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[Effect of low dose 5-fluorouracil and cisplatin intra-arterial infusion chemotherapy in advanced hepatocellular carcinoma with decompensated cirrhosis].

BACKGROUND/AIMS: Advanced hepatocellular carcinoma (HCC) with portal vein thrombosis (PVT) has a poor prognosis. The aim of this study was to evaluate the efficacy and safety of repeated arterial infusions of low dose cisplatin and 5-fluorouracil (FU) in patients with advanced HCC with decompensated cirrhosis. METHODS: Between January 1995 and December 2003, a total of 79 decompensated cirrhotic patients having HCC and PVT were enrolled and divided into 2 groups. Group 1 (n=40) received intra-arterial infusion chemotherapy with cisplatin (10 mg for 5 days) and 5-FU (250 mg for 5 days) via an implanted chemoport every 4 weeks' and group 2 (n=39) was managed with only conservative treatment. RESULTS: The two groups were well matched with respect to the features relating to the prognosis, including age, gender and the Child- Pugh class. Although diffuse tumor involvement, main portal vein tumor thrombosis and bi-lobar involvement were more frequent in group 1, the median survival period of group 1 was significantly longer than group 2 (5 months vs. 3 months, respectively, P=0.016). Also, the 1-year survival rate of group 1 (7.5%) was higher than that of group 2 (5.1%) (P=0.016). When we analyzed the patients with the Child class B, the survival benefits of intra-arterial chemotherapy were more significant (P=0.008). CONCLUSIONS: Intra-arterial chemotherapy consisting of low dose 5-FU and cisplatin achieved favorable results for advanced HCC patients who had decompensated cirrhosis, and it showed better survival in selected patients. This therapy may be useful as a palliative treatment for HCC patients with decompensated cirrhosis.

Adult↗

Persistent high NTpro-BNP concentration as a negative prognostic factor in patients with decompensated heart failure.

INTRODUCTION: Monitoring of natriuretic peptide concentration may be useful for the identification of high-risk patients presenting with decompensated chronic heart failure (CHF). AIM: Assessment of the predicting value of a significant decrease (by > or =20% vs. baseline) of N-terminal proBNP (NTpro-BNP, ROCHE) concentration during hospitalisation in patients with decompensated CHF. METHODS: This study involved 54 patients admitted to our centre because of CHF decompensation. Concentration of NTpro-BNP was measured on admission and at discharge from hospital. Primary end-points of this study were overall mortality and mortality with a number of cardiovascular-related readmissions. RESULTS: Mean NTpro-BNP concentration on admission was 7435+/-10040 pg/ml and at the time of discharge from hospital -- 4816+/-7822 pg/ml. In 31 (57%) patients a significant decrease (> or =20% vs baseline value) in NTpro-BNP level (mean: -58%+/-21%) was noted, while in the remainder (23 patients; 43%) neither an increase nor a decrease in NTpro-BNP levels was observed (mean: +72%+/-132%) despite optimal treatment and stabilisation of the clinical status. The mean follow-up duration was 358+/-240 days. Cox analysis showed that the absence of significant NTpro-BNP level decrease was associated with an increased risk of death -- RR: 3.69 (95% CI: 1.10-12.37; p=0.035) and was the single independent risk factor for readmission due to cardiovascular-related reasons and/or death -- RR: 2.29 (95% CI: 1.20-4.35; p=0.01). In the group of 23 patients with an increase or decrease in NTpro-BNP concentration of more than or equal to 20%, the survival rate was 65% vs. 87% in the remainder (p=0.02). CONCLUSIONS: The lack of a significant (> or =20%) decrease of NTpro-BNP level during hospitalisation correlates with a higher mortality and rate of readmissions. NTpro-BNP level monitoring may be of clinical importance for risk stratification in patients hospitalised for decompensated CHF.

Biological Factors↗

[Comparison of the effects of intravenous recombinant human brain natriuretic peptide and nitroglycerin in patients with decompensated acute heart failure: a multicenter, randomized, open-label, parallel-design study].

