10. Back/neck pain Flashcards
(186 cards)
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
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?
3
Q
examiantion back pain?
A
spine + neuro + abdo
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
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)
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
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.
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)
9
Q
Vascualr causes of back pain?
A
AAA rupture
Aortic dissection
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.
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:
- lipid deposition
- inflammation damages internal and external elastic laminae of the aortic wall
- loss of elastic laminae = difficulty with pressure change from diastole to systole –> dilation
- fibrosis
- aortic wall weaker then systolic pressure –> rupture
(therefore made much worse with HTN)
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.
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
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
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.
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
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.
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
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.
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.
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
22
Q
presentation aortic dissection
A
sudden onset of severe chest pain radiating to the back
syncope, or neurological deficits.
Clinical presentation varies
23
Q
invetsigation ?aortic dissection?
A
CT angiogram
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
25
Associations aortic dissection
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
26
complications of aortic dissection
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
27
what are the infective cuases of back pain?
septic arthritis
osteomyelitis
discitis
epidural abscess
28
what are the most commonly affected joints septic arthritis
hip, knee and ankle
29
typical history septic arthritis
PC: hot red swollen painful joint, stiffness and reduced range of motion, systemic symptoms such as fever and lethargy
any hot/red joint
30
most common causative organism septic arthritis ? other causes
staph aureus
Neisseria gonorrhoea (gonococcus) in sexually active teenagers
Group A streptococcus (Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)
31
young pt presenting with single acutely swollen joint - first ddx?
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.
32
plan ?septic arthritis
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.
33
example first line regime septic arthritis abx
Flucloxacillin for 6 weeks
if pen allergic: clindamycin
If MRSA suspected: vancomycin
If gonococcal arthritis or gram -ve susepcted : cefotaxime or ceftriaxone
34
what criteria can be used in children to distinguish between septic arthritis and transient synovitis of hip
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
35
what is osteomyelitis
an infection in the bone and bone marrow.
This typically occurs in the metaphysis of the long bones.
36
what is the most common causative organism osteomyelitis
staph aureus
37
types of osteomyelitis and how do people get it?
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.
38
In what children is osteomyelitis more common
boys and children under 10 years
39
typical history osteomyelitis
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.
40
best imaging for dx of osteomyelitis
MRI
41
initial invetsigation osteomyelitis
xray
42
plan investigation ?osteomyelitis
1. xray
2. MRI if xray inconclusive
3. inflammatory markers CRP, ESR, WCC
4. blood culture
43
management osteomyelitis
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
44
what is discitis
Discitis is an infection in the intervertebral disc space. It can lead to serious complications such as sepsis or an epidural abscess.
45
typical history discitis
Back pain
General features
pyrexia,
rigors
sepsis
Neurological features e.g. changing lower limb neurology if an epidural abscess develops
46
most common cause discitis
staph aureus
47
plan ?discitis
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
48
what is a spinal epidural abscess?
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.
49
pathophysiology spinal epidural abscess
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.
50
Presentation spinal epidural abscess
fever
back pain
focal neurological deficits according to the segment of the cord affected.
51
invetsigations ?spinal epidural abscess
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.
52
management SEA
1. empirical abx
2. culture based abx
+ if compressive etc consider surgical evaluation
53
whata re some inflammatory cuases of back pain?
ankylosing spondylitis
scheurmann's disease
54
typical history ankylosing spondylitis
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
55
what may you find on examination ank spond
- 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
56
what gene is ank spond associated with ?
HLA B27
57
Investigation ank spond
1. plain xray of sacroiliac joints
2. if negative and still suspected, MRI
58
what may be found on xray in ank spond
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
59
why should you assess resp system in someone with ank spond, what might you find
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
60
first line management ank spond
NSAIDs
61
Management ank spond
1. NSAIDs
2. Paracetamol/codeine if poorly tolerated
3. Seek specialist advice
+ Physio
+ Hydrotherapy
+ OT
62
criteria for rheum referal ank spond
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.
63
complications/associations ank spond
apical fibrosis
anterior uveitis
CVS risk and heart involvement: aortic regurg, AV node block
osteoporosis and fractures
cauda equina
64
what is scheuermann's disease
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.
65
what does anterior wedging mean - spinal imaging
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.
66
presentation scheuermanns disease
progressive kyphosis (at least 3 vertebrae must be involved)
Symptoms include back pain and stiffness
67
management scheuermann's disease
Minor cases may be managed with physiotherapy and analgesia, more severe cases may require bracing or surgical stabilisation
68
x-ray changes scheuermanns
epiphyseal plate disturbance and anterior wedging
69
what are fragility fractures?
