Ambulatory Surgery Patients May Be Discharged before Voiding after Short-acting Spinal and Epidural Anesthesia

Background: Voiding before discharge is usually required after outpatient epidural or spinal anesthesia because of concern about bladder overdistention and dysfunction. Shorter duration spinal and epidural anesthesia may allow return of bladder function before overdistention occurs in low-risk patients (those younger than age 70, not having hernia, rectal, or urologic surgery, and without a history of voiding difficulty), and predischarge voiding may not be necessary.

Methods: After institutional review board approval and informed consent, 201 low-risk ambulatory patients were prospectively studied in either a standard or accelerated pathway after undergoing spinal or epidural anesthesia with procaine, lidocaine, 2-chloroprocaine, or less than 7 mg bupivacaine; epinephrine was not used in any anesthetic. Standard pathway patients (n = 70) were required to void before discharge. Accelerated pathway (n = 131) patients were not required to void. (After randomization of an initial 163 patients to one of the two tracks, 38 additional patients were assigned to the accelerated pathway.) If accelerated pathway patients voided, they were discharged when all other discharge criteria were met. If they did not spontaneously void after block resolution, a bladder ultrasound (BUS) was performed. If the BUS indicated a urine volume of less than 400 ml, the patients were discharged and instructed to return to the emergency department if they were unable to void within 8 h of discharge. If the BUS indicated a urine volume of greater than 400 ml, the patients were reassessed in 1 h and were discharged if they could void spontaneously. If they could not void spontaneously, they were catheterized to facilitate discharge. All patients were contacted the next day to assess the return of normal bladder function.

Results: All standard pathway patients voided without difficulty, and were discharged in 153 +/- 49 (SD) min. 62 patients in the accelerated pathway voided spontaneously after resolution of their block and were discharged in 127 +/- 41 min. 46 patients were discharged with a BUS less than 400 ml in 120 +/- 42 min. 23 patients had a BUS greater than 400 ml: of these, 20 patients voided within an hour and were discharged in 162 +/- 45 min. Three were catheterized after 1 h, and were discharged in 186 +/- 61 min. Mean discharge time for all patients in the accelerated pathway was 22 min shorter than the standard pathway (P = 0.002). No patients had difficulty voiding or returned to the hospital for urinary problems. None reported new urologic symptoms.     

Hypoxic pulmonary vasoconstriction is heterogeneously distributed in the prone dog

Hypoxic pulmonary vasoconstriction (HPV) is thought to protect gas exchange by decreasing perfusion to hypoxic regions. However, with global hypoxia, non-uniformity in HPV may cause over-perfusion to some regions, leading to high-altitude pulmonary edema. To quantify the spatial distribution of HPV and regional PO2 (PRO2) among small lung regions (approximately 2.0 cm3), five prone beagles (approximately 8.3 kg) were anesthetized and ventilated (PEEP approximately 2 cm H2O) with an F1O2 of 0.21, then 0.50, 0.18, 0.15, and 0.12 in random order. Regional blood perfusion (Q), ventilation (VA) and calculated PRO2 were obtained using iv infusion of 15 microm and inhalation of 1 microm fluorescent microspheres. Lung pieces were clustered by their relative blood flow response to each F1O2. Clusters were shown to be spatially grouped within animals and across animals. Lung piece resistance increased as PRO2 decreased to 60-70 mmHg but dropped at PRO2's < 60mmHg. Regional ventilation changed little with hypoxia. HPV varied more in strength of response, rather than PRO2 response threshold. In initially homogeneous VA/Q lungs, we conclude that HPV response is heterogeneous and spatially clustered.     

Damaged chromatin does not prevent the exit from metaphase I in fused mouse oocytes

The presence of checkpoint mechanisms which are able to recognize damaged chromatin and thereafter to prevent exit from metaphase I has been investigated in giant mouse oocytes produced by fusion of a normal metaphase I oocyte with an equivalent oocyte with damaged chromatin. The presence of damaged chromatin did not prevent the onset of anaphase I in both sets of chromatin in the fused cells. Interestingly, fused or unfused cells containing only damaged chromatin failed to enter anaphase and persisted instead in a metaphase-like state. These results demonstrate the fragility of checkpoint controls in mammalian female germ cells.      

