Vascular System - Acute & Chronic Ischaemia Flashcards
What is the Circulatory system transport for
Oxygen
Nutrients
Waste products
What does the circulatory system consist of
Heart
Vessels (arteries, capillaries, veins)
Lymphatics (to a lesser extent)
General structure of arteries and veins
Composed of 3 layers - tunics
Tunica intern, tunica media, tunica externa
Lumen
Lumen
Central blood-containing space surrounded by tunics
What are capillaries composed of
Endothelium with sparse basal lamina
Structure of elastic (conducting) arteries
Large lumen allows low-resistance conduction of blood
Contains elastin all 3 tunics
Where are elastic (conducting) arteries found
Thick-walled arteries near the heart; the aorta and its major branches
Function of elastic (conducting) arteries
Withstand and smooth out large blood pressure fluctuations
Allows blood to flow fairly continuously through the body
Structure of muscular (distributing) arteries and arterioles
Have thick tunica media with more smooth muscle and less elastic tissue
Active in vasoconstriction
Arterioles
Smallest arteries; lead to capillary beds
Control flow into capillary bed via vasodilation and constriction
When are veins formed
When venules converges
What are veins composed of
3 tunics, with a thin tunica media and thick tunica externa consisting of collage fibres and elastic networks
Veins as capacitance vessels
Blood reservoirs
Contains 65% of the blood supply
Special adaptations of veins
Large diameter BP, which offer little resistance to flow
Valves, which prevent back flow of blood
Venous sinuses
Specialised, flattened veins with extremely thin walls (e.g. coronary sinus of the heart and dural sinuses of the brain)
Anastomosis
Connection between two structures that are normally diverging e.g. arteriovenous
What is blood flow equivalent to
Cardiac output (CO), considering the entire vascular system
What is blood flow, or tissue perfusion, involved in
Delivery of oxygen and nutrients to, and removal of waste from tissue cells
Gas exchange in the lungs
Absorption of nutrients from the digestive system
What is blood pressure
Force per unit area exerted on the wall of a blood vessel by its contained blood
Main factors influencing BP
Cardiac output (CO) Peripheral resistance (PR) Blood volume
Blood pressure eqn
CO x PR
What is blood flow directly proportional to
The difference in bp between two points in the circulation
What is blood flow inversely proportional to
Resistance
R is more important than difference in bp between 2 points in the circulation
Systolic pressure
Pressure exerted on arterial walls during ventricular contraction
Diastolic pressure
Lowest level of arterial pressure during a ventricular cycle
Pulse pressure
The difference between systolic and diastolic pressure
Calculating MAP
Diastolic pressure + 1/3 pulse pressure
Venous BP throughout cardiac cycle
Steady and changes little during the cardiac cycle
Factors aiding venous return
Respiratory pump
Muscular pump
Valves prevent back flow during venous return
APBI
Ankle: Brachial Pressure Index
An objective vascular measurement of the vascular supply to the lower limbs
Body sites to palpate pulse
Temporal artery Facial artery Common carotid artery Brachial artery Radial artery Femoral artery Popliteal artery Posterior tibial artery Dorsalis pedis artery
Autoregulation
Automatic adjustment of blood flow to each tissue in proportion to the requirements at any given point in time
What does atherosclerotic disease have a predilection for
Carotid bifurcation LAD Aortic bifurcation Common bifurcation Superficial femoral Aorta just distal to left (subclavian)
Vascular disease - arterial
Narrow and block
Expand and pop
Embolus
What points does an aneurysm have a predilection for
Abdominal aorta
Popliteal Arteries
All the vessels
Embolus
A mass of clotted blood or other material
Brought by the blood from one vessel and forced into a smaller one, obstructing the circulation
What does a decrease in tissue perfusion promote
