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  • 1. Chapter 3: Disorders of Water Balance: Hyponatremia, Hypernatremia, and Polyuria (pp. 67-95) Plasma osmolality can be estimated from two times the plasma sodium concentration (PNa), b/c sodium salts comprise most of the extracellular osmoles: Plasma osmolality ≈ 2 x PNa The plasma osmolality is also equal to the osmolality of the total body water since the osmolality of almost all the body water compartments is the same. The osmolality of the total body water is equal to the ratio of total body solutes to total body water (TBW). The loss of potassium must be balanced by the movement of cation into the cell in order to maintain electroneutrality. The entry of sodium into the cells will tend to lower the plasma sodium concentration. This becomes an important concept with the replacement of intravenous fluids. Maintaining a relatively constant plasma sodium concentration and plasma osmolality is essential for maintance of cell volume, esp in the brain. Acute reduction in the plasma osmolality and plasma sodium concentration over 2 hrs creates an osmotic gradient that promotes the movement of water from the extracellular fluid into the brain. The ensuing cerebral edema leads to severe neurologic symptoms. The only way for the brain cell volume to fall toward nl with persistent hyponatriemia is for the cells to lose solutes, which will be followed by osmotic water loss. In general, only acute hyponatremia or hypernatremia produces neurologic symptoms (lethargy, seizures, coma) d/t cerebral edema and cerebral shrinkage, respectively. The subsequent adaptations that restore brain volume toward nl are so effective that, unless very severe, few if an symptoms are seen in pts with chronic changes in the plasma sodium concentration. The outcome, however, is different when the cerebral edema has been partially corrected by the loss of cell solutes. In this setting, rapid correction can reduce the brain volume below nl and produce an osmotic demyelination syndrome that may include findings of central pointine myelinolysis. This disorder, which may lead to irreversible severe neurologic damage, is characterized by paraparesis or quadriparesis, dysarthia (difficulty speaking), dysphagia (diff. swallowing), and coma. The aim of therapy is different in pts with symptomatic hypo- or hyper- natremia. In these settings, initially rapid correction is safe and may be life-saving. The plasma sodium concentration can at first be returned to nl at 1.5 to 2 mEq/L per hour until the symptoms resolve, followed by slower correction toward nl, again trying to keep the maximal daily change in the plasma sodium concentration from exceeding 12 mEq/L. Hyponatremia - one of the most common electrolyte disorder. Hyponatremia can be induced in only two ways: loss of sodium plus potassium (vomiting, diarrhea) the retention of ingested or infused water. Solute loss (as w/ vomiting or diarrhea) almost always occurs in an isosmotic fluid that has a sodium plus potassium concentration less than that of the plasma. Loss of these fluids cannot directly lower the plasma sodium concentration. Water retention leading to an excess of water in relation to solute is the common denominator in almost all hyponatremic states. The ingestion of water in nl subjects reduces the plasma osmolality and rapidly lowers ADH release, thereby allowing the excess water to be excreted in a dilute urine. The net effect is that water retention resulting in hyponatremia generally occurs only when there is a defect in renal water excretion. A rare exception occurs in pts (often schizophrenics) with primary polydipsia who drink such large volumes of fluid that they can overwhelm even the nl excretory capacity.
