Discuss principles of fluid and electrolyte management of the Presenter Dr Bashiru Aminu Click to edit patient surgicalMaster subtitle

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Moderator Dr Bello

outline
Introduction Anatomy and physiology distribution Classification of body fluid changes Fluid therapy -preoperative -intraoperative -postoperative Complications

Introduction
Fluid and electrolyte management Important part of the perioperative management of the surgical patient Critical factor in some patients as a result of the response to surgery and trauma Understanding of the metabolism of these fluid and electrolyte is essential to the care of surgical patients

Distribution of body water

Water half of adults body TBW 60% of body weight (young men) 50% of body weight (young women and older men) 45% of body weight (older women) TBW Intracellular of TBW Extracellular of TBW

Distribution of body water

Extracellular fluid (ECF) Intravascular 4% of body weight (men) Extravascular Interstitial 15% of body weight Transcellular 1% of body weight Transcellular fluid bone, dense CT, GIT secretions, CSF, synovial fluid, etc.

Distribution of body water

is less in obese patients fat content TBW is less in females relatively smaller muscle mass and higher fat deposits In Children TBW 75 80% at birth, decreases steadily to 65% at 1yr ECF 35% at birth, decreases to 20% at 2yrs ICF changes minimally
TBW

Electrolyte distribution in body fluids

Difference

in ionic composition of ICF and ECF due to the cell membrane semi permeable osmotic pressure contributed to by any substance that does not freely traverse the cell membrane

Effective

Ion Na K

Electrolyte distribution in body fluids

Intravascular mmol/L 140 4 1.25 0.7 0.9 95 105 24 27 0.8 1.4 2 Interstitial mmol/L 143 4 0.625 0.75 115 30 1.6 0 1 3

Intracellular mmol/L 8 140 1 15 8 14 25.8 9 20 -

Ca2+ Mg Cl HCO3PO43Protein

SO421 Organic acids 3

Osmolality
ECF

and ICF contain different types of solute but conc. of solutes inside and outside the cells are equal Concentration difference exists only transiently because they create an extremely strong force for water movement across cell membranes Osmolality no of milliosmoles of solute particles per litre of solution

Osmolality
salts, glucose and urea responsible for most of the solute particles in the ECF Measurement osmometer Plasma osmolality Posm = 2 X Plasma Na+ + Glucose + BUN 18 2.8 2 no of anions accompanying Na+ 18 and 2.8 correction factors in converting Glucose and Urea conc. from mg/dl to mmol/L
Sodium

Body fluid changes

Classified into three groups Disturbances of volume due to loss or addition of isotonic salt solution Disturbances of concentration due to addition or loss of water from the ECF or depletion of Na+ from the ECF Disturbances of composition: Acid base balance

Volume changes
- Excess or deficit of ECF volume can be diagnosed by estimating the blood urea nitrogen (BUN) - BUN rises with sufficient ECF deficit - Concentration of blood cells and plasma proteins increases with ECF deficit and decreases with ECF excess - Concentration of Na+ is not related to the volume status of the ECF

Volume changes
ECF volume deficit is the most common fluid disorder in surgical patients. Seen in : Losses from the GIT due to vomiting, NG suction, diarrhoea and fistula drainage Sequestration of fluid in soft tissue injuries and infections Intra-abdominal and retroperitoneal inflammatory processes Peritonitis Intestinal obstruction

Volume changes
Severe

volume depletion depresses all body systems and interferes with the clinical evaluation of a patient.

Concentration changes
Serum

Na+ level is used to estimate total body fluid osmolality Hypo- and hypernatraemia can be diagnosed clinically but the signs and symptoms are not generally present until derangement is severe. With rapid rate of change, the signs and symptoms tend to occur early and with greater severity

Hyponatraemia
Characterised by : CNS signs of increased intracranial pressure and tissue signs of excessive intracellular water Hypertension induced by the rise in ICP BP usually returns to normal after correction of Na+ level With severe hyponatraemia rapid development of oliguric renal failure irreversible with delayed therapy.

