Lumbar spine Flashcards

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1
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Direction of forces involved (axial compression, axial distraction, translation)

A

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2
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Rotational forces involved

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3
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Position of the spine when the load was applied

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4
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Intensity of force applied

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5
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Presence or absence of direct trauma

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6
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Skin integrity, bruising, haematoma

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7
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Area of pain

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8
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Time of injury, ability to move arms/legs post injury

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9
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Limb symptoms such as numbness, pins and needles, ‘dead leg’, tingling, weakness, foot drop

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10
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Bladder or bowel disturbances

A

Cauda equine syndrome refers to nerve compression within the spinal canal that occurs below L1-2 interspace after the termination of the spinal cord. The clinical picture is that of a lower motor neuron lesion with weakness or paralysis, loss of rectal tone, sensory loss in a dermatomal pattern, decreased deep tendon reflexes, and bladder dysfunction. The classic sensory description is ‘saddle’ anaesthesia, with loss of sensation in the buttocks and perineal areas.
The most common cause of cauda equine syndrome is a large midline disc herniation, usually at L4/5 or L5S1 interspaces. Other causes include spinal metastasis, spinal hematoma, epidural abcess, vertebral fracture, or transverse myelitis.
Urine retention of more than 100-200ml of urine is 90% Sn and 95% Sp for this condition.

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11
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Mental status

A

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12
Q

Discuss the relevance of the following factors with respect to the mechanism of injury with lumbar spine

Other sites for injury and relevant questioning required

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13
Q

What other key information is required to assess for red flags?

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14
Q

What key information is required regarding bladder/bowel function?

A

Cauda equine syndrome refers to nerve compression within the spinal canal that occurs below L1-2 interspace after the termination of the spinal cord. The clinical picture is that of a lower motor neuron lesion with weakness or paralysis, loss of rectal tone, sensory loss in a dermatomal pattern, decreased deep tendon reflexes, and bladder dysfunction. The classic sensory description is ‘saddle’ anaesthesia, with loss of sensation in the buttocks and perineal areas.
The most common cause of cauda equine syndrome is a large midline disc herniation, usually at L4/5 or L5S1 interspaces. Other causes include spinal metastasis, spinal hematoma, epidural abcess, vertebral fracture, or transverse myelitis.
Urine retention of more than 100-200ml of urine is 90% Sn and 95% Sp for this condition.

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15
Q

What key information would you ask to differentiate musculoskeletal low back pain from non musculoskeletal causes?

A

We also ask about constitutional symptoms (eg, unintentional weight loss, fever, or night sweats), history of malignancy, precipitants or precipitating events, therapies attempted, neurologic symptoms (eg, weakness, falls or gait instability, numbness or other sensory changes, or bowel/bladder symptoms), stability or progression of symptoms, history of recent bacterial infections (particularly bacteremia), recent history or current use of injection drugs, history or current use of corticosteroid medications, and recent history of epidural or spinal procedures.

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16
Q

What key information would you ask to differentiate vascular claudication from neurogenic claudication?

A

Peripheral vascular disease may be mistaken for Lumbar spinal stenosis because both are associated with exertional exacerbation. However, symptoms of neurogenic claudication can usually be distinguished from vascular claudication. Neurogenic claudication often persists with rest when standing still in an erect posture but can be relieved by flexed posture. Similarly, cycling is better tolerated with LSS compared with similar intensity walking.

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17
Q

What key information would suggest an upper motor neuron lesion?

A

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18
Q

What key information is required in the setting of chronic low back pain

A

he history should include location, duration, and severity of the pain, details of any prior back pain, and how current symptoms compare with any previous back pain.

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19
Q

What key information in patient’s past medical history in low back pain/injuries?

A

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20
Q

What key information in a patient’s medication history is important in low back pain/injuries?

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21
Q

What key information in a patient’s social history is important in low back pain/injuries?

A

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22
Q

What is the relevance of determining the previous treatment or intervention?

