205502379
Mediastinal mass in an asthmatic patient.
A 52-year-old man with a 2-year history of asthma was referred to theChestClinic becauseofworseningdyspnoea of 1-year duration. He was non-compliant with inhalers and was taking oral prednisolone as needed for control of asthma. There were no other complaints. Physical examinationshowedanobeseman(bodymass index37.8 kg/m) with cushingoid habitus. Examination of the respiratory system showed diffuse bilateral wheeze. Cardiovascular, neurological and abdominal examinations were normal. Spirometry showed moderate airway obstruction with significant bronchodilator reversibility. A chest radiograph showed a superior mediastinal widening. The possibility of upper airway obstruction secondary to the mediastinal mass was considered. Subsequently, high-resolution computed tomography (CT, Fig. 1) showed a low-attenuation unencapsulated mass in the anterior mediastinum (bold arrow), para-aortic (arrow head) and the paratracheal region (small arrow). Also seen was increased extrapleural fat (cleaved arrow head) consistent with a diagnosis of mediastinal lipomatosis. Serum cortisol at 8.00 hours was 55 nmol/L, suggesting suppression of endogenous cortisol secretion. The patient was initiated on inhaled steroids. Prednisolone 20 mg/daywas continued and slowly tapered by 2.5 mg/month. The patient was advised therapeutic lifestyle changes in the form of strict diet control and exercise. He lost 8 kg of weight over the next 6 months and is doing well on follow up. A short Synacthen test with 250 lg Synacthen was carried out at 6 months, which showed an incremental cortisol response of 330 nmol/L at 1 h. Mediastinal lipomatosis is a benign condition that can occur either secondary to obesity and exogenous Cushing’s syndrome, or as a part of symmetrical lipomatosis and is a rare cause of mediastinal mass. Its usual appearance at CT is smooth widening of the upper anterior mediastinum without tracheal deformity. Associated increase in extrapleural fat is a helpful diagnostic feature. At CT the uniform density of fat (270 to 2130 Hounsfield units) is obvious. The importanceof identifying this condition is the fact that except for the radiological opacity, it is an ‘innocent bystander’ and is generally of no pathophysiological consequence to the patient. A condition that resembles mediastinal lipomatosis, but needs to be differentiated, is multiple symmetrical lipomatosis; however, in this condition, multiple masses of benign fat compress the mediastinal structures especially trachea.
33491888
Noninvasive ventilation in ARDS caused by Mycobacterium tuberculosis: report of three cases and review of literature
26068481
Efficacy and safety of iodopovidone pleurodesis through tube thoracostomy.
OBJECTIVE
To evaluate the efficacy and safety of iodopovidone as an agent for pleurodesis through tube thoracostomy in patients with recurrent pleural effusions and pneumothorax.


METHODS
This was a prospective study in which pleurodesis was performed with a solution of 20 mL 10% iodopovidone and 80 mL normal saline solution infused through a tube thoracostomy and left in the pleural cavity for 4 h.


RESULTS
A total of 64 patients (34 men) with a mean (+/-SD) age of 47.1 +/- 15.4 years were included. There were 37 cases of pleural effusion and 27 of pneumothorax. A complete response (neither reaccumulation of fluid nor recurrence of pneumothorax) was obtained in 32 (86.5%) patients with pleural effusion and 25 (92.6%) patients with pneumothorax. A second procedure (i.e. repeated pleurodesis) was attempted successfully in four patients in the pleural effusion group. All patients experienced chest pain to a varying degree as recorded on a Visual Analogue Scale (median 50.5, range 10-95). Seven patients developed fever and one immunocompromised patient developed empyema following the procedure. There were no recurrences at a median follow up of 5 months (range 3-15 months) in the pleural effusion group, and 13 months (range 6-24 months) in the pneumothorax group.


