ABSTRACT
PURPOSE: The use of ultrasound in peripheral blocks has now become the gold standard. Ultrasound is a method that is easy to apply and most importantly does not carry any risk, and its only disadvantage is based on the skill and knowledge of the practitioner. Injury to vascular structures, which is the most common occurrence in peripheral block applications, has been significantly reduced by the use of ultrasound. The aim of this study is to determine the location of nerve branches and to determine the most common anthropometric parameters in the axillary fossa. In this way, the common anatomy of the axillary BP will be determined and will guide the practitioners while performing the axillary plexus block. DESIGN: Observational Clinical Study. METHODS: The patients were positioned with forearm abducted 90 degrees and elbow flexed 90 degrees. Using a high-frequency linear ultrasound probe, it was placed on the lateral border of the pectoralis major muscle in the transverse plane. Pulsation of the axillary artery was visualized and shifted slowly to view the nerves around the artery. The axillary vein was also visualized to facilitate the movement of the transducer and to find the nerve localization more easily. The regions on the prepared wheel were marked. At the same time, demographic information such as gender, age, weight, and height of the patients were also recorded. FINDINGS: 248 patients, 61.3% female and 38.7% male. Our results showed that only 59% were compatible with the most common nerve locations in cadaveric dissections and the locations described in anatomy textbooks. CONCLUSIONS: Since there are many anatomical variations, validation of nerves with a nerve stimulator as well as simultaneous visual application under ultrasound guidance will increase the success chance of axillary brachial plexus block and protect it from unwanted complications.
ABSTRACT
OBJECTIVE: To evaluate the incidence of risk factors for postintubation hypotension in critically ill patients with COVID-19. METHODS: We conducted a retrospective study of 141 patients with COVID-19 who were intubated in the intensive care unit. Postintubation hypotension was defined as the need for any vasopressor dose at any time within the 60 minutes following intubation. Patients with intubation-related cardiac arrest and hypotension before intubation were excluded from the study. RESULTS: Of the 141 included patients, 53 patients (37.5%) had postintubation hypotension, and 43.6% of the patients (n = 17) were female. The median age of the postintubation hypotension group was 75.0 (interquartile range: 67.0 - 84.0). In the multivariate analysis, shock index ≥ 0.90 (OR = 7.76; 95%CI 3.14 - 19.21; p < 0.001), albumin levels < 2.92g/dL (OR = 3.65; 95%CI 1.49 - 8.96; p = 0.005), and procalcitonin levels (OR = 1.07, 95%CI 1.01 - 1.15; p = 0.045) were independent risk factors for postintubation hypotension. Hospital mortality was similar in patients with postintubation hypotension and patients without postintubation hypotension (92.5% versus 85.2%; p = 0.29). CONCLUSION: The incidence of postintubation hypotension was 37.5% in critically ill COVID-19 patients. A shock index ≥ 0.90 and albumin levels < 2.92g/dL were independently associated with postintubation hypotension. Furthermore, a shock index ≥ 0.90 may be a practical tool to predict the increased risk of postintubation hypotension in bedside scenarios before endotracheal intubation. In this study, postintubation hypotension was not associated with increased hospital mortality in COVID-19 patients.
OBJETIVO: Avaliar a incidência de fatores de risco para hipotensão pósintubação em pacientes críticos com COVID-19. METÓDOS: Foi realizado um estudo retrospectivo com 141 pacientes com COVID-19 que foram intubados na unidade de terapia intensiva. Hipotensão pós-intubação foi definida como a necessidade de qualquer dose de vasopressor a qualquer momento em até 60 minutos após a intubação. Pacientes com parada cardiorrespiratória relacionada à intubação e hipotensão antes da intubação foram excluídos do estudo. RESULTADOS: Dos 141 pacientes incluídos, 53 pacientes (37,5%) e 43,6% dos pacientes (n = 17) eram do sexo feminino. A idade mediana do grupo com hipotensão pós-intubação foi de 75 anos (amplitude interquartil: 67,0 - 84,0). Na análise multivariada, índice de choque ≥ 0,90 (RC = 7,76; IC95% 3,14 - 19,21; p < 0,001), níveis de albumina < 2,92g/dL (RC = 3,65; IC95% 1,49 - 8,96; p = 0,005) e níveis de procalcitonina (RC = 1,07, IC95% 1,01 - 1,15; p = 0,045) foram fatores de risco independentes para hipotensão pós-intubação. A mortalidade hospitalar foi semelhante em pacientes com hipotensão pós-intubação e pacientes sem hipotensão pós-intubação (92,5% versus 85,2%; p = 0,29). CONCLUSÃO: A incidência de hipotensão pós-intubação foi de 37,5% em pacientes críticos com COVID-19. Um índice de choque ≥ 0,90 e níveis de albumina < 2,92g/ dL foram independentemente associados à hipotensão pós-intubação. Além disso, índice de choque ≥ 0,90 pode ser uma ferramenta do leito antes da intubação endotraqueal. Neste estudo, a hipotensão pós-intubação não esteve associada ao aumento da mortalidade hospitalar em pacientes com COVID-19.
