Metabolic alkalosis and cystic fibrosis


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Commentary on acid-base status in cystic fibrosis

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Metabolic alkalosis and cystic fibrosis

  1. 1. Metabolic Alkalosis and Cystic Fibrosis Chest 2004;125;1169-1170 DOI 10.1378/chest.125.3.1169 The online version of this article, along with updated information and services can be found online on the World Wide Web at: Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright2004by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. ( ISSN:0012-3692Downloaded from by guest on May 13, 2011 © 2004 American College of Chest Physicians
  2. 2. was detected. However, those studies would presumably be Correspondence to: LCDR Edward M. Omron, MC, USNR,clinically indicated. It is the goal of all of us to reduce the cost of FCCP, Pulmonary Medicine Department, National Naval Medi-testing that does not further the clinical outcome of the patient. cal Center, 8901 Wisconsin Ave, Bethesda, MD 20889; email: Larger studies as well as investigations of different patientpopulations will be needed to answer all the questions surround- Referencesing the topic of routine chest radiographs in patients with 1 Holland AE, Wilson JW, Kotsimbos TC, et al. Metabolicrespiratory failure who are treated with mechanical ventilation. alkalosis contributes to acute hypercapnic respiratory failureSuch studies should be performed in a randomized, controlled in adult cystic fibrosis. Chest 2003; 124:490 – 493protocol, and meaningful clinical outcomes should be sought. 2 Jones NL. Blood gases and acid-base physiology, 2nd ed. New York, NY: Thieme Medical Publishers, 1987; 185 Richard M. Schwartzstein, MD 3 Figge J, Mydosh T, Fencl V. Serum proteins and acid-base equilibria: a follow up. J Lab Clin Med 1992; 120:713–719 Mark Krivopal, MD Beth Israel Deaconess HealthCare To the Editor: Boston, MA We thank Dr. Omron for his interest in our article examiningReproduction of this article is prohibited without written permis- acid-base status in patients with cystic fibrosis (CF) and COPD.1sion from the American College of Chest Physicians (e-mail: His comments focus on two main points: whether the in acid-base balance do in fact represent a primary metabolicCorrespondence to: Mark Krivopal, MD, 330 Brookline Ave, alkalosis in addition to respiratory acidosis in the CF group, andBoston, MA 02215 what the mechanism of the observed changes may be. In the setting of an acute exacerbation of lung disease accompa- nied by hypercapnia, we observed a significantly more alkaline pH inMetabolic Alkalosis and Cystic the CF group than in the group of patients with COPD. AlthoughFibrosis the mean difference in pH between the groups was modest in absolute terms, we noted that 13 of 14 patients with CF (93%) had a pH 7.4, which would be an unusual feature of a partiallyTo the Editor: compensated respiratory acidosis. In addition, in 13 of 14 of the patients with CF (93%), the observed renal response to elevated I read with interest the study by Holland et al (August 2003)1 Paco2 was greater than would be expected to compensate for adescribing the metabolic acid-base status in patients with acute chronic respiratory acidosis.2 We therefore feel confident that theexacerbations of adult cystic fibrosis (CF) and COPD. I congratulate observed differences indicate both primary metabolic alkalosis andthem on an interesting descriptive study of acid-base status and primary respiratory acidosis in the patients with CF.electrolytes in COPD and CF. However, I disagree with their This was a cross-sectional study in which we described acid-conclusion that “metabolic alkalosis contributes to hypercapnic base status in hypercapnic patients with CF and COPD present-respiratory failure with acute exacerbations of CF.” No arterial blood ing with an acute exacerbation of lung disease. As such, ourgas or electrolyte data are provided to establish a premorbid baseline article did not aim to determine the cause of the observedin either the COPD or CF groups to support the inference that one metabolic alkalosis in CF. We concur with Dr. Omron thator both groups are indeed in acute hypercapnic respiratory failure. hypoalbuminemia may play an important role in acid-base dis-The arterial blood gas and electrolyte data on presentation in both turbance, and the data we presented support this hypothesis.groups could be interpreted as chronic hypercapnic respiratory However, in the light of previous work showing an associationfailure with appropriate compensatory metabolic alkalosis. In