Association Between Second Metatarsal Length and Forefoot Loading Under the Second Metatarsophalangeal Joint.

BACKGROUND: Metatarsal length is believed to play a role in plantar plate dysfunction, although the mechanism through which progressive injury occurs is still uncertain. We aimed to clarify whether length of the second metatarsal was associated with increased plantar pressure measurements in the forefoot while walking. METHODS: Weightbearing radiographs and corresponding pedobarographic data from 100 patients in our practice walking without a limp were retrospectively reviewed. Radiographs were assessed for several anatomic relationships, including metatarsal length, by a single rater. Pearson correlation analyses and multiple linear regression models were used to determine whether metatarsal length was associated with forefoot loading parameters. RESULTS: The relative length of the second to first metatarsal was positively associated with the ratio of peak pressure beneath the respective metatarsophalangeal joints ( r = 0.243, P = .015). The relative length of the second to third metatarsal was positively associated with the ratios of peak pressure ( r = 0.292, P = .003), pressure-time integral ( r = 0.249, P = .013), and force-time integral ( r = 0.221, P = .028) beneath the respective metatarsophalangeal joints. Although the variability in loading predicted by the various regression analyses was not large (4%-14%), the relative length of the second metatarsal (to the first and to the third) was maintained in each of the multiple regression models and remained the strongest predictor (highest standardized ß-coefficient) in each of the models. CONCLUSIONS: Patients with longer second metatarsals exhibited relatively higher loads beneath the second metatarsophalangeal joint during barefoot walking. These findings provide a mechanism through which elongated second metatarsals may contribute to plantar plate injuries. LEVEL OF EVIDENCE: Level III, comparative study.

Early response assessment to guide management of methicillin-resistant Staphylococcus aureus bloodstream infections with vancomycin therapy.

BACKGROUND: A subset of vancomycin-treated patients with methicillin-resistant Staphylococcus aureus (MRSA) bloodstream infection (BSI) developed persistent positive blood cultures. Treatment eventually failed. METHODS: A retrospective study was conducted to determine whether early response on day 3 after initiation of vancomycin therapy for MRSA BSI was associated with reduced rates of persistent bacteremia, end-of-treatment failure, and infection-related mortality. Patients' medical charts were reviewed. Susceptibility testing and molecular characterization of bacterial isolates were performed. RESULTS: In this elderly cohort (n = 111; median age 70 years, interquartile range: 57-80 years), early response was observed in 62% of patients and was significantly (P < 0.0001) associated with lower rates of end-of-treatment failure (19% vs 57%) and infection-related death (1% vs 29%), but not with persistent bacteremia (17% vs 29%, P = 0.23). Nearly half (46%; 46 of 100 patients) remained on vancomycin therapy for the entire treatment course; those who continued despite lack of early response had a trend toward a higher risk of death than those who were switched to alternative therapy (38% vs 10%, P = NS). Most (68%) isolates had vancomycin MIC of >1 µg/mL, whereas 10% showed heterogeneous glycopeptide-intermediate Staph aureus (hGISA) phenotype. Nearly half (47%) were typed with staphylococcal cassette chromosome mec IV or V. In a multivariate logistic regression model, lack of response at day 3 was the strongest predictor for end-of-treatment failure, after adjustment for confounders such as age, Acute Physiology And Chronic Health Evaluation II score, intensive care unit admission, vancomycin MIC >1 µg/mL, unbound trough concentration <4 to 5× MIC, and continued vancomycin therapy without change. CONCLUSIONS: Early response assessment after initiation of vancomycin therapy appeared to be useful for considering further diagnostic workup or a switch to alternative therapy to affect a positive outcome in patients with MRSA BSI.

Comparison of bumetanide- and metolazone-based diuretic regimens to furosemide in acute heart failure.

INTRODUCTION: Limited data exist comparing the efficacy and safety of bumetanide- or metolazone-based diuretic regimens to furosemide in acute heart failure (HF). Our purpose was to evaluate the comparative effect on urine output (UO) and renal function between these regimens. METHODS: A retrospective study of hospitalized HF patients treated with continuous infusion furosemide (CIF), combination furosemide plus metolazone (F + M), or continuous infusion bumetanide (CIB). Primary end points were between regimen comparisons for change in mean hourly UO versus baseline and incidence of worsening renal function. RESULTS: Data on 242 patients with acute HF (age 58 ± 12 years, 63% male, left ventricular ejection fraction 38% ± 17%) were analyzed (160 CIF, 42 F + M, 40 CIB). The mean duration of diuretic regimens was 41 ± 32 hours. Compared to baseline, all regimens increased mean hourly UO (P < .0001 for all), with greater increases with F + M (109 ± 171 mL) and CIB (90 ± 90 mL) compared to CIF (48 ± 103 mL; P = .009). Incidence of worsening renal function was not different between regimens; however, blood urea nitrogen (BUN) tended to increase more with F + M (4.4 ± 9.8 mg/dL) and CIB (4.3 ± 9.7 mg/dL) than CIF (1.8 ± 10.8 mg/dL), P = .09. The incidence of hyponatremia was higher with F + M and CIB. Differences in UO, BUN, and hyponatremia were retained in the subgroup analysis limited to patients with baseline serum creatinine <1.5 mg/dL, where renal function between the groups was not different. CONCLUSION: Compared to CIF, F + M or CIB was associated with greater increases in UO. No difference in the incidence of worsening renal function was found; however, electrolyte abnormalities may be more prevalent when furosemide is combined with metolazone or when bumetanide is used. These therapeutic differences warrant prospective study.