OBJECTIVE: To compare the efficacy and safety of intravenous infusion recombinant human brain natriuretic peptide (rhBNP) versus nitroglycerin (NIT) in treating patients with decompensated acute heart failure. METHODS: A total of 209 patients characterized of decompensated acute heart failure were enrolled in this multicenter, randomized, open-label, parallel-design study. The patients were randomly allocated to catheter group and non-catheter group (depending on the use of Swan-Ganz). Each group was then randomly assigned to receive rhBNP (0.15 microg/kg bolus intravenous injection followed by 0.0075 microg.kg(-1).min(-1) for 24 hours, n = 105) or NIT (starting at 10 microg/min and increasing 5 microg/min each time till clinical effective dose for 24 hours, n = 104). Blood pressure, heart rate, dyspnea grade, 24 hours fluid in- and output and improvement in patient symptoms and signs were evaluated and adverse events were documented. RESULTS: Urine output was significantly increased after both rhBNP and NIT treatments. Dyspnea and symptom improvements were more significant in rhBNP group compared to NIT group. PCWP and PAP were both decreased after rhBNP and NIT therapies and there was more significant reduction in PCWP and PAP between 30 min and 2 hours in rhBNP group compared to NIT group. However, RAP and CI were similar between the two groups at various time points. The total adverse events were comparable between the two groups (20.0% vs. 19.2%, P > 0.05) and 7 patients withdrew the study due to adverse events (4 in rhBNP and 3 in NIT group). CONCLUSIONS: rhBNP is superior to nitroglycerin in improving dyspnea and symptoms and decreasing PCWP and PAP in patients with decompensated acute heart failure patients. The safety of rhBNP was comparable to nitroglycerin in treating patients with decompensated acute heart failure.

Adolescent↗

A multivariate model for predicting hospital admissions for patients with decompensated chronic obstructive pulmonary disease.

PURPOSE: To develop a method for predicting hospital admissions for patients with decompensated chronic obstructive pulmonary disease treated in an emergency department. METHODS: A 4-year survey including training and validation periods was conducted. Stepwise logistic regression was used to develop a multivariate model using information from the patient's previous visits and results of baseline pulmonary function tests. MEASUREMENTS AND MAIN RESULTS: During the first 2 years, there were 693 visits to the emergency department for decompensated chronic obstructive pulmonary disease. The patient was admitted to the hospital on 210 occasions (30.3%). Logistic regression showed that the probability of admission was related to the following: the admission and relapse rates for previous visits, the proportion of previous discharges from the emergency department in which "conservative therapy" was given, the highest baseline post-bronchodilator forced expiratory volume in 1 second within 3 years of entry, and the highest baseline pre-bronchodilator forced expiratory volume in 1 second-vital capacity ratio. A relapse was defined as an unscheduled return to the emergency department within 48 hours. "Conservative therapy" was any treatment regimen that did not include parenteral medications. During the next 2 years, the model was validated with patients not previously treated at this medical center. Seventy-six (28.3%) of 269 episodes resulted in hospital admission. The logistic model was used to categorize each visit during the validation phase. "High-risk" visits had calculated probabilities of admission greater than .208, while "low-risk" visits had values that were less. The admission rate for 98 low-risk visits (8.2%) was much lower than the rate for 171 high-risk visits (39.8%). CONCLUSIONS: A multivariate model can be used to identify patients with decompensated chronic obstructive pulmonary disease who are unlikely to need hospitalization. This model could be used to select episodes of decompensated chronic obstructive pulmonary disease for treatment at home.

Aged↗

[Further studies on the functional decompensation of corneal endothelial cells].

30 cases of corneal endothelial decompensation occurred in 241 transparent grafts of penetrating keratoplasty during a 5-year follow-up with the specular photomicroscope. The study indicated that the critical cell density for corneal endothelial decompensation was 786/mm2; the critical cell dimension as represented by the sum of mean maximal and minimal diagonal was 35.43 microns; and the critical difference between the mean maximal and minimal diagonal was 14.70 microns. When these three criteria all approximated the critical values, the endothelium was regarded as in a predecompensation state that heralded impending endothelial decompensation. Therefore, these values may be regarded as a reference standard for diagnosing early stage endothelial decompensation.

