CORRESPONDENCE

1. Schenh P, Mittermayer C, Ratheiser K Inhaled nitric oxide in a patient with severe pulmonary embolism. Ann Emerg Meal. 1999;33:710-714.

2. Tanus Santos JE. Inhaled nitric oxide and pulmona~ embolism. Intensive Care Med. 1998;24:747-748.

3. Tanus-Santos JE, Moreno H jr, Moreno RA, et al. Inhaled nitric oxide improves hemodynamics during a venous air infusion (VAI) in dogs. Intensive Care Med. 1999;25:983-989.

4. Tanus Santos JE, Moreno H Jr, Zappellini A, et aI Small-dose inhaled nitric oxide attenuates hemodynamic changes after pulmonary air embolism in dogs. Anesth Analg. 1999;88:1025-1029.

5. Tanus-Santos dE, Moreno H Jr Inhaled nitric oxide as a coadjuvant therapy after massive pulmonary embolism. Can J Anaesth. 1999;46:906.

In reply:

Tanus-Santos at al 1 recently described an animal model of pulmonary air embolism where stable pulmonary hypertension was induced bya constant venous air infusion. Inhaled nitric oxide (NO) at 3 ppm did not reduce pulmonary artery pressure; the only effect observed was an increase in cardiac index, which was 23% to 24% higher in NO- treated dogs compared with controls. Pulmonary vascular resistance decreased as a consequence of the rise in cardiac index. An increase of the concentration of NO to 40 ppm had similar effects. These authors con- cluded that small doses of inhaled NO (3 ppm) would be as effective as higher doses (40 ppm) in massive pulmonary embolism. However, another animal model of pulmonary embolism by Bottiger et al, 2 where micro- spheres (300 pro)injected into the superior vena cava induced pulmonary hypertension in piglets, showed that 80 ppm NO was even more effective than 40 ppm. The change of pulmonary vascular resistance was only significant at 80 ppm. Both animal models cannot be regarded unequivocally as being comparable models for pulmonarythrom- boembolism because of the different path- omechanism. The present animal models show only small hemodynamic effects of inhaled NO with no or only minor reduction in pulmonary artery pressure. This could be due to a different grade of pulmonary vasocon- striction compared with massive pulmonary thromboembolism, as stated by Bottiger et al. 2 Thus, it would be interesting to study the effect of inhaled NO in an animal model of acute thromboembolism by using the injec- tion of autologous blood clot. We suggested that a higher dose (50 ppm) might have even more effect compared with a low dose (5

ppm) in reducing critically increased right ventricular afterload in the state of severe pulmonary embolism,3 guided bystudies in adult respiratory distress syndrome, where most experience with inhaled NO has been achieved. In patients with adult respiratory distress syndrome, Gerlach et al 4 showed a dose-response curve of inhaled NO (0.01,0.1, 1,10, 1 O0 ppm), demonstrating that higher doses are more effective in lowering pul- monary artery pressure, In addition, in patients with pulmonary hypertension and scleroderma, Williamson etal 5 observed a dose-response curve of inhaled NO.

Experience with inhaled NO in human thromboembolism is scarce; however, in 8 patients the hemodynamic effects of 5 to 50 ppm NO were impressive. 3,6 9 NO reduced pulmonary artery pressure and increased arterial pressure when hypotension was pre- sent. In the study by Capellier et al, 6 in patient No. 2, 10 ppm NO was more effec- tive than 5 ppm; in patient No. 3, 15 ppm was more effective than 5 and 10 ppm; and in patient No. 4, 20 ppm was more effective than 10 ppm. It is clear that controlled trials are needed to confirm the beneficial effects of inhaled NO in this critical, life-threatening setting, as Tanus-Santos et al stated. In addition, dose-response studies are needed to determine the most effective dose.

Peter Schenk, MD Christoph Mittermayer, MD Klaus Ratheiser, MD Department of Internal Medicine 4 Intensive Care Unit University of Vienna Vienna, Austria

47/8/106145 doL 10.1067/mem.2000.106145 1. Tanus-Santos JE, Moreno H Jr, Moreno RA, et al. Inhaled nitric oxide improves hemodynamics dur/ng a venous air infusion (VAI) in dogs. Intensive Care Med. 1999;25:983-989.

2. Bottiger BW, Motsch J, Dorsam J, et al. Inhaled nitric oxide selectively decreases pulmonary artery pressure and pulmonary vascular resistance following acute massive pul- monary microembolism in piglets. Chest. 1996;i 1 O: 1041 - I047.

