20093742
Experience with paraquat poisoning in a respiratory intensive care unit in North India.
INTRODUCTION
Paraquat poisoning is an uncommon entity in India. We report our experience of managing five patients with paraquat poisoning using immunosuppressive therapy.


METHODS
Retrospective analysis of 84 patients admitted with a diagnosis of poisoning over the last eight years was performed. The data were presented in a descriptive fashion.


RESULTS
Five (5.9 percent) out of the 84 patients were admitted with a diagnosis of paraquat poisoning. All patients were mechanically ventilated. All patients had hepatic failure with median peak bilirubin being 22.1 +/- 15.1 mg/dL (range 8.4-45.5). Four of the five patients had renal failure (median peak creatinine 3.8 +/- 1.5 mg/dL; range 3.4-11.1) requiring renal replacement therapy. All patients were treated with intravenous methylprednisolone 15 mg/kg/day for three consecutive days and intravenous cyclophosphamide 10 mg/kg/ day for two consecutive days, followed by intravenous dexamethasone 4 mg thrice a day until recovery or death. Two out of the five patients survived. Three died because of severe acute respiratory distress syndrome and multiorgan dysfunction syndrome.


CONCLUSION
Paraquat poisoning is an uncommon entity in India, and is associated with a high mortality rate. There is a potential role for immunosuppressive therapy in patients with moderate to severe poisoning.
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.
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.
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.
45999589
Noninvasive ventilation in acute heart failure.
30308813
Strategies and feasibility of hypertension control in a prevalent hemodialysis cohort.
BACKGROUND
There are few data to demonstrate the feasibility of long-term blood pressure (BP) control using short dialysis sessions as practiced in the US. Control of hypertension in hemodialysis patients may reduce the risk of cardiovascular events.


METHODS
Forty-two dialysis patients had BPs and weights recorded before and after dialysis for two consecutive weeks and were followed by one physician over three years. Patients were treated by ultrafiltration and conventional antihypertensive drugs and BPs were repeated at three years in the 32 survivors.


RESULTS
93% of the patients (39/42) were African-American. At inception, 85% of the patients were hypertensive with BPs of 154 +/- 23/83 +/- 14 mmHg and 137 +/- 22/74 +/- 14 mmHg pre- and post-dialysis, respectively. The response to ultrafiltration was dependent upon gender, with women having a greater BP reduction compared to men. At three-year follow-up, the BP had dropped significantly in the survivors a mean of 9.4/6.7 mmHg. Pre- and post-dialysis weights, post dialysis BP and interdialytic weight-gain were unchanged. The BP reduction was achieved by an increase in the number of antihypertensive medications from 0.91 +/- 0.86 medications to 1.41 +/- 1.16. Improved BP control did not worsen the efficiency of dialysis (Kt/V). The use of beta-blockers doubled during the period of follow-up. Compared to the USRDS average cardiovascular death rate, the risk of cardiovascular deaths was improved 80% over three years.


CONCLUSION
Long-term BP reduction can be achieved through the use of antihypertensive agents and volume control in a predominantly African-American hemodialysis population. This may impact cardiovascular mortality.
20123228
Selection of initial antihypertensive therapy, regimen design, and goal blood pressure.
Systolic and diastolic blood pressures (BPs) have a strong, continuous, graded, and etiologically significant positive association with cardiovascular disease outcomes. Small reductions in systolic and diastolic BP lead to large and proportionate reductions in ischemic heart disease, stroke, and vascular mortality. A recently reported meta-analysis of nearly a million people without pre-existing vascular disease and participating in clinical trials or observational studies analyzed the relationship between BP and cardiovascular mortality (1). A steep, direct log-linear relationship between systolic and diastolic BP was seen with mortality caused by stroke, ischemic heart disease, and other vascular diseases, including heart failure. The dose-response relationship is seen continuously until 89 years of age. Thus, even the very old have the same relationship between BP and vascular mortality. The million people meta-analysis also was unable to find a threshold at which BP reduction does not yield benefit. The lowest usual BP at any age associated with the best outcomes was 115/75 mmHg. The proportionality of risk reduction also reveals that 20 mmHg systolic BP reduction from 130 to 110 mmHg translates to the same risk reduction as from 180 to 160 mmHg. Vasan et al. (2) analyzed the relationship of high-normal BP with cardiovascular outcomes in men and women in the Framingham cohort. Four BP categories— optimal, normal, high-normal, and hypertension—were studied as defined by the Sixth Joint National Committee. High-normal BP was associated with increased cardiovascular events in both men and women. Even after adjusting for other cardiovascular risk factors (age, body mass index, total cholesterol, diabetes, smoking, and examination year), the risk of first major cardiovascular event was increased 40% in women and 20% in men per change in BP category. A continuous trend for cardiovascular disease across the 3 nonhypertensive BP categories was seen. The authors conclude, “A 20% overall absolute risk of CV events at 10 years currently defines the threshold for treatment of hypertension. In subjects 65 years age, the 10-year absolute risk exceeded 20% in men and approached this in women. Assuming a 25% risk reduction, the estimated number needed to treat over 5 years would be 28 men or 41 women.” These data show that no BP reduction is trivial, and the risk reduction is log-linear. Thus, if the baseline absolute risk is high, the reduction in BP needed to reduce cardiovascular outcomes will be evident with a smaller number of patients.
41975827
Resistant hypertension and the neglected antihypertensive: sodium restriction.
Resistant hypertension is defined as blood pressure (BP) that remains above goal (such as 140/90 mmHg or more) in spite of the concurrent use of three antihypertensive agents of different classes. Ideally, one of the three agents should be a diuretic and all agents should be prescribed at optimal dose amounts. Prevalent among 15% of the treated hypertensives, the risk factors for resistant hypertension include older age, chronic kidney disease (CKD), obesity and diabetes mellitus. Causes of resistant hypertension can be classified into four groups: poor adherence, biological-behavioral factors, CKD and secondary causes, and drugs or exogenous substances. However, before labeling the diagnosis of resistant hypertension, it is important to exclude pseudo-resistant hypertension using home BP monitoring in most patients and ambulatory BP monitoring in a few. Before thinking about the next antihypertensive drug, it is important to restrict dietary sodium. Educating the patient on how to interpret the food label and providing feedback by assessing sodium intake with 24 h urine collection are effective sodium restriction strategies. Sodium restriction can lower BP and among patients with proteinuria can even enhance the anti-proteinuric effects of drugs that block the renin-angiotensin system. Sodium restriction is therefore a valuable but a neglected antihypertensive.
33440140
Supervised atenolol therapy in the management of hemodialysis hypertension.
BACKGROUND
Uncontrolled hypertension continues to be a common problem, particularly in noncompliant hemodialysis patients. Atenolol, a water soluble beta-blocker has a prolonged half-life in renal failure and may serve as a useful antihypertensive agent in these patients.


