FLUID & ELECTROLYTE

MANAGEMENT
&
ACID BASE DISORDERS
ALICE AUGUSTIN
AMINA S
ANAGHA P R
FLUID & ELECTROLYTES
 Fluid intake is derived from both exogenous(consumed liquids) and
endogenous(released during oxidation of foodstuffs) fluids.
 Total body water is 60% of body weight in males and 50% of body
weight in females.
 Intracellular water-2/3rd of plasma.
 Extracellular water-1/3rd of plasma.
PERIOPERATIVE FLUID THERAPY
• A patient undergoing surgery needs intravenous fluids to replace
volume defcit acquired during starvation,normal maintenance for
the duration of surgery and volume lost during surgery.

• Depending on the extent of dissection, fluid accumulates in these

tissues in the form of oedema (third space losses).

• Blood loss also needs to be replaced.

Perioperative fluid therapy in a patient whose body homeostasis is
normal
The replacement is as follows:
1. Fluid requirement during starvation : Patients awaiting anaesthesia and surgery need
to be kept fasting for a few hours prior to and after the surgery.
This volume is calculated at the rate of 2ml/kg/h for the number of hours of fasting
and is then replaced over 2 to 3 hrs.

2.Maintenance requirement : It is calculated as 2ml/kg/h of surgery

3.Third space losses

- 4 ml/kg/h for surgery with minimal dissection, e.g.herniorrhaphy
- 6 ml/kg/h for surgery associated with moderate dissection, e.g.
gastrojejunostomy and vagotomy
-8 ml/kg/h for surgery associated with large amount of dissection,
e.g. Whipple's procedure.
4.Blood loss is replaced :
- if the haematocrit falls below 25% -compatible blood transfusion.
- haematocrit is > 25% - replaced by colloids or three times the volume

with crystalloids.
• Peripoerative fluid therapy in patients with disturbed fluid balance

Dearrangements of fluid therapy can be classified as

1.Disturbances of volume
2.Disturbances of concentration
3.Disturbances of composition
REGULATION OF VOLUME
 Regulating the volume of liquid.
Extracellular fluid volume reduces

Thirst centres in hypothalamus stimulated

Encourages person to ingest more water

 Regulating the volume of urine excreted

Reduction plasma volume

Release of ADH from posterior pituitary

Increased reabsorption of water and reduced

production of urine
DISTURBANCES OF VOLUME
WATER LOSS(VOLUME LOSS)
 A decrease in the whole body fluid volume which includes both ECF
and ICF.
 It can be of two types:

Hypovolemia Dehydration
isotonic volume depletion only water loss with minimal
(both salt and water loss) loss of electrolytes
CAUSES

HYPOVOLEMIA DEHYDRATION
• Diarrhoea • poor fluid intake
• vomiting • diabetes insipidus
• excess diuresis
• fistula
CLINICAL FEATURES

HYPOVOLEMIA DEHYDRATION
• dry tongue • severe thirst
• rapid pulse
• cold clammy extremities • confusion
• sunken eyes • convulsions hypernatremia
• hypotension
• oliguria • normal blood pressure
INVESTIGATIONS
• Evaluate

Serum sodium
Urinary sodium-decrease in hypovolemia
Blood urea-raised in hypovolemia
MANAGEMENT
• HYPOVOLEMIA-infusion of 0.9 % normal saline.
• DEHYDRATION - increased water intake or intravenous 5% dextrose
• Monitor fluid therapy by
1. skin and tongue examination
2. weight gain
3. pulse
4. blood pressure
5. CVP
6. PCWP
WATER EXCESS
• It can be divided into :

water and salt excess water intoxication

Causes: Causes:
CCF Excessive infusion of
Nephrotic syndrome 5% dextrose
Hypoproteinemia SIADH secretion
Cirrhosis TURP
Renal failure Psychogenic polydypsia
Excessive saline infusion
• INVESTIGATION
hematocrit
sodium level
potassium level decrease
blood urea

• TREATMENT

water and salt restriction and observation

monitoring in ICU
management of fluid and electrolyte balance
infusion of hypotonic sodium chloride
DISTURBANCES IN CONCENTRATION
• HYPONATRAEMIA
Sodium level less than 135 mmol per litre
associated with low plasma osmolality
due to water retention,sodium loss or both.
Causes: hypervolaemic hyponatraemia
hypovolaemic hyponatraemia
normovolaemic hyponatraemia
TREATMENT
1. HYPERVOLAEMIC HYPONATRAEMIA

