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Fluid and electrolyte balance ih

This document provides information on fluid and electrolyte balance in the human body. It discusses the daily water intake requirement, where water is distributed in the body, and the three components of body fluids. Key points covered include how the kidneys, hormones, thirst, and osmotic pressures work together to maintain fluid homeostasis and regulate electrolyte concentrations in extracellular and intracellular fluids. Imbalances in sodium, potassium, calcium, and other electrolytes are defined and their causes, signs, symptoms, laboratory findings, and management approaches are summarized.

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Fluid and Electrolyte Balance Presenter : Dr ITRAT HUSSAIN Moderator : Dr. ANUJA AGARWAL
Daily we consume 2250 ml of water but…. • Why do we need to drink water… • Where does all this water go… • Why we drink only this much of water…
We need to drink water because.. 1 All chemical reactions occur in liquid medium. 2 It is crucial in regulating chemical and bioelectrical distributions within cells. 3 Transports substances such as hormones and nutrients. 4 O2 transport from lungs to body cells. 5 CO2 transport in the opposite direction. 6 Dilutes toxic substances and waste products and transports them to the kidneys and the liver. 7 Distributes heat around the body
Where does all this water go… • Water constitutes an average 50 to 70% of the total body weight Young males - 60% of total body weight Older males – 52% Young females – 50% of total body weight Older females – 47% • Variation of ±15% in both groups is normal • Obese have 25 to 30% less body water than lean people. • Infants 75 to 80% - gradual physiological loss of body water - 65% at one year of age
Functional Components of the Body Fluid The water of the body is divided into 3 functional components: (TBW – 60%) Intracellular Fluid – 40% of the body weight Extracellular Fluid – 20% of the body weight Extravascular interstitial fluid 15% of BW Intravascular plasma 5% of BW Rapidly equilibrating / functional component 13-14% of BW Slowly equilibrating / non-functional component 1-2% BW 1. Connective tissue water 2. Transcellular fluid i.e. CSF, joint fluid
We consume only this much fluids because… In HOMOEOSTASIS 1. output = intake 2. Dynamic fluid equilibrium at a) Blood & interstitial fluid level b) Interstitial fluid and cell level 3. Thirst & Satiety 4. Kidney fluid control 5. Hormonal regulation
Dynamic Fluid Equilibrium 1. Interstitial Fluid & cell interface . Ion pumps & carriers 2. Blood & interstitial fluid interface . Starlings forces
Fluid Movement Among Compartments • Compartmental exchange is regulated by osmotic and hydrostatic pressures. • Net leakage of fluid from the blood is picked up by lymphatic vessels and returned to the bloodstream. • Exchanges between interstitial and intracellular fluids are complex due to the selective permeability of the cellular membranes.
Extracellular and Intracellular Fluids • Ion fluxes are restricted and move selectively by active transport. • Nutrients, respiratory gases, and wastes move unidirectionally. • Plasma is the only fluid that circulates throughout the body and links external and internal environments. • Osmolalities of all body fluids are equal; changes in solute concentrations are quickly followed by osmotic changes.
Thirst and Satiety Driving force for intake ...thirst - Baroreceptors and Osmo receptors - detectors - ↓ of 10% plasma volume or ↑ in plasma osmolality by 1% & Hypernatremia ↓ dry mouth ↓ impulses sent to Thirst Control Centers in the Hypothalamus which also controls ADH release ↓ relay information to the Cerebral Cortex where thirst becomes a conscious sensation Urge to drink
Figure 26.5 Hypothalamic Regulation
Kidney Regulation
Factors Controlling Urine Volume 1. Blood Pressure: An increase causes a greater rate of filtration 2. Increased Concentration of Salts or Glucose in Urine: These osmotically draw more water from blood into tubules and urine. 3. Decreased Plasma Protein: failure to osmotically draw water out of tubules into the blood 4. Vasopressin Hormone: Urine volume varies inversely to this hormone. 5. Water Loss from Other Sources: Urine volume varies inversely with water lost from other systems eg. perspiration or diarrhoea. 6. Diuretics
ADH Regulation
Enhances Na+ re-absorption (and K+ secretion) Also stimulated by decrease in plasma Na+ Hormonal Regulation
Composition of Body Fluids • Water is the universal solvent • Solutes – Electrolytes – inorganic salts, all acids and bases, and some proteins. – Non-electrolytes –Most non electrolytes are organic molecules – glucose, lipids, creatinine and urea • Electrolytes have greater osmotic power than non electrolytes • Water moves according to osmotic gradients
Electrolyte Composition of Body Fluids Plasma Interstitial fluid Intracellular fluid Cations (mmol per litre Sodium 140 144 10 Potassium 4 4 155 Calcium 2.5 2 1 Magnesium 1 1 15 Anions (mmol per litre) Chloride 102 114 5 Bicarbonate 27 30 10 Phosphate 1 1 50 Sulphate 0.5 0.5 10 Protein 2 0.1 8 Organic Anions 3 6 2
Electrolyte Composition of Body Fluids
The concentration of osmotically active particles is expressed in ‘osmoles’ • 1 mol of NaCl - 2 osm • Osmolarity - mOsm/L • Osmolality - mOsm/Kg water • Osmolality defines concentration of solution Osmotic Activity of Fluids
Sodium in Fluid and Electrolyte Balance • Normal level : 135-145mEq/L. • It is the single most abundant electrolyte in the ECF • Holds a central position in fluid and electrolyte balance • It is the only electrolyte exerting significant osmotic pressure • Sodium salts: – Account for 90-95% of all solutes in the ECF – Contribute 280 mOsm of the total 300 mOsm ECF solute concentration • Regulated by dietary intake, aldosterone & kidneys
The Integration of Fluid Volume Regulation and Sodium Ion Concentrations in Body Fluids
Sodium imbalance Definiti on Risk factors/ etiology Clinical manifestation Laboratory findings management Hyponatr -aemia It is defined as a plasma sodium level below 135 mEq/ L Kidney diseases Adrenal insufficiency Gastrointestinal losses Use of diuretics (especially with along with low sodium diet) Metabolic acidosis •Weak rapid pulse •Hypotension •Dizziness •Apprehension and anxiety •Abdominal cramps •Nausea and vomiting •Diarrhea •Coma and convulsion •Cold clammy skin •Finger print impression on the sternum after palpation •Personality change •Serum sodium less than 135mEq/ L • serum osmolality less than 280mOsm/kg •urine specific gravity less than 1.010 •Identify the cause and treat *Administration of sodium orally, by NG tube or parenterally *For patients who are able to eat & drink, sodium is easily accomplished through normal diet *For those unable to eat,Ringer’s lactate solution or isotonic saline [0.9%Nacl]is given *For very low sodium 0.3%Nacl may be indicated *water restriction in case of hypervolaemia
