Gilman B. Allen

Background Chest X-rays (CXRs) are traditionally obtained daily in all patients on invasive mechanical ventilation (IMV) in the intensive care unit (ICU). We sought to reduce overutilisation of CXRs obtained in the ICU, using a multifaceted intervention to eliminate automated daily studies. Methods We first educated ICU staff about the low diagnostic yield of automated daily CXRs, then removed the ‘daily’ option from the electronic health records-based ordering system, and added a query (CXR indicated or not indicated) to the ICU daily rounding checklist to prompt a CXR order when clinically warranted. We built a report from billing codes, focusing on all CXRs obtained on IMV census days in the medical (MICU) and surgical (SICU) ICUs, excluding the day of admission and days that a procedure warranting CXR was performed. This generated the number of CXRs obtained every 1000 ‘included’ ventilator days (IVDs), the latter defined as not having an ‘absolute’ clinical indication for CXR. Results The average monthly number of CXRs on an IVD decreased from 919±90 (95% CI 877 to 963) to 330±87 (95% CI 295 to 354) per 1000 IVDs in the MICU, and from 995±69 (95% CI 947 to 1055) to 649±133 (95% CI 593 to 697) in the SICU. This yielded an estimated 1830 to 2066 CXRs avoided over 2 years and an estimated annual savings of $191 600 to $224 200. There was no increase in reported adverse events. Conclusion ICUs can safely transition to a higher value strategy of indication-based chest imaging by educating staff, eliminating the ‘daily’ order option and adding a simplified prompt to avoid missing clinically indicated CXRs.

Posterior reversible encephalopathy syndrome (PRES) is a clinical-radiographic syndrome formally recognized in 1996, which describes specific changes noted on neuroimaging thought to be related to impaired cerebral blood flow autoregulation and endothelial dysfunction. We report a case of PRES in the setting of increased ingestion of ondansetron; complicated by hemorrhagic transformation and refractory intracranial hypertension. We hypothesize an association of 5-HT3 antagonism and PRES. This is a case study report; with review of previously published literature through PubMed search. We describe the case of a 25 year old man following bariatric surgery who increased his ingestion of ondansetron, taking up to 40 tablets/day due to excessive nausea and vomiting. The patient was hospitalized for progressively more severe headache of 1 week’s duration. Computed tomography (CT) revealed bilateral cerebral edema in the parietal and occipital lobes in the setting of elevated blood pressure (BP). Three days into his admission, following improvement in his BP with oral anti-hypertensive but continued use of the ondansetron, the patient developed near complete blindness. CT head imaging revealed progression of the posterior cerebral edema and intraparenchymal hemorrhage. He was admitted to our ICU and despite supportive treatment, his neurological examination worsened while CT head imaging findings remained stable. Invasive multimodality monitoring revealed elevated intracranial pressure. The patient was aggressively treated and after a prolonged hospitalization and rehabilitation course, made a significant recovery. This case highlights a very rare potential neurological complication of ondansetron, a commonly used medication. We hypothesize an underlying association between PRES and 5-HT3 antagonism, via the latter’s potential role in endothelial dysfunction. Prompt recognition and treatment of PRES is essential, in order to prevent secondary cerebral injury and the associated potentially grave consequences.

Aspiration is a common cause of lung injury, but it is unclear why some cases are self-limited while others progress to acute respiratory distress syndrome (ARDS). Sporadic exposure to more than one insult could account for this variable progression. We investigated whether synergy between airway acid and endotoxin (LPS) amplifies injury severity in mice and whether LPS levels in human patients could corroborate our experimental findings. C57BL/6 mice aspirated acid (pH 1.3) or normal saline (NS), followed by LPS aerosol or nothing. Bronchoalveolar lavage fluid (BALF) was obtained 2 to 49 h later. Mice were injected with FITC-dextran 25 h after aspiration and connected to a ventilator, and lung elastance ( H) measured periodically following deep inflation (DI). Endotracheal and gastric aspirates were also collected from patients in the intensive care unit and assayed for pH and LPS. Lung instability (Δ H following DI) and pressure-volume hysteresis in acid- or LPS-exposed mice was greater than in controls but markedly greater in the combined acid/LPS group. BALF neutrophils, cytokines, protein, and FITC-dextran in the acid/LPS mice were geometrically higher than all other groups. BALF from acid-only mice markedly amplified LPS-induced TNF-α production in cultured macrophages. Human subjects had variable endotracheal LPS levels with the highest burden in those at higher risk of aspiration. Acid aspiration amplifies LPS signaling in mice to disrupt barrier function and lung mechanics in synergy. High variation in airway LPS and greater airway LPS burden in patients at higher risk of aspiration could help explain the sporadic progression of aspiration to ARDS.

