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Fluid and Electrolyte Balance (POTASSIUM (Hypokalemia (Causes (Decreased…
Fluid and Electrolyte Balance
POTASSIUM
dominant cation in ICF.
most intracellular K is contained within muscle cells
An average 70-kg adult has about 3500 mEq of K
Resting membrane potential
Normal K+ levels = 3.5 - 5 mEq/L
decrease in plasma K concentration of about 1 mEq/L indicates a total K deficit of about 200 to 400 mEq
Most K+ ingested is excreted by the kidneys
Potasium shifts
Insulin moves K into cells.
β-Adrenergic agonists, especially selective β2-agonists, move K into cells
β-blockade and α-agonists promote movement of K out of cells
Acute metabolic acidosis causes K to move out of cells
acute metabolic alkalosis causes K to move into cell
False K concentrations
Pseudohypokalemia occasionally occurs in patients with chronic myelocytic leukemia with a WBC count > 105/μL when the specimen remains at room temperature before being processed because of uptake of plasma K by abnormal leukocytes in the sample. It is prevented by prompt separation of plasma or serum in blood samples.
Pseudohyperkalemia is more common, typically occurring due to hemolysis and release of intracellular K. To prevent false results, phlebotomy personnel should not rapidly aspirate blood through a narrow-gauge needle or excessively agitate blood samples. Pseudohyperkalemia can also result from platelet count > 400,000/μL due to release of K from platelets during clotting. In cases of pseudohyperkalemia, the plasma K (unclotted blood), as opposed to plasma K, is normal.
Hypokalemia
plasma K concentration < 3.5 mEq/L caused by a deficit in total body K stores or abnormal movement of K into cells
Causes
Decreased intake of K+
Renal losses: excess mineralocorticoid, diuretics
Drugs: Amphotericin B, Penicillin in high doses, Theophylline intoxication
GI tract losses:
Chronic diarrhea, including chronic laxative abuse
Clay (bentonite) ingestion, which binds K and greatly decreases absorption
Vomiting
Rarely, villous adenoma of the colon, which causes massive K secretion
Intracellular shift:
Glycogenesis during TPN (Total Parenteral Nutrition) or enteral hyperalimentation (stimulating insulin release)
After administration of insulin
Thyrotoxicosis (occasionally) due to excessive β-sympathetic stimulation (hypokalemic thyrotoxic periodic paralysis)
Clinical manifestation
Mild hypokalemia (plasma K 3 to 3.5 mEq/L) rarely causes symptoms
Plasma K < 3 mEq/L generally produces muscle weakness and may lead to paralysis and respiratory failure
Other muscular dysfunction: Cramping, Fasciculations, paralytic ileus, Hypoventilation, Hypotension, Tetany, Rhabdomyolysis
Persistent hypokalemia can impair renal concentrating ability, producing polyuria with secondary polydipsia
with severe hypokalemia: P-R prolongation, wide QRS, arrhythmias; increases risk of digitalis toxicity
Diagnosis
Plasma K measurement
ECG (ST segment depression, prolongation of Q-T interval, low amplitude T waves, prominent U waves [most important])
24-h urinary K excretion and plasma Mg concentration
Secretion of > 15 mEq/L suggests a renal cause for K loss
urine K:Cr (should be less than 1 in setting of hypokalemia)
if <1 consider GI loss
if >1 consider a renal loss
Treatment
Oral K supplements
IV K supplements for severe hyperkalemia or ongoing K losses
Because K solutions can irritate peripheral veins, the concentration should not exceed 40 mEq/L
Central vein (> 40 mEq/L or rapid infusion) max 60mmol/L
max infusion 20 mmol/h
usually KCl in saline solutions, avoid dextrose solutions (may exacerbate hypokalemia via insulin release)
Approach to hypokalemia *
Hyperkalemia
plasma K concentration > 5.5 mEq/L resulting from excess total body K stores or abnormal movement of K out of cells.
