1. Fluid, electrolyte & acid – base balance
Fluid intake : derived from 2 sources
Exogenous water ; from drink & solid food, average 2- 3 liters / 24 h
Children needs more fluid requirement due to:
Larger surface area
Greater metabolic activity
Immature kidneys (poor concentrating ability)

2. 2. Endogenous water:
Released during oxidation of ingested food ( during starvation from breakdown of body tissues)
Normally constitutes < 500 ml / 24h

3. Fluid output Water is lost from the body by 4 routes :
By the lungs: about 400 ml/24h lost in expired air, it increased in :
dry atmosphere
tachypnea
tracheostomy
By the skin: average loss ml/24h
In a temperate climate as invisible perspiration

4. Faeces : 60 – 150 ml of water s daily lost, in diarrhea the amount is greatly multiplied
Urine : average 1500ml/24 h
minimum 400ml/24 h is required to excrete end-product of protein metabolism
However, urine output is under control of multiple influences like blood volume, hormonal & nervous factors among which ADH plays a major role in controlling a tonicity of body fluids, by stimulating reabsorption of water from renal tubules, thus varying the amount excreted after the requirement of first three routes have been met.

5. water depletion Diminished intake : due to Lack of availability
Difficult swallowing e.g. any painful conditions of mouth, pharynx
Inability of swallowing e.g. esophageal obstruction, paresis of pharyngeal muscle
2. Increased loss : e.g. after tracheostomy

6. Clinical features :
Weakness & intense thirst (the main symptoms)
diminished U.OP + increased specific gravity
Intracellular dehydration. this delays onset of overt compensated hypovolemia

7. Water intoxication
Excessive water, low sodium intake by any route, excessive hypotonic solutions e.g. overprescribing of dextrose 5% to postoperative pt., also may occur in colorectal washout with plain water or during TURP
SIADH ; occur in association with lung condition (pneumonia, empyema), oat cell carcinoma of bronchus, head injury

8. C/F :
Drowsiness, weakness, sometimes convulsion & coma
Nausea & vomiting of clear fluid
In SIADH, large amount of dilute urine
Lab. Test; low level of PCV, serum Na & other electrolytes concentrations
Tx :
Water restriction, if failed
ICU admission & controlled manipulation of fluid & electrolytes

9. Electrolyte balance 2 kinds :
Cations, electropositive & include sodium, potassium, calcium, magnesium
Anions, electronegative & include
Chloride, phosphate, bicarbonate & sulphate
Described in mmol/litre
Their distribution within fluid compartment of body controls passage of water through the cell walls & maintains acid –base equilibrium

10. Sodium balance It is the principle cation of extracellular fluid
Total body amount = 5000mmol-44% ECF
-9% ICF
-47%bone
daily intake of Nacl =1mmol/kg
=500ml of isotonic0.9% saline
Equivalent amount is excreted daily mainly in urine, some in feces & sweating

11. Control by adrenal corticoids:
The most powerful conservator of Na being Aldosterone (in the renal tubules & sweat gland)
Following trauma there is shutdown of Na excretion due to increased adrenal activity, hence it is inadvisable to give large amount of isotonic saline 0.9% after operation

12. Sodium depletion Causes : Small bowel obstruction
High intestinal external fistula
Severe diarrhea ((hyponatremia+ acidosis)
Adrenocortical insufficiency (hyponatremia+ hyperkalemia)
SIADH
Postoperative dilutional hyponatremia..?
Na robbing by NGT….?

13. Clinical features are due to extracellular dehydration & that :
Sunken eye & drawn face
Depressed anterior fontanelle (in infant)
Coated, dry tongue
Dry, wrinkled skin
Collapsed vein, the S.C. tissue feels lax
pt. Looks older than his age
Thirst is not marked or evident…why?
Scanty, dark urine
Hemoconcentration (high PCV)
Low serum Na, low urinary Na

14. Postoperative hyponatremia
It is also called dilutional hyponatremia in which there is normal or increased extracellular fluid volume
It occurs due to prolonged administration of sodium free solution = water intoxication

