Treatment of esophageal carcinoma with radiation alone or surgery alone has yielded unsatisfactory cure rates and has not had a major impact on survival. The failure to cure or prolong survival of patients with esophageal cancer is because of our inability to eradicate residual disease at the primary site and to early systemic dissemination of disease. Three neoadjuvant approaches involving chemotherapy have been studied in patients with apparently localized esophageal cancer: preoperative chemotherapy followed by surgery, chemotherapy and concurrent radiation therapy followed by surgery, and chemotherapy and radiation therapy without surgery. All of these approaches have shown potential in pilot trials. Large-scale trials comparing surgery alone with chemotherapy prior to operation are underway. For patients with local-regional epidermoid carcinoma who are not able to undergo or who refuse operation, chemotherapy plus concurrent radiation appears, in random assignment trials, to be superior to radiation alone.

Esophageal cancer continues to be a major health problem with an associated poor prognosis. New technology is being applied to the staging of this cancer. The new staging system requires assessment of depth of wall penetration and lymph node status prior to resection. To determine penetration and node status with a high degree of accuracy generally requires some combination of chemotherapy, magnetic resonance imaging, endoesophageal ultrasound, and/or surgical staging. Several variables need to be considered in planning the surgical approach to the patient with esophageal cancer: the intent of the surgeon to either cure or palliate, the anatomic location of the tumor, and the method of reconstruction. Surgery is optimal for localized esophageal cancer. Neoadjuvant chemoradiation has increased survival in specific subgroups. Phase 2 trials have shown the safety and efficacy of chemoradiation. Randomized multi-institutional trials are needed to verify the encouraging results of recent phase 2 trials.

The most critically ill patients in the hospital are located in the ICU. Due to intensive individualized care and monitoring, these patients often suffer from severe sleep deprivation. The amount and continuity of sleep as well as normal sleep architecture are all affected. Moreover, by impairing protein synthesis, cell division, and cellular immunity, sleep deprivation can affect the healing process and thus contribute to an increased morbidity and mortality. Reasons for sleep deprivation appear to be multifactorial and include the following: the patient's chronic underlying illness, an acute superimposed illness or surgical procedure, medications used in treatment of the primary illness, and the ICU environment itself. Therapeutic interventions need to address each of these potential causes, with an emphasis placed on providing an environment that is both diurnal and focused on the importance of uninterrupted sleep.

Recent notable developments have occurred involving radiation therapy (RT) for patients with non-small cell lung cancer (NSCLC). For patients with good performance status with unresected thoracic tumors, induction cisplatin-based chemotherapy followed by RT has resulted in a significant survival advantage over RT alone in two North American trials. However, the best sequence of administration of these two modalities in NSCLC remains to be determined. For palliation of tumor-related symptoms, efforts under way to improve control of brain metastases include the use of twice-daily cranial RT to a higher total dose, the use of focused radiation boost techniques like stereotactic radiosurgery to small metastatic deposits, and increased use of neurosurgical extirpation. For patients with NSCLC with symptomatic bone metastases, use of wider-field irradiation may benefit selected patients. Metastases to the adrenal gland, liver, and subcutaneous tissues can be palliated successfully by brief courses of RT. Intrathoracic tumor symptoms are well palliated by brief courses of thoracic RT. As adjuvant therapy following curative surgery, RT reduces the intrathoracic tumor recurrence rate among patients with metastatic tumor foci in hilar or mediastinal lymph nodes.

Laboratory investigations have begun to elucidate the regulatory molecules that control the processes of blood cell growth and differentiation. Recombinant human colony-stimulating factors are examples of biotechnology-produced molecules that have epitomized the translation of such basic scientific investigation into therapeutic advances. Small cell lung cancer, a malignancy that is overall highly sensitive to aggressive myelosuppressive chemotherapy at initial presentation, has been used as a clinical model in which the activity of human colony-stimulating factors has been tested. In this article, the clinical applications of hematopoietic growth factors are reviewed in brief. The appropriate clinical use of these agents may allow novel therapeutic strategies to be developed in a research setting. Similarly, these agents have the potential to improve supportive care and improve certain clinical outcomes in the non-research clinical care of patients. Issues of cost of treatment are raised by these agents, but the true clinical value of hematopoietic growth factors needs to be studied more rigorously, with emphasis on quality of life and redistribution of care costs outside of hospitals before definitive statements can be made.

Airway liquid balance in asthma is largely determined by active plasma exudation from tracheobronchial microvessels into the interstitial spaces of the mucosa, submucosa, and/or adventitia, and from there into the luminal space. This exuded plasma is rich in proteins and cell mediators capable of initiating several events, including activation of sensory neural pathways, plasma protein cleavage, inflammatory cell recruitment, and inhibition of surfactant function. It can act to amplify the bronchoconstrictor response by increasing mucosal and/or submucosal thickness, altering mechanical properties of airway wall compartments, decoupling the airway wall from parenchymal attachments, filling airway interstices, and by creating an additional inward force because of surface tension, resulting in further airway constriction and possibly closure and thereby significantly increasing airways resistance.

A 61-year-old woman with a history of sarcoidosis presented with acute sarcoid myositis affecting the respiratory muscles. The patient responded to prednisone therapy with improved pulmonary function test results and resolution of her symptoms. Acute myositis is a rare manifestation of sarcoidosis and should be treated with steroids.