Fluid and Electrolyte

Management of the Surgical Patient

Hashmi

ANATOMY OF BODY FLUIDS

Total Body Water Intracellular Fluid Extracellular Fluid Osmotic Pressure

Total Body Water

constitutes 50-70 % of total body weight fat contains little water, the lean individual has a greater proportion of water to total body weight than the obese person total body water as a percentage of total body weight decreases steadily and significantly with increasing age

Total Body Water

% of Body Weight % of Total Body Water

Body Water ICF ECF Intravascular Interstitial

60 40 20 4 16

100 67 33 8 25

Intracellular Fluid
largest proportion in the skeletal muscle potassium and magnesium are the principal cations phosphates and proteins the principal anions

Extracellular Fluid
interstitial fluid: two types
functional component (90%) - rapidly equilibrating nonfunctioning components (10%) - slowly equilibrating
connective tissue water and transcellular water called a third space or distributional change

sodium is the principal cation chloride and bicarb the principal anions

Osmotic Pressure
physiologic and chemical activity of electrolytes depend on three factors: the number of particles present per unit volume (moles or millimoles [mmol] per liter) the number of electric charges per unit volume (equivalents or milliequivalents per liter) the number of osmotically active particles or ions per unit volume (osmoles or milliosmoles [mOsm] per liter)

Terminology
mole: molecular weight of that substance in grams mole eg: sodium chloride is 58 g (Na23, Cl35) equivalent: chemical combining activity; atomic weight expressed in grams divided by the valence divalent ions (calcium or magnesium) 1 mmol equals 2 mEq osmole: used when the actual number of osmotically active particles present in solution is considered millimole of sodium chloride, which dissociates nearly completely into sodium and chloride, contributes 2 mOsm

NORMAL EXCHANGE OF FLUID AND ELECTROLYTES

Water Exchange Salt Gain & Losses

Water Exchange
daily water gains normal individual consumes 2000 to 2500 mL water per day approximately 1500 mL taken by mouth rest is extracted from solid food, either from the contents of the food or as the product of oxidation

Water Exchange
daily water losses
250 mL in stools, 800 - 1500 mL in urine, and 600 mL as insensible loss total losses ~ 2.2 liters Insensible loss: skin (75%) and lungs (25%) increased by hypermetabolism, hyperventilation, and fever 250 mL/day per degree of fever unhumidified tracheostomy with hyperventilation = insensible loss up to 1.5 L/day

Water Exchange

Minimum of 500 to 800 mL urine per day required to excrete the products of catabolism

Salt Gain and Losses

daily salt intake varies 3-5 gm as NaCl kidneys excretes excess salt: can vary from < 1 to > 200 mEq/day Volume and composition of various types of gastrointestinal secretions Gastrointestinal losses usually are isotonic or slightly hypotonic should replace by isotonic salt solution

CLASSIFICATION OF BODY FLUID CHANGES

Volume Changes Concentration Changes Composition Changes
Acid/Base Balance Potassium Abnormalities Calcium Abnormalities Magnesium Abnormalities

Volume Changes
If isotonic salt solution is added to or lost from the body fluids, only the volume of the ECF is changed, ICF is relatively unaffected
If water is added to or lost from the ECF, the conc. of osmotically active particles changes Water will pass into the intracellular space until osmolarity is again equal in the two compartments

Volume Changes
BUN level rises with an ECF deficit of sufficient magnitude to reduce GFR creatinine level may not incr. proportionally in young people with healthy kidneys hematocrit increases with an ECF deficit and decreases with ECF excess sodium is not reliably related to the volume status of ECF a severe volume deficit may exist with a normal, low, or high serum level

Volume Deficit
ECF volume deficit is most common fluid loss in surgical patients most common causes of ECF volume deficit are: GI losses from vomiting, nasogastric suction,diarrhea, and fistular drainage other common causes: soft-tissue injuries and infections, peritonitis, obstruction, and burns

Volume Deficit
signs and symptoms of volume deficit: CNS: sleepy, apathy stupor, coma GI: dec food consumption N/V CVS: orthostatic, tachy, collapsed veins - hypotension Tissue: dec skin turgor, small tongue sunken eyes, atonia

Volume Excess
Iatrogenic or Secondary to renal insufficiency, cirrhosis, or CHF signs & symptoms of volume excess: CNS: none GI: edema of bowel CVS: elevated CVP, venous distension pulmonary edema Tissue: pitting edema anasarca

