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![DETERMINANTS
• Arterial oxygen content
CaO2 = (1.39 x Hb x SaO2) + (PaO2 x 0.0031)
• Oxygen delivery= Cardiac Output x Arterial O2 content
DO2= CO x [(1.39 x Hb x SaO2) + (PaO2 x 0.0031)]
• Oxygen consumption= Cardiac Output x (Arterial O2 content- Venous O2 content)
Vo2= CO x (CaO2- CvO2)
= CO x Hb x 1.39 ( SaO2- SmvO2)](https://image.slidesharecdn.com/sgd1emergencydimasfujiansyah-241107132131-72c55fd6/75/SGD-1-EMERGENCY-DIMAS-FUJIANSYAH-pptx-new-10-2048.jpg)
![References
1. Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013 Oct
31;369(18):1726-34. [PubMed]
2. Cannon JW. Hemorrhagic Shock. N Engl J Med. 2018 Jan 25;378(4):370-379.
[PubMed]
3. Hooper N, Armstrong TJ. StatPearls [Internet]. StatPearls Publishing; Treasure
Island (FL): Sep 26, 2022. Hemorrhagic Shock. [PubMed]
4. Gitz Holler J, Jensen HK, Henriksen DP, Rasmussen LM, Mikkelsen S, Pedersen C,
Lassen AT. Etiology of Shock in the Emergency Department: A 12-Year Population-
Based Cohort Study. Shock. 2019 Jan;51(1):60-67. [PMC free article] [PubMed]
5. Better OS. Impaired fluid and electrolyte balance in hot climates. Kidney Int Suppl.
1987 Aug;21:S97-101. [PubMed]
6. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, Cohen J, Opal SM,
Vincent JL, Ramsay G., SCCM/ESICM/ACCP/ATS/SIS. 2001
SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care
Med. 2003 Apr;31(4):1250-6. [PubMed]](https://image.slidesharecdn.com/sgd1emergencydimasfujiansyah-241107132131-72c55fd6/75/SGD-1-EMERGENCY-DIMAS-FUJIANSYAH-pptx-new-33-2048.jpg)
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SGD 1 EMERGENCY DIMAS FUJIANSYAH.pptx new
- 1. SHOCK CLASSIFICATION, PATHOPHYSIOLOGY, MANAGEMENT DimasFujiansyah 2108260090
- 2. What is Shock? •SAMUEL V GROSS, 1872 said - “Shock is the manifestation of the rude unhinging of the machinery of life” • Shock is a state of acute circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and oxygen demand (consumption) resulting in end-organ dysfunction • A clinical syndrome that results from inadequate tissue perfusion • Failure of circulation centrally or peripherally to meet the metabolic demands of the tissues • A group of life-threatening circulatory syndromes with varying physiological profiles.
- 3. CLASSIFICATION • Hypovolemic Shockor Haemorrhagic Shock • Cardiogenic Shock • Obstructive Shock or Cardiac Compressive Shock • Vasogenic or Distributive Shock 1. Septic Shock 2. Anaphylactic Shock 3. Neurogenic Shock
- 5. HYPOVOLEMIC SHOCK A decreasein circulating volume in relation to the total vascular capacity and characterized by a reduction of diastolic filling pressures resulting in poor tissue perfusion. Commonest cause being trauma resulting in external or concealed haemorrhage from blunt or penetrating injuries.