Sodium imbalan -ce Definiti on causes Clinical manifestation Lab findings management Hypernat -remia It is define d as plasm a sodiu m level greate r than 145m E q/L *Ingestion of large amount of concentrated salts *Iatrogenic administratio n of hypertonic saline IV *Excess alderosteron e secretion • Low grade fever • Postural hypertension • Dry tongue & mucous membrane • Agitation • Convulsions • Restlessness • Excitability • Oliguria or anuria • Thirst • Dry &flushed skin *high serum sodium 135mEq/L *high serum osmolality295 mO sm/kg *high urine specificity 1.030 *Administration of hypotonic sodium solution [0.3 or 0.45%] *Rapid lowering of sodium can cause cerebral edema *Slow administration of IV fluids with the goal of reducing sodium not more than 2 mEq/L for the first 48 hrs decreases this risk *Diuretics are given in case of sodium excess *In case of Diabetes insipidus desmopressin acetate nasal spray is used *Dietary restriction of sodium in high risk clients
Potassium BalancePotassium Balance
Potassium imbalances Definitio n Causes Clinical manifestation Lab findings Management Hypokalemi a It is defined as plasma potassiu m level of less than 3.0 mEq/L *Use of potassium wasting diuretic *diarrhea, vomiting or other GI losses *Alkalosis *Cushing’s syndrome *Polyuria *Extreme sweating *excessive use of potassium free Ivs *weak irregular pulse *shallow respiration *hypotesion *weakness, decreased bowel sounds, heart blocks , paresthesia, fatigue, decreased muscle tone intestinal obstruction * K – less than 3mEq/L results in ST depression , flat T wave, taller U wave * K – less than 2mEq/L cause widened QRS, depressed ST, inverted T wave Mild hypokalemia[3.3to 3.5] can be managed by oral potassium replacement Moderate hypokalemia *K-3.0to 3.4mEq/L need 100to 200mEq/L of IV potassium for the level to rise to 1mEq/ Severe hypokalemia K- less than 3.0mEq/L need 200to 400 mEq/L for the level to rise to l mEq/L *Dietary replacement of potassium helps in correcting the problem[1875 to 5625 mg/day]
Definition Causes Clinical manifestation Lab findings Management Hyperkal emia It is defined as the elevation of potassiu m level above 5.0mEq/L Renal failure , Hypertonic dehydration, Burns& trauma Large amount of IV administration of potassium, Adrenal insufficiency Use of potassium retaining diuretics & rapid infusion of stored blood Irregular slow pulse, hypotension, anxiety, irritability, paresthesia, weakness *High serum potassium 5.3mEq/L results in peaked T wave HR 60 to 110 *serum potassium of 7mEq/L results in low broad P- wave *serum potassium levels of 8mEq/L results in no arterial activity[no p- wave] *Dietary restriction of potassium for potassium less than 5.5 mEq/L *Mild hyperkalemia can be corrected by improving output by forcing fluids, giving IV saline or potassium wasting diuretics *Severe hyperkalemia is managed by 1.infusion of calcium gluconate to decrease the antagonistic effect of potassium excess on myocardium 2.infusion of insulin and glucose or sodium bicarbonate to promote potassium uptake
Calcium imbalan ces Definitio n Causes Clinical manifestation Lab finding s Management hypocal cemia It is a plasma calcium level below 8.5 mg/dl •Rapid administration of blood containing citrate, •hypoalbuminemi a, •Hypothyroidism , •Vitamin deficiency, •neoplastic diseases, •pancreatitis •Numbness and tingling sensation of fingers, •hyperactive reflexes, • Positve Trousseau’s sign, positive chvostek’s sign , •muscle cramps, •pathological fractures, •prolonged bleeding time Serum calciu m less than 4.3 mEq/L 1.Asymtomatic hypocalcemia is treated with oral calcium chloride, calcium gluconate or calcium lactate 2.Tetany from acute hypocalcemia needs IV calcium chloride or calcium gluconate to avoid hypotension bradycardia and other dysrythmias 3.Chronic or mild hypocalcemia can be treated by consumption of food high in calcium
Calcium imbalanc e Definition Causes Clinical manifestation Lab findings Management Hypercal cemia It is calcium plasma level over 5.5 mEq/l or 11mg/dl •Hyperthyro •idism, •Metastatic bone tumors, •paget’s disease, •osteoporosis , •prolonged immobalisatio n •Decreased muscle tone, •anorexia, •nausea, vomiting, •weakness , lethargy, •low back pain from kidney stones, •decreased level of consciousnes s & cardiac arrest •High serum calcium level 5.5mEq/L, • x- ray showing generalized osteoporosis, •widened bone cavitation, •urinary stones, •elevated BUN 25mg/100ml, •elevated creatinine1.5 mg/100ml 1.IV normal saline, given rapidly with Lasix promotes urinary excretion of calcium 2.Plicamycin an antitumor antibiotics decrease the plasma calcium level 3.Calcitonin decreases serum calcium level 4.Corticosteroid drugs compete with vitamin D and decreases intestinal absorption of calcium 5. If cause is excessive use of calcium or vitamin D supplements reduce or avoid the same
Magnesium Balance • Normal conc. 1.5 – 2.4 mg% • Essential for proper functioning of enzyme systems • Depletion characterised by neuromuscular & CNS hyperactivity. Mg+2 Chvostek & Trousseau sign PR & QT interval Treatment if < 1.5mg% = 1 mEq/ Kg if 1.5 – 1.8mg% = o.5mEq/ kg Mg+2 Respiratory Depression BP, Cardiac arrest, Hyporeflexia Treatment -Calcium Infusion -Loop diuretics with NS -MgCl2 / MgSo4
Solute Overview Intracellular v/s Extracellular • Ionic composition very different • Total ionic concentration very similar • Total osmotic concentrations virtually identical Osmolarity is identical in all body fluid compartments
• Body control systems regulate ingestion and excretion: - constant total body water - constant total body osmolarity • Homeostatic mechanisms respond to changes in ECF • No receptors directly monitor fluid or electrolyte balance - Respond to changes in plasma volume or osmotic concentrations Principles of Body Water Distribution
Disorders in the fluid balance are classified in three general categories. Disturbances of - Volume - Concentration - Composition Classification of Body Fluid Changes
• Renal insufficiency, Chronic heart faliure • Iatrogenic • Cirrhosis • Drugs – NSAIDS, Mineralocorticiods • ECF is diluted – sodium content is normal but excess water is present called as Hypotonic Hydration • The resulting hyponatremia promotes net osmosis into tissue cells, causing swelling. ECF Excess
Disorders of Water Balance: Hypotonic Hydration Excessive H2O enters the ECF 1 2 ECF osmotic pressure falls 3 H2O moves into cells by osmosis; cells swell
ECF Deficit CAUSES 1. Loss of GI fluids due to: a. Vomiting b. Diarrhea c. Nasogastric suction d. Fistular drainage 2. Soft tissue injuries and infections 3. Intraabdominal and Intraperitoneal inflammatory processes 4. Burns 5. Insensible losses 6. Sweat
Dehydration Excessive loss of H2O from ECF 1 2 3ECF osmotic pressure rises Cells lose H2O to ECF by osmosis; cells shrink ECF Deficit : When salt depletion is greater, fluid loss is borne by ECF Lab Test: Hematocrit value of 45% indicates an ECF deficit. ICF Deficit : When water depletion is predominant, the greatest fluid loss is sustained by the intracellular compartment Lab Test :The sodium concentration is an indirect measure of the fluid. Higher sodium value indicates an ICF Deficit
Clinical Evaluation Changes in body weight should be recorded accurately and repeatedly on a day to day basis…. Weight loss > 300 to 500gms per day indicate dehydration secondary to decreased fluid intake and / or increased water losses. Water loss Degree of Dehydration 4% of body wt Mild 6% “ “ Moderate 8% “ “ Severe
Principles of Fluid Therapy Whenever fluid therapy is contemplated in a patient, the following basic questions must be considered…. 1. Does the patient need fluid..? 2. Which fluid would be most suitable..? 3. How much fluid is needed..? 4. At what rate..? 5. Which route is to be used..? 6. What are the likely complications..?
