Angioedema

Anesthesia Implications

Anesthesia Implications

Airway obstruction – this is the biggest concern. Do a thorough assessment and secure the airway. This needs to be done EARLY. Have an emergency airway cart at the bedside. If the patient has an enlarged tongue, a nasal trumpet may be utilized to reduce obstruction.

Awake fiberoptic bronchoscopy intubation – this should be considered. Advantages include: In the event the intubation fails the patient will still be able to spontaneously ventilate, direct visualization of the airway and confirmation of direct intubation, and insufflation of oxygen through the suction port of the bronchoscope. Nebulized treatment with 4-5 ml of 4% lidocaine is recommended. LTA kits may be used to provide rapid and effective topical anesthesia to the interior larynx and trachea.

Video laryngoscope – may be an option, but depends on the presentation of the patient.

Acute Treatments – Immediate discontinuation of the ACE inhibitor, Methylprednisolone 125 mg IV, 2 units of fresh frozen plasma (FFP), intramuscular (IM) Epinephrine 0.3 mg, Benadryl 50 mg IV.

Administer IV crystalloid – Angioedema can cause serious fluid shifts.

Extubation – Leave the patient intubated postoperatively. A cuff leak test should be performed every morning to assess laryngeal swelling and readiness for extubation.

Postoperative Treatments – The clinical presentation will typically last 24-72 hours. Consider Dexmethasone 8 mg every 6 hours, 25 mg benadryl every 8 hours, and additional FFP infusions.

Pathophysiology

Angioedema has multiple causes. Drug-induced causes are the focus here.

There are 3 major causes of angioedema: Excess bradykinin, mast cell/basophil degranulation, and idiopathic.

The most common drugs associated with the condition include the categories of NSAIDs, and Angiotensin Converting Enzyme (ACE) inhibitors. Ace Inhibitors are the primary cause in the United States.

35% of antihypertensive medications prescribed in the United States are ACE inhibitors. This accounts for roughly 40 million people. Of these, the overall incidence of developing angioedema is 0.1-2.0%.

Incidence of angioedema is almost 5 times higher in people with African American decent.

The highest incidence is in the 1st month of therapy. However, it can occur anytime after starting therapy.

Angioedema signs and symptoms include localized swelling, nonpitting edema of the dermis, subcutaneous, mucosal, and/or submucosal tissues.

There is no definitive test for ACE-inhibitor induced angioedema. Labs will typically show extremely high bradykinin levels (eg. 10-fold increase in bradykinin levels)

Elevated levels of bradykinin (an inflammatory vasoactive peptide) can initiate the pathological process of angioedema. Bradykinin stimulates the release of Nitric Oxide, Prostaglandins, and Substance P. In short, this leads to potent vasodilation and increased vascular permeability of post capillary venules, which leads to extracellular plasma extravasation.

Additional Notes:

FFP is a beneficial treatement because it contains Kininase II, which is an enzyme with the same mechanism of action as angiotensin-converting enzyme. This generates ANG II and also disposes of bradykinin.

References

Nagelhout. Nurse anesthesia. 5th edition. 2014.
Bruce. An overview of angioedema: clinical features, diagnosis, and management. UpToDate. 2017.
Misra. For allergic and immunologic angioedema, treatment focuses on steroids, antihistamines, and epinephrine. Indian Journal of Anesthesia. 2016.