- 6. ETIOLOGY Hemorrhagic shock -severe blood loss leads to inadequate oxygen delivery at the cellular level. • Traumatic 1.Blunt or penetrating injury 2.Fractures- long bones, pelvic fractures • Non- Traumatic 1. GI bleeds 2. Aortic dissection 3. Rupture of large vessel aneurysm 4. Erosion of a large vessel 5. Diffuse inflammation of mucosal surfaces
- 7. • Due toloss of water and electrolytes, with fall in effective circulating volume. Traumatic i. Burns ii. Crush injuries Non-traumatic i. Fluid loss from vomiting or diarrhoea (eg- cholera) ii. Fluid loss in diabetes mellitus, adrenal insufficiency, excessive sweating, diabetes insipidus iii. Fluid sequestration (eg- intestinal obstruction, pancreatitis) ETIOLOGY
- 8. PATHOPHYSIOLOGY • Ventricular preload- DBP and volume • Decreased SV and CO, hence SBP • CO leads to SVR to maintain perfusion to heart and brain at the expense of other tissues ( muscle, skin, gut) • Autoregulation occurs at heart and brain- maintenance of blood flow over wide range of perfusion pressure (60- 150mm of Hg). Circulating volume Venous return Right and left filling pressures Cardiac output Tissue hypoxemia
- 9. • Neurohumoral CompensatoryMechanisms- 1. Catecholamines 2. Cortisol 3. ADH secretion 4. RAS activation • Shift of fluid from extravascular compartment to vascular compartment 1.PHASE 1- <1 hr of blood loss, shift from interstitium to capillaries (may continue upto 40hrs) 2.PHASE 2- RAS activation- Na+ and water retention to replenish interstitial fluid 3.PHASE 3- Erythropoesis. PATHOPHYSIOLOGY
- 10. DETERMINANTS • Arterial oxygencontent CaO2 = (1.39 x Hb x SaO2) + (PaO2 x 0.0031) • Oxygen delivery= Cardiac Output x Arterial O2 content DO2= CO x [(1.39 x Hb x SaO2) + (PaO2 x 0.0031)] • Oxygen consumption= Cardiac Output x (Arterial O2 content- Venous O2 content) Vo2= CO x (CaO2- CvO2) = CO x Hb x 1.39 ( SaO2- SmvO2)
- 11. • MICROVASCULATURE • Impairmentof microcirculation- central pathophysiology of shock • Imbalance between vasoconstrictors (Angiotensin II, endothelin-1, thromboxane A2) and vasodilators (PGI2, NO, adenosine) • CELLULAR RESPONSE Increased anaerobic metabolism lactate, H+ ion accumulation Acidosis Decrease in interstitial transportation of nutrients Mitochondrial dysfunction- decreased oxidative phosphorylation Decrease in ATP store
- 12. ORGAN RESPONSE • Endocrine 1.Increased gluconeogenesis and lipolysis. 2. In critically ill, cortisol levels and ACTH stimulation is decreased, hence survival rates are low. 3. Pancreas- increased secretion of glucagon- increased gluconeogenesis increasing blood glucose levels. • Renal Response 1. Decreased urine output 2. Hypoperfusion – AKI 3. Acute tubular necrosis Severe pain/stress ACTH stimulation Cortisol secretion Reduced RBF Reduces GFR Reduced U/O Aldosterone Vasopressin
- 13. ORGAN RESPONSE • Cardiovascularresponse 1. Hypovolemia preload SV 2. HR CO(limited) 3. Venoconstriction 4. Shock induced decreased myocardial filling causes decrease in LV end-diastolic volume and fall in SV 5. Hypothermia, myocardial ischemia and acedemia impairs myocardial contractility and SV. 6. Shock Index, SI= HR/SBP (normal= 0.5-0.7)
- 14. • Pulmonary Response ORGANRESPONSE SHOCK Increased PVR PVR> SVR it may lead to RV failure Tachypnoea (reduced TV, high RR) Respiratory Alkalosis
- 16. HAEMORRHAGIC SHOCK • Definitionof Massive Haemorrhage 1. Loss of more than one volume of blood in 24hrs 2. 50% total blood volume lost in 3hrs 3. Bleeding in excess of 150mL/min Lethal Triad
- 18. How does apatient present? • Clinical Features: 1. Pallor 2. Slight anxiety/ restlessness 3. Cold, clammy skin 4. Tachycardia 5. Collapsed neck veins 6. Oliguria (<0.5ml/kg/hr) or anuria “Any patient who is cool and tachycardic is in shock until proven otherwise”(ATLS)
- 19. STAGES COMPENSATED • Hypotension • Tachycardia •Narrow pulse pressure • Peripheral vasoconstriction DECOMPENSATED • Tachypnoea • Altered mental status • Decreased urine output • Myocardial ischemia IRREVERSIBLE • Metabolic derangements • Tissue perfusion critically reduced in vital organs • Acidosis • Hypothermia • Coagulopathy
