Search

Cicatricial pemphigoid (CP) with tracheal involvement is a rare and potentially deadly condition. Here, we report the first case in which Nd:YAG laser (1064nm) laser ablation bronchoscopy was used to treat CP with tracheal involvement. Our patient is a 71-year-old male with a history of CP refractory to medical therapy affecting his trachea who presented to the emergency department with dyspnea. He ultimately underwent bronchoscopy with Nd: YAG laser (1064nm) laser ablation, which resulted in a temporary alleviation of his respiratory symptoms. A repeat laser ablation was planned in hopes of prolonging the patient’s remission, but due to interval changes in the patient’s airway anatomy, it was deemed unsafe. While our patient’s uniquely advanced disease was not amenable to further laser-mediated intervention, it is possible that patients with less advanced disease may experience better outcomes with similar therapy. This case shows the promise laser ablation could hold for patients with tracheal cicatricial pemphigoid.

Mortality rates for pulmonary embolism differ significantly, indicating a need for escalated management. Treatment options include systemic anticoagulation, catheter-directed thrombolysis and/or thrombectomy and surgical thrombectomy. Heparin-induced thrombocytopenia is a severe complication as a result of any form of heparin which limits pharmacologic therapy with thrombolytics and anticoagulation.

Anomalous bronchial arteries originate outside the space bound by the T5 and T6 vertebrae at the major bronchi. Here, we highlight a case of a 37-year-old man with a past medical history of coccidioidomycosis and who presented with massive hemoptysis. A bronchial angiogram showed the patient had a right bronchial artery originating anomalously from the left subclavian artery. The patient ultimately underwent a bronchial artery embolization, after which he achieved symptomatic remission.

Four clinical patterns of diffuse lung disease may be seen with silicosis: acute silicosis or silicoproteinosis (the latter resembling pulmonary alveolar proteinosis), simple nodular sclerosis, accelerated silicosis, and progressive massive fibrosis (PMF). The intensity and duration of exposure as well as host susceptibility dictates the presentation and progression of PMF. Although most cases of PMF in the literature are reported among coal miners in whom this disease has shown a recent increase in prevalence, this disease can also be seen in exposed workers outside the coal industry. In this article, we will review the clinical, physiological, and pathological manifestations of the disease, illustrated by three case examples of PMF among non-coal miners from New Mexico. Diagnosis and management of patients with PMF can be difficult, and carries medicolegal implications for the patient. Physicians and policymakers need to be aware of PMF in workers exposed to silica within and outside the coal industry.

No abstract available. Article truncated after first page. History of Present Illness: A 54-year-old Hispanic male who was incarcerated 3 days prior to hospital admission was brought into the emergency room from prison for alcohol related withdrawal seizures. Physical Examination: Upon arrival to the ER, the patient was noted to be hypoxic with copious thick secretions in his mouth. He was intubated for airway protection, started on propofol and fentanyl drips as well as intravenous thiamine and folic acid. Radiography: A chest radiograph was performed (Figure 1). Which of the following are true regarding management of this patient? 1. Phenytoin should be administered for prevention of seizures; 2. Prophylactic antibiotics for aspiration pneumonia should be administered; 3. Thiamine and folic acid should be administered; 4. 1 and 3; 5. All of the above. …

Obesity increases the risk for asthma, with a disease phenotype characterized by poor clinical control and high frequency and severity of acute exacerbations. Obese asthmatics do not respond well to standard controller asthma therapy; weight loss however helps improve asthma control. Airway hyperresponsiveness, a characteristic of asthma, decreases following surgical weight loss in the subgroup of patients with obesity-associated asthma that is late-onset and nonallergic. Like asthma, obesity is an important comorbidity in patients with chronic obstructive pulmonary disease (COPD). Although COPD is underdiagnosed in the obese population, obese COPD patients have greater dyspnea and physical activity limitation, as well as lower quality of life and lung function than nonobese COPD patients. Some studies show that obese patients with severe COPD have a lower mortality than nonobese patients, constituting the “obesity paradox,” and therefore clinicians may consider accepting a “modest” degree of excess body weight in patients with severe COPD as optimal. Targeted drugs or nutritional interventions that reduce the inflammatory and metabolic activity of fat may open up novel therapies for asthma and COPD in obese subjects.

