Fluid & Electrolytes

Imbalance
Ali Hallal, MD, FRCS
Assistant Professor of Clinical Surgery
AUBMC

Fluids and Electrolytes Imbalance

Common to all medal services.
Frequently encountered
Changes in both occur (pre intra and
post op) as well as in trauma and sepsis

Can be difficult to treat.

Needs monitoring and close follow
up.
Life threatening when severe.

Total Body Water: Weight

/relationship
Fat

Wat
er

Lean tissues and

muscle and solid
organ have the
highest content of
water.
Lower content of
water in female as
opposed to male

Functional Body Fluid Compartments.

Total Body Water =TBW
% TBW
Plasma 5%
Interstitial Fluid
15%

Intracellular
Volume 40%

Volume of
TBW

Male (70 Kg)

(60%) ml

Female (60
Kg) (50%)ml

Plasma

3500

2500

Interstitial

10500

7500

Extracellular
ECF

14000

Intracellular

28000

20000

42000

30000

8%

10000

Body weight %

Total Body Water %

Total

60

100

Intracellular

40

67

Extracellular

20

33

Intravascular

15

25

Interstitial
Transcellular

Chemical Composition of Body Fluid Compartments

153
mEq/L
Cations

153 mEq/L

153
mEq/L

153 mEq/L

Anions

Cations

Anions

200
mEq/L

200 mEq/L

Cations

Anions

K+

15
HPO430
150
SO42-

Na/K
Pump

Na+
H

14
2

Cl-

10
3

HCO3-

27

SO42PO43K+

Ca2

Mg2
+

Na+ 144

K+

Cl-

114

HCO3-

30

SO42PO43-

Organ
ic
acids

Protei
n

16

Ca2

Mg2
+

10

Protei
n

40

Organ
ic
acids

Mg2+

40

Protei
n

Na+

10

HCO3-

Osmotic Activity of Body

Fluids

Osmotic activity = the molar

concentration of the substance
by the number of particles into
which it can freely dissociate in
water . One mole of NaCl
dissociate into Na + Cl and
produce 2 Osm.
The movement of water across
cell membrane depends
primarily on osmosis
Posm=2xNa + Glucose/18 +
Bun/2.8
The osmolality of intracellular
and extracellular fluids is
maintained between 290 and
310 mOsm

Normal Exchange of Fluid and

Electrolytes
The healthy person consumes 2000
ml of H2O/ day (75% liquid, 25%
solid)
Daily water loss (1200 urine, 250
stool 600 insensible loss)
Insensible loss occurs through skin
(75%) and the lungs (25%)
To clear the products of metabolism
the kidney must excrete 500-800 ml/
day

Disturban
ce of Body
Fluid
Volume

Concentrati
on

Compositio
n

Adding NS to ECF will have little effect on ICF but will expand ECF volume
Adding H2O will to ECF will casue water to shift between ECF and ICF and thus
Adding
K+the
willconcentration
affect neitherofvolume
nor concentration
of other solute but will have maj
changing
electrolytes
in compartments
effect on myocardial function

Disturbance in fluid balance

ECF volume deficit is the most
common fluid disorder in surgical
patients.
Signs and symptoms varies
Extent of volume gain or loss
Grade of shock

Acute v/s chronic losses

Cardiovascular neurological
Skin turgor , sunken eyes etc

Extreme of ages.

Signs & Symptoms of Volume Disturbances

System

Volume deficit

Volume gain

Generalized

Weight loss

Weight gain

Decrease skin turgor

Peripheral edema

Tachycardia

Increased CO

Orthostasis

Increased CVP

Collapsed Neck Vein

Distended Neck Vein

Cardiac

Murmur
Renal

Oliguria
Azotemia, urine Na <
20meQ/ L
Urine Osm > Plasma
Osm

GI
Pulmonary

Ileus

Bowel edema
Congestion

Causes of volume excess

Iatrogenic
Renal Dysfunction
Congestive heart failure
Cirrhosis

Signs of Extracellular Fluid Volume

Depletion
10% ECF: 2% wt loss, thirst, U/O less,
Hct mild increase.
20% ECF: 4% wt loss, drowsiness, dry
mucous membranes, HR high,
orthostatic hypotension,
oliguria<30ml/hr, Hct elevated,
specific gravity of urine high, BUN/Cr
> 10:1

