Vascular 2 Flashcards
PAD definition
Narrowing/occlusion of peripheral arteries, reducing blood supply to lower limbs
Chronic limb ischaemia types
Intermittent claudication
Critical limb ischaemia
Chronic limb-threatening ischaemia
Acute limb ischaemia definition
Sudden decrease in limb perfusion due to thrombotic/embolic cause
Atheroma formation
Endothelial dysfunction (LDL/HTN) allows LDL deposits.
LDL enters intima and gets oxidised, activates endothelial cells to recruit leukocytes
Monocytes/Th enter intima.
Monocytes - > macrophages. Take up LDL -> Foam cells (Fatty streak)
foam cells promote myocyte migration from tunica media (collagen synthesis)
Foam cell dies, lipid content released.
Have atheroma plaque formation.
Plaque ruptures and thrombus forms.
High risk plaques have thin cap with large lipid core.
Common atheroma sites
Circle of willis Carotid arteries Popliteal arteries Coronary arteries Abdominal aorta
Athersclerosis sequelae
Weakened vessel wall (arterial aneurysm, dissection)
Demand/supply mismatch (CHD, PAD, vascular dementia)
Thrombosis (ACS, stroke, acute limb ischaemia)
Renovascular hypertension
Atheroma RF
Hypercholesterolaemia, DM, old age, inactivity, HTN, smoking, obesity
Atherosclerosis S+S
Generally asymptomatic, but can have xanthalasma, carotid/ abdo bruit, AAA and loss of peripheral pulse
Intermittent Claudication
Pain on walking (ischaemia), relieved by rest
Gripping calf/thigh/buttock pain. Predominates in one leg, reproducible by walking same distance. If bilateral then internal iliacs often affected and may have ED
Comparison between intermittent claudication and cauda equina
Fixed distance in ID, variable in CE
Pain worse on uphill, better downhill in IC. Worse downhill in CE
Pain disappears in 1-2 mins in IC, takes 15-30 mins in CE
Absent peripheral pulse and reduced ABPI in IC. LMN findings in CE
Chronic peripheral arterial disease epidemiology and RF
Age over 50, but more so over 70
Associated with CHD, cerebrovascular disease and diabetes.
RF: Obesity, HTN, inactivity, smoking, hypercholesterolaemia, DM and older age. Men also higher risk. Smoking is biggest link and correlates to pack years and risk of limb amputation
DM is strong RF (esp poor control) due to accererated atherosclerosis and poor healing
Caused by atherosclerosis (commonly) but can be vasculitis (inflammatory) or fibromuscular dysplasia (non-inflammatory)
Signs of PAD
Pale, cold, hairless leg with reduced Cap refill, weak/absent pulse, arterial bruit and arterial ulceration (deep, punched out, painful, small. Esp over toe joints/heel and lateral aspect (malleolus)
Critical limb ischaemia
Defined as circulation impaired to imminent risk of limb loss. 2 symptoms are rest pain and tissue loss (becomes gangrene if infected and can get osteomyelitis)
Investigations for PAD
Bedside (obs/ECG)
Bloods (FBC, ESR, thrombophilia screen, lipid profile, BM)
Scans (ABPI, duplex USS (non-invasive, determine site/severity)
Can also use MRI/CT
APBI
> 1.2 is abnormally hard/calcified vessel
1.0-1.2 is normal
0.8-0.9 is mild arterial disease/claudication (mod RF)
0.5-0.79 is mod arterial disease/severe claudication (specialist referral)
<0.5 is severe arterial disease and critical ischaemia. Urgent referral
Conservative PAD management
Smoking cessation (atherosclerosis RF but also post stent insertion occlusion)
Diet/exercise mods
Lipid mod/statins
Manage T2D/HTN
Antiplatelet therapy (aspirin/clopidogrel)
Peripheral vasodilators
Chronic limb threatening ischaemia
End stage PAD where there is threatened limb viability
Acute limb ischaemia pathology
Normally thrombotic (blood clot around atherosclerotic plaque) but can also be embolic (15% of cases) Prognosis is linked to severity of arterial disease, acute onset and how rapidly reperfusion achieved
Comparison of thrombotic acute limb ischaemia vs embolic
Embolus is acute onset, severe ischaemia and associated with AF, endocarditis, mitral stenosis, aneurysms, athersclerotic disease and graft presence. Leg pale, other leg unaffected.
