Mortality in Hyperglycemic Crisis

Mortality in Hyperglycemic Crisis

e158 3. Ludmerer KM. The development of American medical education from the turn of the century to the era of managed care. Clin Orthop Relat Res 2004...

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e158 3. Ludmerer KM. The development of American medical education from the turn of the century to the era of managed care. Clin Orthop Relat Res 2004;(422):256–62. 4. Emergency Medicine Milestones. American Board of Emergency Medicine. Available at: https://www.abem.org/public/publications/ emergency-medicine-milestones. Accessed October 21, 2013.

, UTILITY OF DIAGNOSIS OF TUBERCULOSIS IN AN OVERCROWDED EMERGENCY DEPARTMENT , To the Editor: We read the recent article, “Patient factors associated with failure to diagnose tuberculosis in the emergency department” by Geyer et al. with interest (1). It is encouraging that 77% of tuberculosis cases can be diagnosed in the emergency department (ED). They also concluded that homeless, alcoholic, substance abuser, and unresponsive patients are at increased risk of nondiagnosis of tuberculosis in ED visits (1). Delay in diagnosis results in increased infectivity in the community and may lead to more advanced disease and mortality (2). Underutilization of chest radiography, sputum examination, low degree of clinical suspicion, and low socioeconomic and educational level are some of the reasons for diagnostic delay (3). An ED visit provides an opportunity for the diagnosis of tuberculosis, but as suggested by the author, interferon gamma-based diagnostic assay has a limited role in the diagnosis of active tuberculosis (4). Chest radiograph sensitivity and specificity in the diagnosis of tuberculosis are only 80% and 67%, respectively (5). A newer diagnostic test, Xpert MTB/RIF (Cepheid, Sunnyvale, CA), has a high sensitivity of 92.2% in sputum smear-positive cases and 76.9% in sputum smearnegative patients. Xpert MTB/RIF is also suitable for emergency diagnosis because it gives result within 2 h, and its sensitivity does not decrease in human immunodeficiency virus and immune-suppressed states (6). However, cost effectiveness and availability of Xpert MTB/RIF in the ED is a major constraint. Extrapulmonary tuberculosis constitutes 15–20% of immunocompetent and more than 50% of immunesuppressed patients in the ED (7). Hence, the author exclusion of extrapulmonary tuberculosis makes this study less useful in the ED. Delayed ED diagnosis of tuberculosis is seen to be associated with increased mortality in univariate analysis (p = 0.02), but no statistical significance is noted in the final result of stepwise logistic regression analysis (8). To conclude, despite extensive work-up in a crowded ED, diagnostic yield improves only marginally. Final

Letters to the Editor

improvement in the outcome of tuberculosis is also minimal. Nayer Jamshed, MD All India Institute of Medical Sciences, New Delhi Fouzia F. Ozair, MBBS, DO Jawahar Lal Nehru University, New Delhi Praveen Aggarwal, MD All India Institute of Medical Sciences, New Delhi Meera Ekka, MD All India Institute of Medical Sciences, New Delhi http://dx.doi.org/10.1016/j.jemermed.2014.07.044 REFERENCES 1. Geyer BC, Goldwin P, Powell TJ, Moffitt MP, LoVecchio F. Patient factors associated with failure to diagnose tuberculosis in the emergency department. J Emerg Med 2013;5:658–65. 2. Styblo K. Epidemiology of tuberculosis. 2nd edition. The Hague: Royal Netherlands Tuberculosis Association; 1991. 3. Yilmaz A, Boga S, Sulu E, et al. Delays in the diagnosis and treatment of hospitalized patients with smear positive pulmonary tuberculosis. Respir Med 2001;95:802–5. 4. Kang YA, Lee HW, Yoon HI, et al. Discrepancy between the tuberculin test and the whole-blood interferon gamma assay for the diagnosis of latent tuberculosis infection in an indeterminate tuberculosisburden country. JAMA 2005;293:2756–61. 5. van Cleeff MR, Kivihya-Ndugga LE, Meme H, Odhiambo JA, Klatser PR. The role and performance of chest X-ray for the diagnosis of tuberculosis: a cost-effective analysis in Nairobi, Kenya. BMC Infect Dis 2005;5:111. 6. Boehme CC, Nicol MP, Nabetta P. Feasibility, diagnostic accuracy, and effectiveness of decentralised use of the Xpert MTB/RIF test for the diagnosis of tuberculosis and multidrug resistance: a multicentre implementation study. Lancet 2011;377:1495–505. 7. Sharma SK, Mohan A. Extrapulmonary tuberculosis. Indian J Med Res 2004;120:316–53. 8. Tsai TC, Hung MS, Chew G. Delayed diagnosis of active pulmonary tuberculosis in Emergency Department. Am J Emerg Med 2008;26: 888–92.