Signs of Extracellular Fluid Volume

Depletion
30% ECF: Extreme findings: -6% wt
loss -stupor or coma
pale, cyanotic, cool
eyes sunken
pulse rapid, weak, hypotension
-oliguria advanced: <10-15mL/hr
-Hct high,
ATN, BUN/Cr falls

ECF Depletion in Young vs.

Elderly
Areas affected Young adult <
65 yrs
Vascular volume Postural hypo,
HR,pulse,
CVP,oliguria
Interstitial
Dry skin, MM,
volume
tongue,eyes
miscellaneous
Less DTR,
drowsy, ileus
anorexia, coma

Elderly
patients > 65
y
All affected

All affected
Infection,drugs
depression,
hypothyroid

Volume Change
Osmorecept
or
Thirst

Diuresis or
Water
Retention
(vasopressin)

Barorecepto
rs
Neural (symp
parasympathe
tic)

Hormonal
(ReninAngiotensin,
ADH

Causes of volume deficit in surgical

patients

NG Losses
Vomitting
Diarrhea
Enterocutaneous Fistula
Sequestration
Soft tissue injuries
Burns
Peritonitis
Obstruction

Postoperative bleeding

concentration
changes

Composition of Body Fluids

Volume/2
4hrs

[Na+]

[K+]

[Cl-]

[HCO3]

135150

3.5-5

98-106

22-30

10002000

10-150

4-12

120160

Bile

300-800

120170

3-12

80-120

30-40

Pancreas

600-800

135150

3.5-5

60-100

35-110

20003000

80-150

2-8

70-130

20-40

50-100

10-30

80-120

25-30

30-50

30-50

Plasma
Stomach

S.Intestine
Colon
Perspiratio

Maintenance
electrolyte

Maintenance fluid

Fluid Order
Correction for
electrolyte
disturbances

Correction for fluid

deficit

Fluid and Electrolytes Daily

Maintenance
Calculated by
Surface area
fluid

1500mL/m2

sodium

50-75mEq/m2

potassium

50mEq/m2

chloride

50-75mEq/m2

Calculated
by body
weight
Children

1st
10kg:100mL/k
g

2d
>20kg:
10kg:50mL/kg 20mL/kg

Adults

2555yr:35mL/kg

5565yr:30mL/kg

Sodium

1.0-1.5 mEq/kg

>65yr:25mL/k
g

Electrolyte Composition (mEq/L)

HCO

Solution

Na

Cl

ECF

14
2

10
3

LR

13
0

10
9

0.9% NaCl

15
4

15
4

308

D5 0.45% NaCl

77

77

407

253

51
3

51
3

1026

D5W
3% NaCl

Ca

Mg

mOsm

27

280310

28

273

Osmolality / Tonicity
Osmolality

Tonicity

The concentration of
osmotically active
particles in Solution

Effect of the particle

on cell Volume

Permeant solute that

can freely cross across
cell membrane
Permeant solute
contribute to osmolality
but they do not
contribute to tonicity
Urea,ethanol

Impermeant solute that

cannot freely cross cell
membranes
Impermeant solute
contribute to oncotic
pressure across cell
membrane as well as
alteration in cell volume
Na

Osmolality / Tonicity
Both impermeant and permeant
solute can contribute to
hyperosmolar or hyoposmolar state.
However hypososmolar states are
always accompanied by hypotonicity,
whereas hypersomolar state are not
always associated with hypertonicity

