management of hyperkalemia in ckd
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MANAGEMENT OF HYPERKALEMIA IN CKD
Dr.Satchi A.SurendranPost Graduate
General Medicine13/02/2017
Hyperkalemia-Numbers of Interest Potassium >5.5mEq/L 10% of Hospitalised patients 1% with severe hyperkalemia – High
Mortality
In CKD/ESRD patients* 40-50% prevalence 1.9 – 5% of deaths in ESRD
*Arch Intern Med. 2009;169(12):1156-1162
Mortality Risk The study concludes, The risk of hyperkalemia increases with
CKD.
Further more, the Odds Ratio for Mortality at 1 day of the event is also higher with hyperkalemic events in CKD.
Hence, this signifies the importance of Hyperkalemia as a concern to patient safety in CKD.
Causes
Pseudohyperkalemia Increased Intra to extra cellular shift Decreased Excretion
Pseudohyperkalemia – to be ruled out
Cellular Shift
Inadequate Excretion Inhibition of RAAS ACE Inhb/ARBs/ENaC Inhb/Aldo
Inhb. Hyoreninemic
Hypoaldosteronism Diabetic Nephropathy, Tubulo
Interstitial Diseases
Primary Adrenal Insufficiency Autoimmune, Drugs (Heparin),
Infections, Infiltrative,Congenital
Advanced Renal Disease Preservation of normokalemia results from Upto 15ml/min GFR:
An adaptive increase in K+ excretion by remnant nephrons
Below 15 ml/min GFR: Increased colonic excretion.
Three times more colonic excretion of K+ is documented in CKD patients Vs Normal Individuals
Role of Diet in CKD
An impaired GFR combined with a frequently high dietary K+ intake relative to residual renal function
If potassium intake is normal, CKD does not produce significant hyperkalemia until the GFR is < 5 ml/min*
Electrolyte & Blood Pressure 2005; 3:71-78.
CKD Sub Groups with High Risk of Hyperkalemia DM Kidney Transplant Recipients On RAAS Inhibitor Therapy * Metabolic Acidosis Anemia requiring Blood transfusion Acute kindney Injury CardioVascular Co-morbidity * *Drug Induced
Hyperkalemia
Drug induced Hyperkalemia
In an observational retrospective study of nondialyzed patients with serum potassium of 6.5 mmol/L or greater on admission or during hospital stay, more than 60% were taking at least one drug known to cause or worsen hyperkalemia.
CKD + ACE Inhibitors – Patient Profile at risk
Advanced Age > 80 Years Diabetes Heartfailure Increased starting dose of ACE I
(>10mg//day) Concomitant use of K+ Supplements Current use of ARBs/Potassium
Sparing Diuretics Higher Base line Potassium – Higher
the risk
Management Principles
Clinical management for hyperkalemia in patients with CKD requires
Exclusion of pseudohyperkalemia Assessment of the urgency for
treatment, and Appropriate acute and chronic therapy
PseudoHyperkalemia
Important to avoid unnecessary treatment
The most common cause of pseudohyperkalemia is hemolysis, which is usually Easily noted due to a pink tinge to the plasma
resulting from release of hemoglobin from damaged red blood cells
Alternatively, an excessively tight tourniquet surrounding an exercising extremity (e.g., opening and closing a hand) can increase plasma K+ by > 2 mEq/L)
Excessive numbers of either leukocytes > 70,000/cm3, or platelets > 1,000,000/cm3 also can lead to pseudohyperkalemia
Pseudohyperkalemia
When the serum K+ is >0.3 mEq/L as compared with a simultaneous plasma K+ ,
Pseudohyperkalemia should be diagnosed Plasma K+ can be measured by obtaining a
heparinized blood specimen
If pseudohyperkalemia exists, All further K+ levels should be measured using
plasma
ECG Manifestations of True Hyperkalemia
ECGs Considered to be sensitive indicators of
the presence of hyperkalemia
ECG abnormalities consistent with hyperkalemia in the hospitalized hyperkalemia patients were observed in only 14% of episodes
Serum K+ levels > 8 mEq/L are almost invariably associated with ECG abnormalities
ECG Correlation
Clinical Manifestations
Minor ECG abnormalities (tall-peaked T waves) may be the first indication of hyperkalemia but By the time serious changes occur, the
patient usually complains of muscle weakness, paresthesia, and lethargy
Severe hyperkalemia Can cause bilateral flaccid paralysis of
extremities, and weakness of respiratory muscles However unlike hypokalemia, complete
paralysis is uncommon.
