Electrolyte and Metabolic Disturbances AHMED GHALI MD

Lecture Objectives  Review clinical manifestations and management of severe electrolyte disturbances  Recognize acute adrenal insufficiency and appropriate treatment  Describe management of hyperglycemic disturbances  Review clinical manifestations and management of severe electrolyte disturbances  Recognize acute adrenal insufficiency and appropriate treatment  Describe management of hyperglycemic disturbances

Electrolyte Changes – The Principles  Implies an underlying disease process and may produce manifestations  Treat the electrolyte change, but seek the cause  Clinical manifestations usually not specific to a particular electrolyte change, e.g., seizures, arrhythmias  Implies an underlying disease process and may produce manifestations  Treat the electrolyte change, but seek the cause  Clinical manifestations usually not specific to a particular electrolyte change, e.g., seizures, arrhythmias

Electrolyte Changes – The Principles  Changes in ion concentrations affect intracellular reactions, membrane potentials and movement of H 2 O  Symptoms occur most often in tissues/organs dependent upon membrane potentials, e.g., cardiac, neurologic, muscle, GI, etc.  Changes in ion concentrations affect intracellular reactions, membrane potentials and movement of H 2 O  Symptoms occur most often in tissues/organs dependent upon membrane potentials, e.g., cardiac, neurologic, muscle, GI, etc.

Electrolyte Changes – The Principles  Clinical manifestations determine urgency of treatment, not laboratory number  Speed and magnitude of correction dependent upon clinical circumstances  Recheck electrolytes frequently during correction  Clinical manifestations determine urgency of treatment, not laboratory number  Speed and magnitude of correction dependent upon clinical circumstances  Recheck electrolytes frequently during correction

Hypokalemia  Etiology – renal loss, extrarenal loss, transcellular shift, decreased intake  Deficit poorly estimated by serum levels  Manifestations – nonspecific cardiac, neuromuscular, gastrointestinal  Etiology – renal loss, extrarenal loss, transcellular shift, decreased intake  Deficit poorly estimated by serum levels  Manifestations – nonspecific cardiac, neuromuscular, gastrointestinal

Hypokalemia  Titrate administration of K + against serum level and manifestations  ECG monitoring with emergent administration  Allowable maximum iv dose per hour controversial  Treat hypokalemia urgently in acidosis  Titrate administration of K + against serum level and manifestations  ECG monitoring with emergent administration  Allowable maximum iv dose per hour controversial  Treat hypokalemia urgently in acidosis

Hyperkalemia  Etiology – renal failure, transcellular shifts, cell death, drugs, pseudohyperkalemia  Manifestations – cardiac, neuromuscular  Etiology – renal failure, transcellular shifts, cell death, drugs, pseudohyperkalemia  Manifestations – cardiac, neuromuscular

Hyperkalemia – Treatment  Stop intake  Give calcium for cardiac toxicity  Shift K + into cell – NaHCO 3, glucose + insulin, inhaled -agonist  Remove from body – diuretics, dialysis, sodium polystyrene sulfonate  Stop intake  Give calcium for cardiac toxicity  Shift K + into cell – NaHCO 3, glucose + insulin, inhaled -agonist  Remove from body – diuretics, dialysis, sodium polystyrene sulfonate

Hyponatremia  Etiology – euvolemic, hypovolemic, hypervolemic, pseudohyponatremia  Manifestations – nonspecific neurologic, muscular, gastrointestinal  Etiology – euvolemic, hypovolemic, hypervolemic, pseudohyponatremia  Manifestations – nonspecific neurologic, muscular, gastrointestinal

Hyponatremia – Treatment  Hypovolemic Na – give normal saline, rule out hypoadrenalism  Hypervolemic Na – increase free H 2 O loss  Euvolemic Na – restrict H 2 O intake, increase free H 2 O loss  Correct Na slowly due to possibility of demyelinating syndromes  Hypovolemic Na – give normal saline, rule out hypoadrenalism  Hypervolemic Na – increase free H 2 O loss  Euvolemic Na – restrict H 2 O intake, increase free H 2 O loss  Correct Na slowly due to possibility of demyelinating syndromes

Hypernatremia  Etiology –  H 2 O loss, H 2 O intake, Na intake  Manifestations – nonspecific neurologic, muscular  H 2 O deficit (L) = [ 0.6  wt (kg) ]  [ obs Na - 1 ] 140  Etiology –  H 2 O loss, H 2 O intake, Na intake  Manifestations – nonspecific neurologic, muscular  H 2 O deficit (L) = [ 0.6  wt (kg) ]  [ obs Na - 1 ] 140

