Brain Natriuretic Peptide Concentrations After Aneurysmal Subarachnoid Hemorrhage: Relationship with Hypovolemia and Hyponatremia

Mees, Sanne M. Dorhout; Hoff, Reinier G.; Rinkel, Gabriël J.E.; Algra, Ale; Bergh, Walter M. van den

doi:10.1007/s12028-011-9504-0

Cited by 26 publications

(8 citation statements)

References 36 publications

(44 reference statements)

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“…Our study did not distinguish whether polyuria and vasospasm are independent phenomena that have similar etiologies or whether the onset of vasospasm contributes to polyuria or vice versa. The pathophysiology of excessive natriuresis and polyuria after aSAH is not completely understood however numerous studies have demonstrated an increase in natriuretic peptides including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) [ 12 , 13 , 24 , 25 ]. Other less known peptides have been identified such as c-type natriuretic peptide and dendroaspis peptide [ 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

Polyuria and cerebral vasospasm after aneurysmal subarachnoid hemorrhage

et al. 2015

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BackgroundNatriuresis with polyuria is common after aneurysmal subarachnoid hemorrhage (aSAH). Previous studies have shown an increased risk of symptomatic cerebral vasospasm or delayed cerebral ischemia (DCI) in patients with hyponatremia and/or the cerebral salt wasting syndrome (CSW). However, natriuresis may occur in the absence of hyponatremia or hypovolemia and it is not known whether the increase in DCI in patients with CSW is secondary to a concomitant hypovolemia or because the physiology that predisposes to natriuretic peptide release also predisposes to cerebral vasospasm. Therefore, we investigated whether polyuria per se was associated with vasospasm and whether a temporal relationship existed.MethodsA retrospective review of patients with aSAH was performed. Exclusion criteria were admission more than 48 h after aneurysmal rupture, death within 5 days, and the development of diabetes insipidus or acute renal failure. Polyuria was defined as >6 liters of urine in a 24 h period. Vasospasm was defined as a mean velocity > 120 m/s on Transcranial Doppler Ultrasonography (TCDs) or by evidence of vasospasm on computerized tomography (CT) or catheter angiography. Multivariable logistic regression was performed to assess the relationship between polyuria and vasospasm.Results95 patients were included in the study. 51 had cerebral vasospasm and 63 met the definition of polyuria. Patients with polyuria were significantly more likely to have vasospasm (OR 4.301, 95 % CI 1.378–13.419) in multivariate analysis. Polyuria was more common in younger patients (52 vs 68, p <.001) but did not impact mortality after controlling for age and disease severity. The timing of the development of polyuria was clustered around the diagnosis of vasospasm and patients with polyuria developed vasospasm faster than those without polyuria.ConclusionsPolyuria is common after aSAH and is significantly associated with cerebral vasospasm. The development of polyuria may be temporally related to the development of vasospasm. An increase in urine volume may be a useful clinical predictor of patients at risk for vasospasm.

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Section: Discussionmentioning

confidence: 99%

Polyuria and cerebral vasospasm after aneurysmal subarachnoid hemorrhage

et al. 2015

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“…Elevated plasma BNP concentrations may therefore not necessarily mediate the development of hyponatremia. In fact, recent data have suggested that the presence of elevated plasma BNP concentrations cannot be regarded as a reliable predictor of either blood volume status or the development of hyponatremia, within the context of recent subarachnoid hemorrhage [63]. Some previous retrospective studies [4,7] have failed to substantiate cerebral salt wasting as a cause for anything more than a minority of cases of hyponatremia following SAH, and strongly support SIAD as the predominant cause of hyponatremia.…”

