Classification of diseases causing the development of arterial insufficiency. 1.

Chronic arterial insufficiency - obliterating atherosclerosis of aorta and lower extremities - obliterating endarteritis of extremities - nonspecific aorto-arteritis - post-thrombotic occlusion of arteries - post-traumatic occlusion - diabetic angiopathy - Raynauds syndrome 2. Acute arterial insufficiency - embolism of magistral vessel - thrombosis of magistral vessel - post-traumatic occlusion of artery This list mentions main diseases causing ischemia of extremities, but it is not exhaustive. Definition of major chronic arterial diseases. The most common disease causing chronic ischemia of extremity is obliterating atherosclerosis (90%). Atherosclerosis is characterized by specific lesion of arteries of elastic and muscular type in the form of focal proliferation of connective tissue in their wall with lipid infiltration of internal coat. Such thickening afterwards leads to obliteration of the vessel and development of organic lesions. Second to it is obliterating endarteritis. Obliterating endarteritis is chronic inflammation of vessels, mostly arteries, with pronounced hyperplasic process in the area of intima followed by secondary thrombosis. Autoimmune processes play a major role in its pathogenesis. Nonspecific aorto-arteritis occurs more seldom than other vascular diseases. Nonspecific aorto-arteritis (Takayasus disease) is characterized by chronic progressive inflammation; mostly large arteries departing from arch of aorta are involved. The inflammatory process involves all three layers of the artery, the vessel undergoes lymphocytic and plasmocytic infiltration and, afterwards, thrombosis. Raynauds disease is angiotrophoneurosis characterized by specific vasomotor and neurotrophic disorders, mainly manifested by spastic contraction of small digital arteries, sometimes nasal, mental or auricular arteries. Pathologic physiology. Ischemic syndrome underlies all the diseases mentioned above. One of important factors promoting ischemic syndrome is the decrease in blood flow rate. The exchange between capillaries and cells can only proceed if the pressure in magistral arteries is over 60 mm Hg. Is perfusion drops below 20-30 mm Hg the pressure gradient disappears, microcirculation is disrupted, exchange process between blood and tissues stops. Metabolic products accumulate in the tissues. Local metabolism is compensated through increase of anaerobic glycolysis, increased production of lactate and pyruvate. Acidosis develops which has an irritating effect on nerve endings and causes pain syndrome, afterwards trophic disorders to the point of gangrene development. Definition of basic types of acute ischemia of extremities.

Acute arterial insufficiency of arterial flow of extremities is due to acute thrombosis, embolism and traumatic lesion of vessels. Thrombosis is development of blood clots in the lumen of a vessel which disrupts haemodynamics and tissue metabolism. Embolism is a pathological condition in which the lumen is partially or completely obstructed by an embolus formed far away from the place of obstruction. In most cases this embolus is a detached thrombus or its part. It can also be a gas bubble, drops of fat, a solid body (calcium detritus, bullet), accumulation of tumour cells or bacterial cells, or parasites. Pathological physiology. Pathogenesis of arterial embolism consists in migration of solid substrate in the blood stream after it has detached from the point of original location. Then it fixes itself and grows due to thrombotic processes and acute ischemia of the extremity develops. In 1856 Rudolf Virchow determined the triad of thrombogenic factors: slower blood flow, change or damage of inner vascular coat, increased blood clotting. The first factor contributes to thrombogenesis but does not cause it. Ischemia underlies the subsequent processes, like in chronic diseases. The acute process differs in swiftness and more pronounced ischemic changes which is due to the absence of adequate collateral blood supply. Clinical presentations. Clinical presentations depend on the localisation of the process, its extent, development of collateral blood flow and duration of the disease. Pain syndrome is the clinical manifestation; it underlies the classification of chronic arterial insufficiency by A.V. Pokrovsky. Four stages of ischemia are distinguished: stage one pain in lower extremities develops only upon great physical exertion, for instance walking over 1000 metres; stage 2 pain develops upon walking lesser distances, under 1000 metres. If the patient can walk without pain over 200 m, this is stage 2a; if he can walk under 200 m, this is stage 2b. If the patient cannot walk over 25 m without pain, this is stage 3. Stage 4 is characetrised by ulcerative-necrotic changes of tissues. Typical complaints presented by patients with chronic arterial insufficiency also include the sensation of chilliness, paresthesia, pallor of skin, increased perspiration, cramps in lower extremities. Examining the patient note such signs as skin pallor, hair falling out, thickened nails with transverse streaks. In the stage of decompensation the tissues become edematous. Distal parts of extremities can have purple, marble or cyanotic colouration (due to capillary atony). Progressing decompensation leads to the development of trophic changes which include ulcers and gangrene. In obliterating disease of vessels ulcers are typically located in distal parts of extremities; they have characteristic appearance: they are more or less round, their edges and bottom are covered with pale grey incrustation without granulation, without signs of epithelisation or regeneration. The surrounding skin is thinned, parchment-like, slightly inflamed. Around the ulcer the skin is cyanotic or purplish-cyanotic. There is a pronounced edema both around the ulcer and on the foot and shin. The ulcers are very tender. Pains around the ulcers develop at night