15. Sodium excess (hypernatremia)
It arise when excessive amount of 0.9% saline solution is given in early postoperative period resulting in overloading of circulation with salt & its accompanying water

16. C/F :
Puffiness of face is the early sign
Pitting edema especially in sacral region ( at least 4.5 liters of excess fluid is accumulated in tissue spaces to give pitting edema)
In infants who are very susceptible to overhydration, there are tense fontanelle, increased weight, increased frequency of urinations & edema

17. Potassium balance
K is almost entirely intracellular (98%) & only 2% is extracellular
3/4 of total body K (3500 mmol) is found n skeletal muscles
Normal daily requirement = 1 mmol/Kg
After trauma there is augmented excretion of K especially in first 24 hour

18. Hypokalemia It can occur suddenly or gradually
Sudden hypokalemia: occur most frequently in diabetic coma treated by insulin & prolonged infusion of saline solution
Gradual hypokalemia:
It is the type encountered in surgical practice

19. Causes :
Preoperative chronic hypokalemia as result medications e.g. diuretics or cancer pt with cachexia, weight loss & K depletion
Diarrhea from ulcerative colitis, villous tumors of rectum
External fistula e.g. duodenal fistula, ileostomy
Prolonged gastrodoudenal aspiration without replacement of K in IV fluid

20. C/F of hypokalemia
Most pt. are asymptomatic, but at risk of its sequelae like cardiac arrhythmias, more likely during surgery & anesthesia especially n the presence of preexisting myocardial disease
Slurred speech, hypotonia, depressed reflexes & abdominal distention due to paralytic ileus
ECG changes (prolonged QT interval, depressed ST segment, flattened T wave)

21. Treatment Oral K : In form of milk, juices, honey,..
Effervesnt tablets of KCL 2 gm 6 hourly
Intravenous K :
Urine output should be adequate
Administration should be properly controlled & level of K checked daily
Given in form of infusion

22. Estimation of electrolyte balance
Sodium : Na with its equivalent anions account for 90% of osmotic pressure of plasma Normal values: Na mmol/litre Cl mmol/litre Bicarbonate mmol/litre

23. Potassium:
Intracellular deficiency of K may be present in spite of normal plasma concentration
Deficiency is to be expected if oral feeding is withheld for > 4 days
Normally 3.5 – 5 mmol/litre

24. Calcium :
It is an extracelluar cation
Plasma level= 2.2 – 2.5 mmol/litre
It exist in three forms :
Protein bound
Free non-ionised
Free ionised, it is the active form (for blood coagulation, neuromuscular excitability)
Ionised form falls with increasing PH, hence tetany may occur in respiratory alkalosis (as a result of hyperventilation)

25. Also ionisation & solubility is reduced in alkaline urine promoting stone formation
Factors affecting calcium level include vitamin D, phytic acid, parathormone, calcitonin & state of renal & bowel function
Management depends on removal of cause of disturbance.
Prophylactic supplementation of calcium is needed during massive transfusion of blood containing acid citrate dextrose (ACD)

26. Magnesium :
It is an intracellular cation
It shares some of properties of potassium & some of calcium
Normal level= 0.7 – 0.9 mmol/litre
Average daily intake 10 mmol/litre
Its deficiency occur following prolonged loss of GIT secretions due to fistulae, ulcerative colitis, ..,also in liver cirrhosis, diseases of parathyroid

27. C/F of magnesium deficiency:
CNS irritability
ECG changes
Lowered BP
Lowered protein synthesis
P.O. cardiac arrhythmia e.g. de novo atrial fibrillation are commonly associated with both hypokalmia & hypomagnesaemia
Treatment is Mg supplementation e.g. infusion of 20 mmol Mg sulphate

28. Acid-base balance CO2 + H2O ↔ H+ + HCO3 –
Terms acidosis or alkalosis indicate a change or tendency to change the PH of the blood in a particular direction,
in acidosis there is an accumulation of acid or loss of base causing a fall or tendency to fall in the PH, the converse in alkalosis
CO2 + H2O ↔ H+ + HCO3 –

29. Regulatory control By various buffering system :
bicarbonate-carbonic acid ratio
Lungs by removal of carbon dioxide
Kidneys by excretion of both acids & base

30. Normal bicarbonate-carbonic acid ratio is 20:1, a decrease in ratio leads to acidity & vice versa Bicarbonate level is altered by metabolic factors whereas carbonic acid altered by respiratory factors, alteration of one is followed automatically by a compensatory alteration in the other, so that the ratio & therefore PH of blood remains constant

31. Measurement of acid-base disturbance
Normally made on arterial or arterialized capillary blood
Normal blood PH
Normal arterial Pco2 is KPa (35-45 mmHg)
Normal arterial Po2 is KPa ( mmHg)
Normal bicarbonate level=22-25 mmol/l

32. Metabolic alkalosis pH > 7.45 bicarbonate > 26 mEq/L Causes:
Excessive ingestion of absorbable alkali e.g. antacids medication
Loss of acid from the stomach as a result of repeated vomiting or aspiration
Cortisone excess, due to overuse of corticoids medication or a result of Cushing syndrome

33. Compensation by :
Lungs; retention of carbon dioxide
Kidneys; excretion of bicarbonate base (alkaline urine)
C/F:
Chyene-stokes respiration with 5-30 seconds period of apnea
Tetany & late tetany …Trousseaus sign
Usually associated with signs of hypokalemia
In severe alkalosis renal epithelial damage may occur result in renal failure

34. Treatment : Metabolic alkalosis without hypokalemia seldom requires treatment apart from removal the cause of alkalosis & ensuring high urine output

35. Metabolic acidosis pH < 7.35 bicarbonate - < 22 mEq/L
It is a condition in which there is a deficit of base or an excess of any acid other than carbonic acid, occur as a result of :
Increase in fixed acids; due to formation
Ketone bodies….DM, starvation
Metabolites…renal failure
Lactic & pyruvic acid…release of aortic clamp or cardiac arrest
ureterosigmoidostomy

36. 2. Loss of base ; as in sustained diarrhea, ulcerative colitis, gastrocolic fistula, a high intestinal fistula or prolonged intestinal aspiration
C/F :
Rapid, deep noisy breathing ( due to overstimulation of respiratory centre)
Urine is acidic except in renal acidosis
Serum bicarbonate is reduced

37. Treatment Correction of underlying pathology
Ensuring adequate tissue perfusion
Bicarbonate solution is given in severe case of acidosis

38. Hyokalemic alkalosis
Occur as a result of repeated vomiting e.g. pyloric stenosis
Low serum K causes K to leaves the cell & replaced by Na & H leading to IC acidosis, kidneys conserve K & secrete H instead
Tx : replacement with IV fluid & KCL infusion + ECG monitoring, the loss may reach to >1000 mmol

39. Respiratory alkalosis
pH > 7.45
paCO2 < 35 mm Hg
Occur when CO2 tension is below normal level as a result of hyperventilation
Causes :
Excessive pulmonary ventilation during anesthesia
High altitudes, hyperpyrexia, a lesion of hypothalamus & hysteria

40. Compensation by renal excretion of bicarbonate
During anesthesia, alkalosis is accompanied by pallor & hypotension & in severe cases respiratory arrest follows
Tx : respiratory suppression due to alkalosis is corrected by insufflation of CO2 + reverse underlying cause

41. Respiratory acidosis pH < 7.35 paCO2 > 45 mm Hg
It occurs as a result of impaired alveolar ventilation due to
Inadequate ventilation of anesthetized pt.
Inadequate P.O. recovery from muscle relaxant
Preexisting pulmonary diseases e.g. COAD

42. The anion gap
It is a calculated estimation of the undetermined anions in the blood, it also used to establish the cause of metabolic acidosis Anion gap = (Na+K)-(HCO3+Cl) The normal value is mmol

43. Metabolic acidosis + increased anion gap
Ketoacidosis
Lactic acidosis
Salicylates poisoning
Renal failure
Metabolic acidosis + normal anion gap :
RTA
Loss of alkali due to diarrhea, intestinal obstruction or fistula
Hyperchloremia of ureterocolic anastomosis