How to optimize your set-up for a VATS right upper lobectomy

2021 ◽  
Keyword(s):  
Pleural Effusion ◽  
Pulmonary Artery ◽  
Lung Adenocarcinoma ◽  
Histological Analysis ◽  
Lobe Bronchus ◽  
Superior Pulmonary Vein ◽  
Primary Lung Adenocarcinoma ◽  
Set Up ◽  
The Right ◽  
Intercostal Block

A 77-year-old woman with multiple ground-glass opacities, the largest of which measured 21 mm, has a biopsy-proven primary lung adenocarcinoma in her right upper lobe. We performed a 3-port right-sided VATS using the Copenhagen approach. There was no pleural effusion or evidence of pleural metastatic spread. A tumor was identified in the upper lobe. The surrounding lung tissue appeared normal. We performed a multilevel intercostal block using 0.25% levobupivacaine. The inferior pulmonary ligament was divided. The superior pulmonary vein and 2 branches of the pulmonary artery to the right upper lobe were dissected, encircled, and divided using tan reloads of the Endo GIA stapler. The right upper lobe bronchus was dissected, encircled, and divided in a similar fashion using a purple reload of the Endo GIA stapler following a successful test inflation of the lower and middle lobes. The horizontal fissure was completed with further firings of the stapler. Lymph nodes from stations 2, 4, 7, 8, 9, 10, and 11 were sampled and sent separately for histological analysis. There was no parenchymal or stump leak to 20 cm H20 on the test inflation. Hemostasis and pneumostasis were checked and ensured. A single 24 Fr drain was placed in the apex. Hemostasis was complete. The incision was closed in layers.

scholarly journals Localized malignant pleural mesothelioma arising in the interlobar fissure: a unique surgical case masquerading clinicopathologically as primary lung adenocarcinoma

2019 ◽  
Vol 7 ◽  
pp. 2050313X1882480 ◽  
Author(s):  
Xin Guo ◽  
Jiro Watanabe ◽  
Kenji Takahashi ◽  
Tatsuro Hayashi ◽  
Nozomu Kurose ◽  
...  
Keyword(s):  
Lymph Node ◽  
Pulmonary Artery ◽  
Lung Adenocarcinoma ◽  
Malignant Pleural Mesothelioma ◽  
Lower Lobe ◽  
Pleural Mesothelioma ◽  
Hilar Lymph Node ◽  
Primary Lung Adenocarcinoma ◽  
The Right ◽  
Localized Malignant Pleural Mesothelioma

An 80-year-old male with previous workplace exposure to asbestos presented with a history of an increase in the pulmonary-to-hilar mass, measuring more than 50 mm in diameter, likely in the right lower lobe. We first interpreted it as suspicious of primary lung adenocarcinoma with direct invasion to the right hilar lymph node. A right middle and lower lobectomy with partial resection of upper lobe was performed, and gross examination showed a hilar tumor lesion, involving the middle/lower lobe to hilar lymph node and looking whitish to yellow-grayish, partly adjacent to the right pulmonary artery. On microscopic examination, the tumor was located on the extrapulmonary, interlobar pleural fissure, predominantly composed of a proliferation of atypical epithelioid cells, often arranged in an irregular and fused tubular growth pattern with an involvement of pulmonary artery. Immunohistochemically, these atypical cells are positive for several mesothelial markers, including calretinin, cytokeratin 5/6, and WT-1, whereas negative for thyroid transcription factor 1. Furthermore, p16 deletions were specifically detected by fluorescence in situ hybridization, and electron microscopy showed numerous, significantly elongated microvilli. Taken together, we finally made a diagnosis of localized malignant pleural mesothelioma, epithelioid-type, arising in the right interlobar fissure between lower and middle lobes. We should be aware that, owing to its characteristic features, clinicians and pathologists might be able to raise interlobar fissure localized malignant pleural mesothelioma as one of the differential diagnoses, based on careful clinicopathological examinations.

