Fluid & Electrolyte Disorders - Part I : Disorders of sodium balance
A. Clinical Manifestations: Clinical features of hyponatremia are due to brain swelling that accompanies acute dilution of total body water and generally become manifest when the serum sodium concentration falls to 120 mEq per liter or less.
The main symptoms and signs include: Headache, nausea, vomiting, hallucinations, lethargy, weakness, hypoventilation, extra-pyramidal reactions, unreactive pupils, anisocoria, muscle twitching, hyperactive tendon reflexes, seizures and coma.
B. Diagnosis: Hyponatremia is defined as a serum sodium concentration less than 135meq/l. The initial approach to the investigation of the causes of hyponatremia is to determine the serum osmolality as below:
Osmolality = 2 ´ (serum sodium mEq/l) + glucose(mg/dl)/18 + BUN(mg/dl)/2.8
Once established the serum osmolality its also important to measure the urine sodium which helps to distinguish renal from non renal causes of hyponatremia. Urine sodium exceeding 20 mEq/l is consistent with renal salt wasting ( diuretics, ACE inhibitors, mineralocorticoid defficiency, salt-loosing nephropathy).
The fractional excretion should also be calculated using the following parameters:
| FE sodium = | Urine sodium / Plasma sodium |
|---|---|
| Urine creatinine/ Plasma creatinine |
Urine sodium less than 10 mEq or fractional excretion less than 1 %(unless diuretics have been given) implies avid sodium retention by the kidney to compensate for extra-renal fluid losses from vomiting, diarrhea, sweating, or third-spacing, as with ascites.
This test is of value in the setting of Acute Renal Failure to aid in distinguishing a prerenal from a renal parenchimal cause.
C. Types of hyponatremia:
According to the serum osmolality we can divide hyponatremia into the following categories :
C.1 . Isotonic hyponatremia :
The main causes are hyperlipidemia and hyperproteinemia ( as immunoglobulins in Multiple Mieloma).Lipids and proteins occupy a disproportionately large portion of plasma volume,with the serum osmolality and sodium concentration normal. The serum osmolality ranges between 280-295 mOsm/Kg. This condition is termed pseudohypernatremia
C.2 . Hypotonic hyponatremia:
In such cases, the plasma osmolality is usually less then 280 mOsm/Kg.
C.2.1 Hypotonic euvolemic hyponatremia :
Main causes:
C.2.1.1. Syndrome of inappropiate ADH secretion (SIADH) :
This syndrome has as its main features: volume expansion without edema(differing in That respect from patients with Congestive Heart Failure or Cirrhosis), natriuresis (Urinary sodium more than 30 mEq/l), FE sodium more than 1%, hypouricemia, normal or reduced creatinine level, normal tyroid and adrenal function and normal potassium and acid-base balance.
The serum osmolality as mentioned above is less then 280 mOsm/Kg.
When total body water is expanded by about 10% by water retention in SIADH, a natriuresis occurs despite hyponatremia. There is an increase of atriopeptin,which enhances urinary sodium wasting both by enhancing glomerular filtration and probably supressing tubular sodium absorption.
Causes of SIADH :
Pulmonary: Pneumonias, tuberculosis, pulmonary abcess,ventilators with positive pressure. Central Nervous System Disorders: Trauma, infection (Encefalitis, Meningitis), thrombosis, abcesses, hemorrhages, hematomas.
Malignant neoplasia: Carcinoma: bronchogenic (such as small cell lung carcinoma), pancreatic, uretral, prostatic, bladder, lymphoma, leukemia, thymoma, and mesothelioma.Drugs: Drugs leading to increased ADH production:
- Antidepressants ( Amitryptiline, Clomipramine , Desipramine, Imipramine, MAO inhibitors, fluoexitine).
- Antineoplasics (Cyclophosphamide, Vincristine, Vinblastine)
- Carbamazepine
- Clofibrate
- Neuroleptics (Thithixene,Thioridazine, Fluphenazine, Haloperidol, Trifluoperazine)
Drugs leading to potentiated ADH action:
- Carbamazepine, Chlorpropamide, Tolbutamide, Cyclophosphamide, NSAIDs, Somatostatin and analogues.
C.2.1.2 Postoperative hyponatremia:
Severe postoperative hyponatremia can develop in 2 days or less after elective surgery in healthy patients which have received excessive postoperative hypotonic fluid in the setting of elevated ADH levels related to pain , surgery or anesthesia.
