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References 1. 2. 3. 4. 5. 6.
Figure 1: Transesophageal echocardiography (TEE) image (midesophageal bicaval view), demonstrating a thrombus adherent to the superior vena cava and entering the right atrium. SG = Swan–Ganz catheter, C = clot, RA = right atrium, SVC = superior vena cava
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point, the TEE probe was removed, and the patient’s trachea was extubated 2 days later, with intact mental status and improving organ parameters. Based on laboratory testing for antiphospholipid antibodies during admission, her case was likely due to catastrophic antiphospholipid antibody syndrome and complicated by congestive hepatopathy; she was subsequently placed on lifelong anticoagulation.
Guarracino F, Baldassarri R. Transesophageal echocardiography in the OR and ICU. Minerva Anestesiol 2009;75:518-29. Huttemann E, Schelenz C, Kara F, Chatzinikolaou K, Reinhart K. The use and safety of transoesophageal echocardiography in the general ICU: A minireview. Acta Anaesthesiol Scand 2004;48:827-36. Wagner C, Fredi J, Bick J, McPherson J. Monitoring myocardial recovery during induced hypothermia with a disposable monoplane TEE probe. Resuscitation 2011;82:355-7. Kallmeyer IJ, Collard CD, Fox JA, Body SC, Shernan SK. The safety of intraoperative transesophageal echocardiography: A case series of 7200 cardiac surgical patients. Anesth Analg 2001;92:1126-30. Hwang JJ, Shyu KG, Chen JJ, Tseng YZ, Kuan P, Lien WP. Usefulness of transesophageal echocardiography in the treatment of critically ill patients. Chest 1993;104:861-6. Poelaert JI, Trouerbach J, De Buyzere M, Everaert J, Colardyn FA. Evaluation of transesophageal echocardiography as a diagnostic and therapeutic aid in a critical care setting. Chest 1995;107:774-9. Slama MA, Novara A, Van de Putte P, Diebold B, Safavian A, Safar M, et al. Diagnostic and therapeutic implications of transesophageal echocardiography in medical ICU patients with unexplained shock, hypoxemia, or suspected endocarditis. Intensive Care Med 1996;22:916-22. Access this article online Quick Response Code: Website: www.ijccm.org
Our case represents only one of the variety of possible clinical situations where TEE in the ICU may be of benefit. With the advent of smaller, and sometimes disposable, TEE probes, the use of continuous TEE monitoring may increase in the ICU.[3] While the safety of TEE monitoring has been established, demonstrating minimal complications in a large case series,[4] the effectiveness of TEE is also being demonstrated, emphasizing superior diagnostic capability, and improved management of hemodynamics.[3,5] Thus, TEE has emerged as both a diagnostic and therapeutic aid in the ICU.[6,7]
DOI: 10.4103/0972-5229.136086
Methylene blue unresponsive methemoglobinemia
While improved diagnostic capability and altered therapeutic management have been established, improved patient outcomes with a TEE-guided approach have not been studied. Further research at this point should shift away from assessing surrogate outcomes (i.e., change in therapeutic management) to assessing true patient outcomes (i.e., mortality). The time is now to perform high-quality clinical trials of TEE monitoring to assess the next important step: improvement in patient outcomes on a large scale.
Vijay Krishnamoorthy
Sir, I read with great interest the article by Patnaik et al. published recently in your Journal. [1] The authors defined an 18-month-old boy who was presented with central nervous system manifestations (irritability and seizure), cyanosis, metabolic acidosis, and confirmed methemoglobinemia. The major points in this case were: (1) Unknown toxicologic origin despite thorough history taking and (2) the methemoglobinemia unresponsive to methylene blue and vitamin C that then was treated successfully by blood transfusion. I would like to address some missed points in this report.
Correspondence: Vijay Krishnamoorthy, Acting Assistant Professor, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington, USA. E-mail:
[email protected]
The authors stated that they were not able to establish the exact etiology, but according to the situation of patient’s home and history of relatives it was likely that the child was intoxicated with a chemical. If this
Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, Washington, USA
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is true, it is not clear how the child was resuscitated at the presentation with a likely intoxication. Were gastric washing and gavage of an absorbent agent implemented? Was a toxicologist consultation requested for the patient despite the fact methemoglobinemia was not responded to intravenous methylene blue and presence of likely occurrence of a chemical exposure? By the way, how the authors have ruled out one the most important etiologies of methemoglobinemia in toxicologic settings, namely aluminum phosphide, that is the cause of great burden of morbidity and mortality in countries such as India.[2]
5. 6. 7. 8.
