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Fluid & Electrolytes Management of the Surgical Patient

Presenter: Ahmad Nabil B. Md Rosli Supervisor: Dr Aziah

Total Body Water


body wt% total intracellular extracellular intravas interstitial 60 40 20 5 15 Total body water% 100 67 33 8 25

Composition of Fluids Compartment


plasma Cations Na K Ca Mg Anions Cl HCO SO4 HPO4 Protein 140 4 5 2 103 24 1 2 16 interstitial 146 4 3 1 104 27 1 2 5 intracellular 12 150 10 7 3 10 116 40

Normal Water Exchange


Average fluid lost (ml) Sensible urine 1000 intestinal 250 Insensible lungs/skin

600

Control of Volume
Kidneys maintain constant volume and composition of body fluids
Filtration and reabsorption of Na Regulation of water excretion in response to ADH

Water is freely diffusible


Movement of certain ions and proteins between compartments restricted

Osmoregulation
F F F F

osmolality 289 mOsm/kg H20 osmoreceptor cells in paraventricular/ supraoptic nuclei osmoreceptors control thirst and ADH small changes in Posm - large response

Osmoregulation
Excess free water (Posm 280) thirst inhibited ADH declines urine dilutes to Uosm 100

Osmoregulation
Decreased free water (Posm 295)
F thirst increased F ADH increases F urine concentrates to Uosm 1200

Volume Control
osmoreceptors - day to day control

baroreceptors - respond to pressure change neural and hormonal efferents hormonal mediators

Baroreceptors
Hormonal mediators aldosterone renin ANP dopamine Hormonal effect q ECF p Na and water reabsorption

Baroreceptors
Neural mechanism Autonomic nervous system

ReninRenin-angiotensin
Renin secreted when drop BP drop Na delivery to kidney increased sympathetic tone

ReninRenin-Angiotensin

Angiotensin II
Increases vascular tone
F F F F

increases catecolamine release decrease renal blood flow increases Na reabsorption stimulates aldosterone release

Aldosterone
Release stimutlated by
F F F

Angiotensin II increased K ACTH Na and water absorption in distal tubular segments

Effect
F F

Control of Volume
Effective circulating volume
Portion of ECF that perfuses organs Usually equates to Intravascular volume

Third space loss


Abnormal shift of fluid for Intravascular to tissues eg bowel obst, i/o, pancreatitis

Fluid and Electrolyte Therapy


Surgical patients need
1. 2. 3. 4. 5. Maintenance volume requirements On going losses Volume excess/deficits Maintenance electrolyte requirements Electrolyte excess/deficits

1. Maintanence

This includes:insensible, urinary, stool losses

Example: 70 Kg Man Needs


1st 10kg x 100mls 2nd 10kg x 50mls TOTAL = 1000mls = 500mls 2500 mls /d

Next 50kg x 20mls = 1000mls

2. On Going Losses
NG drains fistulae third space losses Concentration is similar to plasma Replace with isotonic fluids

3. Disturbance in Fluid Balance (deficit)


GI lost - nasogastric suction,vomiting, diarrhea, or fistula Skin lost - soft-tissue injuries, burns 3rd space lost - peritonitis, obstruction, or prolonged surgery

3. Disturbance in Fluid Balance (excess)


Iatrogenic Renal dysfunction Congestive cardiac failure Cirrhosis

4. Maintenance Electrolyte Requirements


Na 1-2mEq/Kg/d 1K 0.5 - 1 mEq/Kg/d mEq/Kg/d

Usually no K given until after urine output is adequate and U/E done. Always give K with care, in an infusion slowly - never bolus Ca, PO4, Mg not required for short term

5. Electrolytes Imbalance:
Sodium Potassium Magnesium Calcium

Hyponatremia
Definition: Na < 135 mmol/l Clinical manifestation (<120mmol/l)

Causes
1. Hypotonic (Posmol < 275)
a. Hypovolumic b. Euvolumic

2. Isotonic (pseudo) (Posmol 275-295) 3. Hypertonic 1. Hypervolumic (Posmol >295)


a. Urinary Na >20 b. Urinary Na < 20

Management
General principle: Serum Na should not be increased > 10 mmol/L (asymptomatic) OR 12 mmol/l in symptomatic If Na >120 aggressive correction generally not required If Na <110 urgent treatment is required

Hypervolumic hyponatremia Restriction of Na & water intake Correction of K & promotion of water loss in excess of Na Treat aetiology

Isovolumic hyponatremia a. No or mild symptoms;


Fluid restriction (800-1000cc) until Na rises 0.9% saline with ferusamide may also be used especialy in those with higher urine osmolality

b. Severe symptoms
Seizure & coma require rapid increase of patients extracellular tonicity i.e: 3mmol/L in 3 hours Severe confusion need moderate increment 3-6 mmol in 12 hours The principle is to administer 3% saline at a rate equal to frusemide urinary electrolyte losses This approach avoid dangerous over expansion of ECF & correct primary cause of hyponatremia excessive body water

Example:
60 kg isovolumic male patient presented with grand mal seizure with na: 111mmol/L. How to correct this?

