Impact on cardiac surgery volume of a comprehensive partnership with Integrated Health Solutions.

Background: The New Brunswick Heart Centre (NBHC) entered a contractual partnership with Integrated Health Solutions (IHS) to help address increasing wait times in the province of New Brunswick. Methods: Team leaders were identified from each of the target areas, including surgeons, anesthesiologists, nurses (operating room, intensive care unit [ICU] and postoperative ward), access coordinators and administrators. The methodology used was based on Lean principles and involved exercises by stakeholders aimed at identifying opportunities for improvement. A weekly dashboard was created to monitor and facilitate improvement efforts. No additional hospital beds or operating room theatres were added during the study period. Results: After 2 years, the annual number of cardiac surgical interventions increased from 788 to 873, representing a 10.8% increase in capacity. The best median wait time for patients decreased from 52 to 35 days (35% reduction). The best 90th percentile wait time decreased from 126 to 98 days (22% reduction). The overall increase in capacity could be explained in part by the significant increase in fast tracking from the ICU to the ward (> 2-fold) or bypassing the ICU altogether (4-fold increase reaching 13%). Despite these successes, challenges persist as the number of OR cancellations remained around 7.5% of all cases, mainly because of limited ICU resources. Conclusion: The NBHC-IHS partnership on this project has resulted in excellent engagement by stakeholders and promoted team cohesiveness. Furthermore, it has allowed significant reorganization and realignment of efforts to limit wait times and maximize overall capacity.

Contexte: Le New-Brunswick Heart Centre (NBHC) a conclu une entente contractuelle avec Integrated Health Solutions (IHS) pour remédier aux temps d'attente de plus en plus longs au Nouveau-Brunswick. Méthodes: Des chefs d'équipe ont été identifiés pour chaque domaine cible, notamment la chirurgie, l'anesthésie, les soins infirmiers (en salle d'opération, aux soins intensifs et en soins postopératoires), la coordination des soins et la direction. La méthodologie utilisée se fondait sur l'approche Lean et comprenait des exercices visant à relever les possibilités d'amélioration. Un tableau de bord hebdomadaire a été créé pour suivre et faciliter les mesures d'amélioration. On n'a ajouté aucun lit d'hôpital et aucune salle d'opération pendant la période étudiée. Résultats: Après 2 ans, le nombre de chirurgies cardiaques par année est passé de 788 à 873, une augmentation de 10,8 % de la capacité. Le temps d'attente médian pour les patients est tombé de 52 à 35 jours (réduction de 35 %). Le temps d'attente au 90e centile est passé de 126 à 98 jours (réduction de 22 %). L'augmentation générale de la capacité peut s'expliquer en partie par la réduction significative du temps passé aux soins intensifs avant l'admission en soins généraux (> 2 fois) ou par l'élimination complète du passage aux soins intensifs (augmentation de 400 %; 13 % des cas). Malgré ces réussites, des défis demeurent puisque le taux d'annulation des interventions est resté autour de 7,5 % des cas, surtout en raison des ressources limitées aux soins intensifs. Conclusion: Le partenariat NBHC­IHS sur ce projet a permis de mobiliser efficacement les participants et a favorisé la cohésion au sein de l'équipe. Il a en outre permis une importante réorganisation des ressources pour réduire les temps d'attente et augmenter la capacité générale.

Endothelial molecular changes in a rodent model of arteriovenous malformation.

OBJECT: The cellular and molecular processes underlying arteriovenous malformation (AVM) development and response to radiosurgery are largely unknown. An animal model mimicking the molecular properties of AVMs is required to examine these processses. This study was performed to determine whether the endothelial molecular changes in an animal model of arteriovenous fistula (AVF) are similar to those in human AVMs. METHODS: Arteriovenous fistulas were created in 18 Sprague-Dawley rats by end-to-side anastomosis of the left jugular vein to the common carotid artery creating a model "nidus" of arterialized branching veins that coalesce into a "draining vein" (sigmoid sinus). Six control animals underwent sham operations. RESULTS: After 1 or 3 days, or 1, 3, 6, or 12 weeks, fresh-frozen sections of the fistula, nidus vessels, and contralateral vessels were studied immunohistochemically for thrombomodulin, von Willebrand factor, E-selectin, P-selectin, and vascular endothelial growth factor. CONCLUSIONS: The AVF model has a "nidus" with endothelial molecular changes similar to those observed in human AVMs, supporting its use as a model for studying the effects of radiosurgery on AVMs.

Altered subarachnoid space compliance and fluid flow in an animal model of posttraumatic syringomyelia.

