Surgical fixation of distal ulna neck and head fractures.

OBJECTIVES: Distal ulna plate fixation for ulnar neck and head fractures (excluding ulnar styloid fractures) aims to anatomically reduce the distal ulna fracture (DUF) by open reduction and internal fixation, while obtaining a stable construct allowing functional rehabilitation without need for cast immobilization. INDICATIONS: Severe displacement, angulation or translation, as well as unstable or intra-articular fractures. Furthermore, multiple trauma or young patients in need of quick functional rehabilitation. CONTRAINDICATIONS: Inability to surgically address concomitant ipsilateral extremity fractures, thus, limiting early active rehabilitation. Stable, nondisplaced fractures. Need for bridging plate or external fixator of distal radiocarpal joint. SURGICAL TECHNIQUE: An ulnar approach, with a straight incision between the extensor and flexor carpi ulnaris. Preservation of the dorsal branch of the ulnar nerve. Reduction and plate fixation with avoidance of plate impingement in the articular zone. POSTOPERATIVE MANAGEMENT: Postoperatively, an elastic bandage is applied for the first 24-48 h. In isolated DUF with stable fixation, a postoperative splint is often unnecessary and should be avoided. For the first four weeks, only light weightbearing of everyday activities is allowed to protect the osteosynthesis. Thereafter, heavier weightbearing and activities are allowed and can be increased as tolerated. RESULTS: The best available evidence likely shows that for younger patients with a DUF, with or without concomitant distal radius fractures, open reduction and internal fixation can be safely achieved with good functional outcome and acceptable union and complication rates as long as proper technique is ensured.

[Changes in the bronchial musculature in chronic obstructive respiratory tract diseases]. / Veränderungen der Bronchialmuskulatur bei der chronischen obstruktiven Atemwegserkrankung.

Changes in the bronchial musculature in patients with chronic obstructive lung disease, were submitted to a systematic electron-microscopic investigation. A marked interstitial fibrosis with degenerative changes affecting the muscle cells was observed. The formal pathogenetic course of these changes can be reconstructed on the basis of numerous individual findings. The muscle cells are progressively "ensheathed" in a disorderly fine-filamentous basic structure (matrix), and in collagenous fibres. As a result, the contact surfaces between the muscle cells are disturbed, and the nerve endings "displaced" from the muscle cells. This fibrosis is associated with a protracted "shrivelling" of the individual muscle cells. The changes involving the muscles of the bronchial wall are comparable with those seen in the smooth muscles of blood vessels involved in arteriosclerosis. The morphological changes to the muscles of the bronchi described in this paper strongly suggest that protracted fibrosis formation, coupled with the degradation of muscle cells, contribute to a loss of elasticity of the bronchial wall in chronic obstructive lung disease.

[Value of K+ and Mg2+ in treatment of acute myocardial infarct]. / Stellenwert von K+ und Mg2+ bei der Behandlung des akuten Myokardinfarktes.

A critical role analysis of literature concerning the effects of intravenous magnesium on arrhythmias and mortality in acute myocardial infarction shows discrepant results and often inappropriate methods. So far neither an antiarrhythmic efficacy nor prophylactic effects with respect to mortality could be demonstrated. In contrast, potassium substitution should be performed in the setting of acute myocardial infarction with documented hypokalemia (K+ < 3.5 mmol/l) because of increased risk of ventricular arrhythmias. According to the documented results of the trials reviewed in this article no recommendations for the routine use of magnesium in myocardial infarction can be given.

Arbutamine stress echocardiography.

Arbutamine, a new potent non-selective beta-adrenoceptor agonist with mild alpha 1-sympathomimetic activity, has been developed specifically for pharmacological stress testing. The drug acts like physical exercise, increasing both heart rate and myocardial contractility. Sensitivity, specificity and accuracy in detecting significant stenotic coronary artery disease are 76%, 96%, and 82%, respectively, again similar to those of exercise echocardiography. The drug is delivered by a computerized drug delivery and monitoring device (GenESA) which adjusts the infusion rate according to the patient's heart rate data feedback. The drug is generally well tolerated and has an acceptable safety profile. This article describes recent clinical experience with arbutamine and presents preliminary results of a multicentre multinational study which evaluates the clinical utility and safety of the GenESA system in diagnosing coronary artery disease.

Stress echocardiography: personnel and technical equipment.

In recent years, stress echocardiography has gained broad acceptance as a non-invasive method for the diagnosis of coronary artery disease. Facing different protocols, dosages and instrumentation, official guidelines for the performance, standardization and quality control of stress echocardiograms are needed; however, so far they are not available. This paper recommends the type of personnel and technical equipment needed for stress echocardiography laboratories, based on experience gained during more than 2000 stress echocardiographic procedures. To perform stress echocardiography, a cardiologist and a technical assistant--both well trained over a large number of tests--should be involved. The laboratory must have basic equipment such as a 12-lead ECG, blood pressure monitoring capacity, a treadmill or bicycle for ergometry, a precision intravenous delivery system for pharmacological stress testing as well as an adequate echo table; additionally, emergency equipment is mandatory. The ultrasound machine should contain transducers with high 2-D resolution; most important is a digital image acquisition system which facilitates performance and interpretation through side-by-side display of synchronized rest and stress images. Finally, there is a need for proper patient preparation and the obtaining of informed consent.

-Value of activated blood coagulation time in monitoring anticoagulation during coronary angioplasty-. / Der Stellenwert der aktivierten Gerinnungszeit (ACT) in der Uberwachung der Antikoagulation bei Koronarangioplastie.

Accurate heparin anticoagulation assessment is important to prevent complications (hemorrhage, thrombotic coronary occlusion) during and after coronary angioplasty (PTCA). Paired ACT-, aPTT- and prothrombin time (PT) measurements have not been studied after PTCA using a high dose heparin management. For that reason we analyzed in 150 consecutive patients (115 m., 35 f., 61 +/- 10 y.) immediately after PTCA and at the time of arterial sheath removal aPTT-(Neothromtin, Behring), PT- (Thromborel S, Behring) and ACT-(HR-ACT, HemoTec) values after application of 20,000 U of heparin (5,000 U intravenous, 15,000 U intracoronary) followed by a heparin-infusion (15,000-25,000 U/24 h). Immediately after PTCA in all patients a aPTT above the upper limit of >180 s was found. The average postprocedural ACT was 330 +/- 82 s. Only 9 patients showed an ACT below 200 s. All coronary reocclusions (n = 3) immediately after PTCA occurred in this group. Arterial sheaths were removed 13 +/- 3 h after PTCA. The incidence of minor peripheral bleeding complications at that time was 21% and was related to the anticoagulation level. Major bleeding complications requiring transfusion were noted in only one case. Our findings suggest that after high dose heparinization for PTCA the ACT test provides a reliable and broad range for the assessment of heparin anticoagulation. In contrast to the aPTT the ACT is ideally suited to determine the dosage of heparin infusion and the time of arterial sheath removal after PTCA. ACT measurements are superior to aPTT measurements in heparin anticoagulation assessment during and direct after PTCA.