Abstract
Generally, anaphylactic shock is characterized by an explosive overreaction of the immune system to a triggering event- which can include bee stings, insect bites, peanuts, eggs, drugs given to the body, and others. Derived from the Greek word “ana” or without and “phylaxis” without, the body’s immunity is severely compromised and affects multiple body systems including the skin, upper and lower respiratory, gastrointestinal, and cardiovascular (Anaphylaxis Canada, 2000).
Often, the progression of anaphylactic shock unlike ordinary allergies is rapid and its progression can be progressive with symptoms like swelling (especially lips or tongue and throat), difficulty breathing, abdominal cramps, vomiting, diarrhea, circulatory collapse, coma, and death being the manifestations of shock. Consequently, while most allergens can be avoided, the most common food allergens are peanuts, tree nuts, seafood, eggs, and milk. Exercise, latex, certain drugs, and insect stings can also trigger an anaphylactic response (Mandell, et. al., 2005). Treatment includes epinephrine, H1–receptor blockers/antihistamines, Inhaled beta–agonists (albuterol), H2–receptor blockers and Corticosteroid.
Anaphylaxis and the Body’s Immune System: An Investigation of Anaphylactic Shock
Introduction
Anaphylactic shock is considered to be a dangerous and deadly immunologic reaction that resulted to about 1000 deaths in the United States and an estimated 1.24%-16.8% of the population is considered to be at risk for anaphylactic reaction resulting to exposure to allergens (Neugut, Ghatak and Miller, 2002). Consequently, the most common presentation of those who experienced sever anaphylaxis were presented with sudden cardiovascular collapse.
In this report, we will explore the normal and abnormal physiology, the pathology and path physiology of anaphylactic shock as well as its clinical manifestations. Moreover, an exploration of the medical management as well as the nursing management that can be given to these patients will also be investigated. Furthermore, the progression and the pharmacologic intervention in treating patients with anaphylactic shock will also be explored.
Review of Normal Anatomy
Anaphylactic shock occurs as a result of the immune system’s lack or inability to ward off infection because of severe allergic reaction. Let us first discuss the normal anatomy of the body’s immune system and how it combats allergies to prevent anaphylactic shock and allergies from occurring.
The immune system plays a vital role in protecting the body from infection: for most of us, the immune system serves as the guard in warding off potentially harmful microorganisms such as bacteria and virus that threatens to invade the body. The body has three lines of defense against pathogens. In the first line of defense, the surfaces of the skin, breathing passages, mouth, and stomach function as barriers to pathogens. These barriers trap and kill most pathogens with which you come into contact. Skin forms a physical and chemical barrier against pathogens. Mucus and cilia in your breathing passages trap and remove most pathogens. A sneeze or cough can also remove pathogens. Most pathogens that you swallow are destroyed by chemicals in your saliva or by stomach acid. Pathogens that do get into your body can trigger the inflammatory response, the body’s second line of defense. In the inflammatory response, fluid and white blood cells leak from blood vessels into nearby tissues. The white blood cells then fight the pathogens. The white blood cells involved in the inflammatory response are called phagocytes. A phagocyte engulfs and destroys pathogens by breaking them down. During the inflammatory response, the affected area becomes red, swollen, and warm.
The inflammatory response may also cause a fever. The immune response is the body’s third line of defense. The cells of the immune system can distinguish between different kinds of pathogens. The immune system cells react to each kind of pathogen with a defense targeted specifically at that pathogen. White blood cells that target specific pathogens are called lymphocytes. There are two major kinds of lymphocytes—T cells and B cells. A major function of T cells is to identify pathogens by recognizing their antigens (Tortora, 2003).
However, the immune system when warding off pathogens also releases harmful substances that can also affect the body’s tissues. Thus, the immune system is responsible for protecting the body but when it attacks harmless substances, it can also damage human tissues which are responsible for allergic reactions. Hence, allergic reaction occurs because of the immune system’s attack of harmless substances which are called allergens or substances that in normal immune system will not trigger any reaction (Virtual Medical Center, 2007).
