Management of Life-Threatening

Electrolyte and Metabolic

Disturbances
 Introduction

Common in critically ill & injured patients

Alter physiologic function & contribute to
morbidity & mortality
The most common electrolyte disturban-
ce in critically ill patients are: disturbance
in K, Na, Ca, Mg, P levels
Metabolic disturbance accompany many
systemic disease processes or result of
altered endocrine function
 Electrolyte Disturbances

Potassium: hypo- & hyperkalemia

Sodium : hypo- & hypernatremia
Others:
Calcium : hypo- & hypercalcemia
Phosphate : hypo- & hyperphosphatemia
Magnesium : hypomagnesemia
 Potassium

Essential for maintenance of the electrical

membrane potential

Alteration of K primarily effect the CV,

neuromuscular, and GI systems.
 Hypokalemia

Plasma [K+] <3.5mEq/L (<3.5mmol/L)

Can occur as a result from:
1. increased K loss (renal or extrarenal
losses)
2. intercompartmental shift / transcellular
shift of K
3. inadequate or decreased K intake
Causes of hypokalemia
Transcellular Shifts Renal Losses Extrarenal Decreased Intake
Losses
Alkalosis Diuresis Diarrhea Malnutrition
Hyperventilation Metabolic alkalos Profuse sweating Alcoholism
Insulin Renal tub defects Anorexia nervosa
-adrenergic agonists Diabetic ketoacid
Drugs (diuretics,
aminoglycosides,
amphotericin B)
Hypomagnesemia
Vomiting
Clinical manifestation:

Cardiac system:
arrhythmias (ventricular, & supraventricular,
conduction delay, sinus bradycardia)
ECG abnormalities (U waves, QT prolo-
ngation, flat or inverted T waves)
Neuromuscular system: muscle weakness
or paralysis, paresthesia, ileus, abdominal
cramps, nausea, and vomiting
Effect of hypokalemia
Cardiovaskular
ECG changes/dysrhythmias
Myocardial dysfunction
Neuromuscular
Skeletal muscle weakness
Tetany
Rhabdomyolisis
Ileus
Renal
Polyuria (nephrogenic DI)
Increased ammonia production
Increased bicarbonate reabsorption
Hormonal
Decreased insulin secretion
Decreased aldosteron secretion
Metabolic
Negative nitrogen balance
Encephalopaty in patients with liver disease

Adapted from Schrier RE,ed: Renal and Electrolyte Disorders, 3rd ed. Little, Brown and
Company, 1986.
Treatment (1)

Treatment is aimed:
Correcting the underlying cause
Administering potassium

Stop offending drugs (if possible)

Correct hypomagnesemia & other
electrolyte disturbances
Correct alkalosis
Treatment (2)
K <3 mEq/L (<3 mmol/L) & asymptomatic: K
enterally (orally or NGT) (KCl 20-40 mEq
every 4-6 hrs)
K <2-2.5 mEq/L (<3 mEq/L if on digoxin) or
if symptoms are present: K intravenously
Arrhythmias or paralysis: KCl 20-30 mEq via
central venous catheter (sequential infusion: 10
mEq in 100 mL fluid over 20 mins, infusion rate can
be slowed after symptoms resolve)
Absence of life-threatening manifestation: KCl 10
mEq/hr IV
Treatment (3)

Acidemia is present, correct the

potassium level before correcting pH (K
shift intracellularly as the pH increases)
Monitoring

Continuous ECG monitoring is

necessary (during parenteral
administration of high concentration of
KCl)
Serum K levels must be monitored at
frequent interval during repletion (every
1-2 hrs during initial replacement)
 Hyperkalemia

Potassium >5.5 mEq/L (>5.5 mmol/L)

Most often results from renal dysfunction
Pseudohyperkalemia may result from a
white blood cell count >100,000/mm3 or
platelet count >600,000/mm3.
Causes of hyperkalemia

Renal dysfunction Cell death

Acidemia Rhabdomyolisis
Tumor lysis
Hypoaldosteronism
Burns
Drugs (potassium-sparing diuretics,
ACE inhibitors, etc.) Hemolysis

Excessive intake
Clinical manifestation

Heart:
arrhythmias (heart block, bradycardia, dimi-
nished conduction and contraction)
ECG abnormalities (diffuse peaked T waves,
PR prolongation, QRS widening, diminished P
waves, sine waves)
Muscle: muscle weakness, paralysis, pares-
thesias, and hypoactive reflexes
Treatment (1)
Recognition & treatment of underlying diseases
Removal of offending drugs
Limitation of potassium intake
Correction of acidemia or eletrolyte abnorma-
lities
Any serum potassium level >6 mEq/L should be
addressed, but the urgency of treatment
depends on clinical manifestation
The presence of ECG changes mandates
immediate therapy
Treatment (2)
ECG abnormalities present: CaCl 5-10 mL of a 10%
solution IV over 5-10 mins (the effect lasts only 30-60 mins &
should be followed by additional treatment)
Redistribution of K:
Na bicarbonate 1 mEq/kg (1 mmol/kg) IV over 5-10 mins
(beware of potential Na overload with Na bicarbonate)
50 g of 50% dextrose over 5-10 mins with 10 U of
regular insulin IV
Inhaled 2-agonists in high dose (albuterol 10-20 mg)

