(Chest 1994; 106:275-77) A 49-year-old man was admitted with 3 weeks of progressively stiff dyspnea.


(Chest 1994; 106:275-77)

A 49-year-old man was admitted with 3 weeks of progressively stiff dyspnea. The patient had familial polyposis coli for which he underwent total colectomy with ileorectal anastomosis 15 years previously. pair years before admission, he quick in emergenciesed with iron deficiency anemia fit to adenocarcinoma confined to the rectum and had an abdominal perineal resection.

Physical Examination

Vital signs: temperature, 37[degrees]C; beating [i]or[/i] throbbing of an artery 108/min; respirations, 36/min; and BP 138/92 mm Hg General: rigorous respiratory distress with cyanosis. Chest: normal breath wholes Cardiac: prominent [P.sub.2]. No jugular venous distention. Abdomen: functioning ileostomy. No hepatomegaly or HJ ebb Extremities: cyanotic nail beds. No peripheral edema. Neurologic: normal.

Laboratory Findings



Hemoglobin, 187 g/dl; WBC 16800/[mmsup3] without left shift; electrolyte liver enzyme BUN creatinine, normal. ABG (room air): pH 751; [Pcosub2] 23 mm Hg; [Posub2] 39 mm Hg Chest radiograph: normal. ECG: normal axis, no acute changes. Doppler venous contemplation of both lower extremities: normal. Echocardiogram: dilated right ventricle with hypokinesis, dilated right atrium with tricuspid regurgitation, estimated pulmonary artery systolic constraining force 60 mm Hg. Ventilation-perfusion lung scan: indeterminate for pulmonary thromboembolism (Fig 1) Pulmonary angiogram: "pruning" of vasculature bilaterally without evidence of intraluminal filling blemish measured pulmonary artery pressure, 77/40 mm Hg

[CHART OMITTED]

Hospital Course

hard refractory hypoxemia persisted, and the patient died 48 h after admission after developing intractable hypotension.

What is the probable diagnosis?

Answer: Multiple microscopic tumor emboli to the lung with hypoxic respiratory failure and cor pulmonale.

Pulmonary tumor emboli happen when aggregates of tumor small rooms enter the pulmonary vasculature. Although the pathway for entrance into the pulmonary vasculature is uncertain, emboli are pondering to arise from hepatic vein invasion from liver metastases, venous invasion at the site of the primary tumor, or transit of malignant confined apartments into the venous circulation by means of the thoracic duct. Once in the pulmonary vascular bed, tumor emboli may hut in large pulmonary arteries or in the smaller branches of the pulmonary arterial tree if they are microscopic in size. Histologic sections demonstrate clusters of tumor solitary abode; squalids in association with platelet-fibrin thrombi that may initiate obliterative arteritis. Because chiefly tumor emboli either degenerate or lie dormant within the pulmonary circulation, they are not considered pure metastases.

Tumor embolization as a way of spread of cancer to the lung is singular Tumor emboli were found in solitary 26 of 1,085 (2.4 percent) autopsies of solid malignant neoplasms; there were no cases of tumor emboli to major pulmonary canals In a selected autopsy series of 366 patients who died with breast cancer, gastric carcinoma, hypernephroma, hepatoma, and choriocarcinoma, tumor emboli were lay the foundation of in 26 percent; most tumor emboli from all reported tumors were microscopic. Large tumor emboli, although queer resulted only from hepatoma and choriocarcinoma.

Although tumor emboli may be the initial manifestation of an underlying malignancy, they more commonly come into view in the setting of previously established malignant disease. Of 26 cases of tumor emboli build at autopsy in one series, solely 4 did not have malignancy suspected prior to death.

A wide variety of neoplasms give rise to tumor emboli. In united series of 164 patients, hepatoma was the chiefly frequent (29 percent), followed by the agency of carcinoma of the breast (18 percent) kidney (18 percent) and stomach (9 percent) Carcinoma of the prostate, choriocarcinoma, and multiple other primary sites were reported les frequently

The diagnosis of multiple tumor emboli ofttimes is not considered as the clinical presentation and laboratory data are nonspecific. Dyspnea is the greatest in quantity common symptom, but cough, pleuritic chest pain, and hemoptysis also be met with Autopsy series have also reported that tumor emboli may be silent and discovered as incidental findings in 50 to 70 percent of cases. When the lung are involved according to widespread emboli, as in the not absent patient, respiratory failure, pulmonary hypertension, and cor pulmonale can end Acute pulmonary thromboemboli should always be considered in the differential diagnosis of unexplained respiratory failure, especially in a patient with known malignancy.

Imaging modalities can remind of the diagnosis in patients who not past nor future with acute or subacute dyspnea, hypoxemia, and normal lung fields forward chest radiograph. In cases of microscopic tumor emboli, a ventilation-perfusion lung scan typically exhibits multiple, bilateral, mismatched subsegmental perfusion imperfections Pulmonary angiography fails to present to view intraluminal filling defects, thus excluding acute thromboemboli. However, if large tumor emboli are ready the pulmonary angiogram will point out to filling defects in large utensils similar to those seen in thromboemboli.

...