Use of intravenous magnesium to treat acute onset atrial fibrillation: a meta-analysis.

OBJECTIVES: To assess the effects of intravenous magnesium on converting acute onset atrial fibrillation to sinus rhythm, reducing ventricular response and risk of bradycardia. DESIGN AND DATA SOURCES: Randomised controlled trials evaluating intravenous magnesium to treat acute onset atrial fibrillation from MEDLINE (1966 to 2006), EMBASE (1990 to 2006) and Cochrane Controlled Trials Register without language restrictions. REVIEW METHODS: Two researchers independently performed the literature search and data extraction. RESULTS: 10 randomised controlled trials, including a total of 515 patients with acute onset atrial fibrillation, were considered. Intravenous magnesium was not effective in converting acute onset atrial fibrillation to sinus rhythm when compared to placebo or an alternative antiarrhythmic drug. When compared to placebo, adding intravenous magnesium to digoxin increased the proportion of patients with a ventricular response <100 beats/min (58.8% vs 32.6%; OR 3.2, 95% CI 1.93 to 5.42; p<0.001). When compared to calcium antagonists or amiodarone, intravenous magnesium was less effective in reducing the ventricular response (21.4% vs 58.5%; OR 0.19, 95% CI 0.09 to 0.44; p<0.001) but also less likely to induce significant bradycardia or atrioventricular block (0% vs 9.2%; OR 0.13, 95% CI 0.02 to 0.76; p = 0.02). The use of intravenous magnesium was associated with transient minor symptoms of flushing, tingling and dizziness in about 17% of the patients (OR 14.5, 95% CI 3.7 to 56.7; p<0.001). CONCLUSIONS: Adding intravenous magnesium to digoxin reduces fast ventricular response in acute onset atrial fibrillation. The effect of intravenous magnesium on the ventricular rate and its cardiovascular side effects are less significant than other calcium antagonists or amiodarone. Intravenous magnesium can be considered as a safe adjunct to digoxin in controlling the ventricular response in atrial fibrillation.

Meta-analysis of frusemide to prevent or treat acute renal failure.

OBJECTIVE: To investigate the potential beneficial and adverse effects of frusemide to prevent or treat acute renal failure in adults. DESIGN: Meta-analysis of randomised controlled trials. DATA SOURCES: Cochrane controlled trials register (2005 issue 4), Embase, and Medline (1966 to 1 February 2006), without language restrictions. REVIEW METHODS: Two reviewers checked the quality of the studies and independently extracted data. RESULTS: Nine randomised controlled trials totalling 849 patients with or at risk of acute renal failure were included. Outcome measures not significantly different after frusemide treatment were in-hospital mortality (relative risk 1.11, 95% confidence interval 0.92 to 1.33), risk for requiring renal replacement therapy or dialysis (0.99, 0.80 to 1.22), number of dialysis sessions required (weight mean difference--0.48 sessions, -1.45 to 0.50), and proportion of patients with persistent oliguria (urine output < 500 ml/day: 0.54, 0.18 to 1.61). Stratifying studies that used frusemide to prevent or treat acute renal failure did not change the results on mortality (relative risk ratio 2.10, 95% confidence interval 0.67 to 6.63) and the risk for requiring dialysis (4.12, 0.46 to 37.2). Evidence suggested an increased risk of temporary deafness and tinnitus in patients treated with high doses of frusemide (relative risk 3.97, 95% confidence interval 1.00 to 15.78). CONCLUSIONS: Frusemide is not associated with any significant clinical benefits in the prevention and treatment of acute renal failure in adults. High doses may be associated with an increased risk of ototoxicity.

Maxillofacial injuries and life-threatening hemorrhage: treatment with transcatheter arterial embolization.

BACKGROUND: There are many reasons for hypotension in trauma patients with multiple injuries; one uncommon source is facial fractures. The treatment algorithm is volume replacement and local control of the bleeding. A retrospective study was undertaken to evaluate the treatment of patients with life-threatening hemorrhage secondary to facial fractures, and to develop a treatment algorithm. METHODS: A retrospective chart review was undertaken to determine the incidence of hemorrhagic shock in patients with facial fractures exclusive of others sources, and the use of transcatheter arterial embolization to control the bleeding was evaluated. RESULTS: Over a 4-year period, 7562 patients were treated at Palmetto Richland Memorial Hospital, a Level I trauma center. There were 912 patients with facial injuries, with 11 of these patients presenting with life-threatening hemorrhage secondary to facial fractures. The incidence of life-threatening hemorrhage from facial fracture was 1.2%. The mechanism of injury was blunt in 10 patients and penetrating in 1. The blunt injuries resulted from six motor vehicles crashes, three motorcycle crashes, and one plane crash. The one penetrating injury was a shotgun blast. There were six patients with Le Fort III fractures, two patients with Le Fort II fractures, and three patients with a combination of Le Fort II and III fractures bilaterally. The average volume infused before the embolization was 7 L; this included blood and crystalloid. There were four complications: two minor groin hematomas, one partial necrosis of the tongue, and one facial nerve palsy. There were two deaths, both secondary to concomitant intracranial injury as a result of blunt trauma. CONCLUSION: The incidence of severe hemorrhage secondary to facial fractures is rare; however, it can be life threatening. When common modalities of treatment such as pressure, packing, and correction of coagulopathy fail to control the hemorrhage, transcatheter arterial embolization offers a safe alternative to surgical control.