Thrombotic tends to be slower onset, less severe pain. Associated with PVD, IHD, CVD, graft presence and blood disorders. Often both legs affected to some degree due to atherosclerosis
Acute limb ischaemia classical features
Pain, pallor, paraestheia, pulseless, perishingly cold, paralysis
Pain often not relieved with pain killers. Paralysis is due to nerve damage. Skin may be cyanosed and mottled. Fixed mottling, skin blitering and hard woody muscles is irreversible
Differentials for acute limb ischaemia
Chronic peripheral neuropathy (e.g. diabetic neuropathy, but would have normal temp/pulses)
Compartment syndrome (hard muscles)
DVT (red, hot swollen calf. Pulses normally present)
Management of Acute Limb ischaemia
Surgical emergency (6 hours to save limb) but start with heparinisation to prevent thrombus propagation. Embolus is generally embolectomy. Thombus gets angioplasty, bypass surgery or intra arterial thrombolysis
Acute limb ischaemia complications
Reperfusion of ischaemic muscles leads to oedema (compartment syndrome risk)
Also, products of cell death (KPO4, myoglobin) can cause rhabdymyolysis and AKI.
Necrosis after 6h and amputation needed. If not appropriate then palliative care.
Vasospastic disorder pathology
Mismatch between vasodilation (prostacyclin and NO) and vasoconstriction mediated by atherosclerosis.
Examples include Raynaud’s syndrome, acrocyanosis, livedo reticularis
Raynaud’s disease
Paroxysmal vasospastic and vasodilatory events affecting peripheral arterioles (toes and fingers, thumb spared with clear demarcation of affected skin)
More common in women, precipitated by cold and smotion (but also trauma, smoking and overuse)
Colour changes pale (ischaemia), blue (cyanosis) and red (reactive hyperaemia)
primary raynaud’s
Young female with genetic (no vascular disease)
Secondary Raynaud’s
Phenomenon
Tend to be older with severe symptoms (digital scar, ulceration, gangrene, nail changes). Associated with autoimmunes, environmental exposure (smoking, trauma, chronic vibration, chemicals) endocrine (diabetes, hypothyroidism),
Arterial disease (e.g. Buerger’s), blood disease (lymphoma, polycythaemia),
drugs (beta blocker, coc, cytotoxic)
Management of Raynaud’s
CCB/peripheral dilators
PE S+S
Dyspnoea, tachypnoea. Plueritic chest pain. DVT
Additional symptoms: cough, substernal chest pain, fever, haemoptysis, syncope, unilateral leg pain
WELLS PE
Looks at clinical signs+ symptoms of DVT, tachycardia, haemoptysis
Immobilisation for 3+ days or surgery within 4 weeks, previous DVT/PE, malignancy
Add 3 points is no more likely diagnosis
Score of more than 4- PE likely. 4 or less is unlikely
PE pathway
If Wells score >4, then hospital admission (CTPA or V/Q). If tests not immediately available then give anticoagulation
If less then D dimer within 4h or send to hospital. If D dimer positive then CTPA. If negative then probs not PE
PE diagnostic
CTPA is definitive diagnosis. CI in patients with poor renal function (use scintigraphy instead)
ECG changes non specific and may be normal. Often sinus tachycardia.
PE ECG
Sinus tachycardia
Dominant R wave in V1
T wave inversion in leads V1-V4 or RBBB
Slurred S in Lead 1, Q and T inversion in III (rare, but indicates cor pulmonale)
PE classification: Massive
Massive (large/extensive bilateral.) Shows PE signs, and haemodynamic compromise (syncope, LoC)
Acute with sustained hypotension (<90 sys or drop of 40 from baseline, or 15mins of <40bpm bradycardia)
Submassive PE
Larger thrombus than low risk. Right heart strain (ECG changes/echo changes, elevated troponin)
Low risk PE
Acute PE without clinical markers of massive or submassive PE
Sinus tachycardia might be only abnormality.
Can be asymptomatic, or pleuritic chest pain, SOB, DVT
