Reviewer's report
Title:Sensitivity of intra-abdominal, intra-organ and intravascular pressures in
detecting changes induced by external abdominal pressure with and without
PEEP: an experimental study
Version: 2Date:14 October 2009
Reviewer: Manu Malbrain
Reviewer's report:
I read with interest the paper by Jakob et al. Entitled “sensitivity of
intra-abdominal, intra-organ and intravascular pressures in detecting changes
induced by external abdominal pressure with and without PEEP”
Any further chracterisation on IAP, IAH and ACS is worthwhile and I congratulate
the authors for having performed this study and bringing us more light on this
topic. The article is short and to the point, well written in correct English. I only
have some minor comments.
1) Introduction: please stick to the recently published definitions on IAH and ACS
by the WSACS: IAH is defined as a SUSTAINED increase in iAP above 12
mmHg. While ACS is defined as a sustained increase in IAP above 20 mmHg
(not 25 as stated by the authors) with NEW ONSET organ failure [1, 2].
2) introduction page 5: some reecnt papers alluded to the interactions between
intrathoracic and infrathoracic pressures. I don’t agree with the last paragraph
that these pressure changes are not well defined [3-5].
3) methods: what about the impact of ventilation and thus the respiratory
changes on IAP and other pressures. Recent data show that this may be related
to the compliance of the abdominal wall. Do you have data on end-expiratory,
end-inspiratory and mean values of these pressures; if not this can be discussed
as luimitation and option for future studies.[6]
3) methods: major drawback is that ITP or Peso were not measured – this needs
to be adressed (cfr above)
3) methods: another drawback is that the application of external pressure on the
abdomen is far from a real life situation where the abdomen is either fluid filled
(ascites) or gas filled (laparoscopy) or filled with edematous organs. Making it
difficult to extrapolate these results to other studies or a real life situation. A
recent publication also alluded to the optimal animal model and implicationsand
guidelines for research on IAH and ACS [7, 8].
Methods: some studies alluded to the fact that morphinomimetics (like fentanyl)
can increase IAP by abdominal muscle contraction. Also the level of sedation is
important, the use or not of muscle relaxants and the positioning of the subject or
animal. This could be discussed a little bit more afterwards [9-11].
Methods: pigs were starved with free access to water, later on ringer solution
was given to keep PCWP between 6-12mmHg. This may have introduced a bias
since static barometric tresholds may not reflect true preload status in conditions
of increased ITP or IAP, volumetric monitoring would have given some added
value. What about SVV/PPV?
Methods: regarding zero reference, just a notice that ideally IAP should be
zero-referenced at the mid-abdomen level. It is important to note that the level of
the zero reference used clinically in IAP monitoring may have an impact [12].
Methods: instillation of 50ml into the pigs bladder probably is too much, in
humans a maximal instillation volume of 20mls was recommended – this need to
be discussed.
Methods: just a note regarding the application of external weight, this technique
and its effects on IAP, ICP, … has been studied before and moreover it was in
humans by Citerio, this reference needs to be added [13]
Methods: regarding peep: other studies showed an effect of PEEP on IAP, but
this was related to the magnitude of PEEP (little effect at PEEP levels below 11)
and the baseline IAP. Maybe the results could have been different if PEEP was
increased to a level equal to IAP.
