Goal-Directed Therapy for Shock PDF

GOAL DIRECTED THERAPY FOR THE MANAGEMENT OF SHOCK Andy Bell CP 3.14 Lecture 3 2023 1 ILOS Lecture Content ILOs  Recognise the major indications for fluid therapy and identify clinical cases where fluid therapy may be required  Design a fluid plan (including volume/rate/route & type) based on...

GOAL DIRECTED THERAPY FOR THE MANAGEMENT OF SHOCK Andy Bell CP 3.14 Lecture 3 2023 1 ILOS Lecture Content ILOs  Recognise the major indications for fluid therapy and identify clinical cases where fluid therapy may be required  Design a fluid plan (including volume/rate/route & type) based on a clinical evaluation of a patient in shock  Identify conditions/diseases which may give rise to shock and understand the rationale for treatment  Explain how monitoring of clinical signs, physiological and laboratory data assist in the diagnosis and treatment of shock  Recognise different fluid products and have a basic knowledge of their indications  Discuss common complications which may occur as a result of fluid therapy  Frontiers collection - https://www.frontiersin.org/articles/10.3389/fvets.2021.744080/full - Frontiers collection  www.aaha.org/public_documents/professional/guidelines/fluid_therapy_guidelines.pdf - 2013 Guidelines 2 FLUID COMPARTMENTS Intracellular Fluid Total Body Water (60% BW) Interstitial Fluid Extracellular Fluid Intravascular Fluid 3 MAJOR ELECTROLYTES Extracellular Fluid  Cations  Sodium  Anions Intracellular Fluid  Cations  Potassium  Anions  Chloride  Phosphate  Bicarbonate  Protein • Electrolytes are responsible for osmolarity of the fluid • ~300 mOsm/l in Dogs • ~310 mOsm/l in Cats 4 WHY GIVE FLUIDS? Dehydration Shock  Provide maintenance requirements  Treat electrolyte imbalances  Maintain oncotic pressure (Colloids)  Diuresis 5 DEHYDRATION  Is a deficit in total body water  Strictly refers to loss of water Ins Outs but often used clinically to refer to isotonic and hypotonic losses as well  Normal ‘Maintenance’ requirement is 50ml/kg/day for dogs and cats  This is probably an overestimation in large dogs and an underestimation in small dogs and cats! 6 DEHYDRATION Ins Outs  Due to  Low consumption  Pathological fluid losses  Clinical signs are of skin tenting, dry mucous membranes and sunken eyes  Treatment usually over 24-48 hours  More detail in Alimentary module 7 CIRCULATORY SHOCK  Defined as - A global energy deficit at a cellular level  High morbidity and mortality Shock condition  Presents as the final common pathway of a large number of critical patients Hypovolaemic Circulatory Hypoxic Cardiogenic Distributive (Metabolic) 8 HYPOVOLAEMIC SHOCK  Most common type of shock  Results from loss of intravascular volume  Dehydration (severe)  Blood loss  3rd spacing of fluids  Very common in trauma patients  Low preload reduces cardiac output 9 CARDIOGENIC SHOCK  Essentially this is a failure of the pump  Caused by  Heart disease  Cardiac tamponade  Arrhythmias  Must be differentiated from other types of shock as large volume fluid administration is contra-indicated  Signalment & History  Thoracic auscultation  Heart Murmurs  Pulmonary oedema heard as crackles  Ascites/jugular distention 10 DISTRIBUTIVE SHOCK  Cardiac function and blood volume are not affected but there is a failure of the vascular tree to allow appropriate delivery  Loss of vascular tone  Sepsis/Endotoxaemia  Anaphylaxis  Venous blockage of blood (Obstructive Shock)  GDV  Pulmonary thromboembolism 11 MANY PATIENTS FALL INTO MULTIPLE CLASSIFICATIONS Distributive GDV • Distended stomach limits venous return • Endotoxaemia causes vasodilation Hypovolaemic Cardiogenic • Vomiting • 3rd spacing of fluid into distended stomach • Bleeding