SEMINAR

ON
ANAPHYLAXIS

SUBMITTED TO SUBMITTED BY

MRS. BINDU.K.SANKAR RIYA MARIYAT

ASST. PROFESSOR 1 ST YEAR MSc NURSING

GOVT. COLLEGE OF NURSING GOVT. COLLEGE OF NURSING

THRISSUR THRISSUR
 ANAPHYLAXIS

INTRODUCTION

The term aphylaxis was coined by French physiologist Charles Richet in 1902 in the sense
"lack of protection". Richet himself later changed the term to anaphylaxis on grounds of
euphony. The term is from the Greek word ana-, meaning "against", and, phylaxis, meaning
"protection". In his experiments, Richet injected a dog with sea anemone (Actinia) toxin in an
attempt to protect it. Although the dog had previously tolerated the toxin, on re-exposure, three
weeks later with the same dose, it developed fatal anaphylaxis. Thus instead of inducing
tolerance (prophylaxis), when lethal responses resulted from previously tolerated doses, he
coined the word a (without) phylaxis (protection). He was subsequently awarded the Nobel
Prize in Physiology or Medicine for his work on anaphylaxis in 1913. The phenomenon itself,
however, has been described since ancient times.

Anaphylaxis reactions occur suddenly in hypersensitive patients after exposure to the offending
allergen. They may occur following parenteral injection of drugs (especially antibiotics) or
blood products and following insect stings.

HYPERSENSITIVITY

Hypersensitivity is an altered immune response that results in harm to the client.

ALLERGIC REACTIONS

Allergic reactions are sensitivities to substances called allergens that come into contact with
the skin, nose, eyes, respiratory tract, and gastrointestinal tract. They can be breathed into the
lungs, swallowed, or injected. In an allergic reaction, the immune system starts fighting
substances that are usually harmless as though these substances were trying to attack the body.
Many allergic reactions are mild, while others can be severe and life-threatening and the
manifestation that happen according to the severity of the reaction. An allergic reaction is more
serious when severe allergic reaction (anaphylaxis) occurs.

ANAPHYLAXIS

Anaphylaxis is a sudden, severe allergic reaction that can be life-threatening. It is a medical

emergency case. It can occur within seconds or minutes of exposure to something someone is
allergic to. It is an acute multi-system severe type I hypersensitivity reaction characterized
cardiovascular collapse, bronchospasm & skin changes i.e. urticaria, itching, redness etc. The
clinical presentation of anaphylaxis & Anaphylactoid reactions are same.

DEFINITION

Anaphylaxis is a potentially life threatening systemic allergic reaction caused by the release of
histamines and other vasoactive mediators from mast cells.

ANAPHYLACTIC SHOCK

Anaphylactic shock is anaphylaxis associated with systemic vasodilation which results in low
blood pressure. It is a severe, potentially life-threatening allergic reaction. It can occur within
seconds or minutes of exposure to something person is allergic to, such as the venom from a
bee sting or a peanut.

The flood of chemicals released by immune system during anaphylaxis can cause person to go
into shock; blood pressure drops suddenly and airways narrow, blocking normal breathing.
Signs and symptoms of anaphylaxis include a rapid, weak pulse, skin rash, and nausea and
vomiting. Common triggers of anaphylaxis include certain foods, some medications, insect
venom and latex.

Anaphylaxis requires an immediate trip to the emergency room and an injection of epinephrine.
If anaphylaxis isn't treated right away, it can lead to unconsciousness or even death.

EPIDEMIOLOGY

The incidence is 0.4 cases per million & is increasing. In USA, in 1980 it was 21 per 1,00,000
population, in 1990 it was 50 per 1,00,000 population. It is more common in young female. In
young it mostly food related where as in adults it because of a previous medication or sting
bite.
Worldwide, 0.05–2% of the population is estimated to experience anaphylaxis at some point in
life. Rates appear to be increasing. It occurs most often in young people and females. About
99.7% of people hospitalized with anaphylaxis in the United States survive.

GEL AND COOMBS CLASSIFICATION OF HYPERSENSITIVITIES

Two British immunologists, Coombs and Gell, have classified allergic reactions into four types,
Type I, II, III and IV.

• Type 1 Immediate hypersensitivity IgE – Mediated hypersensitivity

• Type 2 Cytotoxic hypersensitivity IgG/IgM Mediated RBC lysis

• Type 3 immune complex – mediated hypersensitivity IgG Mediated Immune complex

Disease

• Type 4 Delayed hypersensitivity T cell Delayed Type Hypersensitivity

Type I, II and III allergic reactions are called immediate types of allergic reactions because
they occur within twenty-four hours of exposure to the allergen. Type IV reactions typically
occur after 24 hours of exposure and are called delayed allergic reactions.

