Drug:
Route: PO IV SC topical
Prior exposure? Reaction before? Had it since?
Most recent rx?
Sx: wheeze, SOB, rash, angioedema, GI, cardiovascular
Rash - desquam, location, itch,
Timing after exposure:
Duration:
Treatment: hospital, epi, antihist, etc
Other exposures: (ie other drugs, herbals, bites)
Cofactors: alcohol, exercise, nsaids, infection, poor sleep

Impression:

ix:
PEN-FAST score
?histamine / tryptase
Skin test - only penicillin, rest not great
if currently in a Type 4 rx, order markers of end organ damage

Mx:
is it true?
avoid? challenge? desensitizie?

Summary:

WIP

WIP

Basic classifcation

ADRs can be broken down into Type A and B (we are concerned mainly about type B)

• Type A is dose dependent and predictable - expected side effects based on pharmacologic properties of the drug
• Type B is either immunologic or non immunologic
  • Non-immunologic: Idiosyncratic vs mast cell mediated (pseudoallergy)
    • Link to non-ige mediated reactions (ie. direct mast cell, complement activation, IgG mediated, cytokine release reaction)
    • Can occur on first exposure; skin testing is negative; may have atypical symptoms, and may not be reproducible...
  • Immunologic: ie type I - IV

Gel and coombs

This should be listed in a table in the document

Type 1 DHR

Type II

Antibody mediated usually hemolytic anemias you usually will not see this

Type III

Complement mediated reaction and antibody complexes Serum sickness and vasculitis are classic examples

IV

Link to page

The baddie of the world T cell mediated +/- macrophages, eos, or neutrophils DELAYED onset, days to weeks Prominent skin findings are the classic manifestation large variance in clinical severity on presentation

Morbiliform drug reaction, AGEP, DRESS, SJS/TENS

Approach general

History

• rash, mucosa, systemic involvement
• TIMING (latency, recent vs remote)
• treatment - severe or mild, anaphylaxis?
• use before or after

RED FLAGS

• fever
• SCAR type rashes, blistering, desqumation during ACUTE phase (not healing phase)
• other end organ involvement

what's the risk type of allergy additional testing? recommendations

Drug allergy testing basics

SPT, IDT, patch testing,

Immediate reaction history:

• SPT/IDT
• only penicillin (drug major + minor) has good NPV
• other testing has limited evidence

section for other drugs until another page is made:

iron reactions

Mechanisms: IgE (fairly rare), direct mast cell activation, Fishbane reaction (usually consist of acute chest and back tightness and joint pain without severe symptoms, such as hypotension, wheezing, stridor, or laryngeal edema) Testing: no skin tests are reliable in this case. Only an IV challenge is helpful. Management:

1. if direct mast cell => usually try another agent and go very slow
2. if Fishbane, can stop infusion for 15 mins and observe and treat with Tylenol; if improves can run slower

NSAID

generally NSAID induced AAE occurs within 2-3 hours of NSAID ingestion

Ddx is true IgE mediated vs pharmcologic class effect

-Isolated urticaria within 2 hours of NSAID ingestion on repeated exposures is consistent with NSAID induced urticaria which is a cyclo-oxygenase -1 (COX-1) mediated reaction (pharmacologic class effect).
-Consider challenge with celebrex whcih is a cox-2 selective
-As such, we have advised to continue to avoid all NSAIDs moving forward as at higher doses they may cause repeated urticaria. 
-They can continue to take tylenol without issue. 
-Should he require NSAIDs in the future (beyond topical and low doses which can be administered without issue) he can be re-assessed with a supervised challenge

The patient does not have a history of asthma or nasal polyps
The patient does not have a history of chronic urticaria
Their reaction is most in keeping with COX-1 mediated