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Electrolyte Disturbances
Pediatric Critical Care Medicine
Emory University
Children’s Healthcare of Atlanta
Objectives
• Recognize common fluid and electrolyte disorders
• Clinical presentations
• Management
2
Basic Metabolic Panel
Na+ Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
3
Basic Metabolic Panel
Na+ Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
4
Sodium (Na+)
• Bulk cation of extracellular fluid  change in SNa reflects
change in total body Na+
• Principle active solute for the maintenance of intravascular &
interstitial volume
• Absorption: throughout the GI system via active Na,K-ATPase
system
• Excretion: urine, sweat & feces
• Kidneys are the principal regulator
5
Sodium (Na+)
• Kidneys are the principal regulator
– 2/3 of filtered Na+ is reabsorbed by the proximal convoluted tubule,
increase with contraction of extracellular fluid
– Countercurrent system at the Loop of Henle is responsible for Na+
(descending) & water (ascending) balance – active transport with Cl-
– Aldosterone stimulates further Na+ re-absorption at the distal
convoluted tubules & the collecting ducts
– <1% of filtered Na+ is normally excreted but can vary up to 10% if
necessary
6
Sodium (Na+)
• Normal SNa: 135-145
• Major component of serum osmolality
– Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18)
– Normal: 285-295
• Alterations in SNa reflect an abnormal water regulation
7
Sodium (Na+)
• Hypernatremia: Causes
– Excessive intake
» Improperly mixed formula
» Exogenous: bicarb, hypertonic saline, seawater
– Water deficit:
» Central & nephrogenic DI
» Increased insensible loss
» Inadequate intake
8
Sodium (Na+)
• Hypernatremia: Causes
– Water and sodium deficit
» GI losses
» Cutaneous losses
» Renal losses
• Osmotic diuresis: mannitol, diabetes mellitus
• Chronic kidney disease
• Polyuric ATN
• Post-obstructive diuresis
9
Sodium (Na+)
• Hypernatremia Clinical presentation
– Dehydration
– “Doughy” feel to skin
– Irritability, lethargy, weakness
– Intracranial hemorrhage
– Thrombosis: renal vein, dura sinus
10
Sodium (Na+)
• Hypernatremia Treatment
– Rate of correction for Na+ 1-2 mEq/L/hr
– Calculate water deficit
» Water deficit = 0.6 x wt (kg) x [(current Na+/140) – 1]
– Rate of correction for calculated water deficit
» 50% first 12-24 hrs
» Remaining next 24 hrs
11
Sodium (Na+)
• Hyponatremia
– Na+<135
– Seizure threshold ~125
– <120 life threatening
12
Sodium (Na+)
• Hyponatremia: Etiology
– Hypervolemic
» CHF Cirrhosis
» Nephrotic syndrome Hypoalbuminemia
» Septic capillary leak
– Hypovolemic
» Renal losses Cerebral salt wasting
» Extra-renal losses aldosterone effect
• GI losses
• Third spacing
13
Sodium (Na+)
• Hyponatremia: Etiology
• Euvolemic hyponatremia
» SIADH
» Glucocorticoid deficiency
» Hypothyroidism
» Water intoxication
• Psychogenic polydipsia
• Diluted formula
• Beer potomania
• Pseudo-hyponatremia
– Hyperglycemia
– SNa decreased by 1.6/100 glucose over 100
14
-
Sodium (Na+)
• Hyponatremia Clinical presentation
– Cellular swelling due to water shifts into cells
– Anorexia, nausea, emesis, malaise, lethargy, confusion,
agitation, headache, seizures, coma
– Chronic hyponatremia: better tolerated
15
Sodium (Na+)
• Hyponatremia Treatment
