Malattie del rene e delle vie urinarie - Hyponatriemia

PRIMA RY CA RE

· Triggers demyelination of pontine and extrapontinecle cramps, lethargy, restlessness, disorientation, and neurons that can cause neurologic dysfunction, in-depressed reflexes can be observed. Whereas most cluding quadriplegia, pseudobulbar palsy, seizures,patients with a serum sodium concentration exceed- coma, and even death. Hepatic failure, potassium de-ing 125 mmol per liter are asymptomatic, those with pletion, and malnutrition increase the risk of this com-lower values may have symptoms, especially if the plication.disorder has developed rapidly. Complications of se-4 1,37vere and rapidly evolving hyponatremia include sei- MANAGEMENTzures, coma, permanent brain damage, respiratoryarrest, brain-stem herniation, and death. These com- The optimal treatment of hypotonic hyponatremiaplications often occur with excessive water retention requires balancing the risks of hypotonicity againstin patients who are essentially euvolemic (e.g., those those of therapy.

The presence of symptoms and recovering from surgery or those with primary polydipsia); menstruating women appear to be at particular risk. Hypotonic hyponatremia causes entry of water into the brain, resulting in cerebral edema (Fig. 2). Because the surrounding cranium limits expansion of the brain, intracranial hypertension develops, with a risk of brain injury. Fortunately, solutes leave brain tissues within hours, thereby inducing water loss and ameliorating brain swelling. This process of adaptation by the brain accounts forIl testo formattato con tag html sarebbe il seguente:

the relatively asymp- induced expansion of the extracellular-fluid volume.tomatic nature of even severe hyponatremia if it de- Because furosemide-induced diuresis is equivalent tovelops slowly. Nevertheless, brain adaptation is also a one-half isotonic saline solution, it aids in the cor-the source of the risk of osmotic demyelination. rection of hyponatremia, as do ongoing dermal and31-33Although rare, osmotic demyelination is serious and respiratory fluid losses; anticipation of these lossescan develop one to several days after aggressive treat- should temper the pace of infusion of hypertonic sa-ment of hyponatremia by any method, including line. Obviously, electrolyte-free water intake must bewater restriction alone. Shrinkage of the brain withheld. In addition to hypertonic saline, hormone-34-36 F U M HT 2. ORMULAS FOR SE IN ANAGING YPONATREMIAABLE C I .AND HARACTERISTICS OF NFUSATESF * C UORMULA LINICAL SEEstimate the effect of 1 liter ofinfusate Na ¡serum Na+ +1. Change

in serum Na =+ any infusate on serum Na+total body water + 1(infusate Na +infusate K )¡serum Na

Estimate the effect of 1 liter of+ + +2. Change in serum Na =+ any infusate containing Na+total body water + 1 and K on serum Na+ +E -FXTRACELLULAR LUIDI I Na D+NFUSATE NFUSATE ISTRIBUTIONmmol per liter %5% Sodium chloride in water 855 100†3% Sodium chloride in water 513 100†0.9% Sodium chloride in water 154 100Ringer’s lactate solution 130 970.45% Sodium chloride in water 77 730.2% Sodium chloride in 5% dextrose in water 34 555% Dextrose in water 0 40

*The numerator in formula 1 is a simplification of the expression (infusate Na ¡serum Na )¬+ +The estimated total body water1 liter, with the value yielded by the equation in millimoles per liter.38(in liters) is calculated as a fraction of body weight. The fraction is 0.6 in children; 0.6 and 0.5 innonelderly men and women, respectively; and 0.5 and 0.45 in elderly men and women, respectively.39Normally,

