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Electrolyte Abnormalities in
Children
Presenter- Dr Aftab Ahmad Siddiqui
Moderators- Dr. Z Z Rab, Dr. Uzma Firdaus, Dr. Ayesha Ahmad,
Dr Shaad Abqari
Composition of body fluids
 Total body water as a percentage of body weight
declines with age.
 Early fetal life TBW= 90%
 At birth TBW= 75-80%
 By the end of 1st year to puberty TBW= 60%
Body Composition
40% Intracellular
fluid
40%Intracellular
15% Interstitial
5% Intravascular
Body Composition
Intracellular fluid Non Water
Interstitial fluid Intravascular volume
Water balance
Input Output
Water intake:
Fluid 60%
Food 30%
Urine 60%
Stool 8%
Sweat 4%
Water of
oxidation 10
%
Insensible
loss 28%
(skin, lungs)
Water intake is
regulated by
osmoreceptors in
hypothalamus
Water loss is
regulated by ADH
from post.
pituitary
Electrolyte composition of extracellular and intracellular fluid
compartments
140
4 2.5 1.1
104
24
14
6
2
0
20
40
60
80
100
120
140
160
mmol/l
Plasma
140
13
7
107
40
10
3
0
20
40
60
80
100
120
140
160
mmol/l
Intracellular
Osmolality
 Osmolality is the solute concentration of a fluid expressed
as mOsm/kg.
 Fluid/water moves from lower osmolality to higher
osmolality across biological membranes.
 Normal Plasma osmolality = 285 to 295 mOsm/kg
 Tightly regulated within 1-2% of normal.
Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18)
Regulation of sodium and water balance
Maintenance fluid & electrolyte
requirements
 Holliday-Segar method
 Maximum fluid/day = 2400ml/day
Body weight Per day Per hour
0-10 kg 100ml/kg 4ml/kg
10-20 kg 50 ml/kg beyond 10 kg
2ml/kg beyond
10 kg
>20 kg 20ml/kg beyond 20 kg
1ml/kg beyond
20 kg
Maintenance fluid & electrolyte
requirements
 Daily sodium requirement = 3meq/kg (children)
 Daily potassium requirement = 2meq/kg
 Daily chloride requirement = 2meq/kg
Maintenance fluid & electrolyte
requirements
 Fluid/electrolyte requirements calculated on Holliday-segar
method are generally hypotonic (N/4 or N/5)
 Recent evidence shows use of hypotonic fluids esp. in sick
children can cause hyponatremia.
 0.9% NS can be safely used in standard maintenence
volume.
(except in CHF, renal/hepatic failure, diabetes insipidus).
Maintenance fluid & electrolyte
requirements
 No single i.v fluid is suitable in all situations, therapy to be
individualized.
 Monitor with daily wt, input/output, serum electrolytes.
 Maintenance fluids provide only about 20% of calories, therefore
child will lose wt due to catabolism.
Conditions that alter maintenance
fluid requirements
 Increased fluid requirement
 Fever (10-15% per 0C above
380C )
 Radiant warmer/Phototherapy
 Burns
 Excessive sweating
 High physical activity
 Hyperventilation
 Diarrhoea/vomiting
 Polyuria
 VLBW babies
Conditions that alter maintenance
fluid requirements
 Decreased fluid requirement
 Oliguria/Anuria
 Humidified ventilator/incubator
 Hupothyroidism
Sodium
 Most abundant ion of the extracellular compartment
 Normal serum sodium = 135 to 145 mEq/l.
 Daialy sodium requirement is 2 to 3 mEq/kg body weight.
 Requirement is nearly 2 to 3 fold higher in term & VLBW
preterm babies.
 Adult requirements decreases to 1.5mEq/kg/day.
 Extrarenal sodium losses can be significant via profuse
sweating ,burns, severe vomiting or diarrhoea.
Hyponatremia
 Defined as serum Na < 135 meq/l.
 Usually symptomatic when Na is < 125mEq/l or the decline is
acute(<24 hour).
 Early features : headache, nausea, vomiting, lethargy and
confusion.
 Advance manifestations: seizures, coma, decorticate posturing,
dilated pupil, anisocoria, papilledema, cardiac arrhythmias,
myocardial ischemias and central diabetes insipidus.