In today’s era of health care, documentation has become almost as central to patient care as the actual care itself. As far as many credentialing and reimbursement entities are concerned, if it is not documented, it was not done. Unfortunately, these expanding demands for daily medical documentation have led to excessive busywork that frustrates providers in their attempts to achieve the increasingly unrealistic goal of “100% compliance.” More importantly, these demands compete with providers’ time spent in the actual care of their patients. We absolutely must design novel and sensible ways of automating the documentation process.As an example of a poorly met documentation challenge in the intensive care unit (ICU), consider the series of interventions targeted at reducing ventilator-associated pneumonia (VAP). Few experts would argue over the importance of complying with these preventive measures, yet even in high-performing medical centers with incentivized protocols, documented compliance with these best practice measures often falls short of targets. For example, a key element of the VAP prevention bundle, keeping the head-of-bed incline greater than 30°, routinely improves with education and engagement of staff, but can still fall as low as 60% to 70%,1 even when a device is used to continuously record head-of-bed incline and alert providers when this incline drops to less than 28°.2 To make matters worse, even when documented compliance with one or more separate elements of the VAP bundle is maximized through intensive training, comprehensive compliance with the entire bundle falls short of the target. In one study, compliance with head-of-bed elevation climbed to more than 95% following the institution of nurse and physician champions, educational sessions and materials, bedside cues, engagement posters, and regular performance feedback. Yet compliance with all elements of the entire VAP bundle was still only 70%.3 Many possible reasons for this shortcoming include the more appropriately prioritized and time-critical tasks of providing care, which often trump tedious charting and documentation, even though the latter is vital for auditing performance.Given the current workload imposed on health care providers today, how realistic is it to expect them to achieve 100% compliance on the ever-growing list of items they must document, particularly when even the most dedicated and conscientious of our professionals do not always believe that it is a judicious use of their time? Solving this problem requires more than simply saying, “We’ll try harder,” and it is certainly not going to be solved by thinking we are all going to someday magically “get on board” to improve our compliance to 100%. Even the best-intentioned and hardest workers are flawed simply because they are human. Being human, however, is not a problem; it is a statement of fact and one that we must acknowledge and move beyond. The real problem at hand is our failure to properly use existing technology.In today’s era of advanced technology, with digital wireless communication and intuitive user interfaces, it is inexcusable that most important devices used in our ICUs, often designed by several different proprietors, have no standard means of communicating with one another, with our electronic medical records (EMRs), or even in an efficient manner with health care providers themselves.4 This lack of interoperability not only creates unnecessary tedium for personnel, it becomes a threat to patient safety.5 Imagine going to the grocery store today to find that the cashier, instead of swiping each item across a bar code scanner, takes out a pencil and ledger, writes down the price of each item, and then uses longhand addition to calculate the bill. Such a scenario sounds unthinkable to us today because it would waste so much time, as well as introduce an unacceptable allowance for human error. Yet this is what we are asking our physicians and nurses to do every day in the ICU. We manually determine each patient’s weight and height, use a calculator (or possibly a smartphone app) to estimate ideal body weight (IBW), and then calculate the respiratory tidal volume on the basis of 6 mL/kg IBW before plugging it into the ventilator. How many times have these steps led to human error, resulting in deviation from best practice in a patient with sepsis or acute respiratory distress syndrome? Imagine if the patient’s bed could report weight and height directly to the ventilator so that the ventilator could then automatically determine and deliver the 6 mL/kg IBW tidal volume. Imagine this same bed providing a regular update to the EMR on the incline of the patient’s head and upper torso. Imagine software in the pharmacy dispensary automatically telling the EMR every time chlorhexidine kits are checked out and used for oral hygiene. Imagine intravenous infusion pumps and ventilators, respectively, telling the EMR when sedative agents are turned off and when the patient is placed on a spontaneous breathing trial as a “wake and wean” event. The travesty in all of this conjecture is that many providers have already dreamed of these advances, and the technology has long existed to make them possible. Unfortunately, the very people who recognize the need and the market for these advances, we the providers, are not driving the technological design of our own tools and instruments.Many would argue that the fundamental problem is our own failure, as professionals, to put sufficient pressure on the medical equipment industry to provide greater value by having better usability and interoperability.4,5User interface design refers to a process that focuses on simplifying a product’s user interface to most efficiently achieve the user’s goals, a process that is desperately needed in the ICU. Interoperability refers to “the...

The role of gastroesophageal reflux and micro-aspiration as a trigger of airways hyperresponsiveness (AHR) in patients with asthma is controversial. The role of acid reflux and aspiration as a direct cause of AHR in normal subjects is also unclear. We speculated that aspiration of a weak acid with a pH (1.8) equivalent to the upper range of typical gastric contents would lead to AHR in naive mice. We further speculated that modest reductions in aspirate acidity to a level expected during gastric acid suppression therapy (pH 4.0) would impede aspiration-induced AHR. BALB/c female mice were briefly anesthetized with isoflurane and allowed to aspirate 75 μl of saline with HCl (pH 1.8, 4.0, or 7.4) or underwent sham aspiration. Mice were re-anesthetized 2 or 24 h later, underwent tracheostomy, and were coupled to a mechanical ventilator. Forced oscillations were used to periodically measure respiratory impedance (Zrs) following aerosol delivery of saline and increasing doses of methacholine to measure for AHR. Values for elastance ( H), airways resistance (R_N), and tissue damping ( G) were derived from Zrs. Aspirate pH of 1.8 led to a significant overall increase in peak R_N, G, and H compared with pH 4.0 and 7.4 at 2 and 24 h. Differences between pH 7.4 and 4.0 were not significant. In mice aspirating pH 1.8 compared with controls, airway lavage fluid contained more neutrophils, higher protein, and demonstrated higher permeability. We conclude that acid aspiration triggers an acute AHR, driven principally by breakdown of epithelial barrier integrity within the airways.