Diffuse lung disease and lung transplant network: Lung transplant section
Continuous distribution for lung transplant: Overhauling the wait list
Determining how to allocate the scarce resource of donor lungs to patients is a difficult task and evaluated continuously for potential improvement. Since 2005, in the United States, lung transplant recipients have been selected based primarily on location within a Donor Service Area and by lung allocation score (LAS), a composite score of urgency for transplant. This was updated in 2017 to an allocation by highest LAS within 250 nautical miles from the donor hospital. Factors such as blood type compatibility and height are also considered. Implementation of the LAS improved the sickest patients’ access to transplants while not worsening 1-year mortality (Egan TM. Semin Respir Crit Care Med. 2018;39[02]:126-37). Unfortunately, geographic hard boundaries mean a high proportion of low LAS (<50) patients receive local donors while high LAS patients receive national offers or die while on the waitlist (Iribarne A, et al. Clin Transplant. 2016:30:688-93).
Courtesy CHEST
Dr. Grant A. Turner
A new model that employs continuous distribution has been developed based on concerns regarding equity and improving allocation. This model would prioritize patients based on factors including medical priority, efficient management of organ placement (distance), expected posttransplant outcomes, and patient access (equity). By creating a composite of these without a geographic boundary, patients would be considered more on urgency within realistic constraints of distance and outcomes.
Courtesy CHEST
Dr. Laura Frye
The Organ Procurement and Transplantation Network has officially approved continuous distribution, with implementation planned for 2022; details regarding the new scoring system are to be published and further research will need to be undertaken to determine if it meets the goal of overall improvement in patient access, equity, and outcomes.
Grant A. Turner, MD, MHA
Laura Frye, MD
Section Members-at-Large
Critical care network: Non-respiratory critical care section
Update from the non-respiratory critical care section
As you’ve probably noticed, there have been some changes here at CHEST involving the Networks. Leadership here at CHEST has been hard at work restructuring the networks to make them more closely aligned with relevant clinical disciplines, and, ultimately, allow for greater participation. I am proud to have been given stewardship of the new Non-Respiratory Critical Care Section of the Critical Care Network.
Courtesy CHEST
Dr. Deep Ramachandran
So, what exactly is Non-Respiratory Critical Care? Well, that’s where I need your help. You see this network is meant to reflect the needs and wants of CHEST members like you. We need you, dear readers, to join in this venture and help us guide the content that this section will ultimately create for our members.
If you’re interested in critical care, but you don’t see your particular area of interest anywhere else in the current structure ... guess what? You’ve found the right place!
My Infectious Diseases and Nephro peeps? Welcome! Are you a surgical or anesthesia intensivist? Don’t be shy. ECMO people, let’s hear some chatter!Is therapeutic hypothermia your thing? Come on in. The water’s freezing. 33 degrees just like you folks like it. Or is it 36? Not sure. Anyway, see what I’m talking about? We really need your help!You can get involved by clicking on the Membership & Community tab at the CHEST website. Once you’re a member, you can even nominate yourself to run for the Steering Committee elections which are held periodically. Hope to see you soon!
Deep Ramachandran, MD, FCCP
Section Chair
Sleep medicine network: Non-respiratory sleep section
Unusual suspects? Breakthrough in the treatment of idiopathic hypersomnia
Idiopathic hypersomnia (IH) is a rare and debilitating disorder defined by its excessive daytime sleepiness, sleep inertia, prolonged nighttime sleep, and long, unrefreshing naps (AASM. ICSD 3rd ed. 2014). Gamma-aminobutyric acid (GABA) is one of the main inhibitory neurotransmitters in the nervous system. It is through the potentiation of GABA that substances such as alcohol and benzodiazepines yield their effects. It is also hypothesized that the “brain fog” experienced in IH may be a consequence of either higher levels of an endogenous benzodiazepines in the cerebral spinal fluid or the presence of a GABA-enhancing peptide (Rye DB. Science Transl Med. 2012;Med 4:161ra151).
Sodium oxybate (SXB), a compound that likely has its therapeutic effect through the potentiation of GABA receptors, is an effective treatment option for cataplexy and sleepiness in narcolepsy. Although there may be some overlap between narcolepsy and IH in both diagnosis and treatment (Bassetti C, et al. Brain. 1997;120:1423), it would perhaps be entirely counterintuitive (given SXB’s pharmacology) to imagine using SXB as a plausible treatment option in IH. It was, however, investigated in the treatment of refractory hypersomnia and IH. In the retrospective study looking at 46 subjects treated with SXB, 71% experienced improvement of their severe sleep inertia, 55% had a decrease in their excessive daytime sleepiness, and 52% reported a shortened nighttime sleep time (Leu-Semenescu S, et al. Sleep Med. 2016;17:38).
In a recent double-blind, randomized control trial, the lower-sodium oxybate (LXB) was trialed in 154 patients with IH. It demonstrated statistically significant and clinically meaningful improvements (compared with placebo) in the Epworth Sleepiness Scale score (P <.0001) and in the Idiopathic Hypersomnia Severity Scale (P <.0001). The effects were seen both during the up titration of LXB and the benefits were maintained during the stable phase of the intervention (Dauvilliers Y, et al. Lancet Neurol. 2022;21(1):53). In August 2021, LXB (initially launched in 2020 for the treatment of narcolepsy) is now the first FDA-approved medication to treat IH in adults. It is curious, however, that LXB’s understood therapeutic effects are secondary to the “potentiation” of the very GABA receptor we have believed to be the root cause of the debilitating symptoms in IH. Could this discovery lend to further insights into the origins of this condition?
Ruckshanda Majid, MD, FCCP