Israel Medical Association Journal

Background: Multidrug-resistant tuberculosis (MDR-TB) presents a difficult therapeutic problem due to the failure of medical treatment. Pulmonary resection is an important adjunctive therapy for selected patients with MDR-TB.

Objectives: To assess the efficacy of pulmonary resection in the management of MDR-TB patients.

Methods: We retrospectively reviewed the charts of MDR-TB patients referred for major pulmonary resections to the departments of thoracic surgery at Assaf Harofeh and Wolfson Medical Centers. For the period under study, 13 years (from 1998 to 2011), we analyzed patients’ medical history, bacteriological, medical and surgical data, morbidity, mortality, and short-term and long-term outcome.

Results: We identified 19 pulmonary resections (8 pneumonectomies, 4 lobectomies, 1 segmentectomy, 6 wedge resections) from among 17 patients, mostly men, with a mean age of 32.9 years (range 18–61 years). Postoperative complications developed in six patients (35.3%) (broncho-pleural fistula in one, empyema in two, prolonged air leak in two, and acute renal failure in one). Only one patient (5.8%) died during the early postoperative period, three (17.6%) in the late postoperative period, and one within 2 years after the resection. Of 12 survivors, 9 were cured, 2 are still under medical treatment, and 1 is lost from follow-up because of poor compliance.

Conclusions: Pulmonary resection for MDR-TB patients is an effective adjunctive treatment with acceptable morbidity and mortality.
 

Background: Most studies on asbestos-related diseases describe the associations between exposure and disease and the factors influencing that association. It is recognized that there is a long latency period between exposure and disease, but the health status of affected individuals after long-term non-exposure is uncertain.

Objectives: To describe the changes in pulmonary function tests (PFTs) and computed tomographic imaging of the thorax over a 15 year period after cessation of exposure to asbestos in a cohort of Israeli power plant workers.

Methods: Israeli power plant workers whose PFTs and thoracic CT imaging between 1993 and 1998 revealed asbestos-related disease underwent a second clinical, functional and imaging evaluation up to 15 years later. The two sets of results were compared.

Results: Of the original cohort of 59 males, 35 were still alive, and 18 of them agreed to take part in the current study. The mean length of their exposure was 30 ± 10.06 years (range 7–43 years). Comparison of the initial and follow-up examination findings revealed a significant increase in calcification of the pleural plaques (from 37% to 66%, P = 0.008) and a deterioration in PFTs (P = 0.04). Of the 24 men who died, malignant disease was the cause of death in 53%, mostly in sites other than the respiratory system.

Conclusions: PFTs declined and CT findings worsened in subjects who were formerly exposed to asbestos and had not been exposed to it for over a decade. Continued monitoring of individuals exposed to asbestos, even decades after the cessation of exposure, is recommended.
 

Background: The "obesity paradox" is defined as an inverse association of good health, survival and obesity. Usually in healthy persons the more obese you are the more metabolic complications you have; however, thin patients with chronic obstructive pulmonary disease (COPD) have more cardiovascular complications and a higher mortality rate.

Objectives: To explore whether atherosclerosis and peripheral artery disease (PAD) contribute to the higher morbidity and mortality of patients with COPD.

Methods: This prospective study included 87 patients with chronic COPD who were treated in the pulmonary outpatient clinic; all signed a consent form before enrollment. We documented their lung function (FEV1%), body mass index (BMI) and ankle brachial index (ABI). The primary endpoints were to find an association between atherosclerosis and BMI in patients with COPD, and between atherosclerosis and severity of lung disease.

Results: Average ABI[1] was 1.01 ± 0.20, BMI[2] was 29.33 ± 7.48 kg/m2, and the abdominal circumference was 107.34 ± 18.87 cm. A positive correlation was found between BMI and ABI (P = 0.001) and between abdominal circumference and ABI (P = 0.000). Patients with peripheral artery disease were older (73.6 ± 11.5 vs. 68.1 ± 11.6 years old, P = 0.04), were thinner (average BMI 25.5 ± 6.2 vs. 31.06 ± 7.3, P = 0.001), and had a lower abdominal circumference (97.7 ± 18.3 vs. 111.7 ± 17.5 cm, P = 0.001). No such difference was observed for years of smoking. Male PAD patients with COPD had a lower BMI (25.2 ± 5.6 vs. 29.9 ± 7.4, P = 0.016), and their abdominal circumference was smaller (96.1 ± 18.0 vs. 110.2 ± 16.5 cm, P = 0.004). Female PAD patients with COPD had a lower BMI (26.3 ± 8.2 vs. 33.1 ± 7.0, P = 0.045), but their abdominal circumference was not different from females without PAD (102.0 ± 19.7 vs. 114.0 ± 19.4 cm, P = 0.162). Patients with PAD had a worse lung disease (FEV1% 34 ± 8% vs. 45 ± 16%, P = 0.01). During the 1 year of follow-up five patients died: two PAD patients due to acute myocardial infarction and three non-PAD patients died from pulmonary insufficiency (two patients) and pulmonary emboli (one patient).

