NATIONAL UNIVERSITY OF CAJAMARCA

FACULTY OF HEALTH SCIENCES

PROFESSIONAL ACADEMIC SCHOOL OF NURSING

NATIONAL UNIVERSITY OF CAJAMARCA

FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF
NURSING

COURSE:
Emergency Nursing
ISSUE:
NURSING CARE IN EMERGENCIES
ANAPHYLACTIC SHOCK
TEACHER:
Lic. Sick Petronila Bringas Duran
STUDENT:
 Bustamante Gonzales Yuli
 Cabrera Jara Karen

 Chilón Saavedra Jessica

 Gallardo Cojal Diana

 Huamán Tanta Karla Mariela

 Limay Sangay Isamar

 Mestanza Chávez Edit

 Sangay Ayac Maria Sandra

 Ticclia Garcia Rebeca

 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

NURSING CARE IN EMERGENCIES ANAPHYLACTIC SHOCK

I. INTRODUCTION
Anaphylaxis (also called anaphylactic shock) is a serious and life-threatening allergic
reaction. Anaphylaxis is a poor reaction of the body's immune system to the
presence of a foreign body (e.g., food or substance) that it mistakenly interprets as a
threat. The entire body is affected, and it usually happens within minutes of coming
into contact with an allergen, but sometimes the reaction can take hours to occur.
There is a sudden drop in blood pressure and a narrowing of the airways.
Anaphylaxis can be triggered by a wide range of foods or other agents. The most
common are: nuts, sesame seeds, fish, seafood, dairy products, eggs and
strawberries. Likewise, the cause of anaphylaxis can be an allergic reaction to bee or
wasp stings, natural latex (rubber), and certain drugs such as antibiotics with
penicillin.
Anaphylaxis in its advanced phase or without interventions involved, evolves to
shock, which we understand as a state of imbalance between the supply and
demand of oxygen to the tissues and different parenchyma, causing tissue
hypoperfusion, leading to alterations in cellular integrity. and multiple organ
failure, with high associated mortality.

II. GOALS
 Provide the necessary knowledge to detect an anaphylactic reaction early,
establishing emergency measures to minimize secondary complications.
 Provide the necessary knowledge to know how to act in front of a patient and
resolve the anaphylactic reaction, quickly and effectively.
 Define the diagnostic suspicion and establish the management of the clinical
picture
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

III. THEORETICAL FRAMEWORK

A. DEFINITIONS:

1. Allergic reaction: adverse effect resulting from a specific immune response that occurs
upon exposure to a substance (allergen), which comes into contact with the subject
through the skin, lungs, swallowing or an injection. The most common causes are:
drugs, contrasts for diagnostic tests, food, latex and bites. 1

2. Anaphylaxis: is a severe allergic reaction in which more than one system is involved,
with rapid onset and potentially fatal. 1

Anaphylaxis is the syndrome that is triggered in a hypersensitive subject upon

subsequent exposure to a sensitizing antigen. The spectrum of anaphylactic
responses varies from localized to systemic. Systemic anaphylaxis can cause
anaphylactic shock and death. 2

3. Anaphylactic shock: Severe systemic reaction that causes a decrease in systemic

vascular resistance with corresponding hypotension caused by a sensitizing antigen. 1

B. CAUSES OF ANAPHYLACTIC SHOCK

Anaphylaxis is a severe, whole-body allergic reaction to a chemical that has become an
allergen. An allergen is a substance that can cause an allergic reaction.
After being exposed to a substance such as bee sting venom, a person's immune system
becomes sensitive to it. When the person is exposed to the allergen again, an allergic
reaction may occur.
Anaphylaxis happens quickly after exposure. The disease is serious and affects the
entire body.
Tissues in different parts of the body release histamine and other substances. This
causes constriction of the airways and leads to other symptoms.
Some drugs (such as morphine, X-ray contrast dye, aspirin, and others) can cause an
anaphylactic-like reaction (anaphylactoid reaction) upon people's first exposure to them.
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

These reactions are not the same as the immune system response that occurs with true
anaphylaxis. However, the symptoms, risk of complications, and treatment are the same
for both types of reactions.
Anaphylaxis can occur in response to any allergen. Common causes include:
 Drug allergies
 Food allergies
 Insect stings/bites
 Pollens and other allergens that are inhaled very rarely cause anaphylaxis.
Some people have an anaphylactic reaction with no known cause.

Anaphylaxis is life-threatening and can happen at any time. Risks include a history of any
type of allergic reaction. 3

C. RISK FACTOR'S

Adults are at greater risk of allergic reactions compared to children; In this sense,
anaphylactic symptoms caused by general anesthesia, drugs and contrast media are
more common in adults.