Subject(s)
COVID-19 , Hypotension , Shock , Albumins , COVID-19/complications , Critical Illness , Female , Humans , Hypotension/epidemiology , Hypotension/etiology , Incidence , Intubation, Intratracheal/adverse effects , Male , Retrospective Studies , Risk Factors , Shock/etiologyABSTRACT
RESUMO Objetivo: Avaliar a incidência de fatores de risco para hipotensão pósintubação em pacientes críticos com COVID-19. Metódos: Foi realizado um estudo retrospectivo com 141 pacientes com COVID-19 que foram intubados na unidade de terapia intensiva. Hipotensão pós-intubação foi definida como a necessidade de qualquer dose de vasopressor a qualquer momento em até 60 minutos após a intubação. Pacientes com parada cardiorrespiratória relacionada à intubação e hipotensão antes da intubação foram excluídos do estudo. Resultados: Dos 141 pacientes incluídos, 53 pacientes (37,5%) e 43,6% dos pacientes (n = 17) eram do sexo feminino. A idade mediana do grupo com hipotensão pós-intubação foi de 75 anos (amplitude interquartil: 67,0 - 84,0). Na análise multivariada, índice de choque ≥ 0,90 (RC = 7,76; IC95% 3,14 - 19,21; p < 0,001), níveis de albumina < 2,92g/dL (RC = 3,65; IC95% 1,49 - 8,96; p = 0,005) e níveis de procalcitonina (RC = 1,07, IC95% 1,01 - 1,15; p = 0,045) foram fatores de risco independentes para hipotensão pós-intubação. A mortalidade hospitalar foi semelhante em pacientes com hipotensão pós-intubação e pacientes sem hipotensão pós-intubação (92,5% versus 85,2%; p = 0,29). Conclusão: A incidência de hipotensão pós-intubação foi de 37,5% em pacientes críticos com COVID-19. Um índice de choque ≥ 0,90 e níveis de albumina < 2,92g/ dL foram independentemente associados à hipotensão pós-intubação. Além disso, índice de choque ≥ 0,90 pode ser uma ferramenta do leito antes da intubação endotraqueal. Neste estudo, a hipotensão pós-intubação não esteve associada ao aumento da mortalidade hospitalar em pacientes com COVID-19.
ABSTRACT Objective: To evaluate the incidence of risk factors for postintubation hypotension in critically ill patients with COVID-19. Methods: We conducted a retrospective study of 141 patients with COVID-19 who were intubated in the intensive care unit. Postintubation hypotension was defined as the need for any vasopressor dose at any time within the 60 minutes following intubation. Patients with intubation-related cardiac arrest and hypotension before intubation were excluded from the study. Results: Of the 141 included patients, 53 patients (37.5%) had postintubation hypotension, and 43.6% of the patients (n = 17) were female. The median age of the postintubation hypotension group was 75.0 (interquartile range: 67.0 - 84.0). In the multivariate analysis, shock index ≥ 0.90 (OR = 7.76; 95%CI 3.14 - 19.21; p < 0.001), albumin levels < 2.92g/dL (OR = 3.65; 95%CI 1.49 - 8.96; p = 0.005), and procalcitonin levels (OR = 1.07, 95%CI 1.01 - 1.15; p = 0.045) were independent risk factors for postintubation hypotension. Hospital mortality was similar in patients with postintubation hypotension and patients without postintubation hypotension (92.5% versus 85.2%; p = 0.29). Conclusion: The incidence of postintubation hypotension was 37.5% in critically ill COVID-19 patients. A shock index ≥ 0.90 and albumin levels < 2.92g/dL were independently associated with postintubation hypotension. Furthermore, a shock index ≥ 0.90 may be a practical tool to predict the increased risk of postintubation hypotension in bedside scenarios before endotracheal intubation. In this study, postintubation hypotension was not associated with increased hospital mortality in COVID-19 patients.
