Why cerebral edema in hyponatremia

These may include seizures, impaired mental status or coma and death. Brain adapts itself to hyponatremia by generation of idiogenic osmoles. This is a protective mechanism that reduces the degree of cerebral edema; it begins on the first day and is complete within several days. Hence in chronic hyponatremia patients may appear asymptomatic. Mild hyponatremia is characterized by gastrointestinal tract symptoms nausea, vomiting, loss of appetite. Hyponatremia in the elderly may manifest with frequent falls and gait disturbances.

Hyponatremia is classified as pseudo hyponatremia, true and translocational hyponatremia [ Figure 1 ]. Pseudo normo-osmolal or isotonic hyponatremia is due to presence of hypertriglyceridemia or increase in plasma proteins in conditions such as multiple myeloma. In normal subjects, the plasma water is 93 percent of the plasma volume, fats and proteins account for the remaining 7 percent. In renal failure, the elevation in blood urea counteracts the fall in serum osmolality due to hyponatremia.

However, the effective serum osmolality is appropriately reduced in this setting since urea is an ineffective osmole. Translocational hyperosmolal or hypertonic or redistributive hyponatremia is due to presence of osmotically active solutes in the serum e. True hypoosmolal hyponatremia is associated with reduction in serum osmolality and is further classified as euvolemic, hypervolemic and hypovolemic[ 7 , 8 , 9 ] [ Figure 2 ].

It is associated with low plasma volume. The causes of hypovolemic hyponatremia may be renal or non-renal [ Figure 2 ]. Diuretic-induced hyponatremia: Hyponatremia is common with use of thiazides, begins soon after initiation of thiazides, may be severe and is common in elderly females.

Thiazide-induced hyponatremia, occurs due to increased water intake, reduction in diluting ability and water excretion in distal tubule. Sodium plus potassium concentration in urine exceeds that in the plasma, which directly lowers plasma sodium concentration. Hence hyponatremia is not common with loop diuretics. Furosemide-related hyponatremia tends to occur after many months of therapy, often when an intercurrent illness develops. Mineralocorticoid deficiency is another important cause of hypovolemic hyponatremia and may be associated with hyperkalemia.

The final criterion emphasizes that SIADH remains a diagnosis of exclusion and the absence of other potential causes of hypo-osmolality must always be verified.

TBW depends on urine volume. This occurs because of defects in Antidiuretic hormone ADH, arginine vasopressin secretion. Type A — there is unregulated release of ADH that has no relation to plasma osmolality. Plasma ADH levels are above that required for maximum antidiuresis, so urine osmolality is very high. Type C- there is downward resetting of osmostat. Type D- is the least common. Osmoregulation is normal i. ADH secretion varies appropriately with the plasma osmolality , but the urine is concentrated even with suppressed ADH release.

There are 3 mechanisms a germ cell mutation in which the V2 vasopressin receptor is activated. Marathon runners may develop severe hyponatremia due to excessive water intake associated with persistent ADH secretion in some. Beer drinkers or other malnourished patients those with low-protein, high water intake diets have a marked reduction in water excretory capacity despite suppressed ADH.

In a normal person ingestion of a normal diet results in the excretion of mosmol of solute per day primarily sodium, potassium salts and urea. In beer drinkers and those who take a very poor diet there is little or no sodium, potassium, or protein in the diet and the carbohydrate load in beer suppresses endogenous protein breakdown and urea excretion. As a result, daily solute excretion is less than mosmol. Is characterized by increase in thirst and is most often seen in patients with psychiatric illnesses.

However; in the osmotic threshold for thirst is reduced below the threshold for ADH release. The patients continue to drink until the thirst threshold. However; fall in plasma osmolality suppresses ADH secretion with diuresis. This causes continued stimulation of thirst.

Thus normal osmolality is not achieved. Excess water is thus excreted and hence serum sodium concentration is normal or only slightly reduced and hence these patients are usually asymptomatic or may have polydipsia and polyuria. However; they cannot excrete massive water load to mL per hour which may be seen in psychotic patients or acute water load of 3 to 4l. This may cause fatal hyponatremia even though the urine is maximally dilute.

The cause for defective thirst is not known. In some patients hypothalamic lesions that affect the thirst center, infiltrative diseases such as sarcoidosis can result in primary polydipsia. Patients with polydipsia should be evaluated with a computed tomography or magnetic resonance imaging MRI scan of the brain before concluding that excessive water intake is due to a psychiatric cause. There is no specific therapy for primary polydipsia. In long term limiting the use of drugs that cause dry mouth, restricting fluid intake and frequent weighing are useful.

It is seen in congestive heart failure and cirrhosis of liver, nephrotic syndrome and chronic kidney disease. Even though the plasma and extracellular volumes is increased in heart failure and cirrhosis, there is ADH stimulation as described under pathogenesis.

The development of hyponatremia is a poor prognostic sign. Hyponatremia occurs commonly in both acute and chronic renal failure, because the kidneys cannot maximally excrete excess ingested water.