C.2.1.3 Psychogenic polydipsia :
Euvolemia is mantained through the renal excretion of sodium, but unlike SIADH, the levels of ADH are supressed.C.2.2 Hypotonic hipovolemic hiponatremia :
There are two main causes:
C.2.2.1 Due to renal salt loss :
Urinary sodium >20 meq/l: Diuretics (mainly Thiazide diuretics, since they impair diluting capacity,but do not limit concentrating ability to a large extent, because they don’t reduce the solute concentration in the renal medullary intersticium. Medullary osmolality is the principle determinant of urinary concentrating ability when ADH is present),mineralocorticoid defficiency ( in mineralocorticoid defficiency, the major factors resposible for an inability to handle water loads appear to be Extracelullar Fluid contraction, glomerular filtration reduction, enhanced proximal tubular salt absorbtion, and volume-mediated,non-osmotic ADH release), nefropathies and ACE inhibitors.
C.2.2.2 Due to extra-renal salt loss :
Dehydration, diarrhea and vomiting .
C.2.1.4 Hypotonic hipervolemic hiponatremia :
Hyponatremia occurs commonly in advanced stages of disorders characterized by edema formation and a reduced extracellular fluid volume, particularly in intractable heart failure and advanced hepatic cirrosis with ascites. The plasma concentrations of ADH tend to be inappropiately high with respect to plasma osmolality,so that nonosmotic ADH release may contribute to the development of hyponatremia in these disorders, since non osmotic ADH release occurs only with profound reductions in blood volume. The urine sodium is usually low in these conditions, reflecting the edema-forming state
C.3 Hypertonic Hyponatremia :
It is a dilutional hyponatremia, most commonly seen with hyperglicemia and the use of Mannitol which don’t penetrates easily the cellular membranes, leading to an osmotic gradient which in turns results in an increase of the extracelullar volume. For each 100mg/dl of glucose in excess in plasma there is a decline of 1,6 mEq/l of serum sodium. The plasma osmolality is usually more than 295 mOsm/Kg.D.1 Symtomatic Hyponatremia :
Acute hyponatremia associated with a serum sodium concentration below 120 mEq/l and with Central Nervous System manifestations requires immediate therapy. Brain damage, including Central Pontine Myelinolisis, may occur from osmotically induced demyelination from overly rapid correction of serum sodium.The sodium requirement can be calculated as follows :
( 125 - serum sodium)´0.6´body weight = required mEq of sodium
It is thus recommended to correct the serum sodium concentration until it reaches 125 mEq/l at a rate of 1.0 to 1.5 mEq/l per hour, aiming not to exceed 130 mEq/l in the first 48 hours. This correction should be done with hypertonic saline at 3 or 5%.
Another alternative is to use normal saline (0.9%) with furosemide administration. If the patient is euvolemic, if one adds furosemide (0.5- 1.0 mg/Kg intravenously) the diuretic induces salt loss preventing the mechanisms of urinary concentration to work appropiately . So, the urinary salt concentration is lower than that in plasma. This may provide an effective way of raising the serum sodium level in SIADH or in other volume- expanded states.
In the symptomatic edematous states it is a reasonable approach to replace about a ¼ of the urine volume with 3% saline. Isotonic or hypertonic NaCl should no be given without a loop diuretic, since it will correct electrolyte disorder at the expense of an already increased left ventricular end-diastolic pressure.
It is a general rule not to administer isotonic NaCl to patients with the SIADH. Based on the assumption that all of the administered sodium will be retained. Since renal perfusion is characteristically normal in the SIADH, administered solute will be excreted in the urine. Thus, the predominant effect of hypertonic saline in this disorder is not to increase body sodium. Rather, the initial increase in the plasma sodium concentration occurs primarily because the administered NaCl is eliminated in the urine where it enhances water elimination . As a result of these observations, the calculated sodium deficit serves as only a rough guide to hypertonic saline administration.
| SOLUTE | WATER(ml) | |
|---|---|---|
| INPUT | 308 | 1000 |
| OUTPUT | 308 | 500 |
| NET GAIN | 0 | +500 |
D.2 Asymptomatic hyponatremia :
In chronic hyponatremia there has been enough time for cerebral adaption and water restriction or 0.9% saline with furosemide may be used in asyptomatic patients whose serum sodium is less than 120 mEq/l. Mild, asymptomatic chronic hyponatremia is generally managed by correction of the underlying disorder, when the hyponatremia occurs in volume contraction or in salt-retaining states, such as Congestive Heart Failure or Hepatic Cyrrhosis with ascites. Chronic hyponatremia in SIADH may be easily corrected by restricting water intake from 800 to 1000 ml daily.
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