16253913 fluid electro

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PRINCIPLES OF FLUID & ELECTROLYTE BALANCE IN SURGICAL PATIENTS

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PRINCIPLES OF FLUID &

ELECTROLYTE BALANCE INSURGICAL PATIENTS

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NORMAL DAILY LOSSES AND

REQUIREMENTS FOR FLUIDS AND

ELECROLYTES 

Volume Na+ K+ML mmol mmol Urine 2000 80 60 Insensible losses 700 - - Faeces 300 - 10 Minus endogenous 300 - - Water Total 2700 80 70

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ASSESSING LOSSES IN THE

SURGICAL PATIENT 

INSENSIBLE FLUID LOSSES

EFFECT OF SURGERY

The stress response

 ‘Third-Space’ losses 

Loss from the gastrointestinal tract

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INTRAVENOUS FLUID 

5% DEXTROSE

0.9% NaCl

RINGER’S LACTATE (HARTMANN’S

SOLUTION)

HAEMACCEL (SUCCINYLATED GELATIN)

GELOFUSINE (POLYGELINE GELATIN)

HETATARCH HUMAN ALBUMIN SOLUTION 4.5%

(HAS;PPF)

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PROVISION OF NORMAL 24-HR FLUID &

ELECTROLYTE REQUIREMENTS BY

INTRAVENOUS INFUSION

Intravenous fluid Additive Duration

500 ml 0.9% NaCl 20mmol KCl 4hr

500 ml 5% Dextrose - 4hr

500 ml 5% Dextrose 20 mmol KCl 4hr

500 ml 0.9%Dextrose - 4hr

500 ml 5% Dextrose 20 mmol KCl 4hr

500 ml 5% Dextrose - 4hr

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AETIOLOGY OF HYPER AND HYPONATRAEMIA 

Hypernatraemia ------------------- Reduced intake

• fasting• nausea and vomiting• ileus• reduced conscious

level Increased loss *Sweating

(pyrexia,hot environment) *respiratory tract

loss(increased ventilation,administration of drygases)

*administration of dry gases

*burns Inappropriate urinary

water loss• Diabetesinspidus(pituitary ornephrogenic)

• Diabetes mellitus Excessive Sodium load

(hypertonic fluid,parenteral nutrition)

Hyponatraemia

-------------------

- Low extracellular fluidvolume

* Volume depletion(vomiting,diahrrhoea,burns,decreased fluid intake)

* salt losing renaldisease

* Hypoadrenalism

*diuretic use

 

- Normal extracelluler fluidvolume

hypothyroidism

SIADH Increased extracellular fluid

volume

• excessive wateradministration

• excessive mannitol use

• cardiac failure

• cirrhosis

• nephritic syndrome

• renal failure

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CONSEQUENCES OF HYPER

AND HYPOKALEMIA  HYPERKALEMIA

Arrythmias(broad-complexrhythms,bradycardia,heart block,ventricularfibrillation)

Muscle heart blockIleus

Hypokalemia

ECG changesEctopic beats

Muscle weakness

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MANAGEMENT OF SEVERE ACUTE

HYPERKALAEMIA (K+ > 7mmol/L) 

Identify and treat cause 10 – 20 mL intravenous 10% calcium chloride

over 10 min in patients with ECG abnormalities (reduced risk of ventricular fibrillation)

50 mL 50%dextrose plus 10 units short actinginsulin over 2-3min Monitor plasma glucose and K+ over next30-

60 min) Regular Salbutomol nebulizers Consider oral or rectal calcium Resonium (ion exchange resin),although this is

more effective for non-acute hyperkalaemia. Haemodialysis for persistent hyperkalemia

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ACID BASE BALANCE

METABOLIC ACIDOSIS

METABOLIC ALKALOSIS

RESPIRATORY ACIDOSIS RESPIRATORY ALKALOSIS

MIXED PATTERN OF ACID-BASE

IMBALANCE

CO O C S S O O C

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COMMON CAUSES OF METABOLIC

ACIDOSIS IN THE SURGICAL

PATIENT LACTIC ACIDOSIS

Shock (any causes)Severe hypoxaemia

Severe haemorrhage/anaemia

ACCUMULATION OF OTHER ACIDSDiabetic Ketocaidosis

Acute Renal Failure

INCREASED BICARBONATE LOSSDiahrroeaIntestinal FistulaeUreterosigmoidostomy

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COMMON CAUSES OF METABOLIC

ALKALOSIS 

LOSS OF SODIUM AND WATER

VomitingAspiration of gastric secretions

Diuretic administration

HYPOKALEMIA

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CAUSES OF RESPIRATORY

ACIDOSIS

Excessive opiate administration

Pulmonary complications e.gPneumonia

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CAUSES OF RESPIRATORY

ALKALOSIS ENCOUNTERED IN

SURGICAL PRACTICE

Hyperventilation during mechanical

ventilation Pain

Apprehension/hysterical hyperventilation

Pneumonia

Central nervous systemdisorders(meningitis,encephalopathy)

Septicaemia

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Principles of fluid andelectrolyte balance in

surgical patients

Discussions

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1. What are the normal values or serum sodium, potassium,creatinine and urea?

2. What are the normal basal requirements for water, sodiumand potassium?

3. How can this be provided in a patient who is fasting? 4. How is fluid retained in the intravascular compartment? 5. What might cause it to leak out? 6. In clinical practice, it is often desirable to "expand" the

intravascular compartment. Why might this be desirable and howcould it be done?

7. What are the clinical symptoms and signs of fluid depletion?How can the severity of fluid depletion be assessed?

8. How can clinicians assess the patient’s response toresuscitation in severe fluid depletion?

9. What biochemical disturbance might you expect in a patientwith gastric outlet obstruction who has been vomiting for severaldays before admission?

10. What biochemical abnormalities might you expect in a patientwho has had excessive diarrhoea and who has been drinking largeamounts of water because of thirst? (If a house officerinadvertently prescribed too much 5% dextrose and not enough NSaline, you would find the same effect)

In patients with massive burns, fluid losses are impossible tomeasure. How might you assess fluid requirements?