Potassium
cation of intracellular water 98% at concentration of 150mEq/L Normal dietary intake 50100mEq/day Intracellular and extracellular distribution influenced by many factors : Release of significant amount from intracellular space into the extracellular space in response to severe injury, surgical stress, acidosis
Major

Hyperkalaemia
Signs

limited to the CVS and GIT GIT symptoms nausea, vomiting, intermittent intestinal colic and diarrhoea CVS signs apparent on ECG
Tall peaked T waves Widened QRS complex Depressed ST segments

Hyperkalaemia
Treatment - Withhold exogenously administered K+ - Correct the underlying cause - Iron exchange resins - Dialysis when indicated - Give HCO3- , glucose and insulin -Give 1g of 10% calcium gluconate under ECG monitoring to suppress the myocardial effects of K+ temporarily

Hypokalaemia
Due

to excessive renal excretion of K+ Movement of K+ into the cells Prolonged administration of K+ free parenteral fluids with continued obligatory renal loss of K+ (>20mEq/day) Parenteral nutrition with inadequate K+ replacement Loss of GIT secretions

Hypokalaemia
Signs Failure of normal contractility of skeletal, smooth and cardiac muscles i.e. weakness leading to flaccid paralysis, diminished/absent tendon reflexes and paralytic ileus ECG signs arrhythmias, low voltage ECG, flat T waves and depressed ST segments

Hypokalaemia
Treatment Prevention i.e. replace GIT fluid loss volume for volume Give K+ not more than 40mEq/L of fluid Rate not exceeding 20mEq/hour Dont give oliguric patients and within 24hrs post operatively

Calcium
Majority

of Calcium in the body is in the form of PO43- and CO32Normal daily intake : 1 3g/day 200mg excreted in the urine daily, the rest is lost in the GIT Half of the serum calcium exists in unionised form bound to plasma proteins 45% exists in ionised form and is responsible for neuromuscular stability

Calcium
Acidosis

increases the ionised fraction while alkalosis decreases it Disturbances of calcium metabolism are generally not problematic in the postoperative patient Therefore, routine administration of Ca2+ to the surgical patient is not needed in the absence of specific indications

Hypocalcaemia
Serum

levels < 8mg/100ml Features

Circumoral numbness Numbness of fingers and toes Hyperactive tendon reflexes +ve Chvosteks sign Tetany, carpopedal spasms Convulsions (with severe deficits) Prolonged Q-T interval on the ECG

Hypocalcaemia
Causes Acute pancreatitis Massive soft tissue infections necrotising fascitis ARF and CRF Pancreatic and small bowel fistulas Hypoparathyroidism Severe depletion of magnesium Give Calcium salts gluconate and chloride IV , - lactate orally Correct underlying cause and the deficit

Hypercalcaemia
Symptoms

Easy fatigability Lassitude Weakness Anorexia, nausea and vomiting Weight loss In severe cases
-

lassitude, somnambulism, stupor, coma Headaches, skeletal pains, thirst, polydipsia, polyuria

Hypercalcaemia
Causes Hyperparathyroidism Cancer with bony metastasis e.g. Breast Ca Treatment Inorganic PO43- given IV/orally lowers Ca2+ levels Large doses of furosemide Prevention is the main treatment of hypercalcaemia due to metastatic cancer Low calcium diet, adequate hydration to promote urinary excretion of Ca2+

Magnesium
Total

body content 2000mEq Half of this is in bone Distribution similar to potassium mostly intracellular Serum concentration between 1.5 2.5mEq/L Normal dietary intake 20mEq/day Largely excreted in the faeces

Magnesium
Deficiency Seen in starvation, malabsorption syndromes, GIT losses, parenteral nutrition, acute pancreatitis, DKA during treatment , primary aldosteronism and chronic alcoholism Symptoms and signs similar to hypocalcaemia

Magnesium
Treatment Parenteral MgSO4 or MgCl2 solution Monitor HR, BP, respiratory rate and ECG with large doses Never to be given in the phase of oliguria or severe volume deficit to avoid toxicity Excess rare but seen in renal insufficiency - Correct acidosis - Correct pre existing ECF volume deficit

Acid Base Balance

Intracellular Buffers: Proteins Extracellular Buffers: Bicarbonate Carbonic acid system

Respiratory Acidosis
Caused

by retention of CO2 secondary to decreased alveolar ventilation is elevated and plasma HCO3- conc. is normal respiratory acidosis Pco2 , HCO3- with renal compensation

Pco2

Chronic

Respiratory Acidosis
Causes Conditions causing inadequate ventilation Airway obstruction Pneumonia Atelectasis Pleural effusion Hypoventilation due to pain of abdominal incisions or abdominal distension limiting diaphragmatic

Respiratory Acidosis
Management Take measures to ensure adequate ventilation Prompt correction of the pulmonary defect when feasible

Head injury may worsen hypoxic brain damage

Respiratory Alkalosis
Causes hyperventilation due to
Apprehension Pains Hypoxia CNS injury Assisted ventilation They all cause rapid depression of the arterial Pco2 and elevation of pH.

