Electrolytes Hyponatremia What is the serum osmolarity 2Na

Electrolytes

Hyponatremia • What is the serum osmolarity? – 2(Na+) + BUN/2. 8 + Glucose/18 • Hyper-osmolar (>290) – Hyperglycemia – Mannitol • Iso-osmolar (270 -290) – Hyperproteinemia ¦ Multiple myeloma ¦ Amyloidosis ¦ MGUS – Hyperlipidemia – Hyper & Iso-osmolar hyponatremia is also called pseudo-hyponatremia

Hyponatremia • Hypo-osmolar – What is the volume status on physical exam • Hypovolemic – Dehydration ¦ Vomiting ¦ Diarrhea – Treat by calculating and replacing the sodium deficit ¦ body wt in kg x 60% x 10 meq ¦ Select your IV fluid and rate ¦ Watch for central pontine myelinosis during correction • Hypervolemic ¦ CHF ¦ ESLD ¦ Nephrotic syndrome

Hyponatremia • Euvolemic – Addison’s disease – Drugs • HCTZ • SSRI • ACE-I – Hypothyroidism – Psychogenic polydipsia – SIADH

Hyponatremia • SIADH – Etiology • Pulmomary – Small cell carcinoma – TB – Pneumonia – Lung Abscess • CNS – Head injury – CVA – Meningitis / Encephalitis • Drug – Vincristine – Cyclophosphamide – Carbamazepine

Hyponatremia • SIADH – Diagnosis • Urine Sodium or osmolarity – Both should be elevated – Treatment • Treat the underlying cause • Fluid restriction • Demeclocycline • Vaprisol

Hypernatremia • What is the volume status – Hypovolemic • Dehydration – Vomiting – Diarrhea – Insensible and sweat losses • Treatment – Calculate the free water deficit ¦ Total body water x (serum Na+ -140)/140 – Careful for cerebral edema during correction – Hypervolemic • Conn’s syndrome – Renin to Aldosterone ratio

Hypernatremia • Euvolemic – Diabetes Insipidus • Central DI – ADH insufficiency – Caused by ¦ Neoplasm ¦ Infiltrative lesions ¦ Surgery ¦ Radiotherapy ¦ Head injury • Nephrogenic DI – ADH resistance – Caused by ¦ Sickle cell disease ¦ Pyelonephritis ¦ Drugs: lithium, demeclocycline, colchicine

Hypernatremia • Diabetes Insipidus – Diagnosis • Compare plasma and urine osmolarity after dehydration (water deprivation test) and after vasopressin – Treatment • Central DI – Hormone replacement with vasopressin • Nephrogenic DI – HCTZ or amiloride enhances the reabsorption of fluid from the proximal tubule

Hyperkalemia • INCREASED POTASSIUM RELEASE FROM CELLS • Pseudohyperkalemia – Mechanical trauma during venipuncture – Cooling of the sample and specimen deterioration because of increased length of storage – May also represent severe intravascular hemolysis rather than a hemolyzed specimen – Marked leukocytosis or thrombocytosis (white cell or platelet count greater than 100, 000 per mm 3 or 400, 000 mm 3, respectively), as may occur with leukemia or a myeloproliferative disease

Hyperkalemia • INCREASED POTASSIUM RELEASE FROM CELLS • Metabolic acidosis • Insulin deficiency • Increased tissue catabolism – Any cause of increase tissue breakdown result in the release of potassium into the extracellular fluid – hyperkalemia may occur in this setting, particularly if renal failure is also present – Clinical examples include trauma

Hyperkalemia • INCREASED POTASSIUM RELEASE FROM CELLS • Beta-adrenergic blockade • Exercise • Hyperkalemic periodic paralysis • Digitialis • Succinylcholine

Hyperkalemia • REDUCED URINARY POTASSIUM EXCRETION – Hypoaldosteronism • Type 4 RTA – Potassium-sparing diuretics – Renal failure – Effective circulating volume depletion

