Clinical

DIMENSION

Angioedema
Clinical Presentations and
Pharmacological Management
Angela Smith Collins-Yoder, PhD, RN, CCNS, ACNS BC

Angioedema (AE) is a unique clinical presentation of an unchecked release

of bradykinin. The origin of this clinical presentation can be either genetic
or acquired. The outcome within the patient is subcutaneous swelling of the
lower layers of the epidermis. Symptoms are most often localized to the
upper airway or the gastrointestinal tract. A typical course resolves in
5 to 7 days, but in some patients, the clinical manifestations exist up to
6 weeks. Hereditary AE is rare and genetically linked, and typically, the patient
has episodes for many years before diagnosis. Episodes of acquired AE
may be drug induced, triggered by a specific allergen, or idiopathic.
Angioedema can elicit the need for critical care interventions, for advanced
airway management, or unnecessary abdominal surgery. The treatment
for these patients is evolving as new pharmacological agents are developed.
This article addresses subtypes of AE, triggers, pharmacology, and information
for interdisciplinary team planning of individualized case management.
Keywords: Angioedema, Angioedema clinical presentation,
Angioedema outcomes, Bradykinin 2 Receptor Antagonist medications
[DIMENS CRIT CARE NURS. 2016;35(4):181/189]

Angioedema (AE) is an immune-triggered release of cyto-
kines, which can produce subcutaneous swelling of the
face, larynx, tongue, lips, hands, feet, or gastrointestinal
tract.1,2 This swelling, which is nonpitting and localized,
is the extravasation of fluid into the interstitial compart-
ment of the deep dermis and subcutaneous tissues and
typically has no associated urticara.2,3 Clinical mani-
festations result because of an accumulation of vasoactive
elements, particularly bradykinin (BK), histamine, prosta-
glandins, and interleukins (Figure 1).1,4,5 Episodes of AE
may be initiated by genetic predisposition, idiopathic trig-
gers, or allergens or drug induced.1,4 An acute attack of AE
can result in upper airway compromise or unnecessary
surgery for an acute abdomen. Angioedema is considered
a rare disorder, with 5758 deaths from 1979 to 2010
attributed as cause of death in the United States.3 Nurses
play pivotal roles in the care of the acute AE patient. As
part of the interprofessional acute care team, they assess
the AE patient, administer medications, and prepare for
emergency airway support.3 Advanced practice nurses can
act as advocates for these patients and families, assist-
ing them to control the AE episodes. Appropriate case
management, including a rescue treatment plan, assists in
preventing unneeded hospitalization. The purpose of this
article is to increase awareness in acute care nursing prac-
tice, relevant to the etiologies and current treatments of AE.
PATHOPHYSIOLOGY: MEDIATOR INTERPLAY
There are 5 sets of currently identified chemical mediators
interacting within the AE process: the fibrinolytic pathway

