23 May 2014 AST Talk medical, dogma, myths

1. Tan Hon Liang
Singapore General Hospital
Anaesthesiology and Critical Care

2. No conflicts of interest to
disclose

3. Disclaimer
My opinion. Feel free to disagree.

4. The Inevitable Question

5. My Objectives
Dissect Dogma.
Discuss Philosophy.
Revise Stats.
EntertainYou.

7. Illustration of Dogma

8. Illustration of Dogma

9. Illustration of Dogma

10. Illustration of Dogma

11. Illustration of Dogma

12. Illustration of Dogma
"The experiments of Harry Harlow and his associates at
the Primate Laboratory of the University ofWisconsin are
described in the textbook Principles of General
Psychology (1980 JohnWiley and Sons)”

13. Brilliant illustration of
Dogma!

14. Except…
Not described in Harlow’s literature.
Not described in the said textbook.

15. The Reality
1996

16. The Reality
It was made up?!

17. The experiment on Dogma
is itself a
!

18. The Reality
 Monkeys trained to avoid manipulating an object .
 Untrained animal placed in cage with a trained animal and
the object.
 1 trained animal pulled untrained animal away from
object.
 2 trained animals exhibited "threat facial expressions
while in a fear posture" when untrained animal
approached the object.

19. See how dogma can be
perpetuated?

20. Dogma is Learnt Behaviour

21. Dogma is Learnt Behaviour
Deer-ma!

22. Overcoming dogma is
difficult.
Humans also like maintaining old boundaries

23. Dogma in Medicine
 List of Dogma
 Use of CVP to guide fluid resuscitation
 Use of NGT aspirates to determine feed tolerance in ICU
 Use of rapid sequence induction/cricoid pressure, esp in
children
 Use of resonium in hyperkalemia acute management
 Use of fluid boluses to treat oliguria
 Use of IVC ultrasound to determine fluid status
 Pulmonary edema management
 Blah Blah Blah….
 Long list if only you looked.

24. But things are about to
change…

25. Scientometrics
 The science of measuring and analyzing science.
 Facts are not eternal.
 In fact, Fact has a half-life.

26. So what is the half life of
facts in Medicine?

27. Half Life of Surgical Facts
 260 abstracts
 1935 to 1994
 Estimated half-life of facts in surgical literature was 45
years.

28. Half Life of Medical Facts
 Original articles and meta-analyses from 2 journals
(Lancet and Gastroenterology).
 1945 to 1999
 Cirrhosis or hepatitis in adults.
 By 2000, 60% of 474 conclusions were still considered true,
19% obsolete, and 21% false.

29. Half Life of Medical Facts
 Half-life of medical fact (in cirrhosis and hepatitis) was 45 years.

30. Half Life of Medical Facts
 NEJM. 10 years (2001-2010). 2044 original articles: 1344
concerned a medical practice:
 981 (73.0%) examined a new medical practice
 363 (27.0%) tested an established practice.
 146 (40.2%) reversed practice.
 138 (38.0%) reaffirmed it.
 79 (21.7%) inconclusive.
 Half Life of Medical Facts may well be shortening.

31. Overcoming dogma is
difficult.
But someone has to start somewhere.

32. So we begin…
1 of 5

33. Glasgow Coma Scale

34. GCS is a reliable predictor
of outcomes.
True or False

35. GCS is applicable in all ICU
patients.
True or False

36. GCS 8 and below
= no gag
= aspiration risk
= must intubate
True or False

37. AtThe Beginning
 15 point scale.
 E4V5M6
 Original 14 point scale
 revised in 1976 with the addition of a
sixth point in the motor response
 Designed forTraumatic Head Injury
 six hours after head trauma

38. Glasgow Coma Scale
 American College of Surgeons Committee onTrauma
 European Society of Intensive Care Medicine
 Eastern Association for the Surgery ofTrauma
 GCS <9 recommended threshold for intubation

39. Glasgow Coma Scale Problems
 1 year, retrospective review. Blunt trauma patients with
presumed head injury with GCS less than or equal to 13
 120 patients.
 A significant number of patients with a GCS of less than or equal
to 9 required emergent intubation.
 A significant minority of patients with a GCS score of 10-13
required emergent intubation (20%) or had intracranial
pathology on head CT scan (23%).

