Surgery 1 DR.

MILALYN RUTH DELIZO

FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

OUTLINE  Males have higher percentage of TBW than

I. INTRODUCTION
II. BODY FLUIDS
a. FLUID COMPARTMENTS
b. COMPOSITION OF FLUID
COMPARTMENTS
c. PASSIVE TRANSPORT SYSTEM
III. ELECTROLYTE ABNORMALITIES IN SPECIFIC
SURGICAL PATIENTS
a. NEUROLOGIC PATIENTS
b. MALNOURISHED PATIENTS
c. ACUTE RENAL FAILURE PATIENTS
d. CANCER PATIENTS
Black: Powerpoint/PDF
Red: PPT Notes/Recording
Blue: Book (Schwartz Principle of Surgery 10th edition)
INTRODUCTION
Fluid and electrolyte management is paramount to
the care of the surgical patient. Changes in both fluid
and electrolyte composition occur preoperatively,
intraoperatively, and post operatively, as well as in
response to trauma and sepsis.
females, due to a correlation of higher
percentage of adipose tissue and lower
percentage of muscle mass.
 Newborns have the highest percentage of
TBW, 80 % of their total body weight, this
decreases to approximately 65% by 1 year of
age and thereafter remains fairly constant.
Deuterium oxide and tritiated water – have been
used in clinical research to measure TBW by indicator
dilution methods.
FLUID COMPARTMENTS
TBW is divided into three functional fluid
compartments:
1. PLASMA (INTRAVASCULAR)
2. INTERSTITIAL FLUID
3. INTRACELLULAR

BODY FLUIDS
Total Body Water

 Constitutes 50-60% of total body weight

 Relatively constant for an individual and is % Body Volume of
primarily a reflection of body fat. weight TBW MALE
 Muscle and solid organs have higher water (70 kg)
content than bone and fats
Body Water 60 % 42,000 ml
 Lean individuals have greater proportion of
water to TBW than the obese person Intracellular 40 % 28,000 ml
 Total body water decreases steadily and
Extracellular: 20 % 14,000 ml
significantly with increasing age

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 Surgery 1 DR. MILALYN RUTH DELIZO

FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

Interstitial 15% 10,500 ml FILTRATION - Filtration movement of solute and

solvent across a membrane caused by hydrostatic
Plasma 5% 3,500 ml
pressure
(Intravascular)
OSMOSIS - movement of solvent from an area of
lower solute concentration to one of higher
concentration
COMPOSITION OF FLUID COMPARTMENTS
BODY FLUID CHANGES

 Average water intake: 2000 ml

- 75 % from oral intake solid foods
 Daily water losses:
- Urine - 800 to 1200 ml
- Stool - 250 ml
- Insensible losses – 600 ml
o skin 75%
o lungs 25%
 increased by factors as:
 fever
 hypermetabolism
 hyperventilation

 Kidneys must excrete a minimum of 500 to

The ECF compartment is balanced between sodium,
the principal cation; chloride and bicarbonate, the
principal anions.
The ICF is comprised primarily of the cations;
potassium and magnesium, and the anions;
phosphate and proteins.
The concentration gradients between compartments
is maintained by ATP driven sodium-potassium
pumps within the cell membranes (ACTIVE
TRANPORT SYSTEM)
PASSIVE TRANSPORT SYSTEM
DIFFUSION - is the movement of molecules from area
of higher concentration to area of lower
concentration through a biological membrane
800 mL of urine per day to clear products of
metabolism
 Average dietary salt intake per day – 3 to 5 g
Hyponatremia or Hypovolemia:
- Sodium excretion:
 Reduced to: 1mEq/d
 Maximized to: 5000 mEq/d
 to achieve balance except
in people with salt-
wasting kidneys.
 Sweat is hypotonic, and sweating usually
results in only a small sodium loss.
 GI losses are isotonic to slightly hypotonic and
contribute little to net gain or loss of free
water when measured and appropriately
replaced by isotonic salt solutions.