DOI: 10.1097/DCC.0000000000000188 July/August 2016 181

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 AE: Clinical Presentations and Pharmacological Management
Figure 1. Complexities of the multiple pathways that lead to angioedema.1,2,4,5 Images Provided by PresenterMedia and Graphic Figure
rendered by Roger Yoder.
(kinin), XII contact activation pathway (also the intrinsic
pathway of coagulation), complement pathway, eicosanoids,
and immunoglobulin E mast cell mediated (Figure 1).1,4-6
Each of the chemical mediators and acronyms are listed
in Table 1. The cross-talk between the systems is complex
and exponential. The important take away concept is that
BK can be generated by multiple biochemical reactions
with these 5 processes.7 Bradykinin is currently theorized
to have the greatest impact on the clinical manifestations
that present as AE.2 Knowing the pathway that generates
the BK in each clinical presentation is key to matching the
pharmacology to the patient. Having 5 complex pathways
involved, however, makes the specific pathophysiology
of each patient’s AE response difficult to pinpoint in acute
clinical presentation.
ETIOLOGY SUBTYPES OF AE: BOTH
HEREDITARY AND ACQUIRED
There are different etiologies that can lead to AE. Iden-
tification of the etiology is helpful for assisting the patient
to avoid future episodes and allows the health care provider
to individualize care.7,8 There are to nomenclatures for
etiology of AE. The Hereditary AE Association identifies
3 presentations of AE that are genetically linked and 6 for
acquired AE. Table 2 lists Web sites that are appropriate
for use by both patients and health care providers with
182 Dimensions of Critical Care Nursing Vol. 35 / No. 4
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.
tools, on-call support, and resources for diagnosis6,7 The
Hereditary Angioedema International Working Group
(2012) classifies AE into only 7 types of case presenations.8,9
The acronyms used by both groups are summarized in the
sidebar (Table 3).
HEREDITARY AE TYPES I TO III
There are currently 3 identified genetic origins of heredi-
tary AE (HAE). Each genetic mutation creates an inability
of the complement inhibitor (C1-IHN) to shut down an
overactive immune response. C1-INH is a multifunctional
serine protease inhibitor that circulates in an inactive state
in the blood. The reported incidence of HAE varies, but
1 in 50 000 is widely reported.6-8
HAE-I, also called (C1-INH HAE), represents 80% to
85% of HAE cases. HAE-1 is linked to either an inherited
defective gene located on chromosome 11 or an epigenetic
mutation to this gene. The impact of this genetic contribu-
tion is a low C1-inhibitor circulating serum level. Feedback
from interferon-+, interleukin 6, and interleukin 1 increases
production of this complement inhibitor in the liver. C1-INH
functions by inhibition of activated C1r and C1s, inhibi-
tion of activated Hageman factor (XIIa), and inhibition
of activated kallikrein.2,4-6 Kallikrein is the protease that
produces kininogen and releases BK. This chemical reaction
 AE: Clinical Presentations and Pharmacological Management

TABLE 1 Immune Components, Definition, and Acronym2,4-6

Immune Component Definition Acronym

Angiotensin-converting enzyme Enzyme that cleaves the proteins of angioedema I to angioedema II, ACE
resulting in feedback to the kidneys to raise blood pressure.
The ACE is also important to degradation of bradykinin at
the B2 receptor on the cell membrane, extending the life
of bradykinin.
Angiotensin-converting enzyme Pharmacological agents that block the action of the ACE enzyme. ACE-I
inhibitor
Angiotensin receptor blockers Pharmacological agents that block the action of angiotensin II. ARB
Anaphylatoxin Complement fragments that cause histamine release from mast Example: C4a
cells and promote chemotaxis.
Bradykinin Nonpeptide plasma protein derived from kallikrein. BK
Bradykinin receptor 1 G proteinYcoupled receptor site for bradykinin. B1R
Bradykinin receptor 2 Receptor site forms a complex with ACE to promote crosstalk B2R
to the Kinin-Kallikrein system.
C1 esterase inhibitor A protein that limits the activation of complement with inflammatory C1-INH
responses.
Complement A group of 30 or more plasma proteins with immune activity that Each complement has a C
circulate in the blood in an inactive state activated by 1 of 3e and an identified number, eg, C2
pathways (classical, alternate, and lectin).
Complement 4 A protein of the complement system that is involved in the innate C4
immune system. This protein is an early component in immune
activation. Low levels are associated with autoimmune diseases
and angioedema. C4a is an anaphylatoxin.
Eicosanoids Functionally related system of chemicals derived from arachnoic The associated subgroup names
acid. This includes prostaglandins, leukotrienes, lipoxins, and each by the starting initial
thromboxanes. They produce cross talk between the immune, and with subscript numerals.
vascular system, coagulation, and pain responses by the body.
Histamine A chemical compound that causes dilation of capillaries, contraction of Example: H1 receptor
smooth muscle, and stimulation of gastric acid secretion; that is
released during allergic reactions; and that is formed by decarboxylation
of histidine. There are 2 receptor types found in the body.
Immunoglobulin E An antibody released that mediates allergy responses, including IgE
histamine and leukotrienes.
Interleukins A group of proteins released by leukocytes when activated. Example: IL6
Kinin-kallikrein A system of regulatory chemicals involved in mediation and modulation of KKKS
the renin-angiotensin-aldosterone system, prostaglandins, and vasopressin
and in the regulation of sodium-water and particularly blood pressure.
Mast cells Immune system cell type that has granules of histamine and heparin. MC
Plasma contact system (Intrinsic XII coagulation factor (hageman factor) binds to exposed collagen at site XII contact system
pathway of coagulation) of vessel wall injury, activated by high-MW kininogen and kallikrein.
Prostaglandins A type of eicosanoid. One of a number of hormone-like substances that Example: PGD2
participate in a wide range of body functions such as the contraction
and relaxation of smooth muscle, the dilation and constriction of blood
vessels, control of blood pressure, and modulation of inflammation.
Thromboxanes A type of eicosanoid: Any of several substances that are produced especially Example: TXA 2
by platelets, are formed from endoperoxides, cause constriction of
vascular and bronchial smooth muscle, and promote blood clotting.

