Arterial occlusive disease chronic of the extremity arteries I73.9

Author: Prof. Dr. med. Peter Altmeyer

All authors of this article

Last updated on: 14.06.2021

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Synonym(s)

cpAVK; Shovel sickness

Definition
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Most frequent form of chronic arterial occlusive disease.

Etiopathogenesis
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Degenerative arteriosclerosis due to a complex metabolic disorder of the vessel wall, development of intimal edema, atheromatous plaques, ulceration, thrombosis; favoured by nicotine abuse as well as general diseases such as arterial hypertension, diabetes mellitus, lipid metabolism disorders, obesity, hyperuricemia. For rare causes see Table 1.

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Manifestation
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Rapid increase from 45 to 60 years of age; later less frequent. Men are affected 4 times more frequently than women.

Clinical features
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Typical are:
- Changes in pulse quality (attenuated or missing)
- Changes in skin temperature (reduced)
- changes in skin colour (pale, sometimes reddish)
- Skin trophic disorders with circumscribed alopecia
- Sensitivity disorders
- Pain of varying degrees of severity.
Progression in 4 stages (according to Fontaine):
- Stage I: Freedom from symptoms or atypical sensations in the foot, leg.
- Stage II: Latent pain only occurring after certain strains (intermittent claudication).
- Stage III: Pain at rest and possibly beginning trophic disorders (necrosis).
- Stage IV: Gangrene.

Diagnosis
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Clinical picture, medical history, standard examination program.
Palpation and auscultation of the arteries.
Functional tests, mechanical and electronic oscillography, rheography, ultrasound Doppler method, in some cases angiography.

General therapy
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Prophylactic and secondary preventive measures (ban on nicotine, treatment of risk factors: hypertension, diabetes, obesity, fats, cholesterol). Avoidance of exposure to cold and wet, tight footwear and other compression, avoidance of chemical, electrical and thermal stimuli. Avoidance of injuries, toe nail manipulation, etc. Special conservative measures: Occupational therapy: Active muscle training; walking training, groin pulse must be palpable (not for stage III to IV).

Internal therapy
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Vasoactive substances (e.g. Trental, Dusodril, Prostavasin). Vasodilatants, isovolaemic haemodilution (bloodletting and volume replacement with e.g. HAES), viscosity changing drugs (e.g. HAES), aggregation inhibitors (e.g. ASS).
Interventional radiology: Percutaneous transluminal angioplasty followed by marcumarization for short-stretch occlusions.

Operative therapie
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Absolute indication for surgery in stage III and IV:

Transluminal percutaneous catheter dilatation ( yolk technique), best indication in stage II.
Alternatively open TEA (thrombendarteriectomy) or anatomical/extraanatomical bypass surgery.

Tables
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Arterial occlusive disease (AVD) - rare causes

Disease	Etiology/Findings
Pseudoxanthoma elasticum	Pseudoxanthoma of the skin, vascular retinal striations, femoral occlusion (Darier-Groenblad-Strandberg syndrome)
Neurofibromatosis	renal artery stenoses, more rarely stenoses of the aorta, mesenteric and iliac arteries in children and adolescents
Drug abuse (amphetamine, LSD)	Necrotizing angiitis (microaneurysms)
Chronic arsenic poisoning	Fibrous intimal thickening of small and medium-sized arteries (high arsenic content in drinking water)
Carbon disulfide exposure	Premature atheromatosis
Amyloidosis	Arteriolar and arterial amyloidosis, muscle pain, intermittent claudication (preserved foot pulses)
Werner syndrome	Pre-pubertal graying of hair, short stature, hypogenitalism, cataract, scleroderma, osteoporosis, premature arterial occlusion, familial clustering
Retroperitoneal fibrosis	Ureteral, arterial and venous compression in the pelvis due to fibrosis
Osteohypertrophy	Arterial compression due to larger exostoses
Prolonged shock	Acral symmetric gangrene due to extreme centralization, diffuse intravascular coagulation
Endogenous oxalosis	Diffuse visceral and peripheral arterial oxalate deposition in end-stage uremia
Homocystinemia	Thromboembolic tendency
Progressive arterial occlusive disease	Fibrous tissue proliferation between endothelium and lamina elastica interna of small arteries and arterioles. Complications: skin florescence, intestinal perforation, cerebral insult (Degos-Delort-Tricot syndrome).