Compensatory mechanisms e..g vasodilation, development of collateral vessels and anaerobic metabolism
True aneurysm
When an aneurysm involves an intact attenuated arterial wall or thinned ventricular wall of the heart
Involves all 3 layers
When does an arterial dissection arise
Tear in the intima
When blood enters the arterial wall itself, a haematoma dissecting between its layers
False aneurysm (pseudo-aneurysm)
Defect in the vascular wall leading to an extravascular haematoma
Does not consist of the true layers of the arterial wall
Saccular aneurysms
Spherical out pouching
Vary from 5-20 cm in diameter
Often contain thrombus
Fusiform aneurysms
Involve diffuse, circumferential dilation of a long vascular segment
Vary in diameter (up to 20cm)
Factors of pathogenesis of aneurysms
The intrinsic quality of the vascular wall connective tissue is poor
The balance of collagen degradation and synthesis is altered
The vascular wall is weakened through loss of smooth muscle cells
Examples of poor intrinsic quality of the vascular wall
- Marfan syndrome – defective synthesis of fibrillin
- EDS – defective type III collagen causing weak vessel wall
- Vit C deficiency – altered collagen cross-linking
When does ischaemia of the inner media occur
When there is atherosclerotic thickening of the intima “increases the distance that oxygen and nutrients must diffuse”
Factors predisposing weakening of arterial wall
Atherosclerosis HTN Trauma Vasculitis Congenital defects Infections
How can mycotic aneurysms originate
From embolisation of a septic thrombus, usually as a complication of infective endocarditis
By circulating organisms directly infecting the arterial wall
Syphilitic aneurysms
3’ syphilis is now a rare cause of aortic aneurysms
Ischaemic injury can be caused by obliterative endarteritis
What are AAA’s associated with
Atherosclerotic plaque in the intima compresses the underlying media
Risk factors for AAA
Men
Smokers
Age 50+
Atherosclerosis
Where are AAA’s usually found
Usually positioned below the renal arteries and above the bifurcation of the aorta
Can be saccular or fusiform
Consequences of AAA
Rupture into the peritoneal cavity or retroperitoneal tissues with potentially fatal haemorrhage
Obstruction of a branch vessel resulting in ischaemic injury of downstream tissue
Embolism forms atheroma or mural thrombus
Px of AAA
Abdominal mass (pulsating) that simulates a tumour
When can aortic dissection be catastrophic
If the dissection then ruptures through the adventitia and haemorrhages into adjacent spaces
Aortic dissection classification
Type A dissection
Type B dissection
Type A dissection - aortic dissection
More common (dangerous) proximal lesions Involving either both ascending & descending aorta or just the ascending aorta
Type B dissection - aortic dissection
Distal lesions usually beginning distal to the L subclavian artery
Classical clinical symptoms of aortic dissection
Sudden onset of excruciating pain:
Beginning in the anterior chest
Radiating to the back between the scapulae
Moving downward as the dissection progresses
Confused with that of MI
Pathogenic mechanisms of vasculitis
Immune-mediated infl
Direct invasion of vascular walls by infectious pathogens
Infections can indirectly induce non-infectious vasculitis - by generating immune complexes or triggering cross-reactivity
Types of vasculitis
Large vessel
Medium vessel
Small vessel
Thromboangitis Obliterans (Buerger disease)
Distinctive disease that often leads to vascular insufficiency
Segmental, thrombosing, acute and chronic infl of medium-sized and small arteries
Epidemiology of Buerger disease
Occurs almost exclusively in heavy cigarette smokers, usually before the age of 35
Pathogenesis of Buerger disease
Strong rship to cigarette smoking
Genetic influences - certain HLA halotypes
Clinical features of Buerger’s disease
Cold sensitivity of the Raynaud type in the hands
Pain in the instep of the foot
Severe pain, related to the neural involvement
Chronic ulcerations of the toes, feet or fingers
What can bring drastic relief from further attacks of Buerger’s diesase
