Emergency Fluid Therapy

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Emergency Fluid Therapy - Presentation Transcript

1. Fluid Therapy in Emergency Care Dr. Rashidi Ahmad Medical Lecturer/emergentist School Of Medical Sciences USM Health Campus Kelantan 2 nd Regional Fluid Transfusion Workshop 10 February 2007
2. Outline
* Introduction
* Volume therapy in hemorrhagic shock
o Crystalloid versus colloid
o Hypertonic saline/Small volume resuscitation
o Blood
* Fluid therapy – when? How much?
* Fluid therapy in septic shock
* Endpoint of resuscitation
3. “ The Neglected Disease of Modern Society” Trunkey, DD
4. Trauma Chain of survival Fluid therapy is a part of the factors…
5. Polytrauma?
* A syndrome of combined injuries with ISS > 17 & consequent SIRS for at least 1 day, leading to dysfunction, or failure, of remore organs & vital systems, which themselves had not directly been injured.
Marius Keel et al. Pathophysiology of trauma. Injury (2005) 36, 691-71
6. O2 flux = [ C.O X Hb X SaO2 X k] + [ C.O X PaO2 x 0.003] Principle of fluid therapy in Emergency care
7. Shock
* The viability & normal functioning of multiple organ systems & the whole body depends on continuos adjustment of C.O & DO2 to meet VO2
* C.O   VO2 & DO2 imbalance = cumulative O2 debt
Cumulative O2 debt overwhelms the physiologic reserve of CVS & RS to compensates = SHOCK Mohd Y Rady. Em. Med, 1996
8. Traumatic shock
* Tissue oxygenation is compromised by  DO 2 (hemorrhage) &  VO 2 (inflammatory response).
* Occurs in combination (bleeding, pain, tissue edema, neurogenic shock @ tension pneumothorax).
* Bleeding frequently occurs at multiple sites & is self limiting.
* Penetrating trauma, major bleeds rapidly leads to hypovolemic cardiac arrest
9. Marius Keel, Omar Trentz. Pathophysiology of polytrauma. Injury (2005) 36, 691 - 709
10. Pseudo-shock
11. Fluid Balance Consequences in Early Shock
* Mobilization of ECF
* Haemodilution of plasma
* – ?Coagulation effects
* – Gradual fall in Hb
* Maintenance of vascular space at the expense of the ECF
12. Late shock
* • Capillary leak
* • Loss of plasma volume
* • Tissue edema
* • Organ edema (lung, kidney)
* • Multiple organ failure
13. Phases of Resuscitation in Trauma Care
* Pre-hospital Resuscitation
* ED Resuscitation
* Establishment of Definitive Care
* ICU on going resuscitation
14. Aim of volume resuscitation
* • Early, complete restoration of tissue
* oxygenation
* • Minimal biochemical disturbance
* • Preservation of renal function
* • Avoidance of transfusion complications
15. Goals of Fluid therapy in hemorrhagic shock
* First Priority: Restore volume
* Second Priority: Restore blood - oxygen carrying capacity
* Third Priority: Normalize coagulation status
16. Fluid of choices
* Well-balanced resuscitation fluid resembling ECF
* Rapid volume expansion of IVS
* Sustained expansion
* No sugar
17. Options for fluid resuscitation
* Crystalloid – NS, Lactated Ringers’s solution, hypertonic saline
* Colloid – albumin, gelatine, dextran, starch (VOLUVEN)
* Blood – allogenic blood, autologous blood
* Blood substitutes – cross-linked, polymerize @ conjugated Hb
18. Optimal fluid resuscitation
* No ideal fluid resuscitation
* Combination therapy
* Volume expansion
* O2 carrying capacity of blood, without the need for cross matching @ the risk of transmission
* Restore & maintain the normal composition & distribution of body fluid compartment
19. Crystalloids
* • Ringer’s:
* – Low sodium, lactate load
* • Saline:
* – Hyperchloraemic acidosis, no K+
* • Both:
* – Large volume resuscitation needed (3:1)
20. Crystalloid
21. Crystalloids
* Lower cost
* EC expander
* Greater urinary flow
* Replaces interstitial fluid
* Transient haemodynamic improvement (20 – 30 min)
* Peripheral oedema
* Pulm oedema (protein dilution +  PAOP)
22. Colloids
* Greater cost
* IV expander, do not resuscitate ECF
* Smaller volume (1:1)
* Osmotic diuresis
* Longer duration of persistence (2 – 8 hours)
* Less cerebral oedema
* Coagulopathy
* Pulm oedema (cap. leak state)
*  GFR (hyperoncotic kidney failure syndrome
* Improved rheology
* • Allergic risk (gelatin > dextran > HES)
23. Colloid (no capillary leakage)
24. Colloids versus crystalloids for fluid resuscitation in critically ill patients:
* The Cochrane review: Lancet; Issue 2 Oxford 2000 by Alderson P, Schierhout G, Roberts I, Bunn F
* Conclusion: No evidence that resuscitation with colloids reduces the risk of death compared with crystalloid in patient with traumatic injury
25. The crystalloid–colloid debate has evolved into a colloid-colloid debate
26. Ideal colloid National Research Council – USA (1963)
* Rapidly replaces blood volume losses.