Hyponatremia
 CAUSES of hyponatremia
 Hypovolemic hyponatremia
 Renal loss: diuretic use, osmotic diuresis, renal salt
wasting, adrenal insufficiency.
 Extra-renal loss: diarrhoea, vomiting, sweat,cerebral salt
wasting syndrome, third spacing(effusion,ascites)
Hyponatremia
 CAUSES of hyponatremia
 Normovolemic hyponatremia
 Conditions that predispose to SIADH - Inflammatory central
nervous system disease(meningitis, encephalitis), tumors,
pulmonary disease(severe asthma, pneumonia),drugs
(cyclophosphamide, vincristine).
Hyponatremia
 CAUSES of hyponatremia
 Hypervolemic hyponatremia
 CHF, Cirrhosis, Nephrotic syndrome, Acute or chronic
renal failure
Hyponatremia-Treatment
 Determine whether hyponatremia is acute(<24 hr) or chronic(>48hr),
symptomatic/asymptomatic.
 Evaluate the volume status (hypervolemia, euvolemia, hypovolemia).
 Sodium deficit (meq) = 0.6*Body wt(kg) * [desired Na – observed Na]
Hyponatremia-Treatment
 Treat hypotension first (NS/RL/5%albumin), asymptomatic cases
prefer ORS.
 Rate of correction = 0.6 to 1.0 mEq/l/hr till Na is 125 then at slower
rate over 48 to 72 hours.
 For symptomatic cases give 3%NS @ 3-5 ml/kg over 1-2 hr. (increases
serum Na by 5-6mEq/l)
 Stop further therapy with 3%NS when patient is symptom free or
acute rise in serum sodium is 10mEq/l in first 5 hour.
Hyponatremia-Treatment
 Rise in serum Na can be estimated by Adrogue Madias formula-
Δ 𝑁𝑎 =
𝐼𝑛𝑓𝑢𝑠𝑎𝑡𝑒 𝑁𝑎 + 𝐼𝑛𝑓𝑢𝑠𝑎𝑡𝑒 𝐾 −𝑆𝑒𝑟𝑢𝑚 𝑁𝑎
[𝑇𝐵𝑊+1]
Δ[Na]= expected change in serum sodium/L of fluid given
TBW= total body water is 0.6*Body wt (kg)
Hyponatremia-Treatment
 Fluid restriction alone is needed for SIADH.
 Sodium and water restriction for hypervolemic hyponatremia.
 V2-receptor antagonists or vaptans may be used in SIADH &
hypervolemic hyponatremia.
 Diuretics for refractory cases.
Hypernatremia
 Defined as serum Na >150mEq/l
Clinical features
 Lethargy or mental status change which can proceed to coma and
convulsions.
 Acute severe hypernatremia leads to osmotic shift of water from
neurons causing shrinkage of brain and tearing of meningeal vessels -
intracranial hemorrhage.
Hypernatremia
 Causes of Hypernatremia
 Net water loss
 Insensible losses
 Diabetes insipidus
 Inadequate breastfeeding
 Hypotonic fluid loss
 Renal: osmotic diuretics, post obstructive, polyuric phase of acute tubular
necrosis
 GI: vomiting,nasogastric drainage, diarrhea, laxative.
Hypernatremia
 Causes of Hypernatremia
 Hypertonic Sodium gain
 Excess sodium intake
 Sodium bicarbonate, saline infusion
 Hypertonic feeds, boiled skimmed milk
 Ingestion of sodium chloride
 Hypertonic dialysis
 Endocrine: Primary hyperaldosteronism, Cushing syndrome
Hypernatremia- Treatment
 Treat hypotension first (NS/RL/5% Albumin bolus)
 Correct deficit over 48 to 72 hours. Recommended rate of drop is
0.5mEq/l/hr (10-12mEq/l/day)
 Hypotonic infusates are used as N/4 or N/5 saline, avoid sodium free
fluids. ( Calculate expected fall in Na by Adrogue Madias formula ).
Hypernatremia- Treatment
 Seizures during correction of hypernatremia are treated using
3%NS as 5-6ml/kg infusion over 1-2 hr.