- 20. Factors STAGE ISTAGE II STAGE III STAGE IV Blood loss (mL) 750 750-1500 1500-2000 2000 or more Blood loss (% blood volume) 15 15-30 30-40 40 or more Pulse (beats/min) <100 >100 >120 140 or higher Blood pressure Normal Orthostatic Decreased Decreased Pulse pressure (mm Hg) Normal or increased Decreased Decreased Decreased Capillary refill test Normal Positive Positive Positive Respirations per minute 14-20 20-30 30-40 >40 Urine output (mL/hr) 30 20-30 <20 Negligible CNS: mental status normal anxious Anxious, confused Confused, lethargic Fluid replacement Crystalloid Crystalloid Crystalloid + blood Crystalloid + blood Baskett’s Classification of Haemorrhagic Shock
- 21. • Vitals (PR,BP, RR, temp) • Urine output, capillary refill time, JVP, ABG (arterial blood gas or Ph) • Hematocrit • Classic hemodynamic pattern- low CVP, low PCWP (pulmonal capillary pressure), low CO and high SVR. • Oxygen extraction • ETCO2 SaO2 SvO2 O2 extraction (SaO2-SvO2) Normal >95% 65-70% ~30% Hypovolemic >95% 50-65% 30-50% Shock >95% <50% >50% Monitoring a case of hypovolemic shock
- 22. • Bedside USG-assess right-sided filling pressures, IVC diameter and caval index • The Rapid Ultrasound in Shock (RUSH) exam involves a threepart bedside physiologic assessment simplified as 1. the pump (cardiac), 2. the tank (volume status) 3. and the pipes (arterial and venous)
- 24. MANAGEMENT • Fluid Resuscitation-Restoring volume is the keystone VO2= COx Hb x 1.39 x (SaO2- SvO2) • Fluid challenge- 500 or 1000mL NS rapidly infused over 20min and reassess the patient after each bolus • Cannulation Site • Catheter Dimensions and relation to flow rate Infusion Device Length (inches) Flow rate (mL/min) Peripheral 14G catheter 2 195 16G catheter 2 150 Central 16G catheter 5.5 91 16G catheter 12 54
- 25. • Relation tofluid viscosity and flow rate • Estimating volume requirement Male 65ml/kg ; Female 60ml/kg Volume is replaced by calculating the volume deficit crystalloids in 3:1 ratio and colloids and blood at 1:1 ratio Fluid Flow rate (mL/min)* Crystalloids 100 5% albumin 100 Whole blood 65 Packed cells 20
- 26.
- 27. MASSIVE TRANSFUSION PROTOCOL •STEP 1- CONTROL BLEEDING • Minimise time between arrival and surgery if indicated – “Damage Control Surgery” • Use of tourniquet , tamponade techniques, drugs • STEP 2- IDENTIFY THE NEED FOR MASSIVE TRANSFUSION • ABC score (4points) • TASH score (6points) • Identify massive trauma / bleed on purely clinical basis • Based on volume requirements after an initial resuscitation.
- 28. • STEP 3-ACTIVATE HOSPITAL MASSIVE TRANSFUSION SYSTEM • STEP 4-INITIAL EMPIRICAL RESUSCITATION (1ST 15 – 30 MIN) • FBP, cross match, coagulation profile (INR, APTT, fibrinogen), ABG (VBG) • Uncrossmatched (O Rh -) PCV– 2 units. FFP (Fresh Frozen Plasma) (ABO specific)– 2 bags. (1:1 ratio) • STEP 5- CONTINUE VOLUME RESUSCITATION /MONITORING • Target MAP 65-70mm of Hg ; 90-100 in head injury/ raised ICP • Reassess
- 29. • STEP 6:CONSIDER OTHER AGENTS FOR PREVENTION / LIMITATION OF COAGULOPATHY Obstetric haemorrhage: early use of cryoprecipitate is recommended. Platelets: only recommended in thrombocytopenia < 50,000. Tranexamic acid: give 1 g loading dose (over 10 mins) • STEP 7:TARGET THERAPY TO RESULTS • if Hb < 8g/dL- PCV ; if INR > 1.5 or APPT > 50 sec- 2U FFP; if fibrinogen < 1.0 g/dL - 8U of CP • Calcium is < 1.1mmol then, 1 amp of Calcium gluconate 1g/10ml • Maintain temperature > 35 degrees • STEP 8: EVACUATION PLANNING
- 32. ENDPOINTS • ABG- pH,lactate, bicarbonate, SaO2 • Vital Parameters- PR, BP, U/O=>0.5mL/kg/hr • MAP>65mm Hg, CVP- 8-12mm Hg, ScvO2>70% • Bedside Echo- assess intravascular volume and cardiac function • IVC diameter 1.5-2.5cm. Trauma<1cm, <1.5cm volume depletion, >2.5cm overload • Caval index- (IVC exp-IVC insp) diameter/IVC exp*100, volume deletion <50%, >50% fluid responsivesness • Achievement to baseline with in 24hrs-markedly improved survival rate
