1. Fluids and Anaesthesia

2. Table of contents Basic physiology Peri-operative fluid management
Identification and management of hypovolaemic shock
Blood administration and associated complications

3. Basic physiology
Body water: the sum of intracellular water and extracellular water (volume); about 60% of body weight.

4. TBW as % of Total body weight
Basic Physiology
TBW variations with age
Age
TBW as % of Total body weight
Neonate 80
6 months 70
1 year 60
Young adult
Elderly 50

5. Basic physiology Total body water 45 L Extracellular fluid 15L
Intracellular fluid 30 L
Plasma 3.5L
Interstitial fluid 10L
Transcellular fluid 1.5 L

6. How does fluids move between compartments?
The Cell membrane
Movement of solutes across this membrane is via trans-membrane proteins or ion channels.
For water to move between them there must be a difference in the tonicity.
Any change in the ECF or ICF tonicity is caused by a change in the solute concentration. Water then moves passively by osmosis.
The cell membrane is effectively impermeable to Na+ ions. It is the Na+ concentration that effectively governs the distribution of water between ECF and ICF.
Extracellular fluid Na+ concentration is controlled by the kidneys under various neuroendocrine controls. Any net movement of fluid between two compartments can be in either direction depending on the balance of forces.

7. The Capillary wall
Movement of water and solutes across this membrane is largely passive as a result of either filtration or simple diffusion. Filtration results from the balance of Starling forces acting to drive water out of the capillary into the interstitium and in the process taking dissolved solutes with it. Simple diffusion is the movement of solutes from an area of high concentration to an area of lower concentration.
The water crosses the capillary wall via the gaps between cells or directly through the cell membrane.

8. Fluid movement across the capillary
endothelium can be classified into two types:
Type 1 (physiological) occurs continuously with and intact vascular barrier and is returned to the vascular compartment via the lymphatic system, thus avoiding interstitial oedema.
Type 2 (pathological) occurs when the vascular barrier becomes compromised, allowing excessive fluid accumulation leading to oedema.

9. Intake and output in 24 hours in average adult
Drinking 1500ml
Urine 1500 ml
Eating 750 ml
Gastrointestinal 200 ml
Skin (sweat) 400 ml
Metabolism 250 ml
Respiratory 400 ml
Total 2500 ml

10. What is the glycocalyx and why is it important?
The glycocalyx is composed of membrane-bound glycoproteins and proteoglycans and contains glycosaminoglycans. This provides a first line barrier to regulating cellular and macromolecule transport at the endothelium
Hypo- and hypervolaemia both causes release of atrial natriuretic peptide, which damages the glycocalyx and leads to interstitial oedema.

11. Intraoperative fluid management
The aim of intraoperative fluid therapy is to maintain adequate circulating volume and to ensure end-organ perfusion and oxygen delivery to the tissues.
Research has now shown that the aggressive replacement of insensible losses, hypovolaemia due to “prolonged fasting” and “third space” losses is outdated and no longer relevant.
Fluid loading has no influence on anaesthesia-related hypotension and this should rather be treated with vasopressors. Large volume fluid loading is contraindicated as it can lead to hypervolaemia and damage to the glycocalyx, leading to interstitial oedema.

12. Modern evidence-based practice suggests:
Low risk patient undergoing low risk surgery – high volume crystalloid infusions of 20-30ml/kg improves outcomes such as pain, nausea and dizziness.
High risk patients undergoing major surgery one should adjust your fluid regimen to keep the intraoperative urine output between 0.5 – 1.0ml/kg/h.
If possible, one can practice goal directed fluid therapy by using esophageal doppler to measure the blood flow in the descending aorta.

13. Fluid management in hypovolaemic shock
Definition of shock: Abnormality of circulatory system that leads to inadequate organ perfusion and tissue oxygenation.

14. THE DIAGNOSIS OF SHOCK IS A CLINICAL DIAGNOSIS!
Recognition of shock
Tachycardia usually the first measurable sign.
Focus on the patient’s pulse rate and character, respiratory rate, skin colour and pulse pressure A narrow pulse pressure indicates hypovolaemic shock
Do NOT rely on systolic BP – usually a late sign when the patient has already lost >30% of blood volume.
Do NOT rely on laboratory investigations to diagnose hypovolaemic shock – lab results can be unreliable in the presence of massive blood loss – normal hct does NOT exclude massive blood loss.
Lactate and base excess can be useful in monitoring response of hypovolaemia to treatment.
THE DIAGNOSIS OF SHOCK IS A CLINICAL DIAGNOSIS!