 For significant hypernatremia ( >180-200mEq/l ) with concurrent
renal failure and or volume overload, renal replacement therapy
(peritoneal or hemodialysis, hemofiltration) is indicated.
Differentiation b/w few important conditions
Potassium
 Normal serum concentration=3.5-5.0mEq/l and intracellular 150mEq/l .
 Source of potassium include meats, beans, fruits and potatoes.
 Majority in muscles and majority of extracellular K in bones.
 More significant in males around puberty.
 Serum K concentration increases by approximately 0.6mEq/l with each
10 mOsm rise in plasma osmolality
Physiologic function of Potassium
 Electrical responsiveness of nerve and muscle cells.
 Contractility of cardiac, skeletal and smooth muscle cells.
 Maintains cell volume.
Potassium Excretion
 Normally 10% of K is excreted.
 Excretion is increased by aldosterone, loop diuretics, osmotic diuresis,
glucocorticoids, ADH and delivery of negatively charged ions to the
collecting duct(e.g. bicarb).
 Insulin, ß agonists and alkalosis enhance potassium entry into cells.
Hypokalemia
 Serum K<3.5mEq/l.
 Clinical features
 Severe hypokalemia (<2.5mEq/l) cause muscle weakness (neck
flop, abdominal distension, ileus) and arrhythmia.
 Hypokalemia increases the risk of digoxin toxicity by promoting
its binding to myocyte, potentiating its action and decreasing its
clearance.
Hypokalemia
 ECG changes-
Hypokalemia
 The trans-tubular potassium gradient (TTKG) is used to
interpret urinary potassium concentration.
TTKG =
𝑈𝑟𝑖𝑛𝑒 𝐾 ∗ 𝑆𝑒𝑟𝑢𝑚 𝑂𝑠𝑚
𝑆𝑒𝑟𝑢𝑚 𝐾 ∗ 𝑈𝑟𝑖𝑛𝑒 𝑂𝑠𝑚
 TTKG<4 suggest that kidney is not wasting excessive
potassium, TTKG ≥4 signify renal loss.
Causes of Hypokalemia
 Incresed Lossed
 Renal
 Extrarenal
 Decreased intake or stores
 Intracellular shift
Causes of Hypokalemia
 Increased losses
 Renal –
 RTA(proximal or distal)
 Drugs (diuretics, amphotericin B, aminoglycosides,
corticosteroids),
 Cystic fibrosis
 Mineralocorticoid excess (cushing syndrome, CAH, high
renin(renin secreting tumors, renal artery stenosis)
 Gittelman, Bartter and Liddle syndrome
Causes of Hypokalemia
 Increased losses
 Extrarenal –
 Diarrhea/vomiting/nasogastric suction
 Sweating
 Potassium binding resins(sodium polystyrene sulfonate).
Causes of Hypokalemia
 Decreased intake or stores
 Potassium poor parenteral nutrition
 Malnutrition, anorexia nervosa
 Intracellular shift
 alkalosis, high insulin state, drugs (ß agonist, theophylline,
barium, hydroxycholoroquine), refeeding syndrome,
hypokalemic periodic paralysis, malignant hyperthermia.
Hypokalemia-Treatment
 Determine the underlying cause, whether associated with
hypertension and acidosis or alkalosis.
 Hypertension may be due to primary hyperaldosteronism, renal
artery stenosis, CAH, glucocorticoid, liddle syndrome.
 Relative hypotension and alkalosis suggest diuretic use or
tubular disorder (Bartter/Gittelman syndrome).
Hypokalemia-Treatment
 Decrease ongoing losses (stop loop diuretics, replace GI losses). Use K
sparing diuretics, restore i.v volume, correct hypomagnesemia.
 Disease specific therapy , e.g Indomethacin/ACE inhibitors for
Bartter/Gittelman syndrome.
 Correct deficit over 24 hours.
 Replace the deficit : oral route safer. Dose 2-4mEq/kg/day (max-120-
240mEq/day) in 3 or 4 divided doses.
Hypokalemia-Treatment
 IV correction is used under strict ECG monitoring.
 For rapid correction in severe hypokalemia (<2.5 or
arrhythmias) 0.5 to 1.0mEq/kg (max-40 mEq ) is given over 1
hour.
 Infusate K should not exceed 40-60 meq/L.
