Abraham Sanders

Acute Postobstructive Pulmonary Edema

Acute postobstructive pulmonary edema may occur after airway obstruction. A decrease in intrathoracic and intraalveolar pressures causes an increased blood flow into the pulmonary vasculature and favors the development of pulmonary edema. Two mechanisms for the development of acute postobstructive pulmonary edema are proposed: type 1 follows acute airway obstruction, and type 2 follows relief of chronic airway obstruction.

Risk of COPD with obstruction in active smokers with normal spirometry and reduced diffusion capacity.

Smokers are assessed for chronic obstructive pulmonary disease (COPD) using spirometry, with COPD defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as airflow limitation that is not fully reversible with bronchodilators. There is a subset of smokers with normal spirometry (by GOLD criteria), who have a low diffusing capacity of the lung for carbon monoxide (DLCO), a parameter linked to emphysema and small airway disease. The natural history of these “normal spirometry/low DLCO” smokers is unknown. From a cohort of 1570 smokers in the New York City metropolitian area, all of whom had normal spirometry, two groups were randomly selected for lung function follow-up: smokers with normal spirometry/normal DLCO (n=59) and smokers with normal spirometry/low DLCO (n=46). All had normal history, physical examination, complete blood count, urinalysis, HIV status, α1-antitrypsin level, chest radiography, forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), FEV1/FVC ratio and total lung capacity. Throughout the study, all continued to be active smokers. In the normal spirometry/normal DLCO group assessed over 45±20 months, 3% developed GOLD-defined COPD. In contrast, in the normal spirometry/low DLCO group, followed over 41±31 months, 22% developed GOLD-defined COPD. Despite appearing “normal” according to GOLD, smokers with normal spirometry but low DLCO are at significant risk of developing COPD with obstruction to airflow. Smokers with normal spirometry but low DLCO have a higher risk of COPD than smokers with normal spirometry and DLCO http://ow.ly/RWzxB

Bedside sonography for detection of postprocedure pneumothorax.

Bedside sonography for diagnosis of pneumothorax has been well described in emergency and trauma medicine literature. Its role in detection of iatrogenic pneumothorax has not been well studied. We describe the performance of bedside sonography for detection of procedure‐related pneumothorax and highlight some limitations.

Obstructive shock in a 47 year old female with a deep venous thrombosis due to intravascular leiomyomatosis: a case report

IntroductionIntra cardiac tumours and tumour thrombi can present in a manner resembling a massive pulmonary embolism. Intravascular leiomyomatosis with intracardiac extension is one such rare tumour. Survival from obstructive shock in this condition has not been previously reported.Case presentationA case is presented of a female who presented with recurrent syncope, cyanosis and then circulatory shock. An intravascular and intracardiac mass was suspected. Due to refractory shock, she ultimately underwent single stage median sternotomy and exploratory laparotomy, with excision of an intravascular leiomyoma.ConclusionIntravascular leiomyoma with intracardiac extension should be suspected in the differential diagnosis of a female with a history of uterine fibroids or hysterectomy and presenting with right heart obstructive symptoms.

High correlation of the response of upper and lower lobe small airway epithelium to smoking.

The distribution of lung disease induced by inhaled cigarette smoke is complex, depending on many factors. With the knowledge that the small airway epithelium (SAE) is the earliest site of smoking-induced lung disease, and that the SAE gene expression is likely sensitive to inhaled cigarette smoke, we compared upper vs. lower lobe gene expression in the SAE within the same cigarette smokers to determine if the gene expression patterns were similar or different. Active smokers (n = 11) with early evidence of smoking-induced lung disease (normal spirometry but low diffusing capacity) underwent bronchoscopy and brushing of the upper and lower lobe SAE in order to compare upper vs lower lobe genome-wide and smoking-responsive gene expression by microarray. Cluster and principal component analysis demonstrated that, for each individual, the expression of the known SAE smoking-responsive genes were highly correlated in upper and lower lobe pairs, although, as expected, there were differences in the smoking-induced changes in gene expression from individual to individual. These observations support the concept that the heterogeneity observed among smokers in the anatomic distribution of smoking-induced disease are not secondary to the topographic differences in the effects of cigarette smoke on the airway epithelium.

Pulmonary Nocardiosis in the Immunocompetent Host: Case Series.

Pulmonary nocardiosis is commonly recognized as an opportunistic infection in patients with predisposing immunosuppressive conditions. However, reports of pulmonary nocardiosis in the immunocompetent host are rare. Here, we report a case series of four patients with pulmonary nocardiosis without a predisposing condition.

Pulmonary extra-medullary hematopoiesis and pulmonary hypertension from underlying polycythemia vera: a case series:

Myeloproliferative neoplasia (MPN)-associated pulmonary hypertension (PH) is included in group five of the most recent clinical classification of PH. 1 The MPNs are a heterogeneous group of disorders that includes disorders with primary expression of a myeloid phenotype and disorders characterized by expression of the Janus Kinase 2 (JAK2) mutation, p.V617F. The latter includes essential thrombocytosis, polycythemia vera, and idiopathic myelofibrosis. 2 Pulmonary extra-medullary hematopoiesis (EMH) refers to the presence of hematopoietic precursor cells in the lung. It is a rare complication associated with myelofibrosis. Here we present a case series highlighting the clinical–pathological–radiological features of pulmonary EMH and PH from underlying polycythemia vera.

