Anaphylaxis: Difference between revisions
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== Diagnosis == | == Diagnosis == | ||
The clinical picture and the determination of the etiological agent are crucial. | |||
We determine total and [[Laboratory asessment of specific IgE antibodies|specific '''IgE''']] and perform '''skin tests''' (prick tests). Elevation of '''eosinophilic cationic protein''' ([[ECP]]), increase of '''[[histamine]]''' in both plasma and urine, detection of '''[[eosinophils]]''' in bronchial or nasal secretion indicate an allergic cause. Tryptase, a specific [[mast cell]] protease, is determined experimentally. | |||
=== Differential diagnosis === | === Differential diagnosis === | ||
''' | '''Vasovagal [[syncope]]''' is characterized by a response to pain or stress. We find cold acres [[nausea]], a feeling of fainting, on the other hand, we do not see any skin marks or signs of airway obstruction. [[Bradycardia]] is typical , while anaphylaxis induces tachycardia as a compensatory mechanism. Pruritus is not present in '''[[hereditary angioedema]]''', in the family history we often find data on edema or [[suffocation]]. We confirm the diagnosis with decreased levels of C1 complement inhibitor and decreased CH 50 [[complement]] activity. '''[[Arrhythmia]]''' is shown in the ECG. In pacients with '''[[a hysterical attack]]''' we can sometimes also find symptoms of an anaphylactic reaction. Here, a psychiatric-psychological examination is necessary for a correct diagnosis. | ||
== Mechanism == | == Mechanism == | ||
''' | '''Anaphylactic reaction''' is a life-threatening process in which the body reacts excessively to contact with an allergen. It is therefore a special type of an[[Allergy|alergic reaction]]. Contact with an [[allergen]] activates the immune system. Activation of inflammatory factors increases vascular permeability and mass transfer of [[intravascular]] fluid into the interstitium. This reduces the volume of intravascular body fluid, which leads to [[hypotension]] and the pacient falls into [[shock]]. | ||
The anaphylactic reaction is triggered by three well-known mechanisms of the immune response to foreign substance exposure. | |||
=== IgE mediated reaction === | === IgE mediated reaction === | ||
It represents up to 60% of all anaphylactic reactions. IgE antibodies can be formed after a patient's first encounter with a foreign antigen. The antigen may be presented alone or in association with a protein carrier. IgE binds to mast cell and basophil receptors. Upon re-exposure to antigen → antigen leads to bridging of IgE molecules → degranulation of these cells and release of various fast-acting mediators. . | |||
=== Complement mediated reaction === | === Complement mediated reaction === | ||
Immunocomplex-activated complement cascade. The result is the formation of '''anaphylatoxins''' such as C3a and C5a - the direct mechanism triggers the release of mediators from basophils and mast cells. Immunocomplex activated complement is the reaction to [transfusion of blood|blood transfusion]], blood derivatives or plasma. Complement-mediated anaphylaxis occurs, for example, in patients with [[IgA]] deficiency. The formation of [[IgG]] anti-IgA antibodies has been demonstrated in these patients. The complement can also be activated directly by contrast agents and the dialysis membrane. | |||
=== Direct release of mediators and other mechanisms === | === Direct release of mediators and other mechanisms === | ||
* | * The mechanism of a direct mediator release, without the involvement of IgE or complement, is still unknown. Substances capable of this reaction are, for example, hyperosmolar substances such as [[mannitol]], radiocontrast substances, [[opiates]], [[quinolones]] or [[vankomycin]]. | ||
* | * Anaphylaxis after the administration of [[non-steroidal anti-inflammatory drugs ]] (NSAID) is associated with blockade of [[prostaglandin]] synthesiscaused by NSADs, [[leukotriene]] production increases and anaphylaxis is triggered. | ||
* | * Exercise or cold-induced anaphylaxis is based on the principle of direct histaminoliberation or IgE mediated reactions. | ||
=== | === The effect of mediators === | ||
* | * Release of mediators in degranulation – [[histamine]], [[tryptase]], [[heparin]]. | ||
* | * Many mediators of anaphylaxis are formed by ''de novo'' synthesis – prostaglandins D2, leukotrienes, PAF, IL-4, 5, 6, 13, [[TNF]]α and adenosine. | ||
''' | '''Mediators''' → development of clinical signs of anaphylactic reaction: bronchospasm, increased capillary permeability, alterations of systemic and pulmonary vascular smooth muscle. | ||
