DefinitionThis section has been translated automatically.
Most common angiological emergency. Acute PAVK is caused by acute or subacute embolic or thrombotic transverse sectional occlusion of an arterial vessel. Insufficient arterial collateral supply results in acute limb ischemia, which can be organ or life-threatening.
Occurrence/EpidemiologyThis section has been translated automatically.
Acute PAVK has an incidence of about 7 - 14/100,000 inhabitants per year. Its share among all inpatient treated vascular diseases is 10-16% (Dormandy et al. 1999). Despite innovative diagnosis and therapy, acute peripheral arterial occlusive disease is associated with very high morbidity and mortality. In the first 30 days after the onset of acute leg ischemia, the amputation risk is between 10% and 30%. The mortality risk in the first 30 days after the acute event is 15-30%. In Germany, approximately 2000 patients die each year as a result of acute arterial occlusive disease.
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EtiopathogenesisThis section has been translated automatically.
Acute pAVK is mainly caused by embolisms (70-80%), less frequently by acute local thromboses (20-30%). In 10% to 15% of cases, it is not possible to differentiate the cause of occlusion on the basis of the medical history and clinical examination alone. 80-90% of arterial embolisms have a cardiac cause; 10-20% of cases have an extracardial cause.
- absolute arrhythmia in atrial fibrillation (70%)
- Heart Valve Vitae
- Acute myocardial infarction (5%)
- Cardiac wall aneurysm
- Tumours of the left heart
- Atrial myxoma
- prosthetic heart valve replacement
- dilated cardiomyopathy
- paradoxical arterial embolisms over an open Foramen ovale.
- Aneurysms of the aortoiliac and femoro-popliteal region
- atherosclerotic plaques
- Compression Syndrome
- Catheter embolisms or iatrogenic vessel damage
- Tumours (bronchial carcinoma, lung metastases, angiosarcoma)
- Foreign matter
Acute arterial thromboses usually occur in a damaged vascular tract (e.g. in arteriosclerosis); furthermore, dissections, trauma, vasculitis, postoperative vascular damage, paraneoplastic syndromes and medication can be the cause of acute arterial thrombosis. Rarely, cystic adventitia degeneration, phlegmasia coerulea dolens or hypercoagulopathy are causes of acute arterial (non-embolic) thrombosis.
LocalizationThis section has been translated automatically.
Lower extremity > than the upper extremity. In 85% of cases only one limb is affected. The femoral artery is most frequently affected with simultaneous occlusion of 2 or 3 arteries of the lower leg; furthermore, occlusion of the iliac artery (about 13%) and the popliteal artery (12.5%) is also common.
Clinical featuresThis section has been translated automatically.
The extent of the symptomatology of acute arterial occlusion depends on its type, localization and possible collateralization. Complete embolic arterial occlusion usually lacks compensation mechanisms via a pre-existing collateral system, resulting in the typical clinical symptoms (6x "P" according to Pratt) up to critical limb ischemia. In the case of acute thrombotic occlusion at the base of a pre-existing peripheral arterial occlusive disease, the symptoms usually develop more slowly and less severely due to already formed collateral vessels.
Complete ischemia syndrome n. Pratt (6xp):
- Sudden sharpest pain like a whiplash (pain)
- Pulselessnes (pulselessnes)
- Paleness pallor
- Emotional disorder (paresthesia)
- inability to move from about a hand's width below the closure (paralysis)
- Shock (prostration)
The 3 symptoms "sudden pain, pulseless, paleness" are the most reliable clinical symptoms.
An incomplete ischemia syndrome is often found in acute pAVK thrombotic etiology. Clinically, paleness and loss of pulse distal to the arterial occlusion are initial symptoms of acute arterial occlusion. Cooling of the affected extremity often occurs with a time delay. The blue discoloration of the ischemic limb indicates a standstill of blood flow in the capillary flow bed with exhaustion cyanosis and characterizes severe limb ischemia. If sensitivity and motor function are also impaired, the diagnosis is complete ischaemia with imminent loss of the limb. Shock symptoms may develop in cases of aortic or pelvic artery occlusion.
Complications in case of reperfusion too late (>6h): Torniquet or reperfusion syndrome (muscle edema with myoglobinemia or myoglobinuria, acidosis with hyperkalemia, loss of volume as well as acute renal failure in Crushniere and consumption coagulopathy).
Rutherford et al. defined a diagnostically and therapeutically pioneering stage classification of acute PADK (see table).
DiagnosisThis section has been translated automatically.
Of crucial prognostic importance is a quick diagnosis through exact anamnesis, clinical examination with imaging diagnostics. Once the diagnosis has been made, immediate measures must be taken to restore the disturbed arterial circulation.