Most immune system and allergic reactions are hereditary in nature. This is because the genes that affect immunity affect allergy, and genes that affect immunity are important to pass on to children – so that they too will be able to fight infections like their parents can. The tendency to have allergic reactions also called atopy or the presence of an allergic reaction to an allergen can be demonstrated by a skin prick test; or RAST (Virtual Medical Center, 2007).
Review of Normal Physiology
Normally, the immune system’s mast cells and antibodies can combat pathogens and protect the body. In general, the mast cells are responsible in linking the innate immune system (to do with inflammation) and the Acquired Immune System (which is very specific and tightly controlled) – which is normal (Virtual Medical Center, 2007). Consequently, the acquired immune system which also includes the antibodies that is specific to a particular substance.
Antibodies also called immunoglobulins particularly the class of antibody called IgE is often responsible for misdirected attacks on harmful substances. Mast cells are very sensitive to the moment when IgE recognises its target. Antigens are large molecules (usually proteins) on the surface of cells, viruses, fungi, bacteria, and some non-living substances such as toxins, chemicals, drugs, and foreign particles. The immune system recognizes antigens and produces antibodies that destroy substances containing antigens (Medline Plus, 2007). This antibody-antigen attack of harmful substances becomes the precursor for allergic reactions. Thus, when this happens, mast cells release the contents of special granules held inside them; this event may be called degranulation. The granules contain hormones called histamine and leukotrienes. It is histamine and leukotrienes that produce the inflaming response of allergy (Virtual Medical Center, 2007). Atopy begins when the release of histamine and luekotrienes leads to symptoms and becomes an allergic disease.
Pathology of Anaphylactic Shock
Allergic reaction can be provoked by skin contact with poison plants, chemicals and animal scratches, as well as by insect stings. Ingesting or inhaling substances like pollen, animal dander, molds and mildew, dust, nuts and shellfish, may also cause allergic reaction. Medications such as penicillin and other antibiotics are also to be taken with care, to assure an allergic reflex is not triggered (Black and Hawks, 2005; Medline Plus, 2007).
Allergic reaction typically occurs in two phases. The initial phase response usually occurs within 15 minutes of contact with the allergen (Lieberman, 1997). It usually recovers within 2-4 hours. This response involves mast cell degranulation as the primary cause of symptoms. The late phase response occurs several hours later, usually starting 4 hours after contact with the allergen and can last 12 to 24 hours in some individuals. This response occurs after recruitment of white blood cells called eosinophils and T lymphocytes to the site of the allergy (eg. the lungs in asthma) where they release a number of mediators that lead to continued allergic symptoms (Lieberman, 1997).
Pathophysiology of Anaphylactic Shock
Shocks which also include cardiogenic shock, hypovolemic shock and anaphylactic shocks are considered to be medical emergencies because of the rapid and systemic impact on the body. Anaphylactic shock occurs when the body’s antibody-antigen response is triggered by something the person is allergic to. It can happen upon the first exposure or after several exposures to a substance. Histamines and other substances released into the bloodstream cause blood vessels to dilate and tissues to swell. Anaphylaxis may be life-threatening if obstruction of the airway occurs, if blood pressure drops, or if heart arrhythmias occur (Medline Plus, 2007).
Approximately one third of anaphylactic episodes are triggered by foods such as shell-fish, peanuts, eggs, fish, milk, and ree nuts (e.g., almonds, hazelnuts, walnuts, pecans); however, the true incidence is probably under-estimated. Moreover, aspirin and other nonsteroidal anti-inflam-matory drugs (NSAIDs) may produce a range of reactions, including asthma, urticaria, angioedema, and anaphylactoid reactions. Aspirin sensitivity affects about 10 percent of persons with asthma, particularly those who also have nasal polyps. Overall, aspirin accounts for an estimated 3 percent of anaphylactic reactions (Tang, 2003)
The pathophysiology of anaphylactic shock occurs in the figure provided below:
Clinical Presentation/Manifestations
Before we proceed to the clinical manifestations of anaphylactic shock, it should be mentioned that the severity of the shock varies from person to person and that the more rapid the onset of the reaction, the more severe the shock is. While the risk for anaphylaxis typically diminishes over time as exposure or reactions is precipitated, a person at risk for anaphylactic reaction should always be cautious and prepared.
