1. “Excuse Me, Is this
Allergen Free?”
The Food Allergy Phenomenon
and its Anesthesia Implications
Gena L Burnett, CRNA, MSN, BSN, BA
2. Objectives
Describe Elements of:
Immunity - Innate vs. Acquired (Adaptive)
Hypersensitivity reactions
Anaphylaxis
Cross-Reactivity
Understand Food Allergy Basics
Symptoms
Diagnosis
Treatment
Define Differences and give Anesthesia considerations for:
IgE Allergies
FPIES (Food Protein-Induced Enterocolitis Syndrome)
EoE (Eosinophilic Esophagitis)
Oral-Allergy Syndrome (OAS)
Latex-Fruit Syndrome
Food Allergies and Anesthesia Safety – Can we safely administer Propofol?
NPO Guidelines and Food Allergies – are we following the guidelines?
3. Q&A
Below I have listed food allergies/reaction. If a patient
presents with the allergy, would you administer propofol?
1. Peanut – rxn: anaphylaxis
2. Soy – rxn: vomiting/rash
3. Egg – rxn: hives
4. Egg – rxn: profuse vomiting/diarrhea (FPIES)
5. Innate Immunity
Initial response to any infection: FIRST LINE
Recognizes targets common to many pathogens
No memory
Can fight the same toxin over and over and never realize it
Skin Invasion resistance
Includes skin, epithelium, sneeze, sloughing dead cells, vomit,
earwax, mucus, sebaceous fatty & lactic acids, surfactant
Digestive enzymes destroying swallowed organisms
Phagocytosis
Components of Innate Immunity:
Cellular elements: granulocytes, macrophages, monocytes,
natural killer lymphocytes, lysozymes
Non-cellular elements: complement complex, acute-phase
proteins and proteins of the contact activation pathway
6. Leukocytes (WBCs)
Eosinophils
2.3% of WBCs in body
Phagocytize allergen-antibody
complexes
Exhibit chemotaxis
Collect near allergic reactions
Detoxify inflammation
produced by basophils/mast
cells
Reduce the spread of
inflammation
Basophils
0.4% of WBCs in body
IgE has a special propensity to
bind to basophils (and mast cells)
– ½ million molecules of IgE per
cell!
IgE antigen-antibody binding
causes basophils to rupture and
release Heparin, Histamine,
Bradykinin, Serotonin, and
Lysosomal enzymes
Causes most/many of allergic
reaction symptoms
7. Adaptive Immunity
Also known as “acquired immunity”, or SECOND DEFENSE LINE
Onset is delayed: May take days to react to an unfamiliar antigen
Fights lethal bacteria, toxins, and foreign tissues
Works by forming antibodies and/or lymphocytes
Immunizations create acquired immunity
Capable of developing memory
Leading to allergic reactions
Is more rapidly induced by an antigen when memory is present
Components of adaptive immunity:
Humoral: Mediated by B-lymphocytes (they produce antibodies)
Liver and Bone Marrow
Cellular: Mediated by T-lymphocytes (destroy foreign agents)
Thymus gland
8. Antigen-Antibody
Antigen
Foreign
proteins/toxins
evoking production
of Antibodies
Initiate acquired
immunity
Leads to the
production of T-
lymphocytes via
signal transduction
Antibody
What the body makes to
‘remember’ a
disease/toxin
Also termed
immunoglobulins
Every antibody has a
unique shape/class (5)
IgM, IgG, IgA, IgD, IgE
Antibodies act by:
Direct attack on antigen
Activation of the
Complement System
Initiate ANAPHYLAXIS
9. Excessive Adaptive Immunity:
Hypersensitivity Reactions
Time of onset
Immediate hypersensitivity:
Antibody mediated
Delayed hypersensitivity:
T-Cell mediated
Nature of mediator
Type I: IgE mediated
Type II: IgG or IgM, and
complement mediated
Type III: IgG, IgM, and
complement mediated
Type IV: Delayed
hypersensitivity reactions
Type V: Stimulatory
Type I
Immediate
Anaphylaxis
Type II
Cytotoxic
Type III
Immune
Complex
Type IV
Delayed
Hypersensitivity
Hypersensitivity
10. How Anaphylaxis Occurs
Allergen
binds with
mast cell
antibodies
(IgE)
Vasoactive
mediators
released
First wave
of
symptoms
Activated
mast cells
produce
cytokines
Second
wave of
symptoms
6 to 8
hours later
