ANAPHYLAXIS

ANLIDYA PERMATASARI G.
 DEFINITION
• The Joint Task Force on Practice Parameters, representing the American
Academy of Allergy, Asthma and Immunology (AAAAI), the American
College of Allergy, Asthma and Immunology (ACAAI), and the Joint
Council of Allergy, Asthma and Immunology (JCAAI)  defined
anaphylaxis as “a condition caused by an [immunoglobulin E] IgE-
mediated reaction” that is “often life-threatening and almost always
unanticipated.”
• Coomb dan Gell (1963)  anaphylaxis is a type I hypersensitivity
(immediate type reaction).
• Anaphylactoid reactions were defined as non-IgE-mediated reactions with
the same clinical picture as anaphylaxis. When both IgEmediated and non-
IgE-mediated mechanisms were a possible cause, the term anaphylactic
was used to describe the reaction.
EPIDEMIOLOGY
The Rochester Epidemiology Project (2008):
• 75.1 per 100,000 person-years in children aged 9 years
• 65.2 per 100,000 person-years in children aged 10-19-years old
• More common in boys until the age of 15 years
Anaphylaxis
mechanisms
and triggers
MILK, EGGS,
WHEAT, AND SOY
(MEWS)  Most
common
Patient
factors that
contribute to
anaphylaxis
 CLINICAL MANIFESTATION
Skin, subcutaneous tissue, and mucosa
Flushing, itching, urticaria (hives), angioedema, morbilliform rash, pilor erection
Periorbital itching, erythema and edema, conjuncitval erythema, tearing
Itching of lips, tongue, palate, and external auditory canals; and swelling of lips, tongue, and uvula
Respiratory
Nasal itching, congestion, rhinorrhea, sneezing
Throat itching and tightness, dysphonia, hoarseness, stridor, dry staccato cough
Lower airways: increased respiratory rate, shortness of breath, chest tightness, deep cough,
wheezing/bronchospasm, decreased peak expiratory flow
Cyanosis
Respiratory arrest
Gastrointestinal
Abdominal pain, nausea, vomiting (stringy mucus), diarrhea, dysphagia
Cardiovascular system
Chest pain
Tachycardia, bradycardia (less common), other arrhythmias, palpitations
Hypotension, feeling faint, urinary or fecal incontinence, shock
Cardiac arrest
Central nervous system
Aura of impending doom, uneasiness (in infants and children, sudden behavioral change, eg. irritability, cessation of
play, clinging to parent); throbbing headache (pre-epinephrine), altered mental status, dizziness, confusion, tunnel
vision
Other
Metallic taste in the mouth
Cramps and bleeding due to uterine contractions in females
CLINICAL MANIFESTATION
SKIN
EYE
NOSE AND MOUTH
LUNG AND THROAT
HEART AND CIRCULATION
GASTROINTESTINAL
NERVOUS SYSTEM
• Typically, exposure to the triggering allergen is followed by the
rapid development of symptoms over minutes to several hours.
TIME COURSE OF REACTION:
• Uniphasic (occurring immediately after exposure and resolving
with or without treatment in minutes to hours)
• Biphasic (recurring after the apparent resolution of initial
symptoms, usually about 8 h after the first reaction)
• Protracted (persisting for hours or days following the initial
reaction)
• Early recognition of signs and symptoms, timing of the reaction,
and existence of comorbid conditions and concomitant factors can
aid in diagnosis
CLINICAL
CRITERIA
DIFFERENTIAL
DIAGNOSIS
POSITION
• Although it is generally recommended to place the patient in a
recumbent position with lower extremities elevated, individuals
who are experiencing respiratory distress, which is common in
children, and/or vomiting should instead be placed in a comfortable
position with lower extremities elevated. This accomplishes 2
therapeutic goals: 1) preservation of fluid in the circulation (the
central vascular compartment), an important step in managing
distributive shock; and 2) prevention of the empty vena
cava/empty ventricle syndrome, which can occur within seconds
when patients with anaphylaxis suddenly assume or are placed
in an upright position.
EPHINEPHRINE
SECOND LINE MEDICATIONS
• Histamine-1 (H1) blockers such as diphenhydramine can relieve
itching, flushing, urticaria, angioedema, and nasal and eye symptoms,
but do not prevent or relieve upper airway obstruction, hypotension, or
shock have no role as a substitute for epinephrine
• Histamine-2 (H2) blockers such as ranitidine has efficacy for adults
with urticaria. No studies have specifically assessed their efficacy for
treating anaphylaxis
• Beta-2 adrenergic agonist such as salbutamol  additional treatment
for wheezing, coughing, and shortness of breath not relieved by
epinephrine have minimal α-1 adrenergic agonist vasoconstrictor
effects and do not prevent or relieve laryngeal edema and upper airway
obstruction, hypotension, or shock
• Glucocorticoids switch off transcription of a multitude of activated
genes that encode proinflammatory proteins, the onset of action of
systemic glucocorticoids takes several hours  potentially relieve
protracted anaphylaxis symptoms and prevent biphasic anaphylaxis
REFRACTORY ANAPHYLAXIS
• Intubation as indicated
• Patients unresponsive to fluid resuscitation should receive
vasopressors as follows:
• Epinephrine (0.1-1 mcg/kg/min IV) should be considered as the initial
vasopressor in children. Doses at < 0.3 mcg/kg/min will tend to have
more β-activity, whereas α-action becomes more pronounced at higher
doses
• Dopamine (2-20 mcg/kg/min IV) may be used in addition to epinephrine.
Greater α-activity is seen at higher doses
• Norepinephrine (0.1-2 mcg/kg/min IV) is a potent vasopressor. It is
usually considered in children unresponsive to epinephrine
BIPHASIC
• Biphasic anaphylaxis: up to 11% of children with anaphylaxis
• Can occur up to 72 hours (peak 8-10 hours)
Epinephrine auto-injectors (EAIs)
• Children at risk for anaphylaxis may need to carry 2 doses of
epinephrine  the first dose may not be administered effectively,
symptoms may persist despite a successful first injection, or the
patient may experience biphasic anaphylaxis.
• Existing EAIs  EpiPen, TwinJect, Adrenaclick, Anapen, Jext
available in 2 pre-set doses of epinephrine (0.15 and 0.3 mg)  0.15
mg for children who weigh 10–25 kg and 0.3 mg for those who
weigh >25 kg
• Current EAIs have a needle length of 1.27 cm for the 0.15 mg dose
EAI and 1.58 cm for the 0.3 mg dose EAI  may be too short to
penetrate the subcutaneous tissue to achieve intramuscular
injection in children who are overweight or obese
PROGNOSIS
• A 6-fold increase in anaphylaxis hospitalizations with stable
mortality rates (0.047 cases per 100,000 population) was observed
over the past twenty years  this may be due to rising concern
that many patients with anaphylaxis are at risk for biphasic
reactions
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) (ex avoidance of
the drug or therapeutic substitution with a non–cross-reacting
medication)
• 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

Immunomodulation
• Immunomodulation is Immunotherapy with Hymenoptera venoms or
fire ant extracts which are effective therapies to reduce the risk of
anaphylaxis