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A complex case of hyponatremia after TBI forces clinicians to take a cautious approach to diagnosis and treatment.

Hyponatremia is a dangerous complication of major head trauma, and timely diagnosis and treatment can be fraught with “confounding factors” and complexity, say clinicians from the University of Newcastle and John Hunter Hospital in Australia. They reported a case of hyponatremia that required some clinical tightrope walking.

The patient, a 20-year-old university student, had fractured his skull in a skateboard fall while intoxicated. He was started on dexamethasone to reduce the risk of worsening cerebral edema. On day 3, he developed hypo-osmolar hyponatremia, which was worse on day 4, despite treatment, including IV fluid therapy, fluid restriction, and oral salt tablets. Although cognitively the patient was deteriorating, he seemed clinically euvolemic. However, the patient was in negative fluid balance, suggesting renal salt wasting (RSW). After a trial of isotonic normal saline, the patient’s serum sodium level fell further. The patient was then treated for suspected syndrome of inappropriate antidiuretic hormone (SIADH) with a hypertonic saline infusion. The rise in sodium was carefully controlled to avoid rapid overcorrection, which can lead to irreversible neurologic symptoms. Finally, the patient’s sodium level and neurologic status improved.

The clinicians say the case demonstrates the complexity of differentiating between the causes of hyponatremia after head injury. Volume status may be an indicator, they say, but current clinical and laboratory markers of volume status are often limited in accuracy. The hallmark of RSW is volume depletion, whereas diagnosis of SIADH depends on a coexisting euvolemic state (as with the patient).

As many as 10% of victims of traumatic brain injury develop hyponatremia, and it is associated with a worse prognosis, even in mild cases, the clinicians note. Making the right diagnosis is critical—the treatment chosen can easily compromise the outcome. Patients with neurosurgical conditions are often treated with considerable volumes of saline-containing fluid, with consequent dynamic changes in blood and extracellular volumes. Moreover, the patients have elevated levels of adrenergic hormones with their own confounding effects.

In the long term, the patient experienced significant neurologic sequelae, including prolonged posttraumatic amnesia. After extensive rehabilitation he was able to return to the university.

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A complex case of hyponatremia after TBI forces clinicians to take a cautious approach to diagnosis and treatment.
A complex case of hyponatremia after TBI forces clinicians to take a cautious approach to diagnosis and treatment.

Hyponatremia is a dangerous complication of major head trauma, and timely diagnosis and treatment can be fraught with “confounding factors” and complexity, say clinicians from the University of Newcastle and John Hunter Hospital in Australia. They reported a case of hyponatremia that required some clinical tightrope walking.

The patient, a 20-year-old university student, had fractured his skull in a skateboard fall while intoxicated. He was started on dexamethasone to reduce the risk of worsening cerebral edema. On day 3, he developed hypo-osmolar hyponatremia, which was worse on day 4, despite treatment, including IV fluid therapy, fluid restriction, and oral salt tablets. Although cognitively the patient was deteriorating, he seemed clinically euvolemic. However, the patient was in negative fluid balance, suggesting renal salt wasting (RSW). After a trial of isotonic normal saline, the patient’s serum sodium level fell further. The patient was then treated for suspected syndrome of inappropriate antidiuretic hormone (SIADH) with a hypertonic saline infusion. The rise in sodium was carefully controlled to avoid rapid overcorrection, which can lead to irreversible neurologic symptoms. Finally, the patient’s sodium level and neurologic status improved.

The clinicians say the case demonstrates the complexity of differentiating between the causes of hyponatremia after head injury. Volume status may be an indicator, they say, but current clinical and laboratory markers of volume status are often limited in accuracy. The hallmark of RSW is volume depletion, whereas diagnosis of SIADH depends on a coexisting euvolemic state (as with the patient).

As many as 10% of victims of traumatic brain injury develop hyponatremia, and it is associated with a worse prognosis, even in mild cases, the clinicians note. Making the right diagnosis is critical—the treatment chosen can easily compromise the outcome. Patients with neurosurgical conditions are often treated with considerable volumes of saline-containing fluid, with consequent dynamic changes in blood and extracellular volumes. Moreover, the patients have elevated levels of adrenergic hormones with their own confounding effects.

In the long term, the patient experienced significant neurologic sequelae, including prolonged posttraumatic amnesia. After extensive rehabilitation he was able to return to the university.

Hyponatremia is a dangerous complication of major head trauma, and timely diagnosis and treatment can be fraught with “confounding factors” and complexity, say clinicians from the University of Newcastle and John Hunter Hospital in Australia. They reported a case of hyponatremia that required some clinical tightrope walking.

The patient, a 20-year-old university student, had fractured his skull in a skateboard fall while intoxicated. He was started on dexamethasone to reduce the risk of worsening cerebral edema. On day 3, he developed hypo-osmolar hyponatremia, which was worse on day 4, despite treatment, including IV fluid therapy, fluid restriction, and oral salt tablets. Although cognitively the patient was deteriorating, he seemed clinically euvolemic. However, the patient was in negative fluid balance, suggesting renal salt wasting (RSW). After a trial of isotonic normal saline, the patient’s serum sodium level fell further. The patient was then treated for suspected syndrome of inappropriate antidiuretic hormone (SIADH) with a hypertonic saline infusion. The rise in sodium was carefully controlled to avoid rapid overcorrection, which can lead to irreversible neurologic symptoms. Finally, the patient’s sodium level and neurologic status improved.

The clinicians say the case demonstrates the complexity of differentiating between the causes of hyponatremia after head injury. Volume status may be an indicator, they say, but current clinical and laboratory markers of volume status are often limited in accuracy. The hallmark of RSW is volume depletion, whereas diagnosis of SIADH depends on a coexisting euvolemic state (as with the patient).

As many as 10% of victims of traumatic brain injury develop hyponatremia, and it is associated with a worse prognosis, even in mild cases, the clinicians note. Making the right diagnosis is critical—the treatment chosen can easily compromise the outcome. Patients with neurosurgical conditions are often treated with considerable volumes of saline-containing fluid, with consequent dynamic changes in blood and extracellular volumes. Moreover, the patients have elevated levels of adrenergic hormones with their own confounding effects.

In the long term, the patient experienced significant neurologic sequelae, including prolonged posttraumatic amnesia. After extensive rehabilitation he was able to return to the university.

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