Allergic Disorders in Children

PRESENTED TO MAIA KHUKHUNAISHVILI

PRESENTED BY AKANKSHA RANA
DOLLY PAL
HARSHITA
SHWETA THAKRAN
BATCH 7B2 LAB 3
Allergy
 It represents the clinical expression of
IgE-mediated allergic diseases that have a
familial predisposition and that manifest as hyper-
responsiveness in the target organs.

Atopy
It refers to the genetic tendency to develop allergic
diseases
Why Allergy Is Important?
 Allergy affects approximately 15-30% of the
general population around the world, most of
which are children.

 Most allergies interfere with sleep, intellectual

functioning and recreational activities, whereas
food allergy leads to considerable anxieties and
fear of accidentally ingesting some notorious
allergen.

• Allergies are chronic conditions and fighting them

may need a
change of lifestyle, or even profession, adhering
to a diet and to maintain allergen avoidance.
Types of Allergen

• There are 2 types of Allergens

(a) Allergens from the natural environment:

- high molecular weight compounds(> 10 kDa).
- most of these allergens have an enzymatic function
examples are: pollen, fungi , spores, house dust mites,
epidermis of house pets, insect venom, some food
proteins, etc.

(b) Allergens from a chemically contaminated

environment:
- usually low-molecular chemical compounds(<10kDa).
- need to bind to a carbohydrate to attach to IgE.
examples are: metals, drugs, additives to food products,
latex.
 Cells Involved In Allergic
Reactions
• CD4+ T cells play the central role in allergic inflammation.

• Types of CD4+:
 T helper 1 (TH1)
- Secretes IL-2, TNF-b, and interferon-g (IFN-g).
- Antagonize the allergic response.

 T helper 2 (TH2):
- Produces IL-4, IL-5, IL-6,IL-9,IL-10, and IL-13. IL-4 and IL-13
play the
main role in allergic response.

 T-regulatory (Treg) cells

- critical role in expression of allergic and autoimmune diseases.
- These cells have the ability to suppress effector T cells of
either the Th1 or
Th2 phenotypes
Mechanism of action of allergens

• Generally allergic reactions takes place in

following steps:

1) Primary Exposure

2) Secondary Exposure & Release of mediators

Allergic Cascade
Types of allergic reactions
Allergies to be covered....

 Allergic rhinitis
 Atopic dermatitis
 Urticaria and Angioedema
 Insect bites
 Food allergy
 Anaphylaxis
 Allergic Rhinitis

 Inflammatory disorder of the nasal mucosa

marked by nasal congestion, rhinorrhea, and
itching, often accompanied by sneezing and
conjunctival inflammation.
Common allergens
 Pollen

 House dust

 Mite

 Animal dander

 Smoke
 Symptoms of Allergic Rhinitis

• Recurrent episodes of sneezing

• Pruritus, rhinorrhea

• Nasal congestion and lacrimation

• Snorting throat clearing

• Postnasal drip.

• Nasal obstruction unilateral or bilateral

Related Anatomic Structures
Compromised by Allergic Rhinitis
 Sequelae Of Allergic Rhinitis
• Elongated facies
– Allergic shiners, allergic salute

• Nose
– Septal deviation, polyps, drainage, turbinate hypertrophy,
hyponasality

• Mouth
– Cobblestoning of oropharynx

•Chest
– wheezing

• Skin
Classification Of Allergic Rhinitis

•Intermittent allergic rhinitis :

Symptoms present for less than 4 days a week , or
for less than
4 consecutive weeks.

• Persistent allergic rhinitis :

Symptoms present for more than 4 days a week
and for more
than 4 consecutive weeks
Severity Of Allergic rhinitis
Allergic Rhinitis And Quality Of Life

• Sleep loss or disturbance

• Increased daytime sleepiness

• Learning problems

• Reduction in work productivity

Diagnosis
 The 3 most common tests used to confirm
the diagnosis
1)Skin testing
2)Nasal smear
3) In vitro testing for serum levels of specific IgE
antibodies.
Prevention : Avoidance Of Allergens

• Removing a pet from the house

• Covering pillows and mattresses

• Washing bedding with hot water

• Vacuuming mattresses and pillows.

