STUDY - Technical - New Dacian's Medicine
Fluid
and Electrolyte Imbalances (6)
Translation Draft
It's time to talk about hyperpotasemia.
It's time to talk about hyperpotasemia.
It is defined as a plasma
concentration of K+ greater than 5 mmoli/ l and occurs as a
result of both the release of K+ from cells and the decrease in
its renal eliminations. Increased ingestion of K+ is rarely the
only cause of hyperpotasemia due to the phenomenon of potassium
adaptation, which ensures a rapid excretion of K+ in response to
increased intake of K+ from the diet.
Iatrogenic hyperpotasemia may occur with excessive parenteral administration of K+ or in patients with renal impairment. Pseudohyperpotasemia represents false increases in the plasma concentration of K+, caused by the release of K+ from cells immediately from or following a venous puncture. Factors contributing to this are prolonged use of the tourniquet with or without repeated clenching of the fist, hemolysis and leukocytosis or marked thrombocytosis.
The latter two cause elevated levels of K+ in serum by releasing intracellular K+ as a result of blood clot formation. Pseudohyperpotasemia should be suspected in patients with elevated levels of K+ in plasma but who are asymptomatic and have no obvious underlying causes. If a correct venous puncture technique is used under these conditions and the K+ concentration in plasma (not serum) is measured, it must be normal. Intravascular hemolysis, tumor lysis syndrome and rhabdomyolysis lead to the release of K+ from cells as a result of cellular destruction.
Metabolic acidosis, with the exception of that produced by the accumulation of organic anions, may be associated with an average hyperpotasemia resulting from intracellular buffering of H+. As described above, insulin deficiency and hypertonicity (e.g. hyperglycaemia) stimulate the movement of K+ from FIC to FEC. The severity of exercise-induced hyperpotasis is related to the degree of physical exertion. It is determined by the release of K+ from the muscleand is usually rapidly reversible, often associated with a rebound hipposemia.
Treatment with beta blockers rarely causes hyperpotasemia, but may contribute to an increase in the plasma concentration of K+ under other conditions. Hyperpotasemic periodic paralysis is a rare dominant autosomal condition characterized by weakness or episodic muscle paralysis, precipitated by stimuli that normally lead to a medium hyperpotasemia (e.g. exercise). The genetic defect appears to be the substitution of a single amino acid, caused by a mutation in the Gene of The Na+ channels of skeletal muscles. Hyperpotasemia may occur in severe digital toxicity caused by inhibition of the Na+, K+, ATP-ase pump. Muscle depolarization relaxants, such as succinylcholine, can increase the plasma concentration of K+ especially in patients with massive trauma, burns or neuromuscular diseases.
Chronic hyperpotasemia is actually always associated with a decrease in renal secretion of K+ achieved both by impaired secretion and by decreased distal intake of solvents. The latter is rarely the only cause of damage to K+ excretion, but can contribute significantly to the hyperpotasemia of those with protein malnutrition (low urea excretion) and low FEC volume (decrease disintake of NaCl). The decrease in K+ secretion in the main cells is achieved both by an impairment of Na+ reabsorption and by an increase in Cl- reabsorption, both of which result in a decrease in DPCD DPC DPT (by a lower negativity of the lumen).
Hyporenonemic hypoaldosteronism is a syndrome characterized by euvolemia or an expansion of the FEC and a suppression of renin and aldosterone levels. This condition is consistently observed in moderate renal failure, diabetic nephropathy or chronic tubulo-interstitial conditions. Patients frequently have a decrease in kaliuretic response to exogenous mineralocorticoids, suggesting an increase in distal reabsorption of Cl- (due to an electroneutral reabsorption of Na+) may explain many of the features of hyporenenemic hypoaldosteronism. NSAID inhibits the secretion of renin and vasodilating renal prostaglandins. The result is a decrease in RFG and K+ secretion and often manifests as hyperpotasemia.
As a rule, the degree of hyperpotasemia within hyperaldosteronism is average in the absence of increased ingestion of K+ or renal dysfunction. Angiotensin conversion enzyme (ACE) inhibitors block the conversion of angiotensin I into angiotensin II resulting in impaired aldosterone release. Patients at increased risk of ACE inhibitor-induced hyperpotasemia are those with diabetes mellitus, renal failure, decreased actual circulating arterial volume, bilateral renal artery stenosis, or those receiving concomitant diuretics that save K+ or NSAID.
