You are on page 1of 40

Hypokalemia

INTRODUCTION
Potassium is one of the body's major ions.
Nearly 98% of the bodys 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 3.5-5


mEq/L
PATHOPHYSIOLOGY
Total body deficit chronic inadequate intake,
of potassium long-term diuretic or laxative use,
chronic diarrhea, hypomagnesemia & hyperhidrosis

diabetic ketoacidosis,
Acute potassium severe GI losses : vomiting / diarrhea,
depletion dialysis, and diuretic therapy

potassium shifts Alkalosis & hypothermia


from the EC insulin,
to IC space catecholamines
Distal RTA & Bartter syndrome,
Other causes 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 Hormonal assay:
urine):
Amphetamines and
Serum ACTH,
other sympathomimetic Cortisol,
stimulants can cause
hypokalemia. Renin activity,
Other drugs include
verapamil overdose.
Aldosterone
Theophylline.
amphotericin B.
Aminoglycosides.
cisplatin.
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

Cushings 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 high-
potassium

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

You might also like