No dry dusting
 Pharmacotherapy
Drug type Itch / Discharge Blockag Impaire
sneezing e d smell Preparation

Antihistamin +++ ++ + - Fexofenadin

es e
Cetrizine

Anticholinergic - +++ - - Ipratropium

s
Decongesta - +++ ++ - Xylometazoli
nts ne
Oxymetazoli
ne

Mast Cell + + - - Sodium

Stabilizers cromoglycat
e
Atopic Dermatitis
 Chronic Relapsing Skin Disease

 Most commonly during early infancy and

childhood

 AD remains a clinical diagnosis

 Pruritus is a consistent feature

 Family history of atopic disease (asthma, allergic

rhinitis, atopic dermatitis)
Etiology
 Complex integration of environmental and genetic
factors

 Wool, harsh detergents are particularly irritating

 Emotional stress can lead to flares

 Exclusive breast feeding for first 3 months of life

is associated with lower incidence rates of atopic
dermatitis during childhood in children with a
family history of atopy
 In healthy people, the skin acts as a protective
barrier against external irritants, moisture loss, and
infection.

 Proper function of the skin depends on adequate

moisture and lipid content, functional immune
responses, and structural integrity.

 Severely dry skin is a hallmark of AD.

 This results from compromise of the epidermal

barrier, which leads to excess transepidermal water
loss, allergen penetration, and microbial
colonization.
 Filaggrin
 Structural protein in the epidermis

 It is critical to skin barrier function.

 Genetic mutations in the filaggrin gene family have

been identified in up to 50% of patients with severe
AD.
Clinical features
 Vary with the age
 Infancy:
 Ill-defined scaling,
erythematous patches
and confluent,
edematous papules and
vesicles are typical.
 Scalp and face are
most often involved
 When crawling :
extensor surfaces
especially knees are
involved
Childhood

 Lesions are drier, less

eczematous, involve
flexural areas & neck
 Scaling, fissured &
crusted hands
become troublesome
 Infraorbital folds
(Morgan lines)
 Chronic or chronically relapsing

Pruritic, erythematous papulovesicular eruptions that

progress to scaling lichenified dermatitis is common.
Diagnosis
 Radioallergosorbent tests (RASTs) or skin tests
may suggest dust mite allergy.

 Eosinophilia and increased serum IgE levels may

be present but are nonspecific.
 Treatment
 Reduction of trigger factors
 Bland emollients, mild non alkali soaps
 Scented soaps and oil can be irritating
 Cotton clothing is preferable to wool and synthetics
 Topical steroids
 Systemic steroids for severe, acute flares
 Calcineurin inhibitors: tacrolimus, pimecrolimus: no
skin atrophy, therefore, useful on face and neck
 Antihistamines helpful in breaking itch-scratch cycle
Urticaria and Angioedema
 Urticaria (hives) is a vascular reaction of the skin
characterized by wheals surrounded by a red
halo or erythema.

 Cardinal symptom is PRURITUS

 Caused by swelling of the upper dermis

 Up to 20% of the population experience urticaria

at some point in their lives
Rash in urticaria
 Angioedema can be caused by the same pathogenic
mechanisms as urticaria, but the pathology is in the
deep dermis and subcutaneous tissue.

 Swelling is the major manifestation

 Commonly affects the face or a portion of an

extremity

 May be painful or burning, but not pruritic

 May last several days

Angioedema
 COMMON CAUSES OF ACUTE
URTICARIA
 Idiopathic
 Upper respiratory streptococcal infections, helminthes
 Food reactions
 Shellfish, nuts etc.
 Drug reactions
 IV administration Blood products, contrast agents
 ETIOLOGY OF CHRONIC
URTICARIA
 Idiopathic: over 50% of chronic urticaria

 Physical urticarias: many patients with chronic

urticaria have physical factors that contribute to their
urticaria

 These factors include pressure, cold, heat, water

(aquagenic), sunlight (solar), vibration, and
exercise

 Cholinergic urticaria is triggered by heat and

emotion
DERMATOGRAPHISM
 Most common form of
physical urticaria

 Sharply localized
edema or wheal within
seconds to minutes
after the skin has
been rubbed

 Affects 2-5% of the

population
PATHOPHYSIOLOGY
 The mast cell is the major effector cell in urticaria

 Immunologic Urticaria: antigen binds to IgE on

the mast cell surface causing degranulation,
which results in release of histamine

 Histamine binds to H1 and H2 receptors to cause

arteriolar dilatation, venous constriction and
increased capillary permeability.
 Non-Immunologic Urticaria: not dependent on the
binding of IgE receptors

 For example, aspirin may induce histamine

release through a pharmacologic mechanism
where its effect on arachidonic acid metabolism
causes a release of histamine from mast cells.

