Anaphylaxis

1. Hoang Cuong MS-V
HaNoi Medical University

2. CONTENTS
• Introduction
• Triggers and Etiology
• Risk Factors
• Types of Reaction
• Pathophysiology
• Signs and Symptoms
• Diagnostic Criteria
• First Aid and Treatment
• Prevention

3. Definitions
Anaphylaxis is a severe, life-threatening manifestation of a systemic immediate
hypersensitivity reaction that necessitates prompt medical intervention:
• Anaphylaxis is a systemic reaction resulting from the sudden release of multiple
mediators (not just histamine) from mast cells and basophils.
• Anaphylaxis is defined by a wide spectrum of symptoms and their severity
• Although “shock” may occur during anaphylaxis, it most often occurs in the
absence of shock, hypoxia, or collapse
• Quick recognition of anaphylaxis is critical for successful treatment
• Severe immediate (type I) hypersensitivity reaction.
- The term “anaphylaxis” has traditionally → IgE-dependent events, and the term “
anaphylatoid reaction” → IgE-independent events.

5. Triggers and Etiology
• Usual triggers (allergens) are foods, insect stings, medication or Natural latex.
Exercise is a rare trigger.
• Food Triggers: Peanut, milk, shellfish, tree nuts, egg, wheat, soy.
• Medications Triggers: β–lactam antibiotics (ie, penicillins and
cephalosporins), NSAIDs, anesthetics,..
• Stinging Insects Triggers: Stings of Hymenoptera
• Other Triggers: Latex, and idiopathic,…
• Foods are most common trigger in children, teen and young adults.
• Insect stings and medications are relatively common triggers in middle-aged
and elderly adults.

6. Triggers and Etiology
Strenuous exercise can trigger anaphylaxis in some individuals. The
following factors may play a role:
• Food (that can normal be eaten without problem)
• Medication, weather and menses
• Gender (more women than men are affected)
• Having another allergy
Experts usually advice those at risk of exercise–induced anaphylaxis not
to eat for at least four hours preceding exercise

7. Triggers and Etiology
Unknown origin (idiopathic)
• Reactions are classified as idiopathic when an individual has an
anaphylactic reaction and an allergist has been unable to identify a
specific cause.
• These reaction are particularly dangerous since the patient doesn’t know
what to avoid.

8. Triggers and Etiology
Causes of anaphylaxis in a study of 266 patients (Data from Kemp et al)
34%
37%
20%
7% 2%
Food
Idiopathic
Drugs
Exercise
Latex, hormone, Insect Bites

9. Figure:
Anaphylaxis mechanisms
and triggers

10. RISK FACTORS
When anaphylaxis can become worse or fatal?
Potential associated factors that can cause that can cause more severe forms and
fatal allergies includes:
• Age
• Physiologic state (such as pregnancy)
• Concomitant diseases:
 Poorly controlled asthma
 Cardiovascular disease
• Concurrent use of medications:
 Beta-adrenergic blockers
 ACE inhibitors
• Amplifying co-factors:
 Exercise
 NSAIDs
 Infections, emotional stress, peri-menstrual status

11. Figure:
Patient factors that
contribute to anaphylaxis

12. Types of Reaction
• Uni-Phasic ― The most common type, 80-90% of all cases. Isolated reaction producing
signs and symptoms within minutes (typically within 30 minutes) of exposure to an offending
stimulus
• Protracted ― Severe anaphylactic reaction that may last between 24 and 36 hours despite
aggressive treatment
• Bi-Phasic ― Late-phase reactions that can occur 1 to 72 hours (most within 10 hours) after
the initial attack (1%-23%)
Treatment
Initial
Symptoms
Treatment Treatment
8 to 12 hours1
30 minutes to 72 hours2
First Phase Second PhaseAsymptomaticInitial Symptoms
Treatment

13. Types of Reaction
• Biphasic reactions occur in up to 23% of cases of anaphylaxis. In the
largest study, the average time to onset of recurrent symptoms was 10
hours after resolution of initial symptoms.
• The severity of recurrent symptoms is unpredictable. In most patients,
recurrent symptoms are less severe than the initial symptoms, and
isolated urticarial is common. However, recurrent symptoms are not the
same as initial symptoms and in a minority of patients, can be more
severe or even fatal.
• Patients who are discharge following anaphylaxis should be informed
about the possibility of recurrent symptoms for up to three days after the
initial symptoms.

