5. ANAPHYLAXIS Flashcards
Definition of Anaphylaxis:
Anaphylaxis is an acute, potentially-life threatening, multisystem syndrome cause by sudden release of mast cell mediators into the systemic circulation.
It is an IgE-dependent reaction involving 2 or more organ systems
- Cutaneous
- Respiratory
- Cardiovascular
- GI
On the other hand, Anaphylactoid reaction______
On the other hand, Anaphylactoid reaction is a non-IgE dependent reaction which DOES NOT require previous sensitization
This involves direct mast cell activation, complement activation or alteration in arachidonic acid metabolism by Aspirin & NSAIDs
In terms of statistics, the lifetime prevalence of these reactions are estimated to be between
In terms of statistics, the lifetime prevalence of these reactions are estimated to be between 0.05 to 2 percent in the gen population
Etiology of Anaphylaxis:
Some of the common causes of ANAPHYLAXIS include:
- Food - peanuts, walnuts, casher, pistachio, milk, eggs, chicken, fish, shell fish, sesame seeds, wheat, food preservatives
- Drugs - B lactam antibiotics, Sulfonamides, monoclonal antibodies
- Vaccines - tetanus toxoid, mmr, dpt, influenza
- Hymenoptera Venom - honeybee, wasp, hornet, fireant
- Rubber Latex- gloves
It is also important to know the different causes of Anaphylactoid Reactions since more of less the will REQUIRE THE SAME MANAGEMENT
- Physical factors - exercise, cold, heat, sunlight
- Drugs - aspirin, NSAIDs, Opiates, radiocontrast media, ethylene oxide, dialysis tubing
- IVIg
Pathogenesis of Anaphylaxis
Classical mechanism associated with allergic diseases is initiated by an ALLERGEN
Begins with ALLERGIC SENSITIZATION which occurs when an allergen is first encountered
—> allergens are then internalized by Antigen-Presenting Cells (APC) and expressed on their surface through HLA
The products are then presented to other cells involved in the immune response, particulary the T cells and B cells
Through a series of specific cell interactions, B cells are then transformed into plasma cells, undergo class switching, and are able to synthesize IgE antiboies specific to an allergen
- **Once an allergen is reencountered, it binds to the Fab portion of the bound IgE initiating a process of intracellular signaling —> degranulation of mast cells with subsequent release of INFLAMMATORY MEDIATORS
- histamine, proteases, prostaglandins, leukotrienes
(+) vasodilation & dec. peripheral vascular resistance —> HYPO
(+) contraction and separation of endothelial cells —> EDEMA
Bronchoconstriction
Increased gastric acid output
Clinical Manifestations of Anaphylaxis:
Symptoms usually begin within SECONDS to MINUTES and can be divided into EARLY and LATE PHASE reactions
EARLY PHASE REACTIONS:
CUTANEOUS - generalized hives, pruritus, flushing, swollen lips, periorbital edema, conjunctival swelling
RESPIRATORY - rhinorrhea, hoarseness, stridor, shortness of breath, wheeze, cough
GI - nausea, vomiting, diarrhea, crampy abdominal pain
CV - syncope, dizziness, palpitations, chest pain
NEUROLOGIC - anxiety, irritability, sense of impending doom, confusion
LATE PHASE REACTIONS:
Late phase reactions account for the biphasic anaphylaxis seen when EPINEPHRINE administration is DELAYED. It occurs 4-6 hours after the disappearance of the early phase symptoms and can last for days to weeks.
This is brought about by remaining cellular mediators and tissue destruction from sustained allergic response.
There may be increased bronchial reactivity, edema, and further inflammatory cell recruitment.
The primary endangering manifestations of anaphylaxis must be immediately recognized. This includes:
- Laryngeal edema
- Severe bronchial obstruction
- Cardiac dysfunction
- Hypotension
Diagnosis of Anaphylaxis
Criterion 1,2,3
Since there are no definite laboratory work-ups locally available to diagnose or confirm anaphylaxis, diagnosis is CLINICAL and relies on prompt recognition of the syndrome
There are 3 diagnostic criteria for anaphylaxis, each reflecting a different clinical presentation
Criterion 1: Acute onset of an illness (mins to several hours) involving the skin, mucosal tissue such as Generalized hives, pruritus, flushing, swollen lips, tongue, uvula) and at least one of the following:
Respiratory compromise (ex. Dyspnea, wheeze/bronchospasm, stridor, reduced PEFR, hypoxemia)
Reduced blood pressure or associated symptoms and signs of end-organ malperfusion (ex. Hypotonia collapse, syncope, incontinence)
CRITERION 2: two or more of the ff that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours)
Involvement of skin-mucosal tissue
Respiratory compromise
Reduced BP or assoc. symptoms & signs of end-organ malperfusion
Persistent GI symptoms and signs (ex. Crampy abdominal pain, vomiting)
CRITERION 3 - reduced BP after exposure to a known allergen for that patient (mins to hours)
Reduced BP in adults
SBP <90 mmHg
Greater than 30% decrease from person’s baseline
Infants and children
Low SBP (age specific)
1 month - 1 year: <70 mmHg
1 year - 10 years: <70 mmHg x [2 x age]
