FLUID AND ELECTROLYTES

by

Maj Saurabh Khare

SLC Hari J P

GUIDE
Gp Capt Manoj Kumar
Objectives

• Understand daily fluid and electrolyte

requirements for an average adult

• Understand the major components of

replacement fluid

• Maintenance vs. Resuscitation

• Complications of fluid therapy

Fluid Compartments of the Body
Total Body Water (TBW)
Varies with age and gender

60% body weight in males

55% body weight in females
80% body weight in infants

Less in obese: fat contains little water

 Body Fluid Compartments:
2/3
ICF:
55%~75%

X 50~70% TBW
lean body weight

3/4 Extravascular
Interstitial
 Male (60%) > female (55%)
 Most concentrated in skeletal muscle 1/3 fluid
 TBW=0.6xBW ECF
 ICF=0.4xBW
 ECF=0.2xBW

Intravascular
1/4 plasma
 Composition of Body Fluids:
150
Cations Anions

100

ECF
Na+
50
Cl-

0 HCO3-
Ca 2+
Mg 2+
Protein
50 PO43-

ICF
Organic
K+
anion
100

150
 Movement of fluids
Fluid compartments are separated by membranes
that are freely permeable to water.
Movement of fluids:
Starling Forces:
 Capillary filtration (hydrostatic) pressure(Pc)
 Capillary colloid osmotic pressure

 Interstitial hydrostatic pressure

 Tissue colloid osmotic pressure

 Water Input and Output of the “Normal” Adult
• Minimal Obligatory Daily Water input:
– Ingested water: 500mL
– Water content in food: 800mL
– Water from oxidation : 300mL

TOTAL: 1600mL
• Minimal Obligatory Daily water output:
Urine: 500mL
Skin: 500mL
Respiratory tract: 400mL
Stool: 200mL

TOTAL: 1600mL
→ Average adult input/output is 30-35mL/kg/day (2.4L/day)
Regulation of Water and Solute Loss

Under normal conditions, fluid intake and output

is adjusted by
Antidiuretic hormone (ADH)
Atrial natriuretic peptide (ANP)
Aldosterone
12
water requirements increase with:
fever, sweating, burns, tachypnea, surgical
drains, polyuria, or ongoing significant
gastrointestinal losses.
For example, water requirements increase by 100
to 150 mL/day for each C degree of body
temperature elevation.
Daily Electrolyte Requirement
• - Sodium: 100-250meq
– mostly excreted in urine

• - Potassium: 50-100meq
– mostly excreted in urine, 5% in feces

• - Chloride: 60-150meq
– Example: 1/2NS @ 100cc/hr provides ~180mEq of sodium and chloride/day!
- this is why NS should not be used for maintenance fluid in patients
with normal renal function- risk of hyperchloremic metabolic acidosis

• - Bicarb: 1 meq/kg/day
History
Intravenous fluid was first used in 1830’s for treatment of fluid
loss due to cholera.
In1882, Hartog Jakob Hamburger, in his vitro studies of red
cell lysis sugested that 0.9% is concentration of salt in human
blood.
In 1883, Sydney Ringer, through his experiments on hearts cut
out of frogs, found the importance of trace elements in the
blood for effective function of the heart.
In 1924, Rudolph Matas, introduced the concept of continued
IV drip.
In 1932, Alexis Hartmann, modified the ringers solution by
adding sodium lactate.
Index
Aims and indications

Classification of IV fluids

Fluid management
Aims of Fluid Therapy
Correction of shock and establish proper tissue
perfusion
Correct fluid deficit
To provide maintenance requirement of fluid and
electrolyte.
Proper selection of fluid so as to correct electrolyte
and acid base disorders simultaneously
Indications
Coma, anaesthesia, Severe vomiting and diarrhoea.
Dehydration and shock
Hypoglycemia
Vehicle for – antibiotics, chemotherapy agents
Total parenteral nutrition.
Critical problems – anaphylaxis, status asthmaticus or
epilepticus, cardiac arrest , forced diuresis in drug
overdose, poisoning.
Classification
 Maintenance fluids
 Replace insensible loses.
 Replacement fluids
 Correct body fluid deficit after gastric drainage,
vomiting, diarrhoea, infection , trauma, burns.
 Special fluids :
 Hypoglycemia – 25 % dextrose
 Hypokalemia – Inj KCl
 Metabolic acidosis – Inj soda bicarb
Fluids
Crystalloids
Electrolyte solutions with small molecules that can
diffuse freely throughout the extracellular space