The signs and symptoms of anaphylactic shock can occur within seconds or minutes or in some cases where delayed reaction occurs about 15-30 minutes or more after the exposure (this is more typical with drug allergies). Initial symptoms include: flushing (warmth and redness of the skin), itching (often in the groin or armpits), and hives which is often accompanied by a feeling of “impending doom,” anxiety, and sometimes a rapid, irregular pulse (Medicine Net, 2007).
Moreover, after these initial symptoms appear, throat and tongue swelling which results in hoarseness, difficulty swallowing, and difficulty breathing occurs. Consequently, symptoms of rhinitis (hay fever) or asthma may occur causing: a runny nose, sneezing, and wheezing, which may worsen the breathing difficulty, vomiting, diarrhea, and stomach cramps may develop (Brunner and Suddarth, 2006). These are the typical features of anaphylactic shock and in severe cases, the mediators flooding the blood stream cause a generalized opening of capillaries (tiny blood vessels) which results in a drop in blood pressure, lightheadedness, or even loss of consciousness (Medicine Net, 2007).
Medical Treatment and Nursing Management
Anaphylactic shock is a medical emergency and should be treated similar to emergency cases where the ABCs are prioritized. Following an anaphylactic shock, emergency care is given by the nurse through the administration of oxygen through a nasal cannula or a face mask. In severe respiratory distress, mechanical ventilation may be required. Accordingly, if blood pressure is dangerously low, medication to increase blood pressure will be given, an IV catheter may be inserted and an IV is given for medication (Medicine Net, 2007). This is the reason why people with known severe allergic reactions may carry an Epi-Pen or other allergy kit, and should be assisted if necessary (Medline Plus, 2007).
According to the Joint Task Force on Practice Parameters (1998), the treatment for Anaphylaxis includes the following:
Diagnose the presence or likely presence of anaphylaxis. Place patient in recumbent position and elevate lower extremities.
Monitor vital signs frequently (every two to five minutes) and stay with the patient.
Administer epinephrine 1:1,000 (weight-based) (adults: 0.01 mL per kg, up to a maximum of 0.2 to 0.5 mL every 10 to 15 minutes as needed; children: 0.01 mL per kg, up to a maximum dose of 0.2 to 0.5 mL) by SC or IM route and, if necessary, repeat every 15 minutes, up to two doses).
Administer oxygen, usually 8 to 10 L per minute; lower concentrations may be appropriate for patients with chronic obstructive pulmonary disease.
Maintain airway with an oropharyngeal airway device.
Administer the antihistamine diphenhydramine (Benadryl, adults: 25 to 50 mg; children: 1 to 2 mg per kg), usually given parenterally. If anaphylaxis is caused by an injection, administer aqueous epinephrine, 0.15 to 0.3 mL, into injection site to inhibit further absorption of the injected substance. If hypotension is present, or bronchospasm persists in an ambulatory setting, transfer to hospital emergency department in an ambulance is appropriate.
Treat hypotension with IV fluids or colloid replacement, and consider use of a vasopressor such as dopamine (Intropin). Treat bronchospasm, preferably with a beta II agonist given intermittently or continuously; consider the use of aminophylline, 5.6 mg per kg, as an IV loading dose, given over 20 minutes, or to maintain a blood level of 8 to 15 mcg per mL.
Give hydrocortisone, 5 mg per kg, or approximately 250 mg intravenously (prednisone, 20 mg orally, can be given in mild cases). The rationale is to reduce the risk of recurring or protracted anaphylaxis. These doses can be repeated every six hours, as required.
In refractory cases not responding to epinephrine because a beta-adrenergic blocker is complicating management, glucagon, 1 mg intravenously as a bolus, may be useful. A continuous infusion of glucagon, 1 to 5 mg per hour, may be given if required.
In patients receiving a beta-adrenergic blocker who do not respond to epinephrine, glucagon, IV fluids, and other therapy, a risk/benefit assessment rarely may include the use of isoproterenol (Isuprel, a beta agonist with no alpha-agonist properties). Although isoproterenol may be able to overcome depression of myocardial contractility caused by beta blockers, it also may aggravate hypotension by inducing peripheral vasodilation and may induce cardiac arrhythmias and myocardial necrosis. If a decision is made to administer isoproterenol intravenously, the proper dose is 1 mg in 500 mL D5W titrated at 0.1 mg per kg per minute; this can be doubled every 15 minutes. Adults should be given approximately 50 percent of this dose initially. Cardiac monitoring is necessary and isoproterenol should be given cautiously when the heart rate exceeds 150 to 189 beats per minute.
