Overview
Definition:
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is a condition characterized by excessive secretion of antidiuretic hormone (ADH), leading to impaired water excretion and dilutional hyponatremia
In pediatric practice, SIADH is a significant cause of hypotonic hyponatremia, particularly in post-operative or critically ill children, and can manifest with neurological symptoms due to rapid or severe drops in serum sodium levels.
Epidemiology:
SIADH is the most common cause of euvolemic hyponatremia in adults
In pediatrics, its incidence is less well-defined but is frequently seen in association with central nervous system (CNS) disorders, respiratory infections, certain malignancies, and after surgery
Conditions like meningitis, encephalitis, and brain tumors are common triggers in children.
Clinical Significance:
Hyponatremia, especially when severe or rapidly developing, can lead to significant morbidity and mortality in pediatric patients
Neurological symptoms ranging from lethargy and confusion to seizures and coma can occur
Accurate diagnosis and timely, appropriate management, including judicious use of fluid restriction and hypertonic saline, are crucial for preventing irreversible neurological damage and improving patient outcomes
Understanding SIADH management is a high-yield topic for DNB and NEET SS examinations.
Clinical Presentation
Symptoms:
Symptoms are often related to the degree and rapidity of hyponatremia
Mild symptoms may include nausea, vomiting, and malaise
Moderate to severe hyponatremia can manifest as headache, lethargy, confusion, muscle weakness, and irritability
Critical hyponatremia can lead to seizures, stupor, coma, and respiratory arrest
In infants, irritability and poor feeding may be the initial signs.
Signs:
Physical examination may reveal signs of fluid overload (edema, pulmonary congestion) or, more commonly in SIADH, normal or slightly increased extracellular fluid volume due to appropriate ADH action on renal tubules, leading to water retention
Vital signs may be normal or show signs of underlying illness
Neurological examination findings can range from subtle changes in mental status to frank neurological deficits.
Diagnostic Criteria:
The diagnosis of SIADH is typically made based on the presence of the following: 1
Hyponatremia (serum sodium < 135 mEq/L)
2
Hypo-osmolality (serum osmolality < 275 mOsm/kg)
3
Inappropriately concentrated urine osmolality (>100 mOsm/kg), indicating impaired water excretion despite hypotonic plasma
4
Euvolemia (absence of clinical signs of dehydration or volume overload)
5
Elevated urinary sodium excretion (>40 mEq/L) in the absence of diuretic use or salt-wasting conditions
6
Normal renal, adrenal, and thyroid function.
Diagnostic Approach
History Taking:
A detailed history should focus on recent illnesses (especially CNS or pulmonary infections), neurological symptoms, medication use (including over-the-counter drugs that can affect ADH), recent surgeries, and any known underlying chronic conditions
Inquire about fluid intake and output
Assess for symptoms of dehydration or volume overload.
Physical Examination:
A thorough physical examination is essential to assess volume status, including skin turgor, mucous membranes, capillary refill time, peripheral edema, jugular venous distension, and lung auscultation
A detailed neurological examination should be performed to evaluate for any signs of cerebral edema or neurological dysfunction.
Investigations:
Key laboratory investigations include: Serum electrolytes (sodium, potassium, chloride, bicarbonate), serum osmolality, urine electrolytes (sodium, potassium), and urine osmolality
Additional tests may include BUN, creatinine, glucose, and thyroid function tests to rule out other causes of hyponatremia
In specific cases, ADH levels may be measured, though this is not routinely performed
Consider imaging of the brain if a CNS cause is suspected.
Differential Diagnosis:
Differential diagnoses for hyponatremia in pediatrics are broad and include: 1
Psychogenic polydipsia
2
Cerebral salt wasting (CSW) - presents with hyponatremia and natriuresis but typically in the context of CNS injury and hypovolemia
3
Renal salt wasting
4
Hypothyroidism and adrenal insufficiency - typically present with other characteristic symptoms and electrolyte abnormalities
5
Diuretic use
6
Gastrointestinal losses.