July/August 2016 183

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 AE: Clinical Presentations and Pharmacological Management

netic trait is predominantly found in women, but male

TABLE 2 Web Sites
Health care professionals brochure: Hereditary Angioedema Association
Helpful information about subtypes of hereditary angioedema
and treatments
http://www.haea.org/wp-content/uploads/Comprehensive-
Table_chart-only.pdf
Drug manufacturer Web sites
Provides drug insert information, patient stories, and information on
patient enrollment programs
https://www.firazyr.com/
http://www.berinert.com/
http://www.kalbitor.com/index.html
http://www.cinryze.com/hereditary-angioedema-therapy.aspx?s
results in a greater local generation of BK. Episodes of
HAE-I first appear early in life, increasing in number after
puberty. Physical trauma, hormone changes, and emotional
stress can be triggers for an HAE-I episode.
HAE, HAE-II, or U-HAE (HAE of unknown origin)
represents 15% to 20% of the total HAE cases. C1-INH
circulating levels are normal. However, when an antigenic
trigger initiates the immune response, C1-INH is unable to
work effectively. U-HAE is also associated with a low cir-
culating level of serum C4.6,8
HAE-III or FXII-HAE runs in generations of families
and has a lower incidence of overall occurrence. This ge-
family members may also experience adverse clinical events.
There are mutations noted in the XII factor-encoding gene
in reported studies. A published study of 13 families with
29 subjects (26 women and 3 men) in Spain found that
during high estrogen levels, C1-INH activity dropped by
50%.10 Genetic testing of the affected families revealed
that many of the women had asymptomatic men in the
family. These patients are resistant to antihistamines and
have normal levels of C1-INH.11 Episodes may increase
in number during pregnancy and during use of estrogen-
containing oral contraceptives.2,11,12
ACQUIRED AE TYPES
Acquired type I, called C1-INH-AAE, presents with an
etiology associated with autoantibodies that destroy
the C1-INH inhibitor or cause blunting of C1-INH effec-
tiveness. Production of these autoantibodies may rep-
resent the emergence of a lymphoproliferative disease
such as lymphoma or multiple myeloma. This case type
appears when patients are 40 years or older. Labora-
tory tests reveal low levels of C1-INH and C4 proteins.
There are no known genetic links, so family history is not
present.6,8,9
Acquired type II (AAE-II) has autoantibodies that impair
C1-INH function. There is also an associated overproduc-
tion of complement via the classic complement pathway.
This etiology is not linked with cancer presentations or

TABLE 3 Acronyms and Classifications of Angioedema8,9

Hereditary Angioedema International Taskforce on
Name Association Hereditary Angioedema

