Indian Journal of Critical Care Medicine March 2015 Vol 19 Issue 3 5. 6. 7. 8. 9. 10.
11. 12. 13. 14. 15.
Casey CM. The study of activity in older ICU patients: An integrative review. J Gerontol Nurs 2013;39:12‑25. Vollman KM. Understanding critically ill patients hemodynamic response to mobilization: Using the evidence to make it safe and feasible. Crit Care Nurs Q 2013;36:17‑27. Kalisch BJ, Dabney BW, Lee S. Safety of mobilizing hospitalized adults: Review of the literature. J Nurs Care Qual 2013;28:162‑8. Dong ZH, Yu BX, Sun YB, Fang W, Li L. Effects of early rehabilitation therapy on patients with mechanical ventilation. World J Emerg Med 2014;5:48‑52. Abrams D, Javidfar J, Farrand E, Mongero LB, Agerstrand CL, Ryan P, et al. Early mobilization of patients receiving extracorporeal membrane oxygenation: A retrospective cohort study. Crit Care 2014;18:R38. Sricharoenchai T, Parker AM, Zanni JM, Nelliot A, Dinglas VD, Needham DM. Safety of physical therapy interventions in critically ill patients: A single‑center prospective evaluation of 1110 intensive care unit admissions. J Crit Care 2014;29:395‑400. Nydahl P, Ruhl AP, Bartoszek G, Dubb R, Filipovic S, Flohr HJ, et al. Early mobilization of mechanically ventilated patients: A 1‑day point‑prevalence study in Germany. Crit Care Med 2014;42:1178‑86. Kumar SP, Jim A. Physical therapy in palliative care: From symptom control to quality of life: A critical review. Indian J Palliat Care 2010;16:138‑46. Kumar J, Maiya A, Periera D. Role of Physiotherapists in intensive care units of India – A Multicenter survey. Indian J Crit Care Med 2008;11:198‑203. O’Connor ED, Walsham J. Should we mobilise critically ill patients? A review. Crit Care Resusc 2009;11:290‑300. Pattanshetty RB, Gaude GS. Critical illness myopathy and polyneuropathy – A challenge for physiotherapists in the intensive care units. Indian J Crit Care Med 2011;15:78‑81. Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.152782
Hyponatremia management in critically ill: Food (protein) for thought Sir, Hyponatremia is the most common disorder of body fluid and electrolyte balance encountered in clinical critically ill patients and associated with increased morbidity and mortality. A wide range of conditions can cause hyponatremia and, as a result, it is being managed by clinicians from a variety of backgrounds with a variety of approaches to its diagnosis and management. Adding to the complexity is the available treatment options, which
includes normal saline, hypertonic saline, fluid restriction, drugs (demeclocycline and vaptans) and increasing intake of solutes like urea/protein. Treatment decision is based on multiple factors like severity and symptoms of hyponatremia, onset of hyponatremia, underlying disease, and associated illness. Rate of correction and overcorrection are important factors to consider. The decision to administer normal saline or hypertonic saline to patient with hyponatremia is quite clear and easy to practice. Except the use of saline and vaptans, rest of the treatment options are infrequently practiced, sometimes difficult to apply in critically ill patients especially with regard to fluid restriction. Management of the hyponatremia should ensure patient management rather than simply looking at the sodium level. If hyponatremia is serious and symptomatic, it is life‑threatening. In this situation, the first line of treatment will be prompt intravenous infusion of hypertonic saline. For patients with reduced circulating volume, extracellular volume should be replaced with intravenous infusion of 0.9% saline. If the cause is apparent, reversing it may lead to correction as restricting water intake in psychogenic polydipsia, giving glucocorticoid/thyroid replacement in deficient, stopping hypotonic fluids or medications like selective serotonin reuptake inhibitors, nonsteroidal anti‑inflammatory drugs, thiazides or desmopressin and optimization of Congestive heart failure (CHF), hepatic or renal failure. For patients with the syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH), which constitutes about 40% of hyponatremia cases and with moderate or profound hyponatremia, first‑line treatment is fluid restriction. Equal second‑line treatments are increasing solute intake. For moderate or profound hyponatremia, there is no recommendation for the use of lithium, demeclocycline, and even vasopressin receptor antagonist. Overcorrection is major reasons against vaptans.[1] There are not good outcome data either, with vaptans in form of improved survival or improved quality of life.[2] The lack of outcome data also applies to other treatments of hyponatremia. There are a vast majority of hyponatremic patients in the Intensive Care Unit (ICU) who are neither volume deficient nor they have profound and symptomatic hyponatremia. There are also patients in critical care unit where it is difficult to implement fluid restriction. 189
Indian Journal of Critical Care Medicine March 2015 Vol 19 Issue 3
Many patients develop hyponatremia during the course of their ICU management. Such groups of patients can be easily managed by increasing their dietary protein intake. Because of fixed urinary osmolarity in SIADH, increasing the dietary osmoles by increasing their dietary protein intake will lead to increase in urinary output and improvement in hyponatremia.[3] Moreover, increasing protein intake in critically ill will leads to better patient outcome. Studies have suggested that the use of higher protein concentration in nutritional therapy for critically ill patients may help to reduce mortality.[4,5]
Sunil Kumar Garg
Department of Medicine and Critical Care, Sarvodaya Hospital, Sector‑8, Faridabad, Haryana, India
Correspondence: Dr. Sunil Kumar Garg, 219, Pocket‑D, Mayur Vihar, Phase 2, New Delhi ‑ 110091, India. E‑mail: [email protected]
References 1.
