Sometimes the oxymizer is referred to as a “nasal moustache” because the reservoir is positioned under the nose, as in this instructive 1-minute video from RT Clinic.
What’s the conversion between oxymizer and nasal cannula?
Roughly 1:2––For example, 3 L by oxymizer delivers approximately the same amount of FiO2 that 6 L NC does. Some oxymizer devices can provide oxygen at a 1:4 level (so 1 L oxymizer=4 L NC) and deliver up to 20 L NC! Pretty cool.
What are the advantages of using an oxymizer?
For patients at home, oxymizers make portable oxygen tanks last longer (because the flow rate is lower). How much longer? It depends on the individual patient’s O2 needs and activity level. The lower flow rate also decreases nasal dryness and the discomfort of oxygen blasting into the nares all the time. From a pragmatic standpoint, most clinicians would be nervous about keeping patients at 7-8 L NC at all times (especially on a general medical floor), but an oxymizer can be used to keep patients with higher O2 requirements who are otherwise stable on the floor. For most patients with long-term, high-flow oxygen needs, oxymizers just make more sense.
If it’s “better” than nasal cannula, why don’t we use it all the time? Are there any downsides to the oxymizer?
Cost-wise, oxymizers can be expensive. Not all insurance companies cover oxymizers. The retail price of a single device is (as of this post) about $400 and the manufacturers recommend replacing the device every 3-4 weeks to ensure the membrane continues to work properly. In addition, some patients find the heavier tubing uncomfortable to wear. As far as I know, that’s pretty much it.
Disclaimer: I don’t get paid by Big Respiratory to write this. I have noticed more and more patients wearing oxymizers in the past couple of years who have been able to stay out of stepdown units and ICUs just because they “need more than 6 L NC, which is too much for the floor.”
Epistaxis is one of those things that sounds like it’s not a big deal until there’s someone gagging on their own blood, looking like an extra from Carrie. See here for an overview of managing epistaxis. There’s the nasal clip, quick cauterizing and silver nitrate, the Merocel sinus packing, Foley catheters (!), and then…the Rhinorocket.
Rhinorocket=nasal tampon extraordinaire. It is not a “Rapid Rhino” which is another kind of nasal tampon that works just as well. “One-balloon catheter” and “double-balloon catheter” refer to different types of Rhinorocket devices (reference for the image below). The double-balloon is used for posterior bleeds but some believe that it increases the risk of pressure necrosis.
The type of Rhinorocket used depends on what kind of bleeding the patient is presumed to have. It can stay in for 1-3 days (or 3-5 days depending on how bad the bleeding is) before being removed by an ENT. Regardless of what the ED tells you, patients do not have to be admitted just because they have a Rhinorocket in their nose–but they should be if there are concerns about continued bleeding or airway protection.
Some highlights of management:
Most ENTs will also prescribe concurrent antibiotics like amoxicillin or cephalexin (or bacitracin ointment) to prevent toxic shock syndrome
ENTs have told me you can use a whole bottle of Afrin per nare for epistaxis–not just a measly two squirts
Can spray the nares with saline spray several times a day for cleaning purposes
A little oozing immediately after placement is not alarming per se, but if there is ongoing bleeding into the back of the mouth that you can visualize, call ENT
Potential complications of the Rhinorocket: otitis media or ear discomfort, pressure necrosis if not packed correctly, infection like TSS
Example: you have a lovely 68-year old male with a history of two episodes of C. difficile infections after getting antibiotics in the setting of a hip surgery three months ago. He is admitted to your service with pneumonia and you decide he should get a 5-day course of levofloxacin. He has no abdominal pain or diarrhea (yet). Would PO vancomycin would help prevent recurrence of C. diff?
In this case, the answer is a weak “yes.” There is no randomized controlled trial data showing that PO vanc prevents recurrence. However, there is a retrospective study of 172 patients in Quebec with a diagnosis of C. diff who were exposed to antibiotics for whatever reason within 90 days of their diagnosis. Those patients who had at least one recurrence of C. diff who got PO vanc had half the risk of getting C. diff again. Because the study looked at patients within 90 days of diagnosis, it’s unclear whether patients who had C. diff from a longer time ago would get the same benefits. A second study from 2016 of over 200 patients showed that patients who got PO vanc had a 4% risk of recurrence, whereas patients who didn’t had a 27% risk. Notably, this study only surveilled patients for 4 weeks after their antibiotic course, and the patients weren’t randomized–I got the sense that the patients who were offered PO vanc were “sicker.”
