A disorder of cellular and / or extracellular hydration results from a disorder of the water balance and / or of the sodium balance, which justifies the term “hydrosoded equilibrium”.
The regulation of the water balance, based on the control of the effective osmolality, and that of the sodium balance, based on the control of the effective volume, are largely independent: it is thus logical to define simple water balance disorders, not affecting clinically perceptible effective volume, and simple sodal balance disorders, not affecting effective osmolality.However, the existence of interactions between the regulation of effective osmolality and that of effective volemia explains the frequency of disorders associating a water balance disorder and a sodal balance disorder.
Regulation of the hydrosoded balance sheet:
The balance of the hydroelectrolytic balance in general and hydrosodic in particular is obtained thanks to the existence of regulation loops.
WATER BALANCE REGULATION:
It is carried out in such a way as to ensure the stability of the effective osmolality. This term represents the total concentration of all solutes which, due to their unequal distribution between the cellular and extracellular sectors, play a role in the osmotic transfer of water between these two sectors. In practice, the effective osmolality can be estimated in the plasma by the difference between the total osmolality (measured by cryoscopy) minus the molar concentration of the urea. It is normally between 270 and 290 mOsm / kg.
Insofar as the cell membrane is freely permeable to water, the osmotic transfer of water constantly ensures the equality of effective osmolality in all the fluid compartments of the body. Any variation in effective osmolality in a compartment therefore causes a movement of water through the cell membrane causing a variation in cell volume.This variation in cell volume results in a modification of the tension exerted on the cell membrane at the thalamic receptors, a modification which probably represents the detected signal: thus, regulation of the water balance actually ensures the stability of cellular hydration, fundamental for homeostasis.
Any primitive variation of the water balance tends to vary the effective osmolality in the opposite direction. The resulting inhibition or stimulation of the centers of thirst and the secretion of antidiuretic hormone (ADH) makes it possible to reestablish the water balance by adapting the intake and urinary excretion of free water: effective osmolality is thus avoided.
Any decrease (below 270 mOsm / kg defining the hypotonic state) or increase (above 290 mOsm / kg defining the hypertonic state) of the effective osmolality translates into a disorder of water regulation. A primary water balance disorder occurs when control capacities are exceeded or when there is an abnormality in an element of the control loop. The result is a variation of the effective osmolality: a water overload decreases the effective osmolality; a water deficit increases it.
The water balance is not the only determinant of effective osmolality: the determinants of effective osmolality are represented by the water stock but also by the stock of osmotically effective osmoles. Thus, an important osmotic load (significant hyperglycemia, mannitol perfusion, etc.) tends to increase effective plasma osmolality. However, urine remains abundant despite the stimulation of ADH because polyuria is necessary to remove the osmotic load.
REGULATION OF THE SODIUM BALANCE SHEET:
It is carried out in such a way as to ensure the stability of what is known as “effective volume”. This term refers to a blood volume that is in reality poorly identified and whose variations affect the sodium balance: an increase in effective blood volume (effective hypervolemia) causes renal excretion of sodium, a decrease in effective blood volume (effective hypovolemia) renal retention of sodium. Changes in the effective blood volume are detected by changes in the wall tension caused by changes in blood pressure in the baroreceptors, in particular sinocarotid and juxtaglomerular renal, in the arterial system at high pressure, but also in the voloreceptors. the left atrium, the low-pressure system.
Any primitive variation of the sodium balance tends to vary the extracellular volume and therefore the effective volume in the same direction. The result is a variation in the same direction of glomerular filtration and a stimulation or inhibition of the renin-angiotensinaldosterone system and the atrial natriuretic factor which restore the sodium balance by adapting natriuresis: a significant variation in extracellular hydration and of the effective volume is thus avoided.
Any pathological variation of the effective volume of blood leads to a disorder of the sodium regulation. A primary disorder of the sodal balance occurs when the control capacities are exceeded or when there is an abnormality in an element of the control loop. The result is a variation of the effective volume: a sodium overload increases the effective volume; a deficit of sodium decreases it.
Sodium balance is not the only determinant of effective blood volume. The determinants of effective blood volume are the sodal stock, but also the left ventricular function, the value of the peripheral arterial resistances and the oncotic pressure of the plasma. A decrease in plasma oncotic pressure (nephrotic syndrome), a decrease in peripheral resistance (hepatic cirrhosis) or a decrease in cardiac output (heart failure) may be responsible for a decrease in the effective volume: in this case, retention soda is unable to restore the effective volume and the body is in a situation of heavy sodium overload, secondary to the effective hypovolemia.
The regulation of the water balance and that of the sodium balance are largely independent. A water balance disorder affects the effective osmolality but not the effective volumic insofar as the soda balance loop works properly. Similarly, a soda balance disorder, insofar as the water balance regulation loop works correctly, should be associated with an adapted variation of the water stock tending to make the overload or the sodium deficit isotonic in order to ensure stability of the effective osmolality and therefore of the cellular hydration.
