Fluid and Electrolytes

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