Cynthia L. Rapp, BS, RDMS, RDCS

• Vice President of Clinical Program Development
• The Medipattern Corporation
• Toronto, Ontario, Canada

The congenital type includes bronchogenic cysts whose fluid contents have been expelled and congenital cystic disease of the lung gastritis biopsy doxazosin 4mg fast delivery. Blebs are either subpleural or intrapleural gastritis diet �������� 4 mg doxazosin fast delivery, seldom exceed 1 cm in diameter and most frequently develop over lung apices gastritis garlic generic doxazosin 1 mg otc. Bullae are intrapulmonary structures and appear to affect upper and lower lobes equally gastritis diet salad generic doxazosin 4 mg on line. Some bullae develop as a sequela of lung abscess gastritis diet 17 doxazosin 4 mg low price, of either tuberculous or staphylococcal etiology gastritis diet 2 days purchase 2 mg doxazosin free shipping. Post-traumatic pneumatoceles resulting from lung tissue laceration associated with nonpenetrating trauma may present as thin-walled air cysts, with or without an air-fluid level. The cysts are very thinwalled, are small and distributed widely throughout the subpleural zone. Lack of bronchial tapering: the earliest sign of cylindrical bronchiectasis, lack of bronchial tapering, is often subtle. One indication of this finding in crosssection is lack of change in the size of an airway over 2 cm after branching. Visualization of peripheral airways: Visualization of an airway within 1 cm of the costal pleura is abnormal and indicates potential bronchiectasis. Airways may be seen within 1 cm of the mediastinal pleura, should not be seen actually to abut the mediastinal pleura. The assessment of the etiology of bronchiectasis based on the distribution of bronchiectasis on imaging studies is diagnostically helpful. Also, the imaging studies should be interpreted in the presence of specific clinical information. Honeycombing results from destruction of alveoli and loss of acinar architecture and is associated with pulmonary fibrosis. Honeycomb cysts usually share walls with one another and associated findings of fibrosis such as architectural distortion, coarse reticulation, intralobular interstitial thickening and traction bronchiectasis, are also commonly present. Recently, lung cysts have been reported in association with hypersensitivity pneumonitis. The intervening lung parenchyma is typically normal, without evidence of fibrosis or septal thickening. The distribution of findings is usually in upper lungs, with sparing of the costophrenic sulci. Presumably, these are the result of airspace ectasia secondary to progressive airway obstruction. Centrilobular emphysema is found most commonly in the upper lobes and manifests as multiple small areas of low attenuation without a perceptible wall, producing a punched out appearance. Occasionally, a very thin, barely perceptible, wall may be seen in centrilobular emphysema, probably related to some degree of surrounding fibrosis. When centrilobular emphysema becomes more pronounced, area of confluent low attenuation become evident. Centrilobular emphysema and paraseptal emphysema are uncommonly associated with panlobular emphysema. Paraseptal emphysema commonly occurs in smokers and shows upper lobe predominance, although it may be seen with other types of emphysema and even in nonsmokers. Chapter 153 Basic Patterns of Lung Diseases 2535 Spontaneous pneumothorax may occur in association with paraseptal emphysema. Cicatricial emphysema, now termed "irregular airspace enlargement" may be recognized in association with parenchymal scars, especially in the setting of progressive massive fibrosis in patients with pneumoconiosis. Mosaic Perfusion and Inhomogeneous Lung Opacity A mosaic pattern of attenuation, with patchy areas of increased and decreased attenuation, is nonspecific and may be seen when various infiltrative lung, airway, or vascular diseases are present. In the presence of airway obstruction and air trapping, lung remains lucent on expiration and shows little change in cross-sectional area. Areas of air trapping are seen as relatively low in attenuation on expiratory scans. Areas of air trapping can be patchy and nonanatomic; can correspond to individual secondary pulmonary lobules, segments and lobes; or may involve an entire lung. Air trapping in a lobe or lung is usually associated with large airway or generalised small airway abnormalities, whereas lobular or segmental air trapping is associated with diseases that affect small airways. Pulmonary vessels within the low-attenuation areas of air trapping often appear small relative to vessels in the more opaque normal lung regions. In patients with mosaic attenuation resulting from airway disease, attenuation differences are accentuated on expiration. On expiratory scanning, air trapping is not a dominant feature of vascular disease. There are areas of relatively dense parenchyma and lucent areas showing paucity of the normal vasculature-Mosaic perfusion due to bronchiectasis 2536 Section 6 Chest and Cardiovascular Imaging Pulmonary tissue density is in part determined by the blood volume present within lung tissue. Any pathologic process that disturbs the distribution of pulmonary blood volume may alter pulmonary parenchymel attenuation. Two major categories of pathologies producing mosaic perfusions are recognized; air way obstruction and vascular occlusions. Obstructive airway lesions that may produce mosaic perfusion include large air way diseases, such as bronchiectasis and the various forms of bronchiolitis, particularly chronic bronchiolitis with hypersensitivity preumonitis and constrictive bronchiolitis. Vascular occlusion is commonly the result of chronic thromboembolic disease, pulmonary hyperternsion, or capillaritis caused by vasculitis. The presence of lobular low attenuation, in which the outlines of individual secondary pulmonary lobules may be recognized, also favours the presence of mosaic perfusion over ground glass opacity. Once mosaic perfusion is diagnosed, airway and vascular pathologies must then be distinguished; this may be accomplished with expiratory imaging. When the cause of the mosaic perfusion on the inspiratory image is related to bronchiolitis, however, the appearance of the inhomogeneous lung opacity is accentuated. For vascular causes of mosaic perfusion, air trapping is not present and all areas of lung increase in attenuation in a similar fashion. With airway causes of inhomogeneous opacity, however, air trapping impedes the escape of air from some areas of lung, whereas other areas decompress normally. This results in an accentuation of the inhomogeneous opacity with expiratory imaging. As a general rule, small airway causes of mosaic perfusion are far more common than vascular etiologies. This may reflect less extensive physiologic derangements than conditions in which abnormalities are visible on the inspiratory images. The differential diagnosis in such cases include constrictive bronchiolitis, asthma, chronic bronchitis and hypersensitivity pnenumonitis. The objective is to find the planes in which key features are displayed that can help identify the main pattern of diffuse lung disease, any associated findings and the distribution of lesions relative to the secondary pulmonary lobule anatomy. Even when a single diagnosis cannot be established on the basis of available radiographic and clinical information, the next appropriate step in the evaluation of the patient can be suggested. Computed Tomography and Magnetic Resonance Imaging of the Whole Body, 3rd edition. Standardised terms for high-resolution computed tomography of the lung: A proposed glossary. The Radiologic differential diagnosis of diffuse lung diseases characterised by multiple cysts or cavities. Dynamic imaging of lung morphology with ultrafast high-resolution computed tomography. It is responsible for a great amount of morbidity and mortality, particularly in the developing nations. The course of the disease and its corresponding clinicoradiological pattern depends on the interaction between the organism and the host response. Furthermore, due to an altered immunological response in certain groups, such as immunocompromised and elderly patients, an atypical radioclinical pattern may occur. The changing landscape, in which tuberculosis occurs, as well as the global resurgence, and the changed spectrum of the clinical and radiological presentation, justify a renewed interest of radiologists for the imaging features of pulmonary tuberculosis. On the contrary, cases in which the isolates have distinctive genotypes generally represent reactivation of infection. Retro-obstructive inflammation may resorb and evolve to a fibrotic and/ or calcified lesion. Destruction and fibrosis of the lung parenchyma result in formation of traction bronchiectasis. Typically, lesions are located in the apicoposterior lung segments and to a lesser degree in the apical segments of the lower lobes. Coughing may result in bronchogenic spread and contamination of other patients, via inhalation