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Overview |
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Definition |
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Anaphylaxis, meaning "without protection," is a systemic, potentially
life-threatening hypersensitivity reaction. It occurs abruptly and variably, as
a result of an IgE-mediated release of histamine and other mediators from mast
cells and basophils in previously sensitized individuals. The severe allergic
response is a medical emergency and is estimated to be responsible for more than
500 deaths annually. Anaphylactoid reactions (sometimes called
pseudoanaphylaxis) present clinically like anaphylaxis, but their mechanism is
not IgE-mediated. Also, unlike a hypersensitivity reaction, they tend to occur
following initial exposure to an offending agent by direct toxic effect to cell
mediators or indirect activation of the complement cascade. |
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Etiology |
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The number of substances that cause anaphylactic reactions is staggering and
continues to expand as new diagnostic and therapeutic agents are developed. Some
substances are listed below.
Anaphylactic Reactions
- Antibiotics, particularly penicillin (74% of fatalities; 1 fatality
per 7.5 million injections) and cephalosporins (5% to 16% cross-reactivity in
penicillin-allergic individuals); much more common when administered
parenterally
- Hymenoptera venom (e.g., bees, wasps) and other insect (e.g., fire
ants) stings or bites (approximately 40 deaths reported annually in the United
States)
- Foods (e.g., nuts, shellfish, egg whites, chamomile tea, berries).
Chamomile may have cross-reactivity with ragweed pollen
- Allergen extracts for skin testing and immunotherapy
- Egg-embryo–grown vaccines (MMR, yellow fever,
and influenza)
- Blood transfusions, especially in IgA-deficient persons when exposed
to multiple transfusions
- Equine antisera (historically used in rabies and tetanus antitoxins,
but human sera now used for these immunizations without negative response;
equine antisera still used for treatment of botulism, gangrene, and for snake
bites); affects 0.4% to 4% of the population
- Topical or inhaled latex particles; includes anaphylaxis secondary to
condoms; healthcare workers, children, and rubber-industry workers at particular
risk; may have cross-sensitivity with bananas, avocados, and chestnuts as well
as dandelion root
- Glycoprotein in seminal fluid—extremely rare
reaction reported in sexual partners
- Insulin—now extremely rare given the use of
human insulin
- Chymopapain injections for disk herniation; anaphylaxis may occur in
individuals sensitized from exposure to papain (Carica papaya, a crude
fraction of papaya found in meat tenderizer and used to clarify beer as well as
sterilize soft contact lenses)
- Echinacea purpurea pollen—case report
of anaphylaxis from high dose echinacea (two times the recommended amount) in a
woman with a history of allergy to raw fruits and vegetables; she had had
previous exposure to echinacea, but anaphylactoid reactions have also been
reported following initial exposure; it is theorized that the immunomodulatory
properties of echinaea may exacerbate IgE-mediated reactions
- Thiamine (vitamin B1)—anaphylaxis
reported with parenteral administration for ethanol intoxication; vitamins, like
other medicines, can cause either anaphylaxis or anaphylactoid reactions
Anaphylactoid Reactions
- Radiopaque contrast media (some clinical reaction in 4% to 13% of the
population; true anaphylactoid reaction 0.25% with hyperosmolar agents; rates
with low osmolar agents are 1% to 3% for some clinical reaction and <0.04%
for anaphylactoid reaction)
- Aspirin or NSAID use, especially in asthma patients (15% to 20% of
asthmatics have some intolerance to aspirin or NSAIDs; those with nasal polyps
more likely to have an anaphylactoid reaction)
- Opiate analgesics—most commonly from direct
stimulation of histamine release; very rarely IgE mediated, which would be
classified as anaphylaxis
- Food coloring (e.g., tartrazine [FD&C yellow dye No.
