Klaus Meinhof

We report the first known case of malignant pleural effusion (MPE) as the sole presenting feature of clinically occult primary fallopian tube carcinoma (PFTC). A 57-year-old healthy woman was admitted with dyspnea. Evaluation demonstrated a right pleural effusion, fluid of which was malignant. The immunohistochemical profile, including negative calretinin, favored metastatic adenocarcinoma over mesothelioma but could not identify the primary tumour site. Pleural biopsy was not pursued as it would not have helped localize the primary. Chest, abdomen and pelvic computed tomography (CT) demonstrated only borderline lymphadenopathy in the left para-aortic lymph node chain that was hypermetabolic on positron emission tomography. Ultrasound and CT showed normal adnexal anatomy. These findings, coupled with an elevated serum CA-125, prompted empiric neoadjuvant chemotherapy targeting epithelial ovarian carcinoma (EOC) followed by surgery, which revealed a tiny left PFTC with negative peritoneal washings. Sampled left para-aortic lymph nodes were positive. The pleural effusion resolved after chemotherapy. Malignant pleural disease without peritoneal involvement is more characteristic of PFTC than of EOC, in which MPE is common but almost always accompanies peritoneal carcinomatosis. The extensive lymphatic supply of the fallopian tube promotes distant metastasis of small, seemingly localized tumours. This case is a reminder that the clinician should not be dissuaded from considering carcinoma of Müllerian origin, especially PFTC, as the cause of a MPE even in the face of normal gynecologic imaging. Appropriately broad immunohistochemical staining and careful attention to even minimal lymphadenopathy can be invaluable in pinpointing the primary tumour site in such patients.

A 26-year-old previously healthy woman developed sudden-onset hypoxaemic respiratory failure 3 days post partum. During pregnancy, the patient had displayed haematuria (26–50 red blood cells/high-power field on urine dipstick) and proteinuria (30 mg/dL on urine dipstick), which at the time was not further investigated. The pregnancy and vaginal delivery were otherwise uncomplicated. On the morning of planned discharge from the maternity ward, the patient developed sudden dyspnoea, tachypnoea, tachycardia and severe hypoxaemia (PaO2 of 48 mm Hg on room air) accompanied by 5 mL of bright red haemoptysis. Chest auscultation was normal. ECG showed sinus tachycardia with an S1Q3T3 pattern and urgent bedside echocardiogram showed evidence of right heart strain. Respiratory insufficiency in the peripartum period has many potential causes, including PE, amniotic fluid embolism, pulmonary oedema due to tocolytic therapy and peripartum cardiomyopathy. Venous thromboembolism (VTE) is approximately 80 times more common in the first week post partum when compared with the general population1 and PE is a leading cause of maternal mortality in the developed world (whereas postpartum haemorrhage is the most common cause of death in the developing world2). Haemoptysis in the setting of PE occurs in about 5% of patients, and represents pulmonary infarction.3 Given the acute onset of symptoms and echocardiographic findings, PE is the initial concern for this patient. Unfractionated heparin infusion was started. Shortly thereafter, the patient endorsed worsening dyspnoea and coughed up approximately 100 mL of bright red blood. Her heparin infusion was discontinued, and she was emergently intubated for hypoxaemia. Adequate oxygenation on the mechanical ventilator was difficult to maintain despite frequent endotracheal suctioning, use of high positive end-expiratory pressure and fraction of inspired oxygen (FiO2), initiation of neuromuscular blockade and frequent manual recruitment manoeuvres. Chest X-ray (CXR) showed diffuse, predominantly central opacities (figure 1 …

Figure 1. Computed tomography of the chest on axial cuts (left) and sagittal cuts (right) at 10-week follow-up demonstrates central reticular and ground-glass opacities with sparing of both the perihilar and subpleural regions. A 56-year-old man with hepatitis B virus– associated cirrhosis and advanced hepatocellular carcinoma (HCC) presented with dyspnea. He was on therapy with sorafenib and had undergone radioembolization with yttrium 90 (Y) 5 days prior, which was complicated by a high shunt fraction (45%) resulting in an excessive lung radiation exposure of 55 Gy. A technetium-99m macroaggregated albumin (Tc-MAA) scan 1 week prior had demonstrated only a 22% shunt fraction, which would have resulted in a lung radiation dose of less than 30 Gy, the accepted safety standard. Although the initial chest radiograph was normal, given the patient’s symptoms of dyspnea and high dose of radiation exposure, empiric prednisone was prescribed at a dose of 20 mg daily in hopes of preventing radiation pneumonitis (RP). At 1 month follow-up, computed tomography of the chest was normal. Five weeks later, the patient was admitted with worsening dyspnea, and repeat computed tomography demonstrated bilateral ground-glass opacities with sparing of the perihilar regions and periphery (Figure 1). Bronchoscopy with bronchoalveolar lavage and multiple transbronchial biopsies in the affected region were negative for metastatic disease and did not identify any infectious organisms, including Pneumocystis, on special stains and molecular techniques. Histology showed nonspecific inflammation (Figure 2). Sorafenib was discontinued, and the glucocorticoid dose was increased to intravenous methylprednisolone at 60mg daily (equivalent to 1 mg/kg/d) for presumed RP. The patient continued to deteriorate despite therapy, Figure 2. Transbronchial biopsy yielded a 0.43 0.23 0.1–cm sample of alveolar tissue with anthracotic pigment deposition and minor inflammation with no granulomas, malignancy, or microorganisms seen. Cultures were negative (hematoxylin and eosin, 3100).