fact, between chloride depletion and metabolic alkalosis in childrenthe mean inorganic strong ion difference (Na K Cl ) in both with CF,3 along with observed changes in cerebrospinal fluidthe CF and COPD groups is approximately equal (45.7 mmol/L and chloride levels with changes in plasma chloride,4 the contribution45.1 mmol/L or milliequivalents per liter, respectively) and consis- of electrolyte status requires evaluation. We are currently con-tent with appropriate renal compensation for chronic hypercapnea.2 ducting further work in this area.An equal mean inorganic strong ion difference between the CF and We agree with Dr. Omron that the clinical implications of thisCOPD groups reveals that the magnitude of the metabolic alkalosis study are as yet unclear. It is possible that correction of metabolicattributed to electrolyte differences is equal in both groups and does alkalosis in this patient group may not be advantageous; however,not account for the minor difference in mean pH. The CF group this has not been examined. In addition, the effects of noninva-manifested a more severe hypoalbuminemia (less plasma weak-acid sive ventilation on respiratory drive in patients with metaboliccontent) relative to the COPD group, and fully accounts for the alkalosis are unknown. These issues are yet to be examined inalkaline difference in mean pH between the groups when assessed clinical trials. It is clear, however, that acid-base analysis inby physicochemical analysis.3 The inference of the author is of patients with multisystem diseases such as CF needs to encom-clinical concern since overzealous correction of a compensatory pass more than a cursory glance at Paco2.metabolic alkalosis may unmask a severe respiratory acidosis. Aswell, aggressive ventilation for chronic hypercapnic respiratory Anne Holland, BAppScfailure may unmask a severe metabolic alkalosis. Insufficient data are John Wilson, MBBS, PhD, FCCPpresent to support the conclusion that a metabolic alkalosis in adult Tom Kotsimbos, MDCF in this setting contributes to hypercapnic respiratory failure. Matthew Naughton, MD The Alfred Hospital LCDR Edward M. Omron, MC, USNR, FCCP Victoria, Australia National Naval Medical Center Bethesda, MD Reproduction of this article is prohibited without written permis- sion from the American College of Chest Physicians (e-mail:Reproduction of this article is prohibited without written permis- from the American College of Chest Physicians (e-mail: Correspondence to: Anne Holland, BAppSc, The Alfred Hospital, PO Box 315, Prahran, VIC 3181, CHEST / 125 / 3 / MARCH, 2004 1169 Downloaded from by guest on May 13, 2011 © 2004 American College of Chest Physicians
  3. 3. References 1 Holland AE, Wilson JW, Kotsimbos TC, et al. Metabolic alkalosis contributes to acute hypercapnic respiratory failure in adult cystic fibrosis. Chest 2003; 124:490 – 493 2 Jones NL. Blood gases and acid-base physiology. 2nd ed. New York, NY: Thieme Medical Publishers, 1987 3 Mauri S, Pedroli G, Rudeberg A, et al. Acute metabolic alkalosis in cystic fibrosis: prospective study and review of the literature. Miner Electrolyte Metab 1997; 23:33–37 4 Javaheri S, Kazemi H. Electrolyte composition of cerebrospi- nal fluid in acute acid-base disorders. Respir Physiol 1981; 45:141–151 Figure 1. At the end of the plication, the diaphragm should have a normal profile (left, a), avoiding undercorrection (middle, b) and overcorrection (right, c).Plication for DiaphragmaticEventrationA Simple Technique, Not a Simple Problem technique, a partial lateral correction is obtained, without the natural shape of the diaphragmatic dome being restored. More-To the Editor: over, as it was described, the obtained diaphragm may be overcorrected. In our opinion, the best suture line runs from the The case recently reported in CHEST by Hwang et al (July midline of the posterolateral diaphragmatic dome to the level of2003)1 left three important questions open to readers. Even if the phrenic nerve. A good correction shows a diaphragm pro-technically simple, are we justified to propose surgical correction gressively ascending from the attachments just below the poste-of a diaphragmatic eventration only on the basis of progressive rior minithoracotomy, assuming a horizontal portion at the leveldyspnea on exertion and chest radiograph findings? We do not of the cardiophrenic angle. If the diaphragm overcomes thisthink so. angle, it has been undercorrected. If the diaphragm becomes a At least two steps in the evaluation of this patient are missing. linear, flat, oblique, and hard plane between its costodiaphrag- 