“…1 ). This occurs mainly in the context of multiple trauma with severe traumatic brain injury (TBI) [ 1 ], but also in patients with subarachnoid hemorrhage [ 2 ] and acute liver failure [ 3 ]. Acute respiratory syndrome (ARDS) represents altogether a common in-hospital complication after admission for TBI, reaching more than 20% in the adult population [ 1 ].…”
Section: Brain Injury and Severe Lung Disease: A Challenging Combinatmentioning
When intracranial hypertension and severe lung damage coexist in the same clinical scenario, their management poses a difficult challenge, especially as concerns mechanical ventilation management. The needs of combined lung and brain protection from secondary damage may conflict, as ventilation strategies commonly used in patients with ARDS are potentially associated with an increased risk of intracranial hypertension. In particular, the use of positive end-expiratory pressure, recruitment maneuvers, prone positioning, and protective lung ventilation can have undesirable effects on cerebral physiology: they may positively or negatively affect intracranial pressure, based on the final repercussions on PaO2 and cerebral perfusion pressure (through changes in cardiac output, mean arterial pressure, venous return, PaO2 and PaCO2), also according to the baseline conditions of cerebral autoregulation. Lung ultrasound (LUS) and brain ultrasound (BUS, as a combination of optic nerve sheath diameter assessment and cerebrovascular Doppler ultrasound) have independently proven their potential in respectively monitoring lung aeration and brain physiology at the bedside. In this narrative review, we describe how the combined use of LUS and BUS on neurocritical patients with demanding mechanical ventilation needs can contribute to ventilation management, with the aim of a tailored “brain-protective ventilation strategy.”
“…1 ). This occurs mainly in the context of multiple trauma with severe traumatic brain injury (TBI) [ 1 ], but also in patients with subarachnoid hemorrhage [ 2 ] and acute liver failure [ 3 ]. Acute respiratory syndrome (ARDS) represents altogether a common in-hospital complication after admission for TBI, reaching more than 20% in the adult population [ 1 ].…”
Section: Brain Injury and Severe Lung Disease: A Challenging Combinatmentioning
When intracranial hypertension and severe lung damage coexist in the same clinical scenario, their management poses a difficult challenge, especially as concerns mechanical ventilation management. The needs of combined lung and brain protection from secondary damage may conflict, as ventilation strategies commonly used in patients with ARDS are potentially associated with an increased risk of intracranial hypertension. In particular, the use of positive end-expiratory pressure, recruitment maneuvers, prone positioning, and protective lung ventilation can have undesirable effects on cerebral physiology: they may positively or negatively affect intracranial pressure, based on the final repercussions on PaO2 and cerebral perfusion pressure (through changes in cardiac output, mean arterial pressure, venous return, PaO2 and PaCO2), also according to the baseline conditions of cerebral autoregulation. Lung ultrasound (LUS) and brain ultrasound (BUS, as a combination of optic nerve sheath diameter assessment and cerebrovascular Doppler ultrasound) have independently proven their potential in respectively monitoring lung aeration and brain physiology at the bedside. In this narrative review, we describe how the combined use of LUS and BUS on neurocritical patients with demanding mechanical ventilation needs can contribute to ventilation management, with the aim of a tailored “brain-protective ventilation strategy.”
“…Because hepatic dysfunction strongly correlates with intensive care unit mortality, it is essential to determine the correct diagnosis underlying clinical liver dysfunction in order to initiate appropriate therapy. [13] The majority (n = 24, 53%) of our patients presented with an abnormal liver panel 90 days before death. Of those patients, 21 (88%) had a cholestatic pattern and three (12%) were mixed.…”
Section: Discussionmentioning
confidence: 82%
“…Because hepatic dysfunction strongly correlates with intensive care unit mortality, it is essential to determine the correct diagnosis underlying clinical liver dysfunction in order to initiate appropriate therapy. [ 13 ]…”
Hepatic graft‐versus‐host disease (HGVHD) contributes significantly to morbidity and mortality after hematopoietic stem cell transplantation (HSCT). Clinical findings and liver biomarkers are neither sensitive nor specific. The relationship between clinical and histologic diagnoses of HGVHD was assessed premortem and at autopsy. Medical records from patients who underwent HSCT at the National Institutes of Health (NIH) Clinical Center between 2000 and 2012 and expired with autopsy were reviewed, and laboratory tests within 45 days of death were divided into 15‐day periods. Clinical diagnosis of HGVHD was based on Keystone Criteria or NIH Consensus Criteria, histologic diagnosis based on bile duct injury without significant inflammation, and exclusion of other potential etiologies. We included 37 patients, 17 of whom had a cholestatic pattern of liver injury and two had a mixed pattern. Fifteen were clinically diagnosed with HGVHD, two showed HGVHD on autopsy, and 13 had histologic evidence of other processes but no HGVHD. Biopsy or clinical diagnosis of GVHD of other organs during life did not correlate with HGVHD on autopsy. The diagnostic accuracy of the current criteria was poor (κ = −0.20). A logistic regression model accounting for dynamic changes included peak bilirubin 15 days before death, and an increase from period −30 (days 30 to 16 before death) to period −15 (15 days before death) showed an area under the receiver operating characteristic curve of 0.77. Infection was the immediate cause of death in 68% of patients. In conclusion, liver biomarkers at baseline and GVHD elsewhere are poor predictors of HGVHD on autopsy, and current clinical diagnostic criteria have unsatisfactory performance. Peak bilirubin and cholestatic injury predicted HGVHD on autopsy. A predictive model was developed accounting for changes over time. Further validation is needed.
“…The plausible explanation is that in the first 6 months after LT the presence of greater immunosuppressive overload may explain a greater exposure to risk of disease severity due to increased viral load [ 28 , 29 ]. Another argument that would explain the unfavorable impact of early post-LT COVID-19 infection is that the consequences of chronic liver disease, such as malnutrition [ 29 ] and predisposition to secondary infections [ 30 ], as well as in the adult recipient’s renal dysfunction associated with liver disease [ 31 ], are still preponderant in the pediatric liver recipient and may aggravate the clinical evolution of COVID-19. Other studies have shown no correlation between outcomes and the LT interval and COVID-19 infection in adult [ 15 ] and pediatric [ 32 , 33 , 34 ] recipients.…”
Background: The COVID-19 infection has received the attention of the scientific community due to its respiratory manifestations and association with evolution to severe acute respiratory syndrome (SARS-CoV-2). There are few studies characterizing SARS-CoV-2 in pediatric immunocompromised patients, such as liver transplanted patients. The aim of this study was to analyze the outcomes of the largest cohort of pediatric liver transplant recipients (PLTR) from a single center in Brazil who were infected with COVID-19 during the pandemic. Methods: Cross-sectional study. Primary outcomes: COVID-19 severity. The Cox regression method was used to determine independent predictors associated with the outcomes. Patients were divided into two groups according to the severity of COVID-19 disease: moderate–severe COVID and asymptomatic–mild COVID. Results: Patients categorized as having moderate–severe COVID-19 were younger (12.6 months vs. 82.1 months, p = 0.03), had a higher prevalence of transplantation from a deceased donor (50% vs. 4.3%, p = 0.02), and had a higher prevalence of COVID infection within 6 months after liver transplantation (LT) (75% vs. 5.7%, p = 0.002). The independent predictor of COVID-19 severity identified in the multivariate analysis was COVID-19 infection <6 months after LT (HR = 0.001, 95% CI = 0.001–0.67, p = 0.03). Conclusion: The time interval of less than 6 months between COVID-19 infection and LT was the only predictor of disease severity in pediatric patients who underwent liver transplantation.
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