STUDY - Technical - New Dacian's Medicine
Fluid
and Electrolyte Imbalances (3)
Translation Draft
We continue with hyponatremia...
We continue with hyponatremia...
Etiologically, the plasma
concentration of Na+ of less than 135 mmol/ l frequently
reflects a hypotonous status. However, plasma osmolarity may be
normal or increased in some cases of hyponatremia, called
pseudohyponatremia. Plasma contains 93% water, the remaining 7%
being made up of lipids and plasma proteins. Because Na+ ions
are dissolved in plasma water, the increase in the nonaque phase
artificially decreases the concentration of Na+ measured per
liter of plasma (unless Na+ - sensitive glass electrodes are
used). Plasma osmolarity and Na+ concentration remain normal.
This type of hyponatremia has low clinical significance, except for the cause of hyperproteinemia or hyperlipidemia. Isotone or mildly hypotone hyponatremia can complicate transurethral resection of the prostate or bladder, since increased volumes of isoosmotic (manitol) or hypoosmotic (sorbitol or glycine) solutions are used for bladder washing and can be absorbed resulting in dilution hyponatremia.
Metabolism of sorbitol and glycine up to CO2 and water leads to hypotonicity if accumulated fluids and solvents are not quickly excreted. Hypertonic hyponatremia is generally caused by hyperglycaemia or, occasionally, by intravenous administration of mannitol. Relative insulin deficiency causes the impermeability of myocytes to glucose. So, in the case of poorly controlled diabetes, glucose is an effective osmol that draws water from muscle cells and causes hyponatremia. The plasma concentration of Na+ decreases by 1.4 mmol/ l for each 100 mg/ dl increase in plasma glucose concentration.
Most causes of hyponatremia are associated with low plasma osmolarity. In general, hypotonic hyponatremia is given either by primary water gain (and secondary by loss of Na+) or by initial loss of Na+ (and secondary by water gain). Hyponatremia in the absence of water retention is commonly associated with hypovolemic shock. Decrease in FEC volume stimulates athirst and secretion of AVP. Increased water intake and decreased renal excretion cause hyponatremia. It is important to note that diuretic-induced hyponatremia is almost always determined by thiazid diuretics.
Ansa diuretics decrease the tonicity of the medullary interstitial and affect the maximum ability of urine to concentrate. This limits the power of the AVP to promote water retention. In contrast, thiazid diuretics lead to Na+ and K+ deflation and water retention, mediated by AVP. In the presence of an increased K+ deficiency, transcellular ion exchange (K+ exits the cell and Na+ enters) may contribute to hyponatremia. Hyponatremia in the increase in The volume of FEC is commonly associated with edematous conditions such as congestive heart failure, cirrhosis of the liver and nephrotic syndrome.
These conditions share an effective decrease in circulating arterial volume leading to increased thirst and AVP levels. Additional factors that reduce the excretion of water without solvents include a decrease in RFG, a reduction in the supply of ultrafiltered to dilution sites (due to increased proximal fractional reabsorption of Na+ and water) and diuretic therapy. The degree of hyponatremia often correlates with the severity of the underlying conditions and is a prognostic factor. Acute or chronic oligurian renal failure may be associated with hyponatremia if the water ingested exceeds the excretion capacity of an equivalent volume.
Hyponatremia in the absence of a decrease in FEC volume, a decrease in effective circulating arterial volume or renal failure is frequently due to an increase in AVP secretion which causes a decrease in water excretion. Ingestion or administration of water is also necessary when elevated levels of AVP alone are ineffective to produce hyponatremia. This condition, known as inadequate antidiuretic hormone secretion syndrome (ADH or SIADH) is the most common cause of normonolemic hyponatremia and is caused by the nonphysiological release of AVP from the posterior pituitary gland or an ectopic source.
