughing or sneezing)
o localised spinal tenderness
o nocturnal spinal pain preventing sleep.

• Contact the MSCC coordinator immediately to discuss the care of patients with cancer and symptoms suggestive of spinal metastases who have any of the following neurological symptoms or signs suggestive of MSCC, and view them as an oncological emergency:

o neurological symptoms including radicular pain (band-like pain), any limb weakness, difficulty in walking, sensory loss or bladder or bowel dysfunction

o neurological signs of spinal cord or cauda equina compression.

Question 16

Management of spinal cord compression

Answer 16

• Nurse the patient flat with the spine in neutral alignment (eg, using logrolling or turning beds) until spinal stability and neurological stability are ensured.
• Give a course of dexamethasone unless contra-indicated until a definitive treatment plan is made (MSCC as well).
• Insert a catheter to manage bladder dysfunction.
• Use breathing exercises, assisted coughing, and suctioning to clear airway secretions.
• Neurosurgical stabilisation surgery (MSCC)- All patients with cord compression, actual or imminent, or vertebral instability should be discussed with the neurosurgeons. There is evidence that neurosurgical intervention with decompression and stabilisation improves the chance of the patient retaining mobility
• Prophylaxis of VTE (enoxaparin)
• Prevention of gastric stress ulcers (PPI)
• Maintenance of volume and BP
• Bisphosphonates should be offered to all patients with vertebral involvement from myeloma and breast cancer and to patients with prostate cancer in whom conventional analgesia is inadequate.
• Specialised pain control procedures may be needed for intractable pain (eg, epidural analgesia).
• If definitive treatment of the cord compression is appropriate, it should be started before patients lose the ability to walk or before other neurological deterioration occurs, and ideally within 24 hours.
• Definitive treatment may be using surgery (e.g., laminectomy, posterior decompression ± internal fixation) or using radiotherapy.

Question 17

Which medication should be given with dexamethasone?

Answer 17

o High dose dexamethasone is usually started to reduce any additional inflammation around the metastatic deposit and can improve neurological function if actual cord compression is identified.

o Dexamethasone is the most commonly used drug, given orally at a dose up to 16mg a day (in two doses, preferably morning and lunch).

o Always consider gastro-prevention with a PPI such as lansoprazole 30m daily when starting high dose steroids.

Question 18

Complications of spinal cord compression

Answer 18

• Pressure sores
• Hypothermia
• Potential lung complications include aspiration, pneumonia, ARDS, atelectasis.
• Depression.
• Paralysis

Question 19

What is the role of calcium in the body?

Answer 19

• Calcium has a vital role to play in the effective working of the majority of cells in the body and it is therefore important that the optimal level be maintained by the body.
• A reduction in serum calcium can stimulate parathyroid hormone (PTH) release which may then increase bone resorption, increase renal calcium reabsorption, and stimulate renal conversion of 25-hydroxyvitamin D3, to the active 1,25-dihydroxyvitamin D3, which then will increase intestinal calcium absorption.
• These mechanisms restore the serum calcium to normal and inhibit further production of PTH and 1,25-dihydroxyvitamin D3

Question 20

What is corrected calcium level?

Answer 20

• The level for serum calcium is frequently given by laboratories as both an uncorrected level and a corrected level which has allowed for changes in albumin levels.
• It is only the ionised (unbound) calcium, which is physiologically important, taking part in cellular activities such as neuromuscular contraction, coagulation and other cellular activities

Question 21

Presentation of hypercalcaemia at levels<2.8 mmol/L

Answer 21

• At levels <2.8 mmol/L:
o Polyuria and polydipsia
o Dyspepsia - due to calcium-regulated release of gastrin
o Depression
o Mild cognitive impairment

Question 22

Presentation of hypercalcaemia at levels<3.5mmol/L

Answer 22

• At levels <3.5 mmol/L:
o All of the previous plus
o Muscle weakness
o Constipation
o Anorexia and nausea
o Fatigue

Question 23

Presentation of hypercalcaemia at levels>3.5mmol/L

Answer 23

• At levels >3.5 mmol/L
o All of the previous plus
o Abdominal pain
o Vomiting
o Dehydration
o Lethargy
o Cardiac arrhythmias- shortened QT interval
o Coma
o Pancreatitis

Question 24

What happens when hypercalcaemia is long-standing?

Answer 24

• If the hypercalcaemia is long-standing, calcium may be deposited in soft tissues or may result in stone formation - e.g., nephrocalcinosis, nephrolithiasis or chondrocalcinosis.

Question 25

What are the causes of hypercalcaemia?

Answer 25

PTH-mediated hypercalcaemia

Non-PTH mediated hypercalcaemia

Question 26

Causes of PTH-mediated hypercalcaemia

Answer 26

o Primary hyperparathyroidism is the most common cause of raised calcium levels, usually producing a mild hypercalcaemia.