CONCLUSIONS
Iodopovidone can be used as an effective and safe agent for (chemical) pleurodesis (through tube thoracostomy), which is inexpensive and readily available.
22528299
Pulmonary hypertension as a presenting manifestation of allergic bronchopulmonary aspergillosis.
The case of a 46-year-old lady who presented with respiratory failure and pulmonary hypertension in the absence of clinical signs of asthma or bronchiectasis, and in whom a diagnosis of allergic bronchopulmonary aspergilloma [ABPA] was made subsequently on the basis of radiological and laboratory investigations is reported. Symptomatic and objective improvement was seen with corticosteroid therapy. To the best of the authors' knowledge, such an occurrence has not been reported previously. This case highlights the importance of keeping a high index of suspicion while investigating a patient with pulmonary hypertension in whom the aetiology is not apparent on initial evaluation. Identification of the disease, in its early-stage, can prevent progression to bronchiectasis and fibrotic lung disease, and thus, patients can be saved from the morbidity related to end-stage disease.
3038618
Is the mortality higher in the pulmonary vs the extrapulmonary ARDS? A meta analysis.
BACKGROUND AND AIM
ARDS can occur from the following two pathogenetic pathways: a direct pulmonary injury (ARDSp); and an indirect injury (ARDSexp). The predisposing clinical factor can influence the pathogenesis and clinical outcome of ARDS. This metaanalysis was aimed at evaluating whether there is any difference in mortality between the two groups.


METHODS
We searched the MEDLINE, EMBASE, and CINAHL databases for relevant studies published from 1987 to 2007, and included studies that have reported mortality in the two groups of ARDS. We calculated the odds ratio (OR) and 95% confidence interval (CI) to assess mortality in patients with ARDSp vs patients with ARDSexp and pooled the results using three different statistical models.


RESULTS
Our search yielded 34 studies. In all, the studies involved 4,311 patients with 2,330 patients in the ARDSp group and 1,981 patients in the ARDSexp group. The OR of mortality in ARDSp group compared to the ARDSexp group was 1.11 (95% CI, 0.88 to 1.39), as determined by the random-effects model; 1.04 (95% CI, 0.92 to 1.18), as determined by the fixed-effects model; and 1.04 (95% CI, 0.92 to 1.18), as determined by the exact method, indicating that mortality is similar in the two groups. The mortality was no different whether the studies were classified as prospective (OR, 1.15; 95% CI, 0.87 to 1.51) or retrospective (OR, 1.01; 95% CI, 0.61 to 1.69); small (OR, 1.11; 95% CI, 0.77 to 1.60) or large (OR, 1.1; 95% CI, 0.82 to 1.49); or observational (OR, 1.10; 95% CI, 0.82 to 1.49) or interventional (OR, 0.97; 95% CI, 0.79 to 1.19). There was methodological and statistical heterogeneity (I(2), 50.9%; 95% CI, 21.3 to 66.2%; chi(2) statistic, 67.22; p = 0.0004).