However, the independence between the regulation of the water balance and that of the sodium balance is not complete. By stimulating the secretion of angiotensin (strongly dipsogenic) and ADH, effective hypovolemia, when it is large enough, interferes with the mechanisms of regulation of the water balance: it increases the liquid intake in connection with the thirst and decreases l renal elimination of free water due to increased DHA. The result is a water overload, as evidenced by the decrease in effective osmolality.
Primary water balance disorders:
A water balance disorder affects cellular hydration. Diagnosis is essentially based on the measurement of serum sodium.
Disorders of the water balance (overload or water deficiency) are most often secondary to a sodal balance disorder (cf infra).
Otherwise, the water balance disorder is “primitive”.
The primary disorders of the water balance have no effect on the regulation of the sodium balance: consequently the effective volume and the extracellular hydration remain clinically normal; the clinical picture is thus that of a disorder isolated from cellular hydration.
On the biological level, the variation in the effective osmolality induced by a primary water balance disorder results only in a variation in serum sodium, and in parallel with chloraeemia, since, with the exception of serum sodium and chloraemia, the concentration of the osmotically effective solutes usually assayed is regulated independently: a primary disorder of the water balance is biologically translated by hypo- or hypernatremia.
The variation in weight, effective osmolality and serum natality is proportional to the intensity of the water turbidity.However, the variation in weight is often difficult to determine because the initial weight is not always known: it is therefore the measurement of serum nitrate that remains essential in order to confirm the diagnosis.
The primary disorder of the water balance being diagnosed, it is fundamental to determine the etiology and the treatment, to determine the urinary osmolality in order to establish if it is adapted or not to the effective osmolality plasma. The measurement of the only natriuresis is of no interest in this situation where there is no sodal balance disorder: it is very variable and is only a reflection of the intakes.
The total osmolality P of the plasma can be measured by cryoscopy (normal: 275-295 mOsm / kg), but in this situation of primary water turbidity it can be more easily estimated by the formula:
P = 2 (Na + K) + glucose (mmol / L) + urea (mmol / L) (normal value is 290-310 mOsm / L)
The effective osmolality P eff can be calculated by:
P eff = P – urea = 2 (Na + K) + blood sugar
The urinary ionogram on a sample with urea measurement makes it possible to evaluate the urinary osmolality U according to the formula:
U = 2 (Na + K) + urea (mmol / L) to which the urinary glucose concentration (mmol / L) should be added.
PRIMITIVE WATER OVERLOAD:
It results in a table of clinically pure cellular hyperhydration.
Primary water overload is observed in all situations where the kidney is unable to dilute urine sufficiently.
Different etiologies can be distinguished:
– extrarenal causes: the dilution capacity of the urine, otherwise correct, is exceeded due to an excess of liquid intake.
It is the classic “water poisoning” in connection with the absorption of large quantities of beer or with a potomania responsible for a polyurodipsic syndrome (see below);
– renal causes: the dilution capacity of the urine is impaired
We distinguish between intrinsic (chronic renal failure) and extrinsic (unsuitable secretion of ADH [SIADH]). A clinical and biological situation identical to that of SIADH is observed in some elderly people, without any evidence of a disorder of ADH secretion. This situation corresponds to the osmostat reset of the Anglo-Saxons. Finally, a major potassium depletion may be responsible for cellular dehydration at the origin of a stimulation of the secretion of ADH.
Clinical signs suggestive of cellular hyperhydration are not very specific: disgust of the water, even nausea and / or vomiting. Weight gain is constant, but not always easy to assert. The neurological signs, also not very specific (disorders of the consciousness or the behavior, convulsions, coma), appear only in case of severe hyperhydration.The diagnosis of cellular hyperhydration is in fact essentially biological and is based on the observation of hyponatremia.
The absence of clear clinical signs of hyperhydration and of extracellular dehydration attests to the absence of associated disorder of the sodium balance and therefore to the “primitive” character of the water overload. At the very most, does the very slight increase in extracellular volume explain the sometimes infiltrated aspect of the integuments (but without genuine oedemas because there is no sign of the “bucket”) and the possible and slight decrease of the urea, creatinine and especially uric acid.
In view of the finding of a primitive water overload diagnosed on the existence of a hyponatremia reflecting the hypotonic state without appreciable modification of the extracellular hydration, it is first necessary to carry out a urinary ionogramme with urea dosage.
A weak urinary osmolality (urinary / plasma: U / P < 1) is adapted to the water overload: it reflects an excessive liquid intake. The dosage of DHA (which would be collapsed) is not useful.
Inadequate urinary osmolality (U / P > 1) indicates a lack of renal elimination (decreased urine dilution capacity). If the context alone does not allow it, the ADH assay allows an extrinsic decrease in urine dilution capacity (normal or high ADH, unsuitable for hyponatremia, signing the SIADH) to be decided and a decrease intrinsic (collapsed ADH).
