SERUM ELECTROLYTE DERANGEMENTS IN PATIENTS WITH TRAUMATIC BRAIN INJURY
AbstractBackground: Electrolyte derangements are common sequel of traumatic brain injury. Use of intravenous fluids, diuretics, syndrome of inappropriate ADH secretion and cerebral salt washing are some of the factors responsible for this. Proper in time detection followed by appropriate treatment not only improves neurological status but also decrease morbidity and mortality. This study was conducted to know serum derangements of different electrolytes in patients with traumatic brain injury. Methodology: This cross-sectional study was conducted in Pakistan Institute of Medical Sciences, Islamabad, Pakistan from Feb 2009 to Feb 2010. All adult patients with traumatic brain injury who presented to Neurosurgical department with severe head injury (GCS <8) and who need monitoring in high dependency unit, were included in this study. Initially twice daily serum electrolyte monitoring for one week then once daily for remaining period of hospital stay was carried out. All samples were sent to Pathology department of Pakistan Institute of Medical Sciences, Islamabad. Patients who need corrective measures for imbalance had repetition of sampling after giving appropriate therapy. Statistical analysis was performed on SPSS-16. Results: Total 215 patients presented with severe head injury that were managed in high dependency unit. Out of which 127 (59.1%) were male and 88 (40.9%) were females. Most of them were adults between 21–40 years of age (21.4%; 24.7%). Sodium was the main electrolyte that underwent change & out of which hyper-natremia was major abnormality that occurred in 140 (65.1%) of patients. This is followed by hypo-kalemia that occurred in 79 (36.7%) of patients. Serum calcium & magnesium levels show little derangements. Conclusion: Electrolyte imbalance following traumatic head injury is an important cause to look for in patient monitoring. Sodium is the chief electrolytes of concern. Serum potassium and calcium levels also under goes notable changes.Keywords: Traumatic brain injury, serum electrolyte derangements
Childers MK, Rupright J, Jones PS, Merveille O. Assessment of neuroendocrine dysfunction following traumatic brain injury. Brain Inj 1998;12:517–23.
Guggiari M, Georgescu H. The injured brain. Basis for hydro electrolytic and hemodynamic resuscitation. Ann Fr Anesth Reanim 1994;13(1):98–104.
Unterberg AW, Stover J, Kress B, Kiening KL. Edema and brain trauma. Neuroscience 2004;129:1021–9.
Rhoney DH, Parker D Jr. Considerations in fluids and electrolytes after traumatic brain injury. Nutr Clin Pract 2006;21:462–78.
Pomeranz S, Constantini S, Rappaport ZH. Hypokalaemia in severe head trauma. Acta Neurochir (Wien) 1989;97(1–2):62–6.
Gaab M, Knoblich OE, Schupp J, Herrmann F, Fuhrmeister U, Pflughaupt KW. Effect of furosemide on acute severe experimental cerebral edema. J Neurol 1979;220(3):185–97.
Askar A, Tarif N. Cerebral salt wasting in a patient with head trauma: management with saline hydration and fludrocortisone. Saudi J Kidney Dis Transpl 2007;18:95–9.
Gribkov AV, Fraerman AP, Salalykin VI, Salmin AA, Sidorkin VG, Mikhaĭlova EM. Regulation of the water-electrolyte balance during neurosurgical operations with balanced anesthesia using sodium oxybutyrate. Anesteziol Reanimatol 1992;(1):28–31.
Unterberg A, Schneider GH, Gottschalk J, Lanksch WR. Development of traumatic brain edema in old versus young rats. Acta Neurochir Suppl (Wien) 1994;60:431–3.
Ishizaki T, Momota H, Kuwahara K, Tanooka A, Morimoto S. A case of symptomatic traumatic cerebral vasospasm associated with hyponatremia. No Shinkei Geka 1999;27:1031–6. [Article in Japanese]
James HE, Schneider S. Effects of acute isotonic saline administration on serum osmolality, serum electrolytes, brain water content and intracranial pressure. Acta Neurochir Suppl (Wien) 1993;57:89–93.