2. 3. 4.
5.
Malhotra I, Gopinath S, Janga KC, Greenberg S, Sharma SK, Tarkovsky R. Unpredictable nature of tolvaptan in treatment of hypervolemic hyponatremia: Case review on role of vaptans. Case Rep Endocrinol 2014;2014:807054. Dahl E, Gluud LL, Kimer N, Krag A. Meta‑analysis: The safety and efficacy of vaptans (tolvaptan, satavaptan and lixivaptan) in cirrhosis with ascites or hyponatraemia. Aliment Pharmacol Ther 2012;36:619‑26. Berl T. Impact of solute intake on urine flow and water excretion. J Am Soc Nephrol 2008;19:1076‑8. Alberda C, Gramlich L, Jones N, Jeejeebhoy K, Day AG, Dhaliwal R, et al. The relationship between nutritional intake and clinical outcomes in critically ill patients: Results of an international multicenter observational study. Intensive Care Med 2009;35:1728‑37. Weijs PJ, Stapel SN, de Groot SD, Driessen RH, de Jong E, Girbes AR, et al. Optimal protein and energy nutrition decreases mortality in mechanically ventilated, critically ill patients: A prospective observational cohort study. JPEN J Parenter Enteral Nutr 2012;36:60‑8. Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.152784
Rhabdomyolysis in lumbar spinal surgery: Early detection is crucial Sir, Rhabdomyolysis (RM) after neurosurgical procedure is a rare event. We report a case of RM following 190
lumbar surgery and discuss the importance of early recognition. A 22‑year‑old male underwent resection of L3 giant cell tumor in right lateral position. The patient weighed 96 kg with a body mass index (BMI) of 35.6 kg/m2 with no comorbidities. General anesthesia was administered with oxygen, nitrous oxide, isoflurane, propofol, and morphine. Surgery lasted for 9 h. On 1st postoperative day, he developed severe pain with a progressive increase in girth of the right thigh. Doppler study ruled out deep venous thrombosis. Next day, he developed tachycardia, tachypnea, and icterus. Concurrently, he had oliguria. Investigations showed a high serum creatinine (1.63 mg/dl), creatine phosphokinase (CPK) (29,100 U/L) and deranged liver function (total bilirubin 1.5 mg%, direct 0.5 mg%, aspartate aminotransferase 209 U/L, alanine aminotransferase 185 U/L, alkaline phosphate 372 U/L). A diagnosis of RM was made, and the patient was treated with liberal hydration to maintain urine output of at least 100 ml/h along with alkalinization of urine. Clinically and serologically, he started to improve and was ambulated and discharged in a week. There are only a few reported cases of RM after neurosurgical procedures, with several risk factors being proposed. Lateral positioning in posterior fossa tumor resection and minimally invasive spinal surgeries have been reported as probable cause in 9 patients.[1] Van Gompel et al. reviewed 10 cases of RM after neurosurgery in supine or prone positions for cranial and spinal pathologies, and found obesity and prolonged surgery as common risk factors.[2] Woernle et al. studied 150 patients with routine CPK analysis before and after surgery to determine the effect of position. They correlated raised CPK not only with lateral position, but also with the use of intraoperative monitoring, and hypothesized it to be due to the absence of pharmacological relaxation during monitoring.[3] In our case, several of these factors contributed to the development of RM. The patient was obese (BMI of 35.8 kg/m2), had a long surgery (9 h) in right lateral position. Use of isoflurane is thought to stress an unstable sarcolemmal membrane causing increased permeability resulting in an influx of calcium and leak of intracellular potassium and creatinine kinase from myocytes.[4] Acute renal failure (ARF) is the most dangerous complication of RM, with prompt recognition and early therapy determining the outcome. Adequate rehydration to maintain hourly urine output of 100–300 ml is the main component of
Copyright of Indian Journal of Critical Care Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
11. 12. 13. 14. 15.
