10. Back/neck pain Flashcards

1
Q

Differentials for back/eck pain?

A

Vascular
AAA
Aortic dissection

Infective
Osteomyelitis
Spinal epidural abscess
Septic arthritis
Discitis

Inflammatory
Ankylosing spondylitis
RA
OA

Degenerative
Osteoprortic vertebral fractures
Osteoarthritis
Cervical spondylosis

Trauma
C-spine injury major trauma - see major trauma

Neoplastic
Myeloma inc pathological fractures
Metastasis - Neoplastic spinal cord compression

Neuro
Prolapsed disc
Sciatica
Cauda equina
Lumbar spinal stenosis
Myelopathy

GI/renal
Pyelonephritis
Kidney stones
Pancreatitis

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2
Q

History taking back pain?

A

HoPC: location, onset, relieving factors, aggrevating factors, ever get pain in any other bones? morning stiffness? night time pain?

red flags - weight loss, kidney stones, bladder and bowel changes eg unable to control OR retention, any change to sensation when you wipe down below? any weakness in legs? any change to sensation? fever? injuries recently?

MHx: if man over 65 - have you attended screening for AAA?, history of kidney stones? ever had a cancer diagnosis?

SHx: alcohol, smoking, ever injected recreational drugs?

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3
Q

examiantion back pain?

A

spine + neuro + abdo

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4
Q

red flags back pain?

A

Major trauma (spinal fracture)
Stiffness in the morning or with rest (ankylosing spondylitis)
Age under 40 (ankylosing spondylitis)
Gradual onset of progressive pain (ankylosing spondylitis or cancer)
Night pain (ankylosing spondylitis or cancer)
Age over 50 (cancer)
Weight loss (cancer)
Bilateral neurological motor or sensory symptoms (cauda equina)
Saddle anaesthesia (cauda equina)
Urinary retention or incontinence (cauda equina)
Faecal incontinence (cauda equina)
History of cancer with potential metastasis (cauda equina or spinal metastases)
Fever (spinal infection)
IV drug use (spinal infection)
THORACIC PAIN

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5
Q

How many of each vertebrae?

A

Think about meal times… 7am, 12pm, 5pm

Cervical - 7

thoracic - 12

Lumbar - 5

Sacrum (5, fused)

Coxyx (4, fused)

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6
Q

What tool can be used to stratify the risk of developing chronic back pain

A

StarT BAck tool

The tool helps assess the risk of a patient presenting with acute back pain developing chronic back pain. This helps guide the intensity of the initial interventions (e.g., referral for group exercises, physiotherapy and cognitive behavioural therapy).

It involves 9 questions that assess the patient’s function and psychological response to the back pain. It gives a:
Total score (out of 9)
Subscore on the 4 psychosocial questions (out of 4)

total score >3 = medium or high risk
subscore <3 low or medium, >3 is high risk

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7
Q

What is mechanical back pain

A

Mechanical low back pain refers to back pain that arises intrinsically from the spine, intervertebral disks, or surrounding soft tissues. This includes lumbosacral muscle strain, disk herniation, lumbar spondylosis, spondylolisthesis, spondylolysis, vertebral compression fractures, and acute or chronic traumatic injury.1 Repetitive trauma and overuse are common causes of chronic mechanical low back pain, which is often secondary to workplace injury.

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8
Q

Management of no-specific lower back pain?

A

low risk of chronic back pain:
Self-management
Education
Reassurance
Analgesia
Staying active and continuing to mobilise as tolerated

Additional stuff for medium or high risk:
Physiotherapy
Group exercise
Cognitive behavioural therapy

The NICE advise for analgesia:
1. NSAIDs (e.g., ibuprofen or naproxen) first-line
2. Codeine as an alternative
+ Benzodiazepines (e.g., diazepam) for muscle spasm (short-term only – up to 5 days)

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9
Q

Vascualr causes of back pain?

A

AAA rupture
Aortic dissection

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10
Q

What is an AAA

A

An abdominal aortic aneurysm (AAA) is a dilatation of the abdominal aorta greater than 3cm in diameter.

At diameters greater than 5cm there is a significant risk of rupture and this event is life threatening and treated as a time critical medical emergency.

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11
Q

Pathophysiology AAA

A

The underlying cause of a AAA is usually atherosclerotic disease and there is a clear pathophysiological process from aneurysm formation to rupture:

  1. lipid deposition
  2. inflammation damages internal and external elastic laminae of the aortic wall
  3. loss of elastic laminae = difficulty with pressure change from diastole to systole –> dilation
  4. fibrosis
  5. aortic wall weaker then systolic pressure –> rupture

(therefore made much worse with HTN)

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12
Q

Features of a ruptured AAA? time course?

A

Pain - back/loin/ abdo going to back

CVS failure due to haemorrhage - tachycardia, hypotension, may have tamponade features if posterior rupture

Distal ischaemia - haematoma within aneyrysm –> embolise –> distal artery occlusion eg lower limb ischaemia

Death -
Approximately 33% of patients will die at the time of rupture and it should always be kept in mind as a differential for sudden death in middle age. Without treatment all AAA ruptures will eventually lead to death and it can be considered a terminal event.

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13
Q

test to diagnose ruptured AAA or rule it out

A

USS

can be performed by the bedside and gives an instant objective measurement of aortic diameter

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14
Q

tests to plan treatment once a ruptured AAA is diagnosed

A

Once a AAA has been diagnosed (eg USS) or known AAA patient has been admitted with a suspected rupture, the required investigations are used to plan treatment

The gold-standard imaging is a CT angiogram as this allows for a three-dimensional picture of the aneurysm to be created and this can be used to plan for surgery to repair it.

bloods
- FBC - ?low platelts which may require transfusion and affect surgical bleeding risk
- U&E - as if the aneurysm is treated endovascularly the patient will be exposed to large volumes of contrast and pre-existing renal failure may contraindicate this.
- Coagualtion screen
- A coagulation screen should be performed to ensure there is no underlying bleeding risk as during any vascular procedure intravenous heparin is used and the dose may need adjustment if there is a bleeding disorder.
- group and save and cross match

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15
Q

what does the chosen management of an AAA depend on? what are the options?

