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Biomedical subjects

J J Bergin

Publications and source records attributed to J J Bergin.

At least 19 recordsLinked to original sources
PubMed1988

Transfusion therapy in emergency medicine.

Volume replacement is critical to the resuscitation of the hemorrhaging patient, but this usually can be accomplished quickly and safely with crystalloid and/or colloid solutions. Red cells should be used in addition to asanguinous fluids in the treatment of tissue hypoxia due to anemia. The need for whole blood as opposed to packed red blood cells is controversial. However, plasma should not be used as a volume expander, and its use to supplement coagulation factors during the massive transfusion of red cells should be guided by laboratory tests that document a coagulopathy. Similarly, platelet transfusions are indicated to correct documented thrombocytopenia or platelet dysfunction, and routine prophylaxis after fixed volumes of red cells results is unwarranted. Many anticipated complications of massive transfusions, including hemostatic abnormalities, acid-base imbalances, hyperkalemia, and hypocalcemia, are uncommon or of limited clinical significance. The risks of immune hemolysis and transfusion-transmitted diseases, on the other hand, are significant, and argue for judicious use of blood components. In emergencies in which blood is required immediately before compatibility testing can be completed, O-negative uncrossmatched blood can be requested. Careful blood specimen collection and patient identification prior to transfusion are critical. Practices that emphasize blood conservation, including the use of autologous salvaged blood, are always to the patient's advantage.

Blood Grouping and Crossmatching↗
PubMed1975

Aplastic anemia following viral hepatitis: report of two fatal cases and literature review.

Within recent years the combination of aplastic anemia following viral hepatitis has been reported with increasing frequency suggesting the existence of a causal relationship between the two conditions. Two case histories of aplastic anemia following hepatitis are presented in detail, and the information on 193 such patients reported in the literature through 1972 is summarized. A number of parameters were evaluated and extensive cross correlation carried out in order to define criteria which might have diagnostic, prognostic or therapeutic value. Males were more likely to develop bone marrow failure following hepatitis (p congruent to 0.05), but females were less likely to survive the marrow depression (p smaller than 0.025). No other statistically identifiable criteria were detected. The hematologic changes commonly encountered in hepatitis are reviewed. These and other observations support the concept that subclinical hepatitis may be responsible for a significant percentage of so-called idiopathic aplastic anemia, for which, at present, no etiology can be determined in nearly half the cases. Possible pathogenetic mechanisms are discussed as they might relate to chromosomal abnormalities which were found in one of our patients. It is suggested that occasional fortuitious human infection with animal viruses known to be both hepato- and myelotoxic could relate the hepatitis and aplasia.

Adolescent↗