Critical Care - Latest Comments

Paracelsus' wisdom

Giuseppe Citerio — 2013-05-22T11:15:31Z

I¿ve read with interest this paper by Schiefecke and others on parenteral Diclofenac infusion in SAH patients..
Fever is a frequent secondary insult in this setting and strategies for controlling high temperature are more than welcome.
We did publish part of our experience in the use of diclofenac continuous infusion (Neurocritical Care, 6(2), 82¿89. MINERVA ANESTESIOLOGICA, 69(4), 214¿222. Intensive Care Medicine, 26(5), 552¿557) and we are still using it routinely.

The study results of the study need to be commented:
- the drug works: body temperature decreased!
- a decrease in MAP and CPP, necessitated an increase of vasopressors in 26%, colloids in 33% and cristalloids in 5% of interventions, was recored.
- PbtO2 decreased by 13% from a baseline value, resulting in brain tissue hypoxia in 38% (N=8) of patients and 35% (N=43) of interventions.
- Cerebral metabolism showed no significant changes after parenteral diclofenac infusion.

A couple of comments:

- The dose used: 75 mg diclofenac-sodium diluted in 100 ml normal saline in a bouls is too high.
We learned since 1994 that continuous infusion of 0.004¿0.08 mg/kg BW/h (keeping the dose as small as possible and the infusion rate as slow as possible once reached the temperature target) in required for succeeding in fever control with minimal impact on systemic parameters.

- The fall in CPP need to be anticipated (because is a well-known side effect of the drug). In our unit, once the drug is started, noradrenaline is titrated by nurses/residents in order to keep constant CPP.

- The effect on brain oxygen could be due both to a fall in CPP and to hemodilution.

In my opinion the results of the study documented that a very efficacious therapy, when administered without cautions and at a wrong dosage, could have important side effects.
It¿s like to infuse a bolus of 500 ml of mannitol in 10 minutes and to observe polyuria and hypotension and, after the development of hypotension, decide starting fluid administration to counteract it.
As Paracelsus wrote ¿Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.¿
We still think that Diclofenac, used properly, is a remedy not a poison.

BD increase is not always due to shock

Venkatesh Srinivasa — 2013-04-24T10:56:09Z

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.

Toothbrushing for preventing ventilator-associated pneumonia: a live issue worth further investigation

Wan-Jie Gu — 2013-03-07T14:31:59Z

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 believe that research on the field is worthwhile. Large rigorous multicenter trials will help clarify such a live issue, confirming or refuting our prelimary findings.
References
1. Labeau SO, Blot SI: Toothbrushing for preventing ventilator-associated pneumonia. Crit Care 2013, 17:417.
2. Scannapieco FA, Stewart EM, Mylotte JM: Colonization of dental plaque by respiratory pathogens in medical intensive care patients. Crit Care Med 1992, 20:740-745.
3. Ames NJ: Evidence to support tooth brushing in critically ill patients. Am J Crit Care 2011, 20:242¿250.
4. Fitch JA, Munro CL, Glass CA, Pellegrini JM: Oral care in the adult intensive care unit. Am J Crit Care 1999, 8:314¿318.

Sad loss -- I will always remember Professor Traber's resonant voice!

Philip M Kober, JD, MD, PhD — 2012-12-17T10:54:24Z

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

Restful organs

Michael Rodgers — 2012-11-08T13:38:32Z

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 organ.

They claim that "rested" organs have resulted in improvement in outcome in patients with ARDS and cardiogenic shock. However, in the landmark ARDSnet trial, the "rested" group with the lower tidal volumes had in fact a higher minute ventilation compared to the control group. The improvement in outcome in this trial was therefore not due to more "rested" lungs.
In the recent IABP-SHOCK II trial there was no mortality improvement in patients with cardiogenic shock after an acute myocardial infarction placed on an intra-aortic balloon pump The "rested" group had the same mortality as the "un-rested" group.

Furthermore, no trial has ever shown furosemide to improve renal function in any cause of renal failure, despite furosemide reducing oxygen consumption in the renal tubular cells and thus "resting" the kidney.

The trial design the authors offer is interesting, but the likelihood that an outcome difference would be because of a "rested" kidney is unlikely.

In patients with sepsis a moderately high PaCO2 may affect cerebral autoregulation and lead to sepsis-associated delirium over time

Patrice Brassard — 2012-11-05T11:18:33Z

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 patients.

