Occlusive Arterial Diseases
Arterial occlusion refers to the interruption of blood flow within an artery and most commonly results from trauma, thrombi, emboli, arteritis, degenerative lesions such as atherosclerosis, and factors associated with endothelial dysfunction or injury. Arterial thrombosis requires one or more inciting local or systemic conditions: (1) vascular endothelial damage, (2) sluggish blood flow, and (3) changes in blood constituents resulting in a hypercoagulable state. Vascular endothelial injury can be induced by infectious agents (e.g. Dirofilaria immitis), prolonged hypotension, hypoxia, acidosis, inflammation, trauma, and immune mechanisms. Compressive lesions, such as from tumors, may promote thrombosis by a reduction in local blood flow and endothelial injury. Thromboemboli usually represent blood clots that have broken free from a site of thrombus formation. Emboli can also consist of tissue particles, fat, gas, bacterial vegetations, parasites (e.g. heartworms), tumors, or foreign bodies. Entrapped emboli may themselves become thrombogenic. Arterial occlusion can be acute or chronic. Chronic gradual occlusion can occur with mural or extramural hematomas, atherosclerosis, arteriosclerosis, vasculitis, or intimal tears forming valvelike structures.
The potential clinical consequences of arterial occlusion (tissue hypoxemia, ischemia, neuropathy, tissue necrosis) are related to extent and duration of vascular obstruction, and the physiologic consequences of the affected organ or organs. Tissues supplied by the endarteries, which have no connections to collateral vascular beds, undergo greater ischemic injury than organs supplied with collateral circulation. Acute, complete arterial occlusion causes rapid ischemic injury. This is largely due to release of vasoactive substances by the clot, which induces vasoconstriction and reduces collateral circulation. In addition to the acute effects, long-term injury (days or weeks) occurs and includes fibrosis and neuromyopathy.
Feline systemic thromboembolism
Feline systemic thromboembolism is discussed in site.
Canine systemic thrombosis and thromboembolism
Arterial occlusion has been reported in dogs occurring secondary to atherosclerosis, nephrotic syndrome, vegetative endocarditis, neoplastic emboli, dirofilariasis, trauma, and thrombi of left heart origin. The distal aorta, iliac, renal, and femoral arteries are common sites of systemic thromboembolism ().
History Acute arterial occlusion is usually indicative of systemic, metabolic, or cardiovascular disease. Clinical recognition and identification of the cause are enhanced by an insightful history, complete physical examination, and appropriate diagnostic tests. Some animals have a history of intermittent claudication, whereas in others, acute paresis or paralysis is the major presenting sign. Acute, complete arterial occlusion may cause posterior paresis, extreme hindlimb pain, and general distress. In some cases the animal may have an unsteady gait, lameness, progression to stumbling, weakness, or collapse. Other potential signs include weight loss, exercise intolerance, hindlimb licking or chewing, and hypersensitivity over the lumbosacral region and the hindlimbs. Other signs attributable to systemic or metabolic diseases may sometimes be detected.
Clinical signs and physical examination The outcome and clinical signs of arterial occlusion depend on (1) size and number of thrombi, (2) degree and duration of vascular occlusion, (3) pathophysiologic consequences of the organ or organs supplied, (4) whether the clot is infected or sterile, (5) whether the event is solitary or repeated, (6) the adequacy of compensatory mechanisms (e.g. collateral vessel recruitment, vasodilatation, clot lysis, restoration of blood flow), (7) the effects of vasoactive chemicals elaborated by the clot on collateral vessels (i.e. vasoconstriction), and (8) related complications (e.g. tissue necrosis, local infection, hyperesthesia). A slowly progressing arteriosclerotic or atherosclerotic stenosis allows time for the development of collateral circulation and may have minimal clinical consequences. A sudden embolus, however, may not be associated with the development of collateral circulation, and presenting clinical signs may be more severe. Microthrombus formation is common, and rapid clot lysis and abundant collateral circulation usually results in absence of outward clinical signs.
Classic presentation of acute arterial occlusion is described by the seven ft: (1) pain, (2) paleness, (3) paresthesia, (4) pulselessness, (5) polar (cold), (6) paresis or paralysis, and (7) prostration. Physical examination may reveal cool distal limbs and swollen muscles. Segmental and pedal reflexes may be depressed. Hypersensitivity over the lumbar spine may exist. A slow onset and progressive peripheral neuropathy after trauma may be associated with ischemia of peripheral nerves. Arterial thrombosis of a front limb may also occur. Clinical signs are usually less severe than those described for posterior limb thrombosis.
