FLUID AND ELECTROLYTES

Prof. M.C.Bansal. MBBS;MS. FICOG. MICOG.Founder Principal & Controller, Jhalawar Medical college , Jalawar.Ex.Principal&Controller; Mahatma Gandhi Medical College,sitapura , Jaipur.

Normal Physiology Total body water is 60% in male, 50% in female

i.e. 30 litres Inraceullar fluid (ICF) –20 litres water (2/3). Extracellular fluid (ICF)– 10 litres water (1/3). >Plasma –2.2 litres (1/4). > Interstitial fluid – 7.5 litres (3/4).EcF volume and Osmalality regulation is

controlled by 3 hormones –aldosterone, ADH Atrial natriuretic hormone

ION ICF ECF

Sodium 10mml/L 140mml/L

Potassium 150mml/L 4.5mml/L

Chloride Traces 105mml/L

Water Loss (volume Loss) It is decrease in whole body fluid volume

which includes both exta and intracellular fluid loss.

Extracellular fluid loss is more important and has to be assessed .

This fluid loss may be : >Isotonic –Water and salt loss leading to

Hypovolaemia. > Hypotonic – only water loss with

minimal electrolyte loss; leading to dehydration.

Causes And Features of Fluid Loss Isotonic Volume Depletion Occurs due to diarrhea, vomiting and excess

dieresis. > Fluid loss is only of ECF compartment and so

immediate reduction in intravascular volume results leading to hypovolaemia and fall in BP.

> decreased Tissue perfusion. features Dry tongue , rapid pulse, cold

clammy skin , sunken eyes , decreased BP, oliguria , raised blood urea and decreased urinary sodium.

Hypovolaemia –Mild (<2l), Moderate (2-3L) ; severe ( > 3l ) fluid loss.

Causes and features of fluid loss---

Hypotonic Fluid loss > i.e. only water loss , occurs due to decreased

intake of water and diabetes insipidus . > It causes dehydration and appropriate and

decrease in total body water in all fluid compartments ( 2/3rd ICF , 1/3rd ECF ).

>As ECF loss is less ---intravascular fluids loss is also less hence Fall in BP is also less .

Features severe thirst , confusion, convulsions( due to hypernatraemia ), BP relatively normal .

Dehydration : mild (weight loss 5%), moderate (10%) , severe (15% ).

Management Of Fluid Loss

Evaluation is done by estimation of serum Na+, urinary Na+ and blood urea .

Isotonic volume depletion is corrected by o.9% normal saline infusion ,

Pure water depletion is corrected by more water in take / IV 5% dextrose infusion .

Monitoring fluid therapy by skin and tongue examination, weight gain pulse, BP, urine output , CVP and PCWP.

Water Excess (ECF Volume Excess)

Water & Salt excess occurs in CCF , Cirrhosis, nephrotic

syndrome , hypoproteinaemia, renal failure , excessive saline infusion.

Water Intoxication TCRE, excess infusion of 5% dextrose

only, SIADH secretion, Psychogenic polydypsia.

It is managed by stopping fluid infusion or procedure (TCRE), fluid restriction and treating the cause.

Causes of Water excess Excessive amount of intravenous

dextrose(5%). Bowel Wash by plane water in place of

normal saline. In TCRE (TUR in urology ) hydro dissection in

tumour surgery , when excessive fluid Plane water or glycine is used for uterine distension.

In syndrome of inappropriate Anti diuretic hormone secretion which is commonly associated with lobar pneumonia, empyema , oat cell carcinoma and head injury .

Clinical Features Drowsiness , weakness. Convulsions , coma. Nausea and vomiting. Passage of dilute urine. Distended neck veins. Gain in body weight . Circulatory over load –tachycardia,

pulmonary edema, hypertension and pedal edema.

Bilateral basal crepitations , ascites. Raised CVP, PCWP.