5])—5% to 30% of those with aspirin or NSAID allergy
have cross-sensitivity to tartrazine although clinical significance not entirely
clear
- Food preservatives, especially sulfites, bisulfites, and
metabisulfites found in beer, wine, shellfish, fresh fruits, and
vegetables
- Exercise induced anaphylaxis follows ingestion of certain foods to
which a subclinical sensitivity may be present (e.g. celery, shrimp, apples,
squid, wheat, hazelnuts, and chicken); tends to occur in athletes; mechanism
unclear but may be related to endogenous opioids; atopic personal or family
history commonly but not universally associated
- Intravenous induction agents and neuromuscular blockers used during
anesthesia (may cause either anaphylactic or anaphylactoid reactions)
- Elevated progesterone levels during menstrual cycle
- Munchausen's anaphylaxis: purposeful self-induction of anaphylactoid
reaction (very difficult to diagnose and manage)
- Idiopathic
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Risk Factors |
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- Route of administration of the agent (intravenous much more
provocative than oral or topical)
- Frequency and speed of administration (e.g., if immunotherapy is
administered too frequently; however, frequent exposure to an allergen followed
by a long delay and reexposure can also precipitate anaphylaxis)
- Atopy—particularly increased risk for
anaphylactic reaction from latex, exercise, or radiopaque contrast media
- Asthma—particularly if undertreated and
receiving immunotherapy
- Occupational exposure (e.g., rubber industry)
- Therapy with beta-blockers, angiotensin-converting enzyme (ACE)
inhibitors, and angiotensin II receptor blockers (ARBs) (see section entitled
Complications/Sequelae)
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Signs and Symptoms |
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Symptoms, which may range from very mild to fatal, may appear alone or in
combination seconds to minutes after exposure, although a delay of 1 to 24 hours
is not unusual. The sooner that symptoms begin following antigen exposure, the
more severe they tend to be. Most deaths from anaphylaxis occur within 30
minutes. Skin and respiratory symptoms are the most common, while cardiac and
respiratory are the most dangerous.
- Skin: erythema, flushing, pruritus (often the first symptom),
urticaria, angioedema, diaphoresis
- Respiratory system: rhinitis, laryngeal edema, hoarseness, dysphonia,
stridor, dyspnea, bronchospasm, chest tightness, wheezing, asphyxia (from
edematous obstruction)
- Cardiovascular system: tachycardia, hypotension, dysrhythmia (PVCs,
PACs, atrial fibrillation), hypovolemia, vascular collapse (shock), myocardial
infarction
- Gastrointestinal tract: cramping abdominal pain, nausea, vomiting,
diarrhea, incontinence, tenesmus
- Neurologic system: tingling of face, mouth, palms, and soles;
headache, feelings of oppression or impending doom, light headedness,
disorientation, syncope,
seizures
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Differential
Diagnosis |
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A history of exposure to an antigen or an agent that is an identifiable
trigger, in the presence of signs and symptoms of anaphylaxis, typically makes
the diagnosis obvious. In the absence of such conditions, the following should
be considered in the differential diagnosis:
- Acute myocardial infarction
- Pulmonary embolism
- Acute asthma attack; sometimes accompanied by idiopathic urticaria
- Epiglottitis
- Tracheal foreign body
- Other causes of shock (hemorrhagic, cardiogenic, septic)
- Hereditary angioedema, particularly if laryngeal edema and abdominal
pain are present
- Leukemia or mastocytosis; both cause increased production of
histamines; anaphylactic-like reaction can be induced in the presence of
opiates
- Seizure disorder; autonomic epilepsy
- Transfusion reaction
- Vasovagal reaction
- Cold urticaria
- Functional disorders (e.g., panic attacks)
- Pheochromocytoma
- Scombroid poisoning from spoiled fish
- "Chinese Restaurant Syndrome" (MSG ingestion)
- Cardiac arrhythmia
- Hyperventilation
- Other causes of flush: carcinoid syndrome, medullary carcinoma of the
thyroid, menopause
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Diagnosis |
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Physical Examination |
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Physicians must be alert to the most common as well as the most potentially
life-threatening organ systems affected by or involved with anaphylaxis. The
history of an antigenic exposure is helpful for the diagnosis. The skin is often
affected initially, but the progression from urticaria to shock can be rapid
(within minutes). Stridor, hypersalivation, hoarseness, and angioedema generally
coincide with upper respiratory obstruction, while tachycardia and low blood
pressure indicate possible impending shock. |
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Laboratory Tests |
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- Complete blood count with differential, looking for signs of
hemoconcentration as well as eosinophilia
- Urinary histamines
- Serum histamine level if less than or equal to 1 hour from the time of
exposure
- Measurement of serum tryptase levels (peaks 1 to 1˝ hours following
exposure and remains elevated for 5 hours), allergen-specific IgE, or
anaphylatoxins (C3a and C5a)
- CPK, LDH, AST may be elevated in the case of damage to the myocardium
and exercise-induced anaphylaxis
- ECG
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Pathology/Pathophysiology |
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Anaphylaxis
- Allergen binds to IgE antibody on surface membrane of mast cells and
basophils
- IgE-allergen interaction leads to release of inflammatory mediators
including histamine and bradykinins from granules of mast cells and basophils
- Histamine acts at H1 and H2 receptors causing
vasodilation, increased vascular permeability, bronchial constriction, and
enhanced mucus secretion
- Prostaglandins and leukotrienes are synthesized by mast cells, further
exacerbating bronchial constriction, mucus secretion, and increased vascular
permeability
Anaphylactoid Reaction
- Non-IgE mediated release of bioactive mediators from mast cells and
basophils; occurs from direct action of the substance on those cells and via
induction of the complement cascade
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Imaging |
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Chest X ray may show hyperinflation, atelectasis, and/or pulmonary edema;
also, necessary to check endotracheal tube placement if intubation takes place.