Colloids
They contain large, poorly diffusible, solute molecules
that create an osmotic pressure to keep water in the
vascular space.
Crystalloids
 Isotonic saline(0.9 % NS)
 Provide major extracellular electrolytes..
 Corrects both water and electrolyte deficit.
 Increase the iv volume substantially
Indicated in hypovolumic shock, alkalosis with
dehydration, hyponatremia
 Contra indications
Avoid in patients with CHF, renal disease and cirrhosis
Large volume may lead to hyperchloremic acidosis.
5 % dextrose
One liter fluid contains 50 gms glucose
Provides 170 kcal/L
After consumption of glucose water is distributed in
all compartments proportionately therefore it is best
agent to correct intracellular dehydration.
5 % dextrose
 Indications :
 Prevention and treatment of dehydration
 Pre and post op fluid replacement
 IV administration of various drugs
 Prevention of ketosis in starvation, vomiting, diarrhea
Correction of hypernatremia
5 % dextrose
 Contra indications
 Cerebral edema, neuro surgical procedures
 Acute ischaemic stroke
 Hypovolemic shock
 Hyponatremia , water intoxication
Uncontrolled DM , severe hyperglycemia
 Ringer’s lactate
• Most physiological fluid.
• Rapidly expands iv volume.
• Lactate metabolised in liver to bicarbonate useful in
correction of metabolic acidosis.
• Acetate instead of lactate advantageous in severe
shock.
Ringer’s lactate
 Indications
Correction in severe hypovolemia
Replacing fluid in post op patients, burns
Fluid of choice in diarrhoea induced dehydration in
paediatrics
DKA , provides water, correct metabolic acidosis and
supplies potassium
Maintaining normal ECF fluid and electrolyte balance
during and after surgery
Ringer’s lactate
Contraindications
- liver disease
- Addison’s disease
- Metabolic alkalosis
- Along with blood transfusion as calcium in RL binds
with citrate anticoagulant which inactivate
anticoagulant and promote formation of clots in
donor blood.
Isolyte G- gastric replacement solution, Ammonium
ions in solution converted to urea and hydrogen by
liver which corrects metabolic alkalosis.
Isolate-M- richest source of potassium .
Hypertonic saline
Includes 3%, 7.5 % and 23.4 % saline.
Uses
 Alternative to mannitol for treating raised intracranial
pressure in traumatic brain injury.
Treating severe and symptomatic hyponatremia.
Cerebral oedema complicating paediatric diabetic
ketoacidosis
Not recommended for hypovolaemic resuscitation.
Review article: hypertonic saline use in the emergency department. Emerg Med
Australas. 2008 Aug;20(4):294-305.Banks CJ et al
 Effects of large volume crystalloid infusion
 Extravascular accumulation of fluid in skin, connective
tissue and lungs.
 Inhibition of GI motility
 Delayed healing of anastomosis
 Large volume ,rapid infusion crystalloids causes
hypercoagulability. Due to reduction in Antithrombin -3

Ruttmann TG, James MF. Effects on coagulation due to intravenous crystalloid

or colloid in patients undergoing vascular surgery.
Br J Anesth 2002 ; 89 : 999 - 1003
Comparison of Colloids
Fluid Average Oncotic Duration of
Molecular Pressure effect
Weight (mmHg)
25% Albumin 69 70 16 Hr

10% Dextran 40 40 6 Hr
-40
6% Hetastarch 450 30 24 Hr

5% Albumin 69 20 16 Hr
 Albumin
Heat treated preparation of albumin – 5%, 20% and
25% commercially available
Rate of infusion :
• Adults – initial infusion of 25 gm
• 1 to 2 ml/min – 5% albumin
• 1 ml/min - 25% albumin
Albumin
 Indications :
Plasma volume expansion in acute hypovolemic shock,
burns, severe hypo albuminemia
Hypo proteinemia – liver disease, Diuretic resistant
nephrotic syndrome
In therapeutic plasmapheresis , as an exchange fluid

 Contra indications :
 Severe anaemia, cardiac failure
 Hypersensitive reaction
 Dextran
Glucose polymers produced by bacteria(Leucohostoc mesenteroides)
 Dextran 70(6%) and Dextran 40 (10%)
 Expand iv volume but short duration of action due to rapid renal
excretion.
 Dose: In shock – 500 ml bolus; not to exceed 20 ml/kg.
 Indications :
 Hypovolemia correction
 Prophylaxis of DVT and post operative thromboembolism
 Improves blood flow and micro circulation in threatened vascular
gangrene
 Hydroxyethyl starch (Hetastarch)
• Composed of esterified amylopectine (6%)
• Osmolality – 310 mosm/L
• Advantages :
 Non antigenic
 Does not interfere with blood grouping
 Greater plasma volume expansion.
 Action last for 24 hrs.
Side effects
 Increase in S amylase concentration upto 5 days after discontinuation
 Affects coagulation by prolonging PTT, PT and bleeding time by
lowering fibrinogen
 Decrease platelet aggregation , VWF , factor VIII
Dose: Not to exceed 20 ml/kg
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

Colloids vs crystalloids
No significant difference in 28 days mortality.

