Electrolyte and post op fluid requirement

ELECTROLYTESDR NISHMA BAJRACHARYA

FCPS 1ST YR RESIDENT, OB/GYN

Copyright 2009, John Wiley & Sons, Inc.

Body Fluid Compartments

Electrolytes• solutes that are found in various concentrations and

measured in terms of milliequivalent (mEq) units• Can be negatively charged (anions) or positively charged

(cations)

Sodium Na+• 135-145mEq/L• Major Cation, Chief electrolyte of the ECFDetermines ECF & ICF Osmolality Serum osmolality = 2x Na+ + glucose/18 + urea/2.8

Normal – 275-290mOsm/kg

• Regulates volume of body fluids• Needed for nerve impulse & muscle fiber transmission (Na/K

pump)• Regulated by kidneys/ hormones

HYPONATREMIA (Na+< 135mEq/L+)ETIO

LOGY

Hypervolemic Euvolemic•CHF•Cirrhosis•Renal Failure • Excessive administration

of hypotonic fluids

•Psychogenic polydipsia•SIADH•Drugs•Withdrawal of gluococorticoids •Pseudo hyponatremia

HypovolemicRenal Na conservation(urine Na+ <20mEq/L )

Extra renal loss

•GI losses- vomiting, diarrhea•Skin losses- sweating, burn

Renal Na wasting(urine Na+ >20mEq/L)•CRD•Excessive diuretics•Salt losing nephropathy•Adrenal insufficiency

• Mild 135-130 mEq/L• Anorexia, Headache, Nausea, Vomiting, lethargy• Moderate 130-125 mEq/L• Personality Changes, Muscle Cramp Muscular weakness

Confusion, Ataxia• Severe <125mEq/L• Drowsiness, Diminished reflexes, Convulsions,Coma, Death

TREATMENT

HYPONATREMIA (correct underlying etiology)

HYPOVOLEMIA HYPERVOLEMIA EUVOLEMIA

Salt and water No salt Water restriction

supplementation Water restriction

Loop diuretics

ACUTE hyponatremia with severe neurological symptoms

• Rapid correction with hypertonic saline1 – 2mEq/L /hr until Na reaches 125 mEq/LSafe plasma Na+ concentration : 120-125mEq/L

• Correction using 3% NaCL (513 mEq/L)• Na Requirement- 0.6 x total body weight x (desired Na –

actual Na)

TREATMENT

TREATMENT

Chronic asymptomatic hyponatremia (>48hrs):

• Rate of correction - 0.5 to 1.0 mEq/L/hour.

• MAX 8mEq/L per day.• Rapid correction Central pontine demyelination

Dysarthria, dysphagia, flaccid paralysis or coma

Diagnosed by CT or MRI (more accurate)

• Example- 71 Kg woman with neurologic symptoms has serum Na 113 mEq/L,

• correction to serum Na level of 125 is achieved as follows• 0.6 x 71 (weight) x (125- 113) = 511 mEq Na• Patient requires 1 L of 3% saline to increase the level by

12 mEq• Correction In 6-12 hrs appropriate•

HYPERNATREMIA (Na+>145mEq/L)

Etiology – Usually : water deficitHypernatremia associated with formation of concentrated urine (U osm/ Posm >1.5 urine spc >1.015)• Excess nonrenal water loss- Hot environment, fever,

hyperventilation- Urine output <35 ml/h• Solute diuresis- due to inadequate water intake owing

to large volumes of renal solute excretion- Urine output >35 ml/h

• Hypernatremia associated with formation of dilute urine (Uosm/Posm <1, sp gr <1.010)

• Renal loss• Diabetes insipidus

• central (ADH deficiency) urine (Uosm/Posm <0.5, sp gr <1.005)• Nephrogenic –

• Renal tubular Damage- ability to concentrate or dilute the urine is decreased

when water loss exceed water intake- hypernatremia

CLINICAL FEATURES

Polyuria and thirstNeurological symptoms: altered mental status,

weakness, neuromuscular irritability, focal neurological deficit, seizures & coma

Hypertonicity contracts ICF volume brain cell volume subarachnoid or intra-cerebral hemorrhage

TREATMENT

• Restoration of ECF volume using hypotonic solutions• Water deficit :

Plasma Na+ concentration – 140 140

• Rate of correction : 0.5mEq/L/hr and not more than 10-12 mEq/l over 24 hours

X total body water

POTASSIUM (K+)

3.5- 5.5 mEq/LDetermines excitability of nerves and muscle

cells including the myocardium.Most abundant intracellular cation: 98% intracellular.

