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Fluid and Electrolytes. FLUIDS. Fluid homeostasis. Fluid homeostasis is dependent on Basal Inputs Vs. Outputs Our ability during pathologic processes to control Fluid loss Accounting for maintenance fluids Replacing ongoing loss Normal total body water - PowerPoint PPT Presentation
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FLUID AND ELECTROLYTES
FLUIDS
Fluid homeostasis Fluid homeostasis is dependent on
Basal Inputs Vs. Outputs Our ability during pathologic processes to control
Fluid loss Accounting for maintenance fluids Replacing ongoing loss
Normal total body water It is also important to define what we mean by
fluid? Water Vs. Volume Blood
Basal Input Vs. Output
INPUTOral intake ~ 2.5LMetabolic input ~ 200mls
OUTPUTUrine 0.52ml/kg/hourIL insensible loss
Assessing fluid balance Assessing fluid balance is SIMPLE Be calculated and use all the tools
available to you General inspection Physical examination Adjuncts to the physical exam – daily
weighs, inputs vs. outputs Biochemistry
Assessing fluid balance General
inspection Does the patient
look well? Sunken eyes Kussmaul
breathing Conscious state IV
lines/catheter/NIBP/ CVP….
Physical examination Vital signs
BP + Postural HR RR SaO2
JVP – Efficacy? Peripheral
oedema Pulmonary
oedema Cap refill
Assessing fluid balance Adjuncts
Daily weighs Assumes weight
change is due to water change
Inputs Vs. Outputs Oral/Parenteral
Vs. Urine/Faeces/Vomitus/Drain outputs
Biochemistry BUN:Creat ratio
Indicative of pre-renal dysfunction
Sodium Can be used to assess
total body water deficit/surplus
Based on normal TBW Males 0.6% TB weight Females 0.5% TB weight
Contraction alkalosis ?Lactate?
In summary General inspection Physical examination Adjuncts to the exam Biochemistry
So after making you assessment what do you do?
FIRST Don’t meddle too much! Part of your assessment involves knowing when not to do anything Is the process self-resolving/can it be
treated by minimal input from yourself? Is the patient DRY? Give them
appropriate fluid Is the patient WET? restrict
input/remove fluid Why are they dry/wet? How do we fix
this process?
The DRY patient
The DRY patient What has made them dry as compared
to baseline? Reduced intake Fluid loss
Two fluid rules of general medicine (geriatrics) When the elderly become sick, they don’t
drink When they drink, they drink copious
amounts of tea
Causes of fluid loss in the surgical patient
Fasting with inadequate replacement Bowel prep Pre/intra/post operative bleeding Inappropriate post-operative hydration Drains Organ specific
GI – vomiting/diarrhoea/sequestration/NG aspirates/stoma loss
Urology – Post-obstructive diuresis Neuro – Cerebral salt-wasting syndrome
Over-diuresis
Managing the fluid deficit patient; Fluid resuscitation
Replace losses bring the patient to euvolaemia Based on weight Fluid balance charts, estimated blood loss
etc… Biochemistry (will touch on this later)
Ensure adequate maintenance fluids ~ 2.5/3L/day
Replace ongoing losses Look at drains Urine output ANY recordable ongoing output
Sometimes a fluid challenge is the best way to test if someone is DRY
Patients will not shatter, patients will not break
Be calculated and make a calculated decision
Fluid resuscitation in the shocked patient
Primary survey Large bore IV canulas 20ml/kg bolus
500ml/1L bolus take into account left ventricular function
Re-assess fluid status post resuscitation to assess further need for resusc.
Estimating blood loss Total blood volume
66ml/Kg for males, 60mL/Kg for females Class 1 <15%
Minimal signs due to transcapillary refill Class 2 15%-30%
Orthostatic changes in HR/BP, some drop in U/O. Systemic vasoconstriction in play
Class 3 30% - 40% Hypotension, low U/O, tachycardia, loss of systemic
vasoconstriction Class 4 >40%
U/O<5ml/hr, profound shock When do I give blood? Acute phase vs. Delayed phase loss Triggers? HCT? ScvO2?
FIX THE CAUSE Large drain outputs Massive haemorrhage Etc… Fluid will not always save the day Never delay definitive treatment if it is
indicated.
