Disorders of Acid-Base, Fluids,

and Electrolytes
Sean Dineen, MD, and Paul Schumacher, MD

I. ANATOMY OF BODY FLUIDS

A. Total body water (TBW) constitutes approximately 60% (50% to 70%)

of total body weight.

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B. Skeletal muscle contains more water than adipose tissue, and therefore 54
women and obese patients have less TBW.
C. Both women and men lose TBW as they age

DISORDERS OF ACID-BASE, FLUIDS, AND ELECTROLYTES

D. Intracellular fluid (ICF)
1. Two-thirds (67%) of TBW
2. Potassium and magnesium are the major cations of ICF.
3. Phosphates and proteins are the major anions.
E. Extracellular fluid (ECF)
1. Makes up one-third (33%) of total body water
2. ECF is further divided into two compartments: interstitial fluid and plasma.
a. Interstitial fluid is 75% of the extracellular fluid.
b. Plasma is 25% of the extracellular fluid.
3. Sodium and calcium are the major cations of extracellular fluid.
4. Chloride and bicarbonate are the major anions.
F. “Third space” fluid is nonfunctional extracellular fluid sequestration
following surgery, inflammation, burns, and infection. It does not
contribute to the normal ECF or ICF.

II. DAILY FLUID AND ELECTROLYTE REQUIREMENTS

AND MAINTENANCE

A. Water requirements in the hemodynamically normal patient

1. Adults require 35 mL/kg per 24 hours.
2. For children, the following formula can be used for 24-hour requirements:
a. For the first 10 kg of body weight, multiply by 100 mL/kg.
b. For the second 10 kg of body weight, multiply by 50 mL/kg.
c. For each additional kg, multiply by 20 mL/kg.
3. For an hourly basis in children, this is simplified as the “4/2/1” rule.
a. 4 mL/kg/hour for the first 10 kg of body weight
b. 2 mL/kg/hour for the second 10 kg of body weight
c. 1 mL/kg/hour for each additional kg
4. Sustained fever increases insensible fluid losses from the skin by
approximately 250 mL/24 hours for each 1°F over 101°F.
5. Tachypnea increases insensible fluid losses as well.
B. Electrolyte requirements
1. Sodium: 1 to 2 mEq/kg per day for adults; 1 mEq/day for children
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 462 III. Volume Disorders

2. Chloride: 1 to 2 mEq/kg per day for adults; 1 mEq/day for children

3. Potassium: 0.5 to 1 mEq/kg per day

III. VOLUME DISORDERS

A. Hypovolemia. Most common in trauma patients. Primary concern is

loss of intravascular volume. The signs and symptoms are those of
volume depletion:
1. Mild volume deficit
a. 4% to 6% weight loss
b. Agitation
c. Asymptomatic or possibly mildly increased heart rate
d. This degree of volume depletion may be unnoticed.
2. Moderate volume depletion
a. 6% to 8% weight loss
b. Orthostatic hypotension
c. Tachycardia
d. Collapsed veins
e. Apathy
f. Anorexia
g. Drowsiness
h. Decreased skin turgor
i. Oliguria (urine output less than 30 mL/hour)
j. Increase in hematocrit
k. Elevated BUN/Cr ratio
3. Severe volume deficit
a. 8% to 10% weight loss
b. Hypotension
c. Stupor, coma
d. Atonic muscles
e. Sunken eyes
f. Marked decrease in body temperature
g. Anuria
B. Volume overload. The signs and symptoms include:
1. Distended jugular veins
2. Rales
3. Anasarca
C. Monitoring volume status
1. Urine output. Accurate measurement requires placement of a urinary
catheter.
2. Strict intake and output
3. Daily weights
4. Measurement of central venous pressure can aid in assessing volume status.
5. In complex patients with comorbid disease, particularly congestive heart
failure and renal insufficiency, placement of a pulmonary artery catheter
may be necessary to assess volume status
 V. Hypernatremia 463

IV. REPLACEMENT OF FLUID LOSSES

A. Deficit calculation
1. Quantify measurable losses:
a. Urine output
b. Nasogastric tube
c. Drains
d. Output from fistulas
e. Vomiting
f. Diarrhea 54
2. In postoperative patients consider that extracellular fluid losses average
750 to 800 mL/hour during celiotomy.