Hereditary angioedema type I HAE-I C1-INH-deficiency

C1-INH-HAE
Hereditary angioedema type II HAE-II C1-INH levels normal
U-HAE
Hereditary angioedema type III HAE-III Hereditary angioedema with FXII mutations
FXII-HAE
Acquired angioedema I AAE-I C1-INH deficiency
C1-INH-AAE
Acquired angioedema II AAE-II Autoantibodies with no concurrent cancer
Idiopathic acquired angioedema Idiopathic histaminergic
IH-AAE
Nonhistaminergic idiopathic acquired angioedema INAE Idiopathic nonhistaminergic
InH-AAE
Allergic acquired angioedema N/A N/A
ACE-inhibitor acquired angioedema ACEI-AE Acquired angioedema related to ACEI
ACEI-AAE
Drug-induced acquired angioedema N/A N/A

184 Dimensions of Critical Care Nursing Vol. 35 / No. 4

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 AE: Clinical Presentations and Pharmacological Management
other diseases, nor is it linked to drug administration.
The incidence of these acquired C1-INH deficiency dis-
eases is considered rare.6,8,9,12
Idiopathic AE (IH-AAE) has an atypical presentation
because the duration of the swelling may persist up to
6 weeks. The histamine response is predominant in this
clinical presentation. Unlike other subtypes of AE, urticara
can be present. The patient should also be screened for
thyroid dysfunction because the duration of the AE may
be linked to slowed metabolism. Triggers that have been
reported with this case type are extremes in environmental
temperature, anxiety, and minor infections, especially of
the oral cavity.2,6,8,9
Idiopathic AE nonhistaminergic (INHAAE) is believed
to account for 1 of 20 presentations of AE. There is no
decrease in the number or function of the C1-INH levels
and hormones do not appear to impact the resolution of
symptoms. The patient is refractory to antihistamine ad-
ministration. Swelling can occur at any site; however, these
patients rarely have abdominal swelling.6,8,9
Allergic AE is linked to an outside trigger such as cold,
heat, latex, food, aspartame, medication, or a bee sting.
Immunoglobulin E activation of mast cells in response to
an allergen is the initiation etiology. The complement levels
are normal, including C1-INH. There are high circulating
amounts of histamine, and the episode responds to anti-
histamines and epinephrine. Subcutaneous swelling is most
often in the face, tongue, and throat area. This response
can also be a component to an anaphylaxis episode that
includes systemic effects.6,8,12
Angiotensin-converting enzyme inhibitorYinduced
(ACE-I) AE (ACEI-AAE) is associated with the intake of
an ACE-I or angiotensin blocker.13,14 This type of AE is
linked to a blockade in the mediators that degrade BK.
Drug-induced AE occurs in 0.1% to 0.7% of patients who
are prescribed ACE-I.13,14 This blockade leads to a
persistence of BK accumulation, which precipitates the
ACE-associated cough and AE.13,15 The onset of AE can
occur from a range of hours to years after first administer-
ing medication. Even after discontinuation of the medica-
tion, recurrent episodes of ACE-IYassociated AE may
resurface. If episodes occur more than 6 months after
discontinuation of the medication, then testing for a genetic
component would be recommended.
The highest incidence, approximately 50%, of the ad-
verse reaction of ACE-IAE emerges in the first week.14,16
There is a 10% reported rate of AE-induced airway com-
promise that requires intubation, with ACE-I. Angiotensin-
converting enzyme inhibitorYinduced AE prevalence is
5 times higher in African Americans than other ethnic
groups. Angiotensin-converting enzyme inhibitorYinduced
airway compromise leading to death has been documented
by case publication for 7 African Americans.14,17 The total
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.
number of African Americans with ACE-I AE is unknown.
Kupfer et al believe that the airway edema is more refrac-
tory to treatment in elderly black women.14,17
Once a patient has an AE response to an ACE-I,
switching the patient to angiotensin receptor blocking
agents is recommended. Angiotensin receptor blocking
agents are also reported to cause AE, but with a much
lower incidence. The washout timeframe in switching
from an ACE-I to an angiotensin receptor blocking agent
may be key to preventing ACE-I AE reoccurrence.14,17,18
Non-Steroidal Anti-Inflammatory Drug (NSAID)-
related AE is mediated by eicosanoids. Two typologies can
lead to AE.19,20 Angioedema occurs after several hours of
receiving an NSAID. In some patients, only 1 particular
NSAID causes the reaction such as aspirin. Others react to
all medications in the NSAID classification regardless of the
point of prostaglandin suppression. Treatment is focused
on isolating the offending medicine then avoiding the trig-
gering medication.19,20
PHARMACOLOGICAL AGENTS FOR
PROPHYLAXIS AND RESCUE FROM AE
There are 4 drug classifications that are Food and Drug
Administration (FDA) approved for use in AE attacks in
patients with C1-INH deficiency (Table 4).21,22 There is
also 1 additional medication classification, used as a rescue
and preventative medication especially with associated bleed-
ing. The newer pharmacological classifications contain
patented medications that are costly and require exten-
sive justification when selected in either acute or primary
care. Each drug manufacture offers programs specifically
designed to increase affordability of the medication for
eligible patients. There are reports of using additional drug
classifications. If there are randomized control trials of
these medications, the discussion includes that informa-
tion and identified as off-label use.21,22 The mechanism of
action and nursing considerations are presented by phar-
macological classification. Pharmacology specific to HAE
types produces the best clinical outcomes.6
HAE SPECIFIC MEDICATIONS: PROTEINASE
INHIBITORS, KININ-KALLIKREIN INHIBITORS,
BK2 RECEPTOR ANTAGONIST, TRANEXAMIC
ACID, AND ANDROGENS
Proteinase inhibitors are C1-INH repletion medications
that include human-derived C1 esterase inhibitors Cinryze
and Beirnert. These 2 medications are FDA approved and
provide the patient higher circulating levels of C1-INH,
which inhibits Kinin-kallikrein (KK) and diminishes BK
production. Cinryze is indicated for self-administration at
home for prophylaxis against AE in adult and adolescent
patients with diagnosed C1-INH HAE.21,22 Beirnert is a
treatment indicated for acute abdominal, facial, or laryngeal
July/August 2016 185
 AE: Clinical Presentations and Pharmacological Management

