Fluid & Electrolytes

Management

Component & composition of body fluid

Mechanisms of fluid homeostasis
Parenteral fluid therapy
 Body Fluid Compartments:

2/3
ICF:
55%~75%

X 50~70% TBW
lean body weight

3/4 Extravascular
Interstitial
Male (60%) > female (50%) 1/3 fluid
ECF
Most concentrated in skeletal muscle
TBW=0.6xBW Intravascular
ICF=0.4xBW 1/4 plasma
ECF=0.2xBW
Composition of Body Fluids:
Cations Anions
150

100

ECF
Na+
50 Cl-

HCO3-
0
Ca 2+

Mg 2+ Protein
50 PO43-

ICF
K+ Organic
anion

100

150
 Osmolarity = solute/(solute+solvent)
 Osmolality = solute/solvent (290~310mOsm/L)
 Tonicity = effective osmolality
 Plasma osmolility = 2 x (Na) + (Glucose/18) + (Urea/2.8)
 Plasma tonicity = 2 x (Na) + (Glucose/18)
Regulation of Fluids:

Hydrostatic pressure v.s. Oncotic pressure

 Albumin is the major determining oncotic pressure
Regulation of Fluids:
Renal sympathetic nerves
Renin-angiotensin-aldosterone system
ANP / BNP
 Composition of GI Secretions:

Volume
Source Na+* K+ Cl- HCO3-
(ml/24h)
Salivary 1500 (500~2000) 10 (2~10) 26 (20~30) 10 (8~18) 30

Stomach 1500 (100~4000) 60 (9~116) 10 (0~32) 130 (8~154) 0

Duodenum 100~2000 140 5 80 0

Ileum 3000 140 (80~150) 5 (2~8) 104 (43~137) 30
Colon 100-9000 60 30 40 0

Pancreas 100-800 140 (113~185) 5 (3~7) 75 (54~95) 115

Bile 50-800 145 (131~164) 5 (3~12) 100 (89~180) 35

* Average concentration: mmol/L

Parenteral Fluid Therapy:

Crystalloids:
- contain Na as the main osmotically
active particle
- useful for volume expansion (mainly
interstitial space)
- for maintenance infusion
- correction of electrolyte abnormality
Crystalloids:

Isotonic crystalloids
- Lactated Ringer’s, 0.9% NaCl
- only 25% remain intravascularly
Hypertonic saline solutions 3% NaCl
Hypotonic solutions
- D5W, 0.45% NaCl
- less than 10% remain intra-
vascularly, inadequate for fluid
resuscitation
Colloid Solutions:

Contain high molecular weight

substancesdo not readily migrate across
capillary walls
Preparations
- Albumin: 5%, 25%
- Haes-steril 10%
 Common parenteral fluid therapy
Solutions Volumes Na+ K+ Ca2+ Mg2+ Cl- HCO3- Dextrose mOsm/L
ECF 142 4 5 103 27 280-310
Lactated
130 4 3 109 28 273
Ringer’s

0.9% NaCl 154 154 308

0.45%
77 77 154
NaCl

D5W

D5/0.45%
77 77 50 406
NaCl

3% NaCl 513 513 1026

6%
500 154 154 310
Hetastarch
5% 130- 130-
250,500 <2.5 330
Albumin 160 160
25% 130- 130-
20,50,100 <2.5 330
Albumin 160 160
The Influence of Colloid & Crystalloid on
Blood Volume:

Blood volume
Infusion 200 600 1000
volume

1000cc Lactated Ringers

500cc 5% Albumin

500cc 6% Hetastarch

500cc Whole blood

Signs of Hypovolemia:

Diminished skin turgor

Dry oral mucus membrane
Oliguria <500ml/day
- normal: 0.5~1ml/kg/h
Tachycardia
Hypotension
Hypoperfusion  cyanosis
Altered mental status
Clinical Diagnosis of Hypovolemia:

Thorough history taking: poor intake, GI

bleeding…etc
BUN : Creatinine > 20 : 1
BUN↑: hyperalimentation, glucocorticoid
therapy, UGI bleeding
Urine: ↑ specific gravity, FENa < 1%
Increased hematocrit
Electrolytes imbalance
Acid-base disorder (Alkalosis)
Signs of Hypervolemia:

Hypertension
Polyuria
Peripheral edema Especially when
Wet lung hypo-albuminemia

Jugular vein engorgement

Management of Hypervolemia:

Prevention is the best way

Guide fluid therapy with CVP level or
pulmonary wedge pressure
Diuretics
Increase oncotic pressure: FFP or
albumin infusion (may followed by diuretics)
Dialysis
Fluid Management:

Goal:
- to maintain urine output of
0.5~1.0mg/kg/h
Electrolytes require:
- Na+: 1-2mmol/kg/day
- K+: 0.5~1.0mmol/kg/day
Avoid fluid overload, especially in malnutrition,
heart failure and renal insufficiency patient
Fluid Management:

For acute blood loss

- Begin with 2-3L isotonic crystalloid to
restore blood pressure and peripheral perfusion
- Early use of colloid
- Crystalloid + Haes in a ratio of 4:1
- Blood transfusion
- Large borne IV line
Fluid & Electrolytes
Management: Part II
- Homeostasis of Sodium
- Hypernatremia
- Hyponatremia
- Homeostasis of Potassium
- Hyperkalemia
- Hypokalemia
 Homeostasis of Sodium:
60~70% reabsorption 5~10% reabsorption

Filtered
concentration:
142mEq/L
ADH

20~25% reabsorption

Na urine: 20mEq/L
Physiology of Sodium:
Normal individual consumes 3-5g NaCl/day
(50-90mmol of Na+)
Normal concentration: 135~145mmol/L
Potential sources of significant loss include:
sweat, urine, and gastrointestinal secretions
Largely determines the plasma osmolality
Related to the amount of total body water
 a marker of free water balance
Hypernatremia:

Serum Na+>145mEq/L
Hypernatremia:

Etiology:
- loss of fluid with a [Na+] < plasma [Na+]
- gain of a fluid with a [Na+] > plasma [Na+]

Usually hypertonic and typically the result of

water loss in excess of solute
Hypernatremia:
Clinical manifestations - primarily neurogenic:
* lethargy, weakness
* thirst
* hyperpyrexia
* Irritability  fasciculation
* Seizures
* Confusion
* Coma
 Assess ECV
Depleted Expanded

Normal
Hypovolemic Isovolemic Hypervolemic
hypernatremia hypernatremia hyponatremia

Loss of water & sodium Loss of water Gain of water and sodium

Renal Diabetes insipidus Iatrogenic

diuretics Reset osmostat Mineralocorticoid
glycosuria Skin losses excess
urea diuresis Iatrogenic – Hypotonic
ARF or CRF loss with inadequate
Adrenal insufficiency replacement
Extra-renal
partial obstruction
GI loss
Respiratory losses
Skin losses (burns)
Hypernatremia
Hypernatremia:
Treatment:
 Free water deficit (L)
= 0.60 x TBW(kg) x (([Na+]serum/140 )-1)
2. Avoid rapid correction - ½ water deficit should be
corrected over the first 24 hour, and not more than
10mEq/d. the remainder corrected over the
following 2~3 days
Oral replacement is preferable
IVs  D5W, D5 + 0.45%Nacl
Diabetes Insipidus (DI):
large volume of hypotonic urine (Osmourine< 200mOsm/kg)
Hypertonic plasma
CDI (central DI): defect in hypothalamic secretion of ADH
NDI (nephrogenic DI): renal insensitivity to normal ADH
Treatment:
- CDI: add DDAVP
- NDI: remove offending drugs, dietary sodium
restriction + thiazide diuretics.
Hyponatremia
 Serum osmolality

Isotonic Hypertonic
(280~290 mOsm) > 290mOsm
Hypotonic
Measure blood glucose, (< 280 mOsm) Measure blood
lipid and protein glucose
Isotonic hyponatermia Hypertonic hyponatremia
Clinical assess ECV
1. Pseudohyponatremia 1. Hyperglycemia
- hyperlipidemia 2. Hypertonic infusions
- hyperproteinemia - glucose
2. Isotonic infusions - mannitol
- glucose - glycerine
- mannitol 6. TURP
- glycerine
3. TURP

Hyponatremia
Hypovolemic Hypervolemic Isovolemic
Hypotonic Hypotonic Hypotonic
hyponatremia hyponatremia hyponatremia

1. GI losses 1. CHF 1. SIADH

2. Skin losses 2. Cirrhosis 2. Water intoxication
3. Lung losses 3. Nephrotic (↓ Urine osmolality)
4. Third-space losses syndrome • Cortisol deff.
5. Renal losses • K+ defficiency
• Hypothyroidism
• Reset osmostat
Urine Na > 20 Urine Na < 10 • Drugs
- sulfonylureas
- carbamazepine
- antidepressants

Hyponatremia
Hypornatremia:

Clinical manifestations:
- often asymptomatic (if slow until < 120)
- predominant neurologic and result from
hypo-osmolality
* increase intracellular volume  cerebral edema
* lethargy, confusion, nausea, vomiting,
* seizure & coma
* Salivation, lacrimation
Treatment of Hypornatremia:
Slow correction!
up to 2meq/l/h, and not more than 10mEq/day
Hypovolemic: Add 0.9% NaCl to correct volume deficit
Isovolemic:
- correct underlying cause
- water restriction (1000ml/day)
Hypervolemic:
- water restriction (1000ml/day)
- loop diuretics
- optimize cardiac performance in severe CHF patient
- hypertonic saline in severe symptomatic patients
Syndrome of Inappropriate ADH
Secretion (SIADH):
Plasma hypo-osmolality (<290mOsm/L)
Osmo urine > 100~150mOsm/L
Na+ urine > 20mmol/L
Normal adrenal and thyroid function
Normal acid-base balance
Causes:
- pulmonary disorder
- CNS disorder
- drugs
- paraneoplastic syndrome
Treatment of SIADH:
Water restriction (1000mL/day)
If severe hyponatremia ( Na+ < 110mmol/L) 
hypertonic saline (1L of 3% NaCl provide 1026mmol of
Na+); loop diuretics may increase effect
Central Pontine Myelinolysis:
- Goal of correction: 120mmol/L
- Maximal rate 2mEq/h and not more than 10mmol/day
Na+ deficit (mmol) = 0.6 x lean BW (kg) x (120-Na+serum)
Homeostasis & Physiology of K +:
Major intracellular cation, only 2% in the ECF
Normal concentration: 3.3 ~ 4.9mmol/L
Daily ingestion: 50~100mmol
90% renal excretion,
others in the stool
 Causes & Diagnosis of Hyperkalemia:
Pseudohyperkalemia (e.g. hemolysis, Leukocytosis)
cellular shift:
Insulin deficiency
Acidosis (Metabolic, RTA-IV)
Rhambdomyolysis
Cell lysis (after C/T)
Drugs (Digitalis β-adrenergic receptor blockade)
Reperfusion syndrome
Total body overload:
Renal insufficiency
Mineralocorticoid defficiency (Addison’s)
Drugs (K+ sparing, Resprim, Heparin, Ketoconazole)
Clinical Manifestations of
Hyperkalemia:
Mild hyperkalemia (5.0~6.0 mmol/L) is generally
asymptomatic
Primarily cardiovascular (especially > 6.5mmol/L)
Symmetric peaking of T waves, reduced P wave,
widening of QRS complex → Sine-wave, VFib
Treatment of Mild Hyperkalemia
(5.0~6.0mmol/L):

Reduction of daily intake (e.g. banana, orange juice)

Add loop diuretics (e.g. furosemide) to promote
renal elimination
Discontinues drugs that impairing K+ homeostasis
(e.g. nonselective ß blocker, ACE-I, K+-sparing
diuretics, NSAIDs)
Evaluation of Hyperkalemia
TTKG = Kurine * Osmplasma/ Osmurine * Kplasma

TTKG > 10 TTKG < 10

• Decreased EBV
• High K+ intake

↓ Aldosterone ↑Aldosterone

Low renin 1. RTA – IV 1. RTA – I

2. AIDS 2. Severs volume
3. Addison defficiency
N-↑ renin 4. Heparin (Urine Na<15)
5. Ketoconazole
Treatment of Severe Hyperkalemia
(>6.5mmol/L):

Temporizing measures:

0.5g/kg x BW of glucose + 0.3u RI/g of glucose: D20%

6amp or D50% 3amp +6~10u RI
CaCl2 10%: 1amp, i.v. over 2~5minstabilized cell
membranedecrease VF
Inhalated ß agonist: e.g. Ventolin 2~4amp in ½ S 10~20ml
for I.H.
NaHCO3: (1mmol/kg, or 1~2amp of 8.4% NaHCO3), i.v.
over 3~5min, repeat after 10~15min if indicated
Treatment of Severe Hyperkalemia
(>6.5mmol/L):
Therapeutic measures:
Sodium polystyrene sulfonate (Kayexalate):
15~20g in 15~20ml sorbital or lactulose, p.o. or
as retention enema, STAT and keep tid~qid
Hydration: 0.9% NaCl with loop diuretics
Dialysis: for severe, refractory or life-threatening
hyperkalemia
Hypokalemia:
Causes:
- GI loss (e.g. diarrhea, vomiting, persisted NG suction)
- Renal loss (e.g. diuretics, fluid mobilization, Ampho. B)
- Skin loss (e.g. burn)
- Inadequate intake
- Transmembrane shift (e.g. Insulin excess, Alkalosis)
- Drugs (e.g. antibiotics)
- Hypomagnesemia
Clinical Manifestations of
Hypokalemia:
Mild hypokalemia (K+ > 3.0mmol/L) usually asymptomatic
Muscle weakness
Ileus
Primarily cardiovascular
ECG change:
- Ectopy, T-wave depression, and prominent U waves
- Increases susceptibility to reentrant arrhythmias
 Evaluation of Hyporkalemia

Urine K+< 25mEq/d Urine K+>30mEq/d

• GI losses
• Skin losses AB balance
• Prolonged decrease intake
• Cellular shift

Hypertensive
1. Cushing 1. Post TAN 1. RTA I/II
2. Hyperaldosteronism 2. Osmotic diuresis 2. DKA
Normotensive 3. Aggressive diuretics 3. Polydipsia/DI 3. Ampho B
4. Barrter’s /
Gittelman synd
Treatment of Hypokalemia:

For each 1mmol/L decrement  total body

K+ store decrease 200~400mmol/L
Mild: oral replacement (40~100 mmol of KCL
daily, e.g. slow-K 600mg 2# p.o. X3/d)
Parenteral administration: rate < 20mEq/hr
Mg++ supplement - Refractory hypokalemia
should consider hypomagnesaemia
Beware of Digitalis intoxiction!!
Thanks for Your
Attention !!!