14. Types of Reaction
Cases — Protracted
• “A 33-year-old male developed hives in the groin, followed the next day by
abdominal cramps and bloating, vomiting, angioedema of the lip, wheezing,
tightness of the throat, and generalized hives. He attributed these
symptoms to clams eaten 14 hours before the onset of symptoms. On day 3,
the gastrointestinal symptoms continued, and he developed transient
lightheadedness. He presented to the hospital on day 4 with continued
urticarial, gastrointestinal discomfort, and mild tachycardia. Evaluation was
unrevealing, and he was treated with diphenhydramine, cimetidine, and
intravenous fluids, with gradual improvement over the next two days.
Serum tryptase samples drawn on the fourth and fifth days of illness were
elevated, with return to normal immunoassay to clam was negative at the
time of hospitalization but low-positive several months later”

15. Types of Reaction
Cases — Biphasic
• “A 76-year-old atopic male sustained approximately 15 vespid stings.
Within 10 minutes, he developed urticarial, erythema, and hypotension
(90/60mmHg, measured by a family member). A clinician was called to his
home. Upon evaluation, the patient had cutaneous signs and symptoms but
no objective respiratory, CNS, or cardiovascular abnormalities, and his BP
had returned to normal (120/70mmHg). He was treated with parenteral
“antihistamine and corticosteroid” and observed for 45 minutes in his
home. The urticarial subsided, and the clinician left the home.
Approximately 40 minutes after the departure of the clinician, the patient
again developed urticarial, followed by angioedema of the neck. The
symptoms worsened, and the clinician was called back. The patient died,
despite attempts at resuscitation”

16. Pathophysiology
• The mechanism responsible for most cases of human anaphylaxis involves
IgE. Possible alternative mechanisms remain incompletely understood.
• The WAO categorizes anaphylaxis as either immunologic or non-
immunologic:
o Immunologic anaphylaxis ― Immunologic anaphylaxis includes:
 IgE-mediated reactions
 IgG-mediated reactions (which have not been identified in humans)
 Immune complex/complement-mediated reactions
o Non-immunologic anaphylaxis ― caused by agents or events that sudden,
massive mast cell or basophil degranulation, without the involvement of
antibodies.

17. Pathophysiology
• Allergens (aeroallergens) enter the tonsils → taken up
and degraded by APCs (Antigen-presenting cells).
• ACPs then interact with T helper type 2 (Th2) cells and
B cells in the lymph nodes → allergen-specific IgE
production.
• The IgE enters the blood stream and the diffuses
through tissues (especially the skin and mucosal tissues
of the respiratory and gastrointestinal tracts)
• The IgE binds to high-affinity Fc receptors (Fc-epsilon-
RI) on the surface of the tissue mast cells and
circulating basophils

18. Pathophysiology
• When these IgE-coated cells encounter that specific
aeroallergen subsequently, they become activated,
leading to release of inflammatory mediators, which
results in the signs and symptoms of IgE-mediated
allergic reactions.
• In IgE-mediated anaphylaxis, the activation of mast
cells, basophils, and eosinophils→ release of
performed inflammatory mediators, including
histamine, tryptase, chymase, heparin, histamine-
releasing factor, and platelet-activating factor (PAF).
Cellular activation →stimulates the production of
lipid-derived mediators: prostaglandins and
cysteinyl leukotrienes.