Casey CM. The study of activity in older ICU patients: An integrative review. J Gerontol Nurs 2013;39:12‑25. Vollman KM. Understanding critically ill patients hemodynamic response to mobilization: Using the evidence to make it safe and feasible. Crit Care Nurs Q 2013;36:17‑27. Kalisch BJ, Dabney BW, Lee S. Safety of mobilizing hospitalized adults: Review of the literature. J Nurs Care Qual 2013;28:162‑8. Dong ZH, Yu BX, Sun YB, Fang W, Li L. Effects of early rehabilitation therapy on patients with mechanical ventilation. World J Emerg Med 2014;5:48‑52. Abrams D, Javidfar J, Farrand E, Mongero LB, Agerstrand CL, Ryan P, et al. Early mobilization of patients receiving extracorporeal membrane oxygenation: A retrospective cohort study. Crit Care 2014;18:R38. Sricharoenchai T, Parker AM, Zanni JM, Nelliot A, Dinglas VD, Needham DM. Safety of physical therapy interventions in critically ill patients: A single‑center prospective evaluation of 1110 intensive care unit admissions. J Crit Care 2014;29:395‑400. Nydahl P, Ruhl AP, Bartoszek G, Dubb R, Filipovic S, Flohr HJ, et al. Early mobilization of mechanically ventilated patients: A 1‑day point‑prevalence study in Germany. Crit Care Med 2014;42:1178‑86. Kumar SP, Jim A. Physical therapy in palliative care: From symptom control to quality of life: A critical review. Indian J Palliat Care 2010;16:138‑46. Kumar J, Maiya A, Periera D. Role of Physiotherapists in intensive care units of India – A Multicenter survey. Indian J Crit Care Med 2008;11:198‑203. O’Connor ED, Walsham J. Should we mobilise critically ill patients? A review. Crit Care Resusc 2009;11:290‑300. Pattanshetty RB, Gaude GS. Critical illness myopathy and polyneuropathy – A challenge for physiotherapists in the intensive care units. Indian J Crit Care Med 2011;15:78‑81. Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.152782
Hyponatremia management in critically ill: Food (protein) for thought Sir, Hyponatremia is the most common disorder of body fluid and electrolyte balance encountered in clinical critically ill patients and associated with increased morbidity and mortality. A wide range of conditions can cause hyponatremia and, as a result, it is being managed by clinicians from a variety of backgrounds with a variety of approaches to its diagnosis and management. Adding to the complexity is the available treatment options, which
includes normal saline, hypertonic saline, fluid restriction, drugs (demeclocycline and vaptans) and increasing intake of solutes like urea/protein. Treatment decision is based on multiple factors like severity and symptoms of hyponatremia, onset of hyponatremia, underlying disease, and associated illness. Rate of correction and overcorrection are important factors to consider. The decision to administer normal saline or hypertonic saline to patient with hyponatremia is quite clear and easy to practice. Except the use of saline and vaptans, rest of the treatment options are infrequently practiced, sometimes difficult to apply in critically ill patients especially with regard to fluid restriction. Management of the hyponatremia should ensure patient management rather than simply looking at the sodium level. If hyponatremia is serious and symptomatic, it is life‑threatening. In this situation, the first line of treatment will be prompt intravenous infusion of hypertonic saline. For patients with reduced circulating volume, extracellular volume should be replaced with intravenous infusion of 0.9% saline. If the cause is apparent, reversing it may lead to correction as restricting water intake in psychogenic polydipsia, giving glucocorticoid/thyroid replacement in deficient, stopping hypotonic fluids or medications like selective serotonin reuptake inhibitors, nonsteroidal anti‑inflammatory drugs, thiazides or desmopressin and optimization of Congestive heart failure (CHF), hepatic or renal failure. For patients with the syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH), which constitutes about 40% of hyponatremia cases and with moderate or profound hyponatremia, first‑line treatment is fluid restriction. Equal second‑line treatments are increasing solute intake. For moderate or profound hyponatremia, there is no recommendation for the use of lithium, demeclocycline, and even vasopressin receptor antagonist. Overcorrection is major reasons against vaptans.[1] There are not good outcome data either, with vaptans in form of improved survival or improved quality of life.[2] The lack of outcome data also applies to other treatments of hyponatremia. There are a vast majority of hyponatremic patients in the Intensive Care Unit (ICU) who are neither volume deficient nor they have profound and symptomatic hyponatremia. There are also patients in critical care unit where it is difficult to implement fluid restriction. 189
Indian Journal of Critical Care Medicine March 2015 Vol 19 Issue 3
Many patients develop hyponatremia during the course of their ICU management. Such groups of patients can be easily managed by increasing their dietary protein intake. Because of fixed urinary osmolarity in SIADH, increasing the dietary osmoles by increasing their dietary protein intake will lead to increase in urinary output and improvement in hyponatremia.[3] Moreover, increasing protein intake in critically ill will leads to better patient outcome. Studies have suggested that the use of higher protein concentration in nutritional therapy for critically ill patients may help to reduce mortality.[4,5]
Sunil Kumar Garg
Department of Medicine and Critical Care, Sarvodaya Hospital, Sector‑8, Faridabad, Haryana, India
Correspondence: Dr. Sunil Kumar Garg, 219, Pocket‑D, Mayur Vihar, Phase 2, New Delhi ‑ 110091, India. E‑mail: [email protected]
References 1.