Renal excretion of free water is low, while the Na+ balance is unaffected. The most common causes of SIADH include neuropsychiatric and pulmonary diseases, malignant tumors, major surgery (postoperative pain) and pharmacological agents. Severe pain and nausea are physiological stimuli of AVP secretion (these stimuli being inadequate in the absence of hypovolemia or hyperosmolarity). Various disorders of the central nervous system may be associated with SIADH, such as meningitis, encephalitis, haemorrhages, stroke, psychosis, primary and metastatic tumors such as acute porphyria. Pneumonia, empyema, tuberculosis and acute respiratory failure may be complicated by secondary SIADH hyponatremia.
Hypoxemia, hypercapnia and positive pressure ventilation are all nonosmotic stimuli for the release of AVP. Many drugs either stimulate the release of AVP or potentiate its actions on the kidneys. The AVP secretion model can be used to classify SIADH into four subtypes: 1. chaotic autonomic secretion of AVP (ectopic production), 2. normally adjusted aVP secretion around a fixed minimum value of osmolarity or recalibrated osmostat (casexia, malnutrition), 3. normal response of AVP secretion to hypertonicity, but with inability to fully suppress it saddle low osmolarity (incomplete section of pituitary rod and 4. normal secretion) of AVP with increased sensitivity to actions or secretion of another antidiuretic factor (rare).
Hyponatremia can be caused by both excess and hormonal deficiency. Adrenal insufficiency and hypothyroidism may be associated with hyponatremia and should be differentiated from SIADH. Although the decrease of mineralocorticoids may contribute to hyponatremia and adrenal insufficiency, cortisol deficiency is that which leads to hypersecretion of AVP both indirectly (secondary to volume deplation) and directly (by cosecretion with the corticotropin release factor). mechanisms by which hypothyroidism causes hyponatremia include decreased cardiac output and RFG and increased aVP secretion in response to hemodynamic stimuli.
Finally, hyponatremia may occur in the absence of AVP secretion or renal failure if the kidney is unable to excrete the water intake brought through the diet. In primary or psychogenic polydipsia, compulsive water consumption can greatly exceed normal renal excretory capacity of 12 l/ day. These patients often have psychiatric conditions requiring medication, such as phenothiazides, which increase the feeling of thirst through the symptom of dry mouth. The maximum urine production depends on the minimum urinary osmolarity and the need for solvati excretion.
The metabolism of a normal diet generates almost 600 mosm/ day and the minimum urinary osmolarity in humans is 50 mosm/ kg. So the maximum daily urine production will be almost 12 liters. A solvatexcretion excretion rate of more than 750 mosm/day is defined as osmotic diuresis. A low-protein diet can produce about 250 mosm/ day, which corresponds to a maximum urine production of 5 l/ day at a minimum urinary tonicity of 50 mosm/ kg. Beer drinkers typically have a low ingestion of proteins and electrolytes with a high consumption of liquids (beer), which can exceed renal excretory capacity and cause hyponatremia. This phenomenon is known as beer potomania.
Clinical manifestations of hyponatremia are related to osmotic exchange of water, which leads to increased FIC and characteristically causes bloating of brain cells or cerebral edema. So the symptoms are primarily neurological and their severity is dependent on the rapidity of onset and the decrease in absolute concentration of plasma Na+. patients may be asymptomatic or complain of nausea and malaise.
As the concentration of Na+ ions in plasma drops sharply below 120 mmol/l or decreases rapidly. As described above, adaptive mechanisms designed to protect cell volume occur in chronic hyponatremia. Loss of Na+ and K+, followed by organic osmolitions in brain cells, decreases cerebral edema due to a secondary transcellular exchange of water (in FIC in FEC). The net effect is the decrease of cerebral edema and its symptoms.
From a diagnostic point of view, hyponatremia is not a disease, but a manifestation of various diseases. the underlying cause can often be discovered by correct anamnesis and careful physical examination, including an assessment of the status of the FEC volume and the actual circulating arterial volume. Differential diagnosis of hyponatremia, increased FEC volume and decrease in actual circulating volume includes congestive heart failure, cirrhosis of the liver and nephrotic syndrome.
