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 Anaphylaxis is a serious reaction causing a combination of characteristic findings and which is rapid in onset & may cause death.

CLINICAL CRITERIA

Pathophysiology

• Anaphylaxis usually arises from activation of mast cells and basophils. They release performed mediators from secretory granules that include histamine, tryptase, carboxypeptidase A and proteoglycans. Downstream activation of phospholipase A2, followed by cyclooxygenases & lipoxygenases, produces arachidonic acid metabolites including prostagladins, leukotrienes and platelet activating factor. The inflammatory cytokine ,TNF-alpha is released as a performed mediator & also late phase mediator with other cytokine & chemokines. These mediators are responsible for pathophysiology of anaphylaxis.

• Histamine stimulates vasodilation & increases vascular permeability, heart rate, cardiac contraction & glandular secretion.

• Prostaglandin D2 is a bronchoconstrictor , pulmonary & coronary vasoconstrictor & peripheral vasodilator.

• Leukotrienes produce bronchoconstriction, increase vascular permeability and promote airway remodeling.

• Platelet activating factor is also a potent bronchoconstrictor and increases vascular permeability . TNF- alpha actiavtes neutrophoils, recruit other effector cells and enhance chemokine synthesis.

These overlapping & synergestic physiologic effects contribute to the overall pathophysiology of anaphylaxis.

Clinical Feature

• Signs & symptoms begin suddenly, often within 60 minutes of exposure . In general, faster the onset of symptoms , more severe is the reaction – one half of anaphylatic fatalities occur within first hour.

• Classic presentation begins with utricaria, pruritis, cutaneous flushing. They are followed by sense of fullness in throat , anxiety, sensation of chest tightness, shortness of breath and light headedness. This may be followed by abdominal pain or cramping nausea, vomiting , diarrhea, bronchospasm, rhinorrhea and conjunctivitis ,& or hypotension. As it progress respiratory distress, decreased level of consciousness and circulatory collapse may ensue. Severe cases loss of consciousness and cardiorespiratory collapse may result.

MANAGEMENT

First Line Therapy

• Airway & oxygenation :

  • Look for signs and symptoms of angioedema, if angioedema is causing respiratory distress ealry intubation is warranted.

  • Provide O2 to maintain SO2 > 90%.

• Decontamination:

  • Remove the causative agent if it is identified like insect sting.

• Epinephrine:

  • It is the drug of choice & the first drug to be administrated in acute anaphylaxis.

  • Epinephrine is a mixed α1 & β receptor agent. The α1 receptor activation reduces mucosal edema and treats hypotension. Β 1 receptor stimulation increases heart rate and myocardial contractility and β 2 receptor stimulation provides bronchodilation and limits further release.

  • In patients without signs of cardiovascular collapse administer epinephrine IM. Repeat every 5 -10 minutes. Injecting to thigh achieves better peak levels in blood. IV epinephrine is started if refractory .

• IV Crystalloids

  • Hypotension is generally distributive shock and responds to fluid resuscitation.

Second line therapy

• Corticosteroids :

  • Corticosteroids are used to prevent protracted and biphasic reaction.

  • Hydrocortisone and cortisone have strongest mineralocorticoid effects followed by prednisolone. Methylprednisolone and dexamethasone have the lowest mineralocorticoid effect and produce less fluid retention thus preferred in elderly.

• If wheeze is present salbutamol+ ipratropium bromide nebulisation is given.

• Magnesium 2gm IV over 20-30min in 100ml NS can be tried in severe bronchospasm.

• Antihistamine

  • H1 & H2 receptor blocker is recommended for all patients.

• Allergic Bronchospasm

  • A β 2 bronchodilator intermittent or continuous nebulisation is used if wheezing is present.

  • Magnesium is used incase of refractory bronchospasm.

• Glucagon : Patients on beta blockers unresponsive to fluids & adrenaline should receive glucagon 1mg IV every 5min until hypotension is resolved and followed by infusion of 5-10mcg/min.

Updated on 5/3/2019

Reference

• Tintinalli - 8^th Edition

*: Mix 1mg in 500ml NS & infuse @ 0.5ml/min & titrate as needed. Each ml will contain 2mcg/ml .