Anaphylaxis/anaphylactic shock

Tetanus in any combination Anaphylaxis or anaphylactic shock 7 days... 

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. 

Experiments were also made on anaphylaxis. Since young rabbits are said to be more sensitive to anaphylactic shock, the experiments were made with young rabbits weighing about 800 grams. A rabbit was sensitized by a subcutaneous injection of 1.0 cc. of a twenty-two per cent egg-white sol. Twenty-one days later, 0.8 cc. of a ten per cent sodium thiocyanate solution was injected intravenously. This was followed twenty minutes later by the intravenous injection of 2.0 cc. of a twenty per cent egg-white sol. Absolutely no symptoms of shock were noted, while the control rabbit suffered a severe anaphylactic shock. 

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. 

Anaphylaxis, or anaphylactic shock, or anaphylactic reaction—a severe, frightening and life-threatening allergic reaction of the immune system occurring in response to an allergen. The symptoms may include heart rhythm and respiration disorders, lowered blood pressure, swelling, hives, and asthma-like symptoms. 

Anaphylactic shock, the most severe type of anaphylaxis, occurs when an allergic response triggers a quick release from mast cells of large quantities of immunological mediators (histamines, prostaglandins, leukotrienes), leading to systemic vasodilation (associated with a sudden drop in blood pressure) and bronchoconstriction (difficulty in breathing). Anaphylactic shock can lead to death in a matter of minutes if untreated. 

In severe anaphylaxis, hypotension is due to vasodilation and loss of circulating volume through leaky capillaries. Colloid is more effective at restoring blood volume than crystalloid and 1-21 of plasma substitute should be infused rapidly. Oxygen and artificial ventilation may be necessary. Advice on the management of anaphylactic shock may be altered from time to time check the UK Resuscitation Council website (www.resus.org.uk) for current information. 

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. 

Among the anaphylactic reactions to NSAIDs that result in different types of reaction (urticaria, angioedema, asthma, or hypotension), there have been very few reports of anaphylactic shock. However, anaphylaxis has been described in patients taking celecoxib (135,136) or rofecoxib (137). Rofecoxib caused anaphylaxis in a patient who had had a similar reaction to diclofenac, suggesting that COX-2 inhibitors may be not safe in all individuals who have adverse reactions to non-selective COX inhibitors. It also suggests that different mechanisms may be involved in patients with asthma and in those with anaphylactoid reactions to NSAIDs. 

Anaphylactic shock can occur, even after oral administration of penicillin and skin testing. However, anaphylactic shock is less common after oral than parenteral administration (171). In one study the incidence of anaphylactic shock was 0.04% of all patients treated with penicillin (7). It is also low in patients receiving long-term benzathine penicillin (1.2 million units every 4 weeks). Four episodes of anaphylaxis occurred in 0.012% of injections (1.2 reactions to 10 000 injections) (172). Anaphylactic shock resulting in death occurred in 0.002% of all patients treated with penicillin (7) and in 0.003% of those treated with benzathine penicillin (172). 

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). 

Anaphylactic shock occurs rarely with sulfonamides (160,169,170,178,179). Anaphylaxis to a central venous catheter (ARROWg+ard Blue Catheter) coated with chlorhexidine and sulfadiazine has been reported in a... 

Anaphylactic shock is rare, but has been reported with co-trimoxazole (20). However, it is possible that this reaction was due to the sulfonamide compound (21). The case histories of 13 patients (12 women, one man, aged 22-68 years) with anaphylactic reactions to trimethoprim alone that were reported to a national drug safety unit have been analysed (20). Nine were classified as probable anaphylaxis. The casual relation between exposure to trimethoprim and anaphylaxis was classified as definite in three reports, possible in four, and probable in six. In one patient, IgE antibodies against trimethoprim were demonstrated. 

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