Transcript Causes and evaluation of hyperkalemia in adults

The Lethal Electrolyte
Hyperkalemia
‫• مرد ‪ 62‬ساله اي با نارسايي كليه ي مزمن و كراتينين ‪2.1 mg /dL‬‬
‫و پتاسيم نرمال به دليل فشا رخون باال روي رژيم كم نمك قرار مي‬
‫گيرد‪ .‬دو هفته بعد متوجه ضعف عضالني مي شود‪ .‬در معاينه ي‬
‫فيزيكي مختصر كاهش تورگور پوست و ضعف عضالت‬
‫پروگزيمال يافته مي شود ‪ ECG .‬بيمار موج ‪ T‬بلند و پهن شدن‬
‫موج ‪ P‬و كمپلكس ‪ QRS‬رانشان مي دهد‪ .‬آزمايش هاي وي‬
‫بصورت زير مي باشد‪:‬‬
• Plasma Na = 130 meq /L
•
K= 9.8 meq /L
•
Cl= 98 meq /L
•
HCO3= 19meq /L
•
Cr= 2.7 mg/dL
•
Arterial pH= 7.32
‫‪‬محتملترين فاكتور ايجاد كننده ي هايپركالمي درا ين فرد چيست؟‬
‫‪ .1‬نارسايي زمينه اي كليه‬
‫‪ .2‬كمبود حجم‬
‫‪ .3‬اسيدوز متابوليك‬
‫‪ .4‬همه ي موارد باال‬
Causes and evaluation of
hyperkalemia in adults
• Hyperkalemia is a common clinical problem.
• Potassium enters the body via oral intake or intravenous
infusion, is largely stored in the cells, and is then excreted in
the urine.
• The major causes of hyperkalemia are increased potassium
release from the cells and, most often, reduced urinary
potassium excretion
• Total body potassium stores are approximately 3000 meq or
more (50 to 75 meq/kg body weight).
• In contrast to sodium, which is the major cation in the
extracellular fluid and has a much lower concentration in the
cells, potassium is primarily an intracellular cation, with the
cells containing approximately 98 percent of body potassium.
• The intracellular potassium concentration is approximately
140 meq/L compared with 4 to 5 meq/L in the extracellular
fluid.
• The difference in distribution of the two cations is maintained
by the Na-K-ATPase pump in the cell membrane, which pumps
sodium out of and potassium into the cell in a 3:2 ratio.
• The ratio of the potassium concentrations in the cells and
the extracellular fluid is the major determinant of the
resting membrane potential across the cell membrane,
which sets the stage for the generation of the action
potential that is essential for normal neural and muscle
function.
• Thus, both hyperkalemia and hypokalemia can cause
muscle paralysis and potentially fatal cardiac
arrhythmias.
• The plasma potassium concentration is
determined by the relationship among
potassium intake, the distribution of
potassium between the cells and the
extracellular fluid, and urinary potassium
excretion.
• In normal individuals, dietary potassium is absorbed in the
intestines and then largely excreted in the urine, a process
that is primarily determined by potassium secretion by the
principal cells in the two segments that follow the distal
tubule: the connecting segment and cortical collecting tubule
There are three major factors that stimulate principal cell
potassium secretion:
●An increase in plasma potassium concentration and/or
potassium intake
●An increase in aldosterone secretion
●Enhanced delivery of sodium and water to the distal potassium
secretory site
• Ingestion of a potassium load leads initially to the uptake of
most of the excess potassium by cells in muscle and the liver,
a process that is facilitated by insulin and the beta-2adrenergic receptors, both of which increase the activity of
Na-K-ATPase pumps in the cell membrane
• Some of the ingested potassium remains in the extracellular
fluid, producing a mild elevation in the plasma potassium
concentration.
• The increase in plasma potassium stimulates the secretion of
aldosterone, which enhances both sodium reabsorption and
potassium secretion in the principal cells
• The net effect is that most of the potassium load is excreted
within six to eight hours.
• Both cellular uptake and urinary excretion of an acute
potassium load are impaired in patients with advanced acute
or chronic kidney disease
• Potassium adaptation — Hyperkalemia is a rare occurrence in
normal individuals because the cellular and urinary responses
prevent significant potassium accumulation in the
extracellular fluid.