Page 9-10 are difficult to read. I understand the different stages of the study or
given but it would make more sense to presnet the data otherwise: effects on IAP
(stomach vs bladder vs direct); effects on vascular pressures (supradiafragmatic:
CVP, PCWP, PAP – vs infradiafragmatic: IVCP)
Discussion: state definition of APP= MAP – IAP
Page 12 do you mean pulmonary artery oclusion pressure instead of diastolic? I
don’t agree with the statement that your data do not support the use of higher
filling pressure targets in IAH: please omit statement because in general static
pressure targets are useless and volumetric indices or SVV/PPV were not
measured
Conclusions: no data givcen to support statement that bladder, stomach and
direct IAP correlate well: please add results on correlations and bland and altman
analysis
Tables: since a swan ganz was in place can you provide data on SVR, CO, …
Table 2: please also provide data on CVP, PAOP,
Figures are difficult to read: I would replace by correlation plots and bland and
altman plots comparing direct IAP as gold standard with IGP, IVP, IVCP and then
look at correlations between IVP as gold standard vs IGP and IVCP and finally
IGP vs IVCP. Correlations should be looked for for ALL comparisons, for PEEP 0
vs PEEP 10 and fro nl IAP vs IAP >12
Another interesting figure could be to look at delta IAP vs delta IGP/IVP/IVCP
References: a more recent review on “what is normal IAP” has been published
[14], increased mortality in relation to IAH has also been shown in a recent and
the only one so far multicentre study [15]
Regarding abbreviations: please expand all abbreviations when used for the First
time and use them in a concise way afterwards (eg IAP, IAH, ACS,…)
IN CONCLUSIONS: again I want to congratulate the authors for this nice study
that I enjoyed reading. If they take into account the comments above they can
further improve their paper.
Suggested references
1. Cheatham, M.L., et al., Results from the International Conference of Experts
on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II.
Recommendations. Intensive Care Med, 2007. 33(6): p. 951-62.
2. Malbrain, M.L., et al., Results from the International Conference of Experts on
Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I.
Definitions. Intensive Care Med, 2006. 32(11): p. 1722-1732.
3. Valenza, F., et al., Static and dynamic components of esophageal and central
venous pressure during intra-abdominal hypertension. Crit Care Med, 2007.
35(6): p. 1575-81.
4. Wauters, J., A. Wilmer, and F. Valenza, Abdomino-thoracic transmission
during ACS: facts and figures. Acta Clin Belg Suppl, 2007. 62(1): p. 200-5.
5. Talmor, D., et al., Esophageal and transpulmonary pressures in acute
respiratory failure. Crit Care Med, 2006. 34(5): p. 1389-94.
6. Sturini, E., et al., Respiratory variation of intra-abdominal pressure: indirect
indicator of abdominal compliance? Intensive Care Med, 2008. 34(9): p. 1632-7.
7. Schachtrupp, A., J. Wauters, and A. Wilmer, What is the best animal model for
ACS? Acta Clin Belg Suppl, 2007. 62(1): p. 225-32.
8. De Waele, J.J., et al., Recommendations for research from the International
Conference of Experts on Intra-abdominal Hypertension and Abdominal
Compartment Syndrome. Acta Clin Belg, 2009. 64(3): p. 203-209.
9. Drummond, G.B. and M.K. Duncan, Abdominal pressure during laparoscopy:
effects of fentanyl. 2002. 88(3): p. 384-388.
10. De Laet, I., et al., The effect of neuromuscular blockers in patients with
intra-abdominal hypertension. Intensive Care Med, 2007.
11. Cheatham, M.L., et al., The impact of body position on intra-abdominal
pressure measurement: a multicenter analysis. Crit Care Med, 2009. 37(7): p.
2187-90.
12. De Waele, J.J., et al., The effect of different reference transducer positions
on intra-abdominal pressure measurement: a multicenter analysis. Intensive
Care Med, 2008. 34(7): p. 1299-303.
13. Citerio, G., et al., Induced abdominal compartment syndrome increases
intracranial pressure in neurotrauma patients: a prospective study. Crit Care
Med, 2001. 29(7): p. 1466-71.
14. De Keulenaer, B.L., et al., What is normal intra-abdominal pressure and how
is it affected by positioning, body mass and positive end-expiratory pressure?
Intensive Care Med, 2009. 35(6): p. 969-976.
15. Malbrain, M.L., et al., Incidence and prognosis of intraabdominal
hypertension in a mixed population of critically ill patients: a multiple-center
epidemiological study. Crit Care Med, 2005. 33(2): p. 315-22.
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: Yes, and I have assessed the statistics in my report.
Declaration of competing interests:
I declare that I have no competing interests, except as former founding president
of the world society on abdominal compartment syndrome I just have a high
intrest in this topic...