– Rapid correction  central pontine myelinolysis
– Goal 12 mEq/L/day
– Fluid restriction with SIADH
– Hyponatremic seizures
» Poorly responsive to anti-convulsants
» Hypertonic saline
» Need to bring Na to above seizure threshold
16
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Sodium (Na+)
Fill in the blanks
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW
Basic Metabolic Panel
Na+ Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
33
Potassium (K+)
• Normal range: 3.5-4.5
• Largely contained intra-cellular  SK does not reflect total
body K
• Important roles: contractility of muscle cells, electrical
responsiveness
• Principal regulator: kidneys
34
Potassium (K+)
• Daily requirement 1-2 mEq/kg
• Complete absorption in the upper GI tract
• Kidneys regulate balance
– 10-15% filtered is excreted
• Aldosterone: increase K+ & decrease Na+ excretion
• Mineralocorticoid & glucocorticoid  increase K+ &
decrease Na+ excretion in stool
35
Potassium (K+)
• Solvent drag
– Increase in Sosmo  water moves out of cells  K+ follows
– 0.6 SK / 10 of Sosmo
– Evidence of solvent drag in diabetic ketoacidosis
• Acidosis
– Low pH  shifts K+ out of cells (into serum)
– Hi pH  shifts K+ into cells
– 0.3-1.3 mEq/L K+ change / 0.1 unit change in pH in the opposite
direction
36
Potassium (K+)
• Hyperkalemia
– >6.5 – life threatening
– Potential lethal arrhythmias
37
Potassium (K+)
• Hyperkalemia Causes
– Spurious
» Difficult blood draw  hemolysis  false reading
– Increase intake
» Iatrogenic: IV or oral
» Blood transfusions
38
Potassium (K+)
• Hyperkalemia Causes
– Decrease excretion
» Renal failure
» Adrenal insufficiency or CAH
» Hypoaldosteronism
» Urinary tract obstruction
» Renal tubular disease
» ACE inhibitors
» Potassium sparing diuretics
39
Potassium (K+)
• Hyperkalemia Causes
– Trans-cellular shifts
» Acidemia
» Rhadomyolysis; Tumor lysis syndrome; Tissue necrosis
» Succinylcholine
» Malignant hyperthermia
40
Potassium (K+)
• Hyperkalemia Clinical presentation
– Neuromuscular effects
» Delayed repolarization, faster depolarization, slowing of
conduction velocity
» Paresthesias  weakness  flaccid paralysis
41
Potassium (K+)
• Hyperkalemia Clinical presentation
– EKG changes
» ~6: peak T waves
» ~7: increased PR interval
» ~8-9: absent P wave with widening QRS complex
» Ventricular fibrillation
» Asystole
42
Potassium (K+)
43
Potassium (K+)
• Hyperkalemia Treatment
– Lower K+ temporarily
» Calcium gluconate 100mg/kg IV
» Bicarb: 1-2 mEq/kg IV
» Insulin & glucose
• Insulin 0.05 u/kg IV + D10W 2ml/kg then
• Insulin 0.1 u/kg/hr + D10W 2-4 ml/kg/hr
» Salbutamol (β2 selective agonist) nebulizer
44
Potassium (K+)
• Hyperkalemia Treatment
– Increase elimination
» Hemodialysis or hemofiltration
» Kayexalate via feces
» Furosemide via urine
45
Potassium (K+)
• Hypokalemia
– <2.5: life threatening
– Common in severe gastroenteritis
46
Potassium (K+)
• Hypokalemia Causes
– Distribution from ECF
» Hypokalemic periodic paralysis
» Insulin, Β-agonists, catecholamines, xanthine
– Decrease intake
– Extra-renal losses
» Diarrhea
» Laxative abuse
» Perspiration
– Excessive colas consumption
47
Potassium (K+)
• Hypokalemia Causes
– Renal losses
» DKA
» Diuretics: thiazide, loop diuretics
» Drugs: amphotericin B, Cisplastin