A
  • Anatomy of the aneurysm
  • Baseline health of the patient
  • Clinical state of the patient on admission

Open surgical repair - GA, big surgery, risky for pts with significant cardiac disease

Endovascular aneurysm repair (EVAR) - local anaesthetic, only suitable for AAAs not involving the renal arteries, requires large quantities of radiological contrast and is therefore unsuitable for patients with significant renal impairment

Palliative -
Understanding that a ruptured AAA is a terminal event without treatment is important and it is valid to accept this and treat some patients palliatively with best supportive care.
clinical presentation (signif shock) or baseline physiological reserve might make this the only option

It is important to have adequate discussions with family members about the prognosis when patients present with a ruptured AAA, even if surgery is initially intended, as the condition can progress very quickly and become inoperable in a short period of time.

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16
Q

complications of AAA and of treatment for AAA

A

Acute limb ischaemia - esp in EVAR

Bowel ischaemia - Both open and endovascular repair require sacrifice or occlusion of the inferior mesenteric artery and this can lead to bowel ischaemia if the marginal arterial supply to the left colon is inadequate

Abdominal compartment syndrome - more common with open surgery

graft infection –> inadequate graft –> bleed

blood transfusion reactions

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17
Q

what does the screening program for AAA consist of?

A

Screening for an abdominal aortic aneurysm consists of a single abdominal ultrasound for males aged 65.

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18
Q

screening AAA outcome and action?

A

<3m = no further action

3 - 4.4cm = small aneurysm = resan every 12 mo

4.5-5.4 = medium aneurysm = rescna every 3mo

> 5.5cm = large aneurysm = rf to vasc surgery for probable intervention

ALSO OPTOMISE CVS RISKS

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19
Q

what constitutes a high risk AAA at screening? management?

A

symptomatic, aortic diameter >=5.5cm or rapidly enlarging (>1cm/year)

treat with elective endovascular repair (EVAR) or open repair if unsuitable.

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20
Q

what is aortic dissection? pathophysiology?

A

Aortic dissection is a severe, life-threatening condition characterised by the separation of the aortic wall layers, resulting in the formation of a false lumen.

It frequently occurs due to an intimal tear, allowing blood to enter and dissect through the media layer. The aetiology often involves hypertension, connective tissue disorders (e.g., Marfan syndrome), or iatrogenic factors such as catheterization or cardiac surgery.

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21
Q

standford classification of aortic dissection

A

type A - ascending aorta, 2/3 of cases. (type A1 propagates to the aortic arch and sometimes beyond. type A2 is confined to ascending)

type B - descending aorta, distal to left subclavian origin, 1/3 of cases

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22
Q

presentation aortic dissection

A

sudden onset of severe chest pain radiating to the back

syncope, or neurological deficits.

Clinical presentation varies

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23
Q

invetsigation ?aortic dissection?

A

CT angiogram

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24
Q

management aortic dissection?

A

Management depends on the dissection type;
Type A requires emergent surgical intervention due to increased risk of complications like pericardial tamponade, myocardial ischemia, and aortic regurgitation.
surgical management, blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

Type B dissections are primarily managed medically with strict blood pressure control unless exhibiting signs of malperfusion syndromes or impending rupture.
conservative management
bed rest
reduce blood pressure IV labetalol to prevent progression

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25
Q

Associations aortic dissection

A

hypertension: the most important risk factor
trauma
bicuspid aortic valve
collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
Turner’s and Noonan’s syndrome
pregnancy
syphilis

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26
Q

complications of aortic dissection

A

Complications of backward tear
aortic incompetence/regurgitation
MI: inferior pattern often seen due to right coronary involvement

Complications of forward tear
unequal arm pulses and BP
stroke
renal failure

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27
Q

what are the infective cuases of back pain?

A

septic arthritis
osteomyelitis
discitis
epidural abscess

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28
Q

what are the most commonly affected joints septic arthritis

A

hip, knee and ankle

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29
Q

typical history septic arthritis

A

PC: hot red swollen painful joint, stiffness and reduced range of motion, systemic symptoms such as fever and lethargy

any hot/red joint

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30
Q

most common causative organism septic arthritis ? other causes

A

staph aureus

Neisseria gonorrhoea (gonococcus) in sexually active teenagers
Group A streptococcus (Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)

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31
Q

young pt presenting with single acutely swollen joint - first ddx?

A

always think of gonococcus septic arthritis until proven otherwise

Gonorrhoea infection is common and delaying treatment puts the joint in danger. In your exams it might say the gram stain revealed a “gram-negative diplococcus”. The patient may have urinary or genital symptoms to trick you into thinking of reactive arthritis but remember that it is important to exclude gonococcal septic arthritis first as this is the more serious condition.

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32
Q

plan ?septic arthritis

A

Have a low suspicion until joint fluid assessed

  1. Aspiration for gram stain, crystal microscopy, culture and antibiotic sensitivities
  2. If paeds, USS, if shows effusion and with corroborating history, treat as septic arthritis
  3. Bloods inflammatory markers, blood culture
  4. Empirical IV antibiotics (local guidelines)
  5. Continue abx for 3-6 weeks

Patients may require surgical drainage and washout of the joint to clear the infection in severe cases.

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33
Q

example first line regime septic arthritis abx

A

Flucloxacillin for 6 weeks

if pen allergic: clindamycin

If MRSA suspected: vancomycin

If gonococcal arthritis or gram -ve susepcted : cefotaxime or ceftriaxone

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34
Q

what criteria can be used in children to distinguish between septic arthritis and transient synovitis of hip

A

The kocher criteria
fever >38.5 degrees C
non-weight bearing
raised ESR > 40
raised WCC >12

If 0 = very unlikely and can be managed in primary care with close follow up

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35
Q

what is osteomyelitis

A

an infection in the bone and bone marrow.

This typically occurs in the metaphysis of the long bones.

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36
Q

what is the most common causative organism osteomyelitis

A

staph aureus

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37
Q

types of osteomyelitis and how do people get it?

A

Chronic osteomyelitis is a deep seated, slow growing infection with slowly developing symptoms.

Acute osteomyelitis presents more quickly with an acutely unwell pt.

The infection may be introduced directly into the bone, for example during an open fracture.

Alternatively it may have travelled to the bone through the blood, after entering the body through another route, such as the skin or gums.

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38
Q

In what children is osteomyelitis more common

A

boys and children under 10 years

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39
Q

typical history osteomyelitis

A

Osteomyelitis can present acutely with an unwell child, or more chronically with subtle features. Signs and symptoms are:
- Refusing to use the limb or weight bear
- Pain
- Swelling
- Tenderness

They may be afebrile, or may have a low grade fever. Children with acute osteomyelitis may have a high fever, particularly if it has spread to the joint causing septic arthritis.