:* ''' | :* '''Histamine''' causes itching, endothelial dysfunction, erythema, bronchoconstriction and fluid loss; | ||
:* ''' | :* '''Leukotrienes''' lead to endothelial dysfunction, fluid loss, bronchoconstriction or hypotension; | ||
:* ''' | :* '''Adenosine''' causes bronchoconstriction; | ||
:* ''' | :* '''Prostaglandine D2''' induces hypotension; | ||
:* ''' | :* '''Interleukins and TNFα''' cause prolonged anaphylaxis. | ||
== Treatment == | == Treatment == | ||
=== Pre-medical first aid === | === Pre-medical first aid === | ||
If the patient is in shock and his upper airways are not swollen, it is advisable to place him in the Trendelenburg position. <ref name="uptodate ">{{Cite | |||
| type = db | | type = db | ||
| responsibility = Ronna L Campbell, MD, PhD John M Kelso, MD | | responsibility = Ronna L Campbell, MD, PhD John M Kelso, MD | ||
| Line 103: | Line 103: | ||
| cited = 2017-07-18 | | cited = 2017-07-18 | ||
}}</ref> | }}</ref> | ||
Next, we perform the '''correct''' tilting of the head with clearing of the airways and, if necessary, initiate cardiopulmonary resuscitation. If the allergen penetrated the tissue by injection, we cool the limb locally. Ideally, if the affected person has a package with drugs for an anaphylactic reaction, we will use them according to the instructions. <ref name="čls"/> | |||
=== Medical first aid and therapy === | === Medical first aid and therapy === | ||
====== | ====== Respiratory protection: ====== | ||
Early intubation and oxygenation in airway obstruction. <ref name="uptodate">{{Cite | |||
| type = db | | type = db | ||
| responsibility = Ronna L Campbell, MD, PhD John M Kelso, MD | | responsibility = Ronna L Campbell, MD, PhD John M Kelso, MD | ||
| Line 116: | Line 116: | ||
| cited = 2017-07-18 | | cited = 2017-07-18 | ||
}}</ref> | }}</ref> | ||
====== | ====== Circulation: ====== | ||
'''[[Ensuring venous access]]''' is particularly important. <ref name="uptodate"/> | |||
* | * rapid administration of crystalloids and volume expanders; | ||
* | * administration of adrenaline to the lateral vastus muscle at a dose of 0.01 mg / kg (maximum dose 0.5 mg) <ref name="uptodate"/> | ||
** | ** Intravenous administration of adrenaline is reserved for special cases! | ||
* | * Intravenous administration of antihistamines, eg Dithiaden at a dose of 1 mg im, or preferably iv (maximum daily dose is 8 mg). <ref name="čls">{{Cite | ||
| type = academic_publication | | type = academic_publication | ||
| surname1 = Petrů | | surname1 = Petrů | ||
| Line 133: | Line 133: | ||
}} | }} | ||
</ref> | </ref> | ||
* | * [[Corticosteroids]] administration has a limited effect in the acute phase, so it is more suitable for the later phase. <ref name="čls"/> | ||
* | * In bronchospasm, we administer β<sub>2</sub>-mimetics (např. Ventolin) (eg ventolin) in the usual doses as in bronchial asthma. | ||
* | * For local reactions we choose local cooling, local antihistamines, or general antihistamines p.o. | ||
=== | === Aftercare === | ||
Patients with a history of severe anaphylactic reaction after discharge are provided with an '''emergency package''' in case of re-exposure to the antigen. The package should contain an '''''adrenaline pen (Epipene), Prednisone tbl. and peroral antihistamines.'''''. | |||
; | ;The patient should be observed 12–24 hours after the response in the internal medicine or pediatric ward. <ref name="čls"/> | ||
<noinclude> | <noinclude> | ||
Revision as of 08:31, 14 April 2022
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Anaphylactic shock is a severe circulation disorder caused by immunological mechanisms. We distinguish severe forms (anaphylactic shock - with organ systems damage and a distributional shock) and less severe forms (mild skin conditions, urticarial reaction).
- Voice changes, difficulty swallowing and dyspnoea are all signs of a severe course.
Clinical picture
The time etween antigen exposure and the onset of clinical signs is usually less than one hour, the delay depends on several factors: the patient's sensitivity, the route of allergen administration and the amount of allergen. In 20% of patients, we observe a two-phase course of an anaphylactic reaction, in which the symptoms appear 6–24 hours after the initial reaction.
Skin and mucous membranes
- Pruritus and erytematous flush.
- Urticaria, which is mediated by IgE is usually located at the site of the allergen exposure, such as insect bites.
- Angioedema (more severe cases) = swelling of the lower dermis and the subcutaneous layer.