* Restores the haemodynamic balance.
* Normalizes microcirculatory flow.
* Have a sufficiently long intravascular life.
* Be readily metabolized, readily excreted and well tolerated.
* Be free of side effects, especially regarding haemostasis and anaphylactoid reaction
* Be cost effective and contribute to blood savings.
27. Gelatins
* Short acting
* Prevent platelet aggregation induce by ristocetin - minimal effect on coagulation
* May be diuretic
* Allergy risk
* Contain high [Ca 2+ ) ~ facilitate clotting
28.
29. Dextrans
* Good duration of effect
* Good rheological effect (esp Dextran 40)
* Allergy risk
* Significant coagulation effect
* May interfere with cross-match
* Dextran 40 can cause osmotic renal damage
30. Albumin
* Expensive
* • No evidence of benefit
* • Some evidence of harm
* • ANZICS SAFE study:
* – 7000 patients randomized to Alb or NS

31. Starches
* Good duration of effect
* High molecular weight starches impair coagulation
* Medium molecular weight HES has minimal effect
* Possible endothelial benefit
32. Hetastarch (hydroxyethyl starch)
* Derived from corn starch
* Modified natural polymers of amylopectin which breaks down by amylase
*  IV persistence due to substitution of hydroxyethyl group with D – glucose & more of glucose molecules hydroxylated at the C2 position versus the C6 position,
33. Hetastarch evolutionary concept
* A high degree of substitution (> 0.6), a high C2:C6 ratio (> 8), and a high initial MW (> 450 kDa) will maximize the intravascular half-life.
* Polymers with a MW < 50 kDa are eliminated rapidly by glomerular filtration and larger polymers are hydrolysed by amylase into smaller molecules.
34. HAES classification
35. Types of HES
* 1 st HES – marketed in US & Germany, 450kDa, a/w coagulopathy, withdrawn
* Elohes 6% - (200/0.62)
* Lomol 10% - (250/0.45)
* Haes – Steril 6% - (200/0.5)
* Voluven 6% - (130/0.4)
36. Advantages of HES
* Encourages the restoration of cell mediated function and macrophage function after hemorrhagic shock
* Schmand JF et al. Criti Care Med 1995;23:806–14.
* 10% HES (200:0.5) resulted in significantly better systemic haemodynamics and splanchnic perfusion than volume replacement with 20% human albumin
* Boldt J et al. Anesth Analg 1996;83:254–61.
37. HES & allergic reactions Laxenaire MC et al. Anaphylactoid reactions to colloid plasma substitutes: incidence risk factors mechanisms. Annales Francais d’Anesthesie et Reanimation 1994;13:301–10 A French multicenter prospective study.
38. Disadvantages of HES
* Repeated administration of HAES especially high in vivo MW – reduce factor VIII & VWF & renal function (coagulopathy & anuria)
* Haes – Steril solutions, medium MW were widely used for intravascular volume replacement in cardiac surgery.
* Recommended max dose per day: 20 – 33 ml/kg.
39. Voluven
* HES 130/0.4 was developed with the aim of improving the pharmacokinetic & Mw distribution profile of HES 200/0.5
* Their beneficial effects appear to be related more to their action on inflammatory processes than their colloid osmotic power
* It has been shown in few pharmacokinetic studies that voluven solutions were decreased in plasma & tissue storage after repeated administration (50 – 75 ml/kg/d) & less influence on coagulation.