Hyponatremia in relation to primary water overload is usually chronic and therefore generally well tolerated. The treatment consists in imposing a moderate water restriction on the patient as far as possible, in order to avoid the main risk, namely acute decompensation: this may be caused, for example, by the prescription of a diuretic treatment (for hypertension ) or diuresis (for urinary tract infection, etc.) or during hospitalization during which the laying of an isotonic glucose solute of “waiting” is sometimes abusively systematic.
In the case of an acute outbreak of hyponatremia poorly tolerated on the neurological level, when the water restriction, even severe, remains insufficient, the principle of treatment consists in obtaining a negative water balance by forcing the diuresis and compensating the urinary excretion of sodium (by sodium intakes significantly more concentrated in sodium than urine):
– infusion of hypertonic or even simply isotonic sodium chloride (at 9 g / L), at a rate of 0.5 g / h sodium chloride, but not exceeding 15 g on the first day, may be sufficient to cause abundant diuresis and little soda, which allows a gradual correction of hyponatremia. However, the risk of inducing sodium overload is not zero in chronic renal insufficiency and in the elderly (in whom glomerular filtration is physiologically diminished);
– the prescription of a loop diuretic (eg 40 to 80 mg / day furosemide), controlled by natriuresis (to compensate for sodium losses) and serum potassium, increases aqueous diuresis and hence the rapidity of the correction of the hyponatremia, without the risk of a sodium overload. The aim is to raise the serum sodium levels between 125 and 130 mmol / L in 5 to 8 hours: any rapid normalization should be avoided in order to avoid a severe centropontine myelinolysis.
In the case of a SIADH, it has been proposed to use lithium salts (10 to 20 mEq / d of lithium, ie 1 to 2 tablets / d of Téralithe LP t ) which prevent the action of DHA on the collecting tube, but the efficiency is inconstant. Demeclocycline (Ledermycin t ) is interesting because it has an antagonistic effect of that of DHA, but this antibiotic of the tetracycline family is no longer marketed because of its side effects (photosensitivity) and its risks in the l chronic renal insufficiency and in the subject with hepatopathy. As far as possible, the treatment will be etiologic, depending on the cause of SIADH.
PRIMITIVE WATER DEFICIT:
Primary water deficiency results in a clinically pure cell dehydration chart.
A primary water deficit may be related to:
– with insufficient water supply:
– thirst not felt (idiopathic adipsia or more often secondary to a cerebrovascular accident);
– unmet thirst (lack of water, very young age, disability, old age);
– with an excess of renal elimination (diabetes insipidus) or more rarely extrarenal (respiratory losses), but dehydration appears only if this excess is not, or not sufficiently compensated by a polydipsia.
Clinically, thirst is a major sign: present as early as the installation phase of dehydration, it should make it possible to avoid it.
The dryness of the mucous membranes (especially the inner side of the cheeks) is a classic and important sign.Weight loss is constant, but is difficult to quantify if the previous weight is not known accurately. In the case of severe dehydration, other clinical signs, particularly neurological signs, which make it all serious: disorders of consciousness, fever, convulsions … Intracerebral hematomas, especially in the infant, can complicate the most serious forms.
Biologically, hypernatremia, a reflection of hypertonia, makes it possible to affirm the diagnosis.
Cellular dehydration is sometimes associated with a sodal balance disorder (see below). It is the absence of clear clinical signs of hyperhydration and extracellular dehydration which attests to the absence of associated disorder of the sodium balance and therefore of the “primitive” character of the water deficit.
In view of the finding of a primary water deficiency diagnosed on the existence of a hypernatremia without appreciable modification of the extracellular hydration, it is first necessary to practice a urinary ionogramme with dosage of the urea.
A high urinary osmolality (U > 600 mOsm / L) is adapted. It shows a correct capacity of concentration of the urine and signs a liquid intake too weak.
Inadequate urinary osmolality indicates an excess of renal water elimination due to a lack of urine concentration (diabetes insipidus). The ADH assay allows us to decide between central diabetes insipidus (low or normal ADH, in any case unsuitable for hypertonicity) and nephrogenic diabetes insipidus (high ADH). The water restriction test is unnecessary and dangerous in the presence of cellular dehydration (hypernatremia).
It is based on rehydration, carried out as much as possible orally. Cellular dehydration, however, occurs only in the subject incapable of feeling or satisfying his thirst. It is often accompanied by disturbances of consciousness and requires a rehydration by parenteral route based on glucose isoou hypotonic solution (1 L in 6 hours then 1 to 2 L / d) replaced as soon as possible by oral hydrous intakes.
The following relation:
V (L) = 0.6 ‘ weight (kg) (1-140 / serum [mmol / L])
whose demonstration is based on a value of the apparent volume of distribution, also called osmotic distribution volume, of sodium equal to total water (about 60% of the body weight in the absence of hydration disorder) to appreciate the water deficit and therefore to estimate the volume V of solution to be brought. In fact, close monitoring of the natremia, every 4 to 6 hours, makes it possible to adapt the treatment as well as possible and prevent a too rapid decrease: the serum sodium must not decrease by more than 2 mmol / L / h. The addition of insulin (about 4 units of regular insulin per 10 g of glucose) may be useful to avoid the occurrence of osmotic diuresis impeding rehydration.