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Toxic-induced methemoglobinemia occurs in a diverse variety of drug and chemical exposures with oxidizing mechanisms.[3] Although in some reported cases, it has been shown that methemoglobinemia can develop in more rare situations such as acetaminophen overdose,[4,5] metoclopramide overdose,[6] and aluminum phosphide poisoning,[7] but the mechanism of action is more complex and less elaborated. Mostafazadeh et al. in a case series study showed that methemoglobinemia develops in aluminum phosphide poisoning in some degrees, but severe methemoglobinemia requiring therapeutic intervention is a rare finding.[8] Furthermore, Shadnia et al. have described that methemoglobinemia in aluminum phosphide poisoning is unresponsive to methylene blue administration.[7] This poisoning, in this case, could be ruled out by a bedside rapid spot test by silver nitrate impregnated paper.[9] Furthermore, anemia, in this case, has intensified the severity and lack of response to conventional treatment.
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DOI: 10.4103/0972-5229.136087
Role of acidic pH of intravenous fluids in subsequent development of metabolic acidosismay not be what it seems
As noted by authors, chemical exposure is one of the causes of inadequate response to methylene blue therapy in methemoglobinemia, and I think aluminum phosphide poisoning should be borne in mind in cases in which therapy seems to be resistant to methylene blue and ascorbic acid. Thank you for the interesting case discussion.
Sir, We extend our thanks to Singh et al. for drawing attention toward the controversies surrounding the use of acidic intravenous fluids (IVFs) infusion.[1] They have rightly mentioned the propensity of 5% dextrose (D5) and 0.9% saline (NS) to cause thrombophlebitis and other deleterious effects.[1] But unlike mentioned by the authors, current literature discusses the known and putative reasons for the pH of 5.5 of NS.[2] Dissolved CO2 from atmosphere, the ionic composition of the solution and inherent properties of the packaging material in which the solutions are supplied, are thought to determine it.[2] We believe that the same set of reasons may also explain the acidic pH (4.2) of D5.
Seyed Mostafa Mirakbari
Department of Forensic Medicine and Toxicology, Bu Ali Hospital, Qazvin University of Medical Sciences, Qazvin, Iran
Correspondence: Dr. Seyed Mostafa Mirakbari, Department of Forensic Medicine and Toxicology, Bu Ali Hospital, Qazvin University of Medical Sciences, Qazvin 34137-86165, Iran. E-mail:
[email protected]
References 1. 2. 3. 4.
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Pharmacol Ther 2009;32:585-95. Kanji HD, Mithani S, Boucher P, Dias VC, Yarema MC. Coma, metabolic acidosis, and methemoglobinemia in a patient with acetaminophen toxicity. J Popul Ther Clin Pharmacol 2013;20:e207-11. Kearns GL, Fiser DH. Metoclopramide-induced methemoglobinemia. Pediatrics 1988;82:364-6. Shadnia S, Soltaninejad K, Hassanian-Moghadam H, Sadeghi A, Rahimzadeh H, Zamani N, et al. Methemoglobinemia in aluminum phosphide poisoning. Hum Exp Toxicol 2011;30:250-3. Mostafazadeh B, Pajoumand A, Farzaneh E, Aghabiklooei A, Rasouli MR. Blood levels of methemoglobin in patients with aluminum phosphide poisoning and its correlation with patient’s outcome. J Med Toxicol 2011;7:40-3. Chugh SN, Ram S, Chugh K, Malhotra KC. Spot diagnosis of aluminium phosphide ingestion: An application of a simple test. J Assoc Physicians India 1989;37:219-20.
Patnaik S, Natarajan MM, James EJ, Ebenezer K. Methylene blue unresponsive methemoglobinemia. Indian J Crit Care Med 2014;18:253-5. Murali R, Bhalla A, Singh D, Singh S. Acute pesticide poisoning: 15 years experience of a large North-West Indian hospital. Clin Toxicol (Phila) 2009;47:35-8. Rehman HU. Methemoglobinemia. West J Med 2001;175:193-6. McConkey SE, Grant DM, Cribb AE. The role of para-aminophenol in acetaminophen-induced methemoglobinemia in dogs and cats. J Vet
Free acid activity is indicated by pH but the nondissociated acid molecules in a solution may not be characterized by the pH value.[2,3] Thus solutions with high titratable acid have 78
