How to manage chest tubes (5-minute version)

I am no expert in chest tubes, and will add the caveat that for this particular post I really hope everything is correct! If it’s not, let me know! See this post on the different kinds of chest tubes. This is a great but long nursing resource from

You’ve placed a chest tube: great! Now you hook it up to some weird box thing that is called a drainage system…now what? Knowing how chest tubes used to work helps you understand the box thing.

This picture is taken from a truly excellent little video on how chest tube drainage works:

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ThScreen Shot 2017-01-26 at 6.01.21 PM.pngere used to be 3 separate bottles hooked up to the chest tube itself: Bottle #1 is where the patient’s empyema fluid or blood leaked into. Bottle #2 is the waterseal: air is forced to travel through water and can only move in one direction (it cannot move back into the patient). Bottle #3 sets suction power based on how much water is in the bottle–more water=less suction, less water=more suction, and you need to make sure the suction power is just right. You can see how the drainage system has evolved over time on the right.

Should patients be “placed to waterseal” or “placed to -20 suction?” 

“Place to waterseal”= don’t be too crazy with drainage, which is appropriate for most pleural effusions or a mild pneumothorax. If the lung is not fully expanded, you can “turn up the suction.”If you apply suction too aggressively, you put the patient at risk for re-expansion pulmonary edema.

How do I know if there is an “air leak” and what the eff does it mean? 

An air leak is present if there is bubbling in the waterseal chamber when the suction is clamped/on waterseal–this indicates there is positive pressure coming from the pleural space=air getting into the pleural space. Intermittent bubbling with expiration (when pleural pressure is highest in the non-ventilated patient) may be normal, but a continuous air leak is pathological.

Causes include:

  • ruptured bleb (severe emphysema)
  • simple traumatic pneumothorax (from placing the chest tube)
  • a leak in the actual tubing system
  • mechanical ventilation (may see decreased tidal volumes, failure of PEEP increase)
  • bronchopleural fistula (usually more severe or continuous)
  • lung entrapment vs. trapped lung

NB: if your patient has a persistent air leak, think twice about pulling their chest tube because if you do, you may cause a recurrent pneumothorax.

What is “tidaling?” 

You may see movement in the waterseal chamber with respiratory variation. It’s the water being sucked back towards the lung with inspiration due to negative inspiratory pressure. (In mechanically ventilated patients, it’s the opposite.)


How do I know when the tube can be taken out? 

In a 2013 study out of Michigan State, the team found it is reasonable to remove chest tubes when drainage <200 ml/day, on waterseal, with no air leak. In stable patients on the floor, theoretically you don’t need a chest x-ray after removal, but given our litigious society, everyone gets one. In mechanically ventilated patients, you should get a chest x-ray 1-3 hours after removal.

What do I do if the tube falls out? 

Use common sense: cover the area and prepare to re-insert a chest tube. Maintain sterility. The patient is at risk of a tension pneumothorax, so someone should stay with them for close monitoring. More troubleshooting at this nursing website.



Should I use hemoglobin or hematocrit?

Although this will likely not result in life-or-death decisions and is more a matter of intellectual curiosity, I would argue that hemoglobin is superior to hematocrit because it is directly measured and tells you about O2 delivery. Read on.

Hemoglobin is directly measured with spectroscopy (it’s a pigmented dye, so can be directly measured).

Hematocrit can be measured, but in modern times is calculated (RBC count x MCV). It represents a ratio of packed cells: total volume. Conditions that change the osmolarity of the blood will change the MCV temporarily, and affect Hct. It is affected by multiple factors:


  • Polycythemic or macrocytic anemias (larger MCV but less number of RBCs may show a normal Hct but low Hgb)
  • Microcytic anemias would show a reduced MCV and reduced RBC count, so the Hct should still be in line with the reduced Hgb

Hyperosmolar (falsely lowering the Hct):

  • DKA
  • Dehydration
  • Recent blood transfusion

Hypoosmolar (falsely elevating the Hct):

  • High altitude
  • Recent hemorrhage
  • Pregnancy

Some would argue that Hgb and Hct are the same. This paper in J Trauma showed that in their sample, Hgb and Hct had a Pearson’s R=0.99, which is pretty damn close to perfect correlation.

I’ve been told you shouldn’t order both Hgb and Hct, but you want to analyze RBC indices correctly, I think it’s necessary, as these depend on both Hgb and Hct.

From Lab CE

Should I stop vancomycin if my patient has a negative MRSA swab?

Having the time of his life with a MRSA nasal swab…from the New York Times story “A Bug Rises, and With It a Company” 2008

“If your patient has a negative MRSA nasal swab, and you are using vancomycin to empirically cover hospital-associated pneumonia, you can stop the vanc.”

Yes!!! It turns out this is true. There was a study in 2014 from Arizona that looked at how MRSA nasal swab results correlated with MRSA pneumonia: “The MRSA PCR assay demonstrated 88.0% sensitivity and 90.1% specificity, with a positive predictive value of 35.4% and a negative predictive value of 99.2%.” This means that although a positive MRSA swab doesn’t mean your patient will get MRSA pneumonia, if they are negative for MRSA, there is an excellent chance that they will not have MRSA pneumonia and so empiric vancomycin is not indicated unless there are extenuating circumstances. This was also seen in an earlier study.

What about stopping vancomycin for empiric treatment of other infections, like cellulitis? That is more contentious. There is evidence to suggest that very few cases of MRSA infection would be missed if MRSA-negative patients did not receive vancomycin, but many would argue that it is more important to treat any possible MRSA infection.