Anest Analg 2003;96:936 – 43 Anesthesiology, V 99, No 1, Jul 2003
40. Hypertonic saline Stackford SR. J Trauma 1998:44:50-8
* High osmolality (2400 mOsmol/L)
* Small Volume Resuscitation
* Reduced cerebral edema
* Reduced trauma-induced immuno-suppression
* CI: dehydration, oliguric renal failure, cardiogenic shock, DKA, coagulopathies or active hemorrhage
* Central pontine myelinosis : NO clinically significant & were not reported
* Practical dose: 200mls 7.5% NaCl in 10 min
41. Hypertonic Saline
42. Velasco IT et al. Hyperosmotic NaCl and severe hemorrhagic shock. Am J Physiol 1980;239:H664-73
* Severely hemorrhaged dogs (40 ml/kg blood loss) re- sponded with a restored arterial pressure and cardiac output following IV bolus injections of 4 mL/kg of 7.5% NaCl,
* A volume equivalent to only 10% of the volume of shed blood
43. Best evidence
* Wade CE et al. Efficacy of hypertonic 7.5% saline and 6% dextran-70 in treating trauma: a meta-analysis of controlled clinical studies. Surgery 1997;122:609-16.
* 14 trials (1200 patients, 8 HSD, 6 HS)
* Conclusion: No differences in survival with HS, HSD, crystalloid
44. Best evidence
* Wade CE et al. Individual patient cohort analysis of the efficacy of hypertonic saline/dextran in patients with traumatic brain injury and hypotension J. Trauma 1997;42:S61-5.
* RCT comparing HSD & HS alone, as compared to crystalloid.
* Conclusion: some benefit of HS in penetrating injuries and those with combined shock and severe head injury.
45. Blood
* Oxygen flux: CO × O 2 content : CO(SaO2 × Hb × 1.34)
* Blood transfusion is reserved for cases of significant or ongoing bleeding.
* Why?
* - Limited blood supply
* - Need to be re warmed
* - Disease transmission
* - Immunosuppressive effect/ risk of infection
* - I ndependent risk factor for post-traumatic organ dysfunction.
46. Blood
* Limit transfusions
* Transfusion threshold < 7g/dl
* Maintenance level 7 – 9 g/dl
* Older patients and those with ischemic heart disease may need higher Hb
47. Alternative choices
* Autologous blood salvage technique
* Blood substitute
* - modified hemoglobins
* - perfluorocarbons
48. Autologous blood salvage technique
* Example: to reinfuse blood loss secondary to a massive hemothorax.
* Tedious & technical, need experienced personal
* Risk of bacterial contamination
* Micro emboli of platelet plugs and fractured red blood cells.
49. Artificial hemoglobin
* Sloan EP et al. Diaspirin cross linked hemoglobin (DCLHb) in the treatment of severe traumatic hemorrhagic shock. a randomized controlled efficacy trial.
* JAMA 1999; 282:1857-1864
* Study terminated prematurely
* Increased number of death in the experimental group.
50. Hemoglobin based oxygen carrier HBOCs
* Analdo BD, Minei JP. Potential of hemoglobin based oxygen carrier in trauma patients.
* Curr Opin Crit Care 2001; 7: 431-436
* Excellent overview relevant to trauma
* Problem: nitric oxide scavenging effects leading to smooth muscle constriction and subsequent blood pressure elevation
51. HBOC- 201
* McNeil JD, Smith Ld, Jenkins DH, et al.
* J Trauma 2001; 50:1063-1075
* Hypotensive resuscitation using a polymerized bovine hemoglobin-based oxygen carrying solution (HBOC- 201) leads to reversal of anaerobic metabolism.
52. Fluid resuscitation: WHEN & HOW MUCH?
* Traditional strategy: to restore patients to a normovolemic state ASAP
* Based on animal studies (1950 – 60) & Vietnam war.
* Recent strategy: judicious use of fluids, SVR
* Lack of randomized controlled studies, lack of implementation
* ? No documentation support the proposed changes actually will improve patient outcome
53.
* Treatment with IV fluids before hemorrhage was controlled increased the mortality rate, especially if the BP was elevated.
Kowalenko T, Stern S, Dronen S, Wang X. Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma 1992;33:349-53. Stern S, Dronen S, Birrer P, Wang X. Effect of blood pressure on hemorrhage volume and survival in a near- fatal hemorrhage model incorporating a vascular injury. Ann Emerg Med 1993;22:155-63.
54. Postulation
* Increased hydrostatic pressure driving ongoing bleeding or dislodging a clot, as well as the decrease in blood viscosity and dilution of clotting factors.
* - Shoemaker WC et al. Resuscitation from severe hemorrhage. Crit Care Med 1996;24:S12-23 .
* A caveat that also bears consideration when comparing such studies, is the anesthetic used, which can also significantly affect blood loss.
* - Soucy DM et al. Effects of anesthesia on a model of uncontrolled hemorrhage in rats. Crit Care Med 1995;23:1528-32.
55. SBP threshold
* Sondeen JL et al. BP at which rebleeding occurs after resuscitation in swine with aortic injury.
