Fluids_ Electrolytes and Acid-Ba

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					  Fluids and Electrolytes
         Abdulhalim salim Serafi,
             MBChB, MSc, PhD, FESC
Assistant Professor & Consultant Cardiologist.
           Umm Al-Qura University
    Composition of the Human
2            Body
     An average young adult male has:-
     Water = 60-70%(varries age, sex ,&fat contents).
     Protein=18%(mainly skeletal muscles).
     Fat =15% in lean peoples.
     Minerals=7%( mainly Ca++ )These vary in
     concentrations in different compartments.
    The Normal Distribution of
3   Fluids
    The Normal Distribution of Fluids
     Total body water (TBW) forms about
      60% of the lean body mass and is about
      40-42 L
     Intracellular fluid volume (ICF) forms
      60% of TBW and is about 25 L
     Extracellular fluid volume (ECF) forms
      40% of TBW (and 20% of body weight)
      and is about 15-17 L
5   Extracellular Fluid (ECF)
     Extracellular   fluid furtherly consists of:
        Plasma water (IVF)                  3L
        Extravascular fluid (EVF)        12-14 L
         – Interstitial fluid (ISF)           8-9 L
         – Transcellular water                1-2 L
         – Bone and dense connective tissue   4-5 L
6   Transcellular Water
       Special body compartments, separate from ICS,
        ECS, and plasma. It includes:
           Cerebrospinal Fluid (CSF).
           Fluid in potential spaces such as the pericardial, pleural,
           synovial, peritoneal, intraocular spaces.
           Fluid in the GI Tract .

       This volume of fluid is small (1-2 L) & is not normally
        considered in measurements, but should be kept in
        mind, especially in cases of pathology
7   The Normal Distribution of Fluids
               of fluid across the cell
     Distribution
      membrane depends on:
        High protein content of cells (oncotic
        Semi-permeability of the cell membrane
        The Na+-K+ pump, which is energy
        dependent (keeps sodium out of the cells,
        and hence water since water movements
        follow sodium movements)
8   The Normal Distribution of Fluids
     Movements of fluid across the capillary
      bed depends on:
        Hydrostatic pressures at arterial and
        venous ends (10 – 32 mm Hg)
        Semi-permeability of the capillary bed
        Plasma oncotic pressure (25mm Hg)
        Interstitial pressure
9   Normal Fluid Homeostatic Mechanisms:

     Total body fluids are broadly balanced
      by intake and output.
      (Water balance: Intake =output)
    Intake is an expression of drinking as a
      result of thirst which is the function of
      chemoreceptors which detect increased
      circulating and cellular osmolarity
   Normal Fluid Homeostatic
10 Mechanisms

  Total body fluids are broadly balanced
   by intake and output
     Volume receptors are less sensitive to fluid
     depletion as regards increasing intake, but play a
     role in reducing fluid losses by the kidneys, (ADH)
     and stimulating vasoconstriction (Renin-angiotensin-
     aldosterone system) and an increased cardiac output
     to compensate for the shrunken circulating volume
   Normal Fluid Homeostatic
11 Mechanisms

                                                   System for Volume Control
    In hypovolaemia,                                             Vagus


     volume receptors in the                                                                   Pituitary

     heart and great vessels
     stimulate the                  Thyrocarotid

     hypothalamus -
     hypophysis system:           Arterial

        ADH for water retention
        ACTH and hence
        Aldosterone for salt                               ACTH
                                                       Gland                                    JGA
                                                                             Angiotensin II

     The Renin-Angiotensin-Aldosterone Mechanism

        The enzyme „Renin‟ is
         released from the kidney in
         response to a low volume
        This in turn converts
         Angiotensinogen to
         Angiotensin I, which is
         further hydrolyzed to
         Angiotensin II in the lungs
        Aldosterone is then released
         from the adrenal cortex
            Salt and water retention
     The Normal Daily Fluid Turnover
       Action                                                         ml/day
13                                       Intake
       Drink                                                          1300
       Food                                                            850
       Metabolic water                                                 350
             Total(depends   on climate, habits,& level of physical   2500
       Urine (Kidney)                                      1500
       Expired air (lungs)                                  400
       Sweating and perspiration (skin)                     500
       Faeces (GIT)                                         100
             Total(see below)                              2500
             Alimentary secretions (almost all reabsorbed)
       Saliva                                            500-1500
       Gastric juice                                    2000-3000
       Pancreatic juice                                  300-1500
       Bile                                              250-1100
       Intestinal secretions                            about 3000
     Daily loss of body water:
      Insensible water loss (unaware): independent of
       sweating & occurs even in absence of sweat glands.
      - loss by diffusion through the skin ~300-400ml/day
      - loss is minimized by the cornified layer (barrier)
      - extensive burn increases rate of evaporation to
         3-5 L/day( sever dehydration i.v. fluid is indicated)
      Sweating: depends on physical activity & environ-
       mental temperature .
      - normally ~100ml/day → 1-2 L/hour in very hot
       weather & during heavy exercise → depletion of
       body water → dehydration → stimulation of thirst
       centers (hypothalamus)→ increased intake.
     Daily loss of body water:
       Water loss in feces:
     - usually small amount(100ml/day)
     - increases to several liters /day in sever diarrhoea, i.e. can be life-
        threatening (esp. in children G/E) if not corrected quickly .
      Water loss by the kidney: most imp. mech. to maintain water
        balance .
     - could be as low as 0.5 lit/day ( in dehydration) , or as high as
        20 lit/day ( on drinking tremendous amount of water).
     - this variability of intake is also true for most of the electrolytes in
        the body e.g. Na + K +
     Ionic Composition of Body Fluids
      Constituent   ICF(mEq/l)   ECF(mEq/l)
      Na               14           152
      K                157           5
      Ca               0-1           5
      Mg               26            3
      Total            197          163
      Cl-                           113
      HCO3-            10           27
      Protein          74           16
      PO4              113
      Total            197          156
     Summary of Ionic
17   Composition
                                          Organic Phos.
     400                                  Inorganic Phos.
     300                                  Chloride
     200                                  Calcium
     100                                  Sodium

