Hypokalemia & Hypomagnesemia

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Hypokalemia andHypomagnesemia
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Hypokalemia

• Serum level below 3.55.0 mEq/L
• Caused by vomiting, diarrhea, diuretics, gastric
  suctioning
• Hypomagnesaemia
• Muscle weakness, polyuria

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Causes of Hypokalemia
Decrease Intake
Increase Loss
Redistribution into Cells

1. Non-renal
2. Renal

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Causes of Hypokalemia

• I. Decreased intake
• A. Starvation
• B. Clay Ingestion
• II. Redistribution into Cells
• A. Acid-Base (Metabolic Alkalosis)
• B. Hormonal (Insulin, Beta agonist,
  Alpha antagonist)
• C. Anabolic State (folic acid)
• D. Other (Hypothermia, Pseudo
  hypokalemia)

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Causes of Hypokalemia
III. Increased Loss A. Non-renal 1.
Gastrointestinal Los (diarrhea) 2.
Integumentary Loss (sweat) B. Renal
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Cause of Hypokalemia in the patient

• Gastrointestinal losses? diarrhea (secretory)
• Urine potassium level less than 20 mEq/L suggests
  gastrointestinal loss
• Stool has a relatively high potassium content,
  and fecal potassium losses could exceed 100 mEq
  per day with severe diarrhea.

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Gastrointestinal Loss

• Hypokalemia is also due to increased K renal
  excretion
• Loss of Gastric contents results in volume
  depletion and metabolic alkalosis, both of which
  promotes kaliuresis

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Gastrointestinal Loss

• Stimulates aldosterone releaseaugments K
  secretion by principal cells
• There is an increase in distal delivery of NaHCO3
  which enhances the electrochemical gradient
  favoring potassium loss in urine.

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SIGNS SYMPTOMS

• Fatigue
• Muscular weakness paralysis
• Hyporeflexia
• Dyspnea
• Arrhythmia
• Predispose to digitalis toxicity
• Constipation

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SIGNS SYMPTOMS

• Risk of hyponatremia
• resultant confusion, headaches, seizures
• Irritable
• Nervousness

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TREATMENT
Therapeutic goals to correct the K
deficit to minimize on going losses
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• It is safer to correct hypokalemia via oral route
  in order to prevent rebound hyperkalemia if given
  IV
• The plasma potassium concentration should be
  monitored frequently when assessing the response
  to treatment

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• Emergency Treatment of Hypokalemia
• A. Estimated Potassium Deficit
• serum K lt3 mEq/L K deficit gt300 mEq
• serum K lt2 mEq/L K deficit gt700 mEq

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• B. Indications for Urgent Replacement
• ECG abnormalities consistent with severe K
  depletion
• myocardial infarction
• hypoxia
• digitalis intoxication
• marked muscle weakness
• respiratory muscle paralysis.

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IV infusion - for severe hypokalemia or those
who cannot take oral supplementation -
peripheral vein 40 mmol/L (preferred)
central vein 60 mmol/L - rate of
infusion ? 20 mmol/hr - mixed in NSS

• Continuous ECG monitoring
• Serum potassium determination every 3-6 hours

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• Non-Emergency Treatment of Hypokalemia
• attempts should be made to normalize K
  levels if lt3.5 mEq/L
• oral supplementation is significantly safer than
  IV
• KCL elixir, 1-3 tablespoon every day

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Hypomagnesemia

• Hypomagnesemia is an electrolyte disturbance in
  which there is an abnormally low level of
  magnesium in the blood.
• Hypomagnesemia is not necessarily magnesium
  deficiency. Hypomagnesemia can be present without
  magnesium deficiency and vice versa.

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Causes Hypomagnesemia

• 1. Related to decreased Mg intake
• Starvation
• Alcohol dependence
• Total parenteral nutrition
• 2. Related to redistribution of Mg from ECF to
  ICF
• Hungry bone syndrome
• Treatment of diabetic ketoacidosis
• Refeeding syndrome

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• 3. Related to GI Mg loss
• Diarrhea
• Vomiting and nasogastric suction
• Gastrointestinal fistulas and ostomies
• Hypomagnesemia with secondary hypocalcemia (HSH)

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• 4. Related to renal Mg loss
• Gitelman syndrome
• Classic Bartter syndrome (Type III Bartter
  syndrome)
• Familial hypomagnesemia with hypercalciuria and
  nephrocalcinosis (FHHNC)
• Autosomal-dominant hypocalcemia with
  hypercalciuria (ADHH)
• Isolated dominant hypomagnesemia (IDH) with
  hypocalcemia

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DECREASED MAGNESIUM INTAKE

• Alcoholics and individuals on magnesium-deficient
  diets or on parenteral nutrition for prolonged
  periods can become hypomagnesemic without
  abnormal gastrointestinal or kidney function.
• The addition of 4-12 mmol of magnesium per day to
  total parenteral nutrition has been recommended
  to prevent hypomagnesemia.

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REDISTRIBUTION OF MAGNESIUM FROM ECF TO ICF

• Hungry bone syndrome, in which magnesium is
  removed from the extracellular fluid space and
  deposited in bone following parathyroidectomy or
  total thyroidectomy or any similar states of
  massive mineralization of the bones
• Hypomagnesemia may also occur following insulin
  therapy for diabetic ketoacidosis and may be
  related to the anabolic effects of insulin
  driving magnesium, along with potassium and
  phosphorus, back into cells.

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GASTROINTESTINAL LOSSES

• When the small bowel is involved, due to
  disorders associated with malabsorption, chronic
  diarrhea, or steatorrhea, or as a result of
  bypass surgery on the small intestine.
• Patients with ileostomies can develop
  hypomagnesemia as there is some degree of
  magnesium absorption in the colon

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• Hypomagnesemia with secondary hypocalcemia
  (HSH) is a rare autosomal-recessive disorder
  characterized by profound hypomagnesemia
  associated with hypocalcemia.
• Pathophysiology is related to impaired intestinal
  absorption of magnesium accompanied by renal
  magnesium wasting as a result of a reabsorption
  defect in the DCT.

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RENAL LOSSES

• Familial hypomagnesaemia with hypercalciuria and
  nephrocalcinosis (FHHNC), an autosomal-recessive
  disorder, there is profound renal magnesium and
  calcium wasting.
• The hypercalciuria often leads to
  nephrocalcinosis, resulting in progressive renal
  failure.
• Other symptoms reported in patients with FHHNC
  include urinary tract infections,
  nephrolithiasis, incomplete distal tubular
  acidosis, and ocular abnormalities

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• Bartters syndrome
• Autosomal recessive disorder involving impaired
  Thick Ascending Limb salt reabsorption
• Gitelman syndrome
• autosomal recessive disorder involving loss of
  function of the thiazide sensitive
  sodium-chloride symporter located in the distal
  convoluted tubule

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TREATMENT

• Diet
• Can be used alone for mild ? Mg
• Green vegetables, meat, seafood, nuts, seeds,
  legumes, whole grains, peanut butter, cocoa, and
  Spinach (probably one of the best sources)

• Mg replacement
• Assess renal function route of Mg elimination
• IV or IM
• Because the kidneys are main route of excretion,
  make sure to watch BUN and Creatinine levels.
  Renal failure clients have problems with high
  Magnesium

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• The risk of hypomagnesemia can be
  summarized as follows
• 2 in the general population
• 10-20 in hospitalized patients
• 50-60 in intensive care unit (ICU) patients
• 30-80 in persons with alcoholism
• 25 in outpatients with diabetes

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• Thank You