| disease | Anaphylactic Shock |
Anaphylaxis, or anaphylactic shock, is a severe multi-organ syndrome triggered by an immune response when certain antigenic substances enter a sensitized body. The manifestations and severity of anaphylactic shock vary greatly depending on the body's reactivity, the amount of antigen, and the route of entry. It typically occurs suddenly and intensely, and if not treated promptly, can be life-threatening.
bubble_chart Etiology
The antigenic substances that act as allergens to cause this disease include:
(1) Heterologous (foreign) proteins - hormones (insulin, vasopressin), enzymes (chymotrypsin, penicillinase), mongolian snakegourd root extracts (pollen from weeds, trees, grasses), foods (egg white, milk, nuts, seafood, chocolate), antisera (antilymphocyte serum or antilymphocyte gamma globulin), occupationally encountered proteins (rubber products), bee venom.
(2) Polysaccharides - such as iron dextran.
(3) Many commonly used drugs - such as antibiotics (penicillin, cephalosporins, amphotericin B, nitrofurantoin), local anesthetics (procaine, lidocaine), vitamins (thiamine, folic acid), diagnostic agents (iodinated X-ray contrast media, bromsulphalein), occupationally encountered chemicals (ethylene oxide).
The vast majority of anaphylactic shock cases represent the systemic manifestation of a typical type I hypersensitivity reaction affecting multiple organs, particularly the circulatory system. Exogenous antigenic substances (some drugs are incomplete antigens but can combine with proteins to form complete antigens after entering the body) can stimulate the immune system to produce corresponding antibodies. The production of IgE varies significantly among individuals due to constitutional differences. These specific IgEs have strong cytophilic properties and can bind to "target cells" in the skin, bronchi, vascular walls, etc. When the same antigen re-exposes a sensitized individual, it triggers a widespread type I hypersensitivity reaction. The various mediators released during this process, such as histamine and platelet-activating factor, are the direct causes of clinical manifestations like edema and exudation in multiple organs.
During blood transfusion, plasma infusion, or immunoglobulin administration, immediate-type anaphylactic shock may occasionally occur. There are three possible disease causes: ① The donor's specific IgE reacts with medications (e.g., penicillin G) the recipient is receiving. ② Individuals with selective IgA deficiency may develop IgG-class anti-IgA antibodies after multiple transfusions of IgA-containing blood products. Subsequent administration of IgA-containing products may lead to IgA-anti-IgA immune complexes, causing type III hypersensitivity-mediated anaphylactic shock. ③ Intravenous immunoglobulin preparations containing high-molecular-weight immunoglobulin polymers can activate complement, producing anaphylatoxins C3a, C4a, and C5a, which then activate mast cells to cause anaphylactic shock. A few patients may develop clinical manifestations of anaphylactic shock mainly through mast cell degranulation when using drugs such as opium tincture, dextran, highly ionized X-ray contrast media, or antibiotics (e.g., polymyxin B). Recently, cases where no allergen-antibody reaction exists—i.e., anaphylactic shock symptoms and signs occurring through non-immunologic mechanisms—have been termed anaphylactoid reactions.bubble_chart Pathological Changes
The main pathological manifestations of sudden death due to this disease include acute pulmonary static blood and hyperinflation, laryngeal edema, visceral congestion, pulmonary interstitial edema and hemorrhage. Microscopically, edema of the airway mucous membrane root of the nose can be observed, with increased secretions in the small airways, congestion of blood vessels in the bronchi and pulmonary interstitium accompanied by eosinophil infiltration. Approximately 80% of fatal cases also exhibit focal necrosis or lesions in the myocardium. The spleen, liver, and mesenteric membrane vessels are often congested with eosinophil infiltration. A few cases may also present with gastrointestinal bleeding.
The disease mostly occurs suddenly; about half of the patients develop symptoms within 5 minutes of exposure to the disease-causing antigen (such as penicillin G injection), with only 10% of patients experiencing symptoms after half an hour, and very few patients developing the condition during continuous medication.
Anaphylactic shock has two main characteristics: first, there are manifestations of shock, namely a sharp drop in blood pressure to below 10.6/6.6 kPa (80/50 mmHg), with the patient experiencing impaired consciousness, ranging from mild confusion to severe unconsciousness. Second, before or simultaneously with the onset of shock, there are often symptoms related to allergies, as listed below.
(1) Skin and mucosal manifestations — Often the earliest and most common signs of anaphylactic shock, including skin flushing, cutaneous pruritus, followed by widespread urticaria and/or angioedema; sneezing, watery nasal discharge, hoarseness, and even respiratory distress may also occur.
(2) Respiratory obstruction symptoms — The most common manifestation of this condition and the leading cause of death. Due to airway edema, increased secretions, and laryngeal and/or bronchial spasms, patients experience a sensation of throat blockage, chest tightness, shortness of breath, wheezing, suffocation, cyanosis, and even death from asphyxia.
(3) Circulatory failure manifestations — Patients initially experience palpitations, sweating, pale complexion, rapid and weak pulse; then progress to cold limbs, cyanosis, rapid drop in blood pressure, disappearance of pulse, and ultimately unmeasurable blood pressure, leading to cardiac arrest. A few patients with pre-existing coronary artery disease may develop myocardial infarction.
