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LETTERS to the EDITOR

Reactive airways dysfunction after exposure to

teargas

SIR,—To disperse and subdue demonstrators teargas is often used, commonly used agents being CS (o-chlorobenzylidene malononitrile) and CN (chloroacetophenone). Toxicological testing of these agents in the 1960s and 1970s was reassuring but many concerns remain, including the potential for chronic toxicity and for the exacerbation of pre-existing disease. We report the accidental exposure to CS of a previously healthy woman that was followed by reactive airways dysfunction syndrome (RADS). In October, 1989, a 21-year-old healthy woman with no history of wheezing or asthma and no family history of asthma or atopy was in a crowded nightclub when a canister containing CS was discharged 2-3 m away from her, as a malicious prank. The room, measuring 20 x 35 m or so rapidly became cloudy with smoke, but patrons could not escape quickly because of the confusion and

crowding at the exits. The woman spent 5-10 minutes in the room, and experienced intense burning of the eyes, face, throat, and nasal passages. Once outside she was coughing paroxysmally, had tightness and burning in her chest, and felt light-headed. She was taken to hospital by ambulance, receiving oxygen by nasal cannula en route. No remarkable findings were noted on physical examination; and chest radiography was normal. The patient was discharged. However, coughing and shortness of breath persisted. A further radiograph was normal. She was given oral erythromycin. She continued to cough, especially at night, waking up and expectorating phlegm that looked like "cooked egg white". 2 weeks after the CS exposure she was still wheezing and had a deep cough. She was admitted to hospital and treated with intravenous steroids, antibiotics, theophylline, and beta-agonists. 4 weeks after exposure spirometry revealed reduced forced expiratory volume in 1 s (FEV 1) (62% predicted) and forced vital capacity (78%). The patient has continued to have cough and shortness of breath during 2 years of follow-up. These symptoms are worsened by exertion and inhalation of cold air, tobacco smoke, or automobile fumes. She is on continuous inhaled beta-agonists and steroids and intermittent high-dose oral steroids. Pre-exercise spirometry 1½ years after the exposure revealed an FEV1 of 128% (of predicted) but when the patient went for a brisk walk in chilly air this fell by 16%, in association with wheezing, even though she had taken her maintenance medications. Teargas agents consist of a family of fifteen chemicals capable of causing intense sensory irritation that is brief and not usually accompanied by lasting toxicity. The immediate effects are intense irritation of the eyes, mucous membranes, throat and stomach, and skin. In 1971 an official inquiry in Britain reviewed scientific data on CS and concluded that although exposure can be lethal (the most likely form of toxicity being pulmonary damage leading to pulmonary oedema), this would only happen at concentrations several hundred times greater than the exposure "dosages" that produce incapacitating symptoms.1 Nevertheless the possibility of significant pulmonary injury remains an issue. One small volunteer study showed no increase in airway resistance,2 but people with a

history of asthma were excluded. In a community survey of civilians exposed to CS several reported cough and shortness of breath that continued for weeks.3 Exposure to high levels of respiratory irritants similar to CS has been associated with the development of RAD S in some individuals,4,5 and this syndrome is present in this young woman described here. She still has a non-specific bronchial hyperreactivity requiring continuous medications. Channing Laboratory, Brigham and Women’s Hospital, Boston, Massachusetts 02115, USA; Department of Medicine, Harvard Medical School; and Occupational Health Program, Harvard School of Public Health

HOWARD Hu

Pulmonary and Critical Care Unit, Massachusetts General Hospital, Department of Medicine, Harvard Medical School; and Occupational Health Program, Harvard School of Public Health