- 33. References 1. Vincent JL,De Backer D. Circulatory shock. N Engl J Med. 2013 Oct 31;369(18):1726-34. [PubMed] 2. Cannon JW. Hemorrhagic Shock. N Engl J Med. 2018 Jan 25;378(4):370-379. [PubMed] 3. Hooper N, Armstrong TJ. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Sep 26, 2022. Hemorrhagic Shock. [PubMed] 4. Gitz Holler J, Jensen HK, Henriksen DP, Rasmussen LM, Mikkelsen S, Pedersen C, Lassen AT. Etiology of Shock in the Emergency Department: A 12-Year Population- Based Cohort Study. Shock. 2019 Jan;51(1):60-67. [PMC free article] [PubMed] 5. Better OS. Impaired fluid and electrolyte balance in hot climates. Kidney Int Suppl. 1987 Aug;21:S97-101. [PubMed] 6. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, Cohen J, Opal SM, Vincent JL, Ramsay G., SCCM/ESICM/ACCP/ATS/SIS. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med. 2003 Apr;31(4):1250-6. [PubMed]
Editor's Notes
- #6 GI bleeds (eg- peptic ulcer, gastric mucosal erosions, oesophageal varices,typhoid bleeds, DIC) Erosion of a large vessel (eg- pancreatitis, tumour invasion) Diffuse inflammation of mucosal surfaces (eg- ulcerative colitis)
- #8 Shock may occur without hypotension (increased SVR in presence of decreased CO) and hypotension may occur without shock. Autoregulation occurs at heart and brain- However MAP<60mm of Hg will deteriorate function at these tissues too. Autoregulation- anrep effect- increased myocardial contractility to increase in afterload Bowditch- increase in myocardial tension with increase in HR (treppe phenomenon)
- #9 Loss of intravascular volume initiates compensatory mechanisms to maintain perfusion of the vital organs (mainly heart and brain) Effectiveness of these mechanisms depend on rate of fluid loss and degree volume depletion already present Volume depletion stimulates baroreceptors within the intrathoracic vessels and carotids, baroreceptors in the kidneys resulting in release of Catecholamines Cortisol ADH secretion RAS activation The blood volume constitutes 13-15% of total body fluid and an acute loss of 35-40% can be fatal. Shift occurs from interstitial compartment to vascular compartment occurs in three phases: PHASE 1- <1 hr of blood loss, shift from interstitium to capillaries (may continue upto 40hrs) PHASE 2- RAS activation- Na+ and water retention to replenish interstitial fluid PHASE 3- Erythropoesis- stimulation takes few hours, 15-50ml cell volume produced daily, complete replenishment- upto 2-3months. Compensatory responses (mainly in the form or tachycardia and vasoconstriction) may be blunted in elderly patients, diabetics, alcoholics, patients with chronic renal or liver cell dysfunction. Tachycardia may less marked or even absent in such patients and hypotension may occur early with blood loss.
- #10 Cao2- oxygen carried by HB and dissolved plasma in oxygen DO2- amount of O2 delivered to tissue per min. 1000mL of o2/min VO2- amount of O2 consumed by tissue each min is equal to difference in oxygen delivered to tissues and oxygen returning f Oxygen from tissuesto heart. Normal value 250mL of O2/min Oxygen flux refers to amount of O2 leaving the LV per min in the arterial blood
- #11 Functions- transportation of oxygen, carbon dioxide, nutrients and exchange across cell membranes. Impairement of microcirculation- central pathophysiology of shock, leads to deranged cellular metabolism and organ failure. In shock, local perfusion acting on the vascular bed results from balance between the vasoconstrictors and vasodilators As shock progresses, vasodilators take over vasomotor tone causing hypotension and hypoperfusion Metabolic Derangements Disruption in carbohydrate, protein, lipid metabolism Increased anaerobic metabolism- increased lactate production Minimal net energy production, inadequate tissue perfusion leads to acidosis Final stage- dysfunction of cell membrane ( decrease in transmembrane potential), facilitates sodium and water accumulation causing cell swelling. Loss of calcium homeostasis in cell leads to apoptosis.