Management Investigations >Haematocrit and sodium level (will show fall in

level) > Low Potassium and Low blood urea.ECG< X-ray

Chest. Treatment >Water and salt restriction and observation . > Monitoring in ICU. > Management of fluid and electrolyte balance as

per serum electrolyte reports. > Infusion of( ½) hypotonic saline. Administration of diuretics and hypertonic saline

should be avoided as it may de arrange serum electrolytes which may lead to neuronal demylation and FATL OUTCOME.

ECF Loss And Excess ECF Loss > Here only ECF loss occurs , ICF remains Normal. > It is seen in diarrhoea , vomiting, intestinal

obstruction / fistula. > Normal Saline infusion = to calculated ECF loss. ECF excess Only ECF Excess ,ICF remains normal. It occurs when excessive infusion of saline with

impaired excretion as in renal diseases. Raised JVP , cardiac failure and peripheral edema. Treatment is fluid restriction and diuretics like

frusamide.

Hyponatraemia

HYPONNATRAEMIA Definition > Serum Sodium level is < 130mEq/L > Severe degree hyponatraemia, when

serum sodium level < 100 mEq/L in acute type and in chronic type serum sodium level <115 is taken as reference value.

< May be due to water over loading (dilution) or sodium loss.

Types of Hyponatraemia Acute—presents as neurological manifestations. Chronic – cause pontine myelonlysis , presents as behavioral

changes , weakness and central nerve palsies. Other types may be (a) hypervolaemic Hyponatraemia –Rapid absorption of fluid occurs

leading to dilution and decreased Na+ concentration. Decreased osmalality results in migration of ECF in to ICF compartment and hence patient develops cerebral and pulmonary edema ., causing convulsions and respiratory symptoms.

-Urinary Na+ conc. Is 15 mmol/L. -fluid restriction ,hypertonic saline (double strength) infusion and

loop diuratics like frusamide injection are the main lines of management.

- Monitoring is done by Serum Na= estimation and its correction till it reaches above the level of 125mmol/L .

- correction should be slow and gradual at the rate of 2mEq/L /Hr and up to 20 mEq/L in 24 hours. Serum Na+ estimation should be done at 4 hourly interval .

- Rapid correction may lead to irreversible myelinlysis of pontine . - Over correction should always be avoided.

Types of Hyponatraemia (b) Hypovolumaemic hyponatraemia – - Hypovolaemic as in dirrhoea and vomiting ,

hyponatraemic as urinary Na= level is < 20mmol/L.

- Due to forced diuresis and renal causes water is lost and urinary Na+ level is more than 20mmol/L.

- It may be due to over correction of hypovolaemia by only dextrose / hypotonic fluid.

- condition is treated by using Isotonic fluid(normal saline ) therapy.

Types of Hyponatraemia--- (c) Normovolaemic Hyponatraemia— - It may be due to renal failure or

Syndrome of inappropriate ADH secretion - Mild cases fluid restriction (1 litre /day

) will raise the Na+ level . - In severe cases Vasopressin

antagonist ( Demeclocyclin) will increase the diluting ability of kidney . And Na+ level will improve.

Types of Hyponatraemia--- ( d) Pseudo-hyponatraemia –

- Plasma osmalality is mainly achieved by Na+ but small portion of it i.e. 25% is due to other solutes like glucose , proteins, urea and lipids which do not move out easily from vascular compartment, in IC / EC Spaces.

- When concentration of this substances increase , the Na+ level will fall causing Pseudo hyponatraemia.

Correction of increased element will correct the Na+ level.

Causes - Intestinal obstruction, -intestinal fistula, -gastric outlet obstruction with excess of vomiting , -prolonged Ryle’s tube aspiration, -Severe diarrhoea due viral cause –in colitis and cororectal polyposis, -SIADH, -Immediate after surgery / trauma Na+ depletion occurs . -stroke etc.