Hypothyroidism and adrenal insufficiency tend to manifest through an almost normal volume of FEC and an effectively circulating low volume. All these conditions have certain characteristic signs and symptoms. Patients with AIDSH are frequently euvolemic. four laboratory analyses frequently provide useful information and limit differential diagnosis of hyponatremia: 1. plasma osmolarity, 2. urinary osmolarity, 3. urinary concentration of Na+ and 4. urinary concentration of K+. Because FEC tonicity is primarily determined by Na+ concentration, most patients with hyponatremia have low plasma osmolarity.
If plasma osmolarity is not low, pseudohyponatremia should be eliminated. The proper response of the kidney to hypoosmolarity is the excretion of a maximum volume of diluted urine, with osmolarity and density less than 100 mosm/ kg and 1003 respectively. This occurs in patients with primary polydipsia. If this is not present, there is the possibility of an impairment of the excretion of free water due to the action of aVP of the kidney. AVP secretion may be a physiological response to hemodynamic stimuli or may be an inadequate response to the presence of hyponatremia and euvolemia.
Because Na+ is the major cation of the FEC and is largely restricted to this compartment, the decrease in the fEC volume represents a decrease in the total Na+ content of the body. So, volume deletation in patients with normal renal function leads to increased tubular reabsorption of Na+ and a concentration of Na+ in urine below 20 mmol/ l. The discovery of a concentration of more than 20 mmol/ l in hypovolemic hyponatremia implies the presence of nephropathy with loss of salt, diuretic therapies, hypoaldosteronism, or occasionally vomiting.
Both urinary osmolarity and Na+ urinary concentration can be tracked repeatedly when assessing response to therapy. SIADH is characterized by hypoosmolar hyponatremia under conditions of inadequate concentration of urine (urinary osmolarity greater than 100 mosm/ kg). Patients are commonly normonolemic and have a normal Na+ balance.
They tend to have an average volume increase secondary to water retention and have a rate of urinary excretion of Na+ equal to Na+ intake (urinary concentration of Na+ is usually greater than 40 mmol/l). By definition, they have normal and constant renal, adrenal and thyroid function and have a normal K+ and acid-base balance. AIDSH is commonly associated with hypouricemia given by uricosuria induced by volume expansion. In contrast, hypovolemic patients tend to be hyperuricmic, secondary to increased proximal reabsorption of urates.
The aims of therapy are two: 1. increase the plasma concentration of Na+ by restricting water intake and increase its elimination and 2. correction of the underlying conditions.
This type of hyponatremia has low clinical significance, except for the cause of hyperproteinemia or hyperlipidemia. Isotone or mildly hypotone hyponatremia can complicate transurethral resection of the prostate or bladder, since increased volumes of isoosmotic (manitol) or hypoosmotic (sorbitol or glycine) solutions are used for bladder washing and can be absorbed resulting in dilution hyponatremia.
Metabolism of sorbitol and glycine up to CO2 and water leads to hypotonicity if accumulated fluids and solvents are not quickly excreted. Hypertonic hyponatremia is generally caused by hyperglycaemia or, occasionally, by intravenous administration of mannitol. Relative insulin deficiency causes the impermeability of myocytes to glucose. So, in the case of poorly controlled diabetes, glucose is an effective osmol that draws water from muscle cells and causes hyponatremia. The plasma concentration of Na+ decreases by 1.4 mmol/ l for each 100 mg/ dl increase in plasma glucose concentration.
Most causes of hyponatremia are associated with low plasma osmolarity. In general, hypotonic hyponatremia is given either by primary water gain (and secondary by loss of Na+) or by initial loss of Na+ (and secondary by water gain). Hyponatremia in the absence of water retention is commonly associated with hypovolemic shock. Decrease in FEC volume stimulates athirst and secretion of AVP. Increased water intake and decreased renal excretion cause hyponatremia. It is important to note that diuretic-induced hyponatremia is almost always determined by thiazid diuretics.