Acute Vs Chronic Hyperkalemia
ACUTE CHRONICSingular Event; Requires no Ongoing Management
>1 event /year; requires ongoing management
Caused by abnormal net release of K+ from cells (metabolic acidosis/trauma/hemolytic states)
Caused by impairment of K+ excretory process
Acute Management
Acute reduction of serum K+ is required at levels exceeding 7.0 mEq/L, because of the risk of cardiac arrest
For acute therapy of hyperkalemia in an urgent situation, regardless of the underlying cause, following treatments have been recommended
Calcium Gluconate IV
Emergency treatment should be started by the administration of calcium (10-30 mL of 10% calcium gluconate over 10 min intravenously)
Intravenous infusion of calcium is the most rapid and effective way to antagonize the myocardial toxic effects of hyperkalemia
Dextrose Insulin Infusion
Furthermore, intravenous glucose (50 mL dextrose 50 %, preferably by central venous infusion) should be given followed by or combined with 10 units of short-acting regular insulin, because Combined administration of glucose
and insulin results in a greater decline in serum K+ levels
Intravenous insulin rapidly stimulates uptake of K+ into cells, primarily the muscle and liver
Beta Agonists
β2-adrenergic agonists, which also induce cellular K+ uptake, are useful for the acute therapy of hyperkalemia
A direct comparison between Intravenous (0.5 mg) and nebulized (10 mg) albuterol (salbutamol) in ESRD patients revealed a similar potassium-lowering
Beta Agonists
However, 20-40% of ESRD patients are refractory to the K+ -lowering effect of albuterol and Not possible to predict non-responders
Combined use of β2-adrenergic agonists with glucose and insulin will maximize the reduction in
serum K+
Dialysis for Refractory/ Severe Hyperkalemia
Hemodialysis is the most rapid method of K+ removal Removal rates of K+ can
approximate 35 mEq/hr with a dialysate bath potassium concentration of 1-2 mEq/L
A glucose free dialysate is preferable to minimize a glucose-induced shift of K+ into cell, lessening the removal of K+
Dialysis
Peritoneal dialysis and chronic hemodiafiltration are effective in chronic hyperkalemia, but Do not remove K+ fast enough to be
recommended for use in acute, severe hyperkalemia
Although dialysis is the most rapid method available to treat most cases of hyperkalemia, other modes of treatment should not be
delayed while waiting to institute dialysis
Chronic Hyperkalemia
To find modifiable causes of hyperkalemia in CKD patients
Common modifiable causes are Concomitant medications and Excessive dietary intake
A careful history on the dietary habit and the medication is necessary
Treatment Strategies
(1)to avoid or replace drugs that cause hyperkalemia;
(2) to prescribe a low-potassium diet and avoid constipation, and
(3) to enhance potassium excretion by residual functioning nephrons or to remove it more efficiently by dialysis and/or by the gastrointestinal tract
Diuretic Therapy
Chronic treatment of hyperkalemia in CKD
Promoting diuresis with a loop diuretic can control chronic, mild hyperkalemia
Diuretic Therapy
Thiazide and loop diuretics increase the delivery of sodium to the distal tubule, thereby increasing urinary potassium excretion
This may be useful in CKD, especially in patients treated with an ACE inhibitor or ARB
Thiazides effective in GFR >30ml/mt ;Loop diuretics instituted for lower levels.
Cation Exchange Resins
Either after acute hyperkalemia has been corrected or in chronic management of less severe hyperkalemia in CKD patients, the more slowly acting Cation exchange resin may be given orally
or rectally (e.g. sodium/calcium polystyrene sulfonate 15-30 g, with an equal amount of sorbitol to prevent fecal impaction)
Cation exchange resin may be given in order to prevent a further increase in serum K+
Potassium binding resins in hyperkalemia
In hyperkalemic patients, oral SPS mixed in water significantly decreases serum potassium within 24 hours
CJASN ePress. Published on August 26, 2010
Potassium binding resins in hyperkalemia SPS/sorbitol-associated colonic
necrosis is most commonly seen in patients who have received enemas in the
setting of recent abdominal surgery, bowel injury, or intestinal dysfunction
It is a rare event, on the order of 0.2 to 0.3%, almost
exclusively present in patients at risk
CJASN ePress. Published on August 26, 2010
Potassium binding resins in hyperkalemia
SPS ion-exchange resins are the only agents, other than dialysis and diuretics,
Available to increase K+ excretion in hyperkalemia, and when used appropriately,
they appear to be Clinically effective and reasonably
safe
Chronic Hyperkalemia Summary
Either asymptomatic and mild hyperkalemia or chronic hyperkalemia in CKD patients is common
Conclusions
Hyperkalemia is common and life threatening complication of CKD
The effective and rapid diagnosis and management of acute and chronic hyperkalemia is clinically relevant and can be life-saving
Conclusions
In treatment of moderate to severe hyperkalemia, the combination of medications with different therapeutic approaches is usually effective, and often methods of blood purification can be avoided.
In patients with severe hyperkalemia and major ECG abnormalities, conservative efforts should be initiated immediately to stabilize the patient, but management should include rapid facilitation of renal replacement treatment
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