11 years to 17 years: <90 mmHg
Greater than 30% decrease from person’s baseline
Diff Diagnosis for
- Vasovagal collapse - pallor, nausea & diaphoresis with slow pulse but maintained BP
- Hereditary angioedema - strong FH, laryngeal edema, deep localized swelling (hand&foot), cutaenous non-pitting, non-pruritic edema, abdominal pain
- Arrhythmias, MI
- Aspiration
- Pulmonary embolism
- Seizure disorders
- Flushing disorders - alcohol ingestion, mastocytosis, carcinoid syndrome
- Scombroid poisoning - unfresh fish products contaminated with morganella morgagnii (histidine decarboxylase)
- Other causes of shock (cardiogenic, septic)
Management :
Prompt assessment and treatment are critical in anaphylaxis as respiratory cardiac arrest can occur within minutes
The cornerstones of initial management are the ff:
1.) REMOVAL of INCITING ALLERGEN if possible
- ) IM INJECTION of EPINEPHRINE at the earliest opportunity
- ) Placement of patient in a supine position with lower extremities elevated unless there is upper airway swelling wherein patient must be upright
- ) Supplemental o2 & airway management
- ) Volume rescucitation with IV fluids
- ) Continuous monitoring
Management State these 1. IM EPINEPHRINE 2. POSITIONING 3. AIRWAY & OXYGEN 4. FLUIDS 5. MONITORING 6. ADJUNCTIVE AGENTS (H1 receptor antagonists)
- IM EPINEPHRINE
* *Epinephrine is the first and most important Treatment for anaphylaxis. It should be administered as soon as anaphylaxis is recognized to prevent progression of life-threatening symptoms. The pharmacologic actions of epinephrine address the pathophysiologic changes that occur in anaphylaxis better than any medication.
Therapeutic actions of epinephrine include:
A-1 receptor: vasoconstriction, inc. peripherap vascular resistance, inc. blood pressure, decreased mucosal edema
B-1 receptor: inc. heart rate (chronotropy), inc. force of cardia contraction (inotropy)
B-2 receptor: dec. mediator release from mast cells and basophils, inc. bronchodilation
Recommended ROUTE OF ADMINISTRATION is IM on the VASTUS LATERALIS
Dosing would be an aqueous dilution of 1:1000 at 0.01 mL/kg, maximum of 0.5 mL per dose.
IM epinephrine MAY BE REPEATEd at 5 to 15 minutes intervals if there is no response or even sooner if clinically indicated.
- AIRWAY and OXYGEN
Immediate intubation should be done if there is an evidence of impending airway obstruction from angioedema/laryngeal edema
Oxygen can be given 8 to 10 L/min via facemask or up to 100% oxygen as needed - FLUIDS
Two large bore IV catheters should be inserted in preparation for rapid administration of fluids and medications
Adults: 1 to 2 L of NSS at the most rapid flow rate possible in the first minutes. Large volumes of fluid (up to 7L) may be required.
Children: 20 ml/kg bolus of NSS each over 5 to 10 minutes and repeated as needed
Larger volumes of fluid (up to 100ml/kg) may be required
- MONITORING
Contiuous non invasive hemodynamic monitoring and pulse oximetry should be done. UO hsould also be monitored for severe hypotension or shock* - ADJUNCTIVE AGENTS
H1 Receptor Antagonists - mainly used to relieve pruritus and urticaira; does not relieve airway obstruction, hypotension or shock
ADULTS: Diphenhydramine 25-50 mg/IV over 5 minutes (Max dose of 400 mg/day)
CHILDREN: Diphenhydramine 1 mg/kg IV over 5 minutes
Max dose: 50 mg/kg or 200 mg/day
H2 receptor antagonists - used to decrease gastric acid output, decrease vasodilation and decrease mucus gland secretion
ADULTS: Ranitidine 50 mg in 20 mL fluid IV over 5 minutes
CHILDREN: Ranitidine 1 mg/kg in 20 mL fluid IV over 5 minutes
Ranitidine is preferred over cimetidine due to lower drug interactions*
GLUCOCORTICOIDS
Fiancé the function of glucocorticoids take several hours. Therefore, he’s medications do not really the initial symptoms and signs of anaphylaxis. Rational for giving them is theoretically prevent biphasic reactions however randomized controlled trial’s have failed to confirm its effectiveness. The only proven way to prevent biphasic reaction is timely administration of epinephrine.
Nevertheless, a dose of methylprednisolone 1-2 mg/kg/day is sufficient.
Patients on B-blockers may be resistant to epinephrine and can develop _________
Refractory hypotension
Glucagon 1-5 mg/IV over 5 minutes should be adminitered because it has inotropic and chronotropic effects not mediated through B-receptors
This is followed by Infusion-titrated (5 to 14 ug/min) to clinical response.
Most patients with minor signs and symptoms who show marked resolution with ER treatment can be sent home with regular oral antihistamines and follow-up instructions.
Those who present with life-threatening anaphylaxis should be admitted and observed for another 24-48 hours even if their symptoms were easily managed or reverse because of high risk of late phase reactions.
Prevention of Anaphylaxis
- Avoidance of known allergen
- Keep an ADRENALINE KIT (EPIPEN) and instruct how and when to use it
- Advise patient to wear and carry warning identification
- Venom immunotherapy for insect-allergic individuals