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FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

CLASSIFICATION OF BODILY FLUID CHANGES Signs and Symptoms of Volume Disturbances

DISORDERS IN FLUID BALANCE
SYSTEM VOLUME DEFICIT VOLUME
o VOLUME EXCESS
o CONCENTRATION
GENERALIZED Weight loss Weight gain
o COMPOSITION
Decreased skin turgor Peripheral
edema
FLUID VOLUME DISTURBANCES
CARDIAC Tachycardia Increased
 EC volume deficit cardiac
Orthosthasis/hypotension
- most common fluid disorder in output
surgical patients Collapsed neck veins
Increased
- Maybe acute or chronic CVP
o Acute volume deficit is
associated with cardiovascular Distended
and central nervous system neck veins
signs murmur
o Chronic deficits display tissue
RENAL Oliguria
signs, such as a decrease in skin
turgor and sunken eyes, in Azotemia
addition to cardiovascular and
GASTROINTESTINAL ileus Bowel edema
central nervous system signs
- Most Common cause: GI losses
PULMONARY Pulmonary
 Other causes: sequestration edema
secondary to soft tissue
injuries, burns, peritonitis,
prolonged surgery CONCENTRATION CHANGES

 Changes in serum sodium concentration are

inversely proportional to TBW.
 Abnormalities in TBW are reflected by
abnormalities in serum sodium levels

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 Surgery 1 DR. MILALYN RUTH DELIZO

FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

SIGNS AND SYMPTOMS

SODIUM ABNORMALITIES
CENTRAL NERVOUS Headache
HYPONATREMIA SYSTEM
Confusion
Hyperactive/hypoactive
DTRs
Seizures, coma, inc ICP

MUSCULOSKELETAL Weakness, fatigue, muscle

cramps /twitching

GASTROINTESTINAL Anorexia
Nausea, vomiting
 A low serum sodium level occurs when
there is excess of extracellular water Watery diarrhea
relative to sodium. Extracellular
CARDIOVASCULAR Hypertension
volume can be high, normal or low.
 ADH secretion - Increase reabsorption bradycardia
of water
 Drugs that can cause water retention TISSUE Lacrimation
and hyponatremia:
salivation
o Antipsychotics
o Tricyclic antidepressants (TCA) RENAL oliguria
o Angiotensin-converting
enzyme inhibitors
 In most cases of hyponatremia, sodium  Signs and symptoms are dependent on
concentration is decreased as a consequence the degree of hyponatremia and the
of either sodium depletion or dilution rapidity with which it occurred.
 Manifestations primarily have a CNS
origin and are related to water
intoxication and associated increase in
ICP.

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FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

HYPONATREMIA CORRECTION SIGNS AND SYMPTOMS

 Free water restriction CNS Restlessness, delirium
 Administration of Na (severe)
 (+) neurologic s/s – 3% normal saline is used Lethargy, coma
to increase level by no more than 1 mEq/L per Ataxia, irritability, tonic
hour 130 mEq/L spasm
 (-) s/s – 0.5 mEq/L per hour or 12 mEq/L per
day MUSCULOSKELETAL weakness

CARDIOVASCULAR Tachycardia
Seizures, weakness, paresis, akinetic movement,
permanent brain damage and death hypotension

HYPERNATREMIA TISSUE Dry sticky mucus

membrane,
red swollen tongue,
decrease saliva and tears

RENAL oliguria

METABOLIC fever

 Symptoms are rare until the serum

concentration exceeds 160 mEq/L, but once
present, are associated with significant
morbidity and mortality.
SODIUM CORRECTION/HYPERNATREMIA

 Results from either loss of free water
or a gain of sodium in excess of water.
Like hypo natremia, it can be
associated with an increased, normal
or decreased EC volume.
- Treatment of associated water deficit
Water deficit (L) = serum Na - 140 x TBW
140

