The situation: a young woman with opiate use disorder comes into the hospital with a broken arm after a car accident. She tells you she has been been buying methadone off the street and taking 60 mg a day. How do you manage this patient’s pain regimen and what can you do to prevent opiate withdrawal?
Methadone is typically used for maintenance therapy for opiate use disorder (OUD) or chronic pain. If it is for OUD, they must receive their doses from a methadone clinic. You should always try to call the clinic to verify the correct dose. In this patient’s case, she was buying methadone on her own. Therefore, the first step is to do a urine tox test–if the patient has been using methadone in the past week, it should be positive. If she is negative, it is not a good idea to start methadone unless she’s having withdrawal symptoms.
A patient’s home methadone dose does not provide acute pain control. Patients undergoing surgery can continue their methadone perioperatively. A patient who comes in on methadone (or suboxone, for that matter) needs the same kind of pain management as everyone else. For the patient above with the broken arm, you should still start Tylenol, NSAIDs if possible, and opiates like oxycodone or dilaudid for severe breakthrough pain.
Methadone is effective for preventing withdrawal symptoms in the inpatient setting. This Cochrane review shows that compared to placebo, tapered doses of methadone helped prevent withdrawal symptoms. There is no universal methadone tapered dose protocol. This American Pain Society sheet states methadone can be safely and rapidly tapered in 7-14 days. This pamphlet created by Pain Topics (and written by a Univ. Iowa pharmacist) has helpful information on short and long tapers. In general, you want to get the patient to reduce their dose by at most 25% every few days, end on a dose of 10 mg daily, and then stop completely.
For management of symptoms like sweats, muscle cramps, and nausea, check out this sister post.
A speaking valve, commonly called a Passy Muir valve, is a cap that can be put over the trach cannula to allow patients to vocalize more.
Patients often have to practice wearing the Passy Muir valve, and may be more fatigued or have more coughing at first.
The Passy Muir website has a practical and interesting troubleshooting page. Of course, take the company website with a grain of salt, but I did find it helpful overall for understanding the applications and patient perspective better.
Are there contraindications to using a speaking valve?
Yes. Patients with an an inflated cuff, fome cuff trach, history of laryngeal masses, stenosis, total laryngectomy, or thick copious secretions should hold off on a speaking valve.
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.