Publications

Clinical trials of drugs specifically targeting the sepsis response have frequently produced negative or inconclusive results. This has largely been due to the broad heterogeneity of enrolled patient populations, particularly when inclusion was based on the presence of the non-specific systemic inflammatory response syndrome (SIRS) criteria. The heterogeneity may have diluted any possible treatment effect: while some patients may have benefited from the intervention under investigation, others will have been harmed, resulting in an overall null-effect. Furthermore, an underlying infection is not always required for immune-modulating interventions to be effective; for example, patients with severe acute pancreatitis, but no infection, may still benefit from such therapies. There is therefore a need for better patient stratification or subphenotyping to identify those most likely to benefit from a particular therapy. Several trials have already adopted this approach using prognostic and/or predictive enrichment strategies. For example, measurements of triggering receptor expressed on myeloid cells (TREM) could be used to identify candidates most likely to respond to anti-TREM therapies, or patients with coagulopathy or specific inflammatory patterns could be selected for treatments like thrombomodulin or activated protein C. However, challenges remain, including the need for more rapid tools that can be used at the bedside to inform real-time treatment decisions given the rapidly evolving nature of the sepsis response. Nevertheless, the era of broad-spectrum "sepsis drugs" is now giving way to more selective, personalized interventions tailored to individual biological profiles, offering a more promising pathway for future therapeutic development-even in the absence of infection.

We investigated the potential value of vasodilating therapy in critically ill patients with inappropriately low cardiac output during acute illness. In seven patients with low flow state during septic or postoperative state, sodium nitroprusside (20-100 micrograms/min) was compared with nicergoline (NIC) (0.5 to 2.5 mg/min), a new selective alpha 1-blocking agent with negative chronotropic action. Sodium nitroprusside (NP) decreased arterial pressure (from 90 +/- 5 to 68 +/- 5 mm Hg, p less than 0.01) and pulmonary artery balloon-occluded pressure from 20.3 +/- 3.1 to 15.4 +/- 2.8 mm Hg, p less than 0.01) and increased heart rate (from 110 +/- 11 to 120 +/- 13 beats/min, p less than 0.05) but failed to increase stroke volume (from 24.7 +/- 4.8 to 23.4 +/- 4.4 ml, NS). During NIC administration, a comparable decrease in systemic vascular resistance was associated with a significant increase in stroke volume (from 21.6 +/- 3.3 to 25.6 +/- 3.2 ml/m2, p less than 0.01) and cardiac output (CO) (from 2.4 +/- 0.3 to 2.7 +/- 0.3 L/min/m2, p less than 0.025), whereas the decrease in arterial pressure was less significant (from 91 +/- 8 to 84 +/- 7 mm Hg, p less than 0.05). Because NIC has no positive inotropic action, the most likely mechanism is that a baroreceptor-mediated increase in heart rate with NP was prevented by the negative chronotropic action of NIC. Both drugs adversely affected arterial blood oxygenation. By its unique property to decrease heart rate, NIC could represent a valuable vasodilating agent, especially in acute conditions.

Purpose: To describe the epidemiology of the acute respiratory distress syndrome (ARDS) in a Brazilian ICU.

Quantifying organ dysfunction in patients with sepsis can assist in assessing prognosis and determining treatment effectiveness. The simplicity, reliability, and reproducibility of current scores facilitate their widespread use.

info:eu-repo/semantics/published