Hypokalemia

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Hypokalemia
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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.

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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.

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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

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PATHOPHYSIOLOGY
chronic inadequate intake, long-term diuretic or
laxative use, chronic diarrhea, hypomagnesemia
hyperhidrosis
Total body deficit of potassium
diabetic ketoacidosis, severe GI losses
vomiting / diarrhea, dialysis, and diuretic
therapy
Acute potassium depletion
potassium shifts from the EC to IC space
Alkalosis hypothermia insulin, catecholamines
Distal RTA Bartter syndrome, Periodic
hypokalemic paralysis, Hyperaldosteronism
hyperthyroid.
Other causes
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Abnormalities of serum potassium are associated
with well described clinical features

S. K level Clinical features
lt3.5 mmol/l Lassitude
 lt 2.5 mmol/l Possible muscle necrosis
lt2 mmol/l Flaccid paralysis with respiratory compromise
Gennari FJ. Hypokalemia. N Engl J Med 1998 339
451-458
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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 (lt 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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Effects of hypokalemia

• severe (or rapidly occurring) hypokalemia can
  cause muscle weakness and paralysis the paralysis
  mainly affects the proximal lower extremities gt
  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

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Effects of hypokalemia

• hypokalemia produces a carbohydrate-intolerance
  (? due to impaired insulin release and ? impaired
  insulin resistance) gt 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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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.

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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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Investigations

• Drug screen (serum or urine)
• Amphetamines and other sympathomimetic stimulants
  can cause hypokalemia.
• Other drugs include
• verapamil overdose.
• Theophylline.
• amphotericin B.
• Aminoglycosides.
• cisplatin.

• Hormonal assay
• Serum ACTH,
• Cortisol,
• Renin activity,
• Aldosterone

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left adrenal adenoma

Conn syndrome
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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

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Replenishing potassium stores

• cardiac monitoring is necessary in patients with
• profound hypokalemia (lt 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.

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IV infusion rate for severe or symptomatic
hypokalemia
Standard IV replacement rate 10 - 20 meq/h
Serum potassium lt 2.5 meq/L, or Moderate-severe symptoms 20 - 40 meq/h
Serum potassium lt 2.0 Meq/L, or Life-threatening symptoms gt 40 meq/h
If heart block, or Renal insufficiency exists 5 - 10 meq/h

• .

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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 (lt 2.5 meq/L), or
• If the hypokalemia is causing muscle paralysis,
  or
• Malignant cardiac arrhythmias .

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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.

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Medical Decision-Making and Treatment

• The patient should be transferred to ICU for
  severe or symptomatic hypokalemia for
• IV potassium supplementation.
• Continuous cardiac monitoring.

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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).

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what is the next step?
The cause of hypokalemia
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Certain simple combinations of clinical features
and abnormal laboratory values could suggest a
particular diagnosis
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Q.1. Hypertension High Serum Renin High Serum
Aldosterone.

• Renin secreting tumor or
• Bilateral renal artery stenosis or
• Malignant hypertension

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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.

• Liddle syndrome or
• congenital adrenal hyperplasia or
• chronic ingestion of licorice-compounds
  containing glycyrrhizin or
• 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 gt 6.
Distal RTA
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Bartter's syndrome

• Q.7.
• Normotension/hypotension
• Increased serum renin
• Metabolic aklalosis
• Hypomagnesemia
• Hypercalciuria
• Increased urinary chloride (gt 100 meq/l)

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Q.8. Normotension/hypotension metabolic
alkalosis low urinary chloride

• Surreptitious vomiting or
• Prolonged naso-gastric suction and excessive
  gastric fluid loss

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Surgical Care

• Surgical intervention is required only after
  determining that the etiology requires it.
• Etiologies that may require surgery include the
  following
• Renal artery stenosis.
• Adrenal adenoma.
• Intestinal obstruction producing massive
  vomiting.
• Villous adenoma.

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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.

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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.

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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.

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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.

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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