Electrolytes and Metabolic Emergencies Edward Omron MD, MPH Pulmonary Service
Electrolyte and Metabolic Emergencies in Critical Care
May 07, 2015
A review of the more common electrolyte abnormalities and metabolic crises seen in critical care
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Electrolytes and Metabolic Emergencies
Edward Omron MD, MPH
Pulmonary Service
ObjectivesObjectives• Review causes and clinical manifestations of
severe electrolyte disturbances
• Outline emergent management of electrolyte disturbances
• Recognize and treat acute adrenal insufficiency, thyroid storm and myxedema coma
• Describe management of severe hyperglycemic syndromes
• Review causes and clinical manifestations of severe electrolyte disturbances
• Outline emergent management of electrolyte disturbances
• Recognize and treat acute adrenal insufficiency, thyroid storm and myxedema coma
• Describe management of severe hyperglycemic syndromes
Principles of Electrolyte Disturbances
Principles of Electrolyte Disturbances
• Implies an underlying disease process
• 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
• Treat the electrolyte change, but seek the cause
• Clinical manifestations usually not specific to a particular electrolyte change, e.g., seizures, arrhythmias
Principles of Electrolyte Disturbances
Principles of Electrolyte Disturbances
• Clinical manifestations determine urgency of treatment, not laboratory values
• Speed and magnitude of correction dependent on clinical circumstances
• Frequent reassessment of electrolytes required
• Clinical manifestations determine urgency of treatment, not laboratory values
• Speed and magnitude of correction dependent on clinical circumstances
• Frequent reassessment of electrolytes required
HypokalemiaHypokalemia
• K < 3.5 mmol/L
• Etiology – alkalosis, diuresis, dka, ngs, n/v, hypomagnesemia
• Manifestations – life threatening arrhythmias
• Deficit poorly estimated by serum levels
• K < 3.5 mmol/L
• Etiology – alkalosis, diuresis, dka, ngs, n/v, hypomagnesemia
• Manifestations – life threatening arrhythmias
• Deficit poorly estimated by serum levels
Which one of the following ECG changes is least likely to occur with hypokalemia?
• ST-T segment depression
• T wave inversion
• AV Blocks (2nd and 3rd degree)
• PVC’s
• U waves
• QT prolongation
HypokalemiaHypokalemia• Treat aggressively in severe metabolic
acidosis
• Correct hypomagnesemia
• ECG monitoring with emergent administration
• Allowable maximum iv dose per hour controversial– Life threatening arrhythmias: 10 mmols/ 20 minutes
– KCL 20 mmols/hr Central IV or 20 mmol/ PO q1 hour
– KCL 10 mmols/hr peripheral IV (Inefficient)
• Treat aggressively in severe metabolic acidosis
• Correct hypomagnesemia
• ECG monitoring with emergent administration
• Allowable maximum iv dose per hour controversial– Life threatening arrhythmias: 10 mmols/ 20 minutes
– KCL 20 mmols/hr Central IV or 20 mmol/ PO q1 hour
– KCL 10 mmols/hr peripheral IV (Inefficient)
HyperkalemiaHyperkalemia
• K>5.5 mmol/dL
• Etiology – renal failure, acidemia, cell death, drugs(ACE/Succinylcholine)
• Manifestations – arrhythmias: peaked t waves,
QRS widening, sine wave.
• K>5.5 mmol/dL
• Etiology – renal failure, acidemia, cell death, drugs(ACE/Succinylcholine)
• Manifestations – arrhythmias: peaked t waves,
QRS widening, sine wave.
Hyperkalemia – TreatmentHyperkalemia – Treatment
• Urgency of treatment- clinical manifestations
• Stop intake
• Give calcium for cardiac toxicity
• Shift K+ into cell – glucose + insulin, NaHCO3, inhaled 2-agonist (high dose)
• Remove from body – diuretics, sodium polystyrene sulfonate, dialysis
• Urgency of treatment- clinical manifestations
• Stop intake
• Give calcium for cardiac toxicity
• Shift K+ into cell – glucose + insulin, NaHCO3, inhaled 2-agonist (high dose)
• Remove from body – diuretics, sodium polystyrene sulfonate, dialysis
HyponatremiaHyponatremia
• Na < 135 mmol/L• Hypo-osmolar hyponatremia
– Euvolemic (SIADH,Hypothyroidism)– Hypovolemic (Diuretics, Adrenal Insuff.)