11. Vasoactive mediators released during
Antigen/Antibody-Induced Degranulation
Mediator Physiologic Effect
Histamine Increased capillary permeability,
peripheral vasodilation,
bronchoconstriction
Leukotrienes Increased capillary permeability,
intense bronchoconstriction,
negative inotropy, coronary
artery vasoconstriction
Prostaglandins Bronchoconstriction
Eosinophil chemotactic factor Attraction of eosinophils
Neutrophil chemotactic factor Attraction of neutrophils
Platelet activating factor Platelet aggregation and release
of vasoactive amines
Stoelting Table 29-2
13. Type IV Hypersensitivity Reaction
A cell-mediated response where sensitized T-cells release
cytokines causing tissue damage
Repeated exposure causes activated T-helper and T-cytotoxic cells
to move from circulation to the area of toxin (in food allergies, the
GI tract)
Non-IgE
FPIES
EoE
Dermatitis
14. Cross-Reactivity or Cross-Sensitization
90% chance of reacting to other
milks with milk allergy
75% chance of reacting between
shellfish/crustacean
50% chance of reacting between
types of fish
Proteins can react between:
Food to Food
Pollen to Food
Latex to Food
Close structural similarities between any two
allergens from divergent sources can produce
similar allergic reactions in sensitive patients
15. Food Allergy Basics
Definition: hypersensitive, exaggerated,
or adverse immune response towards
food proteins causing tissue injury
Presentation
Myriad of symptoms
Wide variation in severity
Age can play a role
Types include:
IgE Mediated
Mixed IgE/Non-IgE
EoE
Non-IgE – cellular/delayed
OAS
FPIES
16. Food Allergy Testing Options
Medical History and Physical Exam
SPT – Skin Prick Test
IgE specific, non-stand alone
sIgE – Allergen-Specific Serum IgE
Blood draw required, Non-stand alone
APT – Atopy Patch Test
Skin-Contact FA, non-stand alone
FED – Food Elimination Diet
EoE (mixed IgE/non-IgE)
FPIES(non-IgE mediated)
OFC – Oral Food Challenge
When open or single-blind, it must be supported by Pt Hx and Labs
When double-blind placebo-controlled, it is considered diagnostic of FA
Supervised – hospital or office-based and may require IV, labs, etc.
NOTE: not all patients with allergic sensitization have a clinical allergy
17. Types of Food Allergens
Class 1
Primary sensitizers usually through the GI tract
Water-soluble glycoproteins
Heat, acid, and protease stable
Include the ‘Great 8’ and fruits/vegetables
Class 2
Cross-reactivity with Plant Bases
Often leads to Oral Allergy Syndrome or Latex-Fruit Syndrome
Heat Labile/Difficult to isolate
18. The Great 8 for IgE Allergies
Milk
Egg (usually egg white)
Ovalbumin, Ovomucoid, Conalbumin
Soy
Wheat
Peanut (1.1%)
Treenut
Fish/Shellfish (2.3%)
ALLERGENS can be found in medications, vaccines, cosmetics, craft
materials, sunscreen/bug spray, cleansers, lotions, soaps, and diaper
cream (ingredient and cross contamination)
19.
20. Symptoms of a Reaction:
• Mild symptoms may include one or more of the following:
• Hives (reddish, swollen, itchy areas on the skin)
• Eczema (a persistent dry, itchy rash)
• Redness of the skin or around the eyes
• Itchy mouth or ear canal
• Nausea or vomiting
• Diarrhea
• Stomach pain
• Nasal congestion or a runny nose
• Sneezing
• Slight, dry cough
• Odd taste in mouth
• Uterine contractions
• Severe symptoms may include one or more of the following:
• Obstructive swelling of the lips, tongue, and/or throat
• Trouble swallowing
• Shortness of breath or wheezing
• Turning blue
• Drop in blood pressure
• Feeling faint, confused, weak, or passing out
• Loss of consciousness
• Chest pain
• A weak or “thread” pulse
• Sense of “impending doom”
21. Reaction Described by Child
• Pull or scratch tongue
• Put hands in the mouth/Rubbing the face
• Hoarse or squeaky voice
• Crying
• Slurring of words
• "This food is too spicy.”
