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A 68-year-old man was found on CT to have a right lung nodule and paratracheal lymphadenopathy. He was then scheduled for diagnostic bronchoscopy and mediastinoscopy.

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Twenty years ago, he was diagnosed with carcinoma of the right submandibular gland, and underwent excision of the gland, right radical neck dissection, and a course of radiotherapy. He quit smoking several years ago and has had hypertension for about 5 years. He has had a nonproductive cough for several months. His only medication is metoprolol.

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On examination, he is in no distress at rest. His vital signs are: blood pressure (BP) 140/90 mm Hg, heart rate (HR) 70 beats per minute (bpm), and respiratory rate (RR) 18 breaths per minute. Oxygen saturation on room air is 96%. His weight is 94 kg and he is 170 cm tall. Auscultation of the chest reveals decreased breath sounds bilaterally but no rales or rhonchi, and normal heart sounds. No carotid bruits are evident.

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Airway examination reveals a Mallampati IV classification. Mouth opening is 2.5 cm and mandibular protrusion is less than 1 cm. Full upper dentition is present but the mandible is edentulous. The thyromental distance is normal. Cervical spine extension is decreased. Palpation of the submandibular tissues (mandibular space) reveals a woody, indurated consistency. On inspection, telangiectasia and pallor of the submandibular skin are noted. The right neck has the typical appearance of a previous neck dissection. The mucosa of the tongue appears dry.

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Laboratory data reveal normal electrolytes and a hemoglobin of 140 g·L−1. ECG reveals nonspecific ST and T changes.

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The patient has hypertension which is adequately controlled for his surgical procedure. Carcinoma of the lung is suspected on diagnostic imaging. He does not appear to require further medical optimization.

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General anesthesia with endotracheal intubation is required for a brief but stimulating surgical procedure.

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Radiotherapy inflicts a radiochemical injury to both normal and malignant cells.1 The damage is related to the total radiation dose and the method of radiotherapy delivery. In order to achieve adequate tumor control, damage to normal tissues is inevitable.1,2Acute tissue toxicities from radiotherapy are considered to occur within 90 days of the commencement of treatment, and late effects beyond 90 days of treatment.3 The late effects may not be manifested until years following the radiotherapy.4 In general, tissues with rapidly dividing cell populations such as mucous membranes and skin demonstrate acute effects of radiation (mucositis, desquamation), whereas those with slowly proliferating cells such as connective tissue demonstrate late effects.5 The severity of the late effects of radiation therapy in general cannot be predicted by the severity of the acute effects.5 The mechanism of late tissue toxicity may be parenchymal or stromal cell death, or irradiation injury to the microvasculature.5 Increased vascular permeability leads to deposition of fibrin in the perivascular interstitium and subsequent ...

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