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Hypokalemia
INTRODUCTION
Potassium is one of the body's major ions.
Nearly 98% of the body’s potassium is
intracellular.
The ratio of intracellular to extracellular potassium
is important in determining the cellular membrane
potential.
Small changes in the extracellular potassium level
can have profound effects on the function of the
cardiovascular and neuromuscular systems.
The kidney determines potassium homeostasis,
and excess potassium is excreted in the urine.
INTRODUCTION
potassium is necessary for the maintenance
of normal charge difference between
intracellular and extracellular environments.
potassium homeostasis is tightly regulated by
specific ion-exchange pumps (primarily by a
cellular, membrane-bound, sodium-potassium
ATP-ase).
Derangements of potassium regulation often
lead to neuromuscular, gastrointestinal, and
cardiac conduction abnormalities.
Definition

Hypokalemia is defined as a potassium level
less than 3.5 mEq/L.

Moderate hypokalemia is a serum level of 2.5-3
mEq/L.

Severe hypokalemia is defined as a level less
than 2.5 mEq/L.
The reference range for serum potassium level is 3.55 mEq/L
PATHOPHYSIOLOGY
Total body deficit
of potassium
chronic inadequate intake,
long-term diuretic or laxative use,
chronic diarrhea, hypomagnesemia & hyperhidrosis
Acute potassium
depletion
diabetic ketoacidosis,
severe GI losses : vomiting / diarrhea,
dialysis, and diuretic therapy
potassium shifts
from the EC
to IC space
Alkalosis & hypothermia
insulin,
catecholamines
Other causes
Distal RTA & Bartter syndrome,
Periodic hypokalemic paralysis,
Hyperaldosteronism & hyperthyroid.
Abnormalities of serum potassium are associated
with well described clinical features:
S. K+ level
Clinical features
<3.5 mmol/l
Lassitude
< 2.5 mmol/l
Possible muscle necrosis
<2 mmol/l
Flaccid paralysis with
respiratory compromise
Gennari FJ. Hypokalemia. N Engl J Med 1998; 339: 451-458
Effects of hypokalemia


Atrial/ventricular Arrhythmias are more
common in patients with underlying heart
disease (especially CAD) and in patients
taking digoxin.
life-threatening Cardiac Arrhythmias can
occur when the serum potassium is very low
(< 2 meq/L), or when the serum potassium is
relatively low (2 - 3 meq/L) in patients with
underlying heart disease, or when the patient
is digoxin-toxic.
Effects of hypokalemia


severe (or rapidly occurring) hypokalemia can
cause muscle weakness and paralysis the
paralysis mainly affects the proximal lower
extremities => progressing to affect the upper
extremities; dysphagia and dysarthria are
uncommon and cranial nerve palsies are
exceedingly rare)
Rhabdomyolysis can occur in severely
potassium-depleted patients - especially
following vigorous exercise - and muscle
necrosis can rarely occur
Effects of hypokalemia



hypokalemia produces a carbohydrate-intolerance (?
due to impaired insulin release and ? impaired insulin
resistance) => worsening hyperglycemia in diabetics.
hypokalemia also produces a metabolic alkalosis (by ?
stimulation of bicarb absorption by the proximal tubule
and ? renal ammoniagenesis)
hypokalemia can contribute to the development, or
worsen the symptoms, of hepatic encephalopthy (?
due to renal ammoniagenesis)
Investigations


Although ECG changes may be helpful if
present, their absence should not be taken as
reassurance of normal cardiac conduction.
The ECG in hypokalemia may appear normal
or may have only subtle findings immediately
prior to clinically significant dysrhythmias.
During therapy, monitor for changes
associated with over-correction and
hyperkalemia including prolonged QRS,
peaked T waves, bradyarrhythmia, sinus
node dysfunction, and asystole.
The ECG findings in hypokalemia:
Ventricular dysrhythmia, Prolongation of QT interval, ST
segment depression, T wave flattening& U waves.
Investigations

Drug screen (serum or
urine):
– Amphetamines and
other sympathomimetic
stimulants can cause
hypokalemia.
– Other drugs include
»
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verapamil overdose.
Theophylline.
amphotericin B.
Aminoglycosides.
cisplatin.
Hormonal assay:
• Serum ACTH,
• Cortisol,
• Renin activity,
• Aldosterone

left adrenal
adenoma
Conn syndrome
2. Replenishing potassium stores
There is no direct correlation between the serum potassium and the
total body potassium deficit, but a rough estimate is to assume a total
body deficit of ~ 200 - 400 meq of potassium for every 1 meq/L the
serum potassium is below 4 meq/L
consider the possibility of associated magnesium deficiency
Replenishing potassium stores
cardiac monitoring is necessary in patients with
 profound hypokalemia (< 2.5 meq/L), or
 if cardiac arrhythmias are present, or
 if IV potassium is going to be rapidly administered.
IV potassium should normally be diluted in
saline solution so that the maximum
concentration is 40 meq/L (peripheral lines) or 60
meq/L (central lines) and IV potassium.
IV infusion rate for severe or symptomatic hypokalemia
Standard
IV replacement rate
10 - 20 meq/h
.
Serum potassium < 2.5 meq/L, or 20 - 40 meq/h
 Moderate-severe symptoms
 Serum potassium < 2.0 Meq/L, or > 40 meq/h
 Life-threatening symptoms
 If heart block, or
5 - 10 meq/h
 Renal insufficiency exists

