Case Report

Anaphylactic Shock: The Great MimicPatrick F. K. Yong, MBChB, MRCP, Jonathan Birns, BSc, MRCP,and Mohammad A. A. Ibrahim, PhD, MRCPath

Abstract: Anaphylaxis, acute coronary syndrome and pulmonaryembolism are conditions commonly seen in the acute medical settingwhich can be difficult to diagnose. Delay in establishing the correctdiagnosis can result in either delayed or inappropriate treatment, andsubsequent morbidity and mortality. The cases we present highlightthe necessity of good clinical assessment when evaluating such pa-tients.

Key Words: anaphylaxis, acute coronary syndrome, pulmonary em-bolism, troponin, D-dimer

Anaphylaxis, acute coronary syndrome and pulmonaryembolism are conditions commonly seen in the acute

medical setting which can be difficult to diagnose. Delay inestablishing the correct diagnosis can result in either delayedor inappropriate treatment, and subsequent morbidity andmortality.

We present two cases of anaphylaxis which highlight thenecessity of good clinical assessment when evaluating suchpatients.

Case ReportsPatient 1

A 59-year-old woman presented with acute appen-dicitis. At induction of general anesthesia for an ap-pendicectomy, she was given thiopental, fentanyl andsuxamethonium. Within minutes of this, she becametachycardic and hypotensive, with her blood pressuredropping as low as 50/30 mm Hg. No swelling or rashwas noted at that time. She was treated with metaraminoland gelofusine and improved. Postoperatively, an elec-trocardiogram showed lateral ST depression and tropo-nin T was elevated at 0.11 ng/mL (normal range �0.1

ng/mL). Serial electrocardiograms showed inferior Twave inversion. While an inpatient, she developed adiffuse erythematous rash 24 hours after the operation,which was diagnosed as eczema and treated with topicalsteroids and antihistamines.

The patient was initially presumed to have had anacute coronary event in view of the electrocardiogramchanges and elevated troponin level, and plans were madeto investigate her further with coronary angiography.However, a serum tryptase performed retrospectively ona sample taken 1 hour after onset of symptoms was el-evated at 117 ng/mL (normal range 2–14 ng/mL), whichreturned to 2.7 ng/mL. Consequently, allergy testing foranesthetic agents was performed. This showed a suxam-ethonium specific IgE of 0.62 kUA/L and negative skinprick and intradermal tests for fentanyl and thiopental.These results were thought to be consistent with anaphy-laxis due to suxamethonium, complicated by transientmyocardial ischemia presumably due to hypoperfusion.In addition, she had a myocardial perfusion scan whichshowed no coronary obstruction and a low likelihood offuture coronary events.

Patient 2

A 44-year-old man presented with two episodes ofsyncope. After the second episode, he complained ofdyspnea and noticed a rash over both lower legs. Hedenied any chest pain, palpitations, headache, neurologicdisturbance, fever or precipitating events.

On examination, extremities were cool, and therewas an urticarial rash involving the lower limbs. Hisheart rate was 90 bpm and regular, his blood pressurewas 60/40 mm Hg and his respiratory rate was 28/min.Physical examination was otherwise unremarkable.

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From the Departments of Clinical Immunology and Medicine, Kings CollegeHospital, London, United Kingdom.

Reprint requests to Patrick F. K. Yong, Clinical Immunology, Denmark Hill,Kings College Hospital, London SE5 9RS. Email: pyong@doctors.org.uk

Accepted August 22, 2006.

Copyright © 2007 by The Southern Medical Association

0038-4348/0�2000/10000-0295

Key Point• Anaphylaxis can mimic other medical emergencies

and should be considered in the differential diagnosis.

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(Case Report continued from previous page)

Laboratory investigations revealed elevated D-dimer(7832 �g/L, normal range �200) and fibrinogen (5.1g/L, normal range 1.5– 4.5) with normal prothrombintime, full blood count, blood film and serum biochem-istry. Arterial blood gases demonstrated type I respi-ratory failure (pO2 8kPa). Chest x-ray and ECG werenormal. In view of these findings, pulmonary emboluswas suspected but excluded after CT pulmonary an-giography.

He admitted taking a single 75 mg diclofenac tab-let approximately ten hours previously for gout. Hehad no other medical conditions. However, one monthbefore presentation he had experienced a self-limitingurticarial rash over the lower limbs after a 2-weekcourse of diclofenac 75 mg b.i.d. for the first presen-tation of gout.

A diagnosis of anaphylaxis was then made. The pa-tient was treated with IV fluid, steroids, antihistaminesand IM epinephrine. An IV epinephrine infusion wassubsequently required to maintain hemodynamic stabil-ity. The patient was discharged from the hospital one dayafter presentation.