The regimen that I have seen most often is 125 mg PO vancomycin QID, but the second study, for example, reported 125 mg PO vancomycin BID or daily, so regimens are all over the place.
How long should patients continue PO vanc prophylaxis for? Again, no strong right answer. I have seen patients told to take PO vanc for only as long as they are on other antibiotics, for a week after finishing, or to do a slow taper/pulse down. However, there is a clinical trial that has set the time course of PO vanc as 5 days after stopping other antibiotics, which sounds pretty good. What if it’s longer than a week, or a month? I did have a patient who required lifelong oral suppressive antibiotics…and we made the decision to keep her on PO vanc lifelong as well.
Do probiotics prevent recurrence of C. diff? The 2018 IDSA guidelines cite unclear evidence on whether probiotics prevent recurrence. While probiotics are fine for the general population (might as well try it if it won’t hurt), there are rare cases of fungemia/invasive infection that have been reported, in patients who are immunocompromised, have PICC lines, or are otherwise severely ill.
Fecal microbiota transplant (FMT) is an effective and durable method of treating recurrent or refractory C. difficile infections. There are several routes of administration:
Nasogastric tube: patient takes PPI beforehand, NG tube is inserted, 50-60 cc of fecal slurry is pushed into the tube
Endoscopy: 200-250 cc of fecal slurry is delivered by flex sigmoidoscopy or colonsocopy (to the cecum)
Capsules: frozen capsules of slurry taken over several weeks (experimental)
Is there any difference between these different routes of delivery? Capsules were first devised at Massachusetts General Hospital; clinical trials are ongoing and they are not widely available. NG tube vs. endoscopy have been compared, and although some have not found a difference, some conclude that endoscopy is superior. For example, this study of 50 patients from the University of Alabama at Birmingham showed that patients who had endoscopy delivery of FMT had a greater rate of “cure” (improvement of symptoms in 2 weeks) and fewer repeat FMT treatments. However, you do have to evaluate each patient individually: some patients may find the idea of an NG tube too repulsive, some may be too sick to undergo endoscopy, etc. Importantly, FMT is felt to be safe for immunocompromised patients, too.
Tangent: according to the 2018 IDSA guidelines for treatment of C. diff, PO vancomycin or fidaxomicin are now considered agents of choice for a first episode of C. diff, no matter the severity. Keep your metronidazole on the shelves! It’s no longer recommended.
It is a widely held belief that Tylenol (acetaminophen, or paracetamol, depending on where you are) should not be used in patients with chronic liver disease or transaminitis because the drug will worsen liver injury or cause acetaminophen toxicity, the most common kind of drug-induced liver injury. However, underuse of Tylenol may lead to overuse of other pain medications, like NSAIDs or opiates, which come with their own problems.
This review in the British Journal of Clinical Pharmacology goes through studies of healthy adults and adults with liver disease, including cirrhosis to look at the evidence for our fear of Tylenol. Essentially, the studies on Tylenol are small, and ALT naturally fluctuates (thus some of the previous methodology linking rise in ALT and Tylenol may have been questionable). The authors conclude that heavy alcohol use, malnutrition/fasting, underweight status, and sepsis may put patients at risk for acetaminophen toxicity, but Tylenol is still not 100% contraindicated for these groups. They state:
We have not found any case reports of hepatotoxicity secondary to therapeutic doses of paracetamol in adults with pre‐existing CLD who did not have at least one of these risk factors.
Therapeutic dose of acetaminophen is 4 g/24 hours. Therefore, it’s recommended that if you have patients with the above risk factors, aim to give them 2-3 g/24 hours. If they are developing rapidly deteriorating liver function (acute liver injury or failure), then it might be time to stop. Continue reading →