• "My tongue is hot [or burning].”
• "It feels like something’s poking my tongue.”
• "My tongue [or mouth] is tingling [or burning].”
• "My tongue [or mouth] itches.”
• "It [my tongue] feels like there is hair on it.”
• "My mouth feels funny.”
• "There's a frog in my throat.”
• "There’s something stuck in my throat.”
• "My tongue feels full [or heavy].”
• "My lips feel tight.”
• "It feels like there are bugs in there." (to describe itchy ears)
• "It [my throat] feels thick.”
• "It feels like a bump is on the back of my tongue [throat]."
22. IgE Allergy Desensitization
Frequent, repeated intradermal injections of increasing amounts of
an allergen may produce tolerance
Mechanism: development of specific IgG antibodies to the allergen
IgG antibodies bind with the allergen as soon as it enters the body
preventing it from reacting with the IgE antibodies on the surface
of mast cells
IgG coated allergens are then cleared by macrophages
Unfortunately desensitization does not completely eliminate
immediate hypersensitivity reactions, they reduce symptoms
Further, life-threatening anaphylaxis has been known to occur from
desensitization therapy itself!
23. Anesthesia and Anaphylaxis
Dramatic hypotension and CV collapse may be the only signs under general anesthesia
Vasodilation
Decreased Tissue Perfusion
Shock
Bronchospasm
Laryngeal Edema
Vomiting/Esophageal Spasm
Most reactions occur within 5-10 minutes
Proof of anaphylaxis: Increased plasma tryptase within 1-2 hours of the suspected event
Pre-administered antihistamines to mask IgE-mediated anaphylaxis? No
Plasma histamine returns to baseline within 30-60 minutes of the event
Operating Room treatment (ADULTS):
Discontinue Anesthetic Agents
100% FiO2 – intubate/support ventilation
Treat Hypotension – Fluids, Pressors
Epinephrine – 50-100mcg IV, or 0.5-1mg IV in CV collapse
Antihistamines – H1 Diphenhydramine 50mg IV, H2 Ranitidine 50mg IV
Corticosteroids – Hydrocortisone 250mg-1gm IV vs Methylprednisolone 1-2gm IV
Bronchodilators – Albuterol PRN
Consider postponing extubation – cuff leak?
24. Anesthesia and Anaphylaxis:
Pediatrics
WHAT WILL YOU SEE? RASH, BRONCHOSPASM, HYPOTENSION
• Increase O2 to 100%
• Remove suspected trigger(s)
• Ensure adequate ventilation/oxygenation
• If HYPOtensive, turn off anesthetic agents
• To restore intravascular volume: NS or LR 10-30 mL/kg IV/IO rapidly
• To restore BP and ↓mediator release: Epinephrine 1-10 MICROgrams/kg IV/IO, as
needed, may need infusion 0.02-0.2 MICROgrams/kg/min
• Additionally, can give 10MICROgrams/kg IM for depo effect (lingering effects of Epi after
stimulus has been removed)
• To ↓ bronchoconstriction Albuterol (Beta-agonists) 4-10 puffs
• To ↓ mediator release Methylprednisolone 2 mg/kg IV/IO (MAX 100 mg)
• To ↓ histamine-mediated effects: Diphenhydramine 1 mg/kg IV/IO (MAX 50 mg)
• To ↓ effects of histamine: Famotidine or Ranitidine 0.25 mg/kg IV- 1 mg/kg IV
• If anaphylactic reaction requires laboratory confirmation, send mast cell tryptase level
within 2 hours of event
25. EpiPen/EpiPen JR News
EpiPen (0.3mg) dose vs EpiPen JR (0.15mg) dose
2-pack price changes (480% increase!!)
