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

“Why does potassium have to be repleted to 4?”

There is general agreement–but not an official statement that I could find–that in all comers, K <3.0 should be repleted. In patients with a history of past cardiac surgery, heart disease, and definitely in the post-MI population, K<3.5 should be repleted for a goal of 4.0. When there is acute concern for torsades or other arrhythmia, there is again general agreement but no official consensus that the goal is raised to >4.5.

Remember action potentials? The ins and the outs with K, Na, and Ca with the alphabet soup of channels? (Brief review in the first section of this editorial.) In the short-term, having a low serum K affects repolarization and has a chain effect on the action potential, causing increased automaticity, excitability, and QT prolongation, potentially triggering fatal arrhythmia. In the long-term, hypokalemia is associated with cardiovascular mortality in patients with underlying heart disease, arrhythmias like RBBB, and heart failure.

NB: Kind of supporting this are findings that higher doses of thiazide diuretic are linked to sudden cardiac death. Some argue that the mortality benefit of ACE inhibitors and beta-blockers in heart failure comes in part from an ability to better stabilize potassium levels. (Beta-blockers keep potassium extracellular through beta-2 receptors.)

Many studies linking hypokalemia to arrhythmia were relatively smaller studies (it seems like anything fewer than n=5,000 is not impressive in general cardiology) done in the 1980s, with mixed patient populations of mostly acute MI, hypertension (looking specifically at thiazide diuretics), or heart failure. These studies implied that the higher the potassium (K>4.5) the better:

Source

A more recent population-based cohort study of post-MI patients in JAMA (n>38,000), on the other hand, showed the following:

Because the lowest rate of mortality was found in the group with K 3.5-4.5, a goal of 4.0 is generally set for post-MI patients, which was extrapolated to any patient with heart disease. A similar distribution was found in patients who also had renal disease, and this study based on data from MERLIN-TIMI 36. This is a good reminder that hyperkalemia is linked to increased cardiovascular mortality, too.

When is colonoscopy indicated for colonic ischemia (ischemic colitis)?

The underlying pathophysiology of colonic ischemia (frequently called “ischemic colitis”) is much like that of ischemia anywhere else in the body: ischemia of the heart (MI), ischemia of the kidney, ischemia of the brain (stroke), etc. The reason it should be called “colonic ischemia” is because not every case of ischemia results in colitis, but the type of injury is the same.

The incidence of colonic ischemia cannot be accurately stated, because so many cases are relatively “meh” or benign. Someone gets some cramping, maybe they pass a little blood in their stool, things get better after a day or two on their own. That makes strongly evidence-based guidelines hard to come by. This is my caveat for the answers below. My source for this post is the 2015 ACG clinical guideline.

But you’re probably wondering, “Do I need to consult GI for every single case of suspected colonic ischemia? Do I need to ask if colonoscopy is indicated for every single patient?”

Appropriate consultation is an art, of course. GI consultation should not be automatic, but for ischemia, which can be vague and multifactorial, never shy away from consulting GI just because “it’ll get better on its own.” A consultant can help identify contributing factors, like meds that should be discontinued, workup for rheumatologic or hematologic disease, suggest other input from cardiology, etc. Think about the following factors:

  • How confident are you about the diagnosis? Some cases are slam dunks: cramping abdominal pain, some red stools, double halo sign on CT in a patient with a history of vascular disease. But a lot of these findings are non-specific. The differential includes diverticulitis, IBD, infectious colitis, and even malignancy. If you want to rule out another cause and prove it’s ischemic injury, ask GI about more imaging vs. colonoscopy.
  • How severe is the case? Mild cases will likely resolve on their own after a couple of days. Moderately severe cases (see algorithm below) seem most likely to benefit from the additional diagnostic of colonoscopy. Colonoscopy can show the extent of ischemic damage; in particular colonoscopy can visualize right-sided ischemia and pancolitis, which are associated with worse outcomes. As discussed below, anyone with severe findings/peritonitis should NOT have colonoscopy.
  • Is this the first time it happened, or is there a pattern of recurrence? If it’s a mild, first-time case, it’s probably not a big deal. Multiple episodes deserve a more detailed workup with endoscopic evaluation and histopathology to prove ischemic injury.
  • Are there implications for the future? Because of the differential diagnosis above, consider your patient’s other symptoms, medical conditions, and overall state of health. Would it matter for this particular case whether other types of colitis or masses were excluded?
From Brant, Feuerstadt, ACG guideline

NB: no prep is indicated for colonoscopy being done for colonic ischemia.