STUDY DESIGN: A histologic study of cerebrospinal fluid tracers in Sprague-Dawley rats undergoing lumboperitoneal shunt insertion in the excitotoxic animal model of posttraumatic syringomyelia (PTS). OBJECTIVES: To determine the effects of cerebrospinal fluid (CSF) diversion from the subarachnoid space on perivascular flow (PVS) and syrinx formation in posttraumatic syringomyelia. SUMMARY OF BACKGROUND DATA: In an animal model of PTS, fluid enters syringes from the subarachnoid space via perivascular spaces. Preferential PVS flow occurs at the level of the syrinx. It has been suggested that arachnoiditis predisposes to posttraumatic syringomyelia formation by obstructing subarachnoid cerebrospinal fluid flow and enhancing perivascular flow. MATERIALS AND METHODS: Thirty-two male Sprague-Dawley rats were investigated using the CSF tracer horseradish peroxidase (HRP), the excitotoxic model of PTS, and lumboperitoneal shunt insertion. Five experimental groups consisted of normal controls, syrinx only and shunt only controls, and shunt insertion before or after syrinx formation. In all groups except normal controls, CSF flow studies were performed 6 weeks after the final intervention. Grading scales were used to quantify HRP staining. RESULTS: All excitotoxic model animals formed syringes. Perivascular flow was greatest at the level of the syrinx. Cerebral cortex perivascular flow was significantly reduced after shunt insertion in animals with a syrinx (P < 0.05). Shunt insertion did not alter syrinx length or size. There were no significant differences between shunt and syrinx first groups. CONCLUSIONS: Increasing caudal subarachnoid space compliance with a shunt does not affect local CSF flow into the spinal cord and syrinx. These results suggest that localized alterations in compliance, as opposed to obstruction from traumatic arachnoiditis, may act as an important factor in syrinx pathogenesis.

The role of excitotoxic injury in post-traumatic syringomyelia.

Fifty percent of patients with neurological deterioration from post-traumatic syringomyelia do not respond to treatment. Treatment failure is due in part to an incomplete understanding of the underlying aetiology. An animal model that mimics the human disease is required to investigate underlying pathophysiology and treatment options. A previous study was designed to mimic trauma-induced effects on the spinal cord that result in syringomyelia, combining an excitotoxic insult with kaolin-induced arachnoiditis. In this excitotoxic model, syringes were produced in 82% of animals. The aims of the current study were to improve the model to produce syringes in all animals treated, to examine the relative influences of excitotoxic injury and neuronal loss on syrinx formation, and to use magnetic resonance imaging (MRI) to examine syringes non-invasively. A temporal and dose profile of intraparenchymal quisqualic acid (QA) and subarachnoid kaolin was performed in Sprague Dawley rats. MRI was used to study four syrinx and six control animals. In one subgroup of animals surviving for 6 weeks, 100% (eight of eight) developed syringes. Syrinx formation and enlargement occurred in a dose and time dependent manner, whilst significant neuronal loss was only dose dependent. Animal syrinx histology closely resembled human post-traumatic syringomyelia. Axial T2-weighted MR images demonstrated syrinx presence. The results suggest that the formation of an initial cyst predisposes to syrinx formation in the presence of subarachnoid adhesions.

Fluid flow in an animal model of post-traumatic syringomyelia.

More than a quarter of patients with spinal cord injury develop syringomyelia, often with progressive neurological deficit. Treatment options remain limited and long-term failure rates are high. The current poor understanding is impeding development of improved therapies. The source and route of fluid flow into syringes has been investigated using cerebrospinal fluid (CSF) tracers. Previous work using a model of canalicular syringomyelia has shown that fluid enters the dilated central canal from perivascular spaces. The aim of this study was to determine the source and route of fluid flow in an animal model of extracanalicular (post-traumatic) syringomyelia. A model of post-traumatic syringomyelia was established in 25 Sprague-Dawley rats with intraparenchymal injections of quisqualic acid and kaolin-induced arachnoiditis. Rats survived for 6 weeks before injection of the CSF tracer horseradish peroxidase into the cisterna magna. Examination of the spatial distribution of horseradish peroxidase at 0, 3, 5, 10, or 20 min after injection was used to determine the route of fluid flow. Horseradish peroxidase rapidly spread to the ventromedian fissure, perivascular spaces, central canal, and extracanalicular syrinx. Flow occurred into the syrinx prior to significant perivascular flow in the rostral spinal cord. Preferential flow into the syrinx occurred from the perivascular spaces of the central penetrating branches of the anterior spinal artery in the grey matter. Transparenchymal flow into the syrinx was less prominent than perivascular flow. This is the first report of fluid flow within the spinal cord in a model of post-traumatic syringomyelia. Fluid from perivascular spaces moves preferentially into extracanalicular syringes and the surrounding parenchyma. Obstruction to CSF flow and loss of compliance from traumatic arachnoiditis might potentiate fluid flow in the perivascular space.