extracellular and intracellular fluids account for 40 and 60 percent of total body water, respectively. ^39† In addition to its complete distribution in the extracellular compartment, this infusate induces osmotic removal of water from the intracellular compartment. _{1585 Volume 342 Number 21 · The New England Journal of Medicine} can be derived expediently by applying formula 1 in replacement therapy should be given to patients with Table 2, the same formula used for managing hypernatremia, which projects the change in serum sodium elicited by the retention of 1 liter of any infusate. On the other hand, most patients with hypovolemia can be treated successfully with isotonic saline. Patients with seizures also require immediate anticonvulsant-drug therapy andadequate ventilation. determines the volume of infusate required,40 and hence the rate of infusion. Table 2 also presents Patients with symptomatic hyponatremia and dilute the sodium concentrations of commonly used infu-urine (osmolality, <200 mOsm per kilogram of wa-ter) but with less serious symptoms usually require sates, their fractional distribution in the extracellularonly water restriction and close observation. Severe fluid, and clinical estimates of total body water. We39do not recommend use of the conventional formulasymptoms (e.g., seizures or coma) call for infusion for the correction of hyponatremia, as follows:of hypertonic saline.There is no consensus about the optimal treatment sodium requirement=total body water¬(desired serumNevertheless, cor-of symptomatic hyponatremia.28,40-49 sodium concentration¡current sodium concentration).rection should be of a sufficient pace and magnitude The conventional formula requires a complicated pro-to reverse themanifestations of hypotonicity but not cedure to convert the amount of sodium required tobe so rapid and large as to pose a risk of the devel- raise the sodium concentration to an infusion rateopment of osmotic demyelination. Physiologic con- siderations indicate that a relatively small increase in The cases described below illustrate the various the serum sodium concentration, on the order of forms of symptomatic hyponatremia and their man-5 percent, should substantially reduce cerebral ede- agement.Even seizures induced by hyponatremia canma.9,50be stopped by rapid increases in the serum sodium Hyponatremia in the Postoperative State concentration that average only 3 to 7 mmol per Most reported cases of osmotic demyelina- A previously healthy 32-year-old woman has three liter.51,52tion occurred after rates of correction that exceeded grand mal seizures two days after an appendectomy.12 mmol per liter per day were used, but isolated She receives 20 mg of

diazepam and 250 mg of phen-cases occurred after corrections of only 9 to 10 mmol ytoin intravenously and undergoes laryngeal intuba-per liter in 24 hours or 19 mmol per liter in 48 tion with mechanical ventilation. Three liters of 5 per-After weighing the available evi-hours. cent dextrose in water had been infused during the34,35,40,48,53-56dence and the all-too-real risk of overshooting the first day after surgery, and the patient subsequentlymark, we recommend a targeted rate of correction drank an unknown but substantial amount of water.that does not exceed 8 mmol per liter on any day of Clinically, she is euvolemic, and she weighs 46 kg.treatment. Remaining within this target, the initial She is stuporous and responds to pain but not torate of correction can still be 1 to 2 mmol per liter commands. The serum sodium concentration is 112per hour for several hours in patients with severe mmol per liter, the serum potassium concentrationsymptoms. Should severe symptoms not respond

to is 4.1 mmol per liter, serum osmolality is 228 mOsmcorrection according to the specified target, we sug- per kilogram of water, and urine osmolality is 510gest that this limit be cautiously exceeded, since the mOsm per kilogram of water. Hypotonic hyponatre-imminent risks of hypotonicity override the poten- mia in this patient is a result of water retention causedtial risk of osmotic demyelination. Recommended in- by the impaired excretion of water that is associateddications for stopping the rapid correction of symp- with the postoperative state. Planned treatment in-tomatic hyponatremia (regardless of the method used) cludes the withholding of water, the infusion of 3 per-are the cessation of life-threatening manifestations, cent sodium chloride, and the intravenous adminis-moderation of other symptoms, or the achievement tration of 20 mg of furosemide. The estimated volumeof a serum sodium concentration of 125 to 130 of total body water is 23 liters (0.5¬46).mmol per liter

(or even lower if the base-line serum sodium concentration is below 100 mmol per liter).

According to formula 1 of Table 2, it is estimated that the retention of 1 liter of 3 percent sodium chloride will increase the serum sodium concentration by 16.7 mmol per liter ([513÷112]÷[23+1]=16.7).

Long-term management of hyponatremia (described below) should then be initiated. Although faster rates of correction can be tolerated safely by most patients with acute symptomatic hyponatremia, there is no evidence that such an approach is beneficial. Moreover, ascertaining the duration of hyponatremia is usually difficult.

How can the physician determine what the rate of monitoring of the serum sodium concentration?