•
Furthermore, the efficiency of potassium excretion is
enhanced if potassium intake is increased, thereby allowing
what might otherwise be a fatal potassium load to be
tolerated. This phenomenon, called potassium adaptation, is
mostly due to the ability to more rapidly excrete potassium in
the urine
●Increasing potassium intake alone is not a common cause of
hyperkalemia unless it occurs acutely.
Acute hyperkalemia can rarely be induced (primarily in
infants because of their small size) by the administration of
potassium penicillin as an intravenous bolus, the accidental
ingestion of a potassium-containing salt substitute, or the
use of stored blood for exchange transfusions.
In addition, moderate increases in potassium intake can be an
important contributor to the development of hyperkalemia
in patients with impaired potassium excretion due, for
example, to hypoaldosteronism and/or renal insufficiency
●Persistent hyperkalemia requires impaired urinary potassium
excretion.
this is generally associated with a reduction in aldosterone
secretion or responsiveness, acute or chronic kidney disease,
and/or diminished delivery of sodium and water to the distal
potassium secretory site.
 Metabolic acidosis — In patients with metabolic
acidosis other than organic acidosis due to lactic
acidosis or ketoacidosis, buffering of excess
hydrogen ions in the cells leads to potassium
movement into the extracellular fluid, a
transcellular shift that is obligated in part by the
need to maintain electroneutrality
• Smaller effect in lactic acidosis or ketoacidosis — In
contrast to the above finding, hyperkalemia due to
an acidosis-induced shift of potassium from the
cells into the extracellular fluid does not occur in
the organic acidoses lactic acidosis and ketoacidosis
• A possible contributory factor in both disorders is
the ability of the organic anion and the hydrogen
ion to enter into the cell via a sodium-organic anion
cotransporter.
• Smaller effect in respiratory acidosis :
• Hyperkalemia due to respiratory acidosis is not a
common clinical problem.
• The effect of respiratory acidosis on the plasma
potassium is greater with more severe acidosis and
with a longer duration of acidosis
• The mechanisms responsible for the lesser increase
in plasma potassium in respiratory acidosis
compared with metabolic acidosis are not well
defined
 Insulin deficiency, hyperglycemia, hyperosmolality
Insulin promotes potassium entry into cells. Thus, the
ingestion of glucose (which stimulates endogenous insulin
secretion) minimizes the rise in the serum potassium
concentration induced by concurrent potassium intake,
while glucose ingestion alone in patients without diabetes
modestly lowers the serum potassium
• The findings are different in uncontrolled diabetes mellitus.
In this setting, the combination of insulin deficiency and
hyperosmolality induced by hyperglycemia frequently leads
to hyperkalemia
• In addition to hyperglycemia induced by insulin deficiency,
hyperkalemia induced by hyperosmolality has also been
described with hypernatremia /sucrose contained in
intravenous immune globulin /radiocontrast media /and the
administration of hypertonic mannitol
●Fasting is associated with an appropriate reduction in insulin
levels that can lead to an increase in plasma potassium. This
may be a particular problem in dialysis patients.
The risk of hyperkalemia during preoperative fasting can be
minimized by the administration of insulin and glucose in
patients with diabetes, or glucose alone in patients without
diabetes
 Increased tissue catabolism — Any cause of increased tissue
breakdown leads to the release of intracellular potassium
into the extracellular fluid. Hyperkalemia can occur in this
setting, particularly if renal failure is also present.
• Clinical examples include trauma (including non-crush
trauma), the administration of cytotoxic or radiation therapy
to patients with lymphoma or leukemia (the tumor lysis
syndrome), and severe accidental hypothermia
 Beta blockers
• Beta blockers interfere with the beta-2-adrenergic facilitation of
potassium uptake by the cells, particularly after a potassium load
• An increase in serum potassium is primarily seen with nonselective
beta blockers (such as propranolol and labetalol). In contrast, beta1-selective blockers such as atenolol have little effect on serum
potassium since beta-2 receptor activity remains intact
• The rise in serum potassium with nonselective beta blocker therapy
is usually less than 0.5 meq/L. True hyperkalemia is rare unless
there is a large potassium load, marked exercise (or an additional
defect in potassium handling that prevents excretion of the excess
extracellular potassium, such as hypoaldosteronism or renal failure
 Hyperkalemic periodic paralysis — Hyperkalemic periodic
paralysis is an autosomal dominant disorder in which
episodes of weakness or paralysis are usually precipitated by
cold exposure, rest after exercise, fasting, or the ingestion of
small amounts of potassium.