The reason for that consideration is that we (2) and others (3) studied systemic hemodynamics, cerebral blood flow velocity, and dynamic cerebral autoregulation (by transfer function analysis) in healthy volunteers before and after an endotoxin bolus, which represents a model for evaluation of the systemic inflammatory response including vasodilatation (2) without the SAD-associated altered microcirculation. In these healthy volunteers, in whom cerebrovascular reactivity to CO2 seemed intact, endotoxemia was associated with reduced PaCO2 and cerebral perfusion and, in contrast to the patients studied by Schramm et al. (1), with enhanced dynamic cerebral autoregulation. Cerebral autoregulation depends critically on PaCO2 (4-6) and it may be that in septic patients a low PaCO2 would maintain (dynamic) cerebral autoregulation and in turn delay the development of SAD.

Patrice Brassard (a)
Yu-Sok Kim (b,c)
Johannes van Lieshout (b,c,f)
Niels H. Secher (d)
Jaya B. Rosenmeier (e)

a) Department of Kinesiology, Faculty of Medicine, Laval University, Quebec, Canada;
b) Department of Internal Medicine;
c) Laboratory for Clinical Cardiovascular Physiology, Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;
d) Department of Anesthesia, The Copenhagen Muscle Research Center, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark;
e) Department of Cardiology, Gentofte University Hospital, Gentofte, Denmark;
f) School of Biomedical Sciences, University of Nottingham Medical School, Queen¿s Medical Centre, Nottingham, U.K.

References
(1) Schramm P, Klein KU, Falkenberg L, Berres M, Closhen D, Werhahn KJ, David M, Werner C, Engelhard K. Impaired cerebrovascular autoregulation in patients with severe sepsis and sepsis-associated deliriu. Crit Care. 2012;16:R181
(2) Brassard P, Kim YS, van Lieshout J, Secher NH, Rosenmeier JB. Endotoxemia reduces cerebral perfusion but enhances dynamic cerebrovascular autoregulation at reduced arterial carbon dioxide tension. Crit Care Med. 2012;40:1873-1878
(3) Berg RM, Plovsing RR, Ronit A, Bailey DM, Holstein-Rathlou NH, Moller K. Disassociation of Static and Dynamic Cerebral Autoregulatory Performance in Healthy Volunteers After Lipopolysaccharide Infusion and in Patients with Sepsis. Am J Physiol Regul Integr Comp Physiol. 2012 [Epub ahead of print]
(4) Paulson OB, Strandgaard S, Edvinsson L: Cerebral autoregulation. Cerebrovasc Brain Metab Rev 1990; 2:161¿192
(5) Ainslie PN, Celi L, McGrattan K, et al: Dynamic cerebral autoregulation and baroreflex sensitivity during modest and severe step changes in arterial PCO2. Brain Res 2008; 1230:115¿124
(6) Aaslid R, Lindegaard KF, Sorteberg W, et al: Cerebral autoregulation dynamics in humans. Stroke 1989; 20:45¿52

Authors¿ response

Yiyun Lin — 2012-11-05T11:14:54Z

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.
Please note that we have listed several limitations of this study at the end of the manuscript. [1] First, different goals of ideal sedation, and different diagnosis method may not result in the widespread utilization of our results. Second, considering the high cost of dexmedetomidine, additional cost-effective studies are warranted. To enable adequate cost comparisons, proper drug-related cost must be well-defined during clinical study designs, which is generally not the case. However, Gu raised an interesting concern with regard to the lack of high quality randomized controlled studies, which could underscore the value of adequate patient selection for the safe use of dexmedetomidine following cardiac surgery.

Reference
1. Yiyun Lin, Bin He, Jian Chen, Zhinong Wang: Can dexmedetomidine be a safe and efficacious sedative agent in post-cardiac surgery patients: a meta-analysis? Critical Care 2012, 16:R169.

A quick thought from a fellow delirium researcher...

Jiten Patel — 2012-10-22T12:23:35Z

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

Having said this, the fact that earplugs alone were able to prevent "confusion" in this population is an incredible achievement. However, the inability of this tool to reduce the incidence of "true" delirium may lie in the fact that there are several other deliriogenic factors in the intensive care unit. Furthermore, there are other causes of sleep deprivation in this arena, namely light, immobility and the medications employed. Perhaps a more all-encompassing protocol that addresses both sleep disruptive factors and deliriogenic factors could successfully reduce the incidence of delirium?

