Calcified pulmonary nodules in chronic renal failure.
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Biomedical subjects
Publications and source records attributed to W R Webb.
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Expeditious surgical management in serious chest trauma improves survival rates. However, guidelines for emergency thoracotomy that depend on the initial amount of blood loss or continuing blood loss are imprecise and frequently require a period of observation. In an attempt to improve prethoracotomy diagnosis emergency thoracoscopy was used in the operating room in 36 patients who presented with hemothoraces. A diagnostic thoracoscope was inserted through the previously placed incisions for chest tubes. The procedure was well tolerated under local anesthesia and in most patients took less than 15 minutes to complete. No complications resulted from thoracoscopy. When the information obtained did not indicate further operations, the thoracoscope was withdrawn and chest tubes were reinserted through the same incisions. The method provided anatomic definition of the injuries in 35 of 36 patients and allowed the determination of whether blood loss was continuing. Management was altered as a result of thoracoscopy in 16 patients (44.4%). An unnecessary thoracotomy was avoided in 16 patients who had greater than 1,500 ml of blood in the thoracic cavity on admission and allowed a more rapid thoracotomy in one patient. Four patients had wounds located close to the diaphragm and laparotomy was avoided when the diaphragm was found free of injury. Bleeding from lacerated intercostal vessels was stopped with diathermy during thoracoscopy in two of three patients. In addition, 15 patients had 200 ml or more of clotted blood removed. The usefulness of removal of clotted blood remains to be proved but it is hoped that the incidence of empyema will be reduced. Emergency thoracoscopy has proved a valuable diagnostic and therapeutic measure in patients sustaining penetrating chest trauma.
Computed tomography (CT) can be helpful in the preoperative evaluation of patients with a superior sulcus (Pancoast) tumor. The cross-sectional format and tissue resolution of CT better demonstrate the relationship of tumor to significant anterior structures (subclavian artery and vein, trachea, and esophagus) and posterior structures (chest wall and vertebral bodies) than do conventional techniques. Invasion of the subclavian vessels, mediastinum, or vertebral bodies contraindicates surgery.
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A reduction of red cell SA in patients following acute myocardial infarction is reported and the effects of SA-depleted red cells on cardiac index and alveolar capillary blood flow in the dog are described. The mean red cell SA in 26 patients following acute myocardial infarction was 0.021 +/- 0.001 compared with a mean of 0.031 +/- 0.002 mumol./0.1 ml RBC in 12 normal subjects (p less than 0.01). In five dogs injected with neuraminidase, an enzyme which removes SA from the red cell membrane, a 43% decrease in mean cardiac index from 2.3 +/- 0.22 to 1.3 +/- 0.16 (p less than 0.01) occurred. In films of the pulmonary microcircuation the mean widths of typical alveolar capillary beds decreased 42.6% +/- 5% (p less than 0.01). In three other dogs, autotransfusion with SA-depleted stored blood resulted in a 25% decrease in mean cardiac index from 2.0 +/- 0.21 to 1.5 +/- 0.21 (p less than 0.2), and a 21.7% +/- 0.9% (p less than 0.01) decrease in mean widths of typical alveolar capillary beds. We conclude that a reduction of red cell SA follows acute myocardial infarction and that SA-depleted red cells decrease cardiac index and alveolar capillary blood flow in the dogs.
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The pulmonary and systemic hemodynamic response to four hours of hemorrhagic shock and resuscitation has been studied in 17 baboons using both open and closed chest models. No pulmonary artery (PA) hypertension occurred during shock or resuscitation except for an increase in lft ventricular end diastolic pressure (LVEDP) secondary to intravascular volumee overload with Dextran. Pulmonary vascular resistance (PVR) increased during shock but returned to control levels with reinfusion of shed blood and correction of acidosis. PVR was moderately elevated following reinfusion of shed blood if acidosis was not corrected or if volum resuscitation was inadequate. No increase in gradients occurred between PA pressure and left atrial (LA) pressure or LVEDP and there was no gradients between small pulmonary vein and LA pressure. Arterial PO2 uniformly increased during shock and remained at or above control levels of reinfusion. Gross or histologic evidence of "congestive atelectasis" or "shock lung" was not observed. These observations suggest that in the subhuman primate, hemorrhage alone does not produce significant injury to the lung during shock or the immediate postresuscitation interval. Hemorrhage alone did not produce changes in the lung which would result in increased pulmonary microvascular hydrostatic pressure following appropriate resuscitation.
In patients with rheumatoid arthritis who develop symptoms of right heart failure, it is important to consider rheumatoid involvement of the pericardium because untreated rheumatoid pericarditis is often fatal. In addition to echocardiography and right heart catheterization, computed tomography affords a method of detecting pericardial effusion or a markedly thickened pericardium.
