The Rule of SIX in Drug Dosing and Infusion

Source:http://emergencymedic.blogspot.com/2010/08/rule-of-six-in-drug-dosing-and-infusion.html

Supposed as a junior medical officer, you want to start dopamine infusion for a patient in hypovolemic shock (with persistent low BP despite adequate fluid resuscitation). You look up at the drug formulary (just to counter-check) and it states that the dosage for dopamine is "5 mcg/kg/min, increasing gradually using 5-10 mcg/kg/min increments......". Most drug formularies will list dopamine dosages in the form of xxx mcg/kg/min.

So, you decide to start the patient on 10 mcg/kg/min. You remember well what you were taught in med school: dopamine infusion in the range 3 - 5 mcg/kg/min is predominantly for its dopaminergic effect (dopaminergic receptors are present abundantly in the mesenteric vasculature, brain, heart and the kidneys); dosing range from 5 - 10 mcg/kg/min is predominantly for its beta effects and dosage ranges above 10mcg/kg/min up to 20 mcg/kg/min is for its alpha effects.

You inform the staff nurse on duty: "Staff nurse, could you start dopamine infusion for this patient, start with 10 mcg/kg/min, titrating until a desirable blood pressure achieved. Erm.. I think this patient's weight is around 70 kg" Unfortunately, the staff nurse on duty is a junior staff nurse. She looks at you and said "Doctor, can you tell me how do I prepare for the infusion? Each ampoule of dopamine is 200 mg." You look a little bit annoyed, thinking to yourself "you mean you didn't learn that in your nursing school???" Regardless, still the sole responsibility of giving clear, concise and detailed instruction rests on the shoulder of the doctor in charge. You cannot blame the staff nurse of whether she learns that in nursing school or not.

Since you can't get an "answer" from the junior staff nurse, you turn around and ask a senior staff nurse. The senior staff nurse said, "Doctor, I don't know about this 10 mcg/kg/min. But from my experience, if you break open 1 ampoule of dopamine (200 mg) and diluted it into 50 cc, usually most doctors will run the drug at 10 ml/hr.

Huh??? You got more confused!!!

The above scenario is not uncommonly seen. Many nurses, from my experience, either do not understand or have forgotten about the correlation between the xxx mcg/kg/min that is stated in most books and the actual running of how many ml/hr of the diluted dopamine in 100-ml or 50-ml syringe.

The secret of calculating that is by using the RULE of SIX for drug infusion. And I am amazed how many medical students do not know this and how many of them actually do not even know how to derive this formula.

So, in this blog post, I will first prove that this formula is true by deriving it from basic mathematics and then to discuss on the variants of this formula for the ease of practicality.

The Rule of Six for drug infusion states that:

When (6 * body weight of patient) mg of a drug is diluted in 100 ml,

every ml/hr of the drug infused is equal to one mcg/kg/min


In other words,
(6 * BW) mg diluted in 100ml, 1 ml/hr = 1 mcg/kg/min, where BW - body weight

How do we derive that formula? Basic simple algebra......
We break up that equation into two parts:
1 ml/hr ..................... (A)
1 mcg/kg/min ......................(B)

and then we will attempt to prove that (A) = (B)


Now, let's look at the first part of the equation, part (A), namely 1 ml/hr

Let's assume BW = a kg
So,
(6a) mg of Drug A ---- in 100 ml (diluted into 100 ml)

therefore,
1 ml of Drug A = (6a)mg/100

But 1 ml of Drug A is infused over 1 hour (= 60 min)

Therefore, for every min, the amount of drug A infused is:
(6a)mg/(100*60)

But every 1 mg = 1000 mcg.
Therefore, for every min, the amount of drug A infused is:
(6a)*1000 mcg/(100*60)

simplify the equation, for every min, the amount of drug A infused is:
(a) mcg

In other words, part A of the equation (1 ml/hr) can be written as:
(a) mcg...........................(1)


Now, look at part B of the equation, 1 mcg/kg/min

We have assumed that the BW = a kg,

therefore, for every min, the amount of drug A infused is:
(a) mcg............................(2)

Since, (1) = (2), therefore
1 ml/hr = 1 mcg/kg/min if (6*BW) mg of the drug is diluted into 100 ml.