or upon change of weather. Although the ulcers are often infected, you will seldom note the development of phlegmon, abscess, erysipelatous inflammation, severe lymphangitis or osteomyelitis. Local reactivity of tissues is impaired due to circulation disorder. As there are no protective barriers, necrosis progresses and gangrene develops. A slow, gradual spread of the process leads to the dying off and desiccation of tissues, the development of dry gangrene. The toes or foot are black, mummified, dense to the touch, deformed. Dry necrosis usually develops where there are few muscles or little subcutaneous fat. The demarcation line is clear, with ill-defined inflammation ridge with faint granulation. Wet gangrene can be noted when thrombosis of afferent vessels develops against the background of chronic occlusion. The extremity in such cases looks edematous, the skin is taut, blue veins and hemorrhage foci are visible through it. The demarcation line is unclear or absent. Regional lymph nodes are enlarged and painful. The main pathological sign, however, is the developing toxemia syndrome. Topical diagnostics is done with palpation and auscultation of great vessels. You should examine all the vessels accessible to palpation. On lower extremities these are: anterior and posterior tibial arteries, popliteal artery, common femoral artery and the abdominal part of aorta. On upper extremities examine the radial, humeral, axillary and subclavian arteries. No pulsation above these vessels points to occlusion located above. Systolic noise noted over the common tibial, iliac, subclavian, carotid artery or aorta is an important diagnostic sign of lesion of arterial vessels. The presence of systolic noise points to arterial stenosis of over 30%. Various tests that can reveal plantar or palmar ischemia are important in diagnosis. The following function tests are done in lesion of upper extremities: 1. Ratshovs test (1953). The standing patient is asked to raise his slightly bent arms over the head and to flex and unflex the fingers at a amoderate rate for 30 seconds. In healthy people the plams and fingers do not get pale. If there is vascular disorder, the sooner the pallor sets in and the greater its extent, the more peripheral circulation is disrupted. 2. K.N. Bogolepovs test (1957). The standing patient is asked to stretch the arms ahead with straight fingers, then the colouration of fingers, back of the hand, condition of veins (the extent of their dilation, venous stasis) is noted. Then the patient is asked to raise the right arm and to drop the left one. This pose is maintained for 30 seconds and then the arms are returned into the initial position. At this point the stopwatch is started and the character of change of skin colouration, the condition of venous stasis and capillary circulation is watched. If there is no vascular disorder, the changes in vascular filling reverse within 30 seconds. In insufficiency of peripheral circulation the pallor in the raised hand and cyanotic

colouration in the dropped hand disappear the slower, the more arterial and venous circulation is disrupted. In lesion of upper extremities the tests are as follows: 1. V.A. Opels test (1911). The supine patient is asked to raise the straight legs to the angle of 450 and to hold them so for one minute. In insufficiency of arterial circulation pallor develops on the sole on the affected side which does not happen in a normal condition. 2. Samuels test (1943). This test is based on the phenomenon if work hypoxia. The supine patient is asked to bend and unbend his ankle joints. In a normal condition the colouration of foot soles does not change or it is slight pink. A pallor points to circulation insufficiency. 3. Goldflames test (1910). It is made in the same way as Samuels test. The doctor notes the time when the muscles on the affected side get tired. This is done with a stopwatch. 4. D.I. Panchenkos test (1937). The sitting patient is asked to put his bad leg over the healthy one. In some time paresthesia and pains in gastrocnemius muscle develop. The extent and time for paresthesia and pains to set in is in direct relation to the extent of peripheral arterial insificciancy.