ELECTROLYTE ABNORMALITIES

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ELECTROLYTE ABNORMALITIES

• BY Anthony M. Letizio D.O.

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Hyponatremia

• Defn plasma sodium concentration
• less than 134mEq/L.
• Clinical Manifestations vary with the degree of
  hyponatremia, and the rapidity of onset. Moderate
  or gradual onset causes confusion, muscle cramps,
  lethary, anorexia, and nausea. Severe or rapid
  onset can cause seizures and/or coma.

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Etiology and Classifications
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• Hypotonic Hyponatremia
• 1) Euvolemic SIADH, water intoxication, renal
  failure, glucocorticoid deficiency,
  hypothryoidism, thiazide diuretics, NSAIDs,
  carbamazepine, amitriptyline, thioridazine,
  vincristine, cyclophosphamide, colchicine,
  tolbutamide, chlorpropamide, Ace inhibitors,
  clofibrate, oxytocin, SSRIs, and amiodarone.

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• Hypotonic Hyponatremia
• 2) Hypovolemic Renal Losses (diuretics, partial
  urinary tract obstruction, salt-losing renal
  disease), Extrarenal losses gastrointestinal
  (vomiting, diarrhea), extensive burns, third
  spacing (peritonitis, pancreatitis, ileus), and
  adrenal insufficiency.

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• Hypotonic Hyponatremia
• 3) Hypervolemic CHF, nephrotic syndrome,
  cirrhosis, and pregnancy

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• Isotonic Hyponatremia (normal serum osmolality)
• 1) Pseudohyponatremia (increased serum lipids and
  serum proteins).
• 2) Isotonic infusion (glucose, mannitol).

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• Hypertonic Hyponatremia
• 1) Hyperglycemia - each 100 mg/dL increment in
  blood sugar level above normal decreases plasma
  sodium concentration by 1.6 mEq/L.
• 2) Hypertonic infusions (glucose, mannitol)

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Diagnostic Approach

• Useful lab tests serum electrolytes, glucose,
  BUN, creatinine, urine sodium, serum and urine
  osmolality, uric acid, and TSH.
• Urine sodium determines the source. It will be
  low in patients with GI losses or third spacing.
  It will be high in patients taking diuretics.
  Pseudohyponatremia should be suspected when the
  measured and the calculated osmolarities are
  mismatched

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Treatment

• Euvolemic SIADH fluid restriction unless
  acutely symptomatic which you can give hypertonic
  saline infusions.
• The serum sodium concentration should be
  corrected only halfway to normal in the initial
  24 hours, but not faster than 1 mEq/hr to prevent
  cerebral edema, myelinolysis, and seizures.

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Treatment

• Hypovolemic give normal saline infusion
• Hypervolemic strict fliud and sodium restiction.

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Hypernatremia

• Defn Plasma sodium concentration greater than
  144 mEq/L.
• Clinical Manifestations Vary with degree of
  hypernatremia and rapidity of onset they range
  from confusion and lethargy to seizures and coma.

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• Isovolemic Hypernatremia
• (decreased total body water, normal total body
  sodium, and extracellular fluid.
• Causes include diabetes insipidus both neurogenic
  and nephrogenic, and skin loss (hyperhemia),
  iatrogenic, reset osmostat

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• Hypervolemic Hypernatremia
• (increased total body water, markedly increased
  total body sodium and extracellular fluid)
• Causes include iatrogenic (administration of
  hypernatremic solutions), mineralocorticoid
  excess (Conns syndrome, Cushings syndrome) and
  salt ingestion

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• Hypovolemic Hypernatremia
• Loss of water and sodium. (water loss is greater
  than sodium loss)
• Causes include renal losses (diuretics and
  glycosuria), Gastrointestinal, respiratory, skin
  losses, inadequate access to water in the
  disabled or elderly, and adrenal deficiencies.