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40
Q

best imaging for dx of osteomyelitis

A

MRI

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41
Q

initial invetsigation osteomyelitis

A

xray

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42
Q

plan investigation ?osteomyelitis

A
  1. xray
  2. MRI if xray inconclusive
  3. inflammatory markers CRP, ESR, WCC
  4. blood culture
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43
Q

management osteomyelitis

A

Osteomyelitis is treated with antibiotics, usually with surgical debridement

Flucloxacillin for 6 weeks
+ consider fusidic acid or rifmapicin

if pen allergic: clindamycin

If MRSA suspected: vancomycin

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44
Q

what is discitis

A

Discitis is an infection in the intervertebral disc space. It can lead to serious complications such as sepsis or an epidural abscess.

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45
Q

typical history discitis

A

Back pain
General features
pyrexia,
rigors
sepsis
Neurological features e.g. changing lower limb neurology if an epidural abscess develops

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46
Q

most common cause discitis

A

staph aureus

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47
Q

plan ?discitis

A

Invetsigation
Imaging: MRI has the highest sensitivity
blood culture
CT-guided biopsy may be required to guide antimicrobial treatment

transoesophageal/transthoracic echo to assess for endocarditis (seeding)

management
abx based on cultures/biopsy

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48
Q

what is a spinal epidural abscess?

A

A spinal epidural abscess (SEA) is a collection of pus that is superficial to the dura mater (of the meninges) that cover the spinal cord. It is an emergency requiring urgent investigation and treatment to avoid progressive spinal cord damage.

An abscess is a collection of pus encapsulated by a pyogenic membrane.

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49
Q

pathophysiology spinal epidural abscess

A

In SEA, bacteria enters the spinal epidural space by contiguous spread from adjacent structures (e.g. discitis), haematogenous spread from concomitant infection (e.g. bacteraemia from IVDU), or by direct infection (e.g. spinal surgery). Immunosuppression is another major risk factor, which may be caused by congenital immune disorders, acquired immune disorders (such as HIV, diabetes or alcoholism or by iatrogenic means (e.g. chemotherapy or steroids).

SEA is most typically bacterial and the most common causative micro-organism is Staphylococcus aureus.

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50
Q

Presentation spinal epidural abscess

A

fever
back pain
focal neurological deficits according to the segment of the cord affected.

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51
Q

invetsigations ?spinal epidural abscess

A

Investigations
Bloods (including inflammatory markers, HIV, Hep B, Hep C, and preoperative blood tests (coagulation and group and screen))
Blood cultures
Infection screen (including chest x-ray and urine culture)*
MRI whole spine (the entire spine is imaged since skip lesions may be present)

*If the primary source of infection is not clear, a wide search for sources requires investigations including echocardiography and dental x-rays.

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52
Q

management SEA

A
  1. empirical abx
  2. culture based abx

+ if compressive etc consider surgical evaluation

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53
Q

whata re some inflammatory cuases of back pain?

A

ankylosing spondylitis

scheurmann’s disease

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54
Q

typical history ankylosing spondylitis

A

PC: young man with lower back pain and stiffness of insidious onset, stiffness worse in the morning and improves with exercise. may experience pain at night which improves on getting up

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55
Q

what may you find on examination ank spond

A
  • reduced lateral flexion
  • reduced forward flexion - Schober’s test - a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible
  • reduced chest expansion
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56
Q

what gene is ank spond associated with ?

A

HLA B27

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57
Q

Investigation ank spond

A
  1. plain xray of sacroiliac joints
  2. if negative and still suspected, MRI
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58
Q

what may be found on xray in ank spond

A

sacroiliitis: subchondral erosions, sclerosis
squaring of lumbar vertebrae
‘bamboo spine’ (late & uncommon)
syndesmophytes: due to ossification of outer fibers of annulus fibrosus

chest x-ray: apical fibrosis

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59
Q

why should you assess resp system in someone with ank spond, what might you find

A

at risk of apical fibrosis - request CXR if suspected

Spirometry may show a restrictive defect due to a combination of pulmonary fibrosis, kyphosis and ankylosis of the costovertebral joints.

reduced chest expansion o/e

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60
Q

first line management ank spond

A

NSAIDs

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61
Q

Management ank spond

A
  1. NSAIDs
  2. Paracetamol/codeine if poorly tolerated
  3. Seek specialist advice
    + Physio
    + Hydrotherapy
    + OT
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62
Q

criteria for rheum referal ank spond

A

Refer to rheumatology for a spondyloarthritis assessment if a person has low back pain starting before the age of 45 years and lasting longer than 3 months, plus four or more of the following criteria:

Low back pain starting before the age of 35 years.
Symptoms which wake them during the second half of the night.
Buttock pain.
Improvement when moving.
Improvement within 48 hours of taking a nonsteroidal anti-inflammatory drug (NSAID).
Spondyloarthritis in a first-degree relative.
Current or past arthritis.
Current or past enthesitis.
Current or past psoriasis.

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63
Q

complications/associations ank spond

A

apical fibrosis

anterior uveitis

CVS risk and heart involvement: aortic regurg, AV node block

osteoporosis and fractures

cauda equina

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64
Q

what is scheuermann’s disease

A

epiphysitis of verterbral joints

This word describes a condition where the ends of the longer bones of the foal become swollen and painful. The ends of the bones are called the epiphyses, and itis means inflammation = epiphysitis.

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65
Q

what does anterior wedging mean - spinal imaging

A

When the vertebra crushes or collapses, it tends to collapse at the front. This is why compression fractures are sometimes known as anterior wedge fractures. As the bone at the front of the vertebra collapses, it forms a wedge shape.

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66
Q

presentation scheuermanns disease

A

progressive kyphosis (at least 3 vertebrae must be involved)

Symptoms include back pain and stiffness

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67
Q

management scheuermann’s disease

A

Minor cases may be managed with physiotherapy and analgesia, more severe cases may require bracing or surgical stabilisation

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68
Q

x-ray changes scheuermanns

A

epiphyseal plate disturbance and anterior wedging

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69
Q

what are fragility fractures?

A

Asymptomatic: an osteoporotic vertebral fracture may be diagnosed through an incidental finding on X-ray
Acute back pain
Breathing difficulties: changes in the shape and length of vertebrae lead to the compression of organs such as the lungs, heart and intestine
Gastrointestinal problems: due to compression of abdominal organs
Only a minority of patients will have a history of fall/trauma

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70
Q

risk factors osteoporotic fractures?