A

Patients should also be evaluated for social or psychologic distress that may be contributing, Potentially useful items are a history of failed previous treatments

23
Q

What is the relevance of determining compensable status or health insurance status of the patient?

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24
Q

Describe the thoracolumbar spinal column injury classification

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25
Q

Describe common fractures in the thoracolumbar region including mechanism of injury, clinical signs and symptoms

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26
Q

How would you assess the vascular status of the lower limbs?

A

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27
Q

How would you assess for abdominal aortic aneurysm if this was suspected?

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28
Q

How would you assess for cauda equina syndrome if this was suspected?

A

Cauda equine syndrome refers to nerve compression within the spinal canal that occurs below L1-2 interspace after the termination of the spinal cord. The clinical picture is that of a lower motor neuron lesion with weakness or paralysis, loss of rectal tone, sensory loss in a dermatomal pattern, decreased deep tendon reflexes, and bladder dysfunction. The classic sensory description is ‘saddle’ anaesthesia, with loss of sensation in the buttocks and perineal areas.
The most common cause of cauda equine syndrome is a large midline disc herniation, usually at L4/5 or L5S1 interspaces. Other causes include spinal metastasis, spinal hematoma, epidural abcess, vertebral fracture, or transverse myelitis.
Urine retention of more than 100-200ml of urine is 90% Sn and 95% Sp for this condition.

29
Q

What is the relevance of any local skin changes/open wounds to low back?

A

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30
Q

When is an assessment of vital signs indicated?

A

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31
Q

How would you differentiate a lower motor neuron lesion from a peripheral nerve lesion when lower limb pain only is present?

A

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32
Q

How you would differentiate musculoskeletal low back pain from non musculoskeletal low back pain?

A

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33
Q

What are the most common non musculoskeletal presentations of low back pain

A
Among patients who present with back pain to primary care settings, less than 1% will have a serious systemic etiology
Serious systemic etiologies
-Spinal cord or cauda equina compression
-Metastatic cancer
-Spinal epidural Abscess
-Verterbral osteomyelitis 
Less serious, specific etiologies
-Vertebral compression fracture
-Radiculopathy
-Spinal stenosis
-Anklyosing spondylitis
34
Q

When would an X-ray be indicated for a patient with lumbar or thoracolumbar injury? and which views?

A

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35
Q

When would an X-ray be indicated for a patient with a lumbar or thoracolumbar pain without history of trauma?

A

In the ED, imaging is indicated if an alternate diagnosis such as infection or malignancy is suggested based on the history and physical examination.
Emergent imaging should be performed in patients with cauda equine syndrome or acute severe/progressive weakness

36
Q

When would a CT scan be indicated for a patient with a lumbar or thoracolumbar problem/injury?

A

In the ED, imaging is indicated if an alternate diagnosis such as infection or malignancy is suggested based on the history and physical examination.
Emergent imaging should be performed in patients with cauda equine syndrome or acute severe/progressive weakness

37
Q

When would an MRI be indicated for a patient with low back problem/injury?

A

In the ED, imaging is indicated if an alternate diagnosis such as infection or malignancy is suggested based on the history and physical examination.
Emergent imaging should be performed in patients with cauda equine syndrome or acute severe/progressive weakness

38
Q

When would blood investigations be indicated for a patient with lumbar spine problem/injury

A

ost patients with acute low back pain do not require any laboratory testing. In some patients with suspected infection or malignancy, we use the erythrocyte sedimentation rate (ESR) and/or C-reactive protein (CRP) in addition to plain radiographs to determine the need for advanced imaging

The ESR and CRP are also used in the diagnosis of ankylosing spondylitis

39
Q

What are other investigations that may be indicated in a patient with low back pain?

