1. Fluid and electrolytes in children
Also see

2. Composition of Body Fluids
Water is 60% of body mass
(70% in infants, less in obese people, females and elderly).
The water is divided between extracellular (ECF) and intracellular (ICF) compartments.
In an average 70kg person:
Water (L)
Protein (kg)
Na+ (mmol)
K+ (mmol)
Total body 45 6
2550
4560
ICF 15
0.3
2250 60
ECF 30
5.7
300
4500

3. Composition of ECF Water (L) Other constituents Total ECF 15
Contains 230g of albumin and 2250 mmol of Na+
Interstitial compartment 12
Contains 1/4 of the conc. of albumin in plasma (110g of albumin)
Plasma volume 3
Contains 120g of albumin

4. Composition of Fluid in Compartments
Water is held in individual compartments by the osmotic forces generated by the particles restricted to that compartment:
Na+ (along with Cl- and HCO3-) maintain ECF volume
K+ (alongside large macromolecular anions) determines ICF volume
Particles such as urea cross cell membranes rapidly and distribute equally in ICF and ECF. 
Ions which are regulated by transporters and active pumps and therefore have an osmotic effect on the distribution of water between ECF and ICF are:

5. Determinants of water distribution
ECF
ICF (skeletal muscle)
Na+ (mmol/l)
141 10
K+ (mmol/l)
4.1
Cl- (mmol/l)
113 3
HCO3- (mmol/l) 26
Phosphate (mmol/l)
2.0
140 (organic phosphates)

6. Movement of water across cell membranes
Water moves across cell membranes under the action of osmotic forces. 
Movement of water continues until the osmolality on either side of the membrane is equal.
Tonicity is the effective osmolality and equals the total osmolality minus urea and alcohol concentrations (mmol/l). 
Urea and alcohol do not have an osmotic effect as they diffuse freely across cell membranes.
The number of osmotically active particles in the ICF is relatively constant and only changes to help maintain the ICF of brain cells in states of chronic swelling or shrinkage.
As a result: The body content of Na+ determines the ECF volume
The [Na+] in the ECF determines the ICF volume.

7. Distribution of ECF
ECF is distributed between the interstitial and the vascular compartments.  The volumes in each compartment are determined by the forces driving ultrafiltrate across the capillary wall:
Hydrostatic pressure difference
ULTRAFILTRATE
Colloid osmotic pressure difference
Lymphatics

8. Any questions?

9. Water physiology Sensor
In order to maintain the tonicity of body fluids, the body must be able to sense changes in body water and then excrete or conserve electrolyte-free water (EFW).
Sensor
Addition of EFW leads to dilution of solutes. Dilution of the ECF leads to hyponatraemia. However in the ICF, it leads to swelling of cells. Cells in the CNS are sensitive to volume changes and act as a "tonicity receptor". These cells are linked to cells producing antidiuretic hormone (ADH) and to the "thirst" centre.
Effects
Swelling of these cells tells the "thirst" centre to reduce water intake and stops ADH production, thereby causing the kidneys to produce dilute urine.
Thirst is stimulated by an increase in tonicity. Contraction of the ECF volume also stimulates thirst. At the same time the shrinkage of cells in the "tonicity" receptor stimulates the production of ADH by the posterior pituitary.

10. Aquaporins
Collecting duct
H2O
H2O +
ADH
AQP-2

11. Any questions?

12. Sodium physiology
The content of sodium determines the ECF volume, as Na+ and its accompanying anions account for 90% of the ECF osmoles.  As a result, the kidney, through its ability to control the excretion of sodium, is responsible for maintaining ECF volume. 
To maintain the body sodium content there must be a balance between intake and excretion of sodium.  This is achieved through: 1.
monitoring of effective arterial volume 2.
signalling to the kidney 3.
control of sodium excretion

13. Monitoring of effective arterial volume
When NaCl is retained, there is an increase in ECF volume. 
The most important part of the ECF is the effective arterial volume and sensors in the main arteries and central veins send messages to the kidney via renal nerves and hormones to adjust renal sodium excretion accordingly.

