Calculation of fluid rates Flashcards
What are considered “insensible losses” for maintanence
- faeces
- urine
- resp tract evaporation
- skin (less so)
How are maintanence rates roughly calculated ( learn equations)
- (BW x 30) +70 ( 2 - 50kg)
- (BW^0.75) x70 (<2 or >50kg)
How is fluid deficit calculated
- Fluid deficit (ml) = %dehydration (decimel) x BW x 1000
usually replaced over 6 - 24hr
how are fluids discontinued/why
- Should be gradually weaned over 12 - 24hrs, especailly if were at a high rate.
- Fluids can cause medullary solute washout and impair renal concentrationg ability for up to 24hr
What routes are availible for fluid admin
- enteral: by mouth or feeding tube (preferred in stable)
- Parental: intravenous, intraosseous, s/c/ peritoneal
- Peritoneal not recommended due to peritonitis risk. S/c unpredictable absorption in the critically ill
What is the dose for s/c fluids
10 - 20ml/kg: divided over 1 or more sites
What are suggested starting surgical fluid rates?
- 5ml/kg dog 3ml/kg cat.
- can try reducing by 25% each hour until maintanence in longer GA on stable patient.
How would you intially approach hypotension under GA
- 3/10m/kg crystalloid bolus and reassess.
- start pressors if 2 - 3 boluses inadequate.
- check electrolytes and acid/base
What is the target for fluid resusitation in TBI
- MAP 100mmHg
- often hypovolaemic and hypotension is associated with worse outcomes.
What are the most appropriate fluid choices for TBI
- 0.9% saline as has the lowest free water of the isotonics (least likely to exacerbate cerebral oedema)
- hyper osmotic agents (HTS or mannitol) if evidence of increased ICP
What would be an appropriate initial fluid strategy for a patient with TBI and increased intracranial pressure
- 3 - 5ml/kg bolus of hypertonic saline followed by 0.9% saline.
- if there are still signs if increased ICP can give 0.5g/kg mannitol if not hypotensive
What are the considerations for fluid use in chronic hypoalbuminaemia
- may not need IVFT if stable. use minimal possible.
- when COP reduces slowly osmotic gradient between intravascular and interstitum is preserved.
- try and deal with underlying cause
Describe why cerebral oedema can be a complication of treatment for hypernatraemia.
- hypernatraemia increases extracellular osmolality
- intracellular water moves out causing cell shrink
- cells produce indigenic osmoles to increase their osmolality as protection against this.
- if NA falls quickly with treatment there is a relative intracellular hyperosmolality.
- free water moves into cells causing oedema (especially CNS)
How do you calculate the free water deficit
Deficit (l) = ((patient Na/normal na) -1) x (0.6 x BW)
how quickly should hypernatraemia be corrected
maximum 0.5meq/hr in chronic and 1meq/hr in acute
What causes CNS complications with rapid correction of hyponatraemia
- cells reduce numbers of idiogenic osmoles when extracellular space is hypoosmolar to maintain gradient.
- rapid correction results in a hyperosmolar EC space, water moves out of cells = shrinkage.
- causes myelinolysis leading to severe, delayed neuro signs (ataxia, coma, death)
when is it appropriate to correct hyponatraemia quickly
Na <120mmol/l (rapidly correct until at least this level and then slow)
What conditions predispose to fluid overload
- cardiac disease
- pulomnary disease
- oliguria (AKI)
- hypoproteinaemia
What clinical signs could occure with fluid overload
- harsh lung sounds (crackles)
- serous nasal discharge.
- chemosis.
- pitting oedema
- julular distension
- increasing BW
- cats new onset gallop
- (use pocus)
What action is taken if fluid overload due to IVFT is suspected?
- Immediately stop fluids
- supplement O2 if tachypnoeic, dyspnoeic or low SPo2
- if cardiac disease a feature or oliguric with some renal reserve 1mg/kg fruesmide may help.
What is the thinking with limited volume resusitation
- small folmes administered aiming for a MAP of 60mmhg (ie just enough to perfuse vital organs)
- used in patients with uncontrolled haemorrhage
- agressive fluids dilute clotting factors and increased BP may “pop the clot”
What other factors other than overload and coagulopathy should you mention in a question on fluid complications
catheter complications and electrolyte abnormalities
