Management of hyperkalemia in ckd

MANAGEMENT OF HYPERKALEMIA IN
CKD
Dr.SatchiA.Surendran
Post Graduate
General Medicine
13/02/2017

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

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 patientsVs 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
 KidneyTransplant Recipients
 On RAAS InhibitorTherapy *
 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 > 80Years
 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

Clinical Manifestations
 Minor ECG abnormalities (tall-peakedT 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 CHRONIC
Singular 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

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

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

Management of hyperkalemia in ckd

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