URE
A
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A

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A
H

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A

H
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O
H

URE
A

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A

Pseudohyponatremia 2ry to hyperglycemia from DM

Hyponatremia

Sodium
Na+ is main cation of ECF
Always coupled to water
Normal serum [Na+] = 135 145
mEq/L

Hyponatremia - Causes
Common surgical causes include
most
common
PREVENTAB
LE

Iatrogenic
SIADH: closed head injury(CHI),
post bleeding
GI obstruction
GI fistulae
Acute gastric dilatation
Severe protracted diarrhea
Acute pancreatitis. Peritonitis.
Pleural effusion

post craniotomy,
R/O
hypothyroidism
and adrenal
insufficiency,
since they mimic
SIADH

Symptoms and Signs

Dependent on the
degree (120)and the
rapidity of
Hyponatremia .
Clinical manifestations
primarily have a
central nervous
system origin and a re
related to water
intoxication and
associated increase in
ICP

Differentiating the
cause of
hyponatremia can
be difficult

1. Exclude hyperosmolar
hyponatremia
(hyperglycemia, mannitol
contrast agent) ,
pseudohyponatremia.
2. Make a decision
1.
2.

Low Volume
High volume

3. Low Volume
1.

GI losses
(Urine Na < 20 mEq/L)

2.

Renal Losses
(Urine Na > 20 mEq/ L)

4.

High volume
1.

SIADH

Hyponatremia correction
Na should not exceed 8-12
mEq / day (actual Na 120; then
maximum correction till 132)
The rate of correction should
be 0.5-1 mEq/L(body
weight)/hour
Na required= (desired Naactual Na ) x TBW
Choose the correcting Solution
and calculate the
corresponding volume for the
Na required.
Administer either based on
rate if symptomatic or based
maximal allowed correction

Na =120
Correct to Na=130
70 Kg male ; TBW =42 L
Na that need to added =42
x10 meQ =420
3% solution 513 meQ Na/liter
420/513 = 818 cc of 35
NaCl / 24 hrs
818 cc / 24 = 34 cc / hour
The rate allowed
1mEq/L/Hr=42 mEq/hr
(42 /513 ) X 1000= 81 cc
/hour

Hyponatremia Management

What rate of infusion must be

followed?
Rapid development of hyponatremia
Rapid correction <
1mEq/L/hr
Slow time of development

Na =125 mEq

Slow correction <0.5 mEq/L/hr

Hyponatremia Management
Common Infusates
Infusate
5% NaCl in water
3% NaCl in water
0.9% NaCl in water
Ringers lactate solution
0.45% NaCl in water
0.2% NaCl in 5% dextrose in water
5 % dextrose in water

[Na+] mmol/L
855
513
154
130
77
34
0

Hyponatremia - CPM
Central Pontine Myolinolysis or Osmotic
Demyelination
10% extra-pontine: mid brain, thalamus, basal
nuclei, and cerebellum
Proposed mechanisms:
1- osmotic injury to vascular endothelial cells
and release of myelinotoxic factors (vasogenic
edema)
2- brain dehydration resulting in seperation of
the axon from myelin sheath

CPM Typical case

Chronic hyponatremia > 48 hrs
Rapid aggressive correction and
improved mental status of patient
48 72 hrs post Rx, patient suffers
from confusion, gaze paralysis,
spastic quadriplegia & seizures
MRI detects the diagnosis

Central Pontine Myolinolysis-CPM

T2-weighted MRI
scan of the brain

Hyponatremia - CPM

CPM is unlikely to occur following

rapid correction of acute
hyponatremia
Lohr, Am J Med (1994), vol 96 :
HYPOKALEMIA predisposes patients
to CPM following correction of
hyponatremia
Correct
hypokalemia PRIOR to correction of Na
in neurologically stable patient

Hyponatremia Management
Hourly monitoring of the patients
electrolytes is essential
SIADH can be treated with water
restriction (800 ml/day), loop
diuretics, or 600 1200 mg qd
Demeclocycline (V2 receptor
antagonist)

