Blood product wastage reduction by utilising low-cost, low-impact multimodal physician-to-physician communication initiatives.

OBJECTIVES: To assess a multimodal physician-to-physician communication initiative that is low in cost and impact to daily workflow to reduce blood product wastage. BACKGROUND: Blood product stewardship is an important issue in all hospital systems. Previous studies have proposed low-cost interventions to reduce blood product wastage, but few have evaluated improvements in communication between the blood bank and providers. We undertook a prospective quality improvement project focusing on improving communication to reduce blood product wastage. METHODS: We conducted a prospective quality improvement project over the first quarter of 2017, identifying patients with issued but unused blood products. Each service overseeing the care of patients identified on the unit status report was contacted through two possible methods: (i) phone or (ii) proprietary Health Insurance Portability and Accountability Act of 1996 compliant digital messaging application. Collected variables included reserved blood product type and participant time spent. Outcomes included the rate of blood product release and changes in wastage compared with historical data tracked by the blood bank. RESULTS: Eight hundred and forty products were reserved during the study period, of which 436 (52%) were released. Average participant times ranged from 2 ± 1 min to 15 ± 4 min with no significant differences in time spent between participants (P = 0·194). Compared with the average product wastage 10 months prior to project initiation, there were significant reductions in the average wastage for platelets (5·3 ± 2·5 units vs 2·5 ± 1·5 units, P = 0·05), RBCs (6·1 ± 3·7 units vs 0 ± 0 units, P = 0·01) and overall wastage (58·3 ± 14·9 units vs 40 ± 15·7 units, P = 0·05). CONCLUSION: Efforts focusing on improving provider-to-provider communication can reduce blood product wastage.

Non-random maternal X-chromosome inactivation associated with PHACES.

The acronym PHACES is used to describe the association of posterior fossa malformations, hemangiomas, arterial anomalies (cardiovascular or cerebrovascular), coarctation of the aorta and cardiac defects, eye abnormalities, and sternal or ventral defects. We report a female patient with an uncommon variant of this neurocutaneous disorder who manifested a sternal cleft; supraumbilical raphe; hemangiomas of the face, chest, and extremities; micrognathia and cerebrovascular anomalies. A literature review of PHACES patients with both sternal cleft and supraumbilical raphe showed a marked female predilection. Taken together with cases of sternal cleft, supraumbilical raphe and facial hemangiomas tabulated by Gorlin et al. (1994), 91% (40/44) of patients are female. One affected male died shortly after birth. We hypothesized that the gender bias in PHACES results from mutation in an X-linked dominant gene often lethal in males, and performed X-inactivation analysis of the polymorphic androgen receptor locus in this family. We documented consistently skewed X-inactivation (80%/20% in two independent analyses) in the unaffected mother and consistently random X-inactivation (47:53 and 61:39 in independent analyses) in the proband. These findings are consistent with favorably skewed X-inactivation producing a normal maternal phenotype, a phenomenon documented in X-linked dominant Rett syndrome.

Travel vaccines--a review of current thinking.

More controversial aspects of the administration of vaccines are discussed with particular emphasis on the uncertainties surrounding measurement and significance of immunological markers in predicting efficacy. New areas of vaccine development are highlighted, particularly the importance of greater understanding of the gut immune mechanisms which promise oral delivery routes for a variety of immunogens. Emphasis is laid on the requirement for expert administration of intradermal injection if protection is to be reliable. Several new vaccines have been introduced recently and relevant issues relating to typhoid, cholera and hepatitis A vaccines are discussed. New possibilities for immunisation against travellers diarrhoea are appraised. The required frequency of booster doses is discussed for several vaccines where it is found that long term protection has often not been well researched. This is nowhere better demonstrated than with hepatitis B. Finally less commonly used vaccines are discussed and the importance of assessing true risk before deciding on use is emphasized.

Time-resolved fluoroimmunoassay compared with radioimmunoassay of luteinizing hormone.

