A 50–year–old male presented to the emergency department with aphasia and weakness. He had been in his usual state of health until 7 hours prior, when he acutely developed right hand weakness and word–finding difficulties. His exam was notable for dysarthria and a right–sided facial droop. A head CT demonstrated multiple front and parietal lobe hypodensities consistent with infarcts. Incidentally, the caudal images of the scan revealed bilateral lung nodules. A CT of the chest confirmed the presence of innumerable small pulmonary nodules. The patient reported several months of a non–productive cough without hemoptysis, dyspnea, or night sweats. His history was significant for a diagnosis of latent tuberculosis as a young adult. He frequently traveled to developing nations. Transbronchial biopsy of a right middle lobe lung nodule demonstrated a well–differentiated adenocarcinoma. Transthoracic echocardiography was unremarkable save for a patent foramen ovale. Lower extremity venous ultrasound revealed the presence of bilateral, deep venous thromboses. The patient was discharged on anticoagulation with follow–up appointments scheduled in the neurology and oncology clinics.
In this patient presenting with new intracranial lesions and an incidental finding of innumerable pulmonary nodules, initial concern related to a unifying infectious etiology. The patient’s prior history of latent tuberculosis, travel to developing nations, and chest radiography depicting a “miliary pattern” raised concern for disseminated tuberculosis. There is, however, a differential diagnosis for such a finding: other infectious (coccidiomycosis), neoplastic (lung, thyroid, kidney) and inflammatory (sarcoidosis, pneumoconiosis) diseases. Despite the suggestion of tuberculosis on initial history and imaging, this patient’s constellation of symptoms did not fit a typical presentation for any of the above processes. First, the vascular pattern of his cerebral infarctions suggested an embolic source. Second, cardiac imaging demonstrated a patent foramen ovale. Third, deep venous thromboses were found on lower extremity ultrasound. Lastly, immunohistochemical staining was consistent with a primary lung adenocarcinoma. His syndrome was more likely explained by a malignancy–associated hypercoagulable state causing deep venous thromboses, with paradoxical embolization to the brain via an atrial septal defect.
Medical training often emphasizes the classical presentations of an individual diagnosis. In clinical practice, however, such pathognomonic signs are rare. By “anchoring” on individual findings, we run the risk of missing important aspects of a patient’s clinical picture. While complicated mechanisms to explain seemingly disparate clinical findings are tempting to pursue, it is important to remember that Occam’s razor remains as sharp as ever.
Figure 1The appearance of diffuse small diameter pulmonary nodules, commonly referred to as a “miliary pattern”.