Removal of K from body:

Increase urine output with a loop diuretic
Increase GI K loss with Na polystyrene sulfonate 25-50 g
in sarbitol, enterally or by enema
Dialysis
Monitoring

Should be monitored during

evaluation & treatment:
Repeat serum K levels
Continuous cardiac monitoring
and serial ECG tracings
 Sodium

Primary functions:
determinant of osmolality in the body

involved in the regulation of

extracellular
volume
Abnormalities in circulating Na primarily
effect neuronal & neuromuscular function.
 Hyponatremia

Sodium <135 mEq/L (>135 mmol/L)

Most common cause: associated with a low serum
osmolality is excess secretion of ADH (euvolemic
hyponatremia) or associated with hypovolemic and
hypervolemic conditions
The presence of a nonsodium solute: glucose and
mannitol (characterized by an elevated serum
osmolality
Pseudohyponatremia: occurs in the presence of
severe hyperlipidemia, hyperproteinemia, or
hyperglycemia
Causes of hyponatremia

Euvolemia Hypovolemia Hypervolemia

SIADH Diuretic use CHF

Psychogenic polydipsia Aldosterone deficiency Cirrhosis
Hypothyroidism Renal tubular dysfunction Nephrosis
Inappropriate water admi- Vomiting
nistration to infanst/chil- Diarrhea
dren Third-space fluid losses
Clinical manifestation

CNS: disorientation, decreased mentation,

irritability, seizures, lethargy, coma,
nausea and vomiting
Muscle: weakness & CNS-driven
respiratory arrest
Algorithm for treatment of hypernatremia

hypernatremia

water & Na+ loss water loss increased Na+ content

replace isotonic loss replace water deficit loop diuretic

replace water deficit replace any water deficit

Treatment (1)

Treating the underlying disease

Removing offending drugs
Improving the circulating Na level
Hypovolemic hyponatremia: usually responds to IV
volume repletion (with normal saline). Volume is
replaced, ADH is suppressed & free water is
excreted by the kidneys.
Hypervolemic hyponatremia: usually not severe &
improves with successful treatment of the
underlying condition
Treatment (2)
Hyponatremia is acute or symptomatic:
serum Na level should be increased
restricting free-water intake
increasing free-water clearence with loop
diuretics
replacing IV volume with normal saline
(154 mEq/L) or hypertonic 3% saline (513
mEq/L)
The goal of therapy: to remove free water
& not Na
 Hypernatremia

Sodium <145 mEq/L (>145 mmol/L)

Indicates intracellular volume depletion
with a loss of free water, which exceeds
Na loss
Causes of hypernatremia

Water Loss Reduced Water Excessive Sodium

Intake Intake

Diarrhea Altered thirst Salt tablets

Vomiting Impaired access Hypertonic saline
Excessive sweating Sodium bicarbonate
Diuresis
Diabetes insipidus
Clinical manifestation

CNS: altered mentation, lethargy,

seizures, coma
Muscle function: muscle weakness
Polyuria: the presence of diabetes
insipidus or excess salt and water intake
Treatment (1)

Centers on correcting the underlying cause

of hypernatremia
The vast majority of patients require free-
water repletion
The water deficit can be calculated using
equation:
water deficit (L)=0.6 x wt (kg) [(Na2/Na1)-1]
Na1 = the normal sodium level
Na2 = the measured sodium level
METABOLIC DISTURBANCES

Acute Adrenal Insufficiency

Hyperglycemic Syndromes
Acute Adrenal Insufficiency
Lack of specific signs & symptoms makes
early recognition of acute renal insufficiency
difficult
May result from:
Failure of the adrenal glands (autoimmune
disease, granulomatous disease, HIV
infection, adrenal hemorrhage, meningococ-
cemia, ketoconazole)
Failure of the hypothalamic/pituitary axis
(withdrawal from glucocorticoid therapy)
Clinical manifestation
Weakness
Nausea/vomiting
Abdominal pain
Orthostatic hypotension
Hypotension refractory to volume or
vasopressor agents
Fever

Suggestive laboratory findings:

Hyponatremia
Hyperkalemia
Acidosis
Hypoglycemia
Prerenal azotemia
Emergent treatment
Indicated in critically ill patients, even if the
diagnosis is not established
High-risk patients include: AIDS, disseminated
tuberculosis, sepsis, acute anticoagulation,
post CABG patients, patients from whom
glucocorticoid therapy was withdrawn within
the past 12 months
If dexamethasone is used for emergent steroid
replacement, a short adrenocorticotropic
hormone stimulation test can be performed for
diagnosis after resuscitative therapy is
instituted
Short ACTH Stimulating Test
Blood for serum cortisol is drawn at baseline
Synthetic 1-24 ACTH (cortrosyn, cosyntropin), 250 ug,
is administered intravenously
A serum cortisol level is drawn 60 mins after
cosyntropin administration
A cortisol level >20 ug/dL (>552 nmol/L) at 60 mins
indicates adequate adrenal function
Failure to attain adequate cortisol levels indicates the
need for further testing and expert consultation
Since cortisol level may not be reported quickly,
corticosteroid should be administered, pending results,
if the clinical situation is suggestive of acute adrenal
insufficiency
Treatment
Obtain baseline blood samples for cortisol, electrolyte,
etc
Infuse D5 normal saline to support blood pressure
Administer dexamethasone 4 mg IV, then 4 mg IV
every 6 hrs
Perform short adrenocorticotropic hormone stimulation
test if needed for diagnosis
If the diagnosis of adrenal failure is confirmed,
hydrocortisone 100 mg IV, then 100 mg every 8 hrs,
can be administered. Some physicians prefer
administration of hydrocortisone as a continuous
infusion, 300 mg over 24 hrs
Treat precipitating conditions
 Hyperglycemic Syndromes

Results from a relative or absolute lack

insulin
Characterized by: hyperglycemia, keto-
acidosis, and osmotic diuresis-induced
dehydration
Life-threatening hyperglycemic syndromes:
diabetic ketoacidocis (DKA) and hyper-
glycemic hyperosmolar nonketotic syndro-
me (HHNK)
Clinical manifestations
Result from hyperglycemia & excess
ketone production
Hyperglycemia:
Hyperosmolality
Osmotic diuresis-induced dehydration
Fluid & electrolyte loss
Dehydration
Volume depletion
Ketone (DKA):
Acidosis
Osmotic diuresis
Clinical features
Weakness Anorexia
Dehydration Nausea/vomiting
Polyuria Ileus
Polydipsia Abdominal pain
Altered mental status Hyperpnea
Coma Fruity odor to the
Tachycardia breath (DKA)
Arrhythmias
Hypotension
Laboratory investigation
Hyperglycemia
Hyperosmolality (more common in HHNK)
Glukosuria
Ketonemia/Ketonuria (DKA)
Anion gap metabolic acidosis (DKA)
Hypokalemia
Hypophosphatemia
Hypomagnesemia
Leukocytosis
Azotemia
Elevated amylase
Creatine phosphokinase
Treatment (1)

The goal: to restore the fluid & electrolyte

balance, provide insulin, & identify
precipitating factors (infection, stroke, MI,
pancreatitis)
Volume deficits correlate with the severity of
hyperglycemia & are usually greater in HHNK
Normal saline: replenish IV volume & restore
hemodynamic stability (1 L in the first hour,
250-500 mL/hr as needed)
Treatment (2)

After 1-2 L of NS, fluids with less Cl (0.5

saline) should be used to avoid
hyperchloremic metabolic acidosis
Urine output should be maintained at 1-3
mL/kg/hr (ensure adequate tissue
perfusion & clearance of glucose)
Invasive hemodynamic monitoring
(arterial catheter, PA catheter): required
in patients with underlying CV disease
Treatment (3)

DKA:
Loading dose: 5-10 U regular human insulin
IV route is the most reliable & easiest to
titrate
Continuous infusion is necessary with serial
monitoring of the blood glucose &
electrolyte concentration
HHNK:
Smaller doses of insulin are usually
adequate (1-2 U)
Monitor glucose levels

Frequently
Glucose decreases to >250 mg/dL (<13.8
mmol/L), switch to glucose-containing fluids to
avoid hypoglycemia
10% dextrose may be necessary to maintain
glucose levels >150 mg/dL (>8.3 mmol/L)
while continuing insulin infusion
Subcutaneous insulin (BS is controlled,
ketonemia has cleared, the patient is stable)
 Insulin & correction of acidosis shift potassium
intracellularly & may lead to precipitous drops
in K levels
K deficit range from 3-10 mEq/kg
K should be added to fluid therapy as soon as
serum K is recognized or thought to be normal
or low and urine output is documented
K levels should be monitored frequently until
levels stabilize & acidosis is resolved (DKA)
Priorities in initial resuscitation of DKA

Institute crystalloid resuscitation, initially with NS

Institute insulin infusion at 0.1 U/kg/hr
Consider bicarbonate if pH<7.0
Look for precipitating of DKA (infection, MI, GI bleed)
Add KCl to fluid resuscitation when serum K is known or expected
to be low or normal, and urine output is documented
Add glucose to crystalloid infusion when serum glucose is <250
mg/dL. Do not decrease insulin infusion rate unless symptomatic
hypoglycemia or precipitous drops in serum glucose. Administer
10% dextrose if necessary to maintain serum glucose >150
mg/dL
Continue insulin infusion until ketosis is cleared (negative serum
ketones with correction of increased anion gap).
References:
Fundamental Critical Care Support, Course
Text, 3rd edition, Society of Critical Care
Medicine
Lange Clinical Anesthesiology, 3rd edition,
Lange Medical Books/McGraw-Hill Medical
Publishing Division
Physiologic and Pharmacologic Bases of
Anesthesia, 2nd edition, Williams and Wilkins
Textbook of Critical Care, 3rd edition, W.B.
Saunders Company