of bacilliladen droplets. Radiographs show extensive abnormalities, such as apicoposterior infiltrates, cavities, pleural exudates, fibroproductive lesions causing distortion of lung parenchyma, elevation of fissures and hila, pleural adhesions, and formation of traction bronchiectasis. Chest radiograph shows left pleural effusion with an air fluid level and partial atelectasis of the left lung Exudative Pleuritis Bacilli can enter the pleural space from a juxtapleural pulmonary or gangliopulmonary caseating granuloma, or via hematogenous dissemination. Tuberculous pleurisy may become localized, causing a tuberculous empyema, which may break through the parietal pleura to form a subcutaneous abscess, so-called empyema necessitatis. Diagnosis of bronchopleural fistula is based on an increasing amount of sputum production, air in the pleural space, a changing air-fluid level, and contralateral spread of disease. After healing of this focal infection of the bronchial wall, cicatricial bronchostenosis may occur. A healed filled-in cavity and a rounded-off, contracted healing tuberculous lesion are the reported possible mechanisms of tuberculoma formation. Thickening of the walls of a tuberculous cavity or of the adjacent pleura is reported to be an early radiographic sign. It heralds severe and extensive pulmonary involvement by the infectious process, and the onset of bronchopleural fistula and empyema. Tuberculous fibrosing mediastinitis is an uncommon complication and progresses insidiously without significant clinical symptoms. In cases of exogenic reinfection or primary infection, a shift is there from the usual pathogenetic pathway (reactivation) to an unusual pathway for adults, with a presentation similar to that found in children. The clinical spectrum of primary tuberculosis in adults: Confusion with reinfection in the pathogenesis of chronic tuberculosis. Clinical and radiographic correlates of primary and reactivation tuberculosis: a molecular epide miology study. The relationship between pulmonary tuberculosis and bronchogenic carcinoma: A topographic study. Tuberculosis as an endemic and nosocomial infection among the elderly in nursing homes. Inflammatory disease of the lung may be referred to as either pneumonia or pneumonitis. Although these terms are used interchangeably, pneumonia usually implies an infection by pathogenic organisms whereas pneumonitis tends to refer to a noninfective inflammatory process involving the alveolar wall. The radiologist can establish the presence of disease, locate and define the extent of disease, suggest an etiological diagnosis, recognize any underlying pathology, assess the response to treatment and establish the presence of complications. It can give quantitative and qualitative information about pleural fluid collections and serve as a guide for aspiration. Although widely used, these terms have limited value because the same organism may produce several patterns and because patterns often overlap in an individual patient. In lobar/airspace pneumonia the infective organism reaches the acini leading to a rapid production of abundant edema fluid with minimal cellular reaction. There is an initial peripheral localization but as the fluid increases in amount it flows from alveolus to alveolus limited only by pleural boundaries, leading to a confluent involvement of the lung parenchyma. Eventually, the pneumonia may involve the whole lobe, but usually symptoms develop before the entire lobe is consolidated and antibiotic therapy, if started, halts the process. The consolidation is usually confined to one lobe, although multilobar involvement is not uncommon. Because the airways are not primarily affected, there is little or no volume loss and visible air bronchograms are common. A chest radiograph (posteroanterior view) is the basic and most useful imaging tool to establish the presence of pneumonia, determine its location and extent, and monitor its response to therapy. Further, the chest radiograph can detect complications (cavitation, abscess formation, pneumothorax, pleural effusion), detect additional and alternative diagnoses and sometimes guide invasive diagnostic procedures. In bronchopneumonia the mucosal surfaces of the bronchi and bronchioles are affected rather than the terminal airspace. A peribronchiolar focus of infection develops which subsequently spreads along the intralobular airway to the alveolus and then from alveolus to alveolus until the pulmonary lobule is partially or totally involved. More severe disease results in inhomogeneous, patchy, poorly defined opacities with absence of air bronchograms. Often, a radiographic distinction between lobar pneumonia and confluent bronchopneumonia cannot be made. The usual causes of acute interstitial pneumonia are viral or Mycoplasma pneumoniae infection. There is thickening of bronchial walls, centrilobular shadows, acinar and lobular shadows. It is thought by some to represent an early manifestation of the infectious focus that has spread centrifugally.

In cases of significant flow through the azygos vein gastritis juicing recipes discount 4mg doxazosin fast delivery, however gastritis and exercise order 2mg doxazosin overnight delivery, it is beneficial to use stents like the Gianturco stents gastritis diet menus generic 1mg doxazosin visa, which have an open structure to bridge the azygos vein orifice gastritis symptoms in tamil buy doxazosin 1mg. Access from the basilic gastritis diet rice discount 4 mg doxazosin otc, jugular viral gastritis symptoms purchase generic doxazosin, subclavian, or femoral veins is used, depending on disease extent. However, the subclavian access route when compared with others is supposedly the more advantageous and simpler route despite a slight increased risk of pneumothorax. After crossing the obstruction, a standard hydrophilic guide wire is exchanged for a 180- or 260-cm stiff guide wire. In case of strictures, predilatation to allow passage of the stent delivery system may be necessary. However, it is vital to confirm luminal reentry prior to balloon dilatation or stenting. Balloon dilatation should always be performed with caution, however, because this may result in catastrophic venous rupture. Of the 17 deaths 7 (41%) were attributed to severe hemorrhage: 2 cerebral, 3 pulmonary, and 2 unspecified sites. Four deaths (23%) were attributed to cardiac events: two arrhythmias, one myocardial infarction, and one tamponade. One death (6%) was due to documented pulmonary embolism, and in two cases (12%) cause of death was unknown. Fatal hemorrhages were mostly attributed to thrombolytic therapy administration, including streptokinase, urokinase, and tissue plasminogen activator, which were used to dissolve intracaval clot prior to stent insertion. The predisposing factors for stent migration are poor patient selection, inaccurate vessel measurement, inadequate sizing of the stents, inaccurate positioning of the stents, and cardiac motion. These factors should be considered prior to stent deployment to minimize or prevent stent migration. This can lead to acute pulmonary edema, which can be fatal in patients with underlying coronary artery disease and heart failure. Anticoagulation is recommended following stent placement but optimal duration and methods of anticoagulation therapy remain controversial. The main drawback of this technique is that it may increase the risk of perforation of the adjacent aorta and pericardium due to embedment of sharp stent filaments into the vessel wall at the flared ends. Stenting is the treatment of choice for patients with acute life-threatening symptoms. Also outcomes and complications compare very favorably with standard therapies (such as chemotherapy and radiotherapy); therefore, it has been advocated as the first-line treatment option. Prevalence and characteristics of pleural effusions in superior vena cava syndrome. Treatment of malignant superior vena cava obstruction: metal stents or radiation therapy. Superior vena cava syndrome induced by bronchogenic carcinoma: is this an oncological emergency Clinical outcome of stenting in superior vena cava syndrome associated with malignant tumors: comparison with conventional treatment. Superior vena cava obstruction in small cell bronchogenic carcinoma: clinical parameters and survival. Emergency prebiopsy radiation for mediastinal masses: impact on subsequent pathologic diagnosis and outcome. Steroids, radiotherapy, chemotherapy and stents for superior vena caval obstruction in carcinoma of the bronchus: a systematic review. Management of superior vena cava syndrome by internal jugular to femoral vein bypass. Treatment of obstruction of the superior vena cava by combination chemotherapy with and without irradiation in small-cell carcinoma of the bronchus. Small cell lung cancer with and without superior vena cava syndrome: a multivariate analysis of prognostic factors in 408 cases. Cirse guidelines: quality assurance guidelines for superior vena cava stenting in malignant disease. Stenosis of the vena cava: preliminary assessment of treatment with expandable metal stents. Stenting as first option for endovascular treatment of malignant superior vena cava syndrome. Endovascular stenting as a first choice for the palliation of superior vena cava syndrome. Endovascular treatment of superior vena cava obstruction in patients with malignancies. Endovascular stenting in neoplastic superior vena cava syndrome prior to chemotherapy or radiotherapy. Superior vena cava syndrome: treatment with catheter directed thrombolysis and endovascular stent placement. Treatment of malignant superior vena cava syndrome by endovascular stent insertion. Safety and effectiveness of vascular endoprosthesis for malignant superior vena cava syndrome. The use of the Wallstent endovascular prosthesis in the treatment of malignant obstruction of the superior vena cava. Subacute and chronic benign superior vena cava obstructions: endovascular treatment with self expanding metallic stents. Self expanding metal stents for palliative treatment of superior vena caval syndrome. Stent therapy for malignant superior vena cava syndrome: should be first line therapy or simple adjunct to radiotherapy. Vena cava and central venous stenosis: management with Palmaz-balloon-expandable intraluminal stents. Case report: migration and shortening of a self-expanding metallic stent complicating the treatment of malignant superior vena cava stenosis. Endovascular treatment of malignant superior vena cava syndrome: is bilateral wallstent placement superior to unilateral placement Malignant superior vena cava obstruction: stent placement via the subclavian route. Cardiac tamponade: a rare complication of attempted stenting in malignant superior vena cava obstruction. Gianturco-Rosch expandable Z-stents in the treatment of superior vena cava syndrome. Long term results of endovascular stent placement in the superior caval venous system. Use of the Wallstent in the venous system including haemodialysis-related stenosis. Hemodynamic changes after self expandable metallic stent therapy for superior vena cava syndrome. Self-expandable metallic stent therapy for superior vena cava syndrome: clinical observations. Steroids, radiotherapy, chemotherapy and stents for superior vena caval obstruction in carcinoma of the bronchus (Cochrane review). The syndrome was first described by William Hunter, who in 1757 published an account of superior vena cava obstruction secondary to a syphilitic thoracic aortic aneurysm. The superior vena cava and the innominate tributary veins are low-pressure vessels with relatively thin walls. Their anatomic proximity to adjacent structures, such as lymph nodes, lung, and large arteries, makes them susceptible to compression and stenosis. Malignant causes of superior vena cava and innominate vein stenosis include bronchogenic carcinoma, lymphoma, and metastatic disease. Benign causes of superior vena cava and innominate vein stenosis include nonmalignant masses, such as cysts, goiter, teratoma, and thymoma; infectious and inflammatory processes, such as histoplasmosis, tuberculosis, and mediastinitis; vascular aneurysms; postsurgical anastomotic strictures; chronic or repeated central venous catheter use; and cardiac device leads from pacers and defibrillators. Benign causes of central venous stenosis predominated until they were supplanted by increasing rates of lung and mediastinal cancer in the mid- and late 1990s. At their peak, malignant causes accounted for 85% to 97% of all cases of superior vena cava syndrome. In one series benign causes now account for up to 40% of cases of superior vena cava syndrome. However, recent studies have demonstrated that catheter and pacer wire-related stenoses now predominate the benign subset of superior vena cava obstruction (57% to 74%). In the schema set forth by Stanford, superior vena cava obstruction can be stratified into four classes based on the pattern observed at venography (Table 91. The investigators found a correlation between advancing obstruction pattern and the presence of symptoms. Type I is described as up to a 90% stenosis of the superior vena cava with antegrade flow through the azygos vein. Extrinsic compression is the result of mass effect from adjacent structures, such as arterial aneurysm or benign masses. Mediastinitis, either infectious or inflammatory, results in compressive forces as the surrounding fibrosis retracts and collapses the vein lumen. Intrinsic stenosis is the result of intimal trauma and pericatheter thrombus formation, which leads to smooth muscle ingrowth and the development Table 91. The process of thrombus formation further inflames and then scars the vein, resulting in worsening stenosis or occlusion. The obstruction of the superior vena cava leads to impaired venous return from the head and upper extremities. Clinical symptoms include headache, fatigue, dyspnea, cough, dysphagia, dizziness, impaired vision, nausea, syncope, and coma. In the Kishi scoring system grades were assigned to a series of clinical signs and symptoms. By summing the highest grade from each category a score was derived that was used to establish disease severity and evaluate treatment outcome. The primary treatment for malignant superior vena cava syndrome is either external radiation therapy or endovascular intervention with balloon angioplasty or stent placement. Patients with benign causes of superior vena cava syndrome tend to be comparatively younger with longer life expectancies. Initial therapy for superior vena cava obstruction of benign etiology involves anticoagulation to prevent or limit thrombus formation. Indeed some authors have concluded that endovascular intervention is now the first-line treatment for benign superior vena cava syndrome. Early use of thrombolysis for superior vena cava syndrome was focused on occlusions induced by pacemaker wires. Shortly after this initial publication, several other authors published early accounts of balloon angioplasty of the superior vena cava. By drawing on the clinical history, noninvasive imaging findings, and venographic appearance, the interventionist must determine if the vein is stenotic but patent or occluded. B vein is occluded, it is necessary to recanalize the vein because guide wire access across the lesion is fundamental to further intervention. If the vein is occluded with fresh thrombus, the guide wire typically passes without difficulty and the interventionist can proceed with thrombolysis. After excluding relevant contraindications to thrombolytic therapy (bleeding disorder, pregnancy, primary or metastatic disease of the brain or spinal cord, recent surgery, gastrointestinal bleeding, etc. First, by lysing the acute thrombus there is less potential for it to embolize during subsequent balloon angioplasty and stent placement. Second, following a course of thrombolysis, the underlying stenosis or occlusion is often shorter than had been previously appreciated and may require fewer or shorter stents. Recanalization techniques involve using various guide wires and support catheter to cross the occlusion, followed by balloon angioplasty to open the channel in preparation for balloon angioplasty and/or stent placement. In these situations, sharp recanalization can be attempted using a Colapinto needle or other such device. Postangioplasty venogram with restored patency of the previously occluded vein segment. Left arm venogram demonstrates left innominate stenosis secondary to cardiac defibrillator leads. Completion venogram following balloon angioplasty and stent placement documents restored patency of the vein segment. Heparin anticoagulation during the procedure is favored by some, although its use is not universal. By using this technique an inadvertently dislodged stent is constrained by the delivery wire and unable to travel into the heart. When faced with a stenosis or obstruction that involves the superior vena cava as well as both innominate veins, recent publications have indicated that only the superior vena cava and one innominate vein need to be revascularized to achieve clinical benefit. In comparative studies, unilateral innominate vein revascularization is favored because there is shorter procedure time, fewer complications, and less reocclusion. Removal of the pacer wire can be clinically undesirable or technically impossible. One frequently cited concern with the intervention in this setting is the possibility of a harmful interaction between the metallic stent and the pacer wire. First, pacemaker wires are well insulated by a coating of silicone rubber or polyurethane. Second, a pacemaker wire that has incited a venous stenosis is well embedded within the vessel wall and likely has no exposure to the lumen in which the stent is implanted. Whereas the reported primary patency rates of endovascular therapy are in the range of 57% to 79%, the primary assisted or secondary patency to 3 years is 96% to 100%. Major complications include stent migration, pericardial tamponade, superior vena cava rupture, pulmonary embolism, and death.

