A RAPID INCREASE IN FOOT TISSUE TEMPERATURE PREDICTS CARDIOVASCULAR COLLAPSE DURING ANAPHYLACTIC AND ANAPHYLACTOID REACTIONS

Background: Cardiovascular collapse during anaphylactic and anaphylact oid reactions results from release of histamine and other vasoactive s ubstances. Intense arteriolar vasodilation associated with severe alle rgic reactions is likely to increase convective transfer of heat and p eripheral tissue temperature, and finally to provoke cardiovascular co llapse. Therefore the authors tested the hypothesis that during anaphy lactic and anaphylactoid reactions, an acute increase in peripheral ti ssue temperature precedes cardiovascular collapse lapse and that the m agnitude of the increase correlates with the severity of the reaction. Methods: During a 13-yr period, approximately 120,000 patients were s creened for clinical evidence of intraoperative anaphylactic and anaph ylactoid reactions. Core temperature was measured in the distal esopha gus, and ''deep'' foot tissue temperature was measured on the sole of one foot in all these patients. Otherwise unexplained cardiovascular c ollapse accompanied by bronchospasm and/or cutaneous signs such as urt icaria, flushing, or angioedema occurred in 32 patients who ri ere ent ered into a prospective diagnostic protocol. Among these, 15 met labor atory criteria for anaphylactic or anaphylactoid reactions. Anaphylaxi s was confirmed in nine of them by a positive skin test to the suspect ed agent, the in vitro leukocyte histamine-release test, or the Prauni tz-Kustner test. Reactions were considered anaphylactoid in six others when laboratory evidence did not support anaphylaxis, but plasma hist amine or tryptase concentrations were much greater during episodes tha n 6 weeks later. Results: Development of anaphylactic and anaphylactoi d re actions followed a characteristic pattern: (1) Foot temperature, which was initially 3.3 +/- 1.7 degrees C less than core temperature, increased to within 0.3 degrees C of core temperature 3.2 +/- 1.4 min after drug administration; (2) onset of cardiovascular collapse ensued 1.8 +/- 0.8 min later; and (3) core temperature increased from 34.7 /- 1.0 degrees C to peak values 37.1 +/- 0.6 degrees C 13 +/- 5 min af ter drug administration. The most severe reactions were associated wit h shorter times to comparable core and foot temperatures, faster onset of cardiovascular collapse, and higher maximum core temperatures. Con clusions: The normal core-to-peripheral tissue temperature gradient wa s obliterated several minutes before hemodynamic consequences associat ed with anaphylactic and anaphylactoid reactions. Further, a rapid inc rease in deep foot temperature and maximum core temperature correlated with clinical severity.