IV vs. PO steroids for asthma

Treating an asthma exacerbation with steroids–and the sooner the better–is undisputed. And it makes intuitive sense that higher doses of steroids work better, and that IV steroids work better than PO steroids, right?

Well, the answer’s not so simple.

First of all, I see patients >18 years of age (usually). A lot of the literature on asthma was studied in the pediatric population, so while the results might be generalizable, we don’t know for sure.

Is there a maximum dose for steroids?

No, although this Cochrane review suggests that upwards of 100 mg prednisone daily, you’re probably not getting much benefit. This separate Cochrane review concludes most of the evidence is pretty low-quality, so it’s hard to make a strong recommendation. Side effects such as hyperglycemia and agitation/delirium are dose dependent.

Are IV steroids better than PO steroids?

I’ve heard some people suggest that if someone has “failed” PO steroids, then they should get a trial of IV steroids for at least 48 hours. On the one hand, this seems reasonable, because you want to avoid intubating the patient for worsening respiratory distress. On the other hand, there’s no evidence to support the assertion that IV steroids are better. See this pediatric study or this randomized adult study. This review makes the argument that it can be hard to ascertain the true effect of IV steroids in retrospective studies because (1) there is often no true “control” or “placebo” group (2) more severe asthma attacks are more likely to get IV steroids upfront, so you have a “confounding by severity” problem.

IV steroids make sense as a one-time dose for initial therapy in the ED, or for patients who are too obtunded or can’t take PO for some other reason. Then again, I’ve had a couple of cases where we used IV steroids 4-5 days into someone’s asthma treatment, and they got better. There’s the literature, and then there’s practice.

Checking residuals (gastric residuals, that is)

Ah, the fun tradition of “residual 250 cc…hold TF?” This national survey shows that there is very wide variance in how residuals are checked, and how much is “concerning.” 200 cc? 250 cc? 500 cc? Going once, going twice…

Disclaimer: the information below is about adults. Who knows if the answers are the same for a pediatric population? Not me.

This ACG clinical guideline on nutrition in the hospital setting opened my eyes (mostly to how much we don’t know about managing nutrition). The authors write that checking residuals “has been shown to be a poor marker of true gastric volume, gastric emptying, risk of aspiration, pneumonia, and poor outcomes.” The sensitivity of residuals for predicting aspiration is 2-8%. This JAMA study shows that in the ICU, checking residuals didn’t affect development of ventilation-associated pneumonia. In other papers, one of the authors has advocated for the abolishment of checking residuals in nursing practice (see this link for good, practical information).

When is checking residuals useful?

Checking residuals is thought to be most useful in the first 48 hours of initiating tube feeds, as patients are getting increased to goal rate. If the residuals are building up (see below), it might be an indication to pause the tube feeds and make sure there’s nothing wrong with the tube, there are no tube feeds leaking into the peritoneum (this is actually something terrifying that can happen), etc. If your patient is intubated/sedated/obtunded, residuals are the only measure you have–but if the patient is awake and alert, you could talk to them and ask if they’re having worsening nausea, bloating, etc.

How high is too high? When do tube feeds need to be held for residuals?

I don’t know where the adage, “hold TF for residuals >200 cc” comes from. Abbott Nutrition states that when residuals > 500 cc, consider holding tube feeds. (For perspective, the human stomach can accomodate +/- 1 liter.) Check your institutional hospital policy, but…the general message of this post is that you shouldn’t be too worried.

Does checking residuals have harmful effects?

It is known that protein clots when the pH <5.0 (stomach acid pH is usually between 1.5-3.5). Could checking residuals lead to refluxing clotted protein, increasing the likelihood of clogging the tube? This small study (n=30) says, yes. In the group undergoing regular residual checks, there were 10 clogging events, compared to 1 in the no-residual checks group.

Checking residuals can also lead to tube feeds being held unnecessarily–if higher residuals aren’t a good sign of impending aspiration, we’re just holding tube feeds for hours at a time, depriving patients of the nutrition they’re supposed to be getting.

To rule out or not rule out: the TB rule-out

The US is very, very lucky to only have approximately 9,000 cases of TB yearly. But TB can be a “great masquerader” with such serious public health consequences that we have to be constantly vigilant. After all, about ONE-THIRD OF THE WORLD POPULATION is infected with Mycobacterium tuberculosis.

Definitely tuberculosis.

Who needs to be ruled out for TB?

Someone who has clinical +/- epidemiological features of pulmonary TB. Only active pulmonary TB is infectious, so extra-pulmonary TB does not require quarantine. However, extra-pulmonary TB can be infectious if you’re directly biopsying or handling samples from infected lesions.

If the patient in question doesn’t really fit the above features, or you have a strong suspicion for an alternative diagnosis (plain old bacterial pneumonia, pulmonary infarct, DAH, vasculitis, pulmonary sarcoidosis, etc.) then you’re not required to do a rule out. But you better be DAMN SURE because if it turns out the patient does have TB, you could be putting a lot of people at risk of infection.

Who should be put in a negative pressure room “just in case?”