TABLE 4 Angioedema Medications associated with C1-INH and Bradykinin Suppression12,21,22

Pharmacological Black Box Warnings and Most
Name of Medication Classification Reported Adverse Effects Nursing Process Concerns

Human C1-INH (Cinryze)
Human C1-INH (Berinert)
Human kallikrein inhibitor;
ecallantide (Kalbitor)
Icatibant acetate (Firazyr)
Androgens: example,
Danazol
Proteinase inhibitors Headache, nausea, rash
Proteinase inhibitors Dysgeusia (loss of sense of taste),
increased pain, abdominal pain
Kallikrein inhibitor Black Box Warning: anaphylaxis
headache, nausea
Bradykinin B2 receptor Injection site reactions,
antagonist elevated liver enzymes,
pyrexia (fever)
Androgen hormones Emotional labiality,
masculine attributes
(hirsutism), acne
Blood-borne illness.
Thromboembolic events.
Screen for religions that exclude blood products.
Blood-borne illness.
Thromboembolic events.
Screen for religions that exclude blood products.
Instruct about warning signs of a laryngeal attack.
Blood-borne illness.
Thromboembolic events.
Screen for religions that exclude blood products.
Differentiate AE symptoms from anaphylaxis onset.
Teach patient locations of subcutaneous injections.
Teach patients to administer all of the medication
as prescribed typically (3 injection sites).
Patient should be knowledgeable about the
symptoms of laryngeal edema and when to
seek further assistance.
Screen liver enzymes before administration.
Contraindicated in pregnancy or women not
using birth control.
Pharmacist should screen for drug interactions.
Patient should be encouraged to keep a diary of
any break through AE attacks.

