Sunday, April 22, 2018

The Respiratory Rosenhan Experiment on Obese Patients

Normally this post would be on Status Iatrogenicus, but the implications for "evidence" and the EBM movement are too important, so it goes here.

For those not inclined to read about the Rosenhan Experiment, a brief history.  In the early 1970s, Dr. Rosenhan a Stanford psychologist, was concerned about the validity of psychiatric diagnoses.  So he and a half dozen confederates faked mental illness and presented themselves to several prominent psychiatric facilities.  Their feigned symptoms were sufficient to have them admitted with psychiatric diagnoses, usually paranoid schizophrenia.  After admission, they behaved normally.  Nonetheless, they had been diagnosed, put on psychotropic medications, and not allowed to leave until they signed documents swearing to continue the medications upon their release.  The damning report of this experiment was published in Science Magazine in 1973 with the title "On Being Sane in Insane Places."

Psychiatric hospitals were blindsided, having been caught unawares and humiliated.  They challenged Rosenhan to "do it again", but the second time they would be vigilant about these disimulations.  Send us some more fakes, they said.  On the second experiment, they determined that 40 some patients were confederates.  But Rosenhan had the upper RosenHand - he had send no confederates.  Sensitivity, if it can be called that, suffered to specificity on round two.

Previously I have complained about patients who are intubated but needn't have been (see here, and here.)  Oftentimes, after the fact, it is difficult to determine whether the intubation was necessary, especially with alleged upper airway compromise, and with obese patients.  With the latter, roentgenograms of the chest are difficult to interpret because of "fatelectasis" or atelectasis in obese persons,  "flatelectasis" due to recumbency, fluid loading after paralysis and intubation, all which may require high PEEP to counteract.  If you were not present prior to intubation, it is very difficult to determine if respiratory distress preceded the intubation, or if "won't breathe" was mistaken for "can't breathe".  The differentiation between those two entities is "critical".

A man in his late 40s was sent to us recently for "acute respiratory failure" on the ventilator receiving 100% FiO2 and PEEP of 16.  EMS responded to a call to his 18-wheeler that he could not breathe.  His SpO2 was in the 50% range and he was admitted to a local hospital.  There were basilar opacities, and oxygen was administered.   He weighed near 500#.  The opacities were said to represent pneumonia and he was given antibiotics.  Not long after admission, in the middle of the night, he could not be aroused, an ABG was obtained, and his PaCO2 was 90-something with a pH of 7.10 or thereabouts.  This was interpreted to represent acute hypercapneic respiratory failure, on top of his "acute hypoxemic respiratory failure" and an hour-long intubation ensued.  Afterwards he was sent to us on the aforementioned high ventilator settings.

But it didn't make sense.  This man had been driving his truck.  His CT images did not show dense opacification of any segment consistent with pneumonia, nor were there other findings consistent with pneumonia; rather they were consistent with atelectasis.  But - attempts to wean oxygen and PEEP were rapidly met with arterial hypoxemia, though not tachypnea or distress.  Indeed he had been ventilated to normal PaCO2, and had apnea on initial ventilator weaning attempts.  It didn't make sense.

What made sense was that this obese functional man had slowly developed *chronic* respiratory failure, which had become uncompensated.  Then, something happened after admission.  Either oxygen administration or narcotics or both or something else further depressed marginal ventilation, or maybe he was asleep and hypoventilating from OHS or whatever when that ABG was obtained.  It was not possible to tell after the fact with incomplete records and not having been there.  Rosenhan smirks over us as we try to sort it out.

So, we awakened him from massive sedation (soaking into massive adiposity) and he followed commands.  On FiO2 60% and PEEP 15, he had no distress.  PEEP and O2 could not be further weaned.  Positing that this man with depressed respiratory drive from obesity and a propensity for atelectasis from obesity, recumbency, sedation and paralysis could, if allowed, oxygenate and ventilate spontaneously, we planned to extubate to CPAP 15 CM H2O and 60% oxygen.

As has happened in the past, this engendered high anxiety for the nursing and respiratory staff.  Prior to executing the extubation order they attempted to wean the PEEP - no success: the SpO2 declined to the 60% range.

But we did, with my direct supervision and preparation to reintubate, extubate him - to 6 liters nasal cannula.  And he "flew" without a single hiccup and not even requiring the planned CPAP, and he went to the medical floor on nasal canula the next day.  He is the personification of status iatrogenicus.