This is a 1999 multicenter, prospective study of a decision instrument to predict who would be at very low risk of TB and would not require isolation. Not surprisingly, people at low risk included those who were not homeless, did not have recent exposure to TB, were not incarcerated, and did not have suspicious x-ray findings. It stands to reason that you might want to be more cautious with people who do have the risk factors outlined above.

Does everyone getting ruled out for TB require hospitalization?

Theoretically, someone can be ruled out for TB at home if they stay away from other family members and don’t go out into the community. This EM:RAP article has a protocol for setting up outpatient TB rule-out. But because YOU CAN’T TRUST ANYONE (and perhaps because the ED doesn’t want to be held liable if something at home goes wrong), I’ve had even very low-public health risk cases admitted for rule-out. If a patient refuses to be admitted, you cannot legally hold them against their will just for TB rule-out, even if they are a public health hazard. Try to convince them of the merits of being admitted, and if they still refuse and leave AMA, call your local health department, who do have the authority to search for elopers and strong-arm them into getting admitted.

What are the possible outcomes for someone exposed to TB?

Can you rule out someone with a PPD or a quantiferon gold?

It would be so much easier than AFB x3 q8H +/- direct sampling! Alas. PPD and quant golds do not distinguish between latent and active TB. A negative PPD or quant gold could be reassuring, but a positive result doesn’t change management. Plus, up to 25% of people with active pulmonary TB will have a negative test result for these two tests.

CIWA, valium, thiamine, oh my: approaches to treating alcohol withdrawal

I ask myself three questions about patients needing treatment for alcohol withdrawal:
Is it uncomplicated or complicated? (Complicated=delirium tremens, active seizing, cardiovascular compromise)
Are the symptoms relatively under control right now, or is the patient soaking through their sheets/intractably vomiting/having bad hallucinations?
Is the patient willing to stay for treatment of withdrawal, or are they ripping out their IV and promising to avoid withdrawal by getting a post-hospitalization discount from their favorite liquor store?
(True story.)

On CIWA: every medical nurse out there has had a patient try to win the CIWA game. MINDS is an alternative scale that correlates strongly with CIWA and can be used in the ICU setting. However, RASS is thought to be a more objective, simpler scale than CIWA. I prefer to use RASS when thinking about who needs more/faster doses of IV benzos, drug loading, more aggressive care.

Medical floor:

  • Uncomplicated withdrawal: these patients will probably be fine with a light dose of PRN benzo of your choice on a CIWA score.
  • Complicated withdrawal: these patients should be treated more aggressively, and if they have underlying medical problems, bad electrolyte problems, rhabdo, or other issues, warrant consideration for ICU-level care.

On withdrawal seizures: around 15% of patients will have seizures around withdrawal. Of these patients, about 50% have seizures for non-withdrawal reasons like SDH, trauma, electrolyte derangements, infection, etc. So work it up! A patient who just seized (or who has DTs) should be treated more aggressively, and definitely with IV benzos.

Choices of medications:

  • Valium (diazepam): I was taught that patients with cirrhosis should get Ativan instead (L.O.T.!) This review argues that (1) that is not true based on studies of cirrhotics from the 70s and 80s (2) Valium has a shorter acting half-life (more rapid onset of action) but longer elimination half-life (tapers down more easily), which means it can be titrated to symptoms more safely and is a better taper. The review also cites studies reporting better outcomes with “Valium loading.”
  • Ativan (lorazepam): everyone’s favorite.
  • Librium (chlordiazepoxide): there’s older pro-Librium data. Librium, like Valium, is a longer-acting benzo. If you have less familiarity with it, though, prescribe it with guidance.
  • Antipsychotics: studied, and may be useful for acute, howling, punch-throwing agitation but known to lower the seizure threshold so…may not be the best choice.

On scheduled benzos for prophylaxis: UptoDate recommends giving patients who are minimally symptomatic with history of complicated withdrawal prophylactic scheduled benzos to prevent worsening symptoms, but also: “A fixed dose schedule strategy is most useful for preventing withdrawal in patients who are at risk but asymptomatic or minimally symptomatic. The only advantage of this strategy is for the provider, as frequent reassessment is not required.” There are no studies cited for either of these statements. I could only find a couple of studies on giving scheduled benzos (in the surgical literature) which didn’t show improved outcomes with prophylactic benzos. In addition, I’ve had the experience of patients whose real problem was benzo addiction pretend to have alcohol withdrawal and specifically demand scheduled benzos for “history of withdrawal seizures.” I only start scheduled benzos on the floor if a patient had a seizure in the last few weeks-months or has had multiple ICU stays for withdrawal.

On thiamine: given to prevent Wernicke’s. It will feel futile, but there is some evidence that IV/IM thiamine does prevent Wernicke’s in patients who are at risk of thiamine deficiency. If the patient has been on a bender bad enough to make them withdraw, they are probably at risk of malnutrition and thiamine deficiency. Just do it! If your hospital has a shortage of IV thiamine, you can give doses of oral thiamine like 300 mg TID x3 days, but I’m not sure if these higher oral doses have been studied or if it’s just hopeful thinking.

