Abstract 42: Haptoglobin 2-2 Phenotype Is associated with Cerebral Salt Wasting Syndrome in Aneurysmal Subarachnoid Hemorrhage

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Santosh B Murthy ◽  
Justin Caplan ◽  
Shalom Hadar ◽  
Wendy C Ziai ◽  
Andrew P Levy ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebrovascular Disorders ◽  
Demographic Variables ◽  
Continuous Variables ◽  
Chi Square ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Wasting Syndrome ◽  
Genetically Determined

INTRODUCTION: The Haptoglobin (Hp) phenotype has been shown to be a predictor of clinical outcomes in cerebrovascular disorders. We sought to determine if the Hp phenotype was predictive of cerebral salt wasting (CSW) following aneurysmal subarachnoid hemorrhage (SAH). METHODS: Patients admitted with a diagnosis of SAH were divided into three groups based on their genetically determined Hp phenotype: 1-1, 2-1, and 2-2. Outcome measures included CSW, delayed cerebral infarction (DCI) and favorable outcome -Glasgow Outcome score (GOS) of 4-5 at 30 days. CSW was diagnosed by a clinician, and met the following criteria: hyponatremia 4 liters in 12 hours with urine sodium > 40 mEq/L. Pearson’s Chi Square and Wilcoxon-Mann-Whitney tests were used for categorical and continuous variables respectively. Logistic regression was used to assess association between Hp phenotype and SAH outcomes. RESULTS: A total of 133 patients were included in the study. The distribution of Hp phenotype was- Hp 1-1: 29 (21.8%), Hp 2-1: 57 (42.9%), Hp 2-2: 47 (35.3%). The three Hp subgroups did not differ in terms of demographic variables, comorbidities or SAH characteristics. CSW occurred in 1 patient (3.4%) with Hp 1-1, 8 (14.0%) with Hp 2-1 and 15 (31.9%) with Hp 2-2 (p=0.004). In the multivariate analysis adjusted for age, sex, race, Hunt-Hess score and hydrocephalus, Hp 2-2 was associated with CSW (OR: 4.94 CI: 1.78-17.43, p=0.013) but Hp 2-1 was not (OR: 2.92, CI: 0.56-4.95, p=0.150). There were no associations between Hp phenotypes and favorable outcomes or DCI. CSW correlated strongly with development of DCI (OR: 7.16, OR: 2.48-20.62, p<0.001). CONCLUSIONS: Hp 2-2 phenotype was an independent predictor of cerebral salt wasting following SAH. There were no associations between Hp phenotype and DCI or good functional outcome.

Haptoglobin 2-2 Genotype Is Associated With Cerebral Salt Wasting Syndrome in Aneurysmal Subarachnoid Hemorrhage

Neurosurgery ◽  
2015 ◽  
Vol 78 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Santosh B. Murthy ◽  
Justin Caplan ◽  
Andrew P. Levy ◽  
Gustavo Pradilla ◽  
Yogesh Moradiya ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Wasting Syndrome ◽  
Symptomatic Vasospasm ◽  
Baseline Characteristics ◽  
Definition Of ◽  
Salt Wasting Syndrome

Abstract BACKGROUND: Haptoglobin (Hp) genotype has been shown to be a predictor of clinical outcomes in subarachnoid hemorrhage. Cerebral salt wasting (CSW) has been suggested to precede the development of symptomatic vasospasm. OBJECTIVE: To determine if Hp genotype was associated with CSW and subsequent vasospasm after aneurysmal subarachnoid hemorrhage. METHODS: Hp genotypic determination was done for patients admitted with a diagnosis of subarachnoid hemorrhage. Outcome measures included CSW, delayed cerebral infarction, and Glasgow Outcome Score of 4 to 5 at 30 days. Criteria for CSW included hyponatremia &lt;135 mEq/L, and urine output &gt;4 L in 12 hours with urine sodium &gt;40 mEq/L. RESULTS: A total of 133 patients were included in the study. The 3 Hp subgroups did not differ in terms of baseline characteristics. CSW occurred in 1 patient (3.4%) with Hp 1-1, 8 (14.0%) patients with Hp 2-1, and 15 (31.9%) patients with Hp 2-2 (P = .004). In the multivariate regression model, Hp 2-2 was associated with CSW (odds ratio [OR]: 4.94; CI: 1.78-17.43; P = .01), but Hp 2-1 was not (OR: 2.92; CI: 0.56-4.95; P = .15) compared with Hp 1-1. There were no associations between Hp genotypes and functional outcome or delayed cerebral infarction. CSW was associated with delayed cerebral infarction (OR: 7.46; 95% CI: 2.54-21.9; P &lt; .001). CONCLUSION: Hp 2-2 genotype was an independent predictor of CSW after subarachnoid hemorrhage. Because CSW is strongly associated with delayed cerebral infarction, the use of Hp genotype testing requires more investigation, and larger prospective confirmation is warranted. Additionally, a more objective definition of CSW needs to be delineated.

