Immediate anaphylactic shock

Anaphylactic shock is an extremely serious allergic drug reaction that usually occurs shortly after the administration of a drug to which the individual is sensitive This type of allergic reaction requires immediate medical attention. Symptoms of anaphylactic shock are listed in Table 1-2. 

All or only some of these symptoms may be present. Anaphylactic shock can be fatal if the symptoms are not identified and treated immediately. Treatment is to raise the blood pressure improve breathing, restore cardiac function, and treat other symptoms as they occur. 

Anaphylactic shock, which is a severe form of hypersensitivity reaction, also can occur (see Chap. 1). Anaphylactic shock occurs more frequently after parenteral administration but can occur with oral use This reaction is likely to be immediate and severe in susceptible... 

The answer is a. (Hardman, p 224.) Epinephrine is the drug of choice to relieve the symptoms of an acute, systemic, immediate hypersensitivity reaction to an allergen (anaphylactic shock). Subcutaneous administration of a 1 1000 solution of epinephrine rapidly relieves itching and urticaria, and this may save the life of the patient when laryngeal edema and bronchospasm threaten suffocation and severe hypotension and cardiac arrhythmias become life-endangering. Norepinephrine, isoproterenol, and atropine are ineffective therapies Angioedema is responsive to antihis-... 

Do we always have an effective antidote available that can terminate the symptoms Or, will we be at a point of no return, unable to accommodate a volunteer who wants to stop immediately Is there a crash cart available to deal with anaphylactic shock, a sudden dangerous fall in blood pressure or some other unforeseen emergency Is the degree of discomfort likely to be excessive in some cases, going beyond what one or more review authorities would consider humane ... 

Hypersensitivity reactions Serious and occasionally fatal immediate-hypersensitivity reactions have occurred. The incidence of anaphylactic shock is between 0.015% and 0.04%. Anaphylactic shock resulting in death has occurred in approximately 0.002% of the patients treated. These reactions are likely to be immediate and severe in penicillin-sensitive individuals with a history of atopic conditions. 

They are mediated by IgE antibodies. On exposure to the drug, antigen and antibody reaction takes place on mast cells and basophils releasing various mediators e.g. histamine, leukotrienes, 5 hydroxytryptamine (5-HT), prostaglandins etc., which are responsible for immediate immune reactions like skin reaction, anaphylactic shock, asthma etc. These reactions occur immediately after challenge and are termed as immediate hypersensitivity. 

Histamine was synthesized in 1907 and later isolated from mammalian tissues. Early hypotheses concerning the possible physiologic roles of tissue histamine were based on similarities between the effects of intravenously administered histamine and the symptoms of anaphylactic shock and tissue injury. Marked species variation is observed, but in humans histamine is an important mediator of immediate allergic (such as urticaria) and inflammatory reactions, although it plays only a modest role in anaphylaxis. Histamine plays an important role in gastric acid secretion (see Chapter 62) and functions as a neurotransmitter and neuromodulator (see Chapters 6 and 21). Newer evidence indicates that histamine also plays a role in chemotaxis of white blood cells. 

Fig. 6.1 Immediate hypersensitivity reaction. These reactions are the result of the production of IgE antibody in response to an allergen. IgE binds to the mast cells via Fc receptors and its reexposure to the allergen causes degranulation and secretion of endogenous mediators. In allergic responses, TH2 cells are important in recognizing allergens in the context of MHC molecules and secrete IL-4, IL-5 and IL-13. IL-4 induces isotope switching from IgG to IgE, and IL-5 is involved in eosinophil recruitment. IL-8 serves as a chemical signal to attract neutrophils at the site of inflammation. The collective effects of endogenous mediators include rashes, inflammation, smooth-muscle contraction, bronchospasm, asthma and severe anaphylactic shock, which may even cause death (see Color Insert)...

A 40-year-old woman developed anaphylactic shock after receiving depot medroxyprogesterone acetate 150 mg intramuscularly (30). She was not taking any other medications, and there was no history of allergy to food or cosmetics. She responded fully to immediate resuscitation. She had another episode when she received another dose 12 weeks later. 

