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Adult respiratory distress syndrome in a patient with uncomplicated acute myocardial infarction.

A 53-year-old woman was admitted with a diagnosis of acute extensive anterior myocardial infarction. Pulmonary capillary wedge pressure was 17 mmHg, and cardiac index 2.4 l/min.m2. The patient was successfully treated with diuretics and nitrates but on the fifth hospital day moist rales were noted over the entire lung field. A chest roentgenogram showed diffuse bilateral pulmonary infiltration with unchanged cardiac silhouette. Arterial oxygen partial pressure was reduced to 45 mmHg under 3 liters of nasal oxygen inhalation. Pulmonary capillary wedge pressure was 8 mmHg. Diffuse infiltration was not ameliorated by intravenous injection of diuretics. The diagnosis of adult respiratory distress syndrome was finally established by successful treatment with steroids.

Electrocardiography↗

Morbidity of sickle cell trait at high altitude.

A Caucasian with sickle cell trait (54% A, 43% S hemoglobin) had symptoms and signs of chronic hemolytic anemia as well as splenic infarction while living at very high altitude (in excess of 2,800 m). Trips from sea level back to high altitude repeatedly precipitated pulmonary infarctions. All symptoms and evidence of hemolysis resolved at low altitude.

Adult↗

Pulmonary emboli from pulse-spray and mechanical thrombolysis: evaluation with an animal dialysis-graft model.

PURPOSE: To compare pulmonary emboli resulting from pulse-spray pharmacomechanical thrombolysis (PSPMT) and mechanical thrombolysis performed to declot dialysis-access grafts. MATERIALS AND METHODS: Polytetrafluoroethylene arteriovenous shunts were created in eight dogs and were deliberately clotted at monthly intervals. Animals were randomly assigned to treatment with pulse-spray urokinase thrombolysis or a low-speed rotational percutaneous thrombolytic device. Perfusion imaging, pulmonary-artery pressure measurements, and pulmonary arteriography were performed before and after each procedure. RESULTS: A total of 22 procedures were performed (11 PSPMT and 11 mechanical thrombolysis). Declotting was successful in all procedures, with 100% 30-day patency. Segmental defects were seen on perfusion images after 10 (91%) of 11 PSPMT procedures and two (18%) of 11 mechanical thrombolysis procedures (P < .002). Transient increases in pulmonary-artery pressure occurred in the PSPMT group. Complete resolution of emboli and return to baseline pressures were seen in all cases, even after multiple (up to four) procedures in the same animal. There was no histologic evidence of pulmonary infarction in either group. CONCLUSION: The percutaneous thrombolytic device is effective for declotting dialysis grafts in dogs and results in statistically significantly fewer pulmonary emboli compared with PSPMT.

Animals↗

Large right atrial thrombus with pulmonary embolism.

We present the cases of two patients, aged 67 and 77 years, who were admitted for the evaluation of rapidly progressive dyspnea and syncope, respectively. Both patients developed large right atrial thrombi with pulmonary embolism. The first patient received recombinant tissue plasminogen activator and survived with an uneventful result, whereas the second patient received operative thrombectomy followed by intravenous heparin and died 15 days later of pulmonary infarction with pulseless electrical activity. Data from these limited experiences suggest that thrombolytic therapy might be considered in patients with right heart thrombi with pulmonary embolism.

Aged↗

Upstream pressure for systemic to pulmonary flow from bronchial circulation in dogs.

Systemic to pulmonary flow from bronchial circulation, important in perfusing potentially ischemic regions distal to pulmonary vascular obstructions, depends on driving pressure between an upstream site in intrathoracic systemic arterial network and pulmonary vascular bed. The reported increase of pulmonary infarctions in heart failure may be due to a reduction of this driving pressure. We measured upstream element for driving pressure for systemic to pulmonary flow from bronchial circulation by raising pulmonary venous pressure (Ppv) until the systemic to pulmonary flow from bronchial circulation ceased. We assumed that this was the same as upstream pressure when there was flow. Systemic to pulmonary flow from bronchial circulation was measured in left lower lobes (LLL) of 21 anesthetized open-chest dogs from volume of blood that overflowed from pump-perfused (90-110 ml/min) pulmonary vascular circuit of LLL and was corrected by any changes of LLL fluid volume (wt). Systemic to pulmonary flow from bronchial circulation upstream pressure was linearly related to systemic arterial pressure (slope = 0.24, R = 0.845). Increasing Ppv caused a progressive reduction of systemic to pulmonary flow from bronchial circulation, which stopped when Ppv was 44 +/- 6 cmH2O and pulmonary arterial pressure was 46 +/- 7 cmH2O. A further increase in Ppv reversed systemic to pulmonary flow from bronchial circulation with blood flowing back into the dog. When net systemic to pulmonary flow from bronchial circulation by the overflow and weight change technique was zero a small bidirectional flow (3.7 +/- 2.9 ml.min-1 X 100 g dry lobe wt-1) was detected by dispersion of tagged red blood cells that had been injected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Pulmonary artery thrombosis associated with anomalous pulmonary venous connection: an unusual complication following the modified Fontan procedure.