DAVID CHRISTIANI

(chairman). Report of the enquiry into the medical and toxicological aspect of CS (ortho-chlorobenzylidene malononitrile II: enquiry into toxicological aspects of CS and its use for civil purposes. London: HM Stationery Office, 1971. 2. Punte CL, Owens EJ, Gutentag PJ. Exposures to ortho-chlorobenzylidine malononitrile. Arch Environ Health 1963; 6: 366-74. 3. Hu H, Fine J, Epstein P, Walker B, Reynolds P, Kelsey K. Tear gas: harassing agent or toxic chemical weapon? JAMA 1989; 262: 660-63. 4. Brooks SM, Weiss MA, Bernstein IL. Reactive airways dysfunction syndrome (RADS). Chest 1985; 88: 376-84. 5. Brooks SM, Weiss MA, Berstein IL. Reactive airways dysfunction syndrome. J Occup Med 1985; 27: 473-76. 1. Himsworth H

IGE-mediated reaction to hydroxocobalamin

injection in patient with pernicious anaemia SIR,—Although vitamin H12 is widely used, severe reactions are rare.1 There have been vitamin B12 in which

no an

an anaphylactic reaction to IgE-mediated mechanism has been

reports of

demonstrated. A 78-year-old non-atopic woman developed general urticaria and vomiting and collapsed 20 min after an intramuscular injection of 10 mg hydroxocobalamin (HC) (Novobedouze, Bouchara Lab) for pernicious anaemia. 1 month before, she had received HC without reaction. 3 years earlier, after a subtotal resection of the small intestine for generalised stenosis of the small intestine, she had been placed on a monthly maintenance dose of 1 mg cyanocobalamin (CC) intramuscularly (Labaz Lab) without adverse reaction. Skin prick testing with neat HC was positive. Intradermal tests with HC were positive at a dilution of 10-2. A skin prick test was positive when the mean diameter of the wheal (D + d/2) with HC was over 75% that of the mean diameter of the wheal obtained with 9% codeine. Prick and intradermal tests with two different CC preparations or saline were negative. Prick and intradermal tests with HC and CC in two non-atopic patients and two with grass pollen allergy were also negative. In-vitro histamine release by

1536

basophils from the patients with HC demonstrated an IgEmediated reaction. In contrast, no histamine release was seen with CC. Histamine was not detected in the HC vial, whether by manufacturer-performed controls or by radioimmunoassay (Immunotech). The patient was subsequently given increasing doses of CC (0-1, 0-5, 1 mg) intramuscularly, with no allergic reaction. The clinical history, skin test results and the in-vitro histamine release demonstrated an IgE-cell-mediated reaction to HC. Because crossreactions between HC and CC have been described,when intramuscular injection is the only administration route possible in a patient sensitised to vitamin B12’ complete allergic investigations with both HC and CC are warranted. Then, B12 administration should be progressive and under surveillance.

PEEP

days

BLAY M. F. SAGER C. HIRTH M. ALT P. CHAMOUARD R. BAUMANN G. PAULI F.

Hôpitaux Universitaires de Strasbourg, 67091 Strasbourg, France; and Faculté de Médecine de Strasbourg, Université Louis Pasteur, Strasbourg

DE

1.

Hodwing G. Anaphylactic reaction after injection of vitamin B12. Br Med J1968; iii:

2.

James J, Warin R. Sensitivity to cyanocobalamin and hydroxocobalamin. Br Med J 1971; ii: 262.

Pa02/FI02

102.

Extended

(29 days) use of intravascular gas exchanger

a

iu

is

su

sa

s

days excnange

oy

armiciai

uevices

can

oe

mea.

nxiracorporeal

oxygenation (ECMO) is the original approach but it is cumbersome, requiring blood pumps, oxygenators, heat exchangers, tubing, anticoagulants, and round-the-clock supervision by a specialised team. To circumvent this an intravascular gas exchange device has been devised.l It has been used clinically for up to 6 daYS.2 Having done our own experimental evaluationwe report the successful extended use of this device over 29 days. A 21-year-old woman had pneumococcal pneumonia and adult respiratory distress syndrome after shingles. She was cyanotic, hypotensive, and in acute distress, the respiratory rate being 48/min. Blood gases, while she was breathing 4 litres per minute of

PEEP and

Pa02/Fi02 (partial arterial O2 pressure -’- O2 fraction of inspiratory gas). 4h = hours before implant. E day of explant.