Management
Initial Management:
The initial management of SIADH-induced hyponatremia focuses on addressing the severity of symptoms and the chronicity of hyponatremia
Asymptomatic or mildly symptomatic chronic hyponatremia can be managed with fluid restriction alone
Severely symptomatic or rapidly developing hyponatremia requires more aggressive treatment with hypertonic saline, often with careful monitoring in an intensive care setting.
Medical Management:
Fluid restriction is the cornerstone of management for mild to moderate, asymptomatic SIADH
The recommended fluid intake is typically 50-75% of the daily maintenance fluid requirement, aiming to achieve a negative water balance
For severe symptomatic hyponatremia (seizures, coma), intravenous administration of 3% hypertonic saline is indicated
The rate of correction is critical
aiming for a rise of no more than 4-6 mEq/L in the first 24 hours, and a total rise of no more than 10-12 mEq/L in the first 48-72 hours, is crucial to prevent osmotic demyelination syndrome (ODS)
A common initial bolus might be 1-2 mL/kg of 3% saline to raise serum sodium acutely, followed by a continuous infusion tailored to the desired correction rate.
Surgical Management:
Surgical intervention is generally not indicated for SIADH itself
However, if an underlying surgical condition (e.g., brain tumor, intracranial hemorrhage) is the cause of SIADH, surgical management of that condition may be necessary.
Supportive Care:
Supportive care includes close monitoring of neurological status, vital signs, and fluid balance
Electrolyte levels (serum sodium, osmolality) must be monitored frequently, especially during active correction
Nutritional support should be provided as per the patient's requirements
If the underlying cause of SIADH is treatable, addressing that cause is paramount.
Complications
Early Complications:
The most feared early complication is osmotic demyelination syndrome (ODS), also known as central pontine myelinolysis, which can occur if serum sodium is corrected too rapidly, particularly in patients with chronic hyponatremia
Symptoms include dysarthria, dysphagia, spasticity, and even quadriparesis
Seizures and cerebral edema are also risks if hyponatremia is severe or mismanaged.
Late Complications:
Long-term sequelae of ODS can be permanent and devastating
Chronic or recurrent hyponatremia can lead to cognitive impairment and neurological deficits if not managed appropriately.
Prevention Strategies:
Prevention of ODS involves slow and controlled correction of hyponatremia, guided by serial serum sodium measurements
Avoiding rapid increases in serum sodium, especially beyond 10-12 mEq/L in 48-72 hours, is essential
Identifying patients at risk for rapid correction (e.g., those with chronic hyponatremia, malnutrition, or alcoholism) is crucial
Maintaining appropriate fluid balance and addressing the underlying cause of SIADH also plays a vital role.
Prognosis
Factors Affecting Prognosis:
Prognosis is largely dependent on the severity of the hyponatremia, the underlying cause of SIADH, the presence of neurological symptoms, and the promptness and appropriateness of management
Patients who develop ODS have a poorer prognosis.
Outcomes:
With prompt and appropriate management, particularly careful correction of serum sodium, most pediatric patients with SIADH can achieve a full recovery without long-term sequelae
However, severe or rapidly corrected hyponatremia carries a significant risk of permanent neurological damage.
Follow Up:
Patients treated for SIADH-induced hyponatremia, especially those requiring aggressive management, should have regular follow-up to monitor for recurrence and assess for any residual neurological deficits
Continued monitoring of electrolyte balance and fluid intake may be necessary, particularly if the underlying cause of SIADH persists.
Key Points
Exam Focus:
Remember that SIADH causes euvolemic hyponatremia due to excess ADH
Key management strategies are fluid restriction and, for severe symptoms, slow correction with hypertonic saline
Be aware of the risk of osmotic demyelination syndrome with rapid correction.
Clinical Pearls:
Always assess volume status carefully in a hyponatremic patient
If euvolemic, consider SIADH
Differentiate SIADH from cerebral salt wasting by evaluating volume status and urinary sodium
Monitor sodium correction rates diligently
less is often more.
Common Mistakes:
Over-correction of hyponatremia leading to ODS is a critical error
Failing to consider all differential diagnoses of hyponatremia, especially in critically ill children, can lead to delayed or incorrect management
Administering hypotonic fluids in a patient with SIADH will worsen hyponatremia.