Poor intake Non renal loss Renal loss Redistribution

•Anorexia •Starvation•alcoholism

•Vomiting•diarrhea•nasogastric aspiration

•Diuretics•osmotic diuresis• salt wasting nephropathy• Mineralocorticoid excess(primary or secondary), Cushing’s syndrome,• Steroid therapy•Drugs- Gentamicin or Amphotericin B

Metabolic alkalosis, insulin, β2 agonist, Hypokalemic periodic paralysis,

Hypokalemia (K+ < 3.5mEq/L)

Clinical Features

• Commonly : Fatigue, myalgia and muscular weakness of lower extremity

• Smooth Muscle : Constipation, ileus or urinary retention

• Progressive weakness, hyporeflexia, hypoventilation( due to respiratory muscle involvement)

Early changes

Flattening or inversion of T waves Prominent U waves

ST segment depression

Prolonged QT interval U waves

Flattening of T waves

SEVERE HYPOKALEMIA

• Prolonged PR interval

• Decreased voltage

• Widening of QRS

• Ventricular arrythmia :VPC, ventricular tachycardia

TREATMENT

3.5 to 4 mEq/L :

• No potassium supplementation

• Add potassium sparing diuretics or decrease dose of diuretics

3 to 3.5 mEq/L :

• Treat in high risk groups

<3 mEq/L :

• Needs definitive treatment

IV KCl Therapy

Reserved for symptomatic and severe cases

Common Guidelines• Don’t give > 10- 20 mEq/L/ hour (typically 0.5mEq/kg/hr)

• Don’t give more than 240mEq/ day

• Continuous ECG monitoring required if using higher rate

• Use oral replacement whenever possible

TREATMENT

• KCL infusion : In NaCl not in 5% Dextrose D5 insulin release K+ shift ICS aggravates hypokalemia(0.2-1.4mEq/L)

• K deficit-

• Kdeficit (mmol) = (Knormal lower limit - Kmeasured) x kg body weight x 0.4

• Daily K need- 1mmol /kg body weightExample- A 70 Kg female with K+ 2.5 mEq/L requires correction as follows:K deficit= (3.5- 2.5) x 70 x 0.4 = 28 mmolDaily need- 1 x 70= 70 mmolTotal K to replenish over 24 hrs- 98 mmol

HYPERKALEMIA (K+ > 5.5mEq/L)

Etiology

• Increased intake

o I.V fluids containing potassium- RL (4.0 mEq/L), Isolyte M

(35mEq/L)

o Transfusion of blood stored for prolonged periods

o High potassium containing foods

o Potassium containing Drugs- spironolactone

HYPERKALEMIA

• Tissue breakdownHemolysis, RhabdomyolysisCatabolic State

• Shift of potassiumTissue damageMetabolic acidosisUncontrolled Diabetes due to insulin deficiencyHyperkalemic periodic paralysis, Succinylcholine

• Impaired ExcretionAcute renal failure or chronic renal failureDrugs : Potassium sparing diuretic, ACE inhibitors, AT-II

inhibitors,Reduced tubular excretion : Addison’s disease,

hyporeninemic hypoaldosteronism and amyloidosis

• PseuhohyperkalemiaTraumatic haemolysis during blood drawing

HYPERKALEMIA

CLINICAL FEATURES

Muscle weakness hyporeflexia paralysis affecting legs, trunk and arms (in that order) and at last respiratory muscles.

Cardiac Arrythmia6-7 mEq/L : Tall peaked T waves7-8 mEq/L : loss of P waves, widening of QRS complex8-10 mEq/L: QRS merges with T waves forming sine wave >9mEq/L : AV dissociation, Ventricular tachycardia or fibrillation , Diastolic arrest.

