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• BIOCHEMICAL INDICES 
OF WATER-MINERAL 
METABOLISM
• Patients may develop lethargy, 
weakness, confusion, delirium, and 
seizures, especially in the presence of 
an abnormal serum sodium 
concentration. 
• Muscle weakness occurs in patients 
with severe hypokalemia, hyperkalemia, 
and hypophosphatemia; 
• Сonfusion, seizures, and coma may 
develop in those with severe 
hypercalcemia.
• In addition to taking a careful history, 
the diagnosis and treatment of fluid and 
electrolyte disorders are based on: 
• 1) assessment of total body water and 
its distribution 
• 2) serum electrolyte concentrations 
• 3) urine electrolyte conntrations 
• 4) serum osmolality
Body Water 
• Two-thirds of total body water (40 % of body 
weight) is intracellular fluid (ICF), while one-third 
(20 % of body weight) is extracellular fluid 
(ECF). 
• Water may be lost from either or both of the 
fluid compartments. 
• One -fourth of extracellular fluid (5% of 
body weight) is retained within the blood vessels 
as plasma (effective circulating volume)
• Effective circulating volume 
may be assessed by physical 
examination (blood pressure, 
pulse rate, jugular vein dilation).
Serum Electrolytes
Evaluation of Urine 
• Fractional excretion (Fe) of an 
electrolyte X (Fex) is calculated using a 
random urine sample with simultaneously 
obtained serum samples for X and cre­atinine 
(Cr). 
• Fex(%) = UrineX/SerumX × 100 
Urine Cr/Serum Cr
Serum Osmolality 
• Serum osmolality (normally 285-295 
mosm/kg) can be calculated from the 
following formula: 
• Osmolality = 2(Na+ mEq/L) + Glucose mg/dL + BUN 
mg/dL 
18 
2.8
• "Osmoles per kilo­gram 
of 
water" is osmolality; "osmoles 
per liter of solution" is 
osmolarity.
HYPONATREMIA 
• Hyponatremia (defined as a serum 
sodium concentration less than 130 
mEq/L) is the most common elec­trolyte 
abnormality observed in a 
general hospitalized population, seen 
in about 2 % of patients.
• Isotonic hyponatremia can be seen with 
hyperlipidemia and hyperproteinemia. Because 
of marked increases, lipids (chylomicrons, 
triglycerides, which make the blood visibly 
lipemic, and very occasionally cholesterol, 
which may not make the blood visibly lipemic) 
and proteins (> 10 g/dL, eg, intravenous 
immunoglobulin therapy) occupy a 
disproportionately large portion of the plasma 
volume. 
• Plasma osmolality remains normal because its 
measurement is unaffected by the lipids and 
proteins.
• Because the sodium 
concentration in the plasma 
water is actually normal, 
hyperlipidemia and 
hyperproteinemia cause so-called 
"pseudohyponatremia."
• Hypertonic hyponatremia is most commonly 
seen with hyperglycemia. 
• When blood glucose becomes acutely elevated, 
water is drawn from the cells into the 
extracellular space, diluting the serum sodium. 
• The plasma sodium level falls 2 mEq/L for 
every 100 mg/dL rise when the glucose 
concentration is between 200 and 400 mg/dL. 
If the glucose concentration is above 400 
mg/dL, the plasma sodium concentration falls 
4 mEq/L for every 100 mg/dL rise in glucose.
HYPERNATREMIA 
• An intact thirst mechanism usually 
prevents hypernatremia (> 145 mEq/L). 
Thus, whatever the underlying disorder 
(eg, dehydration, lactulose or mannitol 
therapy, central and nephrogenic diabetes 
insipidus), excess water loss can cause 
hypernatremia only when adequate water 
intake is not possible, as with unconscious 
patients
• A. Symptoms and Signs 
• When dehydration exists, orthostatic 
hypotension and oliguria are typical 
findings. Because water shifts from the 
cells to the intravascular space to 
protect volume status, these symptoms 
may be delayed. Hyperthermia, delirium, 
and coma may be seen with severe 
hyperosmolality.
• B. Laboratory Findings 
• 1. Urine osmolality > 400 mosm/kg. Renal 
water-conserving ability is functioning. 
• a. Nonrenal losses. Hypernatremia will 
develop if water ingestion fails to keep up 
with hypotonic losses from excessive 
sweating, exertional losses from the 
respiratory tract, or through stool water. 
Lactulose causes an osmotic diarrhea with loss 
of free water. 
• b. Renal losses. Whereas diabetic 
hyperglycemia can cause pseudohyponatremia, 
progressive volume depletion from the 
osmotic di­uresis 
of glycosuria can result in 
true hypernatremia. Osmotic diuresis can 
occur with the use of mannitol or urea.
• 2. Urine osmolality < 250 mosm/kg. A 
dilute urine with osmolality less than 
250 mosm/kg with hypernatremia is 
characteristic of central and 
nephrogenic diabetes insipidus. 
