Transcript Electrolytes - WordPress.com

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 10meq
 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
mm3 or 400,000 mm3, 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 pH
• 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
• Bisphosphonates
– 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/dL
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-D3 (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-D3
– 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
• Bisphosphonates
• 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