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JOSE RAVELO T. BARTOLOME, MD, FPCS, FPSGS, FPAHNSI ASSISTANT PROFESSOR IN SURGERY DEPARTMENT OF ELECTROLYTES FLUIDS AND SURGERY, FEUNRMF

MANAGEMENT OF THE SURGICAL PATIENTS

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INSTRUCTIONAL LEARNING OBJECTIVES GENERAL OBJECTIVE: At the end of the course, the student must be able to know the basic principles in the recognition and management of the fluids and electrolyte problems of the surgical patient. SPECIFIC OBJECTIVES:
1.

2.

3.

At the end of the course, the student must be able to: Define the different body fluid compartments as to its: 1. Normal distribution 2. Composition 4/28/12 Identify the different avenues of normal fluid loss

5.

6.

7.

Recognize the three main categories of body fluid changes as to its: 1. Etiology 2. Pathophysiology 3. Clinical manifestations 4. Management Identify specific electrolyte abnormalities associated with body fluid changes as to its: 1. Etiology 2. Pathophysiology 3. Clinical manifestations 4. Management Recognize acid-base disorders associated with body fluid changes as to its: 1. Etiology 2. Pathophysiology 3. Clinical manifestations 4/28/12

Anatomy of Body Fluids and Electrolytes

Total Body Water = 60% of total body weight

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Anatomy of Body Fluids and Electrolytes

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Anatomy of Body Fluids and Electrolytes

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Anatomy of Body Fluids and Electrolytes

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Anatomy of Body Fluids and Electrolytes

Total body water
Affected by age and lean body mass Proportion relative to body weight is

higher in infants and children (max. of 75-80% of total body weight in newborn is water)
Lean person has more water; obese

persons has less water

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Anatomy of Body Fluids and Electrolytes

Percentage of Total Body Water in Relation to Age and Sex AGE MALE FEMALE NEWBORN 75 80 75 - 80 10 18 years old 59 57 19 40 years old 41 60 years old > 60 years old 61 55 52 51 47 46
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Water Exchange: Normal exchange of fluids and electrolytes

Daily water requirement: 2000

2500 ml
About 1500 ml taken by mouth;

remaining extracted form solid foods hours

Rule of thumb: 30 ml / kg BW / 24

Daily Water and Salt Losses:

INSENSIBLE

600 1000 ml / day from the skin (perspiration) and 4/28/12

mainly

Water Exchange: Normal exchange of fluids and electrolytes

Daily electrolyte needs:
Sodium: Potassium: Rule of thumb:
K

5 125 meq 40 100 meq

1 meq/ kg BW

and Na / 24 hours =

60

70 meq / day for each

Requirements for other electrolytes

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normally supplied by daily food intake.

Water Exchange: Normal exchange of fluids and electrolytes

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Fluid requirements
typically 35 mL/kg/day insensible loss = 700 mL/day or 0.2

cc/kg/day for every 1 C > 37

1-10 > 21

kg = 100 mL/kg/day {4mL/kg/hr} 50 mL/kg/day {2mL/kg/hr} kg = 20 mL/kg/day {1mL/kg/hr}

11-20 kg =

Trick for hourly maintenance = 40 + weight (kg)

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Daily requirements for electrolytes

Sodium: 1-2 mEq/kg/d Potassium: 0.5-1 mEq/kg/d Calcium: 800 - 1200 mg/d Magnesium: 300 - 400 mg/d Phosphorus: 800 - 1200 mg/d

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Three Main Categories of Body Fluid Changes

VOLUME CHANGES
Water or isotonic salt solution gained or

loss

Water deficit or water excess

CONCENTRATION CHANGES
Changes in the concentration of

osmotically active particles

Mainly involved sodium with

accompanying changes in osmolality

Hypernatremia or hyponatremia
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VOLUME CHANGES
VOLUME DEFICIT or HYPOVOLEMIA VOLUME EXCESS or HYPERVOLEMIA
Primarily an extracellular fluid (ECF)

compartment phenomenon
History

Diagnosis mainly clinical

and Physical Examination; clinical manifestations examination indirect evidence

Laboratory

Serum Sodium concentration

independent of ECF volume status

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VOLUME DISTURBANCES

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VOLUME DEFICIT (HYPOVOLEMIA)

