BackgroundAmiodarone causes less drug-induced torsade de pointes (TdP) compared to other class III antiarrhythmics. Two theories proposed for this finding include that amiodarone has less repolarization heterogeneity, and/or decreases early after depolarization (EADs). Corrected QT (QTc) dispersion as measured on a surface electrocardiogram (ECG) represents spatial heterogeneity of ventricular repolarization. ObjectiveThe purpose of this study was to analyze the difference in QT dispersion between amiodarone and other class III antiarrhythmics and to determine the etiology of TdP. MethodsThis was a retrospective, observational study at Montefiore Medical Center between January 2005 and January 2015. Inclusion criteria were adults >18 years on amiodarone, dofetilide, or sotalol with prolonged QT interval on 12-lead ECG. ECGs were reviewed by three blinded observers. QTc was calculated using the Bazett and Framingham formulas. QTc dispersion was calculated by subtracting the shortest from the longest QTc. Analysis of variance (ANOVA) was applied for comparison between antiarrhythmic groups with Bonferroni correction for multiple comparisons. ResultsA total of 447 ECGs were reviewed and 77 ECGs met inclusion criteria. The average QT dispersion for amiodarone, dofetilide, and sotalol was 0.050, 0.037, and 0.034, respectively (p=0.006) and the average QTc dispersion by Bazett was 0.053, 0.038, and 0.037 (p=0.008) and by Framingham was 0.049, 0.036, and 0.035 (p=0.009), respectively. ConclusionOur results show that given the increase in QT dispersion seen with amiodarone, heterogeneous ventricular repolarization as measured by QTc dispersion likely does not account for the lower incidence of drug-induced TdP seen with amiodarone. The ability of amiodarone to decrease EADs via sodium-channel blockade is more likely the explanation for its lower incidence of drug-induced TdP.
A 50-year-old white man was seen with a chief complaint of abdominal pain of seven hours' duration, which had begun 30 minutes after breakfast. The pain had been preceded by a desire to defecate, after which a knife-like excruciating pain spread from the periumbilical region over the entire abdomen and continued unabated for five hours when the patient began to vomit clear gastric juice. Two weeks previously he had com¬ plained of constipation, and his wife, who was taking a hydro¬ philic bulk-increasing laxative containing synthetic gum methylcellulose (Hydrolose) in plain syrup form, suggested that he use this medicament. He then took 2 tablespoons daily for two days but the constipation was not improved. During the next week he passed small, hard, fecal marbles, and the fulness in the lower abdomen was not relieved. For several days prior to the present acute episode he again took the methylcellulose syrup, 1 tablespoon, at night. The day before he was admitted to the hospital he had passed a huge mass of stool after some straining.The patient's history of illness included occasional instances of sinus tachycardia and an acute suppurative perforated ap¬ pendicitis for which he had been operated on in 1939. During the past five years there had been occasional periods of consti¬ pation that were extremely discomforting. In April, 1951, he had complained of a »ense of fulness in the lower abdomen but an x-ray examination with a barium enema performed by one of us ( A. I. F.) was entirely negative except for moderate spasticity in the sigmoid colon. No diverticula were seen. He had been well until six months prior to this time when, because of several attacks of abdominal pain, he had visited his family physician who advised an x-ray examination with a barium meal. He was then told he had a duodenal ulcer. He was kept on a special diet until three weeks prior to the present illness when he was reexamined by roentgenogram and told that "everything was all right." Physical examination revealed an acutely distressed person doubled up with pain. The heart and lungs showed no ab¬ normalities. Blood pressure was 132/90 mm. Hg. The abdomen was rigid with marked tenderness throughout, especially in the right lower quadrant. When a rectal examination was made, several external bleeding hemorrhoids were discovered but no stool. Proctoscopic examination revealed a small amount of soft brown stool. The patient would not tolerate a sigmoidoscopic examination. The hemoglobin level (Sahli) was 13.6 gm.per 100 cc; there were 4,700,000 red blood cells and 5,200 whiteblood cells with a differential count of 65% polymorphonuclear leukocytes, 30% lymphocytes, 3% monocytes, and 2% eosinophils. The results of urinalysis were normal. A flat film of the abdomen taken with the patient in both erect and prone positions revealed fecal material throughout the descending colon; no definite subdiaphragmatic air pockets were observed. A diagnosis of a perforated duodenal ulcer was made on the basis of the history and clinical findings, and the ...
Abdominal paracentesis is a commonly performed diagnostic and therapeutic procedure with a low complication rate. Previously described complications include injury to the abdominal wall, small bowel perforation, and abdominal hemorrhage. Splenic injury has also been described as a complication from bedside procedures including colonoscopy, upper gastrointestinal endoscopy, thoracentesis, and pleural biopsy. This case highlights a previously unreported complication from an abdominal paracentesis, splenic laceration.
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