           Plasma   Interstitial   Cell
             H2O       H2O         H2O
     Water Depletion:

     Aetiology :
        Pure water depletion may occur in cases of
         reduced intake
           Unavailability, such as loss in the desert
           Incapability, such as in feeble patients or
           patients with swallowing disorders
           Iatrogenic, caused by doctors !!
     Water Depletion:

        Or due to increased losses:
           Losses in urine – such as in diabetes insipidus or
           mellitus, or due to excessive use of osmotic
           Losses from the GIT – as in patients with profuse
           watery diarrhoea
           Losses from the lung – as may occur with
           hyperventilation using unhumidified air
           Losses from the skin - such as increased
           insensible losses associated with fever, burns, or
           excessive sweating in the tropics
     Features of Water Depletion:

        Similar to features of sodium excess, but
         associated with a hypovolaemia:
           Intense thirst.
           Cellular dehydration with loss of tissue elasticity.
           Features of hypovolaemia (rapid pulse, and low BP).
           Lethargy or even coma.
     Management of Water Depletion:

        Slow Rehydration with hypotonic solutions
            Rapid rehydration may induce the development of
            cellular and brain oedema
            Conscious stable patients are rehydrated orally
            Rough estimation of required fluid volume
            calculated by dividing actual serum sodium
            concentration by desired concentration, hence if
            actual [Na] = 150 mEq/L, then fluid requirement
            = 150/140 = 1.07L
22 WaterExcess or Intoxication:
     Basically due to excess administration of
        Inappropriate replacement of fluid losses with low
        sodium content
        Excessive administration of 5% dextrose in water
        Inappropriate fluid balance in renal failure
        Total bowel irrigation with water
        Transurethral resection syndrome
        Inappropriate ADH syndrome
     Water Excess or Intoxication:
        Features are those of a hyponatraemia, but
         associated with a normal or expanded circulating
            Low sodium levels of 118 mmol/L or less
            Neuromuscular features
             – Mental confusion, disorientation, coma and
             – Muscle weakness and lethargy
     Water Excess or Intoxication:
      Stop water intake
      Observe and wait for normal diuresis
      200 ml hypertonic saline may induce diuresis
       if the patient remains oliguric after a few days
      Occasionally dialysis or haemo-filteration may
       become necessary
25   Fluid Management
      Surgicallyimportant fluid losses may be
      in the form of:
         Electrolyte-rich fluids
         Protein-rich fluids
     Loss of Electrolyte-Rich
26   Fluids
      Lossof electrolyte-rich fluid, commonly
      from the GI tract or the GU tract, such
        Vomiting, diarrhoea or losses from fistulae
        Intestinal obstruction (sequestration)
        Diabetes mellitus or insipidus
     Loss of Electrolyte-Rich
27   Fluids
      Pathophysiological        changes:
        Loss of circulating volume, with features of
        hypovolaemia and cellular dehydration
         – Interstitial fluids move into the vascular space,
           thus temporarily correcting hypovolaemia
         – Intracellular fluids move out into the interstitial
           space, with resultant cellular dehydration
        Loss of electrolytes with clinical features
        related to electrolyte deficits
     Loss of Electrolyte-Rich
28   Fluids
        Aims of fluid management include:
           Correction of circulating volume
           Cellular rehydration
           Correction of electrolyte imbalances
      Remember that fluid movements follow
       sodium movements
      Always Replace What Is Lost
      Don’t Forget to Add Normal Requirements
     Loss of Electrolyte-Rich
29   Fluids
        Correction of circulating volume
           For best results use a plasma expander, whence
           circulating volume is expanded equal to
           administered fluid (volume-for-volume)
           Alternately use a crystalloid based mainly on
           sodium (such as normal saline or Ringer‟s
           Lactate) - but only ¼ will remain in the circulation
           and ¾ will load the interstitial space, causing
           peripheral oedema
     Loss of Electrolyte-Rich
30   Fluids
      Never  Use Water or Dextrose for
      Volume Replacement, since only 1/12
      will remain in the circulation, and 8/12
      will enter the cells causing cellular
      oedema and damage
        You may actually drown the patient
     Loss of Electrolyte-Rich
31   Fluids
      Cellular   rehydration
         As seen from the previous slides, plasma
         expanders and saline-containing
         crystalloids are not useful in cellular
         5% dextrose in water, however, is ideal
         (remember 8/12 of the given volume will
         enter the cells), as well as providing
         necessary energy
     Loss of Electrolyte-Rich
32   Fluids
      Correction   of electrolyte imbalances
         Determine imbalance (mostly deficit unless
         iatrogenic excess after over-therapy) by
         biochemical analysis
         Calculate amount of electrolyte(s)
         required, add daily requirements, and
         supplement slowly with volume
         Re-evaluate and manage accordingly
      Constituents of Some
33    Common Replacement Fluids
      Solution Osmolarity Solute    Concentration   Na+   K+   Ca++   Cl-   HCO3-
                                      g/100 ml
     5 % solution   278    Glucose        5          --   --    --     --    --
        5% in       586   Glucose +    5+0.9        154   --    --    154    --
        0.90%               NaCl
     Isotonic 0.9   308     NaCl         0.9        154   --    --    154    --
                            NaCl         0.6
       Ringer's     274      KCl        0.03        130   4    2.2    109    28
       Lactate             CaCl2        0.02
                          Na lactate    0.31
       Human               Protein
       Purified             (95%         4.5        157   2     --    118
       Protein            albumin)
      Macrodex            Dextran 70     6          154   --    --    154
      (Dextran              (MW
         70)               70,000)
34   Loss of Protein-Rich Fluids
                  fluids are usually lost in
      Protein-rich
      association with:
         Infection and inflammation, such as
         Protein-losing enteropathy
         Nephritic and nephrotic syndromes
         Neoplastic disease involving cavities
35   Loss of Protein-Rich Fluids
        Pathophysiological problems include:
           Loss of circulating volume (reduced oncotic
           pressure causes reduced fluid return to the
           circulation from the interstitial space)
           Accumulation of fluids in the interstitial space
           (peripheral oedema or even anasarca)
           Loss of immune bodies and an increased
           susceptibility to infections
           Increased catabolism and reduced wound-healing
36   Loss of Protein-Rich Fluids
      Aims   of fluid management include:
        Correction of circulating volume
        Reduction of interstitial fluid
        Improvement of immunity and correction of
      Always   Replace What Is Lost
37   Loss of Protein-Rich Fluids
      Correction   of circulating volume
         Use a plasma expander. Preferably use a
         protein-containing expander (replace what
         is lost !!)
         Do not use a sodium-containing
         crystalloid solution (except in the case of
         burns in the early phases of fluid management)
         since ¾ of the given volume will enter the
         interstitial space, which is already flooding
38   Loss of Protein-Rich Fluids
      Reduction   of interstitial fluid
        Increase the oncotic pressure of the
        intravascular space by infusing a protein-
        rich fluid
        Increase renal losses of water and sodium
        using diuretics, but not before correcting
        and maintaining circulating volume
39   Loss of Protein-Rich Fluids
      Improvement    of immunity and correction
      of catabolism
        Infuse a protein-rich fluid containing viable
        immunoglobulins (and albumin) – such as
        fresh plasma
        Priority follows correction of circulating
        volume and reduction of interstitial fluids
     Loss of Blood