A

Advancing age is a major risk factor osteoporotic fractures: Women ≥ 65 years old and men ≥ 75 years old should be considered for fracture risk assessment. Women in this age bracket are almost certainly post-menopausal, therefore have reduced oestrogen levels - this is a risk factor for osteoporosis.
Previous history of a fragility fracture
Frequent or prolonged use of glucocorticoids
History of falls
Family history of hip fracture
Alternative causes of secondary osteoporosis e.g. Cushing’s disease, hyperthyroidism, chronic renal disease
Low BMI (< 18.5)
Tobacco smoking
High alcohol intake: > 14 units/week for women, > 21 units/week for men

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71
Q

where is (one of) the commonest sites of osteoporotic fragility frcatures to occur

A

the spine (vertebrae)

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72
Q

how do patients with osteoporotic vertebral fractures present?

A

Asymptomatic: an osteoporotic vertebral fracture may be diagnosed through an incidental finding on X-ray

Acute onset back pain

Breathing difficulties: changes in the shape and length of vertebrae lead to the compression of organs such as the lungs, heart and intestine

Gastrointestinal problems: due to compression of abdominal organs

Only a minority of patients will have a history of fall/trauma

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73
Q

o/e signs of osteoporotic vertebral fracture

A

Loss of height: vertebral osteoporotic fractures of lead to compression of the spinal vertebrae hence a reduction in overall length of the spine and thus the patient becomes shorter

Kyphosis (curvature of the spine)

Localised tenderness on palpation of spinous processes at the fracture site

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74
Q

first line investigation ?osteoprotic vertebral fracture

what does it show

A

X-ray of the spine

This should be the first investigation ordered and may show wedging of the vertebra due to compression of the bone. An X-ray of the spine may also show old fractures (which can have a sclerotic appearance)

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75
Q

why can a cT or MRI be useful in osteoporotic fractures

A

CT spine: gives a more detailed view of the bone structure, therefore can visualise the extent/features of the fracture more clearly

MRI spine: Useful for differentiating osteoporotic fractures from those caused by another pathology e.g. a tumour

76
Q
A
77
Q

What is osteoarthritis

A

Disorder of synovial joints where damage triggers repair processes leading to structural changes within a joint

78
Q

key features of osteoarthritis

A

Slower onset
Activity related pain
Asymmetrical
Fewer joints
Activity related history
Commonly affected joints: hips, knees, sacro-iliac joints, DIPs, CMC joint at base of thumb, Wrist, Cervical spine

79
Q

X-ray changes osteoarthritis

A

LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis (increased density of bone along the joint line)
Subchondral cysts (fluid filled holes within the bone)

80
Q

o/e hand signs osteoarthritis

A

heberden’s nodes (in the DIP joints)
Bouchard’s nodes (in PIP joints)
Squaring at the base of the thumb at carpo-metacarpal joint
Weak grip
Reduced range of motion

81
Q

plan establishing a diagnosis osteoarthrits

A

NICE (2014) suggests that a diagnosis can be made without any investigations if the patient is over 45, has typical activity related pain and has no morning stiffness or stiffness lasting less than 30 minutes.

X-ray

82
Q

Management osteoarthritis

A

Management
1. Patient education and lifestyle advice eg weight loss
+ Physiotherapy to improve strength to support the joint
+ Occupational therapy and orthotics to support activities and function

Analgesia
1. Oral paracetamol and topical NSAID or topical capsaicin
2. Add oral nsaid and consider also prescribing PPI to protect stomach
3. Consider opiates (? i wouldn’t)
4. Intra-articular steroid injections
5. Joint replacement. Knee and hip are most commonly replaced

83
Q

how does osteoarthritis in the spine present? what is it called?

A

Cervical spondylosis is an extremely common condition that results from osteoarthritis.

Cervical spondylosis is a term used to describe degeneration of the vertebral column in the cervical (neck) region. It is otherwise known as cervical osteoarthritis. It most commonly presents in clinical practice as neck pain.

neck pain although referred pain may mimic headaches etc. Pain and/or stiffness in cervical region
Referred pain: retro-orbital, temporal, occipital, interscapular, upper limbs.

84
Q

complications of cervical spondylosis

A

radiculopathy and myelopathy

85
Q

examination findings cervical spondylosis

A

Reduced range of movement of neck (in all directions)
Poorly localised tenderness
Signs of radiculopathy (most commonly affecting nerve roots C5 to C7)
Unilateral neck, shoulder or arm pain, paraesthesia, or hyperaesthesia
Diminished arm reflexes (triceps: C7, biceps: C5/C6, supinator: C5/C6).
A small number (<0.1% of patients with cervical spondylosis) of patients with associated acute myelopathy can develop quadriplegia.

86
Q

red flags cervical spondylosis –> meylopathy

A

any upper motor neuron signs

  • hypertonia
  • babinski
  • hyperreflexia
  • sensory level
87
Q

how does cervical radiulopathy present?

A

PC: pain in the neck with radiation down the shoulder and arm in a dermatomal distribution. Unilateral dermatomal numbness or tingling (C5–C7 levels are most commonly affected). Motor symptoms, although less common, are also usually unilateral and in a myotomal distribution.

88
Q

what spinal levels are most often affected by cervical radiculopathy

A

C5–C7 levels are most commonly affected

89
Q

plan ?cervical radiculopathy

A

Plan:
Management
1. Rule out all red flags, if any red flags: refer immediately

  1. If present for <4-6 weeks and no objective neurological signs: treat conservatively for 4-6 weeks
    Reassurance
    Encourage activity and home exercise
    Analgesia: ibuprofen, paracetamol, codeine
    Consider amitriptyline, duloxetine, pregabalin or gabapentin
    Consider a referral for physiotherapy
  2. If present for more than 4-6 weeks OR there are objective neurological signs
    Refer to confirm diagnosis with MRI and to consider invasive procedures, such as interlaminar cervical epidural injections, transforaminal injections, or spinal surgery.
90
Q

what neoplastic things should you consider when a patient presents with back pain?

A

myeloma

neoplastic spinal cord compression

metastasis

91
Q

what is myeloma

A

Myeloma is a cancer of the plasma cells (type of B lymphocytes that produce antibodies). Cancer in a specific type of plasma cell results in large quantities of a single antibody being produced.

92
Q

what is Monoclonal gammopathy of undetermined significance (MGUS)

A

is where there is an excess of a single type of antibody or antibody components without other features of myeloma or cancer.

