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.

Should I stop Plavix for orthopedic surgery?

A 60 year old woman with a stroke five years ago, who has been on Plavix ever since, gets hospitalized with a broken arm after a fall (it’s been icy this winter!). The orthopedics resident asks you if it’s okay to hold the Plavix, since they’re worried about her bleeding risk in the OR. “For ambulatory surgery,” he says, “We tell them to stop Plavix for 5 days before the procedure.”

Although there are some pretty solid recommendations on aspirin and warfarin in the perioperative setting, there aren’t clear guidelines for Plavix and DOACS….especially when you consider that orthopedic procedures have different bleeding risks than neurosurgical procedures than ophthalmologic procedures. One study of 40 patients undergoing hip fracture surgery reported no difference in bleeding between patients on Plavix versus those who were not. This systematic review of nine studies concludes that delaying hip fracture surgery for Plavix washout did not decrease bleeding and led to more post-op complications.

The American Academy of Neurology sought to provide clarity in this 2013 statement. They stated that while aspirin seems to increase bleeding risk for orthopedic surgeries (but not other kinds of procedures!) there was “insufficient evidence” to make a confident statement about Plavix. However they did point out that when bleeding did occur, most of the time it was mild–but when clotting occurred (like a stroke or PE), it was more morbid.

NB: however, Plavix is known to increase the risk of potential serious complications in spinal anesthesia. You probably want to avoid that. That being said, nothing is impossible, and there are cases of using platelet transfusions during spinal anesthesia to get people on Plavix through the case. It has been generally concluded that aspirin and spinal anesthesia are fine.

Conclusion: there is no one correct answer. For the woman above, if she just had drug-eluting stents put in last week, you should not stop the Plavix (and probably should not do surgery without talking with her cardiologist). If she’s been on Plavix for 5 years, and the surgery is going to be long and complicated, then it might be okay to hold it for a few days? Maybe? I probably wouldn’t because my personal opinion is, bleeding eventually stops, but a clot causes permanent damage. The orthopedics resident is right that holding Plavix for 5 days is general practice (although not clear where the evidence for this comes from). However, that’s in non-hospitalized patients who are functional enough to get to their scheduled surgery and go home after.

What do I do if a trach gets dislodged?!

A nurse runs into the workroom: “Ms. X’s trach is two inches out! She’s desatting to the 70’s on 60% FiO2!”

What do you do for a dislodged trach? This is the situation I faced a week ago, on a patient who wasn’t mine on the floor where I was working.

First, to clarify, dislodged=trach partially out of the stoma, decannulated=trach is all the way out of the stoma. Immature stoma is <1 week, mature stoma >1 week.

I love this slide from Vanderbilt, because it works for me, personally: keep it simple
  1. Your nurses and respiratory therapists are your life line!! Most institutions have protocols to page Anesthesia or a surgical team of some kind for these situations.
  2. Bag valve mask=Ambu bag: whatever you call it, if a patient with a trach is in distress, stabilize them with manual respiration. Apply the bag to the trach itself. If you meet “resistance” while bagging, STOP. It indicates either the trach is in a false tract, or there’s an obstruction, like a plug or extra tissue. (If it’s a false tract, you might be able to feel subcutaneous crepitus develop during bagging!)
  3. If bagging the trach doesn’t work, apply the bag to the patient’s mouth for face bag ventilation. The one caveat is laryngectomy patients: their mouths are not connected to the rest of their airways.
  4. Remove the inner cannula. Insert the suction catheter. If the catheter quickly draws back secretions, it’s still in the right place. If it doesn’t, the trach might be in a false tract.
  5. If you want to be fancy and have the skills, a fiberoptic scope can be passed from the mouth or through the stoma to look for problems.
  6. If the stoma is mature, in an emergency you can replace the trach with one that’s the same size or one size smaller. However, if the stoma is immature, the rate of closure is very high–up to 50% of the hole can close within 12 hours!
  7. Therefore, when dislodgement and definitely decannulation happens in an immature stoma, you may have to reintubate and wait for the surgeons to repair the stoma and reinsert the trach.

In my patient’s case, we ended up bagging her by mouth until respiratory therapy fiddled around with her trach enough to confirm it was in the right place and secured it with the trach collar. Stabilization is always #1! It turned out the patient had a large gap in her stoma, making the trach loose/malpositioned. The thoracic surgery team came by and put in a stitch to close the gap.

References:

Interpreting hypoxia on an ABG: PaO2 and SaO2

Let’s say you have a 57 year old patient breathing comfortably on room air, and when you walk in the next morning, he’s suddenly on 6 L O2 by nasal cannula. He doesn’t look like he’s in respiratory distress, but you decide to investigate by getting an ABG.

Result: 7.27/47/68

He is satting 93% on 6 L NC. Is that good? Is that bad? How does his O2 sat compare to the PaO2 on his ABG?

Normal PaO2=80-100 mm Hg. PaO2 is affected by age (tends to be lower) and altitude (tends to be lower).

PaO2 and O2 sat can be related through the oxygen-hemoglobin dissocation curve! See this table for PaO2 to O2 sat conversion. Remember that from first year of med school?

Straight from Wikipedia

As you can see, under normal conditions, an O2 sat of 90% correlates with a PaO2 of 60 mm Hg  (bonus points if this makes you realize an O2 sat  of 90% is not totally normal, although for sick, hospitalized patients,  it is acceptable). This curve is useful because it shows that giving supplemental O2 is most useful when someone has an O2 sat <90%. The curve also shows that O2 sat falls slower than the PaO2–a change in PaO2 from 96 to 70 may only show up as a change in O2 sat from 97% to 92%.

FiO2 can also affect an ABG reading. The PaO2 on your ABG should equal FiO2 x 500. If it doesn’t, there’s probably an A-a gradient. The PaO2/FiO2 ratio (or P/F ratio) is useful for categorizing hypoxia as potentially severe (when applied to ARDS).

So what about the patient above? His PaO2 of 68 mm Hg correlated perfectly with an O2 sat of 93%. However, he was also on 6 L NC, and the FiO2 was 40%. This implied that there was a significant A-a gradient

Random notes below:

Why are air bubbles bad? The PO2 of room air is 150 mm Hg, which means any air bubbles trapped in the ABG sample will shift the oxygen value towards 150 mm Hg. When does the ABG have to be put on ice? If it can’t be processed in 15 minutes. (Residual blood cells will continue to use oxygen and make the PaO2 seem lower than it really is.) An ABG on ice can still be analyzed for up to an hour after collection. If I get a value like PaO2=213, what does that mean?! At least you know the patient’s not hypoxic? PO2 is measured directly via electrode. The electrode is calibrated for values between 0-140. Therefore values >150 are of unclear accuracy. Remember that FiO2 affects the value as well.

Sources:

UC Denver handout

Clinical Methods (E.P. Trulock III)

American Nurse Today