The following are considered high risk factors:

- Asthma
- Atopy
- Allergy to nuts.
- Coexistence of food allergy and asthma.
- Presence of symptoms after exposure to minimal amounts of food.
- Adolescence.
- High sensitization with specific immunoglobulin E (IgE) (> 50 KU/L).

D. PATHOPHYSIOLOGY

Three separate processes participate in anaphylaxis, each of them being unique and
temporarily different. The first and second are not associated with any clinical manifestation;
The third involves a series of chain reactions of processes that characterize the so-called
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

anaphylactic shock. In the first stage, or sensitization, an antigen is introduced into the
victim, either through the skin or through the respiratory, gastrointestinal or genitourinary
system; or is administered by injection. The antigen stimulates plasma cells to make
antibodies of the IgE class. The second stage is called reversible binding and describes the
interaction between the Fc region of IgE molecules with specific receptors on basophils and
mast cells. These are the effector cells. The final step begins when the antigen is
reintroduced into the body and interacts with IgE molecules. The combination of antigen with
two neighboring receptors of IgE molecules is called cross-linking. This interaction facilitates
the intracellular biochemical phenomena of the effector cells that culminate in the release of
primary mediators. After the activation of basophils and mast cells, there is a biphasic
response in the intracellular levels of cAMP and cGMP. An initial rise in cAMP levels is
followed by a rapid decline. This decrease corresponds to the release of mediators into the
extracellular fluid. After the interaction between IgE and antigens, mast cells and basophils

They release a variety of substances during the acute reaction. These primary mediators are
preformed or synthesized de novo during cellular stimulation. Although most of these
mediators induce significant local effects, only histamine is able to reach the circulation in an
active state. Therefore, the symptoms of anaphylaxis can be attributed primarily to the local
action of multiple mediators released by mast cells, and to the systemic effects of histamine.
In short, most of the changes produced can be attributed to histamine, acting through H1 and
H2 receptors, prostaglandins and leukotrienes. The pathophysiology of the severe
manifestations of anaphylactic shock has been analyzed by several authors. The
consequences of mediator release by mast cells include an increase in vascular permeability
due to the formation of intercellular passageways between endothelial cells in postcapillary
venules. Increased vascular permeability produces tissue edema, leading to urticaria, if the
reaction is limited to the epidermis; angioedema if it extends to the dermis, laryngeal edema,
nasal congestion, and intestinal edema with abdominal pain, distension and diarrhea.
Contraction of smooth muscles produces bronchospasm and abdominal cramps. Vasodilation
is associated with flushing, headaches, reduced systemic vascular resistance, hypotension,
and syncope. Stimulation of nerve endings in the skin is responsible for pruritus, and
stimulation of cardiac histamine receptors produces tachycardia and possibly arrhythmias.

The vasodilatory shock that occurs in anaphylaxis results from multiple mechanisms,
including the excessive activation of vasodilatory mechanisms, such as the upregulation of
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

nitric oxide synthesis that activates soluble guanylate cyclase and produces cGMP, and the
synthesis of prostacyclins that activate soluble adenyl cyclase and produce cAMP, both
causing myosin dephosphorylation and vasorelaxation. Other mediators that are released by
non-IgE-dependent mechanisms can also produce shock by various mechanisms; for
example, protamine induces acute pulmonary vasoconstriction.

E. CLINICAL PICTURE

The clinical manifestations of anaphylactic reactions vary between mild and severe, and
are related to multiple factors, such as the dose, route and absorption of the antigen, as
well as the degree of sensitization of the victim.

GENERAL SYMPTOMS

 Skin: paleness, diaphoresis (sweating), pruritus (itching), hives and generalized

or regional edema (facial, around the eyes or mouth.
 Cardiovascular: tachycardia (heart rate greater than 90/minute), hypotension
(systolic blood pressure < 90 mmHg) and ventricular arrhythmias, manifested
by weak pulse, irregular or weak heart sounds, cold extremities and syncope
(fainting).
 Respiratory: edema of the glottis/epiglottis or severe bronchoconstriction,
manifesting dyspnea (difficult breathing, feeling of lack of air), dysphonia (voice
alteration), stridor (noisy breathing, similar to whistling), wheezing (similar
noises, heard with stethoscope) and cyanosis (dark blue-purple discoloration of
lips, nails, or other sites).
 Digestive: mainly diarrhea and vomiting.
 Nervous: anxiety, disorientation, dizziness, paresthesias (abnormal sensations
such as cold or numbness in the extremities or face), seizures, and loss of
consciousness.

F. DIAGNOSIS
 Physical examination: rapidly progressive manifestations that affect the skin and/or
mucous membranes appear acutely, accompanied by respiratory and/or circulatory
compromise.
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

 Some laboratory tests can help confirm the diagnosis, such as histamine or tryptase in
the blood; the latter is the most used currently. But these tests are not quick to perform,
and therefore you cannot wait for the results before starting treatment; They will serve
to confirm the suspected diagnosis later.