, MORTALITY IN HYPERGLYCEMIC CRISIS , To the Editor: In the clinical review, “Hyperglycemic Crisis,” there are some discrepancies with the literature (1). On page 798, the authors write “In diabetic ketoacidosis (DKA) . is insulin deficiency .. In contrast, patients with hyperosmolar hyperglycemic state (HHS) have some pancreatic beta cell function ..” Since 1977, when the Nobel prize went to Rosalyn Yallow for development of new methods of biochemical analysis that

The Journal of Emergency Medicine

make it possible to measure the concentration of insulin in human plasma, this has been used worldwide. In 1981, the monograph Diabetic Coma: Ketoacidotic and Hyperosmolar was published (2). On page 67 is Figure 6.3, with the names of 12 authors who have reported sufficient amounts of plasmatic insulin in patients with DKA. On the other hand, absolute deficiency of plasmatic insulin has been reported in patients with HHS and also in diabetic patients on routine control, without subjective complaints. Where are published case histories of concrete patients with DKA and absolute deficiency of plasmatic insulin? (3,4). On page 803, the conclusion of the authors is “Hyperglycemic crisis demands . prompt initiation of treatment . to reduce . mortality.” In adult patients, the mortality of comatose patients with DKA is between 100% and 0% (5,6). This extreme difference is explained in the paper of Nyenwe et al.; the immediate cause of coma is very low blood pH (i.e., high concentration of hydrogen ions H+) (7). The glycolytic enzyme phosphofructokinase is pH-dependent, as its activity is decreasing with decreasing pH, and, thus, glucose utilization in brain cells is impaired. The increase of the low blood pH with infusions of sodium bicarbonate (6) makes possible recovery of comatose patients to full alertness (6). Where are published papers with criticism

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of the paper of Nyenwe et al. (7), saying that the results are not correct. Viktor Rosival, PHD SYNLAB Department of Laboratory Medicine De´rer’s Hospital, Limbova´ 5, SK-833 05 Bratislava Slovakia, Europe http://dx.doi.org/10.1016/j.jemermed.2014.07.051

REFERENCES 1. Van Ness-Otunnu R, Hack JR. Hyperglycemic crisis. J Emerg Med 2013;45:797–805. 2. Schade DS, Eaton RP, Alberti KGMM, et al. Diabetic coma: ketoacidotic and hyperosmolar. Albuquerque, NM: University of New Mexico Press; 1981. 3. Vinik A, Seftel LT, Joffe BT. Metabolic findings in hyperosmolar nonketotic diabetic stupor. Lancet 1970;2:797–9. 4. Matsuyama T, Hoffman MH, Dunbar JC, et al. Glucose, insulin, pancreatic glucagon and glucagon-like immunoreactive materials in the plasma of normal and diabetic children. Hormone Metab Res 1975;7:452–6. 5. Basu A, Close CF, Jenkins D, et al. Persisting mortality in diabetic ketoacidosis. Diabet Med 1993;10:282–4. 6. Umpierrez GE, Kelly JP, Navarrete JE, et al. Hyperglycemic crises in urban blacks. Arch Intern Med 1997;157:669–75. 7. Nyenwe EA, Khan AE, Razavi LN, et al. Acidosis: the prime determinant of depressed sensorium in diabetic ketoacidosis. Diabetes Care 2010;33:1837–9.