Cell Count↗

[Piretanide in chronic and acute decompensated heart failure. Effect on hemodynamics and vasoactive hormones].

Eight patients with chronic heart failure classified as NYHA class II to III (group 1) and nine patients with acute decompensated heart failure classified as NYHA class IV (group 2) were treated with piretanide at a dosage of 12 mg administered intravenously. In both groups the level of prostaglandine PGE2 as well as plasma renine activity significantly increased prior to the onset of diuresis. The percentage increase was more pronounced in group 1 which had lower baseline values. With a time-lag, the norepinephrine plasma level also increased significantly. During the first 30 minutes there was only little effect on blood pressure, pulmonary artery pressure and cardiac output in patients with chronic heart failure (group 1). Only after 60 minutes there was a significant decrease in mean pulmonary artery pressure (from 39 +/- 17 to 33 +/- 18 mm Hg; p less than 0.05). In patients with acute decompensated heart failure (group 2) piretanide led to a significant reduction in mean pulmonary artery pressure (from 42 +/- 13 to 37 +/- 12 mm Hg; p less than 0.05) within 15 minutes after administration, i.e. even prior to the onset of diuresis. Thus, the administration of piretanide had a positive effect on hemodynamics in patients with chronic as well as in patients with acute decompensated heart failure. Significant improvement prior to diuresis onset, however, was only found in patients with acute decompensated heart failure. These effects may be explained by a stimulation of prostaglandines which promote vasodilation. They are increased by the diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

Decompensated benign nephrosclerosis and secondary malignant nephrosclerosis.

Using semiquantitative morphometric methods, the clinical picture of decompensated benign nephrosclerosis is distinguished from that of secondary malignant nephrosclerosis, designated as the consequence of high pressure. It is shown that hypertensive glomerulopathy triggered by high pressure and postglomerular interstitial fibrosis with tubular atrophy are in the foreground of pathologic changes in decompensated benign nephrosclerosis, whereas the preglomerular vessel network is most often affected in secondary malignant nephrosclerosis. The preglomerular vascular lesions in secondary malignant nephrosclerosis lead to such heavy stenosis of the afferent vessels that the clinical picture of hypertensive glomerulopathy is rarely observed, while that of ischemic glomerular capillary collapse is frequent. The preferred affliction of the glomeruli and the postglomerular vessel network leads in decompensated benign nephrosclerosis to severe interstitial fibrosis, which has a pyramidal form, decreasing from the base of the pyramid at the corticomedullary boundary to the outer renal cortex. In secondary malignant nephrosclerosis fibrosis of the renal cortical interstitium is homogeneous in all layers of the renal cortex. Clinically, decompensated benign nephrosclerosis and secondary malignant nephrosclerosis, which occur predominantly in young to middle-aged males, manifest malignant hypertension. They are also accompanied by progressive renal insufficiency.

Adult↗

[Excretion of uric acid in cardiac decompensation].

The role of hyperuricemia is confirmed, in literature, as a risk factor in ischemic heart disease and in the development of atherosclerotic complications. The problem of uric acid concentration in serum is still not elucidated as well as the role of the eventual hyperuricemia as a risk factor and its excretion from the kidneys of patients with heart diseases in a decompensation stage. Thirty five patients with different heart diseases in various decompensation stages were observed. In all patients, the uric acid concentration in serum were studied as well as the clearance of uric acid, reabsorption percentage in tubules and glomerular filtration according to the clearance of endogenous creatinine. The results obtained revealed that hyperuricemia (over 7 mg%) is found in a great number of the patients (40%) with heart decompensation. The hyperuricemia established resulted primarily from the reduced filtration of glomeruli. In some of the cases, an increased reabsorption of uric acid in tubules was found. In other, single cases, data exist about uric acid secretion in tubules. The problem of heart patients treatment in decompensation stage with the presence of hyperuricemia is discussed. In those cases, very likely, prophylactic measures should be undertaken due to the fact that hyperuricemia is a factor, secondarily leading to atherosclerotic heart alterations.