Role of monocyte chemoattractant protein-1, tumor necrosis factor-α and interleukin-6 in the control of malignant pleural effusion and survival in patients with primary lung adenocarcinoma

2012 ◽  
Vol 27 (2) ◽  
pp. 118-124 ◽  
Author(s):  
Qian Qian ◽  
Wen-Kui Sun ◽  
Ping Zhan ◽  
Yu Zhang ◽  
Yong Song ◽  
...  
Keyword(s):  
Pleural Effusion ◽  
Lung Adenocarcinoma ◽  
Malignant Pleural Effusion ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Primary Lung Adenocarcinoma ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

This study aimed at assessing the role of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the control of pleural effusion (PE) and survival in patients with primary lung adenocarcinoma. The concentrations of the 3 cytokines were measured in PE from 79 lung adenocarcinoma patients with malignant pleural effusion (MPE) and 23 patients with tuberculosis. Data were correlated with the efficacy of MPE control and patient survival. The level of MCP-1 in PE was significantly higher in patients with lung adenocarcinoma than those with tuberculosis. By contrast, the levels of TNF-α and IL-6 were significantly lower in patients with lung adenocarcinoma than those with tuberculosis. An MCP-1 level greater than 3,187 pg/mL (which was used as a cutoff point) indicated failure to control MPE (odds ratio [OR]=2.82, 95% confidence interval [CI]=1.02–7.82, p=0.04). In multivariate analysis, MCP-1 was confirmed as an independent prognostic factor for progression-free survival (hazard ratio [HR]=2.02, 95% CI=1.24–3.30, p=0.01). The level of MCP-1 in PE appears to be a reliable surrogate marker for evaluating the therapeutic efficacy in the control of MPE and predicting survival in lung adenocarcinoma patients with MPE.

Left atrial hypertension causes pleural effusion formation in unanesthetized sheep

1989 ◽  
Vol 257 (2) ◽  
pp. H690-H692 ◽  
Author(s):  
S. Allen ◽  
J. Gabel ◽  
R. Drake
Keyword(s):  
Pleural Effusion ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Left Atrium ◽  
Left Atrial ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Recovery Period ◽  
Pleural Effusions ◽  
The Right

We studied the effect of left atrial pressure (LAP) elevation on the formation of pleural effusion in unanesthetized sheep. We prepared the animals by placing catheters in the left atrium, pulmonary artery, femoral artery, and vein. We also placed a balloon catheter in the left atrium. After a recovery period of at least 1 wk, we measured LAP, pulmonary artery pressure (PAP), systemic arterial pressure, systemic venous pressure, cardiac output, plasma protein concentration, and plasma colloid osmotic pressure (pi c). We calculated capillary pressure (Pc) as 0.5(PAP - LAP). We then elevated LAP such that Pc-pi c was between -10 and 19.5 mmHg for 6-24 h. At the end of the experiment, we killed the sheep and measured the volume and protein concentration of the right pleural effusion. We also determined the extravascular fluid to blood free dry weight of the right lung. We found that pleural effusions and pulmonary edema formed when Pc-pi c greater than 5 mmHg. We also found that the pleural effusion volume correlated with the amount of pulmonary edema. Our data show that elevated LAP may cause pleural effusions, but only after pulmonary edema has developed.

scholarly journals A Case of Lung Adenocarcinoma with Marked Improvement of Pulmonary Lymphangitic Carcinomatosis by Adding Bevacizumab to Cisplatin and Pemetrexed

2017 ◽  
Vol 10 (3) ◽  
pp. 1065-1069 ◽  
Author(s):  
Maika Natsume ◽  
Takeshi Honda ◽  
Terunobu Haruyama ◽  
Masashi Ishihara ◽  
Yoko Fukasawa ◽  
...  
Keyword(s):  
Pleural Effusion ◽  
Lung Adenocarcinoma ◽  
Marked Improvement ◽  
Pathological Condition ◽  
Progression Free Survival ◽  
Poor Response ◽  
Vegf Receptor ◽  
Response To Chemotherapy ◽  
The Right ◽  
Lymphangitic Carcinomatosis