3. Schenk P, Mittermayer C, Ratheiser K. Inhaled nitric oxide in a patient with severe pulmonary embolism. Ann Ernerg Meal. 1999;33:710-714.

4. Gerlach H, Rossaint R, Pappert D, et al. Time-course and dose-response of nitric oxide inhalation jor systemic oxygenation and pulmonary hypertension in patients with adult respiratory distress syndrome. Eur J Clin Invest. 1993;23:499-502.

.5. Williamson DJ, Hayward C, Rogers P, et at. Acute hemo- dynamic responses to inhaled nitric oxide in patients with limited scleroderma and isolated pulmonary hypertension Circulation. i996;94:477-482.

6. CapelIier Ca, Jacques T, Balvav P, ¢t al. Inhaled nitric oxide in patients with pulmonary embolism. Intensive Care Med. 1997;23:1089-1092.

7. Schenh P, Pernersto,jer T, Mittermayee C, et al. Inhalation oj nitric oxide as a lije-saving therapy in a

patient adter pulmonary embotectomy. Br J Anaesth. I999;82:444-447.

8. Estagnasie P, Le BouMelles G, Mier L, et at. Use oj inhaled nitric o~ide to reverse flow through a patent Jora- men ovale du~ng pulmonary embolism. Ann Intern Med. 1994;120:757-759.

9. Crera¢-Gilbert A, Boots R. Use qf inhaled nitric oxide in pulmonary embolism. Anaesth Intensive Care. 1999;27:4I 2-414

Harmonization of Data Collection on Poisonings

To the Editor.

Buckley et aP (article #101304) have demon- strated the importance of harmonized data collection on poisoning admissions in hospi- tals. By using a standard format of data entry fields for all poisoning admissions, itwas shown that the completion of information on clinical signs at presentation was signifi- cantly greater when a preformatted data entryformatwas used.

The need for standardizing poisoning case and chemical incident data collection was identified as a key role of poison control centers by a group of experts convened by the World Health Organization (WHO)in 1985. 2 This group highlighted the necessity of gen- erating comparable data for the purposes of toxicovigilance and epidemiologic studies that would transcend national boundaries. In response, the WHO has developed Guidelines for Poison Control 3 and initiated what is known as the IPCS INTOX Project, whereby a global network of approximately 100 poison centers in 60 countries has devel- oped a computerized system for such a pur- pose. This system incorporates a series of formats for case registration. Data are entered using control led vocabulary lists of terms and classification systems (of clinical features, agent use/function, agent chemical structure, and biological grouping for toxin- producing organisms). A harmonized system for grading the severity of poisoning cases (Poisoning Severity Score 4) has been incor- porated into the system. The fourth version of

5 1 2 ANNALS OF EMERGENCY MEDICINE 35:5 MAY 2000

CORRESPONDENCE

the system is now being prepared for release and has been modified and improved, based on user feedback. It has been built with Visual Basic(Microsoft; Redmond, CA)using Microsoft Access (relational)(Microsoft) as the back- end database. All of the vocabulary lists and classification terms have been defined and the complete system translated into French, Portuguese, and Spanish by poison center specialists. The case registration format has been translated into Vietnamese, Russian, Polish, and Arabic and issued in hard copy. The system was presented this year at the North American Congress of Clinical Toxicology(La Jolla, CA, October 1999).

Surveillance of poisoning episodes and of the use of chemical products in the commu- nity is well recognized as an important func- tion of poison centers bythe American Association of Poison Control Centers, which operates a Toxic Exposure Surveillance System (TESS). TESS collects data from poi- son centers in a standardized format for these purposes. 5 However, in many develop- ing countries the problems of financing and infrastructure have prohibited the setup of mechanisms for standardized data collection and toxicovigilance activities. The INTOX system attempts to respond to the needs of those countries where mortality from poison- ing remains high, especially due to pesti- cides. 6,7 GIobalization has resulted in an increase in traffic of chemicals around the globe that do not respect national bound- aries. The international group of experts involved in the development and use of this system has guaranteed a global evidence- based mechanism for responding to global problems. 8

The problems encountered when attempting to design epidemiologic studies in clinical toxicology 9,1° would be reduced if those involved agreed on harmonized sever- itygrading and standardized data collection. The INTOX Project provides the basis for such studies, and the WHO is currently coordinat- ing 2 international studies using standard- ized formats of the I NTOX system (one on the burden of acute pesticide poisoning and the other on the treatment of organophospho- rous pesticide poisoning).