Abstinence of cigarette smoking
Varicose veins
Abnormally dilated, tortuous veins
The superficial veins of the upper and lower leg are typically involved
What are varicose veins produced by
Prolonged, increased intraluminal pressure
Loss of vessel wall support
What can happen when legs are dependent for prolonged periods
Venous pressure in these sites can be markedly elevated (up to 10x) and can lead to venous stasis and pedal oedema
Why is there a higher incidence of varicose veins in females
A reflection of the elevated venous pressure in lower legs caused by pregnancy
Most disabling sequelae of varicose veins
Incl persistent oedema in the extremity and ischaemic skin changes manifesting as stasis dermatitis and ulcerations
Where do venous ulcers usually occur
Gaiter areas
Thrombosed deep veins vs superficial
Embolism from the superficial veins is rare but thromboembolism is relatively frequent in thrombosed deep veins
Venous leg ulcers pathophysiology
80-85% of all cases develop when persistently high bp in the veins of the legs (venous htn) causes damage to the skin, which eventually breaks down and forms an ulcer
Interchangable names for venous thrombosis and infl
Thrombophlebitis
Phlebothrombosis
Portal vein thrombosis
Peritoneal infections (peritonitis, appendicitis, salpingitis and pelvic abscesses) Thrombophilic condn associated with platelet hyperactivity (e.g., polycythaemia vera)
Mechanical factors that slow venous return and promote DVT
Congestive heart failure
Pregnancy
Obesity
Trousseau sign
Venous thromboses classically appear at one site, disappear and then reoccur in other veins – migratory thrombophlebitis
Local manifestations of thrombi in legs incl
Distal oedema Cyanosis Superficial vein dilation Heat Tenderness Redness Pain
PE as a serious complication of DVT
Fragmentation/ detachment of the whole venous thrombus
Can be 1st manifestation of thrombophlebitis
Outcome ranges from no symptoms to death
What does Raynaud’s phenomenon result from
Exaggerated vasoconstriction of digital arteries and arterioles
What does secondary Raynaud’s refers to
Vascular insufficiency of the extremities 2’ to arterial disease caused by SLE, scleroderma, Buerger disease or even atherosclerosis
Peripheral Arterial Disease
Term used to describe a narrowing or occlusion of the peripheral arteries, affecting the blood supply to the lower limbs
What is PAD most caused by
Atherosclerosis which narrows the affected arteries. This limits blood flow to the affected limb
Epidemiology of PAD
More common in males
Prevalence rises with age
What diseases are PAD associated with
Coronary artery disease
Cerebrovascular disease
Fontaine classification of PAD
Stage I - Asymptomatic Stage IIa - mild claudication Stage IIb - moderate to severe (short distance) claudication Stage III - ischaemic rest pain Stage IV - ulceration or gangrene
Most common symptom of PAD
IC
Intermittent claudication
Exercise–induced muscle pain
Most commonly in the calf, thighs, buttocks
Worse walking uphill or hurrying
Relieved by rest <10 mins
Possible Intermittent Claudication sites
Buttock and hip
Thigh
Calf
Foot claudication
IC site - buttock and hip
Aortoiliac disease (Leriche syndrome triad)
IC site - thigh
Aortoiliac or common femoral artery
IC site - upper 2/3 of the calf
Superficial femoral artery
IC site - lower 1/3 of the calf
Popliteal artery
IC site - foot claudication
Tibial or peroneal artery
Types of ddx of PAD
Vascular
Neurological pain
MSK
Vascular ddx for PAD
Aneurysm Limb trauma Radiation exposure Vasculitis or ergot use for migraines Popliteal entrapment syndrome Chronic venous disease
Neurological ddx for PAD
Neurospinal (e.g. disc disease, spinal stenosis, tumour) Neuropathic causes (e.g. DM, alcohol abuse)
Prevalence of Chronic Limb Threatening Ischaemia
1 - 2%
When is Chronic Limb Threatening Ischaemia seen
When two or more levels of arterial tree are diseased
Ischaemic rest pain
Severe pain at rest due to inadequate oxygen perfusion
Chronic limb threatening ischaemia and Critical limb threatening ischaemia
