Surgery 1.1 November 8, 2012

Fluid and Electrolyte Management of the Surgical Patient Dr. Rafael Azares

Group 15 |Elizaga, Escano, Esguerra, Eslao Page 1 of 7

OUTLINE

I. Importance to Surgical Patient II. Total Body Water and Fluid Compartments III. Composition of Fluid Compartments IV.Body Fluid Changes V. Disturbances in Fluid Balance VI.Composition Changes

Fluid volume and electrolyte changes can occur:

Preoperatively

Intraoperatively

Postoperatively

In response to trauma

In response to sepsis

Total Body Water (TBW):

o Intracellular Volume (ICV):

Red Cell Volume (2-3% of TBW)

Others

o Extracellular Volume (ECV):

Plasma (5% of TBW)

Interstitial Fluid (15% of TBW)

Total Blood Volume (~7-8%) o RCV (~2-3%) + plasma (~5%) o ~5 L (4.9-5.6 L) in a 70 kg patient

Percentage of body weight (kg): o Male: 60% o Female: 50-55%

Population Fraction (kg)

Infants 0.8

Children 0.65

Adult Men 0.6

Adult Women 0.5

Elderly Men 0.5

Elderly Women 0.45

Exceptions: o Obese: Less TBW per unit of weight ECV > ICV, due to relatively low water content of adipose

tissue o Elderly: Altered body water composition By 80 years of age, TBW only 50% of total body weight

muscle atrophy!

Figure 1. Fluid compartments

Note: The most important among the three is plasma. Plasma can be

interchangeably called intravascular fluid, or the blood, it the one

measured in taking blood pressure and pulse rate.

Figure 2. Normal chemical composition of the body fluid

compartments

I. IMPORTANCE TO SURGICAL PATIENT (from 2014-A Trans)

II. TOTAL BODY WATER AND FLUID COMPARTMENTS

III. COMPOSITION OF FLUID COMPARTMENTS

Extracellular Volume Interstitial Fluid a) Rapidly Equilibrating/Extracellular: volume of IF that participates

mostly in water exchange b) Slowly Equilibrating/Transcellular: CSF, joint fluid, pleural fluid,

peritoneal fluid

Intracellular Volume

Proportional to the amount myocytes, thus leaner and younger have a higher TBW

~40% of an individuals TBW

Skeletal muscle has largest proportion

Adipose tissue hydrophobic; contains little water

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IV. Body Fluid Changes

The concentration gradient between compartments is maintained

by ATP-driven Na-K pumps located in cell membranes.

The movement of ions and proteins between the various fluid compartments is restricted.

Fluid compartments are separated by membranes that are freely permeable to water, so water is freely diffusible and evenly distributed throughout the compartments. Thus, a given volume of water increases the volume of any one compartment by a relatively small amount.

Fluids move due to: o Hydrostatic pressure(pressure generated by fluid present in a

compartment) o Osmotic pressure(dependent solutes presents in the

compartment, solutes can be lipids, proteins, glucose)

The distributionvolumeof various crystalloid or colloid solutions is that volume in which the administered solution will equilibrate over a short term.

There are three resuscitative fluids: isotonic/crystalloid, colloid, plain water. Crystalloids, compared to colloids have lower molecular weight and the amount of sodium and potassium as well as certain electrolytes like bicarbonate, approximates the plasma. Colloids have higher molecular weight. Water in the form of D5 water (50 gm. of glucose present in a solution, example in a litre of water)

Assuming a 70-kg patient has suffered an acute blood loss of 1L, remember: o TBW distribution volume for sodium-free water (D5W) o ECV distributionvolume for crystalloid solution in which

[Na+] approximates 140mEq/L

o PV distributionvolume for mostcolloidsolutions Note: Crystalloids are frequently used in practice because it is less expensive but in this case, colloid solution is a better choice. When sodium-free water is used such as plain water, the distribution volume (DV) is equal to the total body water. Crystalloid solutions DV is equal to the extracellular volume, while colloid solutions is equal to the same as plasma.

