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Today's VeTerinary PracTice | January/February 2016 | tvpjournal.com aHs HearTWorM HoTLine Peer reviewed 64 HISTORY Pets presenting with cs have no or—at best—a poor history of receiving heartworm preventives. cs can occur throughout the year but is more common in the spring and early summer. 2,3 This seasonality may be due to the timing and maturation of a high worm burden acquired during the previous summer. classically, clinical signs occur suddenly, when heartworms relocate to the right heart and cause obstruction. as such, the typical history is that of acute onset—clinically normal yesterday, sick today. Pet owners often report the following: 2,4,5 • s ignificant lethargy and weakness • anorexia • difficulty breathing • cough (occasionally) • "Bloody" urine • Pale gums • distended abdomen (less frequent). CLINICAL FINDINGS Physical examination usually reveals a lethargic, weak, and somewhat anxious pet experiencing mild to severe respiratory distress. since the condition is usually acute at time of presentation, the patient may not yet be clinically dehydrated and often remains in good body condition. other fndings are listed in the Table. DIAGNOSTICS When cs is suspected, the diagnostic approach should be direct. The goal is to quickly confrm or refute the diagnosis by performing a urinalysis, heartworm test, and cardiac ultrasonography. Urinalysis When combined with history and physical fndings, the urinalysis can single out cs as a top diagnostic consideration. The most signifcant fnding is a gross appearance of dark red to black coffee- colored urine, which is a result of severe hemoglobinuria—a consequence of intravascular red cell trauma and subsequent hemolysis. 2,4,6,7 although coffee-colored urine is considered by some to be pathognomonic for cs, any cause of rapid intravascular hemolysis could potentially Clinical signs of CS arise when adult heartworms move retrogradely from the pulmonary arteries to the heart. When this occurs, a mass of worms traverses the tricuspid valve and becomes wrongly located in the right ventricle, atrium, and often the vena cava. In this aberrant location, the worms can become knotted and tangled. As red blood cells regurgitate and squeeze through this tangled mass of worms, they are traumatized and lysed, leading to anemia, hemoglobinemia, and hemoglobinuria. Icterus may or may not be noted, but bilirubinemia secondary to hemolysis is typical. Because the mass of worms traverses the tricuspid valve, the obstruction prevents valve closure and impedes blood fow through the right heart. Cardiac function is further hindered by obstruction of the distal pulmonary arteries by a high number of worms, as well as by endothelial proliferation, fbrosis, and embolic disease within capillaries, arterioles, and arteries. Impeded blood fow through these diseased vessels leads to increased pulmonary artery pressure, further compromising right-sided cardiac output. Cardiac preload also increases, leading to congestion of the liver and spleen and, at times, the formation of ascites. Central lobular necrosis of the liver along with cholestasis has been described, and marked elevations of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferase are common. As one would expect, a reduction in right-heart output diminishes blood volume to the left heart, which, in turn, leads to left-sided output failure. Circulatory collapse ensues. Decreased peripheral arterial pressure results in reduced tissue perfusion. Metabolic acidosis and renal hypotension develop. Hypotension and hemoglobinemia potentiate compromised renal function, which is often represented by increases in blood urea nitrogen, creatinine, and phosphorus levels. Active embolic disease and infammatory changes within the pulmonary arteries and lung parenchyma may incite cough, but more commonly, respiratory signs of polypnea or dyspnea are related to circulatory failure, hypoxia, and respiratory compensation for severe metabolic acidosis. Infammatory mediators may incite the consumption of coagulation factors and platelets, resulting in disseminated intravascular coagulation. As one can see, CS is a complex disease involving both physical and physiologic components. Corruption of homeostasis occurs quickly, and the longer the heartworm mass inhibits cardiac function, the more likely death will ensue. Thus, surgical removal of this obstructive mass is the only means of reestablishing circulation and permitting homeostasis to normalize. Without surgical intervention, the short- term prognosis worsens; affected pets usually die within 1 or 2 days. Caval Syndrome: Disease Overview