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Latex Anaphylaxis: Another Case, Another Cause

Ballantyne, Jane C. MB BS, FRCA; Brown, Emery MD PhD

Case Reports

Department of Anesthesiology, Massachusetts General Hospital, Boston, Massachusetts.

Accepted for publication August 25, 1995.

Address correspondence and reprint requests to Jane C. Ballantyne, MB, BS, FRCA, Department of Anesthesia, Clinics 3, Massachusetts General Hospital, Boston, MA 02114.

Sensitivity to latex (T-cell mediated) manifested by dermatitis, rhinitis, conjunctivitis, and angioedema has been described at least since the early 1960s. More recently, the phenomenon of immunoglobulin E-mediated latex allergy producing urticaria, bronchospasm, and even serious anaphylaxis, has been recognized [1-5]. Serious intraoperative latexinduced anaphylaxis has become a hazard, particularly since the institution of universal precautions requiring the use of gloves for most patient contact. The following case report describes a life-threatening anaphylaxis in a healthy young patient who was not suspected of being allergic to latex. When questioned in detail after the incident about the possibility of latex sensitivity, a previously unrecognized predisposition emerged.

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Case Report

A 29-yr-old woman was scheduled for a laparoscopic cholecystectomy for acute cholecystitis. Her past medical history was remarkable only for infertility, treatment with in vitro fertilization, and delivery of twin girls by cesarean section 1 yr prior to the current admission with cholecystitis. She had several uneventful general anesthetics in the past for gynecologic laparoscopies and for her cesarean section. She was taking no medications at home, but was being treated with cefazolin for cholecystitis in hospital. She had no known drug allergies.

In the operating room, a single intravenous catheter was placed, and she was premedicated with midazolam 2 mg. Standard monitors were applied before induction of anesthesia with propofol 120 mg, atracurium 30 mg, and fentanyl 250 micro gram. Induction of anesthesia and tracheal intubation were unremarkable. Maintenance of anesthesia was continued with 70% nitrous oxide and 0.25% isoflurane.

Twenty minutes after induction of anesthesia, surgery commenced. Having had stable vital signs since induction, she developed a tachycardia (heart rate [HR] 100 bpm) which was not influenced by propofol (50 mg intravenous bolus). Her HR continued to increase (to 140 bpm), her oxygen saturation began to decrease (from 100% to 96%), and her peak airway pressure increased (from 20 cm H2 O to 30 cm H2 O). Ventilation was controlled manually, the FIO2 was changed to 1.0, and the oxygen delivery system was quickly checked. Auscultation of the chest revealed bilateral bronchospasm, and breath sounds markedly reduced on the left. The endotracheal tube was pulled back and suctioned, but no improvement resulted. Twenty-five minutes after induction of anesthesia, when the surgeons were about to begin inflating the abdomen, her HR was 160 bpm, oxygen saturation 96% with an FIO2 of 1.0, and peak airway pressure 60 cm H2 O. She was still normotensive (104/50 mm Hg). The surgeons were asked to discontinue the surgery. Her condition then very rapidly deteriorated. She remained tachycardic (HR 120-180 bpm), with an arterial blood pressure of 70/40 mm Hg and an oxygen saturation of 88%. Breath sounds were now absent on the left. Hypotension was treated initially with intravenous phenylephrine. A 14-gauge Angiocath Registered Trademark (Becton Dickinson, Sandy, UT) was inserted into the left intrapleural space, but there was no obvious air leak, and no improvement. Epinephrine administration was commenced, initially by bolus injection, and then by infusion; she began to improve. Chest radiograph revealed normal lung fields, with no evidence of pneumothorax or aspiration of gastric contents. The Angiocath was removed from the left pleural space. Once she was stable, anesthesia/sedation was restarted with boluses of propofol and she was given 100 mg hydrocortisone. Surgery was abandoned, and she was transferred to the postanesthesia care unit, still tracheally intubated with ventilation controlled. Although the crisis had passed, she was still markedly bronchospastic and dependent on epinephrine for control of bronchospasm and hypotension.

In the postanesthesia care unit, the chest radiograph revealed a total collapse of the left lung. After chest tube placement, the patient gradually improved so that after 2 h, several nebulizer treatments with albuterol, and a gradual decrease in the rate of epinephrine infusion, she had normal breath sounds, was cardiovascularly stable, fully alert and oriented, and the trachea was extubated. Recovery thereafter was uneventful.

Four days later she presented again for laparoscopic cholecystectomy, with chest tube still in place. Because she had recently suffered a serious anaphylaxis, testing was not undertaken (testing being unreliable immediately after serious anaphylaxis). However, a history of possible latex allergy had been elicited; she gave a history of reacting to latex gloves with hives on her hands, and of sneezing and nasal congestion after vaginal examinations. Latex allergy was still thought to be an unlikely cause for her intraoperative collapse, since she was tolerating a latex chest tube. However, for this anesthetic, propofol, atracurium, and latex were avoided, and the operative course and recovery were uneventful. Later, skin tests were strongly positive to latex and negative to all the anesthetics used. The latex radioallergosorbent test test was strongly positive (823.3 ng/mL of immunoglobulin E antibody to latex, the normal being <1.0 ng/mL).

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This is a typical case of intraoperative latex anaphylaxis, with sudden cardiorespiratory collapse occurring well into the course of anesthesia, unlike a drug reaction that occurs immediately after injection of the trigger. It is by no means the first report of its kind [1,4,6-14], but is presented because the patient suffered a life-threatening event which might have been avoided had her risk been appreciated before surgery. The exact mode of latex anaphylaxis is unclear, but skin or mucous membrane contact by latex, drug contamination by latex, injection through latex, or a combination of the above are possible. At the same time, it is not known exactly which latex products are the most antigenic [15]. (Note that this patient actually tolerated a latex chest tube, but still reacted to another latex trigger.) It is becoming clear, however, that patients who are most likely to suffer reactions are primarily those with frequent exposure to latex--particularly mucous membrane exposure--notably health care workers, patients having repeated catheterization with rubber products (those with congenital urologic anomalies, congenital orthopedic anomalies, spina bifida, and spinal cord injury), and industrial workers working with rubber [16-22]. Until more is understood about latex anaphylaxis, the only defense we have is to adequately screen patients and to treat those at risk with broad precautions. It is important, therefore, to be able to recognize patients at risk, and to elicit a careful history of possible latex allergy, especially in patients in known risk categories. Patients having frequent vaginal examinations (particularly those going through an in vitro fertilization program who are examined daily per vagina during midcycle with a latex covered ultrasound probe) should probably be added to the list of individuals at risk.

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© 1995 International Anesthesia Research Society