Hypernatraemia

 &  Potassium  
Imbalances  
Final  Year  CUCMS  Module  
 Hypernatraemia  
•  Hypernatremia  is  high  sodium  in  the  blood  
that  occurs  with  excessive  fluid  loss.    
•  When  fluid  is  lost  and  not  replaced,  sodium  is  
not  adequately  excreted  from  the  body.  
•  DefiniIon:  Na  >  145  mmol/l  
•  Features:  tremulousness,  irritability,  ataxia,  
spasIcity,  mental  confusion  and  coma.  
 Case  6  
•  A  13  year  old  schoolboy  
•  3-­‐day  episode  of  diarrhoea  
•  No  one  else  in  the  family  is  sick  
•  Parents  aVributed  his  diarrhoea  to  eaIng  
kebab  aWer  school  
•  His  parents  thought  the  diarrhoea  and  
vomi,ng  would  pass  away  quickly,  but  in  the  
last  few  hours,  he  has  started  complaining  of  
weakness.  
 Case  6  
•  Clinically  dehydrated  with  loss  of  skin  turgor  
•  Somewhat  sunken  eyes  
•  Drowsy  
•  Mouth  and  tongue  looked  dry  
•  BP  lying  96/60  mmHg,  radial  pulse  94/min  
•  Abdomen  soW,  non-­‐tender,  bowel  sounds  
present  
•  PR  no  malaena  
 Case  6  
•  Blood  invesIgaIons:  
–  Sodium    159  mmol/l  
–  Potassium    3.0  mmol/l  
–  Bicarbonate    17  mmol/l  
–  Chloride    116  mmol/l  
–  Urea      19  mmol/l  
–  CreaInine      130  µmol/l  
–  Random  glucose  4.2  mmol/l  
 Case  6  
•  What  is  the  likely  explanaIon  for  the  plasma  
sodium  results?  
•  Hypernatraemic  dehydraIon  secondary  to  
diarrhoea  
•  PaIent  has  signs  of  hypovolaemia  (fluid  depleIon)  
–  hypotension,  increased  pulse  rate    
•  Hypernatraemia  is  usually  the  result  of  an  
extracellular  sodium  concentraIon  in  excess  to  
that  of  water.  
 Hypernatraemic  dehydraIon  
•  Both  diarrhoea  fluid  and  gastric  juice  have  a  
sodium  concentraIon  of  50  –  70  mmol/l  
•  To  become  hypernatraemic,  this  paIent’s  
water  intake  must  have  been  insufficient  to  
replace  his  water  losses.  
•  Thus,  hypernatraemia  does  not  necessarily  
mean  an  increase  in  total  body  sodium.  
•  In  this  paIent,  hypernatraemia  is  due  to  
haemoconcentraIon.  
 Case  6  
•  Comment  upon  his  electrolytes.  
–  Hypokalaemia  
•  Loss  of  potassium-­‐rich  diarrhoea  fluid  and    
•  Urinary  potassium  loss  as  a  result  of  secondary  
hyperaldosteronism  in  response  to  hypovolaemia.  
–  Hyperchloraemia  
•  Partly  due  to  haemoconcentraIon  
•  Also  hypovolaemia  leads  to  an  increase  of  renal  
reabsorpIon  of  chloride  and  sodium  ions.  
 
 Case  6  
•  Comment  upon  his  electrolytes.  
–  Low  plasma  bicarbonate  
•  Excess  diarrhoea  fluid  also  results  in  loss  of  bicarbonate  
•  Causes  hyperchloraemic  metabolic  acidosis.  
 Case  6  
•  Comment  on  his  renal  funcIon  test.  
–  Elevated  plasma  urea  
•  Due  to  a  decrease  in  intravascular  volume  leading  to  
reduced  GFR  
•  Normally,  plasma  urea:creaInine  raIo  is  about  50:1  
•  In  this  paIent,  the  raIo  has  been  increased  by  a  low  
GFR  (less  urea,  than  creaInine  is  being  excreted  in  the  
urine)  
•  As  a  result  of  reduced  GFR,  there  is  increased  
reabsorpIon  of  urea  by  renal  collecIng  ducts.  
•  In  presence  of  oliguria  (urine  <  400  mls/day),  pre-­‐renal  
renal  failure  should  be  considered.  
 High  urea  to  creaInine  raIo  

•  Pre-­‐renal  acute  renal  failure  

–  Hypovolaemia,  shock,  cardiac  failure  
•  Enhanced  metabolism  of  proteins  
–  Increase  urea  producIon  
–  Seen  with  high  protein  diets,  paIents  on  total  
parenteral  nutriIon,  steroid  use,  burns,  or  fevers.  
•  GastrointesInal  bleeding  
–  nitrogenous  compounds  from  the  blood  are  resorbed  
as  they  pass  through  the  rest  of  the  GI  tract  and  then  
broken  down  to  urea  by  the  liver.  
 Case  6  
•  Why  is  it  important  to  idenIfy  pre-­‐renal  acute  
renal  failure  in  this  paIent?  
–  Risk  of  further  deterioraIon  in  renal  funcIon  
leading  to  acute  tubular  necrosis  (ATN)  
–  Hence  important  to  recognize  as  treatment  of  
dehydraIon  can  reverse  the  impaired  renal  
funcIon.  