• The most common abnormality in hyperkalemic periodic
paralysis is a point mutation in the gene for the alpha subunit
of the skeletal muscle cell sodium channel
 Other — Other rare causes of hyperkalemia due to
translocation of potassium from the cells into the
extracellular fluid include:
● Digitalis overdose; due to dose-dependent inhibition of the
Na-K-ATPase pump .
● Red cell transfusion due to leakage of potassium out of the
red cells during storage. Hyperkalemia primarily occurs in
infants and with massive transfusions
● Use of drugs that activate ATP-dependent potassium
channels in cell membranes, such as calcineurin inhibitors
(eg, cyclosporine and tacrolimus), diazoxide, minoxidil, …
 REDUCED URINARY POTASSIUM EXCRETION — Urinary potassium
excretion is primarily mediated by potassium secretion in the
principal cells in the two segments that follow the distal tubule: the
CS and CCT
•
Three major factors are required for adequate potassium secretion
at these sites: adequate aldosterone secretion, adequate
responsiveness to aldosterone, and adequate distal sodium and
water delivery
•
The widely used term, hypoaldosteronism, applies to both reduced
aldosterone secretion and reduced response to aldosterone.
The four major causes of hyperkalemia due to reduced
urinary potassium secretion are:
●Reduced aldosterone secretion
●Reduced response to aldosterone (aldosterone resistance)
●Reduced distal sodium and water delivery as occurs in
effective arterial blood volume depletion
●Acute and chronic kidney disease in which one or more of
the above factors are present
• EVALUATION — Evaluation of the patient with hyperkalemia
usually begins with a careful history, evaluation for clinical
manifestations of hyperkalemia such as muscle weakness and
characteristic changes on the electrocardiogram, and
laboratory testing for the causes of hyperkalemia
Exclude pseudohyperkalemia
•
Pseudohyperkalemia, refers to those conditions in which the
elevation in the measured serum potassium concentration is
due to potassium movement out of the cells during or after
the blood specimen has been drawn.
• It is usually related to the technique of blood drawing, but it
can also occur in patients with marked elevations in platelet
or white blood cell counts
• Pseudohyperkalemia should be suspected when there is
no apparent cause for the hyperkalemia in an
asymptomatic patient who has no clinical or
electrocardiographic manifestations of hyperkalemia.
• One clue to the possible presence of
pseudohyperkalemia is wide variability in repeated
measurements of the serum potassium concentration
(eg, from 5 to 6.5 meq/L, often including some normal
values).
• Increasing potassium intake is not a major cause of
hyperkalemia in individuals without another risk factor such
as reduced aldosterone secretion or responsiveness or acute
or chronic kidney disease.
• In healthy adults, raising potassium intake from a normal
value of 100 meq/day to a much higher value of 400
meq/day only produces a modest elevation in serum
potassium from 3.8 meq/L at baseline to 4.8 meq/L
• Urinary potassium excretion increases
• Clinical manifestations of hyperkalemia in
adults
• CLINICAL MANIFESTATIONS — The most serious
manifestations of hyperkalemia are muscle weakness or
paralysis, cardiac conduction abnormalities, and cardiac
arrhythmias.
•
These manifestations usually occur when the serum
potassium concentration is ≥7.0 meq/L with chronic
hyperkalemia or possibly at lower levels with an acute rise in
serum potassium
• Severe muscle weakness or paralysis — Hyperkalemia can
cause ascending muscle weakness that begins with the legs
and progresses to the trunk and arms
• This can progress to flaccid paralysis, mimicking Guillain-Barré
syndrome .
