Today's Veterinary Practice provides comprehensive information to keep every small animal practitioner up to date on companion animal medicine and surgery as well as practice building and management.
Issue link: http://todaysveterinarypractice.epubxp.com/i/840151
56 ANAPHYLACTIC SHOCK PEER REVIEWED Histamine acts through 3 receptors (H1R, H2R, H3R) to promote signs of shock. H1R increases smooth muscle contraction, causing vasodilation and increased vascular permeability. It also stimulates the conversion of l-arginine into nitric oxide, which leads to vasodilation and therefore decreases venous return. H2R increases gastric acids, increases heart rate and ventricular contractility, and further promotes vasodilation. H3R inhibits norepinephrine release, thus increasing the degree of systemic shock. Without norepinephrine, vasodilation can persist and lead to clinical hypotension. Clinical signs of histamine release include rhinitis, pruritus, dyspnea, hypotension, and tachycardia. 13 Other Mediators Heparin is also released from mast cell granules. The release of heparin inhibits clot formation by decreasing clotting factors. 13 This may lead to a hypocoagulable state and predispose a patient to clinical bleeding. Cytokines, such as interleukin-4 and interleukin-13, are synthesized and released in response to the arachidonic acid cascade. The release of cytokines leads to an increase in cellular responsiveness to inflammatory mediators, up to 6 times normal. 12 Prostaglandins released may cause bronchoconstriction, pulmonary and coronary vasoconstriction, and peripheral vasodilation. 14 Clinically, airway obstruction, increased airway secretions, and decreased cardiac output may be noted (hypotension). Platelet activating factor decreases coronary blood flow and myocardial contractility and increases pulmonary resistance, vasodilation, hypotension, and platelet aggregation. 13,14 Decreases in myocardial contractility in conjunction with vasodilation can lead to profound hypotension. ANAPHYLACTIC SHOCK Shock is a state of low blood perfusion to tissues that causes inadequate delivery of oxygen and decreased cellular energy production. Shock is often brought on by hypovolemia, maldistribution of vascular volume, or failure of the cardiac pump (cardiogenic shock). Anaphylactic shock results from massive vasodilation secondary to mast cell degranulation, histamine release, and the rapid release of inflammatory and vasoactive mediators. Vasodilation in turn decreases the relative circulatory volume, decreasing perfusion and thus oxygen delivery to tissues. This leads to splenic contraction and tachycardia, and ultimately myocardial and cerebral hypoxemia, cardiovascular collapse, and death. 12 Shock Organs Because of differences in immune response, smooth muscle anatomy, and antigen degradation rates, each species has different physiologic responses to anaphylaxis. 12 Dog: Liver, Gastrointestinal System In dogs, histamine is primarily released from the gastrointestinal tract into the portal vein, thus leading to hepatic arterial vasodilation and an increase in arterial hepatic blood flow. In addition, histamine release into the portal system creates a large venous outflow obstruction that results in a hepatic vascular resistance increase of up to 220% of normal within seconds. 15,16 As a result, venous return to the heart is decreased. Reduced hepatic venous return to the heart decreases cardiac output and therefore contributes to hypovolemia and decreased oxygen delivery to the tissues. Because of decreased oxygen delivery and hypovolemic shock, common clinical signs include collapse and acute onset of gastroenteritis that is sometimes hemorrhagic. 16 Cat: Lungs In cats, anaphylactic reactions are seen primarily in the lungs. Cats typically respond to allergens via profound bronchoconstriction. This leads to reduced blood oxygen levels, increased dissolved carbon dioxide levels, and decreased cardiac output. Acute hypoxemia can increase sympathetic tone, causing splenic contractions and eventually hemoconcentration. 16 CLINICAL SIGNS Signs of anaphylaxis may be categorized based on the affected organ system: cutaneous, respiratory, cardiovascular, or gastrointestinal. 16 Cutaneous Cutaneous signs are the most common initial clinical sign of an allergic reaction but may be a precursor for more severe reactions, such as anaphylaxis. If severe anaphylaxis has a rapidly acute onset, cutaneous signs may be absent. The most common cutaneous clinical signs include erythema, urticaria, pruritus, wheals, and angioedema. These signs are often short in duration.