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Other Diagnostic
Procedures |
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- Intradermal skin testing—to detect
IgE-mediated reactions
- Radioallergosorbent test (RAST)—to detect IgE
antibodies by measuring serum IgE bound to antigen; not as sensitive as skin
testing
- Additional tests may be required to distinguish from conditions in the
differential diagnosis
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Treatment Options |
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Treatment Strategy |
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The most important principle for treatment of anaphylaxis is to initiate
appropriate therapy and supportive care as quickly as possible. Basic life
support and advanced cardiac life support should be initiated by trained
individuals. The keys to caring for the victim of an anaphylactic reaction
include:
- Maintaining adequate oxygenation and normal blood pressure with fluid
expanders
- Treating any cardiac arrhythmias
- Preventing sequelae
Epinephrine is the drug of choice, but high doses may have serious,
life-threatening cardiac effects (particularly in the elderly and those with a
history of heart disease), inducing hypertension and increased myocardial oxygen
demand, and potentially causing cardiac arrhythmias, ischemia, or infarction.
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Drug Therapies |
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The goal of drug therapy in the case of anaphylaxis is to inhibit release of
chemical mediators or reverse their effects on target tissues.
- Epinephrine—generally administered IM by
emergency personnel but can be given SL, IV, or via endotracheal tube if
necessary. Self-administration of preloaded syringe [0.3 cc of 1:1,000 SC in
adults and 0.3 cc of 1:2,000 in children] or aerosolized metered dose inhaler
may occur prior to presentation to EMTs or emergency room staff.
- Diphenhydramine (25 to 100 mg) or
chlorpheniramine—(4 to 10 mg) administered every 4 to 6
hours IM for mild to moderate reactions or IV for severe reactions; pediatric
dose is 5 mg/kg/day in 4 to 6 divided doses—blocks
histamine release, prevents laryngeal edema, and prevents
recurrences
- Corticosteroids, while not necessary for the acute treatment, are
important for preventing later-onset sequelae. Either hydrocortisone (200 mg) or
methylprednisolone (125 to 250 mg) administered IV, followed by a course of oral
prednisone for 7 to 10 days tends to minimize late relapse; oral steroids may
also be used prophylactically, as in the case of known reaction to radiocontrast
material
- Albuterol sulfate—nebulizers for persistent
bronchospasm; anticholinergic agents (e.g., ipratropium bromide) may be
considered as well and aminophylline IV (5 mg/kg over 10 to 30 minutes) followed
by oral maintenance—for asthmatic reactions that do not
respond to epinephrine
- An H2 blocker, namely cimetidine (300 mg IV upon initial
presentation and every 6 hours PO or IV for 2 days); helps to prevent delayed
relapse
- Dopamine (5 mcg/kg/min) may be considered if severe hypotension or
shock persist despite epinephrine and large volumes of crystalloid fluid; other
vasopressors may be tried pending evaluation and progress by trained
professionals in the medical intensive care unit
- Positive pressure 100% oxygen with assisted
ventilation—to treat cyanosis, dyspnea, or
wheezing
- Glucagon IV (1 to 5 mg bolus followed by continuous drip); for
patients on beta-blockers or resistant to the usual approaches
discussed
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Surgical Procedures |
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Endotrachael intubation or tracheostomy with or without mechanical
ventilation maintains the airway in cases of severe laryngeal edema or loss of
consciousness, and assists with progressive hypoxia or status asthmaticus.