Hypovolumic hyponatremia Rehydration over 2-3 days Amount of fluid calculated as:
o Amount depleted: Calculated from degree of dehydration (i.e 5% x BW x 1000cc) o Normal fluid requirement

Rate: o calculated deficit+maintanence+losses may be given in first 24 hours o About of total 24 hours volume may be given in first 8 hours

Hypernatremia
Definition: Na > 150 mmol/l

Clinical manifestation (<160 mmol/l)

Causes
1. Loss of water
a) Reduced water intake b) Water loss in excess of sodium

2. Gain of sodium
a) Increase intake b) Renal salt retention

Management
General principle: Target of fall 10mmol/L/day in all patient* Long standing hyponatremia infusion of hypertonic saline may cause cerebral edema (rate 0.5 mmol/hr) Acute hypernatremia may not increase risk of cerebral edema upon fast correction (i.e 1 mol/hr)

1. Loss of water - see example 2. Salt Gain


The aim is to remove sodium rapidly using potent diuretics & at the same time D5% is infused In severe difficult cases- dialysis is needed

Example:
60kg female hypovolumic patient presented with sever obstundation with Na level of 165 mmol/l? How to correct this

Hyperkalemia
Definition: K > 150 mmol/l Symptoms: nausea, vomitting, intestinal colic, weakness, respiratory failure Signs: peaked T wave, flattened P wave, prolonged PR interval, widened QRS, sine wave formation and VF

Causes
1. 2. 3. 4. 5. 6. Abnormal potassium distribution Factitious Oliguric renal failure Impaired renin / aldosterone axis Inhibition renal potassium secretion Increase intake
a) Endogenous b) Exogenous

Management
Goals: To protect heart from effects of K by antagonizing its effect on cardiac conduction (ca gluconate) To shift K from ECF to ICF (NaChO3, insulin, glucose) To reduce total body K (cation-exchange resin, dialysis)

Recommendation
Mild to moderate hyperkalemia (k: 5,5-6.5) with no ECG changes
Low K diet Stop offending drug Cation exchange resin Correction of acodosis +/- Glucose and insulin infusion

Severe hyperkalemia (k>6.5mmol/L) or ECG changes:


Above treatment Immediate calcium administration Glucose & insulin infusion Other methods i.e dialysis

Method of correction
1. Calcium administration
10 ml of 10% calcium gluconate IV slow bolus

2. Glucose & insulin infusion


Rapid 10U insulin + 50 ml of 50% Dextrose as slo bolus

3. Beta-agonist therapy
- Iv salbutamol 0.5 mg IV in 15 min or 10 mg nebulizer

4. Sodium bicarbonate infusion


Iv NaCH03 100-200 mmol/L over 30 min

5. Cation-exchange resins
Oral kalimate 10g tds

6. Hemodialysis

Hypokalemia
Definition: K > 3.5 mmol/l Symptoms: constipation, ileus, muscle weakness, fatigue Signs: Diminished tendon reflex, U-wave, flattened T-wave, ST segment changes, arrhythmias

Causes
1. Shift into cells 2. Reduced intake 3. Increased loss
a) Renal b) GIT c) Misc

Management
Important facts: 1 g KCL contains 14 mmol K Magnesium depletion should be suspected if K level does not rise after adequate oral therapy K is an extracellular cation; a low serum K level reflects a much greater total K deficit

Oral therapy: Mild to moderate ( K >2.5) Oral KCL 1-2g every 2-4 hourly Slow-release K (1 tab = 8 mmol) or effervescent K (1 tab = 14 mmol) or mist KCL Off/change drug causing hypokalemia

IV therapy: Severe hypokalemia (<2.5 mmol/L), with ECG changes, and in patient who are not able to take orally and who are symptomatic Asymptomatic patient:
Concentration < 40 mmol/L (<3g KCL/l) in dextrose-free carrier Emergency: up to 40 mmol/L (i.e KCL 3g/hr) and in concentration of 200-400 mmol/L*

