ANAPHLATIC SHOCK

ANAPHYLATIC SHOCK

 

Anaphylaxis is an early-type, acute, systemic hypersensitivity reaction mediated by IgE (table 1). If shock symptoms develop in the presence of early type hypersensitivity, this situation is called anaphylactic shock. Peripheral vascular resistance decreases rapidly, resulting in a decrease in preload and cardiac output.

 

When the body, which has previously gained sensitivity through IgEs during the first encounter, encounters the same substance for the second time, the sensitive IgEs become antigenic. It causes the formation of a complex with nutrient and the secretion of mediators from basophils in the circulation and mast cells in the tissues (table 1).

 

Allergic reactions are detected in mast cells in the skin by skin tests, by radioimmunoassay (RIA) tests. It can be predicted by demonstrating IgE binding in basophils. But anaphylaxis is unpredictable. It may also develop during simple tests.

 

 

Table 1: Allergic reaction and anaphylaxis development mechanisms

Clinical Findings and symptoms

·vasodilation,

·increase in bronchial secretion,

·platelet aggregation

·increase in capillary permeability

·Restlessness, feeling of fear,

·Weakness, itching,

·Sweating, dizziness

·Angioneurotic edema in and around the mouth, dyspnea, laryngeal edema, bronchospasm, seizure-like cramps, nausea-vomiting, diarrhea, itching, angioedema, urticaria,

·Tachycardia, hypotension, cardiovascular collapse,

·Change of consciousness

·Cardiac arrest

 

 

Various mediators are secreted during allergic reactions. Some of these are currently stored ones, and some are newly synthesized ones. Mediators stored and released during the reaction are histamine, tryptase, heparin, chymase, chymotryptase, kininogen, hydrolases and cathepsin. Newly synthesized mediators are slow reacting substance (SRS), Seratonin, adenosine and prostaglandins (PGD2 and PGE2: Vasodilation, PGF2: Bronchospasm, PgI2: increase in capillary permeability, Thromboxane: Pulmonary HT, Platelet activating factor: vascular permeability and platelet aggregation).

 

The causes of anaphylaxis are shown in Table 2 .

 

Table 2: Factors causing allergic reaction and anaphylaxis

Causes of anaphylaxis

1. Medicines

·Penicillins, cephalosporins (IgE): Especially in 20-40 years of age,

·Cross reaction to cephalosporins is 3-7%

·Anesthetics, analgesics (thiopental , procaine, lidocaine, morphine, atracurium, succinylcholine)

·Protamine (IgG and complement activation)

·NSAID's (salicylates)

·Chemotherapeutics

2. Blood and serum products

3. Foods

4. Insect poisons

5. Antisera (tetanus, diphtheria, antitoxins)

6. Hormones (insulin, ACTH)

7. Enzymes (pancreatic enzymes, streptokinase)

8. Hydatid cyst fluid (IgE and other Igs)

9. Latex (atopic patients are particularly sensitive - asthma)

10. Pollens

11. Iodinated radiopaque substances

 

Diagnosis:

The most important diagnostic method is anamnesis and clinical findings. There is often no time for diagnosis anyway. Unless urgent treatment is given, it will result in mortality.

Laboratory findings;

• Increased histamine and tryptase in the blood

• Low complement (secondary to increased consumption)

•LTE4 measurement in urine (up to 12 hours): indicates lipoxygenase activation

•Serological tests

•RAST (Radio-Immuno-Allergo-Sorbent) test: IgE detection positive in cases mediated by

•Specific IgG and IgG4 test

 

Treatment:

 

Application of the suspected antigen is stopped. Airway patency is ensured. Respiratory and circulatory support is applied. However, other basic elements of treatment include fluid replacement, catecholamines (adrenaline), histamine antagonists and corticosteroids.

 

Adrenaline increases arteriolar vasoconstriction, increased myocardial contraction, secondary bronchial dilatation and mediator release. provides inhibition. It can be given by subcutaneous, intravenous, intramuscular or endobronchial route.

•For mild reactions, 0.3 – 0.5 mL 1/1000 (0.3-0.5 mg) sc and repeat every 5-10 minutes.

•For moderate to severe reactions (unresponsive bronchospasm or severe circulatory collapse), 0.1-0.2 mL 1/1000 slow IV infusion or 1-2 mL 1/10000 sol.

•Persistent severe hypotension 1 – 4 μg/min infusion in case of sion

 

Corticosteroids are used as adjunctive treatment agents in persistent organ dysfunction to alleviate late phase reactions. Methylprednisolone is administered 1-2 mg/kg IV / 4-6 hours.

RESULT:

In mild reactions:

·Airway is provided

·Toxin is removed

·A bandage is applied to the extremity

·Epinephrine 0.3-0.5 mL (1/1000 sol) at the entrance site

·Supplemental Oxygen

In moderate reactions:

·Epinephrine 0.3-0.5 mL (1/1000 sol) SC,IM / 5-10 min, 1-4 μg/min infusion if necessary

· Methylprednisolone 1-2 mg/kg IV /4-6 hours

·Diphenhydramine 25-100 mg PO or IV /4-6 hours

·Fluid Loading (referring to Htc) : Crystalloid / Colloid

·Inhaled β-agonist drugs

Additionally in severe reactions

·IV Epinephrine / Norepinephrine /Dopamine infusion

·Aminophylline 5-6 mg/kg IV loading, 0.4-0.9 mg/kg/min inf (Resistant bronchospasm)

·Glucagon 1-5 mg IV

·Cimetidine 300 mg / 20 mL IV slow inf.

·Basic and advanced life support CP

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