Anaphylactic Shock after Insect-Sting Challenge in 138 Persons with a Previous Insect-Sting Reaction

1 February 1993 | Volume 118 Issue 3 | Pages 161-168

Objective: To study the rate and severity of anaphylactic reaction in relation to plasma levels of cardiovascular mediators in persons with a history of insect-sting anaphylactic shock who were rechallenged with a sting by the same insect.

Design: A cohort study with measurements before and after intentional sting challenge.

Setting: Intensive care unit of an 830-bed general hospital, a national center of insect-sting anaphylaxis in The Netherlands.

Patients: A total of 138 patients referred after a previous anaphylactic reaction to a Hymenoptera sting; and 8 volunteers.

Measurements: Signs of anaphylaxis and plasma levels of catecholamines and angiotensins.

Main Results: Only 39 of 138 (28%) of patients with a previous insect-sting anaphylactic reaction developed anaphylactic symptoms after sting challenge. Values of cardiovascular mediators and mean arterial pressure did not differ after the challenge from initial values in the volunteers or in the patients with a mild or no reaction after challenge. In the 17 patients with anaphylactic shock, mean arterial pressure decreased from 97 ± 11 (mean ±SD) to 65 ± 17 mm Hg (P < 0.001), epinephrine levels rose from a median of 0.3 nmol/L (range, 0.2 to 2.3 nmol/L) to 2.5 nmol/L (0.2 to 35.7 nmol/L; P < 0.05), norepinephrine from 1.5 nmol/L (0.5 to 6.7) to 5.9 nmol/L (1.6 to 30.9 nmol/L; P < 0.01), and angiotensin II from 61 pmol/L (7 to 217 pmol/L) to 105 pmol/L (11 to 286 pmol/L; P < 0.01), all within 5 minutes after the onset of anaphylactic symptoms. The rise of these mediators correlated with the drop in blood pressure (P < 0.001). Dopamine and angiotensin I levels did not change in any participants.

Conclusions: A recurrent insect-sting anaphylactic reaction occurred in only 28% of patients with a previous reaction. During this recurrent reaction, plasma levels of endogenous epinephrine, norepinephrine, and angiotensin II rose in relation to hypotension.

Author and Article Information

From Eemland Hospital, Amersfoort, The Netherlands; University Hospital Utrecht, Utrecht, The Netherlands; the Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands.
Requests for Reprints: Peter-Willem G. van der Linden, MD, Department of Internal Medicine, Eemland Hospital, Utrechtseweg 160, 3818 ES Amersfoort, The Netherlands.
Acknowledgments: The authors thank Dr. W.H.L. Hackeng and Mrs. B. Seidl-Prech for technical support; Mrs. A.M. van der Linden-Brocker, MA, and Dr. H. Barrowclough for critical review, and Dr. H.J.A. Wijnne for statistical advice.
Grant Support: By Stichting Bijstand Zeiken Eemland, Amersfoort, The Netherlands; and by Fonds Algemene Interne Geneeskunde, Utrecht, The Netherlands.