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Chest Nov 1996Pulmonary vascular inflammatory disorders may involve all components of the pulmonary vasculature, including capillaries. The principal histopathologic features of... (Review)
Review
Pulmonary vascular inflammatory disorders may involve all components of the pulmonary vasculature, including capillaries. The principal histopathologic features of pulmonary capillaritis include capillary wall necrosis with infiltration by neutrophils, interstitial erythrocytes, and/or hemosiderin, and interalveolar septal capillary occlusion by fibrin thrombi. Immune complex deposition is variably present. Patients often present clinically with diffuse alveolar hemorrhage, which is characterized by dyspnea and hemoptysis; diffuse, bilateral, alveolar infiltrates on chest radiograph; and anemia. Pulmonary capillaritis has been reported with variable frequency and severity as a manifestation of Wegener's granulomatosis, microscopic polyarteritis, systemic lupus erythematosus, Goodpasture's syndrome, idiopathic pulmonary renal syndrome, Behçet's syndrome, Henoch-Schönlein purpura, IgA nephropathy, antiphospholipid syndrome, progressive systemic sclerosis, and diphenylhydantoin use. In addition to history, physical examination, and routine laboratory studies, certain ancillary laboratory tests, such as antineutrophil cytoplasmic antibodies, antinuclear antibodies, and antiglomerular basement membrane antibodies, may help diagnose an underlying disease. Diagnosis of pulmonary capillaritis can be made by fiberoptic bronchoscopy with transbronchial biopsy, but thoracoscopic biopsy is often employed. Since many disorders can result in pulmonary capillaritis with diffuse alveolar hemorrhage, it is crucial for clinicians and pathologists to work together when attempting to identify an underlying disease. Therapy depends on the disorder that gave rise to the pulmonary capillaritis and usually includes corticosteroids and cyclophosphamide or azathioprine. Since most diseases that result in pulmonary capillaritis are treated with immunosuppression, infection must be excluded aggressively.
Topics: Anemia; Bronchoscopy; Capillaries; Diagnosis, Differential; Dyspnea; Erythrocytes; Fibrin; Hemoptysis; Hemorrhage; Hemosiderin; Humans; Immunosuppressive Agents; Lung; Lung Diseases; Necrosis; Neutrophils; Pulmonary Alveoli; Pulmonary Embolism; Thoracoscopy; Vasculitis
PubMed: 8915239
DOI: 10.1378/chest.110.5.1305 -
The Journal of Thoracic and... Nov 2018
Topics: Endarterectomy; Hematoma, Subdural; Humans
PubMed: 30057187
DOI: 10.1016/j.jtcvs.2018.06.029 -
Emergency Medicine Clinics of North... Aug 1983Pulmonary parenchymal damage is a frequent consequence of major trauma to the chest. Among the injuries considered in this article are traumatic pulmonary pseudocysts,... (Review)
Review
Pulmonary parenchymal damage is a frequent consequence of major trauma to the chest. Among the injuries considered in this article are traumatic pulmonary pseudocysts, pulmonary hematomas, major pulmonary lacerations, pulmonary contusions, and penetrating pulmonary parenchymal injuries. Also discussed is emergency resuscitation of patients with pulmonary parenchymal injuries.
Topics: Contusions; Cysts; Diagnosis, Differential; Emergencies; Hematoma; Hemoptysis; Hemothorax; Humans; Lung; Lung Diseases; Lung Injury; Oxygen Inhalation Therapy; Positive-Pressure Respiration; Radiography, Thoracic; Resuscitation; Suction; Thoracic Injuries; Wounds, Nonpenetrating; Wounds, Penetrating
PubMed: 6394293
DOI: No ID Found -
Acta Clinica Belgica 2007Pulmonary-renal syndromes or lung-kidney syndromes are clinical syndromes defined by a combination of diffuse alveolar haemorrhage (DAH) and glomerulonephritis.... (Review)
Review
Pulmonary-renal syndromes or lung-kidney syndromes are clinical syndromes defined by a combination of diffuse alveolar haemorrhage (DAH) and glomerulonephritis. Pulmonary-renal syndromes are not a single entity, but are caused by a wide variety of diseases, including various forms of primary systemic vasculitis (especially Wegener's granulomatosis and microscopic polyangiitis), Goodpasture's syndrome (associated with autoantibodies to the alveolar and glomerular basement membrane) and systemic lupus erythematosus. The diagnosis rests on the identification of particular patterns of clinical, radiologic, pathologic and laboratory features. Serologic testing is important in the diagnostic work-up of patients presenting with a pulmonary-renal syndrome. The majority of cases of pulmonary-renal syndrome are associated with ANCAs, either c-ANCA or p-ANCA, due to autoantibodies against the target antigens proteinase-3 and myeloperoxidase respectively. The antigen target in Goodpasture's syndrome is type IV collagen, the major component of basement membranes. Diffuse alveolar haemorrhage is characterized by the presence of a haemorrhagic bronchoalveolar lavage (BAL) in serial BAL samples. In the clinical setting of an acute nephritis syndrome, percutaneous renal biopsy is commonly performed for histopathology and immunofluorescence studies. Treatment of generalized ANCA-associated vasculitis consists of corticosteroids and immunosuppressive agents such as cyclophosphamide (as induction therapy) or azathioprine (as maintenance therapy once remission has been achieved). The combination of plasmapheresis with these cytotoxic agents and steroids is effective in patients with Goodpasture's syndrome, especially if instituted early in the course of the disease. Recent evidence suggests that patients with severe ANCA-associated vasculitis, defined by the presence of diffuse alveolar haemorrhage and/or severe renal involvement (creatinine concentration > 5.7 mg/dl), might benefit from plasma exchange in combination with cyclophosphamide and corticosteroids.