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Treatment

• Isovolemic Replace fliud with dextrose in water
  D5W. Correct half of the estimated water deficit
  in the first 24 hours. The correction rate
  should not exceed 1 mEq/L/hr in acute cases, and
  0.5mEq/L/hr in chronic cases.

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Treatment

• Hypovolemic Replace fluid with isotonic saline
  initially until it is felt that the person is
  becomes euvolemic. This often occurs before the
  sodium concentration is completely corrected.
  Then switch to ½ normal saline or D5W. The rate
  of correction should not exceed 2 mEq/kg/hr

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Treatment

• Hypervolemic Replace fluid with D5W after loop
  diuretics are used to increase excretion of
  sodium. Recommended to monitor electrolytes
  q8-12 hours during this.

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Hypokalemia

• Defn plasma potassium concentration less than
  3.3 mEq/L
• Clinical Manifestations Mild muscle weakness to
  overt paralysis (including respiratory
  paralysis), and rhabdomyolysis. Atrial and
  ventricular arrhythmias may develop and ECG
  changes.

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Hypokalemia

• Mild causes flattening of T waves, ST-segment
  depression, PVCs, prolonged QT intervals.
• Severe causes prominent U waves, atrioventricular
  conduction disturbances, and V-Tach, Fib.

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Hypokalemia
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Causes of Hypokalemia

• Alkalosis (each 0.1 increase in pH decreases
  serum potassium by 0.4 to 0.6 mEq/L
• Insulin administration
• Vitamin B12 therapy for megaloblastic anemias,
  acute leukemias
• Hypokalemic periodic paralysis which is a rare
  familial disorder

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Causes of Hypokalemia

• Beta-Adrenergic agonist (terbutaline),
  decongestants, bronchodilators, theophylline, and
  caffeine.
• Barium poisoning, toluene, verapamil, and
  chloroquine intoxication.
• Correction of digoxin intoxication with digoxin
  antibody fragments (digibind)
• Increased renal excretion due to drugs including
  the diuretic carbonic anhydrase inhibitors such
  as acetazolamide

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Causes of Hypokalemia

• Amphotericin B
• High-dose sodium penicillin, nafcillin,
  ampicillin, or carbenicillin
• Cisplatin
• Aminoglycosides
• Corticosteroids, mineralcorticoids
• Foscarnet sodium

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Causes of Hypokalemia

• Renal tubular acidosis distal type 1 or proximal
  type 2
• Diabetic ketoacidosis
• Magnesium deficiency
• Postobstruction diuresis, diuretic phase of acute
  tubular necrosis
• Osmotic diuresis such as mannitol
• Bartters syndrome which is hyperplasis of the
  juxtaglomerular cells

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Causes of Hypokalemia

• Increased mineralocorticoid activity both primary
  and secondary aldosteronism, Cushings syndrome,
  or physiological increases in mineralocorticoid
  activity during dehydration.
• Chronic metabolic alkalosis from loss of gastric
  fluid
• GI losses including vomiting, nasogartic
  suctioning, diarrhea, laxative abuse villous
  adenomas and fistulas
• Inadequate dietary intake seen in people with
  anorexia nervosa

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Causes of Hypokalemia

• Cutaneous losses such as sweating
• High dietary sodium intake, excessive use of
  licorice
• Hypomagnesemia

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Treatment

• Replace potassium either IV or oral or both.
  Oral increases the potassium more quickly than IV
  because you have to give IV slowly.
• Each 10 meq should raise the potassium level 0.1
  mmol/L
• May have to adjust patients diuretics or other
  drugs such as amphotericin which decrease the
  potassium

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Treatment

• Check a magnesium level which has to be normal
  for maintainence of serum potassium levels.
• Advice patients to eat foods that are high in
  potassium such as fruits.

