OverviewAnaphylaxis is a sudden, severe allergic reaction with multisystem organ damage. If not diagnosed and treated promptly, patients can die rapidly due to severe cardiovascular and respiratory system dysfunction. Anaphylaxis is a condition in which the effective blood volume is insufficient to maintain the function of vital organs, and anaphylaxis is compounded by acute laryngeal edema, tracheospasm, tracheal khat-like secretion, intra-alveolar hemorrhage, and non-cardiogenic hyper-exudative pulmonary edema, a series of serious lesions that can rapidly lead to respiratory system dysfunction.
Anaphylaxis is a manifestation of tachyphylaxis in multiple organs of the body, especially the circulatory system.
I. Pathogenesis
1.IgE-mediated antigen-antibody reaction is a type I rapid allergic reaction.
IgE-mediated antigen acts on mast cells and basophils of the body. Cell degranulation changes, rapid release of large amounts of histamine, resulting in dilation of the blood vessels of the body circulation, increased vascular permeability, hypotension, angioedema, tracheospasm, skin pruritus and increased mucus secretion.
2, penicillin anaphylaxis is a typical type I allergic reaction.
Epidemiological clinical factors most likely to cause anaphylaxis are radioactive iodine contrast agents, β-lactam antimicrobial agents and bee stings.
Clinical manifestations Anaphylaxis can occur rapidly within seconds to minutes after exposure to an allergen, or after one hour. The earlier the onset of allergic symptoms, the more severe the condition.
Anaphylaxis often involves more than 2 of the following organs: skin, respiratory system, cardiovascular and gastrointestinal system.
1. Respiratory system. Laryngeal edema, spasm and tracheal catarrhal secretion cause edematous obstruction of the upper airway, with dyspnea, throat stiffness, hoarseness and cough. Non-cardiogenic pulmonary edema, bronchospasm, and intra-alveolar hemorrhage cause lower respiratory tract edema, which presents as asthma, dyspnea, and cyanosis. Upper airway edema, such as incomplete laryngeal edema, mainly manifests as inspiratory dyspnea, while lower airway edema, such as asthma, mainly manifests as expiratory dyspnea. If edema occurs in both upper and lower respiratory tracts, it can cause rapid deterioration of the condition and endanger life.
2. Cardiovascular system. Due to capillary leakage, vasodilatation leads to absolute or relative lack of blood volume, lack of cardiovascular blood return, cardiac cavity emptiness, and cardiovascular system field trapping, resulting in shock. Tachycardia and syncope are often the main symptoms before cardiac arrest. There can also be supraventricular tachycardia, conduction block, myocardial ischemia and infarction.
3. Skin. Paresthesia, angioedema, sweating, manifested by redness and itching of the skin.
4, Digestive system. Edema of gastrointestinal mucosa and increased secretion of intestinal fluid, liver and spleen congestion, manifested by abdominal pain, abdominal distension, vomiting, diarrhea, severe bloody diarrhea may occur.
5. Central nervous system. Syncope, drowsiness, convulsions, and patients may have a sense of frequent death.
6, Eye and nasal cavity. Conjunctival congestion, itching. Congestion of nasal mucosa, khat-like secretion, allergic rhinitis, itching of the nose.
7, Blood system. Hematoconcentration, diffuse intravascular coagulation (DIC).
The essentials for diagnostic diagnosis are.
1, the presence of allergens.
2, rapid onset of disease.
3, damage to multiple system organs: the essence of the circulatory system is a decrease in effective blood circulation, which is manifested by a drop in blood pressure.
Differential diagnosis
1, vagal syncope (or vagal deficiency): also known as “dizziness”. It mostly occurs after injection, especially when the patient has fever, water loss or hypoglycemic tendency. Patients often pale, nausea, cold sweat, followed by fainting, can be easily misdiagnosed as anaphylaxis, vagal vasovagal coma can be treated with atropine type drugs.
2, hereditary angioedema: angioedema with a family history, not accompanied by pityriasis, but the gastrointestinal mucosa is often significantly edematous, and severe abdominal pain, and there is edema of the respiratory mucosa and cause airway obstruction.
3. Infusion reaction: chills, fever, and increased WBC.
Treatment
1.Basic life support.
(1) Immediately put the patient in a flat position; closely observe respiration, blood pressure, heart rate, and urine output. If there is asthma or respiratory distress, take the head high and feet low position; if there is loss of consciousness, put the patient’s head in the lateral position, lift the jaw, and remove the secretions from the mouth, pharynx, nose and trachea.
(2) Ensure airway patency. If angioedema is present and causes respiratory distress, intubation should be performed immediately. Endotracheal intubation requires a catheter that is more than one times smaller than the normal diameter of the catheter to avoid damage to the narrow airway.
2.Specific drug therapy.
(1) Epinephrine: 0.1% epinephrine 0.5~1.0ml is immediately injected subcutaneously or intramuscularly. Epinephrine is the drug of choice for rescuing anaphylaxis.
(2) Glucocorticoids: dexamethasone, hydrocortisone.
(3) Antihistamines.
H1 receptor blocker: Benadryl 20-40mg (or fexofenadione 50mg or paracetamol 10mg) intramuscular injection.
H2 receptor blockers: ranitidine, famotidine.
Effective for shock not controlled by epinephrine, steroids, infusions, and H1 blockers. Cimetidine prolongs the metabolism of β-blockers and may prolong the allergic state of patients using β-blockers. H2 antihistamines other than cimetidine should be used to treat hypersensitivity reactions.
3, blood volume expansion: fluids can be chosen from low molecular dextrose 500ml, Ringer’s solution, etc.
4. vasoactive drugs: dopamine 10-20 micrograms/.kg.min.
5, release of obvious bronchial spasm: aminophylline 0.25-0.5g plus 5%-10% glucose injection diluted and then administered quietly.
6.Correction of acidosis.
7, symptomatic treatment.