Please  refer  to  your  Nephrology  notes  

for  renal  failure  revision.  
 Case  6  
•  What  are  some  causes  of  hypernatraemia  that  can  
occur  in  hospital  paIents?  
•  The  commonest  cause  of  hypernatraemia  is  negaIve  
water  balance:-­‐  
–  Loss  of  predominantly  hypotonic  fluid,  as  in  this  
paIent  
•  Diarrhoea,  profuse  sweaIng,  vomiIng,  intesInal  fistulae  
–  Result  of  pure  depleIon  of  water  
•  Fever,  hypervenIlaIon  
–  Result  of  reduced  water  intake  
•  Inadequate  IV  replacement,  disorders  of  brain’s  thirst  centre  
(cranial  DI),  or  in  paIents  unable  to  drink  
 Causes  of  hypernatraemia  
•  Water  loss   •  Inappropriate  IV  sodium  
–  Renal  e.g.  central  or   administraIon  
nephrogenic  diabetes   •  Excess  sodium  ingesIon  
insipidus  or  osmoIc  
diuresis  (mannitol  or   •  MineralocorIcoid  excess  
glucose)   –  Cushing’s  syndrome  
–  Water  loss  into  cells   –  Conn’s  syndrome  
•  Rhabdomyolysis,  strenuous  
exercise  or  seizures   •  Rhabdomyolysis  
•  Gut  loss   •  EssenIal  hypernatraemia  
–  Diarrhoea,  malabsorpIon   –  Hypothalamic  disorder  
which  results  in  a  defect  of  
•  Insensible  loss   osmoreceptor  funcIon.  
–  Fever,  sweaIng  
 Case  7  
•  A  22-­‐year  old  unemployed  male  was  brought  to  
A&E  department  following  a  motorcycle  accident  
in  which  he  received  a  head  injury.  
•  He  was  unconscious  and  was  taken  to  the  
intensive  care  for  mechanical  venIlaIon.  
•  He  also  had  fractured  leW  femur  and  right  
clavicle.  
•  He  regained  consciousness  within  12  hours  and  
was  transferred  to  the  orthopaedic  ward  aWer  a  
few  days.  
 Case  7  
•  The  only  drugs  that  he  was  taking  at  this  Ime  
were  analgesics  and  he  was  then  able  to  eat  and  
drink  normally.  
•  It  was  noIced  from  the  fluid-­‐balance  charts  that  
the  paIent  was  passing  large  volumes  of  urine  
and  he  complained  of  thirst.  
•  A  Imed  urine  collecIon  was  made  and  was  
found  to  be  5.1  litres  in  24  hours  with  an  
osmolality  of  106  mOsm/kg.  
•  His  weight  is  70  kg.  
 Case  7  
•  Blood  tests  showed:  
–  Na  159  mmol/l  
–  K  4.5  mmol/l  
–  Urea  7.5  mmol/l  
–  Creat  120  µmol/l  
–  Random  glucose  4.1  mmol/l  
–  Calcium  2.31  mmol/l  
–  PO4  0.88  mmol/l  
–  Albumin  41  mmol/l  
What  is  the  calculated  plasma  osmolality?  
 Case  7  
•  What  is  the  most  likely  
explanaIon  for  the  polyuria?  
–  Polyuria  is  defined  as  the  
passage  of  >  3L  of  urine  per  day  
–  The  paIent  probably  has  cranial  
diabetes  insipidus.  
–  Due  to  deficiency  of  ADH  (acIon  
of  ADH:  to  increase  water  
reabsorpIon  by  the  renal  
tubules)  
 Causes  of  polyuria  
•  Solute  diuresis  (urine  osmolality  >  300  mmol/kg)  
–  Hyperglycaemia  (diabetes  mellitus)  
–  Mannitol  
•  Water  diuresis  (urine  osmolality  <  200  mmol/kg)  