Decreased aldosterone synthesis may be caused by primary adrenal insufficiency (Addison's disease) or congenital adrenal enzyme deficiency. Heparin (including low molecular weight heparin) inhibits aldosterone production in cells in the glomerular area and may lead to severe hyperpotasemia in patients with underlying renal impairment, diabetes mellitus or those receiving K+-saving diuretics, ACE inhibitors or NSAIDs. Pseudohyperaldosteronism is a rare familial condition characterized by hyperpotasemia, metabolic acidosis, renal loss of Na+, hypotension, increased levels of renin and aldosterone and resistance of target organs to aldosterone.
The gene that modifies the mineralocorticoid receptor is normal in these patients, and electrolyte disorders may be reversible with high doses of exogenous mineralocorticoid or 11beta-HSDH inhibitor. The kaliuretic response to aldosterone is affected by k+-saving diuretics. Spironolactone is a competitive antagonist of mineralocorticoid, while amylorid and live land block the apical Na+ channels of the main cell.
Two other drugs that affect the secretion of K+ by blocking the reabsorption of Na+ in the distal nephron are represented by trimetoprim and pentamidine. These antimicrobial agents may contribute to hyperpotasemia that is often observed in HIV-infected patients, patients who have been treated for Pneumocystis carinii pneumonia.
Hyperpotasemia frequently complicates acute oligurial renal failure by increasing the release of K+ from the cellular level (acidosis, catabolism) and decreased excretion. Increased rate of distal flow and secretion of K+ per nephron compensates for decreased renal mass in chronic renal failure. However, this adaptive mechanism is insufficient to maintain the K+ balance when RFG is less than 10-15 ml/ min/ or oliguria occurs. On the other hand, asymptomatic obstruction of the urinary tract is a common cause of hyperpotasemia. Other nephropathy associated with k+ excretion impairment include drug-induced interstitial nephritis, lupus nephritis, sickle cell anaemia and diabetic nephropathy.
Gordon syndrome is a rare condition characterized by hyperpotasemia, metabolic acidosis and normal RFG. These patients consistently have a volemic increase with renin and aldosterone suppression, as well as resistance to the kaliuretic effect of exogenous mineralocorticoids. It has been suggested that these characteristics occur as a result of increased distal reabsorption of Cl- (through electroneutral reabsorption of Na+) or in other words as a result of the Cl-. A similar mechanism may be partially responsible for hyperpotasemia associated with cyclosporin nephrotoxicity. Hyperpotasemic distal ATR (type 4) can be given by both aldosteronism and Cl- shunt (resistant aldosterone).
Let's move on to clinical manifestations! Because the potential resting membrane is related to the ratio of K+ concentrations in FIC to FEC, hyperpotasemia partially depolarizes the cell membrane. Prolonged depolarization affects membrane excitability and manifests itself as muscle weakness that can progress to flaccid paralysis and hypoventilation, if respiratory muscles are involved. Hyperpotasemia also inhibits ammoniogenesis and reabsorption of NH4+ in the thick ascending branch of the Henle anse.
So, net acid excretion is impaired and results in metabolic acidosis, which can then exacerbate hyperpotasemia by exiting K+ from cells. The worst effect of hyperpotasis is cardiac toxicity, which does not correlate well with the plasma concentration of K+. The earliest electrocardiographic changes include increased amplitude of the T-wave or sharp T-waves. More severe hyperpotasemia causes an elongation of the PR interval and duration of the QRS complex, the delay of atrioventricular conduction and the disappearance of P-waves. Finally, it leads to ventricular fibrillation or asystole.
As for diagnosis, with rare exceptions, chronic hyperpotasemia is due to decreased K+ secretion. If the etiology is not obvious and the patient is asymptomatic, pseudohyperpotasemia should be excluded, as described above. Acute oligurian renal failure and severe chronic renal failure should also be excluded. Anamnesis should be focused on medication affecting K+ control and potential sources of K+ ingestion. The assessment of the FEC compartment, actual circulating volume and urine removal is an essential element of the physical examination.
The severity of hyperpotasemia is assessed by symptoms, plasma concentration of K+ and electrocardiographic changes. The appropriate renal response to hyperpotasemia is an excretion of at least 200 mmoli K+ daily. In most cases, the decrease in K+ eliminations is due to the decrease in K+ secretion, which can be assessed by measuring GCTK. A GCTK of less than 10 implies a decrease in K+ secretion due to both hypoaldosteronism and renal resistance to the effects of mineralocorticoid. This can be determined by assessing the kaliuretic response to the administration of mineralocorticoid. Primary adrenal insufficiency can be differentiated from hyporenemic hypoaldosteronism by examining the renin-aldosterone axis.
