Block 4 Flashcards
What is peripheral vascular disease (PVD)
Peripheral vascular disease (PVD) can be noted as an obstruction of the large arteries that supply blood to the peripheries (outside heart and brain)
PVD causes
- Atherosclerosis is the most common cause, this is a thickening of the artery wall due to accumulation of calcium (loss of elasticity)
- Thromboembolism (blood clot)
- Aneurysm, localised blood filled bulge in wall of artery
- Inflammatory processes
PVD risk factors
- Smoking (over 80% are current or ex smokers, risk increase with number of smokes and years of smoking. Causes changes in the lining of blood vessels.
- Diabetes, 2-4 times increased risk of PVD, poor wound healing
- Hypertension (high BP)
- Obesity
- Stroke/CV disease
- Family history
- Dyslipidemia (high cholesterol)
Chronic PVD onset
Begins with claudication (pain with walking secondary to decreased circulation which is relevant with stopping. Cramping, aching, fatigue and numbness).
Remember that some patient may not complain of claudication if their activity is limited by other comorbidities and are not active.
It then progresses to resting pain which represents significant decrease in circulation. Patient report pain relief when limb is lower than heart as gravity will support circulation.
Characteristics of PVD
- Atrophy of calf muscle
- Loss of hair growth over the LL
- Thickening of nails
- Decreased subcutaneous tissue
- Shiny fragile skin
- Dependent rubor
Classification of PVD
0-6 categories each with increases severity of symptoms
0- Asymptomatic
1- Mild claudication
2- Moderate claudication
3- Severe claudication
4- Rest pain
5 - Minor tissue loss, ischemic ulceration not exceeding ulcer of the digits or foot
6- Major tissue loss, sever ischemic ulcers or frank gangrene
Diagnosis of PVD
Major diagnostic tool is the ankle brachial pressure index (ABI). Normal ABI is 1-1.40 in PVD the ABI is <0.9
Conservative management of PVD
Conservative measure are the first line for preventing disease progression after diagnosis. This can include smoking cessation, diabetic management, cholesterol management and exercise in the form of vascular rehabilitation.
Foot care - skin checks, well fitting shoes also important
Vascular rehabilitation
Aims to reduce limb symptoms, improve exercise capacity and prevent or lessen physical disability as well as reduce the occurrence of cardiovascular events.
Walking to near max pain improves intermittent claudication (due to development of collateral blood supply).
Main outcome measure is progressing the treadmill tests. This records claudication pain time (CPT) and maximum walking time (MWT). Altering speed and incline
Types of vascular surgery
Inflow operations
These are used to restore blood flow to the top of the leg
Outflow operations
Restores blood flow below the knee
AAA repair
Inflow operations
- Aorto bifermoal bypass graft
- Used for disease of the aorta below the kidneys and common iliac
- Patient often has sever claudication, non healing ulcers of extremities, aortic aneurisms
- Artificial blood vessel is used rather than natural graft due to large blood vessels involved. This is sewn above and below the diseased artery.
- Axillo bifemoral bypass graft
- Axillary artery is connected to the femoral using artificial graft, this is a large distance so prone to complications
- Iliofemoral bypass
- Cases of isolated or proximal common femoral artery occlusive disease. Graft originates from iliac arteries in pelvis and takes blood to the femoral arteries in groin
- Unilateral or femoral -femoral crossover
- From normal femoral artery in the groin on one legs and goes across to opposite leg
- Femoral endarterectomy
- Removes the atherosclerotic plaque in the lining of artery. This same process can be seen in carotid artery as well
Outflow operations
- Fenoro-popliteal bypass (graft from femoral artery to popliteal)
- Femoro-tibial bypass
- Femoro-crural bypass
AAA repair
Abdominal aortic aneurysm = localised ballooning of the abdominal aorta
Rupture of this is a medical emergency
- Open AAA repair
- Repaired by use of long tube shaped graft, sutured to the aorta
- Endovascular aortic repair (EVAR)
- Less invasive, stent graft inserted but not appropriate for all AAAs
Why do a pre op assessment for amputees
If able to do pre op assessment this is ideal. Gives info about previous level of mobility, home set up, as well as any pre existing respiratory/CV compromises. Helps to build report with patient and are often more receptive to education pre op.
Post op assessment
Circulation, chest and mobility
Need to reinforce foot care, exercise and lifestyle changes. Home exercise program, circulatory exercise and chest therapy.