        Loss of blood may be associated with:
           Acute loss from injury or vascular rupture such as
           bleeding from an external wound, an internal
           bleeding such as splenic rupture, or from
           conditions such as oesophageal varices or peptic
           ulcer, or intra-operatively
           Chronic blood losses from the GIT or the GU
           Damage to RBCs as may occur in burns) in
           addition to plasma volume losses)
     Loss of Blood

        Pathophysiological problems include:
           Loss of circulating volume, particularly in acute
           Loss of oxygen-carrying capacity with higher
           incidence of hypoxia and hypoxic injury
           An increased circulating volume and heart failure
           in cases with chronic bleeding
           Problems associated with massive blood
     Loss of Blood

      Aims   of fluid management include:
        Correction of circulating volume
        Correction of oxygen-carrying capacity
        Minimizing transfusion complications
      Remember  to Always Replace What Is
      Lost (Plus The Daily Requirements)
     Loss of Blood

        Correction of circulating volume
           In acute blood loss with hypovolaemia, volume
           replacement may start with a saline-rich
           crystalloid, but preferrably use a plasma expander.
           Once blood is available, it should be given
           In chronic blood loss associated with heart failure,
           correction of circulating volume (hypervolaemia)
           includes potent diuretics, to be followed by
           transfusion of packed RBCs
     Loss of Blood

      Correction   of oxygen-carrying capacity
         This requires blood transfusion until Hb
         concentration is at least in the range of 10
         Each 500-ml transfusion unit of blood
         will raise the Hb by approximately 1 g/dl
         Oxygen mask
45   Oxygen-Carrying Capacity
        Normal oxygen consumption at rest
           250 ml per minute
        Each gm of Hb can deliver
           1.14 ml oxygen per minute (MAX 80% of 1.36 ml)
        Hence total required arterial-side Hb
           = 250/1.14 = 220 gm of Hb
        Normal arterial-side blood volume (adult)
           = 0.45 x 5L = 2.25L
        Hence required Hb concentration for
         adequate oxygen-carrying capacity
           = 220gm/(2.25x10)dl = 9.8 gm/dl
     Minimizing Transfusion
46   Complications
      Transfuse   only if and when
      Proper grouping and cross-matching
      Meticulous testing for hepatitis and HIV
       and other blood-borne diseases
      Use of aseptic techniques in storing,
       handling and infusing blood, including
       use of proper giving-sets and filters
     Minimizing Transfusion
47   Complications
      Use of fresh blood or blood not older
       than 14 days
      Addition of calcium gluconate with
       massive transfusions
      Careful watch for transfusion reactions,
       and early intervention if necessary
      Careful fluid monitoring to avoid
48   Normal Fluid Requirements
      Thenormal requirements of water, Na+
      and K+ can effectively be given in a
      70Kg man by giving:
        2L dextrsoe 5% in water
        1L normal saline (0.9%)
        Adding 20-30 mmol of K+ in every liter of
        fluid running at 1 liter every 8 hours
49   Normal Fluid Requirements
      This   regimen will supply:
         Water              3L
         Sodium             154 mmol
         Chloride           154 mmol
         Potassium          60-90 mmol
50   Normal Fluid Requirements
        Remember that:
           Fever increases daily fluid requirements by up to
           10% of the daily insensible water loss (800-1000
           Catabolic patients require more fluid intake to
           achieve adequate urinary clearance of waste
           Maintenance needs are less in the immediate
           postoperative period, whence there is water and
           sodium retention
     Monitoring Fluid
51   Replacement Therapy
      The   vital signs
        Pulse rhythm, rate and volume
        Blood pressure
      The   urine output
        Should be in the range of 40-60 ml/hour
        An accurate fluid input-output chart should
        be maintained - including daily weight
     Monitoring Fluid
52   Replacement Therapy
      Clinical   evaluation of:
         Skin turgor and tongue moisture as
         indicators of cellular hydration
         Lungs for evidence of pulmonary oedema
         Lower limbs for evidence of peripheral
         oedema (overload)
     Monitoring Fluid
53   Replacement Therapy
      Central   venous pressure
         Essential in critically ill patients
         Should be maintained at 4-8 mmHg
      Pulmonary    Artery Wedge Pressure
         Useful in patients with right heart failure
         Left atrial and pulmonary arterial wedge
         pressure should be about 25 mmHg
     Monitoring Fluid
54   Replacement Therapy
      Investigations   should include:
         Hb and Hct - dropping levels in absence of
         bleeding indicate haemodilution
         Elevated BUN in presence of a normal
         creatinine level is a feature of dehydration
         Serum electrolytes should be evaluated as
         baseline and daily to guide type of fluid
         required for correction
The Electrolytes
     Gram Molecular Weight
56   (GMW)
      The  number of grams of a substance it
       takes to provide a mole (mol) of that
       substance (i.e., 6.02x1023 molecules)
      The gram molecular weight of a
       molecule can be calculated by summing
       the atomic weight of its individual atoms
     Physiological Molecular
57   Weights
        ATOMIC         Gram Molecular                 MOLECULE               Gram Molecular
      SUBSTANCE         W eight (g/mol)                                        W eight (g/mol)