from splenic rupture • Arrhythmias • Myocardial failure due to severe acidosis 12 CLINICAL SIGNS OF CLASSIC HYPOVOLAEMIC SHOCK  Clinical signs are a reflection of the animal trying to compensate 1. Tachycardia as part of the sympathetic response 2. Poor pulse quality due to vasoconstriction and lack of blood volume 3. Decreased extremity temperature 4. Pale mucous membranes 5. Prolonged capillary refill time 6. Decreased mentation due to inadequate brain perfusion 7. Tachypnoea to increase oxygen uptake (not always evident) 13 WHERE TO FEEL PULSES Auricular artery Lingual artery Brachial artery Femoral artery Coccygeal artery Dorsal pedal artery Metacarpal artery 14 HYPOVOLAEMIA IN DOGS Clinical Sign Mild/ Compensated Moderate Severe/ Decompensated Heart rate 130-150 150-170 170-200, may become bradycardic Mm colour Normal/pinker Pink White/grey CRT <1sec ~2 seconds >2 seconds Pulse amplitude Increased Decreased Severe decrease Pulse duration Mildly decreased Decreased Severe decrease Metatarsal pulse palpable Easily Just Absent 15 EXEMPTIONS FROM THE RULE!  Septic (Distributive) Shock  Due to vasodilation animals may have brick red mucous membranes and bounding pulses (of decreased duration)  Cats  May have increased heart rates in early shock but frequently present with bradycardia in more severe shock! 16 PATHOLOGICAL CONSEQUENCES  Low blood pressure causes activation of the sympathetic nervous system  Tachycardia & vasoconstriction  The renin-angiotensin system is activated Vasoconstriction Fluid retention  Hydrostatic pressure promotes movement of water by Starling’s forces from the interstitium  With these compensatory mechanisms, healthy animals may be able to tolerate fluid losses up to 30-40% of blood volume!!! Intestinal vasoconstriction 17 BUT  Shock can kill animals very rapidly due to lack of perfusion OR  The consequences of shock can cause significant morbidity/mortality in the days following the insult/injury Cellular hypoxia Free radical generation Inflammatory mediators 18 GASTROINTESTINAL HYPOPERFUSION & INFLAMMATION  Sympathetic activation tends to shunt blood away from the GIT  Dispropotionate hypoperfusion and inflammation  May amplify SIRS  May allow bacterial translocation causing sepsis 19 SIRS  A complex immune response follows involving activation of multiple inflammatory mediators throughout the body  This may lead to a syndrome called SIRS – Systemic inflammatory response syndrome – several days after the insult.  SIRS may lead on to multiple organ dysfunction (MODS)  We cannot target the inflammatory response (affordably!) DIC too 20 AIMS OF SHOCK TREATMENT  Rapid yet judicious use of fluid therapy to restore vascular volume, normalise tissue perfusion and reduce secondary injuries  Aggressive, early fluid resuscitation is associated with significantly reduced morbidity and mortality  Identification and control of any haemorrhage is an important component of treatment in hypovolaemic shock  So-called compressible haemorrhage  A different approach may be warranted for patients with ongoing internal bleeding (non-compressible haemorrhage) – This approach is termed hypotensive resuscitation. 