Critical Care最新文献

Background: The assessment of comatose ICU patients presents several challenges with respect to the etiology, depth and ultimate outcome. The acceptance in 1959 of the worst-outcome scenarios of coma, i.e. brain death, and the publication of the Harvard Brain Death Criteria in 1968, were key developments in the management of irreversible coma. Pharmacologic confounders often complicate coma assessments, including brain-death determination. Moreover, associated clinical factors during coma, such as organ failure, hypothermia, prolonged continuous infusions, intoxication, and extreme obesity often alter drug metabolism and clearance. Such circumstances may further complicate standard assessments, and guideline recommendations often do not account for altered pharmacokinetics and pharmacodynamics.

Main text: The assessment of comatose patients involves complex pharmacologic considerations that significantly impact diagnostic accuracy. Accurate differentiation between pharmacologic, metabolic, and structural causes of coma is essential, particularly since drug-related unconsciousness generally carries a more favorable prognosis than other etiologies. Nonetheless, for best outcomes, it is imperative that the etiology of any drug-induced coma be determined as early as possible. It is important to recognize, however, that routine toxicology screens are not comprehensive. Additionally, the interplay between hypothermia and drug metabolism poses unique challenges, as core temperature significantly affects pharmacokinetic parameters such as hepatic metabolism, leading to reduced drug clearance. Multiorgan dysfunction, common after severe neurological injury, further complicates these assessments. Overdose scenarios introduce additional complexity. While ancillary testing may aid in diagnosis of brain death, they have limitations, particularly in cases of profound intoxication. Additionally, premature use of ancillary testing could lead to misdiagnosis. This review is organized into two main sections: Part I examines general coma and its associated pharmacologic considerations, followed by Part II which focuses on brain death.

Conclusion: Accurate assessment of coma and brain death often requires a multidisciplinary approach, integrating expertise in neurology, pharmacy, critical care, and toxicology. Current brain death guidelines provide a framework but leave open critical gaps in pharmacologic and toxicologic confounders. This review article highlights the importance of multidisciplinary approach to the care of coma and brain death patients and further research to refine diagnostic accuracy and mitigate the risks of premature brain death declarations.

Background: Noninvasive evaluation of partial pressure of carbon dioxide (PCO₂) is clinically important for screening and monitoring of hypercapnia, especially in patients with chronic obstructive pulmonary disease (COPD). However, the comparative accuracy of end-tidal PCO₂ (PetCO₂) and transcutaneous PCO₂ (PtcCO₂) monitoring in COPD remains uncertain. This study aimed to evaluate the agreement between PetCO₂ obtained by using modified method of prolonged expiration with an integrated calculation algorithm (PetCO₂-PA) and PtcCO₂ with arterial PCO₂ (PaCO₂) in patients with COPD.

Methods: In this single-center study, 83 patients with COPD (48 at stable phase and 35 during acute exacerbation) underwent arterial blood gas (ABG) analysis followed with simultaneous measurement of PetCO₂-PA and PtcCO₂. Agreement between different measurements was assessed using Bland-Altman analysis (bias and limits of agreement (LOA)), and intraclass correlation coefficients. The receiver operating characteristic curve was used for evaluation of ability to detect hypercapnia, defined as PaCO₂ ≥ 45 mmHg and ≥ 50 mmHg.

Results: Bland-Altman analysis revealed a small bias of - 1.7 mmHg but a relatively wide LOA of - 8.6 to 5.1 for PtcCO₂ and - 2.4 mmHg (LOA: - 9.9 to 5.1) for PetCO₂-PA. The similar results were observed across disease states (stable vs. exacerbation) and degrees of hypercapnia. PetCO₂-PA and PtcCO₂ exhibited comparably diagnostic accuracy for hypercapnia (PaCO₂ ≥ 45 or 50 mmHg), each achieving an area under the curve (AUC) greater than 0.94, with no statistically significant inter-method differences. The proportions of measurements exceeding the clinical acceptability thresholds of ± 4 mmHg and ± 7 mmHg did not differ significantly between techniques.

Conclusion: PetCO₂-PA demonstrated a small bias but a relatively wide LOA with PaCO₂, non-inferior to PtcCO₂, in patients with COPD. Owing to its cost-effectiveness, rapid operation, and portability, PetCO₂-PA represented a practical alternative for screening and monitoring of hypercapnia in COPD patients.

Clinical trial registration: The trial was registered at ClinicalTrials.gov (identifier: NCT04051931).

Background: Intensive Care Unit-acquired weakness (ICUAW) is a common and debilitating complication in critically ill patients, resulting in substantial functional impairment and reduced quality of life. Although early mobilization is widely recommended, the most effective rehabilitation strategy remains unclear. This study aimed to evaluate the short-term clinical efficacy of a suspension-based lower-limb rehabilitation device (SS) combined with conventional rehabilitation in prompt improvement of lower-limb function in patients with ICUAW after diagnosis.

Method: A prospective, within-patient randomized controlled trial with a two-year study period. Sixty patients with ICUAW were enrolled, with one lower limb designated as the intervention side, receiving SS-assisted training plus standard physical therapy, and the opposite limb serving as the control, receiving standard physical therapy alone. Both limbs received 40 min of therapy daily, 5 days per week, for 2 consecutive weeks. Assessments were conducted at baseline (study enrolment), 1 week, and 2 weeks. The primary outcome was the change in lower-limb muscle thickness involving the rectus femoris, vastus intermedius, vastus medialis, vastus lateralis, and tibialis anterior, assessed by musculoskeletal ultrasound. Secondary outcomes included the Medical Research Council (MRC) score, active range of motion (AROM), and limb circumference.

Results: Mixed-effects model analysis of muscle thickness showed a significant interaction between group and time (p < 0.001) and a significant main effect of group (p = 0.001). Post-hoc analysis revealed that at two weeks, muscle thickness in the control limb was significantly lower than in the intervention limb (p < 0.01). In the control limb, muscle thickness was significantly reduced at both 1 week and 2 weeks compared with baseline (p < 0.01), with no significant difference between the two time points (p = 0.06). Notably, no significant within-group changes over time were observed in the intervention limb. Similarly, the control limb showed significantly lower MRC scores than the intervention limb at 1 week (p = 0.05) and 2 weeks (p = 0.003). AROM was also lower in the control limb at 1 week (p = 0.003) and 2 weeks (p < 0.001). No significant interaction or main effect was observed for lower-limb circumference (p = 0.18).

Conclusion: Prompt intervention with SS-assisted rehabilitation combined with conventional therapy may help attenuate muscle atrophy, improve muscle strength, and enhance hip and knee AROM in patients with ICUAW, potentially offering a novel rehabilitation strategy for this population.

Mechanical power has emerged as a unifying metric to quantify the risk of ventilator-induced lung injury (VILI), integrating multiple ventilatory parameters-such as tidal volume, airway pressures, respiratory rate, and inspiratory airflow-into a single measure of the mechanical energy delivered to the lungs. However, total mechanical power alone cannot fully predict the likelihood of injury, as the development of VILI depends not only on delivered energy but also on how this energy interacts with the lung's regional mechanical properties and its intrinsic vulnerability to stress. Critically, only externally measured inflation energy that exceeds one or more local alveolar stress thresholds-termed hazardous elastic power-is likely to contribute to lung damage. In this context, we propose a conceptual method to quantify this damaging component of mechanical power in relation to regional stress thresholds for injury. Once refined and validated, incorporating this approach into clinical practice could enhance individualized, lung-protective ventilation strategies by recognizing that VILI arises from the convergence of mechanical energy, regional stress, and structural vulnerability.