Factors affecting place of death in Washington State, 1968–1981

A study was carried out to determine factors affecting place of death (home, hospital, nursing home or other places) among all 426,115 resident deaths in Washington State during 1968–1981, using death certificate information. Sixteen percent of deaths occurred at home, 74% in institutions (51% in hospitals, 23% in nursing homes) and 9% at other places. Age, marital status and cause of death all strongly affect place of death. Further, the effect of each factor was strongly dependent on the others. Sex had no effect on place of death after controlling for other factors. Elderly people died relatively more frequently in nursing homes, infants and middle aged people in hospitals and young adults in other places. The frequency of deaths at home was quite constant by age. Hospitals were the most common place of death following both vascular disease (including heart attack) and neoplasms, and nursing homes were the most common place of death following cerebrovascular disease (including stroke). Race, socioeconomic status and urban or rural residents affected the place of death only slightly or not at all. The place of death pattern changed little during the time period 1968–1981, except for a slight increase in frequency of home deaths and a corresponding decrease in the frequency of deaths in other places.Among cancer patients, the likelihood of death at home was positively associated with longer periods of survival after diagnosis. Cancer patients of hospitals serving targeted populations, such as veterans, were relatively more likely to die in a hospital and less likely to die in a nursing home compared to other cancer patients, suggesting that the targeted hospitals are sometimes serving a nursing home function. There was a marked difference in the terminal cancer caseload by hospital. The number of cancer deaths per cancer diagnosis varied widely across hospitals (0.1 to 1.6) and was unrelated to size of the hospital or level of services offered.Intervention aimed at affecting place of death, such as increasing the number of deaths at home, will need to take account of the joint effect of age, marital status and disease.Lincoln Polissar, Ph.D., is Associate Member, Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, WA and Associate Professor, Department of Biostatistics, University of Washington in Seattle. Richard K. Severson, M.S., is the Project Coordinator, Fred Hutchinson Cancer Research Center. Norman K. Brown, M.D., is Clinical Professor of Medicine, School of Medicine, University of Washington.This research was supported by NCI Grant Nos. NCI-SR18, CA 29770–03 Requests for reprints should be sent to Lincoln Polissar, Ph.D., Fred Hutchinson Cancer Research Center, 1124 Columbia Street, Seattle, WA 98104     

Thrombopoietin stimulates colony-forming unit-megakaryocyte proliferation and megakaryocyte maturation independently of cytokines that signal through the gp130 receptor subunit

Thrombopoietin (Tpo), the ligand for the c-Mpl receptor, is a major regulator of megakaryopoiesis. Treatment of mice with Tpo raises the platelet count fourfold within a few days. Conversely, c-mpl knock-out mice have platelet counts that are 15% that of normal. The subunit structure of the c-Mpl receptor is not fully understood. Some cytokines that stimulate megakaryopoiesis (IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) bind to receptors that use gp130 as a signal transduction subunit. For these reasons, we determined whether gp130 function was required for Tpo-induced signal transduction. Murine marrow cells were cultured in semi-solid media in the presence of Tpo or IL-3, with or without a neutralizing anti-gp130 monoclonal antibody (RX187) or a soluble form of c-Mpl receptor (soluble Mpl) that blocks Tpo bioactivity, and the numbers of colony-forming unit-megakaryocyte (CFU-Meg) colonies were counted on day 5. Murine marrow cells were also cultured in suspension under serum-free conditions for 5 days, and megakaryocyte DNA content was measured by flow cytometry, as an index of nuclear maturation. The addition of RX187 did not block Tpo-induced CFU-Meg colony growth nor CFU-Meg nuclear maturation in suspension culture. However, IL-3-induced CFU-Meg colony growth and megakaryocyte nuclear maturation decreased in the presence of RX187. Soluble Mpl completely ablated Tpo-induced CFU-Meg growth, and partially blocked IL- 3-stimulated CFU-Meg growth. Thus the effects of Tpo on megakaryopoiesis in vitro do not depend on cytokines that signal through gp130. Furthermore, it is unlikely that gp 130 serves as a beta chain for the c-Mpl receptor, as Tpo signalling is unimpaired in the presence of RX187. In contrast, the effects of IL-3 on CFU-Meg growth are mediated in part through Tpo and through gp130-signalling cytokines.     

A double mobility acetabular implant for primary hip arthroplasty in patients at high risk of dislocation

IntroductionDislocation following total hip replacement continues to be a problem for which no completely satisfactory solution has been found. Several methods have been proposed to reduce the incidence of hip dislocations with varying degrees of success, including elevated rim liners, constrained liners and large diameter bearings. We present our experience with the double mobility acetabular component in patients at high risk of instability.MethodsThis was a retrospective review of 65 primary total hip arthroplasties in 55 patients (15 men, 40 women), performed between October 2005 and November 2009. The majority (80%) of patients had at least two and 26% had at least three risk factors for instability. The mean age was 76 years (range: 44–92 years). The patients were followed up for a mean duration of 60 months (range: 36–85 months).ResultsFourteen patients died and one was lost to follow-up, leaving fifty hips for final assessment. Until the final follow-up appointment, no patients had dislocation and none required revision surgery. The mean Oxford hip score improved from 45.0 to 26.5 (p<0.0001). The mean Merle d’Aubigné pain score improved from 1.4 to 4.9 (p<0.0001), the walking score from 2.3 to 3.1 (p<0.07) and the absolute hip function score from 5.4 to 10.8 (p<0.0001). There were no clinical or radiographic signs of loosening.ConclusionsThe double mobility acetabular component was successful at preventing dislocation during early to medium-term follow-up. However, as data are still lacking with regard to polyethylene wear rates at the additional bearing surface, it would be prudent to restrict the use of this implant to selected patients at high risk of instability.