Cellular dehydration related to diabetes insipidus may justify a specific treatment (see below).
Sodium balance disorders:
A sodal balance disorder affects extracellular hydration.
The diagnosis is essentially based on clinical examination. There is no correlation between natremia and natriuresis: the serum does not give any information on the soda stock.
A sodium balance disorder is “simple” when it does not affect effective osmolality. It then shows a deficiency or isotonic hydrosodic overload. As a result, a simple sodium balance disorder does not result in a change in serum sodium, does not affect cellular hydration, and results in a pure extracellular hyperhydration or dehydration table.
In reality, sodium balance disorders are the most commonly complex disorders, combining a variation in effective volume and an effective osmolality variation, because effective volumics can influence the regulation of the water balance. A complex sodal balance disorder therefore affects both extracellular hydration and cellular hydration. The severity of the disorder of extracellular hydration reveals the importance of sodal balance disorder. Natremia is variable, a function of the possibly associated disorder of the water balance. It provides information on the state of cellular hydration.
A sodium overload results in a clinical picture of extracellular hyperhydration.
Because normal kidneys can eliminate an enormous amount of sodium by reducing the sodium reabsorption rate by a few hundredths, there are no extrarenal causes of sodium overload. The states of extracellular hyperhydration are always of renal cause, in connection with a natriuresis unsuited to the soda overload.
Sodium overload may be the cause of hypervolemia (hypervolemic sodal overload) or the consequence of effective hypovolemia (hypovolemic sodium overload).
The causes of hypervolaemic sodium overloads are:
– intrinsic kidneys, in relation to acute renal failure, chronic terminal renal failure, acute nephritic syndrome;
– extrinsic kidneys, in connection with hyperaldosteronism or hypercorticism.
The causes of hypovolemic sodium overloads are extrinsic kidneys. These are those of the effective hypovolemia which are at the origin: nephrotic syndrome, cardiac insufficiency or cirrhosis.
The diagnosis of sodium overload is based on the clinical signs of extracellular hyperhydration: hypertension and / or generalized edema. Hypertension may reflect hyperhydration in the vascular area: it is constant in hypervolemic sodium overload, but it is very unspecific. The generalized edemas predominating at the declivity points reflect the hyperhydration of the interstitial area, but are clinically detectable only in cases of high sodium overload. Pulmonary acute edema and left ventricular insufficiency are observed only in severe forms.
The intensity of the signs of extracellular hyperhydration is related to the importance of the sodium overload. In contrast, weight gain (often large) and serum sodium are in no way related to the intensity of extracellular hyperhydration. Natremia is variable according to the hypo-, iso- or hypertonic character of the sodium overload.Although its measurement is of no relevance for the positive or etiological diagnosis of extracellular hyperhydration, it is fundamental for determining the state of cellular hydration and defining the behavior to be followed with regard to water intakes.
Normal serum sodium levels reflect a correct adjustment of the water supply, thus ensuring the stability of the effective osmolality and therefore normal cellular hydration: this is a pure extracellular hyperhydration in connection with an isotonic overload due to water regulation . It is only in this case that the weight gain is proportional to the soda overload (weight gain of 1 kg for a sodium overload of about 150 mmol). Although sodium overload may be initially hypertonic, hypernatremia is rare, as it is responsible for intense thirst and stimulation of DHA, causing fluid retention to reduce sodium overload, isotonicity and serum sodium to a normal value.
Hyponatremia is common in cases of effective hypovolemia (which stimulates the secretion of angiotensin and DHA) or in the presence of any other factor that renders the kidney unable to eliminate sufficient free water. It translates cellular hyperhydration which aggravates the weight gain associated with extracellular hyperhydration and requires a restriction of water intake.
Extracellular hyperhydration, especially when it is major, is most often related to a hypovolemic sodium overload whose etiologies are summarized as decompensated nephrotic syndrome, heart failure and cirrhosis. The clinical context makes it easy to decide.
Natriuresis is weak, sometimes almost null and in any case unsuitable, with a urinary Na / K ratio of less than 1 in a context of functional renal insufficiency.
More rarely, extracellular hyperhydration is related to hypervolemic sodal overload. Arterial hypertension is then constant. Hypervolemia is the consequence of the sodium overload that the kidney fails to eliminate and must seek an extrinsic or intrinsic renal cause. Natriuresis is variable, but it is unsuitable for sodium overload. The clinical context (presence or not of edema) and biological (serum potassium, creatinine, proteinuria, and even measurement of plasma and urinary cortisol and aldosterone and of the aldosterone / plasma renin ratio) makes it possible to decide between renal insufficiency, nephritis, hypercorticism or hyperaldosteronism.
The symptomatic treatment of extracellular hyperhydration is that of sodium overload: it consists of decreasing the intakes and increasing renal excretion of sodium.
The disordered diet must be all the more strict as edema and / or ascites are important. A salt-free diet properly followed corresponds to a sodium chloride intake of less than 2 g / d.