Most common fluid disorder in

surgical patients pure water loss (simplest form)

Usually NO significant concentration

changes

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Volume Deficit: Common Causes

External losses
GIT losses vomiting, NGT suctioning,

diarrhea, intestinal fistulas

Hemorrhage/bleeding

Internal losses
Sequestration Soft-tissue injuries/ infections Intestinal obstruction Intra-abdominal and retroperitoneal

inflammatory process

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Volume deficit: gastrointestinal losses

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Volume Deficit: Pathophysiology/Clinical Manifestations

Main defect: Decreased ECF water

volume
CNS and CVS effects

CNS effects:
Due to resulting hypernatremia Restlessness to delirium

CVS effects:
Hypotension and tachycardia Decreased skin turgor and dry mucuous 4/28/12

Volume Deficit: Laboratory/Management

Laboratory tests:
Hemoconcentration = inc. hematocrit Renal insufficiency = elevated BUN &

creatinine

Management:
Volume replacement
Crystalloid Colloidal Blood

solutions / plasma expanders

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Volume and Electrolyte Loss

Combined water and electrolyte loss

(sodium)

Usually GI losses NGT losses, enteric

fistulas, enterostomies, diarrheas

Other causes excess diuretics, adrenal

insufficiencies, profuse sweating, burns, body fluid sequestration

Diagnosis:
Mainly by history and physical

examination
Clinical manifestations similar to pure

volume deficit

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Classification: Hypovolemia/Hemorrhage
Water Loss MILD 4% of TBW CLASS I Hemorrhage 15% of blood volume 15 30% of blood volume 30 40% of blood volume > 40% of blood

MODERATE

6% of TBW CLASS II

SEVERE

8% of TBW CLASS III

Blood volume = 7.5% of total body weight (approx. 5.0 L) SHOCK > 8% of CLASS IV TBW

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Diagnostics: Volume deficit

CBC hemoglobin, hematocrit BUN, Creatinine Chest radiographs Urinalysis Central Venous Pressure; arterial

catheterization and monitoring

Urine Output Arterial Blood Gasses Serum Electrolytes

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Management: Volume Deficit

Fluid and electrolyte resuscitation
Intravenous replacement Intravenous maintenance

Appropriate choice of fluids

CRYSTALOIDS
Plain

and Dextrose containing solutions (eg. D5LRS) containing solutions; dextran

COLLOIDAL SOLUTIONS
Starch 4/28/12 BLOOD AND BLOOD COMPONENTS

Practical replacement strategies

Sweat: D5NS + 5 mEq KCl/L Gastric: D5NS + 20 mEq KCl/L Biliary/pancreatic: LR Small Bowel: LR Colon: LR 3rd space losses: LR

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Resuscitation
Crystalloids
Replace blood loss at a 3:1 ratio Initial bolus 1-2 liters, usually normal

saline

If they have transient response, give

additional fluids. Once 3-4 liters of crystalloid has been given consider blood.
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Indicators of successful resuscitation

PULSE 100 - 120 bpm URINARY OUTPUT
CHILDREN = 1.0 ml/kg/hr ADULT = 0.5 ml/kg/hr

Clearance of lactate Resolution of base deficit BLOOD PRESSURE POOR INDICATOR

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VOLUME EXCESS (HYPERVOLEMIA)

Generally iatrogenic in surgical

patients
Renal insufficiency Increase or excess in extracellular

fluid volume compartment

Etiology:
Parenteral overhydration Fluid retaining conditions (cardiac or

renal)
Mobilization of previously

sequestered fluid

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Clinical manifestations: hypervolemia

Weight gain Pedal / sacral edema Pulmonary rales and wheezes Elevated jugular venous pressure

(JVP)
Elevated CVP or PCWP Seizures, muscle twitching (increase

ICP)
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Laboratory diagnosis: hypervolemia

Decreased hematocrit Decreased albumin Decreased serum sodium
Laboratory manifestations of dilution

effects

Chest radiograph - congestion

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Management: hypervolemia
Water restriction (1500 ml/day) Diuretics Sodium restrictions Albumin infusion Supportive care cardiac, pulmonary,

renal

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CONCENTRATION CHANGES
Changes in the concentration of

osmotically active particles in the body fluid compartments

Mainly changes in sodium ion

concentration in the ECF compartment

May be related to blood glucose

concentration
HYPONATREMIA or HYPERNATREMIA
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HYPONATREMIA
Low or decreased sodium

concentration
Dilutional or overhydration especially

in surgical patients
Hyperglycemia Conditions that expands plasma

volume

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HYPONATREMIA

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HYPONATREMIA
Pathophysiology/Clinical

