Pulmonary veno-occlusive disease: the role of CT

Mineo, Giangaspare; Attinà, Domenico; Mughetti, Martina; Balacchi, Caterina; Luca, Fiorella De; Niro, Fabio; Ciccarese, Federica; Lovato, Luigi; Russo, Vincenzo; Buia, Francesco; Modolon, Cecilia; Manes, Alessandra; Palazzini, Massimiliano; Galiè, N; Zompatori, Maurizio

doi:10.1007/s11547-013-0363-y

Cited by 25 publications

(17 citation statements)

References 25 publications

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“…Pulmonary macrophages ingest these red blood cells, forming cholesterol granulomas that are visualized as centrilobular ground-glass nodules on CT.[25] Centrilobular nodules, ground-glass opacities, smooth thickening of the interlobular septa, enlarged mediastinal lymph nodes, and pleural effusions can be seen in pulmonary veno-occlusive disease (PVOD). [2627] Extensive and larger ground-glass opacities may support the diagnosis of pulmonary capillary hemangiomatosis (PCH). [28] The presence of esophageal dilation may hint to limited scleroderma as the cause of PAH.…”

Section: Determining Etiology Of Pulmonary Hypertensionmentioning

confidence: 99%

A review of imaging modalities in pulmonary hypertension

2017

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Pulmonary hypertension (PH) is defined as resting mean pulmonary artery pressure ≥25 mmHg measured by right heart catheterization. PH is a progressive, life-threatening disease with a variety of etiologies. Swift and accurate diagnosis of PH and appropriate classification in etiologic group will allow for earlier treatment and improved outcomes. A number of imaging tools are utilized in the evaluation of PH, such as chest X-ray, computed tomography (CT), ventilation/perfusion (V/Q) scan, and cardiac magnetic resonance imaging. Newer imaging tools such as dual-energy CT and single-photon emission computed tomography/computed tomography V/Q scanning have also emerged; however, their place in the diagnostic evaluation of PH remains to be determined. In general, each imaging technique provides incremental information, with varying degrees of sensitivity and specificity, which helps suspect the presence and identify the etiology of PH. The present study aims to provide a comprehensive review of the utility, advantages, and shortcomings of the imaging modalities that may be used to evaluate patients with PH.

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Section: Determining Etiology Of Pulmonary Hypertensionmentioning

confidence: 99%

A review of imaging modalities in pulmonary hypertension

2017

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“…A definitive diagnosis of PVOD necessitates surgical lung biopsy, but patients with PVOD often present with advanced disease and surgical lung biopsy is contra-indicated, as it is invasive and at high risk for bleeding, pneumothorax, worsening of respiratory distress, and death [8]. However, high-resolution chest CT scan can help in differential diagnosis, as reported in recent articles [6,11,14]. In consideration of the high negative predictive value of CT scan, the absence of septal thickening and of centrilobular ground-glass opacities excludes the diagnosis of PVOD in the reported case.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary hypertension nosography: are all patients classifiable?