Hypernatremia

Hypernatremia
Clinical conditions associated with
predominant water loss include:
Burns

Diabetes mellitus (uncontrolled)

Intracranial trauma

Water deprivation

Tracheostomy

Sunstroke

Hyperventilation

Hypercalcemia

Fever

Hypocalcemia

Diabetes insipidus

Hypophosphatemia

Hypernatremia
People at most risk are:
-the intubated
-the elderly
-patients with altered mental status
Since their thirst or access to water is impaired

Signs & Symptoms

Hypernatremia Management
What solutions must be used?
- Select the most hypotonic infusate
appropriate so as to use the least
amount of fluid.
- The more hypotonic the infusate is,
the lower the infusion rate required

Hypernatremia Management
Commonly used infusates
Infusate
Free Water
5% dextrose in water
0.2% NaCl in 5% dextrose in water
0.45% NaCl in water ( NSS)
Ringers lactate
0.9% NaCl in water (NSS)

[Na+] mmol/L
0
0
34
77
130
154

Avoid hyperglycemia when using dextrose solution,

because it would aggravate the hypertonicity

Hypernatremia Management
Reassess blood electrolyte at intervals of
at least 6 to 8 hrs
Treat DI with desmopressin (ADH analog)
Correct hypernatremia due to hypertonic
Na+ gain with both furosemide and water
Renal failure => hemodialysis,
hemofiltration, peritoneal dialysis

Hypokalemia

Hypokalemia

K+ is the main cation in ICF

Normal [K+] = 3.5 5.0 mEq/L
Intake = 40 120 mEq/day
Excretion
80% by kidneys
15% by GI
5% by sweat

Signs and Symptoms

 EKG changes do
not correlate with
hypokalemia
Flattened /
inversion of T wave
Prominent U wave
ST segment
depression
Prolongation of QT
interval

Hypokalemia - Causes
Hypomagnesemia
Delays the correction
Associated with increased frequency of
arrhythmias
Mg is the co-factor of Na/K ATPase

Hypokalemia
K level

Serum K in
mEq/L

EKG changes
and arrhythmias

Estimate of K
deficit in mEq

Mild

3.5-3.0

None or
minimal

100-200

Moderate

3.0-2.5

Yes, variable

Severe

2.5-2.0

Yes, dangerous

200- 400
400-800 or
more

With severe hypokalemia, K+ loss from the cells keeps serum K at or above 2.0 mEq/L.

Hypokalemia
Management:
K+ level = 4 to 3.0 mEq/L
-fresh fruit, vegetables, meat
-K+ replacement not necessary

Hypokalemia
Management:
K+ level < 3.0

Potassium replacement is
necessary

Hypokalemia - Management
What salts should be used?
Potassium chloride Salt of choice, esp. with Cl- depletion

Potassium phosphate Preferred if phosphate is depleted

Potassium
bicarbonate
(or precursor)

Used if metabolic acidosis

is present

Hypokalemia - Management
Through what route must the salt be
administered?
-Oral, except in emergencies or if oral
route is not feasible => IV

Hypokalemia - Management
Oral route:
Risk of ulceration and GI bleeding
Dose = 20 60 mEq, 2- 4 times/day
Must be monitored with daily K+
measurements
If serum K+ does not rise by

96

hours => Mg depletion

If Mg< 1.0 mEq/L => 2 ml 50% MgSO4 IM bid 1st day,

bid 2nd day, and qd 3rd day.