* J Trauma 2003;54:S110-7
* Findings: SBP threshold = 90 mmHg, independent of time from start of bleeding.
56.
* Administering large quantities of IV fluids without controlling the hemorrhage results in hemodilution (  HCT,  available Hb (and oxygen- carrying capacity),  clotting factors & ECF compartment
* This effect is found regardless of the fluid used (blood, LR, NS, hypertonic saline).
Hahn RG. The use of volume kinetics to optimize fluid therapy. J Trauma 2003;54:S155-8
57. The optimal volume of IV fluid administered is a balance between improving tissue oxygen delivery against increasing the blood loss by raising SBP MODS CLOTS Major controversy
58. Delayed fluid resuscitation in penetrating trauma
* Bickell WH et al.
* New Engl J Med 1994;331:1105-9.
* Randomized, prospective and blinded comparison of immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries.
* Methods:
o Patients in the immediate resuscitation group received infusion of isotonic infusion of Ringer's acetate solution through two large bore IV catheters inserted at the scene.
59. Delayed fluid resuscitation in penetrating trauma
o Patients in the delayed resuscitation group also had two large bore IV catheters inserted at the scene but these were then flushed and capped.
* After arrival in the operating room, IV crystalloid and packed red cells were given to all patients to maintain SBP > 100 mm Hg, HCT > 25% and urine output > 50 ml per hour.
* The majority of patients were in hospital within 30 min of reported injury and entered the OR < 1H of hospital time.
60. Delayed fluid resuscitation in penetrating trauma
* 598 studied patients, 70 died before reaching the OR.
* Survival rate of delayed resuscitation group (70%) compared with that in the immediate resuscitation group (62%).
* The frequency of complications was similar in the two groups.
* Conclusion: In hypotensive patients with penetrating torso trauma, delay of fluid resuscitation until operative intervention improves outcome.
61. Regel et al, Acta Anaesthesiol.Scand., 1997
* Data limited to penetrating injuries
* No evidence for blunt haemorrhagic trauma
* Decision on field resuscitation relates to type of trauma and likelihood of hospital transfer
62. On going debate/uncertainty
* Best practice for:
o Penetrating versus blunt trauma
o Rural versus urban settings
o Young versus older patients
o Head injured versus non head injured patients
* ? Malaysian Practice
63. Timing of resuscitation
* Do not delay transfer for resuscitation
* Priority is arrest of hemorrhage
* Commence aggressive resuscitation once control of bleeding is imminent
Pepe et al Emerg.Med Clin.North Am., 1998
64. Pre-hospital resuscitation Søreide & Deakin, Injury, 2005
* Set resuscitation targets according to type of trauma
* • Start isotonic crystalloid infusion
* – Rapid 500ml to achieve targets
* • Reassess after each fluid bolus
* • Do not delay transportation for other than life-saving maneuvers
* • Maintain care during transportation
65. Blunt Trauma Søreide & Deakin, Injury, 2005
* • Goals:
o – Perfusion of vital organs without increasing
o bleeding
* • Minimal fluid resuscitation
o – Rapid infusion of rapid 500ml of isotonic crystalloid
* • Targets:
o – Restore peripheral pulses
o – Keep systolic arterial pressure < 90mmHg
66. TBI Søreide & Deakin, Injury, 2005
* • Goals:
o – Limit bleeding risk
o – Maintain CPP
* • Moderate fluid resuscitation
o – Rapid infusion of rapid 500ml of isotonic crystalloid
* • Targets:
o – Restore and maintain SBP > 110mmHg
67. Penetrating injury Søreide & Deakin, Injury, 2005
* • Goals:
o – Perfusion of at least brain and heart without increasing bleeding
o – Rapid transfer
* • Minimal fluid resuscitation
o – Rapid infusion of 500ml of isotonic crystalloid
* • Targets:
o – Restore basal cerebral perfusion
o – Keep systolic arterial pressure < 80mmHg
68. Søreide & Deakin, Injury (2005) 36, 1001 - 1010
* Fluid resuscitation & blood transfusion in the Emergency Department are still essential elements of the early hospital management of critically ill injured patients
69. Rocha-e-Silva et al. CLINICS 60(2):159-172, 2005
* Review paper: Small volume hypertonic resuscitation of circulatory shock.
* Conclusions:
o Safe, but cautious in moribund, or chronic debilitating diseases.
o First treatment for posttraumatic hypotension, particularly in penetrating trauma head trauma.
o Not a/w increased bleeding, clinically significant hypernatremia and allergic reactions
* Commercially available in European countries.
