Discuss Principles of Fluid and Electrolyte Inthe Surgical Patient

8/3/2019 Discuss Principles of Fluid and Electrolyte Inthe Surgical Patient

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scuss pr nc p es o uand electrolyte

management of thesurgical patientPresenter Dr Bashiru AminuModerator Dr Bello


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outline

IntroductionAnatomy and physiology

distribution

Classification of body fluidchanges

Fluid therapy

-preoperative

-intraoperative

-postoperative

Complications


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Introduction

Fluid and electrolyte management

Important part of the perioperativemanagement of the surgical patient

Critical factor in some patients as aresult of the response to surgery andtrauma

Understanding of the metabolism of

these fluid and electrolyte is essentialto the care of surgical patients


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Distribution of body water

Water half of adults body

TBW 60% of body weight (young men)

50% of body weight (young

womenand older men)

45% of body weight (olderwomen)

TBW

Intracellular of TBW

Extracellular of TBW


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Extracellular fluid (ECF)Intravascular 4% of body weight

(men)

ExtravascularInterstitial 15% of body weight

Transcellular 1% of body weight

Transcellular fluid bone, dense CT, GITsecretions, CSF, synovial fluid, etc.


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TBW is less in obese patients fatcontent

TBW is less in females relativelysmaller muscle mass and higher fatdeposits

In Children

TBW 75 80% at birth, decreases

steadily to 65% at 1yrECF 35% at birth, decreases to 20%

at 2yrs

ICF changes minimally


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Electrolyte distribution in bodyfluids

Difference in ionic composition ofICF and ECF due to the cell

membrane semi permeable

Effective osmotic pressurecontributed to by any substancethat does not freely traverse thecell membrane


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fluidsIon Intravascular

mmol/LInterstitialmmol/L

Intracellularmmol/L

Na 140 143 8

K 4 4 140

Ca2+ 1.25 0.625 1

Mg 0.7 0.9 0.75 15Cl 95 105 115 8

HCO3- 24 27 30 14

PO43- 0.8 1.4 1.6 25.8

Protein 2 0 9

SO42- 1 1 20

Organic acids 3 3 -


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Osmolality

ECF and ICF contain different types ofsolute but conc. of solutes inside andoutside the cells are equal

Concentration difference exists onlytransiently because they create anextremely strong force for watermovement across cell membranes

Osmolality no of milliosmoles ofsolute particles per litre of solution


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Osmolality

Sodium salts, glucose and urea responsible for most of the solute particlesin the ECF

Measurement osmometer

Plasma osmolality

Posm = 2 X Plasma Na+ + Glucose +BUN

18 2.8

2 no of anions accompanying Na+

18 and 2.8 correction factors in convertingGlucose and Urea conc. from mg/dl to mmol/L


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Body fluid changes

Classified into three groupsDisturbances ofvolume due toloss or addition of isotonic salt

solutionDisturbances ofconcentration due to addition or loss of waterfrom the ECF or depletion of Na+

from the ECFDisturbances ofcomposition:Acid base balance


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Volume changes

- Excess or deficit of ECF volume canbe diagnosed by estimating the bloodurea nitrogen (BUN)

- BUN rises with sufficient ECF deficit- Concentration of blood cells and

plasma proteins increases with ECFdeficit and decreases with ECF excess

- Concentration of Na+ is not relatedto the volume status of the ECF


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Volume changes

ECF volume deficit is the most common

fluiddisorder in surgical patients.Seen in :Losses from the GIT due to vomiting,

NG suction, diarrhoea and fistuladrainageSequestration of fluid in soft tissue

injuries and infectionsIntra-abdominal and retroperitoneal

inflammatory processesPeritonitis

Intestinal obstruction


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Volume changes

Severe volume depletiondepresses all body systems andinterferes with the clinical

evaluation of a patient.


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Concentration changes

Serum Na+ level is used to estimatetotal body fluid osmolality

Hypo- and hypernatraemia can bediagnosed clinically but the signs andsymptoms are not generally presentuntil derangement is severe.

With rapid rate of change, the signs

and symptoms tend to occur early andwith greater severity


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HyponatraemiaCharacterised by :

CNS signs of increased intracranialpressure and tissue signs ofexcessive intracellular water

Hypertension induced by the rise inICP BP usually returns to normalafter correction of Na+ level

With severe hyponatraemia rapiddevelopment of oliguric renal failure irreversible with delayed therapy.


