FLUID AND ELECTROLYTE

BALANCE
Prof T R Ramachandran
MAHSA
 PLASMA OSMOLALITY
• ECF Osmolality: sum of the concentration
of all dissolved solutes
• Na constitutes 90% of all solutes

• Plasma osmolality = 2X plasma Na

concentration

• ECF and ICF are in osmotic equilibrium

• Plasma Na reflects total body Osmolality

Control of Plasma Osmolality

• Osmo receptors in the

hypothalamus control secretion of
ADH and Thirst mechanism

• Plasma osmolality is maintained

within narrow limits by varying
both water excretion and water
intake
 ADH Secretion
• Supraoptic and Paraventricular nuclei of
hypothalamus sensitive to changes to
plasma osmolality
• Increase in plasma osmolality cells shrink
and release ADH increases water re-
absorption by the collecting tubule
• Corrects the plasma osmolality to normal
 NON OSMOTIC RELEASE OF ADH
• Carotid baroreceptors and probably Atrial
stretch receptors stimulate release of ADH
following 5-10 % reduction in blood volume

• Other stimuli include Pain, Emotional stress

and Hypoxia.
 THIRST MECHANISM
• Osmoreceptors in lateral preoptic
area of Hypothalamus are also
very sensitive to changes to ECF
osmolality.
• Activation of these neurons by
increase ECF osmolality cause
intense thirst forces the individual
to drink water .
• Conversely hypo-osmolality
suppress the thirst mechanism
 Hypernatremia with Low total body
Sodium
• Loss of water and sodium; water more
than sodium
• Hypotonic loss: renal cause- osmotic
diuresis
• Extra renal: Diarrhea, excessive sweating
• Patient has manifest hypovolemia
• Urinary sodium >20 mEq/L ( renal cause)
• Urinary sodium < 10 mEq/L (extra renal)
 Hypernatremia with normal total
body Sodium
• Patient manifest signs of water loss
without hypovolemia
• Common cause Diabetes Insipidus
• Marked impairment of renal concentration
ability either due to decreased excretion of
ADH ( central DI)
• Failure of renal tubules to normally
respond to circulating ADH ( nephrogenic
DI)
 Central Diabetes Insipidus
• Lesions around hypothalamus and pituitary
stalk
• Brain dead patient
• Neurosurgical procedures
• Head injury
• History of polydipsia, polyuria (>6 L/ day)
• Urinary osmolality < serum osmolality
• Increase in urinary osmolality following
administration of s/c or im vasopressin
 Nephrogenic Diabetes Inspidius
• Congenital or acquired chronic Kidney Disease
• Sickle cell disease, hypoprotenemia
• Secondary to drugs amphotericin B,
demeclocyline, mannitol
• ADH secretion normal but renal tubules does
not respond to ADH
• Urinary concentration ability impaired
• Diagnosis confirmed inability of kidneys
inability to produce hypertonic urine in
response to s/c or im vasopressin
Hypernatremia with Increased total
body sodium
• Most common cause adm large
quantities of hypertonic saline
solution such as 3% Na Cl, 7.5% of
NaHCO3
• Primary hyperaldosteronism,
Cushing’s syndrome
 Clinical Manifestations
• Neurological manifestations
predominate because of cellular
dehydration
• Restlessness, lethargy, hyperreflexia,
seizures, progress to coma and death.
• Symptoms correlate with rate of
movement of water out of the cells than
with absolute levels of hypernatremia
• Focal intra-cereberal bleed or
subarachnoid hemorrhage
• Chronic hypernatremia is well tolerated
than acute increase.
Treatment of Hypernatremia
• Aimed at restoring plasma osmolality
and correcting the underlying cause
• Water deficit to be corrected over 48
hours with infusion of 5% dex in
water
• Hypernatremia patients with low Na
should infused with isotonic saline to
restore volume
• Hypernatremia with high Na loop
diuretics and 5% dex in water.
Treatment of Hypernatremia
• Rapid correction of hypernatremia
can result in seizures and
permeant brain damage and death
• Serum Na and plasma osmolality
to be monitored
• Reduction of Sodium
concentration should at the rate of
0.5 mEq/L/ hour
 Example
• 70 kg patient has plasma Na of 160 mEq/L. What
his water deficit?
• Normal Na 140 mEq/L and TBW 60% of body wt.
• Normal TBW X140= present TBWX 160
• (70X.6) X 140 = present TBW X160
• (70x.6) X 140/160 = present TBW X160
• Present TBW = 36.7 L
• (70X.6)– 36.7= 5.3 L
• 5300 ml to be corrected over 48 hours (110
ml/hr)
 HYPONATREMIA