Nephrogenic diabetes insipidus, seen 
with lithium or demeclocycline therapy, 
after relief of prolonged urinary tract 
obstruction, or with interstitial 
nephritis, results from renal 
insensitivity to ADH.
Choice of Type of Fluid 
for Replacement 
• Hypernatremia with hypovolemia— 
Severe hypovolemia should be treated 
with isotonic (0.9%) saline to restore the 
volume deficit and to treat the 
hyperosmolality, since the osmolality of 
isotonic saline (308 mosm/kg) is often 
lower than that of the plasma. This 
should be followed by 0.45% saline to 
replace any remaining free water deficit.
• Hypernatremia with euvolemia—Water 
drinking or 5% dextrose and water 
intravenously will result in excretion of 
excess sodium in the urine. If die GFR is 
decreased, diuretics will increase 
urinary sodium excre­tion 
but may 
impair renal concentrating ability, 
increas­ing 
the quantity of water that 
needs to be replaced.
• Hypernatremia with hypervolemia— 
Treatment consists of providing water 
as 5% dextrose in water to reduce 
hyperosmolality, but this will expand 
vascular volume. Thus, loop diuretics 
such as furosemide (0.5-1 mg/kg) 
should be administered intravenously 
to re­move 
the excess sodium. In 
severe renal insufficiency, 
hemodialysis may be necessary.
HYPOKALEMIA 
• A. Symptoms and Signs 
• Muscular weakness, fatigue, and muscle 
cramps are frequent complaints in mild to 
moderate hypokale­mia. 
Smooth muscle 
involvement may result in consti­pation 
or 
ileus. Flaccid paralysis, hyporeflexia, 
hypercapnia, tetany, and rhabdomyolysis 
may be seen with severe hypokalemia (< 2.5 
mEq/L).
• B. Laboratory Findings 
• The electrocardiogram (ECG) shows 
decreased ampli­tude 
and broadening of 
T waves, prominent U waves, premature 
ventricular contractions, and depressed 
ST segments. Hypokalemia also 
increases the likelihood of digitalis 
toxicity. Thus, in patients with heart 
dis­ease, 
hypokalemia induced by 
certain drugs such as β2-adrenergic 
agonists and diuretics may impose a sub­stantial 
risk
HYPERKALEMIA 
• Many cases of hyperkalemia are 
spurious or associated with acidosis 
(Table 21-6). The common practice of 
repeatedly clenching and unclenching 
a fist during venipuncture may raise 
the potassium concentration by 1-2 
mEq/L by causing acidosis and 
consequent po­tassium 
loss from cells
Biochemical indices of water mineral metabolism
Biochemical indices of water mineral metabolism
Biochemical indices of water mineral metabolism

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Biochemical indices of water mineral metabolism

  • 1. • BIOCHEMICAL INDICES OF WATER-MINERAL METABOLISM
  • 2. • Patients may develop lethargy, weakness, confusion, delirium, and seizures, especially in the presence of an abnormal serum sodium concentration. • Muscle weakness occurs in patients with severe hypokalemia, hyperkalemia, and hypophosphatemia; • Сonfusion, seizures, and coma may develop in those with severe hypercalcemia.
  • 3. • In addition to taking a careful history, the diagnosis and treatment of fluid and electrolyte disorders are based on: • 1) assessment of total body water and its distribution • 2) serum electrolyte concentrations • 3) urine electrolyte conntrations • 4) serum osmolality
  • 4. Body Water • Two-thirds of total body water (40 % of body weight) is intracellular fluid (ICF), while one-third (20 % of body weight) is extracellular fluid (ECF). • Water may be lost from either or both of the fluid compartments. • One -fourth of extracellular fluid (5% of body weight) is retained within the blood vessels as plasma (effective circulating volume)
  • 5.
  • 6. • Effective circulating volume may be assessed by physical examination (blood pressure, pulse rate, jugular vein dilation).
  • 8. Evaluation of Urine • Fractional excretion (Fe) of an electrolyte X (Fex) is calculated using a random urine sample with simultaneously obtained serum samples for X and cre­atinine (Cr). • Fex(%) = UrineX/SerumX × 100 Urine Cr/Serum Cr
  • 9. Serum Osmolality • Serum osmolality (normally 285-295 mosm/kg) can be calculated from the following formula: • Osmolality = 2(Na+ mEq/L) + Glucose mg/dL + BUN mg/dL 18 2.8
  • 10. • "Osmoles per kilo­gram of water" is osmolality; "osmoles per liter of solution" is osmolarity.
  • 11.
  • 12.
  • 13. HYPONATREMIA • Hyponatremia (defined as a serum sodium concentration less than 130 mEq/L) is the most common elec­trolyte abnormality observed in a general hospitalized population, seen in about 2 % of patients.