• Sphincter tone and cranial nerve function are typically intact,
and respiratory muscle weakness is rare
• These manifestations resolve with correction of the
hyperkalemia.
• Cardiac manifestations — Hyperkalemia may be
associated with electrocardiographic changes that, if present,
may suggest the diagnosis before blood test results
• ECG changes — Tall peaked T waves with a shortened
QT interval are usually the first findings
• As the hyperkalemia gets more severe, there is
progressive lengthening of the PR interval and QRS
duration, the P wave may disappear, and ultimately the
QRS widens further to a sine wave pattern.
• Ventricular standstill with a flat line on the ECG ensues
with complete absence of electrical activity.
ECG Changes
Hyperkalemia:
T wave in hyperkalemia is
typically tall and narrow,
but does not have to be tall
(may be just narrow and
peaked pulling ST segment).
Tall T means > 2 big boxes in
the precordial leads or >1
small box in limb leads,
or T wave taller than QRS.
• The progression and severity of ECG changes do not
correlate well with the serum potassium concentration as
illustrated by the following observations:
• Rare patients have a normal ECG despite a serum potassium
above 9.0 meq/L
• ECG manifestations are more likely with rapid onset
hyperkalemia, and the presence of concomitant
hypocalcemia, acidemia, and/or hyponatremia
• Given the unreliable sensitivity, serial measurements of the
serum potassium concentration should guide therapy in
stable patients with hyperkalemia.
• The ECG cannot be reliably used to monitor the efficacy of
hyperkalemia therapy
• In addition, peaked T waves alone are not specific for
hyperkalemia, being seen in the early phase of acute
myocardial infarction and with early repolarization, and some
patients with left ventricular hypertrophy
• Conduction abnormalities and arrhythmias — Hyperkalemia
can lead to a variety of conduction abnormalities and
arrhythmias:
• Conduction abnormalities that may be seen include right
bundle branch block, left bundle branch block, bifascicular
block, and advanced atrioventricular block
• Cardiac arrhythmias associated with hyperkalemia include
sinus bradycardia, sinus arrest, slow idioventricular rhythms,
ventricular tachycardia, ventricular fibrillation, and asystole
• PATIENT ASSESSMENT — Careful monitoring of the ECG and
muscle strength are indicated to assess the functional
consequences of hyperkalemia.
•
Severe muscle weakness and/or marked electrocardiographic
changes, including conduction abnormalities and arrhythmias,
are potentially life-threatening and require immediate
treatment.
• These manifestations usually occur when the serum
potassium concentration is ≥7.0 meq/L with chronic
hyperkalemia or possibly at lower levels with an acute rise in
serum potassium.
• Treatment and prevention of hyperkalemia in
adults
‫خانم ‪ 60‬ساله ي ديابتي به دليل فشا رخون باال مراجعه مي كند‪ .‬در معاينه نكته ي مثبتي ندارد‬
‫‪ BP= 160/90‬دارد و در آزمايشات انجام شده‬
‫‪K: 6.1‬‬
‫‪Na:137‬‬
‫‪Cr:1.1‬‬
‫‪BUN:20‬‬
‫بيمار تحت در مان با لوزارتان و آملوديپين مي باشد‪ ..‬اقدام در ماني شما براي هايپر كالمي چيست؟‬
‫‪.1‬‬
‫‪.2‬‬
‫‪.3‬‬
‫‪.4‬‬
‫قطع لوزارتان و استفاده از داروي ديگر آنتي هايپرتنسيو‬
‫استفاده از پودر كي اگزاالت‬
‫قطع لوزارتان و استفاده از داروي ديگر آنتي هايپرتنسيو‪ +‬استفاده از پودر كي اگزاالت‬
‫نياز به اقدام خاصي ندارد‪.‬‬
‫• مرد ‪ 62‬ساله اي با نارسايي كليه ي مزمن و كراتينين ‪2.1 mg /dL‬‬
‫و پتاسيم نرمال به دليل فشا رخون باال روي رژيم كم نمك قرار مي‬
‫گيرد‪ .‬دو هفته بعد متوجه ضعف عضالني مي شود‪ .‬در معاينه ي‬