–  Diabetes  insipidus  
•  Central/  cranial  (see  next  slide)  
•  Nephrogenic  (due  to  hypercalcaemia,  hypokalaemia,  amyloidosis,  
lithium,  inherited  sex-­‐linked  disorders)  
–  DIDMOAD  syndrome  (DI,  DM,  opIc  atrophy,  deafness)  
•  Chronic  renal  failure  
•  PyelonephriIs  
•  Renal  transplantaIon  
•  Psychogenic  polydipsia  
 Case  7  
•  What  is  the  management  of  this  paIent’s  
hypernatraemia?  
–  Target  fall  in  serum  Na  concentraIon  of  10  mmol/l  
per  day,  except  those  in  whom  hypernatraemia  
developed  over  a  period  of  hours.  
–  If  paIent  with  long-­‐standing  hypernatraemia  is  
infused  with  hypotonic  fluids,  there  is  danger  of  
cerebral  oedema.  
–  It  is  essenIal  to  lower  extracellular  hypertonicity  
slowly  in  hypertonically-­‐dehydrated  paIents,  e.g.  0.5  
mmol/hr  
 Case  7  
•  If  paIent  is  able  to  tolerate  orally,  give  water  
orally.  
•  If  not,  set  up  an  IV  infusion  of  D5%  or  0.45%  
NaCl.    
•  Volume  and  rate  of  infusion  may  be  calculated  
as  follows:-­‐  
•  Change  in  serum  Na  =  Infusate  Na  –  serum  Na  
               Total  body  water  +  1  
 Case  7  
•  Total  body  water  (TBW)  =  0.6  X  70  kg  =  42  L  
•  IdenIfy  Ime  period  of  desirable  correcIon  
e.g.  10  mmol/l  in  24  hour  period  
•  1L  of  0.45%  will  reduce  Na  concentraIon  by:  
(77-­‐  159)  =  1.9  mmol/l  
 (42  +  1)  
•  To  aim  for  10  mmol/l  Na  reducIon,  10/1.9  =  
5.26L  of  0.45%  NaCL  needed  to  be  infused  
over  24  hours  i.e.  219  mls/hour  for  24  hours.    
 Case  7  
•  Total  body  water  deficit  =  
TBW  (0.6  X  70)  X  measured  Na  (159)  –  TBW  (0.6  X    70)  =  2.8L  
                                 Desired  Na  (149)  
•  Water  requirement  =  40  ml/kg/day  =  40  X  70  =  
2.8L  
•  Total  volume  of  water  required  for  1st  day  =  2.8  L  
+  2.8L  =  5.6  L  (assuming  no  more  on-­‐going  losses)  
•  Thus,  addiIonal  5.6  –  5.26  L  i.e.  0.34L  (340  mls)  
may  be  administered  by  NG  feeding/  orally  or  by  
increasing  the  rate  of  hypotonic  soluIon  or  
adding  isotonic  soluIon.      
 Case  7  
•  What  is  the  specific  treatment  for  cranial  
diabetes  insipidus?  
–  Intranasal  DDAVP  (desmopressin)  5  –  10  µg  once  
or  twice  daily  or  
–  SC  aqueous  vasopressin  5  –  10  iu  twice  daily  
–  In  emergency,  IV  DDAVP  1-­‐2  µg  2  or  3  Imes  daily.  
POTASSIUM  IMBALANCES  
 Hypokalaemia    
•  Can  result  from:  
–  Poor  potassium  intake  
–  Increased  translocaIon  into  cells  
–  Increased  losses  in  urine  or  GI  tract  (most  
common)  
•  Kidney  can  lower  excreIon  to  a  minimum  of  5  
mmol  per  day  to  10  mmol  per  day  in  the  
presence  of  decreased  potassium  intake.  
–  Poor  intake  without  excessive  potassium  loss  is  a  
rare  cause  of  hypokalaemia.  
 Hypokalaemia  
•  Excessive  loss  of  potassium  –  common  cause.  