The presence of unrecognized partial anomalous pulmonary venous connection may cause complications of pulmonary infarction and right-to-left shunting in patients undergoing the modified Fontan procedure. These complications can be prevented by identification of any anomalous pulmonary venous connection at preoperative cardiac catheterization.

Adult↗

[Spontaneous pneumomediastinum in adults. 10 cases (author's transl)].

Since it is relatively rare, spontaneous pneumomediastinum is often little known to clinicians. Making the diagnosis, however, presents no problem if the three essential signs are present, that is to say: -subcutaneous emphysema of the base of the neck (7 cases), -Hamman's sign, (6 cases), -a paramediastinal air shadow on chest roentgenograms, (8 cases). The condition is brought about by rupture of perivascular alveoli resulting in the migration of air along the pulmonary vessels. The principal advantage of making the diagnosis is that it enables one to eliminate other pain-causing thoracic syndromes, especially myocardial infarction, pulmonary embolus and acute pericarditis. The clinical course is usually benign necessitating no treatment.

Adolescent↗

Alveolar hemorrhage and pulmonary hypertension in systemic sclerosis: a continuum of scleroderma renal crisis?

Alveolar hemorrhage occurs as a complication of systemic inflammatory diseases. In addition to alveolar hemorrhage, patients with systemic sclerosis (SSc) may suffer from digital infarction, pulmonary hypertension, and renal crisis. Although a common pathogenesis of this disease that explains the variety of problems during a patient's illness has yet to be identified, the unique characteristics of SSc may alter our approach to alveolar hemorrhage in this patient population. We describe a patient with SSc, who presented with pulmonary hypertension and alveolar hemorrhage complicated by features suggesting re-occurrence of scleroderma renal crisis. Our successful management of this patient, with complications that are usually of high morbidity, may be attributed to our judicious use of glucocorticosteroid therapy and maximization of angiotensin-converting enzyme inhibition. In view of the potential for glucocorticoids to precipitate scleroderma renal crisis, we suggest caution in the use of these medications for manifestations that may be similar in their pathogenesis.

Journal Article↗

[Transthoracic sonography in the diagnosis of pulmonary embolism].

In many cases of pulmonary diseases extending up to the pleura, ultrasound helps to identify the etiology of the lesion. There are several sonomorphological criteria to differentiate peripheral pulmonary consolidations. Clinical studies and the sonographic appearance with pathologic correlation showed pulmonary infarctions in location, form and size exactly corresponding with pathological findings. Fresh reperfusable infarcts were homogenous and hypoechoic. Older infarcts were well demarcated, mainly wedge shaped. Triangular pleural based lesions, more roughly structured, were observed with a hyperechoic reflex in the center corresponding to the bronchiole: a sign of segmental involvement. The sensitivity of transthoracic ultrasound in diagnosis of pulmonary embolism was 86 to 94%, the specificity 67 to 87%, positive predictive value 55 to 92%, negative predictive value 91%, accuracy 73 to 91%. In massive central lung embolism, both fresh and old infarctions are found. An imminent larger embolism can be predicted, for instance,in a deep vein thrombosis. With one ultrasound system, we can "kill three birds with one stone": source, way and outcome of pulmonary embolism by bedside examination.

Humans↗

Fatal pulmonary embolism in an adolescent with chickenpox.

A fatal case of pulmonary emboli associated with varicella in an adolescent is reported. Review of the literature revealed confusion between pulmonary infarction and embolization, the latter having been documented with varicella only in adults before this report. Embolic phenomena should be considered in the differential diagnosis of pulmonary symptoms associated with varicella, since their recognition and treatment offers important supportive measures in the care of the frequently critically ill patients.

Adolescent↗

Acute reversible pulmonary ischemia. A cause of the acute chest syndrome in sickle cell disease.

A 6-year-old girl with sickle cell disease was admitted to the hospital with the diagnosis of the acute chest syndrome. The laboratory findings and the radionuclear lung scan supported a diagnosis of pulmonary infarction rather than pneumonia. She improved with intravenous fluids, oxygen, penicillin, and theophylline. The most likely explanation for the rapid resolution of the clinical syndrome, the chest x-ray, and lung scan abnormalities is that masses of sickled cells caused transient pulmonary vascular occlusion leading to perfusion defects and ischemia, and that the sickled cell thrombi were dislodged before the infarction occurred. To our knowledge, this phenomenon has not been described as a cause of the acute chest syndrome in sickle cell disease in children.

Acute Disease↗

Cystic and cavitary lung diseases: focal and diffuse.

