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PubMed1995

[A case report of acute pulmonary valve endocarditis caused by fungi].

A 42 years old female was admitted for evaluation of unrelenting fever and dyspnea on exertion in March, 1991. The patient had a VSD closure in 1968. After admission, serial blood cultures were found to be positive for Candida Parapsilosis and a massive vegetation on the pulmonary valve was demonstrated by echocardiography. Chest X-ray disclosed a wedge-shaped density in the right middle lung lobe that was a compatible finding with pulmonary infarction. At surgery, performed 3 days later the admission, pulmonary valve was entirely resected without replacing it with prosthesis. Antifungal treatment was intensively given afterwards. Her postoperative course was without event and she was sent home on the 51st postoperative day. Right heart catheterization done two years surgery, revealed the pulmonary vascular resistance was 216 dynes sec cm-5. We anticipate that this degree of pulmonary vascular resistance will allow the patient enough to do well without needing valve prosthesis in the near future.

Acute Disease↗
PubMed1997

Pulmonary artery thrombolysis and stenting after a bilateral sequential lung transplantation.

Bilateral sequential lung transplantation was complicated by pulmonary artery anastomotic stenosis and bilateral pulmonary thromboemboli. Pulmonary artery thrombus was eliminated by intrathrombotic but not by systemic administration of urokinase. The pulmonary emboli resulted in localized pulmonary infarctions, supporting the need for thrombolytic intervention to restore pulmonary perfusion in the absence of collateral bronchial blood flow after lung transplantation. Pulmonary artery stenosis was relieved by endovascular stenting, avoiding an early reoperative procedure. This case suggests that direct administration of thrombolytic agent may be superior to intravenous administration in the treatment of pulmonary thromboemboli. Pulmonary arterial anastomotic stenoses after lung transplantation can be relieved by endovascular procedures.

Adult↗
PubMed1991

Rib infarcts and acute chest syndrome in sickle cell diseases.

In the absence of evidence for pneumonia or pulmonary embolus, primary pulmonary infarction has been assumed to be the cause of the syndrome of chest pain, fever, and pulmonary infiltrate on chest X-ray that commonly complicates sickle cell anaemia. To find out whether the syndrome might be due to rib infarction, 99mTc-diphosphonate bone scans were done. In the eleven episodes thus investigated (10 patients) the scans showed segmental areas of increased radionuclide uptake in ribs, indicative of bone infarction. A possible sequence of events is that the rib infarcts are primary and cause bone pain, followed by soft tissue reaction, pleuritis, and splinting. The resultant hypoventilation leads to atelectasis and subsequent development of the radiographic changes of the acute chest syndrome. Prevention of hypoventilation and treatment of bone pain are important therapeutic goals.

Acute Disease↗
PubMed1977

Clinical significance of pulmonary function tests. Pulmonary function after uncomplicated myocardial infarction.

Derangement of pulmonary function following myocardial infarction is related to the severity of hemodynamic dysfunction. Abnormalities of pulmonary function appear even in patients without clinical or radiologic evidence of congestive failure. There is a reduction in vital capacity and rates of air flow. There is evidence for dysfunction of "small airways" and diminished ventilation to dependent parts of the lung. Total lung capacity may be normal or reduced, and residual volume may be increased slightly in uncomplicated myocardial infarction. Residual volume falls with more pronounced pulmonary congestion and edema. Distribution of pulmonary perfusion is altered after myocardial infarction, with a shift of perfusion away from the dependent parts of the lung (bases) towards the apices. Pulmonary gas exchange is impaired, with hypoxemia (due to both ventilation-perfusion inequality and increased shunting); and the diffusing capacity for carbon monoxide is diminished. Dead space is increased. The basic pathophysiologic mechanism responsible for abnormalities of pulmonary function is increased pulmonary water, which may be very minimal with uncomplicated myocardial infarction and stay primarily in the pulmonary interstitial space, but becomes progressively more severe with eventual alveolar flooding and marked impairment of pulmonary function.

Humans↗
PubMed1978

Sternberg-Reed-like cells in a pleural effusion secondary to pulmonary emboli with infarction: a cytological observation.

