Fluid and electrolytes

SOME IMPORTANTSOME IMPORTANT
TERMINOLOGIESTERMINOLOGIES
OSMOLARITYOSMOLARITY : amount of solute dissolved in: amount of solute dissolved in
solution (measured in volume).solution (measured in volume).
Expressed as mOsm/LExpressed as mOsm/L
OSMOLALITYOSMOLALITY : amount of solute dissolved in: amount of solute dissolved in
solvent(measured in KG)solvent(measured in KG)
expressed as mOsm/KGexpressed as mOsm/KG
Osmolality is more accurate than Osmolarity.Osmolality is more accurate than Osmolarity.
9

PLASMA OSMOLALITYPLASMA OSMOLALITY
Largely determined by sodium salts
Normal 275 – 295mOsm/kg
Plasma
osmolality
EFFECTIVE OSMOLALITY
UREA being lipid soluble crosses freely cell membrane
and does not contribute to EFFECTIVE OSMOLALITY
Under normal circumstances glucose accounts for only 5 mOsm/kg
in effective osmolality. So plasma sodium concentration is the
primary determinant of plasma osmolality.
2 x Na + glucose mg/dl+ BUN mg/dl
18 2.8
10

Oral intake + insensible fluid gain due to oxidation
23

OutputOutput
Urine output + insensible loss
24

Maintenance fluidMaintenance fluid
For first 10 kg body weight 4ml /kg /hour
For 10 – 20 kg body weight 2ml / kg /hour
For >20 kg body weight 1ml /kg /hour
For 60 kg body weight
Per hour fluid requirement is 40 +20 + 40 ml=100ml
26

RESPONSE TO WATER DEFICITRESPONSE TO WATER DEFICIT
a)Water intake is regulated by thirst, stimuli for which are
Dehydration
Fall in BP
Increased osmolality
b)Water excretion is regulated by ADH
Regulation: water deficit increases serum osmolality or
decreases circulating blood volume which stimulates
hypothalamus for ADH.ADH acts on distal tubules and collecting
ducts to increase the water permeability and decrease the urine
output.
36

Response to water excessResponse to water excess
1)
2)
3) Decreased ADH
When amount of water in body increases, secretion of ADH
decreases so water absorption by collecting ducts decreases and
urine output increases
2) Increase in ANP
Volume expansion will increase the secretion of ANP which
promotes diuresis and natriuresis.
4)
37

ECFVOLUME EXCESSECFVOLUME EXCESS
Can be divided into two groups
1) Water and salt excess
2) Predominantly water excess (water intoxication)
Water and salt excess
Frequently encountered disorder
ETIOLOGY
SYSTEMIC ILNESS: CHF, cirrhosis, nephrotic syndrome, acute or
chronic renal failure, or hypoproteinaemia
IATROGENIC
Excessive and prolonged administration of saline in traumatic and
post operative patients.
38

..
CLINICAL FEATURES
Weight gain Oedema
Raised JVP with hepatojugular reflex
Tachycardia with bounding pulse
Increase in systolic BP Ascites
Bilateral basal crepitation's
Raised CVP Pulmonary oedema
TREATMENT
§ Treatment of underlying aetiology
§ Water restriction, salt restriction, and diuretics
§ Pulmonary oedema needs extensive treatment i.e. propped up
position, O2 inhalation, i.v aminophylline, nitro-glycerine
infusion and in non responsive patients phlebotomy, dialysis
or ultrafiltration 39

PREDOMINANTLYWATER EXCESSPREDOMINANTLYWATER EXCESS
§ Water intoxication, over hydration or dilutional
syndrome
§ Usually iatrogenic disorder
§ ETIOLOGY
§ Absorption of irrigating fluid in TURP
§ Excessive administration of dextrose in patients with high
ADH secretion
§ Correction of salt and water loss solely by 5% dextrose
solution
§ SIADH
§ Psychogenic polydipsia
40

CLINICAL FEATURESCLINICAL FEATURES
Predominantly neurological due to hyponatremia, hypoosmolality
and increased ICT due to brain cell swelling
Confusion , loss of attention ,altered behaviour, drowsiness,
nausea and vomiting. In severe cases convulsions and coma
On investigations urine is diluted with low specific gravity and
serum sodium and osmolality are low.
TREATMENT
§ Fluid restriction
§ For symptomatic patients vigorous treatment with hypertonic
saline and furosemide
§ Correction of hyponatremia should be done slowly do avoid
cerebral pontine syndrome
§ If patients undergoing TURP show signs of intoxication,
procedure should be terminated and treated promptly.
41

