Disturbances of

body electrolytes
Moderator Prof. Tulsi Nag

Presenter Dr. Satyajit Maity

Disorders of sodium balance
Normal plasma sodium is 135 to 145 meq/l
Hyponatremia
Plasma sodium <135 meq/l
 Types
 Hypovolemic

 Euvolemic

 Hypervolemic
 Hyopovolemic
 Renal
diuretic excess
mineralocorticoid deficiency
salt wasting nephropathies
osmotic diuresis
renal tubular acidosis
 Gastrointestinal
vomiting
diarrhea
fistula
 integumentary
sweating
burns
 Euvolemic
 Primary polydipsia
 SIADH
 Arginine vasopressin release due to
pain,nausea
 Glucocorticoid deficiency
 Hypothyroidism
 Stress
 Hypervolemic
 Congestive cardiac failure

 Cirrhosis

 Nephrotic syndrome

 Acute or chronic renal failure

 Pseudohyponatremia
 Hyponatremia with normal plasma
osmolality
marked hyperlipidemia
marked hyperproteinemia.
TURP syndrome
 Hyponatremia with elevated plasma
osmolality
hyperglycemia
mannitol.
Clinical features
mainly
 Clinical features
 Primarily neurological
 Increased ICF volume
 severity:depends on rapidity of onset
and absolute increase in plasma sodium
concentration
 Asymtomatic or nausea,vomiting
 Depressed level of
consciousness,confusion,agitation
 Stupor,seizures and coma.
 Cerebral edema < 120 meq/l

 Cardiac symptoms < 100 meq/l

diagnosis
 history & physical examination
 3 tests

plasma osmolality
urinary osmolality
urinary sodium excretion

Plasma osmolality = 2 Na + glucose + BUN

18 2.8
 hyponatremia

Assess
extracellular
volume

low normal high

Hypovolemic hyponatremia

URINE
SODIUM

>20mEq/L <20 mEq/L

Diuresis
Adrenal diarrhea
insufficency
Euvolemic hyponatremia

URINE
OSMOLALITY

>100 mOsm/L <100mOsm/L

Psychogenic
SIADH
Polydipsia
Hypervolemic hypernatremia

URINE
SODIUM

>20 <20
mEq/L mEq/L

Renal CHF
failure Cirrhosis
 cont…….
Plasma osmolality low
impaired function
assess renal status primary renal disease
normal
Assess volume status volume depletion volume overload
normovolemic CCF
urinary sodium(meq/l) nephrotic
Adrenal & cirrhosis
thyroid insufficiency <10 >20

normal diarrhea salt wasting nephropathy

vomiting diuretics
Able to dilute urine
In response to water load dilute urine psyhogenic polydipsia
no yes
SIADH
treatment
 Goals of therapy
 To raise plasma sodium concentration
by restricting water intake and
promoting water loss

 To correct underlying disorder

 principles
 0.9% & 3% saline: Hypovolemic

 Water restriction :Euvolemic

&
Hypervolemic
 When to treat....?

 Symptomatic

 Plasma sodium < 120 meq/l

 Cont….
 Rate of correction depends on absence or
presence of neurologic dysfunction.

 In asymptomatic patients :
0.5 to 1 meq/l/hr or 10 to 12 meq/l
over first 24 hours

 Severe symptomatic hyponatremia (<110

meq/l)
hypertonic saline
1 to 2 meq/l/hr for the first 3 to 4
hrs,total not exceeding more than 12meq/l/
24hrs.
 To calculate Na deficit

Sodium deficit=total body water X

(desired Na - present Na)

TBW = body wt x 0.6 males

0.5 females
 Rapid correction can lead to…

 osmotic demyelination syndrome(central

Pontine myelinolysis)

 chronic hyponatremia

 flaccid paralysis,dysarthria,dysphagia.