Patient with acute ischemia of the extremities is considered an emergency and high-risk patient.
The extent of organ damage depends on the ischemia tolerance of the respective tissue and is 12, 6 to 8 for skin, muscles and nerve tissue, respectively. 2 to 4 hours.
Questions about the time of onset of limb pain and pre-existing conditions provide information about the age and cause of arterial occlusion.
An embolism is indicated by a sudden onset of symptoms without previously known intermittent claudication. Patients with embolic acute PAD usually have a history of cardiac dysrhythmia, coronary heart disease or aortic aneurysm.
If intermittent claudication is present or if risk factors for arteriosclerosis are present, an arterial thrombotic occlusion is likely.
Acute PAD can (in rare cases) also develop as paraneoplastic syndrome.
Apparative diagnostics: Since the prognosis of acute PAD depends on the shortest possible time window between the onset of symptoms and the start of treatment, only selected, meaningful and time-saving examination methods should be used in apparative diagnostics. The prerequisite for the optimal management of acute limb is therefore the recognition of the emergency situation by the first attending physician and the immediate admission to a clinic with suitable diagnostic and therapeutic procedures.
Non-invasive apparatus-based procedures that require little time are
- the Doppler pressure measurement,
- the cw Doppler sonography and
- the colour-coded duplex sonography.
The criteria of the Doppler methods are the audible or inaudible signals above the arterial occlusion or above the veins.
The determination of the ankle arm index' (ABI) using the Doppler pressure method provides information about the extent of compensation of the acute peripheral arterial occlusion event (normal ABI > 0.97). A pathological ABI < 0.6 and ankle artery pressures of < 50mmHg in the posterior and anterior tibial arteries indicate critical limb ischemia. Distally of acute arterial occlusion, either no Doppler signal or a monophasic signal with widened curve and increased end-diastolic blood flow can be derived. The lumen in the area of the occlusion may be of variable echogenicity. Measured by DSA, peripheral colour duplex sonography has a high diagnostic accuracy with a positive or negative predictive value of 91% or 100% with a sensitivity and specificity of 92% and 99% respectively.
In comparison to angiography, colour duplex sonography can be used to identify completely or incompletely thrombosed arterial aneurysms as a possible cause of occlusion.
Intra-arterial digital subtraction angiography (DSA) is still considered the "gold standard" of imaging diagnostics in acute arterial occlusive disease. This usually allows the differentiation between arterial embolism and arterial thrombosis. Acute arterial occlusion is angiographically characterized by a sudden stop of the contrast medium column. A so-called "dome phenomenon" is evident (upwardly convex, rounded contrast medium recess in the area of the proximal embolus). Furthermore, in contrast to the acute thrombotic artery occlusion, formed collateral vessels are usually missing (here, pre-existing formed bypass vessels are usually detected).
As an alternative to DSA, contrast-enhanced 3D MRA is indicated for chronic critical limb ischemia (CLI), but not for acute ischemia. Reason: This is not due to the lower significance of 3D-MRA, but rather to patient management, since DSA can be immediately extended to a therapeutic measure.
TherapyThis section has been translated automatically.
In interdisciplinary cooperation between angiologists, radiologists and vascular surgeons, special treatment strategies should be coordinated and initiated quickly and promptly. The special therapeutic measures depend on the genesis of the acute arterial occlusion and the presence of complete or incomplete ischemia (Rutherford's classification of stages).
In stage I of acute PADK (according to Rutherford), the special lumen-opening measures can, under certain circumstances, take place on the day after the acute event after initiation of general therapeutic measures and anticoagulation.
In stages II and III according to Rutherford, all diagnostic and therapeutic measures must be taken immediately as an emergency.
- Inform the vascular surgeon, leave the patient on fasting
- Position limb deep (increased perfusion pressure)
- Extremities padded (cotton wool bandage)
- No cold - no heat applications; no pressure.
- Pain therapy, analgesics i.v. (opiode); do not inject intramucously in order not to endanger a possible lysis therapy
- Immediate intravenous anticoagulation with 10,000 IU unfractionated heparin (prevention of further embolism or thrombus formation)
, thrombectomy (with a Forgarty catheter), thrombendarterectomy and bypass systems.