‫فيزيكي مختصر كاهش تورگور پوست و ضعف عضالت‬
‫پروگزيمال يافته مي شود ‪ ECG .‬بيمار موج ‪ T‬بلند و پهن شدن‬
‫موج ‪ P‬و كمپلكس ‪ QRS‬رانشان مي دهد‪ .‬آزمايش هاي وي‬
‫بصورت زير مي باشد‪:‬‬
• Plasma Na = 130 meq /L
•
K= 9.8 meq /L
•
Cl= 98 meq /L
•
HCO3= 19meq /L
•
Cr= 2.7 mg/dL
•
Arterial pH= 7.32
‫‪‬اولين اقدام درماني شما براي بيمارفوق كدام است؟‬
‫‪ .1‬انفوزيون گلوكونات كلسيم‬
‫‪ .2‬انفوزيون گلوكز و انسولين‬
‫‪ .3‬انفوزيون بيكربنات سديم‬
‫‪ .4‬شروع دياليز‬
‫كداميك از موارد زير در درمان هايپر كالمي اين بيمار كمترين‬
‫تاثير را دارد؟‬
‫‪ .1‬انفوزيون گلوكونات كلسيم‬
‫‪ .2‬انفوزيون گلوكز و انسولين‬
‫‪ .3‬انفوزيون بيكربنات سديم‬
‫‪ .4‬استفاده از پودر كي اگزاالت‬
Principles of Treatment
• Stabilise myocardium
• Move it into cells
• Increase elimination
• URGENCY OF THERAPY — The urgency of treatment of
hyperkalemia varies with the cause and the presence or
absence of the symptoms and signs associated with
hyperkalemia.
• In addition, patients with marked tissue breakdown (eg,
rhabdomyolysis, crush injury, tumor lysis syndrome) release
large amounts of potassium from the cells, which can lead to
rapid and substantial elevations in serum potassium. Thus,
these patients should receive aggressive therapy to remove
potassium even if there is only a mild degree of hyperkalemia
• The most serious manifestations of hyperkalemia are
muscle weakness or paralysis, cardiac conduction
abnormalities, and cardiac arrhythmia
• These manifestations usually occur when the serum
potassium concentration is ≥7.0 meq/L with chronic
hyperkalemia or possibly at lower levels with an acute
rise in serum potassium.
• RAPIDLY ACTING TRANSIENT THERAPIES :
•
Rapidly acting therapies include the administration of calcium, insulin
with glucose, beta-2-adrenergic agonists, and, in selected patients,
sodium bicarbonate.
Indications for use :
• Patients with hyperkalemia and electrocardiographic changes
• Patients with a serum potassium greater than 6.5 to 7 meq/L; some
would not initiate such therapy until the serum potassium is ≥7.0
meq/L in patients who have no clinical or electrocardiographic signs of
hyperkalemia.
• A lesser degree of hyperkalemia in patients with a serum potassium
that is rapidly increasing
• Monitoring — Continuous cardiac monitoring and serial
electrocardiograms are warranted in patients with
hyperkalemia who require rapidly acting therapies.
• The serum potassium should be measured at one to two
hours after the initiation of therapy.
• The timing of further measurements is determined by the
serum potassium concentration and the response to therapy.
• Calcium — Calcium directly antagonizes the membrane
actions of hyperkalemia, while hypocalcemia increases the
cardiotoxicity of hyperkalemia.
• The effect of intravenous calcium administration begins within
minutes but is relatively short-lived (30 to 60 minutes). As a
result, calcium should not be administered as monotherapy
for hyperkalemia but should rather be combined with
therapies that drive extracellular potassium into cells.
• Calcium can be given as either calcium gluconate or
calcium chloride.
• The usual dose of calcium gluconate is 1000 mg (10
mL of a 10 percent solution) infused over two to
three minutes, with constant cardiac monitoring.
• The dose can be repeated after five minutes if the
ECG changes persist or recur.
• Calcium gluconate can be given peripherally, ideally through a
small needle or catheter in a large vein.
•
Calcium should not be given in bicarbonate-containing
solutions, which can lead to the precipitation of calcium
carbonate.