Due to increased K intake, drugs that impair renal K excretion, and acute or chronic kidney disease. It can also occur in metabolic acidosis as in diabetic ketoacidosis
Etiology
most common cause of increased plasma K concentration is probably pseudohyperkalemia caused by hemolysis of RBCs in the blood sample
Increased K intake (usually iatrogenic)
Increased K movement out of cells:
Drugs: β-Blockers, Digoxin toxicity
Increased tissue catabolism: Acute tumor lysis, Bleeding into soft tissues or GI tract, Burns, Rhabdomyolysis
Insulin deficiency
Other: Exercise, Metabolic acidosis
Decreased K excretion
Drugs: ACE inhibitors, Direct renin inhibitor, Heparin, NSAIDs, K-sparing diuretics, Cyclosporine and tacrolimus
Hypoaldosteronism: Adrenal insufficiency
Kidney disorders: failure
Clinical manifestation
hyperkalemia is usually asymptomatic until cardiac toxicity develops
Early: hyperactive muscles, paresthesia
Late: Muscle weakness, flaccid paralysis
Bradycardia >>cardiac arrest
ECG: AV block
Diagnosis
Plasma K measurement
ECG (increased P-R interval, shortening of the QT interval, tall, symmetric, peaked T waves)
Review of drug use
Assessment of renal function
Treatment
Treatment of the cause
mild hyperkalemia
Loop diuretics, ion exchange resins
moderate or severe hyperkalemia
Like mild hyperkalemia
IV insulin and glucose ( 1 u regular insulin per 3,0 g glucose)
IV Ca solution
Sodium bicarbonate solution
possibly an inhaled β2-agonist
usually hemodialysis
C BIG K DROP
C – Calcium gluconate
BIG – β-agonist, Bicarbonate, Insulin, Glucose
K – Kayexalate
DROP – Diuretics, Dialysis
Magnesium
ECF contains only about 1% of total body Mg
required by all enzymatic processes involving ATP and by many of the enzymes involved in nucleic acid metabolism
Normal plasma Mg concentration ranges from 1.4 to 2.1 mEq/L (0.70 to 1.05 mmol/L)
Hypomagnesemia
plasma Mg concentration < 1.4 mEq/L (< 0.70 mmol/L)
Causes
Alcoholism: Due to inadequate intake and excessive renal excretion
GI losses: Chronic diarrhea, Steatorrhea, Small-bowel bypass
Pregnancy-related: Lactation (increased Mg requirements)
Primary renal losses: Rare disorders (eg, Gitelman's syndrome)
Secondary renal losses:
Loop and thiazide diuretics
Hypercalcemia
After removal of parathyroid tumor
Diabetic ketoacidosis
Hypersecretion of aldosterone, thyroid hormones, or ADH
Nephrotoxins (eg, amphotericin B, cisplastin, cyclosporine, aminoglycosides)
Clinical manifestation
Anorexia, Nausea, Vomiting, Lethargy, Weakness, personality change, tetany (eg, positive Trousseau's or Chvostek's sign or spontaneous carpopedal spasm, hyperreflexia), Tremor
tetany, correlate with development of concomitant hypocalcemia, hypokalemia, or both
Severe hypomagnesemia may produce generalized tonic-clonic seizures, especially in children.
arrhythmias including Torsades de pointes
Diagnosis
Plasma Mg concentration < 1.4 mEq/L (< 0.70 mmol/L)
Mg deficiency should be suspected even when plasma Mg concentration is normal in patients with unexplained hypocalcemia or refractory hypokalemia
Mg deficiency should also be suspected in patients with unexplained neurologic symptoms and alcoholism, with chronic diarrhea, or after cyclosporine, cisplatinum-based chemotherapy or prolonged therapy with amphotericin B or aminoglycosides
Treatment
Oral Mg salts
IV or IM Mg sulfate for severe hypomagnesemia or inability to tolerate or be adherent with oral therapy
Hypermagnesemia
plasma Mg concentration > 2.1 mEq/L (> 1.05 mmol/L)
Etiology
most commonly in patients with renal failure after ingestion of Mg-containing drugs, such as antacids or purgatives.
Clinical manifestation
Hyporeflexia, Hypotension, respiratory depression, cardiac arrest
Diagnosis
Plasma Mg concentrations > 2.1 mEq/L (> 1.05 mmol/L)
ECG shows prolongation of the PR interval, widening of the QRS complex, and increased T-wave amplitude
Treatment
Calcium gluconate(IV (Mg2+-antagonist) for acute reversal of magnesium toxicity)
Diuresis
Dialysis
Calcium
required for the proper functioning of muscle contraction, nerve conduction, hormone release, and blood coagulation. In addition, proper Ca concentration is required for various other metabolic processes.
