Evaluation of Serum Electrolytes in Traumatic Brain Injury Patients: Prospective Randomized Observational Study

Traumatic brain injuries (TBIs) is a leading cause of morbidity, mortality, disability and socio economic losses in India and in other developing countries .In India, over 100,000 people die due to road traffic accidents each year [1] and nearly 50-60% of them are hospitalized for brain injury [2]. Electrolyte derangements are common sequel of traumatic brain injury. Dyselectrolytemia is very common in head injuries patients and it is likely due to abnormality in serum sodium, potassium, calcium, phosphate. It may be due to use of intravenous fluids, diuretics, syndrome of inappropriate ADH secretion and cerebral salt washing. Serum Sodium is the most common and important electrolyte abnormality responsible among these electrolytes. Both hyponatremia and hypernatremia can result. More so changes in potassium chiefly Hypokalemia [3] and fluid content [4] are also encountered in clinical practice [5]. There are some different causes and among them most common being syndrome of inappropriate antidiuretic hormone secretion (SIADH) [6], Cerebral salt wasting (CSW) [5] use of diuretics like Furosemide and Mannitol [4]. Age is another important factor that also greatly affects morbidity and mortality. Advancing age has poor outcome [8] appropriate fluid management of patients with traumatic brain injury (TBI) presents a challenge in most part of the world [9] isotonic fluid can be given without significant fluid disturbances in body [10]. However patients may deteriorate after initial improvement even after a week due to electrolyte disturbances chiefly sodium [11]. So proper management of dyselectrolytemia in such patient following a head injury is most important [9]. Apart from Sodium and Potassium, Serum calcium is also is important electrolyte abnormality associated with a variety of clinical manifestations in patients with traumatic brain injury [12]. Initially from the development of tetany [13] to seizures all can happen following derangement in serum calcium. Abnormal responses of neurons to stimulation secondary to accumulation of intracellular calcium in traumatic brain injury are responsible for these features [14]. Both serum hypocalcaemia and hypercalcaemia can occur [12]. Abnormality in serum phosphate following a traumatic brain injury is also been observed. So in our study we also observed the phosphorus level and as we know serum phosphate (Po42) Volume 5 Issue 3 2016