93
Q

pathophysiology myeloma

A

B cells in bone marrow producing antibodies → genetic mutation causing one antibody to be produced uncontrollably (50% of the time this is IgG)

Bone marrow infiltration → anaemia, neutropaenia, thrombocytopaenia
Plasma cells releasing cytokines → increased osteoclast activity → myeloma bone disease → skull, spine, long bones affected → bone pain / pathological fractures → releasing lots of calcium from bones → hypercalcaemia

Kidney failure is common in patients with a monoclonal gammopathy, most frequently due to hypercalcemia or myeloma cast nephropathy. Immunoglobulin crystallization is an uncommon phenomenon that also results in kidney injury
hypercalcaemia can ppt kidney stones,

94
Q

presentation myeloma

A

PC: anaemia
PC: neutropenia
PC: thrombocytopenia
PC: pathological fractures
PC: bone pain, particularly back pain
PC: myeloma renal disease
PC: hyperviscosity
PC: kidney stones

95
Q

Initial tests myeloma

A

FBC: anaemia
Calcium and bone profile: hypercalcaemia
U&Es : renal failure
ESR
Plasma viscosity

If suggetsive –>

then very urgent (within 48hrs)
- protein electrophoresis
- bence-jones urine test

if +ve 2ww
bone marrow biopsy and look at all results

96
Q

diagnostic criteria multiple myeloma

A

The diagnostic criteria for multiple myeloma requires one major and one minor criteria or three minor criteria in an individual who has signs or symptoms of multiple myeloma.

Major criteria
Plasmacytoma (as demonstrated on evaluation of biopsy specimen)
30% plasma cells in a bone marrow sample
Elevated levels of M protein in the blood or urine

Minor criteria
10% to 30% plasma cells in a bone marrow sample.
Minor elevations in the level of M protein in the blood or urine.
Osteolytic lesions (as demonstrated on imaging studies).
Low levels of antibodies (not produced by the cancer cells) in the blood.

97
Q

what is a Autologous hematopoietic cell transplantation

A

involves the removal of a patient’s own stem cells prior to chemotherapy, which are then replaced after chemotherapy

98
Q

what is allogenic haematopoeitic stem cell transplant

A

Allogenic hematopoietic cell transplantation

is not commonly used in myeloma due to high rates of overall mortality and symptoms of graft-ve

99
Q

stages of myeloma treatment

A

A combination of drugs is used to treat myeloma - ‘induction therapy
targeted drugs (such as thalidomide, lenalidomide, bortezomib, daratumumab)
chemotherapy (such as cyclophosphamide or melphalan)
steroids (such as prednisolone or dexamethasone)

The particular combination depends on whether a patient may be suitable for autologous hematopoietic cell transplantation or not.

Autologous hematopoietic cell transplantation
involves the removal of a patient’s own stem cells prior to chemotherapy, which are then replaced after chemotherapy
prolong both event-free and overall survival when compared with non-transplant strategies
typically it is younger, healthier patients who are suitable for stem cell transplantation and rigorous chemotherapy regimes.

100
Q

symptom management and complication avoidance myeloma

A

pain: treat with analgesia (using the WHO analgesic ladder)

pathological fracture: zoledronic acid is given to prevent and manage osteoporosis and fragility fractures as these are a large cause of morbidity and mortality, particularly in the elderly.

infection
patients receive annual influenza vaccinations
they may also receive Immunoglobulin replacement therapy.

venous thromboembolism prophylaxis

fatigue
treat all possible underlying causes
if symptoms persist consider an erythropoietin analogue.

101
Q

Calcium level myeloma

A

Hypercalcaemia,

In cases of myeloma, there is hypercalcaemia secondary to increased osteoclast activity. Additionally, renal impairment causes hypercalcaemia and hyperphosphataemia.

102
Q

Phosphate level myeloma

A

normal / high phosphate

renal impairment causes hypercalcaemia and hyperphosphataemia

103
Q

ALP myeloma

A

normal ALP

ALP enzyme levels remain normal with myeloma but may rise in other conditions such as solid tumours or bony metastases.

104
Q

Pathophysiology neoplastic spinal cord compression

A

Extradural compression accounts for the majority of cases, usually due to vertebral body metastases.

It is more common in patients with lung, breast and prostate cancer

105
Q

most common cancers –> neoplastic spinal cord compression

A

lung, breast and prostate cancer

106
Q

features of neoplastic spinal cord compression

A

back pain - the earliest and most common symptom, may be worse on lying down and coughing
lower limb weakness
sensory changes: sensory loss and numbness
neurological signs depend on the level of the lesion.

Lesions above L1 usually result in upper motor neuron signs in the legs and a sensory level. Lesions below L1 usually cause lower motor neuron signs in the legs and perianal numbness. Tendon reflexes tend to be increased below the level of the lesion and absent at the level of the lesion

107
Q

where does spinal cord end?

A

L1/2

108
Q

what in the history gives away that it is neoplastic spinal cord compression

A

diagnosis/prev diagnosis of cancer !!!! need to ask!!!

109
Q

investigation neoplastic spinal cord compression

A

urgent MRI: the 2019 NICE guidelines recommend a whole MRI spine within 24 hours of presentation

110
Q

management neoplastic spinal cord compression

A

high-dose oral dexamethasone
urgent oncological assessment for consideration of radiotherapy or surgery

111
Q

features of spinal metastases as a cause of back pain?

A

Unrelenting lumbar back pain
Any thoracic or cervical back pain
Worse with sneezing, coughing or straining
Nocturnal
Associated with tenderness!!

112
Q

examination spinal mets - finding?

A

may be tender

also check for any neurological features - if any are present then spinal cord compression must be suspected and acted on promptly

113
Q

invetsigation ?spinal mets

A

Without neurological features, a whole spine MRI should be completed within one week. The whole spine should be imaged as patients commonly present with multi-level disease.

114
Q

how does speed of onset guide ddx spinal cord compression

A

The speed of onset of symptoms varies and can give clues as to the underlying cause. A sudden onset is suggestive of a cord infarction or a disc herniation with compression. Progression over days is suggestive of an inflammatory process, while a slower progression over weeks and months is suggestive of a metabolic, neoplastic or neurodegenerative process.

115
Q

what is radiculopathy

A

nerve root compression

116
Q

how does radiculopathy present?