     Sodium (Na)            2 2. 99       Bicarbonate ( HCO3- )                     6 1.02
     Potassium (K)          3 9. 10       Phosphate, monobasic ( H2PO4- )           9 6.99
     Calcium (Ca )          4 0. 08       Phosphate, dibasic (HPO42- )              9 5.98
     Magnesium (Mg)         2 4. 31       Phosphate (PO43- )                        9 4.97

     Chlorine (Cl)          3 5. 45       Ammonia ( NH3)                            1 7.03
     Phosphorous (P)        3 0. 97       Ammonium ( NH4+ )                         1 8.04

     Carbon (C)             1 2. 01       Glucose ( C6 H12O6 )                     180.16

     Hydrogen (H)           1 . 0 08      Urea ( H2NCONH2)                          6 0.06

     Oxygen (O)             1 6. 00       B.U.N. ( N2 )                             2 8.02

     Nitrogen (N)           1 4. 01
     Expressing Fluid
58   Composition
      Percentage
      Molality
      Molarity
      Equivalence
     Percent Concentrations:
59   (Solute / Solvent) X 100
      Body   solvent is H2O
         1 ml weighs 1 g
      (weight/volume)  percentages (w/v)
      (weight/weight) percentages (w/w)
      Clinical chemistries: mg % or mg / dl

      Concentration   expressed as:
         moles per kilogram of solvent.
      Rarely   used
     Molarity (M)

      Concentration    expressed as:
          moles per liter of solution
      Symbol   “M” means moles/liter not moles
        Physiological concentrations are low
           millimolar (mM)   = 10-3 M
           micromolar (mM)   = 10-6 M
           nanomolar (nM)    = 10-9 M
           picomolar (pM)    = 10-12 M
     Electrochemical Equivalence
62   (Eq)
      Equivalent weight of an ionic substance
       in grams that replaces or combines with
       one gram (mole) of monovalent H+ ions
      Physiological Concentration:
         Milliequivalent (mEq)
     Electrochemical Equivalence
63   (Eq)
      Monovalent    Ions (Na+, K+, Cl-):
         One equivalent is equal to one GMW.
         1 milliequivalent = 1 millimole
      Divalent   Ions (Ca++, Mg++, HPO42-)
         One equivalent is equal to one-half a
         1 milliequivalent = 0.5 millimole
   Complications in Determining
   Plasma Concentrations
  Incomplete    dissociation
     e.g. NaCl
  Protein   binding
     e.g. Ca++
  Plasma    volume is only 93% water.
     The other 7% is protein and lipid
      – Hyperlipidemia
      – Hyperproteinemia
     Osmotic Pressure (p)

         force/area tending to cause water
      The


                     S       S         S
                             S     S   S
                 S       S                 S
                             S     S S
66   Glucose Example

       Initial        Gl Gl Gl           Gl
                             10 L    10 L

       Final     Gl Gl Gl           Gl
                      15 L          5L
67   Osmotic Concentration
      Proportional  to the number of osmotic
       particles formed
      Assuming complete dissociation:
         1.0 mole of NaCl forms a 2.0 osmolar
         solution in 1L
         1.0 mole of CaCl2 forms a 3.0 osmolar
         solution in 1L
68   Osmotic Concentration
      Physiological   concentrations:
         milliOsmolar units most appropriate
         1 mOSM = 10-3 osmoles/L
     Plasma Osmolarity
69   Measures ECF Osmolarity
      Plasma is clinically accessible
      Dominated by [Na+] and the associated
      Under normal conditions, ECF
       osmolarity can be roughly estimated as:
         POSM = 2[Na+]p = 270-290 mOSM
     Clinical Laboratory
70   Measurement
      Includes   contributions from glucose and
      Contribution from glucose and urea
       normally small
         Glucose      normally 60-100 mg/dl
         BUN          normally 10-20 mg/dl
     Clinical Laboratory
71   Measurement