2004> $83.46
2007> Mylan purchases drug from Merck
10/2015> Sanofi US voluntarily recalls Auvi-Q auto-
injector d/t inaccuracies with dose injected
Teva and Adamis auto-injectors not approved by the
FDA
2016> $608.61
The New York Times reports (9/16/2016)
Mylan working to have the drug placed on the
Federal Preventative List (meaning no co-pay)
Mylan offers a co-pay discount program
Mylan contributes to many political campaigns, patient
advocacy groups, and physician groups
CNN.com reports (10/27/2016)
Auvi-Q to re-enter market in first half of 2017
26. FPIES
Food Protein-Induced Enterocolitis Syndrome
Epidemiology
Non-IgE/T-cell mediated GI food hypersensitivity
Prevalence is unknown, but it is rare (0.3% of population in an Israeli study)
Non-Familial
Some studies report slightly more common in boys (52%-60%)
80% of FPIES children are multiple reactors/atopic
90% of children diagnosed outgrow by age 3
Often begins in infancy with introduction of Cow’s milk/Soy and solid foods
(can be delayed in breastfed children)
Triggers
RICE, oat, and barley
Chicken, turkey, and egg white
Green pea
Peanut
Sweet potato, white potato, and corn
Fruit protein
Fish and shellfish
27. FPIES
During episode, Labs show elevated WBC, acidosis, methemoglobinemia, thrombocytosis,
hypoalbuminemia
There are NO diagnostic/predictive tests except OFC
Negative SPTs
Negative sIgE
APT??
Often mis-diagnosed/missed on evaluation and physical exam
Regular follow-up with specialist: GI, Allergist, PT/OT/ST
ACUTE
Repetitive, projectile emesis
1-3hrs after food ingestion
Lethargy
Pallor/Ashen in appearance
Diarrhea with blood/mucous 2-
10hrs after ingestion
Hypothermia
Dehydration
Hypotension/Shock
• CHRONIC
• Intermittent emesis
• Bloody diarrhea
• Poor wt gain/wt loss
• Failure to Thrive
• Abdominal distension
• Irritability
• Same as Acute
28. FPIES Management
Trigger food elimination/Strict Allergen Avoidance
First Line/Acute
REMEMBER: EpiPen won’t help!
Fluid resuscitation
Single Dose Steroids
Zofran
OFC
Considered the ‘gold-standard’, but are not
required for diagnosis
0.15-0.3g protein/kg body weight in 3 doses
every 15-20min
50% reactive OFC requires fluid
resuscitation via IV
Q18-24months/Follow-Up
Delayed Introduction/At-Home Food Trial
Avoid grains, legumes, and poultry until
age 1
Tolerance of one food in each group is
often a good indicator of ‘safes’
Soy – legumes
Oat – grains
Chicken - poultry
Breastfeeding partially digests and
processes the proteins
Protects against CM/Soy FPIES, but not
Solid Food FPIES
Mother’s elimination diets
No Sharing Food, No Restaurant Food, No Party Food
Preschool – allergy table with teacher supervision & separate preparation
ALLERGENS can be found in medication, vaccines, cosmetics, craft materials,
bubbles, sunscreen/bug spray, cleansers, lotions, soaps, and diaper cream
(ingredient and cross contamination)
29.
30. Anesthesia and FPIES
Operative Scenario: A 2yo patient with FPIES to milk, rice, oat,
and soy presents for endoscopy.
Concerns?
Changes in the plan of care?
Changes in your hand-off procedures?
31. EoE: eosinophilic esophagitis
Chronic esophageal dysfunction caused by T-cell inflammatory
response to food/environmental allergens
Activated eosinophils -> cytokine release -> attack healthy tissue
repeatedly -> epithelial/esophageal injury
Endoscopic Features/Histology Reports are characteristic but not
diagnostic (6yr delay in diagnosis reported in one study)
Pediatrics – mostly inflammatory; dysphagia (inaccurately
described), emesis, abdominal pain, GERD
Adults – both inflammatory and fibrostenosis; dysphagia and food
impaction
Most pts have atopic history
IgE food allergies
Allergic Rhinitis
Asthma
Contact Dermatitis
COMMON TRIGGERS
MILK
wheat, egg, soy, nuts, seafood
corn, chicken
33. EoE and Anesthesia
Upper Endoscopy/Biopsy
Foreign Body Extraction
Esophageal Dilation
Pediatric G-tube placement
34. OAS: Oral Allergy Syndrome
Pollen Food Hypersensitivity Syndrome
Considered ‘mild’ IgE reaction limited to the oropharynx
Pruritus
Tingling
Erythema
Swelling of lip, oral mucosa, throat, or tongue
Patient has environmental/pollen allergies and cannot eat
fruits/vegetables with pollen allergen on or in the fruit
Most common with raw or uncooked fruit/vegetable
A Class 2 Type of Food Allergy
In 3% of patients, OAS causes systemic reaction or anaphylaxis
35. Latex-Fruit Syndrome
Food (or seeds) with clinical or immunological
cross-reactivity with latex proteins
2002 study shows 30-50% of patients with NRL
allergy also have some food hypersensitivities
(Wagner and Breiteneder)
IgE vs Non-IgE mediated Food Allergy
concerns?