Manifestations:
Acute hyponatremia
CNS Manifestations
Brain

edema; increased intracranial pressure muscle twitching deep tendon reflex

Seizures,

Increased

Hypertension

Tissue signs of water excess

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HYPONATREMIA
Hyponatremia becomes symptomatic

if the serum sodium level becomes < 120 meq/L (slow) or < 130 meq/L (rapidly)

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HYPONATREMIA
Management
Water restriction Sodium replacement Optimize renal function Control of other contributing factors (eg.

Hyperglycemia)

Water restriction for moderate

hyponatremia complicating volume excess

Water replacement for symptomatic 4/28/12

HYPERNATREMIA
Uncommon; usually dangerous Etiology:
Excessive or unexpected isotonic volume

loss

Evaporative Head

loss in massive burns

injury with diabetes insipidus (SIADH)

Osmotic diuresis Uncontrolled hyperglycemia during TPN High output renal failure
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HYPERNATREMIA

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HYPERNATREMIA
Pathophysiology/Clinical

Manifestations
Profound ECF volume deficit CNS signs and symptoms
Restlessness Dry

and Delirium

mucus membrane skin to anuria fever

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Flushed High

Oliguria

HYPERNATREMIA
Management
Volume replacement to give dilutional

effect

Correct underlying problem Correction should not be too rapid to

avoid abrupt reduction in ECF osmolality (reversal of effect)

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Summary of manifestations in concentration changes

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COMPOSITIONAL CHANGES
ACID-BASE BALANCE SPECIFIC ELECTROLYTE CHANGES
POTASSIUM CALCIUM MAGNESIUM Other electrolytes

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ACID-BASE BALANCE
Goal is to maintain pH between 7.35

7.45 for normal metabolism / enzymatic activities

Metabolism accounts for large

amounts of liberated hydrogen ion or proton load (acid)

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ACID-BASE BALANCE
THREE PRIMARY BODY BUFFER

SYSTEMS
BICARBONATE-CARBONIC ACID BUFFER

SYSTEM
RESPIRATORY BUFFER SYSTEM RENAL BUFFER SYSTEM

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Buffer systems
Bicarbonate-Carbonic Acid Buffer

System
Occurring inside the red blood cells Most important and rapid Based on the Henderson-Hasselbalchs

Equation
pH

= pKa + log (HCO3)/(H2CO3)

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Buffer system
Respiratory buffer system
Function of the ventilation/respiratory

system gas)

Elimination of carbon dioxide (volatile Rapid and inexhaustible system Will function as long as ventilation not

compromised
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Buffer system
Renal buffer system
Function

of the excretory system/kidneys of acid salts of filtered base (HCO3)

Extraction

Reclamation De

novo generation of bicarbonate system

Slow

Compromise

of renal function compromise the buffer system

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ACID-BASE DISORDERS

Diagnosis by clinical history and

minimum of laboratory data (usually starts with the diagnosis of the main disease)
Arterial Blood Gas Analysis is very

important
Serum Electrolyte determination Management principles:
Treat the underlying cause giving rise to

the acid-base problem

Examples: 4/28/12

Normal Arterial Blood Gasses (ABG)

ABG data pH pCO2 pO2 HCO3 O2 saturation Venous O2 saturation Total CO2 Values 7.35 7.45 35 45 mmHg 80 100 mmHg 22 26 mmHg 90% and above 75% 24 29 mEq/L
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Acid-Base Disorders

