Use of Intrapleural Fibrinolytic Therapy in a Trapped Lung following Acute Traumatic Haemothorax.

Retained haemothorax is a common sequela of traumatic haemothorax and refers to blood that cannot be drained from the pleural cavity. We report a case of trapped lung secondary to retained haemothorax in a patient who sustained a penetrating chest injury. Initial chest computed tomography (CT) showed a large haemothorax that was managed with an intercostal drain insertion (ICD). Repeat chest CT and thoracic ultrasonography performed after ICD removal showed an organized pleural space resembling haematoma. ICD was reinserted with administration of intrapleural fibrinolytic therapy (IPFT). Subsequent chest CT showed the development of a pleural rind and trapped lung. A second ICD was inserted, and further IPFT were administered together with aggressive negative pressure suction. Haemoglobin remained stable. The patient made a full recovery and imaging performed two weeks later showed minor blunting of the costophrenic angle. This case highlights the feasibility and safety of IPFT in the management of trapped lung associated with traumatic retained haemothorax as an alternative to surgery

Intrapleural fibrinolysis in acute non‐traumatic retained haemothorax

Abstract: Haemothorax is an accumulation of blood in the pleural space. Retained haemothorax refers to blood that cannot be drained from the pleural cavity and is associated with an increased risk of empyema and fibrothorax often necessitating surgical evacuation. We describe our experience of using intrapleural fibrinolytic therapy in three patients with different bleeding risk and acute non‐traumatic retained haemothorax. The first was a 41‐year‐old female with disseminated Candida guilliermondii sepsis and an iatrogenic haemothorax, second was a 48‐year‐old female with transfusion‐dependent acute myeloid leukaemia and spontaneous haemothorax, and the third was a 72‐year‐old female with spontaneous haemothorax from newly diagnosed lung cancer. All patients received one to two doses of intrapleural alteplase without any bleeding complications and resolution of retained haemothorax. This case series demonstrates the successful application and safety of this approach as an alternative to surgery in a well‐resourced environment with close monitoring and ready access to blood transfusion

Alveolar Macrophages Isolated Directly From Human Cytomegalovirus (HCMV)-Seropositive Individuals Are Sites of HCMV Reactivation In Vivo.

Human cytomegalovirus (HCMV) causes significant morbidity in the immunocompromised host. Following primary infection, the virus establishes latent infection in progenitor cells of the myeloid lineage. These cells exhibit limited viral gene transcription and no evidence of de novo virion production. It is well recognized that differentiation of latently infected myeloid progenitor cells to dendritic or macrophage-like cells permits viral reactivation in vitro. This has been used to support the concept that viral reactivation in HCMV carriers routinely occurs from such terminally differentiated myeloid cells in vivo. However, to date this has not been shown for in vivo-differentiated macrophages. This study is the first to demonstrate that alveolar macrophages from HCMV carriers express immediate early lytic genes and produce infectious virus. This supports the view, until now based on in vitro data, that terminally differentiated myeloid cells in vivo are sites of HCMV reactivation and potential centers of viral dissemination in latently infected individuals with no evidence of virus disease or dissemination.This work was supported by the UK Medical Research Council (grant 0701279 to J. S.) and the National Institute for Health Research UK Biomedical Research Centre (to J. S. and E. R. C.).This is the final published version. It first appeared at http://jid.oxfordjournals.org/content/211/12/1936

Ambulatory Thoracoscopic Pleurodesis Combined With Indwelling Pleural Catheter in Malignant Pleural Effusion.

Background and Objective: Malignant pleural effusion (MPE) often results in debilitating symptoms. Relief of dyspnoea and improvement in quality of life can be achieved with either talc pleurodesis or insertion of an indwelling tunneled pleural catheter (IPC). The former requires a lengthy hospital stay and the latter is associated with lower pleurodesis rates. In response to limited hospital bed capacity, we developed a pragmatic approach in managing MPE by combining thoracoscopic talc poudrage and insertion of IPC into a single day case procedure. We present data on the safety and efficacy of this approach. Methods: Patients who had undergone the abovementioned procedure between 2017 and 2020 were analyzed. Demographic data, hospital length of stay (LOS), histological diagnosis, rates of pleurodesis success and procedural related complications were collated. Patients were followed-up for 6 months. Results: Forty-five patients underwent the procedure. Mean age was 68.5 ± 10.4 years and 56% were male. Histological diagnosis was achieved in all cases. 86.7% of patients were discharged on the day of the procedure. Median LOS was 0 (IQR 0-0) days. Successful pleurodesis was attained in 77.8% at 6-month follow-up. No procedure related deaths or IPC related infections were recorded. Conclusion: Ambulatory thoracoscopic poudrage and IPC insertion is a safe and effective option in the management of MPE. All patients received a definitive pleural intervention with 77.8% pleurodesis success at 6-months and majority of them discharged on the same day. Future randomized trials are required to confirm these findings

Case Report: Indwelling Pleural Catheter Based Management of Refractory Hepatic Hydrothorax as a Bridge to Liver Transplantation