Topics: Glomerulonephritis; Hemorrhage; Humans; Lung Diseases; Pulmonary Alveoli; Syndrome
PubMed: 17547289
DOI: 10.1179/acb.2007.016 -
Current Opinion in Pulmonary Medicine Jul 2016Although thoracentesis is generally considered safe, procedural complications are associated with increased morbidity, mortality, and healthcare costs. In this article,... (Review)
Review
PURPOSE OF REVIEW
Although thoracentesis is generally considered safe, procedural complications are associated with increased morbidity, mortality, and healthcare costs. In this article, we review the risk factors and prevention of the most common complications of thoracentesis including pneumothorax, bleeding (chest wall hematoma and hemothorax), and re-expansion pulmonary edema.
RECENT FINDINGS
Recent data support the importance of operator expertise and the use of ultrasound in reducing the risk of iatrogenic pneumothorax. Although coagulopathy or thrombocytopenia and the use of anticoagulant or antiplatelet medications have traditionally been viewed as contraindications to thoracentesis, new evidence suggests that patients may be able to safely undergo thoracentesis without treating their bleeding risk. Re-expansion pulmonary edema, a rare complication of thoracentesis, is felt to result in part from the generation of excessively negative pleural pressure. When and how to monitor changes in pleural pressure during thoracentesis remains a focus of ongoing study.
SUMMARY
Major complications of thoracentesis are uncommon. Clinician awareness of risk factors for procedural complications and familiarity with strategies that improve outcomes are essential components for safely performing thoracentesis.
Topics: Hematoma; Hemorrhage; Hemothorax; Humans; Incidence; Pleural Diseases; Pneumothorax; Pressure; Pulmonary Edema; Risk Factors; Thoracentesis; Thoracic Wall
PubMed: 27093476
DOI: 10.1097/MCP.0000000000000285 -
Journal of Thrombosis and Haemostasis :... Jul 2017Advances in the management of patients with suspected pulmonary embolism (PE) have improved diagnostic accuracy and made management algorithms safer, easier to use, and... (Review)
Review
Advances in the management of patients with suspected pulmonary embolism (PE) have improved diagnostic accuracy and made management algorithms safer, easier to use, and well standardized. These diagnostic algorithms are mainly based on the assessment of clinical pretest probability, D-dimer measurement, and imaging tests-predominantly computed tomography pulmonary angiography. These diagnostic algorithms allow safe and cost-effective diagnosis for most patients with suspected PE. In this review, we summarize signs and symptoms of PE, current existing evidence for PE diagnosis, and focus on the challenge of diagnosing PE in special patient populations, such as pregnant women, or patients with a prior VTE. We also discuss novel imaging tests for PE diagnosis and highlight some of the additional challenges that might require adjustments to current diagnostic strategies, such as the reduced clinical suspicion threshold, resulting in a lower proportion of PE among suspected patients as well as the overdiagnosis of subsegmental PE.
Topics: Acute Disease; Algorithms; Computed Tomography Angiography; Cost-Benefit Analysis; Dyspnea; Female; Fibrin Fibrinogen Degradation Products; Hematology; Hemorrhage; Humans; Lung; Magnetic Resonance Angiography; Male; Pregnancy; Probability; Pulmonary Alveoli; Pulmonary Embolism; Radionuclide Imaging; Reproducibility of Results; Tomography, X-Ray Computed
PubMed: 28671347
DOI: 10.1111/jth.13694 -
Annals of Cardiac Anaesthesia 2021Dissection of the ascending aorta (AA) represents a life-threatening condition typically treated by emergent surgical repair. A rare, potential complication of AA...
Dissection of the ascending aorta (AA) represents a life-threatening condition typically treated by emergent surgical repair. A rare, potential complication of AA dissection is pulmonary artery (PA) sheath hematoma. Due to the presence of a common adventitial layer between the proximal AA and the PA, dissection can propagate between both vessels, potentially compromising the PA lumen. The resultant acute narrowing of the PA lumen may abruptly increase right ventricular (RV) afterload. Recognition of PA sheath hematoma is important; when seen on echocardiography it is suggestive of AA dissection and has the potential to result in RV hypertension and dysfunction if significant PA compression occurs.
