The SARS-CoV-2 (COVID-19) pandemic has caused unprecedented morbidity, mortality and global disruption. Following the initial surge of infections, focus shifted to managing the longer-term sequelae of illness in survivors. 'Post-acute COVID' (known colloquially as 'long COVID') is emerging as a prevalent syndrome. It encompasses a plethora of debilitating symptoms (including breathlessness, chest pain, palpitations and orthostatic intolerance) which can last for weeks or more following mild illness. We describe a series of individuals with symptoms of 'long COVID', and we posit that this condition may be related to a virus-or immune-mediated disruption of the autonomic nervous system resulting in orthostatic intolerance syndromes. We suggest that all physicians should be equipped to recognise such cases, appreciate the symptom burden and provide supportive management. We present our rationale for an underlying impaired autonomic physiology post-COVID-19 and suggest means of management.
Acute liver failure (ALF) can be complicated by lung dysfunction. The aim of this study was to test the hypothesis that inhibition of oxidative stress through iron chelation with desferrioxamine (DFX) attenuates pulmonary injury caused by ALF.14 adult female domestic pigs were subjected to surgical devascularisation of the liver and were randomised to a study group (DFX group, n57), which received post-operative intravenous infusion of DFX (14.5 mg?kg ?h -1 until completion of 24 h), and a control group (n57). Post-operative lung damage was evaluated by histological and bronchoalveolar lavage fluid (BALF) analysis. DFX resulted in reduced BALF protein levels and tissue phospholipase (PL)A 2 activity. Plasma malondialdehyde and BALF nitrate and nitrite concentrations were lower, while catalase activity in the lung was higher after DFX treatment. PLA 2 , platelet-activating factor acetylhydrolase and total cell counts in BALF did not differ between groups. Histological examination revealed reduced alveolar collapse, pneumonocyte necrosis and total lung injury in the DFX-treated animals.DFX reduced systemic and pulmonary oxidative stress during ALF. The limited activity of PLA 2 and the attenuation of pneumonocyte necrosis could represent beneficial mechanisms by which DFX improves alveolar-capillary membrane permeability and prevents alveolar space collapse.
We report on a rare case of Aggregatibacter aphrophilus brain abscess of odontogenic origin in a 6-year-old previously healthy boy, who had close contact with a pet dog. The poodle was the most likely source of the infecting organism, which subsequently colonized the patient's oral cavity. The abscess was surgically removed and he recovered completely after prolonged antibiotic treatment with meropenem. We also review the relevant medical literature on A. aphrophilus pediatric brain abscesses.
Oxidative mechanisms have been implicated in the pathogenesis of brain edema in acute liver failure (ALF). The aim of this study was to test the hypothesis that inhibition of iron-catalyzed oxidative reactions through iron chelation using deferoxamine could attenuate brain edema in a swine model of ischemic ALF. Following ALF induction (end-to-side portacaval anastomosis and ligation of the hepatoduodenal ligament), 14 animals were randomized to a study group that received an intravenous infusion of 150 mg/kg deferoxamine (group DF; n ϭ 7) or a control group (group C; n ϭ 7). Six sham-operated animals were also assigned to a deferoxamine-treated group (n ϭ 3) or a control group (n ϭ 3). Hemodynamic, neurological, and hematological parameters were monitored postoperatively. All sham animals maintained normal hemodynamics and intracranial pressure. At 18 hours, group DF animals had higher mean arterial pressure (mean Ϯ standard deviation: 98.0 Ϯ 15.9 versus 69.9 Ϯ 15.8 mmHg, P Ͻ 0.004), lower intracranial pressure (18.1 Ϯ 8.6 versus 32.7 Ϯ 13.4 mmHg, P Ͻ 0.032), and higher cerebral perfusion pressure (76.4 Ϯ 16.4 versus 37.1 Ϯ 25.6 mmHg, P Ͻ 0.006) in comparison with group C. Similar differences were recorded up to the 24th postoperative hour, leading to a significant difference in animal survival (88% in group DF versus 17% in group C, P Ͻ 0.001). Furthermore, group DF exhibited an attenuated increase of serum malondialdehyde from the baseline (16% versus 74%, P Ͻ 0.05) and lower brain malondialdehyde concentrations (3.7 Ϯ 1.3 versus 5.7 Ϯ 2.0 M/mg of protein, P Ͻ 0.05) in comparison with controls. In conclusion, deferoxamine delayed the development of intracranial hypertension and improved survival in pigs with ischemic ALF. Liver Transpl 14:1116-1124, 2008. © 2008 AASLD. Received July 30, 2007 accepted February 22, 2008. Cerebral edema and intracranial hypertension continue to be the most serious complications of acute liver failure (ALF) and major determinants of patient outcome. 1 Despite considerable progress in our understanding of the pathophysiology of cerebral edema, 2 liver transplantation remains the only effective treatment of this complication. 3 Pretransplant treatment strategies currently in use include general supportive measures (for example, appropriate patient positioning and hyperventilation) and pharmacological measures (for example, lactulose, mannitol, barbiturates, and hypertonic sodium chloride), 1,4 whereas the application of
It is feasible to map the entire left atrium for AVD-GPs before AF ablation. Aggregated data from multiple patients, producing a distribution probability atlas of AVD-GPs, identified three regions with a higher likelihood for finding AVD-GPs and these matched the histological descriptions. This approach could be used to better characterize the autonomic network.
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