Urgencias en cuidado paliativo oncológico / Emergencies in palliative oncological care

El paciente oncológico de cuidados paliativos puede presentar una variedad importante de condiciones clínicas que producen sufrimiento y disminución en la calidad de vida; esto se presenta como un reto para el clínico en la identificación y correcto abordaje de los pacientes. El dolor se ha considerado por años como el síntoma cardinal a tratar en el paciente oncológico, donde se deben considerar sus condicionantes fisiopatológicos, la farmacología de las intervenciones, los posibles efectos secundarios y los condicionantes familiares, sociales y personales del dolor, pero a pesar de su relevancia, no es el único síntoma, estando acompañado de un abanico de patologías, como las afectaciones gastrointestinales, pulmonares, vasculares, hematológicas y neurológicas, que favorecen la pérdida de capacidad del paciente y, en muchas ocasiones, la muerte. Se realizó una revisión actualizada en bases de datos como EMBASE, PUBMED, SCIELO, además de la revisión de guías de asociaciones internacionales con el objetivo de acercar a todos los médicos, sin distinguir su especialidad o área de trabajo, al abordaje y manejo del paciente oncológico en cuidado paliativo, favoreciendo la sensibilización con estas patologías y la importancia en el curso de vida de los pacientes.

The palliative care cancer patient can present a significant variety of clinical conditions that produce suffering and a decrease in the quality of life. This is a challenge for the clinician in the identification and correct approach of patients. Pain has been considered for years as the cardinal symptom to be treated in cancer patients, where its pathophysiological factors, the pharmacology of the interventions, possible side effects and the family, social and personal conditions of pain must be considered, but despite its relevance is not the onset of symptoms and is accompanied by a range of pathologies such as gastrointestinal, pulmonary, vascular, hematological and neurological affectations that favor the loss of capacity of the patient and in many cases death. An updated review was carried out in databases such as EMBASE, PUBMED, SCIELO in addition to the revision of guides from international associations with the aim of bringing all doctors without distinguishing their specialty or area of work to the approach and management of cancer patients in palliative care favoring awareness of these pathologies and their importance in the life course of patients.

Obstrucción adquirida de vena cava superior derecha en el postoperatorio de cardiopatía congénita. Dos formas de presentación clínica / Obstruction of the superior vena cava in the congenital heart disease postoperative. Two different clinical presentations

Resumen: Se presentan dos casos clínicos de obstrucción de vena cava superior derecha en el postoperatorio alejado de cardiopatía congénita (comunicación interauricular tipo seno venoso asociada a drenaje venoso pulmonar anómalo parcial). Se analizan formas de presentación clínica, procedimiento diagnostico, resolución terapéutica y evolución.

Summary: The study presents the case of two patients who underwent the surgical repair of a congenital heart disease (atrial septal defect and partial anomalous venous drainage), developed in the long term postoperative course, obstruction of the superior vena cava. Clinical features, diagnosis and treatment and long-term follow up are included in this report.

Conducta en el síndrome de vena cava superior (SVCS) / Management in superior vena cava syndrome

Objetivos: Mostrar la conducta realizada en este síndrome. Material y Métodos: Serie retrospectiva de 5 casos tratados entre el 1 de abril de 1995 y el 31 de marzo de 2013. Diagnóstico por imágenes y toma de biopsia con tratamiento específico posterior. Resultados: Todos se debieron a causas tumorales: 2 timomas (uno irresecable), 1 linfoma Hodgkin, 1 leiomiosarcoma de vena cava y 1 caso de cáncer pulmonar a pequeñas células. Fallecieron por progresión de enfermedad 2 casos, 2 están libres de enfermedad a 12 y 11 meses de tratamiento y 1 enfermo se perdió en el seguimiento. Conclusiones: Se define la necesidad de seguir un algoritmo que determine los pasos a seguir ante la presencia de este síndrome.

Objectives: Management in this syndrome. Material and Methods: Retrospective series of 5 cases treated between April 1, 1995 to March 31, 2013. Diagnostic imaging and taking biopsy with subsequent specific treatment. Results: All patients were due to tumor causes: 2 thymomas (one unresectable), 1 lymphoma Hodgkin, 1 Leiomyosarcoma of vena cava and 1 case of small cell lung cancer. Died of disease progression 2 cases, 2 are free of disease to 12 and 11 months of treatment and 1 patient was lost to follow-up. Conclusions: The need to follow an algorithm which determines the steps to follow in the presence of this syndrome is defined.

Síndrome de vena cava superior: forma inicial de presentacion en enfermedades neoplásicas / [Superior Cava Venous syndrome as presentation of neoplasic disease].

Superior Cava Venous Syndrome (SVCS) encompasses a constellation of signs and symptoms resulting from partial or complete obstruction of blood flow through the superior vena cava (SVC) to the right atrium. Thrombosis can be caused by intrinsic (primary) or extrinsic compression (with or without secondary thrombosis). The causes of SVCS can be grouped according to their etiology in non-neoplastic and neoplastic. The causes malignant correspond to 65-90

of them, thrombosis and nonmalignant conditions are another causes. The presentation may be acute, clinically characterized by dyspnea and a characteristic triad (facial, neck and arms edema, cyanosis and collateral circulation). Early detection improves prognosis and is based on clinical data and imaging studies. We describe 8 cases where the SVCS was the first manifestation of neoplastic diseases. Patients were predominantly of middle-aged, male, without association with consumption of tobacco and lymphoma was most frequent diagnosis.

