Anaphylaxis Case File

https://medical-phd.blogspot.com/2021/05/anaphylaxis-case-file.html

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J.
Rosh, MD, MS

Case 10
A 35-year-old woman is brought to the emergency department (ED) by ambulance after collapsing at home. She
had been seen by her regular doctor earlier in the day and prescribed amoxillin for sinusitis. Paramedics report
field vital signs remarkable for a blood pressure of 70/30 mm Hg, heart rate of 140 beats per minute, respiratory
rate of 40 breaths per minute, and an oxygen saturation of 76%. Intravenous fluids and oxygen were
administered during transport. Paramedics are assisting the patient’s breathing with bag-valve mask ventilation,
but oxygen saturations remains low. On physical examination, the patient is obtunded with perioral cyanosis,
tongue swelling, stidor, wheezing, and labored breathing. Her skin is cool and clammy with large urticarial
lesions.

⯈ What are the next steps?

⯈ What treatments should be instituted?

ANSWER TO CASE 10:

Anaphylaxis

Summary: This patient is demonstrating signs and symptoms of anaphylaxis. Anaphylaxis is rapidly progressive
severe allergic reaction which compromises a patient’s airway, breathing, and circulation. Patients may also
exhibit flushing, hives, and swelling of mucous membranes. Successful treatment of anaphylaxis requires early
recognition of the symptoms of anaphylaxis, support of the airway, and administration of epinephrine.

 • Next step: In the presence of symptoms meeting the diagnostic criteria for anaphylaxis, epinephrine
should be administered immediately. The first dose should be administered intramuscularly. In the
setting of a severe reaction like the one described above, moving quickly to intravenous infusion of
epinephrine is recommended.
 • Further treatments: This patient requires rapid resuscitation and stabilization. Airway, breathing, and
circulation (ABCs) should be managed appropriately and in that order, which will mean both procedural
and pharmacological intervention. A definitive airway will need to be immediately established in the
face of impending airway obstruction (see Case 1), and the patient’s cardiovascular compromise must be
supported with epinephrine. Experts have referred to the ABCs of anaphylaxis as A E B C; the E is for
epinephrine.

In addition to airway management and early administration of epinephrine, pharmacologic therapy is tailored to
the other systemic manifestations of the anaphylactic response. These include volume resuscitation with
crystalloid, nebulized beta agonists, nebulized racemic epinephrine, corticosteroids, antihistamines (including
H2 blockers), and removal of any remaining antigen (ie, the bee stinger).

ANALYSIS
Objectives

1. Rapidly recognize the characteristic clinical features of anaphylaxis.

 2. Understand the underlying pathophysiology of anaphylaxis.
3. Become familiar with the available treatment options; most importantly the correct administration of
epinephrine.

Considerations
This patient is brought into the ED with swelling of the tongue and labored breathing. The perioral cyanosis,
diffuse wheezing, stridor, and hypoxia all indicate impending respiratory failure. A delay of even a minute
may be life-threatening. The most important intervention in addition to administration of epinephrine
is securing an airway. This patient likely has edema of the pharynx and larynx making intubation technically
difficult. Airway management in a patient like this often requires a cricothyroidotomy.

Intravenous access with administration of epinephrine is the most important pharmacologic intervention.
Epinephrine should first be given intramuscularly; if that route fails, an intravenous drip should be initiated.
Dosing of epinephrine will be covered below. Identification of the inciting agent is not essential for treatment of
anaphylaxis, but is helpful in preventing further exposures and recurrence of symptoms.

Approach To:
Anaphylaxis

CLINICAL APPROACH

Epidemiology
Millions of people present to emergency departments every year complaining of allergic symptoms ranging
from the minor rashes to multisystem anaphylaxis. Most of the time, it is difficult if not impossible to identify
the trigger. Many reactions may occur in response to medical therapies such as antibiotics and radiologic
contrast agents. Because the spectrum of allergic responses is so broad, anaphylaxis is likely underreported. As
a result it is difficult to calculate a precise incidence of this disease. There are an estimated 30,000 ED visits
every year for adverse food reactions. However, there are far more visits for more vague complaints and
unknown exposures that may be difficult to identify as anaphylaxis. In the emergency department the goal is
rapid diagnosis, symptomatic treatment, and prevention of further episodes.

Pathophysiology
True anaphylaxis is a type 1 hypersensitivity reaction occurring after a previous sensitizing exposure. In its
purest form, this is an immune-mediated activation of basophils and mast cells with subsequent release of
prostaglandins, leukotrienes, and histamine. From a clinical standpoint, an anaphylactoid reaction also
includes release of these compounds but through non–immune-mediated pathways. The only clinical
significance of this difference is that anaphylactoid reactions can occur without prior sensitization. Regardless
of the underlying mechanism, their effects are similar, and early recognition will determine successful clinical
management in these patients (see Table 10–1 for pitfalls).

When first exposed to a substance, binding antibodies trigger class switching and regulatory changes in gene
expression, effectively priming the immune system for its next encounter with the offending agent. In certain
cases, this leads to immunoglobulin (igE) binding mast cells and basophils. In the classically defined
anaphylactic reaction, the antigen again encounters the immune system, binds to the IgE on the mast cells and
basophils, and releases a flood of cytokines that set the clinical response in motion. In an anaphylactoid
reaction, the antigen causes direct release
of cytokines by mast cells and basophils, without need for prior sensitization. In both cases, the end result is the
same, and clinically indistinguishable.