Diagnosis Of Pulmonary Infarction Research Articles

Diagnosis of pulmonary infarction by chest ultrasound in patient with massive pulmonary thromboembolism

Diagnosis of pulmonary infarction by chest ultrasound in patient with massive pulmonary thromboembolism

Clinical characteristics of patients with pulmonary infarction - A retrospective review.

Pulmonary infarction is an infrequent complication of pulmonary embolism. Traditionally, it has been regarded as a sign of worse outcome because ischemia can only occur by the simultaneous failure of all oxygenation sources to the area of infarct, but supporting evidence is limited. We identified 74 cases of pulmonary infarction over 5 years at a single academic center via review of radiographic reports. Contrast-enhanced chest CT scans were examined to confirm evidence of pulmonary infarction, and patient clinical characteristics and imaging results were studied. Survival to discharge was high (97%). Patients most commonly presented with dyspnea (69%), chest pain (46%), and swelling or pain in the lower extremities (31%), while underlying risk factors included history of malignancy (41%) and surgery within 30 days (24%). Many patients had concurrent cardiovascular (59%) and pulmonary disease (22%). Infarction disproportionately affected the lower lobes. Survival after diagnosis of pulmonary infarction is comparable to uncomplicated pulmonary embolism, suggesting that outcome is not worse. While emboli occurred in multiple lobar sites, pulmonary infarction occurred most commonly in the lower lobes, suggesting unique underlying physiological mechanisms in pulmonary infarction development.

Diagnosis of Pulmonary Infarction by Thoracic Ultrasonography

Diagnosis of Pulmonary Infarction by Thoracic Ultrasonography

Predictors of Pulmonary Infarction

In the setting of acute pulmonary embolism (PE), pulmonary infarction is deemed to occur primarily in individuals with compromised cardiac function.The current study was undertaken to establish the prevalence of pulmonary infarction in patients with acute PE, and the relationship between infarction and: age, body height, body mass index (BMI), smoking habits, clot burden, and comorbidities.The authors studied prospectively 335 patients with acute PE diagnosed by computed tomographic angiography (CT) in 18 hospitals throughout central Italy. The diagnosis of pulmonary infarction on CT was based on Hampton and Castleman's criteria (cushion-like or hemispherical consolidation lying along the visceral pleura). Multivariable logistic regression was used to model the relationship between covariates and the probability of pulmonary infarction.The prevalence of pulmonary infarction was 31%. Patients with infarction were significantly younger and with significantly lower prevalence of cardiovascular disease than those without (P < 0.001). The frequency of infarction increased linearly with increasing height, and decreased with increasing BMI. In logistic regression, the covariates significantly associated with the probability of infarction were age, body height, BMI, and current smoking. The risk of infarction grew with age, peaked at approximately age 40, and decreased afterwards. Increasing body height and current smoking were significant amplifiers of the risk of infarction, whereas increasing BMI appeared to confer some protection.Our data indicate that pulmonary infarction occurs in nearly one-third of the patients with acute PE. Those with infarction are often young and otherwise healthy. Increasing body height and active smoking are predisposing risk factors.

Pulmonary infarct as a surgical pathology: morphology and differential diagnosis

The actuality of the work is caused by considerable difficulties of verification of pulmonary infarction of small size in clinical practice, which leads to surgical interventions.Aim. In order to clarify the characteristics of a pulmonary infarction in 4 patients with surgery for «nodule» in the lung and morphologically confirmed diagnosis of «pulmonary infarction» the medical history, clinical and laboratory data were studied and a thorough morphological study of surgical specimens was performed.Methods and results. The data of modern literature were analyzed. It was found that the most frequent surgical pathology is pulmonary infarction of the small size at the stage of the organization. The cause of development, the main histological features characterizing pulmonary infarction, as well as differential diagnostic considerations were determined.Conclusion. The presented material shows that morphological examination is the key in the diagnosis of pulmonary infarction in a number of clinical observations.