Superior vena cava syndrome due to metastasis from urothelial cancer: a case report and literature review

Superior vena cava [SVC] syndrome is caused by compression or obstruction of the SVC. We report here in a case of SVC syndrome due to lymph node metastasis from urothelial cancer to the mediastinum and lung. The origin of metastasis was determined by computed tomography [CT]-guided biopsy of metastases. After radiotherapy to the mediastinum with glucocorticoid failed, anticancer pharmacotherapy including paclitaxel, gemicitabine, and cisplatin proved effective and SVC syndrome resolved. But patient died from cerebral bleeding from newer brain metastases 10 months later

Successful Treatment of Malignant Superior Vena Cava Syndrome Using a Stent-Graft

We report successful outcomes after endovascular placement of a stent graft in a 74- and a 77-year-old men, both of whom had malignant superior vena cava syndrome caused by squamous cell carcinoma. In each patient, successful palliation of the malignant superior vena cava syndrome was achieved by placement of a stent graft. No procedure-related complications were observed. The patients were asymptomatic until their deaths, seven and 14 months after stent graft placement, respectively.

Primary cardiac diffuse large B-cell lymphoma with activated B-cell-like phenotype.

Primary cardiac lymphoma (PCL) is a rare and fatal disorder. It may often mimic other common cardiac tumors like cardiac myxoma because of similarities in the clinical presentation. We report a case of PCL of diffuse large B-cell type, in a 38-year-old, immunocompetent male who presented with superior vena cava syndrome that was excised as a myxoma. Histology revealed a large cell population diffusely and strongly expressing CD45, CD20, MUM1/IRF4 and FOXP1 hinting at an activated B-cell (ABC)-like phenotype. After four cycles of Rituximab with CHOP (cyclophosphamide, hydroxydaunorubicin, Oncovin, and prednisolone) the tumor regressed completely but the patient had a relapse and subsequently succumbed to the disease confirming the aggressive nature. The aggressive behavior of PCL may be possibly linked to its ABC-like origin.

Benign superior mediastinal syndrome due to intrathoracic tuberculosis in a child-association with endobronchial tuberculosis.

A 5-year-old boy presented with fever, cough, breathlessness and facial swelling. He was pale with distended veins over neck and chest, cervical and axillary lymphadenopathy and bilateral expiratory wheeze. Chest radiographs showed superior mediastinal widening. A computed tomography scan of the chest revealed mediastinal lymph nodes compressing superior vena cava and trachea. Bronchoscopy revealed nodular lesions in trachea and bronchi and compression of trachea. Broncho-alveolar lavage revealed acid fast bacilli. Diagnosis of superior mediastinal syndrome (SMS) secondary to tuberculosis was made and child was treated with antitubercular treatment along with oral prednisolone with good response.

Percutaneous extraction of an infected permanent pacemaker in association with superior vena cava obstruction

The procedure of lead removal has recently matured into a definable, teachable art with its own specific tools and techniques. It is now time to recognize and formalize the practice of lead removal according to the current methods of medicine and the health care industry. In this article we report the first case in the United Arab Emirates of infected pacemaker extraction after 9 years of implantation of passive fixation lead for a VVI pacemaker using a locking stylet and countertraction technique with associated superior vena cava obstruction, which had been dilated using the balloon technique with deployment of a stent

Superior Vena Cava Syndrome Caused by Encircling Soft Tissue

Superior vena cava syndrome can occur from benign conditions that might not alter life expectancy. Here we present a case of a superior vena cava (SVC) obstruction caused by soft tissue encircling the SVC, which was strongly suspected of being an unusual focal type of fibrosing mediastinitis. A 39-year-old man with no prior medical history presented with a four-week history of facial plethora, headache and dilated veins of the neck with a dark purple color change on the anterior chest wall. Radiology examinations, including venography, and computed tomography with a 3-dimensional volume-rendering image of the chest, had revealed severe narrowing of the SVC due to tiny encircling soft tissue and collateral vessels. A total occlusion of the SVC occurred as a result of a thrombus that developed within 1 day after the diagnostic SVC angiogram. The patient underwent stent deployment three days after the administration of thrombolytic therapy.

Marcapasso bi-atrial epicárdico subxifóide na obstrução da veia cava superior / Bi-atrial subxiphoid epicardial pacemaker in superior vena cava syndrome / Bi-atrial subxiphoid epicardial pacemaker in superior vena cava syndrome

Um paciente portador de marcapasso definitivo bi-atrial-ventricular por fibrilação atrial paroxística e bradicardia sinusal, em uso crônico de anticoagulante oral, apresentou sinais clínicos da síndrome da veia cava superior. A venografia por subtração digital mostrou obstrução total do tronco braquiocefálico venoso direito e grande dificuldade de fluxo sangüíneo da veia inominada para a veia cava superior. A abordagem terapêutica constou da remoção completa do sistema transvenoso seguida de reimplante do sistema bi-atrial-ventricular por técnica epimiocárdica pela via subxifóide assistida por fluoroscopia.