 Effects of Fluid Resuscitation With Colloids vs Crystalloids on Mortality in Critically Ill Patients
Presenting With Hypovolemic Shock: The CRISTAL Randomized Trial. JAMA. 2013 Nov
6;310(17):1809-17 Annane D et al

There is no evidence from RCTs that resuscitation with

colloids, instead of crystalloids, reduces the risk of death
in patients with trauma, burns or following surgery.

 Colloids versus crystalloids for fluid resuscitation in critically ill patients (Review) Perel P,
Roberts I, Pearson M
Where is my bolus going?
1L D5W distributed into Total Body Water

Free water ICF ECF Interstitial Intravascular Interstiti Intra-

content
al vascula
D5W 1000cc 660cc 340cc 226cc 114cc (11%) r
½ NS 500cc 500cc 500 330cc 170cc + 55cc
+ 55cc from =225cc (22%) 226cc 114cc!!
free water content
NS 0 0 1000cc 660cc 330cc (33%)

Normal saline has no free water and is confined

to ECF space; this is why it is the preferred IVF for
resuscitation!
Steps of fluid therapy
Step 1 – Assesment

Step 2 – Selection of Intravenous Fluid

Step 3 – Determine rate of Fluid Administration

Flow guided Fluid Therapy
Clinical evaluation of hypovolemia:
- Mild: volume loss( < 2 liters) -thirst, concentrated urine
- Moderate volume loss (2 to 3 liters) -above +
dizziness+ oliguria <400 ml/day, postural hypotension
- Severe volume loss( >3liters) –above + confusion, BP<100
mmHg , tachycardia, cold extremities.
- Aim of fluid therapy is to induce positive fluid balance =
50 to 100 ml + urine output + ongoing loss
Pre-op
Elective Emergency
Patients without disorder of Pulse rate, respiratory rate,
gastric emptying undergoing arterial pressure, urine
elective surgery do not output, capillary refill time.
withhold fluids for more than
increasing base deficit or
2 hours.
Preop administration of increased plasma lactate
carbohydrate rich fluids 2-3 concentration on ABG
hrs prior to induction of Resuscitation with balanced
anesthesia. crystalloids.
Patients undergoing bowel
prep should receive iv fluids
like RL
British Consensus Guidelines on Intravenous fluid therapy for Adult surgical
patients
Intra-op
Vasodilatory effects of anaesthesia, blood loss, the
hormonal response to surgery, increased capillary
permeability and albumin escape rate and
increased insensible losses.
Intravenous fluid to achieve an optimal value of
stroke volume during and for the first eight hours
after surgery.

British Consensus Guidelines on Intravenous fluid therapy for Adult surgical

patients
Post-op
Depends upon clinical judgement
AIM: BP >100/70; P <120; UO- 30- 50 ml/hr
Patients who are euvolaemic and haemodynamically
stable a return to oral fluid administration should be
achieved as soon as possible.
Daily maintenance and replacement of any on-going
additional losses

British Consensus Guidelines on Intravenous fluid therapy for Adult surgical

patients
Resuscitation Fluid Therapy
Pre-Op Fluid Therapy
Intra-Op fluid Management
Post Op Fluid management
 Thank you
ELECTROLYTES
 Sodium
Major ECF cation
85-90% extracellular
ECF : 135-145 mEq/l, ICF : 25 mEq/l
Responsible for more than 90% of total osmolality
ECF volume is reflection of TBS
Major function : maintain ECF vol & maintain BP
Daily requirement : 1-2 mEq/kg
 Sodium
Physiology of sodium deficit
decreased Na→ hypovolemia→ angiotensin II and
aldosterone → increase Na absorption
• Renal priority : Na > H > K

• Physiology of sodium excess

increased Na→ increased ECF vol→ decreased
angiotensin II and aldosterone/ increased ANP→
decreased renal absorption and increased excretion
• Hyponatremia
Sodium