Chronic limb threatening limb ischaemia can develop into Critical Limb ischaemia
Where do ischaemic ulcers form
At sites of increased focal pressure
Malleoli, tips of toes, metatarsal heads, heels
Usually dry and punctuate
What condn is dry gangrene most likely seen in
DM
When does dry gangrene develop
When blood flow to the affected area is impaired
The tissue dries up and may be brown to purplish-blue to black in colour
Can be left to auto-amputate or can be amputated after revascularisation
Wet gangrene
Liquefactive necrosis due to infection
The tissue swells and blisters and is called ‘wet’ because of pus
Why is wet gangrene v serious
Infection from wet gangrene can spread quickly throughout the body
Treatment of wet gangrene
Needs IV high dose Abx
Revascularisation, debridement +-/- amputation
Clinical exam for PAD
Inspection (scars, ulcers, gangrene, venous guttering) Buerger's test Palpation of pulses Auscultation for bruits APBI measurement
Vascular ix for PAD
Duplex ultrasound
CT angiography
Magnetic resonance angiography
Lifestyle modifications for asymptomatic PAD pts or mild claudication
Smoking cessation
Exercise
Diet control
Pharmacological therapy for asymptomatic PAD pts and mild claudication
Risk factor modification (control BP, diabetes, dyslipidaemias)
Antiplatelet therapy (clopidogrel 75mg OD)
Cholesterol lowering medication (atorvastatin 80mg OD)
Mx for short distance claudication - Lifestyle modification
Supervised exercise classes
Mx for short distance claudication - Pharmacological
BP/ DM/ Cholesterol control
Antiplatelet and statins
Naftidofuryl/ cilostazol
Mx of short distance claudication - endovascular
Angioplasty +/- stent placement
Mx of short distance claudication - Surgical
Endarterectomy
Peripheral bypass graft: autologous vein, prosthetic (long blockages of vessels)
Angioplasty
Pressure controlled balloon inflation to fracture arterial plaque and remodel the artery
What’s angioplasty most effective for
Short focal stenoses without heavy calcification
Excessive calcification is resistant to angioplasty
Complications of angioplasty
Arterial puncture site haemorrhage Arterial rupture Dissection Distal embolism Contrast induced nephropathy
Stents
Supportive framework that apply radial force to diseased arteries and promotes vessel remodelling
What are stents made from
Stainless steel or Nitinol
2 types of stents
Balloon expandable
Self-expanding stents
Surgical revascularisation
Endarterectomy
Surgical bypass
When is endarterectomy used in surgical revascularisation
For lesions in readily accessible sites, such as common femoral artery
Which surgical bypasses require a prosthetic graft
Infra-inguinals bypasses
Aorta-iliac
Femoral-femoral crossover
Axillo-bifemoral
Complications of surgical revascularisation
Bleeding Infection Distal embolism Limb loss Heart/ lung/ kidney complications DVT Death
Mx of CLTI
Lifestyle modification Pharmacological therapy Wound care - conservative mx Revascularisation Amputation
Leading cause of amputation in western world
PAD
How many more times likely are diabetics to suffer amputation
8-12x
What must be considered before amputation
Rehabilitative potential of the pt
Level and pattern of vascular disease
Likely healing
Common amputation sites
Toe amputation Ray amputation Tran-metatarsal amputation Below knee amputation Above knee amputation
Toe amputation
Removal of toe through proximal phalanx
Ray amputation
Removal of toe through metatarsal bone
Trans-metatarsal amputation
Amputation of all the toes through mid-metatarsal bones
Below knee amputation
Through tibia 10-12 cm distal to tibial tuberosity
Through fibula 2cm proximal to tibia
Above knee amputation
At mid-femoral level >15 cm from tibial plateau
Amputation complications
Failure of wound to heal Flap necrosis Wound infection Post amputation pain Stump haematoma Flexion contractures Psychological problems
Why should rehab be started ASAP after amputationn
Prevents flexion contractures
What happens after stump heals - amputation
