Fluid pdf - د. اياد

Dr. Ayad Abbas

Lec. 3

ELECTROLYTE BALANCE

Tues. 7 / 10 / 2014

Published by : Ali Kareem

مكتب اشور لالستنساخ

5102

Surgery

ELECTROLYTE BALANCE

د. اياد عباس

Lec 3:

7/10/2014

Sodium balance

total body sodium Sodium is the principal cation content of the

extracellular fluid. The amounts to approximately 5000 mmol, of which

44 per cent is in the extracellular fluid,
9 per cent in the intracellular fluid
47 per cent in bone.

The  sodium  housed  in  bone  merits  special  notice:  a  little  more  than  half  of  it  is
osmotically  inactive  and  requires  acid  for  its  solution;  the  remainder  is  water
soluble  and  exchangeable.  Thus,  there  is  a  large  storehouse  of  sodium  ready  to
compensate abnormal loss from the body.
The  daily  intake  of  sodium  is  inconstant.  On  average  it  is  1  mmol/kg  sodium
chloride or 500 ml of isotonic 0.9 per cent saline solution. An equivalent amount
is  excreted  daily,  mainly  in  the  urine  and  some  in  the  faeces.  The  loss  in
perspiration  normally  is  negligible;  however,  in  people  not  acclimatized  to
tropical heat, prolonged profuse sweating results in a considerable loss of sodium
— as much as 85 mmol/hour. If water alone is given to counter-balance the fluid
loss, serious sodium depletion can occur from excessive sweating.

Sodium, with its equivalent anions, accounts for about 90 per cent of

the osmotic pressure of the plasma. Changes in the sodium content coincide
with changes in the osmolality of all the body fluids. The serum sodium value
is normally between 137 and 147 mmol /litre.

The sodium excretion shut down of trauma

Following trauma/surgery there is a variable period of reduced excretion

of sodium. For this reason it may be inadvisable to administer large quantities of
isotonic (0.9 per cent) saline solution after an operation. The period of sodium
excretion shut down can last for up to 48 hours and is due to increased
adrenocortical activity.

Sodium excess (syn. hypernatraemia)

This is likely to arise if a patient is given an excessive amount of 0.9 per cent
saline solution intravenously during the early postoperative period when, as has
been described, some degree of sodium retention is to be expected. The result is
an overloading of the circulation with salt and its accompanying water.

Clinical features:

 Slight puffiness of the face is the only early sign.
 Pitting oedema should be sought, especially in the sacral region, but for

pitting oedema to be present at least 4.5litres of excess fluid must have
accumulated in the tissue spaces.

  The patient’s weight increases with the water-logging.
  There is cellular dehydration.
  Restlessness,  lethargy,  hyperreflexia  and  progress  to  seizure,  comma  and

alternately death.

Signs of overhydration in infancy (infants are very susceptible) are:

  Increased tension in the anterior fontanelle.
  Increased weight.
  An increase in the number of urinations.
  Oedema.

Hypernatraemia

it is of 3 types:

A● Hyper Na

with low total body Na

in which there is loss of H

O + Na

but (H

O > Na

Causes:



Renal: e.g.osmotic diuresis (hyperglycaemia, mannitol).



Osmotic diarrhoea



Sweating

B● Hyper Na

with normal total body Na

in which there is loss of H

Causes:



Renal: Diabetes Inspidus



Burn



↑ respiratory loss

C● Hyper Na

with ↑ total body Na

Causes:



Massive salt ingestion



IV hypertonic saline



NaHCO

therapy



○

hyperaldosteronism



Cushing syndrome

Treatment:

O deficit should be corrected over 48 hrs and rapid correction may → seizure,

brain oedema and death, so plasma concentration of Na

should not ↓ > 0.5

mmol/L/hr.



Type 1                                       Type 2                                             Type 3
H

O +Na

loss H

O loss Loope diuretic

                                                      Lazix (frusemide)

Replace isotonic loss               Replace H

O with

Glucose water Replace any H

Deficit by
Replace H

O loss by Glucose water

Glucose water

Sodium depletion (syn. hyponatraemia)

The most frequent cause of sodium depletion seen in surgical practice is

obstruction  of  the  small  intestine,  with  its  rapid  loss  of  gastric,  biliary,
pancreatic  and  intestinal  secretions  by  antiperistalsis  and  ejection,  whether  by
vomiting  or  aspiration.  Duodenal,  total  biliary,  pancreatic  and  high  intestinal
external  fistulae  also  are  all  notorious  for  bringing  about  early  and  profound
hyponatraemia.  Severe  diarrhoea due  to dysentery, cholera, ulcerative  colitis  or
pseudomembranous colitis will cause hyponatraemia with acidosis. The finding of
hyponatraemia  with  elevated  potassium  would  suggest  adrenocortical
insufficiency. Hyponatraemia is also seen in SIADH.