Type I or anaphylactic reactions: Type I reactions are mediated by proteins called IgE
antibodies produced by the immune system. These are produced in response to the allergens
such as pollen, animal dander or dust mites, or even certain foods. This causes the release of
histamine and other chemicals causing inflammation and swelling. Examples of type
I allergic reactions include

• bronchial asthma,
• allergic rhinitis,
• allergic dermatitis,
• food allergies,
• allergic conjunctivitis (eye inflammation) and
• anaphylaxis (allergic shock).

Anaphylaxis is the most severe form and is a medical emergency because it can lead to a
sudden, life-threatening respiratory failure. People with anaphylaxis have extreme difficulty
in breathing, swelling, low blood pressure, bluish skin and shock.

Type II or cytotoxic reactions: This type of allergic reaction is mediated by proteins called
IgG and IgM antibodies. The antibodies involved in type II reaction damage cells by activating
a component of immunity called the complement system. Type II allergic reactions can be seen
in certain conditions like

• autoimmune hemolytic anemia,

• immune thrombocytopenia and
• autoimmune neutropenia.

Type III or immunocomplex reactions: Type III reactions are also mediated by proteins i.e.
IgM and IgG antibodies. These antibodies react with the allergen to form immunocomplexes
(antigen-antibody complexes). These complexes are responsible for the reaction. Type III
allergic reactions can be seen in

• lupus,
• serum sickness and
• Arthus reaction.
Type IV or cell-mediated reactions: Type IV allergic reactions are also called the delayed
type of hypersensitivity or allergic reactions as they occur after at least 24 hours of exposure
to the allergen. These reactions typically take 48-72 hours or longer to appear after contact with
the allergen. Many long-term infectious diseases, such as tuberculosis and fungal infections,
show cell-mediated reactions. Certain skin sensitivity reactions espescially to metals may also
belong to this type.

WHAT ARE THE TRIGGERS OF ALLERGIC REACTIONS?

Substances that trigger an allergic reaction are called allergens. They include:

• Dust mites
• Animal/pet dander
• Pollen
• Bee/wasp stings
• Certain medications such as penicillin and penicillin-based antibiotics
• Certain foods such as soy, eggs, peanuts, tree nuts, fish, shellfish, milk and wheat
• Mold
• Latex
• Certain metals
• Some plants

TYPES OF ANAPHYLAXIS

It is of two types.

1. True Anaphylaxis or Classical (IgE mediated)

2. Pseudo Anaphylaxis/ Anaphylactoid Reaction (non IgE mediated)

1. True Anaphylaxis
Pathophysiology: - Here the Patient has an previous exposure to an allergen, when he is re
exposed to the same allergen again because of a new challenge an IgE mediated antigen-
antibody reaction takes place and mediator chemical substances are released from the Mast
cells & Basophiles, which act on the skin and mucous membrane to produce severe
vasodilatations leading to cardiovascular collapse, bronchospasm, urticaria, itching, edema etc.

The Mediators are: - On re-exposure, the antigen binds to the antibody, and the receptors are
activated. Clinical manifestations result from release of immune response mediators such as
“histamine, leukotrienes, tryptase, and prostaglandins.”
 2. Pseudo anaphylaxis/ Anaphylactoid reaction
It is not IgE mediated. There is no sensitization by previous exposure, here the substances
directly acting on the mast cells liberate histamine, i.e. Morphine

ETIOLOGY OF ANAPHYLAXIS

Our immune system produces antibodies that defend against foreign substances. This is good
when a foreign substance is harmful (such as certain bacteria or viruses). But some people's
immune systems overreact to substances that shouldn't cause an allergic reaction. When this
occurs, the immune system sets off a chemical chain reaction, leading to allergy symptoms.
Normally, allergy symptoms are not life-threatening. But some people have a severe allergic
reaction that can lead to anaphylaxis. Anaphylaxis usually happens within minutes of exposure
and almost always within two hours. Anaphylaxis can occur in response to almost any foreign
substance.

The most common causes of anaphylaxis are:

• Certain medications, especially penicillin, Cephalosporin, NSAID, Local Anesthetics,
ACE inhibitors.
• Foods, such as peanuts, tree nuts (walnuts, pecans), fish, shellfish, milk and eggs, soy,
legumes
• Insect stings from bees, yellow jackets, wasps, hornets and fire ants
• IV Contrasts- ( 1-3% of patients who receive hyperosmolar & 0.5% with LMW IV
contrast experience a reaction.)