A

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40
Q

Describe the signs, symptoms and management of:

Osteoporotic wedge fracture of the lumbar spine

A

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41
Q

Describe the signs, symptoms and management of:

Pars interarticularis defect or fracture

A

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42
Q

Describe the signs, symptoms and management of:

Lumbar radiculopathy with and without neurological signs

A

Most commonly, the patient is between the ages of 30-50 because in older individuals the nucleus is desiccated and fibrotic and less likely to herniate.
The pain usually originates in the general location of the herniation but frequently the pain from radiculopathy (sciatica) predominates. Sciatica is 95% Sn for lumbar disc herniation.
With an acute rupture, there is severe low back pain that occurs either immediately or several hours later. Any movement exacerbates the pain and it is worse with sitting than standing. The first 30 minutes after awakening are characterised by the worst pain, which later improves.
The back examination reveals significant muscle spasm and flattening of the lumbar curve.
The physical examination should include an examination of the neurologic function in the legs. Sensory loss in a dermatomal distribution is the most reliable predictor of the location of the affected nerve root.
The SLR test exacerbates pain in a patient with a herniation at the L5 or S1 nerve root by stretching the compressed nerve. A positive test is present if sciatica is reproduced between 30-60 degrees of leg elevation. Pain reproduced in the back does not constitute a positive test.

43
Q

Describe the signs, symptoms and management of:

Suspected acute disc herniation with low back pain only

A

The absence of sciatica makes a clinically important disc herniations unlikely, estimated to be present in 1 out of 1000 patients.

44
Q

Describe the signs, symptoms and management of:

Suspected acute disc herniation with neurological signs

A

Most commonly, the patient is between the ages of 30-50 because in older individuals the nucleus is desiccated and fibrotic and less likely to herniate.
The pain usually originates in the general location of the herniation but frequently the pain from radiculopathy (sciatica) predominates. Sciatica is 95% Sn for lumbar disc herniation.
With an acute rupture, there is severe low back pain that occurs either immediately or several hours later. Any movement exacerbates the pain and it is worse with sitting than standing. The first 30 minutes after awakening are characterised by the worst pain, which later improves.
The back examination reveals significant muscle spasm and flattening of the lumbar curve.
The physical examination should include an examination of the neurologic function in the legs. Sensory loss in a dermatomal distribution is the most reliable predictor of the location of the affected nerve root.
The SLR test exacerbates pain in a patient with a herniation at the L5 or S1 nerve root by stretching the compressed nerve. A positive test is present if sciatica is reproduced between 30-60 degrees of leg elevation. Pain reproduced in the back does not constitute a positive test.

45
Q

Describe the signs, symptoms and management of:

Chronic low back pain with signs of centralised pain mechanisms

A

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46
Q

Describe the signs, symptoms and management of:

Acute low back pain with associated yellow flags

A

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47
Q

Describe the signs, symptoms and management of:

Suspected pathological fracture

A

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48
Q

Describe the signs, symptoms and management of:

Discitis

A

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49
Q

Describe the signs, symptoms and management of:

Upper motor neuron lesions

A

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50
Q

Describe the signs, symptoms and management of:

Lumbar sprain

A

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51
Q

Describe the signs, symptoms and management of:

Spinal Epidural Abscess

A

SEA is a rare infection that may result in irreversible paralysis in upto 22% of patients.
Predisposing conditions include immunocompromise (diabetes, HIV, elderly), spinal abnormality (arthritis, trauma, surgery) and an outside source of infection (injection drug use, catheter). The majority of cases are due to hematogenous spread of infection
The symptoms of SEA progress in four classical stages. Initially, back pain at the level of the affected portion of the cord is present followed by nerve root pain. Cord dysfunction in the form of motor weakness, sensory loss and bowel/bladder dysfunction follows. The final stage of untreated disease is paralysis. The rate of progression from one stage to next varies from hours to days.
On physical examination, tenderness is common, especially over the spinous processes.

Laboratory: An elevated leukocyte count is present in 2/3 of cases. C-reactive protein and sedimentation rate are elevated in all cases but these abnormalities are non-specific. Blood cultures should be obtained and will be positive in 60% of cases.

Treatment of SEA includes surgical drainage and systemic antibiotics. Decompressive laminectomy and debridement are ideally performed within 24 hours of presentation.