• High: Avocado, Banana, Chestnut, Kiwi
• Moderate: Apple, Carrot, Celery, Melons, Papaya, Potato, Tomato
• Low/undetermined (40): Apricot, Buckwheat, Cassava/Manioc, Castor bean,
Cherry, Chick pea, Citrus fruits, Coconut, Cucumber, Dill, Eggplant/Aubergine,
Fig, Goji berry/Wolfberry, Grape, Hazelnut, Indian jujube, Jackfruit, Lychee,
Mango, Nectarine, Oregano, Passion fruit, Peach, Peanut, Pear, Peppers
(Cayenne, Sweet/bell), Persimmon, Pineapple, Pumpkin, Rye, Sage, Strawberry,
Shellfish, Soybean, Sunflower seed, Tobacco, Turnip, Walnut, Wheat, Zucchini
www.latexallergyresources.org
36. Gluten
Gluten is a protein found in grains: wheat, rye, barley, and triticale
(wheat/rye cross)
Those with Celiac have to specifically avoid Gluten – even trace
amounts can cause a reaction
Those who are symptomatic with gluten but do not have Celiac have
Non-Celiac Gluten Sensitivity
Cross-contamination during manufacturing
Vitamins lost with Gluten-Free diet: iron, calcium, fiber, thiamin,
riboflavin, niacin, folate
37. MSG
Monosodium glutamate
A meat flavor enhancer often found in Chinese and Asian
foods
Reported System Complex – myalgia, nausea, neck pain,
backache, sweating, flushing, chest tightness
Difficult to reproduce in OCTs
38. Food Allergies and Propofol
Emulsion contains soybean oil, egg lecithin, and glycerol
Soy and Egg Allergy – contamination during processing
Peanut Allergy – cross-reactivity between soy and peanut: review
from 2000 shows a low rate of cross-reactivity
Allergy is thought to be IgE mediated with the 2-isopropyl-group
as the suspect epitope (multiple studies)
(2001) Australia Peds study: 28 egg-allergic children with 43
propofol cases; one atopic child with egg anaphylaxis got
erythema/urticaria, confirmed propofol allergy via SPT/sIgE
(2013) Spanish study: 60 EoE pts had 404 endoscopies with
propofol; 86% had IgE to egg, soy, or peanut via SPT/sIgE (35%
with clinical allergy); No reactions reported
39. Food Allergies and Propofol
(2016) Denmark study (BJA):
Study A: 273 pts with suspected intra-op reactions
154 propofol-exposed pts had SPTs and IV challenge
4 pts tested positive for propofol allergy – but none had allergies to egg, soy, or peanut
Study B: 520 pts with +sIgE to egg, soy, or peanut retrospectively reviewed
171 retrieved records from 99pts – no reactions found
“No evidence for contraindications to the use of propofol in adults allergic to egg, soy, or peanut”
(2016) Polish/Czech review of evidence:
‘References demonstrating safe use of propofol in food allergy pts’
5 retrospective studies, 1 lit review, and 1 consensus statement, includes adults and
pediatrics
‘References demonstrating a potential allergic reaction to propofol’
8 case reports and 1 retrospective study
Limited data does not support avoiding propofol
40. Q&A
Below I have listed food allergies/reaction. If a patient
presents with the allergy, would you administer propofol?
