Acute limb ischaemia

• Acute limb ischaemia:

  • Defined as a sudden decrease in arterial blood flow to a limb that threatens its viability
  • Vascular emergency that can lead to extensive tissue necrosis - may result in limb amputation or death
  • Vast majority of cases involve the lower limbs
• ALI can be as a result of thrombosis, embolism or trauma

  • Thrombosis is the most common cause
  • Commonly due to plaque rupture in an atherosclerotic segment in patients with peripheral arterial disease
  • A thrombus may also form in the context of:
  • Hypovolaemia
  • Thrombophilia
  • Hypotension
  • Malignancy
• Embolism:

  • Next common cause after thrombus
  • Mainly arises from a thrombus in the left atrium (in association with atrial fibrillation) or a mural thrombus following a myocardial infarction
  • Prostheses - heart valves or bypass grafts
  • Aneurysms - especially popliteal and abdominal aortic aneurysms
• Other causes:

  • Trauma (including iatrogenic) can be as a result of iatrogenic injury during interventional procedures, such as percutaneous coronary intervention. Compartment syndrome
  • Phlegmasia cerulea dolen - rare complication of DVT - severe oedema
  • Acute aortic dissection - impaired blood supply
• The risk factors for ALI are similar to the risk factors for peripheral arterial disease (PAD):

  • Smoking
  • Diabetes mellitus
  • Obesity
  • Hypertension
  • Hypercholesterolaemia

  However, not all patients with ALI will have the presence of risk factors.
• The classical features of ALI are summarised as the six P’s (developing over a period of less than 2 weeks):

  • Pain
  • Pallor
  • Pulselessness
  • Perishingly cold (poikilothermia)
  • Paraesthesia
  • Paralysis
• Typical symptoms:

  • Pain in the affected limb usually present at rest
  • Altered sensation (paraesthesia)
  • Paralysis in the affected limb (this is a late sign)
• important areas to cover in the history:

  • Past medical history: if an embolic cause is suspected, history should explore potential sources (e.g. atrial fibrillation, recent myocardial infarction).
  • risk factors: conditions predisposing to PAD, especially diabetes mellitus (a major risk factor), hypertension and hypercholesterolaemia.
  • Medication history: if the patient has established PAD, ask about medications (e.g. antiplatelets), and whether they are compliant
  • Social history: establish the patient’s smoking habits, as smoking is the single biggest risk factor associated with PAD.
• Clinical exam:

  • Thorough peripheral vascular exam
  • Marble white appearance of the skin
  • Absent limb pulses on palpation
  • Cold limb
  • Less common findings which usually appear later:
  • Paraesthesia
  • Paralysis (unable to wiggle toes)
  • Muscle weakness
  • Gangrene
• When assessing for limb ischaemia, a normal contralateral limb with palpable pulses is a sensitive sign for embolic occlusion in the abnormal limb.
• Thrombosis cause clinical features:

  • Onset - gradual, vague
  • Severity - less severe
  • PAD - history of PAD symptoms
  • Previous vascular surgery - likely
  • Cardiac history - unlikely
  • Appearance and feel - less cold, cyanotic
  • Palpation of artery - hard, calcified
  • Contralateral leg pulses - absent
• Embolus cause clinical features:

  • Onset - sudden
  • Severity - severe
  • PAD - unlikely to have history of PAD symptoms
  • Previous vascular surgery - unlikely
  • Cardiac history - history of AF, recent MI
  • Appearance and feel - cold, mottled
  • Palpation of artery - soft, tender
  • Contralateral leg pulses - present
• It is important to try and distinguish embolic from thrombotic ALI.

  As opposed to thrombotic ALI, the sudden nature of embolic ALI does not provide the body with sufficient time to build up compensatory collaterals. This makes urgent intervention in embolic ALI a necessity if the limb is to be salvaged.
• Rutherford classification is used to grade the severity of ALI

  • I
  • IIa
  • IIb
  • III
• The main differential diagnosis to consider is critical limb ischaemia (CLI)

  • Onset: ALI <2 weeks, CLI >2 weeks
  • Pulses: ALI absent, CLI reduced/absent
  • Pain: ALI sudden at rest and calf tenderness, CLI gradual at rest
  • Appearance: ALI pale "marble white", CLI pink
  • Temperature: ALI cold, CLI warm
  • Other: ALI paraesthesia and paralysis, CLI ulcers and gangrene
  • Emergency: ALI yes, CLI no
• Bedside investigations:

  • Duplex ultrasound/doppler: confirm absence of pulses
  • ECG: look for AF
• Lab investigations:

  • Baseline blood tests (FBC, U&E, LFTs, coagulation).
  • Serum lactate: to assess the severity of ischaemia.
  • Thrombophilia screen (if no known risk factors for ALI).
  • Group and save: important to perform as the patient may require emergency surgical intervention.
• Imaging:

  • CT/MR angiography: to guide revascularisation if the limb is viable, where delaying treatment is not threatening to limb viability.
  • Other (e.g. echocardiography if an embolus of cardiac origin is suspected).
• Initial management:

  • Emergency assessment by vascular specialist
  • Systemic anticoagulation with heparin
  • Analgesia: paracetamol and opioid
• Medical management:

  • Infrequently, anticoagulation alone may be sufficient if symptoms are mild or cease
• Surgical revascularisation is first line:

  • Intervention depends on the type of occlusion (thrombus vs embolus)
  • Duration of ischaemia
  • Location
  • Viability of limb
  • Risks associated with treatment
• If the limb is non-viable (i.e. showing signs of irreversible/permanent damage), it will require an amputation.
• Long term management:

  • For all patients with PAD
  • Smoking cessation
  • Diet and exercise
  • Statin therapy and managing cholesterol
  • Antiplatelet therapy
  • Managing comorbidities - diabetes and hypertension
• Complications:

  • High mortality rate of 15-20%, and a similarly high 30 day mortality rate following surgical intervention
  • Around a third of deaths result from reperfusion injury:
  • Massive oedema: resulting in compartment syndrome and hypovolaemic shock.
  • The sudden release of built-up substances which can lead to various systemic complications:
  • Hyperkalaemia due to the release of K+ ions: can cause cardiac arrhythmias.
  • Systemic acidosis from the release of H+ ions.
  • Acute kidney injury due to the release of myoglobin: patients may require emergency renal replacement therapy.
• Endovascular treatment:

  • Percutaneous catheter-directed thrombolytic therapy - inject thrombolytic e.g. alteplase directly into vessel
  • Percutaneous mechanical thrombus extraction - blockage removed via radiology technique e.g. aspirate out with tube
• Surgical management:

  • Thromboembolectomy - vessel opened and blockage removed
  • Bypass surgery