OBJECTIVE: To determine if fluoroimmunoassay (FIA) of serum luteinizing hormone (LH) is more useful clinically than a conventional radioimmunoassay (RIA) because it has been suggested that FIA closely reflects biological activity. DESIGN: Comparison of serum LH measurements by RIA and FIA during various perturbations in normal ovulatory women and in women with polycystic ovarian syndrome (PCOS). SETTING: Normal ovulatory subjects were healthy volunteers and women with PCOS were untreated and newly diagnosed outpatients in our Reproductive Endocrinology/Infertility Clinic, Women's Hospital, at the Los Angeles County+University of Southern California Medical Center. PARTICIPANTS: Fifty-three normal ovulatory women, ages 20 to 35, and 27 women with PCOS, ages 21 to 35. All were in good health and received no other medications during the study period. RESULTS: Fluoroimmunoassay of serum LH reflected status of known altered bioactivity better than with a conventional RIA. This was most evident during conditions of gonadotropin suppression and in patients with PCOS. An excellent correlation was found between values of FIA and RIA. CONCLUSIONS: The measurement of LH by FIA is clinically useful, specifically when a change in biological activity of LH is sought.

Estradiol stimulates the secretion of prostacyclin and thromboxane from endometrial stromal cells in culture.

OBJECTIVE: To determine the production of the vasoactive prostaglandins (PGs), prostacyclin, and thromboxane (TX) in endometrial stromal cell cultures and their steroid modulation by sex steroids. DESIGN: Primary stromal cell cultures with steroid modulation in tissues from the follicular and luteal phases of normal women. SETTING: Laboratories of the Division of Reproductive Endocrinology and tissues obtained from normal patients at the Los Angeles County and University of Southern California Medical Center in Los Angeles, California. MEASURES: Stromal cell tissue culture for 14 days. Radioimmunoassay of 6-keto-PGF1 alpha, TXB2, and prolactin (PRL) as well as determination of protein content. RESULTS: Estradiol stimulated 6-keto-PGF1 alpha production more than TXB2. This effect occurred after day 6 and was as much as 10-fold greater in luteal phase tissue. The effect was eliminated by progestins that alone had no effect. This modulatory response was greater in luteal endometrial tissue than in follicular phase tissue. As expected, in these tissues progestin stimulated PRL, an effect opposite to its negative influence on the vasoactive PGs. CONCLUSION: These data provide evidence for a steroid-related influence on the balance of vasoactive PGs in the stroma of the endometrium.

Is the inappropriate gonadotropin secretion of patients with polycystic ovary syndrome similar to that of patients with adult-onset congenital adrenal hyperplasia?

OBJECTIVE: To assess gonadotropin alterations in adult-onset congenital adrenal hyperplasia (CAH) and to compare these findings with those of patients with polycystic ovary syndrome (PCOS) in an effort to better understand the pathophysiology of these abnormalities. DESIGN: Prospective study of 9 newly diagnosed patients with CAH, 10 with PCOS, and 10 ovulatory controls. INTERVENTIONS: Baseline measurements of serum androgens, progestins, estradiol (E2), estrone (E1), unbound E2, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Serum LH and FSH were measured after intravenous gonadotropin-releasing hormone (GnRH) and in 15-minute blood samples for 6 hours to determine LH pulsatility. RESULTS: Serum androgens were elevated but comparable in the two patient groups. Serum LH was also elevated (P less than 0.05) but was higher in PCOS than CAH. Serum LH:FSH ratios were similar as were the responses to GnRH. Serum E1 was elevated only in PCOS, but unbound E2 was elevated to the same degree in both PCOS and CAH (P less than 0.05). Patients with PCOS had a decreased LH interpulse interval compared with controls and CAH (P less than 0.05), but LH pulse amplitude was increased in both PCOS and CAH (P less than 0.05). Serum E2 and unbound E2 correlated significantly with LH (P less than 0.05), LH responses to GnRH as well as to LH pulse amplitude in CAH (P less than 0.05). The LH interpulse interval did not correlate with estrogen in any group. None of the LH parameters correlated with serum progestin levels in CAH. CONCLUSIONS: The gonadotropin abnormalities of CAH appear to be intermediate between those of controls and PCOS. Although elevated estrogen may explain these abnormalities in CAH, additional factors may be operative in PCOS.

Comparison of norethindrone and medroxyprogesterone acetate with natural progesterone and estradiol in stimulating prolactin production from cultured endometrial stromal cells.