Introduction: Chronic pulmonary hypertension (PH) can display acute elevations in pulmonary arterial pressure (PAP) in the setting of hypoxemia, pulmonary embolism (PE), and possibly sepsis. Case Description: A 68-year-old man with chronic obstructive pulmonary disease, heart failure, recent tobacco cessation, and recent 2-vessel coronary artery bypass grafting (CABG) presented with one to two weeks of respiratory symptoms and syncope on the day of admission. He was found to have a urinary tract infection and Escherichia coli bacteremia. Transthoracic echocardiography found a systolic PAP of 100-105 mmHg, increased from a mean PAP of 32 mmHg before CABG. PE was not seen on computed tomography angiography (CTA). Ventilation-perfusion scan two days later found evidence of subsegmental PE. PAP prior to discharge was 30-35 mmHg plus right atrial pressure. Conclusion: PAP can rise substantially in the acute or subacute setting, particularly when multiple disease processes are involved, and decrease to (near) baseline with proper therapy. Chronic PH may even be protective. In a complex clinical setting with multiple possible etiologies for elevated PAP, clinicians should have a high suspicion for PE despite a negative CTA.

Chronic myeloproliferative disorders (CMPDs) are a heterogenous group of disorders characterized by cellular proliferation of one or more hematologic cell lines in the peripheral blood. Bone marrow histology shows hypercellularity and fibrosis in most of these disorders. The incidence of CMPD is estimated between 6 and 9 new cases per 100,000 yearly. CMPDs are incurable and are associated with a variable clinical course. Pulmonary hypertension (PH) is a well-recognized complication of CMPD, and when present, portends a poorer prognosis with median survival as low as several months, though this varies by the type of PH as well as the severity of the underlying CMPD. This review will serve to summarize the current knowledge of epidemiology, pathophysiology, diagnostic methods, clinical implications, and management of PH in CMPD.

No abstract available. Article truncated after the first page. A 65 year old woman with a history of hypertension and a recent diagnosis of multiple myeloma was admitted to the ICU with septic shock due to Morganella morganii bacteremia. She was treated with cefepime, levophed and dobutamine. During treatment she developed symptoms and a chest x-ray compatible with congestive heart failure. A transthoracic echo is shown below (Figures 1 and 2). Additionally a spectral pulsed-wave Doppler study of the mitral inflow velocities is presented (Figure 3). What is the best explanation for the findings seen in on the echocardiogram? 1. Cardiac amyloidosis; 2. Hypertensive heart disease; 3. Hypertrophic cardiomyopathy; 4. Stress (Takotsubo) cardiomyopathy.

Introduction Chronic lung disease, often characterised by rapid decline in lung function, is associated with vascular endothelial dysfunction (characterised by moderate to severe excess urinary albumin excretion (eUAE) but their longitudinal relationship is inadequately studied. In a bidirectional longitudinal examination of healthy adults, we analysed the following two hypotheses: (1) rapid decline (ie, highest tertile of lung function decline) predicts eUAE and (2) eUAE predicts rapid decline. Methods We performed a secondary data analysis from 3052 eligible participants from the Coronary Artery Risk Development in Young Adults (CARDIA) study. For analysis 1, the predictor was rapid decline in lung function between the peak value (attained at or before CARDIA visit year 10 or Y10 at a mean age of 35 years) and Y20; and the outcome was incident eUAE at Y20 and/or Y25. For analysis 2, the predictor was eUAE at Y10 and the outcome was rapid decline between Y10 and Y20. Results After adjustment for covariates in analysis 1, rapid decline in FEV 1 or FVC between peak and Y20 predicted incident eUAE at Y20 and/or Y25 (OR 1.51 and 1.44, respectively; p≤0.05 for both analyses). In analysis 2, eUAE at Y10 did not predict subsequent rapid decline. Conclusions Healthy adults with rapid decline in lung function are at risk for developing vascular endothelial dysfunction, as assessed by incident eUAE, later in life.