Adolescent↗

Long-term prognosis of patients presenting to the emergency room with decompensated congestive heart failure.

OBJECTIVES: This observational study was done to describe the long term prognosis of patients presenting to an emergency room with decompensated heart failure and to determine the factors that influence their survival. DESIGN: The routine clinical and laboratory characteristics of consecutive patients presenting to an emergency room with decompensated heart failure were documented and the patients followed for an average of 44 months (range 41 to 47). SETTING: One teaching hospital and one community-based hospital in Montreal, Quebec. PATIENTS: A prospective cohort of 153 consecutive patients presenting to the emergency room with decompensated heart failure. OUTCOME MEASURES: Total mortality was the main outcome. Survival status was validated by the government health insurance board. RESULTS: Survival was poor, with 61% dying within the 47-month follow-up. Univariate analysis revealed the following variables to be associated with decreased survival; low sodium (P < 0.001), decreased renal function (P < 0.001), prior hospitalization for decompensated heart failure (P < 0.001), intraventricular conduction defect (P < 0.002), failure despite prior use of angiotensin-converting enzyme (ACE) inhibitors (P < 0.005) and increased cardiac dimensions as determined by increased left ventricular end systolic diameter (P < 0.04). The multivariate analysis using the Cox proportional hazards model showed a prior admission for heart failure (relative risk [RR] 1.9 [P = 0.005], 95% confidence interval [CI] 1.2 to 2.9), hyponatremia (RR 2.1 [P = 0.005], 95% CI 1.2 to 3.5), presence of an intraventricular conduction delay (RR 1.9 [P = 0.003], 95% CI 1.2 to 2.9), and the cumulative required dose of intravenous furosemide (RR 1.7 [P = 0.03], 95% CI 1.1 to 2.8) to be associated with increased mortality. Patients with hyponatremia despite the use of ACE inhibitors were at greatest risk (RR 11.5 [P < 0.001], 95% CI 5.3 to 24.9). CONCLUSIONS: This prospective observational study confirms that the long term prognosis of patients needing hospitalization for congestive heart failure remains poor. Readily available acute-phase clinical variables may assist in predicting prognosis.

Aged↗

The hospital course and short term prognosis of patients presenting to the emergency room with decompensated congestive heart failure.

OBJECTIVES: This observational study was done to describe the characteristics, hospital course and short term prognosis of patients presenting to an emergency room with decompensated heart failure and to determine the parameters influencing the length of their hospital stay. DESIGN: The routine clinical and laboratory characteristics of consecutive patients presenting to an emergency room with decompensated heart failure were documented and the patients followed for six months. SETTING: One teaching hospital and one community-based hospital in Montreal, Quebec. PATIENTS: A prospective cohort of 153 consecutive patients presenting to the emergency room with decompensated heart failure. Follow-up was by clinic visit and telephone survey at one, three and six months. Follow-up was 100%. MEASURES OF OUTCOME: Length of hospital stay, in-hospital mortality, readmissions and after hospital discharge deaths were measured. RESULTS: The average length of hospital stay was 6.2 days with a skewed distribution ranging from one to 56 days. A multivariate analysis showed that the length of hospital stay was associated with increasing left atrial size (P < 0.05), an ischemic etiology of the heart failure (P < 0.03) and a slow response to diuretic therapy (P < 0.001). This mathematical model accounted for only a small amount of hospital stay variability (R2 = 0.22). Six month mortality and morbidity of these patients was high, with 23% dying and 30% readmitted for heart failure, but was independent of the duration of the initial hospitalization. CONCLUSIONS: This prospective study confirms that the hospital course for congestive heart failure is shortening. The six month prognosis of patients presenting to an emergency room for decompensated heart failure is poor and appears independent of the length of hospital stay.

