Lung infarction secondary to infected pulmonary arterial thrombosis in a patient with Eisenmenger's syndrome.

A case is presented where a patient with Eisenmenger's syndrome is successfully treated for infection of chronic pulmonary arterial thrombosis with good effect. The evidence for antibiotic and anticoagulant therapy in this patient group is discussed.

A rare and challenging case of intrapericardial hydatidosis.

BACKGROUND: Hydatid cysts are most frequently located in the liver and lungs and very rarely can be found in the pericardium. Diagnosis and treatment are quite challenging, as the disease can present itself in many forms depending to the location and the complications that it might cause. CASE PRESENTATION: A 22-year-old man presented to our hospital with ongoing dry cough for more than 1 month prior to admission. Other symptoms included chest pain, fatigue, low grade fever, and night sweats, which have worsened in the past 2 weeks. Physical examination revealed normal respiratory and heart function. Chest X-ray demonstrated mediastinal enlargement and left pleural effusion. Contrast-enhanced computed tomography images showed a walled cystic mass lesion measuring up to 56 × 50 mm in close proximity to the upper left atrium, ascending aorta and pulmonary artery, potentially localized in the pericardium, with a 10 mm endoatrial filling defect, findings were compatible with hydatid cyst, left pleural effusion and peripheral pulmonary upper left lobe consolidation. Cardiac involvement was excluded on magnetic resonance imaging and trans-esophageal ultrasound. The patient underwent fine needle aspiration of the affected lung and thoracocentesis. No malignancy was found, meanwhile the biopsy confirmed the presence of pulmonary infarction. In view of the imaging findings were highly suspicious of a hydatid cyst, we performed a test of antibody titers that was negative. The patient underwent left anterolateral thoracotomy, and after the opening of the pericardium, a cystic mass of 5 cm in diameter was found next to the left atrium and in close proximity with the left pulmonary veins. The content of the cyst was completely removed after the surgical area was isolated with gauze impregnated with hypertonic solution (NaCl 10%). The mass resulted to be an echinococcal cyst with multiple daughter cysts within it that did not penetrate/involve (perforate) the cardiac wall. CONCLUSION: Pericardial echinococcosis is a very rare pathology in which a high expertise multidisciplinary approach is required. The compression mass effect caused by the cyst can lead to complications, such as in our case where the pulmonary vein was compressed, leading to pulmonary infarction. The value of radiology studies and transoesophageal ultrasound are very important in the diagnosis. Surgery in these cases is always recommended, but preferred surgical approach is questionable. In cases such as ours, we recommend anterolateral thoracotomy.

Impact of pulmonary infarction in pulmonary embolism on presentation and outcomes.

BACKGROUND: Pulmonary infarction (PI) is relatively common in pulmonary embolism (PE). The association between PI and persistent symptoms or adverse events is largely unknown. AIM: To evaluate the predictive value of radiological PI signs at acute PE diagnosis on 3-month outcomes. METHODS: We studied a convenience cohort with computed tomography pulmonary angiography (CTPA)-confirmed PE for whom extensive 3-month follow-up data were available. The CTPAs were re-evaluated for signs of suspected PI. Associations with presenting symptoms, adverse events (recurrent thrombosis, PE-related readmission and mortality) and self-reported persistent symptoms (dyspnea, pain and post-PE functional impairment) at 3-month follow-up were investigated using univariate Cox regression analysis. RESULTS: At re-evaluation of the CTPAs, 57 of 99 patients (58 %) had suspected PI, comprising a median of 1 % (IQR 1-3) of total lung parenchyma. Patients with suspected PI more often presented with hemoptysis (11 % vs. 0 %) and pleural pain (OR 2.7, 95%CI 1.2-6.2), and with more proximal PE on CTPA (OR 1.6, 95%CI 1.1-2.4) than patients without suspected PI. There was no association with adverse events, persistent dyspnea or pain at 3-month follow-up, but signs of PI predicted more functional impairment (OR 3.03, 95%CI 1.01-9.13). Sensitivity analysis with the largest infarctions (upper tertile of infarction volume) yielded similar results. CONCLUSIONS: PE patients radiologically suspected of PI had a different clinical presentation than patients without those signs and reported more functional limitations after 3 months of follow-up, a finding that could guide patient counselling.

Pulmonary embolism with bilateral pulmonary infarction after surgical correction of Achilles tendon - a rare complication.

INTRODUCTION: Pulmonary embolism (PE) is a potentially fatal disorder that occurs as a result of a thrombus formed in the deep venous system that detaches and obstructs the pulmonary artery or one of its branches. Herein we report a rare, bilateral PE after surgical correction of the Achilles tendon. OBJECTIVES: To report a bilateral PE after calcaneus tendon repair, and to review the literature on this rare condition. MATERIALS AND METHODS: A search of the literature was carried out in electronic databases and a review of medical records. CONCLUSION: PTE, although rare, is a serious and potentially fatal complication, requiring adequate and early treatment. Pharmacological prophylaxis in these situations is still controversial in the medical literature; however, there is consensus for the use of intermittent pneumatic compression in the postoperative period.

