Return to site

Deadly Temperatures: A case study of temperature induced anaphylaxis

· Clinical Education

Words by Tara Jackson and Chiara Hilson

 

Introduction

Anaphylaxis is an acute, type I allergic reaction resulting in a systemic and life-threatening inflammatory response (1-3). This widespread hypersensitivity occurs due to a trigger that produces either an immunological (production of IgE and IgG antibodies) or non-immunological (non-IgE mediated) response (1). In both cases, mast cells and basophils release inflammatory mediators that can cause adventitious changes to the skin, mucosa, respiratory, cardiovascular and/or gastrointestinal systems. Anaphylaxis is commonly recognised by signs and symptoms involving two or more of these systems (1,3). 

With every 3 in 100 adults suffering from anaphylaxis, it is essential that triggers are identified and avoided to prevent these potentially fatal reactions (3). Although uncommon, cholinergic urticaria and cold urticaria are a form of hives that can be induced by an increase or decrease in body temperature, respectively (4-6). Fluctuations in core body temperature can be provoked by factors including exposure to cold or hot environments, exertion, exercise, or even strong emotion (2, 4-6). In some circumstances, cholinergic and cold urticaria have been reported to develop into non-immunological anaphylaxis whereby this inflammatory response manifests from solely urticaria, into signs and symptoms involving multiple systems (4-6).

Due to the infrequent and underreported nature of cholinergic and cold urticaria induced anaphylaxis, health professionals often overlook this trigger as being idiopathic anaphylaxis (4).  As a result, patients can experience a four-to-five-year delay in diagnosis, resulting in a high risk of reoccurrence and poor quality of life in the interim (3-4). As anaphylaxis is commonly encountered in the prehospital setting and with prevalence continuing to rise (1-3), it is essential that paramedics can recognise and thus remove all triggers for the effective treatment of the patient (1). 

The Case

Paramedics were dispatched at approximately 1930 to a 23-year-old female experiencing symptoms of a reaction. Following a hot shower, the patient self-presented to a pharmacy for health advice due to a sudden onset of widespread urticaria, oedema, abdominal cramping, and shortness of breath. Concerned about the patient’s symptoms, the pharmacist called emergency ambulance services. On arrival, the paramedics noted that the patient was hypotensive at 80/50, tachycardic at 120bpm, and she reported feelings of constriction in her throat. . During the assessment, the patient denied any known allergies, however she had experienced a similar urticaria from an unknown trigger two days prior, which was treated and resolved with antihistamines. Following an assessment and consideration of the patient’s signs and symptoms, the attending paramedics administered 500 micrograms of intramuscular adrenaline at 2000 hours to treat a primary diagnosis of anaphylaxis. Despite the adrenaline causing a mild side effect of shaking, it resolved all symptoms and normalised vital signs. This was the patients first experience of anaphylaxis. Allergy testing later showed that this anaphylactic episode was initiated by exposure to heat from the patient’s hot shower; this is commonly referred to as cholinergic urticaria.

Discussion  

Patients with an allergic sensitivity to temperature may experience a spectrum of reactions ranging from mild urticaria to life-threatening anaphylaxis; this is dependent on the size of stimulus and severity of allergy (10). Generally, temperature induced anaphylaxis is triggered by a sudden and large decrease or increase in temperature, such as jumping into cold water or a hot bath (7). While cholinergic urticaria alone is not indicative of anaphylaxis, it can potentially progress into a cascade of multi-system symptoms such as oedema, gastrointestinal upset, bronchospasm, hypotension, and tachycardia, which accompanied this case and made the administration of adrenaline necessary (4). Although the pathophysiology of temperature-induced anaphylaxis is not well understood, the condition’s life-threatening nature requires prompt management from paramedics encountering this in the field (11).

Furthermore, it is essential that recognition and appropriate treatment of anaphylaxis is not delayed when a trigger is unidentified in the patient’s medical history (11). Gabrielli et al. (2019) conducted a study that reported at least 9.8% of anaphylaxis cases presenting to the emergency department had no known trigger. Similarly, the patient in this case exhibited symptoms consistent with the diagnosis of anaphylaxis, however the inability to recognise heat as a trigger resulted in delayed adrenaline administration. 