Less common causes of anaphylaxis include:

• Latex allergy –when we use gloves or other latex products.
• Exercise, often after eating certain foods. Anaphylaxis triggered by exercise varies from
person to person. In some people, aerobic activity such as jogging triggers anaphylaxis.
In others, less intense physical activity such as yard work can trigger a reaction. Eating
certain foods before exercise or exercising when the weather is hot, cold or humid has
also been linked to anaphylaxis in some people
• Muscle relaxants used in general anesthesia

MECHANISM OF ANAPHYLAXIS
The triggers or causes of anaphylaxis may range from insect venom or stings to foods, drugs
and medications. The trigger may be exercising in cold dry climates as well.Most of these
triggers however act via Immunoglobulin E (IgE). The IgE cross links with the mast cells and
basophils binding to FceRI present on these cells.Once bound this gives rise to a chain of
reactions where the complement and coagulation systems are activated and T-cells are
activated along with release of neuropeptide (substance P) release and cytotoxicity.There is
activation of phospholipase A2, Cycloxygenases (COXs), and lipooxygenases that lead to
production of arachidonic acid metabolites like prostaglandins and leukotrienes and platelet-
activating factor (PAF).In addition interleukins like IL-6, IL-33 and TNF-a (Tumor necrosis
factor alpha) are also released as late reactants.The process of autoimmunity may also be
triggered. While the immune system normally attacks invaders, mediators of autoimmunity fail
to distinguish between self and foreign and tend to attack the body’s own tissues.Exercise or
exposure to cold air or cold water can also lead to anaphylaxis. These occur by non-immune
reactions and activations of mast cells and basophils. Thus these reactions are not IgE mediated.
Anaphylaxis is a severe allergic reaction of rapid onset affecting many body systems. It is due
to the release of inflammatory mediators and cytokines from mast cells and basophils, typically
due to an immunologic reaction but sometimes non- immunologic mechanism.

Sensitization stage Antigen (allergens) invades

↓
the body Plasma cells produce large amounts of class IgE antibodies against allergen
↓

IgE antibodies attach to mast cells in body tissues

↓

Subsequent sensory response

↓

More of same allergen invades body

↓

Allergen combines with IgE attached to mast cells, which triggers release of histamine from
mast cell granules
↓

Histamine causes blood vessels to dilate and become leaky which promotes edema; stimulate
release of large amounts of mucus and causes smooth muscles to contract

Rapid onset of increased secretion from mucous membranes, increased bronchial smooth
muscle tone, decreased vascular smooth muscle tone, and increased capillary permeability
occur after exposure to an inciting substance. These effects are produced by the release of
mediators, which include histamine, leukotriene C4, prostaglandin D2, and tryptase. In the
classic form, mediator release occurs when the antigen (allergen) binds to antigen-specific
immunoglobulin E (IgE) attached to previously sensitized basophils and mast cells. The
mediators are released almost immediately when the antigen binds. In an anaphylactoid
reaction, exposure to an inciting substance causes direct release of mediators, a process that is
not mediated by IgE. Increased mucous secretion and increased bronchial smooth muscle tone,
as well as airway edema, contribute to the respiratory symptoms observed in anaphylaxis.
Cardiovascular effects result from decreased vascular tone and capillary leakage. Histamine
release in skin causes urticarial skin lesions.

The most common inciting agents in anaphylaxis are parenteral antibiotics (especially
penicillins), IV contrast materials, Hymenoptera stings, and certain foods (most notably,
peanuts). Oral medications and many other types of exposures also have been implicated.
Anaphylaxis also may be idiopathic.

RISK FACTORS

There aren't many known risk factors for anaphylaxis, but some things that may increase your
risk include:

1. A personal history of anaphylaxis:

If you've experienced anaphylaxis once, your risk of having this serious reaction is increased.
Future reactions may be more severe than the first reaction.

2. Allergies or asthma:
People who have either condition are at increased risk of having anaphylaxis.

3. A family history:
If you have family members who have experienced exercised-induced anaphylaxis, your risk
of developing this type of anaphylaxis is higher than it is for someone without a family history.

Anaphylaxis symptoms are sometimes caused by aspirin, other nonsteroidal anti-inflammatory

drugs — such as ibuprofen (Advil, Motrin, others) and naproxen (Aleve, Midol Extended
Relief) — and the intravenous (IV) contrast used in some X-ray imaging tests.

Although similar to allergy-induced anaphylaxis, this type of reaction isn't triggered by allergy
antibodies. In some cases, the cause of anaphylaxis is never identified. This is known as
idiopathic anaphylaxis

SYMPTOMS

Anaphylaxis typically presents many different symptoms over minutes or hours with an
average onset of 5 to 30 minutes if exposure is intravenous and 2 hours if from eating food.
The most common areas affected include: skin (80–
90%), respiratory (70%), gastrointestinal (30–45%), heart and vasculature (10–45%), and
central nervous system (10–15%)[13] with usually two or more being involved.

