Ventilation heterogeneity does not change following pulmonary microembolism.
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By using the multiple-breath helium washout technique, ventilation heterogeneity (VH) after embolic injury in the lung can be quantitatively partitioned into the conductive and acinar components. Total VH, represented by the normalized slope of the phase III alveolar plateau, Sn(III (total)), was studied for 120 min in three groups of anesthetized and paralyzed mongrel dogs. Group 1 (n = 3) received only normal saline and served as controls. Group 2 (n = 4) received repeated infusions of polystyrene beads (250 microm) into the right atrium at 10, 40, 80, and 120 min. Group 3 (n = 3) was similarly treated, except that the embolic beads used were 1,000 microm in diameter. The data show that, despite repeated embolic injury by polystyrene beads of different diameters, there was no significant increase in total VH. The acinar component of Sn(III), which represents VH in the distal airways, accounts for over 90% of the total VH. The conductive component of Sn(III), which represents VH between larger conductive airways, remains relatively constant and a minor component. We conclude that pulmonary microembolism does not result in significant redistribution of ventilation. (+info)
Pulmonary cytolytic thrombi: a newly recognized complication of stem cell transplantation.
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Over the past 5 years we have recognized a new pulmonary complication of hematopoietic stem cell transplantation (HSCT) associated with fever and pulmonary nodules termed 'pulmonary cytolytic thrombi' (PCT). Retrospective analysis of medical and radiographic records and pathologic material from 13 HSCT recipients with PCT and a review of the Blood and Marrow Transplant Database for all patients with radiographic evidence of pulmonary nodules or who underwent open-lung biopsy from 1 January 1993 to 31 December 1998 (n = 1228) were performed. The median age of patients with PCT was 11.9 years (range, 1.3-29.7 years). All patients developed fever at a median of 72 days (range, 8-343 days) post transplant, followed by pulmonary nodules on chest CT. Eleven patients were receiving therapy for active GVHD (acute, grades I-IV (n = 10); extensive chronic (n = 1)). Biopsy of the pulmonary nodules revealed a unique pattern of necrotic, basophilic thromboemboli with amorphous material suggestive of cellular breakdown products. This was descriptively labeled 'pulmonary cytolytic thrombi'. Immunohistochemical staining revealed entrapped leukocytes and disrupted endothelium, but was negative for histiocytes. Cultures and immunohistochemical stains were negative for infectious agents. Empiric therapy included systemic corticosteroids (n = 9) and amphotericin (n = 7). Nine patients survive with resolution of PCT at a median follow-up of 1.5 years. Bone Marrow Transplantation (2000) 25, 293-300. (+info)
Cavitary pulmonary infarction--a rare cause of spontaneous pneumothorax.
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A 14-year old female was admitted to the hospital with a diagnosis of resolving myocarditis and dilated cardiomyopathy. She developed spontaneous right-sided pneumothorax. Autopsy, revealed rupture of cavitary pulmonary infarction to be the cause of the pneumothorax, a rare finding. (+info)
Guidewire entrapment during deployment of the over-the-guidewire stainless steel Greenfield filter: a device design-related complication.
(52/2239)
The Greenfield filter (Medi-tech/Boston Scientific, Watertown, Mass) is widely used for the prevention of pulmonary embolism. The latest version is a stainless steel over-the-wire filter. The purpose of the guidewire is to facilitate placement of the device down through the atrium or through tortuous vessels and to prevent tilting of the released filter. A case of entrapment of the guidewire in the filter after deployment through the right internal jugular approach and its recovery by reentering it into the sheath is presented. To prevent this complication, the guidewire should be removed completely before releasing this type of filter. The potential risk of tilting the filter does not outweigh the risk of guidewire entrapment. (+info)
Vagal and mediator mechanisms underlying the tachypnea caused by pulmonary air embolism in dogs.
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We investigated the vagal and mediator mechanisms underlying the tachypnea caused by pulmonary air embolism (PAE) in anesthetized and spontaneously breathing dogs. PAE was induced by infusion of air into the right atrium (0.2 ml. kg(-1). min(-1) for 10 min). The first PAE induction caused an increase in respiratory frequency accompanied by a decrease in tidal volume in each of the 30 animals studied. Subsequently, animals were evenly divided into five groups, and a second PAE induction was repeated after various experimental interventions. The tachypneic response to PAE was not significantly altered by pretreatment with a saline vehicle but was largely attenuated by either perivagal capsaicin treatment (a technique that selectively blocks the conduction of unmyelinated C fibers), pretreatment with ibuprofen (a cyclooxygenase inhibitor), or pretreatment with dimethylthiourea (a hydroxyl radical scavenger). Ultimately, the tachypneic response was nearly abolished by a bilateral cervical vagotomy. These results suggest that 1) lung vagal unmyelinated C-fiber afferents play a predominant role in evoking the reflex tachypneic response to PAE and 2) both cyclooxygenase products and hydroxyl radical are important in eliciting this vagally mediated response. (+info)
Postirradiation aortic sarcoma demonstrated by magnetic resonance angiography.
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This is the first ever reported case of a radiation-induced aortic sarcoma. This patient had symptoms and signs initially interpreted as a pulmonary embolus. The extent of the disease was demonstrated with magnetic resonance imaging and magnetic resonance angiography, in particular, allowing rapid surgical intervention. (+info)
Is pulmonary embolism a common cause of chronic pulmonary hypertension? Limitations of the embolic hypothesis.
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The hypothesis that chronic thromboembolic pulmonary hypertension results from unresolved pulmonary embolism has strongly influenced the diagnosis and management of this disease since the 1960s. However, it is nearly impossible to induce chronic pulmonary hypertension in any animal species by means of repeated embolization of thrombotic material. The haemodynamic effects of thrombotic pulmonary embolism of different degrees of magnitude have also been studied in humans and there is little to suggest that chronic pulmonary hypertension is a likely long term outcome. Furthermore many conditions which predispose to venous thromboembolism do not appear to cause thromboembolic pulmonary hypertension. Other arteriopathic and atherosclerotic risk factors, are found in patients with chronic thromboembolic pulmonary hypertension, but not in those with venous thrombosis, suggesting that these may be unrelated conditions. Thrombosis in situ of the pulmonary arteries is common in severe pulmonary hypertension of any cause. Such thrombosis cannot usually be distinguished from pulmonary embolism. It is hypothesized that in situ thrombosis and pulmonary arteriopathy are common causes of vascular occlusion which is usually diagnosed as "chronic thromboembolic pulmonary hypertension" and that venous thromboembolism is unlikely to be a common cause of chronic pulmonary hypertension. It is further hypothesized that pulmonary embolism is seldom the sole cause of "chronic thromboembolic pulmonary hypertension". (+info)
Multiple pulmonary infarctions associated with lung cancer.
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We present a case of right lung adenosquamous cell carcinoma that had obstructed the main pulmonary artery and superior pulmonary vein, causing multiple pulmonary infarctions in the right upper and middle lobes. Multiple peripheral pulmonary nodules showed clinical features that are characteristic of pulmonary infarction: rapid appearance and gradual reduction in size, pleural-based parenchymal density with a truncated apex and a round nodular shadow with a blurred margin and a centrally directed linear shadow. The nodules were more intense than the primary tumor in both T1- and T2-weighted magnetic resonance imaging (MRI). We conclude that pulmonary infarction can look like a nodule when lung cancer invades both the pulmonary artery and vein and that such cases can be distinguished from pulmonary metastasis by MRI, computed tomography and a series of radiological examinations. (+info)