21. Pathophysiology
Two Phases
Immediate (minutes) Late (Hours)
Antigen crosslinks preformed IgE
on presensitized mast cells →
immediate degranulation →
release of histamine (a vasoactive
amine) and tryptase (a marker of
mast cell activation)
Chemokines attract inflammatory
cells, eg, eosinophils) and
cytokines (eg, leukotrienes) from
mast cells → inflammation and
tissue damage

22. Signs and Symptoms
• Temporal course ― Anaphylaxis is usually characterized by the rapid onset
of symptoms over a period of minutes to hours following exposure to a
trigger.
• Factors affecting the time course ― Temporal course of anaphylaxis are not
entirely defined. Several factors appear to be involved:
 The route through which the allergen enters the body→ one factor in
determining the rapidity of onset of symptoms. Injected or Intravenously-
administered allergens cause symptoms in seconds to minutes; while ingested
allergens → in minutes to one hour or two.
 The type of allergen: IgE-mediated anaphylaxis triggered by protein allergens
(the best characterized type of allergen), symptoms usually begin within two
hours of trigger exposure. In contrast, triggered by carbohydrate allergens,
such as some anaphylaxis to mammalian meats and to the monoclonal drug
cetuximab → appear four to six hours after exposure

23. Signs and Symptoms
— Skin
Feeling of warmth, flushing (erythema), itching, urticaria,
angioedema, and pilor erection
— Respiratory
Nose – Itching, congestion, rhinorrhea, and sneezing.
Laryngeal – Itching and tightness in the throat, dysphonia,
hoarseness, stridor
Lower airways – Dyspnea, chest tightness, cough, wheezing,
and cyanosis.
— Gastrointestinal Nausea, abdominal pain, vomiting, diarrhea, and dysphagia.
— Cardiovascular
Felling of faintness or dizziness; syncope, altered mental
status, chest pain, palpitations, tachycardia, bradycardia, or
other dysrrhythmia, hypotension, tunnel vision, hearing,..
— Neurological
Anxiety, apprehension, sense of impending doom, seizures,
headache and confusion...

24. Signs and Symptoms
17%
40%
31%
73%
74%
0% 10% 20% 30% 40% 50% 60% 70% 80%
Gastrointestinal
Neurological
Cardiovascular
Skin
Respiratory
Organ system Involvement Reported by Patients with Anaphylaxis in
Most Recent Reaction (N=344)

25. Signs and Symptoms
66%
58%
54%
46%
40%
33%
20%
20%
20%
17%
13%
1.50%
0% 10% 20% 30% 40% 50% 60% 70%
Increased Breathing Rate or Difficulty Breathing
Skin Reactions
Swelling of Eyes, Lips, Tongue
Coughing, Wheezing, Chest Tightness
Feelings of Uneasiness, Irritability, or Anxiety
Throat Itching
Hoarse Voice
Sudden Behavioral Change
Dizziness, Low Blood Pressure, or Fainting
Cramps, Abdominal Pain, Vomiting, or Diarrhea
Loss of Consciouness
Loss of Bladder or Bowel Control
Symptoms Reported by Patients with Anaphylaxis in their
Most Recent Reaction (n=344)

26. Signs and Symptoms
Anaphylaxis: Causes of Death
• Upper and/or lower Airway Obstruction (70%); Cardiac dysfunction (24%)
“In a review of 56 cases of fatal anaphylaxis for which autopsy data were available, all
food-induced reactions involved difficulty breathing, and respiratory arrest was the cause of
death in 13 of 16 cases [51]. In contrast, shock without respiratory compromise was the
presentation in most cases of venom- or medication-induced anaphylaxis”
Source: Uptodate.com
→ Most fatal food-induced reactions involve difficulty breathing and culminate
in respiratory. In contrast, venom- or medication-induced anaphylaxis more
often cause shock and cardiovascular collapse.