The development of plasminogen activators has mirrored technical improvements in biotechnology gastritis diet 4 believers order doxazosin 1 mg mastercard, protein engineering gastritis que puedo comer buy doxazosin 1 mg low price, and manufacturing techniques gastritis joint pain buy doxazosin 4 mg lowest price. Because of the risk of anaphylactic reaction and/or the need to procure human kidney cells gastritis diet peanut butter order doxazosin mastercard, these agents are no longer manufactured or marketed in the United States gastritis milk order doxazosin australia. The choice of the thrombolytic agent is a matter of regional practices and physician discretion gastritis diet for children buy doxazosin 1 mg without a prescription. Because of its lack of affinity for fibrin, it cleaves both free circulating plasminogen and fibrin-bound plasminogen and can induce systemic fibrinolysis. Its principal advantage is the significantly lower costs (per vial basis) compared to recombinant agents. Derivatives of alteplase can be produced using recombinant techniques involving deletion mutations (reteplase) or substitution mutations (tenecteplase) as described by nordt and bode. Thrombolysis of peripheral arterial and graft occlusions: improved results using high-dose urokinase. Dosage and registered in the United States for massive pulmonary embolism and in Canada for clot lysis and catheter clearance. The principal drawback has been its current limited supply, significantly higher costs compared to the recombinant agents,23 historically longer infusions times, and rare cases of anaphylactoid reactions. Alteplase Tissue plasminogen activator is a naturally occurring glycosylated serine protease produced by human vascular endothelial cells and plays a role in the natural endogenous process of fibrinolysis. Kringle 2 helps to stimulate the protease domain in the presence of fibrin and the fibronectin finger helps bind to fibrin. Alteplase is a direct plasminogen activator but its affinity for fibrin-bound plasminogen is enhanced compared to firstgeneration agents and produces limited conversion of plasminogen to plasmin in absence of fibrin. Alteplase binds to fibrin within the thrombus and converts entrapped plasminogen to plasmin, which then initiates local fibrinolysis. Plasma clearance of alteplase is relatively rapid with a half-life of less than 5 minutes. The fermentation process involves secretion of alteplase from the genetically modified cell lines into the tissue culture medium. The secreted protein is then separated, purified, and lyophilized into powder form. Alteplase is marketed under the trade name Activase (50 and 100 mg, Genentech, Inc. It has a plasma half-life of approximately 13 to 16 minutes and is cleared from the circulation primarily by the liver and kidneys. Use of reteplase in catheter-directed treatment of arterial limb ischemia was initially reported in 2000 in a small doseranging study and has emerged as another thrombolytic alternative. Once an infusion catheter is placed across the length of the thrombosed segment, a steady and constant infusion of thrombolytic agent is administered for several hours (typically overnight). Bolus (or lacing) involves delivery of a large concentration of thrombolytic drug directly into the clot through the intrathrombic catheter in attempts to immediately accelerate and initiate the fibrinolysis process; this is then followed by a lower continuous infusion. Graduated infusions is the process of using stepwise dosing regimen, typically a higher dose continually infused for a fixed period, then empirically lowered to a lower dose for the remainder of the infusion. Pharmacomechanical thrombolysis refers to either the use of high-velocity bursts of small volumes of the thrombolytic agent ("pulse spray") or use of a thrombolytic agent in conjunction with a mechanical device (balloon catheter or mechanical thrombectomy device) to macerate and physically fragment the clot and increase the surface area of clot exposed to the plasminogen activator. Plasminogen Activator There is no consensus on the optimal thrombolytic agent, and selection is based on physician preference and regional practice standards. In treatment of arterial ischemia, doses have ranged from none to sub-therapeutic to full-therapeutic anticoagulation and no consensus position has been established. Contraindications can be classified as absolute and relative and are summarized in Table 99. The goal of therapy is to lyse as much of the thrombus burden as possible, unmask the stenotic iliac vein, and angioplasty and stent the obstructed iliac segment to fully reconstruct the iliofemoral outflow. Monitoring serial fibrinogen levels to assess for potential risk for bleeding complications from systemic fibrinolysis is controversial and no consensus has been established. Historically, maintenance of fibrinogen level greater than 100 mg/dL has been reported but there are no well-controlled studies to confirm that measuring serial fibrinogen levels are predictive of bleeding risk. Although any bleeding complication is undesired, acceptable thresholds of major complications have been proposed for both arterial and venous thrombolysis40,44 (Table 99. Outcomes There are few rigorously designed, prospective, multicenter studies evaluating comparative outcomes from arterial and venous thrombolysis and the body of literature represents mostly single center, nonrandomized observational studies. One of the complexities in analyzing clinical data across published studies is the varying techniques, definitions, patient selection, and outcome parameters used in reporting. Its potential advantage is its very high fibrin specificity and long half-life (~2. Recombinantly derived, it is under investigation for the systemic treatment of acute ischemic stroke (H. Ocriplasmin is a 27 kDa recombinant derivative of human microplasmin (contains only the catalytic domain) that directly acts on fibrin instead of conversion of plasminogen to plasmin. It is a recombinant enzyme that is normally produced from the venom of the southern copperhead snake (Agkistrodon contortrix). Alfimeprase was under investigation for peripheral arterial limb ischemia and catheter clearance but development was discontinued in 2007. Platelet function during and after thrombolytic therapy for acute myocardial infarction with reteplase, alteplase, and streptokinase. Dear Healthcare Provider Letter: Important Drug Warning: Safety information regarding the use of Abbokinase (urokinase). Thrombolytic and antiplatelet therapy in peripheral vascular disease with use of reteplase and/or abciximab. Acute myocardial infarction: intracoronary application of nitroglycerin and streptokinase. The effect in patients of streptococcal fibrinolysin (streptokinase) and streptococcal deoxyribonuclease on fibrinous, purulent, and sanguinous pleural exudations. Randomized trial of intra-arterial recombinant tissue plasminogen activator, intravenous recombinant tissue plasminogen activator, and intra-arterial streptokinase in peripheral arterial thrombolysis. The safety, efficacy, and pharmacoeconomics of low-dose alteplase compared with urokinase for catheter-directed thrombolysis of arterial and venous occlusions. Peripheral artery and bypass graft thrombolysis with recombinant human tissue-type plasminogen activator. Local thrombolytic therapy of acute peripheral arterial ischemia with tissue plasminogen activator: a dose-ranging study. Initial results of reteplase in the treatment of acute lower extremity arterial occlusions. Thrombolysis of occluded peripheral arteries and veins with tenecteplase: a pilot study. Tenecteplase: stability and bioactivity of thawed or diluted solutions used in peripheral thrombolysis. Catheter-directed thrombolytic therapy for limb ischemia: current status and controversies. Quality improvement guidelines for percutaneous management of acute limb ischemia. Society of Interventional Radiology position statement: treatment of acute iliofemoral deep vein thrombosis with use of adjunctive