Symptoms of hyponatremia The changes induced by acute
hyponatremia (developing over 1-3 days) may result in permanent
neurological damage and are primarily duo to cerebral overhydration
Nausea and malaise as the plasma Na+ falls acutely below 125 meq/l
Headache, lethargy, and obtundation may appear in Na+ between
115-120
Slide 7
Symptoms of hyponatremia.. The more sever changes of seizures
and coma are not seen until the plasma Na+ is less than 110-115
meq/l Women particularly premenopausal women,appear to be at much
greater risk of developing sever neurologic symptoms and of
irreversible neurologic damage than men that may be related to
differences in cerebral metabolism and sex hormones.
Slide 8
Slide 9
Treatment There are two basic principles involved in the
treatment of hyponatremia: 1-rasing the plasma Na+ at a safe rate
2-treating the underlying cause
Slide 10
Treatment with Nacl True volume depletion Diuretics Adrenal
insufficiency
Slide 11
Treatment with H2O restriction SIADH Edematous state Renal
failure Primary polydipsia
Slide 12
The risk factors for developing osmotic demyelination 1-More
than a 12 meq/l elevation in Na+ in the first day 2-Over correction
of the Na+ to above 140 meq/l within the first 2 days 3-Hypoxic or
anoxic episodes prior to therapy
TREATMENT OF SIADH Asypmtomatic or Chronic SIADH Water
restriction 0.5-1 liter/day Salt tablets Demeclocycline Inhibits
the effects of ADH Onset of action may require up to one week
Slide 15
Treatment Goal: raise Na by
Slide 16
Central Pontine Myelinosis Correction of Na too FAST more
common w/alcoholism, malnutrition, chronic illness Symptoms:
flaccid paralysis, dysarthria, dysphagia Evolve over days weeks May
extend dorsally Sensory Tracts locked-in syndrome Turn off ADH
& prompt diuresis Sudden & Dramatic Inc serum Na
Slide 17
Slide 18
Example: a 60 kg women with a plasma sodium of 110 meq/L
Formula: SNa = {[Na + K] inf SNa} (TBW + 1) What is the TBW? How
high will 1 liter of normal saline raise the plasma sodium? Answer:
TBW is 30 L Serum sodium will increase by approximately 1.4 meq/L
for a total SNa of 111.4 meq/L
Slide 19
Example: a 90 kg man with a plasma sodium of 110 meq/L Formula:
SNa = {[Na + K] inf SNa} (TBW + 1) What is the TBW? How high will 1
liter of 3% saline raise the plasma sodium? Answer: TBW is 54 L
Serum sodium will increase by approximately 7.3 meq/L for a total
SNa of 117.3 meq/L
Slide 20
Example: 63 y/o female at 75 Kg with N/V/D for 4 days SNa is
108 mEq/L She has had one seizure in the ambulance Plasma
osmolality is 251 mosmol/kg Urine osmolality is 47 mosmol/kg Uric
acid is 6mg/dl What type of hyponatremia does this patient have?
What additional labs/studies would you want?
hollywoodphony.files.wordpress.co m
Slide 21
How will you Tx her? Calculate the total body water 0.5 x
weight = 37.5 L What rate of correction do you want? 8 to 10 mEq/L
in 6 to 8 hours What fluid will you use? 3% Saline How will you
calculate the amount of sodium to give her? SNa = {[Na + K] inf
SNa} (TBW + 1) How will her sodium increase after 1 liter of 3%
saline? By 10.8 mEq/L to 118.8 mEq/L
Slide 22
What other medication will she need? Lasix and a foley Her
sodium increases to 118.8 mEq/L over the next 8-10 hours. How will
you continue to correct her hyponatremia? SNa = {[Na + K] inf SNa}
(TBW + 1) SNa = 154mEq/L 118.8mEq/L 38.5L = 0.9 mEq/L So 2 liters
of normal saline over the next 14 hours
Slide 23
Hypernatremia
Slide 24
HYPERNATREMIA Hypernatremia is defined as a plasma Na+>145
meq/l Hypernatremia represent hyperosmolality that results in water
movement out of the cells into the extracellular fluid that causes
cellular dehydration in the brain that is primarily responsible for
the neurologic symptoms.