Hyperkalemia
 Serum K>5.5mEq/l.
 Factitious or pseudo hyperkalemia: squeezing of extremities during
phlebotomy, sample from limb being infused with K containing fluid or
hemolysed sample.
 Clinical features: nausea vomiting paresthesias, muscle weakness(skeletal,
respiratory), fatigue, ileus, arrhythmia.
Hyperkalemia
 ECG changes-
Causes of Hyperkalemia
 Decreased losses
 Increased intake
 Extracellular shift
 Cellular breakdown
Causes of Hyperkalemia
 Decreased losses:
 Renal failure
 Renal tubular disorder- pseudohypoaldosteronism, urinary tract
obstruction.
 Drugs- ACE inhibitors, ARB, K sparing diuretics, NSAIDS,
heparin.
 Mineralocorticoid deficiency - Addision disease and 21-
hydroxylase deficiency.
Causes of Hyperkalemia
 Increased intake
 IV/Oral intake, PRBC transfusion.
 Extracellular shift
 Acidosis, low insulin state, drugs (ß blocker, digitalis,
succinylcholine, fluoride), hyperkalemic periodic paralysis,
malignant hyperthermia.
 Cellular breakdown
 tumor lysis syndrome, crush injury, massive hemolysis.
Hyperkalemia- Treatment
 It’s a medical emergency.
 Discontinue K+ containing fluids.
 ECG monitoring.
 If K > 7 or symptomatic with ECG changes- Administer Calcium
gluconate to stabilise myocardium (0.5ml/kg of 10%
Ca.gluconate over 5-10 min).
Hyperkalemia- Treatment
 Enhance Cellular uptake of potassium-
 Regular Insulin with glucose i.v (0.3 IU/g glucose over 2 hr).
 NaHCO3 i.v 1-2 meq/kg over 20-30 min.
 ß- agonist (salbutamol/terbutaline nebulized or i.v)
Hyperkalemia- Treatment
 Ensure K elimination
 K binding resin (kayexalate oral/per rectal 1g/kg)
 Loop or thiazide diuretic ( if renal functions maintained )
 Hemodialysis
 Correct hypoaldosteronism if present : steroids.
Thank you

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Electrolytes abnormalities

  • 1. Electrolyte Abnormalities in Children Presenter- Dr Aftab Ahmad Siddiqui Moderators- Dr. Z Z Rab, Dr. Uzma Firdaus, Dr. Ayesha Ahmad, Dr Shaad Abqari
  • 2. Composition of body fluids  Total body water as a percentage of body weight declines with age.  Early fetal life TBW= 90%  At birth TBW= 75-80%  By the end of 1st year to puberty TBW= 60%
  • 3. Body Composition 40% Intracellular fluid 40%Intracellular 15% Interstitial 5% Intravascular Body Composition Intracellular fluid Non Water Interstitial fluid Intravascular volume
  • 4. Water balance Input Output Water intake: Fluid 60% Food 30% Urine 60% Stool 8% Sweat 4% Water of oxidation 10 % Insensible loss 28% (skin, lungs) Water intake is regulated by osmoreceptors in hypothalamus Water loss is regulated by ADH from post. pituitary
  • 5. Electrolyte composition of extracellular and intracellular fluid compartments 140 4 2.5 1.1 104 24 14 6 2 0 20 40 60 80 100 120 140 160 mmol/l Plasma 140 13 7 107 40 10 3 0 20 40 60 80 100 120 140 160 mmol/l Intracellular
  • 6. Osmolality  Osmolality is the solute concentration of a fluid expressed as mOsm/kg.  Fluid/water moves from lower osmolality to higher osmolality across biological membranes.  Normal Plasma osmolality = 285 to 295 mOsm/kg  Tightly regulated within 1-2% of normal. Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18)
  • 7. Regulation of sodium and water balance
  • 8. Maintenance fluid & electrolyte requirements  Holliday-Segar method  Maximum fluid/day = 2400ml/day Body weight Per day Per hour 0-10 kg 100ml/kg 4ml/kg 10-20 kg 50 ml/kg beyond 10 kg 2ml/kg beyond 10 kg >20 kg 20ml/kg beyond 20 kg 1ml/kg beyond 20 kg
  • 9. Maintenance fluid & electrolyte requirements  Daily sodium requirement = 3meq/kg (children)  Daily potassium requirement = 2meq/kg  Daily chloride requirement = 2meq/kg
  • 10. Maintenance fluid & electrolyte requirements  Fluid/electrolyte requirements calculated on Holliday-segar method are generally hypotonic (N/4 or N/5)  Recent evidence shows use of hypotonic fluids esp. in sick children can cause hyponatremia.  0.9% NS can be safely used in standard maintenence volume. (except in CHF, renal/hepatic failure, diabetes insipidus).
