Enhancing Patient Care With the "David and Wendy" Approach: The Effectiveness of Ward Round Documentation Proformas.

Background Surgical ward round documentation, essential for high-quality patient care, is often completed poorly. The advent of electronic medical records offers an opportunity to introduce proformas, aiding junior staff in completing notes both timely and accurately. We aimed to assess whether the introduction of a proforma would improve the quality and speed of ward round documentation. Methods We completed a prospective cohort analysis of ward round documentation at a single institution. Analysis was conducted on the documentation of a single surgical team over a 10-week period, comprising five weeks of baseline data collection followed by five weeks with implementation of a proforma. This proforma was based on the "David & Wendy" acronym, encompassing diet, activity, vital signs, investigations/IV therapy, drains/lines, wound assessment, examination findings, nursing concerns, drugs/deep vein thrombosis (DVT) prophylaxis, and barriers to discharge. Results A total of 711 ward round notes were analyzed, 349 with proforma and 362 without. Statistically significant improvements were observed in the documentation of diet, activity, investigations/IV therapy, drains/lines, wound assessment, nursing concerns, drugs/DVT prophylaxis, and barriers to discharge (p < 0.05) with proforma use. No significant difference was noted in the documentation of vital signs or examination findings. The time taken to finalize ward round notes was significantly reduced with the proforma (M = 31.28 vs. 60.05 minutes, p < 0.001). Conclusion The introduction of the David & Wendy proforma significantly improved the speed and quality of documentation for key surgical ward round information during our study.

Parkinson's disease is not associated with gastrointestinal myenteric ganglion neuron loss.

Gastrointestinal dysfunction is a prominent non-motor feature of Parkinson's disease (PD) that contributes directly to the morbidity of patients, complicates management of motor symptoms, and may herald incipient PD in patients without motor disability. Although PD has traditionally been considered a disease of dopaminergic neurons in the substantia nigra, analyses of gastrointestinal samples from PD patients have consistently revealed pathology in the enteric nervous system. The relationship of PD pathology to GI dysmotility is poorly understood, and this lack of understanding has led to limited success in developing treatments for PD-related GI symptoms. We have quantitatively compared myenteric neuron density and relative abundance of NO, VIP, and catecholamine neurons between patients with PD and control individuals along the length of the GI tract. In addition, we have examined the frequency of GI α-synuclein neuritic pathology and its co-localization with the same neuronal markers. We have included a comparison with a small population of patients with incidental Lewy bodies found at autopsy. These data indicate that there is no neuronal loss in the myenteric plexus in PD. Lewy body pathology parallels parasympathetic autonomic input from the dorsal motor nucleus of the vagus, not the distribution of extrinsic sympathetic input or intrinsic enteric neurons, and is only rarely co-localized with tyrosine hydroxylase. These data provide a critical background to which further analyses of the effect of PD on the GI tract may be compared and suggest that neuropathology in myenteric neurons is unlikely to be a causative factor in PD-related GI dysmotility.

Alpha-synuclein transgenic mice display age-related slowing of gastrointestinal motility associated with transgene expression in the vagal system.

Gastrointestinal (GI) dysfunction is the one of the most common non-motor symptoms of Parkinson's disease (PD) and occurs in nearly every patient afflicted with this common neurodegenerative disorder. While parkinsonian motor symptoms are caused by degeneration of dopamine neurons in the midbrain substantia nigra, the neurological localization of non-motor symptoms in PD is not known. In this study, we examined a transgenic mouse model of PD in which mutant (A53T) human α-synuclein was expressed under control of the prion promoter (AS mice). We found that gastrointestinal expression of human α-synuclein in this transgenic line was limited to efferent fibers projecting from the dorsal motor nucleus of the vagus nerve (DMV) to the enteric nervous system (ENS). Older transgenic mice had a lower density of human α-synuclein expression in the GI tract, suggesting an age-related disruption of efferent vagal fibers in this model. At the same time, mice developed age-related declines in stool frequency and gastric emptying consistent with those seen in human PD. These behavioral and neuropathological patterns parallel those seen in PD patients and suggest the DMV as a target for further investigation into causes for GI neuropathology and symptomatology in parkinsonism.

Neurochemical phenotypes of myenteric neurons in the rhesus monkey.

Understanding the neurochemical composition of the enteric nervous system (ENS) is critical for elucidating neurological function in the gastrointestinal (GI) tract in health and disease. Despite their status as the closest models of human neurological systems, relatively little is known about enteric neurochemistry in nonhuman primates. We describe neurochemical coding of the enteric nervous system, specifically the myenteric plexus, of the rhesus monkey (Macaca mulatta) by immunohistochemistry and directly compare it to human tissues. There are considerable differences in the myenteric plexus along different segments of the monkey GI tract. While acetylcholine neurons make up the majority of myenteric neurons in the stomach (70%), they are a minority in the rectum (47%). Conversely, only 22% of gastric myenteric neurons express nitric oxide synthase (NOS) compared to 52% in the rectum. Vasoactive intestinal peptide (VIP) is more prominent in the stomach (37%) versus the rest of the GI tract (≈10%), and catecholamine neurons are rare (≈1%). There is significant coexpression of NOS and VIP in myenteric neurons that is more prominent in the proximal GI tract. Taken as a whole, these data provide insight into the neurochemical anatomy underlying GI motility. While overall similarity to other mammalian species is clear, there are some notable differences between the ENS of rhesus monkeys, humans, and other species that will be important to take into account when evaluating models of human diseases in animals.