40. Glasgow Coma Scale Problems
 Problem with the Score
 120 mathematical combinations!
 18 possible permutations exist for GCS 9
 17 for scores 8 and 10
 14 for scores 7 and 11
 10 for scores 6 and 12
 Therefore, not all GCS 9 are equal.

41. Stats
What type of scale is GCS?
Nominal
Ordinal
Continuous

42. Ordinal
The difference between unit values is not consistent and compares only better
with worse

43. Glasgow Coma Scale Problems
 Problem with the Score
 E
 Spontaneous (4) : indicative of activity of brainstem arousal
mechanisms but not necessarily of attentiveness
 Vegetative States: Eyes may spontaneously open. “Lights on, but
nobody at home”.
 Noxious stimulus: grimace and eye closure.Then how?
 Eye injury.
 Drugs: muscle relaxants, sedation.

44. Glasgow Coma Scale Problems
 Problem with the Score
 V
 Facial injury.
 Focal neurological injury:
 Broca’s aphasia
 Wernicke’s aphasia
 Conductive aphasia
 Language.
 Intubation, tracheostomy.
 Drugs: muscle relaxants, sedation.

45. Glasgow Coma Scale Problems
 Problem with the Score
 M
 Motor skew
 No correlation to severity:
 M3: internal capsule or cerebral hemispheres injury
 M2: midbrain to upper pontine damage

46. Glasgow Coma Scale Problems
 > 90% publications use 14-item GCS.
 Timing of the initial GCS assessment inconstant.
 GCS components seldom utilized: loss of information.
 Confounders often not reported and, if they are, not in a
standardized manner.
 “current inconsistent and inappropriate use of GCS
diminishes its reliability in both a clinical and a scientific
context.”

47. Glasgow Coma Scale Problems
 French. 60 subjects.
 Observer bias.
 Errors up to 2 points.

48. Glasgow Coma Scale Problems
 Prospective observational study. 208 adult patients.
Emergency Department. Hong Kong.
 Cotton bud and soft tracheal suction catheter to stimulate
the posterior pharyngeal wall (gag reflex)
GCS Gag Present Gag Absent
≤8 36.4% (12/33 ) 63.6% (21/33)
9-14 62.9% (39/62) 37.1% (23/62)
15 77.9% (88/113) 22.1% (25/113)

49. Glasgow Coma Scale Problems
 Designed forTraumatic Head Injury
 six hours after the occurrence of head trauma
 Cannot be used for other pathological states.
 73 patients.Drug or alcohol intoxication. GCS 3 to 14.
 No patient with a GCS <9 aspirated or required intubation.
 1 patient required intubation; this patient had a GCS of 12
on admission to the ward.

50. GCS is a reliable predictor
of outcomes.
False
Not precise.
Many limitations.

51. GCS is applicable in all ICU
patients.
False
Designed for trauma.
May not be applicable to poisoning, medical diseases.

52. GCS <9
= no gag
= aspiration risk
= must intubate
False
Not all need intubation.

53. Summary
 Many limitations.
 GCS for head injury. Be careful about extrapolating to
other conditions.
 Not reliable prognostic factor.
 Not all GCS < 9 require intubation.

54. 2 of 5

55. CentralVenous Pressure
What are the indications for measuring CVP?

56. Indications for CVC
 Hemodynamic monitoring including central venous
pressure (CVP), central venous oxygen saturation (SCvO2)
or for insertion of a pulmonary arterial catheter.
 For infusion of irritants (eg. vasopressors,TPN,
chemotherapy)
 Transvenous cardiac pacing
 Plasmapheresis, apheresis, hemodialysis or CRRT
 Poor peripheral venous access

57. CVP can be used to
monitor hemodynamics
True or False

58. CVP predicts volume
status
True or False

59. CVP predicts fluid
responsiveness
True or False

60. Change in CVP reflects
change in Cardiac Output
True or False

61. CVP
 25 patients.Thoracotomy. 8 on CPB.
 Blood volume estimates with tagged albumin.
 Complex measurement technique.

62. CVP
 Review/case series of 14 different cases, including a
neonate.
 Descriptive: benefit using CVP for additional information.