2. 3. 4.
5.
Malhotra I, Gopinath S, Janga KC, Greenberg S, Sharma SK, Tarkovsky R. Unpredictable nature of tolvaptan in treatment of hypervolemic hyponatremia: Case review on role of vaptans. Case Rep Endocrinol 2014;2014:807054. Dahl E, Gluud LL, Kimer N, Krag A. Meta‑analysis: The safety and efficacy of vaptans (tolvaptan, satavaptan and lixivaptan) in cirrhosis with ascites or hyponatraemia. Aliment Pharmacol Ther 2012;36:619‑26. Berl T. Impact of solute intake on urine flow and water excretion. J Am Soc Nephrol 2008;19:1076‑8. Alberda C, Gramlich L, Jones N, Jeejeebhoy K, Day AG, Dhaliwal R, et al. The relationship between nutritional intake and clinical outcomes in critically ill patients: Results of an international multicenter observational study. Intensive Care Med 2009;35:1728‑37. Weijs PJ, Stapel SN, de Groot SD, Driessen RH, de Jong E, Girbes AR, et al. Optimal protein and energy nutrition decreases mortality in mechanically ventilated, critically ill patients: A prospective observational cohort study. JPEN J Parenter Enteral Nutr 2012;36:60‑8. Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.152784
Rhabdomyolysis in lumbar spinal surgery: Early detection is crucial Sir, Rhabdomyolysis (RM) after neurosurgical procedure is a rare event. We report a case of RM following 190
lumbar surgery and discuss the importance of early recognition. A 22‑year‑old male underwent resection of L3 giant cell tumor in right lateral position. The patient weighed 96 kg with a body mass index (BMI) of 35.6 kg/m2 with no comorbidities. General anesthesia was administered with oxygen, nitrous oxide, isoflurane, propofol, and morphine. Surgery lasted for 9 h. On 1st postoperative day, he developed severe pain with a progressive increase in girth of the right thigh. Doppler study ruled out deep venous thrombosis. Next day, he developed tachycardia, tachypnea, and icterus. Concurrently, he had oliguria. Investigations showed a high serum creatinine (1.63 mg/dl), creatine phosphokinase (CPK) (29,100 U/L) and deranged liver function (total bilirubin 1.5 mg%, direct 0.5 mg%, aspartate aminotransferase 209 U/L, alanine aminotransferase 185 U/L, alkaline phosphate 372 U/L). A diagnosis of RM was made, and the patient was treated with liberal hydration to maintain urine output of at least 100 ml/h along with alkalinization of urine. Clinically and serologically, he started to improve and was ambulated and discharged in a week. There are only a few reported cases of RM after neurosurgical procedures, with several risk factors being proposed. Lateral positioning in posterior fossa tumor resection and minimally invasive spinal surgeries have been reported as probable cause in 9 patients.[1] Van Gompel et al. reviewed 10 cases of RM after neurosurgery in supine or prone positions for cranial and spinal pathologies, and found obesity and prolonged surgery as common risk factors.[2] Woernle et al. studied 150 patients with routine CPK analysis before and after surgery to determine the effect of position. They correlated raised CPK not only with lateral position, but also with the use of intraoperative monitoring, and hypothesized it to be due to the absence of pharmacological relaxation during monitoring.[3] In our case, several of these factors contributed to the development of RM. The patient was obese (BMI of 35.8 kg/m2), had a long surgery (9 h) in right lateral position. Use of isoflurane is thought to stress an unstable sarcolemmal membrane causing increased permeability resulting in an influx of calcium and leak of intracellular potassium and creatinine kinase from myocytes.[4] Acute renal failure (ARF) is the most dangerous complication of RM, with prompt recognition and early therapy determining the outcome. Adequate rehydration to maintain hourly urine output of 100–300 ml is the main component of
Copyright of Indian Journal of Critical Care Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
