|
 
 |
| LETTER TO EDITOR |
|
| Year : 2019 | Volume
: 4
| Issue : 2 | Page : 110-111 |
|
Hyponatremia and traumatic brain injury: An overview
Jamir Pitton Rissardo, Ana Letícia Fornari Caprara
Department of Neurology; Department of Medicine, Federal University of Santa Maria, Santa Maria, Brazil
| Date of Submission | 15-Sep-2019 |
| Date of Acceptance | 17-Dec-2019 |
| Date of Web Publication | 09-Jan-2020 |
Correspondence Address:
Mr. Jamir Pitton Rissardo
Rua Roraima, Santa Maria, Rio Grande Do Sul
Brazil
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/bjhs.bjhs_49_19
How to cite this article:
Rissardo JP, Fornari Caprara AL. Hyponatremia and traumatic brain injury: An overview. BLDE Univ J Health Sci 2019;4:110-1 |
Dear Sir,
We read an article on “BLDE University Journal of Health Sciences” with great interest. Thavara and Veettil report a case of an adult male who presented with traumatic brain injury (TBI) causing a hematoma and hyponatremia observed after 1 week. Sodium reposition was started, and the patient developed extrapontine myelinolysis.[1]
Extrapontine and central pontine myelinolysis are considered osmotic demyelination syndromes. They commonly occur in cases of osmotic disturbances that need correction, and it is this correction that could lead to a myelin injury.
Herewith, we would like to discuss more the hyponatremia in individuals that suffered a TBI.
In the study of Moro et al., an assessment of the incidence, mechanism, and response to sodium supplementation or retention therapy in hyponatremic patients with a TBI was done. Their study found that almost 15% of the individuals presented hyponatremia during the time course. In addition, low sodium levels were related to longer hospital admission and the worst outcome with more complications. It is worthy of mentioning that among the patients with hyponatremia about 70% recovered from the hyponatremia with simple sodium supplementation. However, others required additional sodium retention therapy.[2]
Lohani and Devkota published in 2011 that the most common pathophysiologic mechanism in TBI is hyponatremia due to a syndrome of the inappropriate antidiuretic hormone than the cerebral salt wasting syndrome. However, the fractional excretion of uric acid measurements is probably not consistent enough to distinguish between these two mechanisms. Moreover, their study showed that computed tomography abnormalities scoring of severity is more predictive of low sodium levels than the initial Glasgow Coma Scale.[3]
A prospective study on hyponatremia in TBI revealed that low levels of sodium are a very common electrolyte imbalance occurring in more than 20% of the individuals with TBI. In this context, they proposed that a more aggressive sodium levels clinical monitoring may be required in parenchymal contusions and diffuse axonal injuries since these patients had an increased odds of developing hyponatremia during their hospitalization. Another interesting fact found is that maybe hyponatremia only influences the immediate outcome in TBI, while the long-term outcome is probably not affected.[4]
In a recent study from India, Rajagopal et al. proposed a practical protocol for the management of hyponatremia in TBI. They conclude that in all cases will be needed to added salt. However, in individuals with high urinary sodium and moderate or severe hyponatremia, fludrocortisone should be started. Furthermore, the early initiation of this drug in the setting of hyponatremia with natriuresis decreases the hospital stay, and this is probably even better in tropical countries where fluid restriction might be harmful.[5]
In sum, we agree with the statement of Thavara and Veettil that even though the pontine myelinolysis be a rare pathology, any case that the patient has severe hyponatremia should be managed with a high index of suspicion to avoid possible complications.[1]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Thavara BD, Veettil HP. Hyponatremia correction causing extrapontine myelinolysis. BLDE Univ J Health Sci 2019;4:34-8.  [Full text] |
| 2. | Moro N, Katayama Y, Igarashi T, Mori T, Kawamata T, Kojima J. Hyponatremia in patients with traumatic brain injury: Incidence, mechanism, and response to sodium supplementation or retention therapy with hydrocortisone. Surg Neurol 2007;68:387-93. |
| 3. | Lohani S, Devkota UP. Hyponatremia in patients with traumatic brain injury: Etiology, incidence, and severity correlation. World Neurosurg 2011;76:355-60. |
| 4. | Shanavas C, Basheer N, Alapatt JP, Kuruvilla R. A prospective study on hyponatremia in traumatic brain injury. Indian J Neurotrauma 2016;13:094-100. |
| 5. | Rajagopal R, Swaminathan G, Nair S, Joseph M. Hyponatremia in Traumatic Brain Injury: A Practical Management Protocol. World Neurosurg 2017;108:529-33. |
|
Search Pubmed for