» Hypomagnesemia
» Alkalosis
» Hyperaldosteronism
» Licorice ingestion
» Gitelman & Bartter syndrome
48
Potassium (K+)
• Hypokalemia Presentation
– Usually asymptomatic
– Skeletal muscle: weakness & cramps; respiratory failure
– Flaccid paralysis & hyporeflexia
– Smooth muscle: constipation, urinary retention
ECG changes
» Flattened or inverted T-wave
» U wave: prolonged repolarization of the Purkinje fibers
» Depressed ST segment and widen PR interval
» Ventricular fibrillation can happen
49
Potassium (K+)
Hypokalemia
- Flattened or inverted T-wave
- U wave: prolonged
repolarization of the Purkinje
fibers
- Depressed ST segment and
widen PR interval
- Ventricular fibrillation can
happen
50
Potassium (K+)
• Hypokalemia Treatment
– Address the causes & underlying condition
– Dietary supplements : leafy green vegetables, tomatoes, citrus fruits,
oranges or bananas
– Oral K replacement preferred
– IV: KCl 0.5-1 mEq/kg over 1 hr (rate of 10 mEq/hr)
– K Acetate or K Phos as alternative
– Add K sparing diuretics
– Correct hypomagnesemia
51
Basic Metabolic Panel
Na+ Cl- BUN Ca++
Glu Mg++
K+ HCO3
-- Cr Phos--
52
Bicarb (HCO3
--)
• Normal range: 25-35
• Important buffer system in acid-base homeostasis
• Increased in metabolic alkalosis or compensated respiratory
acidosis
• Decreased in metabolic acidosis or compensated respiratory
alkalosis
• 0.15 pH change/10 change in bicarb in uncompensated
conditions
53
Bicarb (HCO3
--)
• Metabolic acidosis
– Anion gap: Na – (Cl + bicarb)
– Normal range: 12 +/- 2
54
Bicarb (HCO3
--)
• Metabolic acidosis: causes for increase anion gap
– M
– U
– D
– P
– I
– L
– E
– S
55
Bicarb (HCO3
--)
• Metabolic acidosis: causes for increase anion gap
– Methanol
– Uremia
– DKA
– Paraldehyde or propylene glycol
– Isoniazid
– Lactic acidosis
– Ethylene glycol
– Salicylates
56
Bicarb (HCO3
--)
• Metabolic acidosis: causes for normal anion gap
– Diarrhea
– Pancreatic fistula
– Renal tubular acidosis or renal failure
– Intoxication: ammonium chloride, Acetazolamide, bile acid
sequestrants, isopropyl alcohol
– Glue sniffing
– Toluene:
57
Bicarb (HCO3
--)
• Metabolic acidosis Clinical presentation
– Chest pain, palpitation
– Kussmaul respirations
– Hyperkalemia
– Neuro: lethargy, stupor, coma, seizures
– Cardiac; arrhythmias, decreased response to Epinephrine, hypotension
58
Bicarb (HCO3
--)
• Metabolic acidosis Treatment
– pH<7.1, risk of arrhythmias
– IV bicarb
– Dialysis
59
Bicarb (HCO3
--)
• Metabolic alkalosis Causes
– Chloride responsive
» Compensated respiratory acidosis
» Diuretics  contraction alkalosis
» Vomiting
– Chloride resistant
» Retention of bicarb, shift hydrogen ion into IC space
» Alkalotic agents
» Hyperaldosteronism
60
Basic Metabolic Panel
Na+ Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
61
Glucose
• Hypoglycemia Causes
– Complication of DM therapies
– Hyperinsulinemia
– Inborn errors of metabolism
– Alcohol
– Starvations
– Infections, organ failure
62
Glucose
• Hypoglycemia Clinical presentation
– Adrenergic
» Shakiness, anxiety, nervousness, palpitations, tachycardia
» Sweating, pallor, coldness, clamminess
– Glucagon
» Hunger, borborygmus, nausea, vomiting, abd. Discomfort
» Headache
– Neuroglycopenic
» AMS, fatigue, weakness, lethargy, confusion, amnesia.