Elasticated compression, stump socks fitted to shrink stump to an acceptable size for fitting for prosthesis
When is limb fitting usually delayed until
> 6/52 post-op to allow stump oedema to subside
Prognosis for IC
Variable, over 5-years most people continue to have stable claudication
10-20% develop worsening symptoms
5-10% develop critical limb ischaemia
Amputation in required in 1-2%
Prognosis of CLTI
High risk of amputation and premature death
50 - 90% will have a revascularisation procedure
1/3 require LL amputation if no revascularisation
5-yrs all cause mortality of 50%
ALI
A sudden decrease in limb perfusion that causes a potential threat to limb viability in pts who present within 2 weeks of the acute event
Surgical emergency
Incidence of ALI
1.5 cases per 10,000 people per yr but is a frequent missed or delayed dx
Aetiology of ALI
Embolus
Thrombosis
Trauma
Aetiology of ALI - Embolus
Cardiac source - AF, MI, endocarditis, valvular disease, atrial myxoma, prosthetic valves
Arterial source - aneurysms, atherosclerotic plaque
Aetiology of ALI - thrombosis
Vascular grafts Atherosclerosis Thrombosis of aneurysm Entrapment syndrome Hypercoaguable state Low flow state
Aetiology of ALI - Trauma
Blunt
Penetrating
Iatrogenic
6P’s of acute ischaemia
Pain Pulselessness Pallor Paresthesia Paralysis Poikilothermic (perishingly cold)
Imaging for ALI
CT angiography - distinguishes between thrombosis and embolism
Bedside Doppler ultrasound scan
Initial mx for ALI
ABC Analgesia FBC U&Es Baseline clotting profile Heparin IV access and IV resus ECG Catheterise and hourly UO
Giving heparin for ALI
Once the dx of acute arterial occlusion has been made the pt should immediately receive an IV-heparin bolus of 5,000 units followed by continuous infusion
What does mx of ALI depend on
Type of occlusion (thrombosis or embolus)
Location
Duration of ischaemia
Neurological deficit
Co-morbidities
Type of conduit (artery or graft, the risks of treatment and the viability of the limb)
Endovascular therapies for ALI
Percutaneous catheter-directed thrombolytic therapy
Percutaneous mechanical thrombus extraction
Surgical mx for ALI - emboli cause
Surgical embolectomy
Bypass surgery (if there is insufficient flow back)
Local intra-arterial thrombolysis
Amputation if limb is unsalvageable
Thromboembolectomy
Balloon connected to Fogarty catheter inflated removing thrombi
Complications of ALI
Compartment syndrome
Reperfusion injury
Compartment syndrome - complication of ALI
Reperfusion of ischaemic muscles can cause oedema and increased compartmental pressure
Reperfusion injury - complication of ALI
Products of cell death (e.g K, CO2 and myoglobin) are released when blood flow to ischaemic limb is restored
What can reperfusion injury result in
Rhabdomyolysis Cardiac dysrhythmia AKI Multi-organ failure Disseminated IV coagulation
Mortality of ALI
15 - 20% with about a 1/3 of deaths resulting from metabolic complications associated with revascularisation e.g. acidosis and hyperkalemia
Limb prognosis of ALI
Related to the severity of arterial disease, the acuteness of ischaemia onset, and how rapidly perfusion is restored
Causes of lower limb loss in less developed countries
Industrial, railway, farming accidents where safety measures are poor
Causes of lower limb loss in western world
90% vascular (60% PVD/ 30% DM)
Trauma - 5%
Neoplasm - 1%
Other (infection/ psychiatric ) - 4%
Levels of lower limb amputation
Hemi- pelvictomy Hip disartictlatrion Transfemoral Through knee Transtibial Symes (Ankle disarticulation) Chopart (mid-tarsal) Lisfrank (traso-metatrsal)
What does the energy required after amputation depend on
Level of amputation
Length of stump
Pt’s health/ commodity
Reason for amputation
Which level of amputation has the biggest increase in energy needed for gait above normal
Bilateral transfemoral - 200%
ICF
International Classification of Functioning, Disability and Health Framework
Forms basis of rehab med
What does ICF demonstrate the rship between
Health (disorder/ disease)
Function - body functions & structure, activity, participation