63. CVP Myth Buster
 Simultaneous measurement of CVP and PCW in patients
with AMI, during volume expansion or diuresis.
 CVP:
 no consistent relation to PCW.
 Did not predict changes in PCW during fluid therapy.
 3 patients with pulmonary edema had normal CVP.
 “CVP in AMI at best of limited value, and at worst seriously
misleading”.

64. CVP Myth Buster
 500 ml of 5 % albumin. 1 hour. 22 patients with CVP
greater than 15 cm. H2O.
 CVP decreased in 14 (64 percent).
 CVP increased slightly but not significantly in 8 (36
percent).
 “High initial CVP is not a reliable index of either
hypervolemia or cardiac failure in critically ill patients”.

65. Many many other studies
concur.

66. Stats
What is Correlation Coefficient?

67. Correlation Coefficient

68. Correlation Coefficient

69. Guess the correlation of
CVP to hemodynamic
status?

71. CVP Myth Buster
 24 studies. Pooled correlation coefficient between
 CVP and measured blood volume
 0.16 (95% CI, 0.03 to 0.28)
 Baseline CVP and change in stroke index/cardiac index
 0.18 (95% CI, 0.08 to 0.28).
 Delta CVP and change in stroke index/cardiac index
 0.11 (95% CI, 0.015 to 0.21).
 Baseline CVP was 8.7+/-2.32 mm Hg in the responders
compared to 9.7+/-2.2 mm Hg in nonresponders.

72. Stats
What is a Receiver Operating Characteristic Curve (ROC)?

73. Receiver Operating Characteristic
Curve (ROC)
 True positive rate (Sensitivity) plotted against false
positive rate (100-Specificity) for different cut-off points.

74. Receiver Operating Characteristic
Curve (ROC)
 Test with perfect discrimination: ROC curve passes
through the upper left corner (100% sensitivity, 100%
specificity).
 Therefore the closer the ROC curve is to the upper left
corner
 The higher the AUC of ROC curve = higher overall accuracy
of test.

75. CVP Myth Buster
 The pooled area under the ROC curve was 0.56 (95% CI,
0.51 to 0.61).

76. Tale of 7 Mares
 7 Horses. Standing position in “standing dock”
 Bled for 1 hours at 16 mL/kg/h.
 Central venous pressure (CVP), central venous blood gas,
blood lactate concentration, and heart rate measured.
 Only study to show reliable correlation.

77. Half Life of Medical Fact
49 years
46 years
Not too far off!

78. CVP Myth Buster
 43 studies
 AUC 0.56 (95% CI, 0.54-0.58) with no heterogenicity
between studies.
 0.56 (95% CI, 0.52-0.60) for studies done in ICU.
 0.56 (95% CI, 0.54-0.58) for studies in OT.

79. CVP can be used to
monitor hemodynamics
False
No, it cannot and should not.

80. CVP predicts volume
status
False

81. CVP predicts fluid
responsiveness
False
Passive Leg Rising works better

82. Change in CVP reflects
change in Cardiac Output
False

83. Summary
 CVC:
1. For infusion of irritants (eg. vasopressors,TPN,
chemotherapy)
2. Transvenous cardiac pacing
3. Plasmapheresis, apheresis, hemodialysis or CRRT
4. Poor peripheral venous access
5. Liver surgery

84. 3 of 5

85. Treatment of
Hyperkalemia

86. Treatment of hyperkalemia
 Calcium
 Insulin – Dextrose
 Sodium bicarbonate
 Beta agonist
 Resonium
 Hemodialysis

87. Resonium is a resin which
binds only potassium and
aids excretion.
True or False

88. Resonium should be used
to treat acute
hyperkalemia
True or False

89. Resonium is safe and
effective.
True or False

90. Resonium
 Approved by FDA in 1958.
 4 years before drug manufacturers were required to prove
the effectiveness and safety.
 Quoted studies of efficacy:

91. Resonium Myth Buster
 8 patients: 5 given resonium, 3 given sorbitol (laxative)
 0 K+ diet: High sugar syrup only.
 K+ checked on Day 5.
 Resonium 6.6 -> 5.2
 Sorbitol 6.3 -> 4.6

92. Resonium Myth Buster
 Uncontrolled study. 32 patients. Acute and chronic renal
failure.
 23 of 30 cases: K+ fell by at least 0.4 mmol/L in the first 24
hours.
 Low K+ diet.
 20% Dextrose IV. Insulin. NaHCO3.
 No statistical analysis.