How do I give this patient fluid? Oral IV Central line
What type of fluid do I use? Depends on what you are trying to achieve Increasing total body water?
5% dextrose of 4% Dex and 1/5th N/S Increasing total body volume?
Crystalloids/Colloids Replacing blood loss
Blood Augmenting cardiac ouput? In the acidotic patient?
Just to clarify Crystalloids
N/S, hartmann’s, 4% and 1/5th
Based on osmalarity 2/3rd will redistribute into the extravascular space so don’t get excited when your patient’s BP bumps up 5 mins after a fluid bolus!
Colloids Gelofusine, albumin etc... Theoretically to stay in the intravascular
space…but for how long?
The WET patient
The WET patient The WET patient
Too much input Not enough output
OR the fluid is just in the wrong place Distributive shock Crystalloid resuscitation Increased hydrostatic pressure with venous
congestion Decreased colloid oncotic pressure
Treating the wet patient Do you need to? How much fluid O/L is
tolerable? Is this process unlikely to resolve? Is the fluid load going to cause harm to the
patient in the short term? How to treat the wet patient
Fix the underlying cause Fluid restriction Diuresis Physically removing the fluid paracentesis
QUESTIONS?
ELECTROLYTES
So many electrolytes, so little time…
Hypernatraemia Hyponatraemia Hyperkalaemia Hypokalaemia
Hypernatraemia Can be due to Conn’s syndrome or excessive
salt intake (sodium bicarbonate use etc…) But… Almost always water depletion Treatment?
Calculate water deficit cTBW x Current sodium = nTBW x normal sodium nTBW = 0.6 x weight or 0.5 x weight
Replace water deficit BD UEC’s to drop sodium by 0.5mmol/L/hour or
~10mmol sodium/day to prevent cerebral oedema
Hyponatraemia Can occur in a
Hypovolaemic state Euvolaemic state Hypervolaemic state
Do a fluid assessment Do the appropriate investigations
Evaluating hyponatraemia Hypovolaemic
Urinary sodium <20: Diarrhoea with Na loss and renal reabsorption >20: Diuresis, Addison’s disease
Euvolaemic Urinary osmolality (must compare to serum osmolality)
>100: SIADH <100: Psychogenic polydipsia
Hypervolaemic Urinary sodium
>20: Renal failure <20: Heart failure
Correcting hyponatraemia Fluid restriction<urine output If Na change rapid, correct rapidly
Or correct rapidly within limits if patient symptomatic If slow correct slowly ?Sodium replacement?
Sodium deficit = nTBW x (130 – Current Plasma Na) 3% sodium chloride contains 513 mEq of Na/L
Eg. 60kg woman with plasma Na 120 Deficit = 0.5 x 60 x (130-120) = 300mEq 300/513 = 585mL of hypertonic saline Max rate correction of 0.5mmol/L/hr to prevent CPM
Hypokalaemia Causes
Transcellular shift Potassium depletion
Renal loss – diuretics, magnesium depletion (impaired K reabsorption) Extrarenal loss – Diarrhoea
Treatment 10% total body loss for each 1 mEq decrease CHLORVESCENT Slow K/IVT for longer term replacement (diuretics etc…)
Should we be scared of hypokalaemia? It does not in itself produce serious ventricular cardiac
arrhythmias but DOES increase arrhythmogenic potential of associated conditions (magnesium depletion, digitalis, myocardial ischaemia)
Biochemistry to diagnose hypokalaemia
Urine potassium High >30mEq – renal loss
Cl >25mEq – diuretics, Mg depletion Cl <15mEg – Ng drainage, alkalosis
Low <30mEq Diarrhoea
Hyperkalaemia Causes
Pseudohyperkalaemia – beware the 23g needle
Impaired excretion Adrenal insufficiency, drugs (ACEi’s,
spironolactone, NSAIDs) Transcellular shift
Acidosis, rhabdo, drugs (B-blockers, digitalis) Clinical manifestations
ECG changes ~ serum K of 6, definitely at 8
Hyperkalaemia - treatment Treatment
Repeat bloods ECG and monitoring Membrane antagonism
Calcium gluconate Vs. Calcium chloride(x3) Transcellular shift
Insulin/dextrose B-agonists Sodium Bicarbonate
Enhanced clearance Resins Diuretics Haemodialysis
END