Renin and aldosterone levels should be measured in clino and orthostatism after three days of restriction of Na+ ingestion (Na+ ingestion should be less than 10 mmoli/ day) and in combination with a coil diuretic that induces an average volemic decrease. Aldosterone-resistant hyperpotasemia can have various causes of impaired distal reabsorption of Na+ or Cl-shunt. The first leads to loss of salt, decreased FEC volume and increased levels of renin and aldosterone. In contrast, the increase in distal reabsorption of Cl- is associated with volemic expansion and suppression of renin and aldosterone secretion. As mentioned above, hypoaldosteronism rarely causes severe hyperpotasemia in the absence of an increase in K+ intake, renal failure, transcellular exchange of K+ or antikaliuretic drugs.
I will complete this post with the presentation of some elements about the treatment. The therapeutic approach depends on the degree of hyperpotasemia obtained by determining the plasma concentration of K+, the associated muscle weakness and changes in the electrocardiogram. Potentially fatal hyperpotasemia rarely occurs, only when the plasma concentration of K+ exceeds 7.5 mmoli/ l and is frequently associated with severe muscle weakness, and on the electrocardiogram with the absence of P waves, widening of the QRS complex or ventricular arrhythmias.
Severe hyperpotasemia requires emergency treatment, which decreases membrane depolarization, introduces K+ into cells and stimulates K+ losses. In addition, exogenous intake of K+ and antikaliuretic drugs should be discontinued. The administration of calcium gluconate decreases membrane excitability. The usual dose is 10 ml 10% solution injected in 2-3 minutes. The effect occurs within a few minutes, but is short-lived (30-60 min) and the dose should be repeated if no electrocardiogram changes occur after 5-10 min.
Insulin causes K+ to enter cells through a mechanism described above and temporarily decreases the plasma concentration of K+. Although glucose alone stimulates the release of insulin from pancreatic beta cells, a faster response occurs when exogenous insulin is administered (along with glucose to prevent hypoglycaemia). A commonly recommended combination is 10-20 units of regular insulin and 25-50g glucose. Obviously, hyperglycaemic patients will not be given glucose.
As a result, the plasma concentration of K+ will decrease by 0.5-1.5 mmoli/ l in 15-30 in and the effect will last for several hours. Alkalinizing therapy with intravenous NaHCO3 can also introduce K+ into cells. This effect is safe when a 3 ampoule/ l isotone solution (134 mmoli/l NaHCO3) is administered and is particularly reserved for severe hyperpotasemia associated with metabolic acidosis. Patients with terminal renal disease rarely respond to this manoeuvre and do not tolerate Na+ loading and resulting volemic expansion. When administered parenterally or in nebulized form, beta2-adrenergic agonists stimulate the entry of K+ into cells. The onset of their action is at 30 minutes, lowering the plasma concentration of K+ by 0.5 to 1.5 mmoli/ l, and the effect lasts 2-4 hours.
The decrease in the concentration of K+ can be achieved using diuretics, cation-changing resins or dialysis. Ansa and thiazid diuretics, often combined, can increase the excretion of K+ if renal function is adequate. Na+ sulfonate polystyrene is a cation-changing resin that stimulates the exchange between Na+ and K+ in the gastrointestinal tract. Each gram binds a mole to K+ and releases 2-3 moles of Na+.
When administered per bone, the usual dose is 25-50 g mixed with 100 ml sorbitol 20% to prevent constipation. These resins will decrease the plasma concentration of K+ by 0.5 - 1 mmol/ l in 1 - 2 hours and the effect will last 4 to 6 hours. Na+ sulfonate polystyrene can also be given as a retentional enema containing 50 g resin and 50 ml 70% sorbitol mixed with 150 ml of water. Sorbitol should not be administered in the postoperative enema due to the increase in the incidence of the colonic necrosis induced by it, especially following renal transplantation. The best and fastest way to lower the plasma concentration of K+ is hemodialysis.
This should be reserved for patients with renal impairment and those with severe hyperpotasemia who do not respond to conservative measures. Peritoneal dialysis also decreases the concentration of K+, but is only 15-20% effective compared to hemodialysis. Finally, the underlying causes of hyperpotasemia should be treated. This may involve diet modification, correction of metabolic acidosis, careful volemic expansion and administration of exogenous mineralocorticoid.