Aged↗

Characterization of the precipitants of hospitalization for heart failure decompensation.

BACKGROUND: The model for management of patients with heart failure may be a key determinant of morbidity and quality of life. Development of a better management strategy for these patients requires determination of the reasons for decompensation that leads to hospitalization. OBJECTIVES: To ascertain and rank the principal reasons for hospitalization of patients who have heart failure. METHODS: Retrospective audit of all 1992 admissions (N = 1031; 691 patients) coded for heart failure at a Veterans Affairs medical center and a tertiary care university medical center. RESULTS: The diagnosis of heart failure was verified by preset criteria in 72% of the patients. Of the 496 patients with documented heart failure, worsening heart failure was a main reason for admission in 390 (79%). Despite different socioeconomic backgrounds, excessive sodium retention was the leading factor (55%) associated with decompensation in patients at both institutions. Other factors precipitated admission much less often. CONCLUSIONS: Many hospitalizations for heart failure might be avoided by case management directed at lessening sodium overload. Increased use of medications known to be effective in persons with heart failure (angiotensin-converting enzyme inhibitors, digoxin, and adequate diuretic therapy) might reduce the likelihood of decompensation. Implementation of behavioral interventions to assist patients with self-monitoring signs of sodium retention and to improve compliance with medications and dietary sodium restrictions are strategies for further reducing the risk of decompensation.

Aged↗

Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial.

CONTEXT: Decompensated congestive heart failure (CHF) is the leading hospital discharge diagnosis in patients older than 65 years. OBJECTIVE: To compare the efficacy and safety of intravenous nesiritide, intravenous nitroglycerin, and placebo. DESIGN, SETTING, AND PATIENTS: Randomized, double-blind trial of 489 inpatients with dyspnea at rest from decompensated CHF, including 246 who received pulmonary artery catheterization, that was conducted at 55 community and academic hospitals between October 1999 and July 2000. INTERVENTIONS: Intravenous nesiritide (n = 204), intravenous nitroglycerin (n = 143), or placebo (n = 142) added to standard medications for 3 hours, followed by nesiritide (n = 278) or nitroglycerin (n = 216) added to standard medication for 24 hours. MAIN OUTCOME MEASURES: Change in pulmonary capillary wedge pressure (PCWP) among catheterized patients and patient self-evaluation of dyspnea at 3 hours after initiation of study drug among all patients. Secondary outcomes included comparisons of hemodynamic and clinical effects between nesiritide and nitroglycerin at 24 hours. RESULTS: At 3 hours, the mean (SD) decrease in PCWP from baseline was -5.8 (6.5) mm Hg for nesiritide (vs placebo, P<.001; vs nitroglycerin, P =.03), -3.8 (5.3) mm Hg for nitroglycerin (vs placebo, P =.09), and -2 (4.2) mm Hg for placebo. At 3 hours, nesiritide resulted in improvement in dyspnea compared with placebo (P =.03), but there was no significant difference in dyspnea or global clinical status with nesiritide compared with nitroglycerin. At 24 hours, the reduction in PCWP was greater in the nesiritide group (-8.2 mm Hg) than the nitroglycerin group (-6.3 mm Hg), but patients reported no significant differences in dyspnea and only modest improvement in global clinical status. CONCLUSION: When added to standard care in patients hospitalized with acutely decompensated CHF, nesiritide improves hemodynamic function and some self-reported symptoms more effectively than intravenous nitroglycerin or placebo.

Analysis of Variance↗

Lamivudine treatment for decompensated cirrhosis resulting from chronic hepatitis B.

