Perioperative Anaphylaxis

Dr. Manisha Shembekar
Anaesthesiologist, Nagpur
President, ISA Nagpur.

Introduction

Anaphylaxis is defined as severe, potentially life threatening hypersensitivity reaction. Incidence of perioperative anaphylaxis is 1 in 10,000-20,000 procedures, overall mortality is 0.001%. the exact causative agent is difficult to ascertain in the perioperative period as a number of drugs are administered during the procedure.

Pathophysiology

Anaphylaxis can be immunological i.e. IgE mediated, non immunological or idiopathic. Immunological anaphylaxis results due to crosslinking of IgE resulting in degranulation of mast cells and basophils. It causes release of histamine, prostaglandins, proteoglycans and cytokines. Nonimmunological anaphylaxis is caused by direct stimulation of mast cells and release of histamine. It is less severe and present as cutaneous signs only. When no specific causative agent is identified and serum IgE levels are normal, it is labeled as idiopathic. Usually it manifests after second exposure but may occur on first exposure as there may be cross reactivity with many drugs.

History

A detailed history and previous records of allergic reactions should be obtained. Allergy to food items, latex or drugs can cause allergic reactions in perioperative period. Even a small quantity of allergen is sufficient to trigger anaphylaxis. Common agents are antibiotics (58%), latex (17%), neuromuscular blocking agents (11%), colloids, antiseptics like chlorhexidine, adhesive tapes etc.

Transfusion of blood and blood products remains the most important and most dangerous trigger for allergic reactions.

Among muscle relaxants, rocuronium and suxamethonium remain the most common triggering agents. Patients who are allergic to rocuronium or suxamethonium show cross reactivity to other muscle relaxants like atracurium and cis atracurium.

Plasma expanders like colloids, dextran and hydroxyethyl starch cause allergies in 3% cases.

Severity of hypersensitivity reactions can be graded as follows-

1. Generalized cutaneous signs like erythema, urticaria
2. Along with skin manifestations, there may be hypotension, difficulty in breathing, cough, tachycardia
3. Life threatening multiorgan involvement cardiovascular collapse, bronchospasm, arrhythmia, tachy or bradycardia, angioedema, laryngeal edema
4. Cardiac and or respiratory arrest.

Diagnosis

Clinical signs are suggestive of allergic reaction. Investigations are not of much help as they take time to process. Sometimes diagnosing hypersensitivity under anesthesia can be tricky as hypotension, change in heart rate, pruritus may be masked due to effect of anesthetic agents per se. If  in the perioperative period, there is severe hypotension, not responding to vasopressors, anaphylaxis should be suspected.

Diagnosis can be confounded in acute exacerbation of bronchial asthma, myocardial ischaemia, pulmonary embolism, hereditary angioedema.

Investigations 

ABG, kidney and liver function tests to rule out tissue hypoperfusion. Serum tryptase may be elevated more than 25mcg/L in IgE mediate anaphylaxis. However, tryptase levels may also be elevated in other conditions like myocardial infarction, amniotic fluid embolism.

Plasma Histamine levels are raised in hypersensitivity reactions.

Skin testing should be performed 4-6 weeks after the episode. All the agents given just before the reaction should be tested. Cutaneous reactivity should be assessed by positive (codeine/histamine) and negative test. Commercial preparation of diluted or undiluted solutions of drugs are used for prick test and intradermal test. If prick test is negative IDT is performed. IDT is performed with increasing concentration until hypersensitivity to the agent is demonstrated or highest concentration is achieved.

Management

Early diagnosis and prompt treatment is the cornerstone of successful outcome.

Treatment

1. Treatment should start as soon as diagnosis is made. Removal of triggering agent if identified should be done.
2. Oxygen inhalation and securing of airway as edema develop rapidly.
3. Epinephrine – it is a lifesaving drug and forms the mainstay of treatment. The alpha 1 adrenergic effect increases peripheral vascular resistance and decreases mucosal edema. The beta 1 effect causes positive chromotrophic and inotrophic effect. The beta 2 agonist effect causes bronchodilation. Initial dose of epinephrine is 10-20 micrograms IV may increase to 100-200 mcg IV and infusion at 0.05- 0.4 micrograms/ min. Epinephrine should be used judiciously as it may cause ventricular arrhythmias, pulmonary edema.

IV crystalloids to compensate for vasodilatation 20 ml/kg.

If hypotension persists, norepinephrine may be used.  Steroids and antihistamines take longer time to act, can be given after initial resuscitation is over. Hydrocortisone 200 mg IV followed by 100 mg 6 hourly. Chlorphenhydramine 25-50 g IV with H2 blockers can be given for mild symptoms. Steroids take 4-6 hours to act.

Prevention-

Avoid agents which are known to cause hypersensitivity. It is imperative to document any allergic reaction occurring in perioperative period. If specific causative agent is not known, general precautions should be taken viz. optimal perioperative control of asthma, administering drugs slowly, avoiding beta blockers and ACE inhibitors. Regional anesthesia is preferable although anaphylaxis is observed in these cases also.

Conclusion

Perioperative anaphylaxis can be severe and life threatening in otherwise healthy patient. The anesthesiologist plays an important role in managing perioperative anaphylaxis. adrenaline is the drug of choice and should be used earlier than later.