There is one other less obvious, and surreptitious, means whereby the

patient is robbed of sodium and that is by gastric aspiration combined with
allowing the patient to drink as he or she pleases and promptly aspirating the fluid
swallowed. The act of drinking excites the flow of gastric juice, and this is also
aspirated. During this form of therapy, should the patient be receiving intravenous
dextrose solution to maintain fluid balance, he or she will soon become a victim of
hyponatraemia.

Clinical features:

Clinical features of hyponatraemia with salt and water depletion are due to
extracellular dehydration.

 Neurological(↑ IC water)

 Mild-moderate (Na

> 125) → asymptomatic

 Early symptom: nausea, anorexia and weakness
 Progress (Na

< 120) → cerebral oedema, lethargy, confusion, seizure,

comma and death.

  The eyes are sunken and the face is drawn.
  In infants the anterior fontanelle is depressed.
  The tongue is coated and dry; in advanced cases it is brown in colour.
  The skin is dry and often wrinkled, making the patient look older than his or

her years.

 The subcutaneous tissue feels lax.

  Peripheral veins are contracted and contain dark blood.
  The arterial blood pressure is likely to be below normal.
  The urine is scanty, dark in colour, of a high specific gravity and, except in

cases of salt-losing nephritis, contains little or no chloride.

Presuming that the haemoglobin level before the dehydra-tion

commenced was normal, the haematocrit reading (PCV) provides an index of the
degree of haemoconcentration. However, haemoconcentrations can be masked by
pre-existing anaemia.
Laboratory investigations would show normal or slightly reduced serum sodium
with low urinary output and low urinary sodium.

Hyponatraemia

and it is of 3 types:

A● With low total body Na

(↓ extracellualr volume).

Causes:



Renal diuretic



↓ aldosterone



Renal tubular acidosis



Vomiting



Diarrhoea



External Fistulae.



Intestinal Obstruction.



Gastric Aspiration.

B● With normal total body Na

(normal EC volume)
Causes:



Inappropriate ADH syndrome



Glucocorticoid deficiency



Hypothyroidism



Drug induced : chlorpramide, cyclophosphamide, vincristin,

carbamazepine

deficit = BW * Na

deficit

=BW * (Na

desired-Na

present)

C● With ↑ total body Na

(↑ extracellular volume)
Causes:



CHF



Renal failure



Cirrhosis



Nephrotic syndrome

Treatment:

↓ EC vol.                                    Normal EC vol.                           ↑EC vol.


                           cortisol or thyroid hor.     HF& cirrhosis         RF
Replace isotonic deficit                                             + nephrotic synd.
Replace Na

deficit

Restrict H

                                                                     Restrict fluid

                                                  *Restrict fluid
                                                                        *Loop diuretic

Acute symptomatic Hyponatraemia

Requires prompt treatment
● Correct plasma Na

to 130 mmol/L

●  Very  rapid  correct    associated  with  demyelinating  lesion  in  pons  →  serious
neurological sequelae, so according to severity
mild symptoms 0.5 mmol/L/hr or less.
moderate 1 mmol/L/hr or less.
severe 1.5 mmol/L/hr or less.

Postoperative hyponatraemia

Hyponatraemia with a normal or increased extracellular fluid volume

arises as a result of too prolonged administration of a sodium-free solution (cf.
Water intoxication, above).

Potassium balance

Potassium is almost entirely intracellular. No less than 98 per cent is

intracellular,  and  only  2  per  cent  is  present  in  the  extracellular  fluid.  Three
quarters  of  the  total  body  potassium  (approximately  3500  mmol)  is  found  in
skeletal mus-cles. When the body needs endogenous protein as a source of energy,
potassium,  as  well  as  nitrogen,  is  mobilised.  The  mobilised  potassium  passes  to
the  extracellular  fluid,  but  the  surplus  over  and  above  the  normal  content  is  so
rapidly  excreted  by  healthy  kidneys  that  the  concentration  of  potassium  in  the
serum  remains  unaltered.  Each  day  a  normal  adult  ingests  approximately  1.0
mmol/kg of potassium in food; fruit, milk and honey are rich in this cation. Except
for a very small quantity in formed faeces, and a still smaller quantity in sweat, an
amount corresponding to the intake is excreted in the urine.