DISORDERS OF ACID-BASE, FLUIDS, AND ELECTROLYTES

B. Maintenance fluid requirements
1. Insensible losses are 600 to 900 mL per day and must be replaced.
The amount may increase with tachypnea or fever.
2. Replacement for urine output is about 1000 mL per day
C. Ongoing fluid losses should be replaced with a solution of similar
electrolyte composition.
1. Extracellular fluid losses are replaced with a balanced salt solution, such
as Ringer’s lactate.
2. This includes most measurable losses, such as nasogastric output,
vomitus, diarrhea, and fistula drainage, whether biliary or enteric.
3. Fluid losses due to a gastric outlet obstruction are replaced with normal
saline.
4. Maintenance fluids (insensible losses and urine output) are generally
given as half-normal saline but in the absence of a salt-wasting
nephropathy can be supplied as D5W.

V. HYPERNATREMIA

All forms of hypernatremia are hypertonic.

A. Signs and symptoms
1. Thirst
2. Lethargy
3. Convulsion
B. Hypovolemic hypernatremia. Burns, excessive sweating, respiratory
losses, and renal failure are common causes.
1. First need to correct volume depletion with isotonic fluid (lactated
Ringer’s or normal saline)
2. If this does not correct hypernatremia, calculate a free water deficit and
correct with hypotonic fluid. Give only hypotonic fluid (i.e., D5W) when
the patient is euvolemic.
C. Euvolemic hypernatremia
1. A patient that is euvolemic should have free water deficit calculated and
corrected accordingly with hyptonic fluids.
 464 VII. Hyperkalemia

2. Avoid correcting too quickly as this may cause brain edema.

3. Diabetes insipidus is a common cause among brain-injured patients.
a. Characterized by large volume of dilute urine. The patient may
produce as much as 1 L of urine per hour.
b. Urine osmolarity less than 300 mEq/L in a patient with a serum
sodium of >150 is consistent with diabetes insipidus.
c. DDAVP can be given for severe cases.
D. Hypervolemic hypernatremia is caused by excess of sodium and is typically
iatrogenic. It commonly occurs after IV administration of sodium bicarbonate.
1. Administer loop diuretics to reduce load of sodium.
2. D5W may be needed to restore free water.
3. Patients in renal failure who do not respond to loop diuretics will need
dialysis to normalize sodium.
E. Free water deficit should be corrected slowly.

VI. HYPONATREMIA

Hyponatremia reflects an excess of total body water. In contrast to

hypernatremia, hyponatremia may be hypotonic, isotonic, or hypertonic.
A. Hypotonic hyponatremia
1. Hypovolemic –replacement with hypotonic fluids
2. Euvolemic – common with renal failure, SIADH, and adrenal insufficiency
3. Hypervolemic – caused by fluid-retaining states such as in congestive
heart failure, cirrhosis, nephrotic syndrome, or renal failure
B. Isotonic hyponatremia is caused by isotonic infusion of solutions such
as glycine or mannitol. Pseudohyponatremia is caused by
hyperlipidemia or hyperproteinemia but is less common with advances
in laboratory measurements.
C. Hypertonic hypnonatremia is commonly caused by hyperglycemia and
rarely by infusions of hypertonic glycine.
D. Treatment
1. Avoid correcting too fast as this may cause central pontine myelinolysis.
2. Treatment goal is to correct serum sodium to 120.
3. Correct underlying cause if possible.
4. Restrict fluids to <1500 mL/day.
5. If severe may treat with 3% NaCl
a. Aim to correct at 1 to 2 mEq/L per hour initially.
b. Maximum correction in one day should be 8 mEq/L unless the
patient remains symptomatic.