» Ataxia, incoordination, slurred speech
63
Glucose
• Hypoglycemia Treatments
» 0.5-1 g/kg of dextrose
» 5-10 ml/kg of D10W
» 2-4 ml/kg of D25W
» Max 1 amp (50 g)
64
Basic Metabolic Panel
Na+ Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
65
Calcium
• Normal range: 8.8-10.1 with half bound to albumin
• Ionized (free or active)calcium: 4.4-5.4 – relevant for cell
function
• Majority is stored in bone
• Hypoalbuminemia  falsely decreased calcium
– Cac = Cam + [0.8 x (Albn – Alb m)]
66
Calcium
• Roles:
– Coagulation
– Cellular signals
– Muscle contraction
– Neuromuscular transmission
• Controlled by parathyroid hormone and vitamin D
67
Calcium
• Hypercalcemia: Causes
– Excess parathyroid hormone, lithium use
– Excess vitamin D
– Malignancy
– Renal failure
– High bone turn over
» Prolonged immobilization
» Hyperthyroidism
» Thiazide use, vitamin A toxicity
» Paget’s disease
» Multiple myeloma
68
Calcium
• Hypercalcemia: Clinical presentation
– Groans: constipation
– Moans: psychic moans (fatigue, lethargy, depression)
– Bones: bone pain
– Stones: kidney stones
– Psychiatric overtones: depression & confusion
– Fatigue, anorexia, nausea, vomiting, pancreatitis
– ECG: short QT interval, widened T wave
69
Calcium
• Hypercalcemia Treatments
– Fluid & diuretics
» Forced diuresis
» Loop diuretic
– Oral supplement: biphosphate or calcitonine
– Glucocorticoids
– Dialysis
70
Calcium
• Hypocalcemia Causes
– Eating disorder
– Hungry bone syndrome
– Ingestion: mercury , excessive Mg
– Chelation therapy EDTA
– Absent of PTH
– Ineffective PTH: CRF, absent or ineffective vitamin D,
pseudohypoparathyroidism
– Deficient in PTH: acute hyperphos: TLS, ARF, Rhabdo
– Blood transfusions
71
Calcium
• Hypocalcemia: Clinical presentation
– Neuromuscular irritability
– Paresthesias: oral, perioral and acral, tingling or pin & needles
– Tetany (Chvostek & Trousseau signs)
– Hyperreflexia
– Laryngospasm
– Jittery, poor feedings or vomiting in newborns
– ECG changes: prolonged QT intervals
72
Calcium
• Hypocalcemia: Treatments
– Supplements
» IV: gluconate or chloride with EKG change
» Oral calcium with vitamin D
73
Basic Metabolic Panel
Na+ Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
74
Magnesium
• Normal range: 1.5-2.3
• 60% stored in bone
• 1% in extracellular space
• Necessary cofactor for many enzymes
• Renal excretion is primary regulation
75
Magnesium
• Hypermagnesemia: Causes
– Hemolysis
– Renal insuficiency
– DKA, adrenal insufficiency, hyperparathyroidism, lithium intoxication
76
Magnesium
• Hypermagnesemia: Clinical presentation
– Weakness, nausea, vomiting
– Hypotension, hypocalcemia
– Arrhythmia and asystole
» 4.0 mEq/L hyporeflexia
» >5 prolonged AV conduction
» >10 complete heart block
» >13 cardiac arrest
77
Magnesium
• Hypermagnesemia: Treatments
– Calcium infusion
– Diuretics
– Dialysis
78
Magnesium
• Hypomagnesemia Causes
– Alcoholism: malnutrition + diarrhea; Thiamine deficiency
– GI causes: Crohn’s, UC, Whipple’s disease, celiac sprue
– Renal loss: Bartter’s syndrome, postobstructive diuresis,
ATN, kidney transplant
– DKA
– Drugs
» Loop and thiazide diuretics
» Abx: aminoglycoside, ampho B, pentamidine, gent, tobra
» PPI
» Others: digitalis, adrenergic, cisplastin, ciclosporine
79
Magnesium
• Hypomagnesemia: Clinical presentation
– Weakness, muscle cramps
– Cardiac arrhythmias
» Prolonged PR, QRS & QT
» Torsade de pointes
» Complete heart block & cardiac arrest with level >15
– CNS: irritability, tremor, athetosis, jerking, nystagmus
– Hallucination, depression, epileptic fits, HTN, tachycardia,
tetany
80
Magnesium
• Hypomagnesemia: Treatments
– Oral or IV supplement
– Correct on going loss
81
Basic Metabolic Panel
Na+ Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
82
Phosphorus
• Normal range: 2.3 - 4.8
• Most store in bone or intracellular space
• <1% in plasma
• Intracellular major anion, most in ATP
• Concentration varies with age, higher during early childhood
• Necessary for cellular energy metabolism
83
Phosphorus
• Hyperphosphatemia
– Causes
» Hypoparathyroidism
