Extracellular volume depletion

Orai Prevention or treatment of extracellular volume depletion, dehydration, or sodium depletion aid in the prevention of heat prostration. 

The patient discussed in the illustrative case presented with orthostatic hypotension, poor skin turgor, dry mucous membrane, a ketotic odor to the breath, elevations in BUN and creatinine, and ketoacidosis. She had severe extracellular volume depletion, which can be estimated using the following clinical criteria ... 

Diuretic-induced hyponatremia occurs more frequently in patients treated with thiazide diuretics than in patients who are receiving loop diuretics. In addition to causing extracellular volume depletion and nonosmotic stimulation of ADH, thiazides interfere with urinary dilution and water excretion by blocking tubular sodium and potassium reabsorption in the distal tubule. Water is then retained in excess of sodium by virtue of nonosmotic release of ADH and excretion of urine with a concentration of sodium and potassium that exceeds that of the plasma. 

The use of NSAIDs or amiloride to produce mild extracellular volume depletion needs to be evaluated in terms of the risks of an increase in serum creatinine concentration. 

Loop diuretics are useful in treating toxic ingestions of bromide, fluoride, and iodide, which are reabsorbed in the TAL. Saline solution must be administered to replace urinary losses of Na+ and to provide , so as to avoid extracellular fluid volume depletion. 

Sodium balance is integrated with regulation of extracellular fluid volume. Depletional hyponatremia (sodium loss greater than water loss) may result from... 

Dehydration may result from primary water deficiency, usually because of decreased intake, but in some instances (e.g., diabetes insipidus) it may result from increased losses of water. In general, the term dehydration implies intracellular and interstitial fluid depletion, in contrast to volume depletion, which implies extracellular, and particularly intravascular, sodium and water loss. In the case of primary water deficit, cell dehydration occurs, with delayed circulatory failure from decreased circulatory volume with ongoing losses. Initially, the patient may be thirsty and possibly have some mental status changes, such as confusion. If the cellular dehydration occurs slowly, intracellular substances, referred to as idiogenic osmols, develop that firnit progressive comphcations (e.g., cerebral edema or coma). With combined water and salt deficiencies, such as might occur with gastrointestinal... 

Proper attention to plasma expansion must be continued into the intraoperative and postoperative periods. A number of neurohormonal changes take place that affect urine output, and patients may have substantial third-spacing of fluid depending on the operation and the preexisting condition of the patient. Furthermore, postoperative patients are prone to hyponatremia from renal generation of electrolyte-free water and from antidiuretic hormone release. As in acute resuscitation, the administration of hypotonic solutions in the perioperative period does not prevent the decrease in extracellular volume that often occurs. Therefore, although excess fluid administration is to be avoided in the perioperative setting, isotonic crystalloid solutions should be used when fluids are indicated to prevent intravascular depletion and circulatory insufficiency. 

Patients with hypotonic hyponatremia caused by volume depletion should initially receive normal saline followed by 0.45% saline once signs of extracellular fluid volume depletion abate in order to avoid overly rapid correction of the serum sodium concentration. 

Hypermagnesuria is encountered in the case of metabolic and iatrogenic disorders, such as primary and secondary hyperaldosteronism (extracellular volume expansion), hypercalcemia (competition Ca/Mg at the thick ascending loop of Henle), hyperparathyroidism, and phosphate or potassium depletion. Hypermagnesuria may also result from tubulopathy, as the selective defect of the Mg tubular reabsorption (chromosome Hq23), Bartter s syndrome (thick ascending loop of Henle), or Gitelman s syndrome (distal convoluted tubule). 

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

The most serious side effects of diuretics are fluid depletion and electrolyte imbalance.13,88 By the very nature of their action, diuretics decrease extracellular fluid volume as well as produce sodium depletion (hyponatremia) and potassium depletion (hypokalemia). Hypokalemia is a particular problem with the thiazide and loop diuretics, but occurs less frequently when the potassium-sparing agents are used. Hypokalemia and other disturbances in fluid and electrolyte balance can produce serious metabolic and cardiac problems and may even prove fatal in some individuals. Consequently, patients must be monitored closely, and the drug dosage should be maintained at the lowest effective dose. Also, potassium supplements are used in some patients to prevent hypokalemia. 

Because of its powerful action in the kidney, torasemide can rapidly deplete extracellular fluid volume and mobilize tissue oedema, particularly from the lung. This both improves the patient s breathing and improves their ability to exercise. 

Diuretics (see 19.17 Diuretics) are prescribed for hypertension that is not caused by renal-angiotensin-aldosterone involvement because diuretics increase rennin serum level. Diuretics promote sodium depletion decreasing extracellular fluid volume. Commonly prescribed diuretics are ... 

Excessive sweating and lactation Hypercalcemia and hypercalciuria Phosphate depletion Chronic alcoholism Extracellular fluid volume expansion... 

The distal tubule secretes 80% of the uric acid content in urine. The reabsorption of most of the uric acid (98%) in the glomerular filtrate takes place in the proximal tubule. This reabsorption can be inhibited by thiazide diuretics, thus increasing uric acid excretion in urine. The chronic use of diuretics, however, by depleting the extracellular fluid volume provides a stimulus for uric acid reabsorption. Drugs that promote uric acid excretion (uricosuric drugs) include probenecid, sulfinpyrazole, and salicylates in high doses. In low doses salicylates depress uric acid excretion. 

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