2 Hypokalemia

8/12/2019 2 Hypokalemia

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Hypokalemia


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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 thecardiovascular and neuromuscular systems.

The kidney determines potassium homeostasis,

and excess potassium is excreted in the urine.

INTRODUCTION


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potassium is necessary for the maintenanceof normal charge difference between

intracellular and extracellular environments.

potassium homeostasis is tightly regulated byspecific 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.

INTRODUCTION


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Definition

Hypokalemiais defined as a potassium levelless than 3.5 mEq/L.

Moderate hypokalem iais a serum level of 2.5-3

mEq/L.

Severe hypokalem iais defined as a level less

than 2.5 mEq/L.

The reference range for serum potassium level is 3.5-5 mEq/L


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PATHOPHYSIOLOGY

Total body deficit

of potassium

Acute potassium

depletion

potassium shifts

from the ECto IC space

Other causes

chronic inadequate intake,

long-term diuretic or laxative use,chronic diarrhea, hypomagnesemia & hyperhidrosi

diabetic ketoacidosis,

severe GI losses : vomiting / diarrhea,dialysis, and diuretic therapy

Alkalosis & hypothermia

insulin,catecholamines

Distal RTA & Bartter syndrome,

Periodic hypokalemic paralysis,

Hyperaldosteronism & hyperthyroid.


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Abnormalities of serum potassium are associated

with well described clinical features:

S. K+ level Clinical features


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Effects of hypokalemia

Atrial/ventricular Arrhythmiasare morecommon in patients with underlying heart

disease (especially CAD) and in patients

taking digoxin. life-threatening Cardiac Arrhythmiascan

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.


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severe (or rapidly occurring) hypokalemia cancause muscle weakness and paralysistheparalysis mainly affects the proximal lowerextremities => progressing to affect the upperextremities; dysphagia and dysarthria areuncommon and cranial nerve palsies areexceedingly rare)

Rhabdomyolysiscan occur in severelypotassium-depleted patients - especiallyfollowing vigorous exercise - and mus lene rosiscan rarely occur



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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)



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Although ECGchanges may be helpful ifpresent, their absence should not be taken asreassurance of normal cardiac conduction.The ECG in hypokalemia may appear normalor may have only subtle findings immediatelyprior to clinically significant dysrhythmias.

During therapy, monitor for changes

associated with over-correction andhyperkalemia including prolonged QRS,peaked T waves, bradyarrhythmia, sinusnode dysfunction, and asystole.

Investigations


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The ECG findings in hypokalemia:

Ventricular dysrhythmia, Prolongation of QT interval, ST

segment depression, T wave flattening& U waves.


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Drug screen (serum or

urine):

Amphetaminesand

other sympathomimeticstimulants can cause

hypokalemia.

Other drugs include

verapamil overdose. Theophylline.

amphotericin B.

Aminoglycosides.

cisplatin.

Investigations

Hormonal assay:

Serum ACTH,

Cortisol,

Renin activity,

Aldosterone


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left adrenaladenoma

Conn syndrome
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2. Replenishing potassium stores

There is no direct correlation between the serum potassium and thetotal 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


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Replenishing potassium stores

cardiac monitoringis 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 potassiumshould normally be diluted in

saline solution so that the maximumconcentration is 40 meq/L (peripheral lines) or 60

meq/L (central lines) and IV potassium.


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IV infusion rate for severe or symptomatichypokalemia

.

Standard IV replacement rate 10 - 20 meq/h

Serum potassium < 2.5 meq/L, or

Moderate-severe symptoms

20 - 40 meq/h

Serum potassium < 2.0 Meq/L, or

Life-threatening symptoms

> 40 meq/h

If heart block, or

Renal insufficiency exists

5 - 10 meq/h


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Transient, asymptomatic, or mild hypokalemia mayresolve spontaneously or may be treated with enteralpotassium supplements.

Potassium replacement therapy is immediatelyindicated for:

Severehypokalemia (< 2.5 meq/L), or

If the hypokalemia is causing muscle paralysis, or

Malignant cardiac arrhythmias.

Medical Decision-Making and Treatment


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Outpatient therapy and follow-up in 48 - 72hours may be acceptable for mild

hypokalemia patients with no underlying

heart disease.


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The patient should be transferred to ICU

for severe or symptomatichypokalemia

for:IV potassium supplementation.

Continuous cardiac monitoring.



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Magnesium Replacement Therapy

Magnesium replacement therapy is often necessary in

malnourished alcoholicswith hypokalemia.

Hypomagnesemia should be suspected if the serum

potassium does not increase within ~ 96hours of the

commencement of potassium supplementation therapy.

Magnesium can be given orally (3g x 4 doses).


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The cause of

hypokalemia


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Certain simple combinations of

clinical features and abnormal

laboratory values could suggest

a particular diagnosis

Q 1 H i Hi h S


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1. Renin secreting tumor or

2. Bilateral renal artery stenosis or

3. Malignant hypertension

Q.1.Hypertension + High Serum

Renin + High Serum Aldosterone.


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Q.2.Hypertension + Low Serum

Renin+ High Serum Aldosterone.

Primary Hyperaldosteronism


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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


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Q.4.Hypertension + Normal/high Serum

Renin+ Normal Serum Aldosterone

Cushings Syndrome


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Q.5.Hypotension/normotension

+ High Serum Renin + High

Serum Aldosterone.

Secondary Hyperaldosteronism


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Q.6.Normotension + metabolic acidosis

+ hyperchloremia + urine ph > 6.

Distal RTA

Q 7


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Bartter's syndrome

Q.7.

Normotension/hypotension

Increased serum renin

Metabolic aklalosis

Hypomagnesemia

HypercalciuriaIncreased urinary chloride (> 100 meq/l)


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Q.8.Normotension/hypotension +

metabolic alkalosis + low urinary

chloride

1. Surreptitious vomiting or

2. Prolonged naso-gastric suction and

excessive gastric fluidloss


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Surgical Care

Surgical intervention is required onlyafter determining that the etiologyrequires it.

Etiologies that may require surgeryinclude the following:

1. Renal artery stenosis.

2. Adrenal adenoma.

3. Intestinal obstruction producing massivevomiting.

4. Villous adenoma.


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Consultations

The following consultations may be appropriate,depending on the clinical findings:

Nephrologis tfor evaluation of unexplained urinary

potassium losses suggested to be secondary to atubular disorder.

Endocr ino log is tif Cushing syndrome, primaryhyperaldosteronism, glucocorticoid-remediable

hypertension, or congenital adrenal hyperplasia issuggested.

Psychiatr is tfor alcoholism or eating disorders

Surgeon.


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Diet: low-sodium and high-

potassium

The low-sodium diet limits the

amount of sodium reabsorbed at thecortical collecting tubule, thuslimiting the amount of potassiumsecreted.


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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.


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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.

P i Ed i


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Patient Education

Patients should be educated in terms of predisposingconditions.

The importance and risks involved with potassiumsupplementation and

The warning signs of hypokalemia or over-treatmentmust be emphasized in discharge teaching.

Knowledge of cardiopulmonary resuscitation andeducation 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 chronicconditions associated with hypokalemia.


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Medical/Legal Pitfalls

Failure to adequately communicate the risksof treatment

Failure to appropriately monitor patients

receiving potassium supplementation forcomplications,

Failure to follow serum potassium and otherelectrolyte concentrations during or aftertherapy

Treating a patient based on a falsely lowserum potassium value due to sampling orlab error

2 Hypokalemia

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