Does the Patient Need Fluids.. – Pre-existing disease processes • Cancer, cardiovascular, renal, GI – Age • Infants have higher % water- loss felt faster • Elderly –kidneys decreased filtration rate, less functioning nephrons, don’t excrete medications as fast – Acute illness • Surgery, burns, respiratory disorders, head injury – Environmental • Vigorous exercise, temperature extremes – Diet • Fluids and electrolytes gained through diet – Medications • Side-effects may cause fluid and/or electrolyte imbalances
Medications Likely to Cause F&E Imbalances • Diuretics – Metabolic alkalosis, hyperkalemia,hyponatremia. • Steroids – Metabolic alkalosis • Potassium supplements – GI disturbances • Respiratory center depressants (narcotic analgesics) – Respiratory acidosis • Antibiotics – Nephrotoxicity, hyperkalemia, hypernatremia • Calcium carbonate – Metabolic alkalosis • Magnesium hydroxide (Milk of Mag) – hypokalemia
Diagnostics • Hematocrit – If no anemia, can indicate hydration status • Blood creatinine – Measure kidney function • Excreted at constant level if no kidney disease • BUN – Indicates kidney function • May be affected by cell destruction or steroid therapy – Decrease may indicate malnutrition or hepatic damage – Increases with decrease in ECF volume • Serum and urinary electrolyte levels • Urine specific gravity
Assessment of Intravascular Depletion • 5% thirst, dry mucous membranes, UO 1-2 ml/kg/hr • 10% tachycardia, oliguria, UO 0.5-1 ml/kg/hr • 15%-20% tachycardia, hypotension, severe oliguria, UO < 0.5 ml/kg/hr
What Fluids to Give..What Fluids to Give.. • Choice of a particular fluid depends on – Volume status – Concentration abnormality – Compositional abnormality • Crystalloids:Crystalloids: - contain Na as the main osmotically active particle - useful for volume expansion (mainly interstitial space) - for maintenance infusion - correction of electrolyte abnormality
CrystalloidsCrystalloids • Isotonic crystalloids - Lactated Ringer’s, 0.9% NaCl - only 25% remain intravascularly • Hypertonic saline solutions - 3% NaCl - 7% NaCl • Hypotonic solutions - 0.45% NaCl - less than 10% remain intra- vascularly, inadequate for fluid resuscitation
Colloid SolutionsColloid Solutions • Contain high molecular weight substancesdo not readily migrate across capillary walls • Preparations - Albumin: 5%, 25% - Dextran - Gelifundol - Hetastarch
Crystalliod Colloid Intravascular persistance Poor Good Haemodynamic stabilisation Transient t1/2 ~ 30 mins Prolonged t1/2 ~ 90 mins Required infusion volume Large Ratio 4:1 to loss Moderate Ratio 2:1 to loss Risk of tissue oedema Obvious Insignificant Enhancement of capillary perfusion Poor Good Risk of anaphylaxis Nil Low to moderate Plasma colloid osmotic pressure Reduced Maintained Cost Inexpensive Expensive Crystalloids and Colloids
• Oral electrolyte solution: This solution is isotonic and provides a rich source of Na+ , K+ , Cl- and dextrose. The sodium citrate tends to correct any acidosis. • IV fluids: 0.9% Sodium Chloride - iso osmolar with plasma - serves a good replacement solution for ECF volume - chloride content - higher than that of plasma infusion → too much of normal saline may produce hyperchloraemic acidosis - indication : ECF def in the presence of hypernatremia, hypochloremia & metabolic alkylosis… What solution to give…
Dextrose 5% in Water • It provides 50gms of dextrose / L. • slightly hypertonic to plasma • after infusion dextrose is metabolized→ water is left in the ECF… • too much of 5% dextrose may cause dilution and hypotonicity of ECF and water loading, if kidneys are not functioning normally. Dextrose 5% with 0.9% Saline. • Its twice as hypertonic as plasma… • However within a few hours glucose is used and there is no significant change in the plasma tonicity…
Lactated Ringers Solution. • This is slightly hypo osmolar compared to plasma • Minimum effect on pH & normal body fluid composition • Replaces both G.I. & ECF losses • Used in correcting metabolic acidosis…. • Should not be given in patients with liver diseases and in presence of lactic acidosis. Ringers Acetate Solution. - slightly hypo osmolar to plasma… - main use is as a replacement for ECF deficits in patients with damaged liver or lactic acidosis.. - helps in correction of mild to moderate metabolic acidosis.
0.45% Sodium Chloride in 5% Dextrose Solution - It is used as maintenance fluid in postoperative period. - Provides sodium for renal adjustment of sodium concentration in the serum. - Potassium may be added to be used for maintenance requirements in uncomplicated pt requiring only a short period of parenteral fluids. 7.2-7.5 % Sodium Chloride - Studies have shown that even with 50% blood loss, a small volume of 7.2-7.5% NaCl restores the cardiac output and blood pressure within one minute. - This saline is given through a peripheral vein very fast over 2 to 5 mins. And this results in rise in the plasma sodium level and plasma osmolality causing a shift of body water in the vascular tree
Composition of Parental Fluids (Electrolytes Content, mEeq/L)
Practical Crystalloid Therapy • If you infuse NaCl 0.9% 1000ml, all the Na+ will remain in the ECF • As NaCl is isotonic there is no change in ECF osmolality and no water exchange occurs across the cell membrane • NaCl expands ECF only • Intravascular volume will be increased by 250ml
Practical Crystalloid Therapy • If you infuse glucose 5% 1000ml, the glucose will enter the cell and be metabolised • The water expands both ECF and ICF in proportion to their volumes • The ECF volume will increase by 333ml • Intravascular volume will only increase by approximately 100ml
Colloid Solutions Human Plasma - Used for resuscitation of shock patient and for maintenance of I.V. fluid therapy - It has a composition and osmolality similar to ECF. Human Albumin - 20% purified human albumin is commercially available. Its volume expansion capacity is 400 per cent. - Rarely, anaphylactoid reaction has been reported with albumin and may cause post resuscitation hypotension.
Hetastarch • Mixture of derivatized amylopectin of various mol. Wt. • Derivatization increases resistance to enzymatic hydrolysis • Vol. expansion ~ 100 – 172 % of infused volume - seen for 24 – 36 hrs. Dextran • It’s a polysaccharide in 0.9% NaCl / 5% Dextrose • Two types » 40 – lasts for 6 hrs » 70 – lasts for 24 hrs • Facilitates agglutination of RBC. Thus interferes with susequent cross matching of blood
The Influence of Colloid & CrystalloidThe Influence of Colloid & Crystalloid on Blood Volumeon Blood Volume 1000cc1000cc 500cc500cc 500cc500cc 500cc500cc 200200 600600 10001000 Lactated RingersLactated Ringers 5% Albumin5% Albumin 6% Hetastarch6% Hetastarch Whole bloodWhole blood Blood volumeBlood volume Infusion volume Infusion volume
• As in normal health - 0ral Route. - However when rapid correction of hypovolaemia and other electrolyte abnormalities indicated i.v. route provides a quick access to circulation. - Other routes of parenteral therapy include - Subcutaneous - Per Rectal What Route to be Used..