The prognosis of decompensated cirrhosis resulting from chronic hepatitis B is poor, and the benefits of treatment with interferon are outweighed by serious side effects and by the risk of fatal exacerbation of disease activity. Lamivudine rapidly reduces hepatitis B virus (HBV)-DNA in serum to undetectable levels. We have treated 35 patients with chronic hepatitis B and decompensated cirrhosis with lamivudine 100 mg or 150 mg orally once daily. Pretreatment, all were positive for HBV-DNA in serum. Ten had Child-Pugh class B and 25 had Child-Pugh class C liver disease. Seven patients underwent liver transplantation within 6 months of treatment initiation, 5 patients died within 6 months, and 23 patients were treated for at least 6 months (mean = 19 months). In a majority of these 23 cases, there was a slow but marked improvement in liver function, which was most apparent after 9 months of treatment, with a decrease in serum bilirubin from 67 +/- 13 to 30 +/- 4 micromol/L (P <.05, baseline vs. 9 months), an increase in serum albumin from 27 +/- 1 to 34 +/- 1g/L (P <.05), and a decrease in Child-Pugh score from 10.3 +/- 0.4 to 7.5 +/- 0.5 (P <.05). Three patients developed resistance to lamivudine because of a mutation in the YMDD motif, but liver function did not deteriorate. We conclude that inhibition of viral replication with lamivudine results in a significant improvement of liver function in patients with decompensated HBV cirrhosis, but the long-term benefits remain uncertain.

Bilirubin↗

Pharmacokinetics of torsemide in patients with decompensated and compensated congestive heart failure.

Plasma pharmacokinetics of oral furosemide have been shown to be influenced by degree of decompensation in patients with congestive heart failure (CHF). This open-label, sequential comparison trial was conducted to determine whether CHF decompensation also alters the pharmacokinetics and pharmacodynamics of torsemide. Twelve patients with CHF, defined by either hemodynamic parameters or clinical signs and symptoms, were enrolled. On admission for treatment of their CHF, the patients were given 100 mg oral torsemide (phase A). A second dose of oral torsemide 100 mg was administered after hemodynamic parameters and clinical signs and symptoms of decompensated CHF resolved (phase B). Plasma and urine samples were collected over a 24-hour period for determination of torsemide concentrations and urine sodium. Hemodynamic measurements and physical signs and symptoms also were evaluated. During phase A, patients had significantly greater urine output and fractional sodium excretion compared with phase B. A significant increase in the area under the plasma concentration-time curve (AUC) was observed during phase B compared with phase A. However, no significant differences in maximal excretion rate of torsemide were noted between phase A and phase B. Heart failure status slightly affects the plasma pharmacokinetics of torsemide; however, this does not significantly alter the maximal urinary excretion rate of torsemide.

Area Under Curve↗

Spinal imbalance and decompensation problems in patients treated with Cotrel-Dubousset instrumentation.

The basic principles of current idiopathic scoliosis treatment are three-dimensional correction and rigid fixation. Although it is accepted that Cotrel-Dubousset instrumentation (CDI) meets these goals, there is concern about the potential risk of trunk imbalance and spinal decompensation during the derotation manoeuvre. The results of 45 patients with idiopathic scoliosis treated with CDI between December 1988 and August 1992 were retrospectively analysed. Mean age was 14.3 years and mean follow-up period was 48.6 months. An average correction of 49.6% was achieved in the major curves. The best results were obtained in King type III curves, with a 69.4% correction. Spinal imbalance was evaluated by measuring lateral trunk shift (LT), shift of head (SH) and shift of stable vertebra (SS). Decompensation was measured by the increase in secondary curves. When all curve types were included, the average preoperative LT value of 1.96 vertebral units (VU) was brought down to 0.91 VU postoperatively, achieving a 55.9% correction. Fourteen patients had an SH value of zero preoperatively and remained balanced after instrumentation. Of the 41 remaining patients, 21 achieved an SH value of zero postoperatively. When all cases were included, the average preoperative SH value was 1.0 VU, which was corrected to 0.42 VU with CDI (69% correction). An average correction of SS of 75.5% was obtained, with the mean preoperative value of 0.73 VU being corrected to 0.19 VU. At the last follow-up visit, a secondary curve had formed above the major curve in one patient, and three patients had a junctional kyphosis. Loss of correction in the frontal plane correlated with loss of correction of LT. The rigid and semiflexible lumbar curves had a tendency to progress when they were not instrumented, especially in type II curves. Junctional kyphosis could be prevented when concave laminar claws were used in the thoraco-lumbar region. It was concluded that spinal decompensation and imbalance could be minimized with careful preoperative planning, avoidance of overcorrection and use of long instrumentation in double major curves.

