The T lymphocytes, like the B lymphocytes, originate from primitive stem cells and go through stages of maturation (see Fig. 18-1). When the immature lymphocyte leaves the bone marrow, it migrates to the thymus gland, where it is acted on by the hormone thymosin. The T lymphocyte then becomes mature and immunocompetent. The origin of the name T lymphocyte is derived from this thymus-dependent maturation. These mature T lymphocytes can circulate in the blood and lymph, or they may come to rest in the inner cortex of the lymph nodes, where they may form subgroups of T lymphocytes.

These T lymphocytes function overall in the immune system by serving in regulatory, effector, and cytotoxic capacities. The regulatory T lymphocytes are the helper or suppressor T lymphocytes. These lymphocytes amplify or suppress responses of other T lymphocytes or responses of B lymphocytes. The helper T lymphocytes produce a soluble factor that is necessary, in some instances, for antibody formation by B lymphocytes. This helper action is most important for IgE and IgG production. The underproduction of helper cells is associated with AIDS. The suppressor T lymphocytes appear to regulate or suppress the activity of B lymphocytes in the production of antibodies. Evidence indicates that the suppressor T lymphocytes can become pathologically active against helper T lymphocytes and other aspects of cellular immunity. For this reason, these suppressor T lymphocytes may have a role in immune tolerance and in the development of autoimmune disease, such as myasthenia gravis. Effector T lymphocytes are probably responsible for the delayed hypersensitivity reactions, the rejection of foreign tissue grafts and tumors, and the elimination of virus-infected cells. Effector T lymphocytes have antigen receptors on their surfaces that are significant in the initiation of cellular immunity. When an antigen enters the body, it undergoes processing by the phagocytes. The antigen then travels to the regional lymph node, which drains the area of antigen invasion. In this lymph node, the T lymphocyte recognizes the antigen, binds to the antigen, and proliferates. The T lymphocyte becomes sensitized when it comes into contact with the antigen. In addition, memory T lymphocytes result from this interaction. On a second exposure to the antigen, a more intense, efficient, and rapid cellular immunity results. This contact also results in the release of lymphokines by the T lymphocyte. Some of the lymphokines are: (1) chemotactic factor, which recruits phagocytes into the area; (2) migration inhibitory factor, which prevents the migration of phagocytes away from the area; (3) transfer factor, which induces noncommitted T lymphocytes to form T lymphocytes of the same antigen-specific clone as the original cells; (4) lymphotoxin, which is a nonspecific cellular toxin; and (5) interferon, which inhibits the replication of viruses.

The direct cellular cytotoxicity that is mediated by cellular immunity involves cytotoxic lymphocytes, or killer cells, and macrophages. The role of these cytotoxic T lymphocytes is not well established; however, they are believed to be involved in nonspecific killing of viruses, rejection of allografts, and immune surveillance of malignant diseases.

Hypersensitivity reactions

The immune system serves mainly as protection from harmful substances; however, in some instances, the activation of the immune system can cause deleterious effects, which is termed allergic response or hypersensitivity reaction. This response represents a magnified or inappropriate reaction by the host to an antigenic substance; it can result in immunologic disease. Hypersensitivity reactions are divided into four major categories: type I, type II, type III, and type IV hypersensitivity reactions (Table 18-1).

Table 18-1 Categories of Hypersensitivity Reactions

Type I hypersensitivity reaction (anaphylactic, immediate)

Type I hypersensitivity reaction occurs in persons who were previously sensitized to a specific antigen. The antibodies formed against that antigen are of the IgE classification. The term reagins is used to describe these IgE antibodies. Reaginic antibodies bind to mast cells in tissues that surround the blood vessels and to blood basophils. When the previously sensitized host is reexposed to the same antigen, the antigen reacts with the reaginic antibody that is attached to the cell and an immediate swelling, and then rupture of the basophil or mast cell results in a release of chemical mediators into the local environment. These chemical mediators include: (1) histamine, which causes local vasodilatation and increased permeability of the capillaries; (2) slow-reacting substance of anaphylaxis, which causes prolonged contraction of some smooth muscle, such as that of the bronchi; (3) chemotactic factor, which draws neutrophils and macrophages into the area of the antigen-antibody reaction; and (4) lysosomal enzymes, which elicit a local inflammatory reaction. These chemical mediators act on the “shock organs,” such as the mucosa, skin, bronchi, and heart. The resulting clinical manifestations of the type I reaction include urticaria, allergic rhinitis, allergic asthma, and, in severe cases, systemic anaphylaxis.