catheter-directed intrathrombus thrombolysis. A comparison of recombinant urokinase with vascular surgery as initial treatment for acute arterial occlusion of the legs. Dose-ranging trial with a recombinant urokinase (urokinase alpha) for occluded central venous catheter in oncology patients. Randomized, placebo-controlled, dose-ranging clinical trial of intravenous microplasmin in patients with acute ischemic stroke. Development of catheter-directed intrathrombus thrombolysis with plasmin for the treatment of acute lower extremity arterial occlusion. It can occur after any surgical or endovascular intervention including balloon angioplasty, atherectomy, or stent insertion. Because it is the major factor limiting the longevity of endovascular procedures, it significantly impacts the choice between minimally invasive and open procedures for any individual patient. Restenosis after balloon angioplasty is caused by elastic recoil, constrictive remodelling, and neointimal hyperplasia. Neointimal hyperplasia (also called intimal or myointimal hyperplasia) is an overexpression of the normal vascular healing process. These in turn immediately stimulate a healing response that is modulated by a complex interplay of events occurring in the lumen and the vessel wall. Within the vessel wall there is acute inflammation, granulation tissue formation and the local release of chemotactic and growth factors, and oxygen-derived free radicals. In pathologic neointimal hyperplasia (as opposed to appropriately modulated intimal hyperplasia occurring after a normal vessel response to injury), there is excessive proliferation and migration of upregulated vascular smooth muscle cells, and oversecretion of an extracellular proteoglycan matrix. It follows that certain methods of preventing restenosis (such as drug/device combinations) might be more effective in some body regions than others because the degree to which an intimal hyperplasia lesion is composed of vascular smooth muscle cells or proteinaceous matrix varies from vascular bed to vascular bed. These include repetitive deformation, burden of calcification, and vessel wall composition and thickness relative to luminal diameter. Regardless of vascular bed the three most significant determinants of restenosis rates are vessel diameter, length of lesion, and presence of diabetes. In most clinical trials, angiographic restenosis is defined as a recurrent narrowing greater than 50% (the incidence of angiographic restenoses of 51% or greater may also be called the binary restenosis rate). Because patients with angiographic restenosis may be asymptomatic, many consider clinical restenosis the more relevant term. There are multiple ways to define clinical restenosis including recurrence of symptoms or a decline in noninvasive measurements. Prevention of restenosis is more frequently attempted, and successfully performed, than treatment. As the stent remains fully expanded, elastic recoil or constrictive remodeling are not components of in-stent restenosis. In this article we focus on local pharmacologic treatments specifically targeted at the biologic cascade of restenosis. Following implantation, the therapeutic material is released locally into the vessel wall adjacent to the stent as well as into the bloodstream. Multiple factors influence the amount of the active agent that ultimately enters the vessel wall and for how long it stays there. Improved clinical outcomes have resulted in a significant increase in both total number of endovascular coronary procedures and their complexity since that time. In the coronary circulation, surgical bypass to treat a blocked coronary artery involves the morbidity of a thoracotomy and a stay in the intensive care unit; therefore, an endovascular alternative does not have to be more durable to be an acceptable alternative. Drug-eluting coronary stents profoundly decrease restenosis rates in comparison with bare metal stents, and reducing the restenosis rate improves patient clinical outcome. In some peripheral vascular disease states the number of patients is so low that a product purpose-designed to treat that entity would not be commercially viable. This article discusses only coated stents designed for the prevention of restenosis; however, stents that are resistant to thrombosis or designed as reservoirs for the release of agents, such as vasodilators, into the downstream vasculature have also been described. It is ironic that stents have again become a means by which local tissue growth can be modified; Charles R. Stent, an English dentist who died in 1901, devised and lent his name to a curved mold used as a scaffold onto which oral skin grafts were applied to enhance their incorporation. There are coronary stents purpose designed to enhance drug loading and delivery via laser cut reservoirs or slots that act as receptacles for drugs and polymer,10 but no stents of this design have been employed in the peripheral circulation at this time. The coating must be suitable for sterilization, be resistant to abrasion or flaking during stent implantation and expansion, and provide controllable drug release (both in concentration and time), all without thrombogenic or inflammatory effects on the vessel wall. The most commonly used vehicles are nonerodable polymer coatings, but others including phosphorylcholine, biodegradable or bioabsorbable polymers, and ceramic layers have been developed. It was originally isolated in the mid-1930s from Streptomyces hygroscopicus found in Easter Island soil samples (the island is called Rapanui by its natives; hence the name rapamycin). It inhibits cellular proliferation by blocking cell cycle progression from the G1 to S phase. Stents coated with sirolimus analogues have largely supplanted sirolimus-coated stents in the coronary arteries. In practice this classification is somewhat arbitrary because a single agent may affect multiple steps in the restenotic process or have very different mechanisms of action depending on the tissue concentration. Microtubules are intimately related to the functions of intracellular transport, signaling, protein secretion, and motility. Paclitaxel disrupts these cellular processes by forming stable dysfunctional microtubules. Prohealing Agents Agents that accelerate endothelial coverage of a stent after implantation may reduce adverse effects, such as thrombosis. To achieve antirestenotic efficacy in these areas, high drug concentrations on the stent struts are mandatory for stent-based local drug delivery with the consequence of delayed and incomplete endothelialisation of the stent struts. By contrast drug-eluting balloons are coated with free drug and usually an excipient (a polymer that helps in drug delivery). The therapeutic effects appear to be partly due to the fact that the drug is released precisely at the time of vessel wall injury and in part due to the dwell time of the active drug in the vessel wall. Angioplasty is considered to be a transient injury, thus a shorter duration of drug activity is needed. The duration of inhibition of cell proliferation far exceeds the time of balloon inflation, even though typically less than 10% of the drug on the surface of the balloon is actually delivered into the vessel wall. The immunosuppressant everolimus is a semisynthetic sirolimus analogue, also with a similar mechanism of action and a shorter half-life. Abbott Vascular coats its Xience coronary stent systems with this drug in both bioabsorbable polymer and durable polymer carriers. Umirolimus (Biolimus A9) is a highly lipophilic sirolimus derivative; thus, it is more rapidly absorbed into the vessel wall. Terumo (Tokyo, Japan) uses umirolimus on its Nobori coronary stent and Biosensors (Singapore) on the BioMatrix stent system. Taxanes the taxanes are a group of antimitotic agents with profound anti-inflammatory properties acting via a unique ability to interfere with microtubule function. A significant area of stented vessel wall is not covered by the stent, resulting in low tissue concentrations between tynes.