What Rate to be Used.. • Standard recommendation for calculation of Hourly maintenance of Fluid Replacement are : 0 – 10 Kg 4 ml / kg 11 – 20 Kg 2 ml / Kg > 20 kg 1 ml / kg So in a 70 Kg person ( 4×10 ) + ( 2 ×10 ) + ( 1× 50 ) = 110 ml/ hr
Fluid Balance in Pre Op. Period 1. Correct 3rd space losses 2. Correct Na+ balance 3. K+ to be corrected only when adequate urine output maintained 4. Check if blood replacement is required 5. Calculate Allowable Blood Loss 6. Prevention of volume depletion
Third Space Losses • Isotonic transfer of ECF from functional body fluid compartments to non-functional compartments. • Depends on location and duration of surgical procedure, amount of tissue trauma, ambient temperature, room ventilation • Replacement of 3rd space losses Minimum trauma : 3 – 4 ml / kg / hr Moderate trauma : 5- 6 ml / kg /hr Severe trauma : 7 – 8 ml / kg / hr • Surgeon must remember that by 72 hours post op., this 3rd space loss becomes mobilised which results in increased intravascular volume
Intra Op. Fluid Management • If pre-op. volume deficit not addressed --- hypotension • 3rd space losses to be addressed because of » Tissue Trauma » Extensive Dissection » May vary from min. to 3 Lt. • But no lab methods to exactly quantify fluid loss • So, clinically useful guidelines are 1. Replacement of ECF should begin intra op. 2. Blood should be replaced to maintain an acceptable RBC mass irrespective of any additional fluid/ electrolyte therapy 3. Balanced salt sol. needed intra op. ~ 0.5 – 1 Lt/ hr. Only max. of 3 Lt. req. during 4 hr major abdominal surgery
Post Op. Fluid Management 0 – 24 hrs. • Increased secretion of aldosterone & ADH » Na+ & water retention • If blood loss is there, replace it • Replace NPO fluid deficit » DNS or RL • Should not administer K+ unless definitive deficiency present
24 – 48 hrs. • Replace insensible losses which may vary from 900 – 1500 ml/ hr because of - Hyper Ventilation - Fever - Tracheostomy – upto 1200 ml/ day • Loss replaced by DNS since kidneys conserve Na+ even at this stage . • If N-G aspiration is going on then add 1 Lt. of 0.9 NaCl
48 – 72 hrs. • Replace insensible losses • Better to give isotonic DNS & RL • 1 Lt Darrow’s solution to combat K+ loss. This is more important if N-G aspiration is still going on to cover K+ loss via GI secretions Importance of I/O charts Output = urine + vomitus + aspiration + 1000 ml insensible losses + 500 – 1000 ml sweating loss Total this has to be replaced
Post Op. Urine Output • Oliguria is common in immediate post op. period because 1. Surgical stress – affects Adrenal Cortex - increase ADH & Aldosterone 2. Insufficient post op. analgesia – sympathetic activity increased 3. General anesthetics decrease glomerular blood flow & thus GFR • Persistent oliguria – < 20 ml / hr in adults – < 1 ml / hr / kg in children • If urine output < 0.5 ml / hr / kg for 3 or more hrs.– indicative of ARF. Hypovolemia
• Monitoring urine output, heart rate, BP on repeated basis and comparing them to measure fluid intake assists in determining fluid requirement …. • Normal urinary output Adult 0.5-1 ml / kg / hr Child 2 ml / kg / hr End Parameters for Fluid Replacement Therapy
Fluid Regulation in Young • Fluid balance in young is dicey because… • In neonates most significant source of water loss is insensible water loss through skin ~ 7ml / kg / hr • Under normal renal function • Infants & neonates – 2 ml / kg • Toddlers & school age – 1 ml / kg • Daily K+ req. = 2mEq/ kg Na+ req. = 3 mEq/ kg • Maintenance fluid rate  0 – 10 kg - 4 ml / kg / hr 10 – 20 kg - 40 ml + 2 ml / kg / hr  > 20 kg - 60 ml + 1 ml / kg / hr
Blood Replacements Blood weightage – males 66 ml / kg - females 60 ml / kg Indications 1. If Hb. < 6 gm% 2. Ongoing fluid loss of 100 ml/ hr 3. ACS Class IV Haemorrhage 4. Give early in active bleeding Hemodilution • Indicated in surgeries where intra op. blood loss of 2 or more units is anticipated • plasma volume restoration with crystalloids/ colloids • Blood reinfused only after cessation of bleeding
ShockShock Pathophysiology, Classification, andPathophysiology, Classification, and Approach to ManagementApproach to Management
Shock: DefinitionShock: Definition Kumar and Parrillo (1995) - “The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury.”
Classification of Circulatory ShockClassification of Circulatory Shock HYPOVOLEMIC Hemorrhagic • Trauma • Gastrointestinal • Retroperitoneal Fluid depletion (nonhemorrhagic) • External fluid loss - Dehydration - Vomiting - Diarrhea - Polyuria • Interstitial fluid redistribution - Thermal injury - Trauma - Anaphylaxis Increased vascular capacitance (venodilatation) • Sepsis • Anaphylaxis • Toxins/drugs
CARDIOGENIC Myopathic • Myocardial infarction (hibernating myocardium) • Left ventricle Right ventricle Myocardial contusion (trauma) Myocarditis Cardiomyopathy Septic myocardial depression Pharmacologic • Calcium channel blockers Mechanical • Valvular failure (stenotic or regurgitant) • Hypertropic cardiomyopathy • Ventricular septal defect Arrhythmic • Bradycardia • Tachycardia • Classification of Circulatory ShockClassification of Circulatory Shock
Classification of Circulatory ShockClassification of Circulatory Shock EXTRACARDIAC OBSTRUCTIVE Impaired diastolic filling (decreased ventricular preload) • Direct venous obstruction (vena cava) • Increased intrathoracic pressure - Tension pneumothorax - Mechanical ventilation (with excessive pressure or volume depletion) - Asthma • Decreased cardiac compliance - Constrictive pericarditis - Cardiac tamponade Impaired systolic contraction (increased ventricular afterload) • Right ventricle - Pulmonary embolus (massive) - Acute pulmonary hypertension • Left ventricle - Saddle embolus - Aortic dissection
Classification of Circulatory ShockClassification of Circulatory Shock DISTRIBUTIVE Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic • Adrenal crisis • Thyroid storm Toxic (e.g., nitroprusside, bretylium)
TABLE I: CLASSIFICATION OF SHOCK (based on a 70 kg patient) CLASS (mL) up to 750 750-1500 1500-2000 2000 or more Blood Loss (%BV) up to 15% 15-30% 30-40% 40% or more Pulse Rate <100 >100 >120 140 or higher Blood Pressure Normal Normal Decreased Decreased Pulse Pressure Normal/Increased Decreased Decreased Decreased Capillary Refill Normal Decreased Decreased Decreased Respiratory Rate 14-20 20-30 30-40 >35 Urine Output (mL/hr) 30 or more 20-30 5-15 Negligible CNS-Mental Status Slightly-anxious Anxious Anxious - Confused- confused lethargic Fluid Replacement Crystalloid Crystalloid Crystalloid Crystalloid + blood + blood (Modified from: Committee on Trauma of the American College of Surgeons.
Initial Therapeutic StepsInitial Therapeutic Steps A Clinical Approach to ShockA Clinical Approach to Shock Diagnosis and ManagementDiagnosis and Management Admit to intensive care unit (ICU) Venous access (1 or 2 wide-bore catheters) Central venous catheter Arterial catheter ECG monitoring Pulse oximetry Hemodynamic support (MAP < 60 mmHg) • Fluid challenge • Vasopressors for severe shock unresponsive to fluids
Conclusion I.V fluids should be administered with caution Input-output chart should me maintained Electrolyte level should be monitored. The maximum volume is the least volume needed.
References • Clinics in Endocrinology and Metabolism – D. Brian Morgan. • Principles of Surgery – Schwartz • Principles of Surgery – Sabiston • Essentials of Human Anatomy & Physiology – Marieb • Human Physiology – Guyton and Hall • Oral & MaxilloFacial Sugery Clinics of North America – HarryDym
Thank you…

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Fluid and electrolyte balance ih

  • 2.
    Fluid and ElectrolyteBalance Presenter : Dr ITRAT HUSSAIN Moderator : Dr. ANUJA AGARWAL
  • 3.
    Daily we consume2250 ml of water but…. • Why do we need to drink water… • Where does all this water go… • Why we drink only this much of water…
  • 4.