Pulmonary nodules in an infliximab-treated rheumatoid arthritis patient: a clinical pathology conference held by the Division of Rheumatology at Hospital for Special Surgery.

A 78-year-old African-American woman was diagnosed with rheumatoid arthritis (RA) in 1996 after she presented with a symmetrical polyarthritis of the hands. Over the next 4 years, she was treated with multiple disease-modifying antirheumatic drugs including methotrexate, hydroxychloroquine, gold, and leflunomide, all of which were stopped due to side effects or lack of response. She was started on low-dose prednisone in 1998, and was also maintained on low-dose azathioprine, which had been initiated in June. In October 2000, the patient developed a cervical myelopathy, manifested by ataxia and hyperreflexia. Magnetic resonance imaging of the cervical spine showed compression of the ventral cord by an enhancing epidural soft-tissue mass behind the odontoid, which was thought to be pannus, as well as multilevel spondylosis with cord compression at C5– 6. In December 2000, she underwent cervical spine decompression at the C5–6 level but was left with residual ataxia. In early 2000, the patient had begun to lose weight, and this worsened after her spine surgery; she lost 20 lb between August 1999 and April 2001. Computerized tomography (CT) scan of the chest, abdomen, and pelvis without contrast was normal in April 2001. Magnetic resonance imaging of the abdomen was unremarkable except for thickening of the gastric antrum. Endoscopy was normal. Bone-marrow biopsy showed no evidence of malignancy. Testing for antigliadin antibodies and human immunodeficiency virus (HIV) were negative. In May 2001, the patient was started on infliximab for the likelihood that RA activity was contributing to her weight loss and also because of the myelopathy due to the presence of pannus behind the odontoid process. She received the first three infusions but was lost to follow-up. She presented again in September 2001 with a further weight loss of 10 lb and was admitted for further evaluation. The patient_s prior medical history was significant for hypertension, osteoporosis, and a pancreatic cystic mass which, when aspirated in 1998, had revealed no malignant cells. There also was an allergy to contrast dye. Medications at the time of admission were Premarin 0.625 mg daily (qd), prednisone 5 mg qd, furosemide 20 mg qd, and atenolol 50 mg qd. On physical examination, the patient was cachectic, weighing 66 lb. Blood pressure was 110/80 mmHg, and she was afebrile. Significant findings included: chronic swan neck and boutonniere_s deformities of the hands but no active synovitis; hyperreflexia in the lower extremities with mild left-sided dysmetria; and negative Babinski signs. Abdominal examination revealed mild left upper-quadrant abdominal tenderness without masses. Cardiopulmonary examination was within normal limits, and hemoccult stool test was negative. The initial laboratory investigation demonstrated a leukocyte count of 3.7 10/l (normal 3.4–11.2 10/l) with a normal differential, hemoglobin 9.5 g/dl (normal 12–16 g/dl), and platelet count of 201 10/l (normal 150– 450 10/l). Liver, renal, and thyroid function tests, as well as urinalyses, were normal. Serum albumin was 2.9 g/dl, HSSJ (2007) 3: 119–125 DOI 10.1007/s11420-006-9032-1

Progression to COPD in smokers with normal spirometry/low DLCO using different methods to determine normal levels

We thank Drs Quanjer and Miller for their commentaries to our recently published manuscript in the European Respiratory Journal [1]. Our manuscript describes a follow-up study of pulmonary function tests (PFTs) in two groups of healthy smokers with normal post-bronchodilator spirometry and total lung capacity (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and total lung capacity (TLC) ≥80% predicted and FEV1/FVC >0.7, as defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) initiative) [2–5]. The smokers in one group had normal spirometry and normal diffusion capacity of the lung for CO (DLCO) defined as ≥ 80% pred (“normal spirometry/normal DLCO”, n=59) and the smokers in the other group had normal spirometry but low DLCO (<80% pred, “normal spirometry/low DLCO”, n=46). The groups were similar in age, sex and ethnicity, with no difference in exposure to risk factors (i.e., smoking history, pack-year history, packs per day or age of smoking initiation), cough or sputum scores or emphysema score. At the end of the follow-up period (<4 years, on average, for both groups), 2 (3%) out of 59 of the normal spirometry/normal DLCO smokers developed GOLD-defined COPD (FEV1/FVC <0.7) versus 10 (22%) out of 46 of the normal spirometry/low DLCO smokers (p<0.009). We concluded that despite appearing “normal” by GOLD, smokers with normal spirometry but low DLCO are at significantly higher risk for developing COPD with obstruction to airflow. Smokers with normal spirometry/low DLCO are at higher risk of COPD versus those with normal DLCO http://ow.ly/4mQBwZ

Cyclophosphamide responsive interstitial lung disease in "overlap syndrome": a clinical pathology conference held by the division of rheumatology at the hospital for special surgery.

Each author certifies that he or she has no commercial associations (e.g., consultancies, stock ownership, equity interest, patent/licensing arrangements, etc.) that might pose a conflict of interest in connection with the submitted article. Each author certifies that his or her institution has approved the reporting of this case, that all investigations were conducted in conformity with ethical principles of research.