When a standard full dose of a vasopressor fails to normalize blood pressure in a patient with septic shock, escalation begins to yield diminishing returns as the dose and multiplicity of agents approach practical upper limits. Although it is not possible to specify a precise cutoff for limiting vs. intensifying therapy, a mortality of 80% or higher-characterized by two or more concurrent vasopressors at full dose-should prompt shared decision making with the patient's family.

It is very important to suspect Strongyloides infection in a patient presenting with syndrome ofinappropriate antidiuretic secretion as hyperinfection and disseminated disease can be life threatening without antihelmintic therapy.

Recent advances in imaging techniques led to an increase in the incidence of synchronous and metachronous primary lung cancers due to early detection. Management of these patients is challenging and prognosis depends on the stage of the tumor at initial diagnosis and histological type. A 68-year-old African American male patient with medical history of hypertension and diabetes mellitus presented to our emergency department with right sided chest pain, worsening dyspnea and dry cough of 2-week duration. He also reported significant weight loss and was a smoker with 25 pack-years smoking history. Chest radiology showed a large right pleural effusion. Subsequent thoracentesis and fluid analysis revealed a lymphocytic exudate. Patient underwent bronchoscopy with findings of an endobronchial lesion in the left lower bronchus. Microscopic analysis of the biopsy specimen showed a well differentiated carcinoid. It was decided to proceed with VATS and pleural biopsy as part of workup for unexplained exudative pleural effusion. Multiple pleural nodules were detected during the procedure and biopsy of these nodules revealed adenocarcinoma of lung. He was evaluated by Oncology and underwent palliative chemotherapy. The association of carcinoid with adenocarcinoma of lung was infrequently reported in the past. This case also highlights the importance of additional diagnostic workup for primary when the diagnosed malignancy does not explain the clinical presentation.

Idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease with a fatal prognosis. Over the last decade, the concepts in pathobiology of pulmonary fibrosis have shifted from a model of chronic inflammation to dysregulated fibroproliferative repair in genetically predisposed patients. Although new breakthrough treatments are now available that slow the progression of the disease, several newer anti-inflammatory and anti-fibrotic drugs are under investigation. Patients with IPF often have coexistent conditions; prompt detection and interventions of which may improve the overall outcome of patients with IPF. Here, we summarize the present understanding of pathogenesis of IPF and treatment options for IPF in the current landscape of new anti-fibrotic treatment options.