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Hyperkalemia

• Defn plasma potassium concentration greater than
  4.9 mEq/L
• Clinical Manifestations include generalized
  weakness, irritability, paresthesias, decreased
  deep tendon reflexes, flaccid paralysis, cardiac
  arrhythmias, and ileus

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Hyperkalemia

• Mild causes peaking of T waves, and PVCs
• Severe causes peaking of T waves, widening of QRS
  complex, depressed ST segments, prolongation of
  PR interval, sinus arrest, deep S waves, PVCs,
  V-Tach, Fib, and cardiac arrest

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Hyperkalemia
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Causes of Hyperkalemia

• Pseudohyperkalemia Hemolyzed specimen, severe
  thrombocytosis (platelet count of less than 10 x
  6/ml), severe leukocytosis (wbc less than 10 x
  5/ml, fist clenching during phlebotomy, and
  drawing blood from a limb into which potassium is
  being infused.
• Excessive potassium intake
• Decreased renal excretion from potassium sparing
  diuretics, insufficiency, tubular
  unresponsiveness, type 4 RTA, ACE inhibitors,
  heparin administration, NSAIDs, TMP-SMX,
  B-Blockers, and pentamidine.

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Causes of Hyperkalemia

• Acidemia (each 0.1 decrease in pH increases the
  serum potassium by 0.4 to 0.6 mEq/L.
• Insulin deficiency
• Drugs such as succinycholine, markedly increased
  digitalis levels, arginine, and B-adrenergic
  blockers
• Hypertonicity, hemolysis, tissue necrosis,
  rhabdomyolysis, burns

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Treatment

• IV calcium gluconate helps stabilize the
  myocardial cell membranes, it does not lower the
  potassium.
• Give glucose and insulin which will lower plasma
  potassium transiently for 4 to 6 hours.
• Sodium bicarbonate can be used.
• Kayexalate orally or per rectum.
• Remove the cause and patients may need dialysis.

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Hypomagnesemia

• Defn plasma magnesium concentration less than
  1.8mg/dL
• Clinical Manifestations Neuromuscular weakness,
  hyperreflexia, fasciculations, tremors,
  convulsions, delirium, and coma

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Causes of Hypomagnesemia

• Defective absorption (malabsorption)
• Inadequate dietary intake (alcoholics)
• Parenteral therapy without magnesium
• Chronic diarrhea, villous adenoma, prolonged
  nasogastric suction, and fistulas
• Diuretic usage
• Renal tubular acidosis
• Endocrine disturbances such as diabetic
  ketoacidosis, hyperaldosteronism,
  hyperthyroidism, hyperparathryroidism, SIADH,
  bartters syndrome, hypercalciuria, and
  hypokalemia

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Causes of Hypomagnesemia

• Cisplatin, alcohol, cyclosporine, digoxin,
  pentamidine, mannitol, amphotericin B, foscarnet,
  and methotrexate
• Gentamicin, ticarcillin, carbenicillin
• Hypoalbuminemia, cirrhosis, insulin and glucose,
  theophylline, epinephrine, acute pancreatitis,
  CABG, sweating, burns, prolonged exercise,
  lactation, hungry-bones disease.

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EKG Manifestations

• Prolonged QT interval, T-wave flattening,
  prolonged PR interval, A-Fib, torsades de pointes

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Lab Manifestations of Hypomagnesemia

• Hypokalemia refractory to potassium replacement
• Hypocalcemia refractory to calcium replacement

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Treatment Hypomagnesemia

• Correct the magnesium deficiency
• Mild Oral magnesium
• Moderate IV magnesium sulfate over 6 hour
  periods
• Severe serum mag of less than 1 mg/dL give
  2grams magnesium in over 1 hour period
• Monitor ECG, blood pressure, pulse, respiration,
  DTRs, and urine output

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Hypermagnesemia

• Defn plasma magnesium concentration greater than
  2.3 mg/dL
• Clinical Manifestations Paresthesias,
  hypotension, confusion, decreased DTRs
  paralysis, coma, apnea
• Acute hypermagnesemia suppresses parathyroid
  hormone secretion causing hypocalcemia

