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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
8/3/2019 Discuss Principles of Fluid and Electrolyte Inthe Surgical Patient
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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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Distribution of body water
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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Distribution of body water
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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Respiratory Acidosis
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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Respiratory Acidosis
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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Intraoperative fluidtherapy
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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Intraoperative fluidtherapy
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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