The formula describing the effects of fluid infusion on PV expansion is as follows:

Example

If 1 litre of each solution isused, how increment will it produce?

What we need is 1 L increase in plasma,

In water, the expected plasma volume increment: (1 L x 3.5) / 42 =

.08 decilitre); water is distributed evenly, thus even if you dont

want to increase, interstitial fluid and ICV, it will still equilibrate

In crystalloid, (1 L x 3.5) / 14 = 0.25

In colloid, DV is equal to plasma, when it is infused, plasma will

increase by 1L

A healthy person consumes an average of 2L of water per day,

approximately 75% from oral intake and the rest extracted from

solid foods.

Daily water losses:

o 800 to 1200 mL in urine (principal mechanism for maintaining

water balance)

o 250 mL in stool

o 600 mL in insensible losses

Insensible losses:

o 8 to 12mL/kg/day

o Divided into respiratory(25%) and cutaneous(75%) water loss

o Increased by factors such as fever (increases water loss by 10%

in every 1C rise above 37C), hypermetabolism (most often

they are the post-surgical patients), and hyperventilation

Respiratory insensitive water losses tend to be greater with

inspiration of unhumidified air, asmayoccurwith a tracheostomy.

Overall maintenance fluidrequirements are dependent on weight

and are approximated using this table:

The typical individual consumes 3 to 5 g (100 to 250mEq/day) of

dietary salt per day, which is balanced by sodium losses in sweat,

stool, and urine.

o In the perioperativeperiod, adequatemaintenanceofsodium

may be -achieved with an intake of 1-2mEq/kg/day.

o (by virtue of the hormone aldosterone by retaining sodium and

excrete potassium, thereby increasing tonicity of your blood,

attracting water from intracellular going to extracellular

compartment).

From 2014-A Trans:

ECF o Principal cation: Na o Principal anion: Cl and HCO3

ICF o Principal cation: K and Mg o Principal anion: HPO4 and proteins

The slightly higher protein content (organic anions) in plasma results in higher plasma cation composition relative to interstitial fluid and exerts oncotic pressure which draws fluid inside your vascular component maintaining the blood pressure

Water is freely diffusible, does not expend energy, and is distributed evenly throughout the fluid compartments.

Group 15 | Elizaga, Escano, Esguerra, Eslao Page 3 of 7

Normal potassium intake is approximately 40 to 120mEq/day,

approximately 10% to 15% of which is excreted as normal

urinarylosses.

o Body potassium stores can be maintained with an intake of

approximately 0.5 to 1.0mEq/kg/day. (inperioperative period)

Although 0.9% saline is used frequently, the relatively high

concentration of chloride results in a

hyperchloremicmetabolicacidosisbecause of the inability of the

renal tubule to excrete the excess Chloride

Appropriate management of fluids and electrolytes in the

perioperative period requires a flexible yet systematicapproach to

ensure that fluid administration is appropriately tailored to the

patients changing requirements.

o Deficit, maintenance requirements, and anyongoinglosses.

Deficit

o Approximation of intraoperative blood loss

o Fluid losses from evaporative and third-space

fluidsequestration(i.e., extravascular)

Dueto the shiftofcrystalloid from the intravascular space to

the interstitium, crystalloid should replace blood loss in a

ratio of 3-4:1.

Third Spacing

o Extensive dissection at the operative site induces a localized

capillary leak, the result of which is extravasation of

intravascular fluid into the interstitium with edema formation.

Inguinal herniorrhaphy: 4 mL/kg/h

Aortic aneurysm repair: 8 mL/kg/h

o Also, presence of infection, inflammation or burns

o This capillary leak may persist up

to24hoursintothepostoperativeperiodandshould be considered

as part of ongoing losses in the immediate postoperative

period.

On-Going Fluid Losses

o Usuallyrepresent GI lossesfrom stomas, tubes, drains, or

fistulae

o Theelectrolytecompositionof the output depends on the source

of effluent.