                       [glucose] [BUN]
        P = 2  [Na]           
                          18       2.8
72   Effective Osmolarity
      Urea (BUN) crosses cell membranes
      just as easily as water
        [BUN]E = [BUN]i
        No effect on water movement
73   Effective Osmolarity

       POSM (effective) = 2  [Na  ] 

       POSM (effective) = POSM (measured) 
     Osmolar Gap

      Posm(measured) - Posm (calculated)
      Suggests the presence of an
       unmeasured substance in blood
        e.g. following ingestion of a foreign
        substance (methanol, ethylene glycol, etc.)
     Serum Sodium

      Sodium  is the main extracellular cation
      and is involved in fluid volume control
      and fluid movements, as well as in the
      resting membrane potential
     Serum Sodium

      Normal   serum Na+
        135-148 mEq/L
      Normal   total sodium content
        Adults       1.09 g/kg lean body weight
        Neonates     1.78 g/kg lean body weight
      Normal   daily requirements:
        1.5-2.0 mmol/kg body weight
     Serum Sodium

      In   a 70 kg man
            Total body sodium         4000 mmol
            ECF sodium                2100 mmol
            ICF sodium                400 mmol
            Bony skeleton             1500 mmol
            – 700 mmol exchangeable
     Serum Sodium

      Determining   total deficit or excess

       Na = (140 - SNa) TBW in mEq

       Na     = Sodium deficit or excess,
       SNa     = Serum sodium, and
       TBW     = Total Body water = 60% Bwt (kg)
     Serum Sodium

      Determining   serum deficit or excess

       Na = (140 - SNa) ECF   in mEq

       Na     = Sodium deficit or excess,
       SNa     = Serum sodium, and
       ECF     = ECF volume = 20% Bwt (kg)
     Serum Sodium

      Example
        A 65 kg patient with serum sodium level of
        120 mEq/L
        The ECF Na deficit is
        (140-120) x 20% x 65 = 260 mEq
        Each 500 ml bottle of Normal (0.9%)
        Saline contains 75 mEq of sodium
        Therefore number of bottles required to
        correct the deficit = 260/75 = 3.5 bottles
         Sodium Disturbances:
81       Aetiology
         Hyponatraemia                                    Hypernatraemia
         Increased sodium losses                          Sodium excess
        Excessive intestinal losses, such as            Excess steroids - either iatrogenic, or in the
         vomiting or diarrhoea                            Conn‟s or Cushing‟s syndromes
        Excessive sweating such as in cystic            Excessive use of hyperosmolar high-protein
         fibrosis                                         tube feeding
        Excessive infusion of water or diluted salt     Partial drowning in sea water
         solution in patients who are hypovolaemic        Water depletion
         with reduced renal efficiency                   Insufficient water replacement - especially
        Failure of homeostatic mechanisms to             when insensible water loss is increased as
         retain sodium in Addison‟s disease, Renal        in fever, burns, excessive sweating in
         failure, or Use of diuretics                     tropical countries or hyperventilation with
         Water excess                                     unhumidified air
        Inappropriate replacement of fluid losses       Patient too ill, too old, or too lethargic to
         with low sodium content                          respond naturally to thirst, or who are
        Transurethral resection syndrome                 unable to communicate their thirst, such as
        Inappropriate fluid balance in renal failure     infants or comatose patients
        Inappropriate ADH syndrome                      Over administration of osmotic diuretics
        Excessive administration of 5% dextrose in       such as mannitol, or excessive diuresis as
         water intravenous injection                      in diabetes insipidus
        „Appropriate‟ hyponatraemia occurs in           Lesions of the upper GIT which prevent
         presence of hyperglycaemia or acute              swallowing
         uraemia secondary to homeostatic dilution       Profuse watery diarrhoea
         of the whole ECF solutes towards a normal
     Sodium Disturbances:
82   Features
     Hyponatraemia                           Hypernatraemia
      Lowered urine output                   The patient presents with severe
      Loss of skin turgor                     thirst, confusion, lethargy, or even
      Loss of weight                          coma, and if not treated
      Low central venous pressure with        appropriately may be at risk of
       normal or low blood pressure.           death.
      Signs and symptoms of water
       toxicity and over hydration
        Low sodium levels ~ 118 mmol/l.
        Neuromuscular features - such as
         mental confusion, disorientation,
         coma, and convulsions, and muscle
         weakness and lethargy are common
         presenting symptoms.
        Renal features include oliguria.
     Sodium Disturbances:
83   Management
     Hyponatraemia                                  Hypernatraemia
      Restrict water intake.                       Rehydrate patients with appropriate
      Avoid, however, the use of diuretics          fluids in the presence of water depletion;
       which may increase sodium losses and          hypotonic solutions are generally used
       worsen the condition.                         for the gradual reduction in serum
      Correct sodium losses either orally or        sodium concentrations.
       parenterally if the patient is dehydrated  To determine how much water in litres is
      Hypertonic saline may occasionally be       needed to bring back the serum sodium
       needed, but natural correction is the       concentration to normal, determine excess
       norm.                                       sodium (Na) and divide into the expected
                                                   serum sodium concentration (140 mEq/l);
                                                   Example: if the excess sodium was
                                                    determined as 150 mEq, then the amount of
                                                    water needed to bring the concentration
                                                    back to the normal of 140 mEq/litre would
                                                    be 150140 = 1.07 litres
                                                     Avoid rapid fall in serum sodium which
                                                      may otherwise cause cerebral oedema
                                                     Diuretics are useful in the presence of
                                                      sodium excess in normally hydrated
     Serum Potassium
        Normal serum potassium level
           3.8-5.0 mEq/L
        Normal total potassium content
           Adults          2.65 g/kg lean body weight
           Neonates        1.90 g/kg lean body weight
        Daily excretion of potassium:
           50-60 mEq/L
        Normal daily requirements:
           1.0 mmol/kg body weight
     Serum Potassium