Reviewer's report
Title:Sensitivity of intra-abdominal, intra-organ and intravascular pressures in
detecting changes induced by external abdominal pressure with and without
PEEP: an experimental study
Version: 2Date:14 October 2009
Reviewer: Manu Malbrain
Reviewer's report:
I read with interest the paper by Jakob et al. Entitled “sensitivity of
intra-abdominal, intra-organ and intravascular pressures in detecting changes
induced by external abdominal pressure with and without PEEP”
Any further chracterisation on IAP, IAH and ACS is worthwhile and I congratulate
the authors for having performed this study and bringing us more light on this
topic. The article is short and to the point, well written in correct English. I only
have some minor comments.
1) Introduction: please stick to the recently published definitions on IAH and ACS
by the WSACS: IAH is defined as a SUSTAINED increase in iAP above 12
mmHg. While ACS is defined as a sustained increase in IAP above 20 mmHg
(not 25 as stated by the authors) with NEW ONSET organ failure [1, 2].
2) introduction page 5: some reecnt papers alluded to the interactions between
intrathoracic and infrathoracic pressures. I don’t agree with the last paragraph
that these pressure changes are not well defined [3-5].
3) methods: what about the impact of ventilation and thus the respiratory
changes on IAP and other pressures. Recent data show that this may be related
to the compliance of the abdominal wall. Do you have data on end-expiratory,
end-inspiratory and mean values of these pressures; if not this can be discussed
as luimitation and option for future studies.[6]
3) methods: major drawback is that ITP or Peso were not measured – this needs
to be adressed (cfr above)
3) methods: another drawback is that the application of external pressure on the
abdomen is far from a real life situation where the abdomen is either fluid filled
(ascites) or gas filled (laparoscopy) or filled with edematous organs. Making it
difficult to extrapolate these results to other studies or a real life situation. A
recent publication also alluded to the optimal animal model and implicationsand
guidelines for research on IAH and ACS [7, 8].
Methods: some studies alluded to the fact that morphinomimetics (like fentanyl)
can increase IAP by abdominal muscle contraction. Also the level of sedation is
important, the use or not of muscle relaxants and the positioning of the subject or
animal. This could be discussed a little bit more afterwards [9-11].
Methods: pigs were starved with free access to water, later on ringer solution
was given to keep PCWP between 6-12mmHg. This may have introduced a bias
since static barometric tresholds may not reflect true preload status in conditions
of increased ITP or IAP, volumetric monitoring would have given some added
value. What about SVV/PPV?
Methods: regarding zero reference, just a notice that ideally IAP should be
zero-referenced at the mid-abdomen level. It is important to note that the level of
the zero reference used clinically in IAP monitoring may have an impact [12].
Methods: instillation of 50ml into the pigs bladder probably is too much, in
humans a maximal instillation volume of 20mls was recommended – this need to
be discussed.
Methods: just a note regarding the application of external weight, this technique
and its effects on IAP, ICP, … has been studied before and moreover it was in
humans by Citerio, this reference needs to be added [13]
Methods: regarding peep: other studies showed an effect of PEEP on IAP, but
this was related to the magnitude of PEEP (little effect at PEEP levels below 11)
and the baseline IAP. Maybe the results could have been different if PEEP was
increased to a level equal to IAP.
