CONSEQUENCES OF THROMBOEMBOLISM
Tissue injury results not only from ischemia due to occlusion of blood flow but also from reperfusion as blood flow is restored.
Ischemia sets the stage for reactive oxygen species (ROS) formation and oxidative injury through a number of mechanisms.
Glycolysis predominates under anaerobic conditions, leading to lactate production, which results in acidosis. Depletion of
ATP stores eventually leads to cell membrane pump failure, allowing potassium release from the cells and entry of sodium,
calcium, and chloride. This electrolyte shift leads to cellular swelling and death. Hypoxic conditions also result in the
production of various inflammatory mediators and adhesion molecules. Nitric oxide is inactivated and prostacyclin is inhibited,
promoting vasoconstriction and platelet aggregation.25
Reperfusion injury is worse than ischemic injury. As blood flow is re-established, the toxic byproducts and inflammatory mediators
can circulate throughout the body. Potassium released from the cells enters the systemic circulation and can cause life-threatening
hyperkalemia. As oxygen becomes available for ROS formation, ROS react with and damage virtually every molecule in the body
including lipids, proteins, and DNA. The most reactive of these ROS trigger a self-perpetuating reaction of lipid peroxidation
that results in increased membrane permeability and cell death.25
Nitric oxide also plays a role in ROS formation and cellular injury. Nitric oxide is produced by nitric oxide synthase (NOS).
The inducible form of nitric oxide synthase (iNOS) is synthesized in response to hypoxia and inflammation. The iNOS can produce
large amounts of nitric oxide, leading to severe vasodilation and hypotension.26 As NOS requires oxygen as a substrate, the damaging effects of iNOS may not occur until blood flow is re-established.25
Neutrophils are also important in the pathogenesis of reperfusion injury through ROS generation and proteolytic enzyme release.25 Excessive neutrophil recruitment also contributes to the "no reflow" phenomenon that is characterized by a decrease in capillary
perfusion after blood flow is re-established as a result of endothelial cell swelling.27
CLINICAL SIGNS AND PHYSICAL EXAMINATION FINDINGS
Clinical signs of thromboembolism in cats develop acutely. Owners typically are unaware of any prior problems and report the
cats were acting normally before the event.
Most owners first notice vocalization and then find the cats lying on the ground or having difficulty ambulating. Some owners
report their cats may have been hiding before the incident. In many cases, the cat will be tachypneic or panting. Most cats
have no previous history of heart disease. In one retrospective study, 90% of the cats had no prior diagnosis of heart disease.9 Many cats present with concurrent CHF.
Clinical signs depend on the site of the thromboembolus. Since the terminal aorta is the most common site of occlusion, most
cats present for evaluation of pelvic limb paralysis or paresis. Both pelvic limbs are affected in most of these cats.9 On physical examination, the affected limb is usually cool to the touch compared with the other limbs, and the muscles are
firm and painful. Pulses in the affected limb are typically absent but may be weak if the artery is only partially occluded.
Cardiac auscultation findings may support underlying heart disease such as a murmur, diastolic gallop sound, or arrhythmia.
The heart rate is variable: cats may be tachycardic or bradycardic. Fine crackles or increased bronchovesicular sounds may
be heard on auscultation of the lungs if pulmonary edema is present. These cats usually have normal hydration because of the
acute nature of the condition unless presentation has been delayed.