Running head: INTRAOPERATIVE ANAPHYLAXIS
Intraoperative Anaphylaxis
Angelique I Davis
The University of Kansas
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INTRAOPERATIVE ANAPHYLAXIS
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Intraoperative Anaphylaxis
Anaphylaxis is an immediate type I hypersensitivity response that is difficult to diagnose
in the intraoperative setting. Anaphylaxis can present as a multitude of different adverse effects
that occur in response to normal induction proceedings (Norred, 2012). “Immediate
hypersensitivity reactions occur, however, only once in every 5,000 to 10,000 anesthetics”
(Mertes et al., 2010, para. 1). The purpose of this paper is to review the pathophysiologic
process of anaphylaxis, identify the signs and symptoms, recognize the common causes of
anaphylaxis pertaining to anesthesia, and explore the proper treatment regimen.
Type I hypersensitivity is further divided into IgE mediated and non IgE mediated. IgE
mediated anaphylaxis is described as allergic and non IgE mediated immune response is defined
as anaphylactoid. In the perioperative setting differentiating between the two is difficult; the
focus of this paper will be on IgE mediated anaphylaxis (Norred, 2012).
The pathophysiology of a type I hypersensitivity allergic reaction is IgE dependent. An
individual is exposed to an antigen, and through innate and adaptive immunity, activates T-cells,
B-cells, and produces allergen specific IgE antibodies. After reexposure to the antigen, IgE
specific antibodies attach to the surface of the mast cells causing degranulation and subsequent
release of inflammatory mediators into the extracellular fluid compartment. The release of
histamine, tryptase, proteoglycans, carboxypeptidases, prostaglandin, leukotriene, and platelet
activating factor are the cause of the life-threatening symptoms of anaphylaxis (Butterworth IV
et al., 2013). Type I IgE hypersensitivity typically occurs immediately due to intravenous
administration of induction agents, although an allergic reaction can be delayed for an hour or
longer (Norred, 2012).
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Due to the array of mediators released, it is imperative that anesthetic providers recognize
and treat symptoms of anaphylaxis rapidly. Signs and symptoms for the anesthesia provider to
be aware of are the results of mast cell and basophil degranulation. Mast cells are largely located
in heart, vasculature, respiratory, gastrointestinal, and integument systems (Norred, 2012).
The clinical presentation of surgical patients undergoing anaphylaxis may display early
cutaneous symptoms that include pruritus, flushing, erythema, urticaria, or angioedema.
Cutaneous signs are difficult to appreciate in the perioperative setting. The difficulty is due to
patients being draped and the position necessary for the surgery (Mertes et al., 2010). Typically,
the late signs of respiratory distress and cardiovascular instability are, at times, the only
symptoms that the anesthesia provider may recognize. Respiratory symptoms that commonly
occur are wheezing, hypoxia, hypercarbia, angioedema, and increased peak airway pressures.
Cardiovascular symptoms present are hypotension, tachycardia, dysrhythmias, shock, or even
death (Norred, 2012). Some of these symptoms can be mistaken for bronchospasm, pain,
insufficient neuromuscular blockade, bleeding, or light anesthesia (Jacobson et al., 2001).
With respect to symptoms of anaphylaxis, the anesthesia provider must consider the onset
of symptoms in relation to allergens introduced to the patient (Mertes et al., 2010). The most
common allergens in anesthesia are neuromuscular blocking agents, with emphasis on
succinylcholine and rocuronium, followed by latex and antibiotics (O’Donnell, 2014). Causative
factors that attribute to a potential latex allergy in the operating suite are the use of latex
containing gloves, tourniquets, and catheters. Antibiotics that are of primary concern with
anaphylaxis are beta lactams, such as penicillins and cephalosporins. While vancomycin and
quinolones are known to cause anaphylaxis as well, they do so to a lesser extent (Ebo, Fisher,
Hagendorens, Bridts, & Stevens, 2007).
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Anaphylaxis is treated in accordance with the severity of symptoms the patient is
experiencing. The severity of symptoms is quantified using the Ring and Messmer severity
scale. Symptoms can range from mild cutaneous signs to cardiovascular collapse (Norred, 2012)
Treatment of anaphylaxis begins with removing the causative agent, sending for help, and
informing the surgeon of the change in patient status. Maintain or gain access to a patent airway
is imperative, along with administering 100% oxygen. Control of hypotension with epinephrine
is the foundation in anaphylaxis management. Epinephrine’s mechanism of action is primarily
alpha 1, providing vasoconstriction, and beta 2, providing bronchodilation. If
bronchoconstriction is persistent, administration of a direct beta 2 agonist may be indicated.
Salbutamol or albuterol are common beta 2 agonists used in anesthesia. Fluid management with
sodium chloride 0.9% or colloid administration is recommended for the rapid fluid shifts that
occur due to vasodilation and capillary leakage. Management of histamine blockers, both H1 and
H2, and corticosteroids are used to treat angioedema and cutaneous symptoms (Mertes et al.,
2010).
IgE mediated anaphylaxis in the intraoperative setting is primarily caused by
neuromuscular blocking agents, followed by latex and antibiotics (O’Donnell, 2014).
Recognition and treatment is crucial for optimal patient outcomes. The anesthesia provider must
remain vigilant in patient assessment in accordance with medications administered to the patient.
This vigilance will empower the anesthetist to appropriately provide the correct treatment.
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References
Butterworth IV, J. F., Mackey, D. C., & Wasnick, J. D. (2013). Anesthetic Complications. In
Morgan & Mikhail’s Clinical Anesthesiology (5th ed. (pp. 1199-1229). New York, NY:
McGraw-Hill.
Ebo, D. G., Fisher, M. M., Hagendorens, M. M., Bridts, C. H., & Stevens, W. J. (2007).
Anaphylaxis during anesthesia: diagnostic approach. Allergy, 62, 471-487.
Jacobson, J., Lindekaer, A. L., Ostergaard, H. T., Nielsen, K., Ostergaard, D., Laub, M., ...
Johannessen, N. (2001). Management of anaphylactic shock evaluated using a full-scale
anesthesia simulator. ACTA Anaesthesiologica Scandinavica, 45, 315-319.
Mertes, P. M., Tajima, K., Regnier-Kimmoun, M. A., Lambert, M., Iohom, G., GueantRodriguez, R. M., & Malinovsky, J. M. (2010, July). Perioperative Anaphylaxis. Medical
Clinics of North America, 94(4).
Norred, C. L. (2012). Anesthetic-Induced Anaphylaxis. AANA Journal, 80, 129-140.
O’Donnell, M. P. (2014). The Immune System and Anesthesia. In J. J. Nagelhout, & K. L. Plaus
(Eds.), Nurse Anesthesia (5th ed. (pp. 1015-1035). St. Louis, MO: Elsevier.