    We need todrink water because.. 1 All chemical reactions occur in liquid medium. 2 It is crucial in regulating chemical and bioelectrical distributions within cells. 3 Transports substances such as hormones and nutrients. 4 O2 transport from lungs to body cells. 5 CO2 transport in the opposite direction. 6 Dilutes toxic substances and waste products and transports them to the kidneys and the liver. 7 Distributes heat around the body
  • 5.
    Where does allthis water go… • Water constitutes an average 50 to 70% of the total body weight Young males - 60% of total body weight Older males – 52% Young females – 50% of total body weight Older females – 47% • Variation of ±15% in both groups is normal • Obese have 25 to 30% less body water than lean people. • Infants 75 to 80% - gradual physiological loss of body water - 65% at one year of age
  • 6.
    Functional Components ofthe Body Fluid The water of the body is divided into 3 functional components: (TBW – 60%) Intracellular Fluid – 40% of the body weight Extracellular Fluid – 20% of the body weight Extravascular interstitial fluid 15% of BW Intravascular plasma 5% of BW Rapidly equilibrating / functional component 13-14% of BW Slowly equilibrating / non-functional component 1-2% BW 1. Connective tissue water 2. Transcellular fluid i.e. CSF, joint fluid
  • 8.
    We consume onlythis much fluids because… In HOMOEOSTASIS 1. output = intake 2. Dynamic fluid equilibrium at a) Blood & interstitial fluid level b) Interstitial fluid and cell level 3. Thirst & Satiety 4. Kidney fluid control 5. Hormonal regulation
  • 9.
    Dynamic Fluid Equilibrium 1.Interstitial Fluid & cell interface . Ion pumps & carriers 2. Blood & interstitial fluid interface . Starlings forces
  • 10.
    Fluid Movement Among Compartments •Compartmental exchange is regulated by osmotic and hydrostatic pressures. • Net leakage of fluid from the blood is picked up by lymphatic vessels and returned to the bloodstream. • Exchanges between interstitial and intracellular fluids are complex due to the selective permeability of the cellular membranes.
  • 11.
    Extracellular and IntracellularFluids • Ion fluxes are restricted and move selectively by active transport. • Nutrients, respiratory gases, and wastes move unidirectionally. • Plasma is the only fluid that circulates throughout the body and links external and internal environments. • Osmolalities of all body fluids are equal; changes in solute concentrations are quickly followed by osmotic changes.
  • 12.
    Thirst and Satiety Drivingforce for intake ...thirst - Baroreceptors and Osmo receptors - detectors - ↓ of 10% plasma volume or ↑ in plasma osmolality by 1% & Hypernatremia ↓ dry mouth ↓ impulses sent to Thirst Control Centers in the Hypothalamus which also controls ADH release ↓ relay information to the Cerebral Cortex where thirst becomes a conscious sensation Urge to drink
  • 13.
  • 14.
  • 16.
    Factors Controlling UrineVolume 1. Blood Pressure: An increase causes a greater rate of filtration 2. Increased Concentration of Salts or Glucose in Urine: These osmotically draw more water from blood into tubules and urine. 3. Decreased Plasma Protein: failure to osmotically draw water out of tubules into the blood 4. Vasopressin Hormone: Urine volume varies inversely to this hormone. 5. Water Loss from Other Sources: Urine volume varies inversely with water lost from other systems eg. perspiration or diarrhoea. 6. Diuretics
  • 17.
  • 18.
    Enhances Na+ re-absorption (and K+ secretion) Alsostimulated by decrease in plasma Na+ Hormonal Regulation
  • 20.
    Composition of BodyFluids • Water is the universal solvent • Solutes – Electrolytes – inorganic salts, all acids and bases, and some proteins. – Non-electrolytes –Most non electrolytes are organic molecules – glucose, lipids, creatinine and urea • Electrolytes have greater osmotic power than non electrolytes • Water moves according to osmotic gradients
  • 21.
    Electrolyte Composition ofBody Fluids Plasma Interstitial fluid Intracellular fluid Cations (mmol per litre Sodium 140 144 10 Potassium 4 4 155 Calcium 2.5 2 1 Magnesium 1 1 15 Anions (mmol per litre) Chloride 102 114 5 Bicarbonate 27 30 10 Phosphate 1 1 50 Sulphate 0.5 0.5 10 Protein 2 0.1 8 Organic Anions 3 6 2
  • 22.
  • 23.
    The concentration ofosmotically active particles is expressed in ‘osmoles’ • 1 mol of NaCl - 2 osm • Osmolarity - mOsm/L • Osmolality - mOsm/Kg water • Osmolality defines concentration of solution Osmotic Activity of Fluids
  • 24.
    Sodium in Fluidand Electrolyte Balance • Normal level : 135-145mEq/L. • It is the single most abundant electrolyte in the ECF • Holds a central position in fluid and electrolyte balance • It is the only electrolyte exerting significant osmotic pressure • Sodium salts: – Account for 90-95% of all solutes in the ECF – Contribute 280 mOsm of the total 300 mOsm ECF solute concentration • Regulated by dietary intake, aldosterone & kidneys
  • 25.
    The Integration ofFluid Volume Regulation and Sodium Ion Concentrations in Body Fluids
  • 26.
    Sodium imbalance Definiti on Risk factors/ etiology Clinical manifestation Laboratory findings management Hyponatr -aemia Itis defined as a plasma sodium level below 135 mEq/ L Kidney diseases Adrenal insufficiency Gastrointestinal losses Use of diuretics (especially with along with low sodium diet) Metabolic acidosis •Weak rapid pulse •Hypotension •Dizziness •Apprehension and anxiety •Abdominal cramps •Nausea and vomiting •Diarrhea •Coma and convulsion •Cold clammy skin •Finger print impression on the sternum after palpation •Personality change •Serum sodium less than 135mEq/ L • serum osmolality less than 280mOsm/kg •urine specific gravity less than 1.010 •Identify the cause and treat *Administration of sodium orally, by NG tube or parenterally *For patients who are able to eat & drink, sodium is easily accomplished through normal diet *For those unable to eat,Ringer’s lactate solution or isotonic saline [0.9%Nacl]is given *For very low sodium 0.3%Nacl may be indicated *water restriction in case of hypervolaemia
  • 27.
    Sodium imbalan -ce Definiti on causes Clinical manifestation Lab findingsmanagement Hypernat -remia It is define d as plasm a sodiu m level greate r than 145m E q/L *Ingestion of large amount of concentrated salts *Iatrogenic administratio n of hypertonic saline IV *Excess alderosteron e secretion • Low grade fever • Postural hypertension • Dry tongue & mucous membrane • Agitation • Convulsions • Restlessness • Excitability • Oliguria or anuria • Thirst • Dry &flushed skin *high serum sodium 135mEq/L *high serum osmolality295 mO sm/kg *high urine specificity 1.030 *Administration of hypotonic sodium solution [0.3 or 0.45%] *Rapid lowering of sodium can cause cerebral edema *Slow administration of IV fluids with the goal of reducing sodium not more than 2 mEq/L for the first 48 hrs decreases this risk *Diuretics are given in case of sodium excess *In case of Diabetes insipidus desmopressin acetate nasal spray is used *Dietary restriction of sodium in high risk clients
  • 28.
  • 29.
