The pulmonary physician in critical care * Illustrative case 7: Assessment and management of massive haemoptysis.
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Biomedical subjects
Publications and source records attributed to A Gascoigne.
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A case of Pneumocystis carinii pneumonia was induced through immunosuppression following thoracic duct ligation. The patient initially presented with an esophageal adenocarcinoma, which was totally resected. She is human immunodeficiency virus-negative and not undergoing immunosuppressive treatment.
Acute lung injury after oesophagectomy is well recognized but the risk factors associated with its development are poorly defined. We analysed retrospectively the effect of a number of pre-, peri- and post-operative risk factors on the development of lung injury in 168 patients after elective oesophagectomy performed at a single centre. The acute respiratory distress syndrome (ARDS) developed in 14.5% of patients and acute lung injury in 23.8%. Mortality in patients developing ARDS was 50% compared with 3.5% in the remainder. Features associated with the development of ARDS included a low pre-operative body mass index, a history of cigarette smoking, the experience of the surgeon, the duration of both the operation and of one-lung ventilation, and the occurrence of a post-operative anastomotic leak. Peri-operative cardiorespiratory instability (measured by peri-operative hypoxaemia, hypotension, fluid and blood requirements and the need for inotropic support) was also associated with ARDS. Acute lung injury after elective oesophagectomy is associated with intraoperative cardiorespiratory instability.
The vascular endothelium has a central role in the control of microvascular tone, and it has been proposed that vascular endothelial damage occurs in septic shock, producing multiorgan failure. We have developed a method of detecting circulating endothelial cells (EC) that provides direct evidence of EC shedding in human sepsis. Human umbilical vein endothelial cells (HUVEC) were seeded in whole blood and recovered by isopycnic centrifugation to validate the technique. Blood samples were subsequently taken from 11 healthy volunteers, nine ventilated intensive care unit (ICU) control patients without sepsis, eight patients with sepsis but without shock, and 15 patients with septic shock. EC were identified by indirect immunofluorescence, using antibodies to von Willebrand factor (vWf) and the vascular endothelial growth factor receptor KDR. Mean HUVEC recovery was 86% for 20 to 100 seeded cells/ml of blood. vWf-positive EC counts per milliliter were significantly higher (analysis of variance [ANOVA], p < 0.0001) in patients with sepsis (16.1 +/- 2.7 [mean +/- SEM]) and septic shock (30.1 +/- 3.3) than in healthy (1.9 +/- 0.5) or ICU controls (2.6 +/- 0.6). KDR-positive EC counts per milliliter were also significantly higher (ANOVA, p < 0.0001) in patients with sepsis (4.2 +/- 1.1/ml) and septic shock (10.4 +/- 1.2/ml) than in healthy (0.7 +/- 0.3/ml) or ICU controls (0.5 +/- 0.2/ml). Cell counts made with anti-vWf antibody were consistently higher than those made with anti KDR antibody, but correlation between the two counts was high (r(2) = 0.93). The number of circulating KDR-positive EC was significantly higher in patients who died of septic shock than in survivors (12.0 +/- 1.6/ml versus 7.1 +/- 1.2/ml, p = 0.026). An increase in circulating EC can be identified during sepsis and septic shock. This supports the hypothesis that endothelial damage occurs in human sepsis.
We describe two cases of severe constrictive pericarditis arising after allogeneic BMT conditioning involving total body irradiation and melphalan to treat Philadelphia-chromosome positive ALL. Both patients required pericardectomy, resulting in marked improvement in ventricular filling. However, a degree of right-sided cardiac failure persisted in both patients secondary to restrictive cardiomyopathy. Constrictive pericarditis has not been previously described after BMT, but has been observed following thoracic radiotherapy for malignancy, usually involving a substantially higher radiation dose. Pericardial constriction and restrictive cardiomyopathy should be considered as causes of breathlessness and/or oedema occurring late after BMT. Bone Marrow Transplantation (2000) 25, 571-573.
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Re-expansion pulmonary oedema is a recognised but rare complication following the rapid drainage of a large pleural effusion or pneumothorax [1,2], usually occurring on the side of re-inflation. The pathogenesis of the pulmonary oedema is poorly understood but is thought to be due to micro-vascular shearing resulting in neutrophil activation and adhesion to the vascular endothelium resulting in increased micro-vascular permeability [3-7]. Few reports appear in the literature of invasive haemodynamic monitoring following this catastrophe. We describe a patient who sustained fatal pulmonary oedema arising in the contralateral lung, with pulmonary flow catheter data documenting the initial circulatory collapse following the aspiration of a massive pulmonary effusion.
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BACKGROUND: Patients with lung transplantation are prone to respiratory infections. Generally this is attributable to the effects of immunosuppressive drugs but mucociliary clearance has been found to be impaired in these subjects. A study was performed to determine whether this finding is accompanied by a reduction in ciliary beat frequency (CBF). METHODS: Six patients who had undergone single lung transplantation for fibrosing lung disease were investigated. CBF was measured in mucosal samples from native and transplanted bronchi by a videophotometry method. RESULTS: The CBF was reduced in the transplanted bronchi in all cases when both fastest and slowest beating cilia were examined. The fastest beating cilia on the native side had a mean (SD) CBF of 12.1 (1.3) Hz compared with 9.6 (2.0) Hz on the transplanted side. The slowest beating cilia also had reduced CBF on the transplanted side. CONCLUSION: In patients with fibrotic lung disease, CBF is reduced in transplanted bronchi in comparison with native bronchi.
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Bacterial endocarditis after heart-lung transplantation has not been described. We report Staphylococcus aureus bacterial endocarditis in a 12-year-old boy after heart-lung transplantation. He was found to have an apparently free vegetation in his left ventricle, which was surgically removed. After a stormy postoperative period, he successfully recovered and remains well after 6 months.