RESUMEN
Respiratory failure is the leading cause of early death after acute CSCI. Tracheotomy is an effective approach to reduce mortality and improve the clinical outcomes. However, the optimal timing for tracheotomy remains controversial. Hence, the study aimed to compare the clinical outcomes of tracheotomy in patients with acute cervical spinal cord injury (CSCI) at different timing. A retrospectively review was performed of acute CSCI patients who underwent tracheotomy in the intensive care unit of Haian Hospital between January 2014 and June 2019. 124 CSCI patients were included and stratified into three groups based on the timing of tracheotomy: early group (≤4 days from initial intubation), medium group (4-10 days from initial intubation), and late group (≥10 days from initial intubation). The clinical outcomes and functional outcomes were analyzed. No significant intergroup differences in baseline characteristics were observed. The late group needed significantly longer duration of mechanical ventilation, longer ICU stay, and suffered higher ICU mortality, higher pneumonia after tracheotomy than the early and medium groups. More patients in the early and medium groups successfully weaned from mechanical ventilation. The early and medium groups achieved better improvement of JOA and NDI scores than the late group at one year after surgery and at the final follow-up. Early to medium term tracheotomy may lead to better clinical and functional outcomes in patients with acute CSCI who require prolonged mechanical ventilation.
Asunto(s)
Insuficiencia Respiratoria/cirugía , Traumatismos de la Médula Espinal/complicaciones , Traqueotomía , Adulto , Femenino , Mortalidad Hospitalaria , Humanos , Unidades de Cuidados Intensivos , Tiempo de Internación , Masculino , Persona de Mediana Edad , Respiración Artificial , Insuficiencia Respiratoria/etiología , Estudios Retrospectivos , Factores de Tiempo , Resultado del TratamientoRESUMEN
BACKGROUND: The functional improvement following bone marrow stromal cells (BMSCs) transplantation after stroke is directly related to the number of engrafted cells and neurogenesis in the injured brain. Here, we tried to evaluate whether 3-methyl-1-phenyl-2-pyrazolin-5-one (MCI-186), a free radical scavenger, might influence BMSCs migration to ischemic brain, which could promote neurogenesis and thereby enhance treatment effects after stroke. METHODS: Rat transient middle cerebral artery occlusion (MCAO) model was established. Two separate MCAO groups were administered with either MCI-186 or phosphate-buffered saline (PBS) solution to evaluate the expression of stromal cell-derived factor-1 (SDF-1) in ischemic brain, and compared to that in sham group (n = 5/ group/time point[at 1, 3, and 7 days after operation]). The content of chemokine receptor-4 (CXCR4, a main receptor of SDF-1) at 7 days after operation was also observed on cultured BMSCs. Another four MCAO groups were intravenously administered with either PBS, MCI-186, BMSCs (2 × 106), or a combination of MCI-186 and BMSCs (n = 10/group). 5-bromo-2-deoxyuridine (BrdU) and Nestin double-immunofluorescence staining was performed to identify the engrafted BMSCs and neuronal differentiation. Adhesive-removal test and foot-fault evaluation were used to test the neurological outcome. RESULTS: MCI-186 upregulated the expression of SDF-1 in ischemic brain and CXCR4 content in BMSCs was enhanced after hypoxic stimulation. When MCAO rats were treated with either MCI-186, BMSCs, or a combination of MCI-186 and BMSCs, the neurologic function was obviously recovered as compared to PBS control group (P < 0.01 or 0.05, respectively). Combination therapy represented a further restoration, increased the number of BMSCs and Nestin+ cells in ischemic brain as compared with BMSCs monotherapy (P < 0.01). The number of engrafted-BMSCs was correlated with the density of neuronal cells in ischemic brain (r = 0.72 , P < 0.01) and the improvement of foot-fault (r = 0.70, P < 0.01). CONCLUSION: MCI-186 might promote BMSCs migration to the ischemic brain, amplify the neurogenesis, and improve the effects of cell therapy.