•  Most  common  mechanisms:  

–  Increased  urinary  losses  due  to  increased  sodium  
delivery  to  the  distal  nephron  (e.g.  with  diureIcs)  
–  MineralocorIcoid  excess  (e.g.  Conn’s    syndrome)  
–  Non-­‐absorbable  anions  
–  Increased  urine  flow  (e.g.  osmoIc  diuresis)  
 Case  8  
•  A  44-­‐year  old  office  clerk  had  been  urgently  
referred  to  the  hospital  because  of  his  blood  
pressure.  
•  He  smoked  15  cigareVes  per  day  but  does  not  
consume  alcohol.  
•  He  was  on  a  calcium  channel  blocker  for  his  
hypertension.  No  other  medicaIons.  
•  His  previous  health  was  excellent,  with  his  only  
previous  medical  aVendance  due  to  a  broken  
nose  from  a  sporIng  accident.  
 Case  8  
•  He  had  iniIally  presented  to  his  private  doctor  
with  headaches  and  occasional  polyuria.    
•  In  the  clinic,  his  BP  was  160/110  standing  and  
158/104  lying  down.  
•  Physical  examinaIon  was  otherwise  
unremarkable,  apart  from  grade  1  
hypertensive  reInopathy.  
 Case  8  
•  Blood  was  taken  in  the  clinic:  
–  Na    145  mmol/l  
–  K    2.9  mmol/l  
–  HCO3    38  mmol/l  
–  Cl  90    mmol/l  
–  Urea    6.8  mmol/l  
–  Creat    119  µmol/l  
–  RBS    4.4  mmol/l  
•  What  are  your  differenIal  diagnosis?  
 Case  8  
•  He  re-­‐aVended  the  clinic  one  week  later  when  
a  24-­‐hour  urine  test  was  performed.  
•  This  produced  a  total  volume  of  2.8L  with  a  
potassium  excreIon  of  56  mmol/l  
•  A  normal  24-­‐hour  urine  catecholaemine  
excreIon  and  normal  urinary  free  corIsol.  
•  Subsequently,  he  was  admiVed  as  an  in  
paIent  for  invesIgaIons  for  possible  Conn’s  
syndrome.  
 Case  8  
•  Why  was  there  a  suspicion  of  possible  Conn’s  
syndrome?  
–  This  paIent  had  hypokalaemic  metabolic  alkalosis  
with  hypertension  
–  Primary  hyperaldosteronism  (Conn’s  syndrome)  
–  Urinary  potassium  loss  >  30  mmol/l  suggest  renal  
kaliuresis  (provided  not  on  diureIcs,  and  adequate  Na  
intake  >  120  mmol/day)  
•  Hypokalaemia  with  inappropriate  urinary  loss  of  K  =  
mineralocorIcoid  excess.  
–  Commonest  cause  of  Conn’s:  adrenal  adenoma,  
adrenal  hyperplasia,  adrenal  carcinoma.  
 Case  8  
•  What  invesIgaIons  would  you  do  for  this  man?  
§  Plasma  aldosterone  and  renin  early  morning  aWer  
paIent  has  been  supine  for  at  least  half  an  hour  
§  Then  repeat  these  measurements  aWer  4  hours  of  
ambulaIon.  
§  High  plasma  concentraIons  of  aldosterone  and  low  
renin  acIvity  =  primary  hyperaldosteronism  
§  AddiIonally,  if  plasma  aldosterone  concentraIon  falls  
on  standing,  this  is  indicaIve  of  adrenal  adenoma  as  
opposed  to  adrenal  hyperplasia  (a  rise  of  aldosterone  
is  more  usual)  
§  Consider  CT  scan  adrenal  glands.  
 Case  8  
•  How  would  you  correct  his  hypokalaemia  (K  2.9  
mmol/l)?  
§  Oral  therapy:  method  of  choice  for  mild-­‐to-­‐moderate  
hypokalaemia  (K  >  2.5  mmol/l)  
§  Can  also  be  given  as  slow  release  K  (slow  K,  1  tablet  
600  mg  =  8  mmol)    or  liquid  forms  (mist  KCL  10  ml  =  
1g  =  14  mmol)    
§  Slow  K  less  efficacious  in  correcIng  more  severe  degrees  of  
hypokalaemia  (slow  release),  also  shown  to  be  associated  
with  gastric  erosions  
§  40  –  200  mmol  daily  of  KCl  may  be  required  over  
periods  of  days  or  weeks  e.g.  20  –  40  mmol  2  –  4  x  
daily  depending  on  severity  of  depleIon  (as  frequent  
as  2  –  4    hrly  may  be  required)  
3  types  of  mineralocorIcoid  excess  
•  Dependent  on  aldosterone  
–  Primary  hyperaldosteronism  
–  Secondary  hyperaldosteronism  

•  Non-­‐dependent  on  aldosterone  

–  Decreased  renal  enzyme  11-­‐β-­‐hydroxysteroid  
dehydrogenase  
–  Syndrome  of  apparent  mineralocorIcoid  excess  
•  Congenital/  acquired  
•  Liddle’s  syndrome  
 Primary  mineralocorIcoid  excess  
•  Should  be  suspected  in  any  
paIent  with  the  triad  of:  
–  Hypertension  
–  Hypokalaemia  
–  Metabolic  alkalosis  
•  Increased  mineralocorIcoid  
acIvity  can  be  grouped  
according  to:  
–  Plasma  aldosterone  
concentraIon  (PAC)  
–  Plasma  renin  acIvity  (PRA)  
 MineralocorIcoid  excess  
Aldosterone-­‐dependent  
•  Suspect  primary  aldosteronism  
(e.g.  Conn’s  syndrome)  if:  
–  PRA  is  suppressed  and    
–  PAC  is  increased  

•  Suspect  secondary  
hyperaldosteronism  (e.g.  renal  
artery  stenosis,  renin-­‐secreIng  
tumours,  and  coarctaIon  of  
aorta)  
–  Both  PRA  and  PAC  are  increased  and  
–  PAC/  PRA  raIo  is  less  than  10  
 MineralocorIcoid  excess  
Non-­‐aldosterone  dependent  
•  Suspect  non-­‐aldosterone  mineralocorIcoid  
excess  if:  
–  Both  PRA  and  PAC  are  suppressed.  

•  The  renal  enzyme  11-­‐β-­‐hydroxysteroid  

dehydrogenase  provides  mineralocorIcoid  
receptor  specificity  for  aldosterone  by  
metabolizing  glucocor,coids  (corIsol)  to  their  11-­‐
dehydro  derivaIves  (corIsone)  compounds  that  
do  not  bind  to  the  mineralocorIcoid  receptor.  
 MineralocorIcoid  excess  
Non-­‐aldosterone  dependent  
•  Decreased  enzyme  acIvity  allows  glucocor'coids  
to  act  as  mineralocor'coids  and  produce  
hypertension,  hypokalaemia  and  metabolic  
alkalosis  with  low  levels  of  aldosterone.  