Disability - impairment, activity limitation, participation restriction
Role of rehab - pre-amp
Pt education
Defining expectations (ICE)
Determining suitability for artificial limb
Phantom limb prophylaxis
Determining suitability for artificial limb
Energy needed
Contratures
Allodynia
Cognition
PLP prophylaxis
PLP is associated with pre-operative pain and can be reduced with analgesia at least 72 hrs before surgery and 48 hrs after
Role of rehab immediately post-amp
Reduce complications
Maximise independence
Minimise pain and discomfort
Co-ordination and better use of resources
Role of amp rehab on the ward
Post-op care
Artificial limb fitting and training
Long term follow up
What does artificial limb fitting and training involve
Goal establishment
Stump casting and measurement and limb prescription from week 3 post-op
Gait retraining
Education on skincare, and artificial limb maintenance
Long-term follow up - rehab
Checking if new limb is required
Checking for changes in stump size and condn
Checking for changes in residual
Pain management and medical complications
Early walking aids (EWAs)
Used as early 5-7 days post amp
Temporary devices
Useful as part of the assessment process for suitability of artificial limb
Examples of EWA
Post-amputation mobility aid for TT
Femurett for TF
Gait retraining sequence
Full wt-bearing and transfer
Walking with 2 parallel bars
Walking with 2 stick between parallel bars
Walking with 1 stick outside bars
Gait challenges for an amputee
Ground clearance
Times initial (Heel) contact without proprioception
Loss of ability to aboard energy
Maintaining mid-stance on the prosthetic limb
Loss of foot eversion/ inversion AKA stopping knee from buckling
Transmit centre of gravity
Loss of push off in terminal stance
Phantom sensation
Feeling the missing part
Phantom pain
Pain in missing part
Superadded Phantom
Tight band, tight shoes, tight wristwatch over the missing part
Incidence of PLP
54% of all amputees
100% of all LL amputees
Mechanism of PLP
Unknown
Lacking peripheral input
Central cortical reorganisation
Psycho factors - grieving, depression
Why is PLP not a peripheral nervous phenomenon
Changes with time (telescoping)
Changes with interceptive stimuli e.g. micturition
Pharmacological mx of PLP
Analgesic ladder - paracetamol, NSAIDs, opioids
Anticovulsants
Low dose amitriptyline - 10mg then increase gradually up to 50mg
Treatment of clinical depression (if applicable)
Misc - baclofen, botulinum, beta-blockers
Examples of anticonvulsants
Gabapentin
Pregabalin
Carbamazepine
Physical mx of PLP
Massage Heat Accupuncture Electromagnetic TENS Electro-accupunture
Psychotherapy as mx for PLP
Distrcation
Relaxation
Autogenic hypnosis (controlling the phantom hypnosis)
Biofeedback (Ramachandran’s Mirror Box)
Local stump complications after amp
Skin breakdown/ ulcers
Pressure areas
What causes local stump complications
Poor donning technique Poor socket Associated neuropathy Change in stump volume Change in gait pattern Infection with or without ischaemia
Mx for local stump complications
Establish cause
Minimise prothetic use
Dynamic socket fitting/ repeat casting
Abx, regular dressing and reviews
Components of TT artificial limb
Socket Suspension mechanism Adaptor Shin tube Shock/ torque absorber Foot
Factors that would influence unemployment after amputation
Occupational ability
Work environment
What affects occupational ability after amputation
Individual - psychology, physical
Social factors - family support, organisational support
Work environment affecting employment after amputation
Legislations Social security system Welfare rights Labour market Employer - size of firm, work force flexibility
How does ionised state of drug affect passive diffusion
Unionised = lipid soluble = easy passage Ionised = water soluble = difficult passage
What does level of ionisation depend on
Dissociation constant Ka acid or base
pH of bodily fluid
Recommended treatment for aspirin overdose
NaHCO3
Examples of unionised drugs
Digoxin (for AF)
Prednisolone
Major rate-limiting factor for drugs