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FLUID AND ELECTROLYTE MANAGEMENT OF
THE SURGICAL PATIENT
ACUTE SYMPTOMATIC HYPERNATREMIA: CAUSES:
 Titrated to achieve a decrease in serum Na of
no more than 1 mEq/h or 12 mEq/d
CHRONIC SYMPTOMATIC HYPERNATREMIA
 0.7 mEq/h
Cerebral edema and herniation
Water shift from IC to EC space, leading to edema.
POTASSIUM ABNORMALITIES
 Average dietary intake: 50 to 100 mEq/d
 Excreted primarily in the urine
- EC potassium is maintained within a
narrow range, principally by renal
excretion of potassium 10 to 700
mEq/d.
 2 % of the total body Potassium is located
within the ECF
 Normal range: 3.5 to 5.0 Meq/L
1. Hyperkalemia
2. hypokalemia
TREATMENT:
HYPERKALEMIA GOALS
 defined as a serum potassium concentration
above the normal range of 3.5 to 5.0 mEq/L.
 It is caused by:
- excessive potassium intake
- increased release of potassium from
cells
- impaired potassium excretion by the
kidneys
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- Increased intake (supplementation, blood
transfusion, endogenous load/destruction i.e.
hemolysis, rhabdomyolysis, crush injury)
- Increased release from cells (acidosis,rapid
rise of ECF osmolality i.e. hyperglycemia and
mannitol)
- Impaired excretion
o medications (spironolactone, ACE
inhibitors, NSAIDS)
o renal insufficiency/failure
CLINICAL MANIFESTATION OF HYPERKALEMIA
gastrointestinal Nausea, vomiting, colic, diarrhea
neuromuscular Weakness, paralysis, respiratory
failure
cardiovascular Arrythmia, arrest
ECG findings High peaked T waves, widened
QRS complex, flattened P wave,
prolonged PR interval,
ventricular fibrillation
 Reducing total body potassium
 Kayexalate – binds K in exchange for
Na
 Shifting of potassium from EC to IC space
 glucose + insulin IV
 Bicarbonate 1 amp IV
 nebulization with albuterol
 protecting the cell from the effects of
increased K
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 Surgery 1 DR. MILALYN RUTH DELIZO

FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

 CaCl or Ca gluconate 5 to 10 ml of TREATMENT:

10% solution- counteract cardiac
effect  K Level < 4.0 mEq/L
 DIALYSIS  Asymptomatic/tolerates enteral nutrtion:
 kcl 40 mEq per enteral access x 1 dose
 Asymptomatic/not tolerating enteral nut:
HYPOKALEMIA  kcl 20 mEq IV q 2 h x 2 doses
 Symptomatic:
CAUSES:
 kcl 20 mEq IV q 1 x 4 doses
- INADEQUATE INTAKE (dietary, K free IV fluids)
- Excessive renal excretion
Recheck K level 2 hours after the end of infusion
 hyperaldosteronism
 medications ( aminoglycosides,
amphotericin, cisplatin)
- Gastrointestinal losses
 Diarrhea CALCIUM ABNORMALITIES
 Fistula
 Vomiting  Majority of body’s calcium is contained within the
 high NG output bone matrix
 More common in surgical patient  < 1 % in the ECF
 Drugs induce magnesium depletion causing  Daily calcium intake 1 to 3 g/d (most is excreted
renal potassium wastage by the bowel)
 Serum Ca is distributed in 3 forms
CLINICAL MANIFESTATION OF HYPOKALEMIA
1. protein bound 40 %
2. complexed to PO4/anions 10 %
Gastrointestinal Ileus, constipation 3. ionized 50 % - responsible for
neuromuscular stability, measured
Neuromuscular Decreased reflexes, fatigue, directly
weakness, paralysis

Cardiovascular arrest  When total serum calcium levels are measured,

ECG changes U waves, T wave flattening, ST
segment changes, arryhtmias
the albumin concentration must be taken into
consideration:
- Adjust total serum calcium down by 0.8
mg/dL for every 1 g/dL decrease in
albumin.

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FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

HYPERCALCEMIA HYPOCALCEMIA

- Serum Ca level above the normal range (8.5 to  CAUSES

10.5 mEq/L) - Pancreatitis ( sequestration of Ca via
- Ionized Ca level above 4.2 to 4.8 mg/dL chelation with FFA)
- CAUSES: - malignancy (Inc. osteoclastic activity)
1. Primary hyperparathyroidism - massive soft tissue infections
2. malignancy (bony metastasis, - renal failure
secretion of PTHRP) - pancreatic and small bowel fistulas
- hypoparathyroidism
- toxic shock syndrome
CLINICAL MANIFESTATION OF HYPERCALEMIA
- tumor lysis syndrome
gastrointestinal Anorexia,nausea/vomiting,abd
ominal pain CLINICAL MANIFESTATION
neuromuscular Weakness, confusion, coma,  Symptoms do not occur until the ionized
bone pain fraction falls below 2.5 mg/dL
 Chvostek’s sign ( spasm resulting from tapping
cardiovascular Hpn, arryhtmia, worsening of
over the facial nerve)
digitalis toxicity (polyuria)
 Trousseau’s sign ( spasm resulting from
renal polydipsia pressure applied to the nerves and vessels of
the upper extremity with a BP cuff)
ECG changes Shortened QT interval,  Decreased cardiac contractility and heart failure
prolonged PR and QRS interval, t  ECG changes :
wave flattening and widening, - prolonged QT interval
AV block - t wave inversion
- heart block
TREATMENT: - ventricular fibrillation
 Required when symptomatic, usually occurs
when serum levels exceeds 12 mg/dL
 Critical level is 15 mg/dL TREATMENT:
 Initial treatment is aimed at repleting the
 Can be treated with oral and IV calcium
associated volume deficit and then inducing
 Acute symptomatic HypoCa – IV 10% ca
brisk diuresis with normal saline
gluconate (achieve serum conc of 7 to 9
mg/dL)