Cells resembling Sternberg-Reed cells were observed in a pleural effusion that was caused by pulmonary embolus with infarction. Although Hodgkin's disease was suggested on the basis of abnormal pleural fluid cytological preparations, the subsequent evaluation and clinical course did not support that diagnosis. We conclude that first, the cytological diagnosis of Hodgkin's disease should only be made when Sternberg-Reed-like cells are seen in association with a compatible clinical and cytological picture, and second, the cytological diagnosis of Hodgkin's disease or other malignancy should be made with caution in cases in which pulmonary infarction is present.

Adult↗
PubMed1977

Polyarteritis nodosa and hepatitis-B surface antigen: role of angiography in diagnosis.

two patients with polyarteritis nodosa who presented with vague constitutional systems and hepatitis-B antigenemia are reported. Angiography was used as the primary diagnostic procedure and confirmed the diagnosis in each case. Angiography is a relatively simple and direct means for establishing the diagnosis of polyarteritis nodosa. In these patients, the typical finding of aneurysm formation in multiple organs was observed. Arterial narrowing was also widespread. Multiple renal infarcts are shown in one case, and bronchial arteriography revealed aneurysms and narrowing in bronchial and intercostal arteries in one patient who had a recent pulmonary infarction and a normal pulmonary arteriogram. The relationship of the hepatitis-B antigen and polyarteritis is also emphasized.

Adult↗
PubMed1989

Pulmonary microvascular cytology in the diagnosis of lymphangitic carcinomatosis.

The diagnosis of lymphangitic spread of carcinoma in the lungs is sometimes difficult. We studied the cytologic characteristics of blood drawn through a wedged pulmonary-artery catheter from eight patients in whom lymphangitic carcinomatosis was confirmed by subsequent autopsy, lung biopsy, or clinical evaluation. The sites of the primary tumors were the prostate, breast, esophagus, and lung. Malignant cells were found in seven of the eight patients. Cytologic findings were normal in 16 of 17 patients with cancer but without pulmonary metastases and in 22 of 23 patients with nonmalignant pulmonary disorders. In a patient with cancer with tumor embolism to the lungs, the findings were positive, probably because of extensive intravascular tumor in large hepatic veins. One false positive finding occurred in a patient with extensive pulmonary infarction. Megakaryocytes, which are present in large numbers in the pulmonary capillary bed, are the hallmark of a satisfactory pulmonary vascular blood sample for pulmonary microvascular cytologic study. Familiarity with the cytologic characteristics of these cells in Papanicolaou preparations is essential to avoid mistakenly identifying them as malignant. Although transbronchial lung biopsy remains the diagnostic procedure of choice in this disorder, our findings suggest that the presence of malignant cells in pulmonary microvascular-cytology preparations in patients with cancer and unexplained dyspnea constitutes presumptive evidence of lymphangitic carcinomatosis. Pulmonary microvascular cytology may be particularly valuable when lung biopsy is refused or is thought to be too hazardous.

Aged↗
PubMed2001

Right pulmonary artery sarcoma.

A 57-year-old man presented with cough, chest pain and dyspnea. Peripheral lung opacities detected radiologically on admission were surgically resected and histologically confirmed as pulmonary infarcts. Subsequent radiological examinations revealed a stricture of the right pulmonary artery with evidence of pulmonary hypertension. The patient was commenced on anticoagulant therapy, which resulted in some clinical improvement. A hilar mass detected later was resected together with the right lung. Pathological examination of the hilar mass revealed a tumour within the lumen of the pulmonary artery causing almost total occlusion of the artery. Histology showed angiosarcomatous and osteosarcomatous areas. The patient is well and disease-free 9 months following resection.

Disease-Free Survival↗
PubMed1989

[Positive alveolar pressure reduces bronchial systemic-to-pulmonary blood flow in man].

