Acute respiratory distress syndrome is a challenging entity for the intensivist.
The pathological hallmark of the acute phase is diffuse alveolar damage, which
is present in approximately half of living patients with acute respiratory
distress syndrome. It is clear that respiratory support for acute respiratory
distress syndrome has gradually been improving over recent decades. However, it
is also evident that these procedures are beneficial, as they reduce lung injury
and keep the patient alive. This could be interpreted as a time-gaining strategy
until the trigger or causal or risk factor improves, the inflammatory storm
decreases and the lung heals. However, all except two pharmacological treatments
(neuromuscular blockers and steroids) were unable to improve the acute
respiratory distress syndrome outcome. The hypothesis that pharmacological
negative results may be explained by the histological heterogeneity of acute
respiratory distress syndrome has been supported by the recent demonstration
that acute respiratory distress syndrome with diffuse alveolar damage
constitutes a specific clinical-pathological entity. Given that diffuse alveolar
damage is a pathological diagnosis and that open lung biopsy (the most common
technique to obtain lung tissue) has several side effects, it is necessary to
develop surrogate biomarkers for diffuse alveolar damage. The aim of this
narrative review is to address the following three topics related to acute
respiratory distress syndrome: (a) the relationship between acute respiratory
distress syndrome and diffuse alveolar damage, (b) how diffuse alveolar damage
could be surrogated in the clinical setting and (c) how enrichment in diffuse
alveolar damage may improve the results of pharmacological clinical trials tried
out on patients with acute respiratory distress syndrome.
Achalasia is a disease of unknown origin in which there is a denervation of the myenteric plexus on the smooth muscle of the lower oesophageal sphincter, causing a cardial stenosis and a loss of efficacy of oesophageal peristalsis. The predominant symptoms are dysphagia for solids and liquids and regurgitation of the retained food. Occasionally, there may be oesophageal haemorrhage as a consequence of oesophagitis and stasis ulcers. An important but uncommon complication is the development of oesophageal cancer, which is typically squamous cell carcinoma. We report an exceptional case of a 77-year-old woman with a long-term achalasia and mega-oesophagus who presented four episodes of upper gastrointestinal bleeding in a 2 month period. The patient underwent surgical resection of the 10 cm of distal oesophagus, performing a partial fundoplication, and the pathological study revealed an oesophageal infiltration by a low-grade non-Hodgkin's lymphoma. After an insidious outcome, she died on the 47th day after admission.
were 354 (76%) and 114 (24%) women in the pre-Covid and Covid cohorts, respectively. Demographics did not differ between cohorts (table 1). At multidisciplinary team evaluations there were no differences in allocation to primary surgery (PDS), interval surgery (IDS) or chemotherapy only (CT) between cohorts. Surgical complexity scores at PDS and IDS were similar in both cohorts. At PDS significantly more women in the covid cohort had residual disease <10 mm. Type and amount of chemotherapy did not differ between cohorts. Significantly more women in the Covid cohort received PARPi maintenance therapy. A significantly higher cumulative incidence of recurrence was found for the covid cohort (p<0.0003), figure 1a. For women undergoing exploratory laparotomy or IDS the risk of recurrence was higher in the Covid cohort than the pre-Covid cohort during initial 18 months after diagnosis, for IDS HR=2.75 [95% CI, 1.45-5.2], figure 1b. Conclusion Despite equal surgical capacity and favorable prognostic characteristics, women with advanced stage HGSC diagnosed during the Covid pandemic had a significantly higher risk of recurrence when compared to pre-covid cohort, particularly for women undergoing IDS.
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