572
Correspondence Huan-Wen Chen, MD Department of Internal Medicine Far Eastern Memorial Hospital Taipei 100, Taiwan Deng-Huang Su, MD Far Eastern Polyclinic Taipei 100, Taiwan Tzuu-Shuh Jou, MD, PhD Jia-Horng Kao, MD, PhD Department of Internal Medicine National Taiwan University Hospital and National Taiwan University College of Medicine Taipei 100, Taiwan Email address:
[email protected]
doi:10.1016/j.ajem.2004.12.003 Training emergency physicians to perform out-of-hospital ultrasonography
References
To the Editor, We read with interest the paper from Jang et al [1] on training for ultrasonography in emergency cases. Training is a crucial matter when ultrasonographic examination is performed by a nonradiologist operator [2]. Our experience could contribute to this issue as we recently evaluated initial training for emergency physicians performing out-ofhospital ultrasonography. A 4-hour tutorial on focused abdominal sonography for trauma included theoretical lecture, demonstration, and practice. Eight experimented emergency physicians attended 1 to 6 tutorials. Then, ultrasonography was routinely used by emergency physicians in out-of-hospital settings. Patients were followed up to validate out-of-hospital diagnosis. Indeed, it should be noted that, because of outof-hospital settings, patients’ follow-up was indispensable for the physicians to validate their out-of-hospital diagnosis. Two hundred twenty-two examinations were analyzed to evaluate initial training. Diagnostic performance (sensitivity, specificity, and positive and negative predictive values) increased for emergency physicians after attending 2 tutorials (Table 1). Diagnostic performance according to the number of examinations performed using a receiver operator curve showed a cutoff point of 25 examinations. Then, we
Table 1 Comparison of diagnostic performance according to attended formations b2 formations N2 formations
validated the following training protocol associating at least 8 hours of initial tutorial and at least 25 examinations including patients’ follow-up. According to our results, performance reached with such training was similar to the performance reached by hospital emergency physicians. The results we reported are consistent with those of Jang et al whereas ultrasonography indications are different. In both studies, the minimal training seemed to involve 25 examinations or less. Despite the lack of strong evidence, as Jang et al, we concluded that the recommendations of the American College of Emergency Physicians were pertinent as the suggested number of examinations required (25 for each indication) is similar to our results [3]. Such attitude seems to be adequate for emergency physicians willing to reach a high level of performance. It should be noted that, in particular indications, a much shorter tutorial has been proposed with satisfactory results [4,5]. This point illustrates the need to validate tutorials and practical training according to a specific indication, as Jang et al and we undertook.
Sensitivity
Specificity
PPV
NPV
20 92
98 98
67 89
83 99
PPV indicates positive predictive value; NPV, negative predictive value.
[1] Jang T, Aubin C, Naunheim R. Am J Emerg Med 2004;22:439 - 43. [2] Robinson NA, Clancy MJ. Should UK emergency physicians undertake diagnostic ultrasound examinations? J Accid Emerg Med 1999;16:248 - 9. [3] ACEP Board of Directors. ACEP emergency ultrasound guidelines. Available at: www.acep.org [accessed September 24, 2004]. [4] Marshburn TH, Legome E, Sargsyan A, Li SM, Noble VA, et al. Goal-directed ultrasound in the detection of long-bone fractures. J Trauma 2004;57:329 - 32. [5] Kimura BJ, Amundson SA, Willis CL, Gilpin EA, DeMaria AN. Usefulness of a hand-held ultrasound device for bedside examination of left ventricular function. Am J Cardiol 2002;90:1038 - 9.
Fre´de´ric Lapostolle, MD Tomislav Petrovic, MD Jean Catineau, MD Gille Lenoir, MD Fre´de´ric Adnet, MD, PhD SAMU 93, EA 3409, CHU Avicenne 125, rue de Stalingrad 93009 Bobigny, France E-mail address:
[email protected] doi:10.1016/j.ajem.2005.01.008 Spontaneous pneumothorax presenting as epigastric pain To the Editor, Spontaneous pneumothorax is a common disease encountered in hospital practice. It usually occurs in young men and presents with sudden onset of respiratory distress and chest pain. We report on a patient with spontaneous pneumothorax, who presented with epigastric pain,
Correspondence
Fig. 1 Chest radiogram reveals around 80% pneumothorax on the left side without pleural effusion.
