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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Late and progressive respiratory failure after pneumonectomy may result from a variety of causes. Non-specific causes include restrictive failure by loss of alveolar volume; pulmonary hypertension; initial disease recurrence (e.g. bronchogenic cancer, bronchiectasis); side-effects of radio- and chemotherapy; and benign or malignant pleural or pericardial effusions. Acute or subacute conditions are congestive or ischemic heart failure, pulmonary embolism, and pneumonia. Two causes are specific, benign, and curable: the postpnemonectomy syndrome and the platypneaorthodeoxia syndrome. The latter is related to a right-to-left interatrial shunt through a reopened patent foramen ovale. The hemodynamic and anatomical mechanisms are analyzed through an exhaustive review of the literature, together with the particular clinical presentation and the easy diagnosis if suspected.
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PMID:Late complications. Late respiratory failure. 1045 33

A 70-year-old man was admitted with syncope attack on exertion. Ventricular septal defect with pulmonary hypertension and left atrial myxoma were confirmed by ultrasonography and cardiac catheterization. Preoperative Pp/Ps was 0.95 and pulmonary vascular resistance was 16 units. Pulmonary vascular resistance decreased to 9.6 units by the administration of Isoproterenol and decreased to 8.5 units with PGE1. Patch closure of VSD and excision of left atrial myxoma were performed simultaneously. The patient recovered completely, although he suffered from pneumonia and jaundice due to liver congestion postoperatively. Cardiac catheterization before discharge revealed Pp/Ps 0.38 and PVR 10.1 units.
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PMID:[Ventricular septal defect with pulmonary hypertension and concomitant left atrial myxoma in elder patient: a successful surgical case report]. 1066 28

In patients with cardiomegaly and signs and symptoms compatible with CHF, unilateral right-sided or bilateral pleural effusions of similar size are likely to be due to left-sided CHF. Isolated right ventricular failure or chronic pulmonary hypertension is not usually associated with pleural effusions, and unrecognized or new-onset left ventricular dysfunction and other causes should be considered when a patient with cor pulmonale presents with a pleural effusion. Unilateral left-sided pleural effusions with cardiomegaly may be due to pericardial disease. Current hypotheses do not adequately explain the laterality of effusions in CHF or pericardial disease. Clinical and radiographic correlation is always required; however, the associations described occur often enough to make them useful in day-to-day clinical practice. When ascribing pleural effusions to CHF, clinicians must be sure the clinical signs and history "fit the picture," because pneumonia and pulmonary embolism may also cause pleural effusions in patients with heart failure. Typical pleural effusions in patients with uncomplicated CHF (demonstrated by small to medium-sized effusions and the absence of fever, leukocytosis, pleuritic chest pain, or marked asymmetry in bilateral effusions) do not require routine diagnostic thoracentesis for evaluation. A reasonable approach in such cases is treatment of the underlying CHF and follow-up radiography to monitor for resolution of the effusions. Prompt diagnostic thoracentesis is indicated whenever atypical features are present and other diagnoses are under consideration.
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PMID:Pleural effusions in cardiovascular disease. Pearls for correlating the evidence with the cause. 1088 42

Hepatopulmonary syndrome is the most widely recognized of the processes associated with end-stage liver disease. Chronic liver dysfunction is associated with pulmonary manifestations due to alterations in the production or clearance of circulating cytokines and other mediators. Hepatopulmonary syndrome results in hypoxemia due to pulmonary vasodilatation with significant arteriovenous shunting and ventilation-perfusion mismatch. Hepatic hydrothorax may develop in patients with cirrhosis and ascites. Rarely, pulmonary hypertension occurs in the setting of portal hypertension. A second group of disorders may primarily affect the lungs and liver (the hepatopulmonary axis). Among these are the congenital conditions alpha(1)-antitrypsin deficiency and cystic fibrosis. Autoimmune liver disease may be associated with lymphocytic interstitial pneumonitis, fibrosing alveolitis, intrapulmonary granulomas, and bronchiolitis obliterans with organizing pneumonia. Sarcoidosis affects the lung and liver in up to 70% of patients. Medications such as amiodarone can result in a characteristic radiologic appearance of pulmonary and hepatic toxic effects. Knowledge of these associations will assist the radiologist in forming a meaningful differential diagnosis and may influence treatment decisions.
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PMID:Diseases of the hepatopulmonary axis. 1083 22