A

Single dermatome/myotome. Radiating sharp shooting nerve pain

if any objective neuro signs - LMN signs

117
Q

causes of radiculopathy?

A

Spinal degenerative changes eg osteophyte formation

Prolapsed disc (When a spinal disc becomes herniated in the neck, it can leak out into the spinal canal or nerve root tunnel and impinge on the exiting nerve root.)

118
Q

how does cervical myelopathy present?

A

Wide-based spastic gait with clumsy upper extremity function

  • compression of the corticospinal tracts –> resulting in loss of voluntary skeletal muscle control
  • compression of spinocerebellar tracts (proprioception).
119
Q

Presentation sciatica - symptoms and signs

A

PC: unilateral shooting pain in dermatomal distribution down the back of the leg.
- leg pain usually worse than back
- pain often worse when sitting

o/e:
Positive straight leg raise test

120
Q

Management sciatica

A

Management
If red flags present, arrange emergency referral
Arrange 2ww spinal surgery referral if suspicion of tumour or infection w/o neuro dysfunction
If no red flags, use START BACK tool to stratify risk of poor outcome
Self management advice, resume normal activities
Analgesia: NSAIDs, codeine, paracetamol
If high risk, refer to group exercise program +/- physio +/- CBT
Review:
Severe radicular pain at 2–6 weeks (depending on severity and improvement).
Non-tolerable radicular pain at 6 weeks.
Acute and severe sciatica — for consideration for an epidural corticosteroid/local anaesthetic injection.
Sciatica when non-surgical treatment has not improved pain or function — for consideration for spinal decompression.

121
Q

L3 nerve root compression

A

Sensory loss over anterior thigh
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test

122
Q

L4 nerve root compression

A

Sensory loss anterior aspect of knee
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test

123
Q

L5 nerve root compressio

A

Sensory loss dorsum of foot
Weakness in foot and big toe dorsiflexion
Reflexes intact
Positive sciatic nerve stretch test

124
Q

what analgesia should you use sciatica

A
  1. NSAIDs, codeine, paracetamol
  2. if bad at follow up - Amitriptyline or
    Duloxetine

NICE state not to use gabapentin, pregabalin, diazepam or oral corticosteroids for sciatica.

They state not to use opioids for chronic sciatica.

They suggest considering a neuropathic medication if symptoms are persisting or worsening at follow up, but not gabapentin or pregabalin, leaving at the main choices of:
Amitriptyline
Duloxetine

125
Q

S1 nerve root compression

A

Sensory loss posterolateral aspect of leg and lateral aspect of foot
Weakness in plantar flexion of foot
Reduced ankle reflex
Positive sciatic nerve stretch test

126
Q

specialist management options for chronic sciatica

A

Epidural corticosteroid injections
Local anaesthetic injections
Radiofrequency denervation
Spinal decompression

127
Q

causes of cauda equina? most common cause?

A

the most common cause is a central disc prolapse
this typically occurs at L4/5 or L5/S1

other causes include:
tumours: primary or metastatic
infection: abscess, discitis
trauma/fracture
haematoma

128
Q

plan ?cauda equina

A

Investigation
urgent MRI

Management
surgical decompression

129
Q

features cauda equina

A

low back pain

bilateral sciatica - present in around 50% of cases

reduced sensation/pins-and-needles in the perianal area

decreased anal tone

urinary dysfunction

130
Q

Presentation myelopathy

A

Bilateral as spinal cord and bladder/bowel, not always painful “clumsiness” “loss of manual dexterity”
Symptoms such as clumsiness of hands and feet, decreased manual dexterity, and an unsteady gait. Cervical pain may be present but its absence does not exclude this diagnosis.
Signs appear before symptoms

131
Q

what is lumbar spinal stenosis

A

Lumbar spinal stenosis is a condition in which the central canal is narrowed by tumour, disk prolapse or other similar degenerative changes.

132
Q

features lumbar spinal stenosis

A

back pain, neuropathic pain and symptoms mimicking claudication. One of the main features that may help to differentiate it from true claudication in the history is the positional element to the pain. Sitting is better than standing and patients may find it easier to walk uphill rather than downhill.

133
Q

most common underlying cause lumbar spinal stenosis

A

degenerative changes

134
Q

investigation lumbar spinal stenosis

A

MRI scanning is the best modality for demonstrating the canal narrowing.

135
Q

management lumbar spinal stenosis

A

laminectomy

136
Q

How does brown sequard syndrome present?

A

ipsilateral = loss of proprioception and vibration

ipsilateral = paralysis

contralateral = loss of pain and temperature

at spinal cord level ipsilateral loss of all sensation

137
Q

how will anterior cord syndrome present?

A

Damage to the anterior portion of the spinal cord will cause bilateral disruption of the spinothalamic tracts, resulting in bilateral loss of pain and temperature sensation.

The corticospinal tracts are also likely to have been affected, resulting in bilateral spastic paralysis and UMN signs.

Due to its posterior position in the spinal cord, the dorsal columns won’t be affected, meaning that fine touch, proprioception, and vibration sensation will be preserved.

138
Q

common cause of anterior cord syndrome

A

anterior spinal artery stroke

As there is only one anterior spinal artery, blockage of this can damage the whole anterior part of the spinal cord.3 This is analogous to a stroke within the spinal cord but can also be caused by external compression or flexion injuries.

139
Q
A
140
Q

Presentation b12 defieciency

A

Haematological: anaemia and associated symptoms

Neurological: subacute combined degeneration of the spinal cord (SACD) - bilateral dorsal column signs, may have bilateral corticospinal tract signs (affects posterior cord)
and sensory loss peripheral neuropathy

Psychiatric: mild neurosis to severe dementia; depression, personality change, psychosis, bipolar disorder, panic disorder and phobia

141
Q

presentation subacute degeneration of spinal cord

A

bilateral dorsal column signs, may have bilateral corticospinal tract signs (affects posterior cord)

142
Q

prevention subacute combined degeneration of spinal cord

A

Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord

143
Q

management b12 deficieny

A

With neurological involvement
Replacement therapy:
- IM hydroxocobalamin 1mg once daily on alternative days until no further improvement
Maintenance therapy:
- IM Hydroxocobalamin 1mg, which usually lasts for life, once every 2 months

Without neurological involvement
Replacement therapy:
- IM Hydroxocobalamin 1mg three times a week for 2 weeks
Maintenance therapy (diet related):
- IM Hydroxocobalamin 1mg twice a year
Maintenance therapy (non-diet related):
- IM Hydroxocobalamin 1mg once every 2-3 months for life