Ready for today! There will be presentations on acidosis and alkalosis that I'm going to try to finish this weekend.
Iatrogenic hyperpotasemia may occur with excessive parenteral administration of K+ or in patients with renal impairment. Pseudohyperpotasemia represents false increases in the plasma concentration of K+, caused by the release of K+ from cells immediately from or following a venous puncture. Factors contributing to this are prolonged use of the tourniquet with or without repeated clenching of the fist, hemolysis and leukocytosis or marked thrombocytosis.
The latter two cause elevated levels of K+ in serum by releasing intracellular K+ as a result of blood clot formation. Pseudohyperpotasemia should be suspected in patients with elevated levels of K+ in plasma but who are asymptomatic and have no obvious underlying causes. If a correct venous puncture technique is used under these conditions and the K+ concentration in plasma (not serum) is measured, it must be normal. Intravascular hemolysis, tumor lysis syndrome and rhabdomyolysis lead to the release of K+ from cells as a result of cellular destruction.
Metabolic acidosis, with the exception of that produced by the accumulation of organic anions, may be associated with an average hyperpotasemia resulting from intracellular buffering of H+. As described above, insulin deficiency and hypertonicity (e.g. hyperglycaemia) stimulate the movement of K+ from FIC to FEC. The severity of exercise-induced hyperpotasis is related to the degree of physical exertion. It is determined by the release of K+ from the muscleand is usually rapidly reversible, often associated with a rebound hipposemia.
Treatment with beta blockers rarely causes hyperpotasemia, but may contribute to an increase in the plasma concentration of K+ under other conditions. Hyperpotasemic periodic paralysis is a rare dominant autosomal condition characterized by weakness or episodic muscle paralysis, precipitated by stimuli that normally lead to a medium hyperpotasemia (e.g. exercise). The genetic defect appears to be the substitution of a single amino acid, caused by a mutation in the Gene of The Na+ channels of skeletal muscles. Hyperpotasemia may occur in severe digital toxicity caused by inhibition of the Na+, K+, ATP-ase pump. Muscle depolarization relaxants, such as succinylcholine, can increase the plasma concentration of K+ especially in patients with massive trauma, burns or neuromuscular diseases.
Chronic hyperpotasemia is actually always associated with a decrease in renal secretion of K+ achieved both by impaired secretion and by decreased distal intake of solvents. The latter is rarely the only cause of damage to K+ excretion, but can contribute significantly to the hyperpotasemia of those with protein malnutrition (low urea excretion) and low FEC volume (decrease disintake of NaCl). The decrease in K+ secretion in the main cells is achieved both by an impairment of Na+ reabsorption and by an increase in Cl- reabsorption, both of which result in a decrease in DPCD DPC DPT (by a lower negativity of the lumen).
Hyporenonemic hypoaldosteronism is a syndrome characterized by euvolemia or an expansion of the FEC and a suppression of renin and aldosterone levels. This condition is consistently observed in moderate renal failure, diabetic nephropathy or chronic tubulo-interstitial conditions. Patients frequently have a decrease in kaliuretic response to exogenous mineralocorticoids, suggesting an increase in distal reabsorption of Cl- (due to an electroneutral reabsorption of Na+) may explain many of the features of hyporenenemic hypoaldosteronism. NSAID inhibits the secretion of renin and vasodilating renal prostaglandins. The result is a decrease in RFG and K+ secretion and often manifests as hyperpotasemia.
As a rule, the degree of hyperpotasemia within hyperaldosteronism is average in the absence of increased ingestion of K+ or renal dysfunction. Angiotensin conversion enzyme (ACE) inhibitors block the conversion of angiotensin I into angiotensin II resulting in impaired aldosterone release. Patients at increased risk of ACE inhibitor-induced hyperpotasemia are those with diabetes mellitus, renal failure, decreased actual circulating arterial volume, bilateral renal artery stenosis, or those receiving concomitant diuretics that save K+ or NSAID.
Decreased aldosterone synthesis may be caused by primary adrenal insufficiency (Addison's disease) or congenital adrenal enzyme deficiency. Heparin (including low molecular weight heparin) inhibits aldosterone production in cells in the glomerular area and may lead to severe hyperpotasemia in patients with underlying renal impairment, diabetes mellitus or those receiving K+-saving diuretics, ACE inhibitors or NSAIDs. Pseudohyperaldosteronism is a rare familial condition characterized by hyperpotasemia, metabolic acidosis, renal loss of Na+, hypotension, increased levels of renin and aldosterone and resistance of target organs to aldosterone.