Cysts and cavities are commonly encountered abnormalities on chest radiography and chest computed tomography. Occasionally, the underlying nature of the lesions can be readily apparent as in bullae associated with emphysema. Other times, cystic and cavitary lung lesions can be a diagnostic challenge. In such circumstances, distinguishing cysts (wall thickness < or = 4 mm) from cavities (wall thickness > 4 mm or a surrounding infiltrate or mass) and focal or multifocal disease from diffuse involvement facilitates the diagnostic process. Other radiological characteristics, including size, inner wall contour, nature of contents, and location, when correlated with the clinical context and tempo of the disease process provide the most helpful diagnostic clues. Focal or multifocal cystic lesions include blebs, bullae, pneumatoceles, congenital cystic lesions, traumatic lesions, and several infectious processes, including coccidioidomycosis, Pneumocystis carinii pneumonia, and hydatid disease. Malignant lesions including metastatic lesions may rarely present as cystic lesions. Focal or multifocal cavitary lesions include neoplasms such as bronchogenic carcinomas and lymphomas, many types of infections or abscesses, immunologic disorders such as Wegener granulomatosis and rheumatoid nodule, pulmonary infarct, septic embolism, progressive massive fibrosis with pneumoconiosis, lymphocytic interstitial pneumonia, localized bronchiectasis, and some congenital lesions. Diffuse involvement with cystic or cavitary lesions may be seen in pulmonary lymphangioleiomyomatosis, pulmonary Langerhans cell histiocytosis, honeycomb lung associated with advanced fibrosis, diffuse bronchiectasis, and, rarely, metastatic disease. High-resolution computed tomography of the chest frequently helps define morphologic features that may serve as important clues regarding the nature of cystic and cavitary lesions in the lung.

Cysts↗

[A case report of primary pulmonary hypertension: congestive heart failure induced by pregnancy and delivery].

A thirty-year-old woman had complaints of general fatigue and gain in body weight, which had developed since the third trimester of pregnancy. On admission, she had lip cyanosis, general edema, and tachycardia. A chest rentogenogram showed cardiomegaly and dilatation of the pulmonary arteries. On cardiac catheterization, pulmonary artery pressure and pulmonary vascular resistance were elevated moderately. A pulmonary perfusion scintigram revealed a defect in the left lower lung field with no evidence of thrombus in a pulmonary artery angiogram. In this case, an underlying disease which caused pulmonary hypertension might have been the underfined cause. For this reason, primary pulmonary hypertension was the diagnosis. In the present case there is a danger that congestive heart failure may be induced by pregnancy and delivery and, furthermore, there is a possibility that during the clinical course of the illness pulmonary infarction might occur.

Adult↗

Subpleural lung involvement in Behçet's disease: first localization of a systemic entity.

Behçet's disease (BD) is a chronic multisystem vasculitis, affecting many organs and the vascular system, of unknown aetiology. Eyes, skin, joints, the oral cavity, the central nervous system, and, less frequently, heart, lung, kidney, the genital system and the gastrointestinal tract can be involved. Intrathoracic manifestations of BD consist mainly of thromboembolism of the superior vena cava and/or other mediastinal veins; aneurysms of the aorta and pulmonary arteries; pulmonary infarct and haemorrhage; pleural effusion; and, rarely, myocardial and/or hilar lymphoid involvement. In the present case, the patient presented with BD with an asymptomatic subpleural lung mass and bilateral pulmonary artery enlargement. The patient was treated with a combination of surgical and medical therapy with complete resolution of the lung involvement and without any parenchymal relapses after an 8-month follow-up.

Behcet Syndrome↗

The problems of surgical treatment for cardiac myxoma and associated lesions.

Twenty-four patients with cardiac myxomas consisting of 22 left and 2 right atrial myxomas were operated on. All myxomas were removed with an excision of the attachment walls using a cardiopulmonary bypass. Two myxomas required a partial cardiopulmonary bypass from the femoral vein to the artery prior to operation because they were on the verge of becoming stuck in the atrioventricular valves and potentially causing shock. For embolic complications of myxoma, the embolus of the external carotid artery was extirpated before undergoing cardiac surgery. In a patient with pulmonary infarction, the infarcted lung was resected simultaneously. Another patient with a cerebral infarction received a clipping of an aneurysm which later appeared in the infarcted area. For associated cardiac lesions, two patients underwent a coronary artery bypass graft and one mitral valve replacement with tricuspid annuloplasty. In the former two cases, the myxoma was removed prior to coronary artery bypass grafting because the use of retrograde coronary perfusion was considered to be sufficient to protect the heart. In the latter case, the removal of the myxoma first disclosed a significant mitral lesion which had been masked by the huge myxoma. All patients but one, who died of pneumonia, showed a good recovery. In this series, the problems of surgical treatment for cardiac myxoma and associated lesions are also discussed.

Adolescent↗