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 disturbance 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:
Sodium

hypo- & hyperkalemia

: 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
Alkalosis
Hyperventilation
Insulin
-adrenergic agonists

Hypomagnesemia
Vomiting

Renal Losses
Diuresis
Metabolic alkalos
Renal tub defects
Diabetic ketoacid
Drugs (diuretics,
aminoglycosides,
amphotericin B)

Extrarenal
Losses
Diarrhea
Profuse sweating

Decreased Intake
Malnutrition
Alcoholism
Anorexia nervosa

Clinical manifestation:
Cardiac

system:
arrhythmias (ventricular, & supraventricular,
conduction delay, sinus bradycardia)
ECG abnormalities (U waves, QT prolongation, 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, 3 rd 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)
Acedemia

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
Acidemia
Hypoaldosteronism
Drugs (potassium-sparing diuretics,
ACE inhibitors, etc.)

Excessive intake

Cell death
Rhabdomyolisis
Tumor lysis
Burns
Hemolysis

Clinical manifestation
Heart:

arrhythmias (heart block, bradycardia, diminished conduction and contraction)

ECG abnormalities (diffuse peaked T waves,
PR prolongation, QRS widening, diminished P
waves, sine waves)
Muscle: muscle weakness, paralysis, paresthesias, and hypoactive reflexes

Treatment (1)
Recognition

& treatment of underlying diseases

Removal of offending drugs
Limitation of potassium intake
Correction of acidemia or eletrolyte abnormalities
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

SIADH
Psychogenic polydipsia
Hypothyroidism
Inappropriate water administration to infanst/children

Diuretic use
Aldosterone deficiency
Renal tubular dysfunction
Vomiting
Diarrhea
Third-space fluid losses

Hypervolemia
CHF
Cirrhosis
Nephrosis

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

The amount of NaCl necessary to raise plasma [Na+] to

the desired value, the Na+ deficit, can be estimated by the
following formula:

Na+ deficit=TBW x (desired [Na+]-present [Na+] )

Example:
An 80-kg woman is lethargic and found to
have a plasma [Na+] of 118 mEq/L. How much
NaCl must be given to raise her plasma [Na+] to
130 mEq/L?

[Na+] deficit = TBW x (130-118)

TBW is approximately 50% of body weight in
females:
[Na+] deficit=80x0.5x(130-118)
=480 mEq

Normal (isotonic) saline contains 154 mEq/L, the

patient should receive 480 mEq : 154 mEq/L =
3.12 L of normal saline.
For correction rate of 0.5 mEq/L/hour, this
amount of saline should be given over 24 hours
(130 mL/hour)

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

Diarrhea
Vomiting
Excessive sweating
Diuresis
Diabetes insipidus

Reduced Water
Intake
Altered thirst
Impaired access

Excessive Sodium
Intake
Salt tablets
Hypertonic saline
Sodium bicarbonate

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

Example:
A 70-kg man is found to have a plasma
[Na+] of 160 mEq/L. What is his water
deficit?

If one assumes that the hypernatremia if from

water loss only, then total body osmoles are
unchanged. Thus, assuming he had a normal
[Na+] 140 mEq/L and a TBW content that is 60%
of body weight:
Normal TBW x 140 = present TBW x [Na+]plasma
(70 x 0.6) x 140 = present TBW x 160
present TBW = 36.7 ltr
Water deficit = normal TBW present TBW
= (70 x 0.6)- 36.7 = 5.3 L

To replace this deficit over 48 hours, one

would give 5% Dextrose in water intravenously, 5.300 mL over 48 hours, or 110
mL/hour

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, meningococcemia, ketoconazole)
Failure of the hypothalamic/pituitary axis
(withdrawal from glucocorticoid therapy)

Clinical manifestation
Weakness
Nausea/vomiting
Abdominal pain
Orthostatic hypotension
Hypotension refractory

vasopressor agents
Fever

to

Suggestive laboratory findings:

Hyponatremia
Hyperkalemia
Acidosis
Hypoglycemia
Prerenal azotemia

volume

or

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, ketoacidosis, and osmotic diuresis-induced
dehydration
Life-threatening hyperglycemic syndromes:
diabetic ketoacidocis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (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

Altered

Hyperpnea

mental status

Coma
Tachycardia
Arrhythmias
Hypotension

Fruity

pain

odor to the
breath (DKA)

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

route is the most reliable & easiest to titrate
Continuous infusion is necessary with serial monitoring of the blood glucose & electrolyte concentration
IV

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

edition, Society of Critical Care

Text, 3rd
Medicine
Lange Clinical Anesthesiology, 3 rd 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