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
70
risk factors osteoporotic fractures?
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
71
where is (one of) the commonest sites of osteoporotic fragility frcatures to occur
the spine (vertebrae)
72
how do patients with osteoporotic vertebral fractures present?
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
73
o/e signs of osteoporotic vertebral fracture
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
74
first line investigation ?osteoprotic vertebral fracture
what does it show
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)
75
why can a cT or MRI be useful in osteoporotic fractures
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
77
What is osteoarthritis
Disorder of synovial joints where damage triggers repair processes leading to structural changes within a joint
78
key features of osteoarthritis
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
X-ray changes osteoarthritis
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
o/e hand signs osteoarthritis
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
plan establishing a diagnosis osteoarthrits
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
Management osteoarthritis
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
how does osteoarthritis in the spine present? what is it called?
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
complications of cervical spondylosis
radiculopathy and myelopathy
85
examination findings cervical spondylosis
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
red flags cervical spondylosis --> meylopathy
any upper motor neuron signs
- hypertonia
- babinski
- hyperreflexia
- sensory level
87
how does cervical radiulopathy present?
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
what spinal levels are most often affected by cervical radiculopathy
C5–C7 levels are most commonly affected
89
plan ?cervical radiculopathy
Plan:
Management
1. Rule out all red flags, if any red flags: refer immediately
2. 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
3. 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
what neoplastic things should you consider when a patient presents with back pain?
myeloma
neoplastic spinal cord compression
metastasis
91
what is myeloma
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
what is Monoclonal gammopathy of undetermined significance (MGUS)
is where there is an excess of a single type of antibody or antibody components without other features of myeloma or cancer.
93
pathophysiology myeloma
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
presentation myeloma
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
Initial tests myeloma
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
diagnostic criteria multiple myeloma
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
what is a Autologous hematopoietic cell transplantation
involves the removal of a patient's own stem cells prior to chemotherapy, which are then replaced after chemotherapy
98
what is allogenic haematopoeitic stem cell transplant
Allogenic hematopoietic cell transplantation
is not commonly used in myeloma due to high rates of overall mortality and symptoms of graft-ve
99
stages of myeloma treatment
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
symptom management and complication avoidance myeloma
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
Calcium level myeloma
Hypercalcaemia,
In cases of myeloma, there is hypercalcaemia secondary to increased osteoclast activity. Additionally, renal impairment causes hypercalcaemia and hyperphosphataemia.
102
Phosphate level myeloma
normal / high phosphate
renal impairment causes hypercalcaemia and hyperphosphataemia
103
ALP myeloma
normal ALP
ALP enzyme levels remain normal with myeloma but may rise in other conditions such as solid tumours or bony metastases.
104
Pathophysiology neoplastic spinal cord compression
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
most common cancers --> neoplastic spinal cord compression
lung, breast and prostate cancer
106
features of neoplastic spinal cord compression
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
where does spinal cord end?
L1/2
108
what in the history gives away that it is neoplastic spinal cord compression
diagnosis/prev diagnosis of cancer !!!! need to ask!!!
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investigation neoplastic spinal cord compression
urgent MRI: the 2019 NICE guidelines recommend a whole MRI spine within 24 hours of presentation
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management neoplastic spinal cord compression
high-dose oral dexamethasone
urgent oncological assessment for consideration of radiotherapy or surgery
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features of spinal metastases as a cause of back pain?
Unrelenting lumbar back pain
Any thoracic or cervical back pain
Worse with sneezing, coughing or straining
Nocturnal
Associated with tenderness!!
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examination spinal mets - finding?
may be tender
also check for any neurological features - if any are present then spinal cord compression must be suspected and acted on promptly
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invetsigation ?spinal mets
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.
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how does speed of onset guide ddx spinal cord compression
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.
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what is radiculopathy
nerve root compression
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how does radiculopathy present?
Single dermatome/myotome. Radiating sharp shooting nerve pain
if any objective neuro signs - LMN signs
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causes of radiculopathy?
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.)
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how does cervical myelopathy present?
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).
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Presentation sciatica - symptoms and signs
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
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Management sciatica
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.