 no specific treatment.
 Anaesthetic implications
 Plasma Na > 130meq/l for patients
undergoing elective surgery & is
considered safe
 Lower levels can result in signifcant
cerebral edema
Decrease in MAC: intraoperatively
Agitation & confusion :postoperatively
Hypernatremia
Plasma sodium>145meq/l
causes
 Impaired thirst
coma
essential hypernatremia
 Solute diuresis
diabetic ketoacidosis
non-ketotic hyperosmolar coma
 excessive water loss
diabetes insipidus
sweating
 Types
 Hypernatremia with low body sodium
content

 Hypernatremia with normal body

sodium content

 Hypernatremia and increased body

sodium content
 Hypernatremia with low body
sodium content

 Water loss in excess of sodium loss.

eg:osmotic diuresis
diarrhea
sweating
 Hypernatremia with normal total
body sodium content

 Due to water loss

 Diabetes insipidus
central diabetes insipidus
nephrogenic diabetes insipidus
Hypernatremia and increased total
body sodium content

 Following administration of large quantities

of hypertonic saline solutions

Clinical features
mainly
 Mainly due to contracted ICF volume

 Mainly neurological
alered mental status
irritability
weakness
focal neurological deficits
seizures & coma.

 Prone for intracerebral or subarachnoid

haemorrhage.
 Polyuria & thirst.
diagnosis
 ECF volume
not increased increased hypertonic Nacl or
sodium bicarbonate
min volume of max
concentrated urine no
yes
Insensible water loss urine osmole
Gastrointestinal excretion rate
>750 mosmol/d
no yes
renal response diuretic
to desmopressin osmotic diuresis

urine osmolality

increased unchanged

central DI nephrogenic DI
treatment
 Goals of therapy

 To correct water deficit

 To stop ongoing water loss by trating

underlying causes.
 principles
 Correction should be done over 48 to
72 hours.

 Hypotonic solution like 5% dextrose.

 Plasma Na should be lowered by 0.5

meq/l/hr or not more than 12meq/l/
24 hrs.
 To calculate water deficit

Water deficit=plasma Na - 140 X TBW

140
 Rapid correction can lead to…

 Seizures or permanent neurologic damage

 Anaesthetic implications
 Increases MAC, but its clinical
significance is related to fluid deficits
 Enhance uptake of inhalation
anaesthtics by decreasing cardiac
output.
 Predisposes to hypotension &
hypoperfusion of tissues
 Decreases volume of distribution and
reduction in dose of intravenous
agents is required.
Disorders of potassium balance
Normal plasma potassium is 3.5 to 5 meq/l
Hypokalemia
Plasma potassium < 3.5 meq/l
causes
 Redistribution into cells

 Increased loss

 Decreased intake
 Redistribution into cells
 Metabolic alkalosis
 Hormonal
insulin
beta 2 agonist
alpha antagonist
 Anabolic state
vit B12 /folic acid
total parentral nutrition
 others
Hypokalemic periodic paralysis
hypothermia
barium toxicity.
 Increased loss
 Renal
primary hyperaldosteronism
secondary hyperaldosteronism
congenital adrenal hyperplasia
cushings syndrome
bartters syndrome
liddles syndrome
renal tubular acidosis
diabetic ketoacidosis
diuretics,aminoglycosides,penicillin
amphotericin-B
 Gastrointestinal

 integumentary
 Decreased intake

 Starvation

 Anorexia nervosa

 alcoholism
Clinical features
 Manifestations vary between patient

 Asymptomatic

 <3 mq/l

 Fatigue,myalgia & lower extremity

weakness
 Neuromuscular

 Fatigue,myalgia,muscular weakness

 Progressive weakness and hypoventilation

as severity increases

 Rhabdomyolysis

 Paralytic ileus
 cardiovascular
 Abormal electrocardiogram
 Arrhythmias
 Orthostatic hypotension
 Decreased cardiac contractility
 Potentiates arrhythmogenic potential
of digoxin
 Myocardial fibrosis
 ECG Changes
 Appearance of U wave
 Flattening or inversion of T wave
 ST segment depression
 Prolonged QT interval
 Prominent U wave
 Prolonged PR interval
 Widening of QRS complex
 Ventricular arrhythmias
diagnosis
 history
 urinary potassium excretion
<15mmol/d >15mmol/d.