A patient with a bi-atrial-ventricular permanent pacemaker due to paroxystic atrial fibrillation associated to sinus bradycardia, in chronic use of oral anticoagulant, presented clinical signs of superior vena cava syndrome. Digital subtraction venography showed total obstruction of the right brachiocephalic venous trunk and severe stenosis of the connection of the left trunk to the superior vena cava. The therapeutic approach consisted of complete removal of transvenous system followed by re-implant of the bi-atrial-ventricular system using an epicardial subxiphoid access with fluoroscopic assistance

Mediastinite esclerosante no diagnóstico diferencial de tumores mediastinais / Sclerosing mediastinitis in the differential diagnosis of mediastinal tumors

A mediastinite esclerosante é uma doença rara, caracterizada por tecido fibrótico mediastinal extenso, que mimetiza uma neoplasia devido à compressão ou invasão das estruturas mediastinais. Apresentamos três casos de síndrome de veia cava superior em que se comprovou a mediastinite esclerosante. A fisiopatologia relaciona-se a adenomegalias mediastinais, proliferação de fibroblastos e deposição de colágeno. As principais causas são histoplasmose e tuberculose, doenças prevalentes em nosso meio. O diagnóstico histopatológico geralmente é difícil por métodos pouco invasivos. Necessita-se de exploração cirúrgica para o diagnóstico definitivo e resolução da obstrução das vias aerodigestiva e vascular, uma vez que não há tratamento clínico efetivo para esta afecção.

Trombose espontânea de veia subclávia (Síndrome de Paget-Schroetter) / Deep vein thrombosis on left subclavian (paget-Schroetter Syndrome): a case report

Trombose venosa profunda de membros superiores é relativamente incomum, sendo geralmente decorrente de neoplasia ou uso prolongado de cateter venoso. O epônimo Paget-Schroetter se refere à trombose venosa profunda de membros superiores sem fatores aparentes. É descrito o caso de uma mulher de 34 anos que amanheceu com trombose da veia subclávia esquerda. Foram identifi cados os seguintes fatores desencadeantes: apofi somegalia na sétima vértebra cervical, heterozigose do fator V de Leiden e uma provável alteração na percepção de estímulos internos durante o sono. A paciente foi submetida à trombólise e usou cumarínicos por dois meses. Em dez meses de observação, não houve recrudescimento do quadro

Etiology and outcome of superior vena cava (SVC) obstruction in adults.

Between 1997 and 2002, 107 patients with symptoms of superior vena cava (SVC) obstruction presented at a university hospital in Northeast Thailand. Age averaged 50.7 years (range, 1 to 84). The male to female ratio was 5.7:1. Duration of symptoms before diagnosis was 29.4 days (range, 2 to 240), including facial swelling, cough, and chest discomfort. About 20% of cases developed respiratory failure and 11.2% died shortly after admission. The mean hospital stay was 23.7 days. Anteroposterior and lateral chest radiographs and computed chest tomography helped locate the lesion. Transbronchial biopsy through bronchoscopy, transthoracic needle biopsy under computed tomography, lymph node biopsy, pleural fluid cytology and/or biopsy were used for histopathologic sampling. High levels of alpha-fetoprotein and beta-HCG indicated an anterior mediastinal mass. The most common etiology of SVC obstruction was bronchogenic carcinoma (51.8%), followed by an anterior mediastinal mass (14.5%), lymphoma (13.6%--with an LDH of 262 to 1459 U/l), metastatic cancer (9.1%), and acute lymphoblastic leukemia (1.8%). Benign SVC thrombosis was found in four patients with Behcet's disease or some other idiopathy. Mediastinal fibrosis from melioidosis occurred in three patients, which is rare, has not been previouly reported. Most patients (63.6%) received a combination of radiotherapy and corticosteroid and this helped 55.2% improve.

Ponte espiralada de veia safena no tratamento da síndrome de veia cava superior: relato de caso com seguimento de 15 anos / Spiral saphenous vein graft in the management of superior vena cava syndrome: a case report

A síndrome da veia cava superior é uma condição pouco freqüente causada, na maioria das vezes, por tumores malignos. Uma etiologia incomum e benigna é a fibrose mediastinal idiopática. Os autores relatam o caso de um paciente com síndrome da veia cava superior causada por fibrose mediastinal idiopática. O tratamento inicial foi realizado através de uma ponte atriojugular interna direita com politetrafluoretileno, que ocluiu com recorrência dos sintomas após quatro anos. O paciente foi submetido a novo enxerto atriojugular, desta vez, usando veia safena espirilada. Durante o seguimento de 15 anos, o enxerto permaneceu pérvio, conforme comprovação através de eco-Doppler, e o paciente assintomático.