    Potassium imbalances Definitio n Causes Clinical manifestation Lab findingsManagement Hypokalemi a It is defined as plasma potassiu m level of less than 3.0 mEq/L *Use of potassium wasting diuretic *diarrhea, vomiting or other GI losses *Alkalosis *Cushing’s syndrome *Polyuria *Extreme sweating *excessive use of potassium free Ivs *weak irregular pulse *shallow respiration *hypotesion *weakness, decreased bowel sounds, heart blocks , paresthesia, fatigue, decreased muscle tone intestinal obstruction * K – less than 3mEq/L results in ST depression , flat T wave, taller U wave * K – less than 2mEq/L cause widened QRS, depressed ST, inverted T wave Mild hypokalemia[3.3to 3.5] can be managed by oral potassium replacement Moderate hypokalemia *K-3.0to 3.4mEq/L need 100to 200mEq/L of IV potassium for the level to rise to 1mEq/ Severe hypokalemia K- less than 3.0mEq/L need 200to 400 mEq/L for the level to rise to l mEq/L *Dietary replacement of potassium helps in correcting the problem[1875 to 5625 mg/day]
  • 30.
    Definition Causes Clinical manifestation Labfindings Management Hyperkal emia It is defined as the elevation of potassiu m level above 5.0mEq/L Renal failure , Hypertonic dehydration, Burns& trauma Large amount of IV administration of potassium, Adrenal insufficiency Use of potassium retaining diuretics & rapid infusion of stored blood Irregular slow pulse, hypotension, anxiety, irritability, paresthesia, weakness *High serum potassium 5.3mEq/L results in peaked T wave HR 60 to 110 *serum potassium of 7mEq/L results in low broad P- wave *serum potassium levels of 8mEq/L results in no arterial activity[no p- wave] *Dietary restriction of potassium for potassium less than 5.5 mEq/L *Mild hyperkalemia can be corrected by improving output by forcing fluids, giving IV saline or potassium wasting diuretics *Severe hyperkalemia is managed by 1.infusion of calcium gluconate to decrease the antagonistic effect of potassium excess on myocardium 2.infusion of insulin and glucose or sodium bicarbonate to promote potassium uptake
  • 31.
    Calcium imbalan ces Definitio n Causes Clinical manifestation Lab finding s Management hypocal cemia It isa plasma calcium level below 8.5 mg/dl •Rapid administration of blood containing citrate, •hypoalbuminemi a, •Hypothyroidism , •Vitamin deficiency, •neoplastic diseases, •pancreatitis •Numbness and tingling sensation of fingers, •hyperactive reflexes, • Positve Trousseau’s sign, positive chvostek’s sign , •muscle cramps, •pathological fractures, •prolonged bleeding time Serum calciu m less than 4.3 mEq/L 1.Asymtomatic hypocalcemia is treated with oral calcium chloride, calcium gluconate or calcium lactate 2.Tetany from acute hypocalcemia needs IV calcium chloride or calcium gluconate to avoid hypotension bradycardia and other dysrythmias 3.Chronic or mild hypocalcemia can be treated by consumption of food high in calcium
  • 32.
    Calcium imbalanc e Definition Causes Clinical manifestation Labfindings Management Hypercal cemia It is calcium plasma level over 5.5 mEq/l or 11mg/dl •Hyperthyro •idism, •Metastatic bone tumors, •paget’s disease, •osteoporosis , •prolonged immobalisatio n •Decreased muscle tone, •anorexia, •nausea, vomiting, •weakness , lethargy, •low back pain from kidney stones, •decreased level of consciousnes s & cardiac arrest •High serum calcium level 5.5mEq/L, • x- ray showing generalized osteoporosis, •widened bone cavitation, •urinary stones, •elevated BUN 25mg/100ml, •elevated creatinine1.5 mg/100ml 1.IV normal saline, given rapidly with Lasix promotes urinary excretion of calcium 2.Plicamycin an antitumor antibiotics decrease the plasma calcium level 3.Calcitonin decreases serum calcium level 4.Corticosteroid drugs compete with vitamin D and decreases intestinal absorption of calcium 5. If cause is excessive use of calcium or vitamin D supplements reduce or avoid the same
  • 33.
    Magnesium Balance • Normalconc. 1.5 – 2.4 mg% • Essential for proper functioning of enzyme systems • Depletion characterised by neuromuscular & CNS hyperactivity. Mg+2 Chvostek & Trousseau sign PR & QT interval Treatment if < 1.5mg% = 1 mEq/ Kg if 1.5 – 1.8mg% = o.5mEq/ kg Mg+2 Respiratory Depression BP, Cardiac arrest, Hyporeflexia Treatment -Calcium Infusion -Loop diuretics with NS -MgCl2 / MgSo4
  • 34.
    Solute Overview Intracellular v/sExtracellular • Ionic composition very different • Total ionic concentration very similar • Total osmotic concentrations virtually identical Osmolarity is identical in all body fluid compartments
  • 35.
    • Body controlsystems regulate ingestion and excretion: - constant total body water - constant total body osmolarity • Homeostatic mechanisms respond to changes in ECF • No receptors directly monitor fluid or electrolyte balance - Respond to changes in plasma volume or osmotic concentrations Principles of Body Water Distribution
  • 36.
    Disorders in thefluid balance are classified in three general categories. Disturbances of - Volume - Concentration - Composition Classification of Body Fluid Changes
  • 37.
    • Renal insufficiency,Chronic heart faliure • Iatrogenic • Cirrhosis • Drugs – NSAIDS, Mineralocorticiods • ECF is diluted – sodium content is normal but excess water is present called as Hypotonic Hydration • The resulting hyponatremia promotes net osmosis into tissue cells, causing swelling. ECF Excess
  • 38.
    Disorders of WaterBalance: Hypotonic Hydration Excessive H2O enters the ECF 1 2 ECF osmotic pressure falls 3 H2O moves into cells by osmosis; cells swell
  • 39.
    ECF Deficit CAUSES 1. Lossof GI fluids due to: a. Vomiting b. Diarrhea c. Nasogastric suction d. Fistular drainage 2. Soft tissue injuries and infections 3. Intraabdominal and Intraperitoneal inflammatory processes 4. Burns 5. Insensible losses 6. Sweat
  • 40.
    Dehydration Excessive loss ofH2O from ECF 1 2 3ECF osmotic pressure rises Cells lose H2O to ECF by osmosis; cells shrink ECF Deficit : When salt depletion is greater, fluid loss is borne by ECF Lab Test: Hematocrit value of 45% indicates an ECF deficit. ICF Deficit : When water depletion is predominant, the greatest fluid loss is sustained by the intracellular compartment Lab Test :The sodium concentration is an indirect measure of the fluid. Higher sodium value indicates an ICF Deficit
  • 41.
    Clinical Evaluation Changes inbody weight should be recorded accurately and repeatedly on a day to day basis…. Weight loss > 300 to 500gms per day indicate dehydration secondary to decreased fluid intake and / or increased water losses. Water loss Degree of Dehydration 4% of body wt Mild 6% “ “ Moderate 8% “ “ Severe
  • 42.
    Principles of FluidTherapy Whenever fluid therapy is contemplated in a patient, the following basic questions must be considered…. 1. Does the patient need fluid..? 2. Which fluid would be most suitable..? 3. How much fluid is needed..? 4. At what rate..? 5. Which route is to be used..? 6. What are the likely complications..?
  • 43.
    Does the PatientNeed Fluids.. – Pre-existing disease processes • Cancer, cardiovascular, renal, GI – Age • Infants have higher % water- loss felt faster • Elderly –kidneys decreased filtration rate, less functioning nephrons, don’t excrete medications as fast – Acute illness • Surgery, burns, respiratory disorders, head injury – Environmental • Vigorous exercise, temperature extremes – Diet • Fluids and electrolytes gained through diet – Medications • Side-effects may cause fluid and/or electrolyte imbalances
  • 44.