Type II hypersensitivity reaction (cytotoxic)

In the type II hypersensitivity reaction, the antigen and the antibody complex react, thereby injuring the cell membrane or a surface tissue with direct destruction by antibody of cellular elements. The antibodies involved in the type II reaction are either IgG or IgM, and the reaction is enhanced by complement. Hemolytic anemia is an example of a type II reaction that affects the red blood cells (RBCs). For example, when penicillin is absorbed on the RBC membrane, the interaction of antipenicillin antibody, penicillin, and complement causes a reaction that results in the lysis of RBCs.

Type III hypersensitivity reaction (arthus)

The type III hypersensitivity reaction involves the formation of immune complexes of antigen and antibody (IgG or IgM). These immune complexes precipitate in and around small vessels and damage the target tissue by activating complement over several hours. Also involved in this process is an inflammatory reaction that is initiated by the gathering of inflammatory cells and the release of vasoactive amines from platelets. As this process continues, polymorphonuclear leukocytes phagocytize the immune complexes and cause inflammation and necrosis of the blood vessels and surrounding tissue because of the release of lysosomal enzymes. Serum sickness and systemic lupus erythematosus are clinical examples of type III hypersensitivity reactions.

Type IV hypersensitivity reaction (delayed or cell-mediated)

Type IV hypersensitivity reaction is the only hypersensitivity reaction that does not involve antibodies. In the type IV reaction, the exposure to an antigen and the subsequent binding of the antigen with antigen-specific reactive T lymphocytes initiate the production of lymphokines from the T lymphocytes, with tissue damage as the end result. The antigen responsible for the type IV reaction can be bacterial, fungal, protozoan, or viral. Contact dermatitis, allograft rejection, and delayed response in tuberculin skin tests are examples of delayed hypersensitivity reactions.

Latex allergy

The prevalence rate of confirmed allergic reactions among health care workers ranges from 5% to 10%. Similarly, recent studies indicate that 8% to 12% of the health care population becomes sensitized to latex. Since the 1980s when universal precautions were instituted to prevent the spread of human immunodeficiency virus, hepatitis viruses, and other infectious agents, health care workers have routinely worn latex gloves as a protective barrier. In addition, the Occupational Safety and Health Administration instructed health care workers to wear protective material as a barrier. A great demand then occurred for surgical gloves. As a result, the accounts of the amount of latex proteins found in surgical gloves varied.

Many products contain latex; at home, these products include rubber bands, some carpets, earphones, and mouse pads. In the hospital setting, tourniquets, pressure cuff tubing, and urinary catheters often contain latex. In the perianesthesia area, possible routes of exposure include contact with mucosa, direct contact of particles with an open surgical wound, and aerosolized particles that are bound to the powder in the latex article. Interestingly, these particles can stay suspended for up to 5 hours.

The degree of reactions to latex varies; irritant contact dermatitis is basically a nonallergic reaction. Symptoms such as dry, itchy, or irritated areas that may be red and cracked usually occur within the first 6 to 24 hours after exposure. The reaction can be caused by exposure to powders added to the gloves, repeated hand washing and drying, or the use of cleaners and sanitizers. Because this reaction is not a true allergy, it usually clears after the irritant is removed.

Allergic contact dermatitis is also a nonallergic reaction. Symptoms, which usually occur within 24 to 48 hours, include erythema, vesicles, papules, pruritus, blisters, and crusting of the area that touched the latex. This type of response is caused by the chemical additives that are used in the manufacture of latex and are usually thiurams or carbamates.