•  This  occurs  in:  

–  Congenital  adrenal  hyperplasia  (17-­‐α-­‐hydroxylase  
deficiency)      
–  Familial  corIsol  resistance  
–  Severe  Cushing’s  syndrome  
 Case  9  
•  A  49-­‐year  old  man  was  referred  with  leW  loin  pain  
and  haematuria.  
•  He  had  a  long  history  of  renal  stones.  
•  He  had  no  other  medical  problems  and  was  not  
on  any  medicaIons.  
•  T  36.5°C,  pulse  88  regular,  and  BP  148/92  
•  There  was  tenderness  in  the  leW  loin  region  but  
no  organomegaly.  
•  Rectal  examinaIon  was  normal.  
 Case  9  
•  Hb  10.9    MCV  96.4     •  Renin  (upright)  3.4  (N  3.0  
•  WBC  8.6   –  4.3  pmol/ml/hr)  
•  Plt  200   •  Aldosterone  (upright)  420  
(N  330  –  830  pmol/l)  
•  Urea  18.3,  Creat  220  
•  Na  138,  K  3.1,   •  UFEME  
–  pH  6.4,  prot  2+,  blood  1+,  
•  Cl  114,     leuc  1+  
•  pH  7.23,  HCO3  10   •  Abdominal  X-­‐ray:  
•  Ca  2.42,  Alb  38   speckled  calcificaIon  of  
•  PO4  0.98   both  kidneys.  

What  is  the  anion  gap?  