• Acute symptomatic hyponatraemia

-hypertonic saline 1.6% or 3%
-concomitant use of loop diuretics
-goal is to increase serum sodium by 1-2 meqv/l/hr until neurological
symptoms subside.
-correction should be slow and over a period of 12 - 24 hrs
-calculated sodium deficit=(140-current serum Na+)×body
weight(kg)×0.6
2.HYPOVOLEMIC HYPONATRAEMIA
• administer isotonic saline.
• 3.NORMOVOLEMIC HYPONATRAEMIA
• water restriction 1L/day is enough to rise serum sodium.
• Demeclocycline is the drug of choice.

PSEUDOHYPONATRAEMIA
• High level concentrations of glucose, urea, plasma proteins or lipids
leads to reduction in the relative concentration of sodium in unit volume
of serum.

TREATMENT:
Treat the cause
supportive therapy
HYPERNATRAEMIA
•Plasma sodium concentration more than 150mmol/l.
CAUSES
1. Pure water depletion 2. Hypotonic fluid loss
Extra renal loss Extra renal loss
-Failure of water intake -Vomiting
-Mucocutaneous loss(fever) - Diarrhoea
Renal loss - Excessive sweating
-Diabetes insipidus Renal loss
-Chronic renal failure Osmotic diuresis
Salt gain: Iatrogenic,
salt ingestion
DIAGNOSIS
• Urine osmolality > plasma osmolality and decreased urine
output(extrarenal causes)
• Urine osmolality >plasma osmolality and increased urine
output(osmotic diuresis)
• Urine osmolality < plasma osmolality and increased urine
output(increase ADH or renal response to ADH)
TREATMENT
• Administration of water orally or nasogastric tube
• Administration of IV fluid -5% dextrose or 0.45% saline
DISTURBANCES IN COMPOSITION OF
BODY FLUIDS
 POTASSIUM BALANCE
1. HYPOKALAEMIA
• plasma conc. of potassium less than 3.5mEq/l
• Causes: reduced intake
insulin therapy
alkalemia
beta 2 agonist
diarrhoea,vomiting,fistula
diabetes insipidus,cushings syndrome,dialysis
• CLINICAL FEATURES
1. anorexia,nausea
2. muscle weakness
3. reduced reflexes and paralysis
4. cardiac arrhythmias

• MANAGEMENT
1. Syrup potassium chloride 15 ml orally.
2. potassium supplements
3. If patient cannot take orally or severe hypokalaemia-IV potassium
chloride 0.2mmol/kg/hr
HYPERKALEMIA
• Plasma concentration of potassium >5.5mEq/l
CLINICAL FEATURES
Vague muscle weakness
flaccid paralysis
ECG changes- tall peaked ‘T’ waves with shortened QT interval.
wide QRS complex
widening and then loss of ‘P’ wave
wide QRS complex merge into ‘T’ waves
ventricular fibrillation
TREATMENT
• Calcium gluconate 10% 10-30 ml
• sodium bicarbonate 1-2mmol/kg over 10-15 minutes
• 100ml of 50% dextrose with 10-12 units of insulin over 15-20 minutes
• Hyperventilation
• Salbutamol nebulization
• Calcium exchange resins
• peritonal or haemodialysis
MAGNESIUM
HYPOMAGNESAEMIA
• Serum concentration< 0.75mEq/l
CAUSES
Prolonged starvation
malabsorption
inappropriate fluid therapy
excessive losses - nasogastric drainage,diarrhoea,diuresis
CLINICAL FEATURES
• Neurological or neuromuscular abnormalities
• anorexia,lethargy,weght loss
• hyperirritability’hyperexcitability
• muscle spasm, stridor,tetany, convulsion

MANAGEMENT
• Magnesium sulphate 8mmol diluted in 50 ml 5% dextrose
and given over 30 minutes.
HYPERMAGNESAEMIA

• Serum Magnesium >2.5mEq/l

• Most common cause is iatrogenic
CLINICAL FEATURES
4-5mEq/L - muscle weakness and loss of tendon reflexes
6-7.5mEq/l - respiratory arrest
10mEq/l - cardiac arrest.
TREATMENT: Infusion should be stopped if angle jerks become
sluggish.
CALCIUM

HYPERCALCAEMIA
Calcium concentration of ECF above 11mg%
CAUSES :Hyperparathyrodism
Malignant cancers
CLINICAL FEATURES
• fatigue
• confusion
• cardiac arryhthmia
• calcification of kidney and soft tissues
HYPOCALCAEMIA

• Calcium level is <9mg%.