mimicking peptic ulcer disease or acute pancreatitis. The pain subsided after chest tube thoracostomy. A 41-year-old man, smoking for 20 years, had gradual onset of epigastric pain 2 weeks before visit to our hospital. He had no history of heavy alcohol intake. Reviewing his history, the respiratory symptoms, such as cough, dyspnea, chest or shoulder pain, did not occur after the onset. No trauma history was noted. He had no medical history of peptic ulcer disease and pancreatobiliary disease. On arrival, he was clear and ambulatory. The vital signs were stable: blood pressure was 130/80 mm Hg, pulse rate 84 beats per minute, respiratory rate 16 breaths per minute, and body temperature 37.08C. Blood gas analysis at room air was Po2 71.4 mm Hg and Pco2 40.1 mm Hg, and his peripheral oxygen saturation was 94%. Physically, auscultation of the lung revealed clear breath sounds except over the left lung field where breath sounds were diminished. The abdomen was soft but with epigastric tenderness. The remainder of the physical examination was unremarkable. The differential diagnoses were peptic ulcer disease and acute pancreatitis. A peripheral white cell count showed 7100 cells per microliter without a left shift. Serum amylase and lipase were within normal limits. Abdominal ultrasound revealed normal a pancreas without pancreatobiliary tract dilatation. In gastric endoscopy, neither gastric nor duodenal ulcer was found. Posterior-anterior chest radiograph disclosed a left pneumothorax (around 80%) without a mediastinal shift (Fig. 1). Pleural effusion was not observed on the radiograph. Soon after chest tube thoracostomy, his epigastric pain subsided. Full reexpansion of the left lung was achieved, and he was discharged uneventfully 4 days later. No more epigastric pain was reported after discharge. Primary spontaneous pneumothorax is a common disease encountered in hospital practice. It is defined as pneumothorax without underlying lung disease and typically occurs
573 in tall thin boys and men between the ages of 10 and 30 years [1- 4]. It results from rupture of subpleural bullae and air leaks into pleural cavity. Practically, all patients have ipsilateral pleural chest pain or acute dyspnea because reduction of lung volume results in respiratory distress [1- 4]. Other minor symptoms include cough and general malaise [5]. However, our patient presented with epigastric pain, mimicking acute peptic ulcer disease or pancreatitis and, surprisingly, without respiratory symptoms. It is very rare manifestation for spontaneous pneumothorax. In English literature, we found only one report on tension pneumothorax presenting with epigastralgia and epigastric tenderness described by Hollins et al [5]. Very recently, Lien et al [6] reported pneumothorax presenting with right upper quadrant pain and a positive Murphy sign, mimicking acute cholecystitis. The mechanism by which spontaneous pneumothorax causes epigastric pain is still uncertain. In the patients reported by Hollins et al [5], epigastric pain might be elicited by tension pneumothorax that depressed the right hemidiaphragm of the affected side. In the patient reported by Lien et al [6], no tension pneumothorax was found, and therefore, they speculated that right upper quadrant pain might be caused by a small pleural effusion. In our patient, however, there was neither tension pneumothorax nor pleural effusion. We suspected that other mechanism such as influence on diaphragm of the affected side by highly collapsed lung toward pulmonary ligament would be concerned with the epigastric pain. It would be possible in our case rather than tension pneumothorax and pleural effusion. In addition, Lien et al [6] suggested that young age and high pain tolerance were the reason why the patient had no respiratory symptoms. With this phenomenon, we suppose that very slow progression of pneumothorax would be concerned in our patient. In a patient with epigastric pain, an intra-abdominal pathology, especially gastrointestinal and pancreatobiliary diseases, should be sought initially. However, consider a spontaneous pneumothorax if there are negative findings on abdominal sonography and gastric endoscopy.
References [1] Wissberg D, Refaely Y. Pneumothorax: experience with 1,199 patients. Chest 2000;117:1279 - 85. [2] Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med 2000;342:868 - 74. [3] Baumann MH, Strange C, Heffner JE, et al. Management of spontaneous pneumothorax. An American College of Chest Physicians Delphi consensus statement. Chest 2001;119:590 - 602. [4] Noppen M, Baumann MH. Pathogenesis and treatment of primary spontaneous pneumothorax: an overview. Respiration 2003;70:431 - 8. [5] Hollins GW, Beattie T, Happer I, et al. Tension pneumothorax: report of two cases presenting with acute abdominal symptoms. J Accid Emerg Med 1994;11:43 - 4. [6] Lien WC, Yuan A, Tsai KC, et al. Primary spontaneous pneumothorax with clinical manifestation mimicking acute cholecystitis. J Emerg Med 2004;26:354 - 6.
