Anaphylaxis- Summary of Treatment!

APPROACH TO ANAPHYLAXIS

Anaphylaxis is defined as a serious allergic or hypersensitivity reaction that is rapid in onset and may cause death; the diagnosis of anaphylaxis is based primarily upon clinical symptoms and signs, as well as a detailed description of the acute episode, including antecedent activities and events occurring within the preceding minutes to hours. This is a potentially fatal disorder that is not always readily recognised, as it can mimic other conditions and be variable in it’s presentation

Diagnostic criteria: there are three; anaphylaxis is highly likely when any ONE of the following is fulfilled:

Criterion 1 — Acute onset of an illness (minutes to several hours) involving the skin, mucosal tissue, or both (i.e. generalized hives, pruritus or flushing, swollen lips-tongue-uvula) and at least one of the following:

•   Respiratory compromise (i.e. dyspnea, wheeze-bronchospasm, stridor, reduced peak expiratory flow, hypoxemia).

OR

•   Reduced blood pressure (BP) or associated symptoms and signs of end-organ dysfunction (eg, hypotonia [collapse] syncope, incontinence).

Note: Skin symptoms and signs are present in up to 90% of anaphylactic episodes, however; skin and mucosal manifestations may be absent or unrecognized in up to 20% of cases!!!

Criterion 2 — Two or more of the following that occur rapidly after exposure to a LIKELY allergen for that patient (minutes to several hours):

•   Involvement of the skin-mucosal tissue (i.e. generalized hives, itch-flush, swollen lips-tongue-uvula).

•   Respiratory compromise (i.e. dyspnea, wheeze-bronchospasm, stridor, reduced peak expiratory flow, hypoxemia).

•   Reduced BP or associated S&S (hypotonia [collapse], syncope, incontinence).

•   Persistent GI S&S (i.e. crampy abdominal pain, vomiting).

Criterion 3 — Reduced BP after exposure to a KNOWN allergen for that patient (minutes to several hours):

•   Defined as a SBP <90 mmHg or >30% decrease from that person's baseline

Symptoms of anaphylaxis 

• Can be initially non-specific; the onset of symptoms after exposure to the potential allergen may be the strongest clues
•  Anaphylaxis reactions: usually occur within 1h of injection or 2-6h after ingestion

·       DERM: generalized hives, itching, flushing, swollen lips/tongue/uvula, peri-orbital edema, conjunctival swelling

·       RESP (up to 70%): nasal discharge, congestion, change in voice quality, sensation of throat closure/choking, stridor, SOB, wheeze, cough

·       CARDO: syncope, hypotonia, tachycardia, dizziness, incontinence, hypotension

·       Key symptoms prior to the development of hypoxia and hypotension: urticaria, flushing, angioedema, wheezing, throat tightness, cough, abdominal pain, headache, palpitations

·       GI symptoms: if present, often associated with more severe outcomes (N/V/D, crampy abdominal pain)

Triggers-Food allergies (i.e. peanuts, tree nuts), insect stings and medications are the most common cause of anaphylaxis

o   The cause may not be identified

·       In-patient causes:

o   Antibiotics: 75% of all fatal anaphylactic reactions are due to penicillin

o   NSAIDs, including ASA

o   Anesthetics

o   Lasix

o   Iodine contrast

Management

• Cessation of the offending agent (i.e. discontinue the Abx infusion)
• ABCs, IV access (2 large bores), O2 mask, rapid assessment of whether a definitive airway (i.e. ETT intubation) is needed
• Call for respiratory therapist (RT), critical care outreach team (i.e. CCOT)
• Emergent Medical Management:
•  EPINEPHRINE 0.5 mL of 1:1000 (1mg/mL), IM q5 min
• Administer in the antero-lateral thigh, in the middle 1/3
• Use IM route, as SC results in variable absorption and slower onset of action!
• If repeated doses are not improving signs of cardiogenic & vasodilatory shock, consider initiation of an EPI infusion (IV)
•  IV 0.1 mg (1:10000, 0.1mg/mL) over 5 min, may give 5-15 mcg/min infusion
• Delay in EPI IM correlates with higher mortality. TIME IS OF THE ESSENCE.
• There are NO real contra-indications to giving EPI in the setting of presumed anaphylaxis!
• IV FLUID
• Use Normal Saline (i.e. 0.9 NS), as Ringer's lactate has a theoretical risk of contributing to metabolic acidosis; Dextrose is rapidly extra-vasated from the circulation into the interstitial tissues; Colloid products (i.e. starch or albumin) confer no survival advantage and they are costly!
• Continue to run IVF to prevent potential CDV collapse; up to 35% of the intravascular volume can become extra-vascular within 10 minutes of the onset of anaphylaxis
• SABA (i.e. salbutamol): NEB or MDI with aerochamber
• OTHER:
• Positioning: lay the patient supine, with feet elevated, in a Trendelenburg position (this helps promote venous return and reduce the risk of empty ventricle syndrome)
• NON ACUTE MEDICAL MANAGEMENT
•   H1 or H2 antagonists: i.e. Dimenhydramine (Benadryl): 50 mg IV q6h
• Role: alleviates symptoms of pruritis; no other real benefit
• STEROIDS: Methylprednisolone 125 mg IV
•  Reduces bronchospasm, but the effect is NOT immediate
• No immediate benefit
• May reduce the risk of a biphasic reaction (occurs in ~ 23% of patients, approximately 8-10 hours after initial anaphylaxis, despite no further exposure to the presumed stimulus/agent)

NOTE: consider vasopressors if severe shock, crash cart present, may need a definitive airway STAT (earlier—less inflammation of soft tissue and airway—call anaesthesia!)

Long-Term Management for Discharge & Non-Pharmacological Management

• Ensure the patient understands they have a severe allergy to __
•  Documentation of allergy on hospital medical record
• Recommend a Medic-Alert bracelet
•  Prescribe an EpiPEN and instructions on use
• Written action plan (need to inform caregivers, schools, etc)
•  Notify any outside providers (i.e. pharmacy, GP, etc)
• Consider referral to an allergist!* (i.e. if consideration for desensitization was ever needed)                                       

·      Things that may complicate treatment of Anaphylaxis

•      Patient on Beta-Blockers: theoretically block the effect of EPI—making anaphylaxis more severe and refractory! Reversal with glucagon 1-5 mg IV in cases of refractory anaphylaxis
•      ACE inhibitors: can result in more severe or refractory anaphylaxis by blocking the inactivation of bradykinin, which mediates anaphylaxis

Confirming the Diagnosis: The Role of Tryptase measurement?

Elevated levels of total tryptase in the serum can be useful to help distinguish anaphylaxis from other conditions on the DDx (i.e. vasovagal episode, MI, benign flushing, carcinoid syndrome, etc—as these other disorders are normally not associated with an elevation of total tryptase).

An increase in tryptase indicates that mast cell activation has occurred.

Bottom Line: some hospitals allow you to order tryptase levels; collection of tryptase measurements should be considered if the diagnosis of anaphylaxis is being considered. Elevations in tryptase correlate with hypotension and support the diagnosis of anaphylaxis, however; normal levels do not exclude anaphylaxis (especially in food-induced reactions). The specificity and sensitivity of tryptase elevations have not been determined. Try to collect the sample within 1-3 hours of the event. Generaly, large elevations of the tryptase level persist for several hours after the onset of the anaphylaxis.