Page 9-10 are difficult to read. I understand the different stages of the study or
given but it would make more sense to presnet the data otherwise: effects on IAP
(stomach vs bladder vs direct); effects on vascular pressures (supradiafragmatic:
CVP, PCWP, PAP – vs infradiafragmatic: IVCP)
Discussion: state definition of APP= MAP – IAP
Page 12 do you mean pulmonary artery oclusion pressure instead of diastolic? I
don’t agree with the statement that your data do not support the use of higher
filling pressure targets in IAH: please omit statement because in general static
pressure targets are useless and volumetric indices or SVV/PPV were not
measured
Conclusions: no data givcen to support statement that bladder, stomach and
direct IAP correlate well: please add results on correlations and bland and altman
analysis
Tables: since a swan ganz was in place can you provide data on SVR, CO, …
Table 2: please also provide data on CVP, PAOP,
Figures are difficult to read: I would replace by correlation plots and bland and
altman plots comparing direct IAP as gold standard with IGP, IVP, IVCP and then
look at correlations between IVP as gold standard vs IGP and IVCP and finally
IGP vs IVCP. Correlations should be looked for for ALL comparisons, for PEEP 0
vs PEEP 10 and fro nl IAP vs IAP >12
Another interesting figure could be to look at delta IAP vs delta IGP/IVP/IVCP
References: a more recent review on “what is normal IAP” has been published
[14], increased mortality in relation to IAH has also been shown in a recent and
the only one so far multicentre study [15]
Regarding abbreviations: please expand all abbreviations when used for the First
time and use them in a concise way afterwards (eg IAP, IAH, ACS,…)
IN CONCLUSIONS: again I want to congratulate the authors for this nice study
that I enjoyed reading. If they take into account the comments above they can
further improve their paper.
Suggested references
1. Cheatham, M.L., et al., Results from the International Conference of Experts
on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II.
Recommendations. Intensive Care Med, 2007. 33(6): p. 951-62.
2. Malbrain, M.L., et al., Results from the International Conference of Experts on
Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I.
Definitions. Intensive Care Med, 2006. 32(11): p. 1722-1732.
3. Valenza, F., et al., Static and dynamic components of esophageal and central
venous pressure during intra-abdominal hypertension. Crit Care Med, 2007.
35(6): p. 1575-81.
4. Wauters, J., A. Wilmer, and F. Valenza, Abdomino-thoracic transmission
during ACS: facts and figures. Acta Clin Belg Suppl, 2007. 62(1): p. 200-5.
5. Talmor, D., et al., Esophageal and transpulmonary pressures in acute
respiratory failure. Crit Care Med, 2006. 34(5): p. 1389-94.
6. Sturini, E., et al., Respiratory variation of intra-abdominal pressure: indirect
indicator of abdominal compliance? Intensive Care Med, 2008. 34(9): p. 1632-7.
7. Schachtrupp, A., J. Wauters, and A. Wilmer, What is the best animal model for
ACS? Acta Clin Belg Suppl, 2007. 62(1): p. 225-32.
8. De Waele, J.J., et al., Recommendations for research from the International
Conference of Experts on Intra-abdominal Hypertension and Abdominal
Compartment Syndrome. Acta Clin Belg, 2009. 64(3): p. 203-209.
9. Drummond, G.B. and M.K. Duncan, Abdominal pressure during laparoscopy:
effects of fentanyl. 2002. 88(3): p. 384-388.
10. De Laet, I., et al., The effect of neuromuscular blockers in patients with
intra-abdominal hypertension. Intensive Care Med, 2007.
11. Cheatham, M.L., et al., The impact of body position on intra-abdominal
pressure measurement: a multicenter analysis. Crit Care Med, 2009. 37(7): p.
2187-90.
12. De Waele, J.J., et al., The effect of different reference transducer positions
on intra-abdominal pressure measurement: a multicenter analysis. Intensive
Care Med, 2008. 34(7): p. 1299-303.
13. Citerio, G., et al., Induced abdominal compartment syndrome increases
intracranial pressure in neurotrauma patients: a prospective study. Crit Care
Med, 2001. 29(7): p. 1466-71.
14. De Keulenaer, B.L., et al., What is normal intra-abdominal pressure and how
is it affected by positioning, body mass and positive end-expiratory pressure?
Intensive Care Med, 2009. 35(6): p. 969-976.
15. Malbrain, M.L., et al., Incidence and prognosis of intraabdominal
hypertension in a mixed population of critically ill patients: a multiple-center
epidemiological study. Crit Care Med, 2005. 33(2): p. 315-22.
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: Yes, and I have assessed the statistics in my report.
Declaration of competing interests:
I declare that I have no competing interests, except as former founding president
of the world society on abdominal compartment syndrome I just have a high
intrest in this topic...
