Excess ADH as a normal response following Acute Ischaemic Stroke

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 281-290-Comparative Effectiveness/Health Outcomes/Quality Improvement/Patient or Provider Education/Endocrine Emergencies
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-289
Suehazlyn Zainudin*1, Mohd Rahman Omar2, Shahrul Azmin1 and Nor Azmi Kamaruddin1
1Universiti Kebangsaan Malaysia Medical Centre, Malaysia, 2Islamic Science University of Malaysia, Malaysia
Introduction: Electrolyte imbalances, particularly hyponatraemia and hypokalaemia are common findings amongst inpatients. These imbalances are thought to have poor prognostic value. In acute stroke patients, hyponatraemia is often attributed to syndrome of inappropriate antidiuretic hormone (ADH).  The objective of this study was to determine the prevalence of ADH and aldosterone excess and their relationship to acute ischaemic stroke outcome. 

Methods:  This was a prospective study involving all patients with acute ischaemic stroke admitted to the medical wards between March until August 2012. Patients with any diseases that may affect electrolytes, plasma ADH and aldosterone levels were excluded as were patients who were on medications causing similar effects.  Demographic data, neurological characteristics and laboratory parameters were recorded at baseline. Plasma ADH and aldosterone levels were taken at baseline. Levels above normal laboratory values for the respective ADH and aldosterone kits were considered raised or in excess. Outcome was determined at day 7 and day 30 via phone -contact.

Results: Fifty-six patients were recruited. Eighty-nine percent of patients had mild to moderate stroke. Thirteen percent of patients had hypokalemia and 26.8% of patients had hyponatremia. Aldosterone excess was not observed in any patient. All patients had excess ADH. There was no significant difference in ADH levels between hyponatraemic and normonatraemic patients. Plasma ADH levels did not correlate with plasma sodium levels. There were 4 (17%) mortalities at day 7 and 13 (23%) mortalities at day 30. Twenty-six (46.4%) patients had greater functional disability at day 30 as compared to baseline. Baseline plasma aldosterone and ADH levels were not associated with either progression of disability or stroke mortality.

Conclusion: In a cohort of predominantly mild to moderate stroke patients, despite only a quarter of patients had hyponatraemia, all had excess ADH. These findings suggest that ADH release is triggered by acute ischaemic stroke event and may, but not necessarily, result in sodium imbalance. Whether this acute response bears any clinical significance requires further in-depth study.

Nothing to Disclose: SZ, MRO, SA, NAK

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