Journal of intensive medicine最新文献

Sepsis remains a major challenge internationally for healthcare systems. Its incidence is rising due to poor public awareness and delays in its recognition and subsequent management. In sepsis, mortality increases with every hour left untreated. Artificial intelligence (AI) is transforming worldwide healthcare delivery at present. This review has outlined how AI can augment strategies to address this global disease burden. AI and machine learning (ML) algorithms can analyze vast quantities of increasingly complex clinical datasets from electronic medical records to assist clinicians in diagnosing and treating sepsis earlier than traditional methods. Our review highlights how these models can predict the risk of sepsis and organ failure even before it occurs. This gives providers additional time to plan and execute treatment plans, thereby avoiding increasing complications associated with delayed diagnosis of sepsis. The potential for cost savings with AI implementation is also discussed, including improving workflow efficiencies, reducing administrative costs, and improving healthcare outcomes. Despite these advantages, clinicians have been slow to adopt AI into clinical practice. Some of the limitations posed by AI solutions include the lack of diverse data sets for model building so that they are widely applicable for routine clinical use. Furthermore, the subsequent algorithms are often based on complex mathematics leading to clinician hesitancy to embrace such technologies. Finally, we highlight the need for robust political and regulatory frameworks in this area to achieve the trust and approval of clinicians and patients to implement this transformational technology.

Sepsis and septic shock remain the leading causes of death in intensive care units. Some patients with sepsis fail to respond to routine treatment and rapidly progress to refractory respiratory and circulatory failure, necessitating extracorporeal membrane oxygenation (ECMO). However, the role of ECMO in adult patients with sepsis has not been fully established. According to existing studies, ECMO may be a viable salvage therapy in carefully selected adult patients with sepsis. The choice of venovenous, venoarterial, or hybrid ECMO modes is primarily determined by the patient's oxygenation and hemodynamics (distributive shock with preserved cardiac output, septic cardiomyopathy (left, right, or biventricular heart failure), or right ventricular failure caused by acute respiratory distress syndrome). Veno-venous ECMO can be used in patients with sepsis and severe acute respiratory distress syndrome when conventional mechanical ventilation fails, and early application of veno-arterial ECMO in patients with sepsis-induced refractory cardiogenic shock may be critical in improving their chances of survival. When ECMO is indicated, the choice of an appropriate mode and determination of the optimal timing of initiation and weaning are critical, particularly in an experienced ECMO center. Furthermore, some special issues, such as ECMO flow, anticoagulation, and antibiotic therapy, should be noted during the management of ECMO support.

Malaria is responsible for approximately three-quarters of a million deaths in humans globally each year. Most of the morbidity and mortality reported are from Sub-Saharan Africa and Asia, where the disease is endemic. In non-endemic areas, malaria is the most common cause of imported infection and is associated with significant mortality despite recent advancements and investments in elimination programs. Severe malaria often requires intensive care unit admission and can be complicated by cerebral malaria, respiratory distress, acute kidney injury, bleeding complications, and co-infection. Intensive care management includes prompt diagnosis and early initiation of effective antimalarial therapy, recognition of complications, and appropriate supportive care. However, the lack of diagnostic capacities due to limited advances in equipment, personnel, and infrastructure presents a challenge to the effective diagnosis and management of malaria. This article reviews the clinical classification, diagnosis, and management of malaria as relevant to critical care clinicians, highlighting the role of diagnostic capacity, treatment options, and supportive care.

Background

Severe intracerebral hemorrhage (ICH) is the most devastating subtype of stroke resulting in high mortality and disability. At present, the development of targeted treatments to minimize the high morbidity and mortality is limited partly due to the lack of a severe ICH animal model. In this study, we aimed to establish an accurate severe ICH model in rats and examine the pathological and physiological changes associated with ICH.

Methods

A rat model of severe ICH model was established by intrastriatal injection of autologous blood using different blood volumes (ICH 100 µL group, ICH 130 µL group, ICH 160 µL group, ICH 170 µL group, and ICH 180 µL group). The mortality was assessed during the 28-day post-ICH period. Short- and long-term neurological deficits were evaluated using the Longa method, foot fault, falling latency, and Morris water maze tests. Brain water content, hematoma volume, hemoglobin content, and magnetic resonance imaging were assessed to determine the extent of brain injury. Immunofluorescence staining was conducted to examine microglial activation and neuronal apoptosis. Hematoxylin and eosin (H&E) staining, lung water content, and western blotting were used to assess lung injury following ICH.

Results

The mortality of ICH rats increased significantly with an increase in autologous blood injection. The 28-day mortality in the 100 µL, 130 µL, 160 µL, 170 µL, and 180 µL ICH groups were 5%, 20%, 40%, 75%, and 100%, respectively. A significantly higher 28-day mortality was observed in the ICH 160 µL group compared to the ICH 100 µL group. The ICH 160 µL group exhibited significantly increased neurological deficits, brain edema, hematoma volume, and hemoglobin content compared to the sham group. Compared with the sham operation group, the activation of microglia and neuronal death in ICH 160 µL rats increased. The use of H&E staining and western blotting demonstrated that disruption of the intra-alveolar structure, alveolar edema, and infiltration of inflammatory cells and cytokines into the lung tissue were more severe in the ICH 160 µL group than the sham group.

Conclusions

A severe ICH model in rats was successfully established using an injection of autologous blood at a volume of 160 µL. This model may provide a valuable tool to examine the pathological mechanisms and potential therapeutic interventions of severe ICH.