Discussion: We found that COPD patients with PAD were older and thinner and had a lower abdominal circumference and a more progressive lung disease. Extensive atherosclerosis in patients with COPD may partly explain the “obesity paradox” observed in patients with COPD.

Pulmonary epithelioid hemangioendothelioma (PEH), previously known as "intravascular bronchoalveolar tumor," is a rare vascular malignancy with an unpredictable prognosis. Treatment can vary from observation in asymptomatic patients to surgery in patients with resectable disease or chemotherapy in patients with disseminated disease. This report describes the clinical, radiological and pathological features of three cases of PEH and a review of the current literature.
 

Background: Exacerbations of chronic obstructive pulmonary disease (COPD) are a major problem worldwide and are usually the main indication for mechanical ventilation (MV), especially in the intensive care unit (ICU). The rate of weaning failure is also high and prolonged MV leads to complications of intubation. The goal is to wean these patients as soon as possible.

Objective: To determine the optimal time necessary to start the weaning process.

Methods: In an attempt to determine the length of MV and stay in the ICU, we compared the length of MV, weaning, re-intubations and discharge during a 10 month period. This study included 122 patients on MV due to severe exacerbation of COPD who were not suitable for non-invasive ventilation. For each patient serial arterial blood gases were measured at admission and during hospitalization. PeCO₂ (mixed expired CO₂) was tested using a Datex S/5 instrument at follow-up.

Results: The study population comprised all patients who required MV; of these 122, 108 were ventilated from 6 to 140 hours (average 48 ± 42), 9 needed more than 168 hours, and 5 died due to severe ventilation-associated pneumonia. No correlation was found between pH, PCO₂ and length of MV; these findings did not contribute to evaluation of the patient’s condition nor did they enable us to predict the length of treatment necessary.

Conclusion: Most of the patients (93%) ventilated for acute respiratory failure due to COPD required MV for only 6–90 hours.

Background: Community-acquired pneumonia requiring hospitalization is a severe illness with high mortality, especially if the appropriate treatment is delayed. Sometimes diagnosis is difficult due to an equivocal clinical picture or chest film, or to accompanying diseases that mask or simulate pneumonia.

Objectives: To assess the usefulness of certain inflammatory markers to differentiate pulmonary edema from pneumonia throughout the hospital stay in patients admitted for pneumonia or pulmonary edema of non-infectious origin and to monitor the response to treatment.

Methods: The study group comprised 50 patients admitted for pneumonia, 50 admitted for pulmonary edema and 30 healthy individuals. Blood samples for determination of leukocyte count, erythrocyte sedimentation rate (ESR), fibrinogen, C-reactive protein (CRP), albumin, sCD14 and oxidized fibrinogen were drawn upon admission, at 48 and 72 hours after admission, and at discharge from the intensive care unit.

Results: The levels of sCD14 were similar in both patient groups but higher than control levels during the first 48 hours (P < 0.03). They decreased gradually with hospital stay. The concentration of oxidized fibrinogen was similar in both patient groups and significantly lower than that of the healthy control group throughout the hospitalization period.

Conclusions: Oxidized fibrinogen and sCD14 are not reliable markers for the diagnosis of pneumonia, for its differential diagnosis from pulmonary edema, and for patient follow-up throughout hospitalization. The finding of elevated levels of oxidized fibrinogen in the group of healthy controls warrants further study to identify the factors responsible for altering fibrinogen oxidation. The other markers are more indicative.
 

Idiopathic pulmonary arterial hypertension (IPAH) is an isolated small-vessel disease comprising vasoconstriction, remodeling and thrombosis of small pulmonary arteries. However, there is evidence that IPAH[1] does not respect anatomic boundaries and might extend into large vessels such as large central thrombi. On the other hand, chronic thromboembolic pulmonary hypertension (CTEPH) represents a distinct category of pulmonary hypertension as it is thought to be due to an occlusion of the major pulmonary arteries following a thromboembolic event. However, it is currently evident that in most patients, there is a concomitant small-vessel disease. The involvement of both small and large vessels in both IPAH and CTEPH[2] together with a high incidence of silent thromboembolic events might create difficulties in identifying the true cause of pulmonary hypertension. An accurate diagnosis of the cause determines the management and prognosis. Patients with CTEPH can potentially be offered curative surgery in the form of pulmonary endarterectomy; however, oxygen, vasodilators, anticoagulation, and lung transplantation are more feasible options for IPAH.