Surgery 1.

Fluid and Electrolyte Management of the Surgical Patient

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

I.

IMPORTANCE TO SURGICAL PATIENT

(from 2014-A Trans)
Fluid volume and electrolyte changes can occur:
Preoperatively
Intraoperatively
Postoperatively
In response to trauma
In response to sepsis
II. TOTAL BODY WATER AND FLUID COMPARTMENTS
Total Body Water (TBW):
o Intracellular Volume (ICV):

Red Cell Volume (2-3% of TBW)

Others
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

November 8, 2012
Dr. Rafael Azares

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.
III. COMPOSITION OF FLUID COMPARTMENTS

o Extracellular Volume (ECV):

Plasma (5% of TBW)
Interstitial Fluid (15% of TBW)
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

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

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Figure 2. Normal chemical composition of the body fluid

compartments

Page 1 of 7

IV. Body Fluid Changes

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
The
concentration
between
distributed
evenly gradient
throughout
the fluid compartments
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,
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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).

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 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.
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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

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HypervolemicHypoNa: water restriction, with or without loop

diuretics
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.

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

Page 4 of 7

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 <20 mEq/L
Urine osmolarity is <300 to 400 mOsm/L]
[Symptoms occur only in patients with impaired thirst or restricted
access to fluid and only if serum Na+ concentration exceeds 160
mEq/L
o CNS effects predominate (restlessness and irritability, to seizures,
coma, and death)
[Classic signs of hypovolemichypernatremia = tachycardia,
orthostasis, and hypotension]

VI. COMPOSITION CHANGES

Potassium Abnormalities (3.5 to 5meq/L)
A. HYPOKALEMIA
Serum K:<3 mEq/L
Most often the result of abnormal losses (diarrhea, GI fistula,
urinary losses, acidosis), and not of inadequate intake
Often accompanied by HYPOMAGNESEMIA, thus correction of
magnesium is essential
IV potassium replacement should be performed slowly, with
concentrations not exceeding >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

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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 ischemiareperfusion 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).
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), angiotensinconverting 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).

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:

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 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:<8.5mg/dL, or ionized level < 4.5mg/dL
Causes include intracellular shifts caused by infusion of large
volumes of resuscitation fluids, magnesium depletion,
pancreatitis, post-thyroid/ parathyroid surgery
Also, from rapid transfusion of blood products due to the citrate
load (CHELATION)
Clinical manifestations of HYPOCALCEMIA:
o ECG changes: prolonged QT interval, T-wave inversion, heart
block, and ventricular fibrillation
System
HYPOCalcemia
GI
Neuromuscular Hyperactive reflexes (Chvosteks and trousseaus sign),
paresthesia, carpopedal spasm, seizures
CV
Heart Failure
Treatment:
o Aimed at treating the underlying cause
o Replacement should be given to symptomatic patients, and
those with serum Ca <7mg/dL, or ionized Ca <3mg/dL
o Ca gluconate- contains 9mg of elemental Ca per mL
o Ca chloride- contains 27mg/mL
o All patients should have ECG monitoring, as bradycardia and
hypotension are relatively common sequelae
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

B) HYPERCALCEMIA
Ca > 10.4mg/dL or ionized Ca > 5.6mg/dL
In hospitalized patients, MALIGNANCIES account for most cases
In general population, HYPERPARATHYROIDISM and MALIGNANCY
together comprise >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

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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.
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

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 preeclampsia
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

Page 6 of 7

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.

Phosphorus Abnormalities (2.4 to 4.1mg/dl)

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
A)

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.

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
th
Schwartzs Principle of Surgery 9 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

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