Diuretic treatment is the symptomatic treatment of the expansion of extracellular volume, but certain rules must be observed:
– Thiazide diuretics and those of the loop cause an increase in kaliuresis and therefore require monitoring of serum potassium and the possible prescription of potassium supplementation or the combination of a hyperkalaemic diuretic;
– prescription of hyperkalaemic diuretics (spironolactone, …) is logical in any situation of hyperaldosteronism (primary or secondary) or in combination with a hypokalaemic diuretic, but is formally contraindicated in severe renal insufficiency due to the risk of hyperkalaemia;
– loop diuretics are the only ones indicated in renal insufficiency, as they are classically the only ones effective. Their effectiveness decreases as renal insufficiency progresses and their dose must be increased accordingly;
– diuretic treatment, because it decreases the soda stock, tends to decrease the effective blood volume and thus promotes the appearance of hyponatremia. A moderate water restriction can prevent this. In the case of frank hyponatremia, the restriction of water becomes indispensable until it disappears;
– in the presence of effective hypovolemia, etiological treatment is associated as far as possible in order to correct it as well as it is at the origin of the expansion of the extracellular volume:
– improvement of ventricular function (eg by ACE inhibitors) in patients with heart failure;
– stoppage of alcohol and hepatotoxic drugs in cases of cirrhosis;
– a perfusion of albumin will be prescribed only as a last resort in the case of nephrotic syndrome with menacing hypovolemia.
In the case of oligoanuric or preterminal renal insufficiency, sodium overload may be refractory to diuretic therapy, even at high doses (furosemide up to 1500 mg / day per os).
It then imposes an extrarenal purification.
It results in a clinical picture of extracellular dehydration.
Because the normal kidneys can cancel natriuresis if necessary, there is no deficiency soda deficiency. Thus, sodium deficits are usually due to sodium losses.
The losses can be:
– renal origin, intrinsic to the kidney (acute renal failure in diuresis recovery phase, chronic nephropathy, usually interstitial, with compulsory loss of salt) or extrinsic (adrenal insufficiency, diuretic intoxication);
– of extrarenal origin: sodium losses are most often digestive (diarrhea, vomiting, digestive fistula), but they may also be related to the constitution of a third area (intestinal occlusion) or profuse hypersudation (intense fever and prolonged, very high outside temperature), extensive burns, cystic fibrosis.
The diagnosis of sodium deficiency is based on the clinical signs of extracellular dehydration. The key sign is the “skin fold”: loss of the normal elasticity of the skin, more easily seen in the subclavicular regions and the back of the hand. It testifies to the dehydration of the interstitial sector. Tachycardia, feeling tired with standing discomforts of orthostatic hypotension are related to hypovolemia. The eyes are surrounded, sunk into the sockets. Permanent hypotension, or even collapse, occurs only in cases of major sodium deficiency. Biologically, hematocrit and protidemia are elevated, indicative of hemoconcentration. A moderate increase in plasma concentrations of urea, creatinine and uric acid is common, a translation of functional renal failure in relation to renal hypoperfusion.
The intensity of the signs of extracellular dehydration is related to the importance of the sodium deficiency. In contrast, weight loss (often moderate) and serum sodium are in no way related to the intensity of extracellular dehydration.Natremia is variable according to the hypo-, iso- or hypertonic character of the sodium deficiency. Although its measurement is of no relevance for the positive or etiological diagnosis of extracellular dehydration, it is fundamental for determining the state of cellular hydration and defining the behavior to be followed with regard to water intakes.Normal serum sodium corresponds to a correct adaptation of the water stock, which ensures the stability of the effective osmolality and therefore normal cellular hydration: this is a pure extracellular dehydration in relation to a sodium deficiency which has become isotonic due to water regulation . It is only in this case that weight loss is proportional to soda deficiency (weight loss of 1 kg for a sodium deficiency of about 150 mmol). Hypernatremia is due to the usually hypotonic character of sodium losses, but it only appears if the thirst induced by hyperosmolality can not be satisfied. This eventuality is more frequent in the elderly. It corresponds to global dehydration (both extracellular and cellular) and often severe. In reality, natremia is most often diminished, in spite of the originally hypotonic character of the deficit, because hypovolemia stimulates the secretion of angiotensin and ADH. It translates cellular hyperhydration which masks the weight loss associated with extracellular dehydration and requires the prescription of a hypertonic sodium intake by restricting water intake.
In view of a clinical picture of extracellular dehydration, it is first necessary to measure natriuresis on a 24-hour urine ionogram.
Low natriuresis (less than 15 mmol / d) with an Na / K ratio of less than 1 due to hyperaldosteronism secondary to effective hypovolemia, rare and concentrated urine (U / P > 10 urea) due to stimulation of the secretion of ADH by the hypovolemia effective translate an adapted renal behavior and sign the extrarenal origin of the deficit soda.