1. Clinical history: if the patient has no previous chest radio- matic portion and the cardiophrenic angle, it has been overcor- graph, in our opinion the case has to be classified as a rected (Fig 1). recently diagnosed eventration (ie, one known for 2 Finally, a single running suture cannot be enough for a years). In this case, a long period of observation (at least 1 structure such as the diaphragm, which continuously changes its year) is needed to exclude the possibility of diaphragmatic profile. function recovery. Moreover, in the assessment of dia- phragmatic eventration, a detailed clinical history is crucial Francesco Leo, MD, FCCP to determine the most likely cause. The presented case Nicolas Venissac, MD concerns a patient with a mediastinal deviation, which can Fernando Morales, MD cause troubles with cardiac rhythm. Has this aspect been Andres Rodriguez, MD investigated? In cases in which patients are aware of their Jerome Mouroux, MD ´ ˆ eventration, dyspnea can be very difficult to quantify University Hospital of Nice because they can easily translate their anxiety into a wide Nice, France variety of respiratory symptoms. If this is the case, more qualifying signs, such as orthopnea, have to be searched for. Reproduction of this article is prohibited without written permis- 2. Radiologic evaluation: a CT scan is essential to rule out sion from the American College of Chest Physicians (e-mail: thoracic or abdominal disease, to assess the anatomic area Correspondence to: Francesco Leo, MD, FCCP, Thoracic Sur- of the phrenic nerve, and to evaluate lung parenchyma. On gery Department, Pasteur Hospital, 30 Ave de la Voie Romaine, the basis of the presented chest radiograph, how can 06002 Nice, France; e-mail: authors exclude the presence of a left main bronchus lung cancer with lymph node metastases of the aortopulmonary References window? 1 Hwang Z, Shin JS, Cho YH, et al. A simple technique for the thoracoscopic plication of the diaphragm. Chest 2003; 124: The proposed technique is not that different from the video- 376 –378assisted technique that we presented in 19962 and performed in 2 Mouroux J, Padovani B, Poirier NC, et al. Technique for the12 patients in the last 10 years. Do the proposed modifications repair of diaphragmatic eventration. Ann Thorac Surg 1996;improve the technique? This is questionable for several reasons. 62:905–907The only theoretical advantage to the modifications is theavoidance of a 5-cm minithoracotomy by the insertion of two To the Editor:5-mm ports in the eight and ninth intercostal spaces (withpossible injury to two different intercostal nerves). In such a We appreciate the interest in our case report (July 2003)1 andsituation, the surgeon starts the suture in the simplest position the comments made by Leo and colleagues. They pointed outbut ends up in the most difficult one, with the largest part of the several problems, including evaluation of the patient, mini-eventration in the more distant zone. thoracotomy, and direction of the repair. The third question is which is the ideal correction for eventra- The most important step in the evaluation of the patient is thetion? Hwang et al stated that the plication has to be performed search for the cause of disease. In our case, we had beenfrom the anterolateral to the posteromedial costophrenic recess, observing the patient for about 6 years when the operation wasand, at the end of the procedure, the diaphragm has to be tense performed. A chest CT scan obtained with the patient in theon palpation. We disagree with both observations. With such a posteroanterior position 6 years before the operation showed1170 Communications to the Editor Downloaded from by guest on May 13, 2011 © 2004 American College of Chest Physicians
  4. 4. Metabolic Alkalosis and Cystic Fibrosis Chest 2004;125; 1169-1170 DOI 10.1378/chest.125.3.1169 This information is current as of May 13, 2011Updated Information & ServicesUpdated Information and services can be found at: article cites 5 articles, 2 of which can be accessed free at: & LicensingInformation about reproducing this article in parts (figures, tables) or in its entirety can befound online at: about ordering reprints can be found online: AlertsReceive free e-mail alerts when new articles cite this article. To sign up, select the"Services" link to the right of the online article.Images in PowerPoint formatFigures that appear in CHEST articles can be downloaded for teaching purposes inPowerPoint slide format. See any online figure for directions. Downloaded from by guest on May 13, 2011 © 2004 American College of Chest Physicians