- Angioedema accompanied by urticaria is itchy.
- Non-pruritic angioedema is not a sign of hypersensitivity (eg. hereditary angioedema).
- Damage of mucous membranes is characterized by pruritus and congestion of the conjunctiva, nasal mucosa and oral cavity.
- Swelling of the lips or tongue can lead to difficulty swallowing, and in severe cases to respiratory distress.
Respiratory system
In the upper respiratory tract, there is life-threatening edema of the larynx and / or the epiglottis and other adjacent structures.
- Clinically, children may report a feeling of discomfort in the throat, difficult speech, hoarseness of voice.
- Inspiratory stridor may appear.
Lower airway involvement resembles an asthma attack with expiratory dyspnea, cough and chest retractions.
Cardiovascular system
Anaphylactic shock is a type of distributional shock. The cause of hypotension is extreme vasodilation, increased vascular permeability, capillary leak syndrome.
- The result is an intravascular volume depletion, and a toxic effect of released mediators cannot be ruled out pathophysiologically.
Clinically, we find a patient with hypotension, difficult-to-palpate pulsations, tachycardia, but pink periphery. We can often observe arrhythmias, the ECG may show signs of myocardial ischemia.
Central nervous system
Dizziness, syncope, convulsions or alterations of consciousness may appear. Clinical signs are caused by both hypoperfusion and CNS hypoxia and the direct toxic effect of released mediators.
Gastrointestinal system
Damage includes nausea, vomiting, diarrhea and abdominal pain. Other symptoms include rhinorrhoea, profuse sweating, metallic taste in the mouth, feeling hot, skin burning or a feeling of danger.
Severe forms
- Death occurs in the 1. hour after the reaction!
Severe forms occur immediately within minutes of allergen exposure (after drug application, after insect stings).
Symptoms:
- General: nausea, chills, palmar and plantar pruritus, pallor, loss of consciousness, hypothermia, bronchospasm, laryngeal edema, vomiting, diarrhea;
- Breathing: rapid, shallow, wheezing;
- Cardiovascular: tachycardia, hypotension, intangible pulse, inaudible sounds, convulsions,
- ECG changes: atrial fibrillation, ST changes.
Laboratory examination: Hemoconcentration, leucopenia, thrombocytopenia, hypoxemia, hypocapnia, later hypercapnia and acidosis with metabolic predominance also appear. Coagulation disorders in the form of DIC may occur.
Less severe forms
Less severe forms are characterized by generalized erythema and edema, including pharyngeal edema. Symptoms:
- bronchospasm, irritating cough, dyspnoea.
Diagnosis
The clinical picture and the determination of the etiological agent are crucial.
We determine total and specific IgE and perform skin tests (prick tests). Elevation of eosinophilic cationic protein (ECP), increase of histamine in both plasma and urine, detection of eosinophils in bronchial or nasal secretion indicate an allergic cause. Tryptase, a specific mast cell protease, is determined experimentally.
Differential diagnosis
Vasovagal syncope is characterized by a response to pain or stress. We find cold acres nausea, a feeling of fainting, on the other hand, we do not see any skin marks or signs of airway obstruction. Bradycardia is typical , while anaphylaxis induces tachycardia as a compensatory mechanism. Pruritus is not present in hereditary angioedema, in the family history we often find data on edema or suffocation. We confirm the diagnosis with decreased levels of C1 complement inhibitor and decreased CH 50 complement activity. Arrhythmia is shown in the ECG. In pacients with a hysterical attack we can sometimes also find symptoms of an anaphylactic reaction. Here, a psychiatric-psychological examination is necessary for a correct diagnosis.
Mechanism
Anaphylactic reaction is a life-threatening process in which the body reacts excessively to contact with an allergen. It is therefore a special type of analergic reaction. Contact with an allergen activates the immune system. Activation of inflammatory factors increases vascular permeability and mass transfer of intravascular fluid into the interstitium. This reduces the volume of intravascular body fluid, which leads to hypotension and the pacient falls into shock. The anaphylactic reaction is triggered by three well-known mechanisms of the immune response to foreign substance exposure.
IgE mediated reaction
It represents up to 60% of all anaphylactic reactions. IgE antibodies can be formed after a patient's first encounter with a foreign antigen. The antigen may be presented alone or in association with a protein carrier. IgE binds to mast cell and basophil receptors. Upon re-exposure to antigen → antigen leads to bridging of IgE molecules → degranulation of these cells and release of various fast-acting mediators. .