Cholesterol granulomas unrelated to endogenous lipoid pneumonia, pulmonary alveolar proteinosis, or cholesterol pneumonia are a rare finding during pneumectomy or autopsy. They have been occasionally reported in association with pulmonary hypertension. We report a case where these lesions were associated with long-standing pulmonary hypertension and microangiopathic hemolytic anemia and thrombocytopenia. Plexiform lesions were present in the pulmonary vasculature secondary to pulmonary hypertension, causing hemolysis and thrombocytopenia. We suggest that destruction of red blood cells and platelets could provide membrane lipids that are taken up by phagocytic cells, which promotes the formation of these cholesterol deposits.
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PMID:Cholesterol granulomas of the lungs associated with microangiopathic hemolytic anemia and thrombocytopenia in pulmonary hypertension. 1110 63

Pulmonary embolism is nearly always a complication of deep venous thrombosis. The evaluation of risk factors for venous thromboembolism not only aids diagnosis but also guides decisions about the intensity of prophylactic measures. As both the extent and chronicity of pulmonary vascular obstruction vary widely, pulmonary embolism can produce widely differing clinical pictures. From the clinical, pathophysiological and therapeutical point of view, it is convenient to classify pulmonary embolism into four types: acute minor embolism (dyspnoea with or without pleuritic pain or haemoptysis), acute massive embolism (hemodynamic instability), subacute massive embolism (mimicking heart failure or indolent pneumonia), and chronic thromboembolic pulmonary hypertension (slowly progressing dyspnoea). This classification is of importance not only for the rational diagnosis and differential diagnosis, but also for the institution of adequate therapy. Because the disease has many nonspecific manifestations but no pathognomonic symptoms or signs, it is impossible to prove the diagnosis of pulmonary embolism alone on the basis of clinical presentation.
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PMID:[Clinical characteristics of pulmonary embolism]. 1121 69

Inhaled nitric oxide (iNO) has emerged as a promising therapeutic agent in the treatment of persistent pulmonary hypertension of the newborn. Several theories exist regarding causes of both response and nonresponse to iNO. Clinical trials differentiate disease entities (primary vs secondary persistent pulmonary hypertension associated with meconium aspiration syndrome, pneumonia or congenital diaphragmatic hernia) and their specific response rates. iNO combined with high-frequency ventilation appears to be superior to inhalation of nitric oxide (NO) during conventional ventilation. Little is known regarding the role of the degree of lung expansion and its modification -- no matter what mode of ventilation is applied. Gestational age plays an important role in relation to the potential adverse effects of NO. Of particular concern in the premature neonate is the effect of NO on bleeding time and the inhibition of platelet aggregation. Those potentially hazardous effects need to be carefully weighed against early intervention with iNO at a comparably low oxygenation index in order to prevent the vicious cycle of hypoxaemia and subsequent increased right-to-left shunting. Further studies are required to determine the optimal timing, mode of delivery and mode of ventilation used with iNO therapy in order to optimise the response of premature and term neonates.
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PMID:Response to inhaled nitric oxide in premature and term neonates. 1121 69

Pulmonary embolism (PE) was believed to be a rare disease and often misdiagnosed in Thailand. Only a few cases of PE in Thai patients have been reported. The purpose of this study was to describe the characteristics of history, physical examination and laboratory investigations in Thai patients with PE. Forty-nine patients diagnosed as PE in Phramongkutklao Hospital between 1994 and 1998 were included in the study. All patients underwent complete history, physical examination and appropriate laboratory studies. The mean age of this patient group was 53 years. Thirty-four per cent of these patients were first suspected of lung embolism while the others were misdiagnosed as congestive heart failure, myocardial infarction, pneumonia or septic shock. The most common syndrome was isolated dyspnea. Interestingly, chronic thromboembolic pulmonary hypertension which is uncommonly found in western countries was diagnosed in 12 per cent of our patients. Dyspnea, pleuritic pain, leg swelling, cough, tachypnea, tachycardia and increased pulmonary component of second heart sound were common symptoms and signs. A high-probability ventilation/perfusion lung scan and deep vein thrombosis were demonstrated in 93 per cent and 55 per cent of our patients, respectively. The mortality rate was 10 per cent.
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PMID:Clinical and laboratory findings in patients with pulmonary embolism in Phramongkutklao Hospital. 1125 85