Severe elevation (7 mEq/L with toxic ECG changes)

• Calcium Gluconate 10% 10-20ml over 5-10minsto reduce the effects of potassium at the myocardial

cell membrane (lowers risk of ventricular fibrillation)Onset of action- few minAvoid if patient is on digitalis.

TREATMENT

• Infuse 50gm glucose, 10 unit reg insulin and 50mEq Sodium bicarbonate

• Onset- 15 min• IV infusion- 500ml of 10 % dextrose + 15 units

regular insulin + 50 mEq NaHCO3- over several hours

• Nebulized albuterol: 10 to 20 mg nebulized over 15 minutes

Preferred in CRD for rapid lowering

• Na Polystyrene sulfonate (Kayexalate) by mouth, NG tube (20-40 gm every 2-4 hrs)

• - ion exchange resin, that removes K by binding K and releasing Na into body fluids

• Hemodialysis

…TREATMENT

For moderate elevation (6 to 7 mEq/L

- Reduce K intake, diuretics- Kayexalate may be needed- Correct metabolic acidosis/ hyperglycemia if present- Stop administration of medications that can cause

increased K

CALCIUM

8-12 mg/dl99% present in bones, 1% in cells and 0.15%

in ECF.40% bound to Plasma proteinsUnbound form or ionized- physiologic activityTotal calcium- measure of both bound and

unbound form

Mediates :Muscle contraction and nerve conduction

Functions in coagulation cascade• PTH major hormone effecting Ca homeostasis (with

presence of Vit D)

HYPOCALCEMIA Ca <8-8.5mg/dl)

• Weakness• Circumoral and distal paraesthesia• Muscle spasm : carpopedal spasm, tetany.• Mental changes: irritability, depression and psychosis.• ECG- prolonged QT interval- can lead to heartblock or VF

CHOVSTEK’S SIGN

TROUSSEAU’S SIGN

ECG CHANGES

Causes

• Deficiency or absence of PTH• Vit D deficiency• Septic shock (suppression of PTH products)• Renal failure• Hyperphosphatemia

TREATMENT

Treat the underlying cause

Correct abnormalities in magnesium, potassium, and pH simultaneously.

10% calcium gluconate 10 ml IV over 15 minutes.

+ IV infusion of 10-20 mL of 10% calcium gluconate) in 1000 mL D5W @ 0.5 to 2 mg/kg/ hour (10 to 15 mg/kg).

Oral supplements- to treat long term

HYPERCALCEMIA

Serum calcium - 12 to 15 mg/dL.Neurologic symptoms :

• Depression, weakness, fatigue, and confusion at lower levels.

• At higher levels : Hallucinations, disorientation, hypotonicity, seizures, and coma.

Renal• Polyuria , nocturia, stone formation

CLINICAL FEATURES

Gastrointestinal symptoms:• Dysphagia, Constipation, peptic ulcers, and pancreatitis

Cardiovascular symptoms:• Upto 15mg/dl myocardial contractility increases• The QT interval typically shortens when the serum calcium is>

13mg/dL.• PR and QRS intervals are prolonged. • AV block may develop and progress to complete heartblock and even

cardiac arrest when the total serum calcium is > 15 to 20 mg/dL.• Hypercalcemia can worsen digitalis toxicity and may cause

hypertension.

Causes

• Hyperparathyroidism• Thiazide diuretics, Vit D intoxication• Malignancy• - increased bone resorption and decreased renal excretion• -metastasis to bones- increase in osteoclastic activity

TREATMENT

• Treat if• Symptomatic and > 12mg/dl or >15mg/dl

• Immediate therapy• Restore intravascular volume & promote excretion

• infusion of 0.9% saline at 250 to 500mL/h (saline diuresis) until any fluid deficit is replaced and diuresis occurs (urine output 200 to 300 mL/h).