• When hyperkalemia occurs in patients treated with digitalis,
calcium should be administered for the same indications as in
patients not treated with digitalis (eg, widening of the QRS complex
or loss of P waves) even though hypercalcemia potentiates the
cardiotoxic effects of digitalis.
•
In such patients, a dilute solution can be administered slowly,
infusing 10 mL of 10 percent calcium gluconate in 100 mL of 5
percent dextrose in water over 20 to 30 minutes, to avoid acute
hypercalcemia.
• In patients with hyperkalemia due to digitalis toxicity, the
administration of digoxin-specific antibody fragments is the
preferred therapy.
• Insulin with glucose — Insulin administration lowers the
serum potassium concentration by driving potassium into the cells,
primarily by enhancing the activity of the Na-K-ATPase pump in
skeletal muscle
•
Glucose is usually given with insulin to prevent the development of
hypoglycemia.
•
However, insulin should be given alone if the serum glucose is ≥250
mg/dL (13.9 mmol/L).
•
The serum glucose should be measured one hour after the
administration of insulin.
• One commonly used regimen for administering insulin and
glucose is 10 units of regular insulin in 500 mL of 10 percent
dextrose, given over 60 minutes.
• Another regimen consists of a bolus injection of 10 units of
regular insulin, followed immediately by 50 mL of 50 percent
dextrose (25 g of glucose). This regimen may provide a
greater reduction in serum potassium since the potassiumlowering effect is greater at the higher insulin concentrations
attained with bolus therapy.
• However, hypoglycemia occurs in up to 75 percent of patients
treated with the bolus regimen, typically about one hour
after the infusion
•
To avoid this complication, we recommend subsequent
infusion of 10 percent dextrose at 50 to 75 mL/hour and close
monitoring of blood glucose levels
• The administration of glucose without insulin is not
recommended since the release of endogenous insulin can be
variable and the attained insulin levels are generally lower
with a glucose infusion alone.
• Furthermore, in susceptible patients (primarily diabetic
patients with hyporeninemic hypoaldosteronism), hypertonic
glucose in the absence of insulin may acutely increase the
serum potassium concentration by raising the plasma
osmolality, which promotes water and potassium movement
out of the cells
• The effect of insulin begins in 10 to 20 minutes, peaks at 30
to 60 minutes, and lasts for four to six hours
• In almost all patients, the serum potassium concentration
drops by 0.5 to 1.2 meq/L .
• In particular, although patients with renal failure are resistant
to the glucose-lowering effect of insulin, they are not resistant
to the hypokalemic effect because Na-K-ATPase activity is still
enhanced
• Beta-2 adrenergic agonists — Given the potential adverse
effects, intravenous epinephrine should not be used in the
treatment of hyperkalemia.
•
Albuterol is not frequently used but can be considered as
transient therapy in patients who have symptoms or serious
ECG manifestations of hyperkalemia despite therapy with
calcium and insulin with glucose.
• Like insulin, the beta-2 adrenergic agonists drive potassium
into the cells by increasing the activity of the Na-K-ATPase
pump in skeletal muscle .
• Beta-2-adrenergic agonists can be effective in the acute
treatment of hyperkalemia, lowering the serum potassium
concentration by 0.5 to 1.5 meq/L
• Albuterol, which is relatively selective for the beta-2
adrenergic receptors, can be given as 10 to 20 mg in 4 mL of
saline by nebulization over 10 minutes (which is 4 to 8 times
the dose used for bronchodilation).
• Alternatively and where available, albuterol 0.5 mg can be
administered by intravenous infusion
• Albuterol and insulin with glucose have an additive effect,
• reducing serum potassium concentration by approximately 1.2 to
1.5 meq/L
• Thus, although albuterol should not be used as monotherapy in
hyperkalemic patients with ESRD.; it can be added to insulin plus
glucose to maximize the reduction in serum potassium
•
One problem in patients on maintenance hemodialysis is that
lowering the serum potassium concentration by driving potassium
into the cells can diminish subsequent potassium removal during
the dialysis session (from 50 to 29 meq in one report), possibly
leading to rebound hyperkalemia after dialysis
• Potential side effects of the beta-2 agonists include mild
tachycardia and the possible induction of angina in
susceptible subjects. Thus, these agents should probably be
avoided in patients with active coronary disease.
