[64-year-old patient with dyspnea at risk and ankle edema in recurrent tachycardia. Heart failure].
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Diagnosis, Differential↗
Biomedical subjects
W Notheis
Publications and source records attributed to W Notheis.
[Heparin-induced type II thrombocytopenia as the etiology of severe recurrent pulmonary embolism].
Heparin-induced thrombocytopenia (HIT) is a rare complication of anticoagulative heparin therapy. The more severe HIT type II is defined by peripheral thrombocytopenia combined with thrombotic and thromboembolic events. We report the case of a 24 year old male patient who was admitted to our ICU with thromboembolic obstruction of the right central pulmonary artery, and deep venous thrombosis (DVT) of the right superficial femoral vein. Systemic thrombolytic therapy with urokinase for seven days resulted in nearly complete resolution of the thromboembolic material in the pulmonary arteries. Antithrombotic therapy with intravenous heparin and overlapping oral phenoprocoumon was continued on the regular ward. Six days later, the patient had to be readmitted to the ICU with evidence of hemodynamic compromise due to massive bilateral pulmonary thromboembolism that could be confirmed by CT scan--DVT had extended to the right iliacal vein. Additionally, peripheral thrombocyte counts had markedly declined from 112.000 to 35.000/microliter within 3 days, indicating the presence of a Hit type II. This was verified by positive ELISA testing for antibodies against platelet factor 4 (PF4)-heparin-complex. A filter device was temporarily implanted into the inferior vena cava. The patients condition stabilized upon reinitiated systemic thrombolysis and replacement of heparin therapy against recombinant hirudin. Pulmonary artery pressures normalized. Peripheral thrombocytopenia diminished within three days. HIT type II is a severe complication of anticoagulative therapy with heparin. Here we report a case, and discuss diagnostic procedures as well as differential diagnosis to HIT type I.
Adult↗
Recurrence rate after accessory pathway ablation.
OBJECTIVE: To evaluate characteristics of patients and accessory pathways as well as additional technical factors involved in the reappearance of accessory pathway conduction after successful ablation. DESIGN: Analysis of recurrences after radiofrequency ablation. SETTING: 163 consecutive patients with 167 accessory pathways. SUBJECTS: 97 men and 66 women with a mean (SD) age of 36 (14) range (11 to 75) years. RESULTS: After a mean (SD) follow up of 14 (7) range (2 to 27) months, conduction recurred in 13 out of 167 (7.8%) accessory pathways. The initial manifestation of recurrence was circus movement tachycardia in 7 patients and reappearance of delta waves on a 12 lead electrocardiogram in 6 patients. The interval to the return of accessory pathway conduction ranged from 3 hours to 90 days. Age, sex, presence of multiple accessory pathways, criteria to determine the target ablation site, number and duration of radiofrequency applications, and cumulative energy did not significantly differ between the groups with recurrence and without. Recurrence was less common with concealed accessory pathways (2/44) than with overt accessory pathways (11/110). The difference was not significant. The only variable to influence the recurrences in this study group was the location of the accessory pathway. Reappearance of conduction through right sided accessory pathways occurred significantly more often than through left sided ones (8/40 v 5/114, P = 0.01). CONCLUSION: After radiofrequency ablation the recurrence rate of accessory pathways is low and there are no predictors of the risk of reappearance of conduction apart from the right sided location of the accessory pathway.
Adolescent↗