assess acid- base status

metabolic acidosis metabolic alkalosis

lower gastrointestinal loss diuretic

vomiting
k+loss via sweat
 >15 meq/day

assess k+ excretion

TTKG>4 TTKG<2 salt wasting nephropathy

osmotic diuresis
Assess acid-base status diuretic

metabolic metabolic
acidosis alkalosis
yes
DKA hypertension mineralocorticoid
Proximal RTA no excess
Distal RTA vomiting liddles syndrome
bartters
diuretic abuse
hypomagnesemia
treatment
 Therapeutic goals

 To correct potassium deficit

 To minimize ongoing losses

 To prevent life threatening

complications
 principles
 Safer to correct potassium via oral
route

 A decrement of 1mmol/l in plasma

potassium may represent a total body
k+ deficit of 200 to 400meq

 Dextrose containing solutions avoided

 When to treat…..?
 3.5 to 4 mq/l
Increased intake of potassium
containing food.
 3 to 3.5 mq/l
Only in high risk patients.

 < 3 mq/l needs definitive treatment.

 Oral potassium
 Safer
 Potassium chloride preparation of choice
 Potassium bicarbonate and citrate
 Mild to moderate hyperkalemia kcl 60 to
80 meq/day in 3 to 4 divided doses
 Severe or symptomatic – kcl 40 mq 6
hourly under ECG monitoring
 15 ml solution=20 meq
 Rate of infusion should not exceed 20
mEq/L.
 Iv potassium
 Severe symptomatic hypokalemia
 Continous ECG monitoring & frequent k+
estimation.
 KCl should not be directly IV.
 Rapid IV correction can cause dangerous
hyperkalemia.
 Isotonic saline should be used.
 Do not mix with dextrose containing
solutions.
 Cont…..
 15% KCl solution in 10 ml ampoule.

 10 ml = 20 meq of potassium.

 The maximum con. Of administered k+

should not > 40 mq/l : peripheral line
>60 mq/l : central line
 Rate of infusion should not exceed 20
mq/hr
 Anaesthetic implications
 Chronic hypokalemia more succeptible for
arrhythmias
 ECG monitoring
 Glucose free solutions
 Potentiates neuromuscular blockers
 Dose of NMBA should be reduced by 25-
50%.
 Avoid alkalosis
 Hyperventilation should also be avoided.
Hyperkalemia
Plasma potassium >5 meq/l
 causes
 Decreased renal excreation of potassium
 renal failure
 primary hypoaldosteronism
 secondary hypoaldosteronism
drugs:
spironolactone
NSAIDS
ACE inhibitors
Trimethoprim
Triamtreene
Heparin
Amiloride
 Cont…
 Due to extracellular movement of k+
acidosis
hyperkalemic periodic paralysis
succinylcholine
rhabdomyolysis
cell lysis following chemotherapy
digitalis overdose
 Enhanced chloride reabsorption
cyclosporine
Gordons syndrome
 Increased potassium intake
 pseudohyperkalemia
Clinical features
skeletal
 skeletal

 Weakness,flaccid paralysis

 Hypoventilation
CVS
 cardiac
 Increased T-wave amplitude 6 to 7 meq/l
 Prolonged PR interval

 QRS widening 7 to 8 meq/l

 Loss of P wave

 sine wave pattern 8 to 9 meq/l

 Ventricullar fibrillation or asystole > 9meq/l

 diagnosis
Exclude pseudohyperkalemia&transcellular k+ shifts

Exclude oliguric renal failure

stop NSAIDs and ACE inhibitors

assess k+ secretion
 Cont……
TTKG < 5 TTKG > 10
decreased circulating vol
Response to low protien diet
9a-fludrocortisone