VII. HYPERKALEMIA

A. Occurs when serum sodium exceeds 5.0 mEq/L

B. Under normal circumstances extracellular [K+] is tightly controlled.
During trauma, acidosis, or other catabolic states, the intracellular water
concentration of potassium leaks into the extracellular water.
 VIII. Hypokalemia 465

C. Renal failure and rhabdomyolysis can cause rapid increases in plasma

sodium.
D. Hyperkalemia should be anticipated after sudden reperfusion of an
ischemic limb.
E. Succinylcholine may precipitate hyperkalemia.
F. Electrocardiographic changes
1. Peaked T waves
2. Prolonged QRS
3. Depressed ST segments
4. Loss of T waves, heart block, and cardiac arrest are associated with
increasing potassium levels.
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G. Treatment of acute hyperkalemia

DISORDERS OF ACID-BASE, FLUIDS, AND ELECTROLYTES

1. Aim treatment at correcting the underlying cause
2. Stop all potassium supplementation and potassium in IV fluids.
3. Patients in renal failure need dialysis.
4. For patients with potassium levels of 5 to 6.5 and without ECG
changes, loop diuretics or Kayexalate may be given.
5. For patients with ECG changes or K+ > 6.5:
a. Calcium gluconate is given for cardiac protection. Calcium
antagonizes the depolarizing effect of hyperkalemia.
b. Lasix and kayexalate are given.
c. Insulin and glucose will drive K+ into the cells.
d. Bicarbonate will also force K+ into the cells.
e. Albuterol and other beta-agonists may also be used to shift K+ into cells.

VIII. HYPOKALEMIA

A. Causes
1. Gastrointestinal losses. Patients with normal renal function should be
able to reduce urinary excretion to less than 20 mEq/day. If daily
urinary excretion is greater than this, some element of renal failure or
hyperaldosteronism is present.
2. Undersupplementation particularly in the setting of diuretic use
3. Shift of potassium into cells
4. Alkalosis causes excretion of K+ rather than H+ in the kidney and may
cause hypokalemia.
B. Signs
1. U waves on the ECG
2. Atrial tachycardia with or without a block
3. Flattening of ST segments on the ECG
4. Ileus
5. Paralysis
6. Patients on digoxin are at increased risk of toxicity.
C. Treatment
1. Oral supplementation, particularly for patients on loop diuretics
 466 X. Hypocalcemia

2. Intravenous supplementation should be given to correct K+ to greater

than 4.0 in intensive care patients.
3. The dose of potassium that can be administered through a peripheral IV
line should not exceed 10 mEq/L per hour (in 100 mL of normal saline).
More than 10 mEq/L may be given through a central line with ICU
monitoring.

IX. HYPERCALCEMIA

A. Occurs when calcium exceeds 10.5 mEq/L. Ionized calcium levels

better reflect the biochemically active form of calcium. An ionized
calcium greater than 1.4 mmol/L confirms hypercalcemia.
B. Uncommon in trauma
C. Causes
1. Use of thiazide diuretics
2. Thyrotoxicosis
3. Hyperparathyroidism
4. Hypophosphatemia
D. Signs and symptoms
1. Fatigue
2. Lethargy
3. Weakness
4. Polyuria due to a renal concentrating defect. This can lead to volume
depletion.
5. Bradycardia, which may progress to complete heart block
E. Treatment
1. Isotonic fluid
2. Loop diuretics to shed calcium into the urine
3. Bisphosphonates
4. Intranasal or intravenous calcitonin
5. Dialysis

X. HYPOCALCEMIA

A. May be related to citrate accumulation during massive transfusion

B. Ionized calcium less than 0.8 mmol/L is diagnostic of hypocalcemia.
C. Causes
1. Rhabdomyolysis
2. Acute pancreatitis
3. Renal failure
4. Sepsis
5. Hypoparathyroidism (following thyroid surgery)
D. Signs and symptoms
1. Chvostek’s sign – gently tapping along the facial nerve elicits twitching
of facial muscles.
 XII. Hypomagnesemia 467

2. Trousseau’s sign – inflating a blood pressure cuff above the brachial

artery for 3 minutes induces carpopedal spasm.
3. Circumoral numbness and tingling
4. Paresthesias of the hands and feet
5. Prolonged QT interval
6. Decreased myocardial contractility
7. Ventricular fibrillation
E. Treatment
1. Infusion of calcium gluconate or calcium chloride
2. Calcium chloride has a greater amount of elemental calcium per
volume.
54
3. Repleting magnesium is essential to correcting calcium.

