Anaphylaxis is a life-threatening, systemic hypersensitivity reaction and the most severe form of allergic reaction. This is a systemic response to a specific allergen and usually occurs acutely after exposure.6 In children, food-related reactions are the most common mediated by immunoglobulin E (IgE) leading to mast cells and basophils activation and degranulation. Other common mediators released as a result of the reactions include histamine, heparin, tryptase, kallikrein, platelet-activating factor, bradykinin, tumor necrosis factor, nitrous oxide, interleukins and other pro-inflammatory cytokines.3 While manifestations can include neurological response which occur about 15 percent of the time, patients may exhibit headache, dizziness, lightheadedness, confusion, tunnel vision, and loss of consciousness. Prompt intramuscular epinephrine administration is the therapy of choice, along with ensuring proper oxygenation and circulation.4 In severe forms as noted in this case, the patient may require advanced airway and continuous infusion of epinephrine to enhance vasoconstriction, increase peripheral resistance, decrease mucosal edema, increase cardiac inotropy/chronotropy, and bronchodilation to reverse the airway obstruction.5
While complications of anaphylaxis can affect most systems, neurological manifestation post-anaphylaxis is rare. To our knowledge, this is the first description of such a patient case where memory loss occurred after severe anaphylaxis. Prior case studies describing a similar manifestation was reported in an adult patient where memory loss occurred after an insect sting.7 Similarly, this patient also experienced headache, disorientation, and an inability to concentrate or to initiate movement.7 While our patient’s weakness was likely associated with patient’s brief hospital stay, his confusion, agitation and disorientation were persistent for several months after discharge. A proposed pathophysiological explanation in that case report suggested an ischemic necrosis of the Carbonic Anhydrase (CA)-1 area of the hippocampus caused by mediators released during the acute event. Our patient did not have any additional imaging after the hospital course nor an EEG to look for changes compatible with neurological deficits. It is important to note that the adult case described showed no changes on MRI but had a nonspecific abnormality in the temporal region.7
While there were some similarities in the clinical features of both cases, neither could directly associate the ensuing anaphylactic reaction with this neurologic complication post-event and treatment.
Other factors that may have contributed include a sustained inflammatory response which has been documented in previous studies.8–11 While anaphylaxis mediators are generally confined to the airways, cytokines such as Interleukin (IL)-33 may induce an inflammatory state in the central nervous system. IL-33, a member of the IL-1 cytokine family, is described as a key regulator of neuroinflammation8–11 and is associated with different allergic inflammations such as food anaphylaxis and respiratory allergens. Recent study suggest that this cytokine is associated with cognitive impairment in the hippocampus.8 It is not clear whether this could potentially occur in all patients with severe anaphylaxis, nevertheless, these potential pathways to post-anaphylactic neurological complications should be considered in pediatric patients who present with significant anaphylaxis. Further studies to elucidate these factors should be encouraged to further understand the pathophysiology of this neurological post-treatment manifestation to better support patients and their care takers.