BBB - blood brain barrier
First order kinetics - exponential
As conc of drugs increases, rate of reaction (or breakdown of drugs) goes up
Has predictable half life
Zero order kinetics
Saturation = rate limited
Limited capacity of body to process drug
Dose increase - sudden toxicity
Bioavailability
Proportion of parenteral drug that passes into systemic circulation after administration
Improving bioavailability
Change in formulation
Route
Concurrent use of inhibitor
Apparent volume of distribution
Reflects amount of drug in plasma after being taken up
Total amount of drug in body/ plasma conc
Clearance of drugs
Amount of plasma totally cleared of drug
Elimination of drug from plasma
Main parameters of half-life
Clearance
Volume of distribution
How does clearance affect half life
High clearance = shorter half life
How does volume of distribution affect half life
High volume volume of distribution - longer half life
When will a drug reach a steady state
When drugs are given at a constant rate and after 5 half-lives
Either continuous infusion or intermittent chronic dosing
When do you use a large priming or loading dose
Quicker effect
Useful in urgent situation e.g Abx for sepsis
What if drug t 1/2 is short
Give larger dose frequently
Inhibit clearance
Reduce movement of drug to plasma
Modify formulation
Examples of modified release formulations
Sustained release tablets
Depot injectables
Atheroma
Cholesterol plaque
Risk factors of ALI
DM HTN Increased cholesterol & triglycerides AF (a/c blood clots) Obesity Fhx of PVD Trauma (immobilised --> DVT can embolise) Male sex
Spinal stenosis as ddx of IC
Pain gets better when walking uphill due to simian posture (extension) but worse in IC
Why are IC pts advised to exercise to point of pain and past
Hypoxia promotes angiogenesis
Sex difference of venous ulcers
F > M
Sex difference of arterial ulcers
M < F
Sex difference of neuropathic ulcers
F = M
Risk factors of venous ulcers
Previous DVT
Varicose veins
Incompetent valve
Risk factors of arterial ulcers
Smoking
HTN
DM
Risk factor of neuropathic ulcers
DM
Pain levels of different ulcers
Venous - not painful
Arterial - pressure areas
Neuropathic - usually painless, nerves are dead
Site of venous ulcers
Gaitar areas
Site of arterial ulcers
Pressure areas e.g. in between toes, heel
Vein in venous ulcers
Full, dilated
Veins in arterial ulcers
Not visible
Guttering
Veins in neuropathic ulcers
Veins are normal
Temperature of venous ulcers
Normal to warm
Temp of arterial ulcers
Cool
Temp of neuropathic ulcers
Warm or cold
Appearance of venous ulcers
Shallow and flat
Irregular margin
Slough at base
Moderate to heavy exudate
Appearance of arterial ulcers
Punched out
Regular shape
Presence of necrotic tissue
Apperance of neuropathic ulcers
Callous
Trophic
Insensate
Macerated
Site of neuropathic ulcers
Plantar aspect of foot
Tip of toe
Lateral to 5th metatarsal
Condn of leg when venous ulcer is present
Hemosiderin staining
Thickening and fibrosis
Eczematous and itchy skin
Normal CRT
Condn of leg when arterial ulcer is present
Thin, shiny skin
Pallor on leg elevation
Absent/ weak pulses
Delayed CRT
Treatment of venous ulcers
Compression stockings - check ABPI
Leg elevation
Surgical mx
Treatment of arterial ulcers
Revascularisation
Anti-platelet med
Mx of risk factors
Treatment of neuropathic ulcers
Off-loading of pressure
Topical growth factors
Features of asymptomatic PAD
Abnormal/absent pedal pulses
Age 70+
Age 50-69 and hx of smoking and DM
Tunica interna composition
Thin single layer of endothelium
Tunica media composition
Thicker contractile tissue made from circularly arranged elastic fibres, connective tissue and smooth muscle cells
Tunica externa composition
Connective tissue
Bifurcation
Where an artery splits into 2, common site for cholesterol build up and thrombus formation
Mural thrombus
Thrombus attaching two chamber walls
Where is mitral valve found
Between left atrium and left ventricle
Claudication hx
Exercise tolerance - how far can they work
How long to rest for
Rest pain?