Anticoagulants for Cerebral Venous Thrombosis

See related article, p 8. Evidence relating to efficacy and safety of anticoagulants for CVT is only partially available from studies in the peer reviewed medical literature and from the corresponding authors of those studies. Consequently, this article is an opinion piece rather than a systematic review. Cerebral venous thrombosis (CVT) accounts for ≈0.5% of strokes and may occur at any age.1 Risk factors include pregnancy, oral contraceptives, head trauma, malignancy, infection, anemia, and dehydration. In older reports, the incidence of CVT was 3 to 4 per 1 million people per year in Europe and the United States.2 However, a survey published in 2012 found an incidence of CVT of 13.2 per 1 million people per year.3 With modern brain imaging technology, more cases are being discovered that probably would have resolved without medical intervention. Relative to pre-1990 clinical outcomes data, the average prognosis has dramatically improved.4,5 A Cochrane review of anticoagulant therapy for CVT4 based the recommendation in favor of using anticoagulation treatment (full-dose unfractionated heparin [UFH] or low-molecular-weight heparin [LMWH] followed by a vitamin K antagonist [VKA]) on 2 small randomized placebo-controlled trials (RCTs, n=79). These trials demonstrated a non-statistically significant reduction in deaths with anticoagulation (risk ratio, 0.33; 95% confidence interval [CI], 0.08–1.28). Subsequently, the European Federation of Neurological Sciences6 and the American Heart Association/American Stroke Association7 issued clinical practice guidelines calling for full-dose heparin acutely followed by VKAs for ≥3 months. The efficacy and safety of anticoagulants for CVT have not been comprehensively reviewed, with the inclusion of observational studies and the RCTs excluded from the Cochrane review. This review will evaluate published reports from 1990 to 2013 regarding the efficacy and safety of full-dose heparin (UFH or LMWH) during initial hospitalization and subsequent VKA treatment …

Assessing Your Knowledge of Childhood and Adolescent Injuries.

Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma. It is most commonly caused by acute pulmonary embolism (PE), with a reported incidence of around 30%. Following an occlusion of the pulmonary artery, the bronchial arteries are recruited as primary source of perfusion of the pulmonary capillaries. The relatively higher blood pressure in the bronchial circulation causes an increase in the capillary blood flow, leading to extravasation of erythrocytes (i.e. alveolar hemorrhage). If this hemorrhage cannot be resorbed, it results in tissue necrosis and infarction. Different definitions of pulmonary infarction are used in literature (clinical, radiological and histological), although the diagnosis is nowadays mostly based on radiological characteristics. Notably, the infarcted area is only replaced by a fibrotic scar over a period of months. Hence and formally, the diagnosis of pulmonary infarction cannot be confirmed upon diagnosis of acute PE. Little is known of the impact and relevance of pulmonary infarction in acute PE, and whether specific management strategies should be applied to prevent and/or treat complications such as pain, pneumonia or post-PE syndrome. In this review we will summarize current knowledge on the pathophysiology, epidemiology, diagnosis and prognosis of pulmonary infarction in the setting of acute PE. We highlight the need for dedicated studies to overcome the current knowledge gaps.

Magnetic Resonance Imaging in the Diagnosis of Pulmonary Infarction

We report for the first time, to our knowledge, MRI features which could differentiate noninvasively pulmonary infarction from pneumonia. Three subjects with angiographically proven pulmonary infarction showed high T1 weighted MRI signals located in the embolic territory. Three patients with pneumonia and one patient with emboli, but without infarction, did not have these T1 weighted images.

Pulmonary Infarction

The CT appearance of 12 proven pulmonary infarcts in 10 patients was analyzed and correlated with pathologic appearance. The diagnosis of pulmonary infarction was clinically suspected in only 2 of the 10 patients. A pleural based parenchymal density with convex, bulging borders and linear strands directed from the apex of the density toward the hilum was noted in each case (n = 12). Other features were a truncated apex (n = 10), a broad pleural base (n = 10), and scattered areas of reduced attenuation within the lesions (n = 7). This distinctive complex of findings on CT should raise a strong suspicion of pulmonary infarction.

Acute Reversible Pulmonary Ischemia

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.