Ansa diuretics decrease the tonicity of the medullary interstitial and affect the maximum ability of urine to concentrate. This limits the power of the AVP to promote water retention. In contrast, thiazid diuretics lead to Na+ and K+ deflation and water retention, mediated by AVP. In the presence of an increased K+ deficiency, transcellular ion exchange (K+ exits the cell and Na+ enters) may contribute to hyponatremia. Hyponatremia in the increase in The volume of FEC is commonly associated with edematous conditions such as congestive heart failure, cirrhosis of the liver and nephrotic syndrome.
These conditions share an effective decrease in circulating arterial volume leading to increased thirst and AVP levels. Additional factors that reduce the excretion of water without solvents include a decrease in RFG, a reduction in the supply of ultrafiltered to dilution sites (due to increased proximal fractional reabsorption of Na+ and water) and diuretic therapy. The degree of hyponatremia often correlates with the severity of the underlying conditions and is a prognostic factor. Acute or chronic oligurian renal failure may be associated with hyponatremia if the water ingested exceeds the excretion capacity of an equivalent volume.
Hyponatremia in the absence of a decrease in FEC volume, a decrease in effective circulating arterial volume or renal failure is frequently due to an increase in AVP secretion which causes a decrease in water excretion. Ingestion or administration of water is also necessary when elevated levels of AVP alone are ineffective to produce hyponatremia. This condition, known as inadequate antidiuretic hormone secretion syndrome (ADH or SIADH) is the most common cause of normonolemic hyponatremia and is caused by the nonphysiological release of AVP from the posterior pituitary gland or an ectopic source.
Renal excretion of free water is low, while the Na+ balance is unaffected. The most common causes of SIADH include neuropsychiatric and pulmonary diseases, malignant tumors, major surgery (postoperative pain) and pharmacological agents. Severe pain and nausea are physiological stimuli of AVP secretion (these stimuli being inadequate in the absence of hypovolemia or hyperosmolarity). Various disorders of the central nervous system may be associated with SIADH, such as meningitis, encephalitis, haemorrhages, stroke, psychosis, primary and metastatic tumors such as acute porphyria. Pneumonia, empyema, tuberculosis and acute respiratory failure may be complicated by secondary SIADH hyponatremia.
Hypoxemia, hypercapnia and positive pressure ventilation are all nonosmotic stimuli for the release of AVP. Many drugs either stimulate the release of AVP or potentiate its actions on the kidneys. The AVP secretion model can be used to classify SIADH into four subtypes: 1. chaotic autonomic secretion of AVP (ectopic production), 2. normally adjusted aVP secretion around a fixed minimum value of osmolarity or recalibrated osmostat (casexia, malnutrition), 3. normal response of AVP secretion to hypertonicity, but with inability to fully suppress it saddle low osmolarity (incomplete section of pituitary rod and 4. normal secretion) of AVP with increased sensitivity to actions or secretion of another antidiuretic factor (rare).
Hyponatremia can be caused by both excess and hormonal deficiency. Adrenal insufficiency and hypothyroidism may be associated with hyponatremia and should be differentiated from SIADH. Although the decrease of mineralocorticoids may contribute to hyponatremia and adrenal insufficiency, cortisol deficiency is that which leads to hypersecretion of AVP both indirectly (secondary to volume deplation) and directly (by cosecretion with the corticotropin release factor). mechanisms by which hypothyroidism causes hyponatremia include decreased cardiac output and RFG and increased aVP secretion in response to hemodynamic stimuli.
Finally, hyponatremia may occur in the absence of AVP secretion or renal failure if the kidney is unable to excrete the water intake brought through the diet. In primary or psychogenic polydipsia, compulsive water consumption can greatly exceed normal renal excretory capacity of 12 l/ day. These patients often have psychiatric conditions requiring medication, such as phenothiazides, which increase the feeling of thirst through the symptom of dry mouth. The maximum urine production depends on the minimum urinary osmolarity and the need for solvati excretion.