27. Diagnostic Criteria
AND AT LEAST 1 OF
THE FOLLOWING
 Respiratory compromise
(eg, dyspnea, wheeze-
bronchospasm)
 Reduced BP or associated
symptoms of end-organ
dysfunction
Acute onset of an illness with
involvement of the skin,
mucosal tissue, or both
≥2 of the following that
occur rapidly after
exposure to a likely allergen
(minutes to several hours)
Reduced BP after exposure
to known allergen (minutes
to several hours)
OR OR
 Involvement of the skin mucosal
tissue (eg, generalized hives, itch-
flush, swollen lips-tongue-uvula)
 Respiratory compromise (eg,
dyspnea, wheeze-bronchospasm,
stridor, hypoxemia)
 Reduce BP* or associated
symptoms (eg, hypotonia,
collapse, syncope, incontinence)
 Persistent gastrointestinal
symptoms (eg, crampy
abdominal pain, vomiting)
• Infants and children -
Low SBP (age-specific)*
or greater than 30%
decrease in SBP
• Adults – SBP of less than
90mmHg or greater than
30% decrease from that
person’s baseline

28. Figure:
Clinical criteria for the
diagnosis of anaphylaxis

29. First Aid and Treatment
Protocol
1. Place the patient on the back ( or in a position of comfort if there is
respiration distress and/or vomiting)
2. Elevate the lower extremities
3. Administer adrenaline*
4. Assess circulation, airway, breathing, and mental status, skin, and other
visual indictors.
Adrenaline
Intramuscularly administered-adrenaline (epinephrine) is life-saving for the
treatment of anaphylaxis:
o It relieves the symptoms of anaphylaxis including preventing, and
relieving, airway obstruction via beta-2 adrenergic effects caused by
mucosal edema and smooth muscle concentration
o It prevents and relieves fall in blood pressure and shock.

30. o Epinephrine is life-saving in anaphylaxis. It should be injected as early as possible in the episode
in order to prevent progress of symptoms and signs. There are NO absolute contraindication to
epinephrine use, and it is the treatment of choice for anaphylaxis of any severity. We
recommend epinephrine for patients with apparently mild symptoms and sign (eg, a few hives and
mild wheezing) as well as for patients with moderate-to-severe symptoms and sign.
o The route of epinephrine administration depends upon the presenting symptoms. For patients
who are not profoundly hypotensive or in shock or cardiorespiratory arrest, intramuscular (IM)
injection into the mild-outer thigh as the initial route of administration is advised, in preference
to subcutaneous administration or intravenous (IV) administration.
o IV epinephrine is indicated for patients with profound hypotension or symptoms and signs
suggestive of impending shock (dizziness, incontinence of urine or stool) who do not respond to
initial IM injections of epinephrine and fluid resuscitation.
o Massive fluid shifts can occur in anaphylaxis, and all patients with orthostatic, hypotension, or
incomplete response to epinephrine should receive large volume fluid resuscitation with
normal saline. Normotensive patients should receive normal saline to maintain venous access in
case their status deteriorates.
o Supplemental oxygen and bronchodilators should be administered to patients with respiratory
sign or symptoms.
Source: Uptodate.com

32. First Aid and Treatment
• The first and most important treatment in anaphylaxis is epinephrine. The are NO absolute contraindications
to epinephrine in the setting of anaphylaxis.
• Airway: Immediate intubation if evidence of impending airway obstruction from angioedema. Delay may
lead to complete obstruction. Intubation can be difficult and should be performed by the most experienced
clinician available. Criothyrotomy may be necessary.
• Promptly and simultaneously, give:
 IM epinephrine (1mg/mL preparation): Give epinephrine 0.3-0.5 mg IM, preferably in the mid-outer thigh.
Can repeat every 5 to 15 minutes (or more frequently), as needed. If epinephrine is injected promptly IM,
most patients respond to one, two, or at most, three doses. If symptoms are not responding to epinephrine
injections, prepare IV epinephrine for infusion.
 Place patient in recumbent position, if tolerated, and elevate lower extremities.
 Oxygen: Give 8 to 10L/minutes via facemask or up to 100% oxygen, as need.
 Normal saline rapid bolus: Treat hypotension with rapid infusion of 1 to 2 liters IV. Repeat, as needed.
Massive fluid shifts with severe loss of intravascular volume can occur.
 Albuterol (salbutamol): For bronchospasm resistant to IM epinephrine, give 2.5 to 5mg in 3mL saline via
nebulizer. Repeat, as needed.

