Week 5

Context

The number of people in England admitted to hospital because of allergies rose by 7.7% in the 12 months to February 2014. NHS hospitals dealt with 20,320 admissions for allergies during the period, compared with 18,860 in the previous 12 months. Nearly 1 in 5 of admissions were for anaphylactic reactions – an increase of 9.9% from the previous 12 months. Anaphylactic reactions are a severe, potentially life-threatening allergic reaction that can develop rapidly and which is also known as anaphylactic shock (Health & Social Care Information Centre, 2014).

Content

Definition

Anaphylaxis is a severe allergic reaction with a rapid onset of symptoms. It can be either antibody mediated, resulting from exposure to an antigen that promotes the body to produce Immunoglobulin E (IgE), or non-antibody mediated, resulting from substances that directly cause the degranulation of mast cells and basophilic (opiods, vibration, hot and cold extremes, and imaging contrast medium can all cause this reaction. Anaphylaxis is an emergency situation, and can be life threatening within minutes, so early recognition and management is imperative. Watch out for biphasic situations 2-72 hours after first episode.

Dealing with the emergency

The following two videos illustrate the management of anaphylaxis using a real-life situation.

Part 1 (3 minues)

Part 2 (9 minutes)

Classification

IgE antibody mediated systemic anaphylaxis – food, medicines, venoms, blood products
IgE mediated local anaphylaxis with life threatening layngeal obstruction
Immunological but not IgE mediated anaphylaxis
Munchausens anaphylaxis – real or simulated reactions
Anaphylactoid – not IgE mediated but indistinguishable clinically seen in opiods, NSAID and radio opaque contrast reactions
Idiopathic reaction – cause cannot be identified

(BMJ Best Practice, 2014)

Pathophysiology

"Anaphylaxis is believed to arise from the activation of mast cells and basophils through a mechanism generally understood to involve crosslinking of immunoglobulin (Ig) E and aggregation of the high-affinity receptors for IgE, FcRI. Upon activation, mast cells and/or basophils quickly release preformed mediators from secretory granules that include histamine, tryptase, carboxypeptidase A, and proteoglycans. Downstream activation of phopholipase A2 (PLA2), followed by cyclooxygenases and lipoxygenases, produces arachidonic acid metabolites, including prostaglandins, leukotrienes, and platelet activating factor (PAF). The inflammatory cytokine, tumor necrosis factor-α (TNF-α) is released as a preformed mediator, and also as a late-phase mediator with other cytokines and chemokines.

Many of these mediators are believed responsible for the pathophysiology of anaphylaxis. Histamine stimulates vasodilation, and increases vascular permeability, heart rate, cardiac contraction, and glandular secretion. Prostaglandin D2 is a bronchoconstrictor, pulmonary and coronary vasoconstrictor, and a peripheral vasodilator. Leukotrienes produce bronchoconstriction, increase vascular permeability, and promote airway remodeling. PAF is also a potent bronchoconstrictor and increases vascular permeability. TNF-α activates neutrophils, recruits other effector cells, and enhances chemokine synthesis (Ogawa & Grant, 2007).

These overlapping and synergistic physiological effects contribute to the overall pathophysiology of anaphylaxis that variably presents with generalised urticaria and angioedema, bronchospasm, and other respiratory symptoms, hypotension, syncope, and other cardiovascular symptoms, and nausea, cramping, and other gastrointestinal symptoms. Biphasic or protracted anaphylaxis may occur" (Peavy & Metcalfe, 2008). A state of impending doom for the patient may be seen. As in Gary's case Second Chance: Episode 5: Reaction. Hence why we take a mast cell tryptase blood test to see the level in an allergic reaction.

Symptoms

The release of histamine and other chemical mediators (as described above), lead to:

Swelling around mouth and face
Itch eyes
Rash on chest and torso
Urticaria
Noisy breathing and rapid breathing
Chest tightness
Gi disturbances – nausea, vomiting, diarrohea
Feeling of impending doom
Unconsciousness, coma

Adopt an A To E approach in reviewing the patient.

Call for help IMMEDIATELY.

Airway –compromised. Occlusion of the airway, bronchospasm , laryngeal oedema.
Breathing – tachypnoea, reduced oxygenation of the body tissues
Circulation- increased heart rate, hypotension
Disability – collapse, unconsciousness
Exposure – generalised flushing of skin, rash , urticaria

Treatment

The UK Resuscitation Council has produced an algorithm on the emergency treatment of anaphylactic reactions, based on NICE guidance (UKRC, 2013):

References and Further Reading

BMJ Best Practice (2014) Classification of anaphylaxis [WWW] http://bestpractice.bmj.com/best-practice/monograph/501/basics/classification.html

Health & Social Care Information Centre (2014) Provisional Monthly Hospital Episode Statistics for Admitted Patient Care, Outpatients and Accident and Emergency Data - April 2013 to February 2014. Leeds: HSCIC

Ogawa Y, Grant JA. (2007) Mediators of anaphylaxis. Immunology And Allergy Clinics of North America 2007; 27:249-260.

Peavy, RD. & Metcalfe, DD. (2008) Understanding the Mechanisms of Anaphylaxis. Current Opinion in Allergy and Clinical Immunology. 2008;8(4):310-314

UK Resuscitation Council (2013) Emergency treatment of anaphylactic reactions. London: UKRC