1. Peanut – rxn: anaphylaxis
2. Soy – rxn: rash/vomiting
3. Egg – rxn: hives
4. Egg – rxn: FPIES
5. Milk – rxn: causes EoE
41. NPO Guidelines and Food Allergies
ASA Guidelines
2H – clear liquids
4H – breastmilk
6H – non-human milk,
formula, light meal
8H – full, high-fat meal
NPO after midnight
Likely originated in 1946 with an obstetric study on pulmonary aspiration by
Mendelson
1946 study found 0.15% OB patients who received GA had pulmonary
aspiration compared to 0.006% in a 2002 study
Gastric volume and/or pH is unrelated to fasting duration
Benefits of following Guidelines
• Better hydration status
• Improved hemodynamic stability
• Reduction in surgical stress response
Adverse Effects of Prolonged NPO status
• Hunger, thirst, discomfort, crying
• Hypoglycemia
• Dehydration, hypovolemia
• Electrolyte imbalance, ketosis
• Malnutrition
• General malaise
• Delayed recovery, wound healing
• Immune suppression, infection susceptibility
42. Evidence-Based Practice or
Time-Honored Tradition?
(2002) Crenshaw and Winslow – 155 adults, 14hrs solids, 12hrs liquids
(2008) Crenshaw and Winslow follow-up – 275 adults, 14hrs solids, 11hrs liquids
(2011) Engelhart et. Al – 1350 pediatrics, 12hrs solids, 8hrs liquids
(2013) Arun and Korula (INDIA) – 50 pediatrics, ~11hrs solids, ~9hrs liquids
(2013) Williams et. Al – 219 pediatrics
Average Fasting Times to Surgery/Procedure time
Solids: 14.08+6.28hrs
Breastmilk: 9.82+6.6hrs
Clears: 12.61+5.88hrs
Non-compliance w/ guidelines based on MD order
62% for solids
100% for breastmilk
97% for clears
(2016) Brunet-Wood et. Al – 53 pediatrics
No patients allowed clears 2hrs prior and 70% were NPO for 8+ hrs prior
Found 80% (complex) and 65% (non-complex) of pre-op NPO times not within guidelines
Also covered post-operative NPO times: time to first nutrition in complex cases is 63.6hrs and 23.8hrs
for non-complex cases
43. NPO True or False?
My 64yo patient can have a cup of black coffee at 0600 for hernia
surgery at 0900.
The same patient is obese with diabetes and GERD, and added cream to
the coffee. What time can the surgery start?
My 18month old patient can have apple juice at 0700 for oral surgery at
0930.
My 5month old patient can be nursed at 0500 for a T&A at 0800.
The ENT surgeon has been delayed and cannot arrive until 1000. It is
0630 and the patient has arrived in pre-op. It is ok for the parent to give
the child Pedialyte in a bottle.
As a practitioner, I keep my patients NPO for too long.
Pre-op will page me every 5 minutes if we change the rule NPO after
midnight.
MAST CELL – out of the capillaries
BASOPHILS –inside the blood stream
Immune response is a protective phenomenon against any foreign antigen
Humoral or Cell-Mediated
Hypersensitivity is an exaggerated immune response detrimental to the body.
Hence immune response is a double edged sword; at one hand it protects the body, on the other hand it harms the body depending upon the nature of the antigen, antibody produced, and susceptibility of the person.
Hypersensitivity can be induced by environmental antigens in factitious agents, chemicals and drugs.
Sensitization Exposure – excess IgE antibody produced
Active Exposure – Mast cells covered in all these excess IgE antibodies release histamine when re-exposed to the allergen
HISTAMINE, SEROTONIN, PROSTAGLANDINS, LEUKOTRIENES
The development of immediate hypersensitivity is a two step process:
Sensitization phase - When the immune system of atopic individuals is first exposed to an allergen, B lymphocytes produce excess IgE antibodies. These antibodies have a strong affinity for mast cells (and basophils) and coat the surface of these cells by binding to receptors for the heavy chain portion of the IgE molecule (IgE Fc Receptors).