Adrenaline is particularly important in the treatment of anaphylaxis as it has a rapid onset and wide-spread effect on the body. Adrenaline functions by inhibiting alpha-1 receptors causing vasoconstriction thereby relieving hypotension, shock, and airway oedema (8). The beta-2 adrenergic agonist properties also work to palliate urticaria, decrease mediator release and control bronchoconstriction. Intramuscular administration is the preferred route due to its maximal pharmacodynamic effect of adrenaline in 10 minutes, as well as the decreased risk of cardiovascular complications which may present with intravenous adrenaline administration (9). It is also recommended to employ the use of antihistamine drugs and corticosteroids for milder reactions or in conjunction with adrenaline for severe anaphylaxis (9). 

Individuals diagnosed with an allergy or sensitivity to temperature are advised to avoid the trigger, carry an EpiPen and wear a MediAlert bracelet, similarly to those who experience medical or food-related allergies (10). The patient in this case had been removed from the hot environment, however continued to experience symptoms of anaphylaxis until the first administration of adrenaline. Although removal from the trigger is encouraged in the management of all anaphylactic reactions, with temperature-induced anaphylaxis the consideration of environmental conditions is particularly paramount (5). 

Conclusion 

Cholinergic urticaria is underreported, however incidences continue to increase globally and thus it is important to educate health professionals about this allergic reaction and its potential to escalate to temperature induced anaphylaxis. Recognising the trigger of this life-threatening allergic reaction is vital for both the short- and long-term management of this condition. However, it is also essential that paramedics do not delay treatment and the administration of adrenaline when a trigger is not known or can be identified in the pre-hospital setting. It is best practice to have a low threshold for suspecting anaphylaxis and treatment should be based on the patient’s clinical presentation, as opposed to their history.

 

References

1. Johnson M, Curtis J. Anaphylaxis. In Johnson M, Boyd L, Grantham H, Eastwood K. Paramedic principles and practice: A clinical reasoning approach. Australia: Elsevier; 2016. P. 426 – 452                                                                                                                                                                      2. Australasian Society of Clinical Immunology and Allergy. Acute management of anaphylaxis [Internet]. Australia and New Zealand: Australasian Society of Clinical Immunology and Allergy; 2021 [cited 2022 January 15]. 10 p. Available from https://www.allergy.org.au/images/ASCIA_HP_Guidelines_Acute_Management_Anaphylaxis_2021.pdf                                                                                                                                                                  3. Parliament of Australia. Overview of allergies and anaphylaxis in Australia [Internet]. Australia: Parliament of Australia; May 2020 [cited 2022 January 15]. Available from https://www.aph.gov.au/Parliamentary_Business/Committees/House/Health_Aged_Care_and_Sport/Allergiesandanaphylaxis/Report/section?id=committees%2freportrep%2f024422%2f725594. Vadas P, Sinilaite A, Chaim M. Cholinergic urticaria with anaphylaxis: an underrecognized clinical entity. The Journal of Allergy and Clinical Immunology: In Practice. 2016 Mar 1;4(2):284-91.5. Iijima S, Kojo K, Takayama N, Hiragun M, Kan T, Hide M. Case of cholinergic urticaria accompanied by anaphylaxis. The Journal of dermatology. 2017 Nov;44(11):1291-4. 6. Isk S, Arkan-Ayyldz Z, Sozmen SC, Karaman Ö, Uzuner N. Idiopathic cold urticaria and anaphylaxis. Pediatric emergency care. 2014 Jan 1;30(1):38-9. 7. Fernando S. Cold-Induced Anaphylaxis. The Journal of Pediatrics. 2009;154(1):148-148.e1. 8. Mostmans Y, Grosber M, Blykers M, Mols P, Naeije N, Gutermuth J. Adrenaline in anaphylaxis treatment and self-administration: Eexperience from an inner city emergency department. Allergy. 2016;72(3):492-497. 9. Cervellin G, Sanchis-Gomar F, Lippi G. Adrenaline in anaphylaxis treatment. Balancing benefits and harms. Expert Opinion on Drug Safety. 2016;15(6):741-746. 10. Boyce J. Successful treatment of cold-induced urticaria/anaphylaxis with anti-IgE. Journal of Allergy and Clinical Immunology. 2006;117(6):1415-1418. 11. Gabrielli S, Clarke A, Morris J, Eisman H, Gravel J, Enarson P et al. Evaluation of Prehospital Management in a Canadian Emergency Department Anaphylaxis Cohort. The Journal of Allergy and Clinical Immunology: In Practice. 2019;7(7):2232-2238.e3.