DISORDERS OF ACID-BASE, FLUIDS, AND ELECTROLYTES

XI. HYPERMAGNESEMIA

A. This is a rare condition.

B. Causes
1. Renal failure
2. Acidosis
3. Excessive exogenous administration (iatrogenic)
C. Signs and symptoms
1. Lethargy
2. Decreased deep tendon reflexes
3. ECG changes
a. Prolonged PR interval
b. Widened QRS complex
c. Elevated T waves
D. Treatment
1. Calcium may help control symptoms.
2. Dialysis is necessary in renal failure.

XII. HYPOMAGNESEMIA

A. Causes
1. Heavy alcohol intake
2. Chronic diarrhea
3. Long-term use of diuretics
B. Signs and symptoms
1. Hyperactive deep tendon reflexes
2. Tremors
3. Chvostek’s sign
4. Tetany
C. Potassium levels cannot be corrected if hypomagnesemia exists.
D. Treatment consists of replacement with 2 g of intravenous magnesium
sulfate.
 468 XV. Acid-Base Disturbances

XIII. HYPERPHOSPHATEMIA

A. Most commonly caused by renal failure

B. Treatment
1. Stop external supplementation.
2. Oral phosphate-binding agent (Amphojel)
3. Lasix or acetazolamide
4. Dialysis in severe cases

XIV. HYPOPHOSPHATEMIA

A. Causes
1. Gastrointestinal losses
2. Renal losses
3. Starvation
4. Inadequate replacement in total parenteral nutrition
5. Use of phosphate-binding antacids
B. Signs and symptoms
1. Rhabdomyolysis
2. Weakness
3. Erythyrocyte dysfunction
4. Respiratory insufficiency
5. Cardiomyopathy
C. Treatment
1. Severe deficits are corrected with sodium phosphate or potassium
phosphate, depending on the electrolyte composition.
2. Less severe deficits can be corrected with oral agents (Neutrophos or
Fleet’s Phosphosoda).

XV. ACID-BASE DISTURBANCES

A. Regulation of a normal pH is essential for homeostasis. Most cellular

processes function over a narrow pH range. These include enzyme function,
coagulation pathways, oxygen delivery, and cardiovascular function.
B. Normal arterial blood gas values
1. pH 7.36 to 7.44
2. PaCO2 35 to 45 mm Hg
3. PaO2 80 to 100 mm Hg
4. Base excess −3 to 3 mEq/L
C. Buffers
1. The bicarbonate buffer system is the most important in the extracellular
fluid compartment.
2. In the intracellular compartment proteins are the most important
component.
3. Respiratory system regulates CO2 and therefore H+.
 XV. Acid-Base Disturbances 469

4. Renal excretion of HCO3

D. Arterial blood gases are essential to identify the acid-base disturbances
(e.g., pH), to aid in the identification of the disturbance (respiratory vs.
metabolic), and to follow therapeutic interventions.
E. Shock, hemorrhage, and massive transfusion are causes of acid-base
disturbances in trauma patients.
F. Respiratory disturbances
1. Respiratory acidosis
a. Arises from poor ventilation, which causes retained carbon dioxide.
Causes include brain injury, intoxication, oversedation, and agonal
states.
54
b. The pH will decrease by 0.08 for each 10 mm Hg rise in the PaCO2.

