2. Contents
• Water and sodium metabolism
– Hypo- and hyper- osmolarity
– Hypo- and hyper- natremia
• Potassium
– Hypo- and hyper- kalemia
• Acid-base disorder
3. Contents
• Water and sodium metabolism
– Hypo- and hyper- osmolarity
– Hypo- and hyper- natremia
• Potassium
– Hypo- and hyper- kalemia
• Acid-base disorder
4. • Osmotic pressure
– A function of the concentration of all the
solutes in a fluid compartment
Osmotic pressure = total solute
total water
Osmolarity = total solute ; mOsm/Kg H2O
weight of water
Osmolality = total solute ; mOsm / L H2O
volume of water
14. • Hypovolemic
hyponatremia with
UNa >20 (renal loss)
– Diuretic use
– Mineralocorticoid
deficiency
– Salt-losing
nephropathy
– Bicarbonaturia
– Ketonuria
• Hypovolemic
hyponatremia with
UNa <20 (extrarenal
loss)
– Vomiting
– Diarrhea
– Third space loss
• Burn, pancreatitis
15.
16. Causes of SIADH
CARCINOMAS PULMONARY
DISORDERS
CNS DISORDERS OTHERS
Bronchogenic CA Viral pneumonia Encephalitis AIDS
Small cell lung CA Bacterial pneumonia Meningitis Prolonged exercise
CA duodenum Tuberculosis Head trauma idiopathic
CA pancreas Aspergillosis Brain abscess
CA stomach Lung abscess Delerium tremens
Thymoma Asthma Acute psychosis
Lymphoma Pneumothorax Multiple sclerosis
Ewing sarcoma Mesothelioma CVA
CA bladder Cystic fibrosis Guillain-Barre syndrome
Prostate CA
Oropharyngeal tumor
Positive pressure
breathing
17. Symptoms of hyponatremia
• Depend on
– Age
– Gender
– Magnitude and acuteness
• Gastrointestinal symptoms : nausea, vomiting
• Neurological symptoms: headache, lethargy,
muscle weakness, ataxia, psychosis, seizure,
coma, brain herniation
18. Treatment of Hyponatremia
1. Level, duration of hyponatremia
2. Symptoms
3. Volume status
4. Risk of neurological damage
19. Hyponatremic patients at risk for
neurological complications
• Postoperative menstruating female
• Elderly women on thiazide
• Children
• Hypoxemic patients
• Psychiatric polydipsic patients
• Alcholics
• Malnourished patients
• Hypokalemic patients
20. Treatment solution
Depend on volume status
(causes of hyponatremia)
Hypovolemia - isotonic saline
Euvolemia (EM) - hypertonic
Hypervolemia - diuretic ± hypertonic
21. Treatment of hyponatremia
• Acute symptomatic hyponatremia
– Raise SNa 1-2 meq/L
– Not more than 12 meq/L in 24 hours
• Chronic symptomatic hyponatremia
– Raise SNa 0.5-1 meq/L
– Not more than 10 meq/L in 24 hours
• Asymptomatic hyponatremia
– Water restriction
– Drug-induced water diuresis : democlocyclin, lithium, V2 antagonist
– Increase solute intake : urea
22. • A 70-Kg man present diagnosed
bronchogenic carcinoma. He presents with
GTC. BP 130/80 mmHg. JVP 3 cm, lung-
clear. His serum Na is 103 meq/L, Cr 0.7
mg/dl, BS 100 mg/dl
• U/A : sp gr 1.020
Euvolemic hyponatremia
Thyroid function test and cortisol level is normal
SIADH
23. Desired Na = 110 mmol/l
= TBW x (dNa – sNa)
= 0.6 (70) (110 - 103)
= 294 mmol
Na 294 mmol = 3% NaCl 573 ml
Correct Na 1 mmol/l/hr
= 3% NaCl 573/7 = 80 ml/hr iv.drip
24. Approach guideline for hypernatremia
Assess volume status
Hypovolemia
TBW TBNa
Euvolemia
TBW TBNa
Hypervolemia
TBW TBNa
UNa >20 <20 variable >20
Renal loss
Osmotic or loop
diuretics
Postobstructive
diuresis
Intrinsic renal disease
Extrarenal loss
Excessive sweating
Burn
Diarrhea
fistula
Renal loss
DI
hypodipsia
Extrarenal loss
Insensible loss
Sodium gain
Primary hyperaldosteronism
Cushing’s syndrome
Hypertonic dialysis
Hypertonic sodium
bicarbonate
25. Patients at risk of severe hypernatremia
• Elderly patients or infants
• Patients receiving
– Hypertonic infusion
– Osmotic diuresis
– Lactulose
– Mechanical ventilator
• Third space water loss : rhabdomyolysis
• Altered mental status
• Uncontrolled diabetes mellitus
• Unerlying polyuric disorder
26. Hypotonic polyuria
Disorders Urine osmolality SNa
Insufficient AVP
Central diabetes insipidus
+ osmoreceptor dysfunction
Diabetes insipidus in pregnancy
Impaired renal response to AVP
Nephrogenic diabetes insipidus
Primary polydipsia
Dipsogenic polydipsia
psychogenic polydipsia
27. Water deprivation test
• Patients with hypotonic polyuria
– Urine > 50 ml/kg/day
– UOsm < 300 mOsm/kg
– Total osmole <15 mOsm/kg/day, no
glucosuria or other osmoles
28. Protocol for water deprivation test
• Initiation of the deprivation period
• Baseline data
– Body weight, BP
– Serum osmolality, electrolyte
– Urine osmolality
– Serum AVP
• Follow up BW, BP, urine osmolality hourly
• Stop deprivation if BW decrease > 3%, orthostatic hypotension
or urine osmolality changes < 10% in 2-3 consecutive
measrement
• Serum electrolyte, serum osmolality and serum AVP at the
end point
• If SOsm >295, DDAVP 1 ug or AVP 5 ug sc then measure
urine output, urine osmolality 1-2 hours after injection
29. Treatment of hypernatremia
• Reduction of ongoing loss
• Correction of preexisting water deficit
– Rate of correction depends on
• Acuteness
• Severity
• Risk of neurological deficit
30. • If serum osmolality > 330 (SNa > 165),
decrease Sosm to 320-330 mOsm/L in 24
hours then 0.5 meq/L/hour
Water deficit = 0.6 x BW x (SNa – 140)
SNa
31. Treatment of hypernatremia
• Specific treatment
– Central DI
• DDAVP, vasopressin
• Chlorpropamide
– Nephrogenic DI
• Correct cause
• Low salt diet
• Thiazide or amiloride
• NSAIDs
– Pregnancy-induced DI – DDAVP
– Osmoreceptor dysfunction – schedule
– Psychogenic polydipsia – psychotherapy, clozapine
32. Contents
• Water and sodium metabolism
– Hypo- and hyper- osmolarity
– Hypo- and hyper- natremia
• Potassium
– Hypo- and hyper- kalemia
• Acid-base disorder
33. Internal and external K balanceInternal and external K balance
IntakeIntake
(RBC, Muscle, Liver, Bone)(RBC, Muscle, Liver, Bone)
ICFICF
ExcretionExcretion
KidneyKidney 90%90%
ColonColon 10%10%
KK 60-10060-100
mEq/daymEq/day
DistributionDistribution
235235 30003000 200200 300 mEq300 mEq
Sweat <Sweat <10%10%
ECF
50-70 meq
34. Factors - transcellular distribution of KFactors - transcellular distribution of K
NaNa++
KK++
KK++
InsulinInsulin
bb22 -adrenergic-adrenergic
agonistagonist
AldosteroneAldosterone
cAMPcAMP
Na-KNa-K ATPaseATPase
1.1.
HormoneHormone
2. Acid-base status2. Acid-base status
3. Plasma tonicity3. Plasma tonicity
4. Congenital diseases4. Congenital diseases
ThyroidThyroid
40. Rx of hypokalemia
Rx causes
Potassium deficit,
100-200 mEq if S. [K] = 3-3.5 mEq/L
200-400 mEq if S. [K] < 3 mEq/L
> 600 mEq if S. [K] < 2 mEq/L
Caution in periodic paralysis
41. Form:
Oral * Elix. KCl (20 mEq/15 ml)
with metabolic alkalosis
* M Pot Cit oral (10 mEq/15 ml)
with metabolic acidosis
IV * [K] < 60 mEq/L in glucose-free sol.
with the rate of < 10 mEq/h
unless ECG is monitored
43. Treatment of hyperkalemia
Agents Dosage Action Mechanism
10% calcium
gluconate
10 ml IV in 1 min,
repeat q 5 min
immedialtely Stabilze myocardium
insulin 5 units + 50%
glucose 50 ml
15 min Intracellular K+ shift If BS >300 mg/dl,
insulin alone
Aware hypoglycemia
Sodium
bicarbonate
50-100 ml Renal K+ excretion
Intracellular shift
Severe metabolic
acidosis (<10 meq/L)
B2 agonist 20 mg albuterol NB
in 10 min
30 min Intracellular shift
diuretic Furosemide IV 30-60 min Remove K+ For patients with
adequate renal
function
Exchange resin Kayexalate 50 gm
or kallimate
2 hours Remove K+
dialysis Remove K+
44. Contents
• Water and sodium metabolism
– Hypo- and hyper- osmolarity
– Hypo- and hyper- natremia
• Potassium
– Hypo- and hyper- kalemia
• Acid-base disorder
45. METABOLIC ACIDOSIS
• Anion gap = [Na+
] – { [HCO3-
]+[Cl-
] }
– Normal 9 -12 mEq/L
– Each decline in serum albumin by 1 g/dL from
the normal value of 4.5 g/dL, decreases the
AG by 2.5 mEq/L
46. CAUSES OF METABOLIC ACIDOSIS
• High anion gap
– Ketoacidosis
• Diabetic
• Alcoholic
• Starvation
– Lactic acidosis
• L-lactic acidosis (type A
and B)
• D-lactic acidosis
– Drugs and toxin
• Ethanol, Ethylene glycol,
Methanol
• Salicylate
– Uremia
• Normal anion gap
– GI loss of HCO3
• Diarrhea
• Fistula
– Renal loss of HCO3 or
failure to excrete NH4+
• Renal tubular acidosis
• Acetazolamide
– Miscellaneous
• NH4Cl ingestion
• Sulfur ingestion
47. Metabolic acidosis
Anion gap ; Na – (Cl + HCO3)
high normal
Osmolol gap
Measured osmolality – calculated osmolality
high normal
Ethanol
Ethylene glycol
Methanol
Isopropyl alcohol
Ketoacidosis
Lactic acidosis
uremic
Serum potassium
Hypo or
normokalemia
hyperkalemia
Urine anion gap
(Na + K) – Cl
negative positive
GI loss
Drugs
Proximal RTA
Aldosterone resistance
Aldosterone deficiency
dRTA type IV
>5.5
Urine pH
<5.5
48. ACCUMULATION OF LACTATE
Increase lactate production
ischemia
seizure
extreme exercise
leukemia
alkalosis
Decrease lactate utilization
poor blood flow
defective active transport
of lactate into cell
inadequate metabolic
conversion of lactate to
pyruvate
Liver 70%, kidneys 30%
Muscle, gut, brain, skin, RBC
49. LACTIC ACIDOSIS
• TYPE A
– Poor tissue perfusion
– Shock
– Hypoxemia
– Carbon monoxide
poisoning
• TYPE B
– Liver disease
– Leukemia, lymphoma,
large tumor
– Anemia
– Diabetes mellitus
– Drugs : metformin, NRTIs,
sorbital, isoniazid,
salicylate etc
– Inborn error metabolism
– Intravenous fructose
50. Symptoms
• Respiratory symptoms
– Kussmaul respiration
– Oxyhemoglobin dissociation curve
• Left shift in chronic acidosis
• Right shift in acute acidosis
• Cardiovascular systems
– Negative inotropic effect
– Peripheral arterial vasodilatation
– Central venoconstriction
• Neurological systems
– Headache, lethargy, stupor and coma
51. Treatment of metabolic acidosis
• Get rid of cause
– DKA : IV fluid + insulin
– Alcoholic ketoacidosis, starvation : IV fluid (5%D)
– Shock : IV fluid
– Toxin : increase excretion ( kidney, dialysis), antidote
• Bicarbonate replacement
– Causes are not corrected in short period
– Ongoing loss of HCO3
– Severe metabolic acidosis
