Fluid and electrolytes in children

1
Fluid and electrolytes in children

• Also see http/paedstudent.uwcm.ac.uk

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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
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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
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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

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Determinants of water distribution
ECF ICF (skeletal muscle)
Na (mmol/l) 141 10
K (mmol/l) 4.1 120-150
Cl- (mmol/l) 113 3
HCO3- (mmol/l) 26 10
Phosphate (mmol/l) 2.0 140 (organic phosphates)
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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.

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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
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Water physiology

• 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.

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Aquaporins
Collecting duct
H2O
H2O

ADH
AQP-2
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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
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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.

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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
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Control of sodium excretion

• In a normal adult, approximately 27000 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".

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Hyponatraemia

• Hyponatraemia is defined as a plasma sodium lt 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

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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 lt 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.

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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?

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• 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 0.245 L
• Plus any ongoing renal losses of sodium.

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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.

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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

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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.

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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).

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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?

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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

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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.

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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.

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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.

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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.

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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?

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What is the ECF volume?

• Gain of sodium leads to ECF expansion.
• All other causes of hypernatraemia are due
  primarily to water loss.

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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.

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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.

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Is the renal response normal?

• The appropriate response is a low volume of
  concentrated urine (gt 1000 mOsm/kg H2O).
• A failure to produce such a response suggests an
  ADH or renal problem.

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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

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Symptoms

• Mild confusion
• Thirst
• CNS dysfunction
• Polyuria

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Polyuria

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

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Causes of polyuria

• Look at urine osmolality
• Hyperosmolar
• Isosmolar
• Hypo-osmolar

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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.

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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.

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Hypo-osmolar urine

• Most of these patients with very dilute urine
  will have central diabetes insipidus.

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Treatment of a water deficit

• Stop any ongoing water loss
• Replace the deficit slowly, if possible by the
  oral route

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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.

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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.

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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 NaK 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.

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Factors influencing potassium shift from ICF to
ECF

• Hormones
• Acid-Base changes
• Intracellular anions
• Ion channels

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Hormones

• Hormones can affect the activity of the NaK
  ATPase by
• Enhancing the electroneutral entry of sodium into
  cells by activating the Na/H antiporter.
• Stimulating existing NaK ATPase enzymes
  directly.
• Stimulating the production of more NaK 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.

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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.

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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.

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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 NaK ATPase pumps Na
  out of the cell.

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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.

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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.

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The Principal cell
Cl-
Na
Na
ENaC
NaK ATPase
K
K
Lumen
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 NaKATPase, bringing more potassium into
the cell.  The result is a K in the luminal
fluid 10 times higher than in the ECF.
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Hypokalaemia

• Hypokalaemia is a plasma K of lt 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 112.5
  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.

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Aetiology

• Three possible causes
• Inadequate intake
• Shift of potassium into cells
• Loss of potassium from the body

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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.

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2. Shift of potassium into cells

• Metabolic alkalosis
• Action of hormones

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Metabolic alkalosis
As H moves out of cells, K moves in
Additional HCO3-
Respiratory alkalosis does not produce the same
effect.
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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 NaK 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.

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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.

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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.

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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.

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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 (gt 7) if mineralocorticoids
  are acting and will be low (lt 2) if they are not.

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Causes of excess mineralocorticoid activity (1)
High levels of mineralocoticoid
69
Causes of excess mineralocorticoid activity (2)
Low levels of mineralocoticoid
Blockage of breakdown of cortisol by inhibition
of 11ß- hydroxysteroid dehydrogenase eg liquorice
70
Treatment

• The treatment will depend on the cause.
• Indications for initiating therapy

Absolute Digoxin therapyTherapy for diabetic acidosis, because of effect of insulin Presence of symptoms eg. respiratory muscle weaknessSevere hypokalaemia (lt 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
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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.

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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

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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.

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Preparations

• KClThis is the commonest form of potassium
  given.Important to replace chloride in cases of
  hypokalaemia associated with ECF volume
  contraction. Available in various forms.
• KHCO3Use if the patient also needs bicarbonate
  e.g. certain diarrhoeal states.Note that
  bicarbonaturia may promote the renal excretion of
  potassium.
• Potassium phosphateIf 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 potassiumThis is the ideal way to
  replace potassium.Foods rich in potassium
  include meats and fresh fruit.