14. Messages Hormone Stimulus Site of action Effect
Angiotensin II or ß adrenergics via renin release
Low ECF volume
Proximal convoluted tubule
Increased reabsorption of NaHCO3 & NaCl
Aldosterone
Angiotensin II
Hyperkalaemia
Cortical distal nephron
Reabsorption of NaCl
Secretion of K+
Atrial natriuretic peptide
Vascular volume expansion
GFR
Medullary collecting duct
Increased GFR
Reduced reabsorption of NaCl

15. Control of sodium excretion
In a normal adult, approximately mmol of sodium is filtered each day, of which over 99% must be reabsorbed.
In order to maintain ECF volume, filtration and reabsorption of sodium is coordinated such that the correct amount of sodium is excreted, independent of the GFR. 
This is known as "glomerular tubular balance".
The main driving force for the reabsorption of sodium is the generation of a low sodium concentration in the ICF. This is achieved through the action of a Na+-K+ ATPase.  While three sodium ions are pumped out of the cell, only two potassium ions enter the cell and this therefore also generates a negative charge within the cell, which encourages reabsorption of sodium.  The sodium enters through specific transporters in the luminal membrane of the tubular cells which bind sodium alongside a second ligand.  These ligands include glucose, amino acids, phosphate and organic anions.  A sodium-independent glucose transporter (GLUT-2) is present in the basolateral membrane of the tubular cells to allow passage of glucose in to the plasma.
As well as these cotransporters, there is also a Na+-H+ exchanger (NHE-3), whose main role is in the reabsorption of NaHCO3.
When the ECF volume is contracted, there will be virtually no sodium in the urine, while if there is ECF volume expansion, sodium will be excreted.  In a euvolaemic state, sodium excretion will equal dietary intake.

16. Any questions?

17. Hyponatraemia
Hyponatraemia is defined as a plasma sodium < 130 mmol/l.
It is the result of an excess of water in comparison to sodium. 
The increase in electrolyte-free water (EFW) must be accompanied by ADH in order to prevent the excretion of EFW.
There is an expansion of ICF volume, unless the hyponatraemia is secondary to hyperglycaemia.
It is important to differentiate between:
(i) Acute hyponatraemia
(ii) Chronic hyponatraemia

18. Acute hyponatraemia Duration of less than 48 hours.
Need to identify the source of EFW.
Main concern is brain swelling and resultant herniation.
Treatment should be prompt and aim at reducing ICF volume using hypertonic saline for the symptomatic patient with a plasma sodium < 125 mmol/l.  Aim to raise plasma sodium to 130 mmol/l.
When calculating sodium deficit assume that the volume behaves as if the sodium is dissolved in total body water as the cell membrane is permeable to water and not sodium.

19. Clinical problem
How much 5% saline (856 mmol Na+/L) should be given to a 35kg patient to raise the plasma sodium by 10 mmol/l?

20. How much 5% saline (856 mmol Na+/L) should be given to a 35kg patient to raise the plasma sodium by 10 mmol/l?
Total body water = 35 x 0.6 = 21L
21L x 10 mmol/l = 210 mmol
Amount of 5% saline needed = 210 / 856 = L
Plus any ongoing renal losses of sodium.

21. Preventing hyponatraemia
The commonest setting for the development of acute hyponatraemia is in the post-operative period.  The cause is administration of EFW as:
● 5% Dextrose or hypotonic saline
● Sips of water
● The generation of EFW by desalination of isotonic saline solutions.  If excessive amounts of fluids are given in the face of ADH release, then hypertonic urine is produced leaving EFW.