et al. 2017

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A 73-year-old never smoking woman was admitted for exertional dyspnoea to the Respiratory Medicine Section of our hospital in June 2014. The patient's past clinical history revealed systemic arterial hypertension, persistent atrial fibrillation, non-insulin dependent diabetes, hypothyroidism, and hypercholesterolemia. She was taking in treatment with acenocoumarol and metformin. The patient had progressive exercise dyspnoea (NYHA class II) and ankle swelling since 2011. She had been diagnosed with interstitial lung disease with pulmonary hypertension (PAPs of 60 mmHg by transthoracic echocardiography) and hypoxemic respiratory insufficiency. She was referred to our hospital following further worsening of dyspnoea and reduction in exercise tolerance despite long-term oxygen therapy (1 L/min). At admission, she had dyspnoea on minor activities (modified Medical Research CouncilmMRC = 3, NYHA class III), cyanosis, increased respiratory rate (22 breaths/min), and ankle swelling. She had systemic pressure at lower limits of normality (105/ 65 mmHg) and a BMI of 28 (158 cm, 71 kg). At physical examination, fine crackles were audible at both lung bases. She had low (54 mmHg) arterial oxygen tension in oxygen therapy with 1 L/min with CO 2 tension of 50 mmHg, in a framework of compensated respiratory acidosis (HCO 3 -33 mmHg). No alterations of serum electrolytes were found. We got sufficient correction of hypoxia (PaO 2 63 mmHg) by increasing flow oxygen support at 3 L/min with a modest increase of hypercapnia (PaCO 2 54 mmHg). The chest radiograph showed increased cardiac size, bulging of the second arch on the left mediastinal border compatible with enlargement of the pulmonary artery common trunk (Fig. 1). No signs of pulmonary congestion were observed. The electrocardiogram showed atrial fibrillation with average ventricular rate of 77 beats per minute, intraventricular conduction delay, and right axial deviation. Transthoracic echocardiography showed severe tricuspidal regurgitation with TAPSE (tricuspid annular plane systolic excursion) of 15 mm, PAPs of 70 mmHg, right and left atrial enlargement, interventricular septum paradoxical movement, inferior vena cava dilatation with no change on inspiration, mild pericardial effusion, and normal size and wall thickness of the left ventricle, without alteration on the segmental kinesis. Cardiac ejection fraction was preserved (61%). No diastolic relaxation abnormalities were detected. E/A ratio [early transmitral flow (E) and the late flow with atrial contraction (A)] was 0.8 and the ratio E/e 0 [early filling velocity on transmitral Doppler (E) with the early relaxation velocity on tissue Doppler (e 0 )] was 7. Only mild mitral regurgitation was described. Calcification of the cusps of the aortic valve with normal opening was described. Aortic valve peak gradient was 22 mmHg.We decided to treat the patient with furosemide 20 mg iv TID, oxygen therapy (3 L/min) with a partial clinical

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“…Differentiating PVOD from PAH based on clinical observation alone is generally unfeasible because both conditions cause overlapping nonspecific symptoms of dyspnoea, exercise limitation, fatigue and syncope [26,28]. Instead, as in this patient, the diagnosis of PVOD can be established with high probability using a combined approach of clinical suspicion, physical examination, RHC, pulmonary function tests, bronchoscopy with bronchoalveolar lavage, and radiological findings [25,26,34]. Preferred tests for diagnosing PVOD are HRCT and bronchoalveolar lavage along with assessment of partial pressure of oxygen and DLCO [25,35,36], all of which were used in the diagnostic work-up for this patient case.…”

Section: Commentarymentioning

confidence: 98%

“…Preferred tests for diagnosing PVOD are HRCT and bronchoalveolar lavage along with assessment of partial pressure of oxygen and DLCO [25,35,36], all of which were used in the diagnostic work-up for this patient case. HRCT, in particular, is an important diagnostic modality that differentiates PVOD from IPAH with high sensitivity and specificity based on the presence of a triad of ground-glass opacities (centrilobular pattern, thickened interlobular septa and mediastinal lymphadenopathy) in PVOD [25,34]. Bronchoalveolar lavage may be employed to detect signs of haemosiderin-laden macrophages and occult alveolar haemorrhage [25].…”

Section: Commentarymentioning

confidence: 99%

Challenges in pulmonary hypertension: managing the unexpected

Olsson

Palazzini

2015

Eur Respir Rev

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The diverse challenges associated with diagnosis and management of patients with pulmonary hypertension are illustrated in this case-based review. Case 1 describes a patient diagnosed with pulmonary arterial hypertension (PAH) with right heart failure and active systemic lupus erythematosus who was effectively treated with an up-front triple combination of PAH therapies and immunosuppressive therapy. In case 2, a diagnosis of pulmonary veno-occlusive disease was reached after a combined approach of clinical suspicion, physical examination, and invasive and noninvasive tests. Cautious PAH therapy and high-dose diuretics provided clinical benefit in this patient and served as a bridge to lung transplantation. These cases highlight the need for ongoing follow-up of patients with PAH, comprising frequent assessment of treatment success and continued diagnostic evaluation.

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Pulmonary veno-occlusive disease: the role of CT

Abstract: Chest CT can be considered a screening test in the assessment of patients with PAH of unknown aetiology, and the radiologist can help the clinician to identify patients with CT findings that make PVOD highly probable.

Cited by 25 publications

References 25 publications

A review of imaging modalities in pulmonary hypertension

A review of imaging modalities in pulmonary hypertension

Pulmonary hypertension nosography: are all patients classifiable?

Challenges in pulmonary hypertension: managing the unexpected

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