    Medications Likely toCause F&E Imbalances • Diuretics – Metabolic alkalosis, hyperkalemia,hyponatremia. • Steroids – Metabolic alkalosis • Potassium supplements – GI disturbances • Respiratory center depressants (narcotic analgesics) – Respiratory acidosis • Antibiotics – Nephrotoxicity, hyperkalemia, hypernatremia • Calcium carbonate – Metabolic alkalosis • Magnesium hydroxide (Milk of Mag) – hypokalemia
  • 45.
    Diagnostics • Hematocrit – Ifno anemia, can indicate hydration status • Blood creatinine – Measure kidney function • Excreted at constant level if no kidney disease • BUN – Indicates kidney function • May be affected by cell destruction or steroid therapy – Decrease may indicate malnutrition or hepatic damage – Increases with decrease in ECF volume • Serum and urinary electrolyte levels • Urine specific gravity
  • 46.
    Assessment of Intravascular Depletion •5% thirst, dry mucous membranes, UO 1-2 ml/kg/hr • 10% tachycardia, oliguria, UO 0.5-1 ml/kg/hr • 15%-20% tachycardia, hypotension, severe oliguria, UO < 0.5 ml/kg/hr
  • 47.
    What Fluids toGive..What Fluids to Give.. • Choice of a particular fluid depends on – Volume status – Concentration abnormality – Compositional abnormality • Crystalloids:Crystalloids: - contain Na as the main osmotically active particle - useful for volume expansion (mainly interstitial space) - for maintenance infusion - correction of electrolyte abnormality
  • 48.
    CrystalloidsCrystalloids • Isotonic crystalloids -Lactated Ringer’s, 0.9% NaCl - only 25% remain intravascularly • Hypertonic saline solutions - 3% NaCl - 7% NaCl • Hypotonic solutions - 0.45% NaCl - less than 10% remain intra- vascularly, inadequate for fluid resuscitation
  • 49.
    Colloid SolutionsColloid Solutions •Contain high molecular weight substancesdo not readily migrate across capillary walls • Preparations - Albumin: 5%, 25% - Dextran - Gelifundol - Hetastarch
  • 50.
    Crystalliod Colloid Intravascular persistancePoor Good Haemodynamic stabilisation Transient t1/2 ~ 30 mins Prolonged t1/2 ~ 90 mins Required infusion volume Large Ratio 4:1 to loss Moderate Ratio 2:1 to loss Risk of tissue oedema Obvious Insignificant Enhancement of capillary perfusion Poor Good Risk of anaphylaxis Nil Low to moderate Plasma colloid osmotic pressure Reduced Maintained Cost Inexpensive Expensive Crystalloids and Colloids
  • 51.
    • Oral electrolytesolution: This solution is isotonic and provides a rich source of Na+ , K+ , Cl- and dextrose. The sodium citrate tends to correct any acidosis. • IV fluids: 0.9% Sodium Chloride - iso osmolar with plasma - serves a good replacement solution for ECF volume - chloride content - higher than that of plasma infusion → too much of normal saline may produce hyperchloraemic acidosis - indication : ECF def in the presence of hypernatremia, hypochloremia & metabolic alkylosis… What solution to give…
  • 52.
    Dextrose 5% inWater • It provides 50gms of dextrose / L. • slightly hypertonic to plasma • after infusion dextrose is metabolized→ water is left in the ECF… • too much of 5% dextrose may cause dilution and hypotonicity of ECF and water loading, if kidneys are not functioning normally. Dextrose 5% with 0.9% Saline. • Its twice as hypertonic as plasma… • However within a few hours glucose is used and there is no significant change in the plasma tonicity…
  • 53.
    Lactated Ringers Solution. •This is slightly hypo osmolar compared to plasma • Minimum effect on pH & normal body fluid composition • Replaces both G.I. & ECF losses • Used in correcting metabolic acidosis…. • Should not be given in patients with liver diseases and in presence of lactic acidosis. Ringers Acetate Solution. - slightly hypo osmolar to plasma… - main use is as a replacement for ECF deficits in patients with damaged liver or lactic acidosis.. - helps in correction of mild to moderate metabolic acidosis.
  • 54.
    0.45% Sodium Chloridein 5% Dextrose Solution - It is used as maintenance fluid in postoperative period. - Provides sodium for renal adjustment of sodium concentration in the serum. - Potassium may be added to be used for maintenance requirements in uncomplicated pt requiring only a short period of parenteral fluids. 7.2-7.5 % Sodium Chloride - Studies have shown that even with 50% blood loss, a small volume of 7.2-7.5% NaCl restores the cardiac output and blood pressure within one minute. - This saline is given through a peripheral vein very fast over 2 to 5 mins. And this results in rise in the plasma sodium level and plasma osmolality causing a shift of body water in the vascular tree
  • 55.
    Composition of ParentalFluids (Electrolytes Content, mEeq/L)
  • 56.
    Practical Crystalloid Therapy •If you infuse NaCl 0.9% 1000ml, all the Na+ will remain in the ECF • As NaCl is isotonic there is no change in ECF osmolality and no water exchange occurs across the cell membrane • NaCl expands ECF only • Intravascular volume will be increased by 250ml
  • 57.
    Practical Crystalloid Therapy •If you infuse glucose 5% 1000ml, the glucose will enter the cell and be metabolised • The water expands both ECF and ICF in proportion to their volumes • The ECF volume will increase by 333ml • Intravascular volume will only increase by approximately 100ml
  • 58.
    Colloid Solutions Human Plasma -Used for resuscitation of shock patient and for maintenance of I.V. fluid therapy - It has a composition and osmolality similar to ECF. Human Albumin - 20% purified human albumin is commercially available. Its volume expansion capacity is 400 per cent. - Rarely, anaphylactoid reaction has been reported with albumin and may cause post resuscitation hypotension.
  • 59.
    Hetastarch • Mixture ofderivatized amylopectin of various mol. Wt. • Derivatization increases resistance to enzymatic hydrolysis • Vol. expansion ~ 100 – 172 % of infused volume - seen for 24 – 36 hrs. Dextran • It’s a polysaccharide in 0.9% NaCl / 5% Dextrose • Two types » 40 – lasts for 6 hrs » 70 – lasts for 24 hrs • Facilitates agglutination of RBC. Thus interferes with susequent cross matching of blood
  • 60.
    The Influence ofColloid & CrystalloidThe Influence of Colloid & Crystalloid on Blood Volumeon Blood Volume 1000cc1000cc 500cc500cc 500cc500cc 500cc500cc 200200 600600 10001000 Lactated RingersLactated Ringers 5% Albumin5% Albumin 6% Hetastarch6% Hetastarch Whole bloodWhole blood Blood volumeBlood volume Infusion volume Infusion volume
  • 61.
    • As innormal health - 0ral Route. - However when rapid correction of hypovolaemia and other electrolyte abnormalities indicated i.v. route provides a quick access to circulation. - Other routes of parenteral therapy include - Subcutaneous - Per Rectal What Route to be Used..
  • 62.
    What Rate tobe Used.. • Standard recommendation for calculation of Hourly maintenance of Fluid Replacement are : 0 – 10 Kg 4 ml / kg 11 – 20 Kg 2 ml / Kg > 20 kg 1 ml / kg So in a 70 Kg person ( 4×10 ) + ( 2 ×10 ) + ( 1× 50 ) = 110 ml/ hr
  • 63.
    Fluid Balance inPre Op. Period 1. Correct 3rd space losses 2. Correct Na+ balance 3. K+ to be corrected only when adequate urine output maintained 4. Check if blood replacement is required 5. Calculate Allowable Blood Loss 6. Prevention of volume depletion
  • 64.