Intubation may be difficult due to distortion from laryngeal edema. If an airway
cannot be secured quickly enough by this method, cricothyrotomy may be
necessary. |
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Complementary and Alternative
Therapies |
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Because of the need for immediate emergency care, complementary and
alternative therapies are not considered appropriate for first line treatment of
an anaphylactic reaction. CAM therapies may be useful, though, in the prevention
of an allergic response in general and recurrent episodes of anaphylaxis
specifically. Some CAM approaches may also lessen the severity of any allergic
reaction and may improve non–life-threatening symptoms,
such as gastrointestinal dysfunction, that can occur with anaphylaxis.
Substances and approaches that show some promise for possible adjunctive
treatment of anaphylaxis include:
- Flavonoids, such as quercetin—prophylaxis
suggested by traditional use and animal studies; vitamin C potentiates
quercetin
- Omega-3 fatty acids (such as alpha-linolenic
acid)—lower mortality rate in animal
studies
- Zinc—animal study suggests reduced GI
disturbance under anaphylactic conditions
- Certain single and combination herbal remedies (see section entitled
Herbs)
- Acupuncture—small animal study showed lower
mortality rate when used immediately for treatment
(See sections that follow for more details on each of these topics.)
It is important to remember that nutraceuticals and botanicals, like
medications, can cause allergic reactions, including anaphylaxis. In addition to
a few herbs and supplements mentioned in the Etiology section, see
a list of other herbs associated with rare reports of allergic reactions at the
end of the section entitled Herbs. |
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Nutrition |
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Omega-3 Fatty Acids
Omega-3 fatty acids have anti-inflammatory properties that, theoretically,
may be protective from the extreme reaction of anaphylaxis. Animal studies,
however, of IgE antibody response to egg albumin in mice fed alpha-linolenic
acid (an omega-3 fatty acid) versus mice fed linoleic acid (an omega-6 fatty
acid) are somewhat conflicting. Some studies show increased IgE-meditated
reactions in the omega-6 fed animals (as would be expected) and others show
increased IgE-mediated reactions in the omega-3 fed animals. What is consistent,
though, is a lower mortality rate from anaphylactic shock in the mice on a high
omega-3 fatty acid diet compared to those on a high omega-6 diet (Oh-hashi et
al. 1997).
Quercetin & Other Flavonoids
Naturopathic doctors have recommended that people with known allergies take
quercetin (a naturally occurring flavonoid) prior to allergen exposure;
quercetin and other flavonoids stabilize mast cell degranulation, possibly
lessening the severity of a response to an antigen (Pizzorno and Murray 1999).
Allergy-susceptible individuals can take quercetin supplements or eat foods high
in flavonoids on a regular basis.
Animal studies appear to validate this traditional use of quercetin as well
as its mechanism of action. In two separate guinea pig studies,
quercetin:
- Exhibited membrane-stabilizing effects (Wang et al. 1991)
- Inhibited histamine release (Wang et al. 1991)
- Inhibited the anaphylaxis response in smooth muscle cells of guinea
pigs (Nemoto and Okamura 1992)
Vitamin C
Vitamin C is thought to enhance the activity of quercetin (Pizzorno and
Murray 1999).
Zinc
Zinc may be protective against development of gastrointestinal symptoms from
anaphylaxis. As discussed in the section entitled
Pathology/Pathophysiology, anaphylaxis is generally characterized
by contraction of smooth muscle and dilation of capillaries due to release of
active substances such as histamine and bradykinin; in the GI tract these
effects contribute to gastrointestinal disturbances. A small animal study
suggests that zinc has anti-inflammatory and antioxidant properties in the GI
tract under extreme conditions such as malnutrition; similarly, zinc appeared to
protect the malnourished guinea pigs in this trial from anaphylactic intestinal
dysfunction (Darmon et al. 1997). |
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Herbs |
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Several animal studies of medicinal plants used traditionally in South Korea
and other parts of Asia for prevention or treatment of allergic reactions
suggest that the following botanicals, among others, may have merit for
prevention of anaphylaxis and other allergic responses in susceptible
individuals (Kim et al. 1999c; Kim et al. 1999d; Kim and Yang 1999; Lee et al.