Please review this paper.
user
Reviewer's report
Title:Sensitivity of intra-abdominal, intra-organ and intravascular pressures in
detecting changes induced by external abdominal pressure with and without
PEEP: an experimental study
Version: 2Date:14 October 2009
Reviewer: Manu Malbrain
Reviewer's report:
I read with interest the paper by Jakob et al. Entitled “sensitivity of
intra-abdominal, intra-organ and intravascular pressures in detecting changes
induced by external abdominal pressure with and without PEEP”
Any further chracterisation on IAP, IAH and ACS is worthwhile and I congratulate
the authors for having performed this study and bringing us more light on this
topic. The article is short and to the point, well written in correct English. I only
have some minor comments.
1) Introduction: please stick to the recently published definitions on IAH and ACS
by the WSACS: IAH is defined as a SUSTAINED increase in iAP above 12
mmHg. While ACS is defined as a sustained increase in IAP above 20 mmHg
(not 25 as stated by the authors) with NEW ONSET organ failure [1, 2].
2) introduction page 5: some reecnt papers alluded to the interactions between
intrathoracic and infrathoracic pressures. I don’t agree with the last paragraph
that these pressure changes are not well defined [3-5].
3) methods: what about the impact of ventilation and thus the respiratory
changes on IAP and other pressures. Recent data show that this may be related
to the compliance of the abdominal wall. Do you have data on end-expiratory,
end-inspiratory and mean values of these pressures; if not this can be discussed
as luimitation and option for future studies.[6]
3) methods: major drawback is that ITP or Peso were not measured – this needs
to be adressed (cfr above)
3) methods: another drawback is that the application of external pressure on the
abdomen is far from a real life situation where the abdomen is either fluid filled
(ascites) or gas filled (laparoscopy) or filled with edematous organs. Making it
difficult to extrapolate these results to other studies or a real life situation. A
recent publication also alluded to the optimal animal model and implicationsand
guidelines for research on IAH and ACS [7, 8].
Methods: some studies alluded to the fact that morphinomimetics (like fentanyl)
can increase IAP by abdominal muscle contraction. Also the level of sedation is
important, the use or not of muscle relaxants and the positioning of the subject or
animal. This could be discussed a little bit more afterwards [9-11].
Methods: pigs were starved with free access to water, later on ringer solution
was given to keep PCWP between 6-12mmHg. This may have introduced a bias
since static barometric tresholds may not reflect true preload status in conditions
of increased ITP or IAP, volumetric monitoring would have given some added
value. What about SVV/PPV?
Methods: regarding zero reference, just a notice that ideally IAP should be
zero-referenced at the mid-abdomen level. It is important to note that the level of
the zero reference used clinically in IAP monitoring may have an impact [12].
Methods: instillation of 50ml into the pigs bladder probably is too much, in
humans a maximal instillation volume of 20mls was recommended – this need to
be discussed.
Methods: just a note regarding the application of external weight, this technique
and its effects on IAP, ICP, … has been studied before and moreover it was in
humans by Citerio, this reference needs to be added [13]
Methods: regarding peep: other studies showed an effect of PEEP on IAP, but
this was related to the magnitude of PEEP (little effect at PEEP levels below 11)
and the baseline IAP. Maybe the results could have been different if PEEP was
increased to a level equal to IAP.