• Physical stimuli may induce histamine release

through direct mast cell degranulation
 CLINICAL FINDINGS
 Lesions typically appear over the course of minutes,
enlarge, and then disappear within hours
 Individual wheals rarely last >12hrs
 Erythema blanches with pressure

 Urticaria may be acute or chronic

 Acute = new onset urticaria < 6 weeks
 Chronic = recurrent urticaria (most days) > 6
weeks
 Most urticaria is acute and resolves
Diagnosis
 Urticaria is a clinical diagnosis

 A detailed history and physical examination

 If a physical urticaria is suspected, a challenge test with

the respective trigger may be performed

 IgE-mediated food allergy is far more likely to present

with acute urticaria

 A detailed food diary or dietary modification may reveal

foods (or additives) that cause fluctuations in symptoms
of chronic urticaria

 Allergy testing is not routinely performed in patients with

Treatment
The following are examples of H1 antihistamines:
• 1st Generation
- Diphenhydramine
- Hydroxyzine
- Chlorpheniramine
• 2nd Generation
- Cetirizine
- Loratadine
- Fexofenadine
 Epinephrine 1 : 1,000, 0.01 mL/kg intramuscularly
– rarely needed

 Cyclosporine 4-6 mg/kg/day has been effective in

some adults with chronic urticaria but its use is
limited by hypertension and/or nephrotoxicity .
 Insect bites
 Allergic responses to stinging :
1. Localized cutaneous reactions
2. Systemic anaphylaxis

 Allergic reactions that are caused by inhalation of

airborne particles of insect origin result in:
1. Acute or 2.Chronic respiratory symptoms
seasonal or perennial:
i. Rhinitis
ii. Conjunctivitis
iii. Asthma
 Most reactions to biting and stinging insects are
limited to a primary lesion isolated to the area of
the bite and do not represent an allergic
response.

 Occasionally, insect bites or stings induce

pronounced localized reactions or systemic
reactions that may be based on:
1. Immediate or
2. Delayed hypersensitivity reactions.
 Members of the order Hymenoptera include:
i. Apids:
* Honeybee * Bumblebee
ii. Vespids
* Yellow jacket * Wasp * Hornet
iii. Formicids
* Fire ants * Harvester ants
Clinical features
 Insect bites are usually urticarial but may be papular

1.Simple local reactions

i. Involve limited swelling
ii. Pain
iii. Generally last <24 hr.

2.Large local reactions

i. Develop over hours and days
ii. involve swelling of extensive areas (>10 cm)
iii. May last for days
3.Generalized cutaneous reactions
Typically progress within minutes and include cutaneous
symptoms of :
i. Urticaria
ii. Angioedema
iii. Pruritus
beyond the site of the sting

4.Systemic reactions
are identical to anaphylaxis from other triggers and
may includes symptoms of:
i. Generalized urticaria
ii .Laryngeal edema
iii. Bronchospasm
iv. Hypotension
5. Toxic reactions
Stings from a large number of insects at once may
result
in toxic reactions of :
i. Fever ii. Malaise iii. Emesis iv. Nausea

6.Delayed/Late reactions
i. Serum sickness
ii. Nephrotic syndrome
iii. Vasculitis
iv. Neuritis
v. Encephalopathy
Diagnosis
Generally evident from:
i. History of exposure
ii. Typical symptoms
iii. Physical findings
 The primary reasons to pursue skin prick testing
are to confirm reactivity when:

i. Venom immunotherapy (VIT) is being

considered

ii. It is clinically necessary to confirm venom

hypersensitivity as a cause of a reaction
 Treatment
At local site:
i. Cold compresses
ii. Topical medications to relieve itching
iii. oral antihistaminics, analgesic

 Anaphylactic reactions after a sting are treated exactly

like anaphylaxis from any cause

 Stingers should be removed promptly by scraping, with

caution not to squeeze the venom sac because doing so
could inject more venom

 Sting sites rarely become infected, possibly owing to the

antibacterial actions of venom constituents
Venom Immunotherapy(VIT)

 Hymenoptera VIT is highly effective (95-97%) in

decreasing the risk for severe anaphylaxis.

 Immunotherapy against Hymenoptera is indicated

in those ≥17 yr of age who have specific IgE to
venom allergens and a history of generalized
urticaria or a systemic reaction
Prevention
 Avoidance of stings and bites is essential to
reduce the risk of stings, sensitized individuals
should:
1. Avoid attractants – perfumes, bright-colored
clothing outdoors

2. Wear gloves when gardening

3. Wear long pants and shoes with socks when

walking in the grass or through fields
Drug allergy

 Drug allergy is an abnormal response to the

medicine or metabolites through immunological
reactions are known as hypersensitivity reaction
that occurs during or after use of the drug.
Classification of ADR
• Type A (pharmacological 85-90%) –
PREDICTABLE
– Side effects
– Drug interactions
– Drug toxicity

• Type B (Hypersensitivity) – UNPREDICTABLE

– Hypersensitivity
– Idiosyncratic reactions
– Pseudoallergy
CLINICAL FEATURES

 Severe skin reactions, often on the palms and soles.

