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Calculation of "calculated ion gap" (Stella Glasmacher, 09 February 2015)

Dear Dr Leitch, I read your poster presentation with interest and would like to know which formula was used to calculate the "calculated ion gap" and whether the anion gap was also measured? Many thanks Stella read full comment

Comment on: Leitch et al. Critical Care, 11:P451

Quantification of urinary TIMP-2 and IGFBP-7 in cardiac surgery – Applying standards for reporting prognostic accuracy (Azra Bihorac, 23 January 2015)

We read with interest the results of the study by Wetz at el. examining the predictive performance of a novel urinary biomarker test (tissue-inhibitor of metalloproteinase 2 multiplied with urine insulin like growth factor binding protein 7, NephroCheckR) for the diagnosis of acute kidney injury (AKI) after cardiac surgery [1]. This test is the first FDA approved biomarker for risk stratification for AKI in critically ill patients, validated in two large multicenter trials [2-4]. In this study the definition and timing of outcomes, sample size and the reporting of statistical uncertainty all fall below standards in reporting and extrapolating the results of prognostic tests for clinical use [5, 6]. Measuring the occurrence of any stage of AKI up to sixty hours after surgery, as opposed to... read full comment

Comment on: Wetz et al. Critical Care, 19:3

Clinical utilization of TIMP-2 and IGFBP7 for detection of AKI following cardiac surgery (Eric Hoste, 16 January 2015)

We read with great interest the study by Wetz et al on the use of the biomarkers tissue inhibitor metalloproteinase-2 (TIMP-2) and insulin growth factor-binding protein-7 (IGFBP7) for prediction of AKI after cardiac surgery [1]. The authors found that measurement of these biomarkers during the first day after surgery could identify patients at risk for AKI, while measurement 4 h after cardiopulmonary bypass (CPB) surgery or at the end of the procedure could not identify patients at risk for... read full comment

Comment on: Wetz et al. Critical Care, 19:3

Statement in the Methods section to be corrected (Martin Dunser, 09 January 2015)

An important point was brought to the attention of the authors following publication of this manuscript. The point referred to the statement in the Methods section that the electronic patient data management system described uses median filtering to eliminate artefacts from the raw signal. While this was the information of the authors until now, reconfirmation with the company revealed that this was not the case and that the system collects raw signals at one minute intervals. Therefore, the respective statement in the Methods section should correctly read based on this new information: "[...]. Hemodynamic and other vital parameters are collected at one minute intervals. [...]." read full comment

Comment on: Brunauer et al. Critical Care, 18:719

Methodology of echocardiographic measurements. (Lukasz R Nowak, 24 November 2014)

The results obtained by the authors are very promising and a possibility of employing such a small fluid volume for testing the fluid responsiveness is very attractive. Nonetheless I have some doubts about the methodology of echocardiographic measurements employed by the authors. The doubts arose for the first time when I looked at the Figure 1. of the article. It's title: "Photo of an echocardiographic Doppler flow velocity measurement from the level of the aortic annulus from the parasternal long-axis window" immediately raises concerns - it is not possible to measure aortic flow from the parasternal long axis (PLAX) window due to the beam non-alignement with flow direction (such measurements are performed from the apical window as the authors stated elsewhere in the article).... read full comment

Comment on: Wu et al. Critical Care, 18:R108

Amendment acknowledgement (Barbara Bottazzi, 19 November 2014)

The support of EU to AM (FP7-HEALTH-2011- project ADITEC - N°280873) is greatfully acknowledged. read full comment

Comment on: Mauri et al. Critical Care, 18:562

Testing the hypothesis that glucose administration plus tight glucose control is beneficial has the potential to harm (Simon Finfer, 04 November 2014)

In their article Mazeraud and colleagues attempt to explain why tight glucose control was benefiical in the first Leuven trial and not in other trials. They conclude that an interventional study evaluating liberal and restrictive glucose intake during IIT is warranted to provide reliable evidence. While such a trial would provide evidence about the modifying effect of glucose administration on the effects of IIT, it would not provide any information to decide whether IIT was beneficial in the first place. As they note, the EPaNIC study compared two feeding strategies in patients treated with IIT and did not support the further use of the feeding strategy employed in the first Leuven trial. The trial which would be most interesting would be one in which the two feeding... read full comment

