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Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
Travancore Medicity, Kollam
India
editor
Anaphylaxis is a serious reaction causing a combination of characteristic findings and which is rapid in onset & may cause death.
CLINICAL CRITERIA
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2) | Two or more signs or symptoms that occur minutes to hours after allergen exposure :
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3) | Anaphylaxis should be suspected when patients are exposed to known allergen & develop hypotension. |
Pathophysiology
Anaphylaxis usually arises from activation of mast cells and basophils. They release performed mediators from secretory granules that include histamine, tryptase, carboxypeptidase A and proteoglycans. Downstream activation of phospholipase A2, followed by cyclooxygenases & lipoxygenases, produces arachidonic acid metabolites including prostagladins, leukotrienes and platelet activating factor. The inflammatory cytokine ,TNF-alpha is released as a performed mediator & also late phase mediator with other cytokine & chemokines. These mediators are responsible for pathophysiology of anaphylaxis.
Histamine stimulates vasodilation & increases vascular permeability, heart rate, cardiac contraction & glandular secretion.
Prostaglandin D2 is a bronchoconstrictor , pulmonary & coronary vasoconstrictor & peripheral vasodilator.
Leukotrienes produce bronchoconstriction, increase vascular permeability and promote airway remodeling.
Platelet activating factor is also a potent bronchoconstrictor and increases vascular permeability . TNF- alpha actiavtes neutrophoils, recruit other effector cells and enhance chemokine synthesis.
These overlapping & synergestic physiologic effects contribute to the overall pathophysiology of anaphylaxis.
Clinical Feature
Signs & symptoms begin suddenly, often within 60 minutes of exposure . In general, faster the onset of symptoms , more severe is the reaction – one half of anaphylatic fatalities occur within first hour.
Classic presentation begins with utricaria, pruritis, cutaneous flushing. They are followed by sense of fullness in throat , anxiety, sensation of chest tightness, shortness of breath and light headedness. This may be followed by abdominal pain or cramping nausea, vomiting , diarrhea, bronchospasm, rhinorrhea and conjunctivitis ,& or hypotension. As it progress respiratory distress, decreased level of consciousness and circulatory collapse may ensue. Severe cases loss of consciousness and cardiorespiratory collapse may result.
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MANAGEMENT
First Line Therapy
Airway & oxygenation :
Look for signs and symptoms of angioedema, if angioedema is causing respiratory distress ealry intubation is warranted.
Provide O2 to maintain SO2 > 90%.
Decontamination:
Remove the causative agent if it is identified like insect sting.
Epinephrine:
It is the drug of choice & the first drug to be administrated in acute anaphylaxis.
Epinephrine is a mixed α1 & β receptor agent. The α1 receptor activation reduces mucosal edema and treats hypotension. Β 1 receptor stimulation increases heart rate and myocardial contractility and β 2 receptor stimulation provides bronchodilation and limits further release.
In patients without signs of cardiovascular collapse administer epinephrine IM. Repeat every 5 -10 minutes. Injecting to thigh achieves better peak levels in blood. IV epinephrine is started if refractory .
IV Crystalloids
Hypotension is generally distributive shock and responds to fluid resuscitation.
| Adult dose | Pediatric dose |
First Line Therapy | ||
Epinephrine | IM : 0.3 – 0.5mg (1:1000 dilution) | IM : 0.01 mg/kg (.01 ml/kg of 1:1000 dilution) |
IV Bolus : .1mg (.1ml of 1:1000 dilution) in 10ml NS over 10-15 min |
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IV Infusion *: start with 1mcg /min, titrate dose as needed. | IV Infusion : 0.1 -0.3 mcg/kg/min ; titrate dose as needed. Max : 1.5 mcg/kg/min | |
Oxygen | Titrate to maintain SaO2 ≥90% | Titrate to maintain SaO2 ≥90% |
IV fluid | 1-2 L Bolus | 10 -20 ml/kg bolus |
Second line therapy | ||
H1 receptor blocker | ||
Diphenhydramine | 25 -50 mg Q6h IV/IM/PO | 1mg/kg Q6h IV/IM/PO |
H2 receptor blocker | ||
Ranitidine | 50mg IV over 5 minutes | 0.5mg/kg IV over 5 minutes |
Corticosteroids | ||
Hydrocortisone | 250-500 mg IV | 5-10 mg/kg |
Methylprednisolone | 80 – 125 mg IV | 1 -2 mg /kg IV |
Prednisolone | 40 -60 mg/day PO BD or OD | 1-2 mg/day PO BD or OD |
Treatment of patients on beta blockers with refractory hypotension | ||
Glucagon | 1mg IV every 5 minutes until hypotension resolves, followed by 5 -15 mcg/min infusion | 50 mcg/kg IV every 5 min |
Second line therapy
Corticosteroids :
Corticosteroids are used to prevent protracted and biphasic reaction.
Hydrocortisone and cortisone have strongest mineralocorticoid effects followed by prednisolone. Methylprednisolone and dexamethasone have the lowest mineralocorticoid effect and produce less fluid retention thus preferred in elderly.
If wheeze is present salbutamol+ ipratropium bromide nebulisation is given.
Magnesium 2gm IV over 20-30min in 100ml NS can be tried in severe bronchospasm.
Antihistamine
H1 & H2 receptor blocker is recommended for all patients.
Allergic Bronchospasm
A β 2 bronchodilator intermittent or continuous nebulisation is used if wheezing is present.
Magnesium is used incase of refractory bronchospasm.
Glucagon : Patients on beta blockers unresponsive to fluids & adrenaline should receive glucagon 1mg IV every 5min until hypotension is resolved and followed by infusion of 5-10mcg/min.
Updated on 5/3/2019
Reference
Tintinalli - 8th Edition
*: Mix 1mg in 500ml NS & infuse @ 0.5ml/min & titrate as needed. Each ml will contain 2mcg/ml .
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emmedonline
Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
Travancore Medicity, Kollam
India
editor