• Hyponatremia is best classified

according to total sodium content
• Hypoosmolality associated with
hyponatremia ( Na < 135 mEq/L)
Hyponatremia with Increased total body sodium

• Edematous disorders : increase in TBW

and sodium: when the increase in water
more than increase in sodium-
hyponatremia ensues.
• CCF, Cirrhosis of Liver, CKD, nephrotic
syndrome
• Hyponatremia in these settings results
from progressive impairment of free
water excretion and generally parallels
underlying disease condition
• The effective circulating blood volume is
reduced.
Hyponatremia with normal total body
sodium
• Hyponatremia in the absence of
edema or hypovolemia is seen in
glucocorticoid deficiency,
hypothyroidism, drug therapy
(chlorpropamide,
cyclophosphamide) and SIADH
• Urine osmolality > 100 mOsm /Kg
• Urine sodium > 40 mEq /L
 TURP syndrome
• Transurethral resection of prostate
often opens network of venous
sinuses potentially allowing
systemic absorption of irrigating
fluid (20 ml/mt)
• Results in constellation of
symptoms and signs known as
TURP syndrome
Treatment of TURP syndrome
• Early recognition
• Absorbed water must be eliminated
and hypoxemia and hypoperfusion
treated
• Fluid restriction and IV Furosemide
• Symptomatic hyponatremia
resulting in seizures leading to
coma to be treated with hypertonic
saline.
• Slow infusion to avoid exacerbation
of fluid overload.
Manifestation of Hyponatremia
• Primarily neurological and result
from increase in intracellular
water
• Patients with mild to moderate
hyponatremia ( Na >125 mEq /L) :
asymptomatic
• Anorexia, nausea, weakness
progressive cerebral edema –
lethargy, confusion, coma and
death. ( Na < 120 mEq/L)
Treatment of Hyponatremia
• Directed towards correcting
underlying disorder and as well as
plasma sodium
• Isotonic saline is the fluid of choice in
patients with decreased total body
sodium
• Specific treatment of adrenal/ thyroid
deficiency or management CCF
• Demeclocycline antagonizes ADH
activity at the renal tubular level
useful adjunct in SIADH.
Treatment of Hyponatremia
• Rapid correction of hyponatremia
associated central pontine
demyelination resulting in
permeant neurological damage
• Mild symptoms 0.5 mEq/L/ hr
• Mod symptoms 1 mEq/L / hr
• Severe symptoms 1.5 mEq/L/hr
 Example
• 80 Kg woman is lethargic and is
found to have plasma Na 118 mEq/L.
• How much NaCl must be given to
raise her plasma Na to 130 mEq/L?
• Na deficit = TBW X( 130-118)
• = ( 80X.5) X 12
• = 480 mEq
• Isotonic saline 154 mEq/L
• 480/154 =3.1 L of isotonic saline to
given in 24 hours (130 ml/ hr)
•
 HYPOKALEMIA
• Defined plasma K < 3.5 mEq/L
• Inter compartmental shift
• Increased K loss
• Inadequate K intake
• Plasma concentration poorly
correlates to total body K
• K 4 to 3 mEq/L 100-200 mEq deficit
• K < 3 mEq/ L 200-400 mEq/L
deficit
Treatment of Hypokalemia
• Continuous ECG monitoring
• Oral replacement of potassium
chloride over several days 60-80 mEq
/day
• Intravenous replacement reserved
for patient with serious cardiac
manifestation or severe muscle
weakness
• Rapid K replacement (10-20 mEq/hr)
through central vein and continuous
ECG monitoring
 Clinical Manifestations of
Hyperkalemia
• Most important effect on cardiac
and skeletal muscle
• Skeletal muscle weakness
(K>8mEq/L) due to spontaneous
depolarization (due to inactivation of
Na channel ) muscle paralysis
• Cardiac manifestation due to
delayed depolarization (K >7 mEq/l)
• Hypocalcemia, hyponatremia and