 Case  9  
•  The  most  likely  diagnosis  is:  
a.  BarVer’s  syndrome  
b.  Conn’s  syndrome  
c.  Renal  tubular  acidosis  type  1  
d.  Renal  tubular  acidosis  type  2  
e.  Renal  tubular  acidosis  type  4  
 Renal  tubular  acidosis  type  1  
•  This  paIent  had  nephrocalcinosis  (plain  X-­‐ray,  
history  of  repeated  stones)  
•  Autosomal  recessive  
•  Flow  of  urine  is  slowed  from  tubules  into  renal  
pelvis  →  supersaturaIon  of  urine  and  stone  
formaIon.  
•  RTA  1  characterized  by  defect  in  urinary  
acidificaFon  and  renal  ammoniagenesis,  which  
results  in  a  net  accumulaFon  of  acids  within  
body  fluids.  
•  Acid  loading  (ammonium  chloride)  test  –  fail  to  
acidify  urine  
 Renal  tubular  acidosis  type  1  
•  Inability  to  excrete  H+  ions  in  the  distal  
tubule.  
•  Urinary  pH  is  never  <  5.3  
•  Other  features  of  RTA  1  include:  
–  AssociaIon  with  renal  parenchymal  
disease,  such  as  medullary  sponge  kidney  
–  Normal  anion  gap  metabolic  acidosis    
–  Hypokalaemia  due  to  increased  exchange  
between  Na+  and  K+  at  the  distal  tubule.  
 Renal  tubular  acidosis  type  2  
•  DefecFve  bicarbonate  reabsorpFon  in  proximal  
tubule  
•  Leading  to  increased  delivery  of  bicarbonate  to  
distal  nephron  where  it  acts  as  a  non-­‐reabsorbable  
anion  
•  Urine  pH  is  variable,  serum  HCO3  between  14  –  20  
mmol/l  
•  Associated  features:    
–  Fanconi’s  syndrome  (hypophosphataemia,  
hyperuricaemia,  glycosuria,  volume  depleIon)  
–  Osteomalacia    
 Renal  tubular  acidosis  type  4  
•  Hyporeninaemic  hypoaldosteronism  
•  Hyperkalaemia  
•  DiabeIc  nephropathy  
 Other  causes  of  hypokalaemia  
•  Rare  hereditary  defects  of  renal  salt  transporters  
•  Hypomagnasemia  
–  direct  effect  of  low  cytosolic  magnesium  on  potassium  
channels  and  enhanced  potassium  secreIon  
•  DiabeIc  ketoacidosis  
–  Obligate  loss  of  potassium  from  kidney  as  a  caIonic  
partner  to  the  negaIvely  charged  ketone  and  β-­‐
hydroxybutyrate  
•  Rare  hereditary  defects  of  muscular  ion  channels  
and  transporters  
 Rare  hereditary  effects  of  renal  salt  
transporters  
•  Hypokalaemia  without  hypertension  
•  E.g.  BarVer  syndrome  or  Gitelman  syndrome  
•  Similar  to  effect  of  diureIcs  
•  Barrter  syndrome  
–  Defect  in  sodium  transport  in  loop  of  Henle  
–  Associated  with  hypercalciuria  
•  Gitelman  syndrome  
–  Impairment  of  thiazide-­‐sensiIve  sodium-­‐chloride  co-­‐
transporter  in  the  distal  tubule  
–  Associated  with  hypocalciuria  and  hypomagnesemia.  
 Rare  hereditary  defects  of  muscular  
ion  channels  and  transporters  
•  Cause  hypokalaemic  periodic  paralysis    
•  Can  precipitate  severe  hypokalaemia  and  
muscle  weakness  
•  These  defects  cause  an  increased  sensiIvity  to  
catechols  and/or  insulin  and/or  thyroid  
hormone  
•  Leading  to  sudden  influx  of  potassium  from  
extracellular  fluid  into  the  muscle  cells.  
 Case  10  
•  27  year  old  bank  clerk,  smoker  
•  AdmiVed  with  generalised  muscle  weakness  
upon  waking  in  the  morning.  
•  Had  a  heavy  dinner  last  night.  
•  IntermiVent  palpitaIons  with  weight  loss  for  
past  3  months  
•  Brother  had  similar  symptoms  last  year  –  
currently  on  some  sort  of  treatment.  
 Case  10  
•  Appeared  anxious  
•  PR  100  bpm  regular,  BP  110/70  
•  Small  diffuse  goitre  
•  Fine  tremors  of  outstretched  hands  
•  Sweaty  palms  
•  Power  of  both  UL  and  LL  2/5  
•  Reflexes  generally  depressed.  
 Case  10  
•  What  is  the  possible  diagnosis?  
•  Hypokalaemic  periodic  paralysis  secondary  to  
untreated  thyrotoxicosis  
•  DifferenIal  diagnosis:  familial  hypokalaemic  
periodic  paralysis  
 Case  10  
•  What  invesIgaIon  would  you  do  in  the  man  
to  evaluate  his  condiIon?  
o Renal  profile  
o Arterial  blood  gas  
o Urinalysis  in  parIcular  urine  pH  
o ECG  
o Thyroid  funcIon  test  
 Case  10  
•  Urea  4.1    
•  Na  142    
•  K  1.9  
•  Cl  100  
•  pH  7.44,  HCO3  28,  pCO2  34  
•  Urine  pH  5,  no  protein/  RBC/  leuc  
•  T4    70  pmol/l  (N  10  –  25)  
•  TSH  <  0.05  mU/L  (N  0.4  –  5)  
•  Please  comment.  
 Case  10  
•  This  paIent  has  severe  hypokalaemia.  
•  Symptoms  usually  appear  when  K  <  2.5  
mmol/l  
–  Malaise,  faIgue  
–  Neuromuscular  disturbance:  weakness,  
hyporeflexia,  paraesthesias,  cramps,  restless  leg  
syndrome,  rhabdomyolysis,  paralysis  
–  GI:  consIpaIon,  ileus  
–  Polyuria,  polydipsia,  metabolic  alkalosis  
 Important  facts  
•  1g  of  KCL  contains  14  mmol  of  potassium  
•  If  K  level  is  <  3  mmol/l,  potassium  supplements  
should  be  given.  
•  In  paIent  with  hypokalaemia  with  low  urinary  K  
excreIon  (<  20  mmol/l),  hypokalaemia  of  extra-­‐
renal  origin  should  be  suspected  (i.e.  GI  loss).  
•  In  asymptomaFc  paFent  with  K  between  3  -­‐4  
mmol/l,  who  are  vulnerable  to  cardiac  
arrhythmias  e.g.  CCF,  digoxin,  history  of  MI/  IHD,  
potassium  supplements  are  recommended.  
 Case  10  

Sinus  tachycardia.  P  pulmonale,  with  U  waves  present.    

