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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