• Anaphylactic reactions almost always involve the skin or mucous membranes, most of
the patients have some combination of urticaria, erythema, pruritus, or angioedema.
The classic skin manifestation is urticaria. Skin reactions, including hives along with
itching, flushed or pale skin (almost always present with anaphylaxis), . A feeling of
warmth

• The upper respiratory tract commonly is involved, with complaints of nasal congestion,
sneezing, or coryza. Cough, hoarseness, or a sensation of tightness in the throat may
presage significant airway obstruction, The sensation of a lump in your throat

• Eyes may itch and tearing may be noted. Conjunctival injection may occur

• Dyspnea is present when patients have bronchospasm or upper airway edema. Hypoxia
and hypotension may cause weakness, dizziness, or syncope. Chest pain may occur due
to bronchospasm or myocardial ischemia (secondary to hypotension and hypoxia).

• GI symptoms of cramp like abdominal pain with nausea, vomiting, or diarrhea also
occur but are less common, except in the case of food allergy, abdominal cramps, Colic
pain

• Heart and circulation include dizziness, weakness, fainting, rapid, slow, or irregular
heart rate, or Hypotension, coronary artery spasm, myocardial infarction arrhythmia.
 • Nervous system include anxiety, confusion, or a sense of impending doom hives
Swelling of conjunctiva, loss of consciousness, bladder bowel involvement, muscular
weakness

SIGNS

• Abormal heart rhythm (arrhythmia)

• Fluid in the lungs (pulmonary edema)
• Hives
• Low blood pressure
• Mental confusion
• Rapid pulse
• Skin that is blue from lack of oxygen or pale from shock
• Swelling (angioedema) in the throat that may be severe enough to block the airway
• Swelling of the eyes or face
• Wheezing

DIAGNOSTIC EVALUATION

Diagnosis is mainly based on clinical & medical history like exposure to allergens. Allergy
testing is ordered to help in determining the trigger. Skin allergy testing (such as patch testing)
is available for certain foods and venoms.

• Health history and Physical examination

• Allergy testing
• White blood cell count
• Radioallergosorbent test (RAST)

Laboratory Studies- The diagnosis of anaphylaxis is clinical and does not rely on laboratory
testing. The only potentially useful test at the time of reaction is measurement of serum mast
cell tryptase, though the test's availability and slow turn around time greatly limit its clinical
utility. Tryptase is released from mast cells in both anaphylactic and anaphylactoid reactions.
Levels are usually raised in severe reactions.

Sensitivity testing- Testing for sensitivity to penicillin antibiotics may be useful when a
penicillin or cephalosporin antibiotic is the drug of choice for a serious infection in a patient
who has a history of severe allergic reaction.

Blood testing for specific IgE can be useful to confirm milk, egg, peanut, tree nut and fish
allergies.
Specific IgE tests may be preferable to skin prick tests when investigating patients with a
history of anaphylaxis

During an attack, blood tests for tryptase or histamine (released from mast cells) might be
useful in diagnosing anaphylaxis due to insect stings or medications. However these tests are
of limited utility if the cause is food or and they are not specific for the diagnosis.

Anaphylaxis is diagnosed based on clinical criteria.

When any one of the following three occurs within minutes/hours of exposure to an allergen
there is a high likelihood of anaphylaxis:

1. Involvement of the skin or mucosal tissue plus either respiratory difficulty or hypotension.
2. Two or more of the following symptoms:
✓ Involvement of the skin or mucosa
✓ Respiratory difficulties
✓ Low blood pressure
✓ Gastrointestinal symptom
3. Low blood pressure after exposure to a known allergy.

Evaluation of severity

Based on the examination the degree of severity, the anaphylaxis should be evaluated and the
most threatening symptom of anaphylaxis identified. The most life-threatening symptom of
anaphylaxis should be treated with priority.

This may lead to 6 possible scenarios:

1. Cardiac or circulatory arrest (anaphylaxis grade IV)

2. Predominant cardiac and circulatory reaction (anaphylaxis grade II/III)
3. Predominant obstruction of upper airways (anaphylaxis grade II/III)
4. Predominant obstruction of lower airways (anaphylaxis grade II/III)
5. Predominant gastrointestinal involvement (anaphylaxis grade II)
6.Systemic generalized skin manifestations and subjective symptoms (anaphylaxis grade I).