The replacement fluid should be chosen to best approximate the

composition of the ongoing losses.

o Nasogastric losses are typically replaced by Normal Saline

Solution + KCl.

o Losses from a duodenal fistula may best be replaced using

lactated Ringer's solution.

CLINICAL EVALUATION

1.) Intravascular Volume Status

o Evaluation of heart rate, blood pressure and most

importantly, hourlyurine output

o Resting tachycardia (>90 beats/min) is assumed to be a

common occurrence in hypovolemic patients, but

tachycardia in the supine position is absentin majority of

patients with moderate to severe blood loss.

o Hypotension in the supine position is also an insensitive

marker of blood loss (usually appears in the advanced stages

of hypovolemia, where blood loss exceeds 30% of blood

volume).

o Orthostatic Vital Signs

A significant orthostatic change is defined as any of the ff:

o pulse rate of at least 30beats/min

o systolic pressure >20mmHg, or dizziness on standing

There is a shift of 7-8mL/kg of blood to the lower

extremities.

2.) Hematocrit

o Use of hematocrit to estimate blood loss is unreliable and

inappropriate.

o Decreases in hematocrit in the early hours after acute blood

loss is usually the result of volume resuscitation rather than

ongoing blood loss.

3.) Invasive Hemodynamic Measures

o CV catheters, pulmonary artery catheters (allow

measurement of cardiac output and systemic oxygen

transport)

4.) Acid-Base Parameters

o Provide information about the adequacy of tissue

oxygenation

Arterial Base Deficit and Arterial Lactate Concentration

V. DISTURBANCES IN FLUID BALANCE

ECV deficit is the most common fluid disorder in surgical patients

and can be either acute (CV or CNS signs) or chronic (CV, CNS +

decrease in skin turgor and sunken eyes).

ECV excess may be iatrogenic or secondary to renal dysfunction,

congestive heart failure, or cirrhosis (hypoalbuminemia)

Volume changes are sensed by:

o Osmoreceptors: drive changes in thirst and diuresis through

the kidneys

o Baroreceptors: through specialized pressure sensors located in

the aortic arch and carotid sinuses; responses are both neural

(sympathetic and parasympathetic pathways) and hormonal

(renin-angiotensin, aldosterone, atrialnatriuretic peptide, renal

prostaglandins)

Disorders of Sodium Homeostasis

Changes in serum Na concentration are inversely proportional to

TBW.

Values in the range of 125-130 are rarely life-threatening.

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A. HYPONATREMIA

Serum Na:< 135 mEq/L

Severe hyponatremia:< 120mEq/L; associated with irreversible

neurologic complications

Sodium deficit is estimated by:

Na deficit in mEq= (140 serum Na) x 0.6 x (body weight in kg)

Hypertonic:occurs in the setting of hyperglycemia or elevated

BUN, which induces a shift of water from ICV to the extracellular

space.

Each 100 mg/dL rise in serum glucose or 30 mg/dL rise in BUN

correlates to a 1.5-2 mEq/L decrease in serum Na+.

Isotonic:pseudohyponatremia

Extreme hyperlipidemia or hyperproteinemia

Largely artifact NO NEED TO CORRECT

Hypotonic:most common

May occur in the setting of hypovolemia, euvolemia, or

hypervolemia

Hyponatremiacan also be seen with an excess of solute relative to

free water, such as with untreated hyperglycemia or mannitol

administration.

o Glucose exerts an osmotic force in the extracellular

compartment, causing a shift of water from the intracellular to

the extracellular space.