33. First Aid and Treatment
• Adjunctive therapies:
 H1 antihistamine*: Consider giving diphenhydramine 25 to 50 mg IV (for relief of urticarial and itching
only)
 H2 antihistamine*: Consider giving ranitidine 50mg IV.
 Glucocorticoid*: Consider giving methylprednisolone 125 mg IV.
 Monitoring: Continuous noninvasive hemodynamic and pulse oximetry monitoring should be
performed. Urine output should be monitored in patients receiving IV fluid resuscitation for severe
hypotension or shock.
• Treatment of refractory symptoms:
 Epinephrine infusion: For patients with inadequate response to IM epinephrine and IV saline, give
epinephrine continuous infusion.
 Vasopressors: Some patients may require a second vasopressor (in addition to epinephrine)
 Glucagon: Patients on beta-blockers may not respond to epinephrine and can be given glucagon 1 to 5
mg Iv over 5 minutes, followed by infusion of 5 to 15 mcg/minute.

35. Guidelines Clearly Position Epinephrine as First-line Therapy
WAO Anaphylaxis
Guideline
Anaphylaxis
Practice Parameter
NIAID-Sponsored
Expert Panel on Food
Allergy
ICON; Food
Allergy
• Epinephrine has a
primary role in the
management of
anaphylaxis
• Prompt IM injection
of epinephrine, the
first-line medication,
should not be delayed
by taking the time to
draw up and
administer adjunctive
medications, such as
antihistamines and
glucocorticoids
• Epinephrine is the
drug of choice for
the treatment of
anaphylaxis.
• The appropriate dose
of epinephrine
should be given
promptly at the onset
of apparent
anaphylaxis
• Epinephrine is the first-
line treatment in all cases
of anaphylaxis
• When there is suboptimal
response to the initial dose
of epinephrine, dosing
remains first-line therapy
over adjunctive treatments
• Upon discharge, 2 doses
by auto-injector should be
prescribed
• Epinephrine is
the first-line
treatment for
anaphylaxis.
• Upon discharge, 2
doses by auto-
injector should be
prescribed.
• Patients must be
educated on when
and how to use the
epinephrine auto-
injector device.

36. Why Epinephrine?
• Failure to administer epinephrine promptly is most important factor
contributing to death in children and adolescents with anaphylaxis.
• H1 antihistamine → useful for relieving itching and urticaria, but do not
relieve stridor, shortness of breath, wheezing, GI symptoms and signs,
hypotension, or shock → should not be substituted for epinephrine.
• Bronchodilators does not prevent or relieve upper airway edema,
hypotension, or shock → should not be substituted for epinephrine.
• The onset of action of glucocorticoids takes several hours → these
medications do not relieve the initial symptoms and signs of anaphylaxis →
to prevent the biphasic or protracted reactions that occur in some cases of
anaphylaxis.

37. Action of Epinephrine?
• α1-adrenergic receptor:
 ↑ Vasoconstriction (at low doses)
 ↑ Peripheral vascular resistance
 ↑ Heart rate
 ↑ Mucosal edema
• α2-adrenergic receptor:
 ↓ insulin release
• β1-adrenergic receptor:
 ↑ Inotropic
 ↑ Chronotropic (heart rate)
• β2-adrenergic receptor:
 ↑ Bronchodilation
 ↑ Vasodilation
 ↑ Glycogenolysis
 ↓ Mediator release

38. ACE inhibitors, β-blockers, and Anaphylaxis
• Anaphylaxis → allergen cross-linking of IgE on mast cells and basophils
→ Degranulation and release of histamine, tryptase, chymase, platelet-
activating factor, prostaglandins, and leukotrienes → (Histamine)
causes vasodilation leading to ↑ vascular permeability and decreased
peripheral vascular resistance → activation of RAS, a
compensatory mechanism blocked by ACE inhibitors.
• Histamine release also ↑ cardiac rate, cardiac contractility, and
bronchoconstriction → β-blockers mask cardiac signs of anaphylaxis
and lead to unopposed α-adrenergic activity → severe
bronchoconstriction.
• Management of anaphylaxis with concomitant β-blockers use
→ ↓ response to epinephrine and/or inhaled bronchodilators.