TTKG >10 TTK<10

primary/secondary hypotension HTN

hypoaldosteronism high renin & low renin&
aldosterone aldosterone

pseudohypoaldosteronism Gordons syndrome

k+ sparing diuretics cyclosporine
distal RTA, ty 4
treatment
 principles
 >6meq/l should be treated

 To minimize membrane excitability

 To shift potassium into cells

 Promote potassium loss

 Calcium gluconate
 10% solution in 10 ml ampoules
 10ml of 10% calcium gluconate IV over
5 to 10 min
 Repeated if no change in ECG is seen
after 5 to 10 min
 How it helps……?
protects the myocardium
from toxicity to potassium
 Insulin & glucose
 10 to 20 units of regular insulin in 50
ml of 25% dextrose.

 Initial bolus should be followed by

continous infusion of 5% dextrose

 effect begins in 15 min & peak in 60

min
 cont…..
 Sodium bicarbonate
7.5 % of 50 to 100 ml is given as
IV slowly over 10 to 20 min.
 Beta agonist
salbutamol 20 mg in 4 ml saline by
nebulisation

 Loop & thiazide diuretics

 Cont…
 Cation exchange resins
sodium polystyren sulphonate
promote exchange of Na for K in
GIT
25 to 50g with 100ml of 20%
sorbitol 3 to 4 times a day

 Haemodialysis
 Anaesthetic implications
 ECG monitoring
 Succinylcholine avoided
 Potssium free solutions
 Avoid acidosis
 Potentiates neuromuscular blockers
 Mild hyperventilation desirable
Disorders of calcium balance
 Normal plasma calcium 8.5 to 10.5
mg/dl.

 50% in ionized form ,40% protein

bound,10% complexed with anions
hypocalcemia
Plasma calcium <8.5 mg dl
Causes:
 MECHANISM CLINICAL SYNDROME

PTH absent •Hereditary hypoparathyroidism

•Acquired hypoparathyroidism
•Hypomagnesemia

PTH ineffective •Lack of active vit.D

•Defective metabolism from anti convulsant therapy
•Vit.D dependent ricket type 1

Pseudohypoparathyroidim •Ineffective vitD (intestinal malabsorption)

•VitD dependent ricket type II

PTH overwhelmed •Acute hyperphosphatemia

•Tumur lysis syndrome
•ARF
•Rhabdomyolysis
•Ostetis fibrosa after parathyroidectomy
 Hallmark of hypocalcemia is TETANY
 Parasthesia in circumoral region &
extremities
 Laryngospasm,bronchospasm
 Abdominal cramps,urinary frequency
 Hypotension & arrhythmias
 Latent hypocalcemia
Chvosteks sign
Trousseaus sign
 ECG

 Prolongation of QT interval
 treatment
 Symptomatic hypocalcemia – emergency
10 ml of 10% calcium
gluconate IV over 10 minutes.

 Iv calcium should not be given with

bicarbonate or phosphate containing solution

 Serial calcium measurements

 Correction of co-existing alkalosis

 Calcium supplimentation in long term

 Anaesthetic implicatons
 Corrected preoperatively
 Serial ionized calcium level monitored
 Potentiates negative inotropic effect
of barbiturates and volatile
anaesthetics
 Laryngospasm
 Alkalosis should be avoided
hypercalcemia
plasma calcium > 10.5 mg/dl
 causes
 Hyperparathyroidism
 Malignancy
 Pagets disease of bone
 Excessive vitamin D intake
 Granulomatous disorders
 Milk- alkali syndrome
 Drugs
thiazides
lithium
 Clinical features
 Anorexia
 Nausea,vomiting
 Weakness
 Polyuria
 Ataxia
 Irritability
 Lethargy
 confusion
 ECG changes
 Pronged PR interval

 Widened QRS complex

 Shortened QT
 treatment
 Hydration with normal saline
 Loop diuretics like frusemide
 haemodialysis
 Urine output > 3 litres /day
 Severe cases bisphosphonates
pamindronate 60 to 80 mg iv
over 4 hrs
calcitonin 2 to 8 U subcut
 90% due to malignancy &
hyperparathyroidism
 Anaesthetic implications
 Saline diuresis – avoidance of thiazide diuretics