Concentration Changes
Na+ primarily responsible for ECF osmolarity Hyponatremia and hypernatremia s&s often occur if changes are severe or occur rapidly The concentration of most ions within the ECF can be altered without significant osmolality change, thus producing only a compositional change Example: rise of potassium from 4 to 8 mEq/L would significantly effect the myocardium, but not the effective osmotic pressure of the ECF

Hyponatremia (water intoxication)

acute symptomatic hyponatremia (< 130) hypertension can occur & is probably induced by the rise in intracranial pressure signs & symptoms: CNS: twitching, hyperactive reflexes inc ICP, convulsions, areflexia CVS: HTN/brady due to inc ICP Tissue: salivation, watery diarrhea Renal: oliguria - anuria

Hyponatremia (water intoxication)

Hyponatremia occurs when water is given to replace losses of sodium-containing fluids or when water administration consistently exceeds water losses Hyperglycemia: glucose exerts an osmotic force in the ECF and causes the transfer of cellular water into the ECF, resulting in a dilutional hyponatremia

Hypernatremia (water deficit)

The only state in which dry, sticky mucous membranes are characteristic sign does not occur with pure ECF deficit alone signs & symptoms: CNS: restless, weak - delirium CVS: tachycardia - hypotension Tissue: dry/sticky muc membranes swollen tongue Renal: oliguria Metabolic: fever heat stroke

Composition Changes
Acid/Base Balance Potassium Abnormalities Calcium Abnormalities Magnesium Abnormalities

Acid-Base Balance
large load of acid produced endogenously as a by-product of body metabolism acids are neutralized efficiently by several buffer systems and subsequently excreted by the lungs and kidneys Buffers: proteins and phosphates: primary role in maintaining intracellular pH bicarbonatecarbonic acid system: operates principally in ECF

Acid-Base Balance
buffer systems consists of a weak acid or base and the salt of that acid or base Henderson-Hasselbalch equation, which defines the pH in terms of the ratio of the salt and acid: pH = pK + log BHCO3 / H2CO3 = 27 mEq/L / 1.33 mEq/L = 20 / 1 = 7.4 As long as the 20:1 ratio is maintained, regardless of the absolute values, the pH will remain at 7.4

Acid-Base Balance
Four types of acid-base disturbances combinations of respiratory and metabolic changes may represent: compensation for the initial acid-base disturbance or, two or more coexisting primary disorders 10-mmHg PaCO2 change yields a 0.08 pH change

Respiratory Acidosis
retention of CO2 secondary to decreased alveolar ventilation management involves prompt correction of the pulmonary defect, when feasible, and measures to ensure adequate ventilation prevention: tracheobronchial hygiene during the postoperative , humidified air, and avoiding oversedation

Respiratory Alkalosis
PaCO2 should not be below 30 mmHg dangers of a severe respiratory alkalosis are those related to potassium depletion
hypokalemia is related to entry of potassium ions into the cells in exchange for hydrogen and an excessive urinary potassium loss in exchange for sodium

shift of the oxyhemoglobin dissociation curve to the left, which limits the ability of hemoglobin to unload oxygen at tissues

Metabolic Acidosis
Anion gap is a useful aid: normal value is 10 to 15 mEq/L unmeasured anions that account for the gap are sulfate and phosphate plus lactate and other organic anions measured ions are sodium, bicarb, and chloride

Metabolic Acidosis
treatment of metabolic acidosis should be directed toward correction of the underlying disorder sodium bicarbonate is discouraged, attempt to treat underlying cause shifts the oxyhemoglobin dissociation curve left interference with O2 unloading at the tissue level

Metabolic Alkalosis
common surgical patient has hypochloremic, hypokalemic metabolic alkalosis resulting from persistent vomiting or gastric suction in the patient with pyloric obstruction
unlike vomiting with an open pylorus, which involves a combined loss of gastric, pancreatic, biliary, and intestinal secretions

Pathophysiology of Paradoxic Aciduria occurring with GOO

GOO -> hypochloremic, hypokalemic, metabolic alkalosis urinary bicarb excretion to compensate for alkalosis volume deficit progresses aldosterone-mediated sodium resorption is accompanied by potassium excretion kidneys primary goal becomes volume preservation sodium resorption either K+ or H+ must be excreted to keep a balanced due to already excessive hypokalemia, the kidney excretes H+ in place of K+, producing paradoxic aciduria

Potassium Abnormalities
normal daily dietary intake of K+ is approx. 50 to 100 mEq majority of K+ is excreted in the urine 98% of the potassium in the body is located in ICF @ 150 mEq/L and it is the major cation of intracellular water intracellular K+ is released into the extracellular space in response to severe injury or surgical stress, acidosis, and the catabolic state

