Anaphylaxis

What is anaphylaxis

On February 23, 2019 by Ronald S. White

Introduction, epidemiology, history

Anaphylaxis was described in 1901 by Charles Richette and Paul Portier as the result of a study of the poison of a sea urchin (for which the first received the Nobel Prize in Physiology and Medicine in 1913). They administered the poison to dogs and found that they were hypersensitive to the poison when reintroduced.

In the USA, on average, about 100 000 anaphylactic reactions are registered annually, 60 000 of which are registered for the first time and 1500 end in death. Anaphylaxis is most common in summer and the first half of autumn, and is more likely to occur in women over 30 and in boys under 16. 1.6% of the US population has experienced anaphylaxis at least once in their lives, but due to lack of information this figure can be underestimated.

Pathophysiology

Anaphylaxis can be divided into two categories

1. Immune (with the participation of immunoglobulins and activation of complement)

2. Nonimmune, or anaphylactoid, with the participation of substances that directly activate fat cells and cause degradation of basophils.

Mechanism of anaphylaxis development:

1. The allergen-specific IgE produced by B-lymphocytes binds to high affinity IgE receptors on the surface of basophils and fat cells, which is responsible for the release of a large number of biologically active substances such as histamine, tryptaza and tumor necrosis factor.
2. Nonimmune anaphylaxis occurs when complement, basophilus, mast cells are directly activated by a specific substance such as vancomycin (“red man syndrome” for rapid intravenous injection) or opiates.

Typical allergens.

• Food: eggs, peanuts, hazelnuts, clams.
• Medicines: non-steroidal anti-inflammatory drugs, antibiotics.
• Insect poisons: eardrums, fire ants.
• Others: latex.

Diagnostic criteria

Patients with anaphylaxis usually have skin and mucous membrane lesions (90%) or respiratory symptoms (70%). Gastrointestinal and/or cardiovascular symptoms (hypotension) are reported in 45% of patients.

Diagnostic criteria have evolved over the past few years in order to simplify the diagnostic solution. Emergency physicians and allergists have attempted to minimize the likelihood of missed or delayed anaphylaxis diagnoses and thus improve care.

Criteria for anaphylaxis (sensitivity 97%, specificity 82%, prognostic value of positive result 69%, prognostic value of negative result 98%).

1. Acutely developed disease with lesions of the skin / mucous membranes and one of the following signs: respiratory failure or hypotension.

2. Exposure to an alleged allergen followed by two of the following: skin lesion, respiratory impairment, hypotension, gastrointestinal complaints.

3. Hypotension following exposure to a known allergen.

Negative blood test result for tryptase and histamine level do not allow to exclude the diagnosis of anaphylaxis. The level of platelet activation factor is of diagnostic value, but it quickly returns to normal figures within 15 – 20 minutes from the appearance of symptoms.

Treatment algorithm

1. Extraordinary events

As fast as possible adrenaline (MNN epinephrine) intramuscularly into the muscles of the anterior thigh surface. Adults 0.3 to 0.5 mg every 5 minutes (0.3 to 0.5 ml 0.1% solution). Children 0.01 mg/kg of body weight every 5 minutes.

If there is no response to two intramuscular adrenaline injections, proceed to intravenous injection. Intravenous adrenaline injection:

Adults: 1 mg (1 ml 0.1% solution) in 250 ml 5% glucose solution, starting at 0.25 to 1 ml per min. (1 – 4 µg per min.) to 2.5 ml per min. (10 µg per min.)

For children: 0.1 µg/kg min. to 1.5 µg/kg min.

2. Complementary treatment

• Diphenhydramine (dimedrol) 50 mg v/v once.
• Antagonist H2 receptor v/v once.
• Dopamine/dobutamine in treatment-resistant shock: 5 – 20 mg/kg min.
• Glucagon (for patients taking beta-blockers): 1 – 5 mg V/v in 5 min, then 5 – 15 micrograms per min. (20 – 30 µg/kg min. until reaching 1 mg dose for children).

Hemodynamic instability is secondary to the intravascular redistribution of volumes. Infusion therapy in the amount of 2 – 7 liters is prescribed with continuing hypotension. Sodium chloride isotonic solution is preferable to Ringer-Lactate.

Conflicts

• Delayed diagnosis

In most of the cases described, deaths from anaphylaxis stop the blood circulation and breathing shortly after the onset of symptoms: 5 minutes for iatrogenic causes, 15 minutes after insect stinging, 30 minutes for food allergens. Given that antihistamines begin to take effect after 45 minutes, timely recognition of anaphylaxis and adrenaline injection are of great importance.

Up to 20% of anaphylaxis cases go without classic itchy skin rashes. Shock and fatal anaphylaxis can occur without any skin symptoms. There are no absolute contraindications for adrenaline administration, and an anaphylactic reaction in itself can cause myocardial ischemia, arrhythmias and cardiac output reduction.

• Surveillance and transcripts

For medium to severe anaphylaxis with full resolution of symptoms, a 4 to 8 hour observation is recommended. If symptoms do not recur, prescribe a short course of H1/H2 antihistamines and glucocorticoid therapy (despite weak evidence). All patients who have undergone anaphylaxis should be advised to use autoinjection units with adrenaline. Patients with persisting symptoms as well as those requiring further intravenous injection should be hospitalized for further observation.

• Repeated reactions

In most cases, anaphylactic reactions occur monophasically and are resolved within an hour. Less often, they last hours and days. Up to 23% of patients tolerate the renewal of symptoms in the coming hours and days (10 hours on average). The second phase is usually less pronounced than the initial phase. At least one study found that less than 0.25% of repeated reactions were “clinically significant” and no fatalities were found in repeated anaphylaxis. There is no scientific evidence that glucocorticoids reduce the frequency of biphasic reactions.