Hypovolemichyponatremia is a common presentation in the post

surgical patient (inc ADH), in decreased sodium intake, GI losses

vomiting, lose bowel movements, chronic use of diuretics

Treatment of HypoNa:

HypovolemicHypoNa:volume resuscitation with isotonic

(normal saline) fluids

EuvolemicHypoNa: fluid restriction and careful monitoring of

serum Na and volume status

In severe cases, judicious use of 3% NS + Loop diuretics to

increase serum Na by 0.5-1 mEq/hr

HypervolemicHypoNa: water restriction, with or without loop

diuretics

B. HYPERNATREMIA

Serum Na:> 145 mEq/L

Invariably associated with HYPERTONIC STATES

HypovolemicHyperNa:vomiting, diarrhea and forced diuresis

EuvolemicHyperNa:free water loss via lungs, skin or open

wounds or from Diabetes Insipidus

HypervolemicHyperNa: most often iatrogenically induced from

resuscitation with hypertonic fluids

Treatment: regardless of cause is free water replacement

H20 deficit (L) = 0.6 x (Wt. in kg) x (serum Na 140)

140

Half of the water deficit should be given over the 1st

24hrs, while

the remainder given, over the next 24-48hrs.

Serum Na+ should not be reduced by more than 0.5 mEq/L/hr, to

prevent cerebral swelling

FROM 2014 TRANS A

Occurs when there is an excess of extracellular water relative to Na+

either through Na depletion or dilution

DilutionalHyponatremia :results from extracellular water excess;

high extracellular volume

Causes: excessive oral water intake, iatrogenic IV excess,

increased secretion of anti-diuretic hormone, drugs such as

antipsychotics, trcyclic antidepressants, and ACE-I

Physical signs are usually absent; labs reveal hemodilution.

DepletionalHyponatremia:associated with ECF volume deficit

Causes: decrease intake or increased loss of Na+-containing fluid,

GI losses, renal losses]

Extreme elevations in plasma lipids and proteins can cause

pseudohyponatremiabecause there is no true decrease in

extracellular

Na+ relative to water.

Signs and symptoms primarily have a central nervous system origin

and are related to cellular water intoxication and associated

increases in intracranial pressure; they are also dependent on the

degree of hyponatremia and the rapidity with which it occurred.

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VI. COMPOSITION CHANGES

Potassium Abnormalities (3.5 to 5meq/L)

A. HYPOKALEMIA

Serum K:40 mEq/L.

When administering higher concentrations, do cardiac

monitoring(it is a cardiac membrane irritant and may cause

ventricular arrhythmia) because measured extracellular K

represents only a small proportion of total body K, small changes

in serum concentrations lead to significant alterations in body

functions.

Etiology of hypokalemia:

More common than hyperkalemia

May be caused by inadequate potassium intake; excessive renal

potassium excretion; potassium loss in pathologic GI secretions,

or intracellular shifts from metabolic alkalosis or insulin

therapy, and drugs

Symptoms are primarily related to failure of normal

contractility of GI smooth muscle, skeletal muscle, and cardiac

muscle

B. HYPERKALEMIA

Serum K:>5mEq/L

Acute rises in K can cause fatal ventricular dysrhythmias.

Causes: renal failure, acidosis, insulin deficiency, rhabdomyolysis,

cell lysis, drugs (succinylcholine, aldactone) and ischemia-

reperfusion syndromes

PSEUDOHYPERKALEMIA- seen in red blood cell hemolysis in the

collecting tube, false elevation of potassium

Etiology of hyperkalemia:

Treatment:

- Remove all K-containing fluids.

- Obtain ECG and if with changes consistent with hyperK, use

10% Ca gluconate IV to stabilize the cardiac membrane.

- The most rapid (although temporary) treatment is to induce

transcellular shift of K into cells 1amp D50 + 10 u of

regular insulin

- Definitive Tx: eliminate K from the body

- Loop diuretics or, in the case of renal failure, HEMODIALYSIS

- Excretion in the stool is facilitated by POLYSTYRENE

SULFONATE (a Na-K exchange resin).

Calcium Abnormalities

Calcium(8.5- 10.5meq/L)

o Most abundant electrolyte in the human body, 99% found in

bone

o Plasma Ca is divided into:

From 2014-A Trans:

Caused by excessive K+ intake, increased release of K+ from cells, or

impaired K+ excretion by the kidneys

o Oral or IV supplementation

o Hemolysis, rhabdomyolysis, and crush injuries can disrupt cell

membranes and release intracellular K+ into the ECF.

o Acidosis and a rapid rise in extracellular osmolality from

hyperglycemia or IV mannitol can raise causes a shift of K+ ions to

the extracellular compartment

o Drugs: K+-sparing diuretics (spironolactone), angiotensin-

converting enzyme inhibitors, and NSAIDs

Symptoms are primarily GI, neuromuscular, and cardiovascular.