Comment on: Mazeraud et al. Critical Care, 18:232

Authors' comment: Correction to Table One  (Ceri Battle, 03 November 2014)

Column 5 of the data in Table One gives the numbers of patients in the validation sample with no complications. It currently reads 161 and it should read 134. The percentage given (57%) is correct. read full comment

Comment on: Battle et al. Critical Care, 18:R98

Wrong typo in the abstract of the original article leads to a wrong argument in another (Hsiu-Nien Shen, 05 November 2013)

Dear... read full comment

Comment on: et al. Critical Care, 16:R33

Reason for concern (Christian Wiedermann, 03 September 2013)

We had previously noticed the renal replacement therapy (RRT) data listed under "Hemofiltration" in Table 3 of the Critical Care (CC) publication by Boussekey et al. However, only 8 total patients required RRT according to that table compared with a total 82 of patients requiring RRT in the study's entire... read full comment

Comment on: Wiedermann et al. Critical Care, 17:444

Fascinating study which may have more stories to tell (John Pickering, 27 June 2013)

Congratulations to the authors on this fascinating study. We have been waiting a long time for someone to attempt true GFR measurements on AKI patients, not an easy task.... read full comment

Comment on: Bragadottir et al. Critical Care, 17:R108

Paracelsus' wisdom (Giuseppe Citerio, 22 May 2013)

I¿ve read with interest this paper by Schiefecke and others on parenteral Diclofenac infusion in SAH patients..... read full comment

Comment on: Schiefecker et al. Critical Care, 17:R88

BD increase is not always due to shock (Venkatesh Srinivasa, 24 April 2013)

BD value is, when it reflects lactic acidosis. BD can increase during hyperchloremia (hypertonic resuscitation, NS resuscitation) where it is not an indicator of shock. Nonetheless, increased BD from any reason has been shown to have worse outcome. This study emphasizes the need for RCT's. read full comment

Comment on: Mutschler et al. Critical Care, 17:R42

Toothbrushing for preventing ventilator-associated pneumonia: a live issue worth further investigation (Wan-Jie Gu, 07 March 2013)

Reply: We would like to thank Labeau and Blot for their letter and insightful comments.[1] For Critical ill patients with intubation, dental plaque and the oral mucosa can be colonized with potential pathogens associated with ventilator-associated pneumonia (VAP).[2] Observational studies demonstrated that oral care with toothbrushing improved oral hygiene and reduced plaque load.[3,4] Theoretically, toothbrushing may have favorable effect on the development of VAP. However, evidence on this topic still remains limited, which precludes final verdicts and strong clinical recommendations. Moreover, diagnosis is crucial for the prevention of VAP, but debate remains as to the optimal means of diagnosing VAP. In this case, further research on toothbrushing for VAP prevention is warranted. We... read full comment

Comment on: Labeau et al. Critical Care, 17:417

Sad loss -- I will always remember Professor Traber's resonant voice! (Philip M Kober, JD, MD, PhD, 17 December 2012)

I am very saddened to hear of Dr. Dan Traber's death. I am honored to have known him since my days in graduate school in physiology at Loyola University of Chicago. I will always remember his resonant voice -- "Traber, Galveston" -- at American Physiological Society, FASEB, and Shock Society meetings. He will be missed!

Philip M. Kober, JD, MD, PhD read full comment

Comment on: Prough et al. Critical Care, 16:169

Restful organs (Michael Rodgers, 08 November 2012)

Chawla et al make a case for "resting" the kidney. I find this a rather peculiar, non-medical term to use. I presume what they mean is to reduce the metabolism of the... read full comment

Comment on: Chawla et al. Critical Care, 16:317

In patients with sepsis a moderately high PaCO2 may affect cerebral autoregulation and lead to sepsis-associated delirium over time (Patrice Brassard, 05 November 2012)