Complement mediated reaction
Immunocomplex-activated complement cascade. The result is the formation of anaphylatoxins such as C3a and C5a - the direct mechanism triggers the release of mediators from basophils and mast cells. Immunocomplex activated complement is the reaction to [transfusion of blood|blood transfusion]], blood derivatives or plasma. Complement-mediated anaphylaxis occurs, for example, in patients with IgA deficiency. The formation of IgG anti-IgA antibodies has been demonstrated in these patients. The complement can also be activated directly by contrast agents and the dialysis membrane.
Direct release of mediators and other mechanisms
- The mechanism of a direct mediator release, without the involvement of IgE or complement, is still unknown. Substances capable of this reaction are, for example, hyperosmolar substances such as mannitol, radiocontrast substances, opiates, quinolones or vankomycin.
- Anaphylaxis after the administration of non-steroidal anti-inflammatory drugs (NSAID) is associated with blockade of prostaglandin synthesiscaused by NSADs, leukotriene production increases and anaphylaxis is triggered.
- Exercise or cold-induced anaphylaxis is based on the principle of direct histaminoliberation or IgE mediated reactions.
The effect of mediators
- Release of mediators in degranulation – histamine, tryptase, heparin.
- Many mediators of anaphylaxis are formed by de novo synthesis – prostaglandins D2, leukotrienes, PAF, IL-4, 5, 6, 13, TNFα and adenosine.
Mediators → development of clinical signs of anaphylactic reaction: bronchospasm, increased capillary permeability, alterations of systemic and pulmonary vascular smooth muscle.
- Histamine causes itching, endothelial dysfunction, erythema, bronchoconstriction and fluid loss;
- Leukotrienes lead to endothelial dysfunction, fluid loss, bronchoconstriction or hypotension;
- Adenosine causes bronchoconstriction;
- Prostaglandine D2 induces hypotension;
- Interleukins and TNFα cause prolonged anaphylaxis.
Treatment
Pre-medical first aid
If the patient is in shock and his upper airways are not swollen, it is advisable to place him in the Trendelenburg position. [1] Next, we perform the correct tilting of the head with clearing of the airways and, if necessary, initiate cardiopulmonary resuscitation. If the allergen penetrated the tissue by injection, we cool the limb locally. Ideally, if the affected person has a package with drugs for an anaphylactic reaction, we will use them according to the instructions. [2]
Medical first aid and therapy
Respiratory protection:
Early intubation and oxygenation in airway obstruction. [1]
Circulation:
Ensuring venous access is particularly important. [1]
- rapid administration of crystalloids and volume expanders;
- administration of adrenaline to the lateral vastus muscle at a dose of 0.01 mg / kg (maximum dose 0.5 mg) [1]
- Intravenous administration of adrenaline is reserved for special cases!
- Intravenous administration of antihistamines, eg Dithiaden at a dose of 1 mg im, or preferably iv (maximum daily dose is 8 mg). [2]
- Corticosteroids administration has a limited effect in the acute phase, so it is more suitable for the later phase. [2]
- In bronchospasm, we administer β2-mimetics (např. Ventolin) (eg ventolin) in the usual doses as in bronchial asthma.
- For local reactions we choose local cooling, local antihistamines, or general antihistamines p.o.
Aftercare
Patients with a history of severe anaphylactic reaction after discharge are provided with an emergency package in case of re-exposure to the antigen. The package should contain an adrenaline pen (Epipene), Prednisone tbl. and peroral antihistamines..
- The patient should be observed 12–24 hours after the response in the internal medicine or pediatric ward. [2]
References
Related articles
External links
- Template:Akutně
- Anafylaxe (česká wikipedie)
- ALERGIE, ANAFYLAXE, ANAFYLAKTICKÝ ŠOK (článek z časopisu Medicína pro praxi)
References
- ↑ Jump up to: a b c d Anaphylaxis: Emergency treatment [database]. Ronna L Campbell, MD, PhD John M Kelso, MD. The last revision 2017-04-03, [cit. 2017-07-18]. <https://www.uptodate.com/contents/anaphylaxis-emergency-treatment>.
- ↑ Jump up to: a b c d PETRŮ, Vít. Anafylaktické reakce [online]. Praha : ČLS JEP, 2001, Available from <http://www.cls.cz/dokumenty2/postupy/r003.rtf>.
Literature
- HOŘEJŠÍ, Václav – BARTŮŇKOVÁ, Jiřina. Základy imunologie. 3. edition. Praha : Triton, 2008. 280 pp. ISBN 80-7254-686-4.
- HAVRÁNEK, Jiří: Anafylaxe
