Published on 07/02/2015 by admin
Filed under Anesthesiology
Last modified 22/04/2025
This article have been viewed 1068 times
Beth A. Elliott, MD
Equipment and materials containing natural rubber latex (NRL) were once ubiquitous in the modern health care environment. Following the recommendation by the Centers for Disease Control and Prevention for universal precautions in 1987, the use of latex gloves increased dramatically (from 800 million to 20 billion annually). Subsequently, in the 1990s, NRL emerged as a significant cause of allergic reactions in both patients and health care workers. It remains unclear whether this escalation in reactions was the result of increased NRL glove use or abnormally high levels of residual latex antigens in the gloves. Manufacturers, hospitals, and clinics have taken steps to replace NRL with nonallergenic materials wherever possible. However, NRL gloves continue to be used in many operating suites due to their superior tactile properties and fit and a desire for reliable protection against blood-borne pathogens.
Latex is derived from the milky sap of the rubber tree, Hevea brasiliensis, harvested primarily in Malaysia, Indonesia, and Thailand. Approximately 90% of latex is used in the production of “dry” rubber for tires; the remaining 10% is used in the manufacture of “dipped” products, such as gloves, condoms, and balloons. During the manufacturing process, a variety of chemicals are added (e.g., stabilizers, antioxidants, accelerators) to give the rubber the desired characteristics. Once formed, the rubber products are then vulcanized (i.e., cured with heat and sulfur at a temperature of 130°C for 5 to 30 min). For latex gloves, a series of leaching baths are used to rid the gloves of residual water-soluble proteins and excess additives.
Antigenic proteins constitute up to 3% of the final latex product. Antigen levels are typically much higher in dipped latex products than in dry ones, but the levels can vary as much as 1000-fold among lots of gloves by the same manufacturer and as much as 3000-fold among manufacturers. These latex proteins (allergens) are water soluble and can be eluted during contact with moist surfaces (mucous membranes, peritoneal surfaces, and normal skin moisture). Latex allergens also adsorb onto the powder inside gloves. When gloves are donned or discarded, these powders disperse into the air and are inhaled by people nearby.
Irritant contact dermatitis produces a dry scaly irritation of the skin, typically on the hands. This problem is the most common work-related reaction to rubber products (80%). The reaction results from direct irritation by latex and residual chemicals used in the manufacturing process and is exacerbated by frequent handwashing and use of irritant surgical soaps. This reaction is not immune mediated and can be prevented with simple barrier protection or use of a nonlatex alternative.
Allergic contact dermatitis is another common problem associated with exposure to latex products. A red vesicular rash typically appears within 6 to 72 h after contact. The reaction is a type IV cell-mediated immune response to low-molecular-weight accelerators and antioxidants in the rubber product. Antibodies are not involved in type IV reactions. The diagnosis is based on clinical history and on the morphology and distribution of skin lesions. Patch testing confirms the diagnosis. Use of a glove liner or nonlatex alternative should be preventive.
The first case of type I IgE-mediated immediate hypersensitivity reaction to latex was reported in the German literature in 1927. The second case was not reported until 1979. By the 1990s, type I allergy to NRL reached epidemic proportions, with numerous reports of anaphylaxis and death.
Contact urticaria (hives) is the most common manifestation of IgE-mediated latex allergy. Symptoms appear within 10 to 15 min after contact and include itching, redness, and wheal and flare reactions at the site of contact.
Rhinitis and asthma may follow airborne exposure. One study of latex-sensitive individuals found that 51% had experienced rhinitis and 31% dyspnea. Another study found a 73% prevalence of rhinoconjunctivitis and a 27% prevalence of asthma. Most latex-sensitive people have atopic dermatitis and may have a history of seasonal allergic asthma, which may delay the diagnosis.
Anaphylaxis is a life-threatening condition triggered by the interaction between allergen and IgE antibodies attached to mast cells and basophils. Antibodies are formed after the initial exposure. On subsequent exposure, the allergen cross-links two IgE molecules, resulting in degranulation of the mast cell and the release of a host of factors (e.g., histamine, leukotrienes, and prostaglandins) responsible for the anaphylactic response. Capillary dilation, increased vascular permeability, hypotension, edema, clotting defects, bronchoconstriction, and hypoxemia are common manifestations of anaphylaxis. Anaphylactic reactions to latex may be delayed for as long as 60 min after exposure. This delay is thought to be related to the time needed for sufficient antigen to be eluted from surgical gloves and absorbed into the body. When anaphylactic reaction to latex is recognized and treated early, the prognosis is good. Persistent hypotension and bronchospasm may require continued treatment. Intensive care monitoring is warranted for 24 to 48 h because up to 20% of people have relapses, which may occur every l to 8 h.