* A larger prospective, multicenter trials is required to better define the patient population to maximally benefit from hypertonic saline
70.
* SIRS (2 out of 4 criteria) with detection of bacterial focus
* ± /elevated CRP/elevated pro-calcitonin
* Septic shock: sepsis-induced with hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but not limited to lactic acidosis, oliguria or acute alteration of mental status
Sepsis Crit Care Med 1992;20:864-74
71. Fluids in septic shock Marx et al. Int Care Med , 2002
* • 25 fasted, ventilated pigs
* • Faecal peritonitis
* • Fluid titrated to keep CVP 12mmHg
o – Ringer’s solution (RS)
o – Modified fluid gelatin 4% (MFG4%)
o – Modified fluid gelatin 8% (MFG8%)
o – Hydroxyethyl starch 200/0.5 (HES)
* • Haemodynamics and oxygenation measured at 4 and 8 hours
72. Marx et al. Int Care Med , 2002 Fluid requirements
73. Cardiac output Marx et al. Int Care Med , 2002
74. Mixed S v O 2 Marx et al. Int Care Med , 2002
75. Acid base Marx et al. Int Care Med , 2002
76. Fluids in septic shock Marx et al. Int Care Med , 2002
* Conclusions:
* Colloids were significantly better than Ringer’s for resuscitation in this model
* HES appeared to be slightly better than either isotonic or hypertonic gelatin
77. Sepsis
* • Goals:
o – Restore tissue perfusion rapidly
* • Aggressive fluid resuscitation
o – Rapid infusion of 500ml of isotonic crystalloid and colloid
o – Inotropic support as required
* • Targets:
o – Maintain ScvO2 > 70%
o – Keep systolic arterial pressure > 65mmHg
78. End point of resuscitation
* Traditional: Achieved definitive care
* New: Correction of O 2 debt as end point
79. Prehospital care, Arrival to ED Stabilization of vital signs Relieve tissue hypoxia Admission in ICU Phase 1 Phase 2 Phase 3 End point of Resuscitation of Shock
80. RADY ET AL • RESUSCITATION IN THE ED. AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 14, Number 2 • March 1996 . End point of Resuscitation of Shock
81. End point of Resuscitation
82. Davis , Shackford. Base deficit as a guide to volume resuscitation. J. trauma 1988.
o Mild: -2 to -5, moderate: -6 to -14,
o severe: > -14
o Worsening base deficit correlated with ongoing blood loss
o normal base deficit taken as end point of resuscitation
83.
* 76 patients
* Lactate normalized in 24 hr: 100 % survival,
* 24 – 48 hr 78 % survival, > 48 hr: 14 % survivors
* Serum lactate and time to normalization (less
* than or equal to 2 mmol/l) appears to be a
* suitable end point for resuscitation
Abramson et al. Lactate clearance and survival following injury. J. Trauma . 1993
84. Bishop, Shoemaker & colleague J. Trauma 1995
o Prospective randomized trial of survivors values of C.I, O 2 delivery and O 2 consumption as resuscitation end point in severe trauma
o Supranormal values
+ Cardiac Index: CI > 4.5 L/min
+ O 2 Delivery index: DO 2 I > 600ml/min/m2
+ O 2 consumption index: VO 2 I > 170 ml/min/m2
85. Bishop, Shoemaker & colleague J. Trauma 1995
* 50 patients on supranormal variables cf 65 control patients
o lower mortality ( 18 % Vs 37 % )
o fewer organ failures per patient
+ DO 2 I & VO 2 I are strong predictor of multiple organ failure and death
+ Standard hemodynamic measurement MAP, CVP fail to differentiate between survivor and non- survivors.
86. Summary
* Severe hemorrhagic shock
o Aggressive versus judicious fluid therapy (inconclusive)
o Restrictive & permissive hypotension in uncontrolled hemorrhage (clinical evidence is still limited).
o Minimum resuscitation, stop the bleeding (surgical intervention) then maximum resuscitation.
o Future trend may be SVR with HS
o Ringer’s lactate @ NS/ ±Starch is an initial fluid of choice
o Red blood cells if HCT < 25.
o FFP, cryoprecipitate only for coagulation problems
* Septic shock
o Early goal directed, large volume therapy
o Starch is a fluid of choice
87. Conclusions
* Resuscitation should be seen as a continuum in which pre-hospital care, emergency room management and intensive therapy merge.
* Venous access & fluid therapy are a necessary part of this continuum but the optimum timing for fluid administration depends on the circumstances.
* Patient survival is linked to the overall quality, integration, communication & process of care in a trauma system.
88. THANK YOU