CAUSES: Vitamin D Deficiency
chronic renal failure
CLINICAL FEATURES : Muscle spasm
stridor
convulsions
Myocardial depression
cardiac arryhthmias
osteoporosis.
ACID-BASE DISORDERS
Regulation of Acid-Base balance
• Normal pH of blood - 7.35 to 7.45
• pH less than 7.35 - Acidosis
• pH more than 7.45 - Alkalosis
ACIDOSIS

Respiratory Metabolic
Increase in CO2 level Decrease in [HCO3-] reduces the pH

Increase in plasma [H+]

Decrease in pH
 ALKALOSIS

Respiratory Metabolic
Decrease in plasma CO2 Increases [HCO3-] increases the pH

Reduces [H+]
Increases the pH
ACID-BASE DISORDERS
RESPIRATORY ACIDOSIS
Causes :
• CNS : CNS dpression due to trauma, tumour,infections,ischaemia or
drug overdose.
Spinal cord injuries

• Peripheral nervous and muscular systems :

Guillain Barre Syndrome
Tetanus
OP Poisoning
• Primary pulmonary disease:
Asthma
COPD
ARDS
Pnuemonia

• Loss of mechanical integrity:

Flail chest
Clinical Features

• Symptoms of the underlying problem

• If acute : tachycardia,hypertension,arrhythmias,confusion,drowsiness
and coma.
• If gradual in onset: Compensatory metabolic alkalosis
ABG analysis: low PaO2
high PaCO2
high bicarbonate levels
normal pH
Treatment

• Treat the cause

• Maintenance of oxygenation and ventilation using mechanical
ventilatory support
RESPIRATORY ALKALOSIS

Causes
• Head injury
• Cirrhosis
• Pain
• Anxiety , hysteria
• High altiudes
Clinical features

• Features of the underlying disease predominate

• Acute severe hypocarbia - cerebral vasoconstriction, reduced cerebral

blood flow,confusions,seizures and tetany

• Cardiac arrhythmias (due to alkalosis and consequent hypokalaemia)

METABOLIC ACIDOSIS

Causes

1.Over production or retention of non volatile acids in the body

• Diabetic ketoacidosis
• Lactic acidosis
• Salicylate poisoning,methanol poisoning
• Renal failure

2.Loss of bicarbonate ions from the body

• Diarrhoea
• Intestinal fistulae
Clinical feature

• Features of the underlying disease predominant

• Hypotension, reduced cardiac output
• Hyperventilation - rapid deep respiration
• Diabetic ketoacidosis- Kussmaul’s Respiration (deep , gasping type)
• Hyperkalaemia,arrhythmias
• Lethargy , coma
Treatment

• Identify the cause and treat

• Adequate ventilation

• If pH less than 7.1 and patient is unstable- administer sodium bicarbonate

Bicarbonate requirement=body weight × base deficit × 0.3
(mmol) (kg) (mmol/L)

• Half the calculated dose of bicarbonate should be given slowly and should
be followed up with repeat blood pH measurements
 METABOLIC ALKALOSIS

Causes

• Loss of gastric HCl as in vomiting,prolonged nasogastric drainage

• Excessive loss of H+ from kidneys in severe hypokalaemia
• Primary or secondary hyperaldosteronism
• Excessive exogenous administrtion of alkali : indiscrimnate use of NaHCO3
antacid abuse
Clinical features

• Symptoms of underlying cause

• When severe cause hypoventilation and seizures
• When associated with hypokalaemia causes arrhythmias

Treatment
• Treat the primary problem
• Administration of saline and correction of potassium deficit
• Rarely in life threatening metabolic alkalosis :
-rapid correction by administration of H+ in the form of diluted HCl or
ammonium chloride
THANK YOU