Hyperkalemia
signs & symptoms: CVS: peaked T waves, widened QRS complex, and depressed ST segments Disappearance of T waves, heart block, and diastolic cardiac arrest GI: nausea, vomiting, diarrhea (hyperfunctional bowel)

Hypokalemia
K+ has an important role in the regulation of acid-base balance
alkalosis causes increased renal K+/H+ excretion

signs & symptoms:

CVS: flatten T waves, depressed ST segments GI: paralytic ileus Muscular: weakness - flaccid paralysis, diminished to absent tendon reflexes

Calcium Abnormalities
majority of the 1000 to 1200g of calcium in the average-sized adult is found in the bone Normal daily intake of calcium is 1 to 3 gm Most is excreted via the GI tract half is non-ionized and bound to proteins ionized portion is responsible for neuromuscular stability

Hypocalcemia
signs & symptoms (serum level < 8):
numbness and tingling of the circumoral region and the tips of the fingers and toes hyperactive tendon reflexes, positive Chvostek's sign, muscle and abdominal cramps, tetany with carpopedal spasm, convulsions (with severe deficit), and prolongation of the Q-T interval on the ECG

Hypocalcemia
causes: acute pancreatitis, massive soft-tissue infections (necrotizing fasciitis), acute and chronic renal failure, pancreatic and small-bowel fistulas, and hypoparathyroidism

Hypercalcemia
signs & symptoms: CNS: easy fatigue, weakness, stupor, and coma GI: anorexia, nausea, vomiting, and weight loss, thirst, polydipsia, and polyuria

Hypercalcemia
two major causes:
hyperparathyroidism and cancer
bone mets PTH-like peptide in malignancies

Magnesium Abnormalities
total body content of magnesium 2000 mEq about half of which is incorporated in bone distribution of Mg similar to K+, the major portion being intracellular normal daily dietary intake of magnesium is approximately 240 mg most is excreted in the feces and the remainder in the urine

Magnesium Deficiency
causes: starvation, malabsorption syndromes, GI losses, prolonged IV or TPN with magnesium-free solutions signs & symptoms: similar to those of calcium deficiency

Magnesium Excess
Symptomatic hypermagnesemia, although rare, is most commonly seen with severe renal insufficiency signs & symptoms:
CNS: lethargy and weakness with progressive loss of DTRs somnolence, coma, death CVS: increased P-R interval, widened QRS complex, and elevated T waves (resemble hyperkalemia) cardiac arrest

Secretions

FLUID AND ELECTROLYTE THERAPY

Preoperative Fluid Therapy Intraoperative Fluid Therapy Postoperative Fluid Therapy

Preoperative Fluid Therapy

Correction of Volume Changes: Volume deficits result from external loss of fluids or from an internal redistribution of ECF into a nonfunctional compartment
nonfunctional because it is no longer able to participate in the normal function of the ECF and may just as well have been lost externally

Correction of Concentration Changes: If severe symptomatic hypo or hypernatremia complicates the volume loss, prompt correction of the concentration abnormality to the extent that symptoms are relieved is necessary

Postoperative Fluid Management

replace losses & supply a maintenance:
open abdomen losses: 8 cc/kg/hr NGT & urine output Blood loss x 3 Replace with isotonic salt solution (LR or NS) unwise to administer potassium during the first 24 h, until adequate urine output has been established even a small quantity of potassium may be detrimental because of fluid shifts

Fluid Composition

Fluid Replacement Status

Acute Renal Failure

Classified according to its cause: Prerenal: hypotension, hypovolemia, renal artery occlusion/stenosis, cardiac failure Renal: trauma, toxins (contrast, endotoxin), drugs (NSAIDS, aminoglycosides), pigment (myoglobin, hemaglobin) Postrenal: ureteral obstruction, bladder dysfxn (anesthesia, meds, nerve injury), urethral obstruction, foley obstruction

Laboratory Studies
Urinalysis: blood or myoglobin is a positive diagnostic test - can test via Hemoccult card Urinary lytes: urine sodium, creatinine, urea, osmolality, and specific gravity help classify type of renal failure using Renal failure indices

Renal Indices
Indices U Osm U/P osm U/P urea U/P cr Urine Na FENa Prerenal > 500 >1.25 >8 > 40 < 20 < 1% Renal < 350 <1.1 <3 < 20 > 40 > 3% Postrenal Varies Varies Varies < 20 > 40 > 3%

Indications for use of Dialysis in Acute Renal Failure

Severe acidosis Electrolyte abnormalities Inability to clear toxins Volume overload Uremic signs and symptoms (encephalopathy, BUN > 100)