Search PubMed⌕ Search

Biomedical subjects

S Silberman

Publications and source records attributed to S Silberman.

60 records · Page 4Linked to original sources
PubMedDate not supplied

Delayed sternal closure following cardiac operations.

In 13 patients, sternal closure was delayed at the end of open heart procedures. Seven patients underwent coronary artery bypass surgery (CAB), 5 valve replacements, and one left ventricular aneurysmectomy and closure of post myocardial infarction VSD. In all, primary closure of the sternum was considered impossible or inadvisable. The major indications for delaying sternal closure were: cardiac dilatation with tamponade-like behaviour upon attempted sternal closure (8 patients); intractable bleeding (2); intractable arrhythmia (1); insertion of mediastinal assist devices (3) and intraoperative non-cardiogenic pulmonary edema (1). In all, only the skin was closed. Delayed sternal closure (DSC) was performed 36-120 hours later on 10 of the patients, when their condition had stabilized. Nine patients are long term survivors. None of these patients has developed mediastinitis, wound infection, osteomyelitis or instability of the sternum. The judicious use of DSC in selected situations has several advantages: hemodynamic deterioration from pressure upon the heart may be prevented; a quick access to the heart in case of tamponade or intractable arrhythmia is obtained; insertion of mediastinal assist devices is facilitated. With careful technique the risk of infection is low.

Adult↗
PubMedDate not supplied

Heparin-induced thrombocytopenia: use of indirect immunofluorescence.

Sera from 14 patients who developed heparin-induced thrombocytopenia were tested by an indirect platelet immunofluorescent test in an attempt to characterize the serologic reactions between platelets, heparin, and the antibody. Positive results were observed in seven cases with variable patterns of reactions in the tests when performed in the presence or the absence of the offending drug. It was possible to absorb out the antibody in the presence of heparin and recover the antibody in the eluate. Neither complement nor the presence of immune complexes were found to play a role in the thrombocytopenia induced by heparin.

Aged↗
PubMedDate not supplied

A case of rheumatoid hyperviscosity syndrome with characterization of the serum immune complexes.

The clinical and immunologic data in a case of rheumatoid arthritis complicated by serum hyperviscosity are reported. The elevation in the serum viscosity was accompanied by the presence of intermediate immune complexes which were partially purified from the patient's serum by gel filtration chromatography. These complexes had a molecular weight of approximately 510,000 daltons and contained polyclonal IgG and IgA immunoglobulins. The hyperviscosity syndrome in this patient was likely due to the presence of intermediate complexes and unrelated to the rheumatoid factor activity which was found predominantly within the IgM fraction of the serum. This case demonstrates that the hyperviscosity syndrome may, in rare cases, develop as a complication of rheumatoid arthritis. It is important to consider this possibility before the clinical symptoms of increased serum viscosity become manifest.

Antigen-Antibody Complex↗
PubMedDate not supplied

Fast hemoglobins and red blood cell metabolites in citrate phosphate dextrose adenine stored blood.

Blood was drawn from 10 fasted, healthy volunteers and stored under standard blood bank conditions in citrate-phosphate-dextrose-adenine (CPDA-1). Blood was sampled before storage (Day 0) and on Days 5, 12, 19, 26, and 35. Laboratory testing for glucose, HbAla + b, HbAlc, pyruvic acid, lactic acid, adenosine triphosphate (ATP), 2, 3-diphosphoglycerate (2,3DPG), plasma free hemoglobin (Hb) and pH (blood gases) were performed. In addition, P50 was also serially measured in two of the individuals and in their stored blood. Significant elevations of HbAla + b and HbAlc (fast hemoglobins) were found on Days 12 and 19 of storage (p less than 0.05). These elevations of fast hemoglobins are due to hypoxia, acidosis, and hyperglycemia. Following the initial elevation of the fast hemoglobins (Hbs), there was a decline in their concentration, from Day 12, which could partly be explained by cell death.

Adenine↗