Hypokalaemia:

Clinical features

Most patients are asymptomatic. K

< 3.5 mmol/L

Symptoms usually occur < 2.5 mmol/L
Symptoms of hypokalaemia may include:
1.CVS:

 ECG changes:



ST depression



PR & QT prolongation



T inversion



U wave

  Disarrhythmia
  Myocardial dysfunction
  Cardiac arrest may occur
  Orthostatic hypotension

2.Neuromuscular:

  Skeletal muscle weakness.
  Tetany.
  Rhabdomyositis.
  Listlessness and slurred speech.
  Muscular hypotonia
  Depressed reflexes.
  Abdominal distension as a result of a paralytic ileus.

3.Renal:

 Polyurea, nephrogenic DI
 ↑ absorption of HCO

→ metabolic alkalosis

 ↑ Na

retension

4.Postoperative pulmonary complications:

 Weakness of the respiratory muscles may result in rapid, shallow, gasping

respirations.

Causes:

 ↓ intake
 Excessive loss



Renal:

1.  solute diuresis e.g. saline, Glc, mannitol
2.  Diuretic treatment
3.  Hypoaldosteronism and disorder of rennin-angiotensin
4.  Cushing syndrome
5.  Diuretic phase of acute renal failure



GIT: diarrhoea, vomiting, fistula, prolonged gastroduodenal aspiration

with fluid replacement by intravenous isotonic saline solution,
postoperative period following extensive resections for carcinoma of the
alimentary tract, because often the operation has to be undertaken after
months of weight loss and potassium depletion.

 Movement of K

into cells



Alkalosis



Drug: insulin, cathecolamine

 Diabetic coma treated by insulin and prolonged infusion of saline solution.

Treatment

 Oral supplements: 60-80 mmol/day up to 200 mmol/day
 I.V. KCl :



not > 40 mmol/L fluid



not > 20 mmol/hr rapid adminstration may → V.F.



should be under ECG monitoring



not given in unurea

Oral potassium. Potassium can be given in the form of milk, meat

extracts, fruit juices and honey. However, in hospital practice, effervescent tablets
of potassium chloride 2 g can be given by mouth 6-hourly.

Intravenous potassium. Rapid intravenous supplementation (especially

when renal function is impaired) carries the risk of dysrhythmias and cardiac
arrest if the serum concen-tration rises to a dangerous level. Administration
should be properly controlled; the level of potassium should be checked daily; the

urine output must be adequate. When there is no associated alkalosis, the
potassium deficit can be restored by adding 40 mmol potassium chloride to each
litre of 5per cent glucose, glucose—saline or 0.9 per cent saline solution, which is
given 6—8-hourly. Severe hypokalaemia should be treated in a high dependency
or intensive care environment.

Hyperkalaemia:

> 5 mmol/L

Causes:

 ↑ K

intake: I.V adminstration, rapid blood transfusion.

 ↓ renal output

1.  Renal failure (acute, chronic an GFR < 15 ml/min
2.  Adrenocortical insufficiency
3.  Drug: ACE inhibitor, K

sparing diuretic

 Movement of K

out of cell

1.  Acidosis
2.  Trauma
3.  Rhabdomyositis

Effect:

● Nausea, vomiting, diarrhoea, muscle weakness
● ECG changes:
1.peaked T wave
2.absent P wave
3.widened QRS complex
4.sturring ST into T wave

● VF com. > 7 mmol/L
● Cardiac arrest may occur in diastole

Treatment:

● Polystyren sulphate resins: 15 gm 6-8 hourly orally or 30 g rectally
● Insulin 5-10 u in 100 ml of 10-20 dextrose i.v. over 30-60 min (shift K

cell).

● Bicarbonate: 50 mmol i.v (exchange K

for H

across cell membrane)

● Calcium gluconate: 5-10 ml i.v if severe ( act as physiological antagonist of K

● Salbutamol: 5 mg nebulized or i.v (50 Mc bolus and to 5-10 Mc /min infusion
(↑ cellular uptake)
●Dialysis

Calcium

Calcium is an extracellular cation with a plasma concentration of 2.2—

2.5 mmol/litre. It exists in three forms: bound to protein, free nonionised and free
ionised — the last form being the component necessary for blood coagulation and
affecting neuromuscular excitability. The ionised proportion falls with increasing
PH;  thus  in  respiratory  alkalosis  due  to  hyperventilation  there  may  be  tetany  —
with  an  apparently  normal  total  serum  calcium  level.  In  the  urine,  the  ionisation
and  the  solubility  of  calcium  are  similarly  depressed  if  the  pH  is  elevated,  thus
promoting stone formation. The serum level of calcium is likely to be modified by
any  factor  promoting  or  inhibiting  its  absorption  from  the  bowel,  its  storage  in
bone or its elimination by the kidneys: such factors include vitamin D and phytic
acid,  parathormone  and  calcitonin,  and  the  state  of  renal  and  small-bowel
function.

Hypocalcaemia

occurs when total Ca

< 2 mmo/L and/or due to ↓ plasma ionized Ca

Although total Ca

↓ in hypoproteinaemia → the ionized portion is normal and

no clinical features.

Causes:



↓ parathyroid hormone activity:

1.hypoparathyroidism 2.hypomagnesaemia



↓ vit. D activity:1.Inadequate 2.malabsorption 3.or altered vit. D
metabolism: renal failure, hepatic insufficiency



Hyperphosphataemia



Precipitation of Ca

: rhabdomyosistis, pancreatitis



Chelation of Ca

: multiple transfusion, rapid infusion of albumin



Clinical Features:

● Paraesthesia
● Muscle cramps, spasms, tetany
● Stridor
● Chvostek's sign (facial spasm following trapping on facial nerve)
● Trousseau's sign (carpopedal spasm following flat of tourniquet around arm)
● Mental excitability → convulsion
● ECG: prolong QT interval

Treatment:

● Predisposing cause
● i.v calcium if severe 5-10 ml of Ca

chloride or < 10-20 ml of gluconate slowly

● Magnesium if deficient

Hypercalcaemia:

symptom presents when Ca

> 3.5 mmol/L

Causes:



Hyperparathyroidism



Malignancy both 1

○

and bony metastasis



less common:



↑ intake of vit. D or vit A



Other:



Paget disease of bone



hyperthyroidism



adrenocorticoid insufficiency



Sarcoidosis



Thiazide diuretics

Effect:

● Psychatric disturbance
● Dehydration : polyurea, polydipsia
● Nausea, vomiting & constipation

● Muscle weakness
● Drowsiness & comma
● ECG shorten QT interval, prolong interval
● may → renal calculi

Treatment:

● Symptomatic hyper Ca

needs rapid treatment by brisk diuresis (200-300 ml/h)

with i.v normal serum infusion and loop diuretic.
● If severe:
1.Calcitonin 5-10 u/kg/d (i.m subcutaneous) in 1-2 divided doses.
2.Biphosphonate e.g. Na

pamidornate 15-60 mg

● Dialysis may be necessary.

Magnesium

Magnesium is an intracellular cation which shares some of the properties

of potassium and some of calcium. The normal magnesium concentration is 0.7—
0.9 mmol /litre. The average daily intake is approximately 10 mmol. Magnesium
deficien-cy may occur when there is prolonged loss of gastrointestinal secretions
due to fistulae or ulcerative colitis, very prolonged administration of intravenous
fluids  without  magnesium  supplements,  following  massive  small  bowel
resections,  and  in  some  cases  of  cirrhosis  of  the  liver  or  disease  of  the
para-thyroids. The clinical picture of magnesium deficiency is marked by central
nervous  system  irritability,  ECG  changes,  lowered  blood  pressure  and  lowered
protein synthesis. Postoperative cardiac arrythmias (e.g. de novo atrial fibrillation)
are commonly associated with both hypokalaemia and hypomagnesaemia.

Treatment. For the treatment of mild hypomagnesaemia 20 mmol as

magnesium sulphate can be added to 5percent-dextrose or normal saline over a
24-hour period. Magnesium supplements are essential in hyperalimentation.

Hypomagnesaemia:

< 0.75 mmol/L

Causes:



↓ Mg

intake



Malabsorption



↑ loss GIT (diarrhoea, vomiting), renal (diuretic, DM)

Effect:

● Arrhythmia
● Neurological: confusion, irritability, tremor, convulsion

Treatment:

● 1

○

cause

● Acutely: 10-20 mmol/L MgSO

i.v over 1-2 h and repeated as required up to 50

mmol/ day

Hypermagnesaemia:

> 1.05 mmol/L

Causes:



Renal failure



adminstration



Laxatavie, antiacid



Adernocorticoid insufficiency, hypothyroidism

Effect:

● Vasodilatation, hypotension, cardiac conductive defect
● Sedation, comma, weakness & respiratory depression

Treatment:

● Diuresis
● i.v Ca

Printed by :

Ali Malik

Special greetings to: Marwan Zuhair, Mohamed Esam, Sabah Nasir,

Yasir Kasim and to Zaid Fareed