Non-surgical management of an abrupt cavitation and large oval-shaped lung abscess secondary to acute thromboembolic pulmonary infarction: a case report.

Infected cavitating pulmonary infarction is a rare complication of pulmonary embolism with a high mortality rate. Surgical excision for this complication has been used in past decades. Abrupt cavitation and a large oval-shaped lung abscess caused by acute thromboembolic pulmonary infarction during anticoagulation are rare. We present a 70-year-old man who suffered from pleuritic pain and breathlessness, accompanied by nausea and vomiting for 1 day. A physical examination showed tachycardia and tachypnea with moist rales in the left upper chest. High D-dimer levels, leukocytosis, respiratory failure and left upper lobe consolidation were found on plain computed tomography (CT). CT pulmonary angiography was performed 2 days after the previous CT scan because pulmonary embolism was suspected. This scan showed emboli in the main, right upper, middle, lower and left upper pulmonary arteries with deteriorated left upper lobe consolidation and cavitation. Thromboembolic pulmonary infarction and an abscess were diagnosed. Enoxaparin 60 mg was administered every 12 hours for 10 days, followed by rivaroxaban, antibiotics and drainage of the hydrothorax. The patient improved after the strategy of non-surgical treatment and was discharged approximately 1 month later. The patient had an uneventful course during rivaroxaban 20 mg once daily for 1 year.

Pulmonary infarction in acute pulmonary embolism.

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.

Dynamics of CT visible pleural effusion in patients with pulmonary infarction.

Background Pleural effusion remains largely unexplored in patients with pulmonary embolism and concurrent pulmonary infarction. The aim of the study was to investigate the relationship between the size of pulmonary infarction and pleural effusion as well as the time course of pleural effusion in patients with pulmonary infarction. Patients and methods Data from 103 patients with pulmonary infarction was retrospectively analysed along with patient comorbidities, size of pulmonary infarction, presence and size of pleural effusion with the time between the onset of clinical symptoms of pulmonary infarction and CT study. Results Assessment of possible correlations between the size of pulmonary infarction and age revealed a significant negative correlation. There was a highly significant difference (p = 0.005) in the mean size of pulmonary infarction in patients with effusion (34.5 cm3) compared to those without it (14.3 cm3), but the size of the effusion had no correlation with the size of pulmonary infarction. The size of the effusion peaked between 4th-5th day after the onset of clinical symptoms of pulmonary infarction. In the first 5 days after the onset of clinical symptoms of pulmonary infarction a significant correlation was found between the size of the effusion and time with approximation of 1.3 mm/12 h. Conclusions The data shows that patients with a pleural effusion are more likely to have a larger pulmonary infarction than those without it. If present, the effusion can be expected to increase in a relatively slow linear fashion in the first 5 days after the onset of clinical symptoms of pulmonary infarction.

Pulmonary Infarction: Right Upper Quadrant Pain as a Presenting Symptom With Review of Typical Computed Tomography Imaging Features.

The purpose of this case presentation is to discuss right upper quadrant pain as an atypical presenting symptom in pulmonary infarction and review the typical computed tomography (CT) imaging features of pulmonary infarction to improve diagnostic accuracy. Pulmonary infarction results from occlusion of distal arterial vasculature within the lung parenchyma leading to ischemia, hemorrhage, and ultimately necrosis. Patients with lung infarction typically present with pleuritic chest pain and may have associated signs or symptoms of pulmonary thromboembolism or deep vein thrombosis. In this case study, a 34-yr-old female devoid of any symptoms indicative of either pulmonary embolism or deep vein thrombosis presented with right upper quadrant pain 1 mo status post open reduction internal fixation for a left ankle fracture. Multiple clinic visits spanning approximately 7 d were significant for a right lower lobe opacity seen on CT of the abdomen which was presumed to represent community acquired pneumonia as a source for the patient's RUQ pain. The patient presented to the emergency department 1 wk later (6 wk following her initial surgery) complaining of left lower extremity swelling and was subsequently diagnosed with a left lower extremity DVT via ultrasound. CT of the pulmonary arteries was negative for PE but identified a right lower lobe opacity which in retrospect was consistent with pulmonary infarction.

Persistent fever with chills and an endocardial mass in a child: an unusual presentation of Hughes-Stovin syndrome.

A 12-year-old boy with a right atrium endocardial mass was initially diagnosed as having Lemierre's syndrome on the basis of previous mastoiditis and jugular vein and cerebral venous thrombosis. Lack of response to antibiotics, persistent high fever with chills, acute-phase reactants, and peripheral arterial pseudoaneurysms made us reconsider the diagnosis. Only after the late appearance of radiological pulmonary lesions and recognition of pulmonary artery aneurysms, Hughes-Stovin syndrome was diagnosed. Hughes-Stovin syndrome is an exceedingly rare vasculitis, especially in childhood, consisting of multiple pulmonary artery aneurysms and deep venous thromboses. The lack of formal diagnostic criteria and the rarity of the disease make the diagnosis very challenging, especially when respiratory complaints are not present at onset, as in the presented case. The treatment aims to reduce inflammation, although there is debate about anticoagulation therapy because of the risk of pulmonary haemorrhage.