21 ROUTE OF FLUID ADMINISTRATION  As we are expanding the vascular space, intravenous or intraosseous access is mandatory  Intra-osseous cannulation is particulaly suited to small puppies and kittens  Specialised trochars and needle systems are available but a hypodermic needle inserted in a sterile fashion is acceptable in soft boned young animals  Newer intraosseous ‘drill’ devices are available 22 ISOTONIC CRYSTALLOIDS FOR SHOCK  Equilibrate quickly with interstitial fluids  Only 10-25% remains in the circulation after 1 hour  Therefore, high volumes are needed  ‘The shock dose’  80-90 ml/kg/hr in dogs  40-60 ml/kg/hr in cats 23 GOAL-DIRECTED THERAPY  We commonly give a 10-20ml/kg of isotonic crystalloid over 15 minutes and then reassess perfusion parameters; particularly an improvement in mentation, a decrease in heart rate and improving pulse quality  Avoids excessive fluids  Identifies non responders  Fluid administration may be tailored to other measures alongside clinical examination findings  Plasma lactate  Blood pressure  Oxygen delivery  Indices of volume responsiveness 24 AN EXAMPLE – GDT IN HUMANS 25 WHAT FLUID? 26 ISOTONIC REPLACEMENT CRYSTALLOIDS Fluid Na K Cl Ca Normal Saline 154 Ringer’s 147 4 155 2 Hartmann’s 130 4 109 3 Buffer 154 Osmolarity 308 310 Lactate 275 27 Hartmann’s?  Hartmann’s is the obvious choice as it is alkalinising and these patients have a metabolic acidosis (lactic) 28 HARTMANN’S CONTRAINDICATIONS  Lactate cannot be metabolised in SEVERE liver disease  Low osmolarity, therefore not suitable where fluid accumulation may be an issue e.g. cerebral oedema  Contains calcium  Cannot be mixed with blood products  Cannot be mixed with sodium bicarbonate  Not recommended in hypercalcaemic animals Fluid Na K Cl Ca Buffer Osmolarity Hartmann’s 130 4 109 3 Lactate 275 29 Hartmann’s Contraindications  Classically contraindicated in hyperkalaemia (renal/post-renal failure) as contains potassium BUT  Only contains 4mmol/l K+ therefore still dilutional  Bicarbonate buffer in Hartmann’s normalises acid bases status more rapidly than saline in cats with experiental urethral blockage ECF ICF K+ H+ 30 CRYSTALLOIDS  Cheap  Physiological  Few side effects  Widely available BUT  Only transiently expand the vascular compartment  Don’t provide a replacement for albumin (oncotic support)  This is important in hypoalbuminaemic patients, especially those with peripheral oedema 31 COLLOIDS  Contain large molecules which do not cross the vascular endothelium  High oncotic pressure acts to expand and maintain intravascular volume  Smaller volumes required than crystalloids for shock  Max 20 ml/kg/hr in dogs  Max 10 ml/kg/hr in cats  Again, administer to effect ~5ml/kg boluses 32 COMMON COLLOIDS Haemacel (Veterinary licensed product) Pentastarch/Tetrastarch 6% 33 COMMON COLLOIDS Haemacel  Small molecular size  (~25 kDa) Pentastarch/Tetrastarch 6%  Larger molecular size  (~200 kDa)  Rapid volume expansion  Slower volume expansion  Short duration of action  Longer duration of action  ~80% lost after 24 hours  Low risk coagulopathy  Greater risk of anaphylaxis  ~60% lost after 24 hours  Risk coagulopathy at high doses (>20ml/kg/day or up to 50ml/kg/day with certain tetrastarches (voluven)) Higher costs too 34 CRYSTALLOIDS VS COLLOIDS  No definitive evidence exists showing superiority of one over the other  Crystalloids seem effective despite physiological inferiority!  Recent controversy surrounding withdrawal of colloids in human medicine (Renal complications)  Colloids useful with  Hypoalbuminaemia  Large patients  Poor response to crystalloids 35 HYPERTONIC SALINE  7.2% NaCl  High osmotic gradient draws interstitial fluid into the vascular space  Small volumes required – 2-4ml/kg over 10 minutes  May also cause +ve ionotropy, and reduce inflammation  Very valuable in hypovolaemic patients with head trauma  Not to be administered to patients who are already dehydrated  Must be followed by crystalloids to repay the debt  Can be mixed with colloids for shock resuscitation in severe cases Not too fast! 36 BLOOD PRODUCTS  Blood is not a first line treatment for shock as it cannot be administered fast enough while avoiding potential transfusion reactions.  