– hyponatremia ≠ sodium deficit

– hyponatremia ₌ water retention
 Clinical features
Due to cellular swelling
Severity of symptoms depends upon severity and rate
of hyponatremia
Headache, nausea, vomiting, cramps, weakness,
confusion, ataxia, diminished reflexes, convulsions,
coma, death
 Management
Dictum : rapidly developing to be treated rapidly and
slowly to be corrected slowly

Goals :
to raise serum Na at a safe rate
to replace deficit
to correct underlying etiology
Management
 Management
Na deficit (mEq)=([Na]goal- [Na]plasma) X
TBW(Body wt X60%)
Hyper Tonic Saline – 3% infusion (513 mEq/L)

Normal saline – 0.9% infusion (154 mEq/L)

Max rise of 0.5-1 mEq/ml/hr to avoid demyelinating

encephalopathies (CMD)

Plasma Na > 120 mEq/ml Oral Salt 5 g TDS

• Hypernatremia Sodium
– Loss of free water (usually) or gain of sodium
• Iatrogenic administration of sodium-rich fluids
• Mineralocorticoid excess (hyperaldosteronism, Cushing’s syndrome)
• Hypotonic skin losses from fever or tracheostomies during
hyperventilation
• Heat exposure, burns, exercise, mech ventilator
• Renal loss : DI, diuretics
• GI loss : osmotic diarrhoea
• Impaired thirst : comatosed

• Ataxia, tonic spasms, delirium, weakness, tachycardia,

hypotension, syncope, red swollen tongue, decreased
saliva/tears, fever
Management

WATER
 Management
Treat with hypotonic fluids orally,enterally or
parenterally. (Oral water sufficient in mild cases)

ORS may be appropriate in the presence of diarrhoea.

Water deficit = [(plasma Na – 140)/140] x 0.6 x BW (kgs)

Water deficit + ongoing loss

Watch out for cerebral oedema ( initial improvement foll.

by deterioration)
 Potassium
Major intracellular cation
98% is intracellular
Serum : 3.5-4.5 mEq/L
Intracellular : 150 mEq/L
Normal requirement : 1 mEq/kg/day
Role : cellular function & neuromuscular
transmission
 Potassium
Physiology :
- Regulation through renal excretion
- All filtered K is reabsorbed
- K excreted is the one secreted at DCT & CD
-Excretion controlled by aldosterone, distal fluid and
sodium delivery, serum H ion conc.and K ion conc.
- about 20 mEq is lost / day even in absence of K intake
 Potassium
• Hypokalemia – more common than hyperkalemia
• Caused by poor intake, excess renal excretion, diarrhea,
fistulas, emesis, high NG output, intracellular shifts from
metabolic alkalosis or insulin
• Decreases 0.3 mEq/L for every 0.1 increase in pH
• Amphotericin, aminoglycosides, cisplatin, ifosfamide
(induce magnesium wasting)
• Disorders of muscle contractility in GI smooth muscle,
cardiac muscle, skeletal muscle
• Ileus, constipation, weakness, fatigue, dec DTR, paralysis,
cardiac arrest
ECG changes : do not correlate well with serum K
Early changes: - flattening/inversion of T waves
- prominent U waves
- ST depression
- prolonged QT
• Severe depletion: - prolonged PR
- decreased voltage
- widening of QRS
- Ventricular arrythmia
Management
 Management
Goals of therapy
prevent life threatening complications
correct K deficit
minimize Losses
treat underlying pathology
 Management
Infusion through central line

Correct co existing Hypomagnesemia – May lead to

refractory hypokalemia .

IV Infusion – 20 mEq in 100 ml 0.9% NS over 1 hr.

( 10 ml of 15% kcl = 1.5 gm kcl = 20 mEq of K)

Orally available Kesol Solution (1.5 g/15ml =20 mEq),

20 mEq 3-4 times a day
 Remember
Hypokalemia is safer than hyperkalemia (avoid
overzealous Rx)
I V supplementation carries higher risk of hyperkalemia
ECG monitoring must
Avoid IV till U/O established
Don’t give > 10-20 mEq/ hr
Don’t give > 40 mEq/ L
Don’t give > 240 mEq/ day
NEVER GIVE INJ. KCL DIRECTLY I.V.
 Potassium
Hyperkalemia
Uncommon but severe
Often asymptomatic until Serum K > 6.5-7 mEq/l
May lead to fatal cardiac arrythmia “ SILENT KILLER”
• Hyperkalemia
Potassium
– Excessive intake, increased cellular release, extracellular
shift, impaired excretion from kidneys
• PO/IV supplementation, rhabdomyolysis, hemolysis, catabolic
state, post-transfusion RBC lysis, acidosis, insulin deficiency,
ARF/CRF
• K-sparing diuretics, ACE-Is, NSAIDs
– Spironolactone and ACE-Is inhibit aldosterone (renal excretion)