Hypernatremia – Treatment  Provide intravascular volume replacement  Consider giving one-half of free H 2 O deficit initially  Reduce Na cautiously: 12–20 mEq/L over 24 hrs  Secondary neurologic syndromes with rapid correction  Provide intravascular volume replacement  Consider giving one-half of free H 2 O deficit initially  Reduce Na cautiously: 12–20 mEq/L over 24 hrs  Secondary neurologic syndromes with rapid correction

Other Electrolyte Deficits Mg, Ca, PO 4  May produce serious but nonspecific cardiac, neuromuscular, respiratory, and other effects  All are primarily intracellular ions, so deficits difficult to estimate  Titrate replacement against clinical findings  May produce serious but nonspecific cardiac, neuromuscular, respiratory, and other effects  All are primarily intracellular ions, so deficits difficult to estimate  Titrate replacement against clinical findings

Other Electrolyte Disorders  Hypocalcemia Calcium chloride or gluconate Bolus + continuous infusion  Hypercalcemia Rehydration with normal saline Loop diuretics  Hypocalcemia Calcium chloride or gluconate Bolus + continuous infusion  Hypercalcemia Rehydration with normal saline Loop diuretics

Other Electrolyte Disorders  Hypophosphatemia Replacement iv for level < 1 mg/dL  Hypomagnesemia Emergent administration over 5–10 mins Less urgent administration over 10–60 mins  Hypophosphatemia Replacement iv for level < 1 mg/dL  Hypomagnesemia Emergent administration over 5–10 mins Less urgent administration over 10–60 mins

Acute Adrenal Insufficiency  Nonspecific manifestations Abdominal pain, nausea/emesis Orthostatic/refractory hypotension  Laboratory findings Hyponatremia, hyperkalemia Hypoglycemia  Nonspecific manifestations Abdominal pain, nausea/emesis Orthostatic/refractory hypotension  Laboratory findings Hyponatremia, hyperkalemia Hypoglycemia

Acute Adrenal Insufficiency  Baseline blood samples  Volume infusion  Dexamethasone or hydrocortisone  ACTH stimulation test if needed  Treat precipitating conditions  Baseline blood samples  Volume infusion  Dexamethasone or hydrocortisone  ACTH stimulation test if needed  Treat precipitating conditions

Hyperglycemic Syndromes  Diabetic ketoacidosis (DKA)  Hyperglycemic hyperosmolar nonketotic syndrome (HHNK)  Manifestations – dehydration, polyuria/ polydipsia, altered mental status, BP, nausea, emesis, abdominal pain  Diabetic ketoacidosis (DKA)  Hyperglycemic hyperosmolar nonketotic syndrome (HHNK)  Manifestations – dehydration, polyuria/ polydipsia, altered mental status, BP, nausea, emesis, abdominal pain

Hyperglycemic Syndromes – Laboratory  Hyperglycemia/hyperosmolality  Ketonemia/ketonuria (DKA)  Increased gap metabolic acidosis (DKA)  Electrolyte changes (K, PO 4, Na)  Hyperglycemia/hyperosmolality  Ketonemia/ketonuria (DKA)  Increased gap metabolic acidosis (DKA)  Electrolyte changes (K, PO 4, Na)

Hyperglycemic Syndromes – Treatment  Treat precipitating factors  Volume resuscitation  Insulin – iv bolus and infusion  Add glucose to infusion when glucose <250 mg/dL (13.8 mmol/L)  Treat electrolyte changes (K, PO 4 )  NaHCO 3 use rarely needed  Treat precipitating factors  Volume resuscitation  Insulin – iv bolus and infusion  Add glucose to infusion when glucose <250 mg/dL (13.8 mmol/L)  Treat electrolyte changes (K, PO 4 )  NaHCO 3 use rarely needed

Thyroid Storm  Exaggerated manifestations of hyperthyroidism  Supportive measures  Specific measures Propylthiouracil or methimazole Propranolol Potassium or sodium iodide Dexamethasone, sodium ipodate  Exaggerated manifestations of hyperthyroidism  Supportive measures  Specific measures Propylthiouracil or methimazole Propranolol Potassium or sodium iodide Dexamethasone, sodium ipodate

Myxedema Coma  Manifestations of severe hypo-thyroidism  Supportive measures – airway, fluids, glucose, warming  Treat precipitating cause  Hydrocortisone  L-thyroxine  Manifestations of severe hypo-thyroidism  Supportive measures – airway, fluids, glucose, warming  Treat precipitating cause  Hydrocortisone  L-thyroxine

THANK YOU