39. ACE inhibitors, β-blockers, and Anaphylaxis
• Glucagon activates adenylyl cyclase
(CA) directly and can bypass the beta
blockade

40. Fatal asthma or anaphylaxis?
• Case 1:
A 4 year old boy was brought to hospital by ambulance, having suffered a cardiorespiratory arrest at home. He had
asthma that was well controlled with occasional Salbutamol via inhaler and he had had no previous hospital
admissions.
On the day of presentation, he appeared to choke after eating a meal of seafood and rapidly developed gasping
respirations. He also had an episode of profuse diarrhoea. His parents gave Salbutamol via his inhaler and
immediately summoned an ambulance, believing that their child was suffering an asthma attack.
The child became apnoeic and neighbours started CPR. On arrival of the paramedic crew, 30 minutes after the
collapse, the child was asystolic and apnoeic. He was intubated in the field and managed according to standard ALS
guidelines. Cardiac output was obtained within 45 minutes of the initial event. En route to hospital, the child
required a further four doses of intravenous adrenaline (epinephrine) 0.1 ml/kg 1 in 1000 to alleviate
bronchospasm.
He was apnoeic on arrival at the hospital. He was transferred to the paediatric intensive care unit (PICU) for
mechanical ventilation and a dopamine infusion was added for further inotropic support.
Throughout the resuscitation, the child’s pupils were fixed and dilated. In PICU, no spontaneous breaths were noted.
Brain stem death was confirmed clinically and ventilation was ceased 16 hours after the respiratory arrest.
Significantly, his IgE concentration were increased (1271 kU/l) and mast cell tryptase level, taken over 12 hours
after the anaphylactic event began, was 7.9 μg/l (range 0–15 μg/l). No definite trigger was found with RAST testing
for crab, chicken, and peanut being negative. No necropsy was performed in accordance with the parents’ wishes
Source: BMJ journals – Emergency Medicine Journal

41. • Case 2:
A 9 year old girl was diagnosed with asthma at 3 years of age and had required several hospital admissions when the family
lived overseas. One admission necessitated intensive care, but the child had not been ventilated.
Five days before presentation, she developed coryzal symptoms and her general practitioner started cephaclor
suspension. Over the next two days, her cough and fever persisted and she became increasingly breathless, requiring
admission to her local hospital on the third day of the illness. An urticarial rash was noted and was attributed to
intravenous hydrocortisone, which had been administered for the wheeze. The urticaria abated after oral
promethazine (Phenergan) and prednisone. The girl was discharged after 36 hours, with Salbutamol nebulisers every four to
six hours, supplementing her inhaler. Her mother was also advised to stop the cephaclor.
On the day of presentation to our hospital, her mother gave a dose of cephaclor. Within 15 minutes of receiving the
antibiotic, the child complained of abdominal pain and then vomited, accompanied by diarrhoea. She became
increasingly short of breath and collapsed. Her mother initiated CPR and the child was unconscious for 20 minutes until
the paramedic crew arrived.
She was intubated and was asystolic, being managed according to standard ALS guidelines. Nine minutes into the
resuscitation, she developed ventricular fibrillation and received 100 J DC shock. She then went from electromechanical
dissociation to sinus bradycardia and received three doses of intravenous adrenaline 0.1 ml/kg of 1 in 1000 and one
of intravenous atropine 20 μg/kg. On arrival at hospital, she was breathing spontaneously but her chest was noted to be
hyperexpanded with bilateral reduction of air entry. No urticaria was noted before or after the administration of
intravenous hydrocortisone. A Salbutamol infusion was started before transfer to PICU. Her pupils were fixed and dilated
from the time of arrival in the emergency department and her gag reflex was also noted to be absent.
There was no improvement in clinical status despite ventilation and intravenous bronchodilators with corticosteroids. The
clinical finding of brain stem death was confirmed by a cerebral perfusion scan. Care was withdrawn in accordance with
the parents’ wishes.
Her IgE was increased (765 kU/l) and RAST for amoxycillin, cephalothin and cephaclor were weakly positive. RAST for
cephalexin was equivocal. A necropsy was not performed in respect of the parents’ cultural beliefs