ECF VOLUME DEFICITECF VOLUME DEFICIT
§ Severe fluid deficit if untreated can be lethal
Can be divided into two groups
1)Isotonic volume depletion
2)Pure water depletion
Isotonic volume depletion
§ Combined loss of water and salt leading to hypovolemia
§ Causes; diarrhoea, vomiting, excess diuresis
§ Normal or low sodium
§ Reduction only in ECF volume leading to hypotension and
reduction in tissue perfusion
Dry tongue tachycardia postural hypotension
Dizziness oliguria and azotaemia with disproportionate elevation in
BUN
Cold extremities ,shrunken eyes and poor or absent peripheral pulses and
hypotension 42

Pure water depletionPure water depletion
§ Pure water loss leads to dehydration
§ Causes: poor oral intake and DI
§ Characterised by hypernatremia
§ Proportionate reduction in total body water
§ Features : excessive thirst and CNS manifestations secondary to
hypernatremia
§ Blood pressure and tissue perfusion are better maintained
43

TREATMENTTREATMENT
ISOTONIC volume depletion is corrected by .9% NaCl
Pure water depletion is treated with increased oral water intake or 5%
dextrose
44

Renal Loss
Acute or chronic renal insufficiency
Diuretics
50

administration of hypotonic maintenance
intravenous fluids
Infants who may have been given inappropriate
amounts of free water
bowel preparation before colonoscopy or
colorectal surgery
51

Urinary sodium <20mEq/l CHF, Cirrhosis ,nephrotic
syndrome
Urinary sodium >20mEq/l renal failure
52

PSEUDOHYPONATREMIAPSEUDOHYPONATREMIA
Hyponatremia with normal to high osmolality
a) Normal osmolality: hyperlipidaemia, hyperproteinaemia
b)
c) High osmolality: hyperglycaemia
54

DIAGNOSISDIAGNOSIS
Three important diagnostic tests 1) plasma osmolality 2) urinary
osmolality 3) urinary sodium concentration
If plasma osmolality is normal or high, rule out
pseudohyponatremia
Oedematous patient rule out CHF ,cirrhosis, nephrotic
syndrome
Urinary sodium >20mEq/l renal loss of sodium
Urinary sodium<20mEq/l diarrhoea , vomiting, burns
Associated hyperkalemia, renal insufficiency or adrenal
insufficiency with hypoaldosteronism
Associated with hpokalemia and metabolic alkalosis, vomiting or
diuretic theraphy
SIADH –most common cause of euvolemic hyponatremia (high
urinary sodium in spite of low serum sodium)
56

TREATMENTTREATMENT
Treatment must be individualised acc.To etiology, acute/chronic, severity
and signs and symptoms
Hyponatremia which develops quickly, should be treated fast where as
which develops slowly should be corrected slowly
Hypovolumic hyponatremia;;salt and water supplementation (.9% NaCl)
Hypervolumic hyponatremia :: salt and water restriction and loop
diuretics
Normovolumic hyponatremia :: water restriction
Patients with severe hyponatremia are at risk of developing severe and
potentially irreversible neurological demage and sometimes death. On
the other hand rapid correction can produce central pontine myelinosis
or osmotic demyelination syndrome.
57

Osmotic demyelination syndromeOsmotic demyelination syndrome
Occurs after the rapid correction of chronic hyponatremia
Characterised by dysarthria, dysphasia, flaccid paresis and coma
Diagnosis is confirmed by CT or more accurately by MRI
58

GENERAL GUIDLINESGENERAL GUIDLINES
FOR TREATMENT
Chronic asymptomatic hyponatremia
Targeted rate of plasma sodium correction should not be greater
than .5 to 1 mEq/l/hour
Raise the plasma sodium by less than 10- 12 mEq/l on the first day
and less than 18 mEq/l over first two days
If the rate of correction is faster or rise in serum sodium is >25
mEq/48 hours, there is high risk of ODS
Acute hyponatremia with severe neurological symptoms
Require rapid correction with hypertonic saline
Initial rise should be 1.5 – 2 mEq/l/hour for first 3-4 hours or until
the symptoms improve
Besides the initial rapid correction rise in plasma sodium
concentration should not exceed 10-12 mEq in first 24 hours
59

WHEN TO STOPWHEN TO STOP
qPatients symptoms are abolished
q
qSafe plasma sodium 120-125 mEq/l is achieved
q
qA total magnitude of correction of 20 mEq/l is achieved.
q
.9% saline and 3% hypertonic saline are only two
routinely used fluids for hyponatremia
60