Anyone with frequent exposure to NRL-containing materials is at risk for developing latex allergy. The prevalence in the mid-1990s was estimated to be as high as 3% to 9.5% of the general population and as high as 12% of health care workers. With adoption of NRL-avoidance strategies and reduced exposure to NRL, these numbers have fallen to less than 1% and 4%, respectively.
Although latex allergy was originally associated with spina bifida (in whom the incidence approaches 28% to 67%), it has recently come to light that any patient with congenital abnormalities (particularly neuraxial or urogenital) requiring multiple surgical procedures, indwelling catheters, or personal care using latex gloves is at high risk for developing significant latex allergies. There is an established association between latex allergy and allergy to various fruits and nuts, most commonly bananas, avocados, kiwi fruit, chestnuts, papaya, potatoes, and tomatoes.
Individuals with contact dermatitis should avoid unnecessary exposure to latex products. Vinyl and neoprene gloves are available in sterile and nonsterile packaging. Barrier creams and cotton glove liners are alternative methods to limit further exposure. It should be noted that chronic open sores on the hands are a potential site of exposure and sensitization, which can lead to later type I (immediate) hypersensitivity reactions. As many as 79% of individuals with type I hypersensitivity previously had type IV skin eruptions.
IgE-mediated allergic reactions extend across a spectrum from rhinoconjunctivitis to severe life-threatening anaphylaxis. Elimination of further exposure to the antigen should be one of the first steps when responding to an acute problem. Airway management and support, volume resuscitation, and catecholamine therapy (epinephrine) remain mainstays of therapy for anaphylaxis.
Tracheal intubation and mechanical ventilation may be required in cases of significant laryngeal edema, bronchospasm, pulmonary edema, and ventilation/perfusion mismatch. As much as 20% to 40% of the intravascular volume may be lost from acute transcapillary leakage during anaphylactic reactions. Combined with peripheral vasodilation, this can result in severe hypotension. Fulminant noncardiogenic pulmonary edema, pulmonary hypertension, and right-sided heart failure frequently complicate the clinical picture.
Pharmacologic therapy for anaphylaxis is aimed at inhibiting further mediator release, providing competitive blockade of receptors interacting with mediators already released, reversing the end-organ effects of physiologically active substances, and inhibiting the recruitment and migration of other inflammatory cells.
Antihistamines and steroids probably have little effect in acute management but may help attenuate late-phase reactions and secondary inflammatory responses.
Unlike pretreatment for anaphylactoid reactions to intravenously administered contrast dye, pretreatment of latex-sensitive patients with antihistamines, steroids, and catecholamines will not prevent IgE-mediated anaphylaxis.
Careful preoperative questioning of those patients in groups that are at high risk for having latex sensitivity should be done routinely. Patients with spina bifida and congenital urogenital abnormalities are at such high risk for latex allergy that they should completely avoid latex exposure from birth.
A totally latex-free environment is ideal but is achieved only in some hospitals. Recent efforts have focused on creating “latex-safe” environments. Medical equipment and supplies that contain NRL should have a mandated label on the packaging that warns the user of the latex material contained within.
If possible, surgical procedures involving latex-sensitive patients should be scheduled as “first cases” with all latex-containing materials removed the preceding night. Airborne particles containing latex allergens can remain suspended in air for up to 5 h. A readily available supply of nonlatex alternative equipment and supplies should be available in all health care facilities. Regardless of precautions taken to prevent latex exposure, operating personnel should be prepared to treat anaphylaxis in all latex-sensitive patients.
Work environments in which latex gloves are still used should make an effort to eliminate high-allergen products from their inventory to decrease the likelihood of sensitization of employees. Elimination of powdered latex gloves can significantly reduce both sensitization and allergic reactions to latex.
Fausts Anesthesiology Review Expert Consult 4e
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