Enzyme Profiles in the Evaluation of Pulmonary Infarction

The diagnosis of pulmonary infarction is dependent upon the use of multiple diagnostic criteria. These include clinical findings, electrocardiographic changes, pulmonary function changes, serial enzyme change, and radiographic techniques. Increased specificity in the diagnosis of pulmonary infarction was found with a profile of enzyme studies including determinations of creatine phosphokinase, serum lactic acid dehydrogenase, and hydroxy butyrate dehydrogenase. The values obtained from a study of this combination of enzymes eliminated patients whose symptomatology simulated pulmonary infarction but actually represented myocardial infarction. The use of isoenzymes was of minimal value in differential diagnosis of this condition.

Failure to differentiate pulmonary infarction from pneumonia by biochemical tests.

Pulmonary infarction needs to be distinguished from several diseases. In its differentiation from myocardial infarction the electrocardiogram is a very helpful investigation, but it can be difficult to distinguish pulmonary infarction from pneumonia. Evidence of either a potential source of embolus or of a recent infection of the respiratory tract may facilitate the diagnosis, and the chest radiograph may sometimes be helpful, but signifi cant numbers of patients remain in whom a clear-cut distinction cannot readily be made on clinical or radiological grounds. Many serum enzyme determinations have been introduced for the investigation of cardiac and hepatic disease?for example, alkaline phosphatase, alanine and aspartate amino transferase, lactate dehydrogenase and its isoenzymes, isocitrate dehydrogenase, etc.?and the possible value of some of these assays for differentiating between pulmonary infarction and pneumonia has been investigated by various workers?for example, Nikkil? (1959), Wacker and Snodgrass (I960), Wacker, Rosenthal, Snodgrass, and Amador (1961), Stevens and Burdette (1964). So far no single biochemical test has been proposed as a reliable means of differentiating between the two conditions, but combinations of tests have been advocated. Nikkil? (1959) tentatively suggested that measurement of aspartate aminotransferase (G.O.T.), glucose-6-phosphate dehydrogenase, and alkaline phosphatase might prove a helpful triad of investigations, and Wacker and Snodgrass (1960) and Wacker et al. (1961) advocated serial determinations of lactate dehydrogenase (L.D.), G.O.T., and serum bilirubin. In 17 patients diagnosed clinically (12) or at necropsy (5) as having had pulmonary infarction, with or without embolism, L.D. was elevated, whereas G.O.T. remained normal, and in 12 out of the 17 patients serum bilirubin was abnormal at some stage of the illness. Wacker et al. (1961) also applied this combination of tests to seven other patients who subsequently came to necropsy (five with myocardial infarction and two with bacterial pneumonia) ; the patients with myocardial infarction showed abnormal G.O.T. and L.D. values, whereas the patients with pneumonia had normal serum enzyme levels. They therefore proposed that the finding of an elevated L.D. and bilirubin, in association with a normal G.O.T., favoured a diagnosis of pulmonary infarction in patients with a suggestive clinical history. Stevens and Burdette (1964) were unable to confirm the value of the combination of tests advocated by Wacker et al. (1961) ; the only finding consistently observed by Stevens and Burdette (1964) in patients with pulmonary infarction was an elevation of L.D., and they suggested that an elevated L.D. might be a requirement for the laboratory diagnosis of pulmonary infarc tion. However, even this single test is probably not uniformly reliable, as Wr?blewski, Ruegsegger, and LaDue (1956) and Kirkeby and Prydz (1959) have reported normal L.D. values in patients with pulmonary infarction.

Enzymatic Levels in Pulmonary Infarction

Studies of human postmortem material show that pulmonary infarctions are found in 5% to 25% of patients coming to autopsy, and evidence indicates that less than one in three of these pulmonary infarcts found at autopsy is diagnosed prior to the death of the patient. 1-11 Gorham, in calling attention to the syndrome of increasing pulmonary hypertension and cor pulmonale resulting from repeated small emboli to the pulmonary arterial branches, 6 delineates a group of cases with pulmonary infarctions which tax further the diagnostic skills of the surgeon. With surgical procedures available to apply effectively in many patients when embolism can be recognized, many investigators have sought assistance in the diagnosis of pulmonary infarction. Since enzymes have been helpful in the diagnosis of myocardial infarction by virtue of the increased levels of enzymatic activity in the serum when infarcted myocardial tissue is present, the possibility of a parallel in the