    Third Space Losses •Isotonic transfer of ECF from functional body fluid compartments to non-functional compartments. • Depends on location and duration of surgical procedure, amount of tissue trauma, ambient temperature, room ventilation • Replacement of 3rd space losses Minimum trauma : 3 – 4 ml / kg / hr Moderate trauma : 5- 6 ml / kg /hr Severe trauma : 7 – 8 ml / kg / hr • Surgeon must remember that by 72 hours post op., this 3rd space loss becomes mobilised which results in increased intravascular volume
  • 65.
    Intra Op. FluidManagement • If pre-op. volume deficit not addressed --- hypotension • 3rd space losses to be addressed because of » Tissue Trauma » Extensive Dissection » May vary from min. to 3 Lt. • But no lab methods to exactly quantify fluid loss • So, clinically useful guidelines are 1. Replacement of ECF should begin intra op. 2. Blood should be replaced to maintain an acceptable RBC mass irrespective of any additional fluid/ electrolyte therapy 3. Balanced salt sol. needed intra op. ~ 0.5 – 1 Lt/ hr. Only max. of 3 Lt. req. during 4 hr major abdominal surgery
  • 66.
    Post Op. FluidManagement 0 – 24 hrs. • Increased secretion of aldosterone & ADH » Na+ & water retention • If blood loss is there, replace it • Replace NPO fluid deficit » DNS or RL • Should not administer K+ unless definitive deficiency present
  • 67.
    24 – 48hrs. • Replace insensible losses which may vary from 900 – 1500 ml/ hr because of - Hyper Ventilation - Fever - Tracheostomy – upto 1200 ml/ day • Loss replaced by DNS since kidneys conserve Na+ even at this stage . • If N-G aspiration is going on then add 1 Lt. of 0.9 NaCl
  • 68.
    48 – 72hrs. • Replace insensible losses • Better to give isotonic DNS & RL • 1 Lt Darrow’s solution to combat K+ loss. This is more important if N-G aspiration is still going on to cover K+ loss via GI secretions Importance of I/O charts Output = urine + vomitus + aspiration + 1000 ml insensible losses + 500 – 1000 ml sweating loss Total this has to be replaced
  • 69.
    Post Op. UrineOutput • Oliguria is common in immediate post op. period because 1. Surgical stress – affects Adrenal Cortex - increase ADH & Aldosterone 2. Insufficient post op. analgesia – sympathetic activity increased 3. General anesthetics decrease glomerular blood flow & thus GFR • Persistent oliguria – < 20 ml / hr in adults – < 1 ml / hr / kg in children • If urine output < 0.5 ml / hr / kg for 3 or more hrs.– indicative of ARF. Hypovolemia
  • 70.
    • Monitoring urineoutput, heart rate, BP on repeated basis and comparing them to measure fluid intake assists in determining fluid requirement …. • Normal urinary output Adult 0.5-1 ml / kg / hr Child 2 ml / kg / hr End Parameters for Fluid Replacement Therapy
  • 71.
    Fluid Regulation inYoung • Fluid balance in young is dicey because… • In neonates most significant source of water loss is insensible water loss through skin ~ 7ml / kg / hr • Under normal renal function • Infants & neonates – 2 ml / kg • Toddlers & school age – 1 ml / kg • Daily K+ req. = 2mEq/ kg Na+ req. = 3 mEq/ kg • Maintenance fluid rate  0 – 10 kg - 4 ml / kg / hr 10 – 20 kg - 40 ml + 2 ml / kg / hr  > 20 kg - 60 ml + 1 ml / kg / hr
  • 72.
    Blood Replacements Blood weightage– males 66 ml / kg - females 60 ml / kg Indications 1. If Hb. < 6 gm% 2. Ongoing fluid loss of 100 ml/ hr 3. ACS Class IV Haemorrhage 4. Give early in active bleeding Hemodilution • Indicated in surgeries where intra op. blood loss of 2 or more units is anticipated • plasma volume restoration with crystalloids/ colloids • Blood reinfused only after cessation of bleeding
  • 73.
    ShockShock Pathophysiology, Classification, andPathophysiology,Classification, and Approach to ManagementApproach to Management
  • 74.
    Shock: DefinitionShock: Definition Kumarand Parrillo (1995) - “The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury.”
  • 75.
    Classification of CirculatoryShockClassification of Circulatory Shock HYPOVOLEMIC Hemorrhagic • Trauma • Gastrointestinal • Retroperitoneal Fluid depletion (nonhemorrhagic) • External fluid loss - Dehydration - Vomiting - Diarrhea - Polyuria • Interstitial fluid redistribution - Thermal injury - Trauma - Anaphylaxis Increased vascular capacitance (venodilatation) • Sepsis • Anaphylaxis • Toxins/drugs
  • 76.
    CARDIOGENIC Myopathic • Myocardial infarction(hibernating myocardium) • Left ventricle Right ventricle Myocardial contusion (trauma) Myocarditis Cardiomyopathy Septic myocardial depression Pharmacologic • Calcium channel blockers Mechanical • Valvular failure (stenotic or regurgitant) • Hypertropic cardiomyopathy • Ventricular septal defect Arrhythmic • Bradycardia • Tachycardia • Classification of Circulatory ShockClassification of Circulatory Shock
  • 77.
    Classification of CirculatoryShockClassification of Circulatory Shock EXTRACARDIAC OBSTRUCTIVE Impaired diastolic filling (decreased ventricular preload) • Direct venous obstruction (vena cava) • Increased intrathoracic pressure - Tension pneumothorax - Mechanical ventilation (with excessive pressure or volume depletion) - Asthma • Decreased cardiac compliance - Constrictive pericarditis - Cardiac tamponade Impaired systolic contraction (increased ventricular afterload) • Right ventricle - Pulmonary embolus (massive) - Acute pulmonary hypertension • Left ventricle - Saddle embolus - Aortic dissection
  • 78.
    Classification of CirculatoryShockClassification of Circulatory Shock DISTRIBUTIVE Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic • Adrenal crisis • Thyroid storm Toxic (e.g., nitroprusside, bretylium)
  • 79.
    TABLE I: CLASSIFICATIONOF SHOCK (based on a 70 kg patient) CLASS (mL) up to 750 750-1500 1500-2000 2000 or more Blood Loss (%BV) up to 15% 15-30% 30-40% 40% or more Pulse Rate <100 >100 >120 140 or higher Blood Pressure Normal Normal Decreased Decreased Pulse Pressure Normal/Increased Decreased Decreased Decreased Capillary Refill Normal Decreased Decreased Decreased Respiratory Rate 14-20 20-30 30-40 >35 Urine Output (mL/hr) 30 or more 20-30 5-15 Negligible CNS-Mental Status Slightly-anxious Anxious Anxious - Confused- confused lethargic Fluid Replacement Crystalloid Crystalloid Crystalloid Crystalloid + blood + blood (Modified from: Committee on Trauma of the American College of Surgeons.
  • 82.
    Initial Therapeutic StepsInitialTherapeutic Steps A Clinical Approach to ShockA Clinical Approach to Shock Diagnosis and ManagementDiagnosis and Management Admit to intensive care unit (ICU) Venous access (1 or 2 wide-bore catheters) Central venous catheter Arterial catheter ECG monitoring Pulse oximetry Hemodynamic support (MAP < 60 mmHg) • Fluid challenge • Vasopressors for severe shock unresponsive to fluids
  • 83.
    Conclusion I.V fluids shouldbe administered with caution Input-output chart should me maintained Electrolyte level should be monitored. The maximum volume is the least volume needed.
  • 84.
    References • Clinics inEndocrinology and Metabolism – D. Brian Morgan. • Principles of Surgery – Schwartz • Principles of Surgery – Sabiston • Essentials of Human Anatomy & Physiology – Marieb • Human Physiology – Guyton and Hall • Oral & MaxilloFacial Sugery Clinics of North America – HarryDym
  • 85.