When should colonoscopy NOT be performed? The yield decreases substantially >48 hours after symptoms begin (to about 30%) so colonoscopy won’t be as helpful then. Colonoscopy is not recommended in severe cases, peritoneal signs, or diverticulitis because of theoretical risks of insufflation worsening pressure-related injury or causing perforation.

As a corollary–the ACG guidelines from 2015 also state that there is no evidence to support specific rules on when antibiotics are indicated and how long to give them for. Antibiotics not only prevent bacteremia/sepsis, they probably also help reduce the body’s inflammatory response to bowel injury…but there’s not a whole lot of human studies to show how helpful or unhelpful they are. Therefore, the guideline authors recommend antibiotics that cover bowel flora (like a third-gen cephalosporin + metronidazole) in “moderate” and definitely “severe” cases of colonic ischemia. They suggest 72 hours, but I think if someone is rapidly clinically improving, it’s reasonable to stop antibiotics after 1-2 days.

What is pulmonary toilet?

AKA “pulmonary hygiene.” Pulmonary toilet is advocated by many people, and does sound like a good idea in theory. However, the literature on whether pulmonary toilet actually improves outcomes for various patient populations is very mixed. In general, the patients who seem to benefit most are the cystic fibrosis and critically ill/intubated populations.

The purpose is to THIN and LOOSEN secretions. Having an awake, alert patient who can cough on their own is the best kind of pulmonary toilet.

What are the specific components of pulmonary toilet?

  • Bronchodilator (albuterol)
  • Mucolytic (such as NAC or Mucomyst): NAC in particular has become less popular because of lack of demonstrated utility (a good example is    this meta-analysis on cystic fibrosis). I still see it used in the ICU, though.
  • Hypertonic (7%) saline: may cause bronchospasm, coughing
  • Chest PT
    • Vibrating chest vest
    • Percussion (clapping patient on the chest)
    • Postural drainage
  • PEP device and flutter valve (such as Accapella)  
    •       NB: the Accapella =/= incentive spirometer
  • Suctioning
  • Bronchoscopy: using a bronchoscope to “wash out” secretions for atelectasis. This is only helpful in patients who are critically ill/intubated who cannot do any other kind of secretion clearance on their own. My personal observation is that when BAL is used for pulmonary toilet, it turns into a problematic cycle of provoking even more secretions and the need for repeated bronchs. A bronch is also not a completely benign procedure and may be associated with barotrauma, temporarily worsened oxygenation, etc.

When is pulmonary toilet useful? This clinical review is pretty negative. It states that chlorhexidine oral rinses are the only intervention that reduces rates of nosocomial pneumonia, and that other common practices like mucolytics and chest PT are not associated with improved outcomes and may in fact cause harm like bronchospasm and mechanical trauma, respectively. (A lot of evidence comes from pre-2000’s papers/guidelines, though). Let’s look at some common situations:

  • COPD: This meta-analysis reports that daily oral NAC was associated with fewer COPD exacerbations in patients who had a spirometric diagnosis of COPD, but also in patients who did not have a spirometric diagnosis of COPD. However, this joint paper from ACP-ACCP states that multiple trials have not found benefit for mucolytics or chest PT in COPD exacerbations.
  • Cystic fibrosis: Yes to chest PT. There is also good evidence that dornase alfa (DNase) and hypertonic saline have small effects.
  • Atelectasis: for acute atelectasis, if patients cannot cough on their own, chest PT is helpful. (The same review talks about how “bronch for airway clearance” is only indicated in selected cases of atelectasis that are multilobar or severe.)
  • Post-surgical patients :There is very limited objective evidence that pulmonary toilet decreases pulmonary complications (pneumonia, atelectasis, edema, etc.) in the postoperative period. This Cochrane review shows that in patients who underwent  upper abdominal surgery, incentive spirometry didn’t make a difference. Maybe this will make us feel better about all those unused incentive spirometers sitting by patients’ bedsides.