Clinical Features Of Hyponatraemia Dry coated tongue. Sunken eyes. Dry wrinkled skin. Hypotension . Dark scanty urine . Irritability, disorientation , neurological

manifestations. Convulsions. In chronic Hyponatraemia– hypothermia,

reduced tendon reflexes, pseudobulbar palsy.

Investigations In Hyponatraemia

Serum electrolytes --- Low serum Na= Level.

Urinary Na+ level low, Sodium deficit = ( 125- present Na+ ) X body weight in Kg

X 0.6.

Treatment Of Hyponatraemia In acute cases --IV infusion of normal

saline to achieve slow and gradual correction of serum Na+ level at the rate of 2mEq/L / hr. Maximum 20mEq/L in 24 hrs. monitor Na= Level at 4 hrs interval.

In chronic Case--< 1mEq/L/Hr and should not exceed > 10mEq/l in 24 hrs.

Hypertonic saline 1.6 % or 3% can be used in acute severe cases with caution of too early and rapid correction is associated with myelinlysis of pontine.

Cause is also treated simultaneously. Type of Saline fluid NaCl content

0,9% normal saline /L 154mEq/L

3% hypertonic Saline 500 mEq/L

Hypernatraemia

Hypernatraemia

Serum Na+ level >150mEq/L., is taken as hypernatraemia.

Causes >Renal Dysfunction. >Cardiac Failure. >Drug induced like NSAID , Corticosteroids. >Excess infusion of hypertonic saline /intra

amniotic hypertonic saline previously used for mid trimester MTP.

> excess of normal saline infusion causes overloading in circulating salt and water. It is due to when water deficit present in initial stage..

Types Of Hypernatraemia (A) Euvolaemic ( pure water loss ): - It is due to decreased water intake as in coma,

bedridden people , post operative patients when iv therapy has been stoped but pt does not take reqired amount of water, patient in high fever leading to external loss of water. It can also occur in diabetes incipidus / chronic renal failure as renal loss of only water.

( B ) -Hypovolaemic: -( Among loss of water and Na= but water is more lost

than Na+.) as in cases of vomiting ,diarrhoea , more undue sweating ( extra renal ) , osmotic diuresis by high concentration glucose/ mannitol infusion (renal ).

( C ) Hyper volaemic : - (Both water and Na+ gain But Na= gain is more

than water.) as seen in more salt intake, excess steroids , Na HCo3/ hyper tonic saline infusion ( salt gain )

Clinical Features

Pitting edema. Puffiness of face . Increased urination . Often dilated jugular vein. Features of pulmonary Edema.

Management Investigations >Serum Electrolytes. > Plasma and Urinary osmolality. > Renal Function Test. > Haematocrit. Treatment >Restriction of saline , Na+. > Correction should be slow and gradual – Initial infusion of normal saline ,then infusion of ½

strength (0.4.5% ) saline later with 5% dextrose ; otherwise cerebral edema and hyperglycaemia can develop.

> oral / nasogastric administration of water / other fluids as condition improves.

Hypokalaemia

Hypokalaemia Serum Potassium level < 3.5 mEq/L is leveled as

hypokalaemia.( normal range –4.0 to 4.5 mEq /L) 1.Sudden onset It occurs in diabetic coma cases

treated with insulin and saline infusion ; as insulin causes influx of K+ in the cells and saline (containing NO K+) dilutes its concentration in serum.

2. Gradual onset Diarrhoea of any cause, ulcerative colitis, gastric aspiration / vomiting, After trauma or surgery , duodenal fistula/ileostomy , insulin therapy , poisoning , beta blockers , prolong diuretic therapy etc.

Clinical Features

Slurred speech. Muscular hypotonia (physical sign). Depressed reflexes. Paralytic Ileus. Weakness of respiratory muscles. Cardiac arrhythmias. Inability to produce concentrated urine. Nocturia and polyuria.

Management ECG– shows prolonged QT interval, depression of

ST segment , inversion of T wave and prominent U wave.