Topics: Aorta; Echocardiography; Heart Ventricles; Hematoma; Humans; Pulmonary Artery
PubMed: 33884982
DOI: 10.4103/aca.ACA_135_20 -
Archives of Pathology & Laboratory... May 1985Thirteen patients with prominent pulmonary signs and symptoms had pulmonary capillaritis and extensive hemorrhage demonstrated by open-lung biopsy or autopsy. Vasculitis...
Thirteen patients with prominent pulmonary signs and symptoms had pulmonary capillaritis and extensive hemorrhage demonstrated by open-lung biopsy or autopsy. Vasculitis was demonstrated in other organs before or after the lung biopsy or at autopsy. Although there were several suspected causes for the pulmonary capillaritis and different final clinicopathologic diagnoses, the histopathologic features in the lung were similar in all cases and distinctive enough to separate capillaritis from other causes of hemorrhagic lung. All patients were treated with prednisone or cyclophosphamide, or both. Six patients died of their vasculitis, five in respiratory failure and one in renal failure. None of the seven survivors had a clinical recrudescence of pulmonary hemorrhage. By extrapolation from these 13 cases, one may histopathologically recognize pulmonary capillaritis when it causes hemorrhagic lung in a patient without clinically evident extrapulmonary vasculitis. One can then proceed to investigate the patient and possibly determine the nature of the vasculitis.
Topics: Adolescent; Adult; Aged; Capillaries; Child; Female; Hemorrhage; Humans; Lung; Lung Diseases; Male; Middle Aged; Pulmonary Alveoli; Vasculitis
PubMed: 3838654
DOI: No ID Found -
Journal of Ultrasound in Medicine :... Apr 2021Lung ultrasound (LUS) exposure can induce pulmonary capillary hemorrhage (PCH), depending on biological and physical exposure parameters. This study was designed to...
OBJECTIVES
Lung ultrasound (LUS) exposure can induce pulmonary capillary hemorrhage (PCH), depending on biological and physical exposure parameters. This study was designed to investigate the variation in the LUS induction of PCH due to hemorrhagic shock, which itself can engender pulmonary injury.
METHODS
Male rats were anesthetized with isoflurane in air. Shock was induced by withdrawal of 40% of the blood volume and assessed by the blood pressure detected by a femoral artery catheter and by blood glucose tests. B-mode ultrasound was delivered at 7.3 MHz with a low output (-20 dB) for aiming and with the maximal output (0 dB) for exposure. Pulmonary capillary hemorrhage was quantified by an assessment of comet tail artifacts in the LUS images and by measurement of PCH areas on the surface of fresh lung samples.
RESULTS
Tests without shock or catheterization surgery gave results for PCH similar to those of previous studies using different methods. Exposure before hemorrhagic shock gave a mean PCH area ± SE of 24.8 ± 9.2 mm on the ultrasound scan plane, whereas exposure after shock gave 0 PCH (P < .001; n = 7).
CONCLUSIONS
The presence of hemorrhagic shock significantly reduces the occurrence of LUS-induced PCH.
Topics: Animals; Disease Models, Animal; Hemorrhage; Lung; Male; Rats; Rats, Sprague-Dawley; Shock, Hemorrhagic
PubMed: 32856724
DOI: 10.1002/jum.15463 -
The Journal of Pediatrics Apr 1994To assess the possible relationship between exogenous surfactant therapy and pulmonary hemorrhage in premature infants, we compared autopsy findings in 15 infants... (Comparative Study)
Comparative Study
To assess the possible relationship between exogenous surfactant therapy and pulmonary hemorrhage in premature infants, we compared autopsy findings in 15 infants treated with exogenous surfactant and in 29 who died before the introduction of surfactant therapy. Infants who met the following criteria were included: birth weight 501 to 1500 gm, survival 4 hours to 7 days, and no congenital anomalies. Average birth weight, gestational age, and age at death were equivalent for the two groups. High rates of pulmonary hemorrhage were present in both groups (treated 80% vs untreated 83%). The untreated group had higher incidences of interstitial hemorrhage and lung hematomas and significantly more large interstitial hemorrhages: 31% untreated versus 0% treated (p < 0.05). The overall rate of intraalveolar hemorrhage was similar in the two groups, but surfactant-treated infants were more likely to have extensive intraalveolar hemorrhage: 53% versus 14% (p < 0.05). Most surfactant-treated infants who survived more than 24 hours had extensive intraalveolar hemorrhage (8/9). Patients who had extensive intraalveolar hemorrhage, with or without prior surfactant therapy, frequently had clinically significant pulmonary hemorrhage (7/12). These findings indicate that infants who die after surfactant therapy have higher rates of a specific type of pulmonary hemorrhage--extensive intraalveolar hemorrhage.
Topics: Autopsy; Hematoma; Hemorrhage; Humans; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Lung Diseases; Pulmonary Alveoli; Pulmonary Surfactants; Retrospective Studies
PubMed: 8151480
DOI: 10.1016/s0022-3476(05)83145-2