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|Year : 2012 | Volume
| Issue : 4 | Page : 290-293
Upper aerodigestive tract cancer and the lung: A tale of two aspirations
P Vaideeswar, R Ghodke
Department of Pathology (Cardiovascular and Thoracic Division), Seth GS Medical College, Mumbai, India
|Date of Submission||09-Apr-2012|
|Date of Decision||11-Aug-2012|
|Date of Acceptance||28-Aug-2012|
|Date of Web Publication||4-Jan-2013|
Department of Pathology (Cardiovascular and Thoracic Division), Seth GS Medical College, Mumbai
Source of Support: None, Conflict of Interest: None
Patients with upper aerodigestive epithelial cancers frequently develop second primary cancers due to common risk factors or develop distant metastases depending on the locoregional status of the primary tumor. In most instances, the organ affected is the lung. Pulmonary spread usually occurs due to hematogenous or lymphatic dissemination. The following is a report of two patients with upper aerodigestive tract squamous cell carcinomas who developed lung metastases due to aspiration, a route not well documented in recent literature.
Keywords: Lung metastasis, lung primary cancer, upper aerodigestive cancer
|How to cite this article:|
Vaideeswar P, Ghodke R. Upper aerodigestive tract cancer and the lung: A tale of two aspirations. J Postgrad Med 2012;58:290-3
| :: Introduction|| |
Some anatomic sites are prone to the development of synchronous or metachronous second cancers, which pose a threat to the survival of such patients.  One such site is the upper aerodigestive tract, and the cancer can occur in the vicinity of the previous malignancy or can occur at a distant site, especially the lungs.  However, when multiple pulmonary lesions are present in combination with or after treatment of head and neck cancers, they are likely to be metastases. Most metastases to the lung are spread by the hematogenous route. Metastatic deposits are hardly ever attributed to aspiration of tumor cells from the primary site, which appears to be the mechanism in the reported cases.
| :: Case Reports|| |
A 46-year-old male, a chronic tobacco chewer for 16 years, was admitted in the emergency services department for eight hours with altered sensorium. He had a six-day history of painful perianal swelling with high-grade fever and chills, followed by decreased urine output for two days. The patient had been diagnosed as a case of laryngeal cancer five months ago, for which a tracheostomy had been performed; he had refused further treatment. The clinical diagnosis in the current admission was perianal abscess with azotemia and septicemia. An hour prior to death, there had been severe oral and tracheostomy bleeding. There was no recovery despite resuscitative measures. At autopsy, the basal aspect of tongue, epiglottis, and piriform fossae were destroyed by a well-differentiated squamous cell carcinoma. The cancer had formed an ulcerative, nodular gray-white mass, covered by granular necrotic/hemorrhagic material and had infiltrated the supraglottic, glottic, and infraglottic regions. The tracheostomy opening was uninvolved. Loosely adherent blood clots were found in the mouth, larynx, and trachea.
There were interesting findings in the lungs. Both pleurae were patchily opacified and had multiple gray-white firm tumor plaques. Two large nodules (3 × 3× 2.2 cm and 3.9 × 3.5 × 2 cm) were seen close to the hilum of the left lung; one of them abutted the left pulmonary artery. On cut surfaces, there were multiple solid and cavitating metastases ranging in size from 0.5 cm to 3.5 × 2.4 × 2.2 cm, along with fresh hemorrhagic infarcts in the posterior segment of the upper lobe and lateral segment of the middle lobe of the right lung [Figure 1]. These were assumed to be the result of tumorous occlusion of the arteries, seen as glistening, sharply delineated nodules [Figure 1]c. These were, surprisingly, not arteries, but bronchi occluded by aspirated necrotic tumor [Figure 2]. All the solid and cavitated metastases were airwaycentered and showed a well-differentiated tumor. The respiratory epithelium was partially or completely replaced by malignant squamous epithelium with infiltrations of the walls and extension into the alveolated parenchyma [Figure 2]. The arteries also showed stenosis or occlusion by tumor with or without superadded thrombi. There were metastases in the pericardium, hilar lymph nodes, liver, and kidneys.
|Figure 1: (a) External and (b) cut surfaces of the right lung;note patchy pleural thickening, small subpleuralcavitatary metastasis (arrow) and hemorrhagic appearance of middle lobe; (c) Glistening, sharply|
delineated nodules (arrows), thought to be tumorous occlusion of the arteries
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|Figure 2: (a) Scanned section through occluded segments, stained by hematoxylin and eosin (H and E); (b) Luminal occlusion of small bronchus by necrotic tumor (H and E ×250); (c) and (d) Show viable quamous cells surrounded by keratinous/necrotic material (H and E ×400); (e) Scan of section of bronchovascular bundle stained by H and E, showing expansion of bronchus B, abutting pulmonary artery PA; arrow points to the cartilage; (f) Malignant squamous epithelium replacing respiratory epithelium and extending into bronchial wall (H and E ×400)|
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A 55-year-old woman presented with low-grade fever, cough, progressive exertional dyspnea, and a pricking type of left-sided chest pain of three-month duration. The cough, which was initially dry, was associated with episodic hemoptysis for the past 20 days. A right hemimandibulectomy had been performed a year back for a well-differentiated squamous cell carcinoma of the gingivobuccal sulcus. She had been a tobacco chewer for the past 21 years. Details of adjuvant therapy were not known. There was an ulceroproliferative lesion on the buccal mucosa, measuring 1.5 × 1 × 1 cm, covered with slough; biopsy had not been performed. A clinical diagnosis of an irregular cavity in the left lower zone was confirmed on computed tomography.Associated parenchymal opacities and destruction of the left ninth and tenth ribs close to the vertebral bodies were also noted. These were thought to be infective in nature (chronic abscesses), and the patient was put on antibiotics. The patient developed a massive bout of hemoptysis and died.