15. Classification of hypovolaemic shock based on symptoms
Blood loss (ml);% CV (70 kg adult)
< 750
< 15%
15 – 30%
30 – 40%
>2000
> 40%
Heart rate
< 100
>100
>120
>140
Blood pressure
Normal
Decreased
Pulse pressure
Respiration frequency
14-20
20-30
30-40
>40
Urine output (ml/hour)
>30
5-15
< 5
CNS
Agitated
Anxious
Confused
Drowsy

16. Management of hypovolaemic shock
Goals of management: To restore intravascular volume and tissue oxygenation.
Initial management: Airway Breathing Circulation Disability Exposure
Always approach your resuscitative efforts in a trauma in this order. Do NOT jump to the step you think is the most important!!

17. Circulation
Identify the cause of hemorrhage. Remember “4 and on the floor” – chest, abdomen, pelvis and long bones.
2 large bore IV lines >18G IV lines. Take blood for electrolyte studies, ABG, toxicology and crossmatch. Insert urinary catheter and NG tube to monitor resus.
Give warm isotonic fluids: 1-2L of ringers’ lactate in adults and 10-20ml/kg in children.
If patient doesn’t respond fluid management - surgical control of hemorrhage is indicated
Vasopressors are contraindicated in hypovolaemic shock, as it can worsen tissue perfusion.

18. Reassess patient continuously
Reassess patient continuously. Ask yourself: is the patient responding to fluid resus?
Rapid responders:
Responds to initial fluid therapy.
Usually <20% of blood volume lost.
Blood transfusion usually not necessary, but keep crossmatch on standby.

19. Transient responders:
Patients initially respond to fluid therapy, but then deteriorate again.
Usually 20 – 40% of blood volume is lost.
Blood transfusion probably needed.
Reassess your patient and look for other causes of hemorrhage.
Initiate definitive control of hemorrhage.

20. Non responders:
Surgical management of hemorrhage is indicated.
Blood transfusion needed.
Look for non-hemorrhagic causes of shock.

21. Blood transfusion Blood volumes of different age groups Neonates
Blood volumes of different age groups
Neonates
- Prem
- Term
95ml/kg
85ml/kg
Infants
80ml/kg
Adults
- Men
- Women
75ml/kg
65ml/kg

22. 1 Unit of Red Blood cells will increase hb by 1g/dL and hct by 2 – 3%
1 Unit of Red Blood cells will increase hb by 1g/dL and hct by 2 – 3%. Remember to warm blood > 37ᵒC. 

23. Fresh frozen Plasma
Indications of FFP’s - Treatment of isolated factor deficiency - Reversal of warfarin therapy - Correction of coagulopathy
1 unit of FFP’s will increase the level of all clotting factors by 2-3%
Usual dose 10-15ml/kg, remember to warm to > 37ᵒC

24. Platelets <50 000: increased chance of bleeding intraoperatively
Each unit of platelets will increase platelet count by 5000 – 10000
Transfused platelets will usually survive 1-7 days.

25. Complications of Blood transfusions
Immune
Hemolytic immune mediated reactions
Acute: Usually due to an ABO incompatibility. Patient presents with fever, chills, chest and/or flank pain, tachycardia. DIC and shock can rapidly develop.
Management Stop the transfusion immediately. Recheck the unit transfused. Take blood for FBC, crossmatch, coagulation studies Insert a urinary catheter and test for hb in the urine and induce osmotic diuresis. Supportive management: Low dose dopamine to maintain BP and cardiac output.
Delayed: Usually mild. Develops 2-21 days post transfusion. Patient may present with malaise, fever or jaundice. Treatment is supportive

26. Non hemolytic immune mediated reactions
Febrile reactions: 1-3% of transfusions
Utricarial and anaphylactic reactions
TRALI (transfusion related acute lung injury)
Graft versus host disease
Post transfusion purpura
Immune suppression

27. Non-immune
Infections : Viral infections like HIV, EBV, CMV and hepatitis.
Parasitic infections like malaria, toxoplamosis and chaga’s disease
Gram positive infections like staphs and streps.

28. Massive blood transfusions
Coagulopathy
Citrate toxicity
Hypothermia
Disturbance in the acid-base balance
2,3 DPG deficiency
Hyperkalaemia