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Year : 2016  |  Volume : 9  |  Issue : 4  |  Page : 527-530  

A case of severe anaphylaxis following coronary angiography

1 Department of Medicine, Army College of Medical Sciences, New Delhi, India
2 Department of Medicine, 7 Air Force Hospital, Kanpur, Uttar Pradesh, India

Date of Web Publication12-Jul-2016

Correspondence Address:
Anil Kumar
Department of Medicine, Base Hospital, Army College of Medical Sciences, Delhi Cantt, New Delhi - 110 010
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-2870.186055

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Anaphylaxis reactions are not uncommon in routine practice and involve multiple systems usually. Cardiovascular collapse is the severest form of reaction. We present a case of severe anaphylactic reaction with cardiovascular collapse without other systems involvement which had to treat with intravenous adrenaline for a prolonged duration (successfully). The case is presented because of the rarity of presentation (single system involvement) and requirement of prolonged use of adrenaline for more than 24 h.

Keywords: Adrenaline, anaphylaxis, shock

How to cite this article:
Kumar A, Mahesh NK, Bhat KG, Goyal A. A case of severe anaphylaxis following coronary angiography. Med J DY Patil Univ 2016;9:527-30

How to cite this URL:
Kumar A, Mahesh NK, Bhat KG, Goyal A. A case of severe anaphylaxis following coronary angiography. Med J DY Patil Univ [serial online] 2016 [cited 2022 Oct 5];9:527-30. Available from:

  Introduction Top

Anaphylaxis is a severe, systemic allergic reaction characterized by multisystem involvement, including the skin, airway, vascular system, and gastrointestinal tract.[1] Severe cases may result in complete obstruction of the airway, cardiovascular collapse, and death. The term classic anaphylaxis refers to hypersensitivity reactions mediated by the subclass of antibodies immunoglobulins (Igs) IgE, and IgG. Prior sensitization to an allergen has occurred, producing antigen-specific Igs. Subsequent reexposure to the allergen provokes the anaphylactic reaction. Many anaphylactic reactions, however, occur without a documented prior exposure. Anaphylactoid or pseudoanaphylactic reactions display a similar clinical syndrome, but they are not immune-mediated. Treatment for the two conditions is similar.

  Case Report Top

A 68-year-old lady with no modifiable risk factors except diabetes mellitus type II on diet control only was admitted with symptoms of chronic stable angina. Clinically vitals stable with blood pressure (BP) of 130/82 mm Hg. Pulse rate was 80/min. Cardiovascular system and other systems were clinically unremarkable. Hemogram, urine analysis was normal. All biochemical parameters were within normal limits.

Electrocardiogram was done which showed low voltage graph with the poor progression of R waves in anterior leads [Figure 1] with left axis deviation indicating old coronary artery disease (although no history was there indicating an acute coronary event in past). X-ray chest was normal. Two-dimensional echocardiography was done revealed normal size left ventricle (LV) and right ventricle with regional wall motion abnormality in anterior wall and interventricular septum (hypokinesia) with overall LV ejection fraction of 50% (mild LV systolic dysfunction and Stage I diastolic dysfunction. All valves normal. No pericardial effusion or clot [Figure 2] and [Figure 3].
Figure 1: Electrocardiogram

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Figure 2: Normal echocardiogram (Parasternal long axis view)

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Figure 3: Normal echocardiogram (Apical view)

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In view of typical angina, she was taken up for coronary angiography with premedication, and the procedure was done through the right femoral artery route using Judkins left and the right catheters and completed in 15 min with the use of contrast (visipaque) 50 ml. Coronary angiography revealed the right dominant circulation, patent coronaries with having no obstructive lesions [Figure 4] and [Figure 5]. Aortic pressures were 130/80 mm Hg.
Figure 4: Normal left anterior descending/left circumflex

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Figure 5: Normal right coronary artery

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The patient was taken up in post catheterization recovery room where femoral arterial sheath was removed as usual procedure while the patient was on noninvasive BP, cardiac, and SpO2 monitors. The patient developed chest pain and hypotension. She was managed for vasovagal syncope which is not uncommonly seen in cardiac catheterization laboratories during femoral sheath insertion or removal. However, she did not show any response to atropine 1.2 mg and the fluid challenge of 500 ml normal saline. The patient continued having chest pain, giddiness, and started complaining loss of peripheral vision with systolic BP of 40 mm Hg and despite dopamine infusion with 15 µg kg/min and atropine pulse rate of 100/min without improvement in BP. A possibility of iatrogenic complication during coronary angiography was kept, and she was immediately taken up for check coronary angiography via the right femoral route. Check angiography revealed no dissection of coronaries or aorta.

A possibility of anaphylaxis was kept although no urticarial rash, wheezing was there and chest examination did not reveal any rhonchi or crepts clinically. She was then given adrenaline bolus of 50 µg intravenous (IV) which led to a rise in pressure to 150/90 mm Hg but after 10 min dropped back to 50 mm systolic which responded again to a bolus of adrenaline. She was placed on adrenaline infusion which was titrated in around ½ h with continuous invasive arterial BP monitoring to a dose of 0.5 µg/kg/min (0.05-0.5 µg/kg/min). She maintained BP on this dose. In addition, she was given hydrocortisone, antihistamines, and H2 receptor blockers. Serum biochemical parameters renal function test. Liver function test, electrolytes all were within normal limits. Total leukocyte count showed some rise with neutrophilic leukocytosis, possibility effect of steroids. She developed fixed drug eruptions after 24 h [Figure 6].
Figure 6: Fixed drug eruption

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She had to be kept for 36 h on adrenaline infusion which was gradually tapered off with full recovery.