Besides chronic gastritis gastric cancer purchase doxazosin 2 mg mastercard, Doppler is a very operator dependent and time consuming procedure and extensive vessel calcification may prevent insonation of stenosis gastritis diet avoid order doxazosin cheap. Further gastritis meal plan best doxazosin 2mg, when an artery is occluded assessment of distal circulation and collaterals is rarely possible chronic inactive gastritis definition order doxazosin 4 mg on-line. In addition gastritis diet breakfast buy generic doxazosin from india, the ability to simultaneously image the renal arteries is a major advantage as patients may have concomitant renal artery disease gastritis pediatric symptoms order 2mg doxazosin with amex. Not only is the technique accurate for gradation of stenosis but also for evaluating exact lesion length and number of stenoses which are important determinants in choosing the the optimal therapeutic option. However, it provides best results in the arteries of the thigh and below knee plaque subtraction is less accurate. The use of parallel imaging techniques and hybrid dual acquisition techniques has successfully minimized venous contamination. In addition, since contrast sensitivity is heightened at 3T, this allows the use of lesser contrast dose with the potential to diminish contrast dose dependent reactions of importance in patients with impaired renal function. Patients with claudication usually have single level disease, while patients with rest pain or more severe ischemia have multilevel disease. Clinically relevant disease includes stenosis, thrombotic occlusion and ulcerated or exophytic plaques. Plaques may be characterized as focal or long, calcified or noncalcified, concentric or eccentric and smooth or ulcerated. Pitfalls in the interpretation of lower extremity run off studies include: z Relative dilution of contrast medium may be the only sign of an eccentric plaque along the posterior or anterior wall. The pressure gradient across a stenosis proximal to a distal obstruction will be underestimated until downstream flow is re-established. Evaluation of Bypass Grafts10,22-24 Color flow imaging and duplex ultrasound are now the recommended noninvasive examinations for the postoperative monitoring of bypass graft patency. They are used to detect focal stenoses before they progress and lead to graft occlusion. Doppler diagnosis of graft patency vs thrombosis is relatively straight forward since we are dealing with a straight tube, thrombosis is usually complete and color or spectral signal will be absent throughout the graft. Stenotic lesions mostly due to fibrointimal hyperplasia are located at proximal and distal anastomosis, hence stenosis in synthetic grafts occurs almost exclusively at the anastomotic sites. With time, graft failure may be due to progression of peripheral arterial disease in the arteries above or below the anastomosis. Bypass surgery is now almost exclusively performed with autologous vein the reversed vein and in situ vein. The reversed vein approach consists of physical removal of saphenous vein, its reversal so that blood can flow through the valves, placement across the diseased arterial segment and anastomosis to proximal and distal artery. The in situ approach leaves the native superficial vein (greater or lesser saphenous) in its bed, mobilizing a small portion of proximal and distal extent to create anastomotic connections. In addition, the valves are lysed in order to permit downward flow and the side branches which normally communicate with the deep venous system are ligated. In the first month, technical problems such as poor vein selection, placement, poor construction of anastomosis and in case of in situ grafts, arteriovenous fistulas and poor lysis of vein valves are likely to cause graft failure. The second time interval extends from 1 month to 2 years following insertion of graft. This is the interval during which the development of fibrointimal hyperplasia is likely to occur. In 20% of grafts these stenotic lesions as well as fibrotic reactions, typically occurring at the site of vein valves can progress to cause significant stenoses that ultimately lead to graft occlusion. The third time period extends beyond 2 years following surgery after which graft failure is likely to be due to progression of atherosclerotic disease in the arteries proximal and distal to anastomoses. Values above 2 are considered to represent lesions causing 50% diameter narrowing or more. However, in complex grafts, anastomotic sites may have high velocities with no stenosis. These patients frequently have severe symptoms and rest pain is a presenting complaint in 80%. Typically, the disease is segmental and occlusions intervene with normal segments. Cessation of smoking is crucial and amputation is fairly common as reconstructive surgery or endovascular therapies are usually not possible due to lack of distal runoff vessels. Upper Extremities20,21 the brachiocephalic and left subclavian arteries are typically catheterized from the aortic arch. Atherosclerosis and nonspecific aortoarteritis involve proximal portion of subclavian arteries. With proximal subclavian stenosis flow in the ipsilateral vertebral artery may be reversed resulting in subclavian steal syndrome. It is important that the limiting disability is identified and treatment planned accordingly so that the benefits of treatment outweigh the risks. With advances in endovascular interventional techniques such as angioplasty with or without stenting, thrombolysis, atherectomy, etc. This time frame may be altered by many factors including location and degree of obstruction, presence or absence of underlying vascular disease, collateral vessels and spasm. Etiology the most frequent causes of acute extremity ischemia are spontaneous thrombosis of an artery with underlying atherosclerosis, occlusion of bypass grafts and embolism. This difference is primarily explained by the extensive collateral network around scapula and shoulder and by the smaller muscle mass and metabolic needs of the arm. A major diagnostic goal is the distinction between embolic and thrombotic occlusion. Embolic occlusions tend to result in profound ischemia owing to the absence of developed collaterals. Thrombosis of a pre-existing stenosis is tolerated better because the collateral circulation is already established. In the distal anastomoses of aortobifemoral grafts for example, stenosis should not be considered until the ratio exceeds 3 or 4. Doppler is close to 95% accurate for detection of graft stenosis but tends to overestimate the severity of stenosis. Other complications associated with graft placement, such as pseudoaneurysm vs hematoma can also be evaluated with Doppler. Doppler sonography without the need of angiography is typically used as the only guide for surgical correction of these lesions. They, however, provide more thorough evaluation of the inflow and outflow vessels, often obviating the need for catheter angiography before surgery. Clinical Features the patient presents with a cold limb that is painful, pale or cyanotic and numb. Imaging Patients with critically ischemic limbs should proceed directly to surgery while those with less threatened limbs and extensive underlying vascular disease or complex vascular surgical history benefit from preoperative imaging. Angiography Regardless of the anatomic level of ischemia the entire circulation of the extremities should be evaluated to identify potential sources of emboli and to search for occult distal disease. An acute embolus produces a discrete filling defect with reconstitution of the distal vessels. However, it may also appear as a sharp cutoff point that mimics a thrombotic occlusion. Angiographic signs of acute arterial embolism include a meniscus or filling defect, mild or absent disease in other vessels, lack of contralateral disease, poorly developed collaterals and emboli at other sites. In more than 50% cases, emboli lodge in the brachial artery in the upper limb and the Acute Limb Ischemia9,10,20,25 Prompt recognition of acute limb ischemia is vital to proper patient management. Only a narrow window of opportunity may exist in which to salvage the threatened limb. When acute limb ischemia is present, immediate diagnosis and Chapter 179 Imaging of Peripheral Vascular Disease 2909 the etiology of this disorder is varied and includes cervical ribs, congenital fibromuscular bands, anomalies of first rib, muscular hypertrophy, etc. Chronic arterial compression which is made worse with certain arm positions leads to intimal medial injury from high velocity flow and turbulence within the vessel. Over passage of time the result is poststenotic dilatation or frank aneurysm formation, premature atherosclerosis, embolization of platelet fibrin deposits or thrombus from the diseased wall or complete occlusion. Clinical Features Symptoms such as arm pain, weakness, coolness and pallor may be provoked by certain arm positions or exercise. Loss of radial pulse with arm abduction however is a normal feature in minority of the population. Few collaterals are visualized femoral or popliteal artery in the lower limb frequently at major bifurcations. Total occlusion can hide an unusual cause for thrombosis, such as popliteal artery aneurysm. In patients with microembolization syndromes, proximal atherosclerotic disease or aneurysms are often found. In thrombotic occlusions on the other hand, evidence of diffuse atherosclerotic disease in the ipsilateral and contralateral limb is common. Usually collaterals are well developed and thrombosis produces midvessel occlusion rather than at vessel bifurcations. Thrombotic occlusions are treated by direct thrombectomy patch revision or bypass grafting. Percutaneous therapy is especially useful in patients with a clot in small distal vessels inaccessible to surgery or when patient is a poor surgical candidate. Imaging Imaging is directed at evaluating both the lumen of subclavian artery and surrounding structures. The arterial lumen is imaged in order to confirm the compression and diagnose complications such as distal embolization. Imaging should begin with a simple chest X-ray which may reveal a cervical rib or other bony anomalies. The goals of angiograpy in these patients are to evaluate the subclavian artery for stenosis, aneurysmal change presence of thrombus and to detect distal emboli. However, evocative maneuvers can induce arterial compression in half of normal patients. In more than 95% cases, symptoms are caused by compression of the brachial plexus and related nerves; arterial compression is responsible for only 1% of cases. Aneurysms An aneurysm is defined as focal or diffuse dilatation of an artery by more than 50% of its normal diameter. Common sites for degenerative aneurysms in the extremities include iliac, popliteal and common femoral arteries in the lower limb and 2910 Section 6 Chest and Cardiovascular Imaging brachiocephalic and subclavian arteries in the upper limb. The entire popliteal artery may be aneurysmal, but focal aneurysms most often involve the vessel above the joint line. The origin of aberrant right subclavian artery is frequently patulous termed diverticulum of Kommerell. This diagnostic task is so well performed by standard grayscale images that it now serves as a gold standard for the diagnosis of peripheral arterial aneurysms. It can visualize progressive deposition of mural thrombus not appreciated by arteriography. The sensitivity and specificity of ultrasound compared to surgery are close to 100%. Sonography also offers the ability of performing surveys because popliteal artery aneurysms are bilateral in 50% cases and are often associated with abdominal aortic aneurysm. The average diameter of the popliteal artery is 8 mm in patients with abdominal aortic aneurysm. The presence of mural thrombus in a large popliteal artery is diagnostic of an aneurysm. Traditionally, surgical intervention is performed in arteries with focal aneurysm of 2 cm or more in diameter. However, development of symptoms due to distal embolization from thrombus accumulating in the lumen is an absolute indication for surgical intervention, irrespective of the size of aneurysm. Doppler techniques are useful in confirming the continued patency of a channel within the thrombosing aneurysm either at presentation or following surgery. Multiplanar reconstruction are particularly useful in planning surgical intervention providing information about the degree of extension of the aneurysm in sagittal and coronal planes and its relationship with adjacent structures. Aneurysms can be missed by catheter angiography if they are noncalcified and thrombosed or lined by mural thrombus. Catheter angiography is usually reserved for preoperative planning, when percutaneous therapy is being considered or rarely when the diagnosis cannot be made by cross-sectional imaging. The collection of blood remains in communication with the patent artery by means of a channel of variable size and length. The principal etiology is penetrating trauma and includes knife wound, bullet wound and medical intervention. Use of the larger catheters, anticoagulation and obesity may also increase incidence of pseudoaneurysms. The grayscale image shows an echolucent or mixed echogenic collection in close proximity to the artery. This sign is not specific to pseudoaneurysms because saccular aneurysms share similar flow patterns. Color flow mapping helps locate the communicating channel which may be difficult to localize on grayscale imaging. During diastole, the effective pressure within the collection is greater than the systemic arterial pressure thereby pushing blood out from the collection. Within the collection, flow tends to persist and maintain the same direction due to inertia. A variety of therapeutic options are available to treat pseudoaneurysms, including surgery, ultrasound-guided compression repair, thrombin injection and angiographic balloon occlusion. Some pseudoaneurysms may actually thrombose spontaneously, especially when they are small (<3 cm), with a neck length greater than 1 cm. Recently, direct percutaneous thrombin injection has been proposed to treat pseudoaneurysms.