The gene that modifies the mineralocorticoid receptor is normal in these patients, and electrolyte disorders may be reversible with high doses of exogenous mineralocorticoid or 11beta-HSDH inhibitor. The kaliuretic response to aldosterone is affected by k+-saving diuretics. Spironolactone is a competitive antagonist of mineralocorticoid, while amylorid and live land block the apical Na+ channels of the main cell.
Two other drugs that affect the secretion of K+ by blocking the reabsorption of Na+ in the distal nephron are represented by trimetoprim and pentamidine. These antimicrobial agents may contribute to hyperpotasemia that is often observed in HIV-infected patients, patients who have been treated for Pneumocystis carinii pneumonia.
Hyperpotasemia frequently complicates acute oligurial renal failure by increasing the release of K+ from the cellular level (acidosis, catabolism) and decreased excretion. Increased rate of distal flow and secretion of K+ per nephron compensates for decreased renal mass in chronic renal failure. However, this adaptive mechanism is insufficient to maintain the K+ balance when RFG is less than 10-15 ml/ min/ or oliguria occurs. On the other hand, asymptomatic obstruction of the urinary tract is a common cause of hyperpotasemia. Other nephropathy associated with k+ excretion impairment include drug-induced interstitial nephritis, lupus nephritis, sickle cell anaemia and diabetic nephropathy.
Gordon syndrome is a rare condition characterized by hyperpotasemia, metabolic acidosis and normal RFG. These patients consistently have a volemic increase with renin and aldosterone suppression, as well as resistance to the kaliuretic effect of exogenous mineralocorticoids. It has been suggested that these characteristics occur as a result of increased distal reabsorption of Cl- (through electroneutral reabsorption of Na+) or in other words as a result of the Cl-. A similar mechanism may be partially responsible for hyperpotasemia associated with cyclosporin nephrotoxicity. Hyperpotasemic distal ATR (type 4) can be given by both aldosteronism and Cl- shunt (resistant aldosterone).
Let's move on to clinical manifestations! Because the potential resting membrane is related to the ratio of K+ concentrations in FIC to FEC, hyperpotasemia partially depolarizes the cell membrane. Prolonged depolarization affects membrane excitability and manifests itself as muscle weakness that can progress to flaccid paralysis and hypoventilation, if respiratory muscles are involved. Hyperpotasemia also inhibits ammoniogenesis and reabsorption of NH4+ in the thick ascending branch of the Henle anse.
So, net acid excretion is impaired and results in metabolic acidosis, which can then exacerbate hyperpotasemia by exiting K+ from cells. The worst effect of hyperpotasis is cardiac toxicity, which does not correlate well with the plasma concentration of K+. The earliest electrocardiographic changes include increased amplitude of the T-wave or sharp T-waves. More severe hyperpotasemia causes an elongation of the PR interval and duration of the QRS complex, the delay of atrioventricular conduction and the disappearance of P-waves. Finally, it leads to ventricular fibrillation or asystole.
As for diagnosis, with rare exceptions, chronic hyperpotasemia is due to decreased K+ secretion. If the etiology is not obvious and the patient is asymptomatic, pseudohyperpotasemia should be excluded, as described above. Acute oligurian renal failure and severe chronic renal failure should also be excluded. Anamnesis should be focused on medication affecting K+ control and potential sources of K+ ingestion. The assessment of the FEC compartment, actual circulating volume and urine removal is an essential element of the physical examination.
The severity of hyperpotasemia is assessed by symptoms, plasma concentration of K+ and electrocardiographic changes. The appropriate renal response to hyperpotasemia is an excretion of at least 200 mmoli K+ daily. In most cases, the decrease in K+ eliminations is due to the decrease in K+ secretion, which can be assessed by measuring GCTK. A GCTK of less than 10 implies a decrease in K+ secretion due to both hypoaldosteronism and renal resistance to the effects of mineralocorticoid. This can be determined by assessing the kaliuretic response to the administration of mineralocorticoid. Primary adrenal insufficiency can be differentiated from hyporenemic hypoaldosteronism by examining the renin-aldosterone axis.