CALCULATIONCALCULATION
Change in serum infusate Na/L –serum NaChange in serum infusate Na/L –serum Na
sodium conc. Total body water + 1sodium conc. Total body water + 1
Total body water ::Total body water ::
children and non elderly men 0.6xBW kgchildren and non elderly men 0.6xBW kg
elderly men and non elderly women .5xBW kgelderly men and non elderly women .5xBW kg
elderly women .45xBW kgelderly women .45xBW kg
e.g. 45 year male with 60 kg wt with serum sodium of 110 mEq/le.g. 45 year male with 60 kg wt with serum sodium of 110 mEq/l
infusion of 3% NaClinfusion of 3% NaCl
change in Na conc. = 513 – 110 /.6x60 +1change in Na conc. = 513 – 110 /.6x60 +1
= 403/36+1= 403/36+1
=10.9mEq/l=10.9mEq/l
to raise 4 mEq/l in initial 4 hours we need to transfuse 4/10.9x 1000to raise 4 mEq/l in initial 4 hours we need to transfuse 4/10.9x 1000
=366 ml=366 ml 61

Free water deficitFree water deficit
Free water deficit = total body water x (serum Na -140)
140
Half of deficit is corrected over first 24 hours
Rate of correction should not exceed .5 – 1 mEq/l
64

Metabolic acidosis increases the serum potassiumMetabolic acidosis increases the serum potassium
level where as metabolic alkalosis decreases thelevel where as metabolic alkalosis decreases the
serum potassium level.serum potassium level.
unlike sodium, absorption of potassium is neverunlike sodium, absorption of potassium is never
complete, about 20 mEq of K are lost daily even incomplete, about 20 mEq of K are lost daily even in
absence of K intake.absence of K intake.
Whenever body K increases, serum K risesWhenever body K increases, serum K rises
proportionately. But when there is deficit in serum K,proportionately. But when there is deficit in serum K,
reduction in serum K is not proportionate as it isreduction in serum K is not proportionate as it is
compensated by shift from intra cellularcompensated by shift from intra cellular
compartment.compartment. 67

HYPOKALEMIA STEPWISE APPROACHHYPOKALEMIA STEPWISE APPROACH
70

Approach to HypokalemiaApproach to Hypokalemia
Step 1:Step 1: Redistribution or depletionRedistribution or depletion??
Redistribution causesRedistribution causes
Insulin therapy – DKAInsulin therapy – DKA
Beta 2 agonists - SalbutomolBeta 2 agonists - Salbutomol
Metabolic alkalosisMetabolic alkalosis
Beta 2 adrenergic stimulationBeta 2 adrenergic stimulation
increased cell proliferation – Rx ofincreased cell proliferation – Rx of
megaloblatic anaemiamegaloblatic anaemia
Barium poisoiningBarium poisoining
Replacement of potassium in these settings may lead toReplacement of potassium in these settings may lead to
overshoot & hyperkalemiaovershoot & hyperkalemia
71

Approach to HypokalemiaApproach to Hypokalemia
Step 1: Redistribution or depletion?
Depletion causes (common)
GI tract losses (diarrhea, vomiting)
Loop/thiazide diuretic therapy
Other medications (e.g. amphotericin B)
Osmotic diuresis (DKA)
Refeeding syndrome
Endocrinopathies (mineralocorticoid excess)
Salt wasting nephropathies/RTA’s
Magnesium deficiency 72

Approach to Hypokalemia
 Step 2: Estimate the deficit

For every 100 mEq below normal, serum K+ usually drops by 0.3
mEq/L
 Highly variable from patient to patient, however!!
TOTAL 125 -250 250-400 300-600 500 -750
K deficit
(mEq/L,70 kg)
S.K 3.5 3 2 <2
(mEq/L)
73

 Step 3: Choose route to replace K+

In nearly all situations, ORAL replacement is PREFERRED over IV
replacement
 Oral is quicker
 Oral has less side effects (IV burns!)
 Oral is less dangerous

Choose IV therapy ONLY in patients who are NPO (for whatever reason) or
who have severe depletion
I V POTASSIUM
Avoid I v K till urine output is established
Don’t give >10-20mEq/hour
Don’t give >40/l
Don’t give >240/day
Never give inj. KCL directly I v causes sudden hyperkalemia and instant
death
Don’t use D5 as diluent as it aggravates hypokalaemia
74

 Step 4: Choose K+ preparation
 Oral therapy
 Potassium Chloride is PREFERRED AGENT
 Especially useful in Cl-responsive metabolic alkalosis
 ⇑ in ECF K quicker with KCl compared to other salts

Potassium Phosphate useful when co existant
phosphorus deficiency
 Often useful in DKA patients
Potassium bicarbonate, acetate, gluconate, or
citrate useful in metabolic acidosis
ORAL POTTASIUM CHLORIDE SOLUTION
15 ML = 20 mEq/L
10 ml ampoule of 15% kcl = 19.5 mEq 75

 Step 5: Choose dose/timing
 Mild/moderate hypokalemia
 3.0 to 3.5 mEq/L
 60-80 mEq PO (or IV) in divided doses
 Sometimes will require up to 160 mEq per
day (refeeders, lots of diarrhea, IV diuretics)
 Avoid too much PO at once
 GI upset or just poor response
 Usually divide as BID or TID dosing 76