Tryptase in blood: this is the most used currently. It is a substance released by mast cells,
cells that when activated are capable of triggering the allergic reaction. Tryptase is capable
of promoting inflammation and bronchospasm; It rises in severe allergic reactions, reaching
the maximum level in the blood at the hour of the allergic reaction, and is eliminated quickly
(2 hours), so, 24 hours after said reaction, we can detect normal levels in the blood. . The
detection of constantly high levels of tryptase in the blood may be related to the presence
of other diseases, such as kidney or liver failure, as well as systemic mastocytosis, a
disease caused by the proliferation of mast cells.

G. TREATMENT

The sequence that should be followed in a patient with anaphylactic shock is the following:

1. Ensure airway and adequate ventilation.

2. Place the patient horizontally; If hypotension exists, elevate the lower limbs.
3. Discontinue the administration of any drug allegedly responsible for the episode.
4. In the presence of shock, replace blood volume with hydroelectrolyte solutions and 5%
albumin. If shock persists after adequate volume replacement and the administration of
norepinephrine, administer dopamine 5-15 µg/kg/min by intravenous infusion, or
epinephrine 2-4 µg/kg/min.
5. Determine the site of introduction of the allergen; If it is an extremity, a proximal
tourniquet is placed and epinephrine is administered locally: 0.3 to 0.5 ml of a 1:1,000
solution.
6. Infusion of catecholamines: subcutaneous or intravenous epinephrine: 0.3 to 0.5 ml of
1:1,000 solution every 5-10 minutes, or continuous infusion of 1-5 µg/min.
Norepinephrine infusion: 5 to 10 µg/min.
7. For the treatment of bronchospasm: repeat epinephrine, aminophylline 5 mg/kg in 10
minutes followed by 0.4 ml/kg/hour to maintain a plasma level of 10 to 20 µg/ml.
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

Iprapropium may be especially useful for the treatment of bronchospasm in patients who
have received β-blockers.
8. In patients treated with β-blockers, administer glucagon 1 to 2 mg IV or IM.
9. In the presence of ARDS, use mechanical respiratory assistance.
10. Blood pressure monitoring, electrocardiogram, blood gases, lactate, hematocrit, chest x-
ray, coagulation study. In surgery: pulse oximetry and PetCO2.
11. Other usable agents include: diphenhydramine 50-100 mg every 6-8 hours,
hydrocortisone 100 mg IV every 4 hours, cimetidine 300 mg IV every 3 hours.
12. Due to the effectiveness of vasopressin in shock with vasodilation, the drug should be
considered in the treatment of anaphylactic shock that does not respond to conventional
therapy.
13. Observation for 24-48 hours in the ICU due to the risk of repetition of the episode
(biphasic response).

Control of the airway and ventilation. The first priority is ventilation. An adequate airway must be
achieved since high obstruction is a significant risk. In this sense, the initial attempt should be
orotracheal intubation, but if this is not achieved, it is advisable to perform an emergency
cricothyroidotomy. Since these patients may present with pulmonary edema, it is advisable to
perform a chest x-ray using a portable device.

Attempts at tracheal intubation may increase laryngeal edema or compromise the airway with
blood in the oropharynx and further obstruction. Paralyzing patients after a failed attempt at
tracheal intubation can be fatal, because the glottic opening is narrowed and visualization may be
difficult due to lingual and oropharyngeal edema and the patient being apneic. If tracheal
intubation is unsuccessful, even mask ventilation may be impossible, because laryngeal edema
prevents air entry. Pharmacological paralysis at this point can deprive the patient of the only
ventilation mechanism, which is attempts at spontaneous ventilation.

Once endotracheal intubation has been performed, it is advisable to assist ventilation with a
volumetric respirator. FiO2, tidal volume, inspiratory pressure, and respiratory rate should be
adjusted to obtain a PaO2 of more than 60 mm Hg. It may be difficult to obtain an adequate tidal
volume due to the existence of intense bronchospasm that requires high peaks of airway
pressure.

Local treatment
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

When the anaphylactic phenomenon is subsequent to an insect bite or the injection of a drug, it is
advisable to use a local tourniquet on the affected limb in order to delay systemic absorption.
Local injection of epinephrine can also help reduce the absorption of the allergen.