  • 11. Maintenance fluid & electrolyte requirements  No single i.v fluid is suitable in all situations, therapy to be individualized.  Monitor with daily wt, input/output, serum electrolytes.  Maintenance fluids provide only about 20% of calories, therefore child will lose wt due to catabolism.
  • 12. Conditions that alter maintenance fluid requirements  Increased fluid requirement  Fever (10-15% per 0C above 380C )  Radiant warmer/Phototherapy  Burns  Excessive sweating  High physical activity  Hyperventilation  Diarrhoea/vomiting  Polyuria  VLBW babies
  • 13. Conditions that alter maintenance fluid requirements  Decreased fluid requirement  Oliguria/Anuria  Humidified ventilator/incubator  Hupothyroidism
  • 14. Sodium  Most abundant ion of the extracellular compartment  Normal serum sodium = 135 to 145 mEq/l.  Daialy sodium requirement is 2 to 3 mEq/kg body weight.  Requirement is nearly 2 to 3 fold higher in term & VLBW preterm babies.  Adult requirements decreases to 1.5mEq/kg/day.  Extrarenal sodium losses can be significant via profuse sweating ,burns, severe vomiting or diarrhoea.
  • 15. Hyponatremia  Defined as serum Na < 135 meq/l.  Usually symptomatic when Na is < 125mEq/l or the decline is acute(<24 hour).  Early features : headache, nausea, vomiting, lethargy and confusion.  Advance manifestations: seizures, coma, decorticate posturing, dilated pupil, anisocoria, papilledema, cardiac arrhythmias, myocardial ischemias and central diabetes insipidus.
  • 16. Hyponatremia  CAUSES of hyponatremia  Hypovolemic hyponatremia  Renal loss: diuretic use, osmotic diuresis, renal salt wasting, adrenal insufficiency.  Extra-renal loss: diarrhoea, vomiting, sweat,cerebral salt wasting syndrome, third spacing(effusion,ascites)
  • 17. Hyponatremia  CAUSES of hyponatremia  Normovolemic hyponatremia  Conditions that predispose to SIADH - Inflammatory central nervous system disease(meningitis, encephalitis), tumors, pulmonary disease(severe asthma, pneumonia),drugs (cyclophosphamide, vincristine).
  • 18. Hyponatremia  CAUSES of hyponatremia  Hypervolemic hyponatremia  CHF, Cirrhosis, Nephrotic syndrome, Acute or chronic renal failure
  • 19. Hyponatremia-Treatment  Determine whether hyponatremia is acute(<24 hr) or chronic(>48hr), symptomatic/asymptomatic.  Evaluate the volume status (hypervolemia, euvolemia, hypovolemia).  Sodium deficit (meq) = 0.6*Body wt(kg) * [desired Na – observed Na]
  • 20. Hyponatremia-Treatment  Treat hypotension first (NS/RL/5%albumin), asymptomatic cases prefer ORS.  Rate of correction = 0.6 to 1.0 mEq/l/hr till Na is 125 then at slower rate over 48 to 72 hours.  For symptomatic cases give 3%NS @ 3-5 ml/kg over 1-2 hr. (increases serum Na by 5-6mEq/l)  Stop further therapy with 3%NS when patient is symptom free or acute rise in serum sodium is 10mEq/l in first 5 hour.
