Fluids normal intake/output

Fluid restriction is generally unnecessary as long as sodium intake is controlled. The thirst mechanism remains intact in CKD to maintain total body water and plasma osmolality near normal levels. Fluid intake should be maintained at the rate of urine output to replace urine losses, usually fixed at approximately 2 L/day as urine concentrating ability is lost. Significant increases in free water intake orally or intravenously can precipitate volume overload and hyponatremia. Patients with stage 5 CKD require renal replacement therapy to maintain normal volume status. Fluid intake is often limited in patients receiving hemodialysis to prevent fluid overload between dialysis sessions. 

The osmoreceptors of the hypothalamus monitor the osmolarity of extracellular fluid. These receptors are stimulated primarily by an increase in plasma osmolarity they then provide excitatory inputs to the thirst center and the ADH-secreting cells in the hypothalamus. The stimulation of the thirst center leads to increased fluid intake. The stimulation of the ADH-secreting cells leads to release of ADH from the neurohypophysis and, ultimately, an increase in reabsorption of water from the kidneys and a decrease in urine output. These effects increase the water content of the body and dilute the plasma back toward normal. Plasma osmolarity is the major stimulus for thirst and ADH secretion two additional stimuli include ... 

Because no antidote is available, treatment is supportive. A patient s condition should be monitored closely, including fluid intake and output, mental status, and serum levels of lithium, creatinine, and electrolytes. Patients with normal renal function should be able to clear lithium unassisted. If necessary, attempts should be made to remove excess lithium from the body by gastric lavage and emesis. 

Svendsen C K, Hjortkjaer R K, Hesselholt M 1979 Colic in the horse. A clinical and clinical chemical study of 42 cases. Nordisk Veterinaermedicin 31(Suppl) 1-32 Swanson J T, Aldrete J A 1989 Thrombophlebitis after intravenous infusion. Factors affecting its incidence. Rocky Mountain Medical Journal 66 48-51 Tasker J B 1967 Fluid and electrolyte studies in the horse III. Intake and output of water, sodium and potassium in normal horses. Cornell Veterinarian 57 649- 57 Taylor P 1996 Heat stroke, exhaustion and synchronous diaphragmatic flutter (SDF). In Dyson S (ed) A guide to the management of emergencies at equine competitions. Equine Veterinary Journal (A British Equine Veterinary Association Manual), Newmarket, UK, pp. 102-113... 

For those patients with normal to moderately impaired renal function, the cornerstone of initial treatment of hypercalcemia is volume expansion to increase urinary calcium excretion (see Table 49-6). Patients with severe renal insufficiency usually do not tolerate volume expansion they may be initiated on therapy with calcitonin. Patients with symptomatic hypercalcemia are often dehydrated secondary to vomiting and polyuria thus rehydration with saline-containing fluids is necessary to interrupt the stimulus for sodium and calcium reabsorption in the renal mbule. ° Rehydration can be accomplished by the infusion of normal saline at rates of 200 to 300 mL/h, depending on concomitant conditions (primarily cardiovascular and renal) and extent of hypercalcemia. Adequacy of hydration is assessed by measuring fluid intake and output or by central venous pressure monitoring. Loop diuretics such as furosemide (40 to 80 mg IV every 1 to 4 hours) or ethacrynic acid (for patients with sulfa allergies) may also be instiffited to increase urinary calcium excretion and to minimize the development of volume overload from the administration of saline (see Table 49-6). Loop diuretics such as furosemide... 

Regardless of the serotypes, the primary goal of therapy is restoration of fluid and electrolyte losses caused by watery diarrhea. ORT is the preferred method of rehydration, and several studies showed reduction in fluid requirements by 32% to 35% when rice-based instead of glucose-based ORT solutions are used (50-80 g rice instead of 20 g glucose per liter). In patients who cannot tolerate ORT, IV Ringer s lactate solution can be used. Normal saline is not recommended because it does not correct metabolic acidosis. After rehydration, maintenance fluid is given based on accurate recording of intake and output volumes. 

Diuretic medication such as furosemide (Lasix) causes the patient to lose more than the normal volume of fluid in an effort to counteract a disease that results in the retention of fluids. The nurse alerts the patient to the likely increase in urination and also monitors the patient s fluid intake and output to assure that the patient maintains an adequate fluid level. 

Fluid balance in the body is maintained or restored primarily by variations in urine output. Normally, this amounts to about 1400 mL/day, but the total excretion fluctuates according to water intake. The primary factor that controls urine production is the rate of water reabsorption from the renal tubules in the kidneys. This rate is regulated chiefly by the pituitary hormone vasopressin and by the adrenal cortex hormone aldosterone. 

No further renal change was experienced still June 1973, when urine output suddenly stopped. Anuria lasted 48 h Gune 3-5) and in the meanwhile blood urea rose to 87 mg%, blood creatinine to 4 mg% and blood UA to 26 mg%, whereas blood actual pH decreased to 7.29. Once again by stopping adenine, fluid and alkali intake allowed to restore urine output and normalize the blood chemistry. In the first urine specimen after anuria (300 ml), pH was 6.5, UA excretion 210 mg and the ratio of the absorbances of urine sediment at 305/280 m/x was 0.39 this means the presence of considerable amount of dioxyadenine... 

In order that the composition of the other body fluids may be kept constant, that of the urine must be able to vary widely. For this reason, even in a normal individual, the composition of the urine may be quite different according to the times and circumstances and, since the composition of samples collected over short periods may differ significantly from the average, a complete 24 hour sample should be analysed in order to obtain reliable values for the output of its various constituents. In the normal adult the volume excreted is of the order of 1000-2000ml per day and 1500 ml is usually taken as the average figure. The quantity depends on the water intake, the external temperature and the diet as well as on the mental and physical state. 

Large deficits or excesses in the body water are reason for concern. In healthy individuals, the total amount of body water remains reasonably constant. Therefore, an increase or decrease in water intake brings about an appropriate increase or decrease in water output to maintain the balance. Fig. W-4 illustrates the intake of water, the routes of water output, and the movement of fluid between the compartments of the body. Water enters the body as a liquid, and as a component of the food-including metabolic water derived from the breakdown of food. Water is lost from the body by (1) the skin as perspiration, (2) the lungs as water vapor in expired air, (3) the kidneys as urine, and (4) the intestines in the feces. As Fig. W-4 shows, under normal conditions total water intake is approximately equal to total water output by the various routes. 

There are two components to the regulation of ECE sodium the total amount of sodium retained and its concentration. The former is regulated by mechanisms that directly affect sodium, whereas the latter is essentially regulated via water balance. Thus, whatever sodium is retained in ECF is clothed with the appropriate amount of water to maintain the normal plasma sodium concentration within narrow limits deviations of less than 1% (hard to measure in the laboratory) trigger corrective responses. Thus, a raised plasma sodium concentration (e.g., after water loss) stimulates both thirst and renal water conservation antidiuretic hormone (ADH) from the posterior pituitary reduces urine output through its effect on the renal collecting ducts. Even one of these mechanisms can defend body water thus diabetes insipidus (inadequate production or effect of ADH) does not cause severe dehydration but polydipsia (increased fluid intake thirst is a sensation). 

---