ABSTRACT
Background/aim: This study aimed to evaluate the effect of low- and high-pressure pneumoperitoneum pressures applied during robotic-assisted laparoscopic prostatectomy (RALP) using near-infrared spectroscopy (NIRS) on regional cerebral oxygenation saturation (rSO2). Materials and methods: The prospective, comparative, and observational study included patients aged 1880 years, with the American Society of Anesthesiologists (ASA) physical status I-II, who would undergo elective RALP. The patients were divided into two groups (12 mmHg of pneumoperitoneum pressure group, n=22 and 15 mmHg of pneumoperitoneum pressure group, n=23). Patients' demographic data, durations of anesthesia, surgery, pneumoperitoneum, and Trendelenburg position, intraoperative estimated blood loss, fluid therapy, urine output, hemodynamic and respiratory data, and rSO2 values were recorded at regular intervals. Results: The rSO2 values increased significantly during the pneumoperitoneum combined with steep Trendelenburg position (from t3 to t6) and at the end of the surgery (t7) in both groups, compared to the values 5 min after the onset of pneumoperitoneum in the supine position (t2) (P < 0.05), but no statistical significance was observed between the two groups. No cerebral desaturation was observed in any of our patients. Hemodynamic and respiratory parameters were preserved in both groups. The blood lactate levels were significantly higher in patients operated at high-pressure pneumoperitoneum, compared to those with low-pressure pneumoperitoneum (P < 0.05). Conclusion: We believe that low-pressure pneumoperitoneum, especially in robotic surgeries, such as robotic-assisted laparoscopic prostatectomy (RALP), can be applied safely.
Subject(s)
Laparoscopy , Pneumoperitoneum , Robotic Surgical Procedures , Humans , Male , Pneumoperitoneum, Artificial/adverse effects , Prospective Studies , Prostatectomy/adverse effects , Robotic Surgical Procedures/adverse effectsABSTRACT
BACKGROUND: It is important to know whether or not the stroke risk factors and etiologies of patients with multiple acute infarcts are different to those of patients with a single acute infarct. AIM: The frequency of multiple acute infarct was investigated in ischemic stroke patients and a comparison was made of the characteristics of stroke patients with and without multiple acute infarct. PATIENTS AND METHODS: We reviewed the clinical records of 988 ischemic stroke patients who were admitted within 1 week of the onset of stroke and diffusion-weighted imaging (DWI) was performed on first presentation. The clinical characteristics, laboratory, and imaging results were noted from the patient records. According to the DWI findings, the patients were separated into three groups as those with a single acute infarct in a single vascular territory (SI group), those with multiple acute infarcts in a single vascular territory (SMI group) and those with multiple acute infarcts in multiple vascular (MMI group) territories. The frequency of multiple acute infarcts was investigated, and a comparison was made of the characteristics of stroke patients with and without multiple acute infarcts. RESULTS: The SMI group included 119 (12%) patients and the MMI group 126 (12.8%). The most common mechanisms of multiple acute infarcts are large artery atherosclerosis and cardiac origin emboli. Moreover, the risk factors most determined were hypertension, diabetes mellitus, and hyperlipidemia in the MMI group. CONCLUSION: No difference was determined between the groups in respect of stroke etiology and risk factors.
ABSTRACT
Adiponectin is an adipocytokine, and it plays a role in atherosclerosis. The role of adiponectin in the development of ischaemic stroke is controversial. Up to now, adiponectin was not evaluated in transient ischaemic stroke. In this study, we investigated the relationship between adiponectin and transient ischaemic attack. Forty patients with transient ischaemic attack were included into the study. In all patients, traditional risk factors of ischaemic stroke and intima-media thickness of carotid arteries were determined. Also, the relationship between these parameters and adiponectin levels were examined. No difference was found in terms of adiponectin levels between patients and healthy subjects. In addition, there was no association between adiponectin levels and traditional risk factors. Our results suggest that adiponectin may not be a predictive risk factor of transient ischaemic attack.