 Case  10  
•  ECG  changes  in  hypokalaemia:  
–  Small  or  inverted  T  waves  
–  Prominent  U  waves  
–  Depressed  ST  segments  
–  Arrhythmias:  1st  and  2nd  degree  heart  blocks,  atrial  
fibrillaIon,  ventricular  tachycardia,  ventricular  
fibrillaIon  
 Case  10  
•  How  will  you  manage  his  hypokalaemia?  
a.  Increase  his  dietary  potassium  intake    
b.  Mist  KCL  supplements  
c.  Intravenous  potassium  supplements  
d.  Intravenous  magnesium  supplements  
 Management  of  Hypokalaemia  
•  IV  therapy  is  method  of  choice  in:  
–  Severe  hypokalaemia  (K  <  2.5  mmol/l)    
–  With  ECG  changes  
–  PaIent  not  able  to  take  orally  
–  SymptomaIc  e.g.  cardiac  arrhythmias  with  rapid  
ventricular  response,  familial  periodic  paralysis,  
severe  myopathy  
 Management  of  Hypokalaemia  
•  In  asymptomaIc  paIents  without  ECG  
changes,  K  should  be  given  as  follows  
–  At  a  concentraIon  of  <  40  mmol/l  (<  3g  KCL  per  
liter)  in  normal  saline  (avoid  dextrose  fluid)  
–  Given  at  a  rate  of  <  20  mmol/hr  (10  mmol/hr  
recommended)  e.g.  2  g  KCL  in  1  pint  over  3  hour.  
–  Monitor  plasma  K  regularly,  ECG  monitoring  
advised.  
 Management  of  Hypokalaemia  
•  In  emergency  e.g  cardiac  arrhythmias,  severe  
myopathy,  K  can  be  given:-­‐  
–  At  rates  up  to  40  mmol/l  per  hour  (i.e.  KCL  3g/hr)    
–  In  concentraIons  of  200  –  400  mmol/l  (by  mixing  20  –  
40  mmol/l  or  1.5  –  3.0g  KCl  in  100  mls  NS)  
–  IV  administraIon  of  K  at  a  rate  of  >  10  mmol/hr  
requires  conInuous  ECG  monitoring.  
•  As  soon  as  ECG  changes  normalize,  cardiac  
rhythm  returns  to  normal  or  respiratory  muscle  
strength  is  restored,  gradually  taper  IV  infusion  
and  disconInued.  Then,  iniIate  oral  KCL.  
 Management  of  Hypokalaemia  
•  Most  important  potenFal  risk  of  IV  K  
administraIon  =  acute  hyperkalaemia  (most  
likely  in  pts  with  renal  insufficiency)  
•  Use  large  central  vein:  femoral  venous  
infusion  is  preferable  than  upper  body  central  
vein  to  avoid  deleterious  effects  on  cardiac  
conducIon.  
•  ConcentraIon  of  >  60  mmol/l  should  not  be  
given  through  peripheral  vein.  
 Case  11  
•  52  year  old  man  
•  End-­‐stage  renal  disease  under  regular  
haemodialysis  for  past  2  years.  
•  AdmiVed  for  increasing  breathlessness  over  2  
days  duraIon.  
•  Apparently  had  missed  his  dialysis  for  2  
consecuIve  sessions.  
•  Nauseated  and  vomited  3  Imes  since  
morning.  
 Case  11  
•  Pallor,  no  jaundice.  
•  Tachypnoeic  RR  26/min    
•  Flapping  tremor  
•  BP  190/100  PR  80  reg  
•  CVS  S1S2  pericardial  rub  
•  Lungs  bibasal  crepitaIons  
•  Minimal  pitng  pedal  oedema  

•  What  blood  invesIgaIons  would  you  like  to  carry  

out?  
 Case  11  
•  FBC  –  anaemia  (paIent  is  pale),  with  GXM  
packed  cells.  
•  Renal  profile  –  uraemia  (paIent  has  uraemic  
symptoms  and  pericardial  rub),  hyperkalaemia    
•  Arterial  blood  gas  –  metabolic  acidosis  
(paIent  has  Kussmaul  breathing)  
 Case  11  
•  Hb  10.2,  MCV  82,  TWC  4.3,  Plt  219  
•  BU  63,  Na  130,  K  7.6,  Creat  1020  
•  ABG  on  air:   1.  NormocyIc  anaemia    -­‐    most  
–  pH      7.15   likely  anaemia  of  chronic  
disease  
–  pO2      100  mmHg  
2.  Uraemia,    severe  
–  pCO2  20  mmHg   hyperkalaemia,  elevated  
–  HCO3  9  mmol/l   creaInine  –  due  to  ESRD  missed  
dialysis  
•  Please  comment.   3.  Severe  metabolic  acidosis  with  
respiratory  compensaIon  

•  What  is  the  other  important  invesIgaIon?  