DISORDERS OF ACID-BASE, FLUIDS, AND ELECTROLYTES

c. Metabolic compensation occurs
i. In acute hypercapnia, the HCO3 increases by 1 mmol for each
10 mm Hg in PCO2 above 40.
ii. In chronic hypercapnia, the bicarbonate will increase by 4 mmol
for each 10 mm Hg increase of PCO2 above 40.
d. The degree of metabolic compensation is important to estimate so a
mixed acid-base disturbance, which is common in trauma patients,
is not missed.
e. Treatment
i. Correction of underlying cause
ii. If underlying cause is not quickly reversed, mechanical
ventilation is necessary.
2. Respiratory alkalosis
a. Hyperventilation is the most common cause in the trauma patient.
b. For each 10 mm Hg decrease in the PaCO2, the pH will increase 0.08.
c. Metabolic compensation can be estimated by:
i. Acute hypocapnia in which the bicarbonate decreases 2 mmol/L
for each 10 mm Hg decrease of PaCO2 below 40 mm Hg
ii. Chronic hypocapnia in which the bicarbonate decreases 5 to 7
mmol/L for each decrease of PaCO2 below 40 mm Hg
d. Treatment
i. Ventilator control
ii. Possible mechanical ventilation
G. Metabolic disturbances
1. Metabolic acidosis
a. Anion gap = Na – (Cl + HCO3)
b. Normal anion gap is 8 to 14.
c. In trauma, an anion gap acidosis is most commonly caused by
under-resuscitation.
d. Other causes of anion gap acidosis include lactic acidosis;
ketoacidosis; aspirin overdose; ingestion of ethylene glycol,
methylene glycol, or paraldehyde; and chronic renal insufficiency.
e. Common causes of non-anion gap acidosis include diarrhea, fistulas,
and renal tubular acidosis.
 470 XVI. Acute Renal Failure

2. Hyperventilation causes respiratory compensation and inappropriate

compensation may reveal a mixed disorder.
3. Treatment
a. Correct underlying cause.
b. Adequate fluid resuscitation
4. A pH < 7.2 may require bicarbonate administration.
a. Bicarbonate administration may worsen the acidosis if the patient
cannot ventilate the excess CO2.
b. Bicarbonate may be administered using the bicarbonate deficit formula.
i. 0.4 x body weight (kg) x (HCO3 desired – HCO3 measured)
ii. One half of this amount should be administered over 8 hours,
with frequent monitoring of arterial blood gases.
5. Dialysis is indicated for patients in renal failure
H. Metabolic alkalosis
1. Classified as chloride responsive or chloride resistant
2. Chloride responsive
a. Urine chloride <20 mEq/L
b. Causes include
i. Large volume nasogastric output or vomiting with an obstructed
pylorus
ii. Use of diuretics
iii. Volume contraction
c. Treatment
i. Administer chloride-containing fluids such as normal saline.
ii. Acetazolamide 250 to 500 mg IV
3. Chloride resistant
a. Urine chloride >20 mEq/L
b. Causes
i. Hyperaldosteronism
ii. Cushing’s syndrome
iii. Hypokalemia
c. Treatment
i. Correction of underlying cause
ii. Stop exogenous steroids

XVI. ACUTE RENAL FAILURE

A. Classification
1. Oliguric acute renal failure: urine output < 400 mL per 24 hours
2. Nonoliguric acute renal failure: urine output > 400 mL per 24 hours.
Mortality of nonoliguric acute renal failure is one-half that of oliguric
renal failure.
B. Etiology
1. Prerenal
a. Decrease in intravascular volume is common in trauma patients after
hemorrhage, third-space fluid loss, or fluid drainage.
 XVI. Acute Renal Failure 471

b. Impaired cardiac function

c. Renal vascular obstruction
2. Renal
a. Prolonged pre-renal or postrenal states
b. Parenchymal lesions of the glomerulus or tubules due to nephrotoxins
such as aminoglycosides, amphotericin B, and radiologic contrast agents
i. Acute renal failure is more likely to occur after the administration
of radiologic contrast agents if the patient is diabetic or has
preexisting chronic renal failure, decreased intravascular volume,
hypertension, or peripheral vascular disease, or is of increased
age or if other nephrotoxic drugs are being used concomitantly.
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ii. Myoglobin precipitates in the renal tubules, causing obstruction.