Subject(s)
Adiponectin/blood , Ischemic Attack, Transient/blood , Aged , Female , Humans , Ischemic Attack, Transient/metabolism , Male , Middle Aged , Risk FactorsABSTRACT
Histone deacetylases (HDACs) are major epigenetic regulators. We show that HDAC1 and HDAC2 functions are critical for myelination of the peripheral nervous system. Using mouse genetics, we have ablated Hdac1 and Hdac2 specifically in Schwann cells, resulting in massive Schwann cell loss and virtual absence of myelin in mutant sciatic nerves. Expression of Sox10 and Krox20, the main transcriptional regulators of Schwann cell myelination, was greatly reduced. We demonstrate that in Schwann cells, HDAC1 and HDAC2 exert specific primary functions: HDAC2 activates the transcriptional program of myelination in synergy with Sox10, whereas HDAC1 controls Schwann cell survival by regulating the levels of active ß-catenin.
Subject(s)
Histone Deacetylase 1/genetics , Histone Deacetylase 2/genetics , Nerve Fibers, Myelinated/enzymology , Schwann Cells/enzymology , Sciatic Nerve/enzymology , Sciatic Nerve/growth & development , Transcriptional Activation/genetics , Animals , Animals, Newborn , Cell Communication/genetics , Cell Survival/genetics , Cells, Cultured , Gene Expression Regulation, Developmental/physiology , Histone Deacetylase 1/physiology , Histone Deacetylase 2/physiology , Mice , Mice, Knockout , Mutation , Nerve Fibers, Myelinated/pathology , Nerve Fibers, Myelinated/ultrastructure , Rats , SOXE Transcription Factors/genetics , SOXE Transcription Factors/metabolism , SOXE Transcription Factors/physiology , Schwann Cells/pathology , Schwann Cells/ultrastructure , Sciatic Nerve/pathology , beta Catenin/genetics , beta Catenin/metabolism , beta Catenin/physiologyABSTRACT
Patients with Charcot-Marie-Tooth neuropathy and gene targeting in mice revealed an essential role for the SH3TC2 gene in peripheral nerve myelination. SH3TC2 expression is restricted to Schwann cells in the peripheral nervous system, and the gene product, SH3TC2, localizes to the perinuclear recycling compartment. Here, we show that SH3TC2 interacts with the small guanosine triphosphatase Rab11, which is known to regulate the recycling of internalized membranes and receptors back to the cell surface. Results of protein binding studies and transferrin receptor trafficking are in line with a role of SH3TC2 as a Rab11 effector molecule. Consistent with a function of Rab11 in Schwann cell myelination, SH3TC2 mutations that cause neuropathy disrupt the SH3TC2/Rab11 interaction, and forced expression of dominant negative Rab11 strongly impairs myelin formation in vitro. Our data indicate that the SH3TC2/Rab11 interaction is relevant for peripheral nerve pathophysiology and place endosomal recycling on the list of cellular mechanisms involved in Schwann cell myelination.
Subject(s)
Carrier Proteins/metabolism , Endosomes/metabolism , Myelin Sheath/metabolism , Peripheral Nerves/metabolism , rab GTP-Binding Proteins/metabolism , Animals , COS Cells , Carrier Proteins/genetics , Cell Line , Charcot-Marie-Tooth Disease/genetics , Charcot-Marie-Tooth Disease/metabolism , Chlorocebus aethiops , Ganglia, Spinal/metabolism , Humans , Intracellular Signaling Peptides and Proteins , Mice , Mice, Knockout , Mutation , Rats , Schwann Cells/metabolism , Sciatic Nerve/metabolism , rab GTP-Binding Proteins/geneticsABSTRACT
The thickness of the myelin sheath that insulates axons is fitted for optimal nerve conduction velocity. Here, we show that, in Schwann cells, mammalian disks large homolog 1 (Dlg1) interacts with PTEN (phosphatase and tensin homolog deleted on chromosome 10) to inhibit axonal stimulation of myelination. This mechanism limits myelin sheath thickness and prevents overmyelination in mouse sciatic nerves. Removing this brake results also in myelin outfoldings and demyelination, characteristics of some peripheral neuropathies. Indeed, the Dlg1 brake is no longer functional in a mouse model of Charcot-Marie-Tooth disease. Therefore, negative regulation of myelination appears to be essential for optimization of nerve conduction velocity and myelin maintenance.