Unterberg A, Kiening K, Schmiedek P, Lanksch W. Long-term observations of intracranial pressure after severe head injury. The phenomenon of secondary rise of intracranial pressure. Neurosurgery 1993;32:17–23.
Novikov VE, Chemodurova LN. The effect of GABA-ergic agents on the blood electrolyte balance in acute craniocerebral trauma. Eksp Klin Farmakol 1992;55(3):70–2.
Berger S, Schürer L, Härtl R, Deisböck T, Dautermann C, Murr R, et al. 7.2% NaCl/10% dextran-60 versus 20% mannitol for treatment of intracranial hypertension. Acta Neurochir Suppl (Wien) 1994;60:494–8.
Nara I, Shiogai T, Hara M, Saito I. Comparative effects of hypothermia, barbiturate, and osmotherapy for cerebral oxygen metabolism, intracranial pressure, and cerebral perfusion pressure in patients with severe head injury. Acta Neurochir Suppl 1998;71:22–6.
Parkerson JB Jr, Taylor Z, Flynn JP. Brain injured patients: comorbidities and ancillary medical requirements. Md Med J 1990;39:259–62.
Cintra Ede A, Araújo S, Quagliato EM, Castro M, Falcão AL, Dragosavac D, et al. Vasopressin serum levels and disorders of sodium and water balance in patients with severe brain injury. Arq Neuropsiquiatr 2007;65(4B):1158–65.
Goh KP. Management of hyponatremia. Am Fam Physician 2004;69:2387–94.
Steinbok P, Thompson GB. Metabolic disturbances after head injury: abnormalities of sodium and water balance with special reference to the effects of alcohol intoxication. Neurosurgery 1978;3(1):9–15.
Myshkin Ki, ChuenkovVF. Changes in blood serum calcium levels in acute cranio-cerebral injury. Vopr Neirokhir 1963;27:26–8.
Kogan OG, Kaishibaev SK. A case of tetany developing after brain injury. Zdravookhranenie Kazakhstana 1961;21(10):68–70.
Gurkoff GG, Shahlaie K, Lyeth BG. In vitro mechanical strain trauma alters neuronal calcium responses: Implications for posttraumatic epilepsy. Epilepsia 2012;53(Suppl 1):53–60.
Plöchl E, Thalhammer O, Weissenbacher G. Brain damage of acute course in an infant with hyperphenylalaninemia and hypercalcemia. Helv Paediatr Acta 1968;23(3):292–304.
Journal of Ayub Medical College, Abbottabad is an OPEN ACCESS JOURNAL which means that all content is FREELY available without charge to all users whether registered with the journal or not. The work published by J Ayub Med Coll Abbottabad is licensed and distributed under the creative commons License CC BY ND Attribution-NoDerivs. Material printed in this journal is OPEN to access, and are FREE for use in academic and research work with proper citation. J Ayub Med Coll Abbottabad accepts only original material for publication with the understanding that except for abstracts, no part of the data has been published or will be submitted for publication elsewhere before appearing in J Ayub Med Coll Abbottabad. The Editorial Board of J Ayub Med Coll Abbottabad makes every effort to ensure the accuracy and authenticity of material printed in J Ayub Med Coll Abbottabad. However, conclusions and statements expressed are views of the authors and do not reflect the opinion/policy of J Ayub Med Coll Abbottabad or the Editorial Board.
USERS are allowed to read, download, copy, distribute, print, search, or link to the full texts of the articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author. This is in accordance with the BOAI definition of open access.
AUTHORS retain the rights of free downloading/unlimited e-print of full text and sharing/disseminating the article without any restriction, by any means including twitter, scholarly collaboration networks such as ResearchGate, Academia.eu, and social media sites such as Twitter, LinkedIn, Google Scholar and any other professional or academic networking site.