22. To avoid hyponatraemia
Give fluids which are isotonic to the urine if polyuria present and isotonic to the body fluids if the patient is oliguric.
Give fluids only to balance ongoing losses and maintain haemodynamic stability.
If urine output is good, be mindful of conditions which may lead to ADH release:
ECF volume depletion
Blood loss
Hypoalbuminaemia
Low cardiac output
Excessive pain, nausea, vomiting or anxiety
CNS or lung lesions
Neoplasms or granulomas
Drugs that enhance the actions of ADH on the kidney by increasing cAMP activity

23. Hyponatraemia in an infant
The most common cause of hyponatraemia in young children is loss of sodium in conditions such as acute gastroenteritis.  Loss of fluid leads to a decrease in ECF volume and production of ADH.  Commonly hypo-osmolar fluids are given orally and this leads to retention of EFW.
Treatment of the hyponatraemia depends on rapid reexpansion of the ECF volume and a more gradual restoration of ICF volume.

24. Chronic hyponatraemia
Commonly seen in hospitalized patients.
Picked up on routine electrolyte measurement.
Must recognise that adaptive responses have taken place in order to maintain normal ICF volume:
Initially pumping out of K+ and Cl- from cells.
Later, loss of organic molecules such as myo-inositol, amino acids.
Therefore if the sodium concentration rises too quickly in the ECF and time is not allowed for these intracellular osmoles to return, then cells will shrink.  In the CNS this may result in osmotic demyelination syndrome (ODS).

25. Causes of chronic hyponatraemia
There must be:
A source of EFW eg ingestion of water
A restriction in the ability to excrete EFW ie presence of ADH
Main problem to answer is why the secretion of ADH?
What is the stimulus for ADH secretion?

26. Causes of chronic hyponatraemia
The main stimulus for ADH secretion is a low "effective" vascular volume or low ECF volume.  This will also stimulate the "thirst" centre, even in the presence of hyponatraemia. 
The difficulty for clinicians is being able to accurately assess the ECF volume.  However ADH may also be released in the face of a normal ECF volume, if there is an inadequate "effective" vascular volume:
Hypoalbuminaeima - leads to loss of fluid from the vascular compartment
Cardiac dysfunction - results in low arterial volume and high venous blood volume

27. Treatment of chronic hyponatraemia
Firstly, if possible identify and treat the cause.
If possible, correct the hyponatraemia slowly.  Too rapid correction will lead to shrinkage of brain cells.  However more rapid correction may be needed if symptoms are serious i.e coma or seizures.  In this circumstance:
Give hypertonic saline to raise plasma sodium concentration to a level at which seizures cease - usually a rise of around 5 mmol/l.
Do not let the plasma sodium concentration rise by more than 8 mmol/l in any 24 hour period.

28. Gradual correction
Raise plasma sodium by no more than 8 mmol/l/day to prevent development of osmotic demyelination syndrome (ODS).
Reduce rate of correction further if patient may have deficiency of potassium or organic osmolytes eg malnutrition, catabolic states.
Create a negative balance for EFW - Cells have an excess of EFW and this must therefore be lost.  Reduce input of EFW.
Return the composition of the ECF to normal - This will require the provision of adequate amounts of sodium in order to maintain ECF volume as EFW is lost.
Return the composition of the ICF to normal - This will require replacement of potential deficiencies of potassium and organic osmoles to the brain cells.  Administration of KCl will lead to replacement of potassium for sodium in the ICF and an increase in sodium in the ECF with an increase in ECF volume.  If the ECF volume was normal, this must be accompanied by a net excretion of NaCl which is isotonic with the patient.

29. Any questions?

30. Hypernatraemia Plasma sodium greater than 150 mmol/l.
There is an increase in the amount of sodium relative to water and hypernatraemia usually leads to decrease in ICF. The brain is most at risk.
Most people, if their thirst centre is intact, will take in EFW to correct the excessive loss of EFW.
Urine osmolality:
Large volume of hypo-osmolar urine - diabetes insipidus
Large volume of slightly hyper-osmolar urine - osmotic or pharmacologic diuresis
Minimum volume of maximally hyper-osmolar urine - nonrenal water loss without water intake
A rarer cause of hypernatraemia is gain of sodium, in excess of water. This will produce an increase in ECF volume.