Acute phase normal HCO3- conc. Later HCO3- falls with renal compensation

Respiratory Alkalosis
Management Measurement/monitoring of blood gases Appropriate corrections of ventilatory pattern when indicated Severe and persistent respiratory alkalosis difficult to correct and has poor prognosis because of the underlying cause hyperventilation from intracranial injury
Treatment

cause

directed towards the underlying

Metabolic Acidosis
Due

to retention or production of acids or loss of HCO3Causes any condition causing elevated anion gap

Shock or inadequate tissue perfusion Starvation Alcohol intoxication Renal failure Uraemia Aspirin poisoning

Metabolic Acidosis
Most

common cause of severe metabolic acidosis in surgical patients is acute circulatory failure with accumulation of lactic acid

Metabolic Acidosis
Treatment Directed towards correcting the underlying cause Reserve HCO3- therapy for severe metabolic acidosis Discourage routine use of NaHCO3 during resuscitation of patients in hypovolaemic shock particularly after cardiac arrest Frequent measurements of HCO3- and blood pH are the best guides of therapy.

Metabolic Alkalosis
Results

from the loss of fixed acids or gain of HCO3- and is aggravated by any existing K+ deficit. compensation is small but compensation is generally through the renal mechanisms.

Respiratory

Metabolic Alkalosis
Caused

by persistent vomiting as seen in gastric outlet obstruction and intestinal obstruction as well as in prolonged nasogastric drainage

Production Average 2,000 2,500mls/day Orally 1,500mls

Fluid Consumption/Production

The rest from food Stool 250mls Urine 800 1,500mls Insensible losses (skin, lungs): 600 900mls
Increases

Daily fluid losses

with increased environmental temperature 250mls/C rise/day

Fluid and Electrolyte Therapy

Parenteral solutions Vary in composition to satisfy various fluid requirements in the surgical patient. Given a situation, a typical fluid will correct the abnormalities with minimal demands on the kidneys. The choice of a particular fluid depends on the volume status of the patient and the type of concentration or compositional abnormality present.

Fluid and Electrolyte Therapy- an ideal isotonic Ringers lactate

solution/physiological fluid that is close to the plasma compared to isotonic NaCl whose Cl- conc. is 154mEq/L and is higher than the conc. in blood imposing an appreciable load on the kidneys of excess Cl- that cant be excreted rapidly leading to a dilutional acidosis. saline is however good for the correction of an ECF volume deficit in the presence of hyponatraemia, hypochloraemia and metabolic alkalosis.

Normal

Preoperative fluid therapy

Preoperative

and fluid correction an integral part of surgical care approach proper understanding of fluid disturbances associated with surgical illness and adherence to guidelines

Safe

Preoperative fluid therapy

Fluid

replacement depends on existence of concomitant concentration and compositional abnormalities

e.g Hypernatr. + Vol. deficit dextrose Hypernatr. + Vol. excess restrict water

Intraoperative fluid therapy

Inadequate

preoperative ECF Volume replacement can cause hypotension under anaesthesia correction of vol. deficit with a balanced salt solution will remove post operative salt intolerance

Intraoperative

Intraoperative fluid therapy

of intraoperative fluid losses - Blood loss - Oedema from extensive dissection - Fluid collection within the lumen and wall of small bowel - Accumulation of fluid in the peritoneal cavity - Fluid loss from the wound very small
Routes

Intraoperative fluid therapy

The

use of albumin solutions with balanced salt solutions to replace ECF deficits during surgery is not necessary and is potentially harmful

Intraoperative fluid therapy

Guidelines

- Blood should be replaced as lost - Fluid replacement should begin during the operative procedure

Postoperative therapy
postoperative period -Give fluid only after proper evaluation -Correct existing deficit in addition to maintenance as proper replacement during this period will facilitate subsequent fluid management *Do not give potassium within the first 24hrs after surgery unless there is a deficit
Immediate

Postoperative fluid therapy

Late postoperative period - There is a problem of accurate measurement and replacement of all losses during this postoperative convalescent phase - Measure and replace sensible losses (from GIT) - Estimate and replace insensible losses - Identify and correct any electrolyte deficit and give maintenance

Fluid and Electrolyte Management in Surgery

Fluid

and Electrolytes in the Paediatric and Elderly patients need to be administered with caution Essential to the successful management of fluid and electrolyte abnormalities in them is adequate monitoring of their cardiopulmonary status especially the neonates

complications

Conclusion
Fluid

and electrolyte management in surgical patients poses a lot of challenges and could make or mar the outcome of an otherwise successful surgical care. Active anticipation as well as prompt recognition and intervention of disorders is crucial

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