The right paratracheal space and posterior tracheal space are adjacent spaces and are sometimes called stripes gastritis diet 500 order doxazosin with a visa. The importance of these spaces are that they contain lymph nodes gastritis symptoms diarrhoea buy cheap doxazosin line, and therefore treating gastritis naturally discount generic doxazosin uk, likely to be involved by bronchial carcinoma gastritis diet food recipes purchase doxazosin 4 mg. Medical Electrical Equipment gastritis diet ������ buy discount doxazosin 2mg on line, part 2-44: Particular requirements for the safety of X-ray equipment for computed tomography gastritis diet ������ discount doxazosin 4mg on-line, Geneva, International Electrotechnical Commission, 2002. Multi-slice computed tomography as a screening tool for colon cancer, lung cancer and coronary artery disease. Optimization of computed tomography technique to demonstrate the fine structure of the lung. Many lung abnormalities can, therefore, be diagnosed from the plain chest radiograph. Occasionally, findings of increased and decreased opacity may be present on the same imaging study, either reflecting the presence of two or more diseases or, in certain cases, a pathologic process that manifests with both an infiltrative and obstructive process. Airspaces-The air may be replaced by liquids, cells, or a combination of the two (consolidation) or absorbed and not replaced (atelectasis). An alternative approach to pattern recognition is the description of an abnormal radiograph and a differential diagnosis based on the radiographic features of the disease, rather than on its presumed histologic appearance. This system was endorsed by Felson5 in 1979, who believed that it may be easier for radiologists to determine the correct diagnosis by describing the appearance of the radiograph, rather than by attempting to suggest the histology of the lesion. The basic radiographic signs as they indicate the fundamental nature of pulmonary disease are subdivided into three major sections:6 1. Diseases of the pleura Predominantly Airspace Disease Parenchymal Consolidation the acinus is accepted as the basic unit of lung structure for radiographic description, this does not imply that individual acinar shadows must be identified radiologically for a pulmonary shadow to qualify as an airspace filling disease. Margination the edge characteristics of airspace filling processes show poor margination. This is because of spreading and coalescence of the wave of consolidation that partly fills acinar components in a serrated manner. Distribution Characteristics Failure to respect segmental boundaries is a characteristic feature of diseases associated with airspace consolidation. In a widely disseminated process, such as acute pulmonary edema, lack of segmental distribution is expected. However, even in localized disease, intersegmental spread occurs; for example, in acute pneumococcal pneumonia, infection is propagated centrifugally via channels of collateral ventilation. Since segmental boundaries do not impede the passage of gas or liquid via these channels, the exudate of acute airspace pneumonia can spread throughout the lung periphery. Such diseases are nonsegmental in distribution, a finding of importance in establishing the pathogenesis of the disease process and thereby in suggesting an etiologic diagnosis. In contrast, processes that are propogated via the vascular or tracheobronchial tree usually display a striking segmental distribution. Large pleural based pulmonary infarcts also reveal segmental distribution characteristics. Streptococcus pneumoniae, is of low viscosity and therefore spreads rapidly via interalveolar pores, whereas Air Bronchogram Consolidation of lung parenchyma, with little or no involvement of conducting airways, creates this important roentgenographic sign. In acute airspace pneumonia, consolidation usually begins in subpleural parenchyma, the exudate rapidly spreading centrifugally to surround bronchi as it advances towards the hilum. Since the consolidation is entirely parenchymal, air in the bronchi is not displaced. This sign originally described by Fleischner in 1927, was named the air bronchogram sign by Felson. Since the parenchyma may be airless when its air has been replaced by liquid or tissue (consolidation) or when it has been absorbed and not replaced (atelectasis), an air bronchogram may be seen in either situation but only when the supplying bronchus is not occluded. The upper border is smooth and sharply marginated by the horizontal fissure Parenchymal Atelectasis In atelectasis, air is absorbed and not replaced in contrast to consolidation. Since atelectasis has been described essentially in terms of lung volume, it is important to consider the mechanisms that keep the lung expanded. Alternations in these mechanisms provide a suitable basis for classifying atelectasis. Maintenance of Lung Volume the lung has a natural tendency to collapse and while in the thoracic cavity, this tendency is opposed by the recoil of chest wall outwards by contraction of inspiratory muscles and diaphragm. At the resting respiratory position the tendency for the lung to collapse and for the chest wall to expand are equal and opposite. When the lung is stiffer than normal, that is, when its compliance is decreased, lung volume is decreased. When the action of surfactant is interfered with as may occur in the respiratory distress syndrome or after bypass surgery, there may be widespread collapse of alveoli. The most common form of atelectasis is caused by the resorption of gas from the alveoli, as may occur in acute bronchial obstruction. Time Factor An airspace pattern that clears over a period of hours or a couple of days is certain evidence of pulmonary edema or hemorrhage. Airspace disease that persists over time, sometimes for weeks or months, is usually caused by infection, aspiration, bronchioalveolar cell carcinoma, lymphoma, or idiopathic conditions such as alveolar proteinosis. The effect of obstruction of airways depends upon the site and extent of bronchial or bronchiolar obstruction, the pre-existing condition of the lung tissue and collateral air drift. Collateral air drift is the term used to describe ventilation of alveoli other than by direct airway connections. It has been regarded as occurring readily between lobar segments but not between pulmonary lobes. Resorption atelectasis may occur in the absence of occlusion of a major bronchus but cannot develop unless there is interruption of communication between alveoli and a major airway. For example, in lower lobe bronchiectasis consequent upon childhood bronchopulmonary infection, sufficient obliterative and stenosing bronchitis and bronchiolitis results so as to render ventilation through normal channels inadequate. Cicatrization atelectasis designates volume loss resulting from local or general pulmonary fibrosis. The volume of an airless lobe or segment depends not only upon which order of bronchus is obstructed but also upon the amount of sequestered blood and edema fluid within the obstructed parenchyma. Provided the pleural space is free, collapse of any portion of lung is proportional to the amount of air or fluid in the adjacent pleural space. Elevation of the Hemidiaphragm Hemidiaphragmatic elevation is a more prominent feature of lower than of upper lobe collapse. In the lower lung zones, elevation tends to occur in the area contiguous to the lobe involved, posterior elevation in lower lobe collapse and anterior elevation in middle lobe or lingular collapse although it is seldom severe in the latter. It is related to a complex group of forces, of which abnormality of surfactant is probably the most common. Mediastinal Displacement Tracheal and upper mediastinal displacement is a feature of upper lobe collapse. When the lower lobes are involved, the inferior mediastinum undergoes the greatest displacement. Although it may be of some value in cases of chronic loss of volume, it should not be relied upon as an accurate indicator of reduction in hemithoracic volume in