The table below is taken from a very comprehensive paper on trachs in Respiratory Care. As you can see, even trachs that are the same size according to the company actually have different dimensions. So I would recommend discussing with your friendly respiratory therapist if you think a trach needs downsizing and what the right size to go to might be.
A capping trial is performed when you are considering decannulating (removing) a patient’s tracheostomy tube. It is often the final step before someone is able to breathe completely on their own again. It is a test of whether the patient can control secretions and feel comfortable breathing “normally.”
Who can undergo a capping trial?
Anyone who has been successfully weaned from the vent for a good amount of time
At most, they should be on 40% O2
Secretions are not excessive
Patients’ cuffs must be deflated (an inflated cuff will not allow ANY passage of air)
How does the capping trial work?
There is no standardized protocol. Like many aspects related to vent management, this varies by institution. This was a QI study at Hopkins on the creation and implementation of a capping trial protocol. There were two different options:
Cap x24 hours and decannulate if successful (2 days)
Cap x12 hours, rest, cap x24 hours, then decannulate if successful (3 days)
Patients should be monitored for signs of respiratory distress during the capping trial.
This trach weaning form created by St. George’s Hospitals gives you a sense of how to think about the final steps towards decannulating a trach:
Sometimes, you might be told to order a serum ammonia level on a patient who is encephalopathic, whether they have a history of liver disease or not. Why? Does the ammonia level actually matter?
I would argue for most cases, no. There are specific situations in which serum ammonia is a good prognostic or diagnostic test:
Acute liver failure (or acute fatty liver of pregnancy)–associated with risk of cerebral herniation and poorer outcomes
Patients who have inborn errors of metabolism–can suggest a diagnosis of urea cycle disorders
Reyes syndrome–can be suggestive of this diagnosis
Monitoring of ammonia-lowering therapy–in the research phase as far as I know
If you have a patient with cirrhosis or chronic liver disease who comes in with hepatic encephalopathy, though, the serum ammonia level is almost certainly not going to change your management. Ask yourself: If the ammonia level is 20 in a patient with major hand flapping, will you stop their lactulose? If it’s 140 in an alert cirrhotic will you get a head CT to look for cerebral herniation? Probably no, and no. It’s generally agreed that a serum ammonia level >100 is probably bad. And then there’s the question of arterial, venous, or partial pressure–better to just not get it in the first place. It also costs anywhere from $30-50.
Study results vary on whether the serum ammonia level is correlated with encephalopathy. For example, this study of about 120 patients suggests that it is, whereas this study of about 20 patients suggests not, and this study says yes for ALF but not for patients with chronic liver disease. Even if the majority of evidence tips (pun not intended) towards ammonia levels and encephalopathy being correlated, no one has been able to define specific numerical cut-offs for what levels correlate with mild, moderate, or severe hepatic encephalopathy. So ammonia levels remain clinically not useful for managing most cases of hepatic encephalopathy. I rest my case with this clinical vignette and discussion by Phillip Ge and Bruce Runyon.
It is common to set the O2 saturation goal for hospitalized patients with COPD exacerbations at 88-92%, and patients without COPD to 94-98%. This is in accordance with British Thoracic Society guidelines. The O2 sat goals are lower for patients with COPD because of the risk of hypercapnenic respiratory failure.
I’m not questioning the O2 sat goals. What I do want to discuss is one of the oft-cited mechanisms for this respiratory failure: that a higher O2 sat will depress the respiratory drive in these patients. Is this true?
Not really. The explanation is very well stated in LITFL. Patients with COPD suffer from parenchymal damage that increases V/Q mismatch. To compensate for this, those smart pulmonary arterioles vasoconstrict to deliver O2 preferentially to the parts of the lungs with the least damage. Giving someone supplemental O2 in this scenario causes the pulmonary arterioles to dilate, causing increased blood flow to the damaged parts of the lungs, too, which increases V/Q mismatch again. See this article for helpful diagrams and more detailed explanation. In addition, due to the Haldane effect (=introducing more O2 will cause CO2 to dissociate more readily from hemoglobin), adding supplemental O2 theoretically causes COPDers’ CO2 levels to increase. I’m not sure that anyone has actually demonstrated this experimentally, but it makes sense.
This review from Respiratory Care on the use of supplemental O2 cites a 2010 study of about 400 patients with COPD exacerbations. They were randomized into a 88-92% O2 sat group and a non-titrated group (so presumed >94%); each group could get as much supplemental O2 as needed to reach those goals. The titrated group had a 58% reduction in hypercapnea and respiratory failure compared to the non-titrated group.
In conclusion: patients with COPD exacerbations should have a lower target O2 sat, but the justification for this is not that it will affect their respiratory drive–instead, think about V/Q mismatch and CO2 dissociation.
What if a patient has COPD but does not have an exacerbation while they’re in the hospital? I couldn’t find a clear answer but would assume that since the same physiologic properties above are in play, it makes sense to continue the lower O2 sat goal.
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 →