METHODS
Hypertension was diagnosed by ambulatory blood pressure monitoring for 44 hours during an interdialytic interval in eight chronic hemodialysis patients receiving no antihypertensive therapy. An average daytime blood pressure greater than 140/90 mm Hg or an average nighttime blood pressure greater than 120/80 mm Hg was used to define uncontrolled hypertension. Patients were then administered atenolol (25 mg) following hemodialysis three times a week. The efficacy of therapy was judged by ambulatory blood pressure monitoring three weeks after instituting atenolol therapy. Blood pressure loads above the threshold blood pressures during the day or night were also calculated and compared before and after three weeks of atenolol therapy.


RESULTS
The mean 44-hour ambulatory blood pressure (ABP) fell from 144 +/- 14/80 +/- 7 mm Hg to 127 +/- 13/69 +/- 10 mm Hg (P < 0.001). The heart rate fell from 85 +/- 11 to 70 +/- 11 beats per minute. The systolic and diastolic blood pressure load was reduced from 71 +/- 25% and 30 +/- 24% to 35 +/- 26% and 11 +/- 17%, respectively (P < 0.001). There was a persistent antihypertensive effect over 44 hours. The blood pressure reduction was achieved without any increase in intradialytic symptomatic or asymptomatic hypotensive episodes, reduction in delivered dialysis, or statistically significant changes in serum potassium or glucose.


CONCLUSIONS
A supervised administration of atenolol following hemodialysis effectively and safely controls hypertension in chronic hemodialysis patients. This therapy can be particularly valuable for noncompliant hemodialysis patients.
39974976
Antiproteinuric effect of oral paricalcitol in chronic kidney disease.
BACKGROUND
Proteinuria is a marker of cardiovascular and renal disease in patients with chronic kidney disease (CKD), and reduction in proteinuria has been associated with improved cardiovascular and renal outcomes. While active vitamin D and its analogs have been shown to have renal protective effects in animals, these hormones have not been shown to reduce proteinuria in CKD patients.


METHODS
In three double-blind, randomized, placebo-controlled studies to evaluate the safety and efficacy of oral paricalcitol, 220 CKD stage 3 and 4 patients with secondary hyperparathyroidism (SHPT) were randomized to oral paricalcitol (N= 107, mean dose 9.5 microg/week) or placebo (N= 113) and followed for up to 24 weeks. In conjunction with other safety measures, proteinuria was measured by dipstick and read by an automated reader at the beginning and end of trial. We subsequently analyzed the dipstick data to evaluate the effect of paricalcitol on proteinuria.


RESULTS
At baseline, proteinuria was present in 57 patients randomized to oral paricalcitol and 61 patients randomized to placebo (NS). At the final visit, 29/57 (51%) of the paricalcitol patients compared to 15/61 (25%) placebo patients had reduction in proteinuria, P= 0.004 (odds for reduction in proteinuria 3.2 times greater for paricalcitol patients, 95% CI 1.5-6.9). For the patients who had both proteinuria at baseline and parathyroid hormone (PTH) suppression (end point defined as 2 consecutive > or =30% decreases in iPTH from baseline), 27/51 (53%) patients had a reduction in the proteinuria in the paricalcitol group and 0/7 (0%) had a reduction in proteinuria in the placebo group. Reduction of proteinuria favored patients on paricalcitol, regardless of age, sex, race, diabetes mellitus, hypertension, or use of therapies to block the renin-angiotensin-aldosterone system (RAAS).


CONCLUSION
Our results demonstrate that the reduction in proteinuria was associated with paricalcitol treatment, and the reduction in proteinuria was independent of concomitant use of agents that block the RAAS. Paricalcitol as a potential pharmacologic means of reducing proteinuria in CKD patients warrants further investigation.