We are nearing the completion of such a study on a mixed Critical Care Unit in the UK, and will report the results in the near future.

Sedation with dexmedetomidine in post-cardiac surgery patients: practical considerations

Wan-Jie Gu — 2012-10-01T11:36:04Z

To the Editor: I read with interest the paper published in Critical Care by Lin and colleagues, who investigated the effectiveness and safety of dexmedetomidine as a sedative agent in post-cardiac surgery patients [1]. I congratulate the authors on their interesting and important work on this topic. Nevertheless, some concerns need to be discussed. First, inclusion/exclusion criteria: a) In Materials and methods, only randomized controlled trial, non-random controlled trial or cohort study was included this meta-analysis. But a case-control study [2] was also included in Table 2. b) Why exclude the non-English language studies? Though I appreciate the difficulty of assessing a manuscript written in a language you do not speak or write, there is no scientific reason for excluding such manuscripts. It was possible that the exclusion of non-English language studies may lead to bias in effect size. The authors should give a more detailed description of the inclusion/exclusion criteria. Second, outcomes: a) The meta-analysis indicated that there were no significant differences in intensive care unit stay, hospital stay, and morphine equivalents. In fact, these results are not conclusive inasmuch as they are not adequately powered to examine the effect of dexmedetomidine on these endpoints. They were not regarded as the primary outcome and were the only clinically significant endpoints consistently reported in some of the studies included in this meta-analysis. b) Although many outcomes were assessed, there are other equally important variables that can determine the use of dexmedetomidine as a sedative agent (all-cause mortality, myocardial infarction or ischemia, etc.). Third, the real question is why dexmedetomidine is not the ubiquitous sedative agent in post-cardiac surgery patients if it is so good? However, there are many other reasons why it is not widely used and none of these are presented in this review. First, there is no mention of the cost of an ampoule of dexmedetomidine versus other medications. Most institutions cannot split an ampoule of dexmedetomidine among patients and in fact, restrict the use of this medication altogether in the hospital because it is very expensive, far more expensive than other medications. That being the case, how do the authors justify dexmedetomidine? Second, these comparative studies that are cited in the meta-analysis are flawed. Most of them were non-randomized and poor-quality. In conclusion, the use of dexmedetomidine may need practical considerations in post-cardiac surgery patients. References 1. Yiyun Lin, Bin He, Jian Chen, Zhinong Wang: Can dexmedetomidine be a safe and efficacious sedative agent in post-cardiac surgery patients: a meta-analysis? Critical Care 2012, 16:R169. 2. Reichert MG, Jones WA, Royster RL, Slaughter TF, Kon ND, Kincaid EH: Effect of a dexmedetomidine substitution during a nationwide propofol shortage in patients undergoing coronary artery bypass graft surgery. Pharmacotherapy 2011, 31:673-677.

Probiotics' effects on the incidence of nosocomial pneumonia in critically ill patients: a systematic review and meta-analysis

Yi-Zhen Gong — 2012-09-26T09:18:41Z

To the Editor:
We congratulate Liu et al. for their interesting report in a recent issue of the Critical Care, regarding the effects of probiotics on the incidence of nosocomial pneumonia in critically ill patients [1]. There are some issues which need to be ad dressed in the article:
Did only RCTs regarding the effects of probiotics be included this meta-analysis? What about those RCTs regarding the effects of synbiotics? If yes, why the trial conducted by Spindler-Vesel et al. [2] be included? If not, why this trial [3] did not be included? The authors should give a more detailed description of the inclusion/exclusion criteria in their report.
References
1. Liu KX, Zhu YG, Zhang J, Tao LL, Lee JW, Wang XD, Qu JM: Probiotics' effects on the incidence of nosocomial pneumonia in critically ill patients: a systematic review and meta-analysis. Crit Care 2012, 16:R109.
2. Spindler-Vesel A, Bengmark S, Vovk I, Cerovic O, Kompan L: Synbiotics, prebiotics, glutamine, or peptide in early enteral nutrition: a randomized study in trauma patients. JPEN J Parenter Enteral Nutr 2007, 31:119-126.
3. Kotzampassi K, Giamarellos-Bourboulis EJ, Voudouris A, Kazamias P, Eleftheriadis E: Benefits of a synbiotic formula (Synbiotic 2000Forte) in critically Ill trauma patients: early results of a randomized controlled trial. World J Surg 2006, 30:1848-1855.