Search PubMed⌕ Search

PubMed · 14509330

Institutioning a clinical practice guideline to decrease the rate of normal appendectomies.

Abstract

With the advent of laparoscopic appendectomy, the rate of normal appendectomies increased at our institution. To decrease our rate of normal appendectomies, we instituted a clinical practice guideline in January 1999 for the preoperative evaluation and treatment of patients with possible acute appendicitis. The medical records of 464 consecutive patients who underwent either open or laparoscopic appendectomy with a preoperative diagnosis of acute appendicitis between January 1, 1997, and December 31, 2000, were reviewed. The decision of open versus laparoscopic appendectomy was made at the time of surgery by the attending surgeon. Two hundred twelve patients (116 females, 96 males) underwent an appendectomy for acute appendicitis (142 open, 70 laparoscopic) from January 1, 1997 through December 31, 1998, prior to the institution of the guideline. Two hundred fifty-two patients (117 females, 135 males) underwent an appendectomy for acute appendicitis (193 open, 59 laparoscopic) from January 1, 1999, through December 31, 2000 (after the guideline was instituted). Prior to the guideline, the normal appendectomy rate was 21.7 per cent (18.3% open, 28.6% laparoscopic). After the guideline was instituted, the normal appendectomy rate was 16.7 per cent (14.5% open, 23.7% laparoscopic). In females, the normal appendectomy rate prior to the guideline was 31.0 per cent (26.6% open, 36.5% laparoscopic) while the normal appendectomy rate after the guideline was 23.1 per cent (19.0% open, 31.6% laparoscopic), P = 0.172. In males, the normal appendectomy rate prior to the guideline was 10.4 per cent (11.5% open, 5.6% laparoscopic) while the normal appendectomy rate after the guideline was 11.1 per cent (11.4% open, 9.5% laparoscopic), P = 0.861. By instituting a guideline for the diagnosis and treatment of possible acute appendicitis, we were able to decrease our rate of normal appendectomies. Although statistical significance was not reached, there is a trend toward decreasing the rate of normal appendectomies in females after the guideline was instituted.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Deanna Blisard, Joel C Rosenfeld, Fernando Estrada, James F Reed. 2003. Institutioning a clinical practice guideline to decrease the rate of normal appendectomies.. https://pubmed.ncbi.nlm.nih.gov/14509330/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Spinal cord injury-induced expression of TrkA, TrkB, phosphorylated CREB, and c-Jun in rat lumbosacral dorsal root ganglia.

Previous studies have demonstrated increased expression and phosphorylation of tyrosine kinase receptor (TrkA, TrkB) in lumbosacral DRG after chronic (6 weeks) spinal cord (T8-T10) injury. This study examined the effects of acute SCI (48 hours, 2 weeks) on TrkA and TrkB expression and phosphorylation, and CREB and c-Jun expression in DRG. A significant increase in the number of TrkA- (1.5-3-fold; P < or = 0.05), TrkB- (1.3-2.0-fold; P < or = 0.05), and phosphorylated Trk (pTrk)-immunoreactive (1.5-3-fold; P < or = 0.05) cells was observed in the L1, L6, and S1 DRG 48 hours, 2, or 6 weeks after SCI. A significant increase in the number of phosphorylated (p-) CREB-immunoreactive cells was observed in the L1, L2, L6, and S1 DRG 48 hours, 2, or 6 weeks after SCI. The largest changes in p-CREB-immunoreactivity were in L1 and L2 DRG (10-fold; P <or= 0.01) at 48 hours after SCI; however, changes were modest in bladder afferent neurons. After SCI, the overall number of c-Jun-immunoreactive cells in L1, L2, and S1 DRG was dramatically increased (3-10-fold; P < or = 0.01); however, only a low percentage of bladder afferent cells expressed c-Jun-IR before or after SCI. In summary, these results suggest that TrkA or TrkB may be involved in reorganization of micturition pathways after SCI. However, CREB or c-Jun may not be downstream transcription factors in Trk-mediated signaling cascades in micturition reflex pathways after SCI but may play a role in other, nonbladder SCI-induced changes.

Acute Disease↗

Dominant negative effects of the AML1/ETO fusion oncoprotein.

The t(8;21)(q22;q22) translocation, present in 10-15% of acute myeloid leukemia (AML) cases results in the production of the AML1/ETO fusion protein. Expression of AML1/ETO in patients or mouse models is not sufficient to induce AML. Despite convincing evidence that AML1/ETO is directly involved in the pathogenesis of AML, the underlying mechanism is not well understood. Genetic and biochemical experiments suggest that AML1/ETO is a dominant inhibitor of the core binding factor (CBF) transcription complex that includes AML1 (RUNX1), the N-terminal fusion partner in the t(8;21). We generated and recently characterized a novel strain of transgenic mice in which the AML1/ETO cDNA was inserted into the Ly-6A gene that encodes Sca1, a well-characterized marker of murine hematopoietic stem cells. Unexpectedly, transgene expression assessed by flow cytometry was significantly lower than predicted in lymphocytes from these mice. We have confirmed this finding at the mRNA level and suggest that this phenotype is a consequence of dominant inhibition of transgene expression by AML1/ETO. The dominant negative characteristics of AML1/ETO may be important for AML pathogenesis and may provide a molecular target for therapeutic intervention.

Acute Disease↗

Leukemia-associated fusion proteins. Multiple mechanisms of action to drive cell transformation.

Leukemic cells are defined by two main biological features: arrest of differentiation at a specific stage compatible with continued proliferation, and enhanced resistance to stress. Recent work shows that the leukemia-associated fusion protein PML-RAR can mediate both biological effects targeting independent pathways, through a unifying mechanism. Differentiation block is achieved through transcriptional silencing of genes physiologically regulated by RAR, which are involved in hematopoietic differentiation. In contrast, enhanced resistance to stress is due to the capacity of the fusion protein to cause degradation of the tumor suppressor p53, thus explaining the puzzling observation that mutations of p53 are remarkably rare in acute myeloid leukemias (AMLs). Interestingly, this latter phenomenon depends on expression of wild-type PML, acting as a molecular bridge between p53 and the fusion protein. Strikingly, both effects require a unifying molecular mechanism: aberrant recruitment of histone deacetylases (HDACs). Therefore, the study of this form of leukemia appears also of interest for a better understanding of the action of HDAC inhibitors, potential antitumor drugs that are at the early stages of clinical studies.

Acute Disease↗