      In   a 70 kg man
            Total body potassium   3800 mmol
            ECF potassium          60 mmol
            ICF potassium          3740 mmol
     Serum Potassium

      In the absence of acid-base disturbances,
       serum K+ levels closely represent total K+
       (although it forms only 2% of the latter)
      Acidosis may result in an outward shift of
       potassium from the cells into the ECF space,
       with resultant hyperkalaemia, whereas
       alkalosis has the opposite effect with resultant
       hypokalaemia .
     Serum Potassium

      Thus, these changes in serum potassium
       secondary to changes in pH do not reflect the
       true situation regarding the body content of
      However, a loss of 10% of total body
       potassium gives a true drop of serum K+
       levels from 4 to 3 mEq/L at a normal pH.
   Potassium Disturbances:
88 Aetiology

 Hypokalaemia                                               Hyperkalaemia
 Excessive losses of potassium from the body                Increased body gains
 Excessive losses of GIT secretions                         iatrogenic: excessive potassium therapy
  associated with alkalosis due to chloride loss from
                                                            Failure of renal excretion
   the upper GIT such as with vomiting, nasogastric
                                                             reduced Na+/K+ and H+ exchange
   suction, and intestinal fistulas
                                                             potassium-sparing diuretics
  not associated with alkalosis when loss is from the
                                                             Addison‟s disease
   lower GIT-as occurs in diarrhoea, excessive use of
                                                             renal glomerular failure
   purgatives, and in villous tumours of the rectum.
                                                             salt depletion
 Excessive renal losses
  potassium-losing diuretics                               Body redistribution
  osmotic diuresis
                                                            Secondary to acidosis
  high-dose corticosteroids
                                                             diabetic
  Hyperaldosteronism
                                                             renal
  Cushing‟s syndrome
                                                             severe tissue injury
 Reduced intake of potassium                                 burns
 Prolonged administration of potassium-free diet / fluids    crush injuries
 Dietary fads                                                surgical trauma
  anorexia
  alcoholism                                               A haemolyzed blood specimen gives a false rise in
                                                            serum k+ level by 0.5 meq/l: one unit of blood if
                                                            haemolyzed contains 18 meq/l of potassium. This also
 insulin-glucose therapy
                                                            applies to haemolytic diseases such as haemolytic
 over-correction of acidosis (alkalosis)
                                                            sickle-cell crises
   Potassium Disturbances:
89 Features

 Hypokalaemia                                                 Hyperkalaemia
     Personality changes                                      Bradycardia, hypotension, and ECG changes
     Drowsiness and later coma                                 (diminushed P-waves, wide QRS- complexes and
     Cardiac arrhythmias                                       short Q-T intervals, tall peaked T-waves, and
     Muscle weakness and hypotonia - skeletal, smooth          arrhythmias and heart block); hyperkalaemia is
     (such as in paralytic ileus), and particularly cardiac     more dangerous than hypokalaemia as it may
     muscle with changes in the ECG (low flat or                rapidly result in cardiac arrest
     inverted T-waves, wide QRS complexes, prolonged           Intestinal colics, nausea, vomiting, and diarrhoea
     PR intervals, depressed ST segments, and high U-          Parasthaesia and muscle weakness
     waves).                                                   Heart block-Cardiac asystole (arrest in diastole).
     Muscle cramps and tetany secondary to
     hypocalcaemia (intracellular hypo-kalaemia causing
     alkalosis and hence hypocalcaemia)
     Reduced renal blood flow and reduced glomerular
     filtration rate (GFR) - hence caution is needed
     during replacement therapy.
     Aggravation of digoxin toxicity in patients on
     Potassium Disturbances:
90   ECG Changes
   Potassium Disturbances:
91 Management

 Hypokalaemia                                            Hyperkalaemia
    Mild hypokalaemia (K 3.0-3.4 mmol/l) can easily        Dextrose infusion plus insulin: 50 ml of 50%
     be managed by increasing diatary intake with oral       dextrose + 20 units soluble insulin will rapidly
     supplements of potassium - such as Slow-K...etc.        lower serum K+ levels by inducing K+ to enter the
    Severe hypokalaemia (K+ < 2.5 mmol/l) should be         cells with the glucose
     corrected by intravenous therapy. Intravenous          Sodium lactate or bicarbonate (to alkalinize the
     potassium administration should not exceed 10-20        blood): 100 mmol HCO3- (100 ml of 8.4%
     mmol/hour, and even less in the presence of             NaHCO3-) given i.v. will induce an alkalosis which
     oliguria.                                               forces the K+ into the cells.
                                                            Calcium gluconate: 10 ml of 10% calcium
                                                             gluconate given i.v. slowly with ECG monitoring
                                                             will counteract the effects of K+ on tissues -
                                                             particularly cardiac muscle and conductive tissues
                                                            Haemodialysis or peritoneal dialysis or cation
                                                             exchange resins in chronic cases
     Serum Calcium

        Normal serum levels
           4.3-5.3 mEq/L (8.5-10.5 mg/100 ml)
        Daily requirements
           10 mg/kg body weight
        Total body calcium
           Adults             20.1 g/kg lean body weight
           Neonates           9.20 g/kg lean body weight
     Serum Calcium

      In   a 70 kg man
            Total body calcium     30160 mmol
            ECF calcium      35 mmol (2.5 mmol/L)
            ICF calcium      125 mmol (5 mmol/L)
            Bony skeleton 30000 mmol
   Calcium Disturbances:
94 Aetiology