DiscussionEpidemiologic studies estimate that severe anaphylaxis

affects 1 to 3 per 10,000 people, but has a higher incidencein the United States and Australia.1 It is estimated to causedeath in 1 to 3 per million people. Pathophysiologically, itis mediated by substances released systemically duringmast cell and basophil degranulation, which cause in-creased vascular permeability, tachycardia, bronchospasm,pruritus, rhinorrhea, vasodilation, hypotension, flushingand headache.2

The main cardiovascular changes in anaphylaxis are fluidextravasation and vasodilation, which result in a mixed dis-tributive-hypovolemic shock pattern. The increased vascularpermeability in anaphylaxis can result in transfer of 50%of intravascular fluid into the extravascular space within10 minutes.3 In the lung, bronchospasm, tissue edema andhypotension all contribute to impaired gas exchange re-sulting in hypoxia.

Anaphylactic reactions have been reported to trigger car-diovascular events, including myocardial infarction and acutecoronary syndromes, even in patients with normal coronaryvasculature.4 There is evidence to suggest that the chemicalmediators of anaphylaxis have a direct effect on the heart, andthe main proposed mechanism for allergy-induced acute cor-onary syndromes is coronary artery spasm. It is difficult toascertain how large a contribution this has to cardiac dys-function when the usual cause of poor cardiac output is poor

venous return, and diastolic hypotension and hypoxia mayresult in myocardial ischemia.5

Serum tryptase assay can be utilized in distinguishinganaphylaxis from other conditions with similar clinicalmanifestations.6 However, these levels should be obtained1 to 2 hours after the onset of symptoms. If levels are high,they can occasionally be obtained 6 to 12 hours after pre-sentation.7

Diagnosis of anaphylaxis under general anesthesia is dif-ficult unless there is severe bronchoconstriction or hypoten-sion, as cutaneous manifestations can be obscured by drapes;drug-induced hypotension is common and respiratory signscan be masked by inhalational anesthetics. In our first patient,this was the case as there was no marked bronchoconstrictionor immediate skin reaction perioperatively. The most prom-inent abnormalities were the ECG changes and elevated tro-ponin level, which resulted in the delay in diagnosis.

Pulmonary embolism can present with a wide range ofclinical features, including dyspnea, tachypnea, pleuritic pain,apprehension, tachycardia, cough and hemoptysis. Many ofthese features can also be seen in anaphylaxis and were seenin our patient. Both guidelines on pulmonary embolism andanaphylaxis emphasize the need for careful assessment ofprobability in making the diagnosis. D-dimer testing is usefulin excluding pulmonary embolism in patients when used withassessment of clinical probability. However, it has poor spec-ificity and is elevated in a variety of settings, including ana-phylaxis, due to activation of the coagulation pathway byallergic mechanisms.8 It is not surprising that high levels ofD-dimer were found in the second case we report here.

ConclusionAnaphylaxis can present with similar features to other

life-threatening medical emergencies with the cardinal fea-tures of hemodynamic compromise, cardiac dysfunction andhypoxia, as well as abnormal investigation results. Carefulclinical assessment is important so that appropriate treatmentcan be instituted promptly to avoid further morbidity andmortality. Epinephrine is the first and most important treat-ment for anaphylaxis; considering its relative safety, when indoubt, epinephrine should be administered.

References1. Moneret-Vautrin DA, Morisset M, Flabbee J, et al. Epidemiology of

life-threatening and lethal anaphylaxis: a review. Allergy 2005;60:443–451.

2. Lieberman PL. Specific and idiopathic anaphylaxis: pathophysiology andtreatment. In: Bierman CW, Pearlman DS, Shapiro GG, et al, eds. Allergy,Asthma and Immunology From Infancy to Adulthood. Third edition. Phil-adelphia, WB Saunders, 1996, pp 297–319.

3. Fisher MM. Clinical observations on the pathophysiology and treatmentof anaphylactic cardiovascular collapse. Anaesth Intensive Care 1986;14:17–21.

4. Wasserman S. The heart in anaphylaxis. J Allergy Clin Immunol 1986;77:663–666.

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5. Brown SG. Cardiovascular aspects of anaphylaxis: implications for treat-ment and diagnosis. Curr Opin Allergy Clin Immunol 2005;5:359–364.

6. Schwartz LB, Metcalf DD, Miller JS, et al. Tryptase levels as an indicatorof mast cell activation in systemic anaphylaxis and mastocytosis. N EnglJ Med 1987;316:1622–1626.

7. LaRoche D, Vergnaud M, Sillard B, et al. Biochemical markers of ana-phylactoid reactions to drugs: comparison of plasma histamine andtryptase. Anesthesiology 1991;75:945–949.

8. van der Linden PW, Hack CE, Struyvenberg A, et al. Controlled insect-sting challenge in 55 patients: correlation between activation of plasmin-ogen and the development of anaphylactic shock. Blood 1993;82:1740–1748.

Please see Richard D. deShazo’s article on page233 of this issue.

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Case Report

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