Hyperkalemia • Treatment – Antagonism of membrane actions of potassium • Calicum – Drive extracellular potassium into the cells • Insulin and glucose • Sodium bicarbonate, primarily if metabolic acidosis • Beta-2 adrenergic agonists – Removal of potassium from the body • Loop or thiazide diuretics • Dialysis, preferably hemodialysis if severe • Cation exchange resin – Sodium polystyrene sulfonate (Kayexalate)

Hypokalemia • Major causes Decreased potassium intake – Increased entry into cells • An elevation in extracellular p. H • Increased availability of insulin • Elevated Beta-adrenergic activity – Stress or administration of beta-agonists • Hypokalemic periodic paralysis • Marked increase in blood cell production – Administration of vitamin B 12 or folic acid to treat a megaloblastic anemia – Granulocyte-macrophage colony-stimulating factor (GM-CSF) to treat neutropenia • Hypothermia • Chloroquine intoxication –

Hypokalemia • Major causes – Increased gastrointestinal losses • Vomiting • Diarrhea • Laxative abuse – Increased urinary losses • Diuretics • Primary mineralocorticoid excess • Hypomagnesemia • Amphotericin B • Bartter's or Gitelman's syndrome – Increased sweat losses – Dialysis – Plasmapheresis

Hypokalemia • Treatment – 10 meq KCl will raise serum K+ by 0. 1 • Be careful in renal failure

Hyperphosphatemia • Causes – MASSIVE ACUTE PHOSPHATE LOAD • Tumor lysis syndrome • Rhabdomyolysis • Lactic and ketoacidosis • Exogenous phosphate – Renal failure – Increased tubular reabsorption of phosphate • Hypoparathyroidism • Acromegaly – Due to insulin-like growth factor • Vitamin D toxicity • Bisphonates – Pseudohyperphosphatemia • hyperglobulinemia

Hypophosphatemia • Major causes – Internal redistribution • Increased insulin secretion • Refeeding syndrome • Hungry bone syndrome – Decreased intestinal absorption • Inadequate intake • Antacids containing aluminum or magnesium • Steatorrhea and chronic diarrhea • Vitamin D deficiency or resistance – Increased urinary excretion • Hyperparathyroidism • Vitamin D deficiency or resistance

Hypophosphatemia • Signs and symptoms – Mineral metabolism • Release of bone calcium contributes to the hypercalciuria • More prolonged hypophosphatemia leads to rickets and osteomalacia due to decreased bone mineralization – CNS • Metabolic encephalopathy • Confusion, seizures, delirium, and coma – CVS • Myocardial contractility may be impaired with ATP depletion • The reduction in cardiac output may become clinically significant, leading to congestive heart failure, when the plasma phosphate concentration falls to 1. 0 mg/d. L

Hypophosphatemia • Signs and symptoms – Skeletal and smooth muscle • Proximal myopathy, dysphagia and ileus – Hematologic dysfunction • Hypophosphatemia can also affect each of the components of the hematopoietic system • Treatment – Oral (Neutra-Phos) – IV (K-Phos)

Hypermagnesemia • Causes – Renal failure – Magnesium infusion • Severe preeclampsia or eclampsia – Oral ingestion – Magnesium enemas • Substantial quantities of magnesium can be absorbed from the large bowel • Among patients with renal failure, the administration of a magnesium enema can be fatal

Hypermagnesemia • Treatment – Most cases of symptomatic hypermagnesemia can be prevented by anticipation – Dialysis – When the toxic effects of magnesium must be reversed more quickly in a patient with severe symptoms, intravenous calcium can be given as a magnesium antagonist

Hypomagnesemia • Causes – GI losses – Renal losses • Both loop and thiazide diuretic can inhibit net magnesium reabsorption • Alcohol – Appears to reflect alcohol-induced tubular dysfunction that is reversible within four weeks of abstinence • Hypercalcemia – Calcium and magnesium seem to compete for transport in the thick ascending limb of the loop of Henle • Nephrotoxins – Aminoglycoside – Amphotericin B – Pentamidine – Cyclosporine • Loop of Henle or distal tubule dysfunction – Bartter’s syndrome

