{"id":5210,"date":"2011-07-14T20:24:26","date_gmt":"2011-07-14T20:24:26","guid":{"rendered":"http:\/\/crashtext.org\/misc\/sodium.htm\/"},"modified":"2013-01-13T20:35:22","modified_gmt":"2013-01-14T01:35:22","slug":"sodium","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/electrolyte-disorders\/sodium.htm\/","title":{"rendered":"Sodium"},"content":{"rendered":"

<\/span>Hyponatremia<\/span><\/h2>\n

Best review<\/a><\/p>\n

another review<\/a><\/p>\n

Review of Drug-Induced Hyponatremia (Am J Kid Dis 2008;52:144)<\/p>\n

treatment of chronic hyponatremia<\/a><\/p>\n

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\"mechanisms<\/a>from C L E V E L A N D C L I N I C J O U R N A L O F ME D I C I N E V O L UME 7 7 \u0095 N UMB E R 1 0 O C T O B E R 2 0 1 0<\/p>\n

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Stern Review<\/a> and Case Example<\/a> (severe hyponatremia requiring ddavp)<\/p>\n

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lab work-up for SIADH<\/a><\/p>\n

CSW Review<\/p>\n

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if you overcorrect, consider dDAVP 1-2 mcg and possibly D5W 6ml\/kg (see here<\/a> and here<\/a>)<\/p>\n

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hypokalemia repletion<\/a> will raise the sodium<\/p>\n

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Sodium<135 mEq\/L, <120 is severe<\/p>\n

See diabetic section for correction in hyperglycemia<\/p>\n

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caused by non-osmotic secretion of AVP in over 95% of cases<\/p>\n

Hypothalamic osmo-receptors. A decrease in osm of 1-2% stops AVP secretion and we pee water<\/p>\n

Non-osmotic is mediated by arterial stretch baroreceptors in response to 8-10% decrease in blood pressure<\/p>\n

If the kidney is damaged acutely or chronically, FeNa may not be <1 even in volume depletion<\/p>\n

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only hypovolemic hyponatremia should be treated with NS (FeNa <1), but SIADH pts can become volume depleted<\/p>\n

50 ml of 3% should increase Na by ~1 mmol\/L<\/p>\n

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In hypovolemic hyponatremia, there is a deficit of both total body water and sodium, but relatively less deficit of water, thus causing hyponatremia. A history of vomiting, diarrhea, diuretic use, or hyperglycemia with glucosuria, along with increased thirst, weight loss, orthostatic hypotension and tachycardia, and dry mucous membranes, supports the diagnosis of hypovolemic hyponatremia. If the fluid and sodium losses are extrarenal, such as gastrointestinal losses, FENa should be less than 1%. On the contrary, if the source of sodium and water losses is the kidney, for example, diuretics, glucosuria, or bicarbonaturia, then FENa will be greater than 1% [9]<\/a>.<\/p>\n

In euvolemic hyponatremia, total body sodium concentration is near normal so there should be no evidence of ECFV depletion or excess, that is, no peripheral edema, ascites, pulmonary congestion, or pleural effusions. Before turning to the diagnosis of SIADH in patients with euvolemic hyponatremia, several other clinical entities need to be excluded. These include hypothyroidism (measure thyroid-stimulating hormone), hypopituitarism (measure cortisol response to adrenocorticotropic hormone), severe emotional (e.g. psychosis) or physical stress (e.g. anesthesia and surgery), and various medications that stimulate antidiuretic hormone (ADH) release. There are various pharmacological agents associated with SIADH:<\/p>\n

1. Nicotine,2. Chlorpropamide,3. Tolbutamide,4. Clofibrate,5. Cyclophosphamide,6. Morphine,7. Barbiturates,8. Vincristine,9. Carbamazepine (Tegretol),10. Acetaminophen,11. NSAIDs12. Antipsychotics,13. Antidepressants.<\/p>\n