Often hypokalaemia is associated with alkalosis. Serum potassium < 3.5 mEq/L. Treatment > oral potassium 2gm ;6hrly , 15 ml K Cl

syrup(2ommol of K) > Iv K CL 40mmol?L in5% dextrose / normal saline

slowly , often under ECG monitoring . Maximum dose / hr is 20 mmol .

>Hypocalaemic alkalosis if present should be treated carefully by iv Potassium .

Hyper Kalaemia

Hyperkalaemia

Normal serum K+ level ranges from 4.0 to 4.5 mEq/L

Hyperkalaemia menifests when serum K+ exceeds 6.0 mEq/L

Causes of hyperkalaemia Causes Renal Failure. Rapid infusion of potassium. Transfusion of stored blood –K+ diffuse out of stored RBC. Diabetic Ketoacidosis . Adrenal Insufficiency. Potassium sparing drugs like diuretic therapy

(spironolactone), beta blockers , cyclosperine . Massive tissue destruction ,burns , trauma, tumor

necrosis, crush injury –intra cellular K+ is released in blood.

In vitro haemolysis, thrombocytosis , torniquet application exercise cause pseudo hyperkalaemia.

Familial hyperkalaemic periodic paralysis. Note Hyperkalaemia is dangerous state can result in

cardiac arrest.

Investigations And Treatment (A) Investigations > High serum potassium level. > Peak T wave on ECG. ( B ) Treatment > IV infusion of 50 ml of 50% glucose with 10 units of

soluble insulin , slowly . >Infusion of 10% cal gloconate IV ( cardio protection) > CaCl2 is given Iv in severe cases as calcium in this

form is immediately released without hepatic metabolism. > Dieresis using Frusemide –causes K+ excretion. > Haemolysis / dialisis when required. > continuous ECG monitoring , > Salbutamol / Albuterol nebulisation > IV Sodium bicarbonate –shifts K+ in to cells – 50- 100

ml slowly over 10 minutes in 7.5% concentration .

Hypermagnasaemia

Hypermagnesaemia

It is rare: serum magnesium level > 2.5mEq/L(normal level is 1.5- 2.5mEq/L ).

Intracellular magnesium is more 26mEq/L ( 2nd more higher element).

Mg is mainly deposited in bones. It is a co- factor for many enzymes

necessary for phosphorylation of glucose in cell and ATP utilization in muscle fibers.

Daily dietary of Mg is 0.4 gram. It is reabsorbed well in proximal renal

tubules.

High Mg level Advanced renal failure, patient treated with Mg containing

antacids. Diabetic ketoacidosis . Over dose of Mg SO4 in treatment of PIH / Eclampsia. Clinical features > Loss of tendon reflex. > Flaccid quadriplegia. >Neuromuscular depression. > Respiratory depression– muscle paralysis. > Hypotension. > renal out put decreased ; oligourea and anurea. Monitoring urine out put should not go down < 3o ml in one

hour. Knee jerk, planter reflex should not depress. Keep watch on respiration Rate. Serum Mg estimation . Management next dose to be given after checking , respiratory

rate, urinary output and reflexes . - I V inj. Ca gluconate / CaCl2 in 10% concentration, 10-20

ml slowly over 20-30 minutes.

Hypomagnesaemia

Low serum Mg Level Serum MG < 1.5mEq/L Causes Malnutrition , chronic alcoholism,

large GI fluid loss; patient on parenteral fluid therapy for along time.

Clinical Features hyper reflexia, muscle spasm , parasthesia

, tetany, it mimics hypo calcaemia associated with hypokalaemia.

Treatment 2 gm ( 16mEq /L ) of MgSO4 given IV slowly in 10 minutes. Later maintenance dose of 1mEq /kg / day is infused as slow IV drip.