CONCLUSIONS
The results of this study suggest that there is no difference in mortality between these two groups. Further studies should focus on specific etiologies within the subgroups rather than focusing on the broader division of ARDSp and ARDSexp.
45999589
Noninvasive ventilation in acute heart failure.
206196304
Interdialytic hypertension-an update.
The reference standard for diagnosing hypertension among hemodialysis patients is 44-hour interdialytic ambulatory blood pressure (BP) recording. However, a more practical way to diagnose and manage hypertension is to measure home BP over the interdialytic interval. In contrast to pre- and postdialysis BP recordings, measurements of BP performed outside the dialysis unit correlate with the presence of left ventricular hypertrophy and directly and strongly with all-cause mortality. Hypervolemia that is not clinically obvious is the most common treatable cause of hypertension among patients with end-stage renal disease; thus, volume control should be the initial therapy to treat hypertension in most hemodialysis patients. To diagnose hypervolemia, continuous blood volume monitoring is emerging as an effective and simple technique. Reducing dietary and dialysate sodium is an often overlooked strategy to improve BP control. Although definitive randomized trials that show cardiovascular benefits of BP lowering among hypertensive hemodialysis have not been performed, emerging evidence suggests that lowering BP might reduce cardiovascular events. The treatment should be guided by BP obtained outside the dialysis unit because predialysis and postdialysis BP are quite variable and agree poorly with measurements obtained outside the dialysis unit. Although the appropriate level to which BP should be lowered remains elusive, current data suggest that interdialytic ambulatory systolic BP should be lowered to <130 mm Hg and averaged home systolic BP to <140 mm Hg. Antihypertensive drugs will be required by most patients receiving thrice weekly dialysis for 4 hours. Beta blockers, dihydropyridine calcium blockers, and agents that block the renin-angiotensin system appear to be effective in lowering BP in these patients.
11492307
Location Not Quantity of Blood Pressure Measurements Predicts Mortality in Hemodialysis Patients
Background: Blood pressure (BP) measurements obtained outside the dialysis unit are prognostically superior. Whether it is the greater number of measurements made outside the dialysis unit that correlates with prognosis or whether BPs outside dialysis units are ecologically more valid is unknown. Methods and Results: A prospective cohort study was conducted in 133 patients on chronic hemodialysis. BP was measured by the patients at home for 1 week, over an interdialytic interval by ambulatory recording, and by ‘routine’ and standardized methods in the dialysis unit for 2 weeks. Up to 6 BPs were randomly selected from a 44-hour recording of ambulatory or 1-week recording of home BPs, such that the dialysis unit BPs were exactly matched to the number of ambulatory or home BPs. The relationship with left ventricular hypertrophy and all-cause mortality was analyzed using receiver-operating characteristic curves and Cox proportional hazards analysis, respectively. Over a median follow-up of 24 months, 46 patients (31%) died. A BP change of 10/5 mm Hg increased the risk of all-cause mortality by 1.22 (95% CI 1.07–1.38)/1.18 (95% CI 1.05–1.31) with the average of the 44-hour recording and 1.20 (95% CI 1.07–1.34)/1.15 (95% CI 1.03–1.27) when up to 6 random BPs from the same ambulatory recording were drawn and averaged. With home BPs the hazard ratios were 1.17/1.15 per 10/5 mm Hg increase in BP with the average of 1-week recording and 1.18/1.13 when up to 6 random BPs were drawn and averaged. Limited duration ambulatory BP monitoring of any 6-hour interval during the first 24 h or 4-day home BP recorded after the midweek dialysis was similarly predictive of all-cause mortality. Conclusions: In patients on hemodialysis, the location, not the quantity, of the BP recordings obtained outside the dialysis unit is associated with target organ damage and mortality.
30136783
Blood pressure goal in chronic kidney disease: what is the evidence?
PURPOSE OF REVIEW
Most guidelines recommend that seated clinic blood pressure (BP) be targeted to less than 130/80 mmHg in patients with chronic kidney disease (CKD). The evidence underlying these recommendations is the subject of this review.


RECENT FINDINGS
The best evidence to target a certain level of BP in patients with CKD comes from randomized trials. Only three trials have prospectively examined the level to which BP should be lowered. These trials conducted exclusively among patients with CKD have demonstrated that compared to a less aggressive BP goal, a BP goal of less than 130/80 mmHg neither saves lives nor protects the kidney or the cardiovascular system.


SUMMARY
It is reasonable to achieve a goal of less than 140/90 mmHg in most patients with CKD. More aggressive lowering is not firmly supported by current data. Since BP control is important, hypertension therapy should be individualized. Individualization through home BP measurements to diagnose, monitor and treat hypertension appears to be an attractive option.
44919999
Asymptomatic incomplete left ventricular apical rupture diagnosed by cardiac magnetic resonance imaging.
66-year-old man presented with a fever of 103 °F, cough, and dyspnea, despite 3 days' treatment of pneumonia. Chest radiography revealed a normal cardiac silhouette and a small left pleural effusion. A baseline electrocardiogram (ECG) showed normal sinus rhythm with profound ST-segment elevation in the anterolateral leads. An ECG obtained 2 months earlier was normal. An echocardiogram showed severe hypokinesis of the anterior, anteroseptal, and apical segments without evidence of a pericardial effusion. Coronary angiography revealed complete occlusion of the proximal left anterior descending coronary artery with severe distal anterior hypokinesis. 
 