In the absence of these diagnoses, SIADH can be entertained, and a search for pulmonary or central nervous system infections, vascular, or neoplastic diseases should reveal the cause in over 90% of SIADH cases. Because the urine volume in SIADH is low, for example, 500 ml\/24 h, the urinary sodium concentration is generally high even when the patient is in sodium balance. For example, with a very modest daily sodium intake of 100 mmol\/24 h, the urinary sodium concentration in 500 ml of daily urine would have to be 200 mmol\/l of urine for the patient to remain in sodium balance. Thus, a high urine sodium concentration in SIADH should not be called \u0091renal sodium wasting.\u0092<\/p>\n

In hypervolemic hyponatremia, total body sodium concentration and water are increased, but total body water is increased more, and thus hyponatremia occurs. When hypervolemic hyponatremia occurs with cardiac failure or cirrhosis, the patient has advanced and, therefore, readily diagnosed disease. Decreased plasma sodium concentration is a risk factor for poor survival in patients with cardiac failure and cirrhosis [11\u009616]<\/a>. In the absence of diuretics, FENa should be below 1.0% in hyponatremic cardiac or cirrhotic patients, as the kidney is normal and responding to decreased arterial perfusion in these edematous disorders. Specifically, in case of either a successful heart or liver transplant in cardiac or hepatic failure patients, respectively, the kidneys no longer retain sodium and water. The situation in which hypervolemic hyponatremia occurs with a FENa greater than 1.0% is with acute kidney injury or chronic kidney disease, settings in which renal tubular dysfunction is present and neither water nor sodium can be optimally excreted.<\/p>\n

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Drug treatment<\/p>\n

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do not use conivaptan in cirrhotic\/esoph varices pts<\/p>\n

new term is osmotic demyelination<\/p>\n

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for fluid restriction, must be less than output+insensible losses<\/p>\n

average daily insensible ~250 cc<\/p>\n

demeclocycline 600-1200 mg\/day in divided doses<\/p>\n

increase dose only every 3-4 days<\/p>\n

causes nephrogenic DI<\/p>\n

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Beer potomania<\/p>\n

shift into cells. Thiazide-induced hyponatremia occurs most commonly in elderly women, and there is also some evidence that the predisposed women may be drinking more water than normal. One limitation of the urinary excretion of electrolyte-fee water is the amount of solute excreted. With maximal urinary dilution of 50 mmol\/l and diminished daily solute intake of 200 mmol\/l, only 4 l of electrolyte-free water can be excreted. This is the problem that causes hyponatremia with beer drinkers who are not eating. Beer is very hypotonic and contains little solute; therefore, these beer drinkers may develop hyponatremia with an intake of 6\u009610 l of beer\/day. Normal solute intake is 600\u0096800 mmol\/day, thus allowing for substantial electrolyte-free water excretion.<\/p>\n

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Exercise-associated hyponatremia<\/p>\n

With more individuals involved in prolonged and strenuous physical exercise such as marathons, ultramarathons, and triathlons, the entity of exercise-associated hyponatremia has emerged. Risk factors for these individuals include low body mass, less well trained, race time exceeding 4 h, consumption of fluids every mile, and the use of NSAIDs [44]<\/a>. The occurrence of exercise-induced hyponatremia does not seem to be due to sodium imbalance, but rather due to retention of more water. With such vigorous exercise, the nonosmotic stimulation of AVP would be expected, thereby leading to renal water retention [45,46]<\/a>. When hypotonic fluid ingestion exceeds insensible loss due to sweating, the runner actually gains weight and hyponatremia occurs. The symptomatic hyponatremic runners generally have ingested amounts of hypotonic fluid, for example, water or Gatorade, in excess of 400\u0096800 ml\/h. They may develop seizures, ataxia, disturbed level of consciousness, focal neurological deficits, and even mortality can occur. In runners with these symptoms, treatment with 3% hypertonic saline should begin immediately, even before the measurements of serum sodium concentration have returned, and continued until symptoms resolve. Further treatment is generally not needed when serum sodium concentration reaches 130 mmo\/l.<\/p>\n