DISORDERS OF ACID-BASE, FLUIDS, AND ELECTROLYTES

iii. Nonsteroidal anti-inflammatory drugs may increase renal
vasoconstriction in patients with preexisting pre-renal conditions.
3. Postrenal: anatomic obstruction of the urinary tract
C. Diagnosis of acute renal failure
1. Acute renal failure can be assessed by an accurate history and physical
examination focusing on pre-renal or postrenal etiologic factors.
2. Laboratory assessment
a. Blood urea nitrogen (BUN) and creatinine will rise with decreased
renal function.
b. Urine electrolytes should be determined before diuretics are
administered.
c. Fractional excretion of sodium (FENa) is a measure of the kidneys’
concentrating ability.
i. (Urine Na × serum creatinine)/(urine creatinine × serum Na) × 100%
ii. FENa <1 % consistent with prerenal ARF
iii. FENa >3% consistent with renal parenchymal injury
d. Prerenal patients will have unremarkable urinalysis.
i. Urine osmolality >350 mOsm
ii. Urine Na < 10 mEq/L
e. Patients with intrinsic renal failure may have:
i. Proteinuria
ii. Pyuria
iii. Casts (protein, white blood cells, or epithelial) in their urine
iv. Urine osmolality will equal plasma osmolality.
v. Urine Na will be >10 mEq/L.
f. Patients with postrenal failure will have:
i. An unremarkable urinalysis
ii. Unremarkable urine electrolytes
iii. Imaging studies that confirm the diagnosis
g. Patients with rhabdomyolysis will have a positive urine dip for blood
but no microscopic red blood cells.
D. Treatment
1. Prerenal
a. Restoration of intravascular volume
b. Correction of cardiac output
 472 XVII. Suggested Readings

c. Correction of renal vascular perfusion

d. Swan-Ganz catheter may be necessary for hemodynamic monitoring.
e. Establish urine output.
2. Renal
a. Withhold nephrotoxic agents.
b. Myoglobinuria will require vigorous fluid administration until urine is
free of myoglobin.
i. Mannitol is given for osmotic diuresis.
ii. Urine alkalization is achieved with bicarbonate (50 mEq/50 mL).
3. Postrenal. Urinary obstruction should be corrected.
E. Management
1. Establish urine output (0.5 to 1.0 mL/kg per hour).
2. Optimize intravascular volume and hemodynamic status for appropriate
renal perfusion.
3. Use osmotic or loop diuretics to increase urine output for fluid
management.
4. Prevent hyperkalemia.
5. Dialysis for acute renal failure
a. Acidosis
b. Volume overload
c. Hyperkalemia (and other electrolyte disturbances)
d. Ingestion of toxins
e. Signs and symptoms of uremia
6. Intermittent hemodialysis is the standard therapy for acute renal failure.
7. Peritoneal dialysis
a. Inappropriate after recent celiotomy
b. Risk of peritonitis
c. In selected patients has advantages including no need for
anticoagulation; technically easy, less associated hypotension
8. Continuous venovenous hemodialysis and arteriovenous hemodialysis
have benefits over intermittent hemodialysis.
a. Advantages
i. Precise fluid and metabolic control
ii. Less accidental hypotension
iii. Ability to administer nutritional support
b. Disadvantages
i. Need for prolonged anticoagulation
ii. Constant need for surveillance

XVII. SUGGESTED READINGS

Adrogue HJ, Madias NE: Hypernatremia. N Engl J Med 342:1493–1499, 2000.
Adrogue HJ, Madias NE: Hyponatremia. N Engl J Med 342:1581–1589, 2000.
Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group:
Low dose dopamine in patients with early renal dysfunction: A placebo-controlled
randomized trial. Lancet 356:2139–2143, 2000.
Kellum JA, Decker JM: Use of dopamine in acute renal failure: A meta-analysis.
Crit Care Med 29:1526–1531, 2001.
 XVII. Suggested Readings 473

Mehta RL, Pascual MT, Soroko S, Chertow GM for the PICARD Study Group:
Diuretics, mortality, and nonrecovery of renal function in acute renal failure. JAMA
288:2547–2553, 2002.
Mullins RJ: Shock, electrolytes, and fluid. In Townsend CM (ed): Textbook of Surgery:
The Biological Basis of Modern Practice, 17th ed. Philadelphia, Saunder, 2004,
pp 67–112.
O’Brien WJ: Fluids and electrolytes. In Berry SM (ed): The Mont Reid Surgical
Handbook, 4th ed. St Louis, Mosby, 1997, pp 17–31.
Singri N, Ahya SN, Levin ML: Acute renal failure. JAMA 289:747–751, 2003.

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DISORDERS OF ACID-BASE, FLUIDS, AND ELECTROLYTES