Hyperkalemia: used for lethal injection and coronary bypass surgery

(to stop the heart during surgery because you cannot do the

procedure with the heart beating).

From 2014-A Trans:

Results from either a loss of free water or a gain of Na+

HypervolemicHypernatremia

Caused by either iatrogenic administration of Na+-containing fluids,

including Na+ bicarbonate, or mineralocorticoid

Urine sodium concentration is >20 mEq/L

Urine osmolarity is >300 mOsm/L]

NormovolemicHypernatremia

Result from renal causes, including diabetes insipidus, diuretic use,

and renal disease, or from nonrenal water loss from the GI tract or

skin

Urine sodium concentration is

Group 15 | Elizaga, Escano, Esguerra, Eslao Page 6 of 7

Free ionized form (50%): most useful laboratory value,

physiologically active

Complexed to phosphate and other anions (10%)

Protein-bound form (40%): biologically inactive

A) HYPOCALCEMIA

Serum Ca:90% of all cases

Other causes include toxicity from drugs (thiazides, lithium, Vit A

or D), thyrotoxicosis

Clinical manifestations of HYPERCALCEMIA

o ECG changes- shortened QT interval, prolonged PR and QRS

intervals, increased QRS voltage, T-wave flattening and

widening, and atrioventricular block (which can progress to

complete heart block and cardiac arrest).

System HYPERCalcemia

GI Anorexia, Nausea, vomiting, abdominal

pain

Neuromuscular Weakness, confusion, coma, bone pain

CV Hypertension, arrhythmia, polyuria

Renal Polydipsia

Treatment:

o Rapid correction: saline infusion to expand intravascular

volume, IV Furosemide (40- 80mg) to induce calciuresis

o Calcitonin: inhibits bone resorption and decreases renal tubular

reabsorption of Ca

o Corticosteroids: inhibit action of Vit D

o In patients with hypercalcemic crisis, BISPHOSPHONATES are

given to inhibit bone resorption.

Magnesium Abnormalities

Magnesium (1.6- 2.8mg/dL)

o Plays an important role in energy metabolism, protein synthesis

and cell division

o Intimately involved in the regulation of calcium movement

across muscle membranes

A) HYPOMAGNESEMIA

Serum Mg:< 1.6mg/dL

Occurs due to poor dietary intake, diuretic treatment, abnormal

gut losses (biliary or small bowel fistulae and massive diarrhea)

and alcoholism

Often accompanied by K depletion thus hypoK is refractory to K

replacement alone

Treatment:

o MAGNESIUM SO4 (1g=8mEq), can be given in patients with pre-

eclampsia

o Infusion should not exceed 2g/hr or 16mEq/hr to avoid

hypotension

o In life threatening arrhythmias, Magnesium Sulfate may be

given as a bolus of 1-2g IV over 5 minutes

B) HYPERMAGNESEMIA

Serum Mg:>2.8mg/dL

Usually iatrogenic, a result of administration of antacids or

laxatives

Other causes: renal insufficiency and massive hemolysis

Treatment:

o In life-threatening magnesium excess (>12mg/dL) IV Ca

gluconate to reverse cardiac effects, hydration with NS + IV

Furosemide; hemodialysis

From 2014-A Trans:

Usual causes: primary hyperparathyroidism, malignancy or metastasis in bone, secretion of parathyroid hormone-related protein

Symptoms: neurologic impairment, musculoskeletal weakness and

pain, renal dysfunction, GI symptoms, and cardiac symptoms such as

hypertension and arrhythmia

From 2014-A Trans:

Causes: pancreatitis, massive soft tissue infections such as

necrotizing fasciitis, renal failure, pancreatic and small bowel fistulas,

hypoparathyroidism, toxic shock syndrome, abnormalities in

magnesium levels, and tumor lysis syndrome

Malignancies associated with increased osteoclastic activity, such

as breast and prostate cancer, can lead to hypocalcemia from

increased bone formation.

