Investigations
• The diagnosis of hyponatremia: Concentration of sodium in serum
• There may be errors for eg, if sample obtained from site just proximal to infusion of hypotonic saline/ dextrose in water
• Hyperglycemia may lead to low serum sodium levels but it isn’t a true hyposmolar state, as hyperglycemia causes a shift of free water from intracellular to extracellular space thereby diluting the sodium (by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration). Concentration resumed once normoglycemia re-established.
• Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
o In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
o Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
o This phenomenon is known as pseudohyponatremia,
o Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
o Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity: Helpful in establishing the diagnosis of true hyposmolar hyponatremia. Serum osmolarity is abnormally low in patients with hyposmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels
• Hypovolemic hyponatremia: Non-renal: Vomiting, diarrhea, fistulas, GI drainage and third spacing of fluids have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L. Renal: Diuretics, salt-losing nephropathy and aldosterone deficiency have elevated urine sodium levels in excess of 20 mEq/L.
• Hypervolemic hyponatremia: Non-renal: decrease in circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L. Renal: (SIADH) have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH. Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L. Other forms of hyponatremia doesn’t result in such concentrated urine (normal ADH levels)
Serum thyroid-stimulating hormone (TSH) and free thyroxin levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Serum ADH levels are not routinely used in the evaluation of hyponatremia because the assay is technically difficult and not widely available on a stat basis. Recently, a serum peptide known as copeptin has been studied in the evaluation of hyponatremia. Copeptin is the C terminal portion of provasopressin and is released in equimolar amounts with vasopressin (ADH).
Imaging Studies: A head CT scan is indicated in patients with altered mental status to ensure that no other underlying cause for the mental status is present.
Treatments
Emergency Care
• Supply O2 and IV glucose in hypoglycaemic patients who exhibit lethargy.
• Anticonvulsant therapy to patients experiencing seizures but if it is secondary to hyponatremia, unlikely to respond but still should do it until diagnosis is made.
• Intubate and initiate hyperventilation to reduce intracranial pressure in patients exhibiting signs of brainstem herniation (eg: fixed, unilateral, dilated pupil; decorticate posturing) until a more definitive therapy can be initiated.
• Avoid giving hypotonic intravenous fluids because they may exacerbate cerebral edema.
Acute hyponatremia (less common)
• Typically is seen in patients with a history of sudden free water loading (eg, patients with psychogenic polydipsia, infants fed tap water for 1-2 d, patients given hypotonic fluids in the postoperative period).
• Acute evolution of hyponatremia leaves little opportunity for compensatory extrusion of CNS intracellular solutes.
• The ultimate danger for these patients is brainstem herniation when sodium levels fall below 120 mEq/L.
• The therapeutic goal is to increase the serum sodium level rapidly by 4-6 mEq/L over the first 1-2 hours.
• The source of free water must be identified and eliminated.
• In patients with healthy renal function and mild to moderately severe symptoms, the serum sodium level may correct spontaneously without further intervention.
• Patients with seizures, severe confusion, coma, or signs of brainstem herniation should receive hypertonic (3%) saline to rapidly correct serum sodium level toward normal but only enough to arrest the progression of symptoms. An increase in serum sodium level of 4-6 mEq/L is generally sufficient. Any further correction is potentially dangerous and must be avoided unless necessary to correct continued seizures or other severe CNS abnormality.
Chronic hyponatremia (more common)
• Patients with mild symptoms and a serum sodium level of 125 mEq/L or less often have chronic hyponatremia. These patients lack any history of sudden free water loading.
• Chronic hyponatremia must be managed with extreme care; treatment of chronic hyponatremia has been associated with the development of the osmotic demyelination syndrome characterized by focal demyelination in the pons and extrapontine areas associated with serious neurologic sequelae.
• Management should include meticulous attention to adequate oxygenation and a gradual increase in serum sodium level to 120-125 mEq/L. Serum sodium level should not be allowed to reach normal levels or hypernatremic levels within the first 48 hours.
• The risk of osmotic demyelination appears to be minimal in patients whose chronic hyponatremia is corrected at a rate not to exceed 10-12 mEq/L in the first 24 hours and not to exceed 18 mEq/L in the first 48 hours
• Patients with chronic hyponatremia and severe symptoms (eg, severe confusion, coma, seizures) should receive hypertonic saline but only enough to raise the serum sodium level by 4-6 mEq/L and to arrest seizure activity.
o Further correction should proceed at an overall rate that is no greater than 10-12 mEq/L in the first 24 hours and no greater than 18 mEq/L in the first 48 hours.
• In treating patients with chronic hyponatremia and mild to moderately severe symptoms, consider the cause of the hyponatremic state. Patients are classified as having hypovolemic, euvolemic, or hypervolemic hyponatremia based on historical clues and physical examination. Regardless of the therapeutic approach, serum sodium must be monitored closely and corrected no faster than 10-12 mEq/L in the first 24 hours and 18 mEq/L in the first 48 hours.
o Hypovolemic hyponatremia: Patients have decreased total body sodium stores. If symptoms are mild to moderately severe, treat with isotonic saline; monitor serum sodium levels frequently to ensure that the serum sodium level increases slowly.
o Hypervolemic hyponatremia: Patients have increased total body sodium stores. Treatment consists of sodium and water restriction and attention to the underlying cause. The vasopressin receptor antagonists conivaptan (Vaprisol) and tolvaptan (Samsca) are used in hospitalized patients with hypervolemic hyponatremia.
o Euvolemic hyponatremia: This implies normal sodium stores and a total body excess of free water. Treatment consists of free water restriction and correction of the underlying condition. Recently developed AVP (vasopressin) receptor antagonists (eg, conivaptan, tolvaptan) show promise as effective and well-tolerated intravenous therapy for SIADH. Further studies are needed to better define their role in the treatment of hyponatremia associated with SIADH
Hypertonic Saline
Sodium Requirement (mEq) = TBW (Desired Na - Serum Na) where TBW = Body Weight X 0.6
Volume of Hypertonic Saline = Na Requirement (mEq) X 1000 / Infusate Na Concentration (mEq/L)
For example, a 60-kg woman with serum sodium level of 113 mEq/L would require 280 mL of hypertonic saline in order to increase serum sodium by 4 mEq/L (could be administered as 140 mL/h for 2 h)
In general, 200-400 mL of 3% NaCl is reasonable dose in most adult patients with severe symptomatic hyponatremia
Give IV over first 1-2 h until resolution of seizures or herniation
Arginine vasopressin antagonists (Conivaptan: non-selective, Tolvaptam: selective)
These agents treat hyponatremia through V2 antagonism of AVP in the renal collecting ducts. This effect results in aquaresis (excretion of free water).
Arginine vasopressin antagonist Conivaptan (V1A, V2) indicated for euvolemic and hypervolemic hyponatremia. Increases urine output of mostly free water, with little electrolyte loss.
Selective vasopressin V2 -receptor antagonist Tolvaptam, indicated for hypervolemic and euvolemic hyponatremia (i.e., serum sodium level <125 mEq/L) or less marked hyponatremia that is symptomatic and has resisted correction with fluid restriction. Used for hyponatremia associated with congestive heart failure, liver cirrhosis, and syndrome of inappropriate antidiuretic hormone secretion. Initiate or reinitiate in hospital environment only.
http://emedicine.medscape.com/article/767624-treatment
No comments:
Post a Comment