• N/V, intestinal colic, diarrhea, vague muscular weakness,

ascending paralysis leading finally to resp paralysis,
cardiac arrythmias
 Potassium
ECG changes : unlike hypoK it correlates well with
degree of hyperkalemia
 Management
PRINCIPLES:
A. Antagonising membrane effects of
hyperkalemia
- Calcium gluconate
B. Shifting K intracellular
- Insulin + Glucose
- Inj NaHCO3
C. Removal of excess K from body
- Loop/Thiazide diuretics
- Cation exchange resin ( keyxalate)
- Dialysis
 Management
 Ca Gluconate 10% 10 ml IV over 3 min ,can repeat after
5 min OR
Ca chloride 10% 10 ml IV over 3 min (Response only
20 – 30 min)

10 U regular insulin in 50 ml 50% Dextrose over 1 hr,

fast way to lower serum K ( caution in hyperglycemics)

After acute phase/no ECG changes - Kayexelate

Oral 30g in 50 ml 20% sorbitol
 Management
DIALYSIS
most rapid and effective ( hemodialysis)
removal rate around 35 mEq/ hr
reserved for renal failure/ refractory to other
methods
peritoneal only 15-20 % as effective as
hemodialysis
 Calcium
TB Ca : 1.2-1.4 kgs ( most abundant cation in body)
99% in bone, 1% in soft tissue cells, 0.15% in ECF
Serum Ca : 9.5-10.5 mg/dl
40% bound to albumin (physiologically inactive)
50-55% free ionized Ca (physiologically active)
Hypoproteinemia causes decreased protein bound
and total serum calcium but does not reflect upon
ionized Ca ( wrongly diagnosed hypo Ca)
 Calcium
Physiology
PTH and Vit D
Negative feedback
PTH- increases bone resorption, increases
renal reabsorption, promotes conversion of Vit D to
Vit D3 (active form)
Vit D- promotes intestinal absorption, role in
bone marrow formation and reabsorption
• Hypercalcemia Calcium
– Primary hyperparathyroidism, malignancy (bone
metastasis, PTHrP)
• Neurologic impairment, muscle weakness/pain, renal
dysfunction, n/v, abdominal pain, short QT interval, flat T waves,
AV block

• Hypocalcemia
– Pancreatitis, Post thyroidectomy, renal failure, small bowel
fistulas, hypoparathyroidism, abnormal magnesium, tumor
lysis syndrome, breast/prostate cancer, alkalosis
• Perioral tingling, muscle cramps, carpopedal spasm, stridor,
tetany, seizures, hyperreflexia, heart block, prolonged QT
Hypercalcemia
Management
Treatment of cause ( Surgery for PTH adenoma)
Malignancy related (Surgery or Chemo or RT)
Increase urinary excretion (saline infusion followed by
loop diuretic admin)
Bisphosphonate therapy ( pamidronate)

Hypocalcemia
Calcium infusion, correcting coexisting Hypomg
Chronic hypocalcemia oral calcium admin and Vit D
supplementation
 Magnesium
 Fourth most common cation of body
Second most common ICF cation
60% in bones, 1% in ECF and rest within cells
Normal serum Mg : 1.4-2.2 mEq/l
Imp role in neuromuscular function and
cardiovascular tone
 Magnesium
• Hypermagnesemia
– Severe renal insufficiency, magnesium-containing
antacids/laxatives, TPN, massive trauma, severe acidosis
• N/V, neuromuscular dysfunction, weakness, lethargy,
hyporeflexia, impaired cardiac conduction, elevated T waves
• Hypomagnesemia
– Regulated by calcium/magnesium receptors in tubular cells
– Starvation, prolonged IVF therapy, TPN, diuretic use,
amphotericin B, Primary aldosteronism, diarrhea,
malabsorption, acute pancreatitis
• CNS hyperactivity, hyperactive DTRs, muscle tremors, ST
depression
HypermagnesemiaManagement
Stop extraneous supply/infusion of magnesium
Calcium salts to reverse hypotension and respiratory
depression( 100 – 200 mg elemental Ca IV over 5-10 min)
Dialysis

Hypomagnesemia
Mg sulphate 8-12 g/1st 24 hrs -> 4 -6 g/day X 3-4 days
 Management
Hypomagnesemia :
- suspect in refractory/persistent hypocalcemia and
hypokalemia
- replace Mg if present
THANK YOU