Clinical experience with low-dose continuous infusion of furosemide in acute heart failure: assessment of efficacy and safety.

INTRODUCTION: Clinical data are scarce for furosemide administered as a low-dose (<160 mg/24 hours) continuous intravenous infusion in acute heart failure (HF). Our purpose was to evaluate the efficacy and safety of low-dose continuous infusion of furosemide on diuretic response, renal function, and patient outcomes. METHODS: A retrospective study of patients with acute HF who received furosemide administered as a continuous infusion after initial therapy with intermittent boluses (usually 40-80 mg every 12 hours). End points included mean hourly urine output, incidence of acute renal injury, and outcome disparities of patients who developed acute renal injury. Comparison of patients with preserved and reduced left ventricular ejection fraction (LVEF) was also performed. RESULTS: The study included 150 patients (age 57 ± 13 years, male gender 61%, admission weight 87 ± 32 kg, LVEF 37 ± 15%, 28% preserved LVEF). Mean initial and maximum furosemide doses were 5.1 ± 1.1 mg/h and 6.2 ± 2.2 mg/h, respectively. Mean duration of therapy was 51.4 ± 67.5 hours. Continuous infusion of furosemide was associated with a significant increase in mean hourly urine output compared to baseline (150 ± 77 mL/h vs 116 ± 69 mL/h, P < .001). Acute renal injury developed in 19% of patients, with 70% of those occurring within the first 48 hours of therapy. Mean serum creatinine (baseline 1.55 ± 1.50 mg/dL vs at discharge 1.64 ± 1.61 mg/dL, P = .20) and estimated glomerular filtration rate (baseline 67 ± 39 mL/min vs at discharge 67 ± 43 mL/min, P = .89) did not significantly change over the course of the hospitalization. Development of acute renal injury was associated with poorer outcomes, higher furosemide dose, and longer duration of furosemide therapy. Diuretic response and safety were not different between patients with preserved or reduced LVEF. CONCLUSIONS: In patients with acute HF, furosemide administered as a low-dose continuous infusion was effective in achieving diuresis and was not associated with a detectable effect on renal function. This diuretic approach appeared to be similarly effective and safe in patients with preserved LVEF.

Comparative effects of nesiritide and nitroglycerin on renal function, and incidence of renal injury by traditional and RIFLE criteria in acute heart failure.

BACKGROUND: Acute renal insufficiency is associated with poorer outcomes in heart failure. Data regarding the renal effects of vasodilatory therapy in acute heart failure are inconclusive. HYPOTHESIS: Nesiritide and nitroglycerin are associated with differing effects on the incidence of acute renal injury and glomerular filtration rate changes. METHODS: A retrospective cohort study of patients hospitalized with acute congestive heart failure who received intravenous nesiritide or nitroglycerin for ≥6 hours. Acute kidney injury was assessed by risk, injury, failure, loss, and end stage (RIFLE) classification (creatinine/GFR criteria) and by traditional acute rise in creatinine of 0.3 mg/dL or 25%. Secondary endpoints included change in estimated glomerular filtration rate, serum creatinine, serum blood urea nitrogen, blood pressure, and urine output. RESULTS: A total of one hundred and thirty-one patients (age 57 ± 12 years, 67% male, left ventricular ejection fraction 38 ± 35%, 30% ischemic) received nesiritide (N = 37) or nitroglycerin (N = 94). Diuretic regimen and doses were similar in both the groups. Mean duration of therapy was not different (nesiritide 38.6 ± 35.7 h vs nitroglycerin 30.7 ± 22.6 h, P = .13). No differences were detected in incidence of renal injury using either criteria (RIFLE: nesiritide 19% vs nitroglycerin 22%, P = .88; traditional: 22% vs 34%, P = .16); however, glomerular filtration rate declined (-1 ± 18 mL/min vs -9 ± 21 mL/min, P = .03) and blood urea nitrogen increased (-0.2 ± 9.9 mg/dL vs 4.2 ± 9.1 mg/dL, P = .02) to a greater degree with nitroglycerin. Nesiritide was associated with lower hourly blood pressures and a higher incidence of systolic blood pressure <80 mm Hg. CONCLUSION: The incidence of renal injury was not different between nesiritide- and nitroglycerin-treated patients with acute heart failure; however, nitroglycerin was associated with a decline in glomerular filtration rate and increase in blood urea nitrogen despite higher baseline and on treatment blood pressures.