 Case  11  

Tall  tented  T  waves,  absent  P  waves  

 Case  11  
•  What  are  the  ECG  changes  in  hyperkalaemia?  
–  1st  ECG  sign  of  hyperkalaemia  is  peaked  T  waves  
(K  ≥  6  mmol/l)  
–  2nd  sign:  prolonged  PR  interval  (K  ≥  7  mmol/l)  
–  3rd  sign:  absent  P  waves  and  widen  QRS  –  a  VERY  
DANGEROUS  SIGN!  (K  between  8  –  9  mmol/l)  
•  Atrial  acIvity  is  lost  and  the  stage  is  set  for  ventricular  
tachycardia/  fibrillaIon  
–  If  conInue  to  ignore  the  changes  above,  
ventricular  tachycardia/  fibrillaFon  will  ensue.  
 Case  11  
•  What  is  the  next  step  of  management?  
–  LyFc  cocktail  with  conInuous  ECG  monitoring  
•  10  ml  10%  IV  calcium  gluconate  slow  infusion  for  
cardiac  protecIon,  second  dose  may  be  given  if  no  ECG  
changes  aWer  5  minutes  
–  Effect  within  minutes,  lasts  for  1  hour  
•  Rapid  acIng  insulin  10  U  with  50  ml  of  dextrose  50%  
infused  slowly  for  30-­‐60  minutes.  In  paIent  with  renal  
failure,  need  higher  dose  of  glucose  (100-­‐150  ml).    
–  Onset  within  30  –  60  minutes,  lasts  for  several  hours  
–  Can  be  repeated  6  –  8  hrly.  
–  Arrange  for  urgent  dialysis!  
 Case  11  
•  Other  helpful  therapies:  
–  Beta  agonist  therapy  
•  IV  salbutamol  0.5  mg  IV  in  15  mins  or  10  mg  
nebulizaIon  (with  or  without  glucose  and  insulin  
infusion)  has  been  shown  to  be  effecIve  in  
reducing  K  level  (IV  preferred  in  paIent  with  ESRD)  
•  If  effecIve,  plasma  K  will  fall  by  0.5  –  1.5  mmol/l  in  
15-­‐30  mins  and  effect  will  last  for  several  hours  
•  However,  beware  of  tachycardia.  
 Case  11  
•  Sodium  bicarbonate  infusion  
–  IV  infusion  of  bicarbonate  100  –  200  mmol/l  over  30  
mins  produces  metabolic  alkalosis  which  lowers  K  in  
ECF.  
–  Onset  of  acIon  occurs  within  30  mins  and  lasts  for  1-­‐2  
hours.  
–  Less  effecIve  in  paIents  with  renal  failure  and  may  
worsen  sodium  overload  leading  to  pulmonary  
oedema.  
–  Don’t  give  in  the  same  line  with  IV  Calcium  gluconate  
(can  precipitate  calcium),  
 Case  11  
•  CaIon-­‐exchange  resins  (Kalimate  or  Resonium  
A)  
–  Binds  potassium  in  exchange  for  another  caIon  in  
GI  tract,  thereby  removing  K  from  body  
–  Usually  given  orally  
•  Kalimate  (calcium  polystyrene  sulphonate)  5  -­‐10g  TDS  
•  Resonium  A  (sodium  polystyrene  sulphone)  15  –  30g  
three    –  four  Imes  daily  
–  Can  be  given  as  enemas  (Kalimate  30g  in  100  mls  
or  Resonium  30  –  60g  in  200  mls  3  -­‐4  Imes  daily  
 Goals  of  management  of  hyperkalaemia  

1. To protect the heart from effects of

potassium by antagonizing its effects on
cardiac conduction (calcium)
2. To shift potassium from ECF to ICF (Na
bicarb, insulin and glucose)
3. To reduce total body potassium (resins,
dialysis)

•  Urgent treatment if K > 6.5 mmol/l or ECG

shows changes of hyperkalaemia
 Hyperkalaemia  
•  A  medical  emergency!  
•  Usually  occur  when  K  >  6.5  mmol/l  
•  ManifestaIons:  
–  Neuromuscluar:  weakness,  paraesthesia,  
areflexia,  ascending  paralysos  
–  Cardiac:  bradycardia,  prolonged  AV  conducIon,  
complete  heart  block,  wide  complex  tachycardia,  
ventricular  fibrillaIon,  asystole.  
–  Treat  hyperkalaemia  even  in  the  absence  of  ECG  
changes.  
 Causes  of  Hyperkalaemia  
1.  Decreased  renal  excreFon   2.  Increased  potassium  load  
•  Renal  failure:  acute  or  chronic   •  Potassium  chloride:  iatrogenic  
•  MineralocorIcoid  deficiency   and  salt  subsItutes  
–  Addison’s  disease  (primary  
hypoaldosteronism)   •  Potassium  containing  
–  Hyporeninaemic   medicaIons  
hypoaldosteronism  (RTA  type  
4)   •  Transfusion  of  stored  or  
•  Drugs:   irradiated  blood  
–  ACEi/  ARBs  (usually  in  presence  
of  renal  impairment)  
–  Potassium-­‐sparing  diureIcs  
–  NSAIDs  
–  Cyclosporin  therapy  
–  Heparin  therapy  
•  Acidosis  
 Causes  of  Hyperkalaemia  
3.  Increased  release  from  cells   4.  Pseudohyperkalaemia  
•  ShiW  of  K  out  of  cells   •  Increased  in  vitro  release  from  
–  Acidosis   abnormal  cells  
–  Insulin  deficiency  e.g.  DKA  
–  Thrombocytosis  
–  Aldosterone  deficiency  
–  Beta-­‐receptor  antagonists   –  Leucocytosis  
–  Hyperkalaemic  periodic   •  Haemolysis  of  sample  
paralysis   (commonly  encountered)  
•  Tissue  breakdown  
–  Severe  intravascular  
haemolysis  e.g.  severe  malaria  
–  Digoxin  toxicity  
–  Rhabdomyolysis  
–  Tumour  lysis  syndrome  
–  Tissue  necrosis/  crush  injury  
–  Vigorous  exercise  (transient)  
 Mild-­‐moderate  hyperkalaemia  
 (K  5.5  –  6.5  mmol/l)  with  no  ECG  changes  

•  Low  potassium  diet  

•  Stop  drugs  which  may  cause  hyperkalaemia  
•  CaIon-­‐exchange  resins  
•  CorrecIon  of  acidosis  in  paIents  with  metabolic  
acidosis  
•  +/-­‐  glucose  and  insulin  infusion