Abbreviation: AE, angioedema.

attacks of HAE.21,22 Fresh frozen plasma can also be
administered for repletion of C1-INH. One risk of these
medications includes potential for infection because they
are derived from human plasma, which could be an infec-
tious vector for a blood-borne disease. An additional Adverse
Drug Reaction includes arterial thrombi formation. Nurs-
ing considerations include teaching the patient how to
reconstitute and self-administer the medication (including
necessary aseptic techniques) and how to monitor for poten-
tial adverse effects (Table 4).24 Because all of these therapies
are blood derived, religions that object to blood transfu-
sions and products should be informed and additional con-
sent obtained.
Kallikrein inhibitors are the next classification. This
medication is FDA approved for ecallantide (Kalbitor)
and is used subcutaneously to treat acute HAE attacks.12,21
Administration should be limited to health care in acute
care settings with practitioners who are skilled in anaphy-
lactic rescue. Ecallantide selectively binds to KK, thereby
preventing BK production. To receive the needed dosage
to stop an HAE episode, the medication must be admin-
istered as 1 mL in 3 different subcutaneous sites. Nursing
considerations include differential identification of symp-
toms of a refractory HAE episode versus anaphylaxis. There
must be access to rescue medications, a skilled airway pro-
vider, and a crash cart access during the administration and
monitoring timeframe.22,23
There is 1 triple blind study on the off-label use of
ecallantide in the emergency treatment of ACE-induced
AE. The outcome result was an increase in earlier ED dis-
charge due to resolution of symptoms for 10% of the sub-
jects randomized to receive ecallantide.24
Bradykinin B2 receptor antagonist Icatibant is FDA
approved for self-administration by patients during an acute
attack. This medication is administered subcutaneously.21-23
The medication must be stored away from heat. Patients
typically use the refrigerator. Nursing considerations in-
clude teaching the patient how to self-inject and find the
location of subcutaneous sites.25
Use of this medication for ACE-induced AE is con-
sidered off-label. A recent research report of a randomized
control trial describes a quicker resolution of ACE-induced
acute AE using this medication. This study compared
2 treatment protocols: 1 with a glucosteroid and antihis-
tamine and the other with Icatibant. The Icatibant group
had a significantly shorter time till relief of symptoms,
about 8 hours, compared with the other treatment group,
which needed about 27 hours for clinical presentation.13