TREATMENT

The cardinal principle in the therapeutic management of anaphylaxis is, speed in :

• Recognition of signs and symptoms of an anaphylactic reaction
• Maintenance of a patent airway
• Prevention of spread of the allergen by using a tourniquet
• Administration of drugs

During an anaphylactic attack, an emergency medical team may perform cardiopulmonary

resuscitation (CPR) if the patient stops breathing or his heart stops beating. He/she may be
given medications including: 1. Epinephrine (adrenaline) to reduce the body's allergic
response. 2. Oxygen, to help compensate for restricted breathing. 3. Intravenous (IV)
antihistamines and cortisone to reduce inflammation of air passages and improve breathing. 4.
A beta agonist (such as albuterol) to relieve breathing symptoms.

What to do in an emergency ?

If someone who is having an allergic reaction and shows signs of shock caused by anaphylaxis,
a quick reaction is essential. Signs and symptoms of shock caused by anaphylaxis include pale,
cool and clammy skin, weak and rapid pulse, trouble breathing, confusion and loss of
consciousness, take the following steps immediately: - Call 911 or emergency medical help. -
Check the person's pulse and breathing and, if necessary, administer CPR or other first aid
measures.
With injected toxins such as a bee sting, an additional amount equivalent to one half the above
may be injected directly into the site of sting and a tourniquet is applied above it to prevent
further systemic absorption.

If the person has medications to treat an allergy attack, such as an epinephrine auto-injector or
antihistamines, give them right away. Parenteral adrenergic agents- Reverse cardiovascular,
cutaneous, GI, and pulmonary manifestations of anaphylaxis.

Epinephrine- 0.3-1.0 ml 1:1000 solution IM, repeated at 5-10 mins if initial response is
inadequate Inhaled beta-agonists- Used to treat bronchospasm. Doses are identical to those
used in the treatment of asthma. Albuterol - Numerous inhaled beta-agonists are used for
treatment of bronchospasm; albuterol is the most commonly used preparation. 0.5 mL 0.5%
soln in 2.5 cc NS nebulized q15min.

Treatment of anaphylaxis

It is an medical emergency. The main stay of treatments are as follows:-

Stop further administration of the drug.

1. Adrenaline (Epinephrine)
2. IV fluids
3. Maintenance of Air way
4. Oxygen therapy
5. Use of Antihistaminic & Steroids.
6. Bronchodilators
7. IPPV if respiratory failure & Others

Adrenaline

It is the mainstay of treatment in Anaphylaxis. Dose- 1mcg/kg body wt. as bolus IV as diluted
solution, repeated up to 1mg . Never give undiluted adrenaline IV, Can be given intramuscular
/ subcutaneous/ intraoseous/ intratracheal.

Parenteral epinephrine - An adrenergic agonist (sympathomimetic) drug that has both

vasoconstricting and bronchodialating effects mild reactions subcutaneous injection of 0.3ml
to 0.5ml of 1:1000 epinephrine

Intravenous epinephrine is using a 1:100000 concentrations may be used in the client with a
more severe anaphylactic reaction.

Intravenous epinephrine continuous infusion and indications - Patients who do not respond to
several IM injections of epinephrine and aggressive fluid resuscitation . A simple method for
quickly preparing a solution of 1 mcg/mL for adults and adolescents is to add the entire 10 mL
contents of a 0.1mg/mL (1:10,000) prefilled "cardiac" epinephrine syringe (1 mg) to a 1000
mL (1 liter) bag of normal saline, the resultant solution of 1mcg/mL . Infants and children The
dose for IV infusion is 0.1 to 1 mcg/kg/minute with use of an infusion pump. The dose can be
increased after 3-5minutes interval.
Intramuscular Adrenaline - For patients of any age is 0.01 mg/kg (maximum dose of 0.5 mg)
per single dose, injected IM into the mid-outer thigh (vastus lateralis muscle). IM epinephrine
may be repeated at 5- to 15-minute intervals if there is no response or an inadequate response
or even sooner if clinically indicated.

Fluids - Both crystalloids and colloids are administered very fast to make up the volume deficit.
It may be up to 2Lts or 25% of the blood volume. Children 20ml/kg over 15-20 minutes period,
repeat if needed up to 1ooml/kg may be required. If colloids is offending agent it should not be
administered.

Glucagon for patients taking beta-blockers - Beta-blocker therapy, alone or in combination

with angiotensin-converting enzyme inhibitors, has been shown to be refractory to epinephrine,
in such cases glucagon can be administered because it has inotropic and chronotropic effects
that are not mediated through beta-receptors . Adult dosing is 1 to 5 mg slow IV bolus over
five minutes. May be followed by an infusion of 5 to 15 mcg/minute titrated to effect.
Paediatric dosing is 20 to 30 mcg/kg (maximum 1 mg) slow IV bolus over five minutes. May
be followed by an infusion of 5 to 15 mcg/minute titrated to effect (ie, not weight-based). Rapid
administration of glucagon can induce vomiting.