 Maintenance of hydration & urine output with

sodium containing fluids.

 decreased dose of neuromuscular blockers

 Cvp & pulmonary pressure monitoring

 Hyperventilation avoided
Disorders of magnesium balance
hypomangnesemia
Plasma mg+ <1.7 meq/l
 causes
 Inadequate intake
 Reduced gasroinestinal absorption
malabsorption
small bowel /biliary fistula
severe diarrhea
prolonged nasogastric suctionig
 Renal losses
diuresis
hyperparathyroidism
 Drugs
theophylline
diuretics,ethyl alcohol
aminoglycoside,amphotericin B
 clinical features
 Asymptomatic
 Associated with hypocalcemia &
hypokalemia
 Anorexia,weakness,parasthesia
 Confusion,seizures&coma
 Atrial fibrillation
 Potentiates digitalis toxicity
 Prolongation of PR &QT interval
 treatment
 Asymptomatic
2g oral magnesium sulfate

 Symptomatic
magnesium sulfate 1 TO 2 g IV
over 10 min
1 ml of 50% solution contains
4 meq
 Things to be monitored
 Tendon reflexes

 Respiratory rate

 Urine output
 Anaesthetic implications

 No specific anaesthetic interactions

 Coexistent electrolyte imbalances

should be corrected
Hypermagnesemia
Plasma mg > 2.5 meq/l
 causes
 Antacids or laxatives

 Iatrogenic

 Hypothyroidism

 Adrenal insufficiency

 Lithium administration
 Clinical features
 Hyporeflexia ,drowsiness & skeletal muscle
weakness

 Hypotension

 Prolonged PR interval & widening of QRS

complex

 Respiratory arrest
Threshold Serum Mg (mEq/L) MANISFESTATION

>4 Hyporeflexia

>5 1 degree A-V Block

>10 CHB

> 13 Cardiac Arrest

 treatment
 10 ml of 10% calcium gluconate IV
over 10 min

 Loop diuretic with ½ normal saline in

5% dextrose

 Peritoneal / haemodialysis
 Anaesthetic considerations

 tendon reflexes, respiratory rate & urine output

 Potentiates negative inotropic effects of

anaesthetics

 Neuromuscular blockers decreased by 25 to 50%

Hyperphosphatemia

Serum phosphorus > 4.2 mg/dl

 Causes:
 Severe hyperphosphatemia occurs after
tissue damage or cell death.
 Renal insufficiency
 Hypoparathyroidsm
 Hematologic malignancy (plasma cell
dyscrasias).
 Massive liver failure
 Iatrogenic
 Hypothermia.
 Increase in phosphate can lead to Ca2+
 Hypocalcemia due to calcitriol production.
 Precipitation of calcium & phosphate
decreasing serum calcium level further.
 Abdominal calcification & metastatic
calcification.
 Treatment

 Dialysis in renal failure.

 Aluminium hydroxide/carbonate.

 Diuresis induced by acetazolamide.

 hypophosphatemia

plasma phosphate < 2.5 mg/dl

 Clinical manisfestation
 In sever cases (Po4 <1 mg/dl), decreased
level of 2-3 DPG results in increased
affinity of Hb for oxygen.
 Muscle weakness
 Paresthesia
 Encephalopathy
 Platelate & leukocyte dysfunction
 Respiratory failure
 Myocardial dysfunction.
 Treatment

 Prophylaxis is best ( TPM)

 ORAL REPLACEMENT is preferable.

 In sever cases phosphate infusion- 9-10

mmol/ 12 hr.
Key words :
 Referances
 Harrisons ,17th edition

 Millers anesthesia,7th edition

 Clinical anesthesiologyMorgan,5TH edition

 Practical guidelines on fluid therapy ,

sanjay pandya