Within 7 to 10 days of starting treatment, FBC should be performed to check for treatment response.
No response: check serum folate level
Haemoglobin level and reticulocyte index above normal range: adequate treatment

144
Q

other name for b12

A

cobalamin

145
Q

pathophysiology pancreatitis

A

inflammation of the pancreas. Autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis, caused most commonly by gallstones or alcohol

Each cause will trigger a premature and exaggerated activation of the digestive enzymes within the pancreas. The resulting pancreatic inflammatory response causes an increase in vascular permeability and subsequent fluid shifts (often termed “third spacing”).
Enzymes are released from the pancreas into the systemic circulation, causing autodigestion of fats (resulting in a ‘fat necrosis’) and blood vessels (sometimes leading to haemorrhage in the retroperitoneal space). Fat necrosis can cause the release of free fatty acids, reacting with serum calcium to form chalky deposits in fatty tissue, resulting in hypocalcaemia.

146
Q

causes pancreatitis

A

GET SMASHED
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion stings
Hypertriglyceridemia, hypercalcaemia and hyperparathyroidism
ERCP – endoscopic retrograde cholangiopancreatography
Drugs – such as sodium valproate, azathioprine and sulphonamides

147
Q

sudden onset severe constant epigastrium pain radiating to the back/flanks with profuse vomiting

worsen with movement and improve by leaning forwards/in foetal position

A

pancreatitis

148
Q

typical history pancreatitis

A

PC: sudden onset severe constant epigastrium pain radiating to the back/flanks with profuse vomiting
HoPC: worsen with movement and improve by leaning forwards/in foetal position. If caused by gallstones, pain may be described as sudden and knife-like, and may be worse after food.
If alcohol-related, pain may be of less abrupt onset and poorly localized.
Red flags:
Environment: alcohol intake
MHx:
DHx: sodium valproate, azathioprine and sulphonamides

149
Q

o/e pancreatitis

A
  • pain better on leaning forwards
  • fever (inflammation or sepsis)
  • signs of shock
  • Cullen’s sign (bruising around the umbilicus) and Grey Turner’s sign (bruising in the flanks) , representing retroperitoneal haemorrhage.
150
Q

plan ?pancreatitis

A

Plan:
Investigation:
Admit to hospital
Fluid resus, access, abx, o2, parenteral feeding
Bloods: lipase, amylase, liver and renal function, and inflammatory marker levels.
Imaging: USS, CT, MRI
Imaging MRCP

Management:
ERCP if gallstones is the cause
Cholecystectomy

151
Q

which is better amylase or lipase

A

raised serum lipase is more accurate for acute pancreatitis, as it remains elevated longer than amylase

Serum amylase or serum lipase – diagnostic of acute pancreatitis if 3x the upper limit of normal*

Amylase can also be marginally raised in pathologies such as bowel perforation, ectopic pregnancy, or diabetic ketoacidosis

152
Q

LFTs pancreatitis

A

assess for any concurrent cholestatic element to the clinical picture. Patients with acute pancreatitis noted that an alanine transaminase (ALT) level >150U/L has a positive predictive value of 85% for gallstones as the underlying cause

153
Q

What are some GI/renal causes of back pain

A

acute pancreatitis

acute pyelonephritis

renal colic (stones)

154
Q
A
155
Q

what is acute pyelonephritis?

A

Acute pyelonephritis is an infection of one or both of the kidneys.

It occurs as a result of an ascending urinary tract infection (UTI) which has spread from the bladder up towards the kidneys. It is usually caused by bacteria entering the urinary tract through the urethra.

156
Q

Typical history acute pyleonephritis

A
  • fever
  • flank pain usually unilateral
  • nausea and vomiting
  • haematuria
  • foul smelling urine
  • malaise
  • diarrhoea
  • confusion
157
Q

what should you examine for ?acute pyleonephritis

A
  • Tenderness over the loin area
  • Signs of shock

Urosepsis is a life-threatening complication of pyelonephritis and can lead to septic shock. Signs include hypotension tachypnoea, skin changes, oliguria

158
Q

how may acute pyelonephirits present at extremes of age?

A

Young children may have non-specific symptoms such as a fever, irritability and poor feeding

Elderly patients may present with increased confusion or new incontinence.

159
Q

how to make a diagnosis of aucte pyelonephritis?

A

a definitive diagnosis can be made in patients with loin pain and/or fever if a UTI is confirmed by culturing a urinary pathogen from the urine and other causes of loin pain and/or fever have been excluded.

160
Q

Invetsigations ?acute pyelonephritis

A
  1. Mid-stream urine (MSU) / Catheter specimen urine (CSU)

Consider:
- urinalysis
- blood cultures
- fbc, inflammatory markers etc

Imaging in men, children and recurrent
- USS in children (no radiation, quick)
- CT KUB non-contrast = more sensitive
- MRI in preg women

161
Q

what may an USS for ?acute pylepnephritis show?

A

May identify obstruction or stones
May identify complications such as perinephric collections and hydronephrosis

162
Q

Management acute pyleonephritis

A
  1. Admit to hospital if:
    Severe illness (tachy, hypotension, reduced urine output, tachypnoea, confusion
    Severe pain
    Not improving after 48 hours in community
    Pregnant
    Under 3 months or older than 65 years
    Underlying diseases: diabetes or abnormality of genitourinary tract
  2. IV abx, IV fluids, analgesia, anti-emetics

If community :
7-10 days oral abx : co-amoxiclav, cefalexin, trimethorpim or ciprofloxacin

163
Q

What invetsigations are really important to exclude GI/renal cuase of back pain in ED

A
  1. serum amylase or lipase
  2. If normal, consider USS of abdomen to exclude AAA

+ in patientes with ?renal colic, consider abdo USS as this will indicate urteric or renal obstruction and give na aortic diameter to rule out AAA

164
Q

two key complications of kidney stones

A

Obstruction leading to acute kidney injury

Infection with obstructive pyelonephritis

165
Q

most common type of kidney stone?

A

Calcium-based stones are the most common type of kidney stone (about 80%).

There are two types of calcium stones:
Calcium oxalate (more common)
Calcium phosphate

166
Q

risk factors for renal stone

A

dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, polycystic kidney disease
beryllium or cadmium exposure

167
Q

other types (non-calcium based) of kidney stones

A

Uric acid – these are not visible on x-ray
Struvite – produced by bacteria, therefore, associated with infection
Cystine – associated with cystinuria, an autosomal recessive disease

168
Q

what is a staghorn calculus? when does this occur?