  • 2. Etiology -Disorders in which water excretion is impaired: A. Effective circulation volume depletion 1. g.i. losses 2. renal losses 3. skin losses 4. CHF 5. hepatic cirrhosis B. Thiazide diuretics C. Syndrome of inappropriate ADH secretion 1. virtually any neuropsychiatric disorder or severe apin with or without narcotic admin 2. 2. drugs: most often the oral hypoglycemic agent chloropropamide 3. ectopic prdtn by tumors: most often oat cell carcinoma of lung 4. postoperative pt, a response mediated by pain afferents 5. pulmonary diseases (uncommon) D. Advanced renal failure E. Cortisol deficiency F. Hypothryroidis -Primary polydipsia -Reset osmostat Underlying mechanisms responsible for hyponatremia in CHF, SIADH, and a reset osmostat are now to be discussed. CHF Increasing cardiac dysfxn is assoc w/ a progressive fall in CO that promotes the development of hyponatremia in two major ways: 1. the low CO leads to enhanced secretion of the three “hypovolemic hormones”: renin, norepi-, and ADH. ADH directly enhances water retention, whereas Angiotensin II and norepi- endue renal vasocontriction and lower renal bld flow, another factor that can impair water excretion 2. the hypovolemic stiumulus to ADH release also increases thirst. The ensuing elevation in water intake will further enhance the tendency to retain water. Pts w/ advanced CHFwho have a plasma sodium concentration below 137 mEq/L have a mean survival that is only one-half that of normonatremic pt with the same dis. A plasma [Na+] below 125 mEq/L is indicative of almost end-stage disease. SIADH Most often seen w/ neurologic dis, malignancy, and after major surgery. There is typically a gradual reduction in the plasma sodium concentration and most pts are asympt. It is important to emphasize that ADH alon cannot cause hyponatremia in the absence of a source of water to be retained. So aware of the pt who comes into the hosp with a tumor-induced dis with relatively nl plasma sodium b/c of decreased appetite limiting the amt of fluid intake. Once, admitted, however, i.v. fluids administration is begun, hyponatremia develops. Reset Osmostat A subset of pts with mild hyponatremia and SIADH have a reset osmostat. The characteristics of this disorder are determined by the almost nl fxning of the osmoreceptor and therefore of ADH release: - urine can be approp. diluted after a water load, as ADH secretion is shut off - the urine can be approp. concentrated if the plasma osmolality is raised by water restriction, as ADH secretion is increased - the plasma sodium concentration is stable
  • 3. Thus, these pts behave similarly to nl, but they have a reduced threshold for ADH release, occurring at a plasma sodium concentration of 125 mEq/L (nl is 138-140 mEq/L) The main clue to a reset osmostat is that the plasma sodium concentration varies w/in a narrow range of only a few mEq/: over many days of observation. Hyponatremia should not and cannot be treated in this pt. Attempting to raise plasma levels would induce intense thirst and ADH release. Therapy is therefore directed at correcting any underlying problems. Diagnosis 1. H and P 2. Plasma osmoliaty 3. Urine osmolality 4. Urine sodium concentration Plasma Osmolality Pseudohyponatremia can occur in hyperglycemia of uncontrolled DM. The rise in plasma glucose will increase plasma osmolaity and lead to osmotic water mvmt out of the cell and a dilutional reduction in the plasma sodium concentration. Correction of hyperglycemia with insulin will reverse the process and bring sodium levels toward nl. Urine Osmolality Pts w/ primary polydipsia are able to appropriately suppress ADH release, leading to excretion of max. dilute urine with osmolaltity below 100 mosmol/kg. Pts with higher urine osmol. have an impairment in water excretion that is usu. d/t presence of ADH. Urine Sodium Concentration Two major causes of true hyponatremia with inappr. high urine osmolality: 1. effective circulating volume depletion 2. SIADH These disorders are generally distinguished by measuring urine sodium concentration. Pts w/ SIADH are normovolemic and sodium excretion in the steady state is equal to intake. Since nl sodium concentration intake genereally is greater than 80 mEq/day, the urine sodium concentration is typically above 40 mEq/L. Therapy 1. water restriction in edematous pt with CHF, hepatic cirrhosis, or renal disease. These pts also have too much sodium and therefore should not be given sodium unless they have sympt hyponatremia. 2. isotonic saline or oral salt in pts w/ true volume depletion d/t g.i. losses or blding. This regimine will correct hyponatremia in two ways. 1. sodium concentration in saline (154 mEq/L) is higher than plasma 2. saline will reverse volume depletion to eventually remove hypovolemic stimulus to ADH allowing excess water to be excreted 3. water restriction in pts with primary polydipsia and in most pts with SIADH 4. cortisol or thyroid hormone replacement in pts w/ adrenal insufficiency or hypothyroidism 5. no therapy for a reset osmostat Volume distribution of plasma sodium concentration is equal to the TBW which is about 60 and 50% of lean body weight in men and women, respectively. And sodium deficit equals volume of distribution x sodium deficit per liter. Hypernatremia Hypernatremia is defined as plasma sodium concentration above 146 mEq/L. In almost all cases, elevation in the plasma sodium is induced by unreplaced water losses. The nl defense against elevated sodium in the plasma is stimulation of ADH and thirst. Although ADH is important, it is thirst that provides the ultimate protection against hypernatremia. It is when this thirst cannot normally be expressed: as such in mentally altered adults or in children unable to ask for water, that hypernatremia occurs.