Of major concern is the type I immediate hypersensitivity, which is the IgE-mediated response. This response usually occurs within minutes of exposure to the latex; however, it can occur within a few hours in some cases. A mild reaction is characterized by skin redness, urticaria, and itching. Severe reactions can produce acute rhinorrhea, sneezing, angioedema, bronchospasm, and anaphylactic shock.²

Many organizations are investigating latex allergies, and the American Society of Anesthesiologists has a document that can be found on the Internet (http://ecommerce.asahq.org/publicationsAndServices/latexallergy.pdf). Also, the American Association of Nurse Anesthetists has an excellent web site on latex allergies (http://www.anesthesiapatientsafety.com/patients/latex/fact_sheet.asp). Another expert guideline for management of latex allergies and safe latex use is from the American College of Allergy, Asthma, and Immunology (http://www.acaai.org/allergist/allergies/Types/latex-allergy/Pages/latex-allergies-safe-use.aspx).

The best treatment for a latex allergic response is avoidance. Patients who are at risk for an allergic reaction caused by latex are listed in Box 18-1. Health care personnel with known sensitivity should carry their own nonlatex gloves, usually made of vinyl or neoprene. They also should use nonlatex tourniquets and latex-free or glass syringes and should use stopcocks to inject drugs. Intravenous line tubing should have no latex ports, or if the latex ports exist, they should be taped. Box 18-2 summarizes the various recommendations for patients with known latex allergic reactions or a risk of reactions.

BOX 18-1 Patients Who Should Be Strongly Considered at Risk for an Allergic Reaction to Latex

A complete medical history is the most reliable screening examination for prediction of a reaction to latex.

• History of atopic immunologic reactions

• History of contact dermatitis

• History of documented immunologic reactions of unknown etiology during a medical or surgical procedure

• History of allergies to food products, including fruits, nuts, bananas, avocados, celery, figs, chestnuts, and papayas

• Neural tube defects, including spina bifida, myelomeningocele/meningocele, and lipomyelomeningocele

• Multiple operations in the past

• Repeated bladder catheterizations

BOX 18-2 Summary of the Recommendations for Perianesthesia Care of Patients with Known or Risk of Latex Allergic Reactions

Preoperative and intraoperative care

• Remove all latex products from the operating room.

• Use a latex-free reservoir bag on the anesthesia machine, oral airways, endotracheal tubes, and laryngeal mask airways.

• Use a latex-free breathing circuit with plastic mask and bag.

• Anesthesia ventilator must have a latex-free bellows.

• Place all monitoring devices, cords, and tubes (oximeter, blood pressure cuffs, electrocardiograph wires) in stockinet and secure with tape to prevent direct skin contact.

• Cover all rubber injection ports on intravenous bags with tape and label them “Do not inject fluid through ports.”

• Use intravenous tubing without latex ports or cover with tape.

• Use nonlatex gloves.

• Use nonlatex tourniquets.

• Draw medication directly from opened multidose vials.

• Draw up medications immediately before the beginning of the case.

• Use latex-free or glass syringes.

• Use stopcocks to inject drugs.

Postanesthesia phase of care

• Place a sign on the door and flag the chart of the patient to alert personnel to the hypersensitivity.

• Ensure that the patient recovers in a private area.

• Use good handwashing techniques.

• Use only latex-free syringes and gloves.

• Use ampules or remove stoppers from vials before use.

• Cover injection ports on minibags and use latex-free tubings.

• Remain alert for signs and symptoms (hypotension, tachycardia, and bronchospasm) of a latex allergy response and have appropriate emergency drugs and equipment available.

If a reaction to latex develops in the patient in the PACU, the first intervention is removal of the patient from ongoing exposure to the latex. The reactions can vary from mild respiratory reactions that can be treated on a symptomatic level to hives, which can occur immediately to several hours after exposure, and to a type I hypersensitivity anaphylactic reaction.

Treatment for the type I reaction should consist of first carefully looking for the latex allergen, such as rubber drains in the wound, inadvertent use of latex gloves, latex that contains urinary draining tubes, or intravenous tubing. In addition, remove all latex from the patient bedside; change gloves, discontinue antibiotics and blood administration, maintain the airway, administer 100% oxygen, intubate the trachea if necessary, and maintain intravascular volume support. Once the diagnosis of type I IgE-mediated anaphylaxis has been confirmed, epinephrine should be administered intravenously in doses of 0.1 mg/kg and titrated to effect. These small doses stabilize the patient’s condition and avoid ventricular tachycardia and malignant arrhythmias.