Recheck ionized Ca level in 3 days

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FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

PHOSPHORUS ABNORMALITIES TREATMENT:

Phosphorous  Depends on the level of depletion

 primary IC divalent anion, abundant in
metabolically active cells
 involved in energy production during
glycolysis (ATP)
 controlled by renal excretion
 Phosphate level 1.0 to 2.5 mg/dL
- Oral or IV
- Recheck levels in 3 days
 Phosphate level < 1.0 mg/dL
- Oral or IV
- Recheck levels after 4 hours of infusion

HYPERPHOSPHATEMIA

 Most cases are asymptomatic MAGNESIUM ABNORMALITIES

CAUSES:
MAGNESIUM
 INCREASE INTAKE ( IV hyperalimentation,
phosphorous containing laxatives) - 4th most common mineral in the body
 Decreased urinary excretion - Found primarily in the IC compartment
(hypoparathyroidism and hyperthyroidism) - Approximately one half of the total body
 Endogenous mobilization of Phosphorous content of 2000 mEq is incorporated in bone
(hemolysis, severe hypothermia, malignant and is slowly exchangeable.
hyperthermia, sepsis, rhabdomylosis) - Normal dietary intake is 20 mEq/d
- Excreted in both the feces and urine
TREATMENT:
HYPERMAGNESEMIA - RARE
 PHOSPHATE BINDERS (sucralfate and
aluminum containing antacids) CAUSES :
 Ca acetate tablets- useful when hypo Ca is
present  Magnesium containing antacids and laxatives
 Dialysis – for patiets with renal failure  Excessive intake in TPN
 Severe acidosis, massive trauma, thermal
injury
HYPOPHOSPHATEMIA CLINICAL MANIFESTATION:
CAUSES:  Nausea/vomiting, weakness, lethargy,
hyporeflexia, hypotension and arrest
 Decrease intake (malabsorption, adm of
 ECG CHANGES
phosphate binders) CHRONIC
Increased PR interval
 Intracellular shift of Phosphorous ( resp
widened QRS complex
alkalosis, insulin therapy, refeeding
syndrome, hungry bone syndrome) ACUTE elevated T waves
 Increase excretion
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FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

TREATMENT: FLUID AND ELECTROLYTE THERAPY

 Eliminates exogenous sources of magnesium
 Correct concurrent volume deficit
 Correct acidosis if present

(+) Acute symptoms – Ca chloride (5 to 10 ml) to

antagonize cardiovascular effects
Hemodialysis maybe necessary
HYPOMAGNESEMIA - RARE