ACID- BASE BALANCE

Acid –Base Balance Normal pH( - log of H+ ) is 7.36 –

7.44 When H+ increases pH decrases. Factors which Control pH

.> Buffer System –

Bicarbonate Buffer

Protein Buffer

Phosphate Buffer

> Renal Control Of pH

> Respiratory Control of pH

Termnalogies ---

Acid – is a substance that dissociates Waterto release hydrogen Ion .

Base – is a substance that takes hydrogen Ion

Buffer – is combination of weak acid and conjugate base.

These buffers maintain the H+ concentration in blood with in a fine limit / range .

Buffers are 1. Intra cellular . 2. Extracellular.

Buffers ---- Extra Cellular Buffer – Bicarbonate /

Carbonic acid , phosphate buffer and Plasma Protein buffer arte extracellular natural buffers .Bicarbonate / carbonic Acid buffer is most important as carbonic acid level in blood is regulated by lungs which removes excess of Co2 gas. , while bicarbonate pare is contrilled by Kidney.

Intra Cellular Buffer – Haemoglobin and other protein inside cell are playing major role of intra cellular Buffer.

Acidosis---When pH of blood is < 7.35 . Alkalosis ---- when pH is more > 7.45 .

Hydrogen Equation ( Used to Assess Hydrogen Ion Concentration )

H+ (nmol/L ) = K x H2Co3m mol /L _____________ HCO3m mol/L or K x d PCO2 __________ HCO3 m mol/L Here K is coefficien a constant factor =800( for H2 CO3 / HCO3

buffer ) Carbonic acid (H2CO3) is solubility coefficient of CO2 in blood (d)

multiplied by partial pressure of CO2 (pCO2) d is 0.03ml/mmHg / ml blood .

pCO2 is 40 mmHg . H2CO3 = d pCO2 = 0.03 x 40 ==1.2ml . Normal blood Bicarbonate (HCO3) level is 24 m mol /L So H+ is 800 x 1.2 devided by 24 = 40m mol / L

Henderson – Hasselbalch Equation ( used to assess pH )

It is used to find out pH of blood using Logrithm .

Negetive log of K (800 for carbonic buffer ) is called as pKa . It is 6.1 for H2CO3 / HCO# buffer system.

pH = pKa + log HCO3 / H2CO3 means 6,1 + log 24 devided by 1.2 = 6.1

+ log 20 = 6.1 + 1.3 = 7.4

ALKALOSIS

>Metabolic Alkalosis >Respiratory Alkalosis

Metabolic Alkalosis Primary base excess . E.g. HCO3 . A standard

bicarbonate above 27m mol /L. Causes 1. Repeated vomiting as in pyloric stenosis .

Here hypokalaemic alkalosis develop due to loss of K+ and acid in vomit .

2. Excess alkali intake e.g. antacid . 3. Cortisol excess due to over ingestion /injection

or cushing’ syndrome. Clinical Features 1.Chine strokes breathing in

period of apnoea of 5-30 seconds. 2.Tetany due to alkalosis ---latent tetany revealed

by Trousseau’s sign .

Metabolic Alkalosis ---

Investigations Serum electrolytes. Arterial blood gas analysis. Treatment Normal saline or double strength saline IV

with slow IV infusion of KCl 40 m mom/L under ECG monitoring .

pH < 7.7 causes life threatening alkalosis and requires rapid correction by infusing dilute HCl acid or Ammonium chloride with careful monitoring

Respiratory Alkalosis Arterial PCO2 is below normal(45mmHg). Causes 1. Hyperventilation during anaesthesia,

severe pain , hyper pyrexia , head injury . 2. High altitude. 3. encephalitis , hypothalamic tumors ,

salicylates over dose / poisoning , Liver cirrhosis.

4. Hysteria.

Respiratory Alkalosis Clinical Features and Management 1. Headache , tingling , circum oral

anaesthesia ,tightness in chest ,tetany and Arrhythmias are the features.

2.Low PaCO2 , low HCO3, High alkaline Ph .