  Discussion Top

An anaphylactic reaction is not very uncommonly seen in routine clinical practice and has varied presentations. Consider anaphylaxis when responses from 2 or more body systems (cutaneous, respiratory, cardiovascular, neurologic, or gastrointestinal) are noted. The shorter the interval between exposure and reaction, the more likely the reaction is to be severe. Signs and symptoms include the following: Serious upper airway (laryngeal) edema, lower airway edema (asthma), or both may develop, causing stridor, and wheezing. Rhinitis is often an early sign of respiratory involvement.

Cardiovascular collapse is the most common peri-arrest manifestation. Vasodilation produces a relative hypovolemia. Increased capillary permeability contributes to further intravascular volume loss. The patient may be agitated or anxious and may appear either flushed or pale. Additional cardiac dysfunction may result from underlying disease or the development of myocardial ischemia from the administration of epinephrine. Gastrointestinal signs and symptoms of anaphylaxis include abdominal pain, vomiting, and diarrhea.

Severe anaphylaxis only presenting with cardiovascular collapse is not very commonly seen without any other system involvement, and it requires immediate recognition and treatment. Drug of choice is adrenaline and in the case of cardiovascular collapse, it is prudent to give IV instead of the subcutaneous route as the first absorption is slow, erratic, and poorly controlled while IV route is easy to control with assured and quick delivery. Close monitoring is critical because a fatal overdose of epinephrine has been reported.

Aggressive fluid challenge, corticosteroids and antihistamines and H2 receptor blockage are other parts of therapy.

Recommendations to prevent cardiopulmonary arrest are difficult to standardize because etiology, clinical presentation (including severity and course), and organ involvement vary widely. Few randomized trials of treatment approaches have been reported. Providers, however, must be aware that the patient can deteriorate quickly and that urgent support to airway, breathing, and circulation are essential. The following therapies are commonly used and widely accepted but are based more on consensus than evidence:

Oxygen: Administer oxygen at high flow rates.

Epinephrine: Absorption and subsequent achievement of maximum plasma concentration after subcutaneous administration are unpredictable with shock.[2],[3] Thus, the intramuscular (IM) administration is favored:

  • Administer epinephrine by IM injection early to all patients with signs of a systemic reaction, especially hypotension, airway swelling, or definite difficulty breathing.
  • Use an IM dose of 0.3-0.5 mg (1:1000) repeated every 15-20 min if there is no clinical improvement.

Administer intravenous epinephrine: If anaphylaxis appears to be severe with immediate life-threatening manifestations.[1],[2]

  • Use epinephrine 50 µg IV slowly over 5 min.
  • An IV infusion at rates of 0.05-0.5 µg/kg/min may prevent the need to repeat epinephrine injections frequently.

Close monitoring is critical because a fatal overdose of epinephrine has been reported.[4],[5] Patients who are taking blockers have increased incidence and severity of anaphylaxis and can develop a paradoxical response to epinephrine.[3],[5] Consider glucagon as well as ipratropium for these patients.

Aggressive fluid resuscitation: Give isotonic crystalloid (e.g., normal saline) if hypotension is present and does not respond rapidly to epinephrine. A rapid infusion of 1-2 L or even 4 L may be needed initially.

Antihistamines: Administer antihistamines slowly IV or IM (e.g., 25-50 mg of diphenhydramine).

H2 blockers: Administer H2 blockers such as cimetidine (300 mg orally, IM, or IV).[4.5]

Inhaled-adrenergic agents: Provide inhaled albuterol if bronchospasm is a major feature. Inhaled ipratropium may be especially useful for the treatment of bronchospasm in patient's receiving-blockers. Note that some patients treated for near-fatal asthma actually had anaphylaxis, so they received repeated doses of conventional bronchodilators rather than epinephrine.[6]

Corticosteroids: Infuse high-dose IV corticosteroids early in the course of therapy. Beneficial effects are delayed at least 4-6 h.

  Conclusion Top

Anaphylaxis reactions are not very uncommon with the use of newer drugs and procedures in routine practice. These reactions can be life-threatening if not recognized in time while they are preventable and treatable if recognized in time. Adrenaline is drug of choice in shock and should be used intravenously if monitoring is possible.

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Conflicts of interest

There are no conflicts of interest.

  References Top

ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American heart association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2005;112 24 Suppl:IV1-203.  Back to cited text no. 1
Simons FE, Gu X, Simons KJ. Epinephrine absorption in adults: Intramuscular versus subcutaneous injection. J Allergy Clin Immunol 2001;108:871-3.  Back to cited text no. 2
Simons FE, Chan ES, Gu X, Simons KJ. Epinephrine for the out-of-hospital ( first-aid) treatment of anaphylaxis in infants: Is the ampule/syringe/needle method practical? J Allergy Clin Immunol 2001;108:1040-4.  Back to cited text no. 3
Pumphrey RS. Lessons for management of anaphylaxis from a study of fatal reactions. Clin Exp Allergy 2000;30:1144-50.  Back to cited text no. 4
Pumphrey R. Anaphylaxis: Can we tell who is at risk of a fatal reaction? Curr Opin Allergy Clin Immunol 2004;4:285-90.  Back to cited text no. 5
Rainbow J, Browne GJ. Fatal asthma or anaphylaxis? Emerg Med J 2002;19:415-7.  Back to cited text no. 6


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]


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