In contrast, natriuresis greater than 15 mmol / d is unsuitable for sodium deficiency and usually translates into renal deficiency. One exception is the existence of significant vomiting, which is responsible for both sodium deficiency and metabolic alkalosis. The need to remove bicarbonate to control alkalosis may explain the renal excretion of sodium bicarbonate despite the sodium deficiency. In this case, the kidney blocks the renal excretion of sodium chloride in order to spare the sodium: chloruria is then collapsed. This low chloruria makes it possible to differentiate with a sodium deficiency of renal origin, and in particular with an unreported intoxication with diuretics, difficult to differentiate from hidden vomiting because often occurring on the same ground (young woman wanting to lose weight) and driving both with extracellular dehydration with inadequate natriuresis, hypokalaemia and metabolic alkalosis.
Symptomatic treatment consists of correcting the sodium deficiency by the addition of sodium chloride. In hypovolemic shock, macromolecular solutes may be useful for rapidly restoring a stable hemodynamic state.
Sodium may be administered orally if the deficiency is small and without any disturbance of consciousness. Most often, it is carried out intravenously, as a large intake of sodium orally is often a source of vomiting which only aggravate the sodium deficit. The amount of sodium to be perfused can be calculated as if the sodium intake was distributed in total water, ie in about 60% of body weight. If the depletion is of extrarenal origin, the reappearance of a natriuresis testifies to the restitution of the sodic stock.
Intravenous sodium is most often given in isotonic form (9 g / L sodium chloride). In the case of associated hyponatremia, the hydric restriction makes it possible not to aggravate cellular hyperhydration; the use of hypertonic sodium salts is not necessarily justified insofar as the control loop of the water balance is functioning normally, as it may be the cause of a too rapid correction of the hyponatremia. In the presence of hypernatremia in this context of overall dehydration, the intakes will be isotonic until a stable hemodynamic state is reached, then hypotonic in sodium so as to correct hypernatremia and cell dehydration.
In case of associated acidosis (acute diarrhea), all or part of the sodium chloride is replaced with sodium bicarbonate.The etiological treatment depends on the origin of the sodium deficiency.
Natremia refers to the amount of sodium present in 1 L of plasma. It is normally around 140 mmol / L.
A disorder of the natremia, defined by serum sodium outside the range of 135-145 mmol / L, was discovered on the practice of a blood ionogram carried out on the occasion of a systematic assessment or of a symptom generally nonspecific , it is necessary to appreciate both the state of cellular hydration and the state of extracellular hydration in order to specify its mechanism and to deduce the most suitable therapeutic behavior. The treatment is indeed that of the disorders of the extracellular and / or cellular hydration that accompany it. This treatment, considered previously, will not be detailed here.
ETIOLOGICAL DIAGNOSIS OF HYPONATREMIA:
Hyponatremia is defined as a value of plasma sodium concentration of less than 135 mmol / L plasma. The treatment of hyponatremia depends on its aetiology and therefore requires above all to answer successively the following two questions:
– is the effective osmolality of the patient actually decreased (hypotonic hypotensionemia) as is usually the case, or is it found in a more rare situation where the effective osmolality is normal (isotonic hyponatraemia) , or even increased (hypertonic hyponatremia)?
– Is the extracellular volume of the patient approximately normal, markedly decreased or clearly increased?
The answer to the first question depends on the state of cellular hydration of the patient and the way to behave as regards the hydric intakes. From the answer to the second question depend on the value of the soda stock and the behavior to be kept as regards the sodium intakes and the institution of a diuretic treatment.
Appreciation of effective osmolality:
In most cases, hyponatremia is a reflection of a decrease in effective osmolality (hypotonic hyponatraemia). However, the rare cases of isotonic hyponatremia (formerly known as “false hyponatremia”) and hypertonic hyponatremia, which represent less than 5% of hyponatremia in hospitals and probably still much less in town medicine, must be systematically eliminated. Hypertonic hyponatremia is due to an increase in the water supply in relation to hypertonia.Hypertonic hyponatremia is suspected on high blood glucose (greater than 15 mmol / L) or clinical context (decompensated diabetes, mannitol or tris-hydroxy-methylamino-methane (THAM) perfusion, etc.). Isotonic hyponatraemia is a reflection of a decrease in osmolarity (without osmolality modification) in relation to hyperprotidemia or significant hyperlipemia.
It is suspected on biology or clinical context (uncontrolled myeloma, known context of major hyperlipemia …). In case of persistent doubt, the measurement of the effective osmolality (obtained by difference between the total osmolality measured by cryoscopy and the molar concentration of the urea) makes it possible to establish the definitive diagnosis of the type of hyponatremia.
Due to its physiological character, isotonic hyponatraemia must be respected: it does not justify any intake or restriction of water and sodium. Hypertonic hyponatremia is associated with cellular dehydration. Isotonic and hypertonic hyponatraemia will disappear spontaneously when the disturbance at the origin of their installation is corrected, if possible.
In the majority of cases, however, hyponatremia is hypotonic and then responsible for cellular hyperhydration, the neurological consequences of which may be severe if hypernatremia and hyperhydration are severe and abrupt. It is therefore advisable to prescribe a water restriction that is all the more strict as the hyponatremia is deep, because any water supply tends to aggravate cellular hyperhydration and its possible neurological consequences. Thus, with rare exceptions, which are easily ruled out in the clinical context as long as one knows how to think about it, hyponatremia must lead to the reflex prescription of a restriction of fluid intake.