In principle, emergency surgical therapy is indicated if a complete ischemic syndrome with acute occlusion of large extremity arteries proximal to the groin or elbow is present. Artery occlusions distal to the inguinal ligament are suitable for a combined procedure using catheterization and local lysis. In acute PADK with incomplete ischemia syndrome, combined treatment methods such as local catheter-assisted lysis therapy are considered.
local intra-arterial application of urokinase and plasminogen activator (rtPA) is common for lysis treatment of acute arterial occlusion. For local infusion thrombolysis, the fibrinolytic agent is infused locally slowly and continuously up to an appropriate maximum dose via the intra-arterial catheter placed in front of the thrombus. After 6 to 24 hours the angiographic control and possible dose reduction is performed. For infiltration fibrinolysis, the fibrinolytic agent is applied directly into the thrombus by advancing the end-opened catheter. After passage of the thrombus, end-closed catheter systems with lateral openings (multiside-lit catheters) are suitable for wetting the entire thrombus with the fibrinolytic agent. For infiltration thrombolysis of arterial occlusions, lower doses of fibrinolytic agents are used than for local infusion thrombolysis.
In addition to the continuous application of the thrombolytic, pulsed pressure peaks can also be applied during infiltration thrombolysis using automated pulsed spray infusion pumps. In addition to lysis, this "pulsed spray thrombolysis" technique causes additional mechanical destruction of the thrombus. In comparison to simple infiltration thrombolysis and infusion thrombolysis, this procedure achieves much shorter times for thrombus dissolution with lower major complication rates (4% vs. 15-20%) (JJ. Bookstein et al. 1989).
The results of interventional catheter and lysis studies in acute PAVK are inconsistent, as the individual studies included acute, sub-acute and chronic peripheral arterial disease stages. However, the ACC/AHA Guidelines for the Management of Patients With Peripheral Arterial Disease 2006 (AT Hirsch et al. 2006) recommend intra-arterial local fibrinolysis therapy by catheter in patients with high co-morbidity as a low-risk alternative to surgery.
Endoluminal mechanical thrombembolectomyThe
endoluminal therapy of acute limb ischemia comprises several techniques that can be used alone or in combination with local fibrinolytic therapy. Initially, the occlusive thrombembolic material is crushed and removed. Recognised efficient methods of mechanical thrombectomy are percutaneous
,- mechanical fragmentation catheter systems
,- hydro-dynamic catheter systems.
Acute occlusion of the pelvic arteries and bifurcation of the femoral artery are unsuitable for catheter-assisted mechanical thrombembolectomy procedures. They should rather be approached surgically. In contrast, infrainguinal arterial occlusions with acute ischemia syndrome and angiographically poor peripheral outflow ("run off") are an indication for endovascular thrombectomy procedures.
Progression/forecastThis section has been translated automatically.
It is important to identify and eliminate the source of the embolism. The risk factors of arteriosclerosis must be eliminated. For recurrent embolisms, long-term or lifelong oral anticoagulation with vitamin K antagonists is indicated. In addition, oral anticoagulation is also recommended after the application of a knee joint bypass. The long-term administration of antiplatelet aggregation inhibitors is indicated:
- after thrombectomy
- after thrombendarterectomy
- for generalized arteriosclerosis
TablesThis section has been translated automatically.
|I(functional extremity)||not immediately at risk||none||none||audible||
II (endangered extremity)
|IIa (low risk)||Limb preservation with timely restoration of perfusion||minimal (toes)||none||infrasonic||infrasonic|
|IIb (directly threatened)||Limb preservation with timely restoration of perfusion||toe crossing with pain at rest||light to moderate||infrasonic||infrasonic|
|III (irreversibly damaged)||Necrosis or irreversible nerve damage||prolonged hypersensitivity||Paralysis (Rigor)||infrasonic||infrasonic|
LiteratureThis section has been translated automatically.
- Alfke H et al (2003) Radiological diagnostics and therapy for acute ischemia of the extremities. Surgeon 74: 1110-1117.
- Beuckelmann DJ et al (1994) Imaging techniques for the diagnosis of aortic dissection. Internist 35: 999-1005.
- Dormandy JA et al (2000) Management of peripheral arterial disease (PAD). TASC Working Group. Trans Atlantic Inter-Society Concensus (TASC). J Vasc Surg 31: S1 - S296.
- Ludwig M et al (2010) Vascular medicine in clinic and practice. Georg Thieme Publisher Stuttgart-New York S1-S26
- Rutherford RB et al (1997) Recommended standards for reports dealing with lower extremities ischemia:revised version. J Vasc Surg 26: 517-528
Incoming links (4)Arterial occlusive disease; Arterial occlusive disease peripheral; Kawasaki syndrome; Thrombangiitis obliterans;
Outgoing links (6)Duplex sonography; Intermittent claudication; Paraneoplastic syndromes (overview); Phlegmasia coerulea dolens; Platelet aggregation inhibitor; Vitamin k antagonists;
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