A 40-year-old man with a diagnosis of lung adenocarcinoma (cT4N3M1c, stage IVB) experienced worsening of lymphangitic carcinomatosis in the right lung and right pleural effusion after receiving 1 cycle of first-line chemotherapy consisting of cisplatin and pemetrexed. Bevacizumab was thus added from the second cycle of the cisplatin-pemetrexed regimen, leading to a marked improvement in pulmonary lymphangitic carcinomatosis and a decrease in pleural effusion. Subsequently, maintenance therapy consisting of pemetrexed and bevacizumab was continued, successfully leading to long-term progression-free survival. Generally, pulmonary lymphangitic carcinomatosis shows poor prognosis because of poor response to chemotherapy. However, recent studies have been elucidating the role of the vascular endothelial growth factor A (VEGF-A)/VEGF receptor-2 pathway in pulmonary lymphangitic carcinomatosis. Therefore, bevacizumab is expected to be beneficial in the treatment of this pathological condition.

scholarly journals An aberrant mediastinal medial basal segmental pulmonary artery (A7a) in a patient with lung cancer: a case report

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yoshiaki Takase ◽  
Hiroyoshi Tsubochi ◽  
Ei Yamaki ◽  
Osamu Kawashima
Keyword(s):  
Lung Cancer ◽  
Colon Cancer ◽  
Pulmonary Artery ◽  
Main Pulmonary Artery ◽  
Lower Lobe ◽  
Middle Lobe ◽  
Accurate Information ◽  
3D Ct ◽  
Lobe Bronchus ◽  
The Right

Abstract Background Mediastinal branching of the A7a from the right main pulmonary artery (PA) is extremely rare. Herein, we report a patient with an aberrant mediastinal A7a who underwent right basal segmentectomy for lung cancer. Case presentation A 73-year-old man was referred to our department for a right lower lobe nodule measuring 18 mm in diameter on computed tomography (CT). Three-dimensional (3D) CT revealed mediastinal A7a branching from the right main PA. As the patient had undergone colectomy for advanced ascending colon cancer, the nodule was suspected to be a metastasis from the colon primary, and thus, basal segmentectomy of the right lung was performed. Intraoperatively, the A7a was observed behind the V4+5 and middle lobe bronchus. The pathological diagnosis was combined small cell carcinoma with an adenocarcinoma component (p-T1cN0M0, stage IA3). The patient subsequently received adjuvant chemotherapy for colon cancer. At 1-year postoperative follow-up, there was no evidence of disease. Conclusion This is the first report describing an aberrant mediastinal A7a branching from the right main PA. It is important to obtain accurate information about variations of the PA using 3D-CT for safe anatomical pulmonary resection.

Differential sympathetic regulation of automatic, conductile, and contractile tissue in dog heart

1988 ◽  
Vol 255 (5) ◽  
pp. H1050-H1059 ◽  
Author(s):  
J. L. Ardell ◽  
W. C. Randall ◽  
W. J. Cannon ◽  
D. C. Schmacht ◽  
E. Tasdemiroglu
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vein ◽  
Contractile Force ◽  
Right Atrial ◽  
Canine Heart ◽  
Superior Pulmonary Vein ◽  
Right Pulmonary Artery ◽  
The Common ◽  
The Right ◽  
Contractile Tissue

Sympathetic pathways mediating chronotropic, dromotropic, and inotropic responses during ansae subclavia stimulation were determined by sequential dissection around major cardiac vessels. Right sympathetic (RS) projections influencing ventricular contractile force converge at the common pulmonary artery and within the pulmonary artery nerves (PAN). RS projections influencing left atrial contractile force course within the PANs. RS pathways to pacemaker and right atrial contractile tissue were localized between the superior vena cava and ascending aorta. RS projections influencing conductile tissue converge between the common pulmonary artery and proximal right pulmonary artery. Left sympathetic (LS) projections to ventricular contractile tissue were localized at the common pulmonary artery, within the PANs, and in the ventral lateral cardiac nerve (VLCN). LS pathways influencing heart rate and conductile tissue were localized at the left pulmonary artery and coursing between the right pulmonary artery and left superior pulmonary vein. LS projections to atrial contractile tissue were localized within the PANs and coursing between the right pulmonary artery and left superior pulmonary vein. We conclude that there are parallel, yet distinct, projections of sympathetic efferents to automatic, conductile, and contractile tissue of the canine heart.

