Can a traumatic wound cause Syndrome of Inappropriate Antidiuretic Hormone (SIADH)?

Can Traumatic Wound Cause SIADH?

Yes, traumatic wounds, particularly traumatic brain injuries, can cause Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion, which may persist for months after the initial trauma. 1

Mechanism and Pathophysiology

• Traumatic brain injury (TBI) is a common cause of SIADH due to damage to the pituitary stalk or posterior pituitary, resulting in inappropriate non-osmotic hypersecretion of ADH 1
• SIADH leads to water retention, hyponatremia, and increased urinary sodium excretion despite low serum sodium levels 2
• The condition is characterized by:
  • Hyponatremia (serum sodium <135 mEq/L)
  • Inappropriately high urine osmolality
  • Reduced effective serum osmolality
  • Clinical euvolemia 3

Clinical Presentation

• Symptoms typically appear when hyponatremia becomes severe (≤125 mEq/L) 2
• Early symptoms include:
  • Anorexia
  • Vomiting
  • Confusion 2
• Advanced symptoms may progress to:
  • Seizures
  • Coma
  • Death if left untreated 2
• Neurological symptoms are particularly concerning as they can compound the existing neurological deficits from the original trauma 1

Timeframe and Duration

• SIADH typically occurs in the immediate period following traumatic injury 1
• While usually transient, SIADH can become chronic in some cases:
  • Most cases resolve within 12 months 1
  • Rare cases may persist for years (documented cases of up to 4 years) 1
• Recurrent episodes of SIADH can be triggered by subsequent surgeries or additional trauma in patients with a history of TBI-associated SIADH 4

Diagnosis

• Diagnosis requires:
  • Low serum sodium (<135 mEq/L)
  • Low serum osmolality
  • Inappropriately high urine osmolality
  • Urinary sodium >30 mmol/L
  • Clinical euvolemia 3
• Differential diagnosis should exclude:
  • Cerebral salt wasting (CSW)
  • Adrenal insufficiency
  • Other causes of hyponatremia 3, 4

Management

• First-line treatment for confirmed SIADH includes:
  • Discontinuation of implicated medications
  • Fluid restriction
  • Adequate oral salt intake 3
• For severe or symptomatic cases:
  • Immediate treatment with IV furosemide and 3% sodium chloride to produce negative free-water balance 2
• For chronic SIADH when fluid restriction is not tolerated:
  • Demeclocycline can be effective for long-term management 1, 2
  • Fludrocortisone may reduce hospital stay in patients with hyponatremia and natriuresis 5
  • Other options include lithium, which can temporarily impair renal concentrating ability and promote antinatriuresis 6

Important Considerations

• The incidence of hyponatremia in TBI patients is approximately 13.2% 5
• Traumatic subarachnoid hemorrhage is the most common CT finding in patients who develop hyponatremia 5
• Compliance with long-term fluid restriction can be challenging for patients 1
• Early recognition and treatment of SIADH is crucial to prevent neurological deterioration 4

Prevention of Recurrence

• Identifying patients with slow recovery from brain injury who are at risk for SIADH 4
• Monitoring sodium levels closely in TBI patients, especially before subsequent surgeries 4
• Early intervention with appropriate treatment when sodium levels begin to decrease 5