acidosis accentuate effects of
hyperkalemia
Management of Hyperkalemia
• Inj Calcium gluconate 10% 5-10 ml IV
• Inj soda bicarbonate 45 mEq IV
slowly
• IV infusion of 10% glucose with 15
units of regular insulin
• Nebulization with Beta 2 agonist
• Cation ion exchange resin oral/rectal
sodium polysterene (20 gms in 100
ml of 20% sorbitol) each gm binds 1
mEq of K
• Hemodialysis
 Calcium
• Normal calcium 8.5- 10.5 mg/dl
• Approximately 50% ionized, 40%
protein bound 10% complexed
with citrate and amino acids
• The free ionized Ca physiologically
important
• Changes in pH affects degree of
protein binding and thus ionized
Ca concentration
 Clinical manifestations of
Hypercalcemia
• Anorexia, nausea, vomiting, weakness
and polyuria
• Ataxia, irritability, lethargy rapidly
progress to coma
• Hypertension is always present
• ECG shows shortened ST segment and
shortened QT interval
• Hypercalcemia increases sensitivity of the
heart to digoxin
• Pancreatitis, peptic ulcer disease and
kidney failure may complicate
hypercalcemia.
Treatment of Hypercalcemia
• Symptomatic hypercalcemia require
urgent treatment
• Most effective treatment rehydration
followed by brisk diuresis (200-300
ml urine/hr)
• Renal loss of K and Mg may occur
during diuresis and hence to be
monitored and replaced if necessary.
• Additional therapy with
bisphosphonate or calcitonin
• Dialysis rapidreduction of Ca
 Hypocalcemia
• Diagnosed on the basis of ionized
Calcium concentration
Clinical manifesttions of Hypocalcemia
• Paresthesia, confusion, laryngeal
dehydration, carpopedal spasm
(Trousseau’s sign ), masseter
spasm (Chvostek’s sign) and
seizures.
• Biliary colic and bronchospasm
have been reported
• Decreased cardiac contractility –
HF
• Prolongation of QT interval
Treatment of Hypocalcemia
• Symptomatic hypocalcemia medical
emergency needs urgent treatment
• Calcium Chloride 10% solution 3-5
ml slow IV.
• Serial ionized Ca measurement
mandatory
• Rapid infusion or continuous
infusion (1-2 mg/kg/hr)
• Chronic hypocalcemia oral calcium
and vitamin D are usually necessary
 Magnesium
• Plasma Mg 1.7-2.1 mEq/L
• GI absorption, bone storage and
excretion by Kidneys.50-60%
unbound and diffusible
• Hypermagnesemia nearly always
due excessive intake ( antacid or
laxative)
• Renal impairment (GFR <30ml/min
or both
• Adrenal insufficiency ,
hypothyroidism, rabdomylosis.
 Hypermagnesemia
• Neurological, neuromuscular and
cardiac manifestation
• Hyporeflexia, sedation and muscle
weakness and respiratory
depression
• Bradycardia and myocardial
depression may cause
hypotension
• ECG prolongation of PR interval
and widening QRS complex
Treatment of Hypermagnesemia
• Mild case discontinue source
• Moderate to severe case Inj
calcium chloride 10% 5-10 ml IV
(physiological antagonist)
• Loop diuretic with Isotonic
infusion in patient with normal
renal function
• Serial estimation of Mg and Ca
done
• Dialysis necessary in CKD patients
 Hypomagnesemia
• Common and frequently overlooked
in critically patient associated with
low potassium and phosphorous.
• Commonly seen in patients
undergoing cardiac and GI surgery
• Most patients are asymptomatic but
anorexia, weakness, fasciculation
paresthesia and ataxia, coma and
seizures re encountered
• Cardiac manifestation include
arrhythmia
Treatment of Hypomagnesemia
• Asymptomatic patient oral or IM
MgSO4
• Severe cases with cardiac
arrhythmia IV MgSO4 8-16 mmol
given slowly over 15-30 min
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