The mechanism of airflow obstruction was investigated in 21 patients with tracheal stenosis using tantalung tracheograms and pulmonary function studies, including flow-volume (FV) loops. In 4 patients with severe obstructive pulmonary disease, FV loops failed to demonstrate radiographically visible tracheal stenosis. In 17 patients, both FV loops and tracheograms demonstrated central airway obstruction. In three of the 17 patients, the stenotic segment was a rigid lesion at the thoracic outlet with similar limitation of inspiratory and expiratory flow. In nine of the 17 patients, the lesion was extrathoracic (rigid in 6 patients and pliable in 3). The 3 pliable extrathoracic lesions produced marked limitation of inspiratory flow but normal expiratory flow. Three rigid extrathoracic lesions produced inspiratory flow that was more limited than expiratory flow, suggesting dynamic inspiratory compression of the normal extrathoracic trachea. The one rigid intrathoracic lesion caused expiratory flow limitation greater than inspiratory flow limitation, suggesting dynamic compression of the intrathoracic trachea on expiration. The position of the obstructing lesion and dynamic compression of the normal, compliant trachea may be the major determinants of the difference in flow limitation between expiration and inspiration in some patients.
A mediastinal mass can mimic the presence of cardiovascular disease by simulating cardiac or vascular enlargement on chest radiographs, or by compressing the heart or great vessels with resulting symptoms or signs. This problem of misdiagnosis is particularly acute in patients with prior cardiac surgery for repair of congenital heart lesions. Two such cases are reported. In addition tosimulating cardiac disease, at least one, and perhaps both, were related to prior mediastinal surgery.
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A variety of diseases produces or mimics multiple, thin-walled, air-containing cavities or cysts in the lung. Although some causes of this pattern are common (bullous emphysema, multiple pneumatoceles), others are relatively rare (cystic bronchiectasis, histiocytosis X, tracheobronchial papillomatosis, and lucite ball plombage). To some extent, the radiographic features of these lesions allow their differentiation, but differential diagnosis can be difficult. This paper reviews their principal features.
Computed tomography (CT) can provide a noninvasive alternative to pulmonary arteriography for pulmonary embolism in selected circumstances. Three cases that demonstrate the technique and initial clinical experience are reported. Illustrated are: (1) CT detection of massive central pulmonary thromboembolism in a critically ill girl in whom the risk of complications from pulmonary arteriography was considered especially high; (2) the use of CT for serial examinations for follow-up of central thromboembolism, avoiding repeat angiography; and (3) preoperative CT delineation of organized thrombus in the proximal right pulmonary artery, an area not adequately evaluated on selective pulmonary artery injections. CT effectively displayed emboli and thrombi in central pulmonary arteries in each patient. Its application to embolus detection in peripheral arteries was not investigated.
Dogs were made thrombocytopenic (platelet count less than 12,000) with serial intramuscular injections of goat antiplatelet serum (APS), and the hemodynamic response to 1 mg/kg of E. coli endotoxin administered intravenously was studied. Intramuscularly administered APS rendered dogs thrombocytopenic without major alteration in other blood elements or coagulation parameters. The response of normal dogs to endotoxin was a fall in systemic blood pressure and cardiac output (CO) with an increase in pulmonary artery (PA) pressure and an increase in pulmonary vascular resistance (PVR) to 600% of control with a minimal fall in mean left atrial (LA) pressure and pulmonary artery wedge (PAW) pressure. Thrombocytopenic dogs had an identical fall in systemic pressure and CO, but obliteration of the initial PA hypertensive response. LA and PAW pressures fell slightly as in normal dogs, and the obliteration of the PA hypertension was caused by an attenuation of the increase in PVR to a third of that of normals. Cinemicroscopic studies of the lung in vivo showed marked and prolonged slowing of the microcirculation following endotoxin administration in normal dogs. In thrombocytopenic animals slowing of the pulmonary microcirculation was brief and mild. We conclude that platelets are an essential component for the initial pulmonary hypertensive response to infusion of E. coli endotoxin in dogs.
Infection of a pacemaker pocket occurred in a neonate. The infection was eradicated by means of a live omental pedicle graft, even though the pacemaker remained in the original pocket. The case and management are discussed.
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Of 65 patients with intrathoracic metastases from melanomon, 35 had metastasis to hilar or mediastinal nodes. In 28 of these 35, hilar and mediastinal lymph node enlargement was radiographically visible, hilar node enlargement was more commonly seen than mediastinal node enlargement. Pulmonary nodules were demonstrated radiographically in 25 of the 28 patients. Although lymph node enlargement was often asymmetric, symmetric hilar adenopathy mimicking sarcoidosis occurred in five of the 28 patients. Seven patients had unilateral involvement of lung and hilar and mediastinal nodes. In patients with melanoma, indirect metastatic spread via pulmonary nodules to hilar and mediastinal nodes may account for the frequent association of node metastases with lung nodules, the occurrence of intrathoracic adenopathy in the absence of extrathoracic node metastases, and the common finding of unilateral lung and nodal disease.