3. It can be acute or chronic. 4. It is managed by O2 therapy , treating

the cause and tab Aceozolamide in high altitude.

5. respiratory depression is treated by CO2.

Acidosis 1. Metabolic . 2. Respiratory,

1. Metabolic Acidosis - It is state of excess acid / base deficit . A standard Bicarbonate below 21 m mol /L. Causes a. Diabetic Ketoacidosis. b. Starvation. c. Hypoxia—CO2 accumulation. d. Renal efficiency . e. cardiac arrest ---Hypoxia. f. Excessive exercise --- Lactic acid over production . g. Intestinal strengulation , here anion gap is

increased.

1. Metabolic Acidosis– causes-- Loss of base causing metabolic

acidosis a, Diarrhoea. b, Ulcerative Colitis . c, Gastrocolic Fistula . d, Intestinal Fistula . e, Uretero-sigmoidostomy done for

urinary diversion --- results in Hyperchoraemic –Hypokalaemic acidosis , anion gap is normal

1. Metabolic Acidosis Clinical Features a, Rapid, deep, noisy breathing – air hunger; known as KUssMaul’s

Breathing. Cold clammy skin , Tachycardia, right heart strain , altered level of

consciousness. Cardiac Arrhythmia , hypotension . Anorexia, vomiting , muscle weakness. Ph < 7.2 A dangeorus and life threatening level. capillary stassis. Strongly acidic Urine. Low standard HCO3. Base deficit. Evaluation --. Do Arterial blood gas analysis. , showing Low HCO3

level . Low Ph , anion Gap , Urinary anion Gap which is zero or positive ,

Note __ U A G become negative in metabolic acidosis due to GI cause as there is increased NH4Cl excretion .

If it is due to renal orgion UAG will be positive .

1. Metabolic Acidosis Treatment > correction oh hypoxia. > 50M ML OF 8,4 % Sodium bicarbonate iv infusion – NAHCO3 requirement in m Eq/L = Body weight in Kg X base

deficit X 0.3 >Correction of Electrolytes. > Specific Treatment for acidosis depends on .Type A (Shock , Respiratory , CO/ Cynide Poisoning , Anaemia ) . Type B ( Diabetic , hepatic , toxins / drugs .) It needs only careful use of NaHCO3 in severe cases.

Dicholoroacetate therapy will stimulate Pyruvate Dehydrogenase enzymes to reduce Lactate.

> Specific treatment is needed to start in cases of diabetic Ketoacidosis , Alcoholic acidosis , Salicylates poisoning and Renal cause .

Astrup FormulaTotal base deficit / exceesve = Base deficit / excess X Body

Wt In KG X 0.3

2. RESPIRTORY ACiDOSIS It is feature of respiratory insufficiency to breath out CO2

as in respiratory failure ; resulting in High PCO2 and fall in pH.

Causes > During or after anasthesia . > Chronic Bronchitis , obstructive lung disease,

Emphysema. > diseases of Thoracic cage. > Upper abdominal surgery / disease3 decreasing

abdomino –thoracic respiration . > Respiratory air ways obstruction . > Myesthenia Gravis, > Poliomyelits causing paralysis of respiratory muscles

to variable extend. > Stroke, infection , obesity, Hypoventilation.

2. RESPIRATORY ACIDOSIS. Clinical Features > Dyspnoea, confusion , psychosis ,

Hallucinations , sleep disturbances, tremors , jerks and personality changes .

> CNS changes are more common and severe in Respiratory acidosis than in metabolic acidosis . As in respiratory acidosis lipid soluble C)2 crosses brain barrier easily than HCO3.

2. RESPIRATORY ACIDOSIS Treatment > O2 Therapy ; ventilator support . > O2 therapy should not be used in

chronic hypercapnoea unless it is realy indicated as Hypoxia induced respiratory stimulation may be decreased as more CO2 is washed out at faster rate.

> Alkali therapy is also not started unless pH is < 7.15. 0r there is severe bronchospasm .