 Hypocalcaemia                   Hypercalcaemia
    Hypoparathyroidism             Hyperparathyroidism
    Malabsorption                  Bone metastatic carcinoma (particularly from the
    Alkalosis                       breast)
    Acute pancreatitis             Acidosis
    Renal failure                  Osteoporosis
    Small intestinal fistulae      Renal tubular acidosis
                                    Hypervitaminosis D
                                    Sarcoidosis
                                    Tumours secreting parathormone.
   Calcium Disturbances:
95 Features

 Hypocalcaemia                                        Hypercalcaemia
     Numbness, tingling, and hyperactive tendon      Hypercalcaemia is the disease of:
     reflexes                                          Bones
     Positive Chvostek's sign (facial twitching on      generalized osteoporosis
     tapping over the facial nerve)                      Osteitis fibrosa cystica
     Abdominal cramps                                   cyst formation
     Tetany with carpopedal spasm                     Abdominal groans due to
     Convulsions                                        pancreatitis
     ECG changes (prolongation of QT-interval)          peptic ulceration
                                                       Stones
                                                         renal tract stones
                                                         nephrocalcinosis
                                                       Psychic moans
                                                       Fatigue, muscle weakness, and decreased
                                                       Anorexia, nausea, vomiting, and constipation
                                                       Thirst, polyuria, and nocturia
                                                       Corneal calcification
                                                       Lassitude, which may progress to stupor and
                                                        even coma
   Calcium Disturbances:
96 Management

    Hypocalcaemia                      Hypercalcaemia
   Calcium gluconate injections       Emergency Management
   Treat alkalosis                   Saline drip (to cause a dilution)
   Treat the cause                   Chelating agents (EDTA)
                                      Steroids
                                      Sodium sulphate
                                      Dialysis
                                      Mithromycin
     Investigations in
97   Hypercalcaemia
      Hypercalcaemia
      Hypercalciuria
      Hypophosphataemia
      Hyperphosphatiuria
      Elevated serum alkaline phosphatase
      Elevated serum parathyroid hormone
       concentration > 0.5 µgs/L
     Investigations in
98   Hypercalcaemia
      X-rays showing subperiosteal bone resorption
       in the hands, with generalized cystic bone
       disease and renal calculi and/or
      Cortisone suppression test-to exclude
       hypercalcaemia of:
         vitamin D intoxication
         metastatic bone disease
99   Cortisone Suppression Test
        150 mgs are given daily for 10 days (serum
         ionized calcium is measured on the 5th, 8th,
         and 10th days before injection).
           If the serum ionized calcium level is reduced-then
           the likely cause is either sarcoidosis, vitamin D
           intoxication, or metastatic bone disease.
           If the serum ionized calcium level remains high,
           then cause is hyperparathyroidism
      Parathyroid Localization
100   Tests
       Isotopescan-using technetium and
       thallium subtraction imaging is
       extremely sensitive in acurately locating
      Parathyroid Localization
101   Tests
         Other tests (rarely used now) include:
             Cine oesophagography (barium swallow indentation)
             Ultrasound scan
             Arteriography and digital subtraction angiography
             Retrograde venography and venous sampling of
             parathormone levels performed by radiologists via the
             femoral vein
             CT scan
             Nuclear medical radiography
      Surgical Exploration

       Surgical exploration of the neck is
       required for persistent hypercalcaemia
       even if all the tests are negative. The
       failure rate due to incomplete initial
       exploration is 5%, and most undetected
       adenomas are in the neck or the upper
103   Differential Diagnosis
       Primary  hyperparathyroidism
       Sarcoidosis
       Myelomatosis
       Hyperthyroidism
       Milk-alkali syndrome
       Vitamin D intoxication Immobilization
        with Paget's disease
104   Differential Diagnosis
         Malignant disease with endocrine function
            cancer of the bronchus
            renal cancer
         Skeletal metastasis (secondaries) from other
          organs or tissues
            cancer thyroid
            cancer kidney
            cancer prostate
            cancer breast
      Pathways in Calcium
105   Metabolism                     Pathways in Calcium M e tabolism

           Osteolytic tumours   (Vitamin D - sensitive states)
         (Primary or Secondary)      Hypervitaminosis

                          Excessive bone destruction              Increased absorption of calcium

                                                 High blood calcium                M etabolic calcification

        Parathyroid overactivity

                                                    Hypercalcaemia                    Nephrocalcinosis

                                     Phosphate                                         Renal damage
        Low blood calcium                                Stones

                                                                                       Renal failure

        Poor absorption of calcium                  Infections and/or
      Serum Magnesium