membrane

oxygen via nasal prongs, were PaOz5-6 kPa, Sa02 68%, PaC02 60 kPa, and pH 730. Chest radiography revealed bilateral consolidation. Her white cell count was 0-96 x 109/1 with 44%

neutrophils (92% band forms), blood urea 16-4 mmol/l, creatinine 129 umol/1, and aspartate aminotransferase 72 U/1 (normal 60). Penicillin G and acyclovir were started. On adrenaline, noradrenaline, and artificial ventilation (Fi02 of 10, positive end-expiratory pressure [PEEP] 13 cm H2O, inspiration-to expiration ratio 2/1, peak inspiratory pressure 40 cm H2O), the patient deteriorated over the next 24 hours, her blood gases being: P02 (6-5 kPa, Sa02 66%, PC02 65 kPa, and pH 7-2 (lowest arterial oxygen saturation 40%). Cardiac, renal, and hepatic failure ensued. In this precarious situation an intravascular gas exchanger (IVOX size 7; CardioPulmonics, Salt Lake City, Utah) was implanted into the caval axis under fluoroscopic control as a bedside emergency procedure. Despite several complications (haemopneumothorax after drainage of pleural effusions during heparin therapy for prevention of device-related clot formation and a sepsis syndrome requiring antimicrobial therapy), the patient’s general condition and respiratory function improved over the next 29 days of intravascular lung assist (figure). Despite a reduction in FiOand PEEP, her Pa02 progressively increased. Vasoactive and positive inotropic support could be stopped on day 25. The intrapulmonary shunt decreased impressively (not shown), so that the gas exchanger could be removed on day 29 (day E) resulting in an only slight decrease of total gas exchange (El). The patient was later discharged from hospital without neurological sequelae and in good general condition.

=

-

At the time the device was implanted, the patient was getting progressively more hypoxic (final Sa02 40%) and hypotensive with impending multiorgan failure despite conventional intensive care. After the device started to contribute to gas exchange, haemodynamics and organ function recovered, and the conditions of mechanical ventilation could be improved to tolerable settings. Several attempts to remove the gas exchange device within the time limit of two weeks for which the system had originally been designed, failed, due to persistent respiratory incompetence. The device remained fully functional, however, over 29 days. No

problems resulted from the extended

use

of the device. Our

experience indicates that an intravascular gas exchanger is a valid tool, even for prolonged lung assist, allowing a reduction in aggressive mechanical ventilation and permitting recovery of the diseased lung. We do not think that our patient would have survived without artificial membrane oxygenation.

Departments of Surgery and Medicine, University Hospital Zurich, CH-8091 Zürich, Switzerland

L. K. VON SEGESSER A. SCHAFFNER R. STOCKER M. LACHAT R. SPEICH P. C. BAUMANN M. TURINA

1. Mortensen JD. An intravenacaval blood gas exchange (IVCBGE) device. ASAIO Trans 1987; 33: 570-73. 2. Kallis P, Al Saady N, Bennett D, Treasure T. Clinical use of intravascular 3.

oxygenation. Lancet 1991; 337: 549. Segesser LK, Weiss BM, Pasic M, Friedl HP, Leskosek B, Turina M. Temporary lung support using an intravascular gas exchanger. Thorac Cardiovasc Surg (in press).

von

Mycobacterial nucleic acids in sarcoid lesions SIR,—Two contributions in your April 25 issue (pp 1012,1015) report detection of mycobacterial nucleic acids in biopsy specimens and bronchoalveolar lavages (BAL) obtained from patients with sarcoidosis. These results were obtained either by polymerase chain

amplification (PCR) or liquid hybridisation techniques. Using Mycobacterium leprae as a model for organisms that cannot be cultured in vitro, we have developed a PCR for species-specific 16S rRNA sequences of mycobacteria to study M leprae in human cells

IGE-mediated reaction to hydroxocobalamin injection in patient with pernicious anaemia.

1535 LETTERS to the EDITOR Reactive airways dysfunction after exposure to teargas SIR,—To disperse and subdue demonstrators teargas is often...
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