Allergy to latex manifests as a variety of clinical symptoms is often categorized into Type IV Type I hypersensitivity reactions.
Type IV hypersensitivity is a cell-mediated or delayed type reaction. It is often localized to the area of contact occurs 48–72 hours after exposure. Often referred to as allergic contact dermatitis, T-cell-mediated allergy, or chemical allergy.
Type I hypersensitivity is IgE-mediated results in an immediate response. It is systemic ranges from contact urticaria to occupational rhinoconjunctivitis, asthma, or anaphylaxis.
Latex is the second most common cause of anaphylaxis in the operating room. Under general anesthesia it presents as cardiovascular compromise, airway swelling obstruction, flushing, edema.
Epidemiology
Incidence
Sensitivity to latex has been increasing in prominence since the introduction of Universal Precautions.
Life-threatening reactions in the US occur in approximately 1 in 30,000–50,000 people undergoing general anesthesia.
Prevalence
General population in the US (sensitization or allergy): 1–2%
Anaphylactic reactions under anesthesia have a mortality of 3.4%.
Etiology/Risk Factors
Anaphylactoid reaction
Repeated exposure to latex over time (repeated bladder catheterizations, spinal bifida patients, multiple surgeries, especially laparotomies)
Occupational exposure to latex (healthcare workers, latex factory workers)
Urticaria
Asthma
Rhinitis
Spina bifida patients
Atopic patients
Female preponderance
Cross-reactivity with allergies to a variety of fruits (bananas, avocadoes, mangoes, watermelons) chestnuts
Physiology/Pathophysiology
Raw latex is the milky sap from the rubber tree (Hevea brasiliensis), to which ammonia is added as the main preservative.
Type I hypersensitivity is an IgE-mediated reaction to natural rubber latex antigen. It can manifest as mild to life-threatening symptoms that include contact urticaria, occupational rhinoconjunctivitis, asthma, or anaphylaxis.
Latex sensitization occurs when exposure (airborne, parenteral, mucosal routes) to latex antigen induces CD4+ T cells to produce IL-4, IL-5, IL-6, IL-10, granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor (TNF). These cytokines mediators result in the production of IgE antibody specific to latex antigen.
Upon re-exposure (airborne, parenteral, mucosal routes) to latex antigen, there is a cross-linkage of IgE molecules by latex on the surface of mast cells. This results in mast cell degranulation the release of mediators such as histamine, tryptase, slow-reacting substance-A (SRS-A), prostaglin, leukotrienes.
These mediators increase mucous secretion, capillary permeability, bronchial smooth muscle tone (H1 receptor activation bradykinin), as well as decrease arterial tone (H2 receptor activation). Manifests as bronchospasm, V/Q mismatch, hypoxemia, hypotension.
Activation of Hageman factor can start a cascade of disseminated intravascular coagulation.
Transudation of fluid into the extravascular space can lead to a clinical hypovolemia which may result in myocardial ischemia.
Type IV hypersensitivity is a contact dermatitis reaction to chemicals used to process rubber by Langerhans T cells. The patient presents within 48–72 hours of exposure with erythema, vesicles, scaling, hyperpigmentation, lichenification of the contacted areas.
Irritant contact dermatitis is not a latex allergy; it is, however, the most common reaction associated with latex, is not life-threatening. It results from various alkaline chemicals added during rubber production. The dermatitis appears within minutes to hours as a localized abrasion with pruritus, erythema, cracking, dryness, chapping of the skin.
Prevantative Measures
Prevention of exposure to latex in known latex-sensitized patients is the keystone to preventing a potentially life-threatening allergic reaction. A latex-safe protocol in each institution should be in place should consist of identification of patients at risk, establishment of a latex-free environment, close coordination between all staff involved in the management of these patients.
Absolute avoidance of any latex-containing products is essential throughout the perioperative period during the hospital stay. Anesthetic equipments that may contain latex include gloves, some syringe plungers, Foley catheters, medication vials with rubber stoppers, disposable anesthesia bags, bages (adhesives), tourniquets, some endotracheal tubes, bellows, IV ports, blood pressure cuffs, some face masks. All manufacturer packaging should indicate the presence of latex in any medical grade product.
Preoperative prophylaxis with corticosteroids antihistamines is controversial. At best, it may attenuate a reaction but will not prevent true anaphylaxis.
Latex-sensitive patients should be scheduled as first cases because the quantity of latex aeroallergens is likely to be the lowest early in the morning. Airborne latex antigen can be suspended in the air for up to 5 hours after a case.
A latex-free cart should be used that contains non-latex alternatives, all latex gloves products should be removed from the operating room. The room should also be labeled as latex-free.
A resuscitation cart should be placed adjacent to the operating room.
The American Academy of Allergy Immunology recommends that clinical testing should be offered to high-risk patients in a latex-free environment.
Diagnosis⬆⬇
Signs symptoms depend on the type, route, amount of latex exposure as well as the individual's sensitivity.
Awake patients may manifest swelling of contact areas, hives/welts, sneezing, runny nose, ocular redness tears, sore throat, GI cramping, wheezing, shortness of breath, chest tightness. Respiratory manifestations include bilateral rales, stridor, cyanosis.