Acute arterial occlusion
Associated with the 6 P’s - Pain, pallor (pale), pulselessness (pins and needles), paraesthesia, paralysis, poikilothermy (cold skin). Can occur within minutes to hours and are dur to sudden decrease in perfusion.
Foot amputations
- Amputation of toes
- Partial foot (forefoot)
- Ankle disarticulation
Commonly in diabetes with foot wounds. May need multiple follow up where amputation goes up.
NWB post op and require use of bootie (specialised shoe for gait)
Transtibial
- Poorer healing but better functional outcome
- Skin from calf is flapped over the front
- Rigid removeable dressing to protect and help with oedema
Transfemoral
Better healing (more proximal is better as healing closer to major artery) but lower functional outcome
Hip disarticulation
- Rarest and generally due to cancer
- Hip cut down sagittal plane
What is OA
- Disorder that involves multiple joints
- ECM degeneration and cell stress along with maladaptive repair processes
- Begins first as a molecular issue (abnormal joint tissue metabolism) this then progresses to have anatomic and/or physiologic abnormalities such as cartilage degeneration, bone remodelling, osteophyte formation, joint inflammation all of which contribute to loss of normal joint function.
- Important to remember that these issue can but don’t always relate to symptoms
A common misconception is that it is just wear and tear of articular cartilage but OA is a WHOLE joint disease (meniscus, labrum, cartilage, synovium, muscles, subchondral bone). Not just mechanical, also contains inflammatory and metabolic aspects
OA effects on joint components
In OA there is an imbalance between generation and degeneration of articular cartilage which is why there is net degeneration.
The synovial membrane cell involved in inflammation can trigger immune response, which can then affect balance of cartilage matrix degradation and repair. This will lead to more inflammation creating a cycle.
Within the subchondral bone osteophyte formation is a key symptom of OA as well as bone remodelling and bone marrow oedema
Classification of OA
Primary:
- Not resulting from injury or other disease
- Obesity is risk factor for this (even in NWB joint such as hand) and normally start around 55-60
- Can be inherited
Secondary:
- Result from a underlying local or systemic factor such as those with history of ACL injury or ankle sprain
OA risk factors
Non modifiable
- Age - exposure to risk factors as well as ageing related changes
- Sex - women
- Genetics
Modifiable
- Occupation/sport - to much may lead to secondary OA formation
- Trauma and injury - will disrupt articular surface. Increased prevalence after ACL reconstruction
- Alignment - valgus/varus or CAM in hip
- Obesity
- Muscle weakness - quads weakness leads to increased risk for knee
- Inactivity - suboptimal loading for cartilage and other tissues
Pain in OA
Some of the OA risk factors can be directly related to structural pathology which in itself can cause pain
Pain is mostly from nociceptive means, therefore inflammation which will leads to sensitisation. Small amount of people have neuropathic pain with OA.
OA pain is normally intermittent, mechanical (during or after WB) and predictable
Diagnosis of OA
Diagnosis through ACR with involve imaging and clinical tests or could use the NICE criteria which don’t involve these aspects.
Atypical features such as history of trauma, prolonged morning stiffness, rapid worsening of symptoms or presence of a hot swollen joint may indicate alternative diagnosis. These may include gout, other inflammatory arthritis (rheumatoid) or bone pain
NICE tool for OA diagnosis
Must have all:
- Age > 45
- Activity related joint pain
- Either no morning joint related stiffness or morning stiffness that lasts no longer than 30 mins
Most people that meet these will have accompanying imaging signs
Role of imaging in OA
Only imaging patients with OA if suspecting worse pathology or if it will change treatment direction which it probably will not. X-ray and MRI (can see loss of articular cartilage) used for this.
X-ray have grades from 0-4
MRI have knee OA score
However these do not directly relate to symptoms.
Clinical diagnosis without imaging normally sufficient
Clinical features of OA
General:
- Gradual onset, pain with WB and after, stiffness after prolonged rest, poor sleep
- Presences of comorbidities (obesity, diabetes, CV disease) can lead to a cycle as these prevent exercise
- Muscle atrophy and weakness
Knee:
- Pain in knee (either whole or just joint lines)
- Instability and giving way (pain inhibition of quads or from structural deformities)
- Crepitus
- Loss of full ROM (osteophytes, joint shape)
Hip:
- Pain in variety of areas around hip and thigh
Hands:
- Bony enlargement (easy to see)
5 stages of fracture healing
- Tissue damage and haematoma formation
- Inflammation and cellular proliferation
- Callus (woven bone) formation
- Consolidation
- Remodelling