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<\/span>Normotonic<\/span><\/h3>\n

=Pseudohyponatremia<\/p>\n

hyperlipidemia, hyperproteinemia, or the absorption of isotonic glycine during transurethral resection of the bladder or prostate<\/p>\n

<\/span>Hypertonic<\/span><\/h3>\n

hyperglycemia or the administration of hypertonic mannitol: induce osmotic water movement out of the cells and lower the plasma sodium concentration by dilution<\/p>\n

<\/span>Hypotonic<\/span><\/h3>\n

Hypotonic Hyponatremia=true hyponatremia<\/h4>\n

(<285 on Osm)<\/p>\n

Hypervolemic<\/strong><\/p>\n

CHF, Hepatic (UNA<20) Nephrotic (UNa>20)<\/p>\n

Euvolemic<\/strong><\/p>\n

SIADH (fluid restriction, Lithium blocks action of ADH),<\/p>\n

Urine Specific Grav Elevated, Uosm>SerumOsm, Urine Na>18 (elevated),<\/p>\n

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Pyschogenic Polydipsia (Uosm<100), Endocrine (Hypothyroid, Addison’s)<\/p>\n

Will usually have a urine sodium>20 mEq\/L<\/p>\n

Hypovolemic<\/strong><\/p>\n

vomiting, diarrhea(UNa<20), diuretics and adrenal insufficiency (UNa>20), RTA<\/strong><\/p>\n

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The use of electrolyte free irrigation fluid during prostate surgery (TURP) or endometrial ablation has also resulted in hyponatremia<\/p>\n

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The hyponatremic state leads to cerebral edema, if chronic, solute loss will allow equilibrium<\/p>\n

If corrected too quickly, get Central Pontine Myelosis<\/p>\n

RX:\u00a0 Obtain UA, U Lytes, and Uosm.\u00a0 If symptomatic, give 100 cc of 3% Saline along with 10-20 mg of Lasix.\u00a0 Recheck Sodium.\u00a0 If it has not gone up 2 meq\/L repeat 3% saline.\u00a0 Correct .5 meq\/L per hour\u00a0 for non-symptomatic.\u00a0 Raise 1-2 meq\/L per hour for symptomatic.\u00a0 Switch to saline after raising sodium the first couple of points.<\/p>\n

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Change in Serum Na from 1 liter of NS=(154 \u0096 pt\u0092s Na) \/ (1 + (0.5 x weight in Kg))<\/p>\n

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Change in Serum Na from 1 liter of 3% Saline=(513 \u0096 pt\u0092s Na) \/ (1 + (0.5 x weight))<\/p>\n

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Best Review Article:\u00a0 (NEJM 342:21, 2000)<\/p>\n

My review<\/a><\/p>\n

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From: Thomas Bleck<\/strong> <tbleck@gmail.com<\/a>> Date: May 7, 2008 6:49 PM The degree of hypo-osmolality is not as important as the rate at which it develops. \u00a0If this is acute (over hours), then coma and (usually generalized) seizures are a consequence of the rapid drop in osmolality with a concomitant increase in ICP due to brain swelling. \u00a0If it developed over days or weeks, then the brain loses solute to compensate and doesn’t swell. \u00a0Most drug-induced hypo-osmolality is chronic, although if such a patient (or one with SIADH) drinks a lot of free water the osmolality may fall precipitously. \u00a0The low urine osmolality would be more compatible with water intoxication than pure drug effect or SIADH, in which the urine should be inappropriately concentrated.<\/p>\n

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“beer” potomania syndrome: no solutes from poor nutrition. Free water is retained.<\/p>\n

Uosm<100<\/p>\n

new drug for SIADH<\/h4>\n

promotes pure aquaresis, 6 meq rise in Na per liter<\/p>\n

<\/span>Cerebral Salt Wasting<\/span><\/h3>\n

Cerebral Salt Wasting Characteristics<\/p>\n