In contrast, hyponatremia is not very common in the nephrotic syndrome unless associated with a substantial decrease in GFR. Fluid restriction is the cornerstone of therapy. Drug and diet history, history of volume loss i. Determination of volume status i. When available, direct hemodynamic measurements can provide corroboration of the clinical impression. Signs of hypothyroidism or adrenal insufficiency should be noted.

Also a detailed examination should be done to detect any CNS or lung lesion. Pseudohyponatremia falsely low Na with normal plasma osmolality is not seen if ISE with direct potentiometry method is used. However, many laboratory analyzers that measure sodium with ion-selective electrodes utilize indirect potentiometry in which the plasma sample is diluted before measurement; these analyzers will report a low sodium concentration.

Flame photometers may result in low values of serum sodium as they measure the sodium only in aqueous phase. It differentiates true, pseudo or translocational hyponatremia [ Figure 1 ].

Calculated serum osmolality may not reflect serum osmolality if other osmotically active solutes are present in the plasma.

Hence, serum osmolality should be measured by osmometer, IB. If osmometer is not available, random blood sugar, serum triglyceride and serum protein should be helpful in differentiating the three types. Urine osmolality can be used to distinguish between impaired water excretion and hyponatremia with normal water excretion [ Table 5 ].

Values above this level indicate an inability to normally excrete free water, most commonly because of persistent secretion of ADH. This is done by measuring the urinary sodium losses.

If initial urine sodium concentration is equivocal, it could be difficult to differentiate true hypovolemia or euvolemic hyponatremia.

In this situation serial monitoring of the urine osmolality and urine sodium concentration in response to the administration of 1litre 0.

If the patient is hypovolemic, 0. In both disorders, the urine sodium concentration will increase with saline therapy, although the increase in hypovolemic patients will not be seen until the hypovolemia is corrected.

It is the sum of the urine sodium plus potassium concentrations divided by the serum sodium concentration. Fractional excretion of sodium FENa provides an accurate assessment of volume status than the urine sodium alone because it corrects for the effect of variations in urine volume on the urine sodium.

Stimulation of the vasopressor V1a receptor also contributes to the uric acid wasting. Water retention also causes low BUN.

Thiazide diuretic-induced hyponatremia similar reductions in uric acid and urea levels can occur in patients with thiazide diuretic-induced hyponatremia where thiazides are used for water overload.

Evaluation of acid-base and potassium balance may be helpful in some patients. Metabolic acidosis and hyperkalemia - primary adrenal insufficiency in patients without renal failure.

Mild metabolic alkalosis and normal K- is seen in hypopituitarism because of higher plasma aldosterone levels. In case of doubt, one can initiate 0. Hypovolemic hyponatremia improves with 0. Etiology of hyponatremia. Acute hyponatemia is generally symptomatic. The risk of brain herniation is high and rapid correction is needed. Acute hyponatremia is common in marathon runners, patients with primary polydipsia and users of ecstasy. These patients have not had time for the brain adaptations to occur.

Chronic hyponatremia- It is generally asymptomatic or has mild symptoms. However; it may present with seizures if hyponatremia is very severe. Patients with mild symptoms eg, dizziness, forgetfulness, gait disturbance should be treated with less aggressive therapy. Among patients with urine to serum electrolyte ratio greater than 1, in whom fluid restriction will not be sufficient to achieve the desired goal, additional therapy includes salt tablets and if necessary, a loop diuretic.

An alternative approach is the initiation of a vasopressin antagonist without fluid restriction. Rate of correction: In chronic hyponatremia the brain undergoes adaptation and hence the risk of cerebral herniation is very low unlike the risk in acute hyponatremia. Instead very rapid correction can lead to osmotic demyelination syndrome ODS.

Hence, chronic hyponatremia generally needs gradual correction. High risk of ODS is seen esp. Osmotic demyelination-It is a rare, but severe and sometimes irreversible disorder. It presents with locked in syndrome i. This disorder was formerly called central pontine myelinolysis CPM , but the name was changed because demyelination is more diffuse and does not necessarily involve the pons and.

Recently, it has been shown that ODS can be reversed by relowering sodium and giving desmopressin. Potassium added to the solution should be included in the formula i. However, these formulae have limitations and cannot be used to accurately predict the magnitude of change in serum sodium and frequent measurements are necessary.

In the current guidelines these formulae are not used. In addition water restriction, salt, urea, demeclocycline and vaptans are used according to the etiology. Observations on water intoxication in surgical patients. Hyponatremia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women. Ayus J. Postoperative hyponatremic encephalopathy in menstruant women. Baggish M. Fatal acute glycine and sorbitol toxicity during operative hysteroscopy. Hyponatraemia and death or permanent brain damage in healthy children.

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Chronic hyponatremia exacerbates multiple manifestations of senescence in male rats. Age Dordr. Benvenuti S. Low extracellular sodium causes neuronal distress independently of reduced osmolality in an experimental model of chronic hyponatremia. Mancuso C. Heme oxygenase and its products in the nervous system. Redox Signal. Chen K. Neurons overexpressing heme oxygenase-1 resist oxidative stress-mediated cell death.

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