Subject(s)
Adaptor Proteins, Signal Transducing/metabolism , Membrane Proteins/metabolism , Myelin Sheath/physiology , Nerve Tissue Proteins/metabolism , PTEN Phosphohydrolase/metabolism , Schwann Cells/physiology , Adaptor Proteins, Signal Transducing/genetics , Animals , Axons/physiology , Coculture Techniques , Discs Large Homolog 1 Protein , Ganglia, Spinal/cytology , Membrane Proteins/genetics , Mice , Mice, Inbred C57BL , Myelin Sheath/ultrastructure , Nerve Tissue Proteins/genetics , Neural Conduction , Neuregulin-1/metabolism , Proto-Oncogene Proteins c-akt/metabolism , RNA Interference , Rats , SAP90-PSD95 Associated Proteins , Sciatic Nerve/physiologyABSTRACT
Diameter, organization, and length of the myelin sheath are important determinants of the nerve conduction velocity, but the basic molecular mechanisms that control these parameters are only partially understood. Cell polarization is an essential feature of differentiated cells, and relies on a set of evolutionarily conserved cell polarity proteins. We investigated the molecular nature of myelin sheath polarization in connection with the functional role of the cell polarity protein pals1 (Protein Associated with Lin Seven 1) during peripheral nerve myelin sheath extension. We found that, in regard to epithelial polarity, the Schwann cell outer abaxonal domain represents a basolateral-like domain, while the inner adaxonal domain and Schmidt-Lanterman incisures form an apical-like domain. Silencing of pals1 in myelinating Schwann cells in vivo resulted in a severe reduction of myelin sheath thickness and length. Except for some infoldings, the structure of compact myelin was not fundamentally affected, but cells produced less myelin turns. In addition, pals1 is required for the normal polarized localization of the vesicular markers sec8 and syntaxin4, and for the distribution of E-cadherin and myelin proteins PMP22 and MAG at the plasma membrane. Our data show that the polarity protein pals1 plays an essential role in the radial and longitudinal extension of the myelin sheath, likely involving a functional role in membrane protein trafficking. We conclude that regulation of epithelial-like polarization is a critical determinant of myelin sheath structure and function.
Subject(s)
Cell Polarity/physiology , Epithelial Cells/enzymology , Membrane Proteins/physiology , Myelin Sheath/enzymology , Nucleoside-Phosphate Kinase/physiology , Peripheral Nerves/enzymology , Animals , Animals, Newborn , Cells, Cultured , Epithelial Cells/cytology , Mice , Mice, Transgenic , Nerve Fibers, Myelinated/enzymology , Peripheral Nerves/cytology , Protein Transport/physiology , RatsABSTRACT
During development, Schwann cells (SCs) interpret different extracellular cues to regulate their migration, proliferation, and the remarkable morphological changes associated with the sorting, ensheathment, and myelination of axons. Although interactions between extracellular matrix proteins and integrins are critical to some of these processes, the downstream signaling pathways they control are still poorly understood. Integrin-linked kinase (ILK) is a focal adhesion protein that associates with multiple binding partners to link integrins to the actin cytoskeleton and is thought to participate in integrin and growth factor-mediated signaling. Using SC-specific gene ablation, we report essential functions for ILK in radial sorting of axon bundles and in remyelination in the peripheral nervous system. Our in vivo and in vitro experiments show that ILK negatively regulates Rho/Rho kinase signaling to promote SC process extension and to initiate radial sorting. ILK also facilitates axon remyelination, likely by promoting the activation of downstream molecules such as AKT/protein kinase B.
Subject(s)
Axons/physiology , Myelin Sheath/physiology , Peripheral Nervous System/enzymology , Protein Serine-Threonine Kinases/physiology , Regeneration , Schwann Cells/physiology , 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/analogs & derivatives , 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/pharmacology , Animals , Axons/ultrastructure , Cells, Cultured , Integrases , Mice , Mice, Transgenic , Mutagenesis, Site-Directed , Peripheral Nervous System/cytology , Phosphorylation , Protein Kinase Inhibitors/pharmacology , Protein Serine-Threonine Kinases/genetics , Proto-Oncogene Proteins c-akt/metabolism , Schwann Cells/drug effects , Schwann Cells/ultrastructure , Signal Transduction/physiology , rho-Associated Kinases/metabolismABSTRACT
Epileptic nystagmus is a rare, ictal phenomenon characterized by rapid, repetitive eye movements caused by epileptic activity. We report on a patient with cryptogenic focal epilepsy who presented a long-lasting (>30mn) episode of left head and eyes deviation and left-beating nystagmus not crossing the midline. Interictal EEG showed right temporal abnormalities.[Published with video sequences].