cases of acute lobar collapse. Predominantly Interstitial Disease In predominantly interstitial diseases, alveolar air is largely preserved and it is the tissues surrounding the airspaces that are increased in volume. The lung parenchyma is sharply demarcated from the connective tissues of the bronchovascular tree, the interlobular septa and the pleura by a limiting membrane which is composed of dense elastic tissue and collagen that merges into the elastic fibers of alveolar walls. The blood vessels, nerves and lymphatics lie in this compartment of loose connective tissue, called the perivascular or axial interstitial space. In addition there is a small interstitial space in the walls of the alveoli themselves; this is referred to as the parenchymal or acinar interstitial space. The axial interstitial space consists of the sheath of loose connective tissue around the bronchoarterial bundles that form the visible lung markings. This interstitial sheath extends out to the terminal bronchioles, beyond which the airway are intimately related to the parenchyma. A similar sheath exists around the venous radicals within the lung and this interstitial space that contains the veins and lymphatics and drains the peripheral parenchyma; is also continuous with the subpleural interstitial space that lies between the alveolar and capillary basement membranes. Although interstitial diseases of the lung usually affect both compartments to some degree, still their distinction is of some value, because their individual involvement usually produces distinguishable radiographic patterns and different diagnostic considerations. It is of less diagnostic help in the early stages of lobar collapse as compared to diaphragmatic elevation and mediastinal displacement. As the period of collapse lengthens, overinflation becomes more prominent and the diaphragmatic and mediastinal changes regress. There is alteration in vascular markings resulting from the increased lung volume. The vessels are more widely spaced and sparser than in the normal contralateral lung. When greater portion of one lung becomes atelectatic, the tendency is greater for overinflation to involve the contralateral lung; this may progress to the stage in which the opposite lung displaces the mediastinum either generally or locally. These local displacements occur in the three areas of the mediastinum, where the two lungs are separated only by loose connective tissue: (i) the anterior mediastinal compartment, at the level of the first three or four costal cartilages, limited anteriorly by the sternum and posteriorly by the great vessels, (ii) the posterosuperior mediastinum, at the level of the third to fifth thoracic vertebrae, limited anteriorly by the esophagus and trachea and posteriorly by the vertebral column and (iii) the posteroinferior mediastinum, limited anteriorly by the heart and posteriorly by the vertebral column and aorta. Radiographic Patterns of Diffuse Interstitial Disease the normal pulmonary interstitium is not visible on chest radiographs. It is only when the interstitium is involved in disease processes such as edema or fibrosis that its volume and attenuation increase sufficiently to allow its recognition on chest radiographs. The four basic radiographic patterns of interstitial disease are reticular, nodular, reticulonodular and linear. Although reticular and nodular patterns exist in pure forms, most interstitial diseases show a mixed reticulonodular architecture. Since the disease is anatomically interstitial, the Displacement of the Hila this occurs more in collapse of the upper than of the lower lobes and usually is more marked the more chronic the atelectasis. Diffuse interstitial disease is of inhomogeneous radiographic density; this feature alone distinguishes interstitial from airspace disease in most cases. Since there is nothing to prevent air from reaching the lung parenchyma, volume reduction due to airway obstruction is not a feature of interstitial disease. Reticular Pattern this consists of a network of curvilinear opacities-a series of rings surrounding spaces of air density. The precise pattern of reticulation depends upon the degree of thickening of the interstitial space and the effect that the interstitial involvement exerts on parenchymal airspaces. The reticular pattern results from an increase in the amount of tissue in the interstitial space of the lung, both axial and parenchymal. The radiographic pattern of honeycombing may be produced by a number of diseases, including eosinophilic granuloma, fibrosing alveolitis (idiopathic pulmonary fibrosis), rheumatoid lung, pulmonary lymphangiomyomatosis, progressive systemic sclerosis, asbestosis, chronic interstitial fungal infections and sometimes endstage sarcoidosis. Nodular Pattern A nodular pattern is produced when spherical lesions accumulate within the interstitium. The interstitial nodule differs from its airspace counterpart in that it is homogeneous, well circumscribed and of variable size. Since the infecting organism reaches the lung via the circulation and is trapped in the capillary sieve, it must be purely interstitial in location early in its course. Many other diseases of widely differing pathogenesis have similar morphologic changes in the interstitial space. For example intravenous injection of talc particles associated with drug abuse, certain inhalation diseases such as silicosis and sarcoidosis can be associated with multiple, well-defined, nodular shadows throughout the interstitium. Reticulonodular Pattern Although a curvilinear network throughout the interstitial tissue usually presents radiologically as a reticular pattern, orientation of some linear opacities parallel to the X-ray beam sometimes suggests a nodular component in addition to the reticular. Linear Pattern the linear pattern results from thickening in or around the bronchoarterial bundles, the perivenous interstitium, or the interlobular septa (Kerley A and B lines). Septal lines restrict the diagnostic consideration to hydrostatic interstitial edema and lymphangitic malignancy, usually with simultaneous involvement of bronchoarterial sheaths and perivenous spaces. When the linear pattern is localized to the bronchoarterial sheaths, the conditions include cystic fibrosis, bronchiectasis, atopic asthma, dysproteinemia and the increased markings in emphysema. Certain secondary effects sometimes produced by diffuse interstitial disease may modify the basic radiologic pattern. For example, emphysema either secondary to bronchiolar obstruction or compensatory to pulmonary fibrosis, may distort the pulmonary architecture and the original disease pattern is rendered unrecognizable. Their course bears no definite relationship to the anatomic distribution of bronchoarterial bundles. They never extend to the visceral pleura, although their medial extension is usually to the hilum. The visibility of A lines depend upon the accumulation of abnormal amounts of edema fluid or other tissue within the perilymphatic connective tissue and not distention of the lymphatics themselves. Depending upon the disease process that causes them, they may be reversible (as in pulmonary edema) or irreversible (as in pneumoconiosis or lymphangitic carcinoma). Kerley B lines are less than 2 cm long, horizontal, basal peripheral non-branching fine lines visible on the frontal and lateral films. Because of their anatomic location they are sometimes referred to as "septal lines" One of the most. The influence of gravity on pulmonary hemodynamics give rise to interlobular septal edema in the lower portion of the lungs, thus line shadows are seen best just above the Chapter 153 Basic Patterns of Lung Diseases 2517 costophrenic angles on posteroanterior view. When the edema is transient, septal lines appear and disappear with each episode of decompensation. With repeated episodes, or in the presence of chronic and severe pulmonary venous hypertension, fibrosis within the interlobular septa gives rise to permanent, irreversible B lines.

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