The negative fluid balance that causes dehydration results from decreased intake, increased output (renal, GI,

or insensible losses), or fluid shift (ascites, effusions, and capillary leak states such as burns and sepsis). The decrease in total body water causes reductions in both the intracellular and extracellular fluid volumes. linical manifestations of dehydration are most closely related to intravascular volume depletion. !s dehydration progresses, hypovolemic shock ultimately ensues, resulting in end organ failure and death. "oung children are more susceptible to dehydration due to larger body water content, renal immaturity, and inability to meet their own needs independently. #lder children show signs of dehydration sooner than infants due to lower levels of extracellular fluid ($ %). &ehydration can be categori'ed according to osmolarity and severity. (erum sodium is a good surrogate marker of osmolarity assuming the patient has a normal serum glucose. &ehydration may be isonatremic ()*+,)-+ m$./0), hyponatremic (1 )*+ m$./0), or hypernatremic (2)-+ m$./0). Isonatremic dehydration is the most common (3+4). 5ypernatremic and hyponatremic dehydration each comprise -,)+4 of cases. 6ariations in serum sodium reflect the composition of the fluids lost and have different pathophysiologic effects.

Isonatremic (isotonic) dehydration occurs when the lost fluid is similar in sodium concentration to the blood. (odium and water losses are of the same relative magnitude in both the intravascular and extravascular fluid compartments. 5yponatremic (hypotonic) dehydration occurs when the lost fluid contains more sodium than the blood (loss of hypertonic fluid). 7elatively more sodium than water is lost. 8ecause the serum sodium is low, intravascular water shifts to the extravascular space, exaggerating intravascular volume depletion for a given amount of total body water loss.9), :; 5ypernatremic (hypertonic) dehydration occurs when the lost fluid contains less sodium than the blood (loss of hypotonic fluid). 7elatively less sodium than water is lost. 8ecause the serum sodium is high, extravascular water shifts to the intravascular space, minimi'ing intravascular volume depletion for a given amount of total body water loss.9*, <, :;

=eurologic complications can occur in hyponatremic and hypernatremic states. (evere hyponatremia may lead to intractable sei'ures, whereas rapid correction of chronic hyponatremia (2: m$./0/h) has been associated with central pontine myelinolysis. &uring hypernatremic dehydration, water is osmotically pulled from cells into the extracellular space. To compensate, cells can generate osmotically active particles (idiogenic osmoles) that pull water back into the cell and maintain cellular fluid volume. &uring rapid rehydration of hypernatremia, the increased osmotic activity of these cells can result in a large influx of water, causing cellular swelling and rupture> cerebral edema is the most devastating conse.uence. (low rehydration over <3 hours generally minimi'es this risk.

Prerenal azotemia (emedicine)

?rerenal a'otemia refers to elevations in 8@= and creatinine levels resulting from problems in the systemic circulation that decrease flow to the kidneys. In prerenal a'otemia, decreased renal flow stimulates salt and water retention to restore volume and pressure. Ahen volume or pressure is decreased, the baroreceptor reflexes located in the aortic arch and carotid sinuses are activated. This leads to sympathetic nerve activation, resulting in renal afferent arteriolar vasoconstriction and renin secretion through B) ,receptors. onstriction of the afferent arterioles causes a decrease in intraglomerular pressure, which reduces the G%7 proportionally. 7enin converts angiotensin I to angiotensin II, which, in turn, stimulates aldosterone release. Increased aldosterone levels results in salt and water absorption in the distal collecting tubule. ! decrease in volume or pressure is a nonosmotic stimulus for hypothalamic production of antidiuretic hormone, which exerts its effect in the medullary collecting duct for water reabsorption. Through unknown mechanisms, activation of the sympathetic nervous system leads to enhanced proximal tubular reabsorption of salt and water, as well as 8@=, creatinine, calcium, uric acid, and bicarbonate. The net result of these < mechanisms of salt and water retention is decreased output and decreased urinary excretion of sodium (1 :+ m$./0).

Prerenal azotemia (wiki)

?rerenal a'otemia is caused by a decrease in blood flow (hypoperfusion) to the kidneys. 5owever, there is no inherent kidney disease. It can occur following hemorrhage, shock, volume depletion, congestive heart failure, and narrowing of the renal artery among other things.9); The 8@=C r in prerenal a'otemia is greater than :+. The reason for this lies in the mechanism of filtration of 8@= and creatinine. 7enal ?lasma %low (7?%) is decreased due to hypo perfusion which results in a proportional decrease in G%7. In turn, the decreased flow and pressure to the kidney will be sensed by baroreceptors in the Duxtaglomerular ells of the afferent arteriole. If the decrease in blood pressure is systemic (rather than occlusion of the renal artery) baroreceptors in the carotid sinus and aortic arch will be stimulated. This leads to sympathetic nerve activation, resulting in renal afferent arteriolar vasoconstriction and renin secretion through B ) ,receptors. onstriction of the afferent arterioles causes a decrease in the intraglomerular pressure, reducing G%7 proportionally. 7enin is the main effector of the Euxtaglomerular baroreceptors. 7enin is secreted from granules in the DG cells, and once in the blood stream, it acts as a protease to convert angiotensinogen to angiotensin I, which is converted by angiotensin converting en'yme, to angiotensin II, which, in turn, stimulates aldosterone release. Increased aldosterone levels results in salt and water absorption in the distal collecting tubule. ! decrease in volume or pressure is a nonosmotic stimulus for antidiuretic hormone production in the hypothalamus, which exerts its effect in the medullary collecting duct for water reabsorption. Through unknown mechanisms, activation of the sympathetic nervous system leads to enhanced proximal tubular reabsorption of salt and water, as well as 8@=, creatinine, calcium, uric acid, and bicarbonate. The net result of these < mechanisms of salt and water retention is decreased output and decreased urinary excretion of sodium (1 :+ m$./0). The increased reabsorption of =a leads to increased water and urea reabsorption from the proximal tubules of the kidney back into the blood. In contrast, creatinine is actually

secreted in the proximal tubule. This generally leads to a 8@=C r ratio 2 :+ and a fractional excretion of =a of 1 )4 and an elevated urine osmolarity.

(somewebsite) The clinical course of !7% is characteri'ed by the following three phasesC Phase 1. Onset !7% begins with the underlying clinical condition leading to tubular necrosis, for example hemorrhage, which reduces blood volume and renal perfusion. If ade.uate treatment is provided in this phase then the individualFs prognosis is good. Phase 2. Maintenance ! persistent decrease in G%7 and tubular necrosis characteri'es this phase. $ndothelial cell necrosis and sloughing lead to tubular obstruction and increased tubular permeability. 8ecause of this, oliguria is often present during the beginning of this phase. $fficient elimination of metabolic waste, water, electrolytes, and acids from the body cannot be performed by the kidney during this phase. Therefore, a'otemia, fluid retention, electrolyte imbalance and metabolic acidosis occurs. The patient is at risk for heart failure and pulmonary edema during this phase because of the salt and water retention. Immune function is impaired and the patient may be anemic because of the suppressed erythropoietin secretion by the kidney and toxin,related shorter 78 life. Phase 3. Recovery 7enal function of the kidney improves .uickly the first five to twenty,five days of this phase. It begins with the recovery of the G%7 and tubular function to such an extent that 8@= and serum creatinine stabili'e. Improvement in renal function may continue for up to a year as more and more nephrons regain function.