Presentation on theme: "Fluids and Anaesthesia. Table of contents Basic physiology Peri-operative fluid management Identification and management of hypovolaemic shock Blood administration."— Presentation transcript:
Fluids and Anaesthesia
Table of contents Basic physiology Peri-operative fluid management Identification and management of hypovolaemic shock Blood administration and associated complications
Basic physiology Body water: the sum of intracellular water and extracellular water (volume); about 60% of body weight.
Basic Physiology TBW variations with age AgeTBW as % of Total body weight Neonate80 6 months70 1 year60 Young adult60 Elderly50
Basic physiology Total body water 45 L Extracellular fluid 15L Plasma 3.5L Intracellular fluid 30 L Interstitial fluid 10L Transcellular fluid 1.5 L
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.
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.
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.
Intake and output in 24 hours in average adult IntakeOutput Drinking 1500mlUrine 1500 ml Eating 750 mlGastrointestinal 200 ml Skin (sweat) 400 ml Metabolism 250 ml Respiratory 400 ml Total 2500 ml
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.
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.
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.
Fluid management in hypovolaemic shock Definition of shock: Abnormality of circulatory system that leads to inadequate organ perfusion and tissue oxygenation.
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!
Classification of hypovolaemic shock based on symptoms Class 1Class 2Class 3Class 4 Blood loss (ml);% CV (70 kg adult) < 750 < 15% – 30% – 40% >2000 > 40% Heart rate< 100>100>120>140 Blood pressureNormal Decreased Pulse pressureNormalDecreased Respiration frequency >40 Urine output (ml/hour) > < 5 CNSAgitatedAnxiousConfusedDrowsy
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!!
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.
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.
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.
Non responders: Surgical management of hemorrhage is indicated. Blood transfusion needed. Look for non-hemorrhagic causes of shock.
Blood transfusion Blood volumes of different age groups Neonates - Prem - Term 95ml/kg 85ml/kg Infants80ml/kg Adults - Men - Women 75ml/kg 65ml/kg
1 Unit of Red Blood cells will increase hb by 1g/dL and hct by 2 – 3%. Remember to warm blood > 37ᵒC.
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
Platelets <50 000: increased chance of bleeding intraoperatively Each unit of platelets will increase platelet count by 5000 – Transfused platelets will usually survive 1-7 days.
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
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
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.
Massive blood transfusions Coagulopathy Citrate toxicity Hypothermia Disturbance in the acid-base balance 2,3 DPG deficiency Hyperkalaemia