Suprasellar and intraventricular blood predict elevated plasma atrial natriuretic factor in subarachnoid hemorrhage.

Diringer, Michael N.; Lim, Joel Kian Boon; Kirsch, Jeffrey R.; Hanley, Daniel F.

doi:10.1161/01.str.22.5.577

Cited by 43 publications

(13 citation statements)

References 27 publications

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“…ANP is a peptide present at high concentrations in the heart, but is also thought to be biosynthesized in the brain, spinal cord, and autonomic nerve ganglia. Also, there is a strong possibility that apart from ANP natriuretic factors having another structure are present in the brain [2,3]. Even though ANP concentrations did not differ significantly between the two groups in the present study, this does not argue against hormonal involvement in the causation of this selective natriuresis, but rather that future studies will have to focus on other aspects as well.…”

Section: Discussioncontrasting

confidence: 67%

Rapid natriuresis and preventive hypervolaemia for symptomatic vasospasm after subarachnoid haemorrhage

et al. 1996

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To prevent symptomatic cerebral vasospasm, we have used hypervolaemia (HV) or volume expansion in patients with aneurysmal subarachnoid haemorrhage (SAH) in recent years. In these patients we could not perform effective fluid and sodium (Na) replacement because of rapid and overwhelming water and Na loss. Although this phenomenon is characteristic under hypervolaemic states, we regard it important to elucidate the mechanism underlying initiation of vasospasm after aneurysmal SAH. Patients with aneurysmal SAH, operated on within 24 hours of onset, were analysed prospectively. We selected 17 patients in good pre-operative condition. Intravascular volume expansion was accomplished with plasma fractionate or albumin and crystalloid solutions in all patients. We divided the 17 patients into two groups; symptomatic spasm group (S-group) consisting of 4 cases developing transient ischaemic symptoms and non-symptomatic spasm group (NS-group) consisting of 13 cases. In S-group, rapid and marked natriuresis developed characteristically before the onset of ischaemic symptoms. The differences in daily Na balance between the two groups were significant on the 3rd and 5th days (p < 0.05). The mean cumulative Na balance in S-group during the 10 days of the study (-375 +/- 159 mEg) was higher than that of NS-group (-24.4 +/- 225 mEq) (p < 0.05). Rapid natriuresis preceded the development of ischaemic symptoms, and was important as a trigger for symptomatic vasospasm after SAH. We considered that hormonal disorders were implicated in this phenomenon, and atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), renin, and aldosterone were each measured three times during the period, with no significant differences, found between the two groups. It was speculated that another potent natriuretic factor, similar to ANP, induced a rapid selective natriuresis resulting in symptomatic vasospasm.

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Section: Discussioncontrasting

confidence: 67%

Rapid natriuresis and preventive hypervolaemia for symptomatic vasospasm after subarachnoid haemorrhage

et al. 1996

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“…It also decreases plasma volume. Increased BNF is most commonly found in patients with subarachnoid hemorrhage or hemorrhage at the base of the brain or in the third ventricle 21,22. BNF was not measured in this study because the authors did not have the appropriate equipment.…”

Section: Discussionmentioning

confidence: 99%

Serum sodium disorders in patients with traumatic brain injury

Paiva¹,

Bezerra²,

Amorim³

et al. 2011

TCRM

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Sodium disorders are the most common and most poorly understood electrolyte disorders in neurological patients. The aim of this study was to determine the incidence of sodium disorders and its association with different traumatic brain injuries. This prospective study was conducted in 80 patients diagnosed with moderate and severe traumatic brain injuries. All patients underwent cerebral computed tomography. Incidence of sodium disorders, presence of injuries in the first computed tomography after traumatic brain injury, and level of consciousness were analyzed. Patients that presented other potential causes of sodium disorders and systemic trauma were excluded from the study. The incidence of sodium disturbances was 45%: 20 patients presented hypernatremia and 16 hyponatremia. Refers to all patients with sodium disturbances 53% were detected in the first sample. We recorded at least one measurement <125 mEq/L in 50% of the patients with hyponatremia. A greater incidence of sodium disorders was found in patients with subdural, intracerebral hematoma and with diffuse axonal injury. The incidence of sodium disorders among the patients with diffuse lesions was greater than in the group of patients with brain contusion (P = 0.022). The incidence of sodium disorders is higher in patients with diffuse traumatic brain injuries. No association was found between focal lesions and proportion of sodium disorders.

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“…Indeed, in neurosurgical models and clinical studies, 40% to 100% with SAH can have ECG changes or arrhythmias, 16–20 11% to 21% can have myocardial enzyme elevation, 17,19,20 and 2% to 30% may have left ventricular dysfunction manifested by hypokinetic wall-motion abnormalities on echocardiography. 17–20 Compared with AIS, heart–brain interactions in SAH have been more widely investigated, 21–34 with literature describing reversible myocardial stunning, 35 histologic evidence of myocardial necrosis, 36 elevation of natriuretic factors, 37,38 secondary neurogenic pulmonary edema, 39 elevation of systemic plasma catecholamines, 40,41 and impairment of regional myocardial perfusion. 42,43 Additionally, in the neurosurgical literature, hemodynamic manipulations have been more rigorously evaluated, specifically for the management of cerebral vasospasm after SAH 44 …”

Section: Discussionmentioning

confidence: 99%

Cardiac Complications in Acute Ischemic Stroke

Wira¹,

Rivers²,

Martinez-Capolino³

et al. 2011

WestJEM

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IntroductionTo characterize cardiac complications in acute ischemic stroke (AIS) patients admitted from an urban emergency department (ED).MethodsRetrospective cross-sectional study evaluating AIS patients admitted from the ED within 24 hours of symptom onset who also had an echocardiogram performed within 72 hours of admission.ResultsTwo hundred AIS patients were identified with an overall in-hospital mortality rate of 8% (n = 16). In our cohort, 57 (28.5%) of 200 had an ejection fraction less than 50%, 35 (20.4%) of 171 had ischemic changes on electrocardiogram (ECG), 18 (10.5%) of 171 presented in active atrial fibrillation, 21 (13.0%) of 161 had serum troponin elevation, and 2 (1.1%) of 184 survivors had potentially lethal arrhythmias on telemetry monitoring. Subgroup analysis revealed higher in-hospital mortality rates among those with systolic dysfunction (15.8% versus 4.9%; P = 0.0180), troponin elevation (38.1% versus 3.4%; P < 0.0001), atrial fibrillation on ECG (33.3% versus 3.8%; P = 0.0003), and ischemic changes on ECG (17.1% versus 6.1%; P = 0.0398) compared with those without.ConclusionA proportion of AIS patients may have cardiac complications. Systolic dysfunction, troponin elevation, atrial fibrillation, or ischemic changes on ECG may be associated with higher in-hospital mortality rates. These findings support the adjunctive role of cardiac-monitoring strategies in the acute presentation of AIS.

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Suprasellar and intraventricular blood predict elevated plasma atrial natriuretic factor in subarachnoid hemorrhage.

Cited by 43 publications

References 27 publications

Rapid natriuresis and preventive hypervolaemia for symptomatic vasospasm after subarachnoid haemorrhage

Rapid natriuresis and preventive hypervolaemia for symptomatic vasospasm after subarachnoid haemorrhage

Serum sodium disorders in patients with traumatic brain injury

Cardiac Complications in Acute Ischemic Stroke

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