The increasing recognition of latex allergy and accurate testing that is available has led to a decrease in the number of latex allergic persons. Advances in the understanding of these processes should allow this trend to continue.² In the meantime, many health care facilities have become latex free environments to protect both employees and patients.

Immunosuppression

With the advent of organ transplantation, patients often arrive in the PACU in an immunosuppressed state. Consequently, the perianesthesia nurse must have a basic knowledge of the forms of immunosuppression and the appropriate nursing care measures that can be implemented for the patient with immunosuppression.

Forms of immunosuppression

The unresponsive state of the immune system may be caused by a natural tolerance to self-antigens, to a pathologic state, or to induced immunosuppression. Researchers are attempting to understand immunosuppression by artificially manipulating the immune system to produce a natural tolerance to self-antigens. Pathologic states such as lymphoma and leukemia are examples of the second form of immunosuppression, in which the immune system becomes unresponsive because of the pathologic changes in the immunocompetent cells. Induced immunosuppression can be accomplished with the administration of an antigen, antisera, or antibody; hormones and cytotoxic drugs; radiation; or surgery. For the most part, induced immunosuppression is used for tissue and organ transplants.

For patients with allergies, the administration of low-dose antigen provides relief in some instances from the antigen-antibody reaction. This desensitizing process produces antibodies that block the interaction between the antigen and the antibody-producing cells. Another method of providing tolerance to self-antigens is with the administration of antisera or antibody in an attempt to coat the antigenic sites. The object is to prevent immunocompetent cells from combining with the antigen. This method of immunosuppression is 100% effective in the prevention of Rh factor sensitization and ultimately erythroblastosis fetalis. Corticosteroids produce immunosuppression by reducing the amount of T and B lymphocytes that circulate in the blood, by blocking lymphokine release, and by decreasing the number of monocytes. Cytotoxic drugs are used in the treatment of cancer and autoimmune diseases. The most popular drugs are azathioprine and cyclophosphamide. These drugs suppress immune system function by killing unstimulated lymphocytes. X irradiation suppresses most of the immunocompetent cells with the induction of a profound lymphopenia. Surgical removal of the thymus gland, spleen, or lymph nodes may alter the immune response with the removal of tissue needed for the maturation of both the cellular and the humoral immune systems.

Perianesthesia care of the patient with immunosuppression

The major responsibilities of the perianesthesia nurse who cares for the patient with immunosuppression are prevention of infection and early diagnosis and treatment of infection. Opinions differ regarding the placement of the patient who is nonleukopenic in protective isolation. However, if the peripheral leukocyte count is less than 2000 cells/mm³, the patient probably will benefit from protective isolation. Before the patient is admitted to the PACU, sources of cross contamination should be eliminated. Blood pressure cuffs and other equipment that are to be used directly on the patient should be cleaned and disinfected with appropriate solutions. Aseptic technique should be followed at all times. In addition, needle puncture sites and surgical wounds should be cleaned and dressed with appropriate cleaners and ointments. If urinary catheters are used, open skin should be monitored closely for the beginning signs of infection. Patients with immunosuppression might not show the classic symptoms of infection. The temperature of the patient with immunosuppression should be closely monitored, and if it rises above 38° C, the attending physician should be notified immediately. Rectal thermometers should be avoided because they can cause mucosal injury and contamination.

Anesthetics and immune function

The invasive procedures involved in an anesthesia practice compromise many of the physical barriers described previously. Tracheal intubation, venous access devices, central neuraxial access, and mucous membrane contact are all vectors of infection. The inflammatory side effects of surgical procedures provide an ample breeding ground for the newly introduced flora.

Anesthetic agents themselves have long been associated with immune dysfunction. Over two decades ago, Nakagawara and colleagues demonstrated that inflammatory precursors were inhibited when exposed to inhalation anesthetics.³ Macrophage phagocytotic ability is also reduced by the common inhalation anesthetic isoflurane.⁴ Similarly, monocyte, neutrophil, and macrophages are inhibited by intravenous propofol in a dose dependent fashion.⁵ Proper universal precautionsand careful caution against contamination of the described vectors, are crucial for positive patient outcomes.