Asymptomatic hypocalcemia may occur when hypoproteinemia

results in a normal ionized calcium level]

In general, neuromuscular and cardiac symptoms do not occur until

the ionized fraction falls below 2.5 mg/dL.

Clinical findings: paresthesias of the face and extremities, muscle

cramps, carpopedal spasm, stridor, tetany, seizures, hyperreflexia,

positive Chvosteks sign, positive Trosseaus sign

Complications: decreased cardiac contractility and heart failure

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Phosphorus Abnormalities (2.4 to 4.1mg/dl)

A) HYPOPHOSPHATEMIA

intestinal uptake or renal excretion

Treatment:

o Phosphate replacement should be instituted when levels

drop below 2mg/dL

o Na or K PO4 can be given in doses of 0.08- 0.24 mmol/kg over

4- 6 hours

B) HYPERPHOSPHATEMIA

Seen with impaired renal excretion, often associated with

hypocalcemia

Treatment: hydration + diuresis with acetazolamide

Phosphate binders: Al hydroxide will minimize intestinal

absorption.

HD severe, refractory hyperphosphatemia > dialysis

SUMMARY

Proper management of fluid and electrolytes facilitates crucial

homeostasis that allows cardiovascular perfusion, organ system

function, and cellular mechanisms to respond to surgical illness.

Knowledge of the compartmentalization of body fluids forms the

basis for understanding pathologic shifts in these fluid spaces in

disease states.

Alterations in the concentration of serum sodium have profound

effects on cellular function due to water shifts between the

intracellular and extracellular spaces.

Sources:

Dr. Azares lecture

2014-A Trans

Schwartzs Principle of Surgery 9th

ed.

My son, do not despise the Lords discipline,

and do not resent His rebuke,

because the Lord disciplines those He loves,

as a father the son He delights in.

Proverbs 3:11

From 2014-A Trans: Phosphorus Abnormalities

Phosphorus is the primary intracellular divalent anion and is

abundant in metabolically active cells.

Serum phosphate levels are tightly controlled by renal excretion.

Hyperphosphatemia

Can be due to:

o Decreased urinary excretion: in cases of hypoparathyroidism or

hyperthyroidism

o Increased intake: IV or phosphorus-containing laxatives

o Endogenous mobilization of phosphorus seen in anycondition

that results in cell destruction]

Usually asymptomatic but prolonged hyperphosphatemia can lead to

metastatic deposition of soft tissue calcium-phosphorus complexes.

Hypophosphatemia

Can be due to:

o Decreased phosphorus intake: malabsorption or malnutrition

o Intracellular shift of phosphorus: in cases of respiratory alkalosis,

insulin therapy, refeeding syndrome and hungry bone syndrome

o Increased excretion

Usually asymptomatic until levels fall significantly, but in general

symptoms are related to effects of O2 availability to tissue and

decrease in high-energy phosphates (ATP) = cardiac dysfunction or

muscle weakness.

From 2014-A Trans: Hypermagnesemia

Rare, but can be seen in renal insufficiency and changes in K+

excretion

Clinical manifestations: nausea and vomiting; neuromuscular

dysfunction with weakness, lethargy, and hyporeflexia; and impaired

cardiac conduction leading to hypotension and arrest]

Hypomagnesemia

Common problem in hospitalized and critically ill patients

May result from alterations of intake, renal excretion, and pathologic

losses

Depletion is characterized by neuromuscular and CNS hyperactivity

o Symptoms are similar to those of calcium deficiency including

hyperactive reflexes, muscle tremors, tetany, and positive

Chvostek's and Trousseau's signs

o Severe deficiencies can lead to delirium and seizures]

Hypomagnesemia is important not only because of its direct effects

on the nervous system, but also because it can produce

hypocalcemia and lead to persistent hypokalemia.