Cerebral salt wasting syndrome in patients with aneurysmal subarachnoid hemorrhage

2005 ◽  
Vol 27 (4) ◽  
pp. 418-422 ◽  
Author(s):  
Francisco R. Revilla-Pacheco ◽  
Tenoch Herrada-Pineda ◽  
Mauro Loyo-Varela ◽  
Marcos Modiano-Esquenazi
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Salt Wasting Syndrome ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Wasting Syndrome ◽  
Salt Wasting Syndrome

scholarly journals Hyponatremia Following Mild/Moderate Subarachnoid Hemorrhage Is Due To SIAD and Glucocorticoid Deficiency and not Cerebral Salt Wasting

2014 ◽  
Vol 99 (1) ◽  
pp. 291-298 ◽  
Author(s):  
M. J. Hannon ◽  
L. A. Behan ◽  
M. M. C. O'Brien ◽  
W. Tormey ◽  
S. G. Ball ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Clinical Examination ◽  
Plasma Cortisol ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Tertiary Referral Centre ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Wasting Syndrome ◽  
Glucocorticoid Deficiency

Context: Hyponatremia is common after acute subarachnoid hemorrhage (SAH) but the etiology is unclear and there is a paucity of prospective data in the field. The cause of hyponatremia is variously attributed to the syndrome of inappropriate antidiuresis (SIAD), acute glucocorticoid insufficiency, and the cerebral salt wasting syndrome (CSWS). Objective: The objective was to prospectively determine the etiology of hyponatremia after SAH using sequential clinical examination and biochemical measurement of plasma cortisol, arginine vasopressin (AVP), and brain natriuretic peptide (BNP). Design: This was a prospective cohort study. Setting: The setting was the National Neurosurgery Centre in a tertiary referral centre in Dublin, Ireland. Patients: One hundred patients with acute nontraumatic aneurysmal SAH were recruited on presentation. Interventions: Clinical examination and basic biochemical evaluation were performed daily. Plasma cortisol at 0900 hours, AVP, and BNP concentrations were measured on days 1, 2, 3, 4, 6, 8, 10, and 12 following SAH. Those with 0900 hours plasma cortisol &lt;300 nmol/L were empirically treated with iv hydrocortisone. Main Outcome Measures: Plasma sodium concentration was recorded daily along with a variety of clinical and biochemical criteria. The cause of hyponatremia was determined clinically. Later measurement of plasma AVP and BNP concentrations enabled a firm biochemical diagnosis of the cause of hyponatremia to be made. Results: Forty-nine of 100 developed hyponatremia &lt;135 mmol/L, including 14/100 &lt;130 mmol/L. The cause of hyponatremia, and determined by both clinical examination and biochemical hormone measurement, was SIAD in 36/49 (71.4%), acute glucocorticoid insufficiency in 4/49 (8.2%), incorrect iv fluids in 5/49 (10.2%), and hypovolemia in 5/49 (10.2%). There were no cases of CSWS. Conclusions: The most common cause of hyponatremia after acute nontraumatic aneurysmal SAH is SIAD. Acute glucocorticoid insufficiency accounts for a small but significant number of cases. We found no cases of CSWS.