42. • DISCUSSION
- The diagnosis of anaphylaxis is often overlooked in children with asthma.
- The classic clinical picture of anaphylaxis has an acute precipitous – case 1, but a multiphasic reaction –
case 2, is not unusual.
→ Four lessons to be draw from these cases:
• Firstly, when dealing with a child with rapid onset of wheeze or one who is slow to respond to
bronchodilators → enquire about the subtle features of anaphylaxis.
• Secondly, the usual triggers for anaphylaxis are medications and foodstuffs → may be confirmed by
specific RAST and mast cell tryptase levels.
• Thirdly, where anaphylaxis is suspected → early use of adrenaline, whether IM or IV in extremis, is
mandatory.
• Finally, children with features of acute asphyxic asthma → should be screened for allergens and have IM
adrenaline as an element in their asthma management plans

43. Why is the recommendation for epinephrine injection in the
lateral thigh muscle?
• This fast uptake of epinephrine is critical in the treatment of
anaphylaxis
• As opposed to the upper arm, the thigh muscle is one of the body’s
largest muscles with more blood supply → much faster absorption.
• The lateral thigh versus the anterior thigh muscles, because it
provides a skin area with thinner and less fat.
• The subcutaneous body fat tends to be thinner allowing IM access
most readily at this location
• Previously the recommendations → use SQ injections to minimize the
risk of inadvertent intravenous injection, but this minimal risk is more
than compensated by the greater benefit in treating an immediate,
potentially life-threatening condition (The median time to cardiac or
respiratory arrest in fatal food allergy reactions ~ 30 minutes, for
insect anaphylaxis ~ 15 minutes and for in hospital medicine reactions
~ 5 minutes) → Time for treatment is critical.
Source: AAAAI – American Academy of Allergy Asthma & Immunology

45. Intravenous Fluids
• Fluid resuscitation should be initiated immediately in patients who present with orthostasis,
hypotension, or incomplete response to IM epinephrine.
• Adults → receive 1-2 liters of normal saline at the most rapid flow rate possible in the first minutes.
(large volumes of fluid may be required)
• Children should receive normal saline in boluses of 20mL/kg, each over 5-10 minutes, and repeated,
as needed (Large volumes of fluid may be required- up to 100mL/kg)
• Normal saline is preferred over other solutions in most situations because other solutions have
potential disadvantages:
 Lactated Ringer (LR) solution → can potentially contribute to metabolic alkalosis, although large
volumes of normal saline can cause Hyperchloremic metabolic acidosis → change from normal saline
to LR if very large volumes are proving necessary.
 Dextrose → rapidly extravasated from the circulation into the interstitial tissues.
 Colloid solutions (eg, albumin or hydroxyethyl starch) → confer no survival advantage in patients
with distributive shock and are more costly
(Patients should be monitored carefully and continuously for clinical response and for volume overload)
Source: Uptodate.com - Anaphylaxis: Emergency treatment

46. Prevention
• It is important to advise patients about the need to have as-advised regular
follow-up visits with a physician, preferably an allergy/immunology
specialist, to:
• Confirm their specific trigger (s) of anaphylaxis
• Prevent recurrences by avoiding the specific trigger(s)
• Have an emergency action plan and emergency medication on hand
• Have support from the family members
• Receive immunomodulation, where it is clinically approved and relevant

47. Prevention
These are the usual recommendations for patients and their caregivers:
• Learn exactly what allergens have to be avoided
• Be especially careful when eating out, traveling or far from a medical facility
• Make sure friends, family, caregivers, and medical professionals know about the
allergy
• For Food Allergies:
 Wash hands before/after handling food
 Learn how to read a food label and check ingredient labels carefully each time
 Do not share drinking cups, straws, and utensils
 If product ingredients are unlisted, check with manufacturer
 If unsure, DO NOT EAT