Management of Post-Aneurysm Clipping Polyuria
This patient most likely has central diabetes insipidus (DI), not oliguria—the urine output of 100-200 mL/hour represents polyuria, and immediate diagnostic confirmation followed by desmopressin therapy is the definitive treatment. 1
Immediate Diagnostic Confirmation
The clinical picture requires urgent differentiation between central DI and osmotic diuresis from surgical mannitol use:
Obtain simultaneous serum sodium, serum osmolality, and urine osmolality immediately to establish the characteristic triad: polyuria with inappropriately dilute urine (<200 mOsm/kg) and high-normal or elevated serum sodium. 1
Central DI presents with dilute urine (<200 mOsm/kg) and elevated serum sodium, whereas mannitol-induced osmotic diuresis presents with higher urine osmolality despite polyuria. 1
Plasma copeptin levels <21.4 pmol/L can help confirm central DI if the diagnosis remains uncertain, though this is not typically necessary in the post-neurosurgical setting. 1
Definitive Treatment: Desmopressin
Once central DI is confirmed, initiate desmopressin 2-4 mcg in divided doses via subcutaneous or intravenous route. 1 This is the cornerstone of therapy for post-neurosurgical central DI and should not be delayed once the diagnosis is established.
Critical Fluid Management
The fluid management approach is counterintuitive but essential:
Allow free access to water and never restrict fluids—fluid restriction can lead to severe hypernatremic dehydration and death. 1
If IV rehydration is needed, use 5% dextrose in water at maintenance rates, NOT normal saline. 1 Normal saline will worsen hypernatremia in DI.
Allow the patient to drink to thirst rather than calculated requirements, as osmosensors are more sensitive than medical calculations. 1
Avoid intravascular volume contraction, as this increases the risk of delayed cerebral ischemia in the post-SAH period. 2
Monitoring Protocol
Check serum sodium within 7 days of starting desmopressin, then at 1 month, then periodically—the primary risk after treatment is hyponatremia from water intoxication. 1
Initially monitor serum sodium every 2-3 days, then weekly as the patient stabilizes. 1
Continue monitoring for delayed cerebral ischemia, which typically occurs 4-12 days after SAH and can be exacerbated by volume contraction. 3
Common Pitfalls to Avoid
Do not mistake polyuria for oliguria—100-200 mL/hour is excessive urine output (normal is approximately 0.5-1 mL/kg/hour, or ~35-70 mL/hour for a 70 kg patient).
Do not use normal saline for volume replacement in confirmed DI—this worsens hypernatremia. 1
Do not restrict fluids in an attempt to manage polyuria—this is dangerous and can lead to severe hypernatremic crisis. 1
Do not confuse this with the hyponatremia that occurs in 10-30% of SAH patients—that condition requires different management with fludrocortisone or hypertonic saline. 2
Concurrent SAH Management Considerations
While managing the DI, maintain appropriate SAH care: