Common misconceptions and mistakes
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Behaving as if humans are “brittle” with regard to volume status—namely that they transition quickly from total body volume overload to volume depletion (in a dangerous way)
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Not resuscitating hypovolemic individuals for fear that the sodium correction will be too rapid
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Treating hyponatremia based on the calculated Na + deficit and desired rate of increase
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Treating hypernatremia based on the calculated free water deficit, giving half back in the first 24 hours and the remaining half over the next 24–48 hours
Volume status and tonicity
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Life evolved in saltwater; thus humans need constant access to water and salt
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Normal euvolemic (nonedematous) humans store ~ 10 L of saltwater in the interstitium of their bodies, with ~ 3–4 L in the interstitium of their extremities (lower extremity > upper extremity in the upright position)
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This provides at least a 48-hour buffer against dehydration and volume depletion if water is scarce
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The kidneys regulate volume status by adjusting glomerular filtration rate (GFR) and sodium balance, manipulating the amount of NaCl in the urine
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The hypothalamus, pituitary (via anti-diuretic hormone [ADH] secretion and thirst), and the kidneys (by adjusting water reabsorption, responding to ADH) regulate tonicity by manipulating the amount of water or concentration of the urine
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Maintenance of adequate circulating volume (sodium balance ) is the body’s ultimate priority
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Therefore tonicity is sacrificed to maintain adequate volume (resulting in Hyper- and hyponatremia presentations)
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Tonicity (practically speaking, cell size ) is dictated by water balance
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Dehydration is a state of inadequate body water, increased tonicity, and shrunken cells, ultimately causing central nervous system (CNS) dysfunction
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Total body volume status is dictated by sodium balance
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hypovolemia equals total body sodium depeltion, implying = no reserve saltwater in the interstitium, no edema anticipated
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euvolemia equals normal sodium balance , implying > 5 L of reserve saltwater in the interstitium, no edema anticipated
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hypervolemia equals total body sodium overload , implying excessive saltwater in the interstitium, manifesting as peripheral edema
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Volume overload is a problem of NaCl intake, not water intake
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To illustrate, if a human eats 10 g of NaCl in a day he or she will:
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Drink, responding to thirst as tonicity threatens to increase
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Experience a pressure natriuresis in an attempt to prevent volume overload
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Gain 1–2 lbs as he or she expands his or her interstitial fluid volume to the 10 + L maximum of interstitial reserve (often manifesting as sock edema)
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Alternatively, if a human drinks 10 L of water in a day he or she will:
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Urinate 9.5 L of a dilute urine to prevent decreased tonicity
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Not gain weight (or manifest edema)
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The Normal Homeostasis of Volume Status and Sodium Balance
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Hypovolemia leads to a decreased circulating volume, perceived by the kidney as a decreased renal blood flow
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Decreased renal blood flow causes a decreased GFR with subsequent activation of the renin–angiotensin–aldosterone system, leading to:
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Decreased urine output
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Increased sodium reabsorption to conserve salt (urine Na + < 10 mmol/L)
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Increased ADH secretion concentrating the urine to conserve water (> 300 mOsm/kg)
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Hypervolemia leads to an increased circulating volume perceived by the kidney as increased renal blood flow
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Increased renal blood flow leads to an increased GFR leading to sodium spillage “a.k.a. pressure natriuresis”
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Increased urine output
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Sodium spillage to return volume status to normal (urine Na + > 20 mmol/L)
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Decreased ADH secretion diluting the urine to remove water (< 100 mOsm/kg)
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The normal homeostasis of tonicity and water balance
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The hypothalamus, pituitary, and the kidney attempt to maintain tonicity homeostasis by manipulating ADH
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Increased tonicity (ie, hypernatremia) causes increased ADH secretion, concentrating the urine
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Decreased tonicity (ie, hyponatremia) causes decreased ADH secretion, diluting the urine
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Inadequate water intake leads to an increased serum sodium and thus increased tonicity
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Increased tonicity is perceived by the hypothalamus, which creates thirst and activates ADH secretion from the pituitary, leading to:
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Increased water intake
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Increased water reabsorption in the collecting tubule
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Concentrated urine (> 300 mOsm/kg )
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Water excess leads to decreased serum sodium and thus decreased tonicity
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Decreased tonicity inhibits thirst (hypothalamus) and suppresses pituitary ADH secretion, leading to:
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Decreased water intake
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Decreased water reabsorption in the collecting tubule, Increasing urine output
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Dilute urine (< 100 mOsm/kg)
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The pathophysiology and evaluation of hyponatremia
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Hyponatremia represents a state of excessive plasma water
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This is either a result of volume depletion (in an attempt to maintain circulating volume), impaired water excretion (syndrome of inappropriate antidiuretic hormone secretion [SIADH]), or excessive water intake (overcoming the body’s ability to excrete water)
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The most common causes of hyponatremia are:
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Hypovolemic (gastrointestinal [GI] losses) > dilutional (occurring as a complication of volume overload) > SIADH > low sodium intake > excessive water ingestion
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Symptoms of hyponatremia are caused by decreased tonicity
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Decreased extracellular tonicity creates an osmotic gradient, causing water to shift into cells (intracellular tonicity, which is based on potassium, remains normal)
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This shift of water into cells makes them swell (poorly tolerated by central neurons)
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Causing headache, confusion, seizure, coma, and even herniation (water intoxication)
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An acute drop in serum sodium causes:
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Confusion (Na + ≤ 125)
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Seizure, coma, and herniation (Na + ≤ 115)
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A chronic drop in serum sodium is often asymptomatic until the Na + ≤ 115 mEq/L
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When Na + drops gradually, brain cells compensate (over days or weeks) by reducing intracellular osmolality
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This poses a danger if chronic hyponatremia is rapidly corrected
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The previous compensatory decreased intracellular osmolality in the neurons causes them to shrink rapidly as extracellular tonicity normalizes
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This is associated with the devastating osmotic demyelination syndrome (the disease formerly known as “central pontine myelinolysis”)
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The first step in evaluating a low- serum sodium is establishing total body volume status (ie, edema vs no edema) ( Fig. 22.1 )
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The next step is obtaining a urine Na + and a urine osmolality (obtain before IVF is given or expect some Na + spillage)
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Finally, observe the urine output
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Edematous patients are volume overloaded from either heart failure, cirrhosis, or renal failure
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Hyponatremia occurring with volume overload is dilutional :
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Heart failure or cirrhosis lead to decreased renal blood flow and decreased GFR (which directly impairs water excretion)
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Decreased renal blood flow is erroneously perceived by the kidneys as hypovolemia, causing activation of the renin–angiotensin–aldosterone system (which causes sodium retention)
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Angiotensin II leads to nonosmolar -mediated ADH secretion, sacrificing tonicity in an erroneous attempt to increase circulating volume
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Together this signaling causes:
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Low urine output from the “cardio-renal” physiology previously described
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Concentered urine (> 300 mOsm kg) with a low Na + (< 10 mEq/L)
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A low urine osmolality implies concomitant psychogenic polydipsia
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A high urine Na + implies loop diuretic use or acute tubular necrosis (ATN)
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Treat with diuresis (loop diuretics) and water restriction
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Renal failure may impair free water excretion directly
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Treat with loop diuretics, water restriction, and consider renal replacement therapy
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Nonedematous patients with hyponatremia are suffering from volume depletion, impaired water excretion, very low Na + intake, or very high water intake
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Volume depletion (suggested by hypotension, tachycardia, and low urine output )
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Volume depletion (insufficient Na + ) leads to decreased renal blood flow
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This is correctly perceived by the kidneys as hypovolemia, resulting in the activation of the renin–angiotensin system and leading to:
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Nonosmolar -mediated ADH secretion, sacrificing tonicity in an appropriate attempt to increase circulating volume
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Concentered urine (> 300 mOsm/kg)
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Low urine output
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Hypovolemic hyponatremia is caused by NaCl loss (either renal or extrarenal)
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Extrarenal NaCl loss is seen with vomiting, diarrhea, and profound sweating
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Concentrated urine, low urine sodium , and low urine output
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Renal NaCl loss is seen with thiazide diuretics , salt-wasting syndromes, adrenal insufficiency, and distal renal tubular acidosis (RTA)
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Euvolemic patients with hyponatremia either have impaired water excretion from inappropriate ADH secretion (ie, SIADH ) or engage in such voluminous water intake (ie, nonosmotic polydipsia) that they overcome their ability to excrete it (typically > 15 L a day)
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Inappropriately secreted ADH causes water reabsorption from the collecting tubules, leading to:
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An inappropriately concentrated urine (> 300 mOsm/kg)
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A decreased serum sodium (and tonicity)
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An increased circulating volume, increasing renal blood flow and GFR leading to sodium spillage (ie, a high urine Na + [> 20 mEq/L])
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SIADH is common and is caused by myriad medications (eg, selective serotonin reuptake inhibitors [SSRIs]) and conditions, from pulmonary, CNS or thyroid disease to pain
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Very low Na + intake (a.k.a. “tea and toast” or “beer potomania”)
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Very low sodium intake causes decreased tonicity, leading to:
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Inhibition of ADH secretion and a dilute urine (< 100 mOsm/kg)
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Urine Na + remains low because of total body Na + depletion
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Urine output remains normal
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Very low sodium intake is a phenomenon of individuals who eat only “tea and toast” (ie, a diet devoid of salt) or who consume only alcohol (beer potomania)
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Excessive water intake exists in a spectrum, from acute water intoxication to chronic psychogenic polydipsia
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An acute ingestion of a large volume of water (5–10 L) in an hour or two, or a chronic ingestion (10–15 L day), can overcome the body’s maximum water excreting ability, causing decreased tonicity and leading to:
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Osmotic-mediated inhibition of ADH secretion and a dilute urine (< 100 mOsm/kg)
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Urine Na + that remains low (< 10 mEq/L) because plasma volume does not expand when ADH is inhibited (as almost all ingested water is excreted)
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High urine output (500–1000 mL/hr) because ADH is appropriately inhibited
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An acute, massive water ingestion is typically seen in “water-drinking contests” or psychiatric illness
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Chronic, daily ingestion of large volumes of water (> 10 L every 24 hours) is a psychiatric illness known as psychogenic polydipsia
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Assessment of urine output is critical to the evaluation of both volume and ADH status ( Fig. 22.2 )
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Hypovolemic patients have low urine output
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The transition from hypovolemia to euvolemia is demonstrated by the resolution of oliguria (ie, resuscitation is over when the individual starts to urinate)
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Volume-overloaded patients with cardiorenal or cirrhotic physiology will also have low urine output
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When ADH is inhibited , urine volume is high , and dilute
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