Restricted fluid intake

1976 ◽  
Vol 45 (4) ◽  
pp. 432-436 ◽  
Author(s):  
Henry A. Shenkin ◽  
Honorio S. Bezier ◽  
William F. Bouzarth
Keyword(s):  
Water Balance ◽  
Fluid Intake ◽  
Injured Patient ◽  
Fluid Restriction ◽  
Content Type ◽  
Daily Observation ◽  
Brain Injured Patient ◽  
Brain Injured ◽  
The Brain ◽  
Fine Print

✓ Water balance studies in postcraniotomy patients indicate that restriction of fluid intake to 1 liter daily maintains the patient in homeostatic balance. A larger fluid intake will expand the extracellular space and presumably unfavorably influence cerebral edema. Daily observation of serum sodium and osmolarity and blood urea nitrogen, and preserving their normalcy, is a rational way of regulating fluid intake of the brain-injured patient. Fluid restriction should be used with caution if hyperosmolar agents, diuretics, or dexamethasone are also administered.

Intracranial pressure: to monitor or not to monitor?

1982 ◽  
Vol 56 (5) ◽  
pp. 650-659 ◽  
Author(s):  
Raj K. Narayan ◽  
Pulla R. S. Kishore ◽  
Donald P. Becker ◽  
John D. Ward ◽  
Gregory G. Enas ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Injured Patient ◽  
Ct Scans ◽  
Content Type ◽  
Brain Injured Patient ◽  
Monitoring Process ◽  
Brain Injured ◽  
Low Incidence ◽  
Fine Print

✓ The authors have analyzed their experience with intracranial pressure (ICP) monitoring in 207 patients over a 4-year period. Patients with either high-density or low-density lesions on computerized tomography (CT) at admission had a high incidence (53% to 63%) of intracranial hypertension (ICP persistently over 20 mm Hg). In contrast, patients with normal CT scans at admission had a relatively low incidence of ICP elevation (13%). Among these patients, three features were found to be strongly associated with the development of intracranial hypertension: 1) age over 40 years; 2) systolic blood pressure under 90 mm Hg; and 3) motor posturing — unilateral or bilateral. When two or more of these features were noted at admission, the incidence of intracranial hypertension was 60%, as compared to 4% when only one, or none, of these features were present. Thus, the patients at high risk for developing intracranial hypertension after severe head injury are those with abnormal CT scans at admission, and those with normal CT scans who demonstrate two or more of the above-mentioned adverse features. Based on these criteria, only 16% of this series of patients with normal CT scans would have qualified for monitoring. In addition to the three clinical features noted above, multimodality evoked potential (MEP) studies were also found to be strong predictors of ICP elevation in the normal CT scan group, with a 75% incidence of intracranial hypertension in patients with disseminated deficits. There was no statistically significant correlation between the Glasgow Coma Scale score, eye movements, pupillary reaction, hypoxia, or anemia at admission and subsequent ICP elevation in the group with normal CT scans. In this series, an intraventricular catheter was used as the sole monitoring device in 91% of the cases. In the remaining 9%, subarachnoid screws were employed, either alone, or upon failure of the ventriculostomy. While no mortality was directly ascribed to the monitoring process, there was a 7.7% complication rate (infection 6.3% + hemorrhage 1.4%). Eighty-five percent of the infections occurred in patients who had been monitored for 5 days or more, while no infections were noted in those monitored for less than 3 days. Used judiciously, this technique can be valuable in the monitoring and treatment of the brain-injured patient.

ARDS in the brain-injured patient: what’s different?

2016 ◽  
Vol 42 (5) ◽  
pp. 790-793 ◽  
Author(s):  
Mauro Oddo ◽  
Giuseppe Citerio
Keyword(s):  
Injured Patient ◽  
Brain Injured Patient ◽  
Brain Injured ◽  
The Brain

Poster 6 - Functional Vision Evaluation and Management of the Brain-injured Patient

2005 ◽  
Vol 76 (6) ◽  
pp. 366
Author(s):  
Michelle Steenbakkers ◽  
Nicole Hooper ◽  
Danielle Gardner ◽  
Suzanne Wickum ◽  
Kia Eldred
Keyword(s):  
Injured Patient ◽  
Brain Injured Patient ◽  
Brain Injured ◽  
Functional Vision ◽  
The Brain

Pathophysiology of hyponatremia after transsphenoidal pituitary surgery

1997 ◽  
Vol 87 (4) ◽  
pp. 499-507 ◽  
Author(s):  
Beatriz R. Olson ◽  
Julie Gumowski ◽  
Domenica Rubino ◽  
Edward H. Oldfield
Keyword(s):  
Water Balance ◽  
Fluid Intake ◽  
Sodium Intake ◽  
Pituitary Surgery ◽  
Dietary Sodium ◽  
Plasma Sodium ◽  
Water Load ◽  
Content Type ◽  
Transsphenoidal Pituitary Surgery ◽  
Fine Print

✓ Hyponatremia after pituitary surgery is presumed to be due to antidiuresis; however, detailed prospective investigations of water balance that would define its pathophysiology and true incidence have not been established. In this prospective study, the authors documented water balance in patients for 10 days after surgery, monitored any sodium dysregulation, further characterized the pathophysiology of hyponatremia, and correlated the degree of intraoperative stalk and posterior pituitary damage with water balance dysfunction. Ninety-two patients who underwent transsphenoidal pituitary surgery were studied. To evaluate posterior pituitary damage, a questionnaire was completed immediately after surgery in 61 patients. To examine the osmotic regulation of vasopressin secretion in normonatremic patients, water loads were administered 7 days after surgery. Patients were categorized on the basis of postoperative plasma sodium patterns. After pituitary surgery, 25% of the patients developed spontaneous isolated hyponatremia (Day 7 ± 0.4). Twenty percent of the patients developed diabetes insipidus and 46% remained normonatremic. Plasma arginine vasopressin (AVP) was not suppressed in hyponatremic patients during hypoosmolality or in two-thirds of the normonatremic patients after water-load testing. Only one-third of the normonatremic patients excreted the water load and suppressed AVP normally. Hyponatremic patients were more natriuretic, had lower dietary sodium intake, and had similar fluid intake and cortisol and atrial natriuretic peptide (ANP) levels compared with normonatremic patients. Normonatremia, hyponatremia, and diabetes insipidus were associated with increasing degrees of surgical manipulation of the posterior lobe and pituitary stalk during surgery. The pathophysiology of hyponatremia after transsphenoidal surgery is complex. It is initiated by pituitary damage that produces AVP secretion and dysfunctional osmoregulation in most surgically treated patients. Additional events that act together to promote the clinical expression of hyponatremia include nonatrial natriuretic peptide—related excess natriuresis, inappropriately normal fluid intake and thirst, as well as low dietary sodium intake. Patients should be monitored closely for plasma sodium, plentiful dietary sodium replacement, mild fluid restriction, and attention to symptoms of hyponatremia during the first 2 weeks after transsphenoidal surgery.

Sign in / Sign up

Export Citation Format

Share Document