Hypomagnesemia • Signs and symptoms – Neuromuscular • Tetany – Positive Chvostek and Trousseau signs, and generalized convulsions ¦ Can occur in the absence of hypocalcemia – Hypokalemia – Bone and calcium metabolism • PTH resistance • Vitamin D deficiency – CVS • Severe magnesium depletion can lead to prolongation of the PR interval, progressive widening of the QRS complex, and diminution of the T wave • Treatment – PO or IV replacement – Usually under treated

Serum Calcium • Normal value – 8. 0 to 10. 0 • Total body calcium • 99% in stored in bone • 1% in extracellular fluid • 3 forms of calcium in the blood – Bound to protein (40%-45%) • Correct for albumin – Free ionized (45 -50%) • Order ionized calcium – Bound to anions (5 -10%) • Phosphate, bicarbonate, citrate

Calcium physiology • Calcium is: – Absorbed from the gut – Stored in the bone – Excreted by the kidneys • Three endogenous chemicals regulate serum calcium – Parathyroid (PTH) – 1, 25 -(OH)2 -D 3 (Vit D) – Calcitonin • From the thyroid C cells • Can be considered a PTH antagonist • It slows down the osteoclasts causing a decrease in bone resorption

Calcium physiology • Decrease serum calcium, by reduced negative feedback, causes – Increased PTH • Causes a release of bone calcium stores • Decreased renal excretion of calcium • Increases activity of kidney hydroxylase causing increased 1, 25 -(OH)2 -D 3 – Increased Vitamin D • Increases Calcium absorption from the gut

Hypercalcemia • Symptoms (>11. 5 -12) Urinary • Polyuria • Polydipsia • Nephrocalcinosis • Renal failure – CNS • Personality disturbance • Mental obtundation or coma • Neuromuscular weakness • Easy fatigability – GI • Anorexia • Weight loss • Constipation • Nausea / vomiting • Abdominal pain • Pancreatitis – CV • Hypertension • Arrhythmias – Short QT –

Hypercalcemia • Severe hypercalcemia (>15) – Medical emergency • IV fluids • Lasix • Bisphonates • Calcitonin

Hypercalcemia • Causes – Primary hyperparathyroidism • One gland hyperplasia (most common) • Hyperplasia of all four glands • Parathyroid cancer is a rare cause • Can also be part of the MEN 1 & 2 – Maliganancy (PTH like hormone) • Lung (Squamous Cell) • Breast • Myeloma – Activation of osteoclasts – Others • Granulomatos diseases (Sarcoid) – Vit D activation by macrophages • Familial benign hypocalciuric hypercalcemia • Drugs (lithium, Vit D, HCTZ, milk-alkali syndrome) • Immobility

Hypocalcemia • Etiology – Decreased PTH secretion • Thyroid surgery and loss of parathyroid glands – Hypomagnesemia • Alcholics • Patients with bowel disease • Magnesium is required to secrete PTH – Vitamin D deficiency • Osteomalacia – Called rickets when in occurs in youth – Loss of calcium • Occurs with pancreatitis – Severe hyperphosphatemia • Calcium chelates with the phosphate – PTH resistance • Pseudohypoparathyroidism – Albright's hereditary osteodystrophy

Hypocalcemia • Clinical findings – Neuromuscular • Tetany – Chvostek sign (percussion of CN VII) – Trousseau sign • Laryngospasm • Cramping • Seizures – CV • QT prolongation • Refractory CHF • hypotension

Hypocalcemia • Diagnosis – Suggested when the serum calcium is low • Check albumin • Check ionized calcium • PTH may be low or high depending on the etiology • Check serum magnesium • Management – In the acute stages IV calcium can be given – Maintenance therapy includes oral calcium