Hypocalcemia
Definition: corrected Ca < 2.0 Clinical manifestation when Ca < 1.5 Symptoms: Paresthesia, cramp, weakness, confusion, seizure Sign: increase DTR, chvosteks sign, Trouseaus sign, prolonged QT, T wave inversion, VF

Causes

Management
1. Acute symptomatic
10-20cc 10% calcium gluconate over 10 min followed by infusion at 0.5-2mg/kg/hr* Avoid recurrent symptomatic hypocalcemia & maintain calcium at 2-2.25 mmol/l Treat hypomagnesium Cardiac monitoring

2. Long term Oral calcium supplement i.e calcium lactate Vitamin D i.e calcitriol, alfacalcidol

Hypercalcemia
Definition: Ionized Ca > 2.7 mmol/l Symptoms: depression, confusion, stupor, coma, polyuria, polydipsia, nausea, vomitting, abdominal pain, constipation. Sign: QT interval, prolonged PR and QRS intervals, increased QRS voltage, T-wave flattening and widening and AV block.

Causes

Management
Rehydration! Steroids Calcitonin Biphosponates Mithramycin Dialysis

Hypermagnesium
Symptoms: (nause, vomiting, weakness, lethargy, hypotension and cardiac arrest Sign: reduce tendon reflex, ECG changes are similar to thoseseen with hyperkalemia.

Causes
Rare Renal failure with concomittant ingestion of magnesium-containing preparation (antacid & laxative) Total Parenteral Nutrition

Management

Hypomagnisium
Symptoms: delirium seizure Sign: similar to calcium deficiency, including hyperactive reflexes, muscle tremors, and tetany with a positive Chvosteks sign. ECG changes include:prolonged QT and PR intervals, ST-segment depression, flattening or inversion of P waves, Torsades de pointes, and arrhythmias

Causes
Poor intake (starvation, alcoholism, prolonged use of intravenous fluids, and total parenteral nutrition) Renal loss (alcohol, most diuretics, and amphotericin B), GI losses (diarrhea), malabsorption, acute pancreatitis, diabetic ketoacidosis, and primary aldosteronism.

Management
Mild or chronic hypomagnesium
Oral elemental magnesium of 240 mg od-bd A/e: diarrhea

Severe hypomagnesium
Iv magnesium comes in 49.3% 5ml solution (2.47g/5ml) 1-2 g magnesium sulphate over 15 min (MgSo4 at 25-30 mg/kg dilute in normal saline) Then maintain similar dose given in 4-8 hours for a day Monitor Mg, Ca,

Special Surgical Consideration


SIADH Diabetis insipidus Cerebral salt wasting Re-feeding syndrome Malignancy

SIADH
Inclusive criteria:
Plasma Na < 130 mmol/L Plasma osmolality <275 mOsml/kg Urine Na > 20 mmol/L Urine osmolality > plasma osmolality No sign of overload Normal renal, thyroid adrenal function

Refeeding syndrome
Occurs in severely malnourished patient Rapid nutritional repletion leads to:
Severe fluid and electrolytes disturbances Dextrose infusion leads to surge of insulin then leads to K and phosphorus intracellular shift respiratory failure and cardiac decompensation death

Cerebral Salt Wasting Syndrome


CSWS is a volume depleted state with negative Na balance secondary to primary natriuresis As in SIADH, CSWS is common in intracranial disease. Presentation & ix may overlap Treatment - fluid administration to achieve normovolemia

Fluid

Glucose (g)

Na (mmol/l)

K (mmol/l)

Cl (mmol/l)

HCO3 (mmol/l)

Osmolali ty (mOsmol /l)


252 505 2525 154 308 329 406 272 524 330 330

Cal (Kcal/l)

D5% D10% D50% 0.45% NS NS D5/0.22NS D5/NS LR D5/LR ALBUMIN (5%) ALBUMIN (25%)

50 100 500 0 0 50 50 0 50 0 0

0 0 0 77 154 38 154 130 130 145 145

0 0 0 0 0 0 0 4 4 0 0

0 0 0 77 154 38 154 110 110 145 145

0 0 0 0 0 0 0 27 27 0 0

200 400 2000 0 0 200 200 <10 210 200 1000

References
Schwartz Manual of Surgery; 8th edition (2008) Tintinalli Emergency Medicine; 6th Edition Sarawak Handbook of Emergency Medicine; 2nd edition Emergency Medicine (Facts). International Version (2001) Emedicine.medscape.com

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