(5) Other symptoms — More common ones include irritating cough, continuous sneezing, nausea, vomiting, abdominal pain, diarrhea, and ultimately, urinary incontinence may occur.
bubble_chart Treatment Measures
Decisive action must be taken promptly to address the situation without delay. ① Immediately cease exposure to and remove the suspected allergen or causative drug. Apply a tourniquet proximal to the injection or insect bite site to slow absorption, or administer a local injection of 0.005% adrenaline (2–5 ml) at the affected area. ② Administer 0.1% adrenaline immediately, starting with a subcutaneous injection of 0.3–0.5 ml, followed promptly by an intravenous injection of 0.1–0.2 ml, and then maintain an intravenous drip with 5% glucose solution to ensure continuous delivery. Adrenaline rapidly relieves bronchospasm through β-receptor effects and constricts peripheral blood vessels via α-receptor effects. It also counteracts the release of certain mediators in type I hypersensitivity reactions, making it the drug of choice for treating this condition. It may be administered repeatedly during the course of treatment. Typically, after 1–2 adrenaline injections, most patients show gradual improvement in shock symptoms within half an hour. Conversely, if shock persists without improvement, the case is severe, and intravenous dexamethasone (10–20 mg) or hydrocortisone sodium succinate (200–400 mg) should be administered as early as possible. Alternatively, longer-acting and less side-effect-prone anti-shock drugs such as noradrenaline or metaraminol (Aramine) may be selected as appropriate. Concurrently, administer vasoactive drugs and promptly replenish blood volume, with an initial rapid infusion of 500 ml of fluid. The total fluid volume for adults on the first day may generally reach 4000 ml. ③ Anti-allergic and symptomatic treatment typically involves intramuscular injection of chlorphenamine (10 mg) or promethazine (25–50 mg), keeping the patient supine, providing oxygen, and ensuring airway patency.
During anaphylactic shock, the patient’s allergic threshold is significantly lowered, potentially turning previously non-allergenic substances into allergens. Therefore, avoid excessive or indiscriminate use of medications in treating this condition.
Generally, the later the symptoms of this condition appear after antigen exposure, the better the prognosis. Individuals who are highly allergic and experience "lightning-like" anaphylactic shock often have a poorer prognosis. Those with a history of coronary heart disease are more prone to myocardial infarction during this condition due to plasma concentration and blood pressure drop. Patients with pronounced neurological symptoms are also more likely to retain various complications of cerebral hypoxia after recovery.
Since the vast majority of this condition is mediated by specific IgE allergies, each exposure to the corresponding allergen leads to an increase in IgE production, making the likelihood of a severe reaction upon re-exposure even greater. Therefore, patients should be warned to never be exposed to similar allergens again, and contraindicated medications should be recorded on the first page of their medical records.
The most fundamental approach is to identify the allergens that cause this condition and implement effective avoidance measures. However, in clinical practice, it is often difficult to make a specific allergen diagnosis, and many patients experience allergic-like reactions not mediated by immune mechanisms. Therefore, the following precautions should be taken: 1. Before administering medication, thoroughly inquire about the patient's allergy history. Patients with a history of sexually transmitted diseases should have prominent and detailed records on the first page of their medical history. 2. Minimize unnecessary injections and prioritize oral formulations whenever possible. 3. Observe patients with allergic constitutions for 15–20 minutes after injection. If they must receive medications that may trigger this condition (e.g., sulfa contrast agents), consider administering antihistamines or prednisone (20–30 mg) beforehand. 4. Perform intradermal or skin prick tests first and avoid drugs that yield positive results. If unavoidable, attempt "desensitization testing" or "hyposensitization testing." The principle involves gradually increasing the dose of the desensitizing medication under the protection of antihistamines and other drugs until the patient develops tolerance. During desensitization, close medical supervision is essential, with emergency measures such as aqueous epinephrine, oxygen, tracheal intubation, and injectable corticosteroids readily available.
The disease develops rapidly, so timely diagnosis is essential. Whenever systemic reactions occur immediately after exposure (especially after injection) to antigenic substances or certain medications, or after bee stings, and these reactions cannot be explained by the pharmacological effects of the drugs themselves, the possibility of this disease should be immediately considered. Therefore, diagnosis is generally not difficult. However, the following conditions should be excluded.
(1) Vasovagal syncope (or vasovagal collapse) often occurs after injections, especially in patients with fever, dehydration, or a tendency toward hypoglycemia. Patients often exhibit pale complexion, nausea, cold sweating, and may subsequently experience syncope, which can easily be misdiagnosed as anaphylactic shock. However, this condition does not involve cutaneous pruritus or rashes, and syncope improves immediately upon lying down. Although blood pressure is low, the pulse is slow, which differs from anaphylactic shock. Vasovagal syncope can be treated with atropine-like medications.
(2) Hereditary angioedema is a disease inherited through autosomal dominance, characterized by a deficiency of C1 esterase inhibitor. Patients may suddenly develop symptoms under stimulation from nonspecific factors (e.g., infection, trauma, etc.), manifesting as angioedema of the skin and respiratory mucous membranes. Due to airway obstruction, patients often experience wheezing, shortness of breath, and extreme dyspnea, which are quite similar to anaphylactic shock. However, this condition has a slower onset, many patients have a family history or a history of episodes since childhood, and there is usually no drop in blood pressure or urticaria during an attack, which can help differentiate it from anaphylactic shock.
The specific sexually transmitted disease etiology diagnosis is of great significance for the prevention and treatment of this condition. However, allergen testing should be conducted: ① after the shock has been resolved; ② after discontinuing anti-shock and anti-allergy medications; ③ if skin tests are performed, it is best to have necessary anti-shock medications on hand. A small number of patients with negative skin tests may still develop this condition.
