Base deficit and serum lactate concentration in patients with post traumatic convulsion. Academic Article uri icon

Overview

abstract

  • INTRODUCTION: Traumatic brain injury is a major cause of morbidity and mortality worldwide, and has been reported to be one of the risk factors for epileptic seizures. Abnormal blood lactate (LAC) and base deficit (BD) reflects hypoperfusion and could be used as metabolic markers to predict the outcome. The aim of this study is to assess the prognostic value of BD and LAC levels for post traumatic convulsion (PTC) in head injury patients. MATERIALS AND METHODS: All head injury patients with PTC were studied for the demographics profile, mechanism of injury, initial vital signs, and injury severity score (ISS), respiratory rates, CT scan findings, and other laboratory investigations. The data were obtained from the trauma registry and medical records. Statistical analysis was done using SPSS software. RESULTS: Amongst 3082 trauma patients, 1584 were admitted to the hospital. Of them, 401 patients had head injury. PTC was observed in 5.4% (22/401) patients. Out of the 22 head injury patients, 10 were presented with the head injury alone, whereas 12 patients had other associated injuries. The average age of the patients was 25 years, comprising predominantly of male patients (77%). Neither glasgow coma scale nor ISS had correlation with BD or LAC in the study groups. The mean level of BD and LAC was not statistically different in PTC group compared to controls. However, BD was significantly higher in patients with associated injuries than the isolated head injury group. Furthermore, there was no significant correlation amongst the two groups as far as LAC levels are concerned. CONCLUSION: Base deficit but not lactic acid concentration was significantly higher in head injury patients with associated injuries. Early resuscitation by pre-hospital personnel and in the trauma room might have impact in minimizing the effect of post traumatic convulsion on BD and LAC.

publication date

  • January 1, 2016

Identity

PubMed Central ID

  • PMC4802936

Digital Object Identifier (DOI)

  • 10.4103/1793-5482.145117

PubMed ID

  • 27057221

Additional Document Info

volume

  • 11

issue

  • 2