1999; Wu et al. 1991):
- Castanea crenata (Sweet chestnut tree) is an herb that has been
used in Asian countries to treat whooping-cough. According to results of an
animal study, this herbal extract (100 or 200 mg/kg) inhibited percutaneous
anaphylaxis and significantly reduced histamine and serotonin induced vascular
permeability. A bioassay revealed that quercetin was the active component in
C. crenata extract (Lee et al. 1999). (See subsection Quercetin and
Other Flavonoids within the section entitled
Nutrition.)
- Centipeda minima (Spreading sneezeweed) has been used
historically in traditional Chinese medicine for anti-inflammatory and
anti-allergy purposes; contains flavonoids and sesquiterpene lactones. These
active constituents appear to inhibit histamine release from mast cells (Wu et
al. 1991).
- Salviae miltiorrhizae (Danshen root) is an herb
traditionally used for the treatment of allergies. An aqueous extract of salviae
radix root (SRRAE) (0.001 to 1 mg/g) inhibited skin related allergic reactions
but not systemic anaphylaxis in rats (Kim et al. 1999c).
- Rosa davurica (Asian rose spp.) traditionally used to regulate
immune response was tested in rats. Pretreatment with RdF extract (0.0001 to 1
g/kg) inhibited experimentally induced systemic anaphylaxis by reducing
histamine levels in serum and preventing IgE-mediated TNF-alpha production in
mast cells (Kim et al. 1999d).
- Aqueous extracts of Poncirus trifoliata (Hardy orange)
have been traditionally used for the treatment of allergic diseases.
Pretreatment of mice with P. trifoliata fruit extract (PTFE) (200 mg/kg)
inhibited systemic anaphylaxis by arresting IgE production (Kim et al.
1999a).
Some combination herbs have also been tested in animal studies including
Sosiho-Tang (SS-Tang), a Korean medicine traditionally used for allergies, that
contains:
- Bupleurum falcatum (Bupleurum)
- Scutellaria baicalensis George (Skullcap root)
- Panax ginseng (Asian ginseng)
- Pinelliae tenata (Pinelliae tuber)
- Glycyrrhiza uralensis (Glycyrrhiza glabra; Licorice
root)
- Zingiber officinale (Ginger root)
- Zizyphus jujuba (Jujube)
When administered prior to antigen challenge, doses of 1g/kg reduced plasma
histamine levels and inhibited anaphylaxis. However, the large doses of SS-Tang
required to achieve beneficial effects may limit the application of this herbal
remedy for treatment of anaphylaxis (Kim et al. 1999d).
Kumhwang-San, another combination remedy, is traditionally used to treat
allergic skin conditions; in one study, this herbal formula reduced serum
histamine levels in rats in a dose-dependent manner (0.01 to 10 mg/kg).
Ingredients in this formula include:
- Citrus aurantium (Orange peel, bitter)
- Trichosanthis rhosthornii (Snakeground root)
- Atractylodes macrocephalae (Largehead
atractylodis)
- Curcumae longa (Turmeric root)
- Machili cortex
- Arisaema erubescens (Jack-in-the-pulpit tuber)
- Glycyrrhizae glabra (Licorice root)
- Angelicae archangelica (Angelica root)
- Phellodendron amurense (Amur cork-tree)
- Rheum palmatum (Rhubarb)
Other herbs with anti-allergic activity that may also be beneficial when used
alone to prevent reactions include (Tsumura and Kampo 1991):
- Scutellaria baicalensis (Skullcap root)
- Glycyrrhiza glabra or G. uralensis (Licorice root)
- Ganoderma lucidum (Reishi mushroom)
Consultation with an herbalist can help decide what single or combination of
agents is best for an individual patient.
