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Chapter 2: Hypertension and vascular diseases 81
Sex kinase and myoglobin, which can cause acute renal fail-
M > F urebyadirecttoxiceffect(rhabdomyolysis).Volkmann’s
ischaemic muscle contracture may also occur.
Aetiology/pathophysiology
The most common causes are emboli and thrombus.
Investigations
Ninety per cent of emboli arise from the heart, usu-
Angiography may be useful but should not delay surgery
ally due to mural thrombus (e.g. as a complication
incriticallimbischaemia.Incasesofembolifurtherpost-
of atrial fibrillation or post-infarction) or from ab-
operative investigation is required to establish the source
normal, infected or prosthetic heart valves. Less than
of the embolus including ECG, echocardiography and
10% arise from the large vessels, e.g. aortic aneurysm
abdominal ultrasound scan.
or atherosclerotic vessels.
Thrombosis may cause acute ischaemia usually aris-
ing on a pre-existing atherosclerotic plaque or within Management
an aneurysm, causing complete occlusion. Hypo- Following assessment and resuscitation treatment in-
volaemia or hypotension often precipitates complete volves the following:
occlusion. Less commonly thrombosis may arise in Heparintominimisepropagationofthrombus,invery
non-atherosclerotic vessels as a result of malignancy, mild cases this will be sufficient.
polycythaemia or other hypercoagulable states. Early cases and distal arteries may be treated medically
Other causes of acute arterial occlusion include direct initially with thrombolytic therapy delivered directly
trauma and dissection of an aneurysm. to the vessel under radiographic guidance.
Loss of arterial blood supply causes acute ischaemia and Acute occlusion with signs of severe ischaemia is
irreversible infarction occurs if the occlusion is not re- treated with emergency surgery. Embolectomy/thro-
lievedwithin6hours.Aftertheocclusionisrelievedthere mbectomy is usually performed with a Fogarty bal-
maybesecondarydamageduetoreperfusioninjury.This loon catheter under local anaesthetic if possible, and
is due to the production of toxic oxygen radicals, which complex cases may require arterial reconstruction.
cause further cellular damage. Compartment syndrome requires urgent fasciotomy.
Clinical features
Prognosis
Patients present with a cold, pale/white and acutely
Acute upper limb ischaemia tends to have a better prog-
painfullimb,whichbecomesweakandnumbwithlossof
nosis, as there is better collateral supply. Unfortunately,
sensation and paraesthesiae, which starts distally (pain
acute lower limb arterial occlusion is more common.
becoming painless, pallor, paraesthesia, pulseless and
Amputation is uncommonly necessary, but mortality is
paralysed). Paraesthesiae or reduced muscle power are
as high as 20%, depending on the degree of ischaemia at
signs of severe ischaemia. As the condition progresses,
presentation and overall fitness of the patient.
the skin becomes mottled with dusky patches. Muscle
tenderness is a sign of ischaemic damage. Complete loss
of muscle power with tender, firm muscles is a sign of
muscle infarction. Deep vein thrombosis
Definition
Complications
A thrombus forming in a deep vein most commonly
Compartment syndrome may occur (muscle swelling
within the lower limb.
secondary to ischaemia and reperfusion within rigid
compartments between the bones and fascial layers
causes increased tissue pressure, which rises above capil- Aetiology
lary perfusion pressures, such that there is further com- Increased risk of thrombosis may result from blood
promise of blood supply to the affected limb). Muscle stasis, vascular damage or hypercoagulability (Virkoff’s
necrosis leads to the release of high quantities of creatine triad).