Progestins stimulate prolactin production from endometrial stromal cells in culture. We compared the potencies of the synthetic progestins norethindrone and medroxyprogesterone acetate to natural progesterone in inducing stromal prolactin production. Modifications of the culture system provided an increase in stromal cell yield, thus permitting multiple comparisons from the treatment of cells from a common endometrial sample. The effects of high-dose estradiol also were evaluated in this system. The findings suggest relative potencies of 50:1 for medroxyprogesterone acetate and progesterone. Norethindrone gave intermediate and more variable responses. Estradiol potentiated prolactin production from only submaximal progestins doses. The differences between the progestin effects, in large measure, were due to differential culture growth as reflected by culture mass. Compared to controls and estradiol alone, all the progestins induced much greater prolactin production. Thus during decidualization, progestins probably promote both stromal growth and intracellular prolactin production. High-dose estradiol may not interfere with these events.

Comparison of endometrial biopsy and urinary pregnanediol glucuronide concentration in the diagnosis of luteal phase defect.

To determine if pregnanediol glucuronide (PG) excretion is useful in luteal phase assessment, we compared daily first morning urinary PG concentrations during the luteal phase in nine normal and nine deficient cycles. Total luteal pregnanediol excretion (44.1 +/- 11.3 versus 64.0 +/- 11.6 area units +/- SEM) was not different. However, significantly less pregnanediol was excreted by the abnormal group during the 1st 5 days of the luteal phase (12.7 +/- 1.2 versus 18.0 +/- 1.7 area units +/- SEM, respectively). Thus, delayed PG excretion may be characteristic of luteal phase defect and measurement of urinary PG may be useful only if daily samples during the early luteal phase are obtained.

Mifepristone (RU 486) failure in an ovarian heterotopic pregnancy.

A patient treated with mifepristone (RU 486), which successfully induced abortion of an intrauterine pregnancy, was discovered to have a heterotopic ovarian pregnancy resistant to this antiprogesterone. The ovarian pregnancy was removed with operative laparoscopy. This case demonstrates for the first time that an ovarian pregnancy may be resistant to treatment with RU 486 at a dose adequate to abort an intrauterine pregnancy.

Ovine corticotropin-releasing factor and dexamethasone responses in hyperandrogenic women.

Eighteen hyperandrogenic, hirsute women received ovine corticotropin-releasing factor (CRF; 1 microgram/kg) as well as a dexamethasone (DEX) suppression test. Nine of the 18 hirsute women exhibited increased DEX sensitivity. Plasma adrenocorticotropic hormone (ACTH) responses after ovine CRF were significantly lower in the DEX-sensitive subgroup, but serum androstenedione was higher. Baseline serum androgen levels could not predict DEX responses. A significant negative correlation existed between the suppression of androgens after DEX and the increase in ACTH after ovine CRF. The suppression of androgen correlated with the ratio of the increase in androgen to the increase in ACTH after ovine CRF. We conclude that DEX sensitivity occurs frequently and cannot be predicted by levels of serum androgens. Blunted ACTH responses to ovine CRF may reflect enhanced adrenal sensitivity and altered feedback control.

Decreased in vitro production of 6-keto-prostaglandin F1 alpha by uterine arteries from postmenopausal women.

Cessation of ovarian function is associated with a marked increased in morbidity and mortality secondary to ischemic heart disease. Estrogen replacement has been shown to impart protection against ischemic heart disease. We hypothesized that estrogen may influence vascular production of vasodilators such as prostacyclin. To investigate this relationship we have measured the production of 6-keto-prostaglandin F1 alpha, and thromboxane B2 by superfused uterine arteries from pre- and postmenopausal women. Arterial specimens from healthy normotensive premenopausal (n = 5) and postmenopausal women (n = 5) were superfused for 5 hours. Production of 6-keto-prostaglandin F1 alpha reached steady state levels by 120 minutes and remained linear for the length of the experiment. Indomethacin (4 x 10(-5) mol/L) added at 120 minutes significantly decreased prostanoid production. In subsequent experiments, 17 beta-estradiol in concentrations of 10, 100, 1000 ng/ml was added to the superfusion media at 120 minutes. Total production of 6-keto-prostaglandin F1 alpha by premenopausal arteries superfused with neat media during the steady state interval (3 hours) was significantly greater than that of postmenopausal specimens (1.25 versus 0.27 ng/mg dry tissue, p less than 0.05). Thromboxane B2 levels were undetectable in spent media. However, the addition of 17 beta-estradiol did not alter production of 6-keto-prostaglandin F1 alpha. These data suggest that arterial production of prostacyclin is significantly decreased in uterine arteries from postmenopausal women, but in this in vitro model system estrogens did not affect vascular prostanoid production.