Unfortunately, 100-ml syringes are not easily available in my hospitals. Most of the large syringes are 50-ml syringes.

Nevermind, the rule of 6 can still be applied, but for 50-ml dilution,

(3*body weight) mg of drug A in 50 ml, 1 ml/hr = 1 mcg/kg/min

(this simply because 50 = 100/2, therefore we take 6/2, which is 3 !!).

In other words, the rule of 6 can also be written as:

When (3 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to one mcg/kg/min



and, by using the same premise,

When (0.3 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to 0.1 mcg/kg/min



and...


When (0.03 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to 0.01 mcg/kg/min



Now, let's come back to our case scenario.

Let's apply the rule of 6 in our case. The patient's body weight is 70 kg. Most adults' body weight would be in the range of 60 - 70- kg. Assuming that we are going to dilute into 50 ml, therefore we use the variant:


When (3 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to one mcg/kg/min


Therefore,
(3*70) mg of dopamine is diluted in 50 ml, every ml/hr is equal to 1 mcg/kg/min.
In other words, 210 mg of dopamine is diluted in 50 ml, 10 mcg/kg/min requires 10 ml/hr.

210 mg ~ approximately 200 mg. Remember that most dopamine ampoules contain 200 mg each.

Therefore, for convenience sake, break open 1 ampoule of dopamine (200 mg), dilute in 50 ml, and just run 10 ml/hr (that will give you 10 mcg/kg/min). No wonder that's what the senior staff nurse said! You see, most drugs are prepared in such a way that it is convenient to use (especially for adult patients) and most people (especially those in places like emergency departments and ICUs), doctors and staff nurses included, are doing it routinely without really understand the principles behind.

In other words, you would not have much problem, if you are infusing drugs such as dopamine, where the drug ampoules are conveniently prepared.

But you will have troubles when it comes to pediatric patients (where the Rule of 6 is particularly useful) and when it comes to infusing other drugs such as adrenaline or noradrenaline (also known as epinephrine and norepinephrine respectively).

Adrenaline infusion, for example, the dosage range is 0.05 mcg/kg/min - 0.2 mcg/kg/min. So how are you going to prepare the dilution and rate of infusion? Bearing in mind too that most adrenaline ampoules come in 1mg/ml packaging. If you apply the rule of 6, then you will have to take your time to break 200 ampoules!! (while the patient is hanging there in a state of shock). Furthermore, since the dosage range is around 0.05 mcg/kg/min, the rate infused per min will be in the decimals - minute amount!

Therefore, we use this variant of the rule:

When (0.03 * body weight of patient) mg of a drug is diluted in 50 ml,

every ml/hr of the drug infused is equal to 0.01 mcg/kg/min


So, for adrenaline, (0.03 * 70) mg of adrenaline diluted in 50 cc, 1 ml/hr = 0.01 mcg/kg/min.

Therefore, for convenience, you just need to break 2 or 3 ampoules (2 - 3 mg) of adrenaline, dilute it to become 50 ml, and infuse at the rate of 5 ml/hr (if you are aiming for 0.05 mcg/kg/min). Bearing in mind too that the rule need not to be applied rigidly, because in the first place, the weight that you estimate is just as it is - an estimation. You can always titrate the infusion rate up and down. But the decimal point and the variant of the rule you are going to use must be decidedly correct because there has been anecdotal report that states that a baby died as a result of "misplaced decimal point (when applying the rule of 6) and the preparation of a dopamine infusion that was 10 times more concentrated than required" (Click on the link to read the article).

I disagree with the writer of that article that the use of the Rule of 6 should be abandoned. The rule of 6 is just a scientific, standalone formula that can be derived objectively from first principles. It is neutral. It is only when we do not understand the principles behind properly, then we will just follow blindly and thus, courting disaster!

Happy infusing!

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Emergency Fluid Therapy

Source:http://www.slideshare.net/drcd2009/emergency-fluid-therapy
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

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