A

Most commonly, this occurs with stones made of struvite. In recurrent upper urinary tract infections, the bacteria can hydrolyse the urea in urine to ammonia, creating the solid struvite.

A staghorn calculus is where the stone forms in the shape of the renal pelvis, giving it a similar appearance to the antlers of a deer stag. The body sits in the renal pelvis with horns extending into the renal calyces. They may be seen on plain x-ray films.

169
Q

Presentation kidney stones

A

Renal stones may be asymptomatic and never cause an issue.

Renal colic is the presenting complaint in symptomatic kidney stones.

Renal colic is:
Unilateral loin to groin pain that can be excruciating (“worse than childbirth”)
Colicky (fluctuating in severity) as the stone moves and settles

170
Q

Invetsigations ?kidney stones

A
  • urine dip = usually shows haematuria and is useful for excluding infection. a normal urine dip doesn’t exclude stones
  • Non-contrast computer tomography (CT) of the kidneys, ureters and bladder (CT KUB) is the initial investigation of choice for diagnosing kidney stones. within 14 hours of admission
    OR immediately if fever, one kidnet, diagnosis uncertain

urine dipstick and culture
serum creatinine and electrolytes: check renal function
FBC / CRP: look for associated infection
calcium/urate: look for underlying causes
also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis

171
Q

three causes of raised calcium

A

calcium supplementation

hyperparathyroidism

cancer (e.g., myeloma, breast or lung cancer).

172
Q

Management kidney stones

A

Analgesia
1. NSAID eg IM diclofenac
or IV paracetamol. Opiates are not very helpful for pain management and are not routinely used.

Antiemetic

Antibitoic if infection present

Renal stones
- watchful waiting if < 5mm and asymptomatic
- 5-10mm shockwave lithotripsy
- 10-20 mm shockwave lithotripsy OR ureteroscopy
> 20 mm percutaneous nephrolithotomy

Uretic stones
- <10mm shockwave lithotripsy +/- alpha blockers
- 10-20 mm ureteroscopy

If causing hydronephrosis and sepsis, need to relieve obstruction and treat infection before distrupting stone –> nephrostomy if acute. ureteric stent if chronic

173
Q

when is surgical intervention indicated for kidney stones? what interventions?

A

required in large stones (10mm or larger), stones that do not pass spontaneously or where there is complete obstruction or infection.

Extracorporeal shock wave lithotripsy (ESWL):
ESWL involves an external machine that generates shock waves and directs them at the stone under x-ray guidance. The shockwaves break the stone into smaller parts to make them easier to pass.

Ureteroscopy and laser lithotripsy:
A camera is inserted via the urethra, bladder and ureter, and the stone is identified. It is then broken up using targeted lasers, making the smaller parts easier to pass.

Percutaneous nephrolithotomy (PCNL):
PCNL is performed in theatres under a general anaesthetic. A nephroscope (small camera on a stick) is inserted via a small incision at the patient’s back. The scope is inserted through the kidney to assess the ureter. Stones can be broken into smaller pieces and removed. A nephrostomy tube may be left in place after the procedure to help drain the kidney.

Open surgery

174
Q

how do you advise patients with a kidney stone to prevent recurrent stones

A

Increase oral fluid intake (2.5 – 3 litres per day)

Add fresh lemon juice to water (citric acid binds to urinary calcium reducing the formation of stones)

Avoid carbonated drinks (cola drinks contain phosphoric acid, which promotes calcium oxalate formation)

Reduce dietary salt intake (less than 6g per day)

Maintain a normal calcium intake (low dietary calcium might increase the risk of kidney stones)

For calcium stones – reduce the intake of oxalate-rich foods (e.g., spinach, beetroot, nuts, rhubarb and black tea)
For uric acid stones – reduce the intake of purine-rich foods (e.g., kidney, liver, anchovies, sardines and spinach)
Limit dietary protein

175
Q

what medicatuons can be used to prevent recurrence of kidney stones?

A

Potassium citrate in patients with calcium oxalate stones and raised urinary calcium

Thiazide diuretics (e.g., indapamide) in patients with calcium oxalate stones and raised urinary calcium

176
Q

drug causes kidney stones

A

drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline

177
Q

pathophysiology syringomyelia

A

Development of a fluid-filled cyst (a syrinx) around the spinal canal.
Causes: Chiari malformation, tumour, trauma

178
Q

presentation syringomyelia

A

‘central cord syndrome’ bilateral spinothalamic and/or bilateral corticospinal tract symptoms. The upper limbs are affected first whilst the lower limbs are spared until much later.

classically said to be a “cape-like” loss of pain and temperature sensation.

179
Q

plan ?syrinfomyelia

A

Investigation: full spine MRI with contrast and brain MRI
Management: treat cause. If persistent : shunt

180
Q

causes iliopsoas abscess

A

Primary
Haematogenous spread of bacteria
Staphylococcus aureus: most common

Secondary
Crohn’s (commonest cause in this category)
Diverticulitis, colorectal cancer
UTI, GU cancers
Vertebral osteomyelitis
Femoral catheter, lithotripsy
Endocarditis
intravenous drug use

181
Q

prognosis iliopsoas abscess

A

mortality rate can be up to 19-20% in secondary iliopsoas abscesses compared with 2.4% in primary abscesses.

182
Q

examination iliopsoas abscess

A

Patient in the supine position with the knee flexed and the hip mildly externally rotated
Specific tests to diagnose iliopsoas inflammation:
Place hand proximal to the patient’s ipsilateral knee and ask patient to lift thigh against your hand. This will cause pain due to contraction of the psoas muscle.
Lie the patient on the normal side and hyperextend the affected hip. This should elicit pain as the psoas muscle is stretched.

183
Q

investigation of choice ?iliopsoas abscess

A

CT abdomen

184
Q

MAnagement of iliopsoas abscess

A

Antibiotics
Percutaneous drainage is the initial approach and successful in around 90% of cases

Surgery is indicated if:
1. Failure of percutaneous drainage
2. Presence of an another intra-abdominal pathology which requires surgery

185
Q

features iliopsoas abscess

A

Fever
Back/flank pain
Limp
Weight loss

186
Q

spondylolisthesis vs slipped disc

A

spondylolisthesis = slipped verterbrae
- pain when moving

slipped disc = herniated disc, can compress nerves
- pain all the time