H1 antihistamines - Relieve itch and hives. These medications do not relieve upper or lower
airway obstruction, hypotension or shock, and in standard doses, do not inhibit mediator release
from mast cells and basophils. Only first-generation H1 antihistamines are available in
parenteral formulations, and rapid IV administration may increase
hypotension.(Diphenhydramine & Avil).

Diphenhydramine HCL/Avil - For 25 to 50 mg can be administered IV over five minutes,

which may be repeated up to a maximum daily dose of 400 mg per 24 hours. For children
weighing less than 50 kg, diphenhydramine 1 mg/kg (maximum 50 mg) can be administered
IV over five minutes, which may be repeated up to a maximum daily dose of 5 mg/kg or 200
mg per 24 hours.

Avil - 22.75mg/ml Injection. An alkylamine derivative is a histamine H1-receptor antagonist

with anticholinergic and moderate sedative effects. It is used for treating allergic conditions
like Pruritus, urticaria or hay fever ,allergic conjunctivitis and also as an over-the-counter
sleeping pill similar to other sedating antihistamines.
Contraindications: Pregnancy, below 5years, glaucoma, Prostatic Hypertrophy, on MAO
inhibitors, with Alcohol. Dose: IV/IM/SC ( 0,25mg/kg).

Pharmacodynamic properties - Antihistamines, including chlorphenamine, used in the

treatment of allergy act by competing with histamine for H1-receptor sites on cells and tissues.
Chlorphenamine also has anticholinergic activity. The mechanism by which chlorphenamine
exerts its anti-emetic, anti- motion sickness and anti-vertigo effects is not precisely known but
may be related to its central actions. Further, most antihistamines, including chlorphenamine,
cross the blood-brain barrier and probably produce sedation largely by occupying H1-receptors
in the brain.

Glucocorticosteroids - Due to their slow onset of action, glucocorticosteroids play a minor role
in the acute phase of anaphylaxis treatment . There are no systematic clinical trials regarding
this indication. However, glucocorticosteroids are effective in the treatment of asthma and
against protracted or biphasic anaphylactic reactions. An unspecific membrane stabilizing
effect within the first 10–30 minutes of application of high dose glucocorticosteroids (500–
1,000 mg) independent of the potency of the glucocorticosteroids has been postulated in review
article. When there is no intravenous catheter, glucocorticosteroids may be applied rectally,
especially in small children (e.g. prednisolone suppositories) or orally.

Steroids( Glucocorticosteroids) - Corticosteroid-( hydrocortisone hemesuccinate) 100-

1000mg, Methyl Prednisolone -30mg/ kg body wt. The prophylactic use of these substances
are of doubtful value.

Bronchodilators - For the treatment of bronchospasm not responsive to epinephrine, inhaled

bronchodilators (eg, albuterol, salbutamol) should be administered by mouthpiece (or facemask
for those whose age or condition requires) and nebulizer/compressor, as needed.
Aminophyline - as infusion if there is bronchospasm (250mg in 500ml 5% dextrose).
Bronchodilators are adjunctive treatment to epinephrine because they do not prevent or relieve
mucosal edema in the upper airway or shock, for which the alpha-1-adrenergic effects of
epinephrine are required

Oxygen Therapy - To improve saturation, Ventilatory support if needed.

Combination of antihistamines and sympathomimetic agents are also used.

OTHER TREATMENT

Airway management takes the highest priority for clients with an acute anaphylactic reaction.
Insertion of an endotracheal tube or emergency tracheostomy may be required to maintain
airway patency with severe laryngospasm

Plasmapheresis: Removal of harmful components in the plasma may be used to treat immune
complex responses such as glomerulonephritis.

NURSING MANAGEMENT

1. Ineffective airway clearance related to bronchospasm or laryngeal edema

• Administer oxygen
• Assess respiratory rate and pattern, level of consciousness and anxiety, use of accessory
muscles for respiration, chest wall movement, audible stridor; auscultate lung sounds
and any adventitious sounds.
• Insert a nasopharyngeal tube or oropharyngeal airway and arrange for immediate
intubation if indicated
• Administer subcutaneous epinephrine as prescribed.
• Provide calm reassurance

2. Decreased cardiac output related to peripheral vasodialation and increased capillary

permeability from the release of histamine

• Monitor vital signs frequently Assess skin colour, temperature, capillary refill, edema
and other indicators of peripheral perfusion
• Monitor level of consciousness
 • Administer warmed intravenous solutions of ringer lactate or normal saline as
prescribed
• Insert an indwelling catheter and monitor urinary output frequently
• Once breathing is established place the client with legs elevated

COMPLICATION OF ANAPHYLAXIS

✓ Pulmonary edema, pulmonary hemorrhage, and pneumothorax , Respiratory arrest (no

breathing), Airway blockage
✓ Laryngeal edema with or without airway obstruction
✓ Myocardial ischemia and infarction, Cardiac arrest (no effective heartbeat)
✓ Death may result from asphyxiation from upper airway obstruction or profound shock
or both.