- #12 Prompt resuscitation reduces risk of AKI Splanchnic organs---due to vasoconstriction there can be Ileus, GI bleeding, pancreatitis, acalculous cholecystitis, and mesenteric ischemia can occur due to low flow states. Enteric bacteria and antigens translocate from the gut lumen into the systemic circulation during gut ischemia causing irreversible shock Centrilobular injury with mild increases of transaminases and lactate dehydrogenases
- #13 Restoring intravascular volume promptly increases stroke volume and cardiac output , in turn improves tissue perfusion. Venoconstriction- increased ventricular filling SI> persistently >1= impaired LV function as a result of blood loss or cardiac depression, high mortality rate
- #14 Increased pulmonary vascular resistance due to Inflammatory damage from Resuscitation induced ROS Causes acute lung injury and ARDS Decrease compliance, increased interstitial edema causes increased work of breathing and respiratory muscle fatigue Infusion of cold fluids exacerbates the heat lost from hemorrhage, depleted energy stores, and environmental exposure and leads to decreased function of the enzymes in the clotting cascade.
- #17 Sites that can harbor sufficient extra-vascular volume: Intrathoracic (2-3L/ pleural cavity) Intraabdominal (2-5L) Retroperitoneal # long bones (1L or more)
- #18 Relative bradycardia (paradoxical bradycardia):- pulse<90/min with SBP <90mmhg,occurs in 45% of all hypotensive trauma
- #19 An initial preshock/ compensated , during which reflex compensatory mechanisms are activated and vital organ perfusion is maintained • A decompensated stage, characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis • An irreversible stage, in which cellular and tissue injury is so severe that even if the hemodynamic defects are corrected, survival is not possibleAcute loss of 10% of circulating volume results in tachycardia and increased SVR with maintenance of BP.
- #21 HCT- helpful if insidiousbleed, or if recognition of blood loss is delayed or if fluid resuscitation has been prompt, low HCT Oxygen extraction- As a response to decreased CO, there is an increased O2 extraction from the blood. This can continue only to a point, after which oxygen debt occurs and there is a switch of aerobic to anaerobic metabolism ETCO2- decrease in CO results in decrease in PCO2 of expired gas. Normally ETCO2 differs from arterial PCO2 by 3-4mm of Hg. It may drop to below 10mmof Hg in severe shock and shows a progressive rise with successful resuscitation. IVC diameter 1.5-2.5cm. Trauma<1cm, <1.5cm volume depletion, >2.5cm overload Caval index- (IVC exp-IVC insp) diameter/IVC exp*100, volume deletion <50%, >50% fluid responsivesness Invasive monitoring in Hypovolemia complicating other forms of shock Cause of the shock is not clear Hypovolemia in patients with poor cardiac function When inotropic support is needed inspite of volume replacement.
- #22 IVC diameter 1.5-2.5cm. Trauma<1cm, <1.5cm volume depletion, >2.5cm overload Caval index- (IVC exp-IVC insp) diameter/IVC exp*100, volume deletion <50%, >50% fluid responsivesness
- #23 The Rapid Ultrasound in Shock exam involves a threepart bedside physiologic assessment simplified as the pump (cardiac), the tank (volume status), and the pipes (arterial and venous) ABCDE airway, controlling the work of breathing, optimizing the circulation, assuring adequate oxygen delivery, and achieving end points of resuscitation.
- #24 Ultimate objective is to restore and maintain oxygen uptake in vital organs and preserve organ function. VO2 is compromised by both CO and Hb. First objective is to restore CO , later Hb deficit. Replacement of haemoglobin with blood transfusions Monitoring fluid and blood resuscitation clinically Determining the cause of hypovolemic shock Two large bore (16G) IV lines to be secured in peripheral veins. In case of collapsed peripheral veins, large bore catheter can be placed in the femoral vein or a central line has to be secured. Due to long length and smaller lumen of central lines it may not permit rapid fluid replacement. Venous cutdown can also be done. Rate of infusion is directly proportional to pressure gradient along the catheter and the fourth power of radius of the catheter. It is inversely related to the length of catheter and viscosity of the fluid infused.
