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Biomedical subjects

M Sezer

Publications and source records attributed to M Sezer.

3 recordsLinked to original sources

Blunt and penetrating traumatic ruptures of the diaphragm.

BACKGROUND: The difficulties in diagnosing traumatic diaphragmatic rupture (TDR) at the first admission are the most common causes of morbidity and mortality. The purpose of this study was to review our experience with the management of TDR in order to identify the factors contributing to diagnostic delay and associated morbidity and mortality. METHODS: Fourteen patients with TDR were treated in our hospital between January 2000 and June 2005. They have been investigated retrospectively. RESULTS: The study identified 9 men (64 %) and 5 women (36 %), with ages ranging from 19 to 65 years (mean 35.3 years). Rupture of the diaphragm was left-sided in 10 (71 %) and right-sided in 4 (29 %) of the patients. Blunt trauma accounted for the injuries of 11 patients (79 %). Early diagnosis was obtained in 9 patients (64 %). The diagnosis was established preoperatively in 8 patients (57 %), and intraoperatively in 4 (29 %). The diagnosis was missed in 2 (14 %) patients in the first operation. Multiple associated injuries were observed in 12 patients (85 %). Postoperative complications were encountered in five patients (35 %), and the overall mortality was 7 %. CONCLUSIONS: Diaphragmatic rupture should be suspected in all blunt or penetrating traumas of the thorax and abdomen, and the presence of such an injury should be excluded before terminating the exploratory procedure.

Abdominal Injuries↗

New support for clarifying the relation between ST segment resolution and microvascular function: degree of ST segment resolution correlates with the pressure derived collateral flow index.

OBJECTIVE: To investigate the relation between the degree of ST segment resolution (STR) after thrombolysis and the pressure derived collateral flow index (CFIp), determined using an intracoronary pressure measurement technique in patients with recent myocardial infarction. METHODS: 33 patients were studied. TIMI grade III flow was achieved in the infarct related artery by thrombolysis. A surface ECG was obtained on admission and 90 minutes later. The sum of ST segment elevations was measured by summing all leads with ST elevation on the baseline ECG and on the 90 minute ECG (after thrombolysis) and calculating the percentage recovery. The study population was divided into two groups, with good STR (> or = 50%; group 1) or poor STR (< 50%; group 2). After angiography, a fibreoptic pressure monitoring guidewire was advanced to the stenosis to be dilated. The CFIp was determined as the ratio [coronary wedge pressure - central venous pressure]/[mean aortic pressure - central venous pressure]. RESULTS: The mean STR on the surface ECG was 54.6% and mean (SD) CFIp was 0.25 (0.12) (range 0.10-0.41). There was an inverse correlation between the individually calculated percentage of STR and CFIp (r = -0.64, p < 0.01). The mean CFIp was lower in patients with a good STR than in those with a poor STR (0.18 (0.07) v 0.27 (0.10), p < 0.02). CONCLUSIONS: Although TIMI grade III flow was achieved after thrombolysis, a worse STR on the surface ECG was associated with higher CFIp measured in the infarct related artery. CFIp appears to reflect the degree of microvascular obstruction by quantifying impedance of the microvasculature.

Blood Pressure↗

Hemostatic changes in active pulmonary tuberculosis.

OBJECTIVE: Severe pulmonary tuberculosis (PTB) is sometimes complicated by deep vein thrombosis (DVT). We have searched for possible hemostatic disturbances that are predisposing factors for venous thrombosis in patients with PTB. DESIGN: Coagulation and platelet function tests were studied in 45 patients with active PTB and 20 healthy control volunteers before therapy. Findings were compared with results at 30 days. RESULTS: Analysis in patients with active PTB showed anemia, leucocytosis, thrombocytosis, elevation in plasma fibrinogen, factor VIII, plasminogen activator inhibitor 1 (PAI-1) with depressed antithrombin III (AT III) and protein C (PC) levels. On the 30th day of treatment, anemia, leucocytosis and thrombocytosis were improved. Fibrinogen and factor VIII levels had decreased to normal levels, PC and AT III levels had increased to normal levels, and there was no difference in PAI-1 levels. We found no activated protein C resistance. Platelet aggregation studies demonstrated increased platelet activation. However, DVT was not detected in patients during the follow-up period. CONCLUSION: Decreased AT III, PC and elevated plasma fibrinogen levels and increased platelet aggregation appear to induce a hypercoagulable state seen in PTB and improve with treatment.

Adult↗