Forty-eight hours after admission, the patient had recurrent fever. A repeat transthoracic echocardiogram (Fig. 1) revealed a thin, aneurysmal, left ventricular (LV) apex with pericardium apparently adherent to the apex. In addition, a moderate-to-large, echo-free pericardial effusion was noted. Out of clinical concern for a possible contained LV rupture, cardiac magnetic resonance imaging (CMR) was performed for definitive evaluation and tissue characterization. 
 
 
 
Fig. 1 Transthoracic echocardiogram (4-chamber view at end-systole) reveals an apex-sparing pericardial effusion and an aneurysmal left ventricular apex. 
 
 
 
The CMR (Figs. 2 and 3) revealed evidence of a large myocardial infarction (MI) with subsequent aneurysm formation involving the distal half of the left anterior descending artery distribution and the entire apex, with an extensive amount of thrombus in the apex. A “hinge-point” involving the lateral and anterolateral walls was noted, raising the concern of a possible contained rupture of the LV apex. A large, predominantly simple-appearing pericardial effusion was noted circumferentially, but the apex was spared. The pericardium was hyperenhanced on viability/ scar imaging in the regions of infarct, suggesting post-MI pericarditis. 
 
 
 
Fig. 2 Cine cardiac magnetic resonance imaging demonstrates a large aneurysmal area involving the distal half of the left anterior descending coronary artery distribution with an extensive amount of thrombus at the apex. A hinge-point involving the lateral ... 
 
 
 
 
 
Fig. 3 Viability/scar imaging reveals a transmural infarction of the affected area. The remainder of the left ventricular myocardium appears to be of full thickness and viable. There is also hyperenhancement of the pericardium in the infarct regions, ... 
 
 
 
A follow-up echocardiogram performed 1 week later showed a slight decrease in the size of the pericardial effusion. Repair of the LV was deferred until effective surgical suturing could be performed on the infarcted area. 
 
Eight weeks later, the patient underwent successful LV endoaneurysmorrhaphy with a Dacron patch. Intraoperatively, a 3- × 4-cm balloon-like aneurysm was found to be fused to the pericardial sac. The aneurysm was excised, and subsequent microscopic evaluation revealed necrotic myocardium and reactive connective tissue (Fig. 4). The patient had an uneventful hospital course and was discharged from the hospital in stable condition. At a follow-up visit 2 months later, he reported a substantial increase in exercise tolerance and a return to usual daily activities. 
 
 
 
Fig. 4 Photomicrograph illustrates necrotic myocardium and adjacent reactive connective tissue. (H & E, orig. ×100)
37096406
Diagnosing obesity by body mass index in chronic kidney disease: an explanation for the "obesity paradox?".
Although obesity is associated with poor outcomes, among patients with chronic kidney disease (CKD), obesity is related to improved survival. These results may be related to poor diagnostic performance of body mass index (BMI) in assessing body fat content. Accordingly, among 77 patients with CKD and 20 controls, body fat percentage was estimated by air displacement plethysmography (ADP), skinfold thickness, and body impedance analysis. Defined by BMI ≥30 kg/m(2), the prevalence of obesity was 20% in controls and 65% in patients with CKD. Defined by ADP, the prevalence increased to 60% among controls and to 90% among patients with CKD. Although sensitivity and positive predictive value of BMI to diagnose obesity were 100%, specificity was 72%, but the negative predictive value was only 30%. BMI correctly classified adiposity in 75%. Regardless of the presence or absence of CKD, subclinical obesity (defined as BMI <30 kg/m(2) but excess body fat by ADP) was often missed in people with low lean body mass. The adjusted odds ratio for subclinical obesity per 1 kg of reduced lean body mass by ADP was 1.14 (95% CI: 1.06 to 1.23; P<0.001). Skinfold thickness measurements correctly classified 94% of CKD patients, but bioelectrical impedance analyzer-assessed body fat estimation did so in only 65%. Air displacement plethysmography-, skinfold thickness-, and bioelectrical impedance analyzer-assessed body fat all provided reproducible estimates of adiposity. Skinfold thickness measurements may be a better test to classify obesity among those with CKD. Given the low negative predictive value of BMI for obesity, our study may provide an explanation of the "obesity paradox."