» Chronic renal failure
» Osteomalacia
– Presentations
» Ectopic calcification
» Renal osteodystrophy
– Treatments
» Dietary restriction
» Phosphate binder
84
Phosphorus
• Hypophosphatemia Causes
– Re-feeding syndrome
– Respiratory alkalosis
– Alcohol abuse
– Malabsorption
85
Phosphorus
• Hypophosphatemia
– Clinical presentation
» Muscle dysfunction and weakness: diploplia, low CO, dysphagia,
respiratory depression
» AMS
» WBC dysfunction
» Instability of cell membrane  rhabdomyolysis
– Treatments
» supplementation
86

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Electrolyte-Disturbances ppt.ppt

  • 1. Electrolyte Disturbances Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta
  • 2. Objectives • Recognize common fluid and electrolyte disorders • Clinical presentations • Management 2
  • 3. Basic Metabolic Panel Na+ Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 3
  • 4. Basic Metabolic Panel Na+ Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 4
  • 5. Sodium (Na+) • Bulk cation of extracellular fluid  change in SNa reflects change in total body Na+ • Principle active solute for the maintenance of intravascular & interstitial volume • Absorption: throughout the GI system via active Na,K-ATPase system • Excretion: urine, sweat & feces • Kidneys are the principal regulator 5
  • 6. Sodium (Na+) • Kidneys are the principal regulator – 2/3 of filtered Na+ is reabsorbed by the proximal convoluted tubule, increase with contraction of extracellular fluid – Countercurrent system at the Loop of Henle is responsible for Na+ (descending) & water (ascending) balance – active transport with Cl- – Aldosterone stimulates further Na+ re-absorption at the distal convoluted tubules & the collecting ducts – <1% of filtered Na+ is normally excreted but can vary up to 10% if necessary 6
  • 7. Sodium (Na+) • Normal SNa: 135-145 • Major component of serum osmolality – Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18) – Normal: 285-295 • Alterations in SNa reflect an abnormal water regulation 7
  • 8. Sodium (Na+) • Hypernatremia: Causes – Excessive intake » Improperly mixed formula » Exogenous: bicarb, hypertonic saline, seawater – Water deficit: » Central & nephrogenic DI » Increased insensible loss » Inadequate intake 8
  • 9. Sodium (Na+) • Hypernatremia: Causes – Water and sodium deficit » GI losses » Cutaneous losses » Renal losses • Osmotic diuresis: mannitol, diabetes mellitus • Chronic kidney disease • Polyuric ATN • Post-obstructive diuresis 9
  • 10. Sodium (Na+) • Hypernatremia Clinical presentation – Dehydration – “Doughy” feel to skin – Irritability, lethargy, weakness – Intracranial hemorrhage – Thrombosis: renal vein, dura sinus 10
  • 11. Sodium (Na+) • Hypernatremia Treatment – Rate of correction for Na+ 1-2 mEq/L/hr – Calculate water deficit » Water deficit = 0.6 x wt (kg) x [(current Na+/140) – 1] – Rate of correction for calculated water deficit » 50% first 12-24 hrs » Remaining next 24 hrs 11
  • 12. Sodium (Na+) • Hyponatremia – Na+<135 – Seizure threshold ~125 – <120 life threatening 12
  • 13. Sodium (Na+) • Hyponatremia: Etiology – Hypervolemic » CHF Cirrhosis » Nephrotic syndrome Hypoalbuminemia » Septic capillary leak – Hypovolemic » Renal losses Cerebral salt wasting » Extra-renal losses aldosterone effect • GI losses • Third spacing 13
  • 14. Sodium (Na+) • Hyponatremia: Etiology • Euvolemic hyponatremia » SIADH » Glucocorticoid deficiency » Hypothyroidism » Water intoxication • Psychogenic polydipsia • Diluted formula • Beer potomania • Pseudo-hyponatremia – Hyperglycemia – SNa decreased by 1.6/100 glucose over 100 14 -
  • 15. Sodium (Na+) • Hyponatremia Clinical presentation – Cellular swelling due to water shifts into cells – Anorexia, nausea, emesis, malaise, lethargy, confusion, agitation, headache, seizures, coma – Chronic hyponatremia: better tolerated 15
  • 16. Sodium (Na+) • Hyponatremia Treatment – Rapid correction  central pontine myelinolysis – Goal 12 mEq/L/day – Fluid restriction with SIADH – Hyponatremic seizures » Poorly responsive to anti-convulsants » Hypertonic saline » Need to bring Na to above seizure threshold 16