  • 4. Etiology Major Causes of Hypernatremia: 1. Increased water losses that are unreplaced d/t impaired thirst A. insensible and sweat losses: fever, resp infxns B. urinary losses: central or nephrogenic diabetes insipidus, osmotic diuresis d/t glucose or mannitol C. g.i. losses D. hypothalamic lesions affecting thirst center (rare) 2. Admin of hypertonic sodium chloride or sodium bicarbonate Most comoon cause of hypernatremia is infection in the elderly pt wit diminished mental status. Loss of water in excess sodium plus potassium also occurs in uncontrolled DM. The plasma glucose is so high that the filtered glucose load exceeds glucose reabsorptive capacity in proximal tubule. The ensuing presence of large amts of nonreabsorbed glucose in tubular lumen carries water w/ it = osmotic diuresis. Net effect is sodium plus potassium concentration in urine is well below that of the plasma, thereby raising both the plasma sodium [] and plasma osmolality. Note that plasma [Na+] is often not elevatedon admission in unctrolled DM b/c of the counteracting hyponatremic effect of hyperlycemia. Diagnosis Assuming hypernatremia is not d/t admin of hypertonic sodium or salt tablets, DDx is aimed at identifying source of water loss. 1. H and P 2. plasma glucose concentration 3. test urine for glucose with dipstick 4. urine osmolality 5. response to ADH by admin dDAVP (analog of ADH) Upon admin of dDAVP, urine osmolality should rise by at least 50% in the first 2 hrs in pts w/ central diabetes insipidus who are ADH-deficient. Treatment Slowly (just like in hyponatremia) develop elevation in plasma sodium [ ] so as to not elicit neurologic symptoms. The recommendation is that the plasma sodium concentration be reduced at a max rate of 12 mEq/L per day, similary to that of hyponatremia. Water deficit must be calculated using: Total body osmoles = TBW x plasma osmolality The TBW is normally 60-50% of lean body wt (LBW) in men and women, respectively. However it is probably reasonable to use valsue about 10% lower in hypernatremic pts who are water-depleted. Polyuria Polyuria is an increase in urine ouput that exceeds 3 L/day. One cause is decreased sodium reabsorption in the proximal nephron. This is most often d/t glucose –induced osmotic diuresis in uncontrolled DM. Other than in DM, most cases of polyuria represent a water diuresis in which urine osmolality is less than that in the plasma d/t decreased water reabsorption in the collecting tubules. Polyuria in this setting is d/t diminished ADH effect, which can be induced in three ways: 1. decreased ADH prdtn in central diabetes insipidus (CDI). This disordered often idiopathic, but can also be d/t trauma, pituitary surgery, or hypoxic encephalopathy. 2. reduced reanal response to ADH in nephrogenic diabetes insipidus (NDI). ADH resistance that is severe enough to produce polyuria in adults is rare except for in two settings: chronic lithium ingestion and hypercalcemia.
  • 5. 3. decreased ADH prdtn is d/t a primary increase in water intake. Initial water retention lowers plasma [Na+], thereby reducing ADH release. Note that the polyuria in this disorder is inappropriate. Diagnosis 1. H and P 2. raising plasma osmolality using either water restriction or 3. admin of hypertonic saline Test to raise plasma osmolality is continued until one of two points is reached: the urine osmolality reaches a level that represents clearly adequate concentrating ability (above 500-600 mosmol/kg); or the plasma osmolality exceeds 295-300 mosmol/kg, the level at which there is sufficient circulating ADH in nl subjects to induce a max increase in urine osmolality. At this point, exogenous ADH is given and urine volume and osmolality is monitored for 2 hrs. Only pts with ADH release impairment should respond with a further elevation in urine osmolality. Both primary polydipsia and CDI are assoc with usu. modest impairment in max concentrating ability. Primary Polydipsia pts have relatively intact ADH-renal axis; as a result raising the plasma osmolality will lead to a nl increase in ADH release and urine osmolality. Pts with CDI, will have submaximal increase in urine osmolality as the plasma osmol rises. However, the admin of ADH will, in mod to severe cases, raise the urine osmolality and lower urine volume by more than 50%. In NDI, pts show initial response to raising plasma osmolality that is similary to that seen in CDI. These pts however, are resistant to ADH with urine osmolality generally increasing by less than 10%. Treatment There is generally no therapy for primary polydipsia unless a drug is responsible. In comparison, the polyuria can usu be corrected n CDI by the admin of the ADH analog dDAVP by nasal insufflation. The two most widely studied are chlorpropamide and carbazepine. ADH or drugs that depend uon ADH typically ineffective in nephrogenic diabetes insipidus. The major drug useful in this setting is thiazide diuretic. Thiazides act by inducing mild volume depletion. The ensuing activation of the renin- angiotensin-aldosterone and sympathetic nervous systems will increase proximal sodium and water reabsorption, limiting water delivery to the ADH-sensitive site in the collecting tubules.