Medical ICU:

  • Benzo drip: I don’t know what the record for an Ativan drip is, but I’ve had patients running at 25 ml/hr (so…600 mg of IV Ativan in a day?). The stalwart of ICU withdrawal treatment. Coming down from the drip can be prolonged if patients develop signs of benzo withdrawal, though.
  • Phenobarbital: Research from my old hospital shows it’s effective, self-tapering, and easy to administer, with shorter length of stay and no adverse outcomes–as long as the nurses and ED docs agree on giving it up front. This PulmCrit piece by Josh Farkas provides an excellent overview. If a patient is going to leave AMA and already got a dose of phenobarb, I don’t worry about it, because the half-life is very long.
  • Ketamine?

The bleeding heart in me reminds you: whenever you have the opportunity to care for someone with ETOH withdrawal, you also have the opportunity to prescribe a medication to assist with sobriety, or encourage the patient to think about an intensive substance abuse program.

What is an oxymizer?

What does this thing even look like?

Glad you asked:

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.”

What is a Rhinorocket? (and what do I need to know about them)

Reference– UpToDate

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

Are orthostatics useful?

Yes. But only in certain situations. Read on.

Typical case: 80-year old woman with severe ILD and pulmonary hypertension on 6 L nasal cannula coming in with dizziness and presyncope. “I feel fine now,” she says after one day of being in the hospital (her son warns you she is eager to get home to see a new grandchild). She has been on Lasix for several months for leg edema (which on exam is 3+), and despite saying she’s not dizzy anymore, her orthostatic vital signs (VS) are positive by SBP and DBP. Should you stop Lasix? Can you send her home?

Orthostatic symptoms include lightheadedness, dizziness, confusion, weakness, blurry vision, etc. Orthostatic VS are positive if after 1-3 minutes, the heart rate increases >30, systolic BP decreases >20, diastolic BP decreases >10 (the 30-20-10 rule). For patients who have hypertension, using a cutoff of systolic BP decreases >30 is more specific. This paper provides a great physiologic review of orthostatic hypotension (OH). In up to 1/3 of cases, the cause of orthostasis will not be identified.

Studies such as this meta-analysis and this prospective population study have linked OH to increased all-cause mortality as well as stroke, CHF, and MI. Positive orthostatic VS can be linked to serious chronic illnesses, but these studies showed patients with OH had worse outcomes independently of other conditions.

Just some of the diseases associated with OH:

  • Neurodegenerative disease: primary autonomic failure, MSA, Parkinson’s, MS
  • Neuropathies: diabetes, amyloidosis, renal failure, stroke
  • Cardiovascular disease: heart block, pulmonary HTN, heart failure
  • Endocrinopathies: adrenal insufficiency, hypothyroidism
  • Cancer: paraneoplastic syndromes, multiple myeloma

Known factors that can make OH worse:

  • Fever
  • Dehydration, excessive urination
  • Increased venous pooling
  • Immobilization and deconditioning
  • Post-prandial state
  • Certain medications (diuretics, some antipsychotics, etc…)

The above information shows that not all orthostasis will be fixed by fluids. Don’t overload patients if they’re not responding.

More recently, orthostatic VS have been critiqued. Anand Swaminathan’s presentation on the “urban legend” of orthostatics in the ED is very informative. He cites a study showing that in a population of 900 nursing home residents, 50% had orthostatic VS changes. The numbers are similar for young, healthy adults. Positive orthostatics could indicate a new problem…or not. See this: a letter to the editor on the lack of evidence showing positive orthostatic VS in syncope require additional diagnostic testing/admission. For triaging purposes, orthostatic VS are not as useful as orthostatic symptoms (getting so lightheaded they might fall or injure themselves at home).

Orthostatic VS should only be obtained if they will change decision-making or result in new treatment. I propose that orthostatic VS are useful for:

  • in certain presenting complaints, like pre-syncope or syncope, which based on a patient’s background, may lead to cardiac testing (I say this as an internal medicine doctor dealing with patients already admitted to the hospital)
  • determining how aggressively someone’s supine hypertension should be treated
  • determining if someone’s lightheadedness, dizziness, or hypotension should be treated with compression stockings or meds like droxidopa or midodrine
  • evaluating functional status or quality of life in patients with above-mentioned chronic illnesses (very specific situations)

Returning to the case: the patient’s positive orthostatic VS were thought to be due to underlying pulmonary HTN and deconditioning. Lasix was thought to be necessary for pulmonary and peripheral edema. She was sent home. She was re-admitted <48 hrs later with syncope and found to be normotensive lying on her back, but profoundly hypotensive (SBP 50s) with just turning in bed; this failed to improve with IV fluids. TTE showed new RV dilation and a thrombus vs. vegetation on a pacemaker lead. In retrospect, this TTE should have been performed during her first hospitalization. This case is a good example that the significance of positive orthostatics depends on the clinical context, and while you may not need to treat the orthostatics per se, they can be a warning sign of a high-risk patient or a brewing problem.