Animals in shock do not die of anaemia, they die of a lack of vascular volume!  Once initial resuscitation has been carried out, transfusion may be required to maintain a PCV of greater than 20-25%. 37 HYPOTENSIVE RESCUSITATION  May be indicated in ongoing internal hemorrhage  Restores blood pressure to acceptable limits (60 mmHg) without “popping the clot”  Definitive volume restoration delayed until bleeding is surgically managed Permissive hypotension!! Not head injuries 38 ADDITIONAL SHOCK THERAPIES  Vasopressors/Inotropes (e.g. Noradrenaline)  Shouldn’t be required in the vast majority of hypovolaemic cases – more used in severe sepsis  (Bicarbonate)  Glucocorticoids  Have been used at high doses to treat shock in the past  No beneficial effects are documented  Potential to cause harm via immunosuppression and GI irritation  Physiological doses may be useful in septic shock (when non responsive to vasopressors!) 39 ADDITIONAL MONITORING  Physical findings essential (e.g., mucous membrane color, capillary refill time, pulse rate and quality, heart rate, respiratory rate)  Arterial blood pressure  May be normal in early shock due to compensation and not fall until the syndrome is severe  Can also be influenced by pain  Monitoring of trends is still valuable 40 BLOOD LACTATE  Produced by anaerobic metabolism in hypoxic cells  Useful to assess oxygen delivery to tissues  Normal levels < 2.0 mmol/L  Mild increase 2-5  Moderate 5-8  Severe >8 41 42 GUIDE TO THERAPY  Reductions of >10% plasma lactate in patients treated for shock are considered significant  Serial Lactate measurements aid ‘goal-directed’ therapy  Both the initial level and the magnitude of reduction are considered prognostic in GDV Imp outcome in humans Direct measure tissue ox 43 INTRAOPERATIVE BLOOD LOSS  8yo Bulldog weighing 20kg, normal haematocrit  Undergoing ear surgery  No evidence pre/intra-op fluid deficits UNTIL!  Loss of approximately 300ml blood from surgical site Causing drop bp and inc hr 44 BLOOD LOSS UNDER ANAESTHESIA  Bruno’s blood volume  Percentage loss = 90ml/kg x 20kg = 1800ml = 300/1800 x 100 = 17% Guidelines (Vary depending on patient health & PCV) <10% blood loss - Replace with 3x volume crystalloids 10-20% blood loss - Replace with equal volume colloid >20% blood loss - Consider whole blood + colloid Colloid limit 20ml/kg 45 COMPLICATIONS OF FLUID THERAPY  Iatrogenic electrolyte disturbances  Overzealous use of fluids may lead to volume overload  Characterised by chemosis, serous nasal discharge, increased respiratory rate, effort and noise, restlessness, peripheral oedema, and polyuria  Pulmonary and interstitial oedema  Most likely in patients with  Renal disease  Cardiac Disease  Hypoalbuminaemia  Pulmonary contusions  Catheter related issues  Complications associated with individual products (e.g. coaguloptahy with colloids) 46 ILOS Lecture Content ILOs  Recognise the major indications for fluid therapy and identify clinical cases where fluid therapy may be required  Design a fluid plan (including volume/rate/route & type) based on a clinical evaluation of a patient in shock  Identify conditions/diseases which may give rise to shock and understand the rationale for treatment  Explain how monitoring of clinical signs, physiological and laboratory data assist in the diagnosis and treatment of shock  Recognise different fluid products and have a basic knowledge of their indications  Discuss common complications which may occur as a result of fluid therapy  Frontiers collection - https://www.frontiersin.org/articles/10.3389/fvets.2021.744080/full - Frontiers collection  www.aaha.org/public_documents/professional/guidelines/fluid_therapy_guidelines.pdf - 2013 Guidelines 47