• After adequate rehydration, 3-6 L/day.• Addition of loop diuretics – increase urine calcium excretion

TREATMENT

Biphosphonates – inhibit osteoclast precursorsEg- Etidronate Disodium, pamidronate, zoledronic acidCalcitonin- inhibit renal excretion of calcium and inhibits

osteoclastic activity Glucocorticoids- decrease intestinal absorption of Ca,

promote urinary excretion

MAGNESIUMMagnesium is the fourth most common mineral second most abundant intracellular cation Normal serum Mg2+ 1.2 – 2.2mg/dlMagnesium is necessary for the

• movement of sodium, potassium, and calcium into and out of cells• magnesium plays an important role in stabilizing excitable

membranes.• Enzyme co-factor in protein and carbohydrate metabolismReabsorbed in ascending limb of Loop of Henle, less in PCT and DT

Obstetric practice• Powerful tocolytic – Manage premature labour.• Prophylaxis and treatment of eclampsia.

HYPOMAGNESEMIA <1.8mg/dl

Result from decreased GI absorption due to chronic diarrhea, malabsorption , NG suction

Muscular tremors and fasciculations, TetanyAltered mental state Cardiac arrhythmias such as torsades de pointes.

Often seen together with hypocalcemia, hypokalemia

ECG findings- prolonged PT and QT intervals

TREATMENT

For severe or symptomatic hypomagnesemia:

1 to 2 g of IV MgSO4 over 5 to 20 minutes.• Followed by continuous infusion of 1mEq/kg/24hours.

For seizures (Eclampsia) – loading dose 4 g IV MgSO4 (20%) over 5 mins followed by 10 gm MgSO4( 50%) deep IM

Maintenance- 5gm MgSO4 (50%) IM 4 hrly

Administration of calcium is usually appropriate because most patients with hypomagnesemia are also hypocalcemic.

Caution and monitoring MgSO4 therapy• Check deep tendon reflex every 15mins (knee jerk)• Periodic monitoring of serum Mg concentration.• Reduce dose in renal failure.• Contraindicated in heart block or extreme myocardial

damage• Maintain urine output – >30ml/hr• Overtreatment 10% calcium gluconate 10-20ml

followed by fluid loading and diuretics.

TREATMENT

HYPERMAGNESEMIA (>3mg/dl)

Etiology• Renal failure patients : most common

cause• Treatment of pre-eclampsia with I.V

MgSO4.

• Therapy with Mg containing antacids, laxatives.

CLINICAL FEATURES

• Nausea vomiting, somnolence• Muscular weakness muscular paresis leading to

respiratory depression and respiratory failure. • Hypotension: peripheral vasodilatation• Bradyarrhythmia, asystole

• ECG changes- Prolonged PR interval, QRS duration and

QT interval, Complete heart block

TREATMENT

Eliminate source

10% calcium gluconate 10-20 ml IV over 10 min

IV saline diuresis (administration of IV normal saline and furosemide [1 mg/kg]) can be used to increase renal excretion of magnesium until dialysis can be performed.

Dialysis is the treatment of choice for severe hypermagnesemia.

Artificial respiration

PHOSPHORUS3-4.5 mg/dlMajor Buffer anion for ICF & ECF

• Rapid shifting can occur

Functions• Muscle, red blood cells & nervous system• Maintains acid-base balance

Adequate renal function necessary to maintain normal balance by PTH 90% excreted by kidneys

HYPOPHOSPHATEMIA<2.5mg/dl

• Paresthesia, Muscle pain/weakness

• Confusion/coma

• Causes- malabsorption, Vit D deficiency,

Hyperparathyrodism

TREATMENT

Diet/supplements (mild)IV replacement (severe)- infusion 2.5 – 5 mg

elemental phosp/ kg every 6 hrs • Concomitant Ca supplements

HYPERPHOSPHATEMIA (> 4.5mg/dl)• Tachycardia, Restlessness• Anorexia, Nausea and vomiting• Tetany, Tingling & numbness of fingers/lips• Muscle spasms

• Causes- renal failure, rhabdomyolysis, tumor lysis syndrome, hypoparathyroidism

TREATMENT

Diet restrictionsAdminister phosphate binding products

• Calcium acetate and calcium carbonate or aluminum hydroxide

Dialysis in severe renal failure.

