1310 Correspondence / American Journal of Emergency Medicine 33 (2015) 1305-1322

these cases concerned solid (mainly lung) tumors. In the remaining cases analyzed in our study, pulmonary embolism was considered as idiopathic or the result of trauma, fracture, or other form of immobilization of the patient. Clearly, the possibility of occult hematologic disease cannot be completely ruled out, especially in cases considered as idiopathic. Nevertheless, the analysis of the data coming up from patients’ medical record, clinical examination, or laboratory tests does not support such a possibility.

On the other hand, second-hand smoking could represent an additional limitation of our retrospective study, although it is difficult to estimate the extent of this limitation. We should also take into account the difficulty in assessing passive smokers’ exposure to environmental tobacco smoke. Although medical History taking in our hospital checks for exposure to cigarette smoking, it does not comprise a standard questionnaire for the semiquantitative evalua- tion of passive smoking. Two patients who spontaneously reported a very high exposure to passive smoking were classified as smokers and were excluded from the study. Ideally, the quantification of exposure to passive smoking should be based on the information reported by parents and verified by the measurement of cotinine levels in saliva or urine to support their statements [3]. Of course, this was impossible in our study due to its retrospective nature.

Furthermore, although passive smoking has been repeatedly reported to acutely increase COHb levels, most of these measurements have been carried out during participants’ exposure to second-hand smoking or shortly after this. Moreover, this effect appears to be dose dependent. Thus, lower levels or shorter durations of smoke exposure fail to significantly increase COHb levels [4]. Generally, exogenously delivered CO presents a half-life of 5 to 6 hours without supplemental Oxygen administration [5]. Therefore, it is not surprising that COHb had poor discriminating ability for passive smoking in when evaluated later after the exposure during the preoperative process [6,7]. We consider this clinical setting to present more similarities with our study compared with other studies involving the acute effects of environmental tobacco smoke exposure under experimental conditions.

Yours sincerely

Sotirios Kakavas, MD, MSc, PhD? Aggeliki Papanikolaou, MD Evangelos Balis, MD, PhD Nikolaos Tatsis, MD Christina Goga, MD Georgios Tatsis, MD

Pulmonary Department, Evangelismos General Hospital of Athens

Ypsilanti 45-47, 10676, Athens, Greece

?Corresponding author. Tel.: +30 213 2041 631; fax: +30 210 7232 370 E-mail addresses: [email protected] (S. Kakavas) [email protected] (A. Papanikolaou) [email protected] (E. Balis), [email protected] (N. Tatsis)

[email protected] (C. Goga) [email protected] (G. Tatsis)

http://dx.doi.org/10.1016/j.ajem.2015.05.006

References

1. Sotirios Kakavas, Aggeliki Papanikolaou, Evangelos Ballis, Nikolaos Tatsis, Christina Goga, Georgios Tatsis. Carboxyhemoglobin and methemoglobin levels as Prognostic markers in acute pulmonary embolism. Am J Emerg Med 2015. http://dx.doi.org/10. 1016/j.ajem.2015.01.046.
2. Nielsen VG, Pearson EC, Smith MC. Increased carbon monoxide production by hemeoxygenase-1 caused by device-mediated hemolysis: thrombotic phantom menace? Artif Organs 2013;37(11):1008-14.
3. Jarvis M, Tunstall-Pedoe H, Feyerabend C, Vesey C, Salloojee Y. biochemical markers of smoke absorption and self reported exposure to passive smoking biochemical markers of smoke absorption and self reported exposure to passive smoking. J Epidemiol Community Health 1984;38(4):335-9.
4. Yarlioglues M, Kaya MG, Ardic I, Dogdu O, Yarlioglues H, Zencir C, et al. Dose- dependent acute effects of passive smoking on left ventricular Cardiac functions in healthy volunteers. J Investig Med 2012;60:517-22.
5. Scherer G. Carboxyhemoglobin and thiocyanate as biomarkers of exposure to carbon monoxide and hydrogen cyanide in tobacco smoke. Exp Toxicol Pathol 2006;58:101-24.
6. Cardwell K, Pan Z, Boucher R, Zuk J, Friesen RH. Screening by pulse CO-oximetry for environmental tobacco smoke exposure in preanesthetic children. Paediatr Anaesth 2012;22:859-64.
7. Yee BE, Ahmed MI, Brugge D, Farrell M, Lozada G, Idupaganthi R, et al. Second-hand smoking and Carboxyhemoglobin levels in children: a prospective observational study. Paediatr Anaesth 2010;20(1):82-9.

