Osmotic gradient develops across blood brain barrier causing water to move into brain. -Two protective mechanisms: - Movement of interstitial fluid into the CSF - Loss of cellular potassium and organic osmolytes Acute hyponatremia (Na < 120) developing < 24 hours OR rate of fall of > 0.5 meq/L per hour: -Muscular twitching, seizures, coma Acute severe hyponatremia with CNS changes – mortality rate 50%. CPM – correction of hyponatremia faster than the brain can recover solute.
Protective mechanism – ADH - Released in response to decreased blood volume - Increased ADH present in almost all hyponatremic conditions - Increases water reabsorption by renal tubules (seems counterproductive) - Potent vasoconstrictor: - Increased peripheral vascular resistance - Increased blood flow to liver and kidneys at expense of skin and muscle
Movement of water from ICF to ECF dilutes the ECF. Volume replacement with sodium containing fluids.
Results in intracellular volume expansion with derangement of cellular function. Obtain serum and urine electrolytes Obtain plasma and urine osmolality
Clinical manifestations due to volume deficit rather than hyponatremia.
Unequal loss of electrolyte and water loss produces a contracted ECF volume with hyponatremia. Maintained by effect of volume depletion on kidneys inhibiting free water excretion. - Decreased GFR. - Increased proximal tubular resorption of solute and water. - Decreased deliver of fluid to the diluting segment of the nephron. - ADH released by nonosmotic stimuli.
Slightly expanded ECF No clinical edema, near normal total body Na Sx usually relative to CNS hypotonicity
CHF – perceived as low flow state, stimulates ADH Nephrotic Syndrome – low serum protein due to urinary loss Cirrhosis – low intravascular oncotic pressure due to decreased protein production
Comatose or bedridden patients susceptible since they are unable to obtain adequate fluid. All hypernatremic states are hyperosmolar.
ADH response to low volume and hypertonicity UO < 20 mL/h
Doughy abdominal skin when pinched between fingers Accumulation of amino acids in the brain
Iatrogenic Na – NaHCO3, hypertonic saline Mineralocorticoid/Glucocorticoid excess Primary aldosternoism Cushing’s syndrome Ectopic ACTH hormone production
Iatrogenic Na – NaHCO3, hypertonic saline Mineralocorticoid/Glucocorticoid excess Primary aldosternoism Cushing’s syndrome Ectopic ACTH hormone production
Mortality rate Overall 10% 25 to 50% if plasma osmolality > 350
Mortality rate Overall 10% 25 to 50% if plasma osmolality > 350
Cerebral edema due to presence of idiogenic osmoles
6.5 to 7.5 meq/L 7.5 to 8.0 meq/L 10 to 12 meq/L
Membrane stabilization Effect w/in 1 to 3 min, active for 1 hour Central line Glucose/Insulin 50 g glucose with 5-10 units regular insulin Onset 30 min, durastion 4 to 6 hrs NaHCO3 Onset 5 to 10 min, duration 1 to 2 hrs
Membrane stabilization Effect w/in 1 to 3 min, active for 1 hour Central line Glucose/Insulin 50 g glucose with 5-10 units regular insulin Onset 30 min, durastion 4 to 6 hrs NaHCO3 Onset 5 to 10 min, duration 1 to 2 hrs Kaexalate Given with Sorbital to avoid constipating effects and speed bowel transit time
Most abundant mineral in the body
In presence of albumin, total Ca may be low but ionized Ca remains normal Vit D deficiency Sunlight/dietary deficiency Malabsorption (Gastrectomy)
Chvostek – Twitch at corner of mouth when tapped over facial nerve just in front of ear. Trosseau – Carpal spasm produced when BP cuff to upper arm maintains a pressure above systolic for 3 min. Fingers spastically extend at the IP joints and flex at the MCP joints. Wrist flexed, forearm pronated,
Give over 10 to 20 min, then drip 1g CaCl over 6-12 hrs