Respiratory Acidosis BE = 0 HCO3 = 24 Metabolic Acidosis

Metabolic Alkalosis

Respiratory Alkalosis

7. 4

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Respiratory Acidosis
Retention of carbon dioxide =

increased formation of H2CO3

Acute or chronic hypercapnia due to

inadequate ventilation

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Respiratory Acidosis
Etiology:
Any condition that may cause

inadequate ventilation
Airway COPD Pneumonia CNS

obstruction

injuries depression (eg. In patients on

Respiratory

morphine)
Thoracic

injury
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Respiratory acidosis
Diagnosis:
Clinical history and physical examination ABG: decresed pH, increased pCO2 Acute state: normal HCO3 Chronic state: elevated HCO3 Clinical manifestations largely depends

on the symptoms of the underlying disease

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Respiratory acidosis
Management:
Treatment of underlying etiology Any measure to improve ventilation
Intubation Mechanical

ventilator

Supportive measures
Manage

fluids and electrolyte problem

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Respiratory Alkalosis
Acute or chronic hyperventilation Increased in expulsion of CO2 Etiology:
Apprehension/anxiety Pain (postoperative) Hypoxia Pulmonary embolism CNS injuries/infections Assisted/mechanical ventilation
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Respiratory alkalosis
Diagnosis:
ABG: decreased pCO2, increased pH

Dangers / Complications:
Potassium depletion = cardiac

complications

Ventricular arrhythmias and fibrillation Cerebral ischemia & acidosis due to

cerebral vasoconstriction

Others:
Depressed O2 delivery to tissues
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Respiratory alkalosis
Management:
Difficult and with poor prognosis in

severe and persistent cases measures

Treat underlying cause and supportive Rebreathing device

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Metabolic Acidosis
Retention / overproduction of acids
Azotemia Diabetic ketoacidosis Lactic acidosis

Loss of bicarbonate
Diarrhea Pancreatic or small bowel fistulas

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Metabolic acidosis
Characterized by calculated anion

gap as to possible cause

Normal anion gap
Loss of bicarbonate Gain of chloride

Increased anion gap

Increased production of organic acids Retention of sulfuric and phosphorus

acid
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Metabolic acidosis
Management:
Correct the underlying cause Volume resuscitation Treatment of sepsis/infection

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Metabolic Alkalosis
Loss of acid and gain of base Usually aggravated by hypokalemia

and volume contraction

Two types
Chloride responsive Chloride resistant

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Metabolic alkalosis
Diagnosis:
ABG: increased HCO3 and pH Compensatory hypercapnia (increased

pCO2)

Hypokalemia

Management:
Treat underlying cause Correct hypovolemia with chloride-

containing fluids function)

Correct hypokalemia (assure good renal

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Potassium Abnormalities
K+ is the major ICF cation; the small

ECF conc. Is critical for cardiac and neuromuscular functions

Normal serum potassium = 3.5 5.5

mEq/ L

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HYPOKALEMIA (decreased serum potassium)

Etiology:
Redistributional losses from intracellular

uptake esp. in acute alkalosis, insulin treatment and anabolism steroids use, renal tubular acidosis

External losses GI, renal (diuretics) ,

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Hypokalemia
Diagnosis:
S / S: Muscle weakness, hyporeflexia,

paralytic ileus, Insulin resistance depression, ( + ) U-waves

EKG:decrease voltage, flat T-waves, ST-

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Hypokalemia
Management:
Check renal function before treatment Treat alkalosis if present; decrease

sodium intake
Enteral replacement is preferred: 20 40

mEq

KCl elixir : 15 cc = 20 mEq KCl Potassium tablet = 8 mEq KCl Parenteral replacement:
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HYPERKALEMIA (increased serum potassium)

Etiology:
Pseudo-hyperkalemia: in leukocytosis,

hemolysis, thrombocytosis

Redistributional: as in cases of acidosis,

hypoinsulinism, repefusion syndrome, digitalis toxicity, post-operative period (1st 24 48 hours)

Spironolactone use as diuretics

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Hyperkalemia
Diagnosis:
Clinical S / S: nausea, vomiting,

intestinal colic, weakness, diarrhea segments, wide QRS

EKG: peaked T-waves, depressed STCardiac-arrest in diastole

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Hyperkalemia
Management:
Remove exogenous source of

bicarbonate or base

Hydration Treat acidosis Emergency: calcium, NaHCO3, Kayexalate

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hemodialysis or peritoneal dialysis