We studied in humans during total cardio-pulmonary by-pass the effects of positive alveolar pressure on systemic to pulmonary bronchial blood flow. Systemic to pulmonary bronchial blood flow is the entire bronchial blood flow to the lung and was measured as the volume of blood which accumulates in the left heart when there is no pulmonary flow. Systemic to pulmonary bronchial blood flow was vented by gravity via a cannula (18 French) introduced in the upper superior pulmonary vein and advanced into the lower most portion of the left heart. In Group A (10 patients) systemic to pulmonary bronchial blood flow was measured with alveolar pressure constant at 4.0 +/- 0.4 cm H2O for 53.5 +/- 6.2 min (range 25 to 95 min), and ranged between 0.32 and 2.76% of cardiac output (pump flow) remaining constant with time. In Group B (10 patients) systemic to pulmonary bronchial blood flow was measured for 2 periods of 20 min each with alveolar pressure equal 4.1 +/- 0.2 and 14.1 +/- 0.4 cm H2O respectively. The increase of alveolar pressure reduced systemic to pulmonary bronchial blood flow by almost 40%. The reduction of systemic to pulmonary bronchial blood flow we observed may be deleterious for the survival of the lung parenchyma particularly in some circumstances. This is the case of pulmonary embolism, when bronchial blood flow is the major source of blood to the lung parenchyma and serves to prevent pulmonary infarction, or the case of acute respiratory distress syndrome, when pulmonary flow is compromised and systemic to pulmonary bronchial blood flow increases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1980

[Adrenal cortex hormones in acute myocardial infarct complicated by pulmonary edema].

The results of the study of adrenal cortical function in 94 patients (including 20 patients with acute myocardial infarction and pulmonary edema) and in 20 practically healthy persons are discussed. Marked activation of adrenal cortical hormones was noted in patients with acute myocardial infarction and edema of the lungs.

Adrenal Cortex Function Tests↗
PubMed1975

Radiology of the Swan-Ganz catheter and associated pulmonary complications.

Radiographic features of the Swan-Ganz catheter and the complications associated with its use are described. Pulmonary infarcts develop subsequent to wedging of the catheter in a peripheral position, failure to deflate the balloon after use, and maintenance for morethan 72 hours. The radiology of the infarct is usually classical in appearance, i.e., pleural-based density which resolves in 14-21 days. The frequency of pulmonary ischemia may BE related to compromise of the venous and collateral arterial circulation in intensive care unit patients in whom the catheter is used.

Aged↗
PubMed2002

Pulmonary embolism of polymethylmethacrylate after percutaneous vertebroplasty: a report of three cases.

STUDY DESIGN: Three cases of pulmonary embolism caused by polymethylmethacrylate (PMMA) after percutaneous vertebroplasty are reported, and the literature is reviewed. OBJECTIVES: To report on three cases of pulmonary embolism caused by polymethylmethacrylate after percutaneous vertebroplasty, and to review the literature briefly for reduction of this complication. SUMMARY OF BACKGROUND DATA: Pulmonary embolus caused by polymethylmethacrylate during percutaneous vertebroplasty is a rare complication. However, there is always a potential risk of this complication, which may result in pulmonary infarction. METHODS: Three of 27 patients with malignant spinal tumor experienced pulmonary embolism caused by polymethylmethacrylate after percutaneous vertebroplasty. Cement migration into the venous channel was observed in two patients, but not during the procedure. Two patients had mild dyspnea and chest discomfort, and one was asymptomatic. Pulmonary embolism was confirmed on chest radiographs. Ventilation perfusion scanning was performed to detect perfusion defect in all cases. RESULTS: Ventilation perfusion scanning showed no perfusion defects in any case. The symptoms of dyspnea and chest discomfort in two patients subsided after treatment using supplemental oxygen inhalation and anticoagulants. CONCLUSIONS: Three cases of pulmonary embolism caused by polymethylmethacrylate after percutaneous vertebroplasty are reported. Proper techniques can minimize the risk of pulmonary embolism caused by poly-methylmethacrylate during percutaneous vertebroplasty.

Anticoagulants↗
PubMed1985

Malignant fibrous histiocytoma of the lung.

