Thanks to Audris for presenting the case of a middle-aged man with vasculopathy on ACEi who presented with angioedema requiring intubation! We discussed the diagnostic work up and management of angioedema as well as hyperkalemia!
- First order of business when suspecting angioedema is the ABCs!
- Treat angioedema in the acute setting with H1 blockers and steroids, even if you are suspicious of a non-histaminergic pathway.
- Always assess for concurrent anaphylaxis (hypotension or bronchospasm in addition to hives or angioedema). If anaphylaxis is present, then treatment involves IM 0.3-0.5 mg of 1:1000 dilution epinephrine (1mg/mL), repeat every 20 minutes until symptoms resolve (max 3 doses)
- If you have access to a functioning kidney, favor loop diuretics over cation exchange binders (i.e. kayexalate) to lower serum potassium!
- Patiramer is much better tolerated than kayexalate and has a more favorable side effect profile.
- Calcium gluconate has a role in the treatment of hyperkalemia when EKG changes are present. Give a dose and repeat the EKG. If no improvement, repeat to a maximum of 3 doses until EKG has normalized.
- 3 pathophysiologic subtypes:
- Mast cell/histamine mediated
- Allergic reactions: food/insect stings, latex, drugs. Can also be idiopathic. IgE type 1 hypersensitivity
- Direct mast cell release: drugs (opiates, contrast). IgE is not involved.
- ASA/NSAIDs: via IgE or direct mast cell release
- Chronic urticaria w/w/o angioedema
- S/sx affecting organ systems other than the skin? Suspicious for anaphylaxis ⇒ give epi
- Treatment: H1 blockers, glucocorticoids.
- Bradykinin mediated
- Inhibition of enzymes involved in the degradation of bradykinin, or deficiency/dysfunction of complement C1 inh
- More prolonged time course, develops over 24-46 hours and resolves within 2-4 days
- Relationship between trigger and onset of symptom is not as apparent
- Not associated with other s/sx. More common to have abdominal pain due to bowel wall involvement.
- Treatment: bradykinin pathway mediators (ecallantide, icatibant), C1 inhibitor concentrate, or plasma replacement.
- Unknown mechanism
- Idiopathic angioedema
- Infections (in children)
- Other drugs: sirolimus, everolimus, amiodarone, metoprolol, risperidone, paroxetine, and etanercept, inhaled cocaine.
- Herbal meds
- Urticarial vasculitis
- Hypereosinophilic syndrome and Gleich syndrome
- Mast cell/histamine mediated
Agents that reduce serum potassium via transient intracellular shift:
- Insulin: give with D50 if normoglycemic to avoid hypoglycemia and be sure to check FSG hourly for 4 hours after to ensure no hypoglycemia develops
- Albuterol (10-20 mg) nebs: this is significantly higher than the dose we give in COPD (2.5 mg) and is equal to ~8 treatments! So make sure to continue the nebs when the patient arrives on the floor from the ER if they are still hyperkalemic.
- NaHCO3: best for management of chronic hyperkalemia in the outpatient setting. In the acute management of hyperkalemia, alkalinization of serum with a large bicarb load can lead to a reduction in serum calcium levels. Lower serum calcium can lead to more cardiac membrane instability and fatal arrhythmias!
Agents that eliminate potassium from the body:
- Loop diuretics: first choice if a functioning kidney is available!
- Cation exchange binders: preferred when kidneys are not available
- Patiramer (available at VMC), much more tolerable than kayexalate and highly effective at lowering serum potassium. Like kayexalate, it works over hours to days.
- Sodium zirconium: similar to patiramer but not currently available
- Kayexalate: not pleasant to take orally. Also carries with it the slight risk of colonic ischemia especially in post renal transplant patients and those with baseline colonic dysfunction (due to infection or inflammation).
Indication for using calcium gluconate: when EKG changes are noted. Repeat doses (maximum 3) until EKG changes have resolved.