Renin and aldosterone levels should be measured in clino and orthostatism after three days of restriction of Na+ ingestion (Na+ ingestion should be less than 10 mmoli/ day) and in combination with a coil diuretic that induces an average volemic decrease. Aldosterone-resistant hyperpotasemia can have various causes of impaired distal reabsorption of Na+ or Cl-shunt. The first leads to loss of salt, decreased FEC volume and increased levels of renin and aldosterone. In contrast, the increase in distal reabsorption of Cl- is associated with volemic expansion and suppression of renin and aldosterone secretion. As mentioned above, hypoaldosteronism rarely causes severe hyperpotasemia in the absence of an increase in K+ intake, renal failure, transcellular exchange of K+ or antikaliuretic drugs.
I will complete this post with the presentation of some elements about the treatment. The therapeutic approach depends on the degree of hyperpotasemia obtained by determining the plasma concentration of K+, the associated muscle weakness and changes in the electrocardiogram. Potentially fatal hyperpotasemia rarely occurs, only when the plasma concentration of K+ exceeds 7.5 mmoli/ l and is frequently associated with severe muscle weakness, and on the electrocardiogram with the absence of P waves, widening of the QRS complex or ventricular arrhythmias.
Severe hyperpotasemia requires emergency treatment, which decreases membrane depolarization, introduces K+ into cells and stimulates K+ losses. In addition, exogenous intake of K+ and antikaliuretic drugs should be discontinued. The administration of calcium gluconate decreases membrane excitability. The usual dose is 10 ml 10% solution injected in 2-3 minutes. The effect occurs within a few minutes, but is short-lived (30-60 min) and the dose should be repeated if no electrocardiogram changes occur after 5-10 min.
Insulin causes K+ to enter cells through a mechanism described above and temporarily decreases the plasma concentration of K+. Although glucose alone stimulates the release of insulin from pancreatic beta cells, a faster response occurs when exogenous insulin is administered (along with glucose to prevent hypoglycaemia). A commonly recommended combination is 10-20 units of regular insulin and 25-50g glucose. Obviously, hyperglycaemic patients will not be given glucose.
As a result, the plasma concentration of K+ will decrease by 0.5-1.5 mmoli/ l in 15-30 in and the effect will last for several hours. Alkalinizing therapy with intravenous NaHCO3 can also introduce K+ into cells. This effect is safe when a 3 ampoule/ l isotone solution (134 mmoli/l NaHCO3) is administered and is particularly reserved for severe hyperpotasemia associated with metabolic acidosis. Patients with terminal renal disease rarely respond to this manoeuvre and do not tolerate Na+ loading and resulting volemic expansion. When administered parenterally or in nebulized form, beta2-adrenergic agonists stimulate the entry of K+ into cells. The onset of their action is at 30 minutes, lowering the plasma concentration of K+ by 0.5 to 1.5 mmoli/ l, and the effect lasts 2-4 hours.
The decrease in the concentration of K+ can be achieved using diuretics, cation-changing resins or dialysis. Ansa and thiazid diuretics, often combined, can increase the excretion of K+ if renal function is adequate. Na+ sulfonate polystyrene is a cation-changing resin that stimulates the exchange between Na+ and K+ in the gastrointestinal tract. Each gram binds a mole to K+ and releases 2-3 moles of Na+.
When administered per bone, the usual dose is 25-50 g mixed with 100 ml sorbitol 20% to prevent constipation. These resins will decrease the plasma concentration of K+ by 0.5 - 1 mmol/ l in 1 - 2 hours and the effect will last 4 to 6 hours. Na+ sulfonate polystyrene can also be given as a retentional enema containing 50 g resin and 50 ml 70% sorbitol mixed with 150 ml of water. Sorbitol should not be administered in the postoperative enema due to the increase in the incidence of the colonic necrosis induced by it, especially following renal transplantation. The best and fastest way to lower the plasma concentration of K+ is hemodialysis.
This should be reserved for patients with renal impairment and those with severe hyperpotasemia who do not respond to conservative measures. Peritoneal dialysis also decreases the concentration of K+, but is only 15-20% effective compared to hemodialysis. Finally, the underlying causes of hyperpotasemia should be treated. This may involve diet modification, correction of metabolic acidosis, careful volemic expansion and administration of exogenous mineralocorticoid.
Ready for today! There will be presentations on acidosis and alkalosis that I'm going to try to finish this weekend.
Pleasant, restful, fun
weekend, full of understanding, love and gratitude!
Dorin, Merticaru