When should duplex ultrasound not be done when investigating ischaemia
Absent limb pulses
Pre op work for vascular surgery
NTProBNP
LFT
Fibroscan
Consultant anaesthetic review
How is chronic limb ischaemia clinically defined
Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia
Presence of ischaemic lesions or gangrene
ABPI less than 0.5
Acute-on-chronic ischaemia
There is an acute often embolic event in a pt w/ previous PAD
What can cause a falsely high ABPI
Calcification and hardening of the arteries so any ABPI value >1.2 should be interpreted with caution
What can chronic limb ischaemia result in
Sepsis (2’ to infected gangrene)
Acute-on-chronic ischaemia
Amputation
Reduced mobility and QoL
Signs of Chronic Limb Ischaemia
Pale and cold limbs Weak/ absent pulses Limb hair loss Skin changes (atrophic skin, ulceration or gangrene) Thickened nails
Sensitive sign of ALI caused by emboli occlusion
A normal, pulsatile contralateral limb
What can cause a mural thrombus
Recent MI
Surgical mx for ALI - thrombotic cause
Local intra-arterial thrombolysis
Angioplasty
Bypass surgery
Thrombolectomy
Irreversible limb ischaemia
Mottled, non-blanching appearance
Requires urgent amputation or taking a palliative approach
What can release of substances in reperfusion injury cause
K+ - hyperkalemia
H+ - acidosis
Myoglobin - significant AKI
Leriche syndrome triad
Claudication
Absent femoral pulses
Erectile dysfunction
Conditions for use of compression stockings (venous)
Patent arteries and ABPI above 0.8
What does an ABPI of 1.3+ indicate
Abnormally hard vessel e.g. calcification
Common in diabetics
When would we hear biphasic signals on the Doppler
Beginning of arterial disease
Old age - vessels losing elasticity
Lipodermatosclerosis
Induration, pigmentation and infl of skin
When does an ulcer become chronic
4 weeks
Ulcers in which areas suggest pressure sores
Sacrum
Greater trochanter
Heel
Slough
Mixture of fibrin, cell breakdown products, serous exudate, leukocytes and bacteria
Does not always imply infection
Granulation tissue
Deep, pink, gel-like matrix contained within a fibrous collagen network
Evidence of a healing wound
What does associated lymphadenopathy w/ ulcers suggest
Infection or malignancy
Signs of high cholesterol in eyes
Corneal arcus
Xanthelasma
Signs of central cyanosis
Blue tongue and mouth
What can radio-radial delay be caused by
Aortic dissection (Type A) Difference in bp (>20 mmHg)
What can radio-femoral delay be caused by
Type B aortic dissection
Coarctation of the aorta
Differentiating between thrombotic and embolic cause of ALI
Pts with cardiac sources will have no hx of IC or PAD, and ABPI will not be low in both limbs
ABCDE approach - A
Voice, breath sounds
ABCDE approach - treatment of A
Head tilt, chin lift
Oxygen (15 litres)
Suction
ABCDE approach - B
Resp rate Chest wall movements Chest percussion Lung auscultation Pulse oximetry
ABCDE approach - treatment of B
Rescue breaths
Bag-mask ventilation
ABCDE approach - C
Skin colour, sweating CRT Pulse rate Heart auscultation BP ECG
ABCDE approach - treatment of C
Cannulate:
Give 500ml IV bolus for hypotension (saline or Hartmann’s)
Take bloods - FBC, cross-match, LFTs, U&E’s, ESR/CRP, ABG/VBG
ABCDE approach - D
Level of consiousncess - GCS
AVPU
Limb movements
Blood glucose
ABCDE approach - E
Expose skin - looking for lesions, erythema, wounds, fractures, rashes etc
Temp
What is key in ABCDE approach
Checking to see if interventions have helped
Leriche syndrome triad
IC
Erectile dysfunction
Absence of femoral pulse
Types of thrombotic ischaemia
Incomplete
Complete
Mx of incomplete ischaemia - thrombotic
Angiography to map out occlusion and plan intervention
Mx of complete ischaemia - thrombotic
Surgical bypass
Angio and thrombolysis delays mx - takes too long