FOLLOW UP

1. Patients not admitted to the hospital should be observed for several hours, because late
“biphasic” reactions can begin as late as 24 hours after the initial anaphylaxis.
2. Should be treated with steroids during the acute treatment, and they should be given a
short course of oral corticosteroids to finish at home.
3. Must be discharged with autoinjectable epinephrine (this will provide temporary relief
so the patient will have time to seek medical assistance).
4. Patients must know to seek medical help if symptoms reappears.

REFRACTORY ANAPHYLAXIS

Anaphylactic shock displays features of both distributive (vasodilatory) and hypovolemic

shock. Further Management – Shifting to ICU & Treat Shock as per protocol.( Fluid &
Vasopressors) "Norepinephrine, vasopressin, Dopamine and other vasopressors have been used
with success in patients in anaphylaxis with refractory hypotension“.

Methylene blue - Vasoplegia (profound vasodilation) may be present in some cases of

refractory anaphylaxis. A few case reports and other publications support the use of methylene
blue, an inhibitor of nitric oxide synthase and guanylate cyclase, in severe anaphylaxis, mostly
in perioperative settings

Dose of Methylene Blue - The efficacy and ideal dose of methylene blue is unknown, but a
single bolus of 1 to 2 mg/kg given over 20 to 60 minutes has been used in cardiac surgery.
Improvement of vasoplegia (eg, increased systemic vascular resistance, reduced vasopressor
dose) has been observed within one to two hours in the setting of cardiac surgery, but few data
are available about anaphylaxis. This drug should not be given to patients with pulmonary
hypertension, underlying glucose-6-phosphate dehydrogenase deficiency, or acute lung injury.
We also advise caution regarding potential drug interactions with serotonergic agents.

Extracorporeal membrane oxygenation - Patients suffering from refractory anaphylaxis have

been resuscitated with extracorporeal membrane oxygenation (ECMO) or operative
cardiopulmonary bypass. ECMO is becoming increasingly available in emergency departments
and should be considered in patients unresponsive to complete resuscitative efforts in
institutions with experience in this technology. The decision to initiate ECMO should be
considered early in patients unresponsive to traditional resuscitative measures, before
irreversible ischemic acidosis develops

PROGNOSIS

• Excellent, provided the trigger can be avoided.

• Establishment of IV line
• Intraoseous Needle Placement

PREVENTION

The best way to prevent anaphylaxis is to avoid substances that cause this severe reaction.

FIRST AID

If you're with someone having an allergic reaction with signs of anaphylaxis:

1. Immediately call your local medical emergency number.

2. Ask the person if he or she is carrying an epinephrine autoinjector to treat an allergic
attack (for example, EpiPen, Twinject).
3. If the person says he or she needs to use an autoinjector, ask whether you should help
inject the medication. This is usually done by pressing the autoinjector against the
person's thigh.
4. Have the person lie still on his or her back.
5. Loosen tight clothing and cover the person with a blanket. Don't give the person
anything to drink.
6. If there's vomiting or bleeding from the mouth, turn the person on his or her side to
prevent choking.
7. If there are no signs of breathing, coughing or movement, begin CPR. Do uninterrupted
chest presses — about 100 every minute — until paramedics arrive. Get emergency
treatment even if symptoms start to improve. After anaphylaxis, it's possible for
symptoms to recur. Monitoring in a hospital setting for several hours is usually
necessary.

CONCLUSION

Anaphylaxis is a life-threatening condition. Prompt identification, assessment and management

is vital for positive outcomes. Rapid transport is key to definitive treatment. Do not delay on
scene time. Be aware of future treatment options. Anaphylaxis is a severe allergic reaction to
venom, food, or medication. Most cases are caused by a bee sting or eating foods that are
known to cause allergies, such as peanuts or tree nuts. Anaphylaxis causes a series of
symptoms, including a rash, low pulse, and shock, which is known as anaphylactic shock.
RELATED RESEARCH STUDIES

Prevalence and Severity of Food Allergies Among US Adults

IMPORTANCE : Food allergy is a costly, potentially life-threatening condition.

Although studies have examined the prevalence of childhood food allergy, little
is known about prevalence, severity, or health care utilization related to food
allergies among US adults.

OBJECTIVE : To provide nationally representative estimates of the distribution,

severity, and factors associated with adult food allergies.