31. Hypernatraemia - Aetiology
The true normal plasma [Na+] is 152 mmol/kg water.
If measured per litre of plasma, the plasma [Na+] is 140 mmol/L because plasma contains 6-7% of nonaqueous fluids (lipids, proteins) while sodium is only present in the aqueous part.
If blood proteins or lipids are raised, the measured plasma [Na+] may be lower than the actual [Na+] in the aqueous phase, depending on the laboratory method used.
If the lab use a Na+-selective electrode or a conductance method, which measures the ratio of sodium to water in the plasma, the result will not be affected.
However if a method such as flame photometry is used, which measures the [Na+] per volume of plasma, a ''factitious" hyponatraemia will be recorded.
Thirst is stimulated by a rise in the plasma [Na+] of 2 mmol/l. For hypernatraemia to develop, this thirst response must fail.

32. To assess the cause of hypernatraemia ask:
What is the ECF volume?
Has the body weight changed?
Is the thirst response to hypernatraemia normal?
Is the renal response to hypernatraemia normal?

33. What is the ECF volume? Gain of sodium leads to ECF expansion.
All other causes of hypernatraemia are due primarily to water loss.

34. Has the body weight changed?
Rarely fluid moves from the ECF to the ICF  e.g. following a convulsion or rhabdomyolysis.
Hypernatraemia then occurs with no change in body weight.

35. Is the thirst response normal?
A 2% increase in plasma tonicity stimulates thirst.
Failure to take on EFW may occur in a baby who does not have control over access to fluids.
The absence of thirst suggests a CNS lesion.

36. Is the renal response normal?
The appropriate response is a low volume of concentrated urine (> 1000 mOsm/kg H2O).
A failure to produce such a response suggests an ADH or renal problem.

37. Causes of hypernatraemia
Hypernatraemia due to water loss
Nonrenal water loss - Hypotonic solutions may be lost through the skin, respiratory or GI tracts.
Renal water loss.  Usually polyuria - diabetes insipidus or an osmotic diuresis.
Hypernatraemia due to sodium gain
Use of replacement solutions containing more sodium than in the fluids being lost ie urine.
Salt poisoning
Ingestion of sea water
Dialysis error

38. Symptoms
Mild confusion
Thirst
CNS dysfunction
Polyuria

39. Polyuria
Polyuria is the excretion of too much water for a given physiological state.
When assessing polyuria consider:
Urine volume
Osmole excretion
Urine osmolality

40. Causes of polyuria Look at urine osmolality: Hyperosmolar Isosmolar
Hypo-osmolar

41. Hyperosmolar urine
If a large volume of hyperosmolar urine is excreted there must be the same number of osmoles being taken in. Normally adults excrete approx. 900 mOsm/day. If amounts greater than this are being excreted, an osmotic diuretic such as urea or glucose must be present. During an osmotic diuresis, Na+ (50 mmol/l) and K+ (25-50 mmol/l) will also be found in the urine. This can lead to a depletion of these ions and ECF contraction.

42. Isosmolar urine
These patients are characterised by a loss of medullary hypertonicity. The main cause is renal damage secondary to infection, hypoxic injury, obstructive uropathy or drug-induced. The use of loop diuretics will produce a similar temporary picture. There is no significant increase in osmolality following administration of ADH.

43. Hypo-osmolar urine
Most of these patients with very dilute urine will have central diabetes insipidus.

44. Treatment of a water deficit
Stop any ongoing water loss
Replace the deficit slowly, if possible by the oral route

45. Stop any ongoing water loss
If this is the result of ADH deficiency then administer ADH.
If the cause is an osmotic diuresis then remove source and address any sodium or potassium deficit.