Evaluation of extracellular volume:
A hypotonic hyponatraemia shows a hydric retention. This retention can be primitive, without associated disorder of the sodal balance, and then corresponds to a pure cellular hyperhydration. Water retention is more frequently associated with deficiency or sodium overload. This is why the estimation of the soda stock by the evaluation of the extracellular volume is essential in the presence of hypotonic hyponatremia to specify its mechanism and adapt the therapy. This assessment is based on clinical criteria.
The association of hyponatremia and extracellular dehydration leads to the diagnosis of hyponatremia of sodium deficiency. When the signs of extracellular dehydration are not clear, the dosage of urea and uric acid may make it possible to distinguish hyponatremia from sodic deficiency of hyponatraemia of primary water overload: in the first case, urea and uric acid are generally elevated due to functional renal insufficiency induced by hypovolemia; in the second case, they are generally lowered due to the slight subclinical increase in blood volume. The therapeutic behavior is the same as before any sodium deficiency of renal or extrarenal origin.
In contrast, the association of hyponatremia and extracellular hyperhydration causes the diagnosis of hyponatremia of overload. Hyponatremia comes from the association with the sodium overload of a hydric retention, of which the generally rapid weight gain measures the importance. The therapeutic behavior is the same as for any sodium overload: it is based on diuretics, but the presence of hyponatremia also requires a restriction of water.
Hyponatremia can be aggravated by the diuretic treatment which must then be carried out in hospital with a monitoring of the natremia every 4 to 6 hours.
The absence of a clinically perceptible disorder of extracellular hydration testifies to an almost normal soda stock.
Hyponatremia is then related to a primary water deficit.
ETIOLOGICAL DIAGNOSIS OF HYPERNATREMIA:
Hypernatremia is defined as serum sodium greater than 145 mmol / L. It is associated with a hypertonic state and therefore with cellular dehydration. Normally, any effective hyperosmolality causes a thirst. Consequently, the persistence of hypernatremia is always related to the fact that thirst can not be expressed (disorders of thirst corresponding to an abnormally high osmotic threshold, disorders of consciousness, very young child) or satisfied (disability, lack of water, extreme ages of life).
Hypernatremia is an indication of insufficient water stock adjustment. This deficiency can be primitive, without associated disorder of the sodal balance, and then corresponds to pure cellular dehydration. Water deficiency can also be secondary to a sodal balance disorder, and in this case much more often a deficit than a sodium overload. The treatment of hypernatremia depends on its etiology, which should therefore be clarified before anything else, by appreciating the effective volume of blood pressure and the state of extracellular hydration. This assessment is based on clinical criteria.
The absence of a clinically detectable disorder of the effective volume and extracellular hydration testifies to a suitable soda stock.
Hypernatremia is then related to a primary water deficit.
If there are signs of extracellular dehydration associated with hypernatremia, this is related to a hydrosodic deficiency.The severity of the signs of extracellular dehydration reveals the importance of sodium deficiency. The importance of hypernatremia provides information on the severity of cell dehydration. Weight loss, when it can be estimated, measures water deficit. The patient is threatened by both cellular dehydration and extracellular dehydration: this is the serious picture of overall dehydration occurring more frequently in an elderly patient.
The association of hypernatremia and clinical signs of extracellular hyperhydration is in favor of hypervolemic sodium overload (although sodium overload is rarely responsible for hypernatremia). Moderate hypernatremia (between 145 and 150 mmol / L) can be explained by the elevation of the osmotic threshold of thirst and by the increase in excretion of free water in relation to the inhibition of angiotensin and DHA by hypervolemia. Sometimes severe hypernatremia can be observed in intensive care in patients with renal insufficiency (with limited capacity for sodium excretion) in parenteral nutrition too high in sodium and unable to satisfy their thirst. The etiologies of these hypernatremia are those of hypervolemic soda overload. Symptomatic treatment is based on diuretics, but the presence of hypernatremia requires the addition of hydrous intake, if possible per os, if not with glucose solutes, so as to reduce hypernatremia and correct dehydration cellular.
Diuresis is usually between 1 and 2 L / d. It varies according to the fluid intake.
Polyurodipsic syndrome is defined by the association of polyuria (diuresis greater than 3 L / d) and intense thirst (polydipsia). Hypotonic polyures (aqueous diuresis) defined by a urinary osmolality of less than 200 mOsm / L or an osmolar flow rate of less than 50 mOsm / h and the isotonic polyuria (osmotic diuresis) defined by a urinary osmolality greater than 200 mOsm / L or an osmolar flow rate greater than 50 mOsm / h. The polyurodipsic syndrome becomes responsible for a water balance disorder, and therefore an effective osmolality disorder, only when thirst and polyuria can no longer compensate.