Explicit political recognition of the role of poison centers was achieved during the United Nations Conference on Environment and Development held in Rio de Janeiro,

Brazil, in June 1992 (Agenda 21, Chapter 19). By the year 2002, countries will be expected to report on their achievements since the Rio Earth Summit concerning the sound manage- ment of chemicals and the reduction of toxic exposures. The harmonized data collection tools developed by the INTOX Project are enabling countries to collect the evidence required to plan effective prevention cam- paigns and to report on the progression of exposures to toxic substances.

Michael Ruse, PhD John Haines, PhD Jenny Pronczuk, MO International Programme on Chemical Safety World Hea/th Organization Geneva, Switzerland

47/8/106144 doi: 10.1067/mem.2000.106144 1. BuclelEy NA, Whyte L\.I, Dm~son AH, et al Prejormatted

admission char ts fin poisoning admissions.facilitate chemi cell assessment and research Ann Emerg Med. 1999;34:476 482.

2. World Health O~gan<ation. Organization of a Poison Control Programme: Roles and Responsibilities of Poison Control Centres, Meeting Report. Geneva, Switz.erland: World Health Organization; 1985.

3. World Health Organization Guidelines for Poison Control. Gene;a, Switzerland: World Health Organization: 1997

4. Persson HE, 5jobetg GK, Haines JA, et al. Poisoning Seven(,, Score Grading of acute poisoning J Toxicol Clin ToxicoI 199&.36:20.'>213.

5. 1.itovitz T The TESS database. Use in product saleU assessment Drug Saf. 1998;18:9-19.

6. Ga~cia ]E. Acute poisonings lrom pesticides: human and economic costs [in Spanish/ Rev Panam Salud Publica 1998;4:38.3-387.

7 Murrqy CJL, Lopez AD. The Global Burden of Disease Boston, MA: Harvard School of Public Health, Harvard University P~ess; 1996.

8. Meredith T, Haines JA. International data collection and e~idence-based clinical to~xicologv. J Toxicol Clin Toxicol. ] 996;34:647-649.

9 Buckley NA, Smith AJ. Evidence based medicine in taxi- cology: where is the evidence? Lancet 1996;347: I 157-1169.

10 Whyte IM, Buckler NA Pragress in clinical toxicoloxv: j iom case tcpo~ts to toxkoepidemiolox'v. Med J Aust 1995;163:340-34i.

Meeting the SAEM Ultrasound Guidelines

To the Editor.

Witting et al 1 (article #102245) have studied a focus of extreme importance in the devel- opment of emergency ultrasonography.

Currently the only emergency medicine train- ing guideline is the Society for Academic Emergency Medicine (SAEM)model curricu- lum published in 1994. 2 As the authors cor- rectly state, these guidelines recommend 40 hours of teaching and 150 proctored exami- nations, yet their survey revealed significant heterogeneity at training programs with only one reaching these guidelines. The imple- mentation of a successful ultrasound pro- gram is a formidable task at any hospital and achieving the model curriculum can be chal- lenging. Immense work is required, but justi- fied as we are responsible for training physi- cians for tomorrow's practice.

Developing a successful ultrasound pro- gram and completing the SAEM guidelines requires full departmental and training pro- gram support. Complete integration of ultra- sound into the residencytraining program is necessary. Early devoted time for introduc- tory 1- to 2-day courses allows for a founda- tion on which ultrasonography skills can be taught during the 36-month emergency medicine training period. Ongoing teaching must occur in a lecture format and consis- tently at the bedside. Residents should be given assigned readings and receive self- study modules/examinations in an effort to learn ultrasonography as they would any other emergency medicine content. Integral to this is a well-developed quality improve- ment program that provides consistent feed- backto the resident in training. Research is both stimulating and necessary for ultra- sound development in emergency medicine and completes the evolution of an academic program. Within this framework, graduating residents should achieve the model curricu- lum guidelines and be given a certificate to that effect.

The aforementioned components have taken years to develop within the specialty but can occur in reasonable time frame at new programs with available resources. Programs and departments needing help in developing an ultrasound program should contact the SAEM Ultrasound Interest Group orthe American College of Emergency Physicians Ultrasound Section for assis- tance. Our cooperative efforts will help develop the field of emergency ultrasonogra- phy within training centers, but implementa- tion of bedside ultrasound in the community

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