 Step 5 (con’t): Choose dose/timing
 Severe hypokalemia (< 3.0 mEq/L)
 Can use combination of IV and PO, again with PO
preferred if at all possible
 Avoid more than 60-80 mEq PO in a single dose
 Avoid IV infusion rates faster than 20 mEq/hour—can
cause arrhythmia!!!
 Most protocols won’t allow more than 10 mEq/hour rates on the
floors (ICU’s too?)
77

 Step 6: Monitor/reassess
 Severe hypokalemia, DKA patients
 Reassess labs 4-6 hourly
 Moderate hypokalemia, IV diuresis patients
 Reassess labs BID to TID as needed
 Mild hypokalemia
 Reassess labs OD or less as needed
78

Treatment of hypocalcemiaTreatment of hypocalcemia
Acute management
10-20 ml of 10% ca. glu i.v over 10 min followed by infusion of 60
ml of ca glu in 500 ml of d5
If I.v calcium does not relieve tetany rule out hypomagnesemia
Long term management
Oral elemental calcium 1 to 3 grams per day
Vitamin d (calcitriol)
86

Treatment of hypercalcemiaTreatment of hypercalcemia
ü Measures to increase urinary excretion
0.9% NaCl for volume expansion and natriuresis
furosemide
hemodialysis
ü Measures to inhibit bone resorption
bisphosphonates like pamidronate
calcitonin
Measures to decrease intestinal absorption
glucocorticoids
oral phosphate

Due to dilution of serum bicarbonate. Many argue that in acidotic pts
body offloads O2 from Hb better than in alkalosis, atleast to a milder
degree.
98

PLASMA-LYTEPLASMA-LYTE
Balanced crystalloid containing additional electrolytes such as
acetate and gluconate.
Chloride level is lower
Also contains magnesium.
Safe in priming of extracorporeal circulation pumps, cold ischemia,
circulatory arrest, organ transplantation, and organ preservation.
100

112
Higher rates may be
needed in shock
500 ml of 5% alb
or 100 ml of 25%

122
DR
DROP RATE/MIN VOLUME TO BE INFUSED IN ML
DURATION OF INFUSION IN HRS X 4
Suppose 500 ml of NS is to be infused over 3 hrs
500/3x4 = 500/12 = 40 drops per min

Potassium is avoided in first twoPotassium is avoided in first two
post op days why????post op days why????
q Oliguria or azotemia unless urine output is established K is risky
q
q Tissue trauma releases K from intracellular stores __ hyperkalaemia
q
q Intra or imm. post op blood transfusions add large amount of K
q Post op metabolic acidosis will shift K extracellular
q Body has large stores of K intracellular so hypokalaemia will not occur 129

FLUIDTHERAPY INFLUIDTHERAPY IN
BURNBURN
PATIENTS

General PrinciplesGeneral Principles
>10% total BSA - IV fluid resuscitation & urinary>10% total BSA - IV fluid resuscitation & urinary
catheter.catheter.
In major injury - nasogastric tube toIn major injury - nasogastric tube to
decompress the stomach.decompress the stomach.
During transport - maintain body temperature.During transport - maintain body temperature.

Fluid ResuscitationFluid Resuscitation
§ Burn leads to intravascular volume depletion
§ Major losses occur during the first 24 hrs – crystalloids used.
§ Myocardial depression - 24-“36 hrs after injury.
§ The goal of resuscitation is to maintain adequate intravascular
volume to support tissue perfusion and thereby preserve organ
function.
§ The adequacy of resuscitation - based on observation of blood
pressure, heart rate, and urine output.
§ Fluid to maintain normal blood pressure, heart rate, and hourly
urine output of 1 mL/kg/hr in the infant and young child and 0.5
mL/kg/hr in the child >12 years of age or >50 kg in weight.

Parkland formula - crystalloid-based formula - with
RL - based on the BSA of burn and the patient's body
weight.
Maintenance fluids (5% dextrose in lactated
Ringer solution)
= (4ml/kg+ BSA of burn) + Maintainance fluids
 (For adults and children who weigh >40 kg,
maintenance fluids are not included in the estimate of
fluid requirements.)
 Half of this - in the first 8 hrs after injury, and other
half is given in the following 16 hrs.

After the first 24 hrs, - maintenance requirements + to
replace ongoing losses.
The hourly evaporative fluid loss from wounds can be
estimated as:
= ( 25 + Burn surface area) x total BSA
The evaporative losses are primarily free water.
However, to avoid rapid changes in sodium concentration
in children, this loss is replaced with - 5% dextrose in 0.2%
normal saline.
loss of serum protein occurs in > 40% BSA burns.
When the injury is larger, the loss is replaced in the second
24 hrs after injury with 5% albumin.

Ultimate goal – to maintain normal blood
pressure,
heart rate, urine output, and serum
sodium

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