Electrolyte and Metabolic

Disturbances

A. Salahuddin, M.D
Anesthesiologist

Dept. of Anesthesiologi, ICU and Pain Management

Faculty of Medicine Hasanuddin University

Introduction

Common in critically ill & injured patients

Alter physiologic function and 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

Objectives

Review causes and clinical manifestations

of severe electrolyte disturbances

Outline emergent management of

electrolyte disturbances

Recognize acute adrenal insufficiency and

appropriate treatment

Describe management of severe

hyperglycemic syndromes

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

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

Electrolyte Disturbances
Potassium: hypo- & hyperkalemia
Sodium
: hypo- & hypernatremia
Others:

Calcium
: hypo- & hypercalcemia
Phosphate : hypo- & hyperphosphatemia
Magnesium : hypomagnesemia

Metabolic Disturbances
Severe hyperglycemic syndromes
Acute adrenal insufficiency

Potassium (K)

Essential for maintenance of the electrical

membrane potential

Alteration of K primarily effect the CV,

neuromuscular, and GI systems.

Overview of Potassium Balance

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

Alkalosis
Hyperventilation
Insulin
-adrenergic agonists

Diuresis
Metabolic alkalos
Renal tub defects
Diabetic ketoacid
Drugs (diuretics,

Hypomagnesemia
Vomiting

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

Hypokalemia
Neuromuscular manifestations:
weakness, fatigue, paralysis, respiratory
dysfunction
GI: constipation, ileus
Nephrogenic DI
ECG changes: U waves, flattened T
waves
Arrhythmias

Box 26-1.Symptoms of hypokalemia.

Mosby items and derived items 2005, 2002 by Mosby, Inc.

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.

Due to Delayed ventricular repolarization:

T wave flattening and inversion

Prominent U wave
ST segment depression
Increased P wave amplitude
Prolongation of the PR interval

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 <3mEq/L (<3mmol/L) & asymptomatic: K
enterally (orally or NGT) (KCl 20-40mEq
every 4-6 hrs)
K <2-2.5mEq/L (<3mEq/L if on digoxin) or if
symptoms are present: K intravenously

Arrhythmias or paralysis: KCl 20-30mEq via central

venous catheter (sequential infusion: 10mEq 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)

K+ deficit (mEq/L) =
fluid deficit (L) x proportion from ICF x K+
concentration (mEq/L) in ICF.

Lund GJ. Fluid and electrolyte. The Harriet Lane Handbook. 8th Ed, 2009

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)

Blood-Gas Analysis

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

ECG change:

Peaked T-wave
Widening of QRS complex
PR prolongation
Loss of P wave
Loss of R wave amplitude
ST depression (occationally elevation)
Sine wave
Ventricular fibrillation and asystole

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.

Overview of Sodium Balance

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,
nausea and vomiting
Muscle:
weakness
respiratory arrest

lethargy,

&

coma,

CNS-driven

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+] )

TBW : 0,6 x BB

Example:
Koreksi Na : 0,6x 60 ( 130 126 ) = 144 meq.
Koreksi Na 3% : 144/513 = 280 ml
syarat 0,5 meq/jam atau 10 meq/ 20 jam
Jadi yang dibutuhkan : 280/20 = 14 ml per jam
NaCl 3 %

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 freewater 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

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
Fluid & electrolyte loss
Dehydration
Volume depletion
Ketone (DKA):
Acidosis
Osmotic diuresis

dehydration

Clinical features

Weakness
Dehydration
Polyuria
Polydipsia
Altered mental status
Coma
Tachycardia
Arrhythmias
Hypotension

Anorexia
Nausea/vomiting
Ileus
Abdominal pain
Hyperpnea
Fruity 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

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
adequate (1-2 U)

insulin

are

usually

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