dysnatremias Flashcards
ICF=
66% tbw
ECF=
33 % tbw
blood volume=
12% tbw
hypovolemic hypernatremia
most common. renal losses (osmotic diuresis by means of glucose, urea, mannitol use). insensible losses (through sweating, fever, respiration). GI losses (through diarrhea).
euvolemic hypernatremias
renal losses (through diabetes insipidus nephrogenic or central). variable hypothalamic disorder (primary hypodipsia, resetting of osmostat). normal intravascular status but sodium is high
hypervolemic hypernatremia
hypertonic saline administration. sodium bicarbonate administration. primary hyperaldosteronism. Too much na related fluid such as IV hypertonic saline.
the 2 defense mechanisms against hypernatremias
stimulation of ADH release (resulting in maximal urinary concentraton) and thirst.
hypernatremia
almost never found in an alert patient who has access to water and a normal thirst mechanism.
concentration of urine requires two basic conditions:
a hypertonic medullary interstitium. osmotic equilibrium of urine in the collecting duct that has the hypertonic interstitium (requiring ADH).
Central diabetes insipidus
occurs when secretion of ADH is impaired through disruption of the hypothlamic neclei, osmoreceptors. through disruption supraopticohypophysial tract.
central DI common causes
head trauma, hypoxic or ischemic encephalopathy, idiopathic conditions
nephrogenic diabetes insipidus
the countercurrent mechanism in the kidney is disrupted or the ability to respond to ADH is impaired. lithium. osmotic diuresis. sickle cell anemia.
clinical manifestations of hypernatremia
neurologic manifestations. lethargy, weakness, irritability, hyperreflexia, seizures, coma, and even death, are the result. patients with DI usually do not present with neurologic sxs because of the powerful thirst mechanism which protects them from hypernatremia. instead, these pts complain of polydipsia, polyuria, and nocturia.
diagnosis of hypernatremia
H and P:
recent fluid losses, alteration in mental status, and thirst.
assessing the pts volume status and measuring urine osmolality and urine sodium concentration can be helpful in establishing the cause of hypernatremias and in guiding therapy
treatment of hypernatremia
rapid correction should be avoided because of the brain’s adaptive response to hypernatremia and the potential risk of cerebral edema. the current recommendation is to lower the serum sodium concentration by about .5 meq/l per hour and to replace no more than half the water deficit in the first 24 hours.
hypovolemic hypernatremia treatment
normal saline solution is indicated initially to correct the intravascular volume deficit. when that is accomplished, more hypotonic fluids can be used.
hypervolemic hypernatremia treatment
removing the source of salt excess, administering diuretics, and replacing water are important to successful therapy.
manifestations of hyponatremia
correlate with the serum sodium concentration and more important, with how rapidly the condition developed. anorexia, nausea, lethargy, and apathy. more advanced sxs include disorientation, agitation, seizures, depressed reflexes, focal neurologic deficits.
diagnosis of hyponatremia
important hx: medications (particularly thiazide diuretics), recent vomiting, diarrhea or excessive sweating with hypotonic fluid ingestion, recent surgery, and a history of psychiatric illness, CHF, cirrhosis, or nephrotic syndrome with renal failure.
hyponatremia physical exam findings
assessment of volume status. orthostatic vital signs, skin turgor, mucous membrane appearnace, jugular venous distension, findings of edema, and wedge pressure and central venous pressure.
euvolemic hyponatremia
adh excess (through syndrome of inappropriate ADH, use of thiazide diuretics or oral hypoglycemic agents). pain, postoperative state, cortisol deficiency. hypothyroidism. decreased solute intake. psychogenic polydispsia. resetting of osmostat (pregnancy, psychiatric disorders)
hypovolemic special mention
pyschogenic plydispsia. ingest rapidly too much water. related to psychiatric disease or psychiatic drugs. rarely see on other drugs that cause severe dryness of the mouth.
treatment failure central pontine myelinolysis
demyelination of the pons. mutism, dysphasia, spastic quadriparesis, psedobulbar palsy, delirium, coma, and even death. Key point: raising the serum sodium concentration more than 25 or to a normal or above normal level in the first 48 hours increases the liklihood of central pontine myelinolysis.
treatment of hyponatremia
eliminate the cause. restrict water. normal saline. may correct up to about 120 fairly rapidly then slow down and increase sodium by about 12 meq every 12-24 hours.