 Common problem in hospitalized patients

particularly in the critically ill
 Results from alterations of intake, renal
excretion and pathologic losses
 Increase renal excretion from alcohol abuse,
diuretic use
 GI losses from diarrhea, malabsorption and
acute pancreatitis
CLINICAL MANIFESTATION:
- Hyperactive reflexes
- Muscle tremors
- Tetany
- Positive Chvostek’s and trousseau’s sign
- Delirium
- ECG changes : prolonged QT and PR intervals,
flattening or inversion of p waves, arryhtmias
- Hypomagnesemia is important not only
because of it’s direct effect on the nervous
system but also because it can produce
hypocalcemia and persistent hypokalemia
TREATMENT:
 Asymptomatic and mild – oral
 Symptomatic with severe deficit ( <1 mEq/L)
- 1 to 2 g of magnesium sulfate IV over
15 minutes
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 The type of fluid administered depends on the
patient’s volume status and the type of
concentration or compositional abnormality
present.
 Both lactated Ringer’s solution and normal
saline are considered isotonic and are useful
in replacing GI losses and correcting
extracellular volume deficits.
 Lactated Ringer’s is slightly hypotonic in that
 it contains 130 mEq of lactate.
 Resuscitation using lactated Ringer’s may be
deleterious because it activates the
inflammatory response and induces
apoptosis. [significantly lower levels of
apoptosis in lung and liver tissue after
resuscitation.]
 Sodium chloride is mildly hypertonic,
containing 154 mEq of sodium that is
balanced by 154 mEq of chloride.
 The high chloride concentration imposes a
significant chloride load on the kidneys and
may lead to a hyperchloremic metabolic
acidosis.
 Sodium chloride is an ideal solution for
correcting volume deficits associated with
hyponatremia, hypochloremia, and metabolic
alkalosis.
 0.45% sodium chloride, are useful for
replacement of ongoing GI losses as well as
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for maintenance fluid therapy in the
postoperative period. [dextrose added to
0.45% NaCl solutions to maintain osmolality
and prevent lysis of RBC.]
ALTERNATIVE RESUCITATIVE FLUIDS
 Hypertonic saline (3.5 % and 5 %)
 Hypertonic saline (7.5%) has been used as a
treatment modality in patients with closed
head injuries. [increased cerebral perfusion +
decrease intracranial pressure = decrease
brain edema.] [ hypertonic saline has a risk of
bleeding ->arteriolar vasodilator]
 Colloids –(used on surgical patients) transient
plasma volume expansion (confined in the IV
space)
albumin
dextran
hetastarch
gelatins
PREOPERATIVE FLUID TREATMENT
 MAINTENANCE FLUIDS
first 0 to 10 kg - 100 ml/kg per day
next 10-20 kg – additional 50ml/kg/day
weight > 20 kg – additional 20ml/kg/day
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For example, a 60-kg female would receive a total of
2300 mL of fluid daily: 1000 mL for the first 10 kg of
body weight (10 kg × 100 mL/kg per day), 500 mL for
the next 20 kg(10 kg × 50 mL/kg per day), and 800
mL for the last 40 kg (40 kg× 20 mL/kg per day).
 Volume deficits
obvious GI losses
poor oral intake
third space or non functional ECF
losses (GI obstruction, peritoneal or bowel
infalmmation, burns, severe soft tissue
injuries, ascites)
INTRAOPERATIVE FLUID THERAPY
 Loss of compensatory mechanism are lost
with the induction of anesthesia
(hypotension will develop if not corrected)
 Replacement of ECF during surgery often
requires 500 to 1000 ml/h – isotonic solution
to support homeostasis
 Major open abdominal surgeries, complex
fractures, large soft tissue wounds, burns
third space losses/parasitic losses
POSTOPERATIVE FLUID THERAPY
 Volume excess is a common disorder in the
postoperative period
 Based on patient’s current estimated volume
status and projected ongoing fluid losses
 Initial post op period – isotonic solution
 After 24 to 48 H – 5 % dextrose in 0.45 %
saline
 Potassium maybe added if with normal urine
output
 Continued sequestration of EC fluids into the
site of injury or operative trauma can
continue for 12 h or more after operation
 Adequacy of resuscitation
-acceptable values for v/s
- adequate urine output
-correction of base deficit or lactate in
complicated cases
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ELECTROLYTE ABNORMALITIES IN SPECIFIC
SURGICAL PATIENTS
NEUROLOGIC PATIENTS
SYNDROME OF INAPPROPRIATE SECRETION OF ADH
(SIADH)
 SIADH can occur after head injury or surgery to the
CNS, but it is also seen in association with
administration of drugs (e.g. morphine,
nonsteroidals, and oxytocin) and in a number of
pulmonary and endocrine diseases (e.g.
hypothyroidism, glucocorticoid deficiency).
