Biomedical subjects

R M Sinow

Publications and source records attributed to R M Sinow.

7 recordsLinked to original sources

PubMed1995

Endovaginal ultrasonographically guided transvaginal drainage for treatment of pelvic abscesses.

OBJECTIVE: This study assessed the ability of endovaginal ultrasonographically directed transvaginal drainage of pelvic abscesses to treat patients who failed intravenous antibiotic therapies and whose abscesses were not amenable to percutaneous or colpotomy drainage. STUDY DESIGN: Thirty-one women who would otherwise have required surgery to treat their pelvic abscesses underwent the procedure. Immediate clinical response and longer-term follow-up results were collected retrospectively. RESULTS: Thirty-four procedures were performed on 31 women. Purulent material (10 to 350 ml) was aspirated in every case. Twenty-six of the 31 women (84%) were successfully treated by drainage. In the 6- to 21-month follow-up period, 10 women remained without problems, eight had sequelae related to pelvic infection, and eight were lost to follow-up. CONCLUSION: Endovaginal ultrasonographically guided transvaginal drainage is a safe, effective procedure for treatment of pelvic abscesses and should be considered the route of choice for draining collections not amenable to percutaneous or colpotomy drainage.

Abscess↗

PubMed1993

MR mammographic localization. Work in progress.

The authors present phantom test results for a stereotaxic device that may permit simple, rapid, and accurate needle biopsy and localization of breast lesions detected at contrast material-enhanced magnetic resonance (MR) mammography. The mechanical accuracy of this prototype MR breast localizer is approximately plus or minus 3.5 mm at 5 cm.

Biopsy, Needle↗

PubMed1992

Subcapsular hematoma as a predictor of delayed splenic rupture.

Over the past 46 months at a level I trauma center, 966 computed tomography (CT) scans were performed for blunt abdominal trauma. Eighty-three (8.6%) demonstrated splenic injury, and 31 (3.2%) of these showed a subcapsular hematoma with or without associated parenchymal damage. Of the 31 patients, 23 were managed conservatively, based initially upon surgeons' preference (14 patients) and after March 1990 to conform to the authors' splenic trauma protocol (nine patients). The eight patients operated upon were hemodynamically stable and all underwent splenectomy. Subcapsular hematoma, as diagnosed by preoperative CT scan, was confirmed in each of the eight celiotomies. Parenchymal involvement, which had also been identified in these eight patients by CT, was evident at operation in all, and hilar involvement occurred in three. None of the 23 observed patients developed delayed splenic rupture. All were discharged home with outpatient follow-up in surgical clinic to at least 1 month without further complication. The authors came to the following conclusions: 1) Subcapsular hematoma is neither a predictor for delayed splenic rupture, nor by itself an indication for operative management of the injured spleen in the hemodynamically stable patient; 2) Degree of parenchymal injury based on CT morphology, specifically hilar involvement, signifies the need for laparotomy with splenectomy; 3) Splenorrhaphy has a reduced role in splenic trauma because most injuries now operated upon are severe.

Blood Transfusion↗

PubMed1988

Food cobalamin malabsorption occurs frequently in patients with unexplained low serum cobalamin levels.

Malabsorption of food-bound or protein-bound cobalamin with normal absorption of free cobalamin has been described in studies of patients with gastric dysfunction. We used the egg-yolk cobalamin absorption test to study 47 patients selected not because of known gastric disorders but because they had low serum cobalamin levels with normal Schilling test results. Their egg test results were significantly lower than in normal controls, while Schilling test results were normal. Twenty of the subjects had egg test excretion below 1.5%. No features distinguished them from the 27 who excreted more than 1.5% other than the presence of lower pepsinogen I:II ratios. Eight of 19 tested patients with food cobalamin malabsorption had no evidence of abnormal gastric status by blood tests and/or gastric analysis. Also noteworthy was the finding of food cobalamin malabsorption in 60% of tested patients who had neurologic, cerebral, or psychiatric abnormalities. Food cobalamin malabsorption appears to be associated frequently with otherwise unexplained low cobalamin levels. Low cobalamin levels in patients with normal Schilling test results cannot be dismissed as insignificant without also testing for food cobalamin malabsorption, whether or not the patients have known gastric dysfunction.

Adult↗

PubMed1987

Low serum cobalamin levels occur frequently in the acquired immune deficiency syndrome and related disorders.

Low serum cobalamin levels in 10 patients with AIDS or AIDS-related complex led us to also prospectively survey 40 homosexual men in our AIDS clinic. 8 of the latter (20%) had low cobalamin values. We found no evidence of megaloblastic changes in the blood or bone marrow. Assessment disclosed malabsorption of cobalamin in only 1 of 6 cases tested for it. 6 of the patients were treated with cobalamin and had no hematologic response. It appears that low serum cobalamin levels in AIDS and related disorders do not usually represent overt cobalamin deficiency. While malabsorption is occasionally responsible for the low cobalamin level, in most cases the cause is unknown and may reflect a serum abnormality similar to that in multiple myeloma. AIDS and related disorders should be considered in the differential diagnosis of unexplained low cobalamin levels.

AIDS-Related Complex↗

PubMed1987

Unsuspected pernicious anemia in a patient with sickle cell disease receiving routine folate supplementation.

Although the issue of folate supplementation in sickle cell anemia remains controversial, routine supplementation has become common. The major drawback to indiscriminate folate therapy is the potential of masking findings of vitamin B12 (cobalamin) deficiency. This has been dismissed as a problem in sickle cell anemia because of the generally young age of the patients. However, because young blacks, especially women, are at higher risk for developing pernicious anemia than whites, sickle cell anemia and pernicious anemia can be expected to coexist occasionally. In this article we describe such a patient and recommend that routine folate supplementation should not be given in sickle cell anemia before determining the vitamin B12 status.

Adult↗

PubMed1987

Atypical cobalamin deficiency. Subtle biochemical evidence of deficiency is commonly demonstrable in patients without megaloblastic anemia and is often associated with protein-bound cobalamin malabsorption.

We performed studies in 25 patients with low serum cobalamin levels who had few if any clinical or hematologic findings of cobalamin deficiency. All but three had morphologically normoblastic hematopoiesis, and 15 were not even anemic. None of those tested excreted methylmalonic acid or homocystine. Nevertheless, the dUST identified metabolic abnormalities in 18 of the 25 cases. In vitro additives were essential in the dUST. Especially noteworthy was MTHF, whose addition unmasked an otherwise undetectable dUST abnormality in four cases. Why MTHF appears to act as a "stress test" in this setting is unknown but deserves further attention. Seven patients had early forms of classical malabsorptive states such as pernicious anemia, defined by abnormal Schilling test results. Among the rest, seven of 13 patients displayed malabsorption of protein-bound cobalamin despite normal absorption of free cobalamin by the Schilling test. In two patients, initially normal Schilling test results became abnormal the following year. These findings demonstrate that seemingly falsely low serum cobalamin levels often indicate subtle biochemical cobalamin deficiency. Early stages of pernicious anemia or other classical malabsorptive states are sometimes responsible for such subtle deficiency. However, malabsorption confined to protein-bound cobalamin is an equally common cause. Current concepts of cobalamin deficiency and the absorptive defects that can cause it should be expanded to include atypical defects requiring newer methods of identification.

Adult↗