ANION GAP It is a calculated estimation of the

undetermined or unmeasured ANIONS in blood . ANION GAP = ( Na+ + K+ ) – ( HCO3- + Cl - ). e.g. Total ANION – total Cation in bloodNormal anion gap is 10-16m mol /L. Important unmeasured are +ve charged proteins

, phosphate , sulphate and organic acids . Important unmeasured Cations –Ve charged CA

and Mg. Albumin is main component of Anion Gap . When albumin level in blood decreases by 1

gm / dl –anion gap decreases by 2m Eq /L .

ANION GAP

Increased Anion Gap Is seen In

Normal Anion Gap Is seen in

Metabolic acidosis due to Ketoacidosis.

Diuarrhoea.

Lactic acidosis. GIT Fistula .

Poisoning ( CO / salicylates/ cynide

Hyper chloraemic acidosis .

Renal Failure

FLUID THERAPY

Fluid therapy

Osmolality of a solution is assessed by the amount of solute dissolved in a solvent like water measured in weight (Kg).

Osmolality of a solution is assessed by amount of solute dissolved in solvent like water measured in volume (litre) .

Normal plasma is 285 mOsm / Kg (275 -295 ).

Calculation of Osmolality* Plasma Crystalliod osmolality --2 Methods a. Osmolality of plasma = 0.54/1.86 X 1o rase to power 3

mOsmol / Kg. It is based on the fact that solution of 1mOsmol/ Kg

freezes at -1.86 degree Centigrade ; where as plasma freezes at -0.54 degree Centigrade .

b . Osmolality of plasma= 2X(Na) +( Glucose mg%/18) + ( Blood urea mg % /6) It is based on the concentration of major solutes ( Na ,

glucose and urea) in plasma. Na+ contributes maximum in plasma osmolality.

*Colloidal Osmotic Pressure It is difference in plasma osmotic pressure and interstitial fluid pressure = 25 mmHg.

This is mainly due to concentration of Albumin in plasma. Plasma proteins do not go out of capillary wall and do not enter in interstitial compartment.

Principles Of Fluid Therapy Indications > For rapid restoration of fluid and electrolite

deficit as in dehydration as in cases of diarrhoa, vomiting , burns, Haemorrhagic shock and sepsis.

> Total parentral nutrition. > anaphylaxis, cardiac arrest , hypoxia. > Post operative period . > for maintenance , replacement of loss or as a

special fluid.Advantage Controlled , accurate , adjustable,

rapid , predictable and specfic in terms of solutes and solvent as per need of clinical situation.

Problems In Fluid Therapy Needs Hospitalisation : costaly ; needs to

practice universal aseptic measures. Fluid over load; pulmonary edema;

cardiac failure . Infection , thrombophlebitis ,

haematoma;cellulitis ion local area. Pyogenic infection , air embolism ,

bacteraemia . Discomfort , poor acceptance by patient

and relatives.

Fluid and electrolyte and callories therapy

Daily requirement > Na –100mEq ; K– 60mEq ; Ca –5mEQ ; Mg 1mEq.

Crystalloid Solutions(fluids) .

Name of fluid

NA + mEq/L

K+ mEq/l

Cl- mEQ /L

Lactate (HCO3)mEq/L

Ca+ mEq/L

Normal Saline

154 - - - -

Ringer lactate

130 4 109 28 3

Dextrose Saline

5% dextrose

Isolyte P

Isolyte G

Isolyte M

Colloids –Solutions (fluids) Colloids are large molecules which shift

the fluid (solvent/ Water ) from interstitial compartment to intravascular compartment., used as plasma volume expanders.

name Na K Cl Ca bicarbonate

Molecular size

Remarks

Special Purpose Fluids

Isolyte G Isolyte P Islyte M NS RL½ NS Hypertonic saline GDW 5% GDW10% GDW 40%

Fructodex Lomodex Hamaccoele Invertase