– Hypervolemic (CHF, Cirrhosis, NS)• Normo- or hyperosmolar hyponatremia
• Pseudohyponatremia• Manifestations – neurologic (brain edema)
• Na < 135 mmol/L• Hypo-osmolar hyponatremia
– Euvolemic (SIADH,Hypothyroidism)– Hypovolemic (Diuretics, Adrenal Insuff.)
– Hypervolemic (CHF, Cirrhosis, NS)• Normo- or hyperosmolar hyponatremia
• Pseudohyponatremia• Manifestations – neurologic (brain edema)
65 yo wm POD 2 TURP presents lethargic to ICU
• HR =90, BP = 120/80, RR = 15• Na = 114, K =3.8, Cl = 78, HCO3 = 20, Cre = 1.2
– Free Water Restriction– Isotonic Saline– Hypertonic Saline– Furosemide– Ringers Lactate
• (infusate Na - serum Na)/ (TBW+1)
• NS(154 mmol/L)– (154 - 114) / (42L + 1) = Delta 0.9 mmol
• Hypertonic Saline– (514 - 114) / (42+1) = Delta 9.3 mmol– Given over 24 hours (40 cc/hr)– Correct 0.5 mmol/hr until Na > 120 mmol/L
Delta Plasma Na from 1 liter of fluid
Hyponatremia – TreatmentHyponatremia – Treatment• Hypovolemic Na – give normal saline,
rule out adrenal insufficiency
• Hypervolemic Na – increase free H2O loss
• Euvolemic hyponatremia
– Restrict free water intake
– Increase free water loss
– Normal or hypertonic saline
• Correct slowly due to possibility of demyelinating syndromes
• Hypovolemic Na – give normal saline, rule out adrenal insufficiency
• Hypervolemic Na – increase free H2O loss
• Euvolemic hyponatremia
– Restrict free water intake
– Increase free water loss
– Normal or hypertonic saline
• Correct slowly due to possibility of demyelinating syndromes
HypernatremiaHypernatremia• Na > 145 mmol/L
• Causes: diarrhea, vomiting, diuresis, thirst, diabetes insipidus
• Manifestations- neurologic
• Na = 160 mmol, 70 kg male
– 1 L D5W changes Na by 4 mmol/L
– H2O deficit (L) = [ 0.6 wt (kg) ]
[ observed Na/140 - 1 ] = 6 Liter Free H2O
Urine Osmolality > 500 mOsmol/kg extrarenal or osmotic diuresis, < 300 mOsmol/kg diabetes insipidus
• Na > 145 mmol/L
• Causes: diarrhea, vomiting, diuresis, thirst, diabetes insipidus
• Manifestations- neurologic
• Na = 160 mmol, 70 kg male
– 1 L D5W changes Na by 4 mmol/L
– H2O deficit (L) = [ 0.6 wt (kg) ]
[ observed Na/140 - 1 ] = 6 Liter Free H2O
Urine Osmolality > 500 mOsmol/kg extrarenal or osmotic diuresis, < 300 mOsmol/kg diabetes insipidus
Hypernatremia – TreatmentHypernatremia – Treatment• Provide intravascular volume
replacement
• Consider giving one-half of free H2O deficit initially
• Reduce Na cautiously: 0.5-1.0 mmol/L/hr
• Secondary neurologic syndromes with rapid correction
• Provide intravascular volume replacement
• Consider giving one-half of free H2O deficit initially
• Reduce Na cautiously: 0.5-1.0 mmol/L/hr
• Secondary neurologic syndromes with rapid correction
Other Electrolyte DeficitsCa, PO4, Mg
Other Electrolyte DeficitsCa, PO4, Mg
• 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 DisordersOther Electrolyte Disorders
• Hypocalcemia
– Calcium chloride or gluconate
– Bolus + continuous infusion
– Albumin correction is useless
• Hypercalcemia
– Rehydration with normal saline
– Loop diuretics
• Hypocalcemia
– Calcium chloride or gluconate
– Bolus + continuous infusion
– Albumin correction is useless
• Hypercalcemia
– Rehydration with normal saline
– Loop diuretics
Other Electrolyte DisordersOther Electrolyte Disorders
• Hypophosphatemia
– PO4 < 2.5 mg/dL
– Replacement iv for level < 1 mg/dL
• Hypomagnesemia
– Emergent administration over 5–10 mins– Less urgent administration over
10–60 mins
• Hypophosphatemia
– PO4 < 2.5 mg/dL
– Replacement iv for level < 1 mg/dL
• Hypomagnesemia
– Emergent administration over 5–10 mins– Less urgent administration over
10–60 mins
What is most likely to present in a patient with severe magnesium deficiency?