At autopsy, both lungs showed scattered small gray-white bronchocentric nodules and multiple, firm pale yellow-to-brown foci of consolidation, predominantly distributed in the lower lobes [Figure 3]a. The histology of the bronchocentric nodules was similar to that in Case 1 with the presence of an aspirated necrotic tumor within the airway lumina. Other nodules showed replacement of the respiratory epithelium by malignant squamous epithelium with or without extension of the tumor through the bronchial walls into the lung parenchyma [Figure 3]b and c. The yellow foci of consolidation revealed a prominent giant cell reaction [Figure 3]d and e, which was due to aspiration of the secretions of the upper digestive tract; vegetable matter was seen at places. The posterobasal segment of the left lower lobe also showed a cavitatary metastasis of a well-differentiated squamous cell carcinoma. The cavity was large (5 × 4 × 4 cm), irregular with a gray-white irregular inner surface, variably thick gray-white wall, and a few blood clots. Part of the cavity was continuous with markedly thickened, nodular pleura, which in turn was adherent to thickened nodular white adventitia of the distal thoracic aorta. A sample of the mucosal growth revealed a recurrent well-differentiated squamous cell carcinoma.
|Figure 3: (a) Slice of left lung showing small gray-white nodules (arrows) and geographic pale yellow foci of consolidation; (b) Small part of respiratory epithelium flanked by malignant squamous epithelium; (c) quamous cell carcinomainvades bronchial subepithelial tissue; (d) Scan of section of boxed area stained by hematoxylin and eosin (H and E) revealed small areas of consolidation around bronchovascular bundle, bronchus B contains hemorrhage; (e) Consolidation showing prominent giant cell reaction (H and E ×400)|
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| :: Discussion|| |
Multiple primary neoplasms (MPN), once considered as rare entities, are now well-recognized phenomena. Apart from some well-described genetic syndromes that predispose to synchronous or metachronous second or more malignant tumors, a more common and acquired pathway of MPN is through 'field cancerization'-a concept introduced in 1953-where multifocal epithelial histological alterations occur in response to common risk factors.  This explains the development of second primary cancers at an annual rate of 3 to 7% in patients with upper aerodigestive tract malignancies, especially in the lungs, where tobacco is the common risk factor.  Further, survival of these patients is also affected by the development of distant metastases. The incidence of this complication is, however, small in comparison to other cancers and depends on positive nodal status and presence of locoregional recurrence.  Lung again remains the common site for distant metastases, with an incidence of 10%.  Distinction between pulmonary metastases and a new primary lung cancer may be difficult, especially if the lung nodule is solitary. The problem may be solved to some extent if certain clinical criteria are taken into consideration, that is, when the aerodigestive cancer is of a higher stage, and lung lesions are multiple, peripherally located, developing within three years, diagnosis of metastases would be favored; diagnosis at times may require to be substantiated by sophisticated molecular techniques.  The metastases occur through the 'standard' hematogenous route and/or lymphatic permeation. Both our patients undoubtedly had metastatic lung lesions which were multiple, peripheral in location, and developed five months and one year after diagnosis/therapy of primary lingual and bucccal cancers, respectively. The peculiar feature of intraparenchymal lung lesions in both cases was centering on airways with luminal occlusion by necrotic tumor (nonfatal endobronchial embolism), replacement of respiratory epithelium, invasion of wall by malignant epidermoid cells, and formation of cavities. Considering this unusual histological picture, we considered development of these endobronchial metastases through the phenomenon of aspiration, in addition to the vascular dissemination. Though this pattern is considered as one of the routes for metastases,  it is hardly reported; in fact, the common primary tumors cited to produce endobronchial metastases are breast, renal, and colorectal carcinomas.  Both the cases satisy the criteria for 'aspirational' metastases-put forward by Pickren et al. in 1958  -which are a route for neoplastic cells, displacement of these cells from their attachement to the primary site, aspiration of tumor cells, followed finally by implantation of tumor cells. This pattern may also explain the so-called metastasis of even benign tumors in the upper aerodigestive tract.  Aspiration (especially during sleep) and consequent aspiration pneumonitis occur in untreated  and untreated patients  of head and neck cancers. A swallowing dysfunction results due to the impaired mobility of structures, loss of sensation, and disrupted sphincter mechanism produced by the tumor and its associated therapeutic modalities, which were present in our cases. Though pneumonia was not documented, one of the patients had giant cell aspiration pneumonitis. We feel that aspirational metastases should be kept in mind as a unique mode of tumor spread in patients of upper aerodigestive cancers and lung metastases.
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[Figure 1], [Figure 2], [Figure 3]