18 Mar 07

When is dead really dead – on the legitimacy of using neurologic criteria to determine death

Posted in Brain death at 9:56 by Laci

By L M Whetstine

Critical Care 2007, 11:208

This review explores the legitimacy of the whole brain death (WBD) criterion. I argue that it does not fulfill the traditional biologic definition of death and is, therefore, an unsound clinical and philosophical criterion for death. I dispute whether the clinical tests used to diagnose WBD are sufficient to prove all critical brain functions have ceased, as well as examine the sets of brain functions that persist in many WBD patients. I conclude that the definition of death must be modified from a biologic to an ontologic model if we intend to maintain the WBD criterion.

Differences in one-year health outcomes and resource utilization by definition of prolonged mechanical ventilation: a prospective cohort study

Posted in Mechanical ventilation at 9:55 by Laci

By C E Cox, S S Carson, J H Lindquist, M K Olsen, J A Govert  and L Chelluri  for the Quality of Life After Mechanical Ventilation in the Aged (QOL-MV) Investigators

Critical Care 2007, 11:R9

See related commentary by Combes.

The outcomes of patients ventilated for longer than average are unclear, in part because of the lack of an accepted definition of prolonged mechanical ventilation (PMV). To better understand the implications of PMV provision, we compared one-year health outcomes between two common definitions of PMV as well as between PMV patients and those ventilated for shorter periods of time.

Methods
We conducted a secondary analysis of prospectively collected data from medical and surgical intensive care units at an academic tertiary care medical center. The study included 817 critically ill patients ventilated for ≥ 48 hours, 267 (33%) of whom received PMV based on receipt of a tracheostomy and ventilation for ≥ 96 hours. A total of 114 (14%) patients met the alternate definition of PMV by being ventilated for ≥ 21 days. Survival, functional status, and costs were measured at baseline and at 2, 6, and 12 months after discharge. Of one-year survivors, 71 (17%) were lost to follow up.

Results
PMV patients ventilated for ≥ 21 days had greater costs ($140,409 versus $143,389) and higher one-year mortality (58% versus 48%) than did PMV patients with tracheostomies who were ventilated for ≥ 96 hours. The majority of PMV deaths (58%) occurred after hospital discharge whereas 67% of PMV patients aged 65 years or older had died by one year. At one year PMV patients on average had limitations in two basic and five instrumental elements of functional status that exceeded both their pre-admission status and the one-year disability of those ventilated for < 96 hours. Costs per one-year survivor were $423,596, $266,105, and $165,075 for patients ventilated ≥ 21 days, ≥ 96 hours with a tracheostomy, and < 96 hours, respectively.

Conclusion
Contrasting definitions of PMV capture significantly different patient populations, with ≥ 21 days of ventilation specifying the most resource-intensive recipients of critical care. PMV patients, particularly the elderly, suffer from a significant burden of costly, chronic critical illness and are at high risk for death throughout the first year after intensive care.

Four-day antithrombin therapy does not seem to attenuate hypercoagulability in patients suffering from sepsis

Posted in Sepsis at 9:50 by Laci

By C Gonano, C Sitzwohl, E Meitner, C Weinstabl  and S C Kettner

Critical Care 2006, 10:R160

See related commentary by Hoffmann and Schick.

Sepsis activates the coagulation system and frequently causes hypercoagulability, which is not detected by routine coagulation tests. A reliable method to evaluate hypercoagulability is thromboelastography (TEG), but this has not so far been used to investigate sepsis-induced hypercoagulability. Antithrombin (AT) in plasma of septic patients is decreased, and administration of AT may therefore reduce the acquired hypercoagulability. Not clear, however, is to what extent supraphysiologic plasma levels of AT decrease the acute hypercoagulability in septic patients. The present study investigates the coagulation profile of septic patients before and during four day high-dose AT therapy.

Methods
Patients with severe sepsis were randomly assigned to receive either 6,000 IU AT as a bolus infusion followed by a maintenance dose of 250 IU/hour over four days (n = 17) or placebo (n = 16). TEG, platelet count, plasma fibrinogen levels, prothrombin time and activated partial thromboplastin time were assessed at baseline and daily during AT therapy.

Results
TEG showed a hypercoagulability in both groups at baseline, which was neither reversed by bolus or by maintenance doses of AT. The hypercoagulability was mainly caused by increased plasma fibrinogen, and to a lesser extent by platelets. Plasmatic coagulation as assessed by the prothrombin time and activated partial thromboplastin time was similar in both groups, and did not change during the study period.

Conclusion
The current study shows a distinct hypercoagulability in patients suffering from severe sepsis, which was not reversed by high-dose AT treatment over four days. This finding supports recent data showing that modulation of coagulatory activation in septic patients by AT does not occur before one week of therapy.

Distal airways in acute respiratory distress syndrome

Posted in ALI/ARDS, Mechanical ventilation at 9:42 by Laci

By M Jain and J I Sznajder

Critical Care 2007, 11:206     doi:10.1186/cc5159

See related commentary by Pelosi and Rocco.

Distal airways are less than 2 mm in diameter, comprising a relatively large cross-sectional area that allows for slower, laminar airflow. The airways include both membranous bronchioles and gas exchange ducts, and have been referred to in the past as the ‘quiet zone’, in part because these structures were felt to contribute little to lung mechanics and in part because they were difficult to study directly. More recent data suggest that distal airway dysfunction plays a significant role in acute respiratory distress syndrome. In addition, injurious mechanical ventilation strategies may contribute to distal airway dysfunction. The presence of elevated airway resistance, intrinsic positive end-expiratory pressure or a lower inflection point on a pressure–volume curve of the respiratory system may indicate the presence of impaired distal airway function. There are no proven specific treatments for distal airway dysfunction, and protective ventilation strategies to minimize distal airway injury may be the best therapeutic approach at this time.

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