  • 21. Hyponatremia-Treatment  Rise in serum Na can be estimated by Adrogue Madias formula- Δ 𝑁𝑎 = 𝐼𝑛𝑓𝑢𝑠𝑎𝑡𝑒 𝑁𝑎 + 𝐼𝑛𝑓𝑢𝑠𝑎𝑡𝑒 𝐾 −𝑆𝑒𝑟𝑢𝑚 𝑁𝑎 [𝑇𝐵𝑊+1] Δ[Na]= expected change in serum sodium/L of fluid given TBW= total body water is 0.6*Body wt (kg)
  • 22. Hyponatremia-Treatment  Fluid restriction alone is needed for SIADH.  Sodium and water restriction for hypervolemic hyponatremia.  V2-receptor antagonists or vaptans may be used in SIADH & hypervolemic hyponatremia.  Diuretics for refractory cases.
  • 23. Hypernatremia  Defined as serum Na >150mEq/l Clinical features  Lethargy or mental status change which can proceed to coma and convulsions.  Acute severe hypernatremia leads to osmotic shift of water from neurons causing shrinkage of brain and tearing of meningeal vessels - intracranial hemorrhage.
  • 24. Hypernatremia  Causes of Hypernatremia  Net water loss  Insensible losses  Diabetes insipidus  Inadequate breastfeeding  Hypotonic fluid loss  Renal: osmotic diuretics, post obstructive, polyuric phase of acute tubular necrosis  GI: vomiting,nasogastric drainage, diarrhea, laxative.
  • 25. Hypernatremia  Causes of Hypernatremia  Hypertonic Sodium gain  Excess sodium intake  Sodium bicarbonate, saline infusion  Hypertonic feeds, boiled skimmed milk  Ingestion of sodium chloride  Hypertonic dialysis  Endocrine: Primary hyperaldosteronism, Cushing syndrome
  • 26. Hypernatremia- Treatment  Treat hypotension first (NS/RL/5% Albumin bolus)  Correct deficit over 48 to 72 hours. Recommended rate of drop is 0.5mEq/l/hr (10-12mEq/l/day)  Hypotonic infusates are used as N/4 or N/5 saline, avoid sodium free fluids. ( Calculate expected fall in Na by Adrogue Madias formula ).
  • 27. Hypernatremia- Treatment  Seizures during correction of hypernatremia are treated using 3%NS as 5-6ml/kg infusion over 1-2 hr.  For significant hypernatremia ( >180-200mEq/l ) with concurrent renal failure and or volume overload, renal replacement therapy (peritoneal or hemodialysis, hemofiltration) is indicated.
  • 28. Differentiation b/w few important conditions
  • 29. Potassium  Normal serum concentration=3.5-5.0mEq/l and intracellular 150mEq/l .  Source of potassium include meats, beans, fruits and potatoes.  Majority in muscles and majority of extracellular K in bones.  More significant in males around puberty.  Serum K concentration increases by approximately 0.6mEq/l with each 10 mOsm rise in plasma osmolality
  • 30. Physiologic function of Potassium  Electrical responsiveness of nerve and muscle cells.  Contractility of cardiac, skeletal and smooth muscle cells.  Maintains cell volume.
  • 31. Potassium Excretion  Normally 10% of K is excreted.  Excretion is increased by aldosterone, loop diuretics, osmotic diuresis, glucocorticoids, ADH and delivery of negatively charged ions to the collecting duct(e.g. bicarb).  Insulin, ß agonists and alkalosis enhance potassium entry into cells.
  • 32. Hypokalemia  Serum K<3.5mEq/l.  Clinical features  Severe hypokalemia (<2.5mEq/l) cause muscle weakness (neck flop, abdominal distension, ileus) and arrhythmia.  Hypokalemia increases the risk of digoxin toxicity by promoting its binding to myocyte, potentiating its action and decreasing its clearance.
  • 34. Hypokalemia  The trans-tubular potassium gradient (TTKG) is used to interpret urinary potassium concentration. TTKG = 𝑈𝑟𝑖𝑛𝑒 𝐾 ∗ 𝑆𝑒𝑟𝑢𝑚 𝑂𝑠𝑚 𝑆𝑒𝑟𝑢𝑚 𝐾 ∗ 𝑈𝑟𝑖𝑛𝑒 𝑂𝑠𝑚  TTKG<4 suggest that kidney is not wasting excessive potassium, TTKG ≥4 signify renal loss.