Sometimes, polydipsia is primitive (significant fluid intake): hypotonic polyuria (aqueous diuresis) is the logical consequence of the tendency to plasma hypotonia. In contrast, in diabetes insipidus, polyuria is primitive: polydipsia is the logical consequence of the tendency to plasma hypertension secondary to aqueous diuresis.
A polyurodipsic syndrome may also be secondary to an osmotic load exceeding the ability to concentrate urine, which tends to increase effective plasma osmolality. The consequences are an osmotic diuresis (isotonic polyuria) essential to eliminate the osmotic load and a polydipsia in connection with the tendency to plasma hypertonia.
Positive diagnosis is based on questioning. Etiologic diagnosis is often difficult: it is to establish whether polyuria is primitive and responsible for thirst, or whether thirst is primitive and responsible for polyuria.
The measurement of serum sodium is essential because it is a fundamental element of the diagnosis when it reveals a disturbance of effective osmolality. Hypotonic hyponatraemia translates secondary polyuria to an excess of fluid intake (water poisoning). An effective hyperosmolality (hypernatremia or hypertonic hyponatremia) is in favor of diabetes insipidus or an osmotic diuresis, easily differentiated by the clinical and biological context, or even by the assessment of urinary osmolality.
However, natremia usually remains within normal limits, reflecting a correct adaptation of polyuria and polydipsia.Measurement of urinary osmolality is then necessary to differentiate between aqueous diuresis (U < 200 mOsm / L) and osmotic diuresis (U > 200 mOsm / L).
The etiological diagnosis of osmotic diuresis is generally easy. The clinical context and the measurement of urinary osmolality usually make it possible to distinguish between situations in which the (otherwise normal) capacity of the urine concentration (high hyperglycemia, mannitol perfusion, etc.) and related situations with impaired concentration (chronic renal failure).
The etiological diagnosis of aqueous diuresis (excess intake or diabetes insipidus) is often more difficult. The determination of ADH allows the diagnosis of nephrogenic diabetes insipidus if it returns high. Otherwise, the water restriction test becomes necessary to differentiate polyuria secondary to excess fluid intake and polydipsia secondary to central diabetes insipidus.
In the case of central diabetes insipidus, there is no clear elevation of urinary osmolality in response to water restriction.
The water restriction test (which must therefore be carried out under hospital supervision) should be stopped in good time, otherwise dehydration and the corresponding hypernatremia which may be severe may occur.
In case of polyuria secondary to an excess of intakes, the renal response is adapted: the hydric restriction should always cause an elevation of the urinary osmolality. However, this elevation is often limited in the case of chronic polyuria because of the decreased kidney capacity to concentrate urine: the corticomedullary concentration gradient required for maximum urine concentration does not immediately recover. The study of the secretion of ADH under water restriction and that of the renal response to vasopressin, normal in case of polyuria secondary to an excess of intake, can then be useful.
Central diabetes insipidus may require replacement therapy with a nasal ADH (desmopressin) analogue. If the ADH deficiency is not complete, clofibrate (1.5 to 2 g / d, ie 3 to 4 capsules / day of Lipavlon t ) and carbamazepine (200 to 600 mg / d, ie 1 to 3 tablets / d of Tegretol t ) could be used successfully, as they appear to potentiate the effect of DHA.
Diabetes insipidus of nephrogenic origin requires treatment of the cause when this is possible. The association of a restricted salt diet and thiazide diuretics may decrease the aqueous diuresis. More recently, inhibitors of prostaglandin synthesis (indomethacin, ibuprofen) have been shown to be effective.
It is defined as a diuresis of less than 500 mL / d in the absence of acute retention of urine.
Oliguria is always pathological: the healthy subject always eliminates at least 500 mL of water per day due to the production of endogenous water by carbohydrate catabolism and the need to eliminate the osmolar load. Oliguria is related to kidney failure, most often acute. Indeed, chronic renal insufficiency does not lead to oliguria, but rather osmotic polyuria, except in case of dehydration added or end stage requiring dialysis.
Acute renal failure may be:
– functional, secondary to an effective hypovolemia, or in a table of hydrosoded overload as a consequence of effective hypovolemia (nephrotic syndrome, cardiac insufficiency, cirrhosis) or, conversely, in a table of sodium deficiency causing effective hypovolemia ;
The positive diagnosis is obvious, but it is important to eliminate a false oliguria (the patient does not remember to have urinated) by a serum creatinine dosage that objectively demonstrates the absence of renal insufficiency, on the other hand, a retention of urine on the absence of urge to urinate and globe bladder. In case of doubt, a bladder ultrasound shows an empty bladder.
The etiologic diagnosis is that of acute renal failure.
Dark urine with a high U / P urea ratio ( > 10), low natriuresis ( < 15 mmol / d) with a urinary Na / K ratio of less than 1, are in favor of functional renal failure secondary to effective hypovolemia the cause of which must be sought. In contrast, clear urine with a low urinary urea / urea ( < 10), unblocked natriuresis ( > 15 mmol / d) ratio with a urinary Na / K ratio greater than 1 renal insufficiency.