• Respiratory Depression
• Bradycardia
• Tetany
• Hypotension
• Loss of patellar reflex
• 35 yo with fever, hypotension, and syncope– 2 months of fatigue, weight loss– BP 70/40, HR 110, temp 103, RR 18– Na = 128, K = 5.6, Cl = 102, HCO3 = 16– Glucose = 60, BUN = 28, Creat = 1.2– Bolus 3L NS, BP 80/50 Dopamine started
1. Norepinephrine and decrease dopamine 2. Dexamethasone 4 mg IV 3. Infuse 1 liter hetastarch 4. Thyroxine IV and hydrocortisone 100 mg IV
Acute Adrenal InsufficiencyAcute Adrenal Insufficiency
• Nonspecific manifestations– Abdominal pain, nausea, emesis– Orthostatic/refractory hypotension
• Laboratory findings– Hyponatremia, hyperkalemia– Hypoglycemia– metabolic acidosis– Hypereosinophillia
• Nonspecific manifestations– Abdominal pain, nausea, emesis– Orthostatic/refractory hypotension
• Laboratory findings– Hyponatremia, hyperkalemia– Hypoglycemia– metabolic acidosis– Hypereosinophillia
Acute Adrenal InsufficiencyAcute Adrenal Insufficiency
• Baseline blood samples
• Volume and glucose infusion
• Dexamethasone or hydrocortisone
• ACTH stimulation test if needed
• Treat precipitating conditions
• Baseline blood samples
• Volume and glucose infusion
• Dexamethasone or hydrocortisone
• ACTH stimulation test if needed
• Treat precipitating conditions
Hyperglycemic SyndromesHyperglycemic Syndromes
• Diabetic ketoacidosis (DKA)
• Hyperglycemic hyperosmolar state (HHS)
• Manifestations – dehydration, polyuria/polydipsia, altered mental status, BP, nausea, emesis, abdominal pain
• Diabetic ketoacidosis (DKA)
• Hyperglycemic hyperosmolar state (HHS)
• Manifestations – dehydration, polyuria/polydipsia, altered mental status, BP, nausea, emesis, abdominal pain
Hyperglycemic Syndromes – Laboratory
Hyperglycemic Syndromes – Laboratory
• Hyperglycemia/hyperosmolality
• Ketonemia/ketonuria (DKA)
• Increased anion gap metabolic acidosis (DKA)
• Electrolyte changes (K, PO4, Na)
• Hyperglycemia/hyperosmolality
• Ketonemia/ketonuria (DKA)
• Increased anion gap metabolic acidosis (DKA)
• Electrolyte changes (K, PO4, Na)
Hyperglycemic Syndromes – Treatment
Hyperglycemic Syndromes – Treatment
• Identify and treat precipitating factors
• Restore fluid/electrolyte balance
• Insulin – iv bolus and infusion
• Add glucose to infusion when glucose <250-300 mg/dL (13.9-16.7 mmol/L)
• Treat electrolyte changes (K, PO4)
• NaHCO3 rarely needed
• Lactated Ringers preferred crystalloid
• Identify and treat precipitating factors
• Restore fluid/electrolyte balance
• Insulin – iv bolus and infusion
• Add glucose to infusion when glucose <250-300 mg/dL (13.9-16.7 mmol/L)
• Treat electrolyte changes (K, PO4)
• NaHCO3 rarely needed
• Lactated Ringers preferred crystalloid
• 28 yo with schizophrenia, acute delirium– HR 120, T 101.6, BP 96/50– bibasilar rales, 2/6 systolic murmur– ECG with atrial fibrillation– WBC 10,000, CK 150, (-) LP, UA, and head
CT
1. Dantrolene 2. Haloperidol 3. Antibiotics 4. Propylthiouracil, propranol
Thyroid StormThyroid 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
• 56 yo obese female minimally responsive– HR 64, RR 10, BP 160/100, T 96.5– Distant heart sounds, 3+ LE non-pitting edema– CXR: bilateral effusions/ cardiomegaly– Na = 130, Hb = 10.2, CK = 500, WBC =13000– (-) head ct and lumbar puncture
– 1. Intravenous thyroxine, hydrocortisone– 2. TTE– 3. Neurology consult– 4. flumazenil
Myxedema ComaMyxedema 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
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