Question 27

Causes of Non-PTH-mediated hypercalcaemia

Answer 27

o Malignancy - the most common cause of non-PTH-mediated hypercalcaemia.
-Hypercalcaemia of malignancy can occur as a result of four different mechanisms: ectopic production of parathyroid hormone-related peptide by tumour cells, osteolytic hypercalcaemia, ectopic calcitriol (1,25-dihydroxyvitamin D), and ectopic PTH produced by tumour cells.

o Granulomatous conditions - e.g., sarcoidosis and tuberculosis.

o Endocrine conditions - e.g., thyrotoxicosis, pheochromocytoma and primary adrenal insufficiency.

o Drugs - e.g., thiazide diuretics, vitamin D and vitamin A supplements.

o Familial - e.g., familial hypocalciuric hypercalcaemia.

o Other - e.g., prolonged immobilisation, calcium-alkali syndrome, AIDS.

Question 28

Investigations for hypercalcaemia

Answer 28

• Corrected calcium level - this will by definition be raised.
• Compared with the hypercalcaemia of malignancy, hyperparathyroidism tends to be associated with lower serum calcium levels (<3 mmol/L) and a longer duration of hypercalcaemia (more than six months).

• In the presence of a raised corrected calcium:
o A raised albumin level in the presence of a raised urea indicates dehydration.
o A raised albumin level in the presence of a normal urea suggests a cuffed specimen.
o A normal alkaline phosphatase is indicative of myeloma (raised plasma protein), calcium-alkali syndrome (formerly milk-alkali syndrome), thyrotoxicosis or sarcoidosis.
o A raised alkaline phosphatase suggests bony metastases, sarcoidosis or thyrotoxicosis.
o A raised calcitonin level is suggestive of B-cell lymphoma.

•PTH levels

• Radio-imaging:
o Plain X-rays may show features indicative of bone abnormalities, such as demineralisation, bone cysts, pathological fractures or bony metastases.

o Ultrasound scan, computerised tomography (CT) scan or intravenous pyelogram (IVP) may be required to detect abnormalities of the urogenital tract, such as calcification or stones.

o Ultrasound or technetium scan of the parathyroid glands may be indicated if hypertrophy or adenoma is suspected.

Question 29

How do you interpret PTH levels in the context of hypercalcaemia?

Answer 29

Interpreting PTH levels:
o Raised PTH levels are suggestive of primary, secondary or tertiary hyperparathyroidism, or familial hypocalciuric hypercalcaemia.

o Low PTH levels are seen in granulomatous disease, iatrogenic causes (e.g., renal dialysis), adrenal insufficiency, thyrotoxicosis, and vitamin D intoxication.

o The levels in malignancy may be low, normal or high.

Question 30

Management of hypercalcaemia due to malignancy

Answer 30

o Increasing the circulating volume with 0.9% saline, helping to increase the urinary output of calcium.

o A loop diuretic such as furosemide. This is occasionally used where there is fluid overload, but it does not reduce serum calcium .

o After rehydration, bisphosphonates (which act by reducing bone turnover) should be administered intravenously. Pamidronate and zoledronic acid are commonly used. Salmon calcitonin may also be given. It has fewer side-effects than bisphosphonates but is less effective in reducing hypercalcaemia

o Glucocorticoids are useful for hypercalcaemia due to vitamin D toxicity, sarcoidosis and lymphoma.

o Gallium was identified as a useful drug when it was found that patients with malignancy having gallium scans did not develop hypercalcaemia. It may be given intravenously to patients with malignant hypercalcaemia who do not respond to bisphosphonates.

o Denosumab, a human monoclonal antibody, is licensed for the prevention of osteoporotic fractures but is also useful for patients with persistent or relapsed hypercalcaemia of malignancy.

Question 31

Management of hypercalcaemia for other causes

Answer 31

o Cinacalcet hydrochloride is a calcimimetic (= mimicking the action of calcium) agent that effectively reduces parathyroid levels in patients with secondary hyperparathyroidism.

o Paricalcitol is also licensed for the prevention and treatment of secondary hyperparathyroidism associated with chronic kidney disease.

o Patients with advanced underlying kidney disease and refractory severe hypercalcaemia should be considered for haemodialysis.

Question 32

Management of PTH-mediated hypercalcaemia

Answer 32

o Asymptomatic patients may be treated conservatively with regular monitoring of bone density, renal function and serum and urinary calcium levels.

o For symptomatic patients, dietary calcium should be reduced - e.g., minimise the intake of dairy products and leafy vegetables.

o Bed-bound patients should be mobilised if possible.
o Symptomatic patients will respond well to having the affected part of the parathyroid gland removed.