186 Dimensions of Critical Care Nursing Vol. 35 / No. 4

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 AE: Clinical Presentations and Pharmacological Management
Tranexamic acid is an antifibrinolytic medication used
to prevent bleeding in patients with hemophilia. The labeled
FDA indication is specific to hemophilia.21 Tranexamic
acid is a competitive inhibitor of plasminogen activation
and diminishes BK by blocking the contact pathway of
coagulation. Research studies report using tranexamic
acid for AE, but it is an off-label use in the United States.18
Before the approval of other medication classes, this medi-
cation was used off-label as an agent to prevent AE in the
etiologies of U-HAE and InH-AAE.6,18
Attenuated androgens have been found to increase in-
trinsic production of C1-INH by the liver. Androgens are
considered first-line for HAE prophylaxis. These medications
have a reduced cost and decrease the severity and frequency
of HAE episodes.2,12 Screening of liver function is advised
before starting this medication. Follow-up laboratory moni-
toring should guide the dosages. This hormone is associated
with emotional lability and dermatological issues, including
acne and oily skin. The adverse effect of hirsutism makes
use of this product more problematic in women.21,22
PRESENTATION IN THE EMERGENCY ROOM
OR RECOVERY ROOM
Assessment and rapid response to an AE episode with upper
airway manifestations are vital to reduce morbidity and
Figure 2. Flowchart diagram of possible interdisciplinary team interventions.12,14 Images Provided by PresenterMedia and Graphic Figure
rendered by Roger Yoder.
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.
mortality of these patients. Patients with AE should be
rapidly moved from triage to a location capable of han-
dling a difficult airway.6,12,14 Priority 1 for treatment in
acute AE is to break the cycle of Kinin-Kallikrein System
activation and maintain a patent airway. If an allergic
etiology pattern is present, then treatment with steroids,
antihistamines, and sympathomimetic medications is
indicated. The offending allergen should be eliminated, if
known to the providers. If an HAE or ACE-I etiology
pattern is assessed, then first-line treatment with protease
inhibitors is recommended. If these are unavailable, then
administration of Fresh Frozen Plasma may provide the
needed C1-INH to reduce the KK and BK response.25 The
patient is then continuously assessed for any progression
of tissue edema. If the response is unabated, then the
second round of medication indicated is a B2 receptor
antagonist (Figure 2).6,8,12,14 The patient should be
monitored for patency of airway and increased work of
breathing. The most skilled practitioner in difficult air-
ways should make the decision when intubation or tra-
cheostomy interventions will be required. Monitoring the
degree of tongue enlargement and inability to control oral
secretions can be helpful cues for increased upper airway
edema. Increased upper airway edema may require that
a series of arterial blood gases be obtained to assess
July/August 2016 187
 AE: Clinical Presentations and Pharmacological Management
oxygenation status. Vigilance of the provider in assessment
of the airway is paramount to prevent a code due to hypoxia.
If excessive vasodilation associated with a decrease in mean
arterial pressure is noted, then use of a vasoconstriction
agent such as epinephrine is appropriate.
Presentation of AE to the ED as an acute abdomen is a
diagnostic challenge. Clinicians arrive at diagnosis through
exclusion and thoughtful history taking. Angioedema in
the abdomen has been primarily linked to a history of
HAE, but there are isolated case reports of ACE abdomi-
nal AE as well.26 Clinical findings include swollen abdomi-
nal viscera upon examination and computed tomography
evaluation. Symptoms would improve upon administration
of protease inhibitors and discontinuation of the trigger-
ing medication.26 The drug allergy associated with this
type of clinical manifestation should be highlighted pro-
minently in the electronic medication record to guide fu-
ture providers.
Disposition of the AE patient would be guided by the
patient’s response to interventions. After stabilization of
the suspected HAE patient, appropriate referrals to an
allergy specialist or HAE treatment centers are indicated.
This provider would then assess the patient for ability to
manage future episodes by self-rescue.12 Patients report
greater satisfaction and convenience when they are trained
to recognize and self-administer the prescribed medica-
tion.27 Patients with HAE may need additional follow-up
for genetic testing. Awareness among the extended family
would aid in identifying other persons who might benefit
from early diagnosis.8 A patient with drug-induced AE
benefits from referral to a clinical pharmacist to have de-
velopment of an individual alert profile for all medications
in a particular classification. Teaching patients to both read
and identify the category within the over the counter medi-
cation ingredients is vital.
Patients who have an episode linked to allergen expo-
sure would also need referral to an allergist. A strategy of
allergen avoidance and self-injection of epinephrine would
be developed collaboratively by the patient and the inter-
disciplinary team. The patient would then be knowledge-
able about the optimal prophylaxis and rescue regimen,
promoting self-efficacy.
CONCLUSION
Angioedema is a diagnosis with a high risk of airway com-
promise and a significant cause of pain and suffering.
Nurses, as part of an interdisciplinary team, are in a key
position to help connect these patients to specialized care
providers, teach them self-management strategies, and assist
in referrals to high reliability internet and infusion resources.
As genetic patterns are identified, the treatment of these
individuals can become individually prescriptive. The de-
sired outcomes are prevention of further AE episodes,
188 Dimensions of Critical Care Nursing Vol. 35 / No. 4
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.
decreased utilization of emergency services, and greater
patient empowerment.
Acknowledgments
The author expresses her thanks to Dr Crystal Lewis
for stimulating this author’s interest in this complex
pharmacology. Becky Edwards, RN, MSN, was the
sounding board for pathophysiology and pharmacology
clarity.
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ABOUT THE AUTHOR
Angela Smith Collins-Yoder PhD, RN, CCNS, ACNS BC, is a clinical
professor at the University of Alabama Capstone College of Nursing
and is a critical care clinical nurse specialist.
The author has disclosed that she has no significant relationships
with, or financial interest in, any commercial companies pertaining to
this article.
Address correspondence and reprint requests to: Angela Smith
Collins-Yoder, PhD, RN, CCNS, ACNS BC, The Capstone College of
Nursing, University of Alabama, 12 650 University Boulevard,
Tuscaloosa, AL 35401 (acollins-yoder@ua.edu).
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