574
Correspondence Ryoko Ogawa, MD Yusuke Yamamoto, MD Norihiro Haraguchi, MD Hiroaki Satoh, MD Kiyohisa Sekizawa, MD Division of Respiratory Medicine Institute of Clinical Medicine University of Tsukuba Tsukuba City Ibaraki, 305-8575, Japan E-mail address:
[email protected]
doi:10.1016/j.ajem.2004.12.007 A cross-sectional ED survey of infantile subclinical methemoglobinemiaB To the Editor, The prevalence of clinically significant methemoglobinemia (MHb) is unknown among previously healthy infants presenting to the emergency department (ED) with diarrhea and dehydration. However, it is well described in these infants and, when present, can be associated with significant morbidity [1-4]. Nevertheless, it may not be clinically apparent until levels reach almost 7 times normal levels [5]. Based on this, we hypothesized that dehydrated infants younger than 3 months with diarrhea would commonly have MHb levels above normal but below that causing cyanosis and obvious distress. We conducted a cross-sectional study of MHb in acyanotic dehydrated infants with diarrhea and a comparison group of well-hydrated febrile infants, all 3 months old or younger, presenting to an urban pediatric ED. The age group and severity of illness of the dehydrated patients were chosen for the highest likelihood of MHb [3]. A sample size of 10 was needed in each group, with a one-tailed a level of .05 and power of 80% to detect a mean group MHb level of 5% F 5%. (An MHb level of 5% was chosen as a cutoff level for which symptoms are likely to occur but clinical signs will not be evident.) A convenience sample was enrolled during 1 year from among age-appropriate patients with diarrhea and diagnosis of dehydration as determined by the on-duty attending pediatric emergency physician. Diarrhea was defined as 3 or more loose or watery stools in the prior 24 hours. Degree of dehydration was established by the use of a generally accepted pediatric emergency dehydra-
Presented in part at the Clinical Research 2003 National Meeting (March 23, 2003), the National Meeting of the Pediatric Academic Societies (May 3, 2003), and the National Meeting of the Society for Academic Emergency Medicine (May 29, 2003). B This research was supported by GCRC grant M01-RR13297 from the National Center for Research Resources, National Institutes of Health, Bethesda, MD.
Table 1
Demographics and clinical variables by group Dehydrated Febrile
Male sex [n (%)]
7 (70)
Breastfed [n (%)]
4 (40)
RR = 0.99 (0.59 to 1.64) 13 (76) RR = 0.53 (0.24 to 1.18) 52 [32-81] P = .69
Median age 64 [38-84] (d [IQR]) Mean weight 52 F 36 61 F 30 (percentile) Mean temperature 38.2 F 1 38.4 F 1 (8C) Mean pulse 175 F 24 164 F 16 (beats/min) Mean respirations 41 F 8 41 F 10 (beats/min) Mean oxygen 99 F 2 99 F 1 saturation (arterial) (%) Median dehydration 5 [5-10] 0 [0-0] level (% [IQR]) Total 10 17 a
Significance
12 (71)
P ( P ( P ( P ( P (
= .55 22 to 39)a = .66 1 to 1)a = .23 30 to 8)a = .98 7 to 7)a = .33 1 to 2)a
P b .001
The 95% CI of the difference in the means.
tion scale [6]. Well-hydrated comparison patients were selected from a convenience sample of well-hydrated infants in the same age range undergoing a fever evaluation. Patients were excluded if they had a history of MHb, an acidemia-inducing illness (eg, metabolic disorder), or received oxidizing medication via breast milk or direct ingestion. The research was approved by the hospital’s institutional review board. Written informed consent was obtained from the parents of all infants. The study was conducted at the Children’s National Medical Center General Clinical Research Center. Thirty patients were approached for enrollment and 3 parents refused (1 in the dehydration group and 2 in the fever group). We enrolled a total of 27 subjects: 10 with dehydration and 17 febrile patients. The mean age of the entire study population was 59 F 29 days; 70% were boys. The 2 groups were demographically similar (Table 1). The prevalence of subclinical MHb (sMHb) (ie, MHb N1.5%) was 2 of 10 (20%; 95% CI, 2.5-55.6) dehydrated subjects and 1 of 17 (5.9%; 95% CI, 0.2-28.7) well-hydrated comparison patients ( P = NS). It is noteworthy that of the patients with sMHb, the 2 dehydrated patients had levels of 5.9% and 6%, whereas the single well-hydrated patient had a level of 1.9%. None of the potential risk factors for sMHb were significantly associated with group designation. Among all 27 patients enrolled, v 2 analysis and the Student t test revealed the following factors significantly associated with sMHb: lower mean body weight percentile ( P = .027) and higher mean chloride level ( P = .033) (Table 2).