   Endogenous and exogenous factors affecting the levels of carboxyhemoglobin

   

   To the Editor,

   We read with great interest the article “Carboxyhemoglobin and methemoglobin levels as prognostic markers in acute pulmonary embolism” written by Kakavas et al [1]. We think that the factors affecting the Carboxyhemoglobin level were not expressed clearly, and some patients who should be excluded from the study may have been included in this research that examined the COHb and methemoglobin level in patients with pulmonary embolism. There- fore, COHb levels were higher than expected, and the study results could be affected.

   Carbon monoxide poisoning is a condition that affects many systems especially the cardiovascular and central nervous systems [2-6]. Older erythrocytes are removed from the circulation, and when the Heme they contain are demolished, CO occurs. Carbon monoxide originating from the human body generates 1% of COHb. Endogenous CO rises to the level of 4% to 6% in some Hematologic diseases [7]. Otherwise, COHb level of patients being smoker and also passive smoker rises. Carboxyhemoglobin level of a passive smoker has been reported to be twice as much than the normal level of COHb in studies [8,9].

   Therefore, we consider that not questioning the conditions causing an increase in COHb levels such as passive smoker and hematologic diseases in addition to smokers in study exclusion criteria was one of limitations of study, and this situation should be explained in the study.

   Y. Emrah Eyi, MD

   Department of Emergency Medicine, Gulhane Military

   Medical Academy, Ankara, Turkey Corresponding author at: Gulhane Military Medical Academy Etlik, Ankara, Turkey. Tel.: +90 532 582 2802; fax: +90 312 304 1194.

   E-mail address: [email protected]

   Memduh Yetim, MD

   Van Military hospital, Van, Turkey

   Sukru Tekindur, MD Department of Anesthesiology and Reanimation Gulhane Military Medical Academy, Ankara, Turkey

   http://dx.doi.org/10.1016/j.ajem.2015.05.005

   References

   Sotirios Kakavas, Aggeliki Papanikolaou, Evangelos Ballis, Nikolaos Tatsis, Christina Goga, Georgios Tatsis. Carboxyhemoglobin and methemoglobin levels as prognostic markers in acute pulmonary embolism. Am J Emerg Med 2015. http://dx.doi.org/10. 1016/j.ajem.2015.01.046.

   Correspondence / American Journal of Emergency Medicine 33 (2015) 1305-1322 1311

   Eyi YE, Aksoy Y, Zorlu E, Kaya A, Ozturk K, Colakoglu K. Is S100B protein level really not an indicator of brain damage due to carbon monoxide poisoning in children? Am J Emerg Med 2013;31(10):1531.

8. Clower JH, Hampson NB, Iqbal S, Yip FY. Recipients of Hyperbaric oxygen treatment for carbon monoxide poisoning and Exposure circumstances. Am J Emerg Med 2012;30(6):846-51.
9. Kaldirim U, Yolcu U, Arziman I, Eyi YE, Tuncer SK. The relationship between blood lactate, carboxy-hemoglobin and clinical status in CO poisoning. Eur Rev Med Pharmacol Sci 2014;18(19):2777.
10. Zengin S, Oktay MM, Al B, Yavuz E, Yildirim C. An Unusual Cause of Supraventricular Tachycardia: acute carbon monoxide poisoning. J Clin Anal Med 2015;6(3):377-9.
11. Akdemir HU, Kati C. Bilateral Globus Pallidus Ischemia: Carbon Monoxide Poisoning. J Clin Anal Med 2013. http://dx.doi.org/10.4328/JCAM.1683.
12. Nielsen VG, Pearson EC, Smith MC. Increased carbon monoxide production by hemeoxygenase-1 caused by device-mediated hemolysis: thrombotic phantom menace? Artif Organs 2013;37(11):1008-14.
13. Bentur L, Hellou E, Goldbart A, Pillar G, Monovich E, Salameh M, et al. Laboratory and clinical acute effects of active and passive indoor group water-pipe (narghile) smoking. Chest 2014;145(4):803-9.
14. Akhter S, Ali Warraich U, Rizvi N, Idrees N, Zaina F. Comparison of end tidal carbon monoxide (eCO) levels in shisha (water pipe) and cigarette smokers. Tob Induc Dis 2014;12(1):10.

    fluid management decisions should not be guided by fixed central venous pressure targets

    

    To the Editor,

    In the March issue of the journal, Sirvent et al [1] published an article entitled “fluid balance in sepsis and septic shock as a determining factor of mortality.” In this study, they demonstrated that a positive fluid balance in the first days after admission is independently linked to adverse outcome. Two of us (K.H.P. and J.V.) wrote an accompanying editorial entitled “Do not drown the patient: appropriate fluid management in critical illness” [2]. One of the points that we tried to make, forcefully, was that central venous pressure is completely unreliable as a parameter to assess volume status or to predict fluid responsiveness [1,2]. We strongly urged the readers never to target specific CVP values in their fluid management.