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Calcium Abnormalities
Calcium is essential for

neuromuscular activities and as cofactors in various metabolic pathways

Normal serum calcium = 9 11 mg /

dL
2 types :
Non-ionized form
55%

of total body calcium

bound

to albumin and other interstitial protein

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Ionized form

HYPOCALCEMIA
Etiology:
Acute pancreatitis Necrotising fascitis Acute and chronic renal failure Pancreatic and small intestinal fistulas Hypoparathyroidism After surgical removal or

devscularization of the parathyroid glands

Transient hypocalcemia in

hyperparathyoid patient after4/28/12 removal of

Hypocalcemia
Clinical manifestations:
Usually asymptomatic until level is below

8 mg / dL

Numbness, tingling sensation of the

circumoral area and tips of fingers and toes

Muscular and abdominal cramps Tetany, seizures, hyperreflexia Chvosteks sign Trosseaus sign
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Hypocalcemia
Management:
Correction of underlying cause and

replacement of deficit

Acute treatment: intravenous calcium

(Ca chloride or Ca gluconate in 10% solution)

Chronic treatment: oral calcium (calcium

lactate tabs), supplemental vitamin D

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HYPERCALCEMIA
Etiology:
Malignancy Hyperparathyroidism Acute adrenal insufficiency Pagets disease Prolonged immobilization Hyperthyroidism

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Hypercalcemia
Clinical manifestations:
Acute

crisis = if calcium > 12 mg/ dL (critical: 16 20)

Bones Moans Abdominal groans Psychic overtones Nausea, vomiting, anorexia Constipation, polyuria Confusion, lethargy
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Hypercalcemia
Management:
Acute crisis must be managed urgently Hydration; rapid ECF volume repletion to

lower serum calcium by dilution

Loop diuretics furosemide Mithramycin intravenously Hemodialysis Calcitonin Parathyroidectomy (if due to

hyperparathyroidism)

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MAGNESSIUM ABNORMALITIES
Magnessium ion needed in most

enzymatic systems and depletion may lead to neuromuscular and CNS hyperactivity

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MAGNESSIUM DEFFICIENCY
Etiology:
Complication of malnutrition Starvation Malabsorption syndromes Acute pancreatitis Diabetic ketoacidosis GI fluid losses Prolonged parenteral nutrition and

hyperalimentation

Primary aldosteronism

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Magnessium deficiency
Clinical manifestations:
Diagnosis based on high index of Similar to calcium deficiency

suspicion clinical and laboratory hyperreflexia, muscle tremors, and tetany with Chvosteks sign

Delirium and convulsions Cardiac arrhythmias

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Magnessium deficiency
Management:
Magnessium replacement : parenteral

administration of Mg sulfate or Mg Chloride solutions

Check renal function Monitor cardiac activity, blood pressure

and respiration when giving Mg sulfate

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MAGNESSIUM EXCESS
Etiology:
Renal failure Antacid overuse Hypothyroidism Adrenal insufficieny

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Magnessium excess
Clinical manifestations:
Nausea and vomiting Weakness Mental status changes Hyper-reflexia Hyperventilation

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Magnessium excess
Management:
Remove or discontinue possible external

sources cases

IV calcium gluconate for emergency Dialysis in renal failure

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Electrolyte replacement therapy protocol

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Electrolyte replacement therapy protocol

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Phosphate
HYPOPHOSPHATEMIA
Etiology:
TPN DM

nutrition

ketoacidosis

Malabsorption Alcoholism Acute

renal tubular necrosis alkalosis

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Starvation Prolonged

Phosphate
HYPOPHOSPHATEMIA
Clinical manifestations:
Myocardial Anorexia Bone

depression

pain

Weakness Rhabdomyolysis CNS

changes replacement

Management:
Parenteral 4/28/12

Phosphate
HYPERPHOSPHATEMIA
Etiology:
Renal

insufficiency

Hypoparathyroidism Catabolism Vit

D metabolites

May produce metastatic calcification Management:

Restrict

source antacids
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Phosphate-binding

Zinc
Enzyme activator; 1 2 gm in the

whole body
Concentrated in the brain, pancreas,

liver, kidney, etc

Adjunct in wound healing S / S of zinc deficiency:
Diarrhea Dermatitis Depression
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Planning daily fluids and electrolyte requirements

VOLUME OF WATER (replacement of

acute and ongoing loss)

TONICITY or CONCENTRATION SPECFIC ELECTROLYTES ACID-BASE BALANCE CALORIC INTAKE

FOR Surgical patients:

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