Anesthetized patients may have a more dubious presentation. Dermatologic symptoms (hives, welts, flushing, swelling) may not be immediately recognized under drapes warming devices. Hypotension is the first presenting sign in approximately 1/3rd of patients in anaphylactic shock. Additionally, respiratory manifestations such as bilateral rales, may not be immediately recognized.
Monitors
Noninvasive blood pressure monitoring: Look for worsening hypotension over a few minutes, although some patients will present with a more precipitous decline in blood pressure.
EKG: Tachycardia, dysrhythmias, ST changes; pulseless electrical activity may be the first manifestation in anaphylactic shock.
Airway pressure monitors: High peak plateau inspiratory pressures may be seen in the mechanically ventilated patient. If the bronchospasm is severe, the patient may also have auto-PEEP which will further contribute to hypotension. Decreased pulmonary compliance may not be immediately recognized with LMAs.
End-tidal carbon dioxide: May be increased with upsloping of capnograph tracing. It should be noted that complete airway obstruction may occur with a supraglottic device, mask GA, or supplemental oxygen modality (nasal canula, face mask) for a sedation case; this will result in the extinguishment of the capnograph tracing.
Pulmonary artery catheter (PAC) or pulse contour cardiac output monitoring (PiCCO): If present, a low systemic vascular resistance will be present.
Serum tryptase levels should be sent at the time of the event, at 1 hour, 6–24 hours after the episode.
Serologic testing: Carries no risk of anaphylaxis is the test of choice if the history reveals a high probability of allergic reaction.
Radioallergent absorbent testing (RAST) is capable of measuring the level of drug-specific IgE antibody in the serum. It is highly specific (80–87%), but has a low sensitivity (50–60%); false-negatives occur 25% of the time.
Skin testing: Carries the risk of inducing systemic anaphylaxis should only be performed by physicians with training resources to respond to an emergency situation.
Skin prick testing uses an antigen solution at a variety of dilutions. It has been found to be very sensitive specific.
Intradermal testing uses an antigen solution.
Patch testing may be useful in establishing the diagnosis of contact dermatitis (Type IV allergic reaction).
Differential Diagnosis
Anaphylaxis due to other antigens (neuromuscular blocking agents, antibiotics, protamine, blood transfusions):
Asthma
Angioedema
Cardiogenic shock
Septic shock
Carcinoid syndrome
Pulmonary embolism
Treatment⬆⬇
Management of anaphylaxis due to latex does not differ from any other type of anaphylactic reaction.
Discontinue the exposure to latex.
Communicate the emergency situation with the operating room team.
Administer 100% oxygen; maintain a clear airway with a low threshold for intubation.
Administration of epinephrine 10–100 µg IV
Inhaled bronchodilators may be necessary.
IV crystalloid fluid as clinically indicated
Diphenhydramine 50–75 mg IV
Hydrocortisone up to 200 mg IV or methylprednisolone 1–2 mg/kg
Consideration of sodium bicarbonate if severe acidosis persists
Consider central line placement for monitoring therapy if not already in place.
Follow-Up⬆⬇
After an episode of anaphylaxis, the patient should be closely monitored in an ICU setting since symptoms can recur in up to 20% of patients.
If the patient experienced their first allergic reaction, then they should be referred to an allergist or dermatologist for further testing. They should also be fully informed of the situation wear a Medic-Alert bracelet indicating their allergy.
If no episode of anaphylaxis occurred in a latex-sensitive patient, they can likely be discharged to the ward with continued latex precautions.
References⬆⬇
HepnerDL, CastellsMC.Latex allergy: An update. Anesth Analg. 2003;96:1219–1229.
KamPC, ThompsonJF.Latex allergy: An emerging health hazard for operating theatre staff. Anaesthesia. 1997;84(3):570–575.
FarleyCA, JonesHM.Latex allergy. Contin Educ Anaesth Crit Care Pain. 2002;2(1):20–23.
RyderSA.Anaphylaxis. Contin Educ Anaesth Crit Care Pain. 2004;4(4):111–113.
Additional Reading⬆⬇
American latex allergy association
See Also (Topic, Algorithm, Electronic Media Element)
Latex allergies have increased since the introduction of Universal Precautions in the healthcare setting.
Known latex allergies allow the operating room team to make preparations to avoid a potentially life-threatening reaction. In addition to absolute avoidance of latex-containing products, patients should be scheduled as first cases since aeroallergens can be suspended in the air for up to 5 hours.
Unknown allergies pose the greatest threat since signs symptoms are not specific to latex anaphylaxis may also be delayed. Dermatologic signs may not be immediately obvious under surgical drapes cardiovascular collapse (hypotension, PEA) may be the first presenting symptom. Furthermore, inadequate circulation may delay dermatologic manifestations.
Latex antigens are found in several products in the operating room should be well known to the anaesthetist. Additionally, the anaesthetist is responsible for clearing out items specific to their care (disposable anesthesia bag, tourniquets, syringe plungers, medication vials with rubber stoppers, some face masks, ETTs, etc.).