Persistent pulmonary hypertension of the newborn (PPHN) remains one of the most challenging situations in the neonatal intensive care unit, and it is associated with high mortality and morbidity. The optimal treatment for PPHN is controversial. We report our 9-year experience in the management of PPHN through a retrospective review of 29 neonates with persistent pulmonary hypertension. The diagnosis of PPHN is made by echocardiography and/or preductal and postductal oxygen tension difference. The treatment modalities include supportive medical care, vasodilator therapy, mechanical ventilation and correction of underlying conditions. The wide diversity of etiologies of PPHN, the complications of vasodilator therapy, the management of assisted ventilation, the mortality and the morbidity are evaluated. There are 29 patients enrolled in this study, including 18 male and 11 female babies. Twenty-two patients (72%) are referred from other hospitals. The mean birth body weight is 2707 +/- 693 grams (range: 1450-4100 grams) and the mean gestational age is 37.1 +/- 3.1 weeks (range: 31-41 weeks). The underlying clinical conditions include meconium aspiration syndrome (n = 8), perinatal asphyxia (n = 7), respiratory distress syndrome (n = 5), sepsis and/or pneumonia (n = 4), congenital diaphragmatic hernia (n = 3) and idiopathic persistent fetal circulation (n = 2). In addition to supportive medical care and correction of underlying clinical conditions, most of the patients receive vasodilator therapy (Tolazoline) and nonhyperventilation respirator management. The overall mortality rate is 27.6% (8/29). The duration on ventilator therapy in the survival group (9.3 +/- 8.6 days) is not significantly different from in the mortality group (6.0 +/- 7.1 days) (p = 0.13). There is also no statistically significant difference between these two groups both in the maximal alveolar-arterial oxygen tension difference (594 +/- 53 mmHg and 613 +/- 37 mmHg, p = 0.145) and in the maximal oxygenation index (49.7 +/- 29.6 and 61.1 +/- 36.9, p = 0.172) before vasodilator therapy. However, twenty-four hours after treatment, these two parameters change significantly with the former changes to 426 +/- 198 mmHg and 643 +/- 7 mmHg, respectively (p < 0.001), and the latter changes to 21.6 +/- 15.8 and 82.3 +/- 54.8, respectively (p < 0.001). Skin rash, gastrointestinal hemorrhage, hypotension and hyponatremia are the most common complications of Tolazoline therapy. Eight patients have pulmonary complications including pneumothorax (n = 5) and pulmonary interstitial emphysema (n = 3). Two patients develop chronic lung disease. Three patients have neurodevelopmental handicap. In conclusion, we achieve a survival rate of nearly 75% in PPHN mainly with the administration of Tolazoline therapy and the nonhyperventilation respirator approach. Further well-controlled and multicenter studies with newer treatment modalities are crucial for the improvement of survival of PPHN in Taiwan.
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PMID:Persistent pulmonary hypertension of the newborn: experience in a single institution. 1135 72

We report an autopsy case of elderly-onset anticentromere antibody-positive pulmonary-renal syndrome. An 84-year-old woman was admitted to our hospital with complaints of leg edema and general malaise. Neither skin rush nor arthritis was seen. Because of hematuria, proteinuria with various casts, renal dysfunction and anemia, a clinically diagnosis of rapidly progressive glomerulonephritis was made. Slight pulmonary hypertension was observed in ultrasonic cardiography. Hypocomplementemia was not seen. Tests for MPO- and PR 3-anti-neutrophil cytoplasmic antibodies and anti-glomerular basement membrane antibody were negative, but a high titer of antinuclear antibody with a discrete speckled pattern on immunofluorescent staining was disclosed. Results for anticentromere antibody and anti-Ki antibody were positive, but for anti-Sm antibody and anti-double stranded DNA antibody were both negative. She did not present any clinical features of systemic sclerosis or CREST syndrome. Subsequently, prednisolone was administered, but pulmonary alveolar hemorrhage occurred and the patient died of acute respiratory failure caused by massive pulmonary hemorrhage. Autopsy revealed crescentic glomerulonephritis including glomerular capillaritis and pulmonary capillaritis with positive granular deposits of immunoglobulins and compliment on the glomerular and pulmonary capillary walls. Immunologically mediated crescentic glomerulonephritis and pulmonary capillaritis was then diagnosed histopathologically. The main pathological feature of the case was small-vessel vasculitis with immune-complex deposition. Although this case did not fulfill the clinical criteria for systemic lupus erythematosus (SLE), its histological features resembled those of lupus nephritis and acute lupus pneumonitis. We speculated that anticentromere antibody-positive pulmonary-renal syndrome without any other symptoms or signs of connective tissue disease, such as our case, is a clinical entity distinct from typical SLE or CREST syndrome.
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PMID:[Elderly-onset anticentromere antibody-positive pulmonary-renal syndrome: report of an autopsy case]. 1157 30


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