A 75-year-old woman was admitted to a hospital for diagnosis of pulmonary infarction and died during treatment. An autopsy revealed a tumor 5 cm in diameter in the hilus of the left lung, spreading into the posterior mediastinum, and a metastasis was also found in the right lung. Histologically, this tumor consisted of two kinds of cells; one of fibroblast-like cells and the other of histiocyte-like cells, showing a storiform pattern. Furthermore, a positive staining for alpha 1-antitrypsin, but negative for CEA, keratin or S-100 protein was seen. Therefore, it was diagnosed as malignant fibrous histiocytoma (MFH) originating in the hilus of the left lung. In addition, many foci of hemorrhagic infarction due to metastasis and infiltration of the tumor into the pulmonary arteries were observed in the right lung. MFH is one of the rarest primary tumors of the lung.

Aged↗
PubMedDate not supplied

[Helical CT as preferred imaging modality in the diagnosis of pulmonary embolism].

PURPOSE: We investigated the role of Helical Computed Tomography (CT) as primary screening imaging modality in the diagnosis of pulmonary embolic disease. MATERIAL AND METHODS: We retrospectively reviewed the CT examinations, resulted positive for pulmonary embolism, performed in 134 patients (69 men and 65 women, ranging in age 23-83 years) from June 1998 to June 1999. CT was performed with a helical unit (thickness 3 mm, reconstruction interval 2 mm, pitch 1.5) after intravenous contrast agent (120 mL) rapid infusion (4 mL/s, 15s acquisition delay from bolus starting) and using a power injector. The spiral acquisition was performed from the apex of the pulmonary trunk to the diaphragm. Pulmonary embolism was considered as complete when a filling defect was present in a main pulmonary artery, as moderate when a filling defect was observed in an interlobar pulmonary artery and as very small when a filling defect was identified in a segmental pulmonary artery. RESULTS: Helical CT allowed us to identify the presence of a filling defect in the main pulmonary artery in 60.4% of cases (complete pulmonary embolism), in an interlobar pulmonary artery in 27.6% of cases (moderate pulmonary embolism) and in a segmental pulmonary artery in 11.9% of cases (very small pulmonary embolism). At helical CT study, pulmonary embolus was identified as complete filling defect (92.5% of cases), thromboembolic mass floating freely in the lumen (28.3%) and partial filling defect (19.4%). Pleural effusion and pulmonary infarction were associated in 46.2% and 20.1% respectively. DISCUSSION AND CONCLUSIONS: Pulmonary embolic disease continues to be a major cause of morbidity and mortality. The clinical diagnosis of pulmonary embolism remains an important challenge: among the different imaging modalities, contrast-enhanced helical CT can be used as primary screening imaging modality in the diagnosis of pulmonary embolism, allowing us to detect the presence of pulmonary embolus in the main, lobar and segmental artery, as demonstrated in our experience.

Adult↗
PubMed1991

[A case of myocardial infarction associated with pulmonary edema during curettage for hydatidiform mole].

We experienced a case of myocardial infarction associated with pulmonary edema in a patient with hydatidiform mole probably due to methylergometrin and prostaglandin F2 alpha (PGF2 alpha) administered during the operation. A 26-year-old woman was scheduled to have curettage for hydatidiform mole under general anesthesia. She had no previous history of cardiopulmonary disease. During the operation, 0.4 mg of methylergometrin was administered intravenously to induce uterine contraction. Because the contraction was not sufficient, 2 mg of PGF2 alpha was given into the uterine muscle. A few minutes later blood pressure and heart rate increased abruptly and arterial blood gas analysis showed hypoxia and respiratory acidosis. Pulmonary edema was confirmed by chest X-P. After ordinary treatment for pulmonary edema, she was transferred to ICU. Postoperative examinations of ECG, serum enzymes and echocardiography revealed anterior subendocardial infarction. About one month later, methylergometrin test was performed during coronary angiography and this induced coronary vasospasm. PGF2 alpha is also known to cause peripheral as well as pulmonary vasoconstriction. Acute myocardial infarction induced by methylergometrin and PGF2 alpha may be a possible cause of this episode.

Adult↗