• In addition, all patients with ESRD should be monitored
carefully since they may have subclinical or overt coronary
disease
• Sodium bicarbonate — Raising the systemic pH with sodium
bicarbonate results in hydrogen ion release from the cells as
part of the buffering reaction. This change is accompanied by
potassium movement into the cells to maintain
electroneutrality.
•
The use of bicarbonate for the treatment of hyperkalemia
was mainly based upon small uncontrolled clinical studies
• However, in a study that compared different potassiumlowering modalities in 10 patients undergoing HD, a
bicarbonate infusion for up to 60 minutes had no effect on
the serum potassium concentration .This lack of benefit was
confirmed in several subsequent studies of hemodialysis
patients
• Given the limited efficacy, we do not recommend the
administration of sodium bicarbonate as the only therapy for
the acute management of hyperkalemia, even in patients with
mild to moderate metabolic acidosis
• However, prolonged bicarbonate therapy appears to be
beneficial in patients with metabolic acidosis.
• TREATMENT OF REVERSIBLE CAUSES — A variety of factors
can contribute to or cause hyperkalemia. These include
reversible causes of impaired renal function, such as
hypovolemia, nonsteroidal anti-inflammatory drugs, urinary
tract obstruction, and inhibitors of the (RAAS), each of which
can also directly cause hyperkalemia
• These abnormalities often cannot be corrected quickly, and
their correction may not be sufficient to induce a large fall in
serum potassium. Thus, when there is more than mild
hyperkalemia, modalities directed at potassium removal
should not be delayed
• POTASSIUM REMOVAL — The effective modalities described
above only transiently lower the serum potassium
concentration. Thus, additional therapy is typically required
to remove excess potassium from the body.
• The three available modalities for potassium removal are
diuretics, cation exchange resin, and dialysis.
• Loop or thiazide diuretics — Loop and thiazide diuretics
increase potassium loss in the urine in patients with normal or
mild to moderately impaired renal function, particularly when
combined with saline hydration to maintain distal sodium
delivery and flow.
• However, patients with persistent hyperkalemia typically have
impaired renal potassium secretion, and there are no data
demonstrating a clinically important short-term kaliuretic
response to diuretic therapy.
• Cation exchange resins — The major available cation
exchange resin is sodium polystyrene sulfonate.
• Cation exchange resins, which are effective in lowering the
serum potassium after multiple doses, are usually not
effective immediately and do not appear to be more
effective in removing potassium from the body than
laxative therapy.
• Although uncommon, cation exchange resins can produce
severe side effects, particularly intestinal necrosis, which
may be fatal.
• When to use cation exchange resins — Clinicians are often
faced with a choice between using sodium sulfonate therapy
and dialysis in patients with kidney disease and hyperkalemia.
• cation exchange resins are usually not effective after a single
dose and may produce fatal side effects (particularly in
postoperative patients or those with ileus or bowel
obstruction and in patients who have received a kidney
transplant).
• Given these concerns, dialysis is the preferred treatment in
patients with severe kidney disease and potentially lifethreatening hyperkalemia, particularly in patients who have
a vascular access.
• In patients with less severe hyperkalemia, diuretic therapy, a
low-potassium diet, and removal of potentially reversible
causes (such as discontinuation of an angiotensin inhibitor)
may be sufficient
• Thus, we suggest that sodium polystyrene sulfonate be used
(in conjunction with the rapidly acting transient therapies
mentioned above) only in a patient who meets all of the
following criteria:
• Potentially life-threatening hyperkalemia
• Dialysis is not readily available.
• Other therapies to remove potassium (eg, diuretics, rapid
restoration of kidney function) have failed or are not
possible.
• Sodium polystyrene sulfonate with or without sorbitol should
not be given to the following patients because they may be at
high risk for intestinal necrosis:
• Postoperative patients
• Patients with an ileus or who are receiving opiates
• Patients with a large or small bowel obstruction
• Even if restoration of renal function or dialysis are not
possible or immediately available, sodium polystyrene
sulfonate should not be given in these high-risk settings;
• such patients can be managed with repeated doses of insulin
and glucose (or continuous infusions) until dialysis can be
performed.