Section: Hyponatremia Following Subarachnoid Hemorrhagementioning

confidence: 99%

Neurosurgical Hyponatremia

Hannon

Thompson

2014

JCM

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Hyponatremia is a frequent electrolyte imbalance in hospital inpatients. Acute onset hyponatremia is particularly common in patients who have undergone any type of brain insult, including traumatic brain injury, subarachnoid hemorrhage and brain tumors, and is a frequent complication of intracranial procedures. Acute hyponatremia is more clinically dangerous than chronic hyponatremia, as it creates an osmotic gradient between the brain and the plasma, which promotes the movement of water from the plasma into brain cells, causing cerebral edema and neurological compromise. Unless acute hyponatremia is corrected promptly and effectively, cerebral edema may manifest through impaired consciousness level, seizures, elevated intracranial pressure, and, potentially, death due to cerebral herniation. The pathophysiology of hyponatremia in neurotrauma is multifactorial, but most cases appear to be due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Classical treatment of SIADH with fluid restriction is frequently ineffective, and in some circumstances, such as following subarachnoid hemorrhage, contraindicated. However, the recently developed vasopressin receptor antagonist class of drugs provides a very useful tool in the management of neurosurgical SIADH. In this review, we summarize the existing literature on the clinical features, causes, and management of hyponatremia in the neurosurgical patient.

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“…We then used published values of BNP and EPO concentrations in similar patients [21, 30] to calculate the number of patients needed (three groups of patients with hypervolemia, normovolemia and hypovolemia, respectively, considering the initial protocol with a 50 % between-group difference and power of 80 %). Data were analyzed using R [31].…”

Section: Methodsmentioning

confidence: 99%

Mid-regional pro-adrenomedullin (MR-proADM), a marker of positive fluid balance in critically ill patients: results of the ENVOL study

et al. 2016

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BackgroundThe optimal control of blood volume without fluid overload is a main challenge in the daily care of intensive care unit (ICU) patients. Accordingly this study focused on the identification of biomarkers to help characterize fluid overload status.MethodsSixty-seven patients were studied from ICU admission to day 7 (D7). Blood and urine samples were taken daily and sodium and water balance strictly calculated resulting in a total cumulative assessment of ∆Na+ and ∆H2O. Furthermore, plasmatic biomarkers (cortisol, epinephrine, norepinephrine, renin, angiotensin II, aldosterone, pro-endothelin, copeptine, atrial natriuretic peptide, erythropoietin, mid-regional pro-adrenomedullin (MR-proADM)) and Sequential Organ Failure Assessment (SOFA) scores were measured at D2, D5 and D7. Blood volumes were measured with 51Cr fixed on red blood cells at D2 and D7.ResultsThe ∆Na+ or ∆H2O were increased in all patients but never related to blood volumes at D2 nor D7. Total blood volumes were at normal values with constantly low red blood cell volumes and normal or decreased plasmatic volume. Weight, plasmatic proteins, and hemoglobin were weakly related to ∆Na+ or ∆H2O. Amongst all tested biomarkers, only MR-proADM was related to sodium and fluid overload. This biomarker was also a predictor of SOFA scores.ConclusionsPlasmatic concentration in MR-proADM seems to be a good surrogate for evaluation of ∆Na+ or ∆H2O and predicts sodium and extracellular fluid overload.Trial registrationClinicalTrials.gov: NCT01858675 in May 13, 2013.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1540-x) contains supplementary material, which is available to authorized users.

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Brain Natriuretic Peptide Concentrations After Aneurysmal Subarachnoid Hemorrhage: Relationship with Hypovolemia and Hyponatremia

Abstract: High BNP concentrations are related to the occurrence of severe hypovolemia and possibly hyponatremia. These data do not support a role for BNP measurements to differentiate between hypovolemic and non-hypovolemic hyponatremia in SAH patients.

Cited by 26 publications

References 36 publications

Polyuria and cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Polyuria and cerebral vasospasm after aneurysmal subarachnoid hemorrhage

Neurosurgical Hyponatremia

Mid-regional pro-adrenomedullin (MR-proADM), a marker of positive fluid balance in critically ill patients: results of the ENVOL study

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