Normal total plasma Ca concentration ranges from 8.8 to 10.4 mg/dL (2.20 to 2.60 mmol/L). About 40% of the total blood Ca is bound to plasma proteins, primarily albumin. The remaining 60% includes ionized Ca plus Ca complexed with phosphate (PO4) and citrate
Hypercalcemia
total plasma Ca concentration > 10.4 mg/dL (> 2.60 mmol/L) or ionized plasma Ca > 5.2 mg/dL (> 1.30 mmol/L)
Etiology
Excessive bone resorption:
Cancer with bone metastases (Multiple myeloma)
Immobilization
Parathyroid hormone excess
Vitamin toxicity (vit A and D)
Excessive GI Ca absorption, intake, or both:
Sarcoidosis and other granulomatous diseases
Milk-alkali syndrome
Vitamin D toxicity
Clinical manifestation
mild hypercalcemia (Ca < 12 mg/dL)
Constipation, Anorexia, Nausea, Vomiting,abdominal pain, Ileus, Impairment of the renal concentrating mechanism leads to polyuria, nocturia, and polydipsia
moderate hypercalcemia (Ca > 12 mg/dL):
muscle weakness, arrhythmias, emotional lability, Nephrolithiasis (stones), Confusion, Delirium, Psychosis, Stupor, coma
Severe hypercalcemia (Ca > 18 mg/dL)
Shock, renal failure, death
“Bones, stones, groans, and psychiatric overtones”
Diagnosis
Total plasma Ca concentration
Chest x-ray, measurement of electrolytes, BUN, creatinine, ionized Ca, phosphate, and alkaline phosphatase, and serum protein immunoelectrophoresis to determine the cause,ECG (Short QT)
PTH and urinary excretion of Ca with or without phosphate
Treatment
Oral phosphate for plasma Ca < 11.5 mg/dL with mild symptoms and no kidney disease
IV saline and furosemide for more rapid correction for plasma Ca < 18 mg/dL
Bisphosphonates or other Ca-lowering drugs for plasma Ca < 18 mg/dL and > 11.5 mg/dL or moderate symptoms
Hemodialysis for plasma Ca > 18 mg/dL
Surgical removal for moderate, progressive primary hyperparathyroidism and sometimes for mild disease
phosphate restriction and binders and sometimes calcitriol for secondary hyperparathyroidism
Differential diagnosis of hypercalcemia*
Hypocalcemia
total plasma Ca concentration < 8.8 mg/dL (< 2.20 mmol/L) in the presence of normal plasma protein concentrations or a plasma ionized Ca concentration < 4.7 mg/dL (< 1.17 mmol/L)
Etiology
Hypoparathyroidism, Pseudohypoparathyroidism, Vitamin D deficiency, Renal disease
Mg depletion (can cause relative PTH deficiency and end-organ resistance to PTH action, usually when plasma Mg concentrations are < 1.0 mg/dL (< 0.5 mmol/L); Mg repletion improves PTH concentrations and renal Ca conservation)
Acute pancreatitis (when lipolytic products released from the inflamed pancreas chelate Ca)
Hypoproteinemia (reduces the protein-bound fraction of plasma Ca; hypocalcemia due to diminished protein binding is asymptomatic—because ionized Ca is unchanged, this entity has been termed factitious hypocalcemia)
Transfusion of > 5 units of citrate-anticoagulated blood and use of radiocontrast agents containing the divalent ion-chelating agent (can decrease the concentration of bioavailable ionized Ca while total plasma Ca concentrations remain unchanged)
Infusion of gadolinium (may spuriously lower Ca concentration)
Clinical manifestation
frequently asymptomatic
Major clinical manifestations of hypocalcemia are due to disturbances in cellular membrane potential, resulting in neuromuscular irritability
Neurologic manifestations
Muscle cramps
Mild encephalopathy
Severe hypocalcemia with plasma Ca < 7 mg/dL (< 1.75 mmol/L) may cause hyperreflexia, tetany, laryngospasm or generalized seizures
Tetany characteristically results from severe hypocalcemia but can result from reduction in the ionized fraction of plasma Ca without marked hypocalcemia, as occurs in severe alkalosis. Tetany is characterized by the following:
Sensory symptoms consisting of paresthesias of the lips, tongue, fingers, and feet
Carpopedal spasm, which may be prolonged and painful
Generalized muscle aching
Spasm of facial musculature
Chvostek's and Trousseau's signs are easily elicited at the bedside to identify latent tetany
Chvostek's sign: involuntary twitching of the facial muscles elicited by a light tapping of the facial nerve just anterior to the exterior auditory meatus. It is present in ≤ 10% of healthy people and in most people with acute hypocalcemia but is often absent in chronic hypocalcemia.
Trousseau's sign: precipitation of carpopedal spasm by reduction of the blood supply to the hand with a BP cuff inflated to 20 mm Hg above systolic BP applied to the forearm for 3 min. Trousseau's sign also occurs in alkalosis, hypomagnesemia, hypokalemia, and hyperkalemia and in about 6% of people with no identifiable electrolyte disturbance
diagnosis
Estimation or measurement of ionized Ca
PTH, PO43-, Mg2+, Urine Ca2+, creatinine
Treatment
IV Ca gluconate for tetany
Oral Ca for postoperative hypoparathyroidism
Oral Ca and vitamin D for chronic hypocalcemia
For tetany, Ca gluconate 10 mL of 10% solution IV over 10 min is given. Response can be dramatic but may last for only a few hours. Repeated boluses or a continuous infusion with 20 to 30 mL of 10% Ca gluconate in 1 L of 5% glucose over the next 12 to 24 h may be needed. Infusions of Ca are hazardous in patients receiving digoxin and should be given slowly and with continuous ECG monitoring