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HYPOKALEMIA
Serum K level < 3.5 mmol/L (normal: 3.5 5.0 mmol/L)
True hypokalemia : decreased of serum K level
False (spurious) hypokalemia :
false in laboratory result
in extreme leucocytosis (in vitro), wbc uptake kalium
in the test tube
Transcelular shift
insulin therapy
beta2 agonists
alkalosis
Kalium depletion
Metabolic acidosis
RTA
Diabetic ketoacidosis
Viarable PH
post obstructive
ATN recovery
aminoglycoside
CLINICAL MANIFESTATIONS
Cardiac
ventricular irritability
abnormal ECG
predisposition of digitalis intoxication
coronary artery spasm
Neuromuscular
muscle spasm, tetany, paralysis
gastrointestinal (constipation, ileus)
Renal
polyuria
increased amoniogenesis
Endocrene
carbohydrate intolerance
MANAGEMENT
Emergency or not emergenny ?
clinical manifestation
ECG
degree of hypo K
Estimated degree of decreases in total body kalium
decreased in average of 0,3 mmol/L for each 100 mmol of
kalium depletion
Serum K level
Deficit
Mild
Moderate
< 2 meq/L
Severe
MANAGEMENT
Treat the underlying causes
In mild hypo K : oral K preparation 600 -1200 meq/day
- small risk of hyper K
HYPERKALEMIA
Definition :
Plasma potassium consentration > 5. meq/L
(N. 3.5 -.5 meq/L)
----- excess concentration K ion in extracellular fluid
Causes of Hyper K
1. Extrarenal
2. Renal
B. Compartment shift
a. inhibition of Na/K ATPase
insulin resistance/deficiency
B2 adrenergic deficiency/resistance
Familial hyperkalemic periodic paralysis
b. Altered transcellular electrochemical
K gradient
inorganic metabolic acidosis
ECF hypertonicity/hyperosmolar state :
(hyperglycemia, mannitol
Clinical feature
often asymptomatic
neuromuscular disturbance (K>6.5 meq/L)
distal parasthesia
generalized muscle weakness
ascending flaccid paralysis
ventilatory failure
sudden cardiac death (K>7-7.5 meq/L)
ECG changes
K+, 5-6 meq/L
50% no ECG changes
peaked T, shortened QT
K+, 6-7 meq/L
Prolonged QR, AV dissociation
flattening and loss P
widening QRS complex
K+ > 7 8 meq/L - VT
Pseudo Hyper K
hemolysis
thrombocytosis
leukocytosis
familial psudohyper K
MANAGEMENT
Hyper K >6.5 meq/L : medical emergency
- therapy should begin immediately
1. Stabilization of cardiac membrane
- 10 ml Ca gluconas 10% over 2-3 min into large vein
- evident within minutes and lasts for 30 to 60 min
- represents a temporizing measure only
- plasma K concentration is unaltered
Management
2. Transcellular redistribution
a. insulin and dextrose
--- activated insulin receptor stimulates N+/K+-ATPase
driving cellular uptake of K
- 1 iu insulin setiap 5 gr glukosa
- each 10 iu insulin can expected to lower K by 0.5-1.5
meq/l within 15 min, lasting 2-4 hrs
b. sodium bicarbonate
- increasing the pH of ECF (100 mmol over 1-2 hrs)
- when hyper K associated by severe inorganic acidosis
c. Salbutamol
- meter dose inhaler, nebulized, intravenous
Management
3. Removal of excess
- loop diuretic
- cation exchange resin (kayexilate)
- hemodialysis or CRRT
- laxantia (MgS04)
HYPONATREMIA
Plasma sondium (Na+) concentration :
the ratio between sodium and water in the plasma
Normal
Hyponatremia
Hiponatremia
Low osmotic
(true hyponatremia)
Translocational
Pseudohyponatremia
protein
hyperglycemia
lipid
irrigation fluids
(mannitol, sorbitol)
surgical
(transurethral prostatectomy)
Urinary osmolality
<100 mosm/kg
Urinary osmolality *)
> 100 mosm/kg
Euvolaemia
Hypervolaemia
Syndrome of
inappropriate
antidiuretic
Psychogenic
Hypothyroid
Drugs
Heart failure
Liver failure
Nephrotic syndrome
Urinary sodium
concentration
Urinary
osmolality
Treatment
Normal saline
Water restriction
Essential
Clinical euvolemia
Supplemental
CLINICAL MANIFESTATION:
Symtoms of hyponatremia due to the
consequences of plasma hypoosmolality
Hypoosmolality
intracellular
edema
Particularly in CNS
Symptoms:
- Lethargy
- confusion
- nausea-vometing
- muscle cramps
- seizures- coma
Note:
Permanent neurologic damage may be occur in premenopausal women
- the cause is not well understood
- so: hyponatremic women must be watched carefully
children
hypoxemic patients
MANAGEMENT
Important questions must be answered :
1. Is the patients symptomatic ?
2. is the hyponatremia
- acute (before 48 hrs) ?
- chronic (after 48 hrs) ?
MANAGEMENT
Acute
Symptomatic
Chronic
SEVERE
HYPONATREMIA
(Na+ <120 mmol/L)
Asymptomatic
Chronic
Mechanism
Fluid restriction
Demeclocycline
V2 receptor antagonist
Antagonises vasopressin
Urea
Osmotic diuresis
THE LANCET, Vol 352, July 18, 1998)
HYPERNATREMIA
Definition
Serum Na consentration > 145 meq/L
Classification
1. Decreased total body sodium
Extracelular water and sodium loss with
excess water loss
Extra renal loss
Renal loss
Vomiting
Diarrhea
Excessive sweating
Dialysis
Renal loss
Unconscious state
Mechanical obstruction
Inappropriate intravenous
therapy
No access to water
Hypertonic saline
Mineralocorticoid excess
Clinical presentation
not seen until serum Na >155 meq/L
fever, restlessness, lethargy, confusion
Treatment
Note
A rapid decreased of serum Na could be detrimental
--- decrease of serum Na by 2 meq/L/hr