Endocrine response after severe subarachnoid hemorrhage related to sodium and blood volume regulation.
BACKGROUND
Hyponatremia is often associated with, and worsens, the prognosis of severe aneurysmal subarachnoid hemorrhage (SAH). Several possible endocrine perturbations of variable severity and variable sodium and water intake have been described in SAH. However, a comprehensive study of the different hormonal systems involved in sodium and water homeostasis and circulating blood volume modifications is still needed. Our aim was to assess water and sodium regulation after severe SAH by investigating blood volume and several hormonal regulatory systems in the context of hyponatremia prevention by controlled sodium intake.


METHODS
Nineteen mechanically ventilated patients with severe SAH, were prospectively studied. Replacement of sodium was at least 4.5 mmol x kg(-1) x d(-1) and adjusted on natriuresis. Hormones involved in electrolyte and water homeostasis: vasopressin, renin, angiotensin, aldosterone, and natriuretic peptides were assessed every 3 days for 12 days. Red blood cell volume was measured by the isotopic method (technetium-labeled red blood cells), in the first 48 h after admission and at day 7. Cardiac function was assessed using electrocardiogram, transthoracic echocardiography, and troponin Ic (cTnI). Outcome was assessed at 3 mo.


RESULTS
After SAH onset, hyponatremia, but not decreased circulating blood volume, was prevented by high sodium and water infusion adapted to renal excretion. The hormonal profiles were characterized by an increase in renin, angiotensin II, natriuretic peptide concentrations associated with increased troponin Ic, stable low levels of vasopressin, and the absence of increased aldosterone concentrations. There were no correlations between hormone concentrations and natriuresis.


CONCLUSIONS
After severe SAH, in the context of multiple clinical interventions, increased natriuresis and low blood volume are consistent with cerebral salt wasting syndrome, probably related to the sequence of severe SAH, highly increased sympathetic tone, hyperreninemic hypoaldosteronism syndrome, and increased natriuretic peptides release.
Audibert
Gérard
G
Department of Anaesthesia and Critical Care, Hôpital Central, 29 Avenue de Lattre de Tassigny, 54035 Nancy Cedex, France.
Steinmann
Gaëlle
G
de Talancé
Nicole
N
Laurens
Marie-Hélène
MH
Dao
Pierre
P
Baumann
Antoine
A
Longrois
Dan
D
Mertes
Paul-Michel
PM
D000328:Adult; D000758:Anesthesia; D001810:Blood Volume / Q000502:physiology*; D003422:Critical Care; D004702:Endocrine Glands / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D023261:Glasgow Outcome Scale; D006400:Hematocrit; D006706:Homeostasis / Q000502:physiology; D006728:Hormones / Q000097:blood; D006801:Humans; D007010:Hyponatremia / Q000378:metabolism / Q000517:prevention & control; D020896:Hypovolemia / Q000378:metabolism / Q000517:prevention & control; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D009318:Natriuresis / Q000502:physiology; D019635:Neurosurgical Procedures; D012084:Renin-Angiotensin System / Q000502:physiology; D012964:Sodium / Q000378:metabolism*; D013345:Subarachnoid Hemorrhage / Q000378:metabolism / Q000503:physiopathology* / Q000601:surgery; D014057:Tomography, X-Ray Computed; D016896:Treatment Outcome; D014882:Water-Electrolyte Balance / Q000502:physiology
D006728:Hormones; D012964:Sodium