In chemotherapy-induced lung injury, pulmonary permeability is altered because of alveolar epithelial disruption with fluid and protein leakage into the alveolar spaces and focal necrosis of type I pneumocytes and fibrosis. Permeability can be assessed using ^99mTc-DTPA aerosols. The inhalated aerosol is deposited in the alveoli, permitting the acquisition of scintigraphic images that show different patterns of ventilation. In the noninflammed lung there is minimal permeability of the DTPA from the air space to the vasculature, hence minimal activity in the systemic circulation. The inflammed lung has greater permeability, allowing passage of the tracer from the air space to the vasculature. The clearance time decreases as epithelial ­permeability [14, 15] increases. In untreated patients, permeability was reduced, possibly because of tumoral infiltration, while it was increased in treated patients, suggesting early injury [16, 17].

In radiation therapy of the thorax, radiation pneumonitis can appear 2–8 months after treatment. Radiation lung injury occurs in proportion to the amount of lung that is exposed to doses of >20 Gy. Symptoms vary from none, when radiation is delivered to a small region of the lung, to systemic signs and symptoms of fever, dyspnea, cough, and respiratory distress syndrome, when radiation is delivered to >20% of the total lung volume. Following lung radiation there are two phases of cytokine expression: one occurring hours to days or weeks after radiation, typically returning to normal after ∼2 weeks and a second phase at 6–8 weeks, leading to pulmonary parenchymal and vascular damage [18], which may progress for 6–24 months following radiation exposure. Within 1–3 months of exposure, acute radiation lung injury can occur, manifested by dyspnea, cough, and hypoxia. Six to twenty-four months after radiation lung fibrosis can occur, leading to progressive impairment of pulmonary function. Early detection of radiation pneumonitis enables adequate treatment with a reasonable chance to prevent or limit late sequelae [19]. Clinical manifestations, chest radiographs and pulmonary function tests may help to establish an early diagnosis, but scintigraphic abnormalities can be demonstrated in the acute phase often before radiologic changes become apparent. ⁶⁷Ga-citrate is also a sensitive method for the early detection of radiation pneumonitis [20], although the delineation of lung injury may be hampered due to the normal ⁶⁷Ga uptake in sternum and thoracic spine.

Pentetreotide, a synthetic somatostatin analog with strong affinity for the somatostatin receptor subtypes 2 (sst2) and 5, can be labeled with ¹¹¹In. Somatostatin has been shown to modulate fibroblast activation and to have antifibrotic properties also [21], although the exact mechanisms of such antifibrotic action of octreotide still remains unclear. ¹¹¹In-pentetreotide may have a role in the differential diagnosis of patients with complaints after radiotherapy and in the monitoring of the response to corticosteroid therapy [19]. Some false-positive studies have been reported with increased pulmonary uptake in patients with neuroendocrine tumors which eventually was due to pulmonary fibrosis (Fig. 30.2) [22, 23]. [¹⁸F]FDG-PET has also been recently proposed to detect radiation pneumonitis [24] and may be used use as a predictor for acute radiation pneumonitis [25] (Fig. 30.3).

There may be significant [¹⁸F]FDG uptake in the irradiated region up to about 2 months following therapy. Persistence of significant focal activity beyond 8 weeks raises the likelihood of persistence of disease within the irradiated region.

Radiation-induced lung damage may lead to decreased lung perfusion, lung ventilation, and diffusion of gases in the irradiated region. A decrease in pulmonary blood flow in the irradiated areas has been reported in breast cancer patients receiving radiotherapy [26]. Lung scintigraphy with ^99mTc-DTPA aerosol or ^99mTc-MAA (macroaggregates of albumin) have been performed to assess abnormal ventilation/­perfusion patterns. A reduction in both ventilation and perfusion was observed 3 months after radiotherapy. Other radiotracers used in different studies include ¹³³Xe, ^81mKr gas, or ¹³¹I-MAA with reduced perfusion in the irradiated areas as the common finding [26–28].

Chemotherapeutic drugs (cisplatin and ifosfamide) can cause renal damage, while abdominal radiation in the treatment of abdominal malignancies can lead to renal nephropathy. Several radionuclide techniques have been proposed to evaluate the effect of these treatments over the kidneys.

Nausea, vomiting, diarrhea, and enteritis often occur due to radiotherapy and chemotherapy. Nuclear medicine examinations can play a role in the detection of radiation-induced late injury on the small bowel.