Interesting aside: another study looking at rates of MRSA disease found that patients can still develop MRSA infections even if their nasal swab is negative though: “nearly a third of MRSA-infected patients were not nasally colonized, suggesting that nasal colonization need not precede disease and that a negative test for nasal colonization would not rule out MRSA disease in settings of moderate or high prevalence.”

What’s the difference between ESR and CRP? Which is better?

It is helpful to first define what these measures are:

What does biological processes do ESR or CRP actually reflect? ESR: How quickly red blood cells fall in a vertical tube: more immunoglobulins and fibrinogens, which are positively charged, cause RBCs to form rouleaux “rolls” and fall faster
CRP: Levels of C-reactive protein, a hepatic acute phase reactant released by macrophages that rises in response to IL-1, IL-6, TNF-alpha and activates complement
May remain elevated for:  Weeks  Days
Falsely low if: Anemia, polycythemia, sickle cell, hypofibrinogenemia or hypogammaglobulinemia
Falsely high if: received IVIG, affected by age, gender, smoking, certain meds like steroids or NSAIDs Liver failure, late pregnancy

This study in Hematology looked at levels of ESR and CRP in several thousand healthy adults in the community and concluded that ESR levels varied more after the age of 40, but that both tests were good screening tests for inflammation.

It has been suggested that because ESR is an indirect measure of fibrinogen, which has a longer half-life than CRP, that ESR is more useful for monitoring chronic inflammatory conditions and CRP is more useful for measuring response for acute inflammation. Although this was written for a pediatric crowd, it is worth considering that ESR correlates better with lupus and chronic infections like osteomyelitis, and CRP correlates better with acute infections, Crohn’s, and rheumatoid arthritis.

Why continue to get both tests? Because the results can be telling. For instance, lupus flares tend to present with elevated ESR but normal-mildly elevated CRP. If the CRP is also sky-high, it may suggest there is underlying infection. In Kawasaki disease, ESR and CRP are both elevated, which would support that diagnosis. And in a process like osteomyelitis, ESR and CRP are both elevated to begin with, but CRP is monitored for response to antibiotic therapy.


Which QTc is the right one?


This post is for the psychiatry resident who asked me about a patient who had a Bazett’s QTc in the 510’s, but a Hodges QTc of 470:

Generally, we are concerned about QTc because torsades=bad.Practically speaking, a QTc >500 is something to be worried about.

A really shocking number of medications prolong the QTc, and just as a reminder, include things like antiarrhythmics, ondansetron, and haloperidol, but also Benadryl, erythromycin, tacrolimus, and TCAs.

What are the different formulas for QTc?

  • Bazett’s formula: QTC = QT / √ RR
  • Fredericia’s formula: QTC = QT / RR 1/3
  • Framingham formula: QTC = QT + 0.154 (1 – RR)
  • Hodges formula: QTC = QT + 1.75 (heart rate – 60)

Based on my expert Internet search, it is unclear which is the “best.” I also asked a couple of our attending cardiologists and cards enthusiasts, who didn’t have strong opinions.

The current clinical standard is the most widely used Bazett formula, but with this formula, there is a known overcorrection at high heart rates and undercorrection at lower heart rates. The Fridericia and Framingham correction formulae showed the best rate correction and significantly improved prediction of 30‐day and 1‐year mortality. With current clinical standards, Bazett overestimated the number of patients with potential dangerous QTc prolongation, which could lead to unnecessary safety measurements as withholding the patient of first‐choice medication.

That all being said: use the QTc that will give your patient the safest plan. And if you remain skeptical of a prolonged QTc in a clinically stable patient, get repeat EKGs until it’s…less prolonged…and your problem is solved.

When does someone need a long term chronic urinary catheter?

I asked this question after meeting a patient with spinal cord injury who intermittently self-cathed who had repeated bouts of acute prostatitis. Would a long term Foley help him?

A urinary catheter is considered “chronic” when a patient maintains a need for a catheter >4 weeks.

Here are the two situations in which long term urinary catheter placement might be indicated:

  • inability to void urine
  • incontinence that affects daily function

These issues might be more common in people with underlying conditions:

  • spinal cord injury
  • cauda equina syndrome
  • multiple sclerosis
  • stroke
  • prostatic enlargement that cannot be surgically improved
  • pelvic surgery (such as hysterectomy, colectomy, etc)

Note: None of these are ABSOLUTE indications to place a long term catheter. Because long term catheters are associated with higher risk of infection, they should only be used when intermittent catheterization has not been working or the patient is unable to manage intermittent catheterization.

Unfortunately, there might be other reasons for my patient to have recurrent prostatitis, and a long term catheter would not necessarily help.

A related question is, how frequently do chronic indwelling catheters need to be exchanged? Medscape has an article on this; the conclusion is that it may be 2-6 weeks depending on the patient, and reasons to exchange are obstruction, either by encrustation or mucus, symptomatic infection, or leakage around the catheter. Catheters should NOT be exchanged unless there is a reason to do so–otherwise, patients are put at higher risk of infection.

* ** When assessing a patient with a chronic indwelling urinary catheter, ask yourself, what is the indication for this catheter? Would it be possible to remove it? Patients are not necessarily doomed to a catheter forever; they should be subjected to multiple trials of void if possible.

I also ran across a condition I’d never heard of before: Fowler’s Syndrome, an uncommon cause of urinary retention in younger (<30 years) women.