FLUID AND ELECTROLYTES IN POST OPERATIVE PERIOD

• After surgery modification in normal physiology of fluid and electrolytes balance.

• ACUTE STRESS increased sympathetic stimuli- tachycardia, vasoconstriction & stress.

• Increased ACTH stimulate adrenal gland • --secretes large amount of hydrocortisone to fight

acute stress and aldosterone which leads to Na retention and urinary loss of K.

• Increased ADH secretion causes water retention , reduction in U.O to as low as 500 ml on 1st post op day.

• NPO status leads to hypovolemia prior to surgery, pt becomes hypotensive during surgery & anaesthesia.

• Fluid loss • Surgical stress or direct damage of kidney,

brain ,lung , skin or GI tract.

Goal of fluid therapy

• Aim to maintain • B.P >100/70 mm of Hg• Pulse rate of less than 120 bpm• Hourly U.O between 30 and 50 ml• Normal temperature, warm skin , normal

respiration and sensorium.

When and how long to give post-op iv fluid ?

• Short operative procedure ( no handling of intestine or viscera ) – maintenance i.v fluid to correct deficit due to NPO state.

• After 4-5 hours oral fluid is restarted & iv fluid is not needed.

• Major surgeries ( handling of intestinal viscera ) – requires post op iv fluid for few days.

• After ensuring normal movement of intestine oral fluid intake is restarted.

• Major surgery ( handling of intestinal viscera not done ) • Most of OBS/GYNE surgeries – I.V fluid is required for only 24 to 48

hrs.

Factors to consider for post op iv fluid

• Age , weight , vital data, hydration status and U.O.• Nature of surgery, blood loss , nature and vol of fluid

and blood replaced intraoperatively.• Drain output , fluid lost at operative site.• Renal status, associated illness ( HT,DM) and

associated electrolytes and acid base disorders, if any.• Insensible loss due to atmospheric temp, pyrexia,

hyperventilation etc.

On the 1st post op day

Increased ADH and aldosterone secretion –salt and fluid retention by the kidney .

K is avoided in I.V fluidsSo preferred- 5% dextrose, isotonic saline• Maintenance fluid - steady rate over an 18 to 24

hrs period.

Volume Excess

• Blood excess – pulmonary congestion.• Saline excess- weight gain, periorbital puffiness,

hoarseness or dysnoea on exertion.• Hypotonic fluid excess ( 5% dextrose) –

hyponatremia

Fluid volume deficit

• Decreased U.O < 30 ml/hr• Postural hypotension• Tachycardia• Diminished skin turgor• Decreased capillary refill time• Inc BUN out of proportion to creatinine

TREATMENTDepends on the type of fluid lost , can be done with isotonic solutions –NS or

LR.

Electrolyte Imbalances

• Hyponatremia- • Excess ADH- retention of water In excess of sodium.• Excess 5% dextrose• Water administration consistently which exceeds water loss.• Nausea without vomiting, drowsy, weak, confused or gets

convulsion.

TREATMENTAvoid using hypotonic solution.Avoid excessive use of electrolyte free solutions during the first 2-4

post op days.

• Hypokalemia – most common• Lost through urine or GI.• Post op infusion of mannitol or diuretics.• Prolonged administration of potassium free i.v fluids.• Extreme weakness , muscular hypotonia , paralytic ileus. Treatment Daily supplement 60 -100 mEq QD.• Hypernatremia and Hyperkalemia – Uncommon

Fluid management in Hypertension

• Strictly over 24 hrs and not faster.• Sodium containing fluids cause water retention and rise in

B.P • Strict B.P monitoring should be done on 1st post op day.• Furesemide will drop the b.p , increase the urine output but

can cause disturbance in electrolyte levels.

Fluid management in Diabetes

• high chances of development of diabetic ketoacidosis.

• Avoid using dextrose on 1st post op day as already due to excess glucocorticoids the level of glucose is on the higher side.

• GKI drip.

References

• Te linde’s Operative Gynecology, 11th Edition• UpToDate.com

Thank you