Successful non-myeloablative allogenic bone marrow transplantation in a child with severe congenital neutropenia complicated by chronic pulmonary infection.

We herein describe a 2-year-old boy with severe congenital neutropenia (SCN) who was successfully treated with reduced-intensity bone marrow transplantation (HSCT). He had suffered recurrent episodes of bacterial pneumonia from 12 months of age, and was found to have severe neutropenia with white blood cell counts below 100/µl. The patient harbored a heterozygous missense mutation in ELANE exon 4 (p.Gln134Pro, NM_001972.2: c.401A>C). This was a novel mutation. Due to intractable pneumonia and severe persistent neutropenia, reduced-intensity HSCT was performed from an HLA-matched sibling donor. The preparative regimen consisted of melphalan, fludarabine, and 4 Gy of total body irradiation. Hematopoietic engraftment was rapidly obtained, i.e., by day +14, and complete donor chimerism was subsequently achieved. The lung complications observed pre-transplantation markedly improved after neutrophil recovery, i.e., by day +60. We concluded that HSCT is a useful treatment for SCN patients, especially for those at high risk of leukemic transformation. Fludarabine-based reduced-intensity HSCT may represent a safe and effective therapeutic option for patients with SCN who need HSCT even if they have intractable infectious complications.

Takayasu Arteritis With Antiphosphatidylserine/Prothrombin Antibody-Positive Antiphospholipid Syndrome: Case Report and Literature Review.

A relationship between Takayasu arteritis (TA) and positive antiphospholipid antibody states has been pointed out, but patients with TA complicated with antiphospholipid antibody syndrome (APS) are rare. Here we report the case of a 17-year-old Japanese man diagnosed with TA based on pulselessness of the left brachial artery, discrepancy of blood pressure between the upper extremities, and arterial wall thickening and narrowing of artery in contrast computed tomography. He was also diagnosed with provisional APS based on a pulmonary infarction without narrowing of the pulmonary artery and positive antiphosphatidylserine/prothrombin antibody. The patient also had concurrent Crohn's disease (CD) based on histopathological findings, which may have been associated with TA. We started high-dose corticosteroid therapy and anticoagulation therapy, and his symptoms including fever, dizziness, chest pain, and lower-right uncomfortable abdomen improved.We reviewed 9 cases of TA with APS including our patient by conducting a PubMed search. Based on past reports, we considered the relationship among TA, APS, and CD.Clinicians should bear in mind that many etiologies can exist in 1 patient, and differential diagnoses are essential.

Masa cavitada en paciente con disnea súbita / Cavited mass in a patient with sudden onset dyspnea

No disponible

Intrauterine fetal death of a monochorionic twin with peripheral pulmonary infarcts: potential thromboembolic events following death of co-twin.

In utero fetal lung infarction has rarely been reported. We present a case of intrauterine lung infarction in a 28-3/7 weeks' gestation monochorionic twin following intrauterine fetal demise of the co-twin at 20 weeks. This case highlights the potential for thromboembolic events (TBEs) associated with monochorionic gestations to include pulmonary TBE and infarction among the risks for fetal morbidity and mortality.

Diagnostic approach of pneumonia in an elderly patient with comorbidities--case report.

Dyspnea is one of the symptoms that has a major impact on patients' health, with a negative influence on the quality of life. The main causes of dyspnea are cardiac, pulmonary and mixed (cardiac or pulmonary). There are several other causes such as metabolic conditions (acidosis), pain, neuromuscular disorders, otorhinolaryngeal disorders, anxiety, panic disorders and hyperventilation. Acute pneumonia in the elderly is a common occurrence and its incidence grows as the elderly population increases. We report the case of a 76 years old patient with a known cardiovascular condition, recently hospitalized for right pulmonary infarction. He presented to our clinic for influenced general state, rest dyspnea, fever, shiver, and productive cough in the last two days. Current medication included oral anticoagulants and triple antihypertensive treatment (responsible for his low blood pressure). Laboratory results showed a nonspecific inflammatory syndrome with leukocytosis and neutrophilia and mild normochromic normocytic anemia; D-dimers were within normal range, fibrin degradation products 1+; myocardial enzyme testing showed no alteration, and BPN (beta natriuretic peptide) was 790 pg/ml. Chest X-ray showed diffuse bilateral reticular shadows (more pronounced on the right side) and left costodiafragmatic opacification. It appears that age-related increase in morbidity and mortality in community-acquired pneumonia is not due to age per se, but to interactions between the immune system, systemic diseases and nutritional factors. Community-acquired pneumonia in the elderly is known to have a high mortality. Although the diagnosis can be easy, the physician must also investigate for less obvious causes of dyspnea such as the presence of comorbidities and fragility of the elderly patient.