- #25 In obese patients, 10% has to be deducted from the calculated value. Fluids used in volume replacement Increase in cardiac index- Dextran-40 > whole blood > ringer lactate > packed cells. Generally used crystalloids include NS and RL for rapid replacement, however shift to extravascular compartment occurs and 25% are presumed to retain in vascular compartment. Colloids may be equally good or even better but disadvantages include anaphylaxis, more expensive solutions, renal failure and bleeding ( inhibit platelet adhesion and aggregation).
- #26 Vasopressors are most effective when the vascular space is “full” and least effective when the vascular space is depleted. Patients with chronic hypertension may be at greater risk of renal injury at lower blood pressures; however, in others, there appears to be no mortality benefit in raising MAP above the 65 to 70 mm Hg range.
- #27 Massive transfusion- >1 blood volume/ 10pcv in 24hrs or >50% blood volume replenished in 4 hrs This may require early Evacuation planning---torniquets -control peripheral bleeding vessels; Tamponade eg. Pelvic binders, direct pressure, suture scalp lacerations; Intrauterine balloon devices for PPH, manual compression, oxytocics ABC score: 4 points – Penetrating injury , Positive FAST exam (Focussed Assessment with Sonography for trauma), HR > 120/min, Systolic BP <90 0= 1% risk of MTP, 1=10% risk, 2= 41% risk, 3= 48% risk, 4= 100%. Activate MTP if 3 + criteria met TASH(Trauma Associated Severe Haemorrhage) 7point scale Hb< 7g/dL ,Base Excess <-10mmol/L, SBP<100mm of Hg, HR>120, Positive FAST Clinically unstable pelvic fracture or open/displaced femur fracture, male gender Multitrauma with multiple system injuries and unstable haemodynamics Massive post-partum haemorrhage ( blood loss > 1500 ml) Post-surgical bleeding from major vessels GI bleeding with shock
- #28 Lab team need to know early – they will need to prep products and process your incoming blood samples. Orderly to run samples and bloods to the lab for processing Early thawing of 2 units FFP if large volumes are expected. Dedicated nurse / team member to run the rapid infusion device Take bloods for URGENT processing: FBP, cross match, coagulation profile (INR, APTT, fibrinogen), ABG (VBG) Request immediately available blood products. Crystalloids – aim to minimise the use of crystalloids – they will make coagulopathy, temperature and possibly acidosis worse Uncrossmatched (O Rh -) packed red cells – 2 units. FFP (ABO specific)– 2 bags. (recommend 1:1 ratio where possible) NOTE: thawing FFP takes ~ 30 minutes – lab has to be alerted. target MAP is 65 – 70 mmHg (prior to definitive intervention) ; target MAP is 90 –100 in patients with traumatic brain injury / raised ICP suspected Monitoring- invasive monitoring (arterial line) if available Send repeat investigations every ~ 30 minutes: FBP, coags, fibrinogen, ABG / lactate, Ca++, Frequent / continuous temperature monitoring
- #29 Warfarinised / known coagulopathy : give Vit K 10 mg, Dabigatran / thrombin inhibitor Obstetric haemorrhage: early use of cryoprecipitate is recommended. Platelets: only recommended in thrombocytopenia < 50,000. Tranexamic acid: give 1 g loading dose (over 10 mins) as early as possible in traumatic bleeding Target MAP = 65 mmHg Give fluid volume; if Hb < 8g/dL-RBCs; if INR > 1.5 OR APPT > 50 sec- 2U FFP; if fibrinogen < 1.0 g/dL Give 8U of CP Calcium is < 1.1mmol then, 1 amp of Calcium gluconate 1g/10ml Optimise acidosis Consider intubation / ventilation - normocapnea Maintain temperature > 35 degrees IV fluid warmer, airblanket, limit exposure & operation time. In smaller centres the early evacuation must be planned in the absence of a definitive surgical service. Suggest early liason receiving hospital surgeon and clinical Haematologist.
- #31 TRALI- Transfusion related acute lung injury-
- #32 VITALS-fall in heart rate, improvement in blood pressure, improved urine output, warm skin, good capillary refill, correction of metabolic acidosis are good indicators of improving circulatory function. Overinfusions result in pulmonary edema and can be clinically detected by noting increased respiratory rate, crackles at base of the lungs.