46. Replace the deficit slowly
If hypernatraemia is acute or there are serious CNS symptoms, then initial reduction of plasma sodium may have to be rapid.  However aim to replace total water deficit over 2-3 days. 
Oral replacement is best, unless unable to administer fluids orally.  Can give water.

47. Any questions?

48. Potassium physiology
Potassium ions are important in the maintenance of resting membrane potentials across cell membranes.  Imbalances of potassium homeostasis affect many biologic processes which rely on these membrane potentials.
This is important with respect to cardiac muscle cell contractility and changes in plasma [K+] may lead to arrythmias.
The kidneys are responsible for maintaining plasma [K+].
Potassium is the main intracellular cation.  98% of body potassium is inside cells.  It is held inside cells by a charge gradient which maintains a negative charge within cells.  This is achieved by:
A Na+K+ ATPase creates a high intracellular [K+].  3 Na+ are pumped out and only 2 K+ enter the cell.
K+ diffuses out of cells, down the concentration gradient. 
Potassium ions diffuse through cell membranes more rapidly than sodium ions. 
The majority of the intracellular anions are large macromolecules and therefore cannot diffuse out of the cells.

49. Factors influencing potassium shift from ICF to ECF
Hormones
Acid-Base changes
Intracellular anions
Ion channels

50. Hormones Hormones can affect the activity of the Na+K+ ATPase by:
Enhancing the electroneutral entry of sodium into cells by activating the Na+/H+ antiporter.
Stimulating existing Na+K+ ATPase enzymes directly.
Stimulating the production of more Na+K+ ATPase.
The main hormones involved are insulin and catecholamines. 
Insulin and ß-adrenergics lead to a fall in plasma [K+]
Alpha-adrenergics lead to movement of potassium out of cells.

51. Acid-Base changes
Metabolic acidosis, caused by a loss of bicarbonate or gain of HCl causes movement of potassium out of cells the K+ being displaced from the cell by the entry of H+. 
If the kidneys are working normally, via the action of aldosterone, the acidosis will be corrected and the plasma [K+] return to normal.
In contrast, accumulation of organic acids does not lead to hyperkalaemia, as the associated anions (lactate in the case of lactic acid) move into the cells alongside the H+ and K+ ions are not displaced out.
Respiratory acid-base problems do not produce any significant change in plasma potassium.

52. Intracellular anions
Within the cell there is a balance between negative and positive charges. 
Most of the anions are large molecules (organic phosphates such as DNA and RNA). 
The number of these molecules remains relatively constant except in specific diseases such as diabetic ketoacidosis. 
If there is a lack of insulin, organic phosphates are degraded to maintain protein synthesis and this fall in anions leads to a parallel loss of K+.

53. Ion channels
Some problems of potassium homeostasis are the result of abnormalities of ion channels.  Such a disease is periodic paralysis. 
Normally the voltage-gated Na+ channel in muscle cells is inactive, because of the negative potential within the cell.  Nerve stimulation leads to opening of these Na+ channels allowing Na+ to rapidly enter the cell.  This results in a transient depolarization of the muscle cell.  There is a rapid restoration of the resting potential because:
the fall in the negative charge within the cell switches off the Na+ channels
voltage-gated K+ channels open, causing K+ to exit cells down its concentration gradient restoring the negative charge within the cell
Increased activity of the Na+K+ ATPase pumps Na+ out of the cell.

54. Periodic Paralysis Hyperkalaemic periodic paralysis –
This condition is caused by an abnormality of the skeletal muscle Na+ channel.  When the [K+] in the ECF is raised, some of these voltage-gated Na+ channels remain active and the cell becomes inexcitable.
Hypokalaemic periodic paralysis –
This is an autosomal dominant condition presenting as hypokalaemia and weakness in the second decade of life.  The resting membrane potential is less negative than normal.  The precise molecular abnormality is unknown.