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Causes of Hypermagnesemia

• Renal failure due to a decreased GFR
• Decreased renal excretion due to salt depletion
• Abuse of antacids and laxatives which contain
  magnesium
• Endocrinopathies including mineralocorticoid and
  thyroid horomone
• Rhabdomyolysis

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Causes of Hypermagnesemia

• Acute diabetic ketoacidosis
• Pheochromocytoma
• Lithium, volume depletion, familial hypocalciuric
  hypercalcemia

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EKG Manifestations

• Shortened PR interval, heart block, peaked
  T-waves, and increased QRS duration

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Treatment for Hypermagnesemia

• Identify and correct the underlying disorder
• Dialysis is needed for severe hypermagnesium

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Hypophosphatemia

• Defn plasma phosphate concentration less than
  2.5 mg/dL
• Clinical Manifestations Proximal muscle
  weakness, waddling gait, bone pain, myalgias,
  osteopenia, apprehension, paresthesia, seizures,
  coma, ataxia, encephalopathy, hemolytic anemia,
  leukocyte and platelet dysfunction,
  rhabdomyolysis, ventilator dependence,
  respiratory failure, dysrhythmias, hypotension,
  cardiomyopathy, decreased contractility, CHF, and
  metabolic acidosis

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Causes of Hypophosphatemia

• Decreased intake
• Malabsorption, vomiting, diarrhea
• Phosphate-binding antacids
• Renal loss including RTA, Met acidosis, Fanconis
  syndrome, vitamine D- resistant rickets, ATN,
  hyperparathyroidism, familial hypophosphatemia,
  acute volume expansion, glycosuria, acetazolmide,
  and kidney transplantation

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Causes of Hypophosphatemia

• Transcellular caused by withdrawal of alcohol,
  DKA, glucose, insulin and/or catecholamine
  infusion, anabolic steriods, and other hormones
  such as insulin, glucagon, epinephrine and
  dopamine. Total parenteral nutrition,
  theophylline overdose, severe hyperthermia, acute
  leukemias and Burkitts lymphoma.

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Treatment

• Mild to moderate can be oral replaced daily.
• Severe cases require IV phosphate salts until
  serum phosphate is greater than 1.5 mg/dL

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Hyperphosphatemia

• Defn plasma phosphate concentration greater than
  5mg/dL
• Clinical Manifestations Soft tissue
  calcifications in the kidney, cornea, lung, blood
  vessels, and skin.

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Treatment

• Renagel (Sevelamer) is the agent of choice. It
  is an oral agent given TID with meals. It binds
  phosphate in the gut and prevents its absorption.
• May also use insulin and glucose infusion to
  prompt cell phosphate uptake when rapid phosphate
  decreases are needed.
• May also need dialysis.

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Hypercalcemia

• Symptoms constipation, anorexia, nausea,
  vomiting, pancreatitis, ulcers, confusion,
  obtundation, pyschosis, lassitude, depression,
  coma, nephrolithiasis, renal insufficiency,
  polyuria, decreased urine-concentrating ability,
  nocturia, nephrocalcinosis, myopathy, weakness,
  osteoporosis, pseudogout, bone pain, HTN,
  metastatic calcifications, pruritis

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EKG changes

• Shortening of the QT interval

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Treatments

• Vigorous IV hydration, bisphosphonates, loop
  diuretics, phosphate repletion, calcitonin,
  mithramycin, glucocorticoids, and indomethacin

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Hypocalcemia

• Symptoms neuromuscular irritability with the
  Chvosteks and Trousseaus sign, tetany,
  paresthesias, myopathy, seizures, muscle spasm or
  weakness, soft tissue calcifications, ocular
  cataracts, arrhythmias, CHF

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ECG changes

• Increases QT interval

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Treatment

• IV calcium gluconate, improve nutritional status,
  replace calcium orally, treat underlying diseases.