The metabolism of a normal diet generates almost 600 mosm/ day and the minimum urinary osmolarity in humans is 50 mosm/ kg. So the maximum daily urine production will be almost 12 liters. A solvatexcretion excretion rate of more than 750 mosm/day is defined as osmotic diuresis. A low-protein diet can produce about 250 mosm/ day, which corresponds to a maximum urine production of 5 l/ day at a minimum urinary tonicity of 50 mosm/ kg. Beer drinkers typically have a low ingestion of proteins and electrolytes with a high consumption of liquids (beer), which can exceed renal excretory capacity and cause hyponatremia. This phenomenon is known as beer potomania.
Clinical manifestations of hyponatremia are related to osmotic exchange of water, which leads to increased FIC and characteristically causes bloating of brain cells or cerebral edema. So the symptoms are primarily neurological and their severity is dependent on the rapidity of onset and the decrease in absolute concentration of plasma Na+. patients may be asymptomatic or complain of nausea and malaise.
As the concentration of Na+ ions in plasma drops sharply below 120 mmol/l or decreases rapidly. As described above, adaptive mechanisms designed to protect cell volume occur in chronic hyponatremia. Loss of Na+ and K+, followed by organic osmolitions in brain cells, decreases cerebral edema due to a secondary transcellular exchange of water (in FIC in FEC). The net effect is the decrease of cerebral edema and its symptoms.
From a diagnostic point of view, hyponatremia is not a disease, but a manifestation of various diseases. the underlying cause can often be discovered by correct anamnesis and careful physical examination, including an assessment of the status of the FEC volume and the actual circulating arterial volume. Differential diagnosis of hyponatremia, increased FEC volume and decrease in actual circulating volume includes congestive heart failure, cirrhosis of the liver and nephrotic syndrome.
Hypothyroidism and adrenal insufficiency tend to manifest through an almost normal volume of FEC and an effectively circulating low volume. All these conditions have certain characteristic signs and symptoms. Patients with AIDSH are frequently euvolemic. four laboratory analyses frequently provide useful information and limit differential diagnosis of hyponatremia: 1. plasma osmolarity, 2. urinary osmolarity, 3. urinary concentration of Na+ and 4. urinary concentration of K+. Because FEC tonicity is primarily determined by Na+ concentration, most patients with hyponatremia have low plasma osmolarity.
If plasma osmolarity is not low, pseudohyponatremia should be eliminated. The proper response of the kidney to hypoosmolarity is the excretion of a maximum volume of diluted urine, with osmolarity and density less than 100 mosm/ kg and 1003 respectively. This occurs in patients with primary polydipsia. If this is not present, there is the possibility of an impairment of the excretion of free water due to the action of aVP of the kidney. AVP secretion may be a physiological response to hemodynamic stimuli or may be an inadequate response to the presence of hyponatremia and euvolemia.
Because Na+ is the major cation of the FEC and is largely restricted to this compartment, the decrease in the fEC volume represents a decrease in the total Na+ content of the body. So, volume deletation in patients with normal renal function leads to increased tubular reabsorption of Na+ and a concentration of Na+ in urine below 20 mmol/ l. The discovery of a concentration of more than 20 mmol/ l in hypovolemic hyponatremia implies the presence of nephropathy with loss of salt, diuretic therapies, hypoaldosteronism, or occasionally vomiting.
Both urinary osmolarity and Na+ urinary concentration can be tracked repeatedly when assessing response to therapy. SIADH is characterized by hypoosmolar hyponatremia under conditions of inadequate concentration of urine (urinary osmolarity greater than 100 mosm/ kg). Patients are commonly normonolemic and have a normal Na+ balance.
They tend to have an average volume increase secondary to water retention and have a rate of urinary excretion of Na+ equal to Na+ intake (urinary concentration of Na+ is usually greater than 40 mmol/l). By definition, they have normal and constant renal, adrenal and thyroid function and have a normal K+ and acid-base balance. AIDSH is commonly associated with hypouricemia given by uricosuria induced by volume expansion. In contrast, hypovolemic patients tend to be hyperuricmic, secondary to increased proximal reabsorption of urates.
The aims of therapy are two: 1. increase the plasma concentration of Na+ by restricting water intake and increase its elimination and 2. correction of the underlying conditions.
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