We are interested in the study by Schramm et al. (1) on a relationship between the incidence of sepsis-associated delirium (SAD) and cerebral autoregulation. Cerebral autoregulation was found impaired one day after the diagnosis of sepsis and several patients developed SAD (after four days). SAD was attributed to the impaired cerebral autoregulation detected on day 1 suggesting that impaired dynamic cerebral autoregulation might trigger SAD. As mentioned by the authors, PaCO2 levels were at the upper normal range and increased from day 1 to 4. We consider that these high PaCO2 levels could have impaired dynamic cerebral autoregulation in these... read full comment

Comment on: Schramm et al. Critical Care, 16:R181

Authors¿ response (Yiyun Lin, 05 November 2012)

We thank Gu for his comments. Indeed, our results indicate that sedation with dexmedetomidine is associated with shorter length of mechanical ventilation and lower risk of delirium following cardiac surgery. Further, dexmedetomidine may decrease the risk of postoperative ventricular tachycardia and hyperglycemia, and not increase length of hospital stay and mortality at hospital discharge. [1] Thus, we hypothesized that dexmedetomidine would be a safe and efficacious sedative agent in cardiac surgical patients.... read full comment

Comment on: Lin et al. Critical Care, 16:R169

A quick thought from a fellow delirium researcher... (Jiten Patel, 22 October 2012)

I was fascinated to read that the simple use of earplugs could impact on patient morbidity during Critical Care Unit... read full comment

Comment on: Van Rompaey et al. Critical Care, 16:R73

Sedation with dexmedetomidine in post-cardiac surgery patients: practical considerations (Wan-Jie Gu, 01 October 2012)

To the... read full comment

Comment on: Lin et al. Critical Care, 16:R169

Probiotics' effects on the incidence of nosocomial pneumonia in critically ill patients: a systematic review and meta-analysis (Yi-Zhen Gong, 26 September 2012)

To the... read full comment

Comment on: Liu et al. Critical Care, 16:R109

Fluid overload after cardiac surgery: too much or the right therapy? (Andrea Rossi Zadra, 26 September 2012)

The work of Stein and colleagues addresses a key issue in cardiac anesthesia and critical care: optimal fluid management may deeply impact on prognosis. The conclusions may suggest cautious intake of fluids to prevent complications, including kidney failure. Despite extensive literature warns against fluid overload, we suggest that correct fluid management should be titrated to reach adequate volemia. After cardiac surgery the question about fluid status may change compared to preoperative conditions: what is now the correct volemia for the patient? Type of surgery, e.g. aortic valve replacement, and inflammation after extracorporeal circulation deeply impact on volume distribution and cardiac preload. Inadequate volemia is associated to poor perfusion and low cardiac output. Thus, the... read full comment

Comment on: Stein et al. Critical Care, 16:R99

Postflight evaluation of inflight emergency cases (Ashok Devkota, 06 June 2012)

To the... read full comment

Comment on: Sand et al. Critical Care, 16:R42

excellent paper (H M, 28 May 2012)

metformin is a uncoupling agent causes uncoupling of oxidative phosphorylation; due to an increase in permeability of the inner mitochondrial membrane, protons heat is generated without atp, (not using ATP synthase ligated channels) reactions involving NADH, FADH increase, H+'s used, generating heat. other uncoupling agents include Salicyates, Alcohol, Dinitrophenol, and of course Metformin. , "SAD-M". Perhaps induced hypothermia would be of benefit in cases with malignant hyperthermia. read full comment

Comment on: Protti et al. Critical Care, 16:R75

Metformin-induced effects in oxygen consumption (Heikki Savolainen, 14 May 2012)

Dear Editor,

The authors of this study have to be congratulated for their elegant experiments and reaching the correct conclusions.

The drug is, in fact, an inhibitor of the complex I in the mitochondrial respiratory chain. This seems to be the main reason for the deleterious effects. Two other circumstances may, however, contribute and aggravate it. D-lactate produced excessively from glucose is slowly metabolized by the D-lactic acid oxidase prolonging the metabolic acidosis, and acidotic excessive protons impair the the terminal cytochrome oxidase which is essentially a proton pump to molecular oxygen.

Thus, metformin interferes with the oxidative phosphorylation at several stages. read full comment

Comment on: Protti et al. Critical Care, 16:R75