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2 Hypokalemia
2 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
PATHOPHYSIOLOGY
Total body deficit of potassium
chronic inadequate intake, long-term diuretic or laxative use,
diabetic ketoacidosis, severe GI losses : vomiting / diarrhea, dialysis, and diuretic therapy Alkalosis & hypothermia insulin, catecholamines Distal RTA & Bartter syndrome, Periodic hypokalemic paralysis, Hyperaldosteronism & hyperthyroid.
Other causes
Abnormalities of serum potassium are associated with well described clinical features:
S. K+ level
<3.5 mmol/l < 2.5 mmol/l <2 mmol/l
Clinical features
Lassitude Possible muscle necrosis Flaccid paralysis with respiratory compromise
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.
Investigations
Hormonal assay:
Serum ACTH, Cortisol, Renin activity, Aldosterone
Conn syndrome
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 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
Severe hypokalemia (< 2.5 meq/L), or If the hypokalemia is causing muscle paralysis, or Malignant cardiac arrhythmias .
therapy and follow-up in 48 - 72 hours may be acceptable for mild hypokalemia patients with no underlying heart disease.
The patient should be transferred to ICU for severe or symptomatic hypokalemia for: IV potassium supplementation. Continuous cardiac monitoring.
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.
Certain simple combinations of clinical features and abnormal laboratory values could suggest a particular diagnosis
Primary Hyperaldosteronism
Cushings Syndrome
Secondary Hyperaldosteronism
Distal RTA
Q.7. Normotension/hypotension Increased serum renin Metabolic aklalosis Hypomagnesemia Hypercalciuria Increased urinary chloride (> 100 meq/l)
Bartter's syndrome
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.
Matching potassium intake to losses. Monitoring for Hypokalemia or Hyperkalemia Due to Therapy By:
periodic testing of serum potassium levels EKG.
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