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Potassium

Major cation of intracellular water 98% at concentration of 150mEq/L

Normal dietary intake 50-100mEq/day

Intracellular and extracellulardistribution influenced by manyfactors :

Release of significant amount fromintracellular space into theextracellular space in response to

severe injury, surgical stress, acidosis


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Hyperkalaemia

Signs limited to the CVS and GITGIT symptoms nausea,

vomiting, intermittent intestinal

colic and diarrhoeaCVS signs apparent on ECG

Tall peaked T waves

Widened QRS complex

Depressed ST segments


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Hyperkalaemia

Treatment- Withhold exogenously administeredK+

- Correct the underlying cause

- Iron exchange resins

- Dialysis when indicated

- Give HCO3- , glucose and insulin

-Give 1g of 10% calcium gluconateunder ECG monitoring to suppress themyocardial effects of K+ temporarily


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Hypokalaemia

Due to excessive renal excretion of K+Movement of K+ into the cells

Prolonged administration of K+ free

parenteral fluids with continuedobligatory renal loss of K+(>20mEq/day)

Parenteral nutrition with inadequate

K+ replacementLoss of GIT secretions


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Hypokalaemia

SignsFailure of normal contractility of

skeletal, smooth and cardiac musclesi.e. weakness leading to flaccidparalysis, diminished/absent tendonreflexes and paralytic ileus

ECG signs arrhythmias, low voltage

ECG, flat T waves and depressed STsegments


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Hypokalaemia

TreatmentPrevention i.e. replace GIT fluid

loss volume for volume

Give K+ not more than 40mEq/Lof fluid

Rate not exceeding 20mEq/hour

Dont give oliguric patients andwithin 24hrs post operatively


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Calcium

Majority of Calcium in the body is inthe form of PO43- and CO32-Normal daily intake : 1 3g/day 200mg excreted in the urine daily,

the rest is lost in the GITHalf of the serum calcium exists in

unionised form bound to plasmaproteins45% exists in ionised form and is

responsible for neuromuscular stability


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Calcium

Acidosis increases the ionised fractionwhile alkalosis decreases it

Disturbances of calcium metabolismare generally not problematic in thepostoperative patient

Therefore, routine administration ofCa2+ to the surgical patient is not

needed in the absence of specificindications


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Hypocalcaemia

Serum levels < 8mg/100mlFeatures

Circumoral numbness

Numbness of fingers and toes

Hyperactive tendon reflexes

+ve Chvosteks sign

Tetany, carpopedal spasms

Convulsions (with severe deficits) Prolonged Q-T interval on the ECG


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Hypocalcaemia

CausesAcute pancreatitisMassive soft tissue infections necrotising

fascitis

ARF and CRFPancreatic and small bowel fistulasHypoparathyroidism

Severe depletion of magnesiumGive Calcium salts gluconate and chloride IV ,

- lactate orally

Correct underlying cause and the deficit


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Hypercalcaemia

Symptoms Easy fatigability Lassitude Weakness Anorexia, nausea and vomiting Weight loss

In severe cases

- lassitude, somnambulism, stupor, coma- Headaches, skeletal pains, thirst,

polydipsia, polyuria


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Hypercalcaemia

CausesHyperparathyroidismCancer with bony metastasis e.g. Breast

Ca

TreatmentInorganic PO43- given IV/orally lowers

Ca2+ levelsLarge doses of furosemide

Prevention is the main treatment ofhypercalcaemia due to metastatic cancer Low calcium diet, adequate hydration to

promote urinary excretion of Ca2+


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Magnesium

Total body content 2000mEqHalf of this is in boneDistribution similar to potassium

mostly intracellularSerum concentration between

1.5 2.5mEq/LNormal dietary intake

20mEq/dayLargely excreted in the faeces


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Magnesium

DeficiencySeen in starvation, malabsorption

syndromes, GIT losses, parenteral

nutrition, acute pancreatitis, DKAduring treatment , primaryaldosteronism and chronicalcoholism

Symptoms and signs similar tohypocalcaemia


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Magnesium

TreatmentParenteral MgSO4 or MgCl2 solutionMonitor HR, BP, respiratory rate and

ECG with large doses

Never to be given in the phase ofoliguria or severe volume deficit toavoid toxicity

Excess rare but seen in renalinsufficiency

- Correct acidosis

- Correct pre existing ECF volume

deficit


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Acid Base Balance

Intracellular Buffers: Proteins

Extracellular Buffers:Bicarbonate

Carbonic acid

system


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Respiratory Acidosis

Caused by retention of CO2secondary to decreased alveolarventilation

Pco2 is elevated and plasmaHCO3- conc. is normal

Chronic respiratory acidosis -Pco2 , HCO3- with renal compensation


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CausesConditions causing inadequate

ventilation

Airway obstruction Pneumonia Atelectasis

Pleural effusion Hypoventilation due to pain ofabdominal incisions or abdominal

distension limiting diaphragmatic


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ManagementTake measures to ensure

adequate ventilation

Prompt correction of thepulmonary defect when feasible Head injury may worsen hypoxic

brain damage


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Respiratory Alkalosis

Causes hyperventilation due to Apprehension Pains Hypoxia CNS injury Assisted ventilation

They all cause rapid depression of the

arterial Pco2 and elevation of pH.Acute phase normal HCO3- conc.