    The same issue of the journal contains a letter by Sarlak et al [3],

    written in response to the article by Sirvent et al and our accompanying editorial. The letter is entitled “Fluid necessity should be followed by central venous pressure.” It argues that CVP should be measured as an indicator of volume responsiveness, with a target pressure of 8 to 12 cm water.

    Of course, we strongly disagree with the title and content of this letter, because (as our editorial discussed) more than 40 studies have conclusively demonstrated that CVP is completely unreliable as a parameter of volume status or as predictor of fluid responsiveness [2,4].

    More importantly, Sarlak et al cite 2 articles in support of their statement, which, in reality, support the opposite view. One is a review written by 2 of us, P.M. and J.V. [5]; this review forcefully argues against use of CVP in the way advocated by Sarlak et al. To quote from this review, “titrating fluid based on the CVP is equally likely to result in either hypovolemia or pulmonary edema.” Nothing in our review supports the use of fixed CVP targets to guide fluid therapy, and we do not understand how it could be misinterpreted in this way.

    The other study cited by Sarlak et al is as study by Coen et al [6], investigating inferior vena cava and Lung ultrasounds as an alternative to invasive CVP monitoring. Again, this study does not support using CVP targets to guide fluid administration in any way whatsoever.

    The letter by Sarlak et al wrongly suggests that we and others

    support use of fixed CVP targets to guide fluid management. The exact

    dangerous. Central venous pressure is one of the least reliable methods to assess volume status, and basing decisions regarding fluid administration on fixed CVP targets is only marginally better than flipping a coin to guide the decision [2,4]. Our editorial lists numerous alternative methods that are much more reliable [2].

    We hope this letter corrects any possible misinterpretation of our views and take this opportunity to once again urge the reader to avoid “iatrogenic submersion” of the patient.

    Kees H. Polderman, MD, PhD Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA 15261

    Corresponding author.

    E-mail address: [email protected]

    Joseph Varon, MD, PhD

    The University of Texas Health Science Center at Houston

    Houston, TX 77030

    Paul E. Marik, MD, PhD Department of Internal Medicine, Eastern Virginia Medical School, Norfolk, VA 23507

    http://dx.doi.org/10.1016/j.ajem.2015.05.015

    References

    Sirvent JM, Ferri C, Baro A, Murcia C, Lorencio C. Fluid balance in sepsis and septic shock as a determining factor of mortality. Am J Emerg Med 2015;33:186-9.

15. Polderman KH, Varon J. Do not drown the patient: appropriate fluid management in

    critical illness. 2015;33:448-50.

    Sarlak H, Tanriseven M, Duran E. Fluid necessity should be followed by central venous pressure. Am J Emerg Med 2015;33:471.

16. Marik PE, Cavallazzi R. Does the central venous pressure predict fluid responsive- ness? An updated meta-analysis and a plea for some common sense. Crit Care Med 2013;41:1774-81.
17. Marik PE, Varon J. Early goal-directed therapy: on Terminal life support? Am J Emerg Med 2010;28:243-5.
18. Coen D, Cortellano F, Pasini S, Tombini V, Vaccaro A, Montalbetti L, et al. Towards a less invasive approach to the early goal-directed treatment of septic shock in the ED. Am J Emerg Med 2014;32:563-8.

    Fluid Management Dilemma in Patients with Severe Sepsis and Septic Shock?

    

    To the Editor,

    We read the letter “Fluid management decisions should not be guided by fixed central venous pressure targets” written by Polder- man and Varon [1] with great interest. We thank them for their valuable contributions and criticisms. First of all, we did not cite the article number 4 that they had stated in their response. In that meta-analysis, 191 studies have been evaluated, 43 of them have been included in the study, and only 4 of them were associated with the patients who were in sepsis [2].

    The title of our letter is questionable, but we do not agree with Polderman and Varon on the content [3]. Creatinine and lactate levels should be monitored closely for renal functions initially and after. Intravenous fluids, along with antibiotics, source control, vasopressors, inotropic agents, and mechanical ventilation are the key components in early management of septic shock [4,5]. For improving outcome in severe sepsis, early diagnosis, early antibiotics, and early and appropriate fluid resuscitation targeting is necessary for adequate tissue perfusion [6].

    opposite is the case; as we have argued repeatedly, the literature

    clearly shows that such use of the CVP is misguided and even

    ? There is no conflict of interests.