Adolescent↗

Decompensation following scoliosis surgery: treatment by decreasing the correction of the main thoracic curve or "letting the spine go".

Coronal decompensation following correction of adolescent idiopathic scoliosis (AIS) has been reported to be due to the Cotrel-Dubousset rod derotation maneuver, or to a hypercorrection of the main thoracic curve. The treatment of such decompensation consists classically in observation, bracing, or extension of the instrumentation in the lumbar spine for a King 2 curve, or in the upper thoracic spine for a King 5 curve. As the postoperative decompensation is related to a hypercorrection of the main thoracic curve (relative to the compensatory curve), we hypothesized that if we were to "let the spine go" to some of its initial deformity, the balance of the patient would be improved. The purpose of the study was therefore to report on two cases where a postoperative imbalance following scoliosis surgery was successfully treated by decreasing the correction of the main thoracic curve. Two patients with AIS were found to have significant imbalance after scoliosis surgery. Both patients had been treated for a right thoracic curve (82 degrees and 85 degrees respectively) with an anterior release and posterior instrumentation. The revision surgery consisted for both patients in removing all the hooks between the end vertebrae of the main thoracic curve. This was done before the 3rd postoperative month for both patients. After revision surgery, the balance of both patients improved dramatically within a few weeks. The shoulders became almost level, and the trunk shift improved concomitantly. The Cobb angle increased by 8 degrees and 10 degrees, and the apical vertebra shifted to the right by 15 and 10 mm for the respective patients. These results were stable at 1-year follow-up. In the event of a persisting imbalance, we recommend, in selected cases, letting the spine go by removing all the implants located between the end vertebrae of the main thoracic curve. This adjustment or fine-tuning of the instrumentation should be done before the fusion takes place, and is best achieved with an instrumentation in which the hooks can be easily removed from the rod.

Adolescent↗

Emergency department management of patients with acute decompensated heart failure.

The Acute Decompensated HEart Failure National REgistry (ADHERE(R)) confirms that the management of decompensated heart failure is an emergency department (ED) problem, as more than 75% of patients admitted to the hospital with heart failure arrive through the ED. This emphasizes the need for collaboration among emergency medicine, cardiology, nephrology, and hospitalists in the management of acute decompensated heart failure. Such collaboration is important for several reasons, including the enhancement of patient care. It is also known that most hospitals lose money on heart failure admissions. Strategies that can be employed to limit hospital losses on heart failure include reducing admissions from the ED; decreasing the length of hospital stay; increasing the use of the observation unit; reducing re-admissions, particularly through the first 30 days; and reducing the use of high-resource areas such as the intensive care unit (ICU). This article will focus on initiatives that can be implemented in the ED to help with these strategies. In particular, we will discuss early initiation of therapy and its ability to improve length of stay, reduce re-admissions, and reduce ICU admissions. Use of the observation unit for the management of heart failure will also be discussed as a way of decreasing admissions from the ED.

Acute Disease↗

Hepatic decompensation associated with hepatitis B e antigen clearance in chronic type B hepatitis.

To examine hepatic decompensation associated with acute exacerbation preceding hepatitis B e antigen clearance in chronic type B hepatitis, 376 patients with chronic hepatitis who were hepatitis B e antigen-positive were prospectively studied for up to 7 yr (mean 25 mo). Among the 165 patients who underwent hepatitis B e antigen clearance, 4 patients experienced hepatic decompensation and one of them eventually developed hepatic encephalopathy and died. The incidence of hepatic decompensation associated with hepatitis B e antigen clearance was 2.4%. We suggest that such an event in previously unrecognized chronic hepatitis B carriers could have been erroneously interpreted as acute or subacute hepatic failure, and that it might have been the result of a stronger enhancement of the host immune response.

Acute Disease↗