DESIGN, SETTING, AND PARTICIPANTS : In this cross-sectional survey

study of US adults, surveys were administered via the internet and telephone from
October 9, 2015, to September 18, 2016. Participants were first recruited from
NORC at the University of Chicago’s probability-based AmeriSpeak panel, and
additional participants were recruited from the non–probability-based Survey
Sampling International (SSI) panel.

EXPOSURES : Demographic and allergic participant characteristics.

MAIN OUTCOMES AND MEASURES : Self-reported food allergies were the

main outcome and were considered convincing if reported symptoms to specific
allergens were consistent with IgE-mediated reactions. Diagnosis history to
specific allergens and food allergy–related health care use were also primary
outcomes. Estimates were based on this nationally representative sample using
small-area estimation and iterative proportional fitting methods. To increase
precision, AmeriSpeak data were augmented by calibration-weighted, non–
probability-based responses from SSI.

RESULTS : Surveys were completed by 40 443 adults (mean [SD] age, 46.6
[20.2] years), with a survey completion rate of 51.2% observed among
AmeriSpeak panelists (n = 7210) and 5.5% among SSI panelists (n = 33 233).
Estimated convincing food allergy prevalence among US adults was 10.8% (95%
CI, 10.4%-11.1%), although 19.0% (95% CI, 18.5%-19.5%) of adults self-
reported a food allergy. The most common allergies were shellfish (2.9%; 95%
CI, 2.7%-3.1%), milk (1.9%; 95% CI, 1.8%-2.1%), peanut (1.8%; 95% CI, 1.7%-
1.9%), tree nut (1.2%; 95% CI, 1.1%-1.3%), and fin fish (0.9%; 95% CI, 0.8%-
1.0%). Among food-allergic adults, 51.1% (95% CI, 49.3%-52.9%) experienced
a severe food allergy reaction, 45.3% (95% CI, 43.6%-47.1%) were allergic to
multiple foods, and 48.0% (95% CI, 46.2%-49.7%) developed food allergies as
an adult. Regarding health care utilization, 24.0% (95% CI, 22.6%-25.4%)
reported a current epinephrine prescription, and 38.3% (95% CI, 36.7%-40.0%)
reported at least 1 food allergy–related lifetime emergency department visit.

CONCLUSIONS AND RELEVANCE : These data suggest that at least 10.8%

(>26 million) of US adults are food allergic, whereas nearly 19% of adults believe
that they have a food allergy. Consequently, these findings suggest that it is
crucial that adults with suspected food allergy receive appropriate confirmatory
testing and counseling to ensure food is not unnecessarily avoided and quality of
life is not unduly impaired.

Incidence Rate of Hypersensitivity Reactions to Bee-Venom Acupuncture

INTRODUCTION: Bee-venom acupuncture (BVA) has been widely applied to

various disorders including pain-related diseases; however, patients are often
warned of adverse reactions such as anaphylaxis. This study aimed to estimate
the risk of hypersensitivity reactions to BVA and to determine their clinical
features.

METHODS: We retrospectively surveyed the medical records of patients treated

by BVA between January 2010 and April 2019 in Dunsan Hospital of Daejeon
University, and all cases of allergic reactions and their clinical symptoms were
analyzed.

RESULTS: A total of 8,580 patients (males 4,081 and females 4,499) were
treated with BVA which amounts to a total of 60,654 treatments (average 7.1 ±
14.8 times). A total of fifteen patients (7 males and 8 females) reported an allergic
reaction (0.175%, 95% CI, 0.086-0.263) of type 1 hypersensitivity, indicating a
rate of allergic reaction in 0.025% (95% CI, 0.012-0.037) of the total BVA
treatments. The average number of BVA treatments in those patients was 6.9 ±
6.5 (males: 4.1 ± 3.4 and females: 9.3 ± 7.9). Among the cases of hypersensitivity
reactions, 4 involved anaphylactic shock; therefore, the incidence rate of
anaphylaxis was 0.047% (95% CI, 0.001-0.092) for the 8,580 subjects and
0.007% (95% CI, 0.000-0.013) for the 60,654 treatments. All grade 1 cases were
recovered within 1 day, whereas others took up to 30 days for complete recovery.
CONCLUSION: Our results may emphasize paying attention to unforeseeable
risks of anaphylaxis after bee-venom acupuncture. This study could be essential
reference data for the guidelines of appropriate use of bee-venom acupuncture
and bee-venom-derived interventions in clinical applications.

BIBLIOGRAPHY

• Levis’s Medical Surgical Nursing, Assessment and management of clinical

problems Second South Asia Edition , Elsevier publications.

• Brunner and Siddarth. Text book of Medical Surgical Nursing, 13th

Edition. Philadelphia : Wolters Kluwer, Elsevier publications.