93. Won’t get published in
NEJM now!

94. But does Resonium work?
“I swear I have seen it work acutely”

95. Resonium – Does it work?
 1 mmol K+ binds 1 g of resin.
 In vivo, sodium only partially released: efficiency is 33%.
 Bind any cation: Calcium, hydrogen, Magnesium
 10 mmol of K+ bound and excreted per 30-g dose.
 What doses have you seen prescribed in your hospital?
 How much K+ would that clear?

96. Resonium – why it seems to
work?
 Given with laxatives/sorbitol – poop works.
 Sodium exchanged: possibly absorbed: plasma expansion
= dilution!
 Other things you did worked.
 Low K+ diet
 Insulin-Detrose
 Dialysis
 Spurious in the first place?

97. Resonium Myth Buster
 Increase insoluble K+ output but decrease soluble K+
output: no significant effect on total K+ output.
 Did not decrease serum K+ at 4, 8 and 12 hr.
 Single-dose resin-cathartic therapy produces no or only
trivial reductions in K+.

98. Resonium Myth Buster
 FDA warning:
 Severe constipation.
 Colonic necrosis.
 Wisdom of using Resonium challenged.

99. Resonium is a resin which
binds potassium and aids
excretion.
False

100. Resonium should be used
to treat acute
hyperkalemia
False

101. Resonium is safe and
effective.
False

102. Resonium works and
should be given to treat
acute hyperkalemia.
No, it does not.
No, it has no role.

103. Summary
 No role in acute hyperkalemia.
 Can be harmful.
 Avoid in constipated patient, uremia, critically ill or post
abdominal surgery.

104. 4 of 5

105. UterineTilt in Obstetric
Patients
Is it your OT routine?

106. The gravid uterus causes
IVC and aortic
compression.
True or False

107. IVC compression and the
fetus is harmed.
True or False

108. Left lateral tilt is a
solution.
True or False

109. So how much do you tilt?
5, 10, 15, 30, 90?

110. 2 Questions
Maternal vs fetal

111. Fetal Effects

112. Left LateralTilt averts fetal harm?
 20 term parturients
 Neither the left or the right pelvic-tilt position associated
with a significant change in leg blood flow or maternal
heart rate compared to the supine position.
 Fetal heart rate and umbilical Doppler resistance did not
change in any position.

113. Left LateralTilt averts fetal harm?
 25 term parturients.
 Supine and in both right and left 5 degrees and 10 degrees
lateral tilt positions.
 No significant difference among fetal variables in the
various maternal position.

114. Left LateralTilt averts fetal harm?
 25 term parturients.
 4 positions (random order): supine with a 15-degree left
tilt, sitting, and left lateral and right lateral positions.
 No significant differences in fetal heart rate, pulsatility
index, or resistivity index among positions.

115. Maternal Effects

116. Maternal Harm?
 157 term parturients. Suprasternal doppler. NIBP of upper
and lower limbs
 11 patients CO decreased >20%, without changes in SBP,
when tilted to <15°: attributable to IVC compression.
 Only 1 patient in the supine had aortic compression with
the SBP in the upper limb 25 mm Hg higher than the lower
limb

117. Maternal Harm?
 573 pregnant subjects undergoing antepartum Non-Stress
Test.
 Only 2% had presyncopal symptoms when supine
 (did not affect the NST, either in terms of reactivity or any
pathological findings)

118. The Angle Matters
Often too little.

119. Angle Matters
 157 term parturients. Random position : 0°, 7.5°, 15°, and
full left lateral tilt.
 CO 5% higher when patients were tilted at ≥15° compared
with <15°.

120. Angle Matters
 16 anaesthetists. Almost all less than 15 degree tilit
 Visually guess was grossly inaccurate in 42 of 43 patients.
 Average tilt given was only 8.09 degrees

121. How you position might
matter.

122. How to get the tilt matters
 51 term parturients
 Random left lateral, supine-to-tilt and left lateral-to-tilt
positions using a Crawford wedge.
 Femoral vein area, femoral vein velocity, femoral artery area,
pulsatility index, resistance index and right arm MAP and HR.
 Moving from the full left lateral to the lateral tilt position may
prevent aortocaval more than when from a supine to left lateral
tilt position.