55. The Kidneys and Potassium
In order to maintain potassium content in the body, the kidneys must excrete the 1-2 mmol/kg of potassium ingested each day.
Control of potassium excretion takes place primarily in the cortical collecting duct.  This is carried out by the principal cell.

56. The Principal cell Cl- Na+ Lumen Na+ ENaC Na+K+ ATPase K+ K+
Aldosterone stimulates the activity of the epithelial sodium channel (ENaC).  This effect is blocked by amiloride.  If reabsorption of sodium is in excess of that of chloride this leads to creation of an electrical gradient which augments the net secretion of potassium.  Increased sodium in the principal cell also enhances the activity of the Na+K+ATPase, bringing more potassium into the cell. 
The result is a [K+] in the luminal fluid 10 times higher than in the ECF.

57. Any questions?

58. Hypokalaemia Hypokalaemia is a plasma [K+] of < 3.5 mmol/l.
The main concerns are cardiac arrythmias, respiratory failure and hepatic encephalopathy.
The main effect is on the resting membrane potential of cells, which become hyperpolarized as the ratio between the ICF and ECF [K+] increases:
The ECF potassium comprises only 2% of the total potassium in the body and this is reflected in the relative [K+] of the ICF and ECF. 
If the ECF [K+] falls from 4 to 3 a comparable fall in ICF [K+] would take it from 150 to mmol/l. 
The actual change is less than half this and as a result the ratio of ICF to ECF [K+] must rise. 
The resting membrane potential therefore rises as more K+ diffuses out of cells down an exaggerated concentration gradient.

59. Aetiology Three possible causes: Inadequate intake
Shift of potassium into cells
Loss of potassium from the body

60. 1. Inadequate intake
Hypokalaemia is rarely due to inadequate intake alone.
The kidneys are able to greatly reduce potassium excretion in the face of low intake.
However low intake may exacerbate the problem in the presence of excess loss of potassium.

61. 2. Shift of potassium into cells
Metabolic alkalosis
Action of hormones

62. Metabolic alkalosis As H+ moves out of cells, K+ moves in:
Additional HCO3- HB
B- + H+ H+
CO2 x
Na+ K+
Na+K+ATPase
HCO3-
Respiratory alkalosis does not produce the same effect.

63. Actions of hormones
The hormones which cause potassium to move into cells are insulin and beta-2-adrenergics.
Insulin
Insulin makes the resting membrane potential more negative. This is the result of increased activity of NHE-1.  The extra sodium in the ICF is pumped out by the Na+K+ ATPase which exchanges 3Na+ for 2K+ i.e. a net loss of positive charge from the ICF. 
This effect of insulin is important to recognise when treating poorly controlled diabetes mellitus.
Beta-2-adrenergic actions
Increased beta-2-adrenergic activity leads to movement of potassium into cells.  This is seen in conditions associated with stress, hypoglycaemia etc.  Also seen in association with beta-2-agonists used for the treatment of asthma.
Aldosterone
The main action of aldosterone is on the kidney, leading to potassium wasting.  However, in patients who have lacked aldosterone, there appears to be a reduced ability to retain potassium within cells, such that when aldosterone is administered there may be a sudden drop in plasma [K+].

64. 3. Loss of potassium from the body
The main route for potassium to be lost from the body is via the kidneys. 
However certain diarrhoeal illnesses can lead to loss of potassium from the GI tract.

65. Non-renal loss of potassium
Gastric secretions only contain approx. 15 mmol/L of potassium. Therefore relatively little potassium is lost directly through vomiting.
However colonic losses can amount to 50 mmol/L of potassium in diarrhoea, increased further if the losses are from the distal colon eg villous adenoma of the rectum.  This can lead directly to hypokalaemia.
In addition, any excessive loss of fluid, leading to ECF volume contraction will cause renal potassium wasting.

66. Urinary potassium loss
Causes
Diuretics
Hypermineralocorticoid action
Potassium excretion is high when there is a high [K+] in the cortical collecting duct or a high volume of urine passing through the cortical collecting duct.
In virtually all cases of chronic hypokalaemia, the underlying cause is renal loss of potassium.