In another dimension or warp zone, he may have been enrolled in an ARDS trial, or spent 1-2 weeks getting his PEEP weaned, or maybe even received a tracheostomy and a "discharge" to an LTACH.

His successful extubation was exhilarating to me insomuch as it saved him from those indignities. He was intubated based on a misunderstanding of basic respiratory physiology and prior probabilities, placing too much emphasis on a test result outside of this understanding.   There is no amount of evidence based medicine that can save a patient or his physician from this kind of misconception.   Proper treatment of this patient is founded on experience which is a form of evidence that has received short shrift in the EBM movement.  For all the benefits of deductive reasoning and "evidence", they are out in the cold if the diagnosis is not firmly established on the basis of "inductive" experience predicated upon a sound understanding of prior probabilities and the natural history of disease - the lifeblood of diagnosis.

"Never make unnecessary assumptions" said Marshall Goldberg in his 10 commandments of diagnosis.  With obese folks, you always have to worry about the respiratory Rosenhan experiment:  Is somebody trying to pass off to you a person whose chronic diseases are being misinterpreted as an acute illness?

It is a good question to ask, and patients benefit immeasurably if the answer is affirmative.


  1. Very interesting scenario. I have seen these kinds of patients and they can be challenging - one has to take a small leap of faith at times. A couple things I was curious about: you say that the pt wasn't able to be weaned from his PEEP and FiO2 (presumably during spontaneously breathing trial)and yet you were able to extubate him to nasal cannula immediately afterwards. That doesn't make a lot of sense to me if you're diagnosis is that the pt has baseline obesity-induced atelectasis - but perhaps I missed something there. Also, you postulate that this pt has "chronic respiratory failure" that became clinically manifest. What, if anything did you/could you do to prevent such an episode from happening again? Or is this gentleman doomed for another intubation down the road with a predictably poor eventual outcome?
    Thanks for your blog - I find it very interesting and well thought-out. Cheers

    1. Thanks for this comment! In the past I have used post-extubation CPAP to replace the PEEP. In this case, he was clearing his airway of blood and secretions post extubation on 6 liters NC, so we did not immediately apply it. After he had cleared the secretions and was sitting upright on nasal cannula, (negative pressure breathing) it was clear with SpO2 94% and RR 16 that he did not "need" the CPAP for positive pressure.

      I think that this guy was chronically hypoxemic for a long time - he was also polycythemic - and that the proverbial "bottom fell out" and he had to call 911 to his truck. Had he been on oxygen and maybe some diuretics, that would not have happened.

      I think that all obese patients are at grave risk of having their blood gasses misinterpreted, and so are all chronica respiratory failure patients. I was recently called to admit a patient with COPD for "hypercapnic respiratory failure" who had "become somnolent" in the ED from "CO2 narcosis". Her blood gas showed: 7.35/70/85/35. Totally compensated chronic respiratory acidosis. She had received a dose of morphine for abdominal pain - that was the cause of her somnolence. It is my position that very few physicians can properly interpret an ABG in the context of a specific clinical scenario, especially when respiratory drive is part of the equation.

  2. An esteemed colleague and mentor emailed me this anecdote:

    A 22 yo M weighing 600 # came to the ED c/o his scrotum swelling. To examine his scrotum the ED team had him lie down on a gurney, supine. Within about 5 minutes he had lost his sensorium. He was intubated and rocketed up to the MICU, where he was wide awake, with pH ~7.30 and PaCO2 ~75 mmHg. I asked him, “Lenny, do you sleep in a bed?” He nodded no. His mother, standing there with him, explained that he sleeps with his knees on the floor, his arms crossed over the side of the bed, and his head resting on his arms. We found a large, sturdy chair, had him get out of bed to the chair, and extubated him. He breathed just fine after extubation.

    Some very obese patients have not been supine for years. They can’t breathe when they are supine, but our repertoire of body positions for patients is limited.

    His whole body, including his scrotum, was swollen, anasarcic, from chronic cor pulmonale. We gave him a little O2 by nasal cannula and touched him with one dose of furosemide. The flood gates then opened and he peed out many, many gallons of urine. He lost 100 # of edema weight and went home a happy customer.

  3. Here is a similar case reported in AJRCCM in August 2018:


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