• Despite modest efficacy and the risk of catastrophic
consequences, sodium polystyrene sulfonate remains the
most widely used treatment for hyperkalemia
• Sodium polystyrene sulfonate is also frequently used as
chronic therapy to control hyperkalemia in patients with CKD
who do not have other indications for dialysis and whose
hyperkalemia is not controlled adequately with a lowpotassium diet, diuretic therapy, and removal of potentially
reversible causes.
• Mechanism of action — In the gut, sodium polystyrene
sulfonate takes up potassium (and calcium and magnesium to
lesser degrees) and releases sodium.
•
Each gram of resin may bind as much as 1 meq of potassium
and release 1 to 2 meq of sodium.
• Thus, a potential side effect is exacerbation of edema due to
sodium retention.
• Administration and dose — Sodium polystyrene sulfonate
without or with sorbitol can be given orally and sodium
polystyrene sulfonate without sorbitol can be given as a.
retention enema .
• Oral dosing is probably more effective if intestinal motility is
not impaired.
• The oral dose is usually 15 to 30 g, which can be repeated
every four to six hours as necessary.
• Single doses are probably ineffective
• Sorbitol — the occurrence of intestinal necrosis in some
patients treated with cation exchange resins led the FDA to
issue a recommendation in September 2009 that sodium
polystyrene sulfonate should no longer be administered in
sorbitol
• Cation exchange resins do not appear to have superior
efficacy as compared with laxatives alone.
• A major concern with sodium polystyrene sulfonate in sorbitol is
the development of intestinal necrosis, usually involving the colon
and ileum which is frequently a fatal complication
• In such cases, sodium polystyrene sulfonate crystals can often be
detected in pathological specimens, adherent to the injured
mucosa
• Sodium polystyrene sulfonate in sorbitol can also injure the
esophagus and stomach when given orally, possibly resulting in
manifestations such as bleeding and esophageal necrosis
• Other complications of sodium polystyrene sulfonate include
hypocalcemia, volume overload and hypokalemia
• Intestinal necrosis in the absence of sorbitol — The
association of sodium polystyrene sulfonate in sorbitol with
intestinal necrosis may be coincidental since sorbitol is so
widely used in conjunction with sodium polystyrene
sulfonate.
• Multiple cases of intestinal necrosis with sodium polystyrene
sulfonate and similar cation exchange resins without sorbitol
have been reported
Thus, intestinal necrosis may be a complication of sodium
polystyrene sulfonate independent of sorbitol.
• Dialysis — Dialysis is indicated if the measures listed above
are insufficiently effective or the hyperkalemia is severe or is
expected to increase rapidly as could occur with marked
tissue breakdown, leading to the release of large amounts of
potassium from injured cells
• Hemodialysis is preferred, since the rate of potassium
removal is many times faster than with peritoneal dialysis
• Hemodialysis can remove 25 to 50 meq of potassium per
hour, with variability based upon the initial serum potassium
concentration, the type and surface area of the dialyzer used,
the blood flow rate, the dialysate flow rate, the duration of
dialysis, and the potassium concentration of the dialysate
• Postdialysis potassium rebound — A rebound increase in
serum potassium concentration occurs after hemodialysis in
all patients in whom potassium is removed, since the
reduction in serum potassium during dialysis creates a
gradient for potassium movement out of the cells.
• the serum potassium concentration should usually not be
measured soon after the completion of hemodialysis, since
the results are likely to be misleading.
• PREVENTION — There are several measures that can help to
prevent hyperkalemia in patients with (CKD), particularly (ESRD):
• In addition to a low-potassium diet, the following modalities have
been effective in stable maintenance hemodialysis patien
• Avoid episodes of fasting, which can increase potassium movement
out of the cells due, at least in part, to reduced insulin secretion
• Avoid, if possible, drugs that raise the serum potassium
concentration. These include inhibitors of the (RAAS), such as ACEI
/ ARB, aldosterone antagonists, and nonselective beta blockers
• Beta-1-selective blockers such as metoprolol and atenolol are much
less likely to cause hyperkalemia
Thanks for your
attention