2Table of contents Basic physiology Peri-operative fluid management Identification and management of hypovolaemic shockBlood administration and associated complications
3Basic physiologyBody water: the sum of intracellular water and extracellular water (volume); about 60% of body weight.
4TBW as % of Total body weight Basic PhysiologyTBW variations with ageAgeTBW as % of Total body weightNeonate806 months701 year60Young adultElderly50
5Basic physiology Total body water 45 L Extracellular fluid 15L Intracellular fluid 30 LPlasma 3.5LInterstitial fluid 10LTranscellular fluid 1.5 L
6How does fluids move between compartments? The Cell membraneMovement 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.
7The Capillary wallMovement 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.
8Fluid 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.
9Intake and output in 24 hours in average adult Drinking 1500mlUrine 1500 mlEating 750 mlGastrointestinal 200 mlSkin (sweat) 400 mlMetabolism 250 mlRespiratory 400 mlTotal 2500 ml
10What 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 endotheliumHypo- and hypervolaemia both causes release of atrial natriuretic peptide, which damages the glycocalyx and leads to interstitial oedema.
11Intraoperative 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.
12Modern 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.
13Fluid management in hypovolaemic shock Definition of shock: Abnormality of circulatory system that leads to inadequate organ perfusion and tissue oxygenation.
14THE DIAGNOSIS OF SHOCK IS A CLINICAL DIAGNOSIS! Recognition of shockTachycardia 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 shockDo 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!
15Classification 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>140Blood pressureNormalDecreasedPulse pressureRespiration frequency14-2020-3030-40>40Urine output (ml/hour)>305-15< 5CNSAgitatedAnxiousConfusedDrowsy
16Management of hypovolaemic shock Goals of management: To restore intravascular volume and tissue oxygenation.Initial management: Airway Breathing Circulation Disability ExposureAlways approach your resuscitative efforts in a trauma in this order. Do NOT jump to the step you think is the most important!!
17CirculationIdentify 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 indicatedVasopressors are contraindicated in hypovolaemic shock, as it can worsen tissue perfusion.
18Reassess 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.
19Transient 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.
20Non responders:Surgical management of hemorrhage is indicated.Blood transfusion needed.Look for non-hemorrhagic causes of shock.
21Blood transfusion Blood volumes of different age groups Neonates Blood volumes of different age groupsNeonates- Prem- Term95ml/kg85ml/kgInfants80ml/kgAdults- Men- Women75ml/kg65ml/kg
221 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.
23Fresh frozen PlasmaIndications of FFP’s - Treatment of isolated factor deficiency - Reversal of warfarin therapy - Correction of coagulopathy1 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
24Platelets <50 000: increased chance of bleeding intraoperatively Each unit of platelets will increase platelet count by 5000 – 10000Transfused platelets will usually survive 1-7 days.
25Complications of Blood transfusions ImmuneHemolytic immune mediated reactionsAcute: 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
26Non hemolytic immune mediated reactions Febrile reactions: 1-3% of transfusionsUtricarial and anaphylactic reactionsTRALI (transfusion related acute lung injury)Graft versus host diseasePost transfusion purpuraImmune suppression
27Non-immuneInfections : Viral infections like HIV, EBV, CMV and hepatitis.Parasitic infections like malaria, toxoplamosis and chaga’s diseaseGram positive infections like staphs and streps.
28Massive blood transfusions CoagulopathyCitrate toxicityHypothermiaDisturbance in the acid-base balance2,3 DPG deficiencyHyperkalaemia