Case Study: Management of Antidiuretic Hormone Abnormalities in Traumatic Brain Injury
Patient Information: The patient, a 45-year-old male, was admitted to the emergency department following a motor vehicle accident resulting in severe traumatic brain injury (TBI). Initial assessment revealed Glasgow Coma Scale (GCS) score of 6, bilateral pupil dilation, and evidence of diffuse axonal injury on computed tomography (CT) scan. In addition to neurological injuries, the patient presented with altered fluid balance, prompting further investigation into antidiuretic hormone (ADH) abnormalities.
Clinical Presentation: Upon admission, the patient exhibited signs of fluid imbalance, with hyponatremia (serum sodium level of 129 mEq/L) and decreased urine output. Given the severity of the TBI and the potential impact of ADH dysregulation on neurological outcomes, prompt assessment and management of ADH abnormalities were prioritized.
Diagnostic Workup: Laboratory evaluation revealed low serum osmolality and high urine osmolality, suggestive of syndrome of inappropriate antidiuretic hormone secretion (SIADH). Further investigations, including brain imaging and neurological assessments, confirmed the presence of TBI with associated cerebral edema and elevated intracranial pressure (ICP). These findings supported the diagnosis of SIADH secondary to TBI.
Management Strategy: The patient was initially managed with fluid restriction (1,000 mL/day) and close monitoring of serum sodium levels to prevent further hyponatremia and cerebral edema. Hypertonic saline was administered cautiously to correct hyponatremia and stabilize serum sodium levels while minimizing the risk of osmotic demyelination syndrome. Additionally, pharmacological interventions, including demeclocycline and tolvaptan, were considered to further mitigate ADH-mediated water retention.
Outcome: Over the course of hospitalization, the patient’s fluid balance and serum sodium levels were closely monitored, with adjustments made to fluid management strategies based on ongoing assessments of neurological status and laboratory parameters. Despite initial challenges in achieving optimal fluid balance, the patient’s serum sodium levels gradually normalized, and signs of cerebral edema improved. Repeat imaging studies demonstrated resolution of cerebral edema, with stabilization of ICP within acceptable limits.
Long-Term Follow-Up: Following discharge from the hospital, the patient underwent intensive rehabilitation to address residual neurological deficits and optimize functional outcomes. Long-term follow-up assessments revealed gradual improvement in cognitive function and motor abilities, with no evidence of persistent ADH abnormalities or recurrent fluid imbalance.
Conclusion: This case highlights the importance of recognizing and managing ADH abnormalities in traumatic brain injury to optimize patient outcomes. Through a multidisciplinary approach incorporating neurocritical care, endocrinology, and fluid management expertise, effective strategies can be implemented to restore fluid balance, minimize neurological complications, and facilitate recovery. Ongoing research is needed to further refine management protocols and improve outcomes in this complex patient population.
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