In the central nervous system (CNS), arterial occlusion is rarely diagnosed. For signs to be recognizable, several arteries have to be occluded simultaneously, as can occur in severe atherosclerosis or with embolization after arterial catheteriza-tion. Cerebrovascular occlusions may lead to sudden disorientation, weakness, anisocoria, and hemiamaurosis. Infarction may follow thromboembolism to a localized area of the brain. Stroke is a generic term denoting any acute, nonconvulsive, focal neurologic deficit stemming from cerebrovascular disease. The classic presentation includes hemiparesis, but a broad spectrum of neurologic injuries may result. Neurologic signs depend on site, extent, and time course of vascular occlusion. In a series of 17 affected dogs, cerebrovascular disease was associated with coagulopathy, metastatic brain tumor, trauma, sepsis, atherosclerotic thrombus, unknown cause, and vascular malformation. A cerebellar infarction caused by meningeal arterial thrombosis has also been described in a German shepherd dog with acute onset of seizure and neurologic deficits. We have occasionally observed neurologic signs related to stroke in cats associated with severe systemic hypertension. Affected animals usually present acutely blind and show signs of retinal hemorrhage and detachment. Neurovascular disorders may be more common than the literature suggests. Increasing availability of advanced imaging techniques should facilitate the diagnosis of these conditions.
With endocarditis, a heart murmur of mitral or aortic insufficiency may be auscultated. Bacterial embolization from these valves may cause a systemic shower of emboli, which frequently affect abdominal organs, especially the kidneys and small intestines. Complete unilateral or bilateral renal artery occlusion invariably causes severe renal infarction. Affected dogs are depressed and may exhibit an arched back, sublumbar pain, and hematuria.
Acute occlusion of a major mesenteric artery may cause initial gastric hyperactivity, followed by ileus and intestinal infarction. Sudden anorexia, vomiting, bowel evacuation, and abdominal pain may be present. Feces may contain blood. With bowel infarction, bloody diarrhea, severe signs of an acute abdomen, and shock may develop.
Diagnosis When peripheral arterial thrombosis is suspected, a survey thoracic radiograph is indicated to evaluate cardiac size and shape and to assess for pulmonary changes including edema, thrombosis, or dirofilariasis. Chest and abdominal radiographs should be evaluated for orthopedic lesions, which could result in posterior paresis. In addition, radiographs of the pelvic and hindlimb region may be indicated to check for masses that could exert pressure on the aorta and for periosteal reactions in the sublumbar area. Doppler echocardiography may be useful for identifying vascular disturbances.
Clinical pathology data may help characterize the underlying primary disease. Coagulation profiles are variable. Some cases of glomerulopathies and hypoproteinemia have been associated with reduced levels of antithrombin HI. Assessment of protein C and protein S levels should be considered when these tests are available. A clinical pathology data base is also advised to evaluate and detect renal or hepatic disease, dirofilariasis, DIC, and systemic and metabolic disorders. Blood cultures are indicated if endocarditis, bacteremia, or sepsis is suspected.
Confirmation of diagnosis may require proof of a vascular occlusion. This can be accomplished in some cases by physical examination, whereas in others, arteriography or diagnostic ultrasound are required. The arteriogram can indicate the exact location of the thrombus or illustrate the extent of vascular occlusion and collateral vascular supply (). Furthermore, radiolucent emboli such as heart-worms may be outlined when present as longitudinal filling defects. Contrast angiography and other alternative imaging methods (thermography, perfusion scanning) in human medicine are being replaced by MRA and advanced ultrasound techniques such as intravascular ultrasound.
Differential diagnoses Differential diagnoses include trauma; peripheral neuropathy; spinal, pelvic or vascular tumors; infections; toxoplasmosis; degenerative myelopathy; interventricular disc protrusion; fibrocartilaginous embolic myelopathy; and the cauda equina compression syndrome. Radiographs should be systematically evaluated for signs related to these disorders.
Prognosis The prognosis depends on the cause, extent, and severity of occlusion, presence or absence of local complications (ischemic neuromyopathy, ulcers), and concurrent embolization to visceral organs. Even in cases with spontaneous recovery, relapses must be expected. Rapid diagnosis and treatment are essential to avoid severe or even irreversible tissue injury.