  • 17. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 18. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 19. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 20. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 21. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 22. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 23. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 24. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 25. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 26. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 27. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 28. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 29. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 30. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 31. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 32. Sodium (Na+) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW
  • 33. Basic Metabolic Panel Na+ Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 33
  • 34. Potassium (K+) • Normal range: 3.5-4.5 • Largely contained intra-cellular  SK does not reflect total body K • Important roles: contractility of muscle cells, electrical responsiveness • Principal regulator: kidneys 34
  • 35. Potassium (K+) • Daily requirement 1-2 mEq/kg • Complete absorption in the upper GI tract • Kidneys regulate balance – 10-15% filtered is excreted • Aldosterone: increase K+ & decrease Na+ excretion • Mineralocorticoid & glucocorticoid  increase K+ & decrease Na+ excretion in stool 35
  • 36. Potassium (K+) • Solvent drag – Increase in Sosmo  water moves out of cells  K+ follows – 0.6 SK / 10 of Sosmo – Evidence of solvent drag in diabetic ketoacidosis • Acidosis – Low pH  shifts K+ out of cells (into serum) – Hi pH  shifts K+ into cells – 0.3-1.3 mEq/L K+ change / 0.1 unit change in pH in the opposite direction 36
  • 37. Potassium (K+) • Hyperkalemia – >6.5 – life threatening – Potential lethal arrhythmias 37
  • 38. Potassium (K+) • Hyperkalemia Causes – Spurious » Difficult blood draw  hemolysis  false reading – Increase intake » Iatrogenic: IV or oral » Blood transfusions 38
  • 39. Potassium (K+) • Hyperkalemia Causes – Decrease excretion » Renal failure » Adrenal insufficiency or CAH » Hypoaldosteronism » Urinary tract obstruction » Renal tubular disease » ACE inhibitors » Potassium sparing diuretics 39
  • 40. Potassium (K+) • Hyperkalemia Causes – Trans-cellular shifts » Acidemia » Rhadomyolysis; Tumor lysis syndrome; Tissue necrosis » Succinylcholine » Malignant hyperthermia 40
  • 41. Potassium (K+) • Hyperkalemia Clinical presentation – Neuromuscular effects » Delayed repolarization, faster depolarization, slowing of conduction velocity » Paresthesias  weakness  flaccid paralysis 41
  • 42. Potassium (K+) • Hyperkalemia Clinical presentation – EKG changes » ~6: peak T waves » ~7: increased PR interval » ~8-9: absent P wave with widening QRS complex » Ventricular fibrillation » Asystole 42
  • 44. Potassium (K+) • Hyperkalemia Treatment – Lower K+ temporarily » Calcium gluconate 100mg/kg IV » Bicarb: 1-2 mEq/kg IV » Insulin & glucose • Insulin 0.05 u/kg IV + D10W 2ml/kg then • Insulin 0.1 u/kg/hr + D10W 2-4 ml/kg/hr » Salbutamol (β2 selective agonist) nebulizer 44
  • 45. Potassium (K+) • Hyperkalemia Treatment – Increase elimination » Hemodialysis or hemofiltration » Kayexalate via feces » Furosemide via urine 45
  • 46. Potassium (K+) • Hypokalemia – <2.5: life threatening – Common in severe gastroenteritis 46
  • 47. Potassium (K+) • Hypokalemia Causes – Distribution from ECF » Hypokalemic periodic paralysis » Insulin, Β-agonists, catecholamines, xanthine – Decrease intake – Extra-renal losses » Diarrhea » Laxative abuse » Perspiration – Excessive colas consumption 47
  • 48. Potassium (K+) • Hypokalemia Causes – Renal losses » DKA » Diuretics: thiazide, loop diuretics » Drugs: amphotericin B, Cisplastin » Hypomagnesemia » Alkalosis » Hyperaldosteronism » Licorice ingestion » Gitelman & Bartter syndrome 48
  • 49. Potassium (K+) • Hypokalemia Presentation – Usually asymptomatic – Skeletal muscle: weakness & cramps; respiratory failure – Flaccid paralysis & hyporeflexia – Smooth muscle: constipation, urinary retention ECG changes » Flattened or inverted T-wave » U wave: prolonged repolarization of the Purkinje fibers » Depressed ST segment and widen PR interval » Ventricular fibrillation can happen 49
  • 50. Potassium (K+) Hypokalemia - Flattened or inverted T-wave - U wave: prolonged repolarization of the Purkinje fibers - Depressed ST segment and widen PR interval - Ventricular fibrillation can happen 50
  • 51. Potassium (K+) • Hypokalemia Treatment – Address the causes & underlying condition – Dietary supplements : leafy green vegetables, tomatoes, citrus fruits, oranges or bananas – Oral K replacement preferred – IV: KCl 0.5-1 mEq/kg over 1 hr (rate of 10 mEq/hr) – K Acetate or K Phos as alternative – Add K sparing diuretics – Correct hypomagnesemia 51
  • 52. Basic Metabolic Panel Na+ Cl- BUN Ca++ Glu Mg++ K+ HCO3 -- Cr Phos-- 52
  • 53. Bicarb (HCO3 --) • Normal range: 25-35 • Important buffer system in acid-base homeostasis • Increased in metabolic alkalosis or compensated respiratory acidosis • Decreased in metabolic acidosis or compensated respiratory alkalosis • 0.15 pH change/10 change in bicarb in uncompensated conditions 53
  • 54. Bicarb (HCO3 --) • Metabolic acidosis – Anion gap: Na – (Cl + bicarb) – Normal range: 12 +/- 2 54
  • 55. Bicarb (HCO3 --) • Metabolic acidosis: causes for increase anion gap – M – U – D – P – I – L – E – S 55
  • 56. Bicarb (HCO3 --) • Metabolic acidosis: causes for increase anion gap – Methanol – Uremia – DKA – Paraldehyde or propylene glycol – Isoniazid – Lactic acidosis – Ethylene glycol – Salicylates 56
  • 57. Bicarb (HCO3 --) • Metabolic acidosis: causes for normal anion gap – Diarrhea – Pancreatic fistula – Renal tubular acidosis or renal failure – Intoxication: ammonium chloride, Acetazolamide, bile acid sequestrants, isopropyl alcohol – Glue sniffing – Toluene: 57
  • 58. Bicarb (HCO3 --) • Metabolic acidosis Clinical presentation – Chest pain, palpitation – Kussmaul respirations – Hyperkalemia – Neuro: lethargy, stupor, coma, seizures – Cardiac; arrhythmias, decreased response to Epinephrine, hypotension 58
  • 59. Bicarb (HCO3 --) • Metabolic acidosis Treatment – pH<7.1, risk of arrhythmias – IV bicarb – Dialysis 59
  • 60. Bicarb (HCO3 --) • Metabolic alkalosis Causes – Chloride responsive » Compensated respiratory acidosis » Diuretics  contraction alkalosis » Vomiting – Chloride resistant » Retention of bicarb, shift hydrogen ion into IC space » Alkalotic agents » Hyperaldosteronism 60
  • 61. Basic Metabolic Panel Na+ Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 61
  • 62. Glucose • Hypoglycemia Causes – Complication of DM therapies – Hyperinsulinemia – Inborn errors of metabolism – Alcohol – Starvations – Infections, organ failure 62
  • 63. Glucose • Hypoglycemia Clinical presentation – Adrenergic » Shakiness, anxiety, nervousness, palpitations, tachycardia » Sweating, pallor, coldness, clamminess – Glucagon » Hunger, borborygmus, nausea, vomiting, abd. Discomfort » Headache – Neuroglycopenic » AMS, fatigue, weakness, lethargy, confusion, amnesia. » Ataxia, incoordination, slurred speech 63
  • 64. Glucose • Hypoglycemia Treatments » 0.5-1 g/kg of dextrose » 5-10 ml/kg of D10W » 2-4 ml/kg of D25W » Max 1 amp (50 g) 64
  • 65. Basic Metabolic Panel Na+ Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 65
  • 66. Calcium • Normal range: 8.8-10.1 with half bound to albumin • Ionized (free or active)calcium: 4.4-5.4 – relevant for cell function • Majority is stored in bone • Hypoalbuminemia  falsely decreased calcium – Cac = Cam + [0.8 x (Albn – Alb m)] 66
  • 67. Calcium • Roles: – Coagulation – Cellular signals – Muscle contraction – Neuromuscular transmission • Controlled by parathyroid hormone and vitamin D 67
  • 68. Calcium • Hypercalcemia: Causes – Excess parathyroid hormone, lithium use – Excess vitamin D – Malignancy – Renal failure – High bone turn over » Prolonged immobilization » Hyperthyroidism » Thiazide use, vitamin A toxicity » Paget’s disease » Multiple myeloma 68
  • 69. Calcium • Hypercalcemia: Clinical presentation – Groans: constipation – Moans: psychic moans (fatigue, lethargy, depression) – Bones: bone pain – Stones: kidney stones – Psychiatric overtones: depression & confusion – Fatigue, anorexia, nausea, vomiting, pancreatitis – ECG: short QT interval, widened T wave 69
  • 70. Calcium • Hypercalcemia Treatments – Fluid & diuretics » Forced diuresis » Loop diuretic – Oral supplement: biphosphate or calcitonine – Glucocorticoids – Dialysis 70
  • 71. Calcium • Hypocalcemia Causes – Eating disorder – Hungry bone syndrome – Ingestion: mercury , excessive Mg – Chelation therapy EDTA – Absent of PTH – Ineffective PTH: CRF, absent or ineffective vitamin D, pseudohypoparathyroidism – Deficient in PTH: acute hyperphos: TLS, ARF, Rhabdo – Blood transfusions 71
  • 72. Calcium • Hypocalcemia: Clinical presentation – Neuromuscular irritability – Paresthesias: oral, perioral and acral, tingling or pin & needles – Tetany (Chvostek & Trousseau signs) – Hyperreflexia – Laryngospasm – Jittery, poor feedings or vomiting in newborns – ECG changes: prolonged QT intervals 72
  • 73. Calcium • Hypocalcemia: Treatments – Supplements » IV: gluconate or chloride with EKG change » Oral calcium with vitamin D 73
  • 74. Basic Metabolic Panel Na+ Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 74
  • 75. Magnesium • Normal range: 1.5-2.3 • 60% stored in bone • 1% in extracellular space • Necessary cofactor for many enzymes • Renal excretion is primary regulation 75
  • 76. Magnesium • Hypermagnesemia: Causes – Hemolysis – Renal insuficiency – DKA, adrenal insufficiency, hyperparathyroidism, lithium intoxication 76
  • 77. Magnesium • Hypermagnesemia: Clinical presentation – Weakness, nausea, vomiting – Hypotension, hypocalcemia – Arrhythmia and asystole » 4.0 mEq/L hyporeflexia » >5 prolonged AV conduction » >10 complete heart block » >13 cardiac arrest 77
  • 78. Magnesium • Hypermagnesemia: Treatments – Calcium infusion – Diuretics – Dialysis 78
  • 79. Magnesium • Hypomagnesemia Causes – Alcoholism: malnutrition + diarrhea; Thiamine deficiency – GI causes: Crohn’s, UC, Whipple’s disease, celiac sprue – Renal loss: Bartter’s syndrome, postobstructive diuresis, ATN, kidney transplant – DKA – Drugs » Loop and thiazide diuretics » Abx: aminoglycoside, ampho B, pentamidine, gent, tobra » PPI » Others: digitalis, adrenergic, cisplastin, ciclosporine 79
  • 80. Magnesium • Hypomagnesemia: Clinical presentation – Weakness, muscle cramps – Cardiac arrhythmias » Prolonged PR, QRS & QT » Torsade de pointes » Complete heart block & cardiac arrest with level >15 – CNS: irritability, tremor, athetosis, jerking, nystagmus – Hallucination, depression, epileptic fits, HTN, tachycardia, tetany 80
  • 81. Magnesium • Hypomagnesemia: Treatments – Oral or IV supplement – Correct on going loss 81
  • 82. Basic Metabolic Panel Na+ Cl- BUN Ca++ Glu Mg++ K+ CO3 -- Cr Phos-- 82
  • 83. Phosphorus • Normal range: 2.3 - 4.8 • Most store in bone or intracellular space • <1% in plasma • Intracellular major anion, most in ATP • Concentration varies with age, higher during early childhood • Necessary for cellular energy metabolism 83
  • 84. Phosphorus • Hyperphosphatemia – Causes » Hypoparathyroidism » Chronic renal failure » Osteomalacia – Presentations » Ectopic calcification » Renal osteodystrophy – Treatments » Dietary restriction » Phosphate binder 84
  • 85. Phosphorus • Hypophosphatemia Causes – Re-feeding syndrome – Respiratory alkalosis – Alcohol abuse – Malabsorption 85
  • 86. Phosphorus • Hypophosphatemia – Clinical presentation » Muscle dysfunction and weakness: diploplia, low CO, dysphagia, respiratory depression » AMS » WBC dysfunction » Instability of cell membrane  rhabdomyolysis – Treatments » supplementation 86