Page 9-10 are difficult to read. I understand the different stages of the study or
given but it would make more sense to presnet the data otherwise: effects on IAP
(stomach vs bladder vs direct); effects on vascular pressures (supradiafragmatic:
CVP, PCWP, PAP – vs infradiafragmatic: IVCP)
Discussion: state definition of APP= MAP – IAP
Page 12 do you mean pulmonary artery oclusion pressure instead of diastolic? I
don’t agree with the statement that your data do not support the use of higher
filling pressure targets in IAH: please omit statement because in general static
pressure targets are useless and volumetric indices or SVV/PPV were not
measured
Conclusions: no data givcen to support statement that bladder, stomach and
direct IAP correlate well: please add results on correlations and bland and altman
analysis
Tables: since a swan ganz was in place can you provide data on SVR, CO, …
Table 2: please also provide data on CVP, PAOP,
Figures are difficult to read: I would replace by correlation plots and bland and
altman plots comparing direct IAP as gold standard with IGP, IVP, IVCP and then
look at correlations between IVP as gold standard vs IGP and IVCP and finally
IGP vs IVCP. Correlations should be looked for for ALL comparisons, for PEEP 0
vs PEEP 10 and fro nl IAP vs IAP >12
Another interesting figure could be to look at delta IAP vs delta IGP/IVP/IVCP
References: a more recent review on “what is normal IAP” has been published
[14], increased mortality in relation to IAH has also been shown in a recent and
the only one so far multicentre study [15]
Regarding abbreviations: please expand all abbreviations when used for the First
time and use them in a concise way afterwards (eg IAP, IAH, ACS,…)
IN CONCLUSIONS: again I want to congratulate the authors for this nice study
that I enjoyed reading. If they take into account the comments above they can
further improve their paper.
Suggested references
1. Cheatham, M.L., et al., Results from the International Conference of Experts
on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II.
Recommendations. Intensive Care Med, 2007. 33(6): p. 951-62.
2. Malbrain, M.L., et al., Results from the International Conference of Experts on
Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I.
Definitions. Intensive Care Med, 2006. 32(11): p. 1722-1732.
3. Valenza, F., et al., Static and dynamic components of esophageal and central
venous pressure during intra-abdominal hypertension. Crit Care Med, 2007.
35(6): p. 1575-81.
4. Wauters, J., A. Wilmer, and F. Valenza, Abdomino-thoracic transmission
during ACS: facts and figures. Acta Clin Belg Suppl, 2007. 62(1): p. 200-5.
5. Talmor, D., et al., Esophageal and transpulmonary pressures in acute
respiratory failure. Crit Care Med, 2006. 34(5): p. 1389-94.
6. Sturini, E., et al., Respiratory variation of intra-abdominal pressure: indirect
indicator of abdominal compliance? Intensive Care Med, 2008. 34(9): p. 1632-7.
7. Schachtrupp, A., J. Wauters, and A. Wilmer, What is the best animal model for
ACS? Acta Clin Belg Suppl, 2007. 62(1): p. 225-32.
8. De Waele, J.J., et al., Recommendations for research from the International
Conference of Experts on Intra-abdominal Hypertension and Abdominal
Compartment Syndrome. Acta Clin Belg, 2009. 64(3): p. 203-209.
9. Drummond, G.B. and M.K. Duncan, Abdominal pressure during laparoscopy:
effects of fentanyl. 2002. 88(3): p. 384-388.
10. De Laet, I., et al., The effect of neuromuscular blockers in patients with
intra-abdominal hypertension. Intensive Care Med, 2007.
11. Cheatham, M.L., et al., The impact of body position on intra-abdominal
pressure measurement: a multicenter analysis. Crit Care Med, 2009. 37(7): p.
2187-90.
12. De Waele, J.J., et al., The effect of different reference transducer positions
on intra-abdominal pressure measurement: a multicenter analysis. Intensive
Care Med, 2008. 34(7): p. 1299-303.
13. Citerio, G., et al., Induced abdominal compartment syndrome increases
intracranial pressure in neurotrauma patients: a prospective study. Crit Care
Med, 2001. 29(7): p. 1466-71.
14. De Keulenaer, B.L., et al., What is normal intra-abdominal pressure and how
is it affected by positioning, body mass and positive end-expiratory pressure?
Intensive Care Med, 2009. 35(6): p. 969-976.
15. Malbrain, M.L., et al., Incidence and prognosis of intraabdominal
hypertension in a mixed population of critically ill patients: a multiple-center
epidemiological study. Crit Care Med, 2005. 33(2): p. 315-22.
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: Yes, and I have assessed the statistics in my report.
Declaration of competing interests:
I declare that I have no competing interests, except as former founding president
of the world society on abdominal compartment syndrome I just have a high
intrest in this topic...
assistant