       Normal   serum levels
          1.6-2.1 mEq/L
       Total   body magnesium
          Adults      0.30 g/kg lean body weight
          Neonates    0.27 g/kg lean body weight
    Magnesium Disturbances:
     Hypomagnesaemia               Hypermagnesaemia
       Serum Mg < 1 mEq/L              Serum Mg > 3 mEq/L
       (1.2 mg/dl)                     (3.6 mg/dl)
       Frequently associated
       with hypocalcaemia, and
       must be sought in all
       patients with
       Magnesium Disturbances:
108    Aetiology
                       Hypomagnesemia                                       Hypermagnesemia
      Diminished absorption or intake                    It is usually due to acute or chronic renal failure
     Malabsorption, chronic diarrhoea, laxative abuse   associated with increased intake of magnesium
     Prolonged gastrointestinal suction                 (magnesium-containing antacids, magnesium
     Small bowel bypass                                 sulphate).
     Malnutrition
     Alcoholism
     Parenteral alimentation with inadequate Mg2+
      Increased loss
     Diabetic ketoacidosis
     Diuretic therapy
     Diarrhoea
     Hyperaldosteronism, Bartter‟s syndrome
     Associated with hypercalciuria
     Renal magnesium wasting
     Hyperparathyroidism
     Postparathyroidectomy
     Vitamin D therapy
     Induced by aminoglycoside antibiotics, cisplatin
       Magnesium Disturbances:
109    Features
                         Hypomagnesemia                                         Hypermagnesemia
      Features may also be contributed to by the associated    Symptoms and signs vary according to the degree of
      hypocalcaemia:                                           hypermagnesemia:
     Carpopedal spasm, Tetany, Athetoid movements,            Serum concentration 3-5 meq/L:
      jerking, coarse and flapping tremors, and               Peripheral vasodilatation and hypotension
      hyperexcitability.                                      Nausea and vomiting
     Positive Bainski‟s sign, seizures, and weakness          Serum concentration 5-10 meq/L:
     Tachycardia, ventricular arrhythmias, hypertension      Drowsiness, confusion and lethargy
      and vasomotor changes.                                  Deep tendon reflexes are depressed
     Confusion, disorientation and psychotic behaviour.       Serum concentration > 10 meq/L:
                                                              Progressive weakness,
                                                              Skeletal muscle paralysis,
                                                              Depression of respiratory centers
                                                              Coma and death
                                                               ECG changes include a prolonged PR interval,
                                                               widened QRS complexes, and elevated T-waves.
        Magnesium Disturbances:
110     Management
                         Hypomagnesemia                                                 Hypermagnesemia
                                                                   Dialysis using a magnesium-free dialysate in patients
      Extracellular magnesium deficit can be determined by the      with severe renal impairment
      following formula:                                           Volume expansion with normal saline infusion may
                                                                    enhance renal clearance in patients with normal renal
                    0.2 x bwt in kg x (1.6 - SMg)                   function.
                                                                   This may also be enhanced by the use of potent
                                                                    diuretics, such as furosemide (0.5-1.0 mg/kg
                 where SMg is the observed serum                    intravenously)
                          magnesium                                The intravenous infusion of calcium will temporarily
                                                                    neutralize the neuromuscular effects of
      Replacement of this deficit should then be given              hypermagnesemia
      cautiously over 48 hours

      Oral Replacement
     For adults, give magnesium oxide, 250-500 mg 4
      times daily orally
      Parenteral Replacement
     For the intramuscular route, 0.1-0.4 ml per kilogram of
      50% solution of magnesium sulphate is given 6
     For the intravenous route, magnesium chloride is
      given as an infusion at a rate no more than 0.1-0.2
111   Chloride Balance
         Normal serum levels (in venous serum or
            Men        100-106 mEq/L
            Women      102-108 mEq/L
       Cell water contains up to 25 mEq/L chloride
       Total body chloride
            Adults     1.56 g/kg lean body weight
            Neonates   2.00 g/kg lean body weight
112   Chloride Balance
       In   a 70 kg man
             Total body chloride    2200 mmol
             ECF chloride      1500 mmol (100
             ICF chloride      700 mmol (28 mmol/L)
113   Chloride Balance
       Chlorideand potassium follow each
       other, hence a deficiency of one is
       followed by a deficiency of the other
114   Chloride-Bicarbonate Shift
       When  blood is oxygenated, chloride
       leaves the RBCs and bicarbonate
       enters; water follows the chloride and
       hence RBCs become dehydrated when
       oxygenated (hence alkaline venous
       blood has a lower chloride content than
       well oxygenated blood)
115   Bicarbonate Balance
       Normal   serum levels
          Men              24-28 mmol/l
          Women            22-26 mmol/l
       The ratio of dissolved CO2 to
        undissociated carbonic acid is 700-
       1 mEq of HCO3- will release 1 mmol of
      Treatment of Acidosis Due
116   to Lowered Bicarbonate
         mEq of HCO3- required
            = base deficit x body weight x 0.3
         Bicarbonate may be given i.v. either as
          sodium bicarbonate injection (1 ml of 8.4%
          sodium bicarbonate solution is equivalent to 1
          mEq HCO3-) or as sodium lactate injection (4
          ml/kg of M/6 sodium lactate are equivalent to 1
          mEq HCO3-)
      Treatment of Alkalosis Due
117   to Increased Bicarbonate
       Incase of alkalosis with base excess
        more than 5 mEq/L use ammonium
        chloride (NH4Cl)
             2 ml/kg of M/6 NH4Cl lowers the HCO3- by 1
       mEq     of chloride required
             = base excess x body weight x 0.3
118   Phosphorous Balance
       Normal   serum levels
          Adults     3-4 mg/100 ml (1.7-2.4 mEq/L)
          Children   4-6 mg/100 ml (2.3-3.5 mEq/L)
       Total   body phosphorous
          Adults   11.6 g/kg body weight
          Neonates 5.40 g/kg body weight
119   Phosphorous Balance
       About  30 mEq of PO43- are excreted in
        the urine daily (equivalent to 0.93 grams
        of phosphorous).
       Phosphorous is the largest anion
        component of cells (80 mEq/L of cell
      Disturbances of
120   Phosphorous Balance
         Increased                   Reduced
          phosphorous levels           phosphorous levels
            Hypoparathyroidism           Hyperparathyroidism
            In children during           During transfer of
            active growth due to         blood sugar to cells
            increased growth             (sugar enters in the
            hormone                      form of Glucose-6-
                                         phosphoric acid,
                                         possibly as a salt of