Later HCO3- falls with renal

compensation


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Respiratory Alkalosis

ManagementMeasurement/monitoring of blood

gasesAppropriate corrections of ventilatory

pattern when indicatedSevere and persistent respiratory

alkalosis difficult to correct and has

poor prognosis because of theunderlying cause hyperventilationfrom intracranial injuryTreatment directed towards the underlying

cause


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Metabolic Acidosis

Due to retention or production ofacids or loss of HCO3-Causes any condition causing

elevated anion gap Shock or inadequate tissue perfusion Starvation Alcohol intoxication Renal failure Uraemia Aspirin poisoning


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Metabolic Acidosis

Most common cause of severemetabolic acidosis in surgical

patients is acute circulatoryfailure with accumulation of lacticacid


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Metabolic Acidosis

TreatmentDirected towards correcting the

underlying causeReserve HCO3- therapy for severe

metabolic acidosisDiscourage routine use of NaHCO3

during resuscitation of patients inhypovolaemic shock particularly after

cardiac arrestFrequent measurements of HCO3- and

blood pH are the best guides oftherapy.


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Metabolic Alkalosis

Results from the loss of fixedacids or gain of HCO3- and is

aggravated by any existing K+deficit.

Respiratory compensation is

small but compensation isgenerally through the renalmechanisms.


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Metabolic Alkalosis

Caused by persistent vomiting asseen in gastric outlet obstruction

and intestinal obstruction as wellas in prolonged nasogastricdrainage

Fl id


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FluidConsumption/Production

ProductionAverage 2,000 2,500mls/dayOrally 1,500mls

The rest from food

Daily fluid losses Stool 250mls Urine 800 1,500mls

Insensible losses (skin, lungs): 600 900mlsIncreases with increased environmental

temperature 250mls/C rise/day

Fl id d El t l t


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Fluid and ElectrolyteTherapyParenteral solutions Vary in composition to satisfy various

fluid requirements in the surgicalpatient.

Given a situation, a typical fluid willcorrect the abnormalities with minimaldemands on the kidneys.The choice of a particular fluid

depends on the volume status of thepatient and the type of concentrationor compositional abnormality present.

Fl id d El t l t


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Fluid and ElectrolyteTherapy

Ringers lactate - an ideal isotonicsolution/physiological fluid that is close tothe plasma compared to isotonic NaClwhose Cl- conc. is 154mEq/L and is higher

than the conc. in blood imposing anappreciable load on the kidneys of excessCl- that cant be excreted rapidly leadingto a dilutional acidosis.

Normal saline is however good for thecorrection of an ECF volume deficit in thepresence of hyponatraemia,

hypochloraemia and metabolic alkalosis.


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Preoperative fluid therapy

Preoperative and fluid correction an integral part of surgical care

Safe approach properunderstanding of fluiddisturbances associated with

surgical illness and adherence toguidelines


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Preoperative fluid therapy

Fluid replacement depends onexistence of concomitant

concentration and compositionalabnormalities

e.g Hypernatr. + Vol. deficit

dextroseHypernatr. + Vol. excess

restrict water

I t ti fl id


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Intraoperative fluidtherapy

Inadequate preoperative ECFVolume replacement can cause

hypotension under anaesthesia

Intraoperative correction of vol.deficit with a balanced salt

solution will remove postoperative salt intolerance

I t ti fl id


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Intraoperative fluidtherapyRoutes of intraoperative fluid losses

- Blood loss

- Oedema from extensive dissection

- Fluid collection within the lumen andwall

of small bowel

- Accumulation of fluid in the

peritonealcavity

- Fluid loss from the wound very

small

I t ti fl id


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The use of albumin solutions with

balanced salt solutions to replaceECF deficits during surgery is notnecessary and is potentially

harmful

Intraoperati e fl id


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Guidelines

- Blood should be replaced as

lost- Fluid replacement should begin

during

the operative procedure


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Postoperative therapy

Immediate postoperative period-Give fluid only after proper evaluation

-Correct existing deficit in addition to

maintenance as proper replacementduring this period will facilitate

subsequent fluid management

*Do not give potassium within the first24hrs after surgery unless there is adeficit

Postoperative fluid


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Postoperative fluidtherapy

Late postoperative period- There is a problem of accurate

measurement and replacement of alllosses during this postoperativeconvalescent phase

- Measure and replace sensible losses(from GIT)

- Estimate and replace insensible losses- Identify and correct any electrolyte deficit

andgive maintenance

Fl id and Electrol te


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Fluid and ElectrolyteManagement in Surgery

Fluid and Electrolytes in thePaediatric and Elderly patientsneed to be administered with

cautionEssential to the successful

management of fluid andelectrolyte abnormalities in themis adequate monitoring of theircardiopulmonary statusespecially the neonates


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complications


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Conclusion

Fluid and electrolytemanagement in surgical patientsposes a lot of challenges and

could make or mar the outcomeof an otherwise successfulsurgical care.

Active anticipation as well asprompt recognition andintervention of disorders is crucial


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Discuss Principles of Fluid and Electrolyte Inthe Surgical Patient

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