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Evaluation of development of diabetes insipidus in the early phase following traumatic brain injury in critically ill patients
© BioMed Central Ltd 2008
- Published: 13 March 2008
- Traumatic Brain Injury
- Injury Severity Score
- Brain Death
- Diabetes Insipidus
- Plasma Sodium
The purpose of this study was to define the prevalence and outcome of diabetes insipidus (DI) in the early post-traumatic brain injury (TBI) period in ICU patients. Inadequate antidiuretic hormone secretion, which results in DI, is a well recognized complication of TBI, owing to post-traumatic posterior pituitary dysfunction.
This prospective study was performed in 73 ICU-TBI patients (with or without multisystem trauma) admitted to a general ICU at a tertiary center between December 2005 and November 2007. Patients had suffered severe TBI, according to the initial GCS score (≤ 8). DI was diagnosed if plasma sodium exceeded 145 mmol/l in the presence of inappropriate dilute urine with 24-hour urine volume >30 ml/kg body weight, urine specific gravity <1,005 or urine osmolality <300 mOsm/kg with a simultaneous plasma osmolality ≥ 300 mOsm/kg. The age, gender, GCS, Injury Severity Score (ISS), onset of DI, peak recorded plasma sodium and outcome were noted. Statistical analysis was computed by t test and Fischer exact test. P < 0.05 was considered statistically significant.
Twenty-one ICU-TBI patients (28.7%) developed acute DI. Comparison was made between two groups of these patients: Group A, nine survivors and Group B, 12 nonsurvivors of TBI. There was no statistical significance between them with respect to age, gender (P > 0.05). Group B had a lower GCS (4.5 ± 1.5) as compared with Group A (7.8 ± 3, P = 0.003). The ISS was significant greater in Group B: 38 ± 8 versus 17 ± 7 in Group A, P < 0.001. Peak plasma sodium was significantly greater in Group B: 167 ± 4 mmol/l versus 156 ± 3 mmol/l in Group A, P < 0.05. The mean onset time of DI in Group B (1.7 ± 0.9 days) was shorter than in Group A (7.4 ± 3.3 days), P = 0.004. Overall mortality was 57.1%. The mortality rate for the development of DI within the first 3 days after TBI was 90% versus 27.2% if DI occurred later. Nonsurvivors died from brain death and not as a result of their associated injuries.
Our results demonstrate that DI is common, following severe TBI. ICU-TBI patients presenting with features of DI have an overall high mortality. This study shows that the development of DI within the first 3 days of TBI is associated with high mortality rate and impending brain death. On the contrary, ICU-TBI patients who develop DI later have a better prognosis.
This article is published under license to BioMed Central Ltd.