  • 14.
  • 15. • Isotonic hyponatremia can be seen with hyperlipidemia and hyperproteinemia. Because of marked increases, lipids (chylomicrons, triglycerides, which make the blood visibly lipemic, and very occasionally cholesterol, which may not make the blood visibly lipemic) and proteins (> 10 g/dL, eg, intravenous immunoglobulin therapy) occupy a disproportionately large portion of the plasma volume. • Plasma osmolality remains normal because its measurement is unaffected by the lipids and proteins.
  • 16. • Because the sodium concentration in the plasma water is actually normal, hyperlipidemia and hyperproteinemia cause so-called "pseudohyponatremia."
  • 17.
  • 18. • Hypertonic hyponatremia is most commonly seen with hyperglycemia. • When blood glucose becomes acutely elevated, water is drawn from the cells into the extracellular space, diluting the serum sodium. • The plasma sodium level falls 2 mEq/L for every 100 mg/dL rise when the glucose concentration is between 200 and 400 mg/dL. If the glucose concentration is above 400 mg/dL, the plasma sodium concentration falls 4 mEq/L for every 100 mg/dL rise in glucose.
  • 19. HYPERNATREMIA • An intact thirst mechanism usually prevents hypernatremia (> 145 mEq/L). Thus, whatever the underlying disorder (eg, dehydration, lactulose or mannitol therapy, central and nephrogenic diabetes insipidus), excess water loss can cause hypernatremia only when adequate water intake is not possible, as with unconscious patients
  • 20. • A. Symptoms and Signs • When dehydration exists, orthostatic hypotension and oliguria are typical findings. Because water shifts from the cells to the intravascular space to protect volume status, these symptoms may be delayed. Hyperthermia, delirium, and coma may be seen with severe hyperosmolality.
  • 21. • B. Laboratory Findings • 1. Urine osmolality > 400 mosm/kg. Renal water-conserving ability is functioning. • a. Nonrenal losses. Hypernatremia will develop if water ingestion fails to keep up with hypotonic losses from excessive sweating, exertional losses from the respiratory tract, or through stool water. Lactulose causes an osmotic diarrhea with loss of free water. • b. Renal losses. Whereas diabetic hyperglycemia can cause pseudohyponatremia, progressive volume depletion from the osmotic di­uresis of glycosuria can result in true hypernatremia. Osmotic diuresis can occur with the use of mannitol or urea.
  • 22. • 2. Urine osmolality < 250 mosm/kg. A dilute urine with osmolality less than 250 mosm/kg with hypernatremia is characteristic of central and nephrogenic diabetes insipidus. Nephrogenic diabetes insipidus, seen with lithium or demeclocycline therapy, after relief of prolonged urinary tract obstruction, or with interstitial nephritis, results from renal insensitivity to ADH.
  • 23. Choice of Type of Fluid for Replacement • Hypernatremia with hypovolemia— Severe hypovolemia should be treated with isotonic (0.9%) saline to restore the volume deficit and to treat the hyperosmolality, since the osmolality of isotonic saline (308 mosm/kg) is often lower than that of the plasma. This should be followed by 0.45% saline to replace any remaining free water deficit.
  • 24. • Hypernatremia with euvolemia—Water drinking or 5% dextrose and water intravenously will result in excretion of excess sodium in the urine. If die GFR is decreased, diuretics will increase urinary sodium excre­tion but may impair renal concentrating ability, increas­ing the quantity of water that needs to be replaced.
  • 25. • Hypernatremia with hypervolemia— Treatment consists of providing water as 5% dextrose in water to reduce hyperosmolality, but this will expand vascular volume. Thus, loop diuretics such as furosemide (0.5-1 mg/kg) should be administered intravenously to re­move the excess sodium. In severe renal insufficiency, hemodialysis may be necessary.
  • 26.
  • 27. HYPOKALEMIA • A. Symptoms and Signs • Muscular weakness, fatigue, and muscle cramps are frequent complaints in mild to moderate hypokale­mia. Smooth muscle involvement may result in consti­pation or ileus. Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis may be seen with severe hypokalemia (< 2.5 mEq/L).
  • 28. • B. Laboratory Findings • The electrocardiogram (ECG) shows decreased ampli­tude and broadening of T waves, prominent U waves, premature ventricular contractions, and depressed ST segments. Hypokalemia also increases the likelihood of digitalis toxicity. Thus, in patients with heart dis­ease, hypokalemia induced by certain drugs such as β2-adrenergic agonists and diuretics may impose a sub­stantial risk
  • 29.
  • 30. HYPERKALEMIA • Many cases of hyperkalemia are spurious or associated with acidosis (Table 21-6). The common practice of repeatedly clenching and unclenching a fist during venipuncture may raise the potassium concentration by 1-2 mEq/L by causing acidosis and consequent po­tassium loss from cells