Subarachnoid Hemorrhage

2018 ◽  
pp. 44-53
Author(s):  
Sherry Hsiang-Yi Chou
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Complex Disease ◽  
Hormone Secretion ◽  
Delayed Cerebral Ischemia ◽  
Early Brain Injury ◽  
Neurogenic Pulmonary Edema ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Wasting Syndrome

Subarachnoid hemorrhage (SAH) affects over 30,000 Americans per year, leaves over half of its survivors in severe disability, and has a mortality rate of approximately 20%. SAH syndrome presents with a complex disease course and symptoms involving both the central nervous system (CNS) as well as extra-CNS systems. SAH may lead to early brain injury, cerebral vasospasm, and delayed cerebral ischemia, which increases SAH morbidity and mortality. SAH-related extra-CNS organ injuries include neurogenic stunned myocardium, neurogenic pulmonary edema, syndrome of inappropriate antidiuretic hormone secretion, cerebral salt wasting syndrome, systemic inflammatory response syndrome, fever, and venous thromboembolism, all of which require careful critical care management. Though multiple randomized trials in the recent years have not successfully identified any effective neuroprotective therapy in SAH, the overall SAH outcome has significantly improved over the past two decades.

Neurovascular Critical Care

2018 ◽  
Author(s):  
Jose Manuel Sarmiento ◽  
Shouri Lahiri
Keyword(s):  
Ischemic Stroke ◽  
Subarachnoid Hemorrhage ◽  
Acute Ischemic Stroke ◽  
Cerebral Vasospasm ◽  
Cerebral Edema ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
High Morbidity ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Decompressive Hemicraniectomy

Ischemic stroke and intracranial hemorrhage are among the most devastating and debilitating injuries in medicine. Initial management principles for acute ischemic stroke rely on prompt revascularization before the brain parenchymal is infarcted. Large hemispheric infarctions and malignant cerebral edema occur uncommonly in a subset of patients with acute ischemic stroke and are associated with high morbidity and mortality rates. The indications for decompressive hemicraniectomy for malignant cerebral edema are reviewed. Medical management of intraparenchymal hematomas and aneurysmal subarachnoid hemorrhage in the intensive care setting is emphasized. Important clinical sequelae of subarachnoid hemorrhage such as rebleeding, cerebral vasospasm, and cerebral salt wasting are reviewed.   This review contains 5 figures, 4 tables and 52 references Key Words:  acute ischemic stroke, cerebral aneurysm, cerebral vasospasm, decompressive hemicraniectomy, intracerebral hemorrhage, large hemispheric infarctions, subarachnoid hemorrhage, malignant cerebral edema

Prevalence and clinical demographics of cerebral salt wasting in patients with aneurysmal subarachnoid hemorrhage

Pituitary ◽  
2009 ◽  
Vol 12 (4) ◽  
pp. 347-351 ◽  
Author(s):  
Lily Kao ◽  
Zahraa Al-Lawati ◽  
Joli Vavao ◽  
Gary K. Steinberg ◽  
Laurence Katznelson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Salt Wasting ◽  
Salt Wasting

scholarly journals Cerebral Salt-Wasting Syndrome in Subarachnoid Hemorrhage: A Primer for Interventional Neuroradiologists

2018 ◽  
Vol 02 (01) ◽  
pp. 051-054
Author(s):  
Adhithyan Rajendran ◽  
Santhosh Kannath ◽  
Smitha Vimala ◽  
Jayadevan Rajan
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Clinical Setting ◽  
Biochemical Parameters ◽  
Present Report ◽  
Cerebral Salt Wasting Syndrome ◽  
Optimal Care ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Wasting Syndrome ◽  
Salt Wasting Syndrome

AbstractHyponatremia due to several causes could occur in subarachnoid hemorrhage (SAH), and cerebral salt-wasting syndrome (CSWS) is one of the frequent causes of hyponatremia in this clinical setting. Appropriate clinical diagnosis is important as the treatment is entirely different in various etiologies. In the present report, the authors highlight various clinical and biochemical parameters that help in the recognition of CSWS and discuss its clinical management using a clinical prototype. As neurointerventional radiologists are becoming increasingly involved in the management of intra-cranial aneurysms and SAH, awareness of this entity and its appropriate management is essential in providing optimal care to these patients.

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