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Hasanul Arifin

Objectives
• Recognize common fluid and electrolyte
disorders
• Clinical presentations
• Management
Basic Metabolic Panel

Na + Cl- BUN Ca++


Glu Mg++
K+ CO3-- Cr Phos--
• 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
• 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
• 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
– Na+<135
– Seizure threshold ≤ 125 mEq/L
– < 120  life threatening
– Hypervolemic
• CHF Cirrhosis
• Nephrotic syndrome Hypoalbuminemia
• Septic capillary leak
– Hypovolemic
• Renal losses Cerebral salt wasting
• Extra-renal losses aldosterone effect
– GI losses
– Third spacing
• Euvolemic hyponatremia
• SIADH • Pseudo-hyponatremia
• Glucocorticoid deficiency – Hyperglycemia
• Hypothyroidism – SNa decreased by 1.6/100
• Water intoxication glucose over 100
– Psychogenic polydipsia
– Diluted formula
Clinical Manifestation
CNS dysfuntion
( large or rapidly)

headache, nausea, vomiting, muscle cramps,


lethargy, restlessness, disorientation.

severe and rapidly  seizure, coma, brain damage,


respiratory arrest, brain stem herniation, death
management

• The optimal treatment of


hypotonic hyponatremia requires
balancing the risks of
hypotonicity against those of
therapy
There is no consensus about the optimal
treatment of symptomatic hyponatremia
Management (cont’)
• Reverse the manifestation of hypotonicity, but not be so rapid
and large as to pose a risk of the development of osmotic
demyelination (CPM)

Recommend :
•The initial rate of correction can still be 1 to 2 mmol/L/hr for several
hours in patients with severe symptoms
•A targeted rate of correction that does not exceed 10-12 mmol/L/day.
Formula
Change in serum Na+
Infusate Na+ - serum Na+
=
Total body water +1

Clinical use :
Estimate the effect 1 liter of any infusate on serum Na+
case : 3-year-old boy, hyponatremia
(serum Na+ 113 mmol/L), BW :10 kg,

• 1L of NaCl 3%  513 mEq Na+


• Retention 1L of NaCl 3%  formula
 (513-113) : (0.6x10 + 1) = 57 mmol/L
 to raise the serum Na+ concentration by 3 mEq/L
over the next three hours =( 3:57 )x1000ml = 53 ml
  = 17-18 ml NaCl 3%/hr
•  17-18 gtt (micro)/min.
After 3 hours

• Serum Na+  116 mEq/L

• 126 mEq/L
• (513-116) : (6+1) = 55 mEq/L
• (10 :55) x 1000 mL = 180 ml/24 hours
•  = 7.5ml/hours = 7 – 8 drips (micro)/min.
– Rapid correction  central pontine myelinolysis
– Goal 10 - 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
definition

Na+ > 145 mmol/L


 Excessive intake
• Improperly mixed
 Water and sodium
formula deficit
• Exogenous: bicarb, • GI losses
hypertonic saline, • Cutaneous losses
seawater • Renal losses
 Water deficit: – Osmotic diuresis:
mannitol, diabetes
• Central & nephrogenic
mellitus
DI
– Chronic kidney disease
• Increased insensible loss – Polyuric ATN
• Inadequate intake – Post-obstructive
diuresis
Clinical Manifestation
CNS dysfuntion
( large or rapidly)
hyperpnea, muscle weakness,
restlessness, insomnia, lethargy, coma

Brain shrinkage induced by hypernatremia 


vascular rupture, cerebral bleeding, SAH, neurologic
damage, & death

CPM
Volume 343:817-818 September 14, 2000 Number 11
management
• Underlying cause
• Correcting hypertonicity, without
cerebral edema and convulsion

reducing rate : 0.5 mmol/L/hr , or 10


mmol/L/d
Target  serum Na+ : 145 mmol/L
Formula
Change in serum Na+
Infusate Na+ - serum Na+
=
Total body water +1

Clinical use :
Estimate the effect 1 liter of any infusate on serum Na+
case,
Pure Water Loss

• A4-year-old children,,BW 15 kg,


presents with dry mucous membranes,
decreased skin turgor, fever, tachypnea ,
Na+ serum : 168 mEq/L.
• Dx ; Hypernatremia caused by pure
water depletion due to insessible losses.
• Th/ Infusion of D5W
• Estimated TBW = 9L (0.6x15)
• The formula  (0-168) : (9+1) = -16.8mEq/L
• The goal of treatment  -10 mEq/L/d
(10:16.8) x 1000 mL = 595 mL (600 mL) ,
with added (IWL)
• IWL = 30-45 mL/kg/d = 450-675 ml (500
mL)
• Therefore the total require D5W solution is
600+500 = 1100 m L/d
 = 1100 : 24 = 45 mL/hr
 = 45 drips/min. D5W
• Estimated TBW = 9L (0.6x15)
• The formula  (0-168) : (9+1) = -16.8mEq/L
• The goal of treatment  -10 mEq/L/d
(10:16.8) x 1000 mL = 595 mL (600 mL) ,
with added (IWL)
• IWL = 30-45 mL/kg/d = 450-675 ml (500
mL)
• Therefore the total require D5W solution is
600+500 = 1100 m L/d
 = 1100 : 24 = 45 mL/hr
 = 45 drips/min. D5W
Basic Metabolic Panel

Na + Cl- BUN Ca++


Glu Mg++
K+ CO3-- Cr Phos--
• 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
• 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
• 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
– >6.5 – life threatening
– Potential lethal arrhythmias

• Causes
• Spurious
– Difficult blood draw  hemolysis  false reading

• Increase intake
– Iatrogenic : IV or oral
– Blood transfusions
• Decrease
excretion  Trans-cellular shifts
– Renal failure • Acidemia
– Adrenal insufficiency • Rhadomyolysis; Tumor
or CAH lysis syndrome; Tissue
– Hypoaldosteronism necrosis
– Urinary tract • Succinylcholine
obstruction • Malignant hyperthermia
– Renal tubular disease
– ACE inhibitors
– Potassium sparing
diuretics
– Neuromuscular effects
• Delayed repolarization, faster depolarization, slowing of
conduction velocity
• Paresthesias  weakness  flaccid paralysis

– EKG changes
• ~6: peak T waves
• ~7: increased PR interval
• ~8-9: absent P wave with widening QRS complex
• Ventricular fibrillation
• Asystole
• 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

• Increase elimination
– Hemodialysis or hemofiltration
– Kayexalate via feces
– Furosemide via urine
< 2.5 mEq/L  life threatening
Common in severe gastroenteritis
Causes :
– Distribution from ECF – Renal losses
• Hypokalemic periodic • DKA
paralysis • Diuretics: thiazide, loop
• Insulin, Β-agonists, diuretics
catecholamines, xanthine • Drugs: amphotericin B,
– Decrease intake Cisplastin
– Extra-renal losses • Hypomagnesemia
• Alkalosis
• Diarrhea
• Hyperaldosteronism
• Laxative abuse
• Licorice ingestion
• Perspiration
• Gitelman & Bartter
– Excessive colas syndrome
consumption
– 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
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
– 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
Basic Metabolic Panel

Na + Cl- BUN Ca++


Glu Mg++
K+ HCO3-- Cr Phos--
• 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
–Anion gap : Na – (Cl + Bicarb)
–Normal range: 12 +/- 2
causes for increase anion gap
– Methanol
– Uremia
– DKA
– Paraldehyde or propylene glycol
– Isoniazid
– Lactic acidosis
– Ethylene glycol
– Salicylates
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:
– Chest pain, palpitation
– Kussmaul respirations
– Hyperkalemia
– Neuro: lethargy, stupor, coma, seizures
– Cardiac; arrhythmias, decreased response to
Epinephrine, hypotension
– pH<7.1,  risk of arrhythmias
– IV bicarb
– Dialysis
– Treat the causes
– Chloride responsive
• Compensated respiratory acidosis
• Diuretics  contraction alkalosis
• Vomiting
– Chloride resistant
• Retention of bicarb, shift hydrogen ion into IC space
• Alkalotic agents
• Hyperaldosteronism
Basic Metabolic Panel

Na + Cl- BUN Ca++


Glu Mg++
K+ CO3-- Cr Phos--
– Complication of DM therapies
– Hyperinsulinemia
– Inborn errors of metabolism
– Starvations
– Infections, organ failure
• 0.5-1 g/kg of dextrose
• 5-10 ml/kg of D10W
• 2-4 ml/kg of D25W
• Max 1 amp (50 g)

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