 It should be considered in patients who are
euvolemic and hyponatremic with elevated urine
sodium levels.
 In chronic SIADH, when long-term fluid restriction
is difficult to maintain or is ineffective,
demeclocycline and lithium can be used to induce
free water loss.
DIABETES INSIPIDUS (DI)
 DI is a disorder of ADH stimulation and is
manifested by dilute urine in the case of
hypernatremia.
 Central DI – results from a defect in ADH secretion,
frequently seen in association with pituitary
surgery, closed head injury, and anoxic
encephalopathy.
 Nephrogenic DI – results from a defect in end-
organ responsiveness to ADH, associated with
hypokalemia, administration of radiocontrast dye,
and use of drugs such as aminoglycosides, and
amphotericin B.
CEREBRAL SALT WASTING
 Cerebral salt wasting is a diagnosis of exclusion
that occurs in patients with a cerebral lesion and
renal wasting of sodium and chloride with no
other identifiable cause.
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 Natriuresis in patients with a contracted
extracellular volume should prompt the possible
diagnosis of cerebral salt wasting
 Hyponatremia is frequently observed but is
nonspecific and occurs as a secondary event,
which differentiates it from SIADH.
MALNOURISHED PATIENTS: REFEEDING SYNDROME
 Refeeding syndrome is a potentially lethal
condition that can occur with rapid and excessive
feeding of patients with severe underlying
malnutrition due to starvation, alcoholism delayed
nutritional support, anorexia nervosa, or massive
weight loss in obese patients.
 It can be associated with enteral or parenteral
refeeding, and symptoms from electrolyte
abnormalities include cardiac arrhythmias,
confusion, respiratory failure and even death.
 Thiamine should be administered before the
initiation of feeding.
ACUTE RENAL FAILURE PATIENTS
 A number of fluid and electrolyte
abnormalities are specific to patients with
acute renal failure.
 Oliguric renal failure – requires close
monitoring of serum potassium levels.
 Hypocalcemia, hypermagnesemia, and
hyperphosphatemia also are associated with
acute renal failure.
 Metabolic acidosis is commonly seen with
renal failure.
CANCER PATIENTS
 Fluid and electrolyte abnormalities are
common in patients with cancer.
 Hyponatremia in cancer patients, is
frequently hypovolemic due to renal loss of
sodium caused by diuretics or salt-wasting
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nephropathy as seen with some
chemotherapeutic agents such as cisplatin.
 Hypernatremia in cancer patients, is caused
by poor intake or GI volume losses, which are
common side effects of chemotherapy.
 Hypokalemia can develop from GI losses
associated with diarrhea caused by radiation
enteritis or chemotherapy, or from villous
adenomas of the colon.
 Hypocalcemia can be seen after removal of a
thyroid or parathyroid tumor or after a central
neck dissection, which can damage the glands.
Acute hypocalcemia can also occur with
hyperphosphatemia because phosphorus
complexes with calcium.
 Hypomagnesemia a side effect of ifosfamide
and cisplatin therapy.
 Hypophosphatemia can be seen in
hyperparathyroidism. Acute
hypophosphatemia can occur as rapidly
proliferating malignant cells take up
phosphorus in acute leukemia.
 Malignancy is the most common cause of
hypercalcemia due to increased bone
resorption or decreased renal excretion.
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ABDUL RAZAKASISTINBISTAYANDEOQUINODETABALIANDOYBILAOEN
DR. MILALYN RUTH DELIZO
AUGUST 11, 2019
 Humoral hypercalcemia of malignancy is a
common cause of hypercalcemia.
 Bisphonates etidronate and pamidronate –
inhibit bone resorption and osteoclastic
activity.
 Calcitonin – effective in inhibiting bone
resorption and increasing renal excretion of
calcium.
 Corticosteroids - may decrease tachyphylaxis
in response to calcitonin and can be used
alone to treat hypercalcemia.
 Gallium nitrates - potent inhibitors of bone
resorption.
 Mithramycin – an antibiotic that blocks
osteoclastic activity, but it can be associated
with liver, renal, and hematologic
abnormalities, which limits its use to the
treatment of Paget’s disease of bone.
 Tumor lysis syndrome – results when the
release of intracellular metabolites
overwhelms the kidney’s excretory capacity.
Most commonly develops during treatment
with chemotherapy or radiotherapy.
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 Surgery 1 DR. MILALYN RUTH DELIZO

FLUID AND ELECTROLYTE MANAGEMENT OF

THE SURGICAL PATIENT
AUGUST 11, 2019

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BATCH 2022 AB
ABDUL RAZAKASISTINBISTAYANDEOQUINODETABALIANDOYBILAOEN