Partial anomalous left pulmonary artery: report of two cases and review of literature

2014 ◽  
Vol 25 (5) ◽  
pp. 1012-1014 ◽  
Author(s):  
Supratim Sen ◽  
David S. Winlaw ◽  
Gary F. Sholler
Keyword(s):  
Pulmonary Artery ◽  
Lower Lobe ◽  
Left Pulmonary Artery ◽  
Primary Diagnosis ◽  
Left Lower Lobe ◽  
Lobe Bronchus ◽  
First Child ◽  
Right Pulmonary Artery ◽  
The Right ◽  
Aortic Arch Hypoplasia

AbstractWe describe two cases of anomalous origin of the left lower-lobe pulmonary artery from the right pulmonary artery. The primary diagnosis was mitral atresia, hypoplastic left ventricle, aortic arch hypoplasia in the first child, and tetralogy of Fallot in the second. In both cases, the pulmonary trunk gave rise to a left pulmonary artery in the normal position. In addition, a second branch of the left pulmonary artery arose from the right pulmonary artery, and passed posterior and inferior to the left main or upper-lobe bronchus to supply the left lower lobe. In this review, we compare our findings with previously reported examples of this extremely rare cardiac malformation, and discuss possible embryological explanations for the lesion.

Tracheostenosis and Bronchial Abnormalities Associated with Pulmonary Artery Sling

1976 ◽  
Vol 85 (5) ◽  
pp. 582-590 ◽  
Author(s):  
Seymour R. Cohen ◽  
Benjamin H. Landing
Keyword(s):  
Pulmonary Artery ◽  
Tracheal Stenosis ◽  
Main Bronchus ◽  
Left Pulmonary Artery ◽  
Surgical Correction ◽  
Left Main ◽  
Pulmonary Artery Sling ◽  
Lobe Bronchus ◽  
Normal Number ◽  
The Right

Three patients with aberrant left pulmonary artery (sling artery) are reported to illustrate associated tracheobronchial abnormalities. The clinical picture was that of severe episodic or progressive respiratory distress without dysphagia in early infancy. Striking narrowing of the trachea by complete “ring cartilages,” unrelated to compression by the abnormal pulmonary artery, was present. Tracheotomy and intubation failed to relieve the obstruction. In one patient the bronchi and bronchial segmentation pattern were normal, but in the other two patients, bronchial abnormalities included wide irregular cartilages in the main bronchi, forming more complete rings than is normal. In both, the right main bronchus was relatively longer than normal, and the bronchus intermedius showed poor cartilage ring formation and was relatively short compared to the main bronchus. This discrepancy did not appear to be due to distal displacement of the right upper lobe bronchus. In these two patients the left main bronchus was relatively short and wide with reduced number of cartilage rings (five-six vs usual normal number of nine), so that the right and left main bronchi were almost of equal length. However, the branch patterns of the lobar bronchi were within normal range. Bronchoscopy seems essential to demonstrate such ring tracheal cartilages (absence of the pars membranacea of the trachea), which when found should alert the examiner to the possible presence of an abnormal left pulmonary artery. Since surgical correction of tracheal stenosis of this type is not possible at present, the ultimate prognosis of patients with sling artery may depend more on the severity of the tracheal anomaly rather than on success of surgical correction of the abnormal left pulmonary arterial course. Although aberrant (sling) left pulmonary artery can occur in patients without respiratory tract symptoms, tracheal stenosis due to ring tracheal cartilages occurs in a significant fraction of patients with this arterial anomaly. Bronchoscopic study of the trachea, and possibly air or contrast bronchography of right and left main bronchi, can be of aid in diagnosis of this complex.

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