Hypokalemia - Management
IV:
-Peripheral vein

-Central vein

For maintenance of daily

requirements
Infusate concentration
=
20 40 mEq/L
Maximum= 60 mEq/L
For moderate and
severe
hypokalemia
Maximum rate 40
mEq/hr

Hypokalemia - Management
What solutions must be used for the
correction?
- Quarter or half NSS
Dextrose induces insulin response that drives K+ into cells

Add 40 mEq/L to D5W to prevent the drop in serum K+

Hypokalemia - Management
In what rate must the solutions be
infused?
- Usual maximum rate = 1020
mEq/hr
- 40 mEq/hr can be used for only 2-3
Higher rates predispose the patient to
hrs
hyperkalemia and cardiac arrhythmias
Monitor serum K+ every 2-4 hrs and
ensure adequate urine output

Hypokalemia - Management
K+ sparing drugs:
1- spironolactone
2- triamterene
3- amiloride
If used, normal renal function must be ensured

Hypokalemia - Management
Metabolic alkalosis must be corrected
if present along with the
hypokalemia, especially if serum K+
< 2.5 mEq/L
Dehydration must also managed,
since further stress would aggravate
the hypokalemia.

Hyperkalemia

Etiology

Drugs that can cause

Hyperkalemia
Family of agents

Individual drugs

K-sparing

Spironolactone,Triamterene,
Amiloride

ACE inhibitors

Captopril,
Fosinopril

NSAIDS

Indomethacin,
Ketorolac

Anti-infective

Trimethoprimsulfamethoxazole
(Bactrim), Pentamidine

Anticoagulant

Heparin

Cardiac glycoside

Digitalis

Antihypertensives

-blockers, and
blockers (labetolol)

Enalapril,
Ibuprofen,

Hyperkalemia - Causes
Heparin:
Unfractionated native

Cause reversible Aldosterone

production inhibition =>
hyperkalemia in 7 to 8 %

LMWH
Heparinoids

You should rule out heparin-induced adrenal

hemorrhage by cortisol level and CT

Signs and Symptoms

EKG changes
ECG changes do
not correlates
closely with K
levels.
Peaked T wave
Prolonged Pr and
QRS
AV conduction
delay
Sine wave that
might terminate in

Treatment of Hyperkalemia

Is hyperkalemia associated with physiologic

effect such as cardiac arrhythmias ??

Treatment of Hyperkalemia

Treatment of Hyperkalemia

Treatment of Hyperkalemia
Drug

Dose

Onset of Action

Calcium gluconate

10-30 ml of 10% solution Few minutes

at 2 ml/min over 2 3 min

NaHCO3

44-132 mEq

Glucose and insulin

Glucose: 25-50 gm/hr by 15-30 min

continuous IV drip; regular
insulin: 5U IV q 15 min

Albuterol

IV: 0.5 mg in 100 ml D5W 20 30 min

over 10 15 min
30 min
Nebulized: 20 mg in 4 ml
NSS over 10 min

Kayexalate

Enema (50 100 gm)

Oral (40 gm)

4 hours

60 min
120 min

Hyperkalemia- Mnemonic
C alcium
B icarbonate
I nsulin
G lucose
K ayexalate
D ialysis

See Big Potassium Drop

Hypochloremia
Respiratory acidosis: tubular
resorption of bicarbonate and less Cl Causes: loss of gastric acid by
vomiting or NG, renal losses from
diuretics, ARF and CRF non-oliguric
Important to correct deficit with
other deficits like hypochloremic
hypokalemic metabolic acidosis

Hyperchloremia
Uncommon in surgical patients
In association with hypernatremia, in
RTA, excess KCL intake or ammonium
chloride.
Ileal urinary conduits,
ureterosigmoidostomy. Mucosa
absorbs Cl- in exchange of Bicarb.

Calcium
40% of Ca++ in ECF bound to proteins,
10% complex with bicarb, citrate, and
phosphate
50% ionized, hormonally regulated are
active. Neuromuscular activity
8.5-11.0 Nl, ionized: 4.75-5.3.Most are
bound to Albumin. PTH regulated
Corrected total Ca++ = [ 0.8 x (4- alb)] +
total serum Ca++

Hypocalcemia

Artifactual : low Albumin

Acute pancreatitis
Surgically induced
Necrotizing fasciitis
Inadequate intestinal absorption
Fistulae with excessive losses
Chronic diarrhea
Renal insufficiency
Low Mg++, high PO4--

Hypocalcemia
Circumoral tingling, numbness
fingertips cramps
Hyperactive DTRs, Chvostek sign,
tetany and Trousseaus sign. Seizures
.
Confused or Depressed. Prolonged QT
Calcium gluconate or chloride IV
Oral calcium lactate. Vitamin D.
Thiazide diuretics

Hypercalcemia - Causes

Hyperparathroidism
Malignancy
Granulomatous disease
Excessive dietary intake
Thiazide Diuretics
Immobilization
Endocrine: thyrotoxicosis, adrenal
insuf.