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L3 nerve root compression
Sensory loss over anterior thigh
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test
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L4 nerve root compression
Sensory loss anterior aspect of knee
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test
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L5 nerve root compressio
Sensory loss dorsum of foot
Weakness in foot and big toe dorsiflexion
Reflexes intact
Positive sciatic nerve stretch test
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what analgesia should you use sciatica
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
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S1 nerve root compression
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
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specialist management options for chronic sciatica
Epidural corticosteroid injections
Local anaesthetic injections
Radiofrequency denervation
Spinal decompression
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causes of cauda equina? most common cause?
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
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plan ?cauda equina
Investigation
urgent MRI
Management
surgical decompression
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features cauda equina
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
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Presentation myelopathy
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
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what is lumbar spinal stenosis
Lumbar spinal stenosis is a condition in which the central canal is narrowed by tumour, disk prolapse or other similar degenerative changes.
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features lumbar spinal stenosis
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.
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most common underlying cause lumbar spinal stenosis
degenerative changes
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investigation lumbar spinal stenosis
MRI scanning is the best modality for demonstrating the canal narrowing.
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management lumbar spinal stenosis
laminectomy
136
How does brown sequard syndrome present?
ipsilateral = loss of proprioception and vibration
ipsilateral = paralysis
contralateral = loss of pain and temperature
at spinal cord level ipsilateral loss of all sensation
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how will anterior cord syndrome present?
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.
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common cause of anterior cord syndrome
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
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Presentation b12 defieciency
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
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presentation subacute degeneration of spinal cord
bilateral dorsal column signs, may have bilateral corticospinal tract signs (affects posterior cord)
142
prevention subacute combined degeneration of spinal cord
Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord
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management b12 deficieny
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
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other name for b12
cobalamin
145
pathophysiology pancreatitis
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.
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causes pancreatitis
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
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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
pancreatitis
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typical history pancreatitis
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
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o/e pancreatitis
- 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.
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plan ?pancreatitis
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
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which is better amylase or lipase
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
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LFTs pancreatitis
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
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What are some GI/renal causes of back pain
acute pancreatitis
acute pyelonephritis
renal colic (stones)
154
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what is acute pyelonephritis?
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.
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Typical history acute pyleonephritis
- fever
- flank pain usually unilateral
- nausea and vomiting
- haematuria
- foul smelling urine
- malaise
- diarrhoea
- confusion
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what should you examine for ?acute pyleonephritis
- 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
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how may acute pyelonephirits present at extremes of age?
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.
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how to make a diagnosis of aucte pyelonephritis?
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.
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Invetsigations ?acute pyelonephritis
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
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what may an USS for ?acute pylepnephritis show?
May identify obstruction or stones
May identify complications such as perinephric collections and hydronephrosis
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Management acute pyleonephritis
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
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What invetsigations are really important to exclude GI/renal cuase of back pain in ED
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
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two key complications of kidney stones
Obstruction leading to acute kidney injury
Infection with obstructive pyelonephritis
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most common type of kidney stone?
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
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risk factors for renal stone
dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, polycystic kidney disease
beryllium or cadmium exposure
167
other types (non-calcium based) of kidney stones
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
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what is a staghorn calculus? when does this occur?
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.
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Presentation kidney stones
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
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Invetsigations ?kidney stones
- 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
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three causes of raised calcium
calcium supplementation
hyperparathyroidism
cancer (e.g., myeloma, breast or lung cancer).
172
Management kidney stones
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
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when is surgical intervention indicated for kidney stones? what interventions?
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
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how do you advise patients with a kidney stone to prevent recurrent stones
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
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what medicatuons can be used to prevent recurrence of kidney stones?
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
drug causes kidney stones
drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline
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pathophysiology syringomyelia
Development of a fluid-filled cyst (a syrinx) around the spinal canal.
Causes: Chiari malformation, tumour, trauma
178
presentation syringomyelia
‘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
plan ?syrinfomyelia
Investigation: full spine MRI with contrast and brain MRI
Management: treat cause. If persistent : shunt
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causes iliopsoas abscess
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
prognosis iliopsoas abscess
mortality rate can be up to 19-20% in secondary iliopsoas abscesses compared with 2.4% in primary abscesses.
182
examination iliopsoas abscess
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
investigation of choice ?iliopsoas abscess
CT abdomen
184
MAnagement of iliopsoas abscess
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
features iliopsoas abscess
Fever
Back/flank pain
Limp
Weight loss
186
spondylolisthesis vs slipped disc
spondylolisthesis = slipped verterbrae
- pain when moving
slipped disc = herniated disc, can compress nerves
- pain all the time
