Chapter 046. Sodium and Water (Part 4) ppt

Chapter 046. Sodium and Water (Part 4) Extrarenal Nonrenal causes of hypovolemia include fluid loss from the gastrointestinal tract, skin, and respiratory system and third-space accumulations (burns, pancreatitis, peritonitis). Approximately 9 L of fluid enters the gastrointestinal tract daily, 2 L by ingestion and 7 L by secretion. Almost 98% of this volume is reabsorbed so that fecal fluid loss is only 100–200 mL/d. Impaired gastrointestinal reabsorption or enhanced secretion leads to volume depletion. Since gastric secretions have a low pH (high H + concentration) and biliary, pancreatic, and intestinal secretions are alkaline (high HCO 3 – concentration), vomiting and diarrhea are often accompanied by metabolic alkalosis and acidosis, respectively. Water evaporation from the skin and respiratory tract contributes to thermoregulation. These insensible losses amount to 500 mL/d. During febrile illnesses, prolonged heat exposure, exercise, or increased salt and water loss from skin, in the form of sweat, can be significant and lead to volume depletion. The Na + concentration of sweat is normally 20–50 mmol/L and decreases with profuse sweating due to the action of aldosterone. Since sweat is hypotonic, the loss of water exceeds that of Na + . The water deficit is minimized by enhanced thirst. Nevertheless, ongoing Na + loss is manifest as hypovolemia. Enhanced evaporative water loss from the respiratory tract may be associated with hyperventilation, especially in mechanically ventilated febrile patients. Certain conditions lead to fluid sequestration in a third space. This compartment is extracellular but is not in equilibrium with either the ECF or the ICF. The fluid is effectively lost from the ECF and can result in hypovolemia. Examples include the bowel lumen in gastrointestinal obstruction, subcutaneous tissues in severe burns, retroperitoneal space in acute pancreatitis, and peritoneal cavity in peritonitis. Finally, severe hemorrhage from any source can result in volume depletion. Pathophysiology ECF volume contraction is manifest as a decreased plasma volume and hypotension. Hypotension is due to decreased venous return (preload) and diminished cardiac output; it triggers baroreceptors in the carotid sinus and aortic arch and leads to activation of the sympathetic nervous system and the renin- angiotensin system. The net effect is to maintain mean arterial pressure and cerebral and coronary perfusion. In contrast to the cardiovascular response, the renal response is aimed at restoring the ECF volume by decreasing the GFR and filtered load of Na + and, most importantly, by promoting tubular reabsorption of Na + . Increased sympathetic tone increases proximal tubular Na + reabsorption and decreases GFR by causing preferential afferent arteriolar vasoconstriction. Sodium is also reabsorbed in the proximal convoluted tubule in response to increased angiotensin II and altered peritubular capillary hemodynamics (decreased hydraulic and increased oncotic pressure). Enhanced reabsorption of Na + by the collecting duct is an important component of the renal adaptation to ECF volume contraction. This occurs in response to increased aldosterone and AVP secretion and suppressed atrial natriuretic peptide secretion. Clinical Features A careful history is often helpful in determining the etiology of ECF volume contraction (e.g., vomiting, diarrhea, polyuria, diaphoresis). Most symptoms are nonspecific and secondary to electrolyte imbalances and tissue hypoperfusion and include fatigue, weakness, muscle cramps, thirst, and postural dizziness. More severe degrees of volume contraction can lead to end-organ ischemia manifest as oliguria, cyanosis, abdominal and chest pain, and confusion or obtundation. Diminished skin turgor and dry oral mucous membranes are poor markers of decreased interstitial fluid. Signs of intravascular volume contraction include decreased jugular venous pressure, postural hypotension, and postural tachycardia. Larger and more acute fluid losses lead to hypovolemic shock, manifest as hypotension, tachycardia, peripheral vasoconstriction, and hypoperfusion—cyanosis, cold and clammy extremities, oliguria, and altered mental status. Diagnosis A thorough history and physical examination are generally sufficient to diagnose the etiology of hypovolemia. Laboratory data usually confirm and support the clinical diagnosis. The blood urea nitrogen (BUN) and plasma creatinine concentrations tend to be elevated, reflecting a decreased GFR. Normally, the BUN:creatinine ratio is about 10:1. However, in prerenal azotemia, hypovolemia leads to increased urea reabsorption, a proportionately greater elevation in BUN than plasma creatinine, and a BUN:creatinine ratio of 20:1 or higher. An increased BUN (relative to creatinine) may also be due to increased urea production that occurs with hyperalimentation (high-protein), glucocorticoid therapy, and gastrointestinal bleeding. The appropriate response to hypovolemia is enhanced renal Na + and water reabsorption, which is reflected in the urine composition. Therefore, the urine Na + concentration should usually be <20 mmol/L except in conditions associated with impaired Na + reabsorption, as in acute tubular necrosis (Chap. 273). Another exception is hypovolemia due to vomiting, since the associated metabolic alkalosis and increased filtered HCO 3 – impair proximal Na + reabsorption. In this case, the urine Cl – is low (<20 mmol/L). The urine osmolality and specific gravity in hypovolemic subjects are generally >450 mosmol/kg and 1.015, respectively, reflecting the presence of enhanced AVP secretion. However, in hypovolemia due to diabetes insipidus, urine osmolality and specific gravity are indicative of inappropriately dilute urine. . Chapter 046. Sodium and Water (Part 4) Extrarenal Nonrenal causes of hypovolemia include fluid loss from the gastrointestinal tract, skin, and respiratory system and third-space. concentration) and biliary, pancreatic, and intestinal secretions are alkaline (high HCO 3 – concentration), vomiting and diarrhea are often accompanied by metabolic alkalosis and acidosis,. or increased salt and water loss from skin, in the form of sweat, can be significant and lead to volume depletion. The Na + concentration of sweat is normally 20–50 mmol/L and decreases with