Hypercalcemia - Treatment

Calcium intake restricted

Hydration
Loop diuretics
Oral or IV Phosphate supplements
Corticosteroids
Plicamycin (mithramycin), DNAbinding antibiotic

Hypomagnesemia
Low Mg++: common with starvation, GI
losses, alcoholism and Drugs.
Accompanied with low K+, PO4 and low
Ca++
Neuromuscular problems: cramps,
fasciculations, tetany,confusion and
arrythmias.
Oral or IV magnesium sulfate.
1-2 mEq/kg/day

Hypermagnesemia
Renal failure
Crush injury, burns: rhabdomyolysis
Dehydration, acidosis, adrenal insuff.,
cathartics, eclampsia and antacids
Nausea, weakness, hypoventilation,
decreased DTRs. Then hypotension,
bradycardia, paralysis, respiratory dep.
And coma
Rx: hydration, IV calcium, diuretics,
dialysis

Phosphorus
Phosphorus is important in energy
production during glycolisis
The level is tightly controlled by renal
excretion

Hypophosphatemia
Etiology
Inadequate uptake
increased renal
excretion or
compartmental shifts
as result of insulin
release, resp.
alkalosis, alcoholism,
burns ,
parathyroidectomy
Treatment of DKA
Refeeding syndrome

Effect
Platelet aggregation
Impaired WBC
chemotaxis and
phagocytosis
Impairs 02 release to
tissue due to decrease
in 2-3 DPG
Cardiac dysfunction
Bone pain, anorexia
Tremors

Hypophosphatemia
Treatment
Adequate nutrition
Correction depends on the level of
depletion and tolerance to oral
supplementation

Hypophosphatemia
PO4 < 1 md/dL
Tolerating enteral nutrition
KPHO4 or NaPO4
0.25mmol/kg over 6hrs x1
dose
Not tolerating enteral
nutrition
KPHO4 or NaPO4 0.25
mmole/kg IV x 1dose .
Recheck level
0.15mmole/kg if PO4 <
2.5mg/dL

PO4 level 1.0-2.5

mg/dl
Tolerating enteral
nutrition
Neutra-Phos 2 pack Q
6hrs per NG
Not tolerating enteral
nutrition
KPHO4 or NaPO4
0.15mmole/kg IV

Hyperphosphatemia
Etiology
Low renal excretion, increased GI absorption or
iatrogenic
Hyperthyroidism or Hyperparathyroidism
Clinical condition associated with cell destruction
Rhabdomyolisis
Tumor lysis syndrome
Hemolysis
Sepsis
Severe hypothermia
Malignant hyperthermia

Excessive PO4 administration in hyperalimentation

Hyperphosphatemia
Treatment:
Aluminum-based antacids, diuretics
Calcium acetate tablet when
hypocalcemia is present
Hemodialysis

Conclusion
Proper management of fluid and electrolytes
facilitates crucial homeostasis that allows
cardiovascular perfusion, organ system function
and cellular mechanism to respond to surgical
illness
Knowledge of the compartmentalization of body fluid
forms the basis for understanding pathologic shifts
in theses fluid spaces in disease states. Although
difficult to quantify a deficiency in the functional
ECF fluid compartment often requires resuscitation
with isotonic fluids in surgical and trauma patients.

Conclusion
Alteration in the concentration of
serum Na have profound effects on
cellular function due to water shifts
between intracellular and extracellular
spaces

Questions?
Thank you