On the other hand, certain herbal remedies may induce allergic reactions,
although this happens much less frequently with herbs than it does with
pharmaceutical preparations. Herbs for which there have been rare reports of
hypersensitivity include (Blumenthal et al. 2000):
- Arnica Montana (frequently used as a homeopathic
remedy)
- Cynara scolymus (Artichoke
leaf)—should not be used in case of an allergy to
artichokes; Cnicus benedictus (Blessed Thistle herb)
- Capsicum spp. (Cayenne pepper)
- Cinnamomum verum (Cinnamon bark)
- Taraxacum officinale (Dandelion
root)—rare cross-reactivity with latex allergy due to
sesquiterpene lactone present in the both the latex and dandelion
- Echinacea purpurea (Echinacea)
- Foeniculum vulgare (Fennel oil and fennel seed)
- Tanacetum parthenium/Chrysanthemum parthenium
(Feverfew)
- Ginkgo biloba (Ginkgo biloba leaf extract)
- Populus spp.(Poplar bud)—may
cross-react with salicylate sensitivity
- Plantago spp. (Psyllium seed)—reaction
more common with powder or liquid
- Achillea millefolium
(Yarrow)
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Homeopathy |
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While standard medical care should not be delayed in the case of anaphylaxis,
there are several homeopathic remedies that have been used for allergic
reactions including symptoms of anaphylaxis; these may, therefore, prove of
value for adjunctive care (Morrison 1993):
- Aconite napellus—helps in the setting
of tremendous anxiety and fear of dying that may accompany or follow an
anaphylactic reaction.
- Arnica montana—may be used for
adjunctive treatment of anaphylactic shock
- Apis—for skin related symptoms
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Acupuncture |
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Mice randomized to control (n = 15) or electroacupuncture (EA; n = 25) were
sensitized to and subsequently challenged with bovine serum. The animals in the
treatment group were immediately treated with EA applied to renzhong (GV 26) and
chengjiang (CV 24) points for 20 minutes. The control group had a 60% mortality
rate and the EA group had a significantly reduced mortality rate of 20% (Jian
1985). Again, while treatment of anaphylaxis should never be delayed, this study
raises the question as to whether acupuncture may be a useful adjunct to
conventional treatment for anaphylaxis. More research is needed, including in
humans. |
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Patient Monitoring |
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Continuous cardiac monitoring should be started as soon as possible;
admission to an intensive care unit may be necessary and in some cases,
Swan-Ganz catheterization may be required.
On occasion, persistent or delayed-onset reactions occur 4 to 12 hours after
the initial event (known as a biphasic response). Patients who have experienced
anaphylaxis should be observed for at least 24 hours following recovery. They
should also be given steroids, H1 and H2 blockers, and
metered-dose inhalers, if used in initial treatment, to prevent delayed
reactions. |
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Other
Considerations |
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Prevention |
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- Avoidance of any known or suspected etiologic agents including
avoidance of new medications unless absolutely necessary, particularly in
susceptible individuals
- Avoidance of cephalosporins with history of anaphylaxis from
penicillin
- Administration of antibiotics and other medications orally whenever
possible
- Pretreatment with antihistamines and systemic corticosteroids before
studies using radiocontrast material
- Avoidance of products made with echinacea flowers in allergy-prone
individuals may be warranted (see section on Etiology)
- Referral to an allergist for skin and other testing
- Appropriate individuals should carry preloaded epinephrine-containing
syringes with 0.3 ml of 1:1,000 solution for adults and 0.3 ml of 1:2,000
solution for children for self-treatment in case of exposure to antigen;
especially for insect stings and food allergies
- Medic-Alert bracelet for patients who have had previous anaphylactic
reactions
- Skin testing before antiserum or allergenic extracts are
administered
- Desensitization and immunotherapy when appropriate with observation
for at least 30 minutes following treatments; in such settings of controlled
administration of antigens, emergency equipment must be readily available;
consider checking FEV1 in asthmatics prior to immunotherapy and avoid this
treatment when FEV1 is <70%.
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Complications/Sequelae |
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- Beta-blockers may worsen an anaphylactic reaction and inhibit the
effects of epinephrine
- Monoamine oxidase inhibitors interfere with the degradation of
epinephrine, increasing its half-life and therefore its risks
- ACE inhibitors and ARBs can cause life-threatening pharyngeal edema
and inhibit angiotensin II, an endogenous compensatory mechanism for
hypotension; levels of angiotensin I and II are inversely related to severity of
an anaphylactic reaction
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Prognosis |
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Most patients treated aggressively and appropriately for anaphylaxis do quite
well. Airway obstruction and irreversible vascular collapse result in
approximately 400 to 800 deaths annually from anaphylaxis. Not everyone who is
re-exposed to an inciting agent develops anaphylaxis again; however, a high
percentage do, and the risk is too great to warrant the chance of repeat
exposure. |
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Pregnancy |
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Several of the medications used to treat anaphylaxis may pose a risk to the
fetus; however, this life-threatening circumstance requires immediate response
and administration for the ultimate protection of both the mother and the
fetus. |
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References |
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