 Fever, sometimes as high as 104 degrees F, is
always present and usually appears before the skin
rash.
 Joint pain (50%) - usually seen in the larger joints,
but occasionally the finger and toe joints may also be
involved.
 Swelling of lymph nodes, particularly around the
site of the injection, is seen in 10-20% of cases.
 Urine analysis may show traces of blood and protein
in the urine.
 Other symptoms may include changes in vision, and
Erythema multiforme and Steven Johnson
Syndrome:
Cotrimoxazole
Penicillin
Tetracyclines
NSAIDs
Anticonvulsant
Toxic epidermal necrolysis

 Aspirin
 Penicillin
 Phenytoin
 Sulfasalazine
Acneform eruptions :

 Corticosteroids
 Iodides
 Isoniazid
Fixed Drug Eruption
 Patients may complain of burning in the affected area
before the appearance of lesions but systemic
symptoms are usually absent.
 The period required for sensitization
ranges from weeks to years and
the time between drug administration
& eruption can be anything from a
day or two to a few weeks.

 It is so named because the site of

the eruption is FIXED

 It occurs in exactly the same place

when the same drug is again
encountered
Treatment
 Discontinuation of the drug.

 When the drug is considered to be very important

and cannot be replaced, can continue to be
provided with the approval of the family, and by
way of desensitization.

 Mild clinical manifestations – no treatment

needed.

 For pruritus, urticaria or edema -antihistamines

 When very severe clinical symptoms - supportive

treatment with corticosteroids and maintain fluid
and electrolyte needs, transfusion, antibiotic
Food allergy
 Adverse reactions to foods consist of any
untoward reaction following the ingestion of a
food or food additive and are classically divided
into
 food intolerances which are adverse physiologic
responses
 food allergies which are adverse immunologic
responses

 When allergens are encountered in the GI

system, they activate an immune response. The
allergic cascade is activated and response is
Common food allergens

 Peanuts

 Sea food

 Cow’s milk

 Egg

 Wheat

 Soy products

 Fruits
Clinical features
 Gastrointestinal :

1) Food protein–induced enterocolitis syndrome

(FPIES) typically manifests in the first several
months of life as irritability, intermittent vomiting and
protracted diarrhoea

2) Food protein-induced proctocolitis

presents in the first few mo of life as blood-streaked
stools in otherwise healthy infants
3) Food protein–induced enteropathy
often manifests in the first several months of
life as diarrhea, often with steatorrhea and
poor weight gain

4) Eosinophilic gastroenteropathies may

appear from infancy through adolescence,
more frequently in boys manifests as chronic
gastroesophageal reflux, intermittent emesis,
food refusal, abdominal pain, dysphagia,
irritability, sleep disturbance, and failure to
respond to conventional reflux medications
 Oral allergy syndrome
 Skin Manifestations
Atopic dermatitis , Acute urticaria and angioedema
 Perioral dermatitis & perioral flushing
 Respiratory manifestations : Food induced
rhinoconjunctivitis
 Anaphylaxis
Treatment
 Appropriate identification and elimination of foods
responsible for food hypersensitivity reactions are
the only validated treatments for food allergies.
Anaphylaxis
 Anaphylaxis is defined as a serious allergic
reaction that is rapid in onset and may cause
death.

 Anaphylaxis in children, particularly infants, is

underdiagnosed.

 Anaphylaxis occurs when there is a sudden

release of potent biologically active mediators
from mast cells and basophils leading to
symptoms
Diagnosis of Anaphylaxis
 Anaphylaxis is highly likely when any 1 of the following 3 criteria
is fulfilled:
1. Acute onset of an illness (minutes to several hours) with
involvement of the skin and/or mucosal tissue
AND AT LEAST 1 OF THE FOLLOWING:
a. Respiratory compromise
b. Reduced BP or associated symptoms of end-organ dysfunction

2. Two or more of the following that occur rapidly after exposure to

a likely allergen for that patient (minutes to several hours):
a. Involvement of the skin/mucosal tissue
b. Respiratory compromise
c. Reduced BP or associated symptoms
d. Persistent gastrointestinal symptoms

3. Reduced BP following exposure to known allergen for that

Thank you