Medications commonly given include the following (Medicine Net, 2007):
Epinephrine
Given in severe allergic reactions, epinephrine is extremely effective and fast–acting; it acts by constricting blood vessels, which increases blood pressure, and widening the airway. Epinephrine is given by injection into the muscle, through an IV line, or by injection under the skin.
H1–receptor blockers/antihistamines
Usually diphenhydramine (Benadryl); these drugs do not stop the reaction but relieve some of the symptoms. They may be given by IV, by injection in the muscle, or by mouth
Inhaled beta–agonists (albuterol)
Used to treat bronchospasm (spasms in the lung) and dilate the airways; inhaled
H2–receptor blockers
Usually cimetidine (Tagamet); given by IV or by mouth
Corticosteroids (examples are prednisone, Solu–Medrol
These drugs help decrease the severity and recurrence of symptoms; may be given orally, injected in muscle, or by IV line
Prognosis
Anaphylaxis is a severe disorder which has a poor prognosis without prompt treatment. Symptoms, however, usually resolve with appropriate therapy, underscoring the importance of action. Complications may include: shock, cardiac arrest (no effective heartbeat), respiratory arrest (absence of breathing), and airway obstruction (Medline Plus, 2007).
Conclusion
Anaphylactic shock can occur at any time and a rapid phase. Thus, parents and patients who have experienced anaphylactic shock or have allergies are advised to wear or carry a medical alert bracelet, necklace, or keychain to warn emergency personnel of anaphylaxis risk. Moreover, it also important that patient keeps epinephrine self-injection kit and oral diphenhydramine (Benadryl) for future exposures. Anaphylactic shock can be prevented if the patient will not be exposed or will be kept away from exposure of the allergen.
References
Anaphylaxis Canada. (2000). What is anaphylaxis? Retrieved October 10 2007. Available at http://www.anaphylaxis. org/content/whatis/anaphylaxis_is.asp
Black, J. and Hawks, J.H. (2005) Medical Surgical Nursing-Clinical Mangement for positive outcomes,7 th edition. Elsevier.
Brunner and Suddarth’s Text Book of Medical Surgical Nursing: 9th edition. (2005)
Lippincott Raven Publishers.
Joint Task Force on Practice Parameters. (1998) The diagnosis and management of anaphylaxis. Journal of Allergy Clinical Immunology. 01(6 Pt 2):S465-528.
Kemp SF, Lockey RF, Wolf BL, Lieberman P. (1995) Anaphylaxis. A review of 266 cases. Arch Intern Med;155:1749-54.
Lieberman P. (1998) Anaphylaxis and anaphylactoid reactions. In: Middleton E. Allergy: principles and practice. 5th ed. St. Louis: Mosby:1079-89.
Mandell, D., Curtis, R., Gold, M. and Hardie, S. (2005) Anaphylaxis: How Do You Live with It? Health and Social Work. 30(4): 325-333.
Medicine Net. (2007) Anaphylaxis: Signs of Anaphylaxis. Retrieved 10 October 2007 at http://www.medicinenet.com/anaphylaxis/page4.htm.
Medline Plus. (2007) Anaphylaxis. US National Library of Medicine. Retrieved 10 October 2007 at http://www.nlm.nih.gov/medlineplus/ency/article/000844.htm.
Neugut, Alfred, Anita Ghatak and Rachel Miller. (2001)Anaphylaxis in the United States: An Investigation Into Its Epidemiology. Arch Intern Med. 161.108 January 2001 15-21.
Tang, A. (2003) A Practical Guide to Anaphylaxis. American Family Physician. 68: 1325-1332.
Tortora, G. (2003) Principles of Anatomy &Physiology. 10 th ed.,Wiley inter.
Virtual Medical Center. (2007) Allergy and the Immune System. Retrieved 10 October 2007 at http://www.virtualallergycentre.com/anatomy.asp?sid=4.