Introduction: Liver transplantation is the treatment of choice for decompensated liver disease, and by extension for hepatic hydrothorax. Persistent pleural effusions make it challenging for patients to maintain physiological fitness for transplantation. Indwelling pleural catheters (IPCs) provide controlled pleural fluid removal, including peri-operatively. The immune dysfunction of cirrhosis heightens susceptibility to bacterial infection and concerns exist regarding the sepsis potential from a tunnelled drain. Method: Six patients were identified who underwent IPC insertion for hepatic hydrothorax before successful liver transplantation, between November 2016 and November 2017. Results: All patients had recurrent transudative right sided pleural effusions. Mean age was 49 years (range 24–64) and mean United Kingdom Model for End-Stage Liver Disease score was 58. Four patients required correction of coagulopathy before insertion. There were no complications secondary to bleeding. Three patients were taught self-drainage at home of up to 1 litre (L) daily. A protocol was developed to ensure weekly review, pleural fluid culture and drainage of larger volumes in hospital. For every 2–3 L of pleural fluid drained, 100 mls of 20% Human Albumin Solution (HAS) was administered. On average an IPC was in situ for 58 days before surgery and drained 19 L of fluid in hospital. There was a small increase in average BMI (0.2) and serum albumin (2.1 g/L) at transplantation. There was one episode of stage one acute kidney injury secondary to high volume drainage. No further ascitic or pleural procedures were needed while an IPC was in situ. One thoracentesis was required after IPC removal. On average IPCs remained in situ for 7 days post transplantation and drained a further 2 L of fluid. Pleural fluid sampling was acquired on 92% of drainages in hospital. Of 44 fluid cultures, 2 cultured bacteria. Two patients had their IPCs and all other lines removed post transplantation due to suspected infection. Conclusion: Our case series describes a novel protocol and successful use of IPCs in the management of refractory hepatic hydrothorax as a bridge to liver transplantation. The protocol includes albumin replacement during pleural drainage, regular clinical review and culture of pleural fluid, with the option of self-drainage at home

Food for Thought: Dietary Intervention in a Rare Cause of Severe Ventilatory Failure

Plastic bronchitis is a rare condition characterised by endobronchial cast formation. We report the case of a 53-year-old women who deteriorated following an elective bronchoscopy procedure. She developed refractory ventilatory failure and required repeated bronchoscopy, which identified thick tenacious casts as the cause of her airway compromise. She did not respond to conventional therapies including endoscopic clearance, mucolytic therapy and nebulised tissue plasminogen activator (TPA). Total parenteral nutrition and a fat-free enteral diet were instituted while the patient was on extracorporeal membrane oxygenation (ECMO), which led to substantial improvement in her condition and demonstrated the importance of dietary strategies in this case

Phenotype of ARDS alveolar and blood neutrophils

RATIONALE: Acute respiratory distress syndrome is refractory to pharmacological intervention. Inappropriate activation of alveolar neutrophils is believed to underpin this disease's complex pathophysiology, yet these cells have been little studied. OBJECTIVES: To examine the functional and transcriptional profiles of patient blood and alveolar neutrophils compared with healthy volunteer cells, and to define their sensitivity to phosphoinositide 3-kinase inhibition. METHODS: Twenty-three ventilated patients underwent bronchoalveolar lavage. Alveolar and blood neutrophil apoptosis, phagocytosis, and adhesion molecules were quantified by flow cytometry, and oxidase responses were quantified by chemiluminescence. Cytokine and transcriptional profiling were used in multiplex and GeneChip arrays. MEASUREMENTS AND MAIN RESULTS: Patient blood and alveolar neutrophils were distinct from healthy circulating cells, with increased CD11b and reduced CD62L expression, delayed constitutive apoptosis, and primed oxidase responses. Incubating control cells with disease bronchoalveolar lavage recapitulated the aberrant functional phenotype, and this could be reversed by phosphoinositide 3-kinase inhibitors. In contrast, the prosurvival phenotype of patient cells was resistant to phosphoinositide 3-kinase inhibition. RNA transcriptomic analysis revealed modified immune, cytoskeletal, and cell death pathways in patient cells, aligning closely to sepsis and burns datasets but not to phosphoinositide 3-kinase signatures. CONCLUSIONS: Acute respiratory distress syndrome blood and alveolar neutrophils display a distinct primed prosurvival profile and transcriptional signature. The enhanced respiratory burst was phosphoinositide 3-kinase-dependent but delayed apoptosis and the altered transcriptional profile were not. These unexpected findings cast doubt over the utility of phosphoinositide 3-kinase inhibition in acute respiratory distress syndrome and highlight the importance of evaluating novel therapeutic strategies in patient-derived cells.This work was funded by a non-commercial grant from GSK, with additional support from The Wellcome Trust, Papworth Hospital, The British Lung Foundation and the NIHR Cambridge Biomedical Research Centre. DMLS holds a Gates Cambridge Scholarship; CS is in receipt of a Wellcome Trust Early Postdoctoral Research Fellowship for Clinician Scientists [WT101692MA].This is the author accepted manuscript. The final version is available from ATS Journals via http://dx.doi.org/10.1164/rccm.201509-1818O

A delayed identification of compound heterozygous (Phe508del/Arg117His) cystic fibrosis variants in a patient awaiting liver transplantation

A man in his 60s undergoing liver transplant assessment was referred to the respiratory team after a thoracic computerised-tomography (CT) scan revealed diffuse tree-in-bud changes. He had a history of infertility, chronic pancreatitis and liver cirrhosis with portal hypertension. Broncho-alveolar lavage (BAL) was positive for Pseudomonas aeruginosa. Genetic screening found two cystic fibrosis transmembrane conductance regulator (CFTR) variants: Phe508del and Arg117His-7T. The patient was referred to the regional cystic fibrosis (CF) centre for follow-up but died from hepatobiliary complications. The atypical presentation with relatively late onset of pulmonary disease and hepatobiliary disease predominance created a diagnostic challenge. This case is a reminder that whilst CF is a monogenic disorder, its manifestation, natural history and extent can be highly variable. Taking a thorough medical history in any chronic illness is essential and patients with the appropriate clinical presentation, regardless of age, should be investigated for CF.non