123. The gravid uterus causes
IVC and aortic
compression.
True
But not all symptomatic.

124. IVC compression and the
fetus is harmed.
Maybe.
Current evidence suggest not.

125. Left lateral tilt is a
solution.
True
But correct angle needed.
Full left lateral is better if you need it.

126. Summary
 ~1-4% of term parturient affected.
 Majority not symptomatic.
 Fetal compromise might be over-emphasized.
 Visual estimated (agar agar) token tilt is pointless.
 Tilt often overestimated visually.
 Want to do it, then do it properly: full lateral (then possibly
tilt back).

127. 5 of 5
hallelujah

128. Treating Oliguria/AKI in
ICU
Preventing dialysis dependence/progression of renal failure

129. Treating Oliguria/AKI in ICU
 Diuretic
 Fluid bolus
 Increase blood pressure
 Dialysis
 (Do nothing)

130. Theoretical Basis
 Diuretic
 Paralyze energy dependent ion exchangers: Reduce oxygen
consumption in kidneys.
 Fluid bolus
 Improve preload
 Increase blood pressure
 Improve renal perfusion
 Dialysis
 Partial replacement of kidney function.
 (Do nothing)

131. Loop diuretics/frusemide
can treat/prevent AKI.
True or False

132. Loop Diuretic/Frusemide
 54 critically ill surgical patients.
 Frusemide increased urine output, COsm, and CNa.
 Produced no change in GFR, RPF, RBF, and RBF
distribution.

133. Loop Diuretic/Frusemide
 In-hospital mortality RR 1.11 (95% CI 0.92 to 1.33)
 Renal replacement therapy RR 0.99 (95% CI 0.80 to 1.22),
 Possibly increased risk of temporary deafness and tinnitus
with high doses RR 3.97 (95% CI 1.00 to 15.78).

134. Frusemide
 Loop diuretics increased incidence of AKI (NNH = 8 (95%
CI: 5 to 15).

135. Loop diuretics/frusemide
can treat/prevent AKI.
False
Urine for the sake of urine is not useful acutely.

136. Loop diuretics/frusemide
may still have a role.
But not acutely.
In volume management in latter stages.

137. AKI/Oliguria can be
treated with fluid boluses.
True or False

138. Fluid Bolus
 Theory:
 Increase preload. Prevent ischemia.
 Prevent renal hypoperfusion.
 Reality:
 Post-mortem kidney biopsy
 Capillary leukocytic infiltration and apoptosis predominate.
 Not ischemic necrosis

139. Fluid Bolus
 Reality:
 No consistent renal histopathological changes in human or
experimental septic AKI.
 Majority of studies reported normal histology or only mild,
nonspecific changes.
 ATN was relatively uncommon.

140. Fluid Bolus
 Reality
 Renal vasculature cannulated: hyperdynamic instead of
ischemic.

141. Not much point giving
fluid bolus thinking it will
improve renal perfusion!
Except in acute hypovolemia/hemorrhagic shock

142. Excessive fluid is not
harmless

143. Excessive Fluid
 Less fluid, better oxygenation.
 Although no difference in mortality.
 Less fluid, but no increase risk in dialysis rates.
 Infer: fluid does not affect dialysis rate.

144. Excessive Fluid
 10 ICU. Italy.
 601 patients: 132 had AKI. Mortality 50% in this group.
 Non-survivors had higher mean fluid balance (1.31 ± 1.24
versus 0.17 ± 0.72 L/day; P <0.001) compared to survivors.

145. Beyond initial
resuscitation, fluid bolus
maybe pointless and
potentially harmful.

146. AKI/Oliguria can be
treated with fluid boluses.
False
And it might even be harmful.
Avoid “therapeutic drowning”

147. Summary
 In the treatment of oliguria/AKI in ICU:
 Diuretic: no acute role.
 Fluid bolus: no role unless acute hypovolemia/hemorrhage.
 Increase blood pressure: yes, if baseline BP is high.
 Dialysis: trend to mortality benefit if started early.
 Doing nothing is not unreasonable.

148. Conclusion

149. Half of what we do is
wrong
We just don’t know which half.

150. Trust no one
(and everything you were ever told)
Including what I just told you.

151. ThankYou
tan.hon.liang@sgh.com.sg

152. In case you are not convinced
 The abstract that says it all.