Pharmacotherapy

Epinephrine is the drug of choice for the acute treatment of anaphylaxis since it allows reversing
severe manifestations such as bronchoconstriction and hypotension through increasing cAMP
levels in mast cells and basophils. The β-agonist effects of epinephrine improve the inotropic and
chronotropic conditions of the heart, and the α-agonist properties raise blood pressure by
increasing peripheral resistance. It should be used in subcutaneous or intramuscular doses of 0.3
to 0.5 ml of the 1:1,000 solution in mild reactions in adults, repeated every 10 to 15 minutes. In
the presence of severe reactions with cardiovascular manifestations, 1 mg of the drug should be
diluted in 10 ml of physiological solution and inject 0.1 to 0.2 mg intravenously every 5 to 10
minutes or less, depending on the effect obtained. It can also be administered intratracheally in
doses of 1-4 mg or by constant infusion in doses of 0.1-0.5 µg/kg/min. The dosage in children is
0.01 ml/kg up to a maximum of 0.3 ml of a 1:1,000 dilution.

Aminophylline is a very useful drug if bronchospasm persists after administration of epinephrine.

During an acute and severe reaction, aminophylline should be administered intravenously, using
a loading dose of 5-6 mg/kg in 20 minutes, followed by a continuous infusion of 0.4-0.9
mg/kg/hour.

Antihistamines block the peripheral effects of histamine through competitive inhibition at the level
of H1 and H2 receptors. The recommended drugs are diphenylhydramine in doses of 50-100 mg
IV and cimetidine in doses of 300 mg IV every 5 minutes.

Corticosteroids are useful to treat or prevent anaphylaxis reactions. They are also useful in
managing the urticarial reactions that accompany anaphylaxis. The recommended dose is 100 to
200 mg of hydrocortisone at four to six hour intervals.

Shock treatment. A fundamental therapeutic maneuver in the treatment of anaphylactic shock is

the administration of fluids in order to compensate for hypovolemia. The liquids to be
administered include electrolyte solutions and in severe cases albumin or plasma expanders. In
general, large volumes of fluids are required: 1,000 to 2,000 ml should be administered quickly,
depending on blood pressure.
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

In patients with β-adrenergic blockade, up to five to seven liters may be required to achieve
hemodynamic stability. If rapid resolution of shock is not achieved, placement of a pulmonary
artery catheter is recommended to monitor cardiac function.

If the shock state persists despite the administration of plasma expanders, additional use of
adrenergic agents should be resorted to. For this purpose, the preferred drug is epinephrine in
repeated intravenous doses of 0.1-0.2 µg every 5 to 10 minutes. When hypotension persists
despite this treatment, some authors recommend continuous intravenous infusion of 2 to 4
µg/min, with continuous monitoring of blood pressure and electrocardiogram. Dopamine infusion,
at doses of 5 to 15 µg/kg/min, is also a useful option for the treatment of shock refractory to
treatment with volume expanders.

H. NURSING CARE IN ANAPHYLACTIC SHOCK

a) Previous Considerations:
 Always know, record and highlight the existence or not of the patient's allergies
in the nursing assessment upon admission, the treatment sheet and in the care
plan.
 Avoid contact of the patient with the declared allergen.
 Take special caution with food allergies, both when requesting the diet and when
administering it.
b) Anaphylactic Reaction Detection
 The most frequent symptoms in an anaphylactic reaction are: 80% cutaneous
(urticaria, angioedema, pruritus), respiratory (bronchospasm, dyspnea),
cardiovascular (hypotension, altered heart rate), gastrointestinal (nausea,
vomiting) and/or neurological ( headache, confusion mint).
 The factors to take into account regarding the form of appearance and the nature
of an anaphylactic reaction are:
- The route of administration of the allergen.
- The amount that has been administered.
- The time elapsed since the last administration.
- Symptoms may appear within minutes or hours.
- The degree of hypersensitivity of the person.
 NATIONAL UNIVERSITY OF CAJAMARCA
FACULTY OF HEALTH SCIENCES
PROFESSIONAL ACADEMIC SCHOOL OF NURSING

 Keep in mind that if the patient is being treated with antihistamines or tricyclic
antidepressants, the anaphylactic reaction may be altered.

c) Immediate Care for the Patient With Anaphylactic Reaction

Once the anaphylactic reaction is confirmed, the following measures will be taken.
 Reassure the patient and provide emotional support throughout the process.
 Remove the allergen if possible:
- Discontinue any medication that is being administered.
- In case of anaphylaxis caused by food, do not induce vomiting, and try to
remove food remains from the mouth.
 Seek nursing support and notify the responsible doctor.
 Place the patient in a safety position.
 Maintain the airway patent.
 Administer oxygen.
 Simultaneously monitor vital signs while the emergency situation lasts.
 Have the stop car nearby.
 Cannulate a large-caliber peripheral vein if possible, and administer the prescribed
medication.
 The most common drugs prescribed in anaphylactic reactions are: adrenaline,
bronchodilators, glucagon, atropine, vasopressor drugs and antihistamines.
 Initiate cardiopulmonary resuscitation if cardiopulmonary arrest occurs.
 Accompany the patient in his transfer to the intensive care unit if necessary.