Histamine was synthesized in 1907 and later isolated from mammalian tissues. Early hypotheses concerning the possible physiologic roles of tissue histamine were based on similarities between histamine s actions and the symptoms of anaphylactic shock and tissue injury. Marked species variation is observed, but in humans histamine is an important mediator of immediate allergic and... 

If there is any inkling of anaphylactic shock, immediately call 911 medical help is absolutely necessary and can be lifesaving The best thing is to administer rescue breathing until the ambulance or medical aid arrives. Find more information about anaphylaxis at www.foodal lergy.org. 

Very strong and immediate reactions, including anaphylactic shock, following consumption of even the smallest amounts of peanuts or their derived products. In extreme cases even a trace amount of peanut protein added to other food products may bring about death of particularly sensitive individuals (Burks et al. 1999, Wiithrich 2000). 

The use of adrenahne is largely limited to subcutaneous administration for the immediate relief of anaphylactic shock. Intramuscular doses of 0.1 ml of a 1 1000 solution are often given repeatedly, up to a maximum of some 2 ml in 5 minutes. Although the sensitivity of individuals to adrenahne varies considerably, the adverse reactions to such doses are generahy hmited to mild cardiovascular effects. 

Once sensitivity has been established, that is, once hapten-specific IgE-producing B cells have been formed, exposure to even small amounts of hapten can induce a cascade of events that lead to immediate reactions, such as anaphylaxis (210). Briefly, preformed IgE antibodies to drug determinants recognize the hapten-carrier complex and fix to the surface of mast cells or basophils, triggering the release of a series of mediators, such as histamine, neutral proteases, biologically active arachidonic acid products, and cytokines. This ultimately leads to a clinical spectrum that ranges from a mUd local reaction to anaphylactic shock. 

Co-administration of beta-blockers has been associated with an increased risk of severe allergic drug reactions and reduces the effect of adrenaline in the immediate treatment of anaphylactic shock. The mechanism involves changes in the regulation of anaphylactic mediators (281). 

Anaphylactic shock associated with cinoxacin was reported in three patients by the Netherlands Center for Monitoring of Adverse Reactions to Drugs (97). Another 17 cases were reported to the WHO Collaborating Center for International Drug Monitoring. In some cases the reaction was observed immediately after the first dose of a repeat cycle of treatment. Anaphylactoid reactions to ciprofloxacin have been reported in patients with cystic fibrosis (98-100). 

Antimuromonab IgE antibodies have been identified after 10-25 days of treatment in six of 181 patients, and only in those with high titers of antimuromonab IgG antibodies (34). Immediate IgE-mediated anaphylactic reactions, namely anaphylactic shock, bronchospasm, urticaria, have been rarely reported and have sometimes been difficult to differentiate from the cytokine-release syndrome (35,36). Late-onset reactions after the first week of treatment, including cutaneous erythema, a fall in blood pressure, or serum sickness-hke reactions, are infrequent (37). 

For acute anaphylaxis, immediate treatment is essential, with adrenaline followed by intravenous histamine Hi receptor antagonists, glucocorticoids, fluids, and electrolytes. In view of the frequency of cardiac dysrhythmias and conduction disturbances in patients with anaphylactic shock, they should immediately be monitored (198,199). 

A 35-year-old woman who had received monthly intramuscular hydroxocobalamin for 6 years developed anaphylactic shock immediately after a dose. Later she was given cyanocobalamin with terfenadine 120 mg/day for 2 days before each injection. After 3 years she had not had any allergic reactions. 

Severe immediate hypersensitivity reactions (tjrpe 1), sometimes accompanied by anaphylactic shock and circulatory collapse, have been described very rarely (1). AUergic reactions of the Arthus phenomenon type, characterized by local swelling and necrosis following less than 24 hours after immunization, have occurred in rare instances. Some of these cases have been fatal. 

Anaphylactic This is an immediate allergic reaction that can result in anaphylactic shock, which can lead to sudden drop in blood pressure and edema of the bronchial mucosa causing bronchoconstriction. 

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