  • 35. Causes of Hypokalemia  Incresed Lossed  Renal  Extrarenal  Decreased intake or stores  Intracellular shift
  • 36. Causes of Hypokalemia  Increased losses  Renal –  RTA(proximal or distal)  Drugs (diuretics, amphotericin B, aminoglycosides, corticosteroids),  Cystic fibrosis  Mineralocorticoid excess (cushing syndrome, CAH, high renin(renin secreting tumors, renal artery stenosis)  Gittelman, Bartter and Liddle syndrome
  • 37. Causes of Hypokalemia  Increased losses  Extrarenal –  Diarrhea/vomiting/nasogastric suction  Sweating  Potassium binding resins(sodium polystyrene sulfonate).
  • 38. Causes of Hypokalemia  Decreased intake or stores  Potassium poor parenteral nutrition  Malnutrition, anorexia nervosa  Intracellular shift  alkalosis, high insulin state, drugs (ß agonist, theophylline, barium, hydroxycholoroquine), refeeding syndrome, hypokalemic periodic paralysis, malignant hyperthermia.
  • 39. Hypokalemia-Treatment  Determine the underlying cause, whether associated with hypertension and acidosis or alkalosis.  Hypertension may be due to primary hyperaldosteronism, renal artery stenosis, CAH, glucocorticoid, liddle syndrome.  Relative hypotension and alkalosis suggest diuretic use or tubular disorder (Bartter/Gittelman syndrome).
  • 40. Hypokalemia-Treatment  Decrease ongoing losses (stop loop diuretics, replace GI losses). Use K sparing diuretics, restore i.v volume, correct hypomagnesemia.  Disease specific therapy , e.g Indomethacin/ACE inhibitors for Bartter/Gittelman syndrome.  Correct deficit over 24 hours.  Replace the deficit : oral route safer. Dose 2-4mEq/kg/day (max-120- 240mEq/day) in 3 or 4 divided doses.
  • 41. Hypokalemia-Treatment  IV correction is used under strict ECG monitoring.  For rapid correction in severe hypokalemia (<2.5 or arrhythmias) 0.5 to 1.0mEq/kg (max-40 mEq ) is given over 1 hour.  Infusate K should not exceed 40-60 meq/L.
  • 42. Hyperkalemia  Serum K>5.5mEq/l.  Factitious or pseudo hyperkalemia: squeezing of extremities during phlebotomy, sample from limb being infused with K containing fluid or hemolysed sample.  Clinical features: nausea vomiting paresthesias, muscle weakness(skeletal, respiratory), fatigue, ileus, arrhythmia.
  • 44. Causes of Hyperkalemia  Decreased losses  Increased intake  Extracellular shift  Cellular breakdown
  • 45. Causes of Hyperkalemia  Decreased losses:  Renal failure  Renal tubular disorder- pseudohypoaldosteronism, urinary tract obstruction.  Drugs- ACE inhibitors, ARB, K sparing diuretics, NSAIDS, heparin.  Mineralocorticoid deficiency - Addision disease and 21- hydroxylase deficiency.
  • 46. Causes of Hyperkalemia  Increased intake  IV/Oral intake, PRBC transfusion.  Extracellular shift  Acidosis, low insulin state, drugs (ß blocker, digitalis, succinylcholine, fluoride), hyperkalemic periodic paralysis, malignant hyperthermia.  Cellular breakdown  tumor lysis syndrome, crush injury, massive hemolysis.
  • 47. Hyperkalemia- Treatment  It’s a medical emergency.  Discontinue K+ containing fluids.  ECG monitoring.  If K > 7 or symptomatic with ECG changes- Administer Calcium gluconate to stabilise myocardium (0.5ml/kg of 10% Ca.gluconate over 5-10 min).
  • 48. Hyperkalemia- Treatment  Enhance Cellular uptake of potassium-  Regular Insulin with glucose i.v (0.3 IU/g glucose over 2 hr).  NaHCO3 i.v 1-2 meq/kg over 20-30 min.  ß- agonist (salbutamol/terbutaline nebulized or i.v)
  • 49. Hyperkalemia- Treatment  Ensure K elimination  K binding resin (kayexalate oral/per rectal 1g/kg)  Loop or thiazide diuretic ( if renal functions maintained )  Hemodialysis  Correct hypoaldosteronism if present : steroids.