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Angioedema

by Carlo Raj, MD
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    00:01 We’ll continue our discussion of dermatology by looking at angioedema.

    00:06 Take a look at these lovely lips.

    00:08 Well, this was not implantation.

    00:11 This was not a patient that went in for cosmetic surgery and had it enhanced.

    00:17 So, what do you think happened here? Well, there are two ways in which your patient may develop what’s known as angioedema.

    00:22 To begin with, by definition, when you have angioedema, it is the fact that you have edema that’s taking place.

    00:28 Obviously, it’s leaving, or should I say the fluid is escaping from the angio, which refers to your blood vessels.

    00:36 And when it does, in terms of its location, most likely, it would be deep into your skin, so you’re thinking about dermis, and maybe perhaps even, your subcutaneous tissue.

    00:49 With that said, our topic is angioedema.

    00:53 It could be acquired or hereditary.

    00:55 And with skin, the last time we talked about this was, in fact, a type 1 hypersensitivity in which you would be releasing histamine, and that would be a type of acquired angioedema.

    01:09 And at some point in time, we’ve also discussed hereditary type of angioedema, which from immunology, will be more or less considered to be a complement type of pathology, in which your patient is then deficient of C1-inhibitor.

    01:22 All those should come in mind, and we have swelling of the lips, airways, or eyes when dealing with angioedema The causes include -- well, in order for you to understand this, it’s the concept that you want to keep in mind.

    01:38 The concept here is going to be the fact that you are not able to properly control with hereditary.

    01:45 Your complement system.

    01:48 And by this, we mean, for example, we’ve talked about a few complement pathologies, in which you have unrestricted or unopposed complement activity.

    01:55 These include paroxysmal nocturnal hemoglobinuria.

    02:00 These also include your dense deposit disease that we saw with membranoproliferative glomerulonephritis type 2.

    02:08 And then here, normally, you require a C1-inhibitor so that you keep things under control, so that you do not have excessive complement activation.

    02:18 Let’s say that you’re missing the inhibitor.

    02:20 If you’re missing the inhibitor of C1, then you have unopposed complement activation.

    02:27 C1 esterase inhibitor deficiency, hereditary angioedema, and you would not consider this to be hives.

    02:34 So therefore, this is not considered to be urticaria.

    02:37 Patients will present with, well, this is important, low C4 levels.

    02:42 And the reason for that is because, well, as I told you, if you have unopposed complement activity, guess what you’re going to do with your complement.

    02:49 You’re activating it, or activating them, and you’re also consuming them.

    02:54 So therefore, you can expect your complement levels to be decreased, but this is a concept we’ve seen earlier, when in fact we did glomerulonephritis.

    03:03 Then we move on to acquired type.

    03:05 Acquired type, obviously, would be more common.

    03:08 And with the acquired type, what if there was a patient who had hypertension, and with hypertension, this patient was then put on ACE inhibitor, and all of a sudden, started having dry cough? In addition to dry cough, there was also angioedema that was also developing.

    03:25 Remember that with ACE, it’s an enzyme that normally knocks out or metabolizes bradykinin.

    03:31 And so therefore, if you inhibit the ACE, then there could be increase levels of bradykinin.

    03:36 This bradykinin then brings about, at this point, the theory that you want to take with you, is a dry cough and the fact that the patient may present with angioedema.

    03:44 Do not confuse this with urticaria.

    03:47 This is twice now that I’ve asked you not to confuse this with urticaria.

    03:51 Why? Urticaria means hives, thinking about wheal formation.

    03:55 Urticaria would be a type 1 hypersensitivity in which that histamine is then causing vasodilation.

    04:01 This is either hereditary or acquired type of angioedema, and this is deep down beyond the skin so you will not have urticarial hives.

    04:12 Remember, edema, it’s taking place, affecting the mucosal membrane.

    04:17 Then the allergy acquired, which we talked about extensively.

    04:21 So, still under acquired type of angioedema, your patient has been, perhaps, exposed to drugs or maybe perhaps associated with urticaria.

    04:29 Keep the two separate, please.

    04:31 By that, we mean urticaria would be more superficial in nature.

    04:35 And so therefore, it is the blood vessels in the epidermis undergoing wheal or hive formation.

    04:41 Whereas here, we’re talking about blood vessels deeper down in perhaps the subcutaneous tissue.

    04:47 Management here: Well, epinephrine if airway is compromised.

    04:52 Remember, please, that if it is in fact the acquired type, there’s every possibility that you would have severe involvement of your airways.

    05:00 So therefore, epinephrine is something that you want to keep in mind.

    05:04 If it’s allergic that you’re thinking about, then obviously, antihistamine or IV steroids so that you can remove the effects of your constriction, or in this case, vasodilation.

    05:15 And if it’s hereditary, well, in this case, you want to try to replenish some of that C1-inhibitor that was deficient to begin with.

    05:23 Another name for that C1-inihibitor is technically called C1 esterase inhibitor, and this then has to be replenished, you’re thinking about FFP, which stands for fresh frozen plasma.

    05:36 And then if it’s ACE inhibitor associated angioedema, obviously, remove the offending agent and stop administering to ACE inhibitor.


    About the Lecture

    The lecture Angioedema by Carlo Raj, MD is from the course Inflammatory Skin Diseases.


    Included Quiz Questions

    1. Urticaria or hives
    2. Swelling of lips and tongue
    3. Low C4 levels
    4. C1 esterase inhibitor deficiency
    5. Unopposed complement activity
    1. Stop Lisinopril
    2. Stop Amlodipine
    3. Continue current regimen and add antihistamines
    4. Add IV steroids
    5. Continue current treatment and transfuse FFP
    1. contact dermatitis
    2. PNH (paraoxysmal nocturnal hematuria)
    3. MPGN Type 2
    4. Hereditary angioedema
    5. Dense deposit disease

    Author of lecture Angioedema

     Carlo Raj, MD

    Carlo Raj, MD


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