Traumatic brain injury (TBI) is on the rise, especially in today’s fast-paced world. TBI requires not only neurosurgical expertise but also neurointensivist involvement for a better outcome. Disturbances of sodium balance are common in patients with brain injury, as the central nervous system plays a major role in sodium regulation. Hyponatraemia, defined as serum sodium <135 meq/L is commonly seen and is especially deleterious as it can contribute to cerebral oedema in these patients. Syndrome of inappropriate antidiuretic hormone secretion (SIADH), is the most well-known cause of hyponatraemia in this subset of patients. Cerebral Salt Wasting Syndrome (CSWS), leading to renal sodium loss is an important cause of hyponatraemia in patients with TBI. Although incompletely studied, decreased renal sympathetic responses and cerebral natriuretic factors play a role in the pathogenesis of CSWS. Maintaining a positive sodium balance and adequate hydration can help in the treatment. It is important to differentiate between SIADH and CSWS when trying to ascertain a case for patients with acute brain injury, as the treatment of the two are diametrically opposite.
in approximately 50%, decreases brain blood flow by directly acting on post-synaptic α 2 receptors, decreases CSF pressure without ischemic suffering and effectively decreases brain metabolism and intracranial pressure and also able to decrease injury caused by focal ischemia. Materials and Methods: A prospective randomized study was done on 50 patients (ASA grade 1, 2) scheduled for intracranial tumor surgeries were divided into study or control group (25 each). Both group received Midazolam (0.02 mg/kg) iv, Glycopyrrolate (0.005 mg/kg) iv, Inj Fentanyl (2 μg/kg) iv and group D received dexmedetomidine 0.8 μg/kg iv in 20 ml saline over 10 mins and group C received 20 ml Normal saline iv for same time period without dexmedetomidine in Premedication. Patients were induced with inj. Propofol (iv) after giving test drug and dose was calculated by BIS values between 40-60, followed by inj. Vecuronium 0.1 mg/kg after recording hemodynamic measurements. Patients were ventilated with 100% oxygen for 180 seconds. Hemodynamic measurements were recorded two minutes before test drug and placebo, two minutes before and one minutes after induction and just after and one minutes, two minutes, five minutes and 10 minutes of intubation. Change in intraocular pressure with the help of schiotz tonometer is also noted during this period. The groups were compared with heart rate, systolic blood pressure, and diastolic blood pressure and mean arterial pressure, IOP and IV dose of Propofol requirement for induction. Results: Groups were well matched for their demographic data (P > 0.05) and preoperative vitals. Heart rate and mean arterial blood pressure decreased significantly in patients of group D (Dexmedetomidine group) compared to group C (placebo group) (P < 0.05), and patients were more hemodynamicaly stable before induction, and at T-1, T-2, T-5, T-10 minutes after induction in group D (P value < 0.05). The total propofol requirements for induction is more in patients of group C than in patients of group D (128.6± 15.5 mg vs. 91.8± 20.41 mg, P < 0.05). The intraocular pressure in right eye and left eye decreases significantly from pre-induction value of 21.97 ± 4.75 mm Hg and 22.08 ± 4.94 mm Hg to 18.02 ± 4.30 mm Hg at intubation and 17.78 ± 4.15 mm Hg one minutes after intubation in both the eyes in group D after the test drug. In Group C IOP at pre-induction, intubation and one minute after intubation are 20.96 ± 3.80 mm Hg, 26.55 ± 4.08 mm Hg and 25.99 ± 3.78 mm Hg in right eye and 21.05 ± 3.72 mm Hg, 26.38 ± 4.14 and 25.90 ± 3.75 mm Hg in left eye respectively and the difference is statistically significant between the groups. Bradycardia and hypotension incidences were higher in group D. Conclusion: Dexmedetomidine is an excellent drug when used as an adjunct to general anesthesia for attenuation of pressor response. It not only decreased the magnitude of stress response to intubation but also decreased the intraocular pressure and induction dose requirement of propofol.Background: This randomized, double-blind placebo c...
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