Activation phase - Later when sensitized mast cells, coated with IgE antibodies, are re-exposed to the allergen, they rapidly release vasoactive mediators such as histamine and serotonin from cytoplasmic granules. A requirement for activation of mast cells appears to be the cross-linking of surface IgE molecules by the inciting allergen. Later, prostaglandins and leukotrienes are also synthesized from the mast cell plasma membrane. Among other things, this leads to the accumulation of neutrophils and eosinophils at the site of antigenic stimulation.. This stage of the immediate hypersensitivity reaction is sometimes referred to as a late phase response.
The clinical manifestations of immediate sensitivity reactions depend on whether the antigen is introduced into the skin, lung, or blood stream.
Immediate Hypersensitivity Reactions in the Lung:
Immediate hypersensitivity reactions to inhaled allergens can lead to bronchospasm and some forms of asthma.
Other drugs such as epinephrine and theophylline which relax bronchial smooth muscle or drugs such as cromolyn and corticosteroids which block mast cell degranulation are also effective
Not all asthma is allergic or IgE mediated. In some people the smooth muscle cells lining the airways are "hyper-reactive" and constrict in response to non-immunologic stimuli.
Histamine seems to be the primary mediator of immediate hypersensitivity reactions involving the skin and mucous membranes
These reactions can be blocked by the administration of anti-histamines
Histamine causes dilation of capillary venules which results in increased blood flow to the skin (redness and warmth) with the extravasation of plasma into the interstitial spaces (wheal)
Histamine does not produce significant bronchospasm. Instead, it is the late phase mediators prostaglandins and leukotrienes that are responsible for the intense bronchospasm and increased mucous secretion of immediate hypersensitivity reactions in the lung.
The late phase response in the skin seems to be one mechanism for producing certain forms of eczema. This reaction is not blocked by antihistamines.
There are multiple processes by which biologically active mediators can be generated to produce an anaphylactoid reaction.
There are 2 pathways:
Classical: initiated through IgG or IgM (transfusion reactions) or plasmin.
Alternative pathway: activated by lipopolysaccharides (endotoxin), drugs, and Xray contrast dye, vascular graft material, latex or latex-containing products and nylon membranes on bubble oxygenators. Blood coagulation, fibrinolytic or complement activation all are apart of the classic route.
Histamine can be liberated independent of immunologic reactions. Mast cells and basophils release histamine in response to chemicals or drugs. What makes patients susceptible to release of histamine in response to drugs in unknown but hereditary and environment may play a role.
Pre-treatment with diphenhydramine, ranitidine and corticosteriods has been reported to be useful for reducing anaphylactoid symptoms associated with contrast reactions (and narcotics)
Non-IgE mediated "Allergy": There are a number of substances which can directly activate mast cells in the absence of IgE and produce so called anaphylactoid (anaphylaxis-like) reactions. They include morphine, shellfish, iodinated radiocontrast agents, certain berries, and aspirin. Anaphylactoid reactions have the same clinical significance as IgE mediated anaphylaxis. They are also managed the same way.
TYPE IV: T CELL-MEDIATED HYPERSENSITIVITY:
Delayed Type Hypersensitivity (DTH) reactions are mediated by CD4 Helper T Lymphocytes. Injury results from the hydrolytic enzymes and toxic oxidants secreted by macrophages activated by CD4 lymphocytes. Later, chronic inflammation (manifested by granuloma formation) and fibrosis dominates the clinical picture.
Contact dermatitis - Poison ivy, some drugs, and occasionally cosmetics can bind to certain cell surface proteins and become the target for CD4 Helper lymphocytes producing local inflammation, fibrosis and edema.
FPIES
NOTE:
REFERENCE: The state of GA student learning website
Profits exceed 1Billion last year with 99% of the market purchasing this product exclusively
Heather Bresch – chief exec of Mylan – the daughter of WV Senator
Most of Mylan’s employees are major contributors to Capitol Hill and are considered ‘well-connected’
First described 4 decades ago
MEN??
Acts similarly to Asthma – multiple ongoing clinical trials of medications
Monoclonal Antibody therapy – no symptom improvement but reduction in effector cell (mast cells and eosinophil counts) proliferation at esophagus found
Concerns – friable tissue/perforation, aspiration
Lecithin – a purified egg phosphatide (lipid vehicle) – NOT a protein (greek word meaning yolk)