Medical Decision-Making and Treatment
Transient, asymptomatic, or mild hypokalemia may
resolve spontaneously or may be treated with enteral
potassium supplements.
Potassium replacement therapy is immediately
indicated for:
 Severe hypokalemia (< 2.5 meq/L), or
 If the hypokalemia is causing muscle paralysis, or
 Malignant cardiac arrhythmias .
Medical Decision-Making and Treatment
 Outpatient
therapy and follow-up in 48 - 72
hours may be acceptable for mild
hypokalemia patients with no underlying
heart disease.
Medical Decision-Making and Treatment
The patient should be transferred to ICU
for severe or symptomatic hypokalemia
for:
IV potassium supplementation.
Continuous cardiac monitoring.
Magnesium Replacement Therapy

Magnesium replacement therapy is often necessary in
malnourished alcoholics with hypokalemia.

Hypomagnesemia should be suspected if the serum
potassium does not increase within ~ 96 hours of the
commencement of potassium supplementation therapy.

Magnesium can be given orally (3g x 4 doses).
The cause of
hypokalemia
Certain simple combinations of
clinical features and abnormal
laboratory values could suggest
a particular diagnosis
Q.1. Hypertension + High Serum
Renin + High Serum Aldosterone.
1. Renin secreting tumor or
2. Bilateral renal artery stenosis or
3. Malignant hypertension
Q.2. Hypertension + Low Serum
Renin + High Serum Aldosterone.
Primary Hyperaldosteronism
Q.3. Hypertension + Low Serum
Renin + Low Serum Aldosterone.
1. Liddle syndrome or
2. congenital adrenal hyperplasia or
3. chronic ingestion of licorice-compounds containing
glycyrrhizin or
4. ingestion of other exogenous mineralocorticoids
Q.4.Hypertension + Normal/high Serum
Renin + Normal Serum Aldosterone
Cushing’s Syndrome
Q.5. Hypotension/normotension
+ High Serum Renin + High
Serum Aldosterone.
“Secondary Hyperaldosteronism”
Q.6. Normotension + metabolic acidosis
+ hyperchloremia + urine ph > 6.
Distal RTA
Q.7.
Normotension/hypotension
Increased serum renin
Metabolic aklalosis
Hypomagnesemia
Hypercalciuria
Increased urinary chloride (> 100 meq/l)
Bartter's syndrome
Q.8. Normotension/hypotension +
metabolic alkalosis + low urinary
chloride
1. Surreptitious vomiting or
2. Prolonged naso-gastric suction and
excessive gastric fluid loss
Surgical Care


Surgical intervention is required only
after determining that the etiology
requires it.
Etiologies that may require surgery
include the following:
1. Renal artery stenosis.
2. Adrenal adenoma.
3. Intestinal obstruction producing massive
vomiting.
4. Villous adenoma.
Consultations
The following consultations may be appropriate,
depending on the clinical findings:




Nephrologist for evaluation of unexplained urinary
potassium losses suggested to be secondary to a
tubular disorder.
Endocrinologist if Cushing syndrome, primary
hyperaldosteronism, glucocorticoid-remediable
hypertension, or congenital adrenal hyperplasia is
suggested.
Psychiatrist for alcoholism or eating disorders
Surgeon.
Diet: ‟low-sodium and highpotassium”
The low-sodium diet limits the
amount of sodium reabsorbed at the
cortical collecting tubule, thus
limiting the amount of potassium
secreted.
Further Inpatient Care
Matching potassium intake to losses.
 Monitoring for Hypokalemia or
Hyperkalemia Due to Therapy By:

» periodic testing of serum potassium levels
» EKG.

Alleviation of aggravating conditions.
Further Outpatient Care
Patients should receive follow-up
medical care for home management if
the condition is expected to persist
beyond inpatient care.
 Additional medical follow-up must be
obtained for associated medical
conditions.

Patient Education





Patients should be educated in terms of predisposing
conditions.
The importance and risks involved with potassium
supplementation and
The warning signs of hypokalemia or over-treatment
must be emphasized in discharge teaching.
Knowledge of cardiopulmonary resuscitation and
education on timely access to emergency medical
services may prevent morbidity or mortality.
Ongoing communication is essential in reducing the
risks and therapy, especially in patients with chronic
conditions associated with hypokalemia.
Medical/Legal Pitfalls




Failure to adequately communicate the risks
of treatment
Failure to appropriately monitor patients
receiving potassium supplementation for
complications,
Failure to follow serum potassium and other
electrolyte concentrations during or after
therapy
Treating a patient based on a falsely low
serum potassium value due to sampling or
lab error