Hypokalemic Periodic Paralysis
Pediatrics in Review
Volume 18 Number 10 October 1997
Copyright 1997 American Academy of Pediatrics
This section of Pediatrics in Review reminds clinicians of those conditions that can present in a misleading fashion and require suspicion for early diagnosis. Emphasis has been placed on conditions in which early diagnosis is important and that the general pediatrician might be expected to encounter, at least once in a while.
Case 3 Presentation
A 16 year-old boy is referred to the emergency department for evaluation of generalized weakness. He reports that 2 days ago, following 2 days of “flu-like” symptoms, he became weak while climbing stairs. His weakness progressed rapidly; soon he was unable to move his extremities or sit up. His mother has helped him eat, drink, and urinate. He uses no medications, alcohol, or illicit drugs. He has no history of ingestions, fever, dyspnea, dysphagia, or paresthesias. He had a similar episode of weakness 4 years ago that was less severe and resolved spontaneously within 2 days. His grandmother has had similar episodes.
Hypokalemic Periodic Paralysis
Index of suspicion. Case 3. Hypokalemic periodic paralysis
This section of Pediatrics in Review reminds clinicians of those conditions that can present in a misleading fashion and require suspicion for early diagnosis. Emphasis has been placed on conditions in which early diagnosis is important and that the general pediatrician might be expected to encounter, at least once in a while.
Hypokalemia, or Low Potassium
By Shawna Kopchu R.N.
Hypokalemia refers to a below normal serum potassium concentration. It usually indicates a real deficit in total potassium stores; however, it may occur in patients having normal potassium stores when alkalosis is present (since alkalosis causes a temporary shift of serum potassium into the cells).
Hypokalemia is frequently encountered in clinical medicine and has been estimated to occur in approximately 20% of patients admitted to general internal medicine service. Symptoms may be absent, identified only on routine electrolyte screening, or may range from neuromuscular weakness, rarely progressing to frank paralysis or sudden cardiac death. Usually correction of hypokalemia is not difficult, but if therapy is not appropriate, symptoms may worsen with potentially severe, even lethal, consequences.
Magnesium and Potassium Deficiency
Magnesium is an essential cation, involved in many enzymatic reactions, as a cofactor to adenosine triphosphatases. It is critical in energy- requiring metabolic processes, as well as protein synthesis and anaerobic phosphorylation. Serum Mg concentration is maintained within a narrow range by the kidney and small intestine since under conditions of Mg deprivation both organs increase their fractional absorption of Mg. If Mg depletion continues, the bone store contributes by exchanging part of its content with extracellular fluid (ECF).
Magnesium Increases Potassium
Does magnesium play a role in the hypokalemia of Bartter’s syndrome?
A patient with Bartter’s syndrome manifested hypomagnesemia in addition to hypokalemia. Under conditions of maximal free water production, he had a fractional distal solute reabsorption of 0.65, a value consistent with a renal defect in sodium chloride reabsorption in the thick ascending limb of the loop of Henle. This is also the site of 65% to 70% of urinary magnesium reabsorption.
Magnesium and Potassium Balance
Magnesium repletion and its effect on potassium homeostasis in critically ill adults: Results of a double-blind, randomized, controlled trial
Objectives: The aims of this study were to evaluate the safety and efficacy of magnesium replacement therapy and to determine its effect on potassium retention in hypokalemic, critically ill patients.
Metabolic Alkalosis
Metabolic alkalosis is common–half of all acid-base disorders as described in one study [1] . This observation should not be surprising since vomiting, the use of chloruretic diuretics, and nasogastric suction are common among hospitalized patients. The mortality associated with severe metabolic alkalosis is substantial; a mortality rate of 45% in patients with an arterial blood pH of 7.55 and 80% when the pH was greater than 7.65 has been reported [2] . Although this relationship is not necessarily causal, severe alkalosis should be viewed with concern, and correction by the appropriate intervention should be undertaken with dispatch when the arterial blood pH exceeds 7.55.
Potassium Sparing Medications
Amiloride works by inhibiting sodium reabsorption in the distal convoluted tubules and collecting ducts in the kidneys. This promotes the loss of sodium and water from the body, but without depleting potassium. The drug is often used in conjunction with thiazide or loop diuretics. Patients with Bartter or Gitelman Syndromes benefit from this by keeping their potassium levels up.
Potassium-sparing diuretics are commonly used to help reduce the amount of water in the body. Unlike some other diuretics, these medicines do not cause your body to lose potassium.
Amounts of Potassium & Magnesium in Snack Foods
If you have Bartter’s or Gitelman’s Syndrome you should know that diet alone cannot come close to correcting the potassium and magnesium deficiencies. At the same time, if you are going to eat a snack, you might as well have something that adds rather than detracts from your levels. Looks like a bag of peanuts would be a good choice, and popcorn would be a poor choice.
You may also be interested in a Chart of Foods High in Magnesium
Potassium Dosing
Potassium is essential for life, growth, development & life span.
Not enough attention is paid to the potassium in our diets or in our supplements. Your daily dietary need for potassium is 2000-4000 mg. A typical modern diet only supplies 1500-5000 mg of potassium. Low potassium diets produce great fatigue & muscle weakness.