67. Assessment of potassium excretion
Potassium excretion is controlled primarily by events in the cortical collecting duct.
K+ excretion = Urine [K+]  x Urine volume
Transtubular potassium gradient (TTKG)
Assesses the driving force behind potassium secretion.
TTKG = (Urine [K+] / Plasma [K+]) x (Plasma osmolality / Urine osmolality)
This calculation makes a number of assumptions:
That the quantity of water reabsorbed in the medullary collecting duct can be estimated by comparing the rise in the osmolality of the fluid in the terminal cortical collecting duct (which is equal to that of the plasma) with that of the final urine.
Potassium is not reabsorbed or secreted in the meduallary collecting duct.
The osmolality of the fluid in the terminal cortical collecting duct is known.  This is only true if the urine osmolality is greater than the plasma osmolality.
The TTKG will be high (> 7) if mineralocorticoids are acting and will be low (< 2) if they are not.

68. Causes of excess mineralocorticoid activity (1)
High levels of mineralocoticoid:
Angiotensin II
ACE
Renal artery stenosis, or a tumour
Angiotensin
Renin +
Low ECF volume K+
ACTH
Aldosterone

69. Causes of excess mineralocorticoid activity (2)
Low levels of mineralocoticoid:
CCD
Na+
Principal cell
Abnormal ENaC (Liddle’s syndrome)
Channel always open.
Insertion of an artificial Na+ channel eg amphotericin
Blockage of breakdown of cortisol by inhibition of 11β- hydroxysteroid dehydrogenase eg liquorice

70. Treatment The treatment will depend on the cause.
Indications for initiating therapy:
Absolute
Digoxin therapy Therapy for diabetic acidosis, because of effect of insulin Presence of symptoms eg. respiratory muscle weakness Severe hypokalaemia (< 2 mmol/l)
Strong
Myocardial disease
Anticipated hepatic encephalopathy
Anticipated increase in another factor that causes a shift of potassium intracellularly eg. salbutamol
Modest
Development of glucose intolerance
Mild hypokalaemia
Need for better antihypertensive control

71. How much potassium?
Aim:  Acute correction to avoid serious complications.  Then more gradual correction.
Emergency administration should be via a large vein and with the patient on a cardiac monitor.
As most of the body's potassium is intracellular, it is difficult to assess the potassium deficit from plasma potassium levels.   Specific amounts are therefore difficult to calculate and it is therefore important to follow the replacement with regular measurements.

72. Methods of potassium administration
The safest route of administration is orally.
Intravenous therapy is indicated if:
GI problems limit absorption or intake
there is severe hypokalaemia with either respiratory muscle weakness or cardiac arrhythmias
therapy is likely to cause a shift of potassium into cells e.g. treatment of DKA

73. Rate of administration
The concentration of potassium in fluids given through a peripheral intravenous cannula should not exceed 60 mmol/l because of local irritation to veins.
The rate of infusion should not normally exceed 0.2 mmol/kg/hr although rates up to 0.5 mmol/kg/hr may sometimes be justified.  This does not apply to acute episodes which may require larger doses to be administered via a central line.

74. Preparations
KCl This is the commonest form of potassium given. Important to replace chloride in cases of hypokalaemia associated with ECF volume contraction. Available in various forms.
KHCO3 Use if the patient also needs bicarbonate e.g. certain diarrhoeal states. Note that bicarbonaturia may promote the renal excretion of potassium.
Potassium phosphate If the potasium loss is accompanied by loss of intracellular anions (phosphate), the potassium deficit will only be corrected when phosphate is given.
Examples:- Anabolism associated with total parenteral nutrition Recovery from diabetic ketoacidosis
Dietary potassium This is the ideal way to replace potassium. Foods rich in potassium include meats and fresh fruit.