Slide 25
Generation of hypernatremia Water loss: hypernatremia due to
water loss occurs only in patients who have hypodipsia, in adults
with altered mental status, and in infants. Na+ concentration >
150 is virtually never seen in an alert adult with a normal thirst
mechanism and access to water.
Slide 26
Hypernatremia Fluid volume status assessed by physical eaxam
Hypervolemic Gain H 2 O and Na+ Isovolemic Loss of H 2 O
Hypovolemic Loss of H 2 O>Na+ loss >20 mEq/L Renal loss
Diabetic insipidis Central Nephrogenic 20 mEq/L Renal loss Diuretic
Glycosuria Renal failure Extrarenal loss GI-vomiting GI-diarrhea
Excess sweating Respiratory loss Hypertonicdialysis Hemodilysis
Peritoneal dialysis Treatment Water replacement D5W at 1-2 mEq/L/hr
vasopressin for Central DI Mineralocorticoid 1 Hyperaldosteronism
Cushing disease Adrenal o Treatment Diuretics dialysis Treatment
Saline then hypotonic solution
Slide 27
Symptoms of hypernatremia Lethargy,weakness, irritability, are
the earliest findings which can then progress to
twitching,seizures, coma, and death that are more related to
cellular dehydration in the brain. Patients with chronic
hypernatremia may be relatively asymptomatic despite a plasma Na+
>170 The severity of the neurologic symptoms is related to the
both the degree and more importantly,the rate of rise in the
effective plasma osmolality.
Slide 28
Treatment of hypernatremia Rapid correction of hypernatremia
can induce cerebral edema, seizures, permanent neurologic damage,
and death therefore the plasma Na+ must be slowly lowered unless
the patient has symptomatic hypernatremia.
Slide 29
Treatment of hypernatremia Water deficit= 0.4 LBW( plasma
Na-140/ 140) The maximum safe rate at which the plasma Na+ should
be lowered (in the absence of hypernatremic symptoms) is 0.5
meq/L/h or 12 meq/L/per day
Slide 30
CLINICAL USE Estimate the effect of 1 liter of any infusate on
serum Na + Estimate the effect of 1 liter of any infusate
containing Na + and K + on serum Na + FORMULA* 1.Change in serum Na
+ = 2.Change in serum Na + = infusate Na + - serum Na + total body
water + 1 (infusate Na + + infusate K + ) -serum Na + total body
water + 1
Slide 31
InfusateInfusate Na + Extracellular-Fluid Distribution mmol per
liter % 5% Dextrose in H 2 0 0 40 0.2% NaCl in 5% dextrose in H 2 O
34 55 0.45% NaCl in H 2 O 77 73 Ringers lactate130 97 0.9% NaCl in
H 2 O154100
Slide 32
Isotonic saline unsuitable except in ECF volume depletion
causing hemodynamic instability Switch to hypotonic solutions as
soon as circulatory status stabilized Avoid excessive rapid
correction or over correction Select the most hypotonic infusate
suitable with appropriate allowances for ongoing fluid losses Most
important - reassess infusion prescriptions at regular intervals
based on pts clinical status and electrolyte values
Slide 33
Slide 34
POTASSIUM
Slide 35
Slide 36
POTASSIUM BALANCE Potassium is the major intracellular cation
that is essential for a variety of cellular and neuromuscular
functions. The total body K+ stores in a normal adult are 3000-4000
meq(50-55meq/kg) and the normal plasma concentration is 3.5-5 meq/l
and inside cells is about 140 meq/l
Slide 37
Regulation of potassium balance The maintenance of K+ balance
involves two functions: 1-the normal distribution of K+ between the
cells and extra cellular fluid 2-the renal excretion of the K+
added to the extra cellular fluid from dietary intake and
endogenous cellular breakdown
Slide 38
Factors influencing the distribution of K+ between the cells
and extra cellular fluid Physiologic: 1-Na+k+ ATPase
2-catecholamines 3-insulin 4-plasma potassium concentration
5-exercise Pathologic: 1-chronic disease 2-extra cellular PH
3-hyperosmolality
Slide 39
Renal excretion of k+ The urine is major route by which the K+
derived from diet and endogenous cellular breakdown, is eliminated
from the body. The primary event in urinary K+ excretion is the
SECRETION of K+ from the tubular cell in to the lumen in the distal
nephron.
Slide 40
Renal Handling of K+ Glomerulus: freely filtered PCT, Thick As
limb LOH : reabsorbed
Symptoms of hypokalemia Marked symptoms are unusual unless the
plasma K+ concentration is below 2.5-3 meq/l,but in susceptible
patients even mild reductions in the plasma potassium can
predispose to potential fatal arrhythmia.
Slide 47
Mild hypokalemia : generally asymptomatic Increased risk of
mortality for pts with cardiovascular disease trigger ventricular
tachycardia / ventricular fibrillation (decrease K+ : d/t
sympathetic stimulation) Digitalis induced arrhythmias can occur
with normal drug levels if hypokalemia is present Diuretic induced
hypokalemia & hypomagnesemia must be avoided in pts on drugs
that prolong QT interval : as it predisposes to polymorphic VT /
Torsade de pointes Hypokalemia < 3 mEq/L : Symptomatic Clinical
Features
Abnormalities induced by hypokalemia Muscle weakness or
paralysis Cardiac arrhythmias Rhabdomyolysis Renal dysfunction
1-impaired concentrating ability 2-increased ammonia production
3-impaired urinary acidification 4-increased bicarbonate
reabsorption 5-renal insufficiency Hyperglycemia
Slide 55
ECG : Initially : flattening of t wave depression of ST Segment
development of prominent u waves Severe hypokalemia : increased
amplitude of p wave increased QRS duration S.Potassium Basic
Investigations
Slide 56
Slide 57
Treatment of hypokalemia Monitoring of ECG and muscle strength,
is an essential part of the management of patients with sever
hypokalemia There is no definite correlation between the PLASMA k+
and BODY K+ stores. A reduction in the plasma K+ from 4 to 3 meq/l
requires the loss of 200-400 meq of K+
Slide 58
Urinary K+: > 20 mEq/L Renal loss Urinary K + : < 20
mEq/L Extrarenal loss TTKG : Transtubular Potassium Gradient (
Urine K+ / Plasma K+ ) ( Urine Osm / Plasma Osm ) TTKG : Renal loss
: > 4 Extra renal loss : < 4 Renal Vs Extra renal loss
Slide 59
Extra Renal Loss Urinary K+ < 20 mEq/L Metabolic Acidosis GI
Loss Diarrhoea Laxative Abuse Normal pH Villous Adenoma Laxative
Abuse Geophagia Metabolic Alkalosis GI Loss: rare Laxative abuse :
rare
Slide 60
Urinary loss K+ > 20 mEq/L Metabolic Acidosis RTA DKA
Ureterosigmoidost omy Variable pH ATN recovery Post obstructive
diuresis Drugs Metabolic Alkalosis Urinary chloride level Renal
Loss
Slide 61
Amphotericin B : tubular damage increased excretion of K+
Aminoglycosides : renal wasting of K+ Thiazides, Furosemide,
Acetazolamide : renal loss K+ Cisplatin HYPOMAGNESEMIA :
Significant renal K+ wasting Renal loss - Drugs
Slide 62
Urinary Chloride < 20 mEq/L Diuretics Vomiting > 20 mEq/L
Check BP Renal Loss + Metabolic Alkalosis
Treatment of hypokalemia. A variety of potassium preparations
are available for oral and IV use including the CL-, HCO3-,
phosphate,gluconate. In metabolic alkalosis and hypokalemia KCL
preparation is choice In metabolic acidosis and mild degree of
hypokalemia KHCO3 is preferred ORAL: KCL can be given orally in
salt substitutes as a liquid or in a slow release tablet or
capsule
Slide 65
Treatment of hypokalemia. IV: the standard IV kcl solution
contains 2meq/ml each of k+ and cl-. 20-40 meq of k+(10-20 ml) is
added to each liter of saline solution. In general,no more than 60
meq/l should be given through a peripheral vein,since higher
concentration of k+ are very irritating,resulting in pain and
sclerosis of the vein.
