Anaphylaxis Flashcards
Half of fatalities occur with in
First hour
Anaphylaxis caused by
Activation of mast cells + basophils through a mechanism crosslinking IgE and aggregation of high affinity receptors for IgE
Upon activation of mast cells and basophils
Several chemical mediations released, including histamine
Common systems involved in anaphylactic reaction
Heart lungs GI skin
4 routes of entry
Injection Ingestion Absorption Inhalation
3 ways to develop tolerance
Natural
Acquired
Artificially introduced
4 classes of immunogoblins (AKA antibodies)
Type 1 - IgE mediated
Type 2 - Tissue specific reactions
Type 3 - Immune-complexed mediated reactions
Type 4 - Cell mediated reactions
Antigens
Each have one antibody which will disable it, they were developed in a protective response by the body
IgE dependent
Normal ones
Nuts, seafood, milk, stings, MSG, penicillin, pets, NSAIDS
IgE INdependent reactions
Radio contract materials
Blood products
Non-immunologic
Opioids
Dextrans
Vancomycin
Primary response
Large amounts of IgE are produced, which bind to cell membranes of basophils and mast cells
IgE mediated hypersensitivity Type I
Ag induces crosslinking -
IgE binds to mast cells and basophils which release vasoactive mediators
IgG mediated cytotoxic Type II
Ab directed against cell surface antigens mediates cell destruction via complement activation
From blood transfusions, erthroblastosis fetalis, autoimmune hemolytic anemia
Type III Immune complex-mediated
Ag-Ab complexes deposited in various tissue induce complement activation and ensuing inflammatory response mediated by massive infiltration of neutrophils
Arthus reaction, serum sickness, necrotizing vasculitis, glomerulenephritis, RA and lupus
Ag =
Antigen generator
Ab =
Antibody
Arthus reaction
Localized vasculitis from type III reactions
Type IV Cell-mediated
Sensitized Th1 cells release cytokines that activate macrophages or Tc cells which mediate direct cellular damage
Contact dermitits, tubercular lesions, graft rejection
Histamines
Causes bronchoconstriction, increases intestinal motility, vasodilation, increased vascular permeability
Main culprit on anaphylaxis
Two classes H1 bronchoconstriction, contraction of intestines
H2 peripheral vasodilation and secretion of gastric acids
Leukotrienes
SRS-A (slow reacting substances of anaphylaxis)
Smooth muscle contraction and increased vasc perm, but takes longer than histamine to act
CNS effects
Anxiety/agitated Tremor Sensation of cold Dizziness Weakness Obtunded Unconscious
Airway effects
Stridor Hoarseness Larygneal/epiglottic edema Rhinorrhea Bronchospasm Increased mucus production Accessory muscle use Wheezing Decreased or absent air entry
CVS effects
Tachy, hypotension, arrhythmias, shock, bradycardia, cvs collapse, cardiac arrest
GI GU
N/V cramps diarrhea
Integumentary
Angioedema, uticaria, pruritus (itchy), erythema
Differential for anaphylaxis
Angioedema, PE/edema, asthma, epilgottitis, foregin body airway, poisoning, non-organic disease
Tx keys
Early recognition, rapid evaluation, prompt intervention
How does epi work
Reverses symptoms and inhibits release of mast cells/ basophils
Epinephrine
1:1000 0.3mg IM q 5 max 0.9
Benadryl
H1 antihistamine
25-50mg IM/IV/IO q 4-6 prn
H2 blockers
Ranitidine or cimetidine after a severe reaction, or during episode if circulatory collapse
Steroids - 3rd line
Clinical effect delayed 4-6 hours
Do reverse bronchospasm and skin effects
Don’t reverse cardiovascular effects
Can prevent biphasic
Solumderol/Methylprenisolone
125mg IV/IO once
Dexamethasone
8MG IM/IV/IO once
Prenisone
50mg PO
Epi 1:10 000
Refractory to 1st/2nd line therapies
0.1mg of 1:10000 SIVP/IO given q 2 prn max 1mg
Epi infusion
Persistent symptoms greater than 30 min transport
1mcg/min titrate to BP 90 max dose 8mcg/min
Glucagon
Hypotensive and on BB 1mg SIVP/IO q5 max 5mg
Ventolin
2.5-5mg q 4-6 hours (thats silly)
Nebbed epi
May help reduce laryngeal swelling, does not replace IM/IV
BP
Lots of epi, lots of crystalloids consider pressors with alpha activity (levophed, epi, dope)
Consider glucagon if on BB
Biphasic response
1-8 hours despite being asymptomatic, up to 36 hours
Anaphylaxis tins pathology
IgE activates preformed mediators from secretory granules (histamine, tryptase, carboxypeptidase A, proteoglycans.
Downstream activation of phospholipase A2, followed by cyclooxygenases and lipoxygenases, produce AA metabolites including prostaglandins, leukotrienes, PAF.
Histamine
Vasodilation, increased cap perm, increased heart rate and contraction, increased glandular secretion
Prostaglandin
Bronchocontrictor
Pulm and coronary vasoconstrictor
Peripheral vasodilator
AHS anaphylaxis criteria
Exposure plus 1 of: Sudden resp syndromes Sudden hypotension or signs of end organ perfusion OR BOTH: Sudden skin & GI
Timing of anaphylaxis
Quicker onset = more serious
1/2 of fatalities in first hour
Small risk for secondary reaction 8-11 hours later from cysteinyl leukotrienes 4-5% experience this (some studies say 20%)
Differential for anaphylaxis
Vasovagal Myocardial ischemia, arrhythmias Sever acute asthma, epiglottitis Seizure HAE FBAO non-IgE- mediated reactions
Approach to anaphylaxis
Examine mouth, pharynx and neck for S&S of angioedema.
Assess for stridor, resp distress, hypoxia
If angioedema present consider tubing
Remove decontamination
EPI, benadryl, Neb, steroid,
2L fluid
1mg glucagon if on BB
IV EPI
after 500mL 1mcg/min to 8mcg/min greater than 30 minute transport time
IV EPI setup
1.5mg to 250mL D5W, concentration is 6mcg/mL
60 drop set, 1mcg/min = 10 drops per minute (Start at 10/min go to 80/min
B blockers, CCB maybe
Severe hypotension due to unopposed alpha agonism so only B blockers need it
Strongest to weakest steroid effects of mineralcorticoid
Hydrocortisone and cortisone are strongest, then pred followed by methylprednisolone and dex
ACE inhibitor induced angioedema managament
Not IgE so standard meds don’t work
Tins says steroids won’t work either for this reason
Icartibant (bradykinin-2 antagonist) is tx
1000 IU of C1 esterase inhibitor may help as well
Hereditary angioedema
C1 esterase inhibitor deficiency Last from few hours to 1-2 days Minor trauma often precedes attack Stanozolol 2mg/d C1 esterase inhibitor FFP if no C1 available