Slide 66
Treatment of hypokalemia.. 1-If k+ is between 3 to 3.5 meq/l
treatment is not urgent and these patients can usually be treated
with oral kcl at an initial dose of 60-80 meq/day 2-In patients
with sever symptoms or marked hypokalemia,k+ must be give more
rapidly. The plasma k+ will acutely rise by as much as 1-1.5meq/l
after 40-60 meq oral kcl and by 2.5-3.5 meq/l after 135- 160 meq/l
but these maximum effect is transient,why?
Slide 67
Rate of potassium repletion IV potassium is administered at a
maximum rate of 10-20 meq/h although as much as 40-60 meq/h has
been given to patients with paralysis or life threatening
arrhythmias. This solution containing as much as 200 meq of k+ /L
and are best tolerated if given into a large vein such as femoral
vein (infusion through a central venous line should probably be
avoided, why?
Slide 68
Rapid administration of k+ is potentially dangerous even in
severely k+ depleted patients and should be used only in life
threatening situation
Slide 69
HYPERKALEMIA
Slide 70
Hyperkalemia defined as a k+>5meq/l occurs as a result of
either k+ release from cells or decreased renal loss. There is an
adaptive response in hyperkalemia
Symptoms of hyperkalemia 1-Muscle weakness : most often begins
in the lower extremities and ascends to the trunk and upper
extremities. *The respiratory muscles and those supplied by the
cranial nerves are usually spared 2-Abnormal cardiac conduction:
the cardiac toxicity is enhanced by hypocalcemia, hyponatremia,
acidemia, and a rapid elevation in the plasma k+ concentration
Slide 73
EKG Changes Peaked T Waves
Slide 74
Slide 75
EKG Changes Widening of QRS Complex
Slide 76
EKG Changes Ventricular Tach/Torsades
Slide 77
Treatment of hyperkalemia Modality Mechanism of action
OnsetDurationPrescription K+ Removed From Body Calcium Antagonizes
cardiac Conduction abnor- malities 0-5 minutes 1 hour Calcium
gluconate 10%,5-30 mL IV; Or calcium chloride 5%,5-30 mL IV 0
Bicarbonat e Distributes K+ into cells 15-30 minutes 1-2 hours
NaHCO 3, 44-88 meq (1-2 ampules) IV 0 Insulin Distributes K+ into
cells 15-60 minutes 4-6 hours Regular insulin, 5-10 units IV,plus
glucose 50%,25 g (1 ampule) IV 0 Albuterol Distributes K+ into
cells 15-30 minutes 2-4 hours Nebulized albuterol, 10-20 mg in 4 mL
normal saline,in Haled over 10 minutes 0 Emergency
Slide 78
No emergency Modality Mechanism of action Duration of Treatment
Prescription K+ removed From body Loop diuretic Renal K+ excreation
Renal K+ excreation 0.5-2 hours Furosemide,40-160 mg IV or orally
with Or without NaHCO 3, 0.5-3 meq/ kg daily Variable Sodium
polystyrene Sulfonate(kayexalate) Lon exchange resin binds K+ 1-3
hours Oral: 15-30 g in 20% Sorbitol (